Clinical Guide To The Diagnosis and Treatment of Mental Disorders PDF

CLINICAL GUIDE TO THE
DIAGNOSIS AND TREATMENT

OF MENTAL DISORDERS
Clinical Guide to the Diagnosis and Treatment of Mental Disorders. M. B. First and A. Tasman
© 2006 John Wiley & Sons, Ltd. ISBN 0-470-01915-8
• FIRST
• TASMAN
CLINICAL GUIDE TO THE
DIAGNOSIS AND TREATMENT
OF MENTAL DISORDERS
Michael B. First
Associate Professor of Clinical Psychiatry
Department of Psychiatry
Columbia University College of Physicians and Surgeons
New York, NY
USA
Allan Tasman
Professor and Chair
Department of Psychiatry and Behavioral Sciences
University of Louisville School of Medicine
Louisville, KY
USA
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Library of Congress Cataloging-in-Pub1ication Data
Clinical guide to the diagnosis and treatment of mental disorders/edited by Michael B. First, Allan Tasman.
p. ; cm.
Includes bibliographical references and index.
ISBN-13: 978-0-470-01915-3 (pbk. : alk. paper)
ISBN-10: 0-470-01915-8 (pbk. : a1k. paper)
1. Mental illness. 2. Psychiatry. I. First, Michael B., 1956–
II. Tasman, Allan, 1947–
[DNLM: 1. Mental Disorders–diagnosis. 2. Mental Disorders–therapy.
WM 140 C6405 2006]
RC469.C555 2006
616.89–dc22 2006008578
British Library cataloguing in Publication Data
A Catalogue record for this book is available from the British Library
ISBN 0-470-01915-8
ISBN 978-0-470-01915-3
Typeset in 9.5/11.5pt Times Roman by Thomson Press (India) Limited, New Delhi, India
Printed and bound in Great Britain by Antony Rowe Ltd, Chippenham, UK
This book is printed and acid-free paper responsibly manufactured from sustainable forestry
in which at least two trees are planted for each one used for paper production.
Dedications
To Leslee, my bashert
Michael
With love and thanks to my family, in particular to my

father, Goodman Tasman, for your support and inspiration
Allan
Table of Contents
Preface xvii
Acknowledgments xix
Chapter 1 Psychiatric Diagnosis 1

Chapter 2 Childhood Disorders: Mental Retardation 18
Diagnosis 18
Treatment 21
Comparison of DSM-IV-TR and ICD-10 Diagnostic Criteria 25
Chapter 3 Childhood Disorders: Learning and Motor Skills Disorders 26

Diagnosis 26
Treatment 30
Chapter 4 Childhood Disorders: Communication Disorders 32

Diagnosis of Communication Disorders 32
Diagnosis of Expressive Language Disorder and Mixed
Receptive–Expressive Language Disorder 34
Diagnosis of Phonological Disorder and Stuttering 34
Diagnosis of Communication Disorder Not Otherwise Specified 35
Treatment of Communication Disorders 35
Chapter 5 Childhood Disorders: Pervasive Developmental Disorders 38

Diagnosis 38
Treatment 42
Chapter 6 Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders 49

Diagnosis 49
Treatment 53
Chapter 7 Childhood Disorders: Feeding and Eating Disorders of Infancy or Early Childhood 57
Feeding Disorder of Infancy or Early Childhood 57
Diagnosis 57
Treatment 59
Rumination Disorder 61
Diagnosis 61
Treatment 61
Pica 62
Diagnosis 62
Treatment 62
viii Table of Contents
Chapter 8 Childhood Disorders: Tic Disorders 64

Diagnosis 64
Treatment 67
Chapter 9 Childhood Disorders: Elimination Disorders and Childhood Anxiety Disorders 71

Enuresis 71
Diagnosis 71
Treatment of Nocturnal Enuresis 72
Treatment of Diurnal Enuresis 74
Encopresis 75
Diagnosis 75
Treatment 76
Separation Anxiety Disorder 77
Diagnosis 77
Treatment 78
Selective Mutism 79
Diagnosis 79
Treatment 79
Chapter 10 Childhood Disorders: Reactive Attachment Disorder of Infancy or Early Childhood 81

Diagnosis 81
Treatment 83
Chapter 11 Delirium, Dementia, and Amnestic Disorders 85

Delirium 85
Diagnosis 85
Treatment 90
Dementia 91
Diagnosis 91
Dementia of the Alzheimer Type 96
Diagnosis 96
Treatment 98
Vascular Dementia 99
Diagnosis 99
Treatment 100
Dementia Due to HIV Disease 100
Diagnosis 100
Treatment 102
Dementia Due to Other General Medical Conditions 102
Substance-Induced Persisting Dementia 105
Diagnosis 105
Treatment 105
Dementia Due to Multiple Etiologies 106
Amnestic Disorders 106
Diagnosis 106
Treatment 107
Chapter 12 Mental Disorders Due to a General Medical Condition 109

Psychotic Disorder Due to a General Medical Condition 111
Table of Contents ix
Diagnosis 111
Treatment 113
Mood Disorder Due to a General Medical Condition with Depressive Features 113
Diagnosis 113
Treatment 114
Mood Disorder Due to a General Medical Condition with Manic Features 114
Diagnosis 114
Treatment 116
Anxiety Disorder Due to a General Medical Condition with Panic Attacks or with Generalized
Anxiety 116
Diagnosis 116
Treatment 117
Anxiety Disorder Due to a General Medical Condition with Obsessive–Compulsive
Symptoms 117
Diagnosis 117
Treatment 117
Catatonic Disorder Due to a General Medical Condition 118
Diagnosis 118
Treatment 119
Personality Change Due to a General Medical Condition 119
Diagnosis 119
Treatment 122
Chapter 13 Substance-Related Disorders: General Approaches to Substance and Polysubstance Use

Disorders/Other Substance Use Disorders 123
Diagnosis 123
Treatment 131
Polysubstance Dependence 133
Other Substance-Use Disorders: Anabolic Steroids and Nitrites 134
Chapter 14 Substance-Related Disorders: Alcohol 136

Diagnosis 136
Treatment 141
Chapter 15 Substance-Related Disorders: Amphetamine 147

Diagnosis 147
Treatment 150
Chapter 16 Substance-Related Disorders: Caffeine 153

Caffeine Intoxication 153
Diagnosis 153
Treatment 155
Caffeine Withdrawal 156
Diagnosis 156
Treatment 157
Caffeine Dependence 157
Diagnosis 157
Treatment 158
Caffeine-Induced Anxiety Disorder 158
x Table of Contents
Diagnosis 158
Treatment 158
Caffeine-Induced Sleep Disorder 159
Diagnosis 159
Treatment 159
Chapter 17 Substance-Related Disorders: Cannabis 160

Cannabis-Use Disorders 161
Diagnosis 161
Treatment 162
Cannabis-Induced Disorders 163
Diagnosis 163
Treatment 165
Chapter 18 Substance-Related Disorders: Cocaine 166

Diagnosis 166
Treatment 171
Chapter 19 Substance-Related Disorders: Hallucinogens and MDMA 175

Hallucinogen Intoxication 176
Diagnosis 176
Treatment 177
Hallucinogen-Induced Psychotic Disorders 177
Treatment 177
Hallucinogen Persisting Perception Disorder (HPPD) 177
Diagnosis 177
Treatment 178
MDMA (“Ecstasy’’)-Related Disorders 178
Diagnosis 178
Treatment 179
Chapter 20 Substance-Related Disorders: Inhalants 180

Diagnosis 180
Treatment 184
Chapter 21 Substance-Related Disorders: Nicotine 186

Diagnosis 186
Treatment 188
Chapter 22 Substance-Related Disorders: Opioids 196

Diagnosis 196
Treatment 200
Chapter 23 Substance-Related Disorders: Phencyclidine 206
Diagnosis 206
Treatment 208
Table of Contents xi
Chapter 24 Substance-Related Disorders: Sedatives, Hypnotics, and Anxiolytics 210

Diagnosis 210
Treatment 216
Chapter 25 Schizophrenia and Other Psychotic Disorders 219

Schizophrenia 219
Diagnosis 219
Treatment 228
Schizoaffective Disorder 242
Diagnosis 242
Treatment 243
Brief Psychotic Disorder 244
Diagnosis 244
Treatment 245
Schizophreniform Disorder 246
Diagnosis 246
Treatment 246
Delusional Disorder 247
Diagnosis 247
Treatment 249
Shared Psychotic Disorder 249
Diagnosis 249
Treatment 250
Chapter 26 Mood Disorders: Depressive Disorders 252

Major Depressive Disorder 252
Diagnosis 252
Treatment 263
Dysthymic Disorder 271
Diagnosis 271
Treatment 273
Chapter 27 Mood Disorders: Premenstrual Dysphoric Disorder 274

Diagnosis 274
Treatment 276
Chapter 28 Mood Disorders: Bipolar Disorders 278

Diagnosis 278
Treatment 285
Chapter 29 Anxiety Disorders: Panic Disorder with and without Agoraphobia 292
Diagnosis 292
Treatment 296
Chapter 30 Anxiety Disorders: Social and Specific Phobias 301
Diagnosis 301
Treatment 307
xii Table of Contents
Chapter 31 Anxiety Disorders: Obsessive–Compulsive Disorder 316

Diagnosis 316
Treatment 321
Chapter 32 Anxiety Disorders: Traumatic Stress Disorders 326
Posttraumatic Stress Disorder 326
Diagnosis 326
Treatment 328
Acute Stress Disorder 331
Diagnosis 331
Treatment 333
Chapter 33 Anxiety Disorders: Generalized Anxiety Disorder 335
Diagnosis 335
Treatment 340
Chapter 34 Somatoform Disorders 345
Somatization Disorder 345
Diagnosis 345
Treatment 352
Undifferentiated Somatoform Disorder 353
Diagnosis 353
Treatment 354
Conversion Disorder 355
Diagnosis 355
Treatment 357
Pain Disorder 358
Diagnosis 358
Treatment 360
Hypochondriasis 362
Diagnosis 362
Treatment 363
Body Dysmorphic Disorder 364
Diagnosis 364
Treatment 366
Somatoform Disorder Not Otherwise Specified 367
Chapter 35 Factitious Disorders 368
Diagnosis 368
Treatment 371
Chapter 36 Dissociative Disorders 373
Dissociative Amnesia 373
Diagnosis 373
Treatment 374
Dissociative Fugue 374
Diagnosis 374
Treatment 375
Depersonalization Disorder 375
Table of Contents xiii
Diagnosis 375
Treatment 376
Dissociative Identity Disorder (Multiple Personality Disorder) 376
Diagnosis 376
Treatment 378
Dissociative Trance Disorder 380
Diagnosis 380
Treatment 381
Chapter 37 Sexual Disorders 382
Sexual Dysfunctions 382
Problems of Sexual Desire 382
Diagnosis 382
Treatment 384
Problems with Arousal 385
Diagnosis 385
Female Sexual Arousal Disorder 385
Male Erectile Disorder 385
Treatment 386
Problems with Orgasm 387
Female Orgasmic Disorder 387
Diagnosis 387
Treatment 388
Male Orgasmic Disorder 388
Premature Ejaculation 388
Diagnosis 388
Treatment 389
Sexual Pain Disorders 389
Dyspareunia 388
Diagnosis 388
Vaginismus 390
Diagnosis 390
Treatment of Dyspareunia and Vaginismus 390
Sexual Dysfunction Due to a General Medical Condition 390
Substance-Induced Sexual Dysfunction 391
Sexual Dysfunction Not Otherwise Specified (NOS) 391
Gender Identity Disorder 391
Diagnosis 392
Treatment 393
The Paraphilias 394
Diagnosis 394
Treatment 397
Sexual Disorder Not Otherwise Specified 398
Chapter 38 Eating Disorders 399
Anorexia Nervosa 399
Diagnosis 399
Treatment 402
Bulimia Nervosa 404
Diagnosis 404
Treatment 406
xiv Table of Contents
Binge-Eating Disorder 407

Diagnosis 407
Treatment 409
Chapter 39 Sleep and Sleep–Wake Disorders 410

Diagnosis 410
Dyssomnias 411
Primary Insomnia 411
Diagnosis 411
Treatment 413
Primary Hypersomnia 415
Diagnosis 415
Treatment 416
Narcolepsy 416
Diagnosis 416
Treatment 417
Breathing-Related Sleep Disorder 417
Diagnosis 417
Treatment 418
Circadian Rhythm Sleep Disorder (Sleep–Wake Schedule Disorders) 418
Delayed Sleep Phase Type 418
Diagnosis 418
Treatment 419
Shift-Work Type 419
Diagnosis 419
Treatment 419
Jet Lag Type 419
Diagnosis 419
Treatment 419
Periodic Limb Movements in Sleep 420
Diagnosis 420
Treatment 420
Parasomnias 420
Nightmare Disorder 420
Diagnosis 420
Treatment 421
Sleep Terror Disorder 421
Diagnosis 421
Treatment 421
Sleepwalking Disorder 421
Diagnosis 421
Treatment 421
REM Sleep Behavior Disorder 422
Diagnosis 422
Treatment 422
Nocturnal Panic Attacks 422
Sleep-Related Epilepsy 422
Sleep Disturbances Related to Other Mental Disorders 422
Diagnosis 422
Treatment 423
Sleep Disorder Due to a General Medical Condition 423
Substance-Induced Sleep Disorder 423
Table of Contents xv
Chapter 40 Impulse Control Disorders 425

Intermittent Explosive Disorder 425
Diagnosis 425
Treatment 427
Kleptomania 428
Diagnosis 428
Treatment 429
Pyromania and Fire-Setting Behavior 429
Diagnosis 429
Treatment 430
Pathological Gambling 430
Diagnosis 430
Treatment 431
Trichotillomania 432
Diagnosis 432
Treatment 433
Chapter 41 Adjustment Disorders 435

Diagnosis 435
Treatment 436
Chapter 42 Personality Disorders 439

Personality Disorder 439
Diagnosis 439
Treatment 440
Paranoid Personality Disorder 441
Diagnosis 441
Treatment 442
Schizoid Personality Disorder 443
Diagnosis 443
Treatment 444
Schizotypal Personality Disorder 444
Diagnosis 444
Treatment 445
Antisocial Personality Disorder 446
Diagnosis 446
Treatment 447
Borderline Personality Disorder 448
Diagnosis 448
Treatment 448
Histrionic Personality Disorder 450
Diagnosis 450
Treatment 451
Narcissistic Personality Disorder 452
Diagnosis 452
Treatment 453
Avoidant Personality Disorder 453
Diagnosis 453
Treatment 454
xvi Table of Contents
Dependent Personality Disorder 455

Diagnosis 455
Treatment 456
Obsessive–Compulsive Personality Disorder 456
Diagnosis 456
Treatment 457
Personality Disorder Not Otherwise Specified 458
Chapter 43 Psychological Factors Affecting Medical Condition 459
Diagnosis 459
Treatment 462
Index 465
Preface
The publication of DSM-III in 1980 revolutionized psychiatry. Among its many accomplishments (e.g., increased
diagnostic reliability), it provided both a common language for naming, describing, and identifying the complete
range of mental disorders seen in clinical practice, as well as an organizational plan embodied in the diagnostic
groupings contained in the DSM-III classification (i.e., grouping together Organic Mental Disorders, Psychotic
Disorders, Mood Disorder, Anxiety Disorders, etc.) Its appeal is several-fold: (1) it is authoritative; the information
contained in the DSM is authored by the leading experts in psychiatry and psychology; (2) it is comprehensive: all
disorders seen by mental health professionals are covered in the DSM; (3) it is clinically useful: material included
in the DSM is intended to be of practical use in making psychiatric diagnoses; (4) it is educational: material is
included also for the purpose of educating the reader about mental disorders, such as how they present, sex ratio,
prevalence rates; and (5) it is relatively concise: all the information is contained in a single volume, of around 900
pages in length.
Although the DSM is indispensable in the evaluation and treatment of individuals with mental disorders, arriving
at a psychiatric diagnosis is only the first step in the process. Once the clinician determines the diagnosis, he or she
must then choose from among a range of available treatment options. Certainly the biggest limitation of the DSM-
IV-TR is its omission of any information about the management and treatment of individuals with mental disorders.
DSM-IV-TR users must turn elsewhere for information about which treatment to choose—either to books written
specifically about the treatment of a disorder or books covering treatment in general. DSM-IV-TR Mental Disorders:
Diagnosis, Etiology, and Treatment (edited by First and Tasman), adapted from Section 5 of the two-volume textbook
Psychiatry, 2nd edition (edited by Tasman, Kay, and Lieberman), was published in May 2004 and combined informa-
tion about the diagnosis, etiology, and treatment of mental disorders into a single volume. Unfortunately, its length
and cost greatly limited its utility as a helpful guide for students and practicing clinicians. This Clinical Guide to the
Diagnosis and Treatment of Mental Disorders arises from our efforts to create a more concise and more clinician-
friendly version of the original First and Tasman book.
This book retains the breadth of the Diagnosis, Etiology, and Treatment book but not the depth—we will continue
to have the same number of chapters which cover all of the disorders in the DSM-IV-TR but the content has been
edited to meet the clinical needs of the readership. Rather than serving as a reference book about mental disorders,
we see this book as an accessible clinical guide to diagnosis and treatment. As such, the “Etiology’’ sections from
the original book have been eliminated and the “Diagnosis’’ and “Treatment’’ sections have been condensed with
the goal of retaining only information which is clinically relevant. In addition, details of studies establishing the
epidemiology of the disorders or the efficacy of treatments have been removed, as have all of the references. Readers
interested in this information should refer to the corresponding chapters in the original book.
The organization of the chapters in this book closely parallels the layout of disorders in the DSM-IV-TR. The
amount of space allocated to each disorder in this book varies according to clinical importance. Thus, unlike DSM-
IV-TR, in which all of the anxiety disorders are covered in the same chapter, the book splits up the major anxiety
disorders among several different chapters. Within each chapter, this book for the most part follows a consistent
structure. The “Diagnosis’’ section for each disorder begins with introductory material describing the features of the
disorder and includes information about assessment issues, comorbid conditions, associated features, epidemiology,
course (which includes age at onset, prognosis, and outcome), and differential diagnosis. The “Treatment’’ sections
summarize the available treatments for the disorders, and often are broken down into “Somatic Treatments’’ and
“Psychosocial Treatments’’ for ease of reference.
The factual content of the chapters in this book has been adapted from the “Disorders’’ section of the 2nd edition
of the two-volume Tasman, Kay, and Lieberman textbook Psychiatry, which was published by Wiley in 2003. We
would like to acknowledge the excellent contributions made by the original contributors to these chapters, who are
listed in the Acknowledgments of this book. Two new chapters, covering Amphetamine-Related Disorders by Kevin
xviii Preface
Sevarino and Reactive Attachment Disorder by Brian Stafford and Charles Zeanah were developed for the original
First and Tasman book (and thus are included in an edited form here), as no chapters covering these disorders were
included in the original two-volume textbook. We would also like to express our gratitude to Deborah Russell and
Andrea Baier at John Wiley & Sons for their help in the editing and production of this book.
Michael B. First
Allan Tasman
April 2006
Acknowledgments
We would like to gratefully acknowledge the authors of those chapters in Psychiatry, 2nd edition from which mate-
rial in this book was adapted.
Henry David Abraham Substance Abuse: Hallucinogen- and MDMA-Related Disorders

Sonia Ancoli-Israel Sleep and Sleep–Wake Disorders
Martin M. Antony Anxiety Disorders: Social and Specific Phobias
Gordon J. G. Asmundson Anxiety Disorders: Panic Disorder with and without Agoraphobia
Thomas F. Babor Substance Abuse: Alcohol Use Disorders
Mark S. Bauer Mood Disorders: Bipolar (Manic–Depressive) Disorders
Jean C. Beckham Anxiety Disorders: Traumatic Stress Disorders
Olga Brawman-Mintzer Anxiety Disorders: Generalized Anxiety Disorder
Alan Breier Schizophrenia and Other Psychoses
Edwin H. Cook Childhood Disorders: The Autism Spectrum Disorders
Jonathan R. T. Davidson Anxiety Disorders: Traumatic Stress Disorders
Jane L. Eisen Obsessive–Compulsive Disorder
Stuart Eisendrath Factitious Disorders
Rif S. El-Mallakh Substance Abuse: Hallucinogen- and MDMA-Related Disorders
Milton Erman Sleep and Sleep–Wake Disorders
Susan J. Fiester Substance Abuse: Nicotine Dependence
Anne Fleming Factitious Disorders
Robert L. Frierson Delirium and Dementia
Paul J. Fudala Substance Abuse: Opioid Use Disorder
J. Christian Gillin Sleep and Sleep–Wake Disorders
Reed D. Goldstein Mood Disorders: Depression
Roland R. Griffiths Substance Abuse: Caffeine Use Disorders
Amanda J. Gruber Substance Abuse: Cannabis-Related Disorders
Alan M. Gruenberg Mood Disorders: Depression
Jeffrey M. Halperin Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders
John H. Halpern Substance Abuse: Hallucinogen- and MDMA-Related Disorders
Carlos A. Hernandez-Avila Substance Abuse: Alcohol Use Disorders
Charles Y. Jin Substance Abuse: Cocaine Use Disorders
William M. Klykylo Childhood Disorders: Communication Disorders
Thomas R. Kosten General Approaches to Substance and Polydrug Use Disorders
Henry R. Kranzler Substance Abuse: Alcohol Use Disorders
James L. Levenson Psychological Factors Affecting Medical Condition
Bennett L. Leventhal Childhood Disorders: The Autism Spectrum Disorders
Stephen B. Levine Sexual Disorders
Walter Ling Substance Abuse: Sedative, Hypnotic, or Anxiolytic Use Disorders
Joyce H. Lowinson Substance Abuse: Phencyclidine Use Disorders
xx Acknowledgments
Christopher P. Lucas Childhood Disorders: Elimination Disorders and Childhood Anxiety Disorders
R. Bruce Lydiard Anxiety Disorders: Generalized Anxiety Disorder
José R. Maldonado Dissociative Disorders
John S. March Anxiety Disorders: Traumatic Stress Disorders
Randi E. McCabe Anxiety Disorders: Social and Specific Phobias
Elinore F. McCance-Katz Substance Abuse: Cocaine Use Disorders
Laura F. McNicholas Substance Abuse: Opioid Use Disorders
Jeannine Monnier Anxiety Disorders: Generalized Anxiety Disorder
David P. Moore Mental Disorders due to a General Medical Condition
Stephanie Mullins Personality Disorders
Jeffrey H. Newcorn Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorder;
Adjustment Disorders
Thomas Owley Childhood Disorders: The Autism Spectrum Disorders
Jayendra K. Patel Schizophrenia and Other Psychoses
Michele T. Pato Obsessive–Compulsive Disorder
Teri Pearlstein Mood Disorders: Premenstrual Dysphoric Disorder
Katharine A. Phillips Obsessive–Compulsive Disorder
Debra A. Pinals Schizophrenia and Other Psychoses
Harrison G. Pope, Jr Substance Abuse: Cannabis-Related Disorders
Mark A. Riddle Childhood Disorders: Tic Disorders
Neil Rosenberg Substance Abuse: Inhalant-Related Disorders
Kurt P. Schulz Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders
David Shaffer Childhood Disorders: Elimination Disorders and Childhood Anxiety Disorders
Vanshdeep Sharma Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders
Charles W. Sharp Substance Abuse: Inhalant-Related Disorders
Larry B. Silver Childhood Disorders: Learning and Motor Skills Disorders
Daphne Simeon Impulse Control Disorders
David E. Smith Substance Abuse: Sedative, Hypnotic, or Anxiolytic Use Disorders
David Spiegel Dissociative Disorders
Eric C. Strain Substance Abuse: Caffeine Use Disorders
James J. Strain Adjustment Disorders
Ludwik S. Szymanski Childhood Disorders: Mental Retardation
Steven Taylor Anxiety Disorders: Panic Disorder with and without Agoraphobia
Jane A. Ungemack Substance Abuse: Alcohol Use Disorders
John T. Walkup Childhood Disorders: Tic Disorders
B. Timothy Walsh Eating Disorders
Donald R. Wesson Substance Abuse: Sedative, Hypnotic or Anxiolytic Use Disorders
Thomas A. Widiger Personality Disorders
Maija Wilska Childhood Disorders: Mental Retardation
Ronald M. Winchel Impulse Control Disorders
George E. Woody Substance Abuse: Opioid Use Disorder
Yoram Yovell Impulse Control Disorders
Sean H. Yutzy Somatoform Disorders
Douglas Ziedonis Substance Abuse: Nicotine Dependence
Stephen R. Zukin Substance Abuse: Phencyclidine Use Disorders
Ilana Zylberman Substance Abuse: Phencyclidine Use Disorders
CHAPTER
1 Psychiatric Diagnosis
There is a natural human predilection to categorize DSM-IV-TR also facilitates the identification and
and classify in order to simplify and organize the wide management of mental disorders in both clinical
range of observable phenomena and experiences that and research settings. Most of the DSM-IV-TR di-
one is confronted with, thus facilitating both their un- agnostic labels provide considerable and important
derstanding and their predictability. Many (if not most) predictive power. For example, making a diagnosis
of the mental disorders that afflict contemporary indi- of bipolar disorder suggests the choice of treatment
viduals have occurred in antiquity. For example, the options (e.g., mood stabilizers), that a certain course
first recorded depiction of mental illness dates to 3000 may be likely (e.g., recurrent and episodic), and that
B.C. Egypt, with a description of the syndrome senile there is an increased prevalence of this disorder in
dementia attributed to Prince Ptah-hotep. The current family members. By defi ning more or less homoge-
system for the diagnosis of mental disorders, the Di- neous groups of individuals for study, DSM-IV-TR
agnostic and Statistical Manual of Mental Disorders, can also further efforts to understand the etiology of
Fourth Edition Text Revision (DSM-IV-TR), is just the mental disorders. DSM-IV-TR also plays an impor-
latest example from the long and colorful history of tant role in education. In its organization of disorders
psychiatric classification. into major classes, the system offers a structure for
teaching phenomenology and differential diagnosis.
DSM-IV-TR is also useful in psychoeducation by
GOALS OF THE DSM-IV-TR
showing individuals suffering from symptoms of a
Perhaps the most important goal of the DSM-IV-TR mental disorder that their pattern of symptoms is not
is to allow mental health practitioners and research- mysterious and unique but rather has been identified
ers to communicate more effectively with each other and studied in others.
by establishing a convenient shorthand for describ-
ing the mental disorders that they encounter. For ex-
DSM-IV-TR OVERVIEW
ample, telling a colleague that an individual whom
you have just evaluated has major depressive disorder The remainder of this chapter provides an overview of
can convey a great deal of information in only a few the DSM-IV-TR multiaxial system as well as a presen-
words. First of all, it indicates that depressed mood tation of some of the organizational principles of the
or loss of interest is a central aspect of the presenting various diagnostic groupings included in the DSM-IV-
problem and that the depression is not the kind of TR classification. The chapters in this book are organ-
“normal” mood fluctuation that lasts for only a few ized according to their presentation in the DSM-IV-TR
days but rather that it persists every day for an ex- classification and provide detailed information regard-
tended period of time, for at least 2 weeks. Further- ing the diagnosis, epidemiology, course, and treatment
more, one can expect to fi nd a number of additional of these disorders.
symptoms occurring at the same time, like suicidal
ideation and changes in appetite, sleep, energy, and
DSM-IV-TR MULTIAXIAL SYSTEM
psychomotor activity. Finally, information is also
communicated about what is not to be found in this The multiaxial system was first introduced by DSM-III
individual—specifically, that the depression is not in order to encourage the clinician to focus his or
caused by the direct physiological effects of alcohol, her attention during the evaluation process on issues
other drugs, medications, or a general medical condi- above and beyond the psychiatric diagnosis. Use of
tion; and that there is no history of schizophrenia or the multiaxial system requires that information be
manic or hypomanic episodes. noted on each of the five different axes, each axis
2 Clinical Guide to the Diagnosis and Treatment of Mental Disorders
devoted to a different aspect of the evaluation proc- impact on the options for the choice of antidepressant
ess. Axes I, II, and III are the diagnostic axes that medication.
divide up the diagnostic pie into three separate do- Psychosocial stressors are well known to play an im-
mains. Axis I is for “clinical syndromes and disor- portant role in the etiology, maintenance, and manage-
ders,” an admittedly confusing name since Axis II ment of a number of mental disorders. Axis IV provides
and Axis III also include clinical disorders. The most the clinician with the opportunity to list clinically rel-
accurate name for Axis I is “diagnoses not coded on evant psychosocial and environmental problems (e.g.,
Axis II and Axis III,” since Axis II and Axis III were homelessness, poverty, divorce). To facilitate a com-
carved out of Axis I specifically to draw attention to prehensive evaluation of such problems, DSM-IV-TR
certain disorders that clinicians were more likely to includes a psychosocial and environmental checklist
overlook. that allows the clinician to indicate which types of
That said, Axis II is designated for coding per- problems are present and relevant (Figure 1-1).
sonality disorders and traits and mental retarda- Mental disorders differentially impact on the individ-
tion. There have been many recent criticisms of the ual’s level of functioning. For example, one individual
coding of personality disorders on Axis II. Critics with schizophrenia may function quite well, being able
correctly point out that there is no fi rm conceptual to live in the community, marry and have a family, and
basis for this division. Although disorders on Axis II maintain a steady job, whereas another individual with
tend to be lifelong and pervasive, a number of disor- schizophrenia may function quite poorly, requiring
ders on Axis I (e.g., schizophrenia, autistic disorder, chronic institutionalization. Since both of these indi-
dysthymic disorder) fit this description as well. Oth- viduals have symptoms that meet the diagnostic criteria
ers have made the incorrect assumption that catego- for schizophrenia, their important differences in func-
ries on Axis II are unresponsive to medication treat- tioning are not captured by the clinical diagnosis alone.
ment, which is at odds with more recent evidence Some of the differences in functioning may be due to
that medications are often helpful in the treatment different symptom profiles or symptom severities.
of personality disorders. The fact is that the Axis Other differences may be related to resilience factors
I/Axis II division is strictly pragmatic. First intro- or different levels of psychosocial support. Whatever
duced in DSM-III, Axis II was designed to draw at- the reason, the DSM-IV-TR multiaxial system provides
tention to certain disorders that were thought to be the clinician with the ability to indicate the individual’s
overshadowed in the face of the more florid Axis I overall level of functioning in addition to the diagnosis
presentations. In DSM-III, Axis II was reserved for
personality disorders in adults and specific develop-
mental disorders in children. In DSM-III-R, all of Check:
the developmental disorders (i.e., mental retardation, Problems with primary support group (childhood, adult,
pervasive developmental disorders, specific devel- parent−child). Specify:
opmental disorders) were coded on Axis II along Problems related to the social environment.
with the personality disorders. In DSM-IV-TR, Axis Specify:
II was modified once again so that only personality Educational problems. Specify:
disorders and traits and mental retardation remain
on Axis II. Certainly the placement of personality Occupational problems. Specify:
disorders on a separate axis has increased both their Housing problems. Specify:
clinical visibility and their importance as a subject
for research studies. Whether the Axis I/Axis II di- Economic problems. Specify:
vision has fi nally outlived its usefulness remains a Problems with access to health care services.
topic of heated debate and will be revisited during Specify:
the DSM-V deliberations. Problems related to interaction with the legal system/crime.
Axis III, like Axis II, is intended to encourage clini- Specify:
cians to pay special attention to conditions that they Other psychosocial problems. Specify:
tend to overlook, in this case, clinically relevant gen-
eral medical conditions. The concept of “clinically Figure 1-1 DSM-IV-TR Axis IV: psychosocial and environmental
relevant” is intended to be broad. For example, it checklist. (Reprinted with permission from the Diagnostic and
would be appropriate to list hypertension on Axis III Statistical Manual of Mental Disorders, Fourth Edition, Text Revision,
even if its only relationship to an Axis I disorder is its pp36, Copyright 2000. American Psychiatric Association.)
Chapter 1 • Psychiatric Diagnosis 3
on Axis V, using the Global Assessment of Functioning severe obsessional rituals, frequent shoplifting) or any
(GAF) Scale (Figure 1-2). This GAF Scale has been serious impairment in social, occupational, or school
criticized because it is not actually a “pure” measure of functioning (e.g., no friends, unable to keep a job).
an individual’s ability to function since it incorporates For this reason, the DSM-IV-TR includes a scale (the
symptom severity into the scale; for example, level 41 Social and Occupational Functioning Scale [SOFAS])
to 50 is for serious symptoms (e.g., suicidal ideation, that relies exclusively on functioning in its appendix
Global Assessment of Functioning (GAF) Scale

Consider psychological, social and occupational functioning on a
hypothetical continuum of mental health-illness. Do not include
impairment in functioning due to physical (or environmental) limitations.
Code (Note: Use intermediate codes when appropriate, e.g., 45,68,72.)

100 Superior functioning in a wide range of activities, life’s problems never seem
to get out of hand, is sought out by others because of many positive qualities.
91 No symptoms.
90 Absent or minimal symptoms (e.g., mild anxiety before an examination),
good functioning in all areas, interested and involved in a wide range of
activities, socially effective, generally satisfied with life, no more than
everyday problems or concerns (e.g., an occasional argument with family
81 members).
80 If symptoms are present, they are transient and expectable reactions to
psychosocial stressors (e.g., difficulty concentrating after family argument); no
more than slight impairment in social, occupational, or school functioning
71 (e.g., temporarily falling behind in school work).
70 Some mild symptoms (e.g., depressed mood and mild insomnia) OR some
difficulty in social, occupational, or school functioning (e.g., occasional
truancy, or theft within the household), but generally functioning pretty
61 well, has some meaningful interpersonal relationships.
60 Moderate symptoms (e.g., flat affect and circumstantial speech, occasional
panic attacks) OR moderate difficulty in social, occupational, or school
51 functioning (e.g., few friends, conflicts with peers or coworkers).
50 Serious symptoms (e.g., suicidal ideation, severe obsessional rituals, frequent
shoplifting) OR any serious impairment in social, occupational, or school
41 functioning (e.g., no friends, unable to keep a job).
40 Some impairment in reality testing or communication (e.g., speech is at times
illogical, obscure, or irrelevant) OR major impairment in several areas, such as
work or school, family relations, judgment, thinking, or mood (e.g., depressed
man avoids friends, neglects family, and is unable to work; child frequently beats up
31 younger children, is defiant at home, and is failing at school).
30 Behavior is considerably influenced by delusions or hallucinations OR serious
impairment in communication or judgment (e.g., sometimes incoherent, acts
grossly inappropriately, suicidal preoccupation) OR inability to function in almost
21 all areas (e.g., stays in bed all day; no job, home or friends).
20 Some danger of hurting self or others (e.g., suicide attempts without clear
expectation of death, frequently violent, manic excitement) OR occasionally fails to
maintain minimal personal hygiene (e.g., smears feces) OR gross impairment in
11 communication (e.g., largely incoherent or mute).
10 Persistent danger of severely hurting self or others (e.g., recurrent violence) OR
persistent inability to maintain minimal personal hygiene OR serious suicidal
1 act with clear expectation of death.
0 Inadequate information
Figure 1-2 DSM-IV-TR Axis V: Global Assessment Functioning Scale. (Reprinted with permission from the Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition, Text Revision, pp34, Copyright 2000. American Psychiatric Association.)
Example of DSM-IV-TR Multiaxial DSM-IV-TR Classification

Table 1-1
Evaluation
NOS ⫽ Not Otherwise Specified.
Axis I 296.23 Major depressive disorder, single
episode, severe but without psychotic An x appearing in a diagnostic code indicates that a
features, with postpartum onset. specific code number is required.
307.51 Bulimia nervosa An ellipsis (…) is used in the names of certain disor-
Axis II 301.6 Dependent personality disorder
Frequent use of denial ders to indicate that the name of a specific mental dis-
Axis III Rheumatoid arthritis order or general medical condition should be inserted
Axis IV Partner relational problem when recording the name (e.g., 293.0 Delirium Due to
Axis V GAF ⫽ 35 (current)
Hypothyroidism).
If criteria are currently met, one of the following se-
of Criteria Sets and Axes Provided for Further Study. verity specifiers may be noted after the diagnosis:
An example of a DSM-IV-TR multiaxial evaluation for
a hypothetical individual with depression is shown in Mild
Table 1.1. Moderate
Severe
DSM-IV-TR CLASSIFICATION If criteria are no longer met, one of the following

AND DIAGNOSTIC CODES specifiers may be noted:
In Partial Remission
The “DSM-IV-TR Classification of Mental Disorders”
In Full Remission
refers to the comprehensive listing of the official diag-
Prior History
nostic codes, categories, subtypes, and specifiers (see
below). It is divided into various “diagnostic classes”
that group disorders together on the basis of common Disorders Usually First Diagnosed in Infancy,
presenting symptoms (e.g., mood disorders, anxiety Childhood, or Adolescence
disorders), typical age at onset (e.g., disorders usually
first diagnosed in infancy, childhood, and adolescence), MENTAL RETARDATION
and etiology (e.g., substance-related disorders, mental
Note: These are coded on Axis II.
disorders due to a general medical condition).
317 Mild Mental Retardation
The diagnostic codes listed in the DSM-IV-TR are
318.0 Moderate Mental Retardation
derived from the International Classification of Dis-
318.1 Severe Mental Retardation
eases, Ninth Revision, Clinical Modification (ICD-
318.2 Profound Mental Retardation
9-CM), the official coding system for reporting mor-
319 Mental Retardation, Severity Unspecified
bidity and mortality in the United States. That is the
reason the codes go from 290.00 to 319.00; they are
actually derived from the mental disorders section of LEARNING DISORDERS
a much larger coding system for all medical disor- 315.00 Reading Disorder
ders that extend from 001 to 999. Clinicians working 315.1 Mathematics Disorder
in the United States are required to use ICD-9-CM 315.2 Disorder of Written Expression
in order to get reimbursement from both govern- 315.9 Learning Disorder NOS
ment agencies (e.g., Medicare and Medicaid) and
private insurers. To insure that users of the DSM-
IV-TR are able to meet this requirement without do- MOTOR SKILLS DISORDER
ing any cumbersome code conversions, the DSM-IV- 315.4 Developmental Coordination Disorder
TR contains the current ICD-9-CM codes. Because
the ICD-9-CM codes are updated on a yearly basis
(i.e., every October 1), the DSM-IV-TR codes have COMMUNICATION DISORDERS
to be similarly updated as changes to the codes in 315.31 Expressive Language Disorder
the ICD-9-CM mental disorder section occur. Suc- 315.32 Mixed Receptive–Expressive Language
cessive printings of DSM-IV-TR have been modified Disorder
to include these updated codes. In addition, updated 315.39 Phonological Disorder
diagnostic codes are available on the DSM-IV-TR 307.0 Stuttering
web site (www.dsm4tr.org) 307.9 Communication Disorder NOS
PERVASIVE DEVELOPMENTAL DISORDERS OTHER DISORDERS OF INFANCY,

CHILDHOOD, OR ADOLESCENCE
299.00 Autistic Disorder
299.80 Rett’s Disorder 309.21 Separation Anxiety Disorder
299.10 Childhood Disintegrative Disorder Specify if: Early Onset
299.80 Asperger’s Disorder 313.23 Selective Mutism
299.80 Pervasive Developmental Disorder NOS 313.89 Reactive Attachment Disorder of Infancy or
Early Childhood
Specify type: Inhibited Type/Disinhibited
ATTENTION-DEFICIT AND DISRUPTIVE Type
BEHAVIOR DISORDERS 307.3 Stereotypic Movement Disorder
314.xx Attention-Deficit/Hyperactivity Disorder Specify if: With Self-Injurious Behavior
.01 Combined Type 313.9 Disorder of Infancy, Childhood, or
.00 Predominantly Inattentive Type Adolescence NOS
.01 Predominantly Hyperactive-Impulsive
Type Delirium, Dementia, and Amnestic and Other
314.9 Attention-Deficit/Hyperactivity Disorder Cognitive Disorders
NOS
312.xx Conduct Disorder DELIRIUM
.81 Childhood-Onset Type
.82 Adolescent-Onset Type 293.0 Delirium Due to … [Indicate the General
.89 Unspecified Onset Medical Condition]
313.81 Oppositional-Defiant Disorder —.— Substance Intoxication Delirium (refer to
312.9 Disruptive Behavior Disorder NOS Substance-Related Disorders for
substance-specific codes)
— .— Substance Withdrawal Delirium (refer to
FEEDING AND EATING DISORDERS Substance-Related Disorders for
OF INFANCY OR EARLY CHILDHOOD substance-specific codes)
—.— Delirium Due to Multiple Etiologies (code
307.52 Pica each of the specific etiologies)
307.53 Rumination Disorder 780.09 Delirium NOS
307.59 Feeding Disorder of Infancy or Early
Childhood
DEMENTIA
294.xx Dementia of the Alzheimer’s Type, With
TIC DISORDERS Early Onset (also code 331.0 Alzheimer’s
307.23 Tourette’s Disorder disease on Axis III)
307.22 Chronic Motor or Vocal Tic Disorder .10 Without Behavioral Disturbance
307.21 Transient Tic Disorder .11 With Behavioral Disturbance
Specify if: Single Episode/Recurrent 294.xx Dementia of the Alzheimer’s Type, With
307.20 Tic Disorder NOS Late Onset (also code 331.0 Alzheimer’s
disease on Axis III)
.10 Without Behavioral Disturbance
ELIMINATION DISORDERS .11 With Behavioral Disturbance
290.xx Vascular Dementia
—.— Encopresis
.40 Uncomplicated
787.6 With Constipation and Overflow
.41 With Delirium
Incontinence
.42 With Delusions
307.7 Without Constipation and Overflow
.43 With Depressed Mood
Incontinence
Specify if: With Behavioral Disturbance
307.6 Enuresis (Not Due to a General Medical
Condition) Code presence or absence of a behavioral disturbance
Specify type: Nocturnal Only/Diurnal Only/ in the fifth digit for Dementia Due to a General
Nocturnal and Diurnal Medical Condition:
294.10 ⫽ Without Behavioral Disturbance 293.9 Mental Disorder NOS Due to … [Indicate
294.11 ⫽ With Behavioral Disturbance the General Medical Condition]
294.1x Dementia Due to HIV Disease (also code
042 HIV on Axis III)
294.1x Dementia Due to Head Trauma (also code Substance-Related Disorders
854.00 head injury on Axis III)
294.1x Dementia Due to Parkinson’s Disease The following specifiers apply to Substance
(also code 331.82 Dementia with Lewy Dependence as noted:
a
Bodies on Axis III) With Physiological Dependence/Without
294.1x Dementia Due to Huntington’s Disease (also Physiological Dependence
b
code 333.4 Huntington’s disease on Axis III) Early Full Remission/Early Partial Remission/
294.1x Dementia Due to Pick’s Disease (also Sustained Full Remission/Sustained Partial
code 331.11 Pick’s disease on Axis III) Remission
c
294.1x Dementia Due to Creutzfeldt–Jakob Dis- In a Controlled Environment
d
ease (also code 046.1 Creutzfeldt–Jakob On Agonist Therapy
disease on Axis III) The following specifiers apply to Substance-Induced
294.1x Dementia Due to … [Indicate the General Disorders as noted:
I
Medical Condition not listed above] (also With Onset During Intoxication/ WWith Onset During
code the general medical condition on Withdrawal
Axis III)
—.— Substance-Induced Persisting Dementia
(refer to Substance-Related Disorders for ALCOHOL-RELATED DISORDERS
substance-specific codes) Alcohol Use Disorders
—.— Dementia Due to Multiple Etiologies
(code each of the specific etiologies) 303.90 Alcohol Dependencea,b,c
294.8 Dementia NOS 305.00 Alcohol Abuse
AMNESTIC DISORDERS Alcohol-Induced Disorders

294.0 Amnestic Disorder Due to … [Indicate the 303.00 Alcohol Intoxication
General Medical Condition] 291.81 Alcohol Withdrawal
Specify if: Transient/Chronic Specify if: With Perceptual Disturbances
—.— Substance-Induced Persisting Amnestic 291.0 Alcohol Intoxication Delirium
Disorder (refer to Substance-Related 291.0 Alcohol Withdrawal Delirium
Disorders for substance-specific codes) 291.2 Alcohol-Induced Persisting Dementia
294.8 Amnestic Disorder NOS 291.1 Alcohol-Induced Persisting Amnestic
Disorder
291.x Alcohol-Induced Psychotic Disorder
OTHER COGNITIVE DISORDERS .5 With DelusionsI,W
294.9 Cognitive Disorder NOS .3 With HallucinationsI,W
291.89 Alcohol-Induced Mood DisorderI,W
291.89 Alcohol-Induced Anxiety DisorderI,W
Mental Disorders Due to a General Medical 291.89 Alcohol-Induced Sexual DysfunctionI
Condition Not Elsewhere Classified 291.82 Alcohol-Induced Sleep DisorderI,W
291.9 Alcohol-Related Disorder NOS
293.89 Catatonic Disorder Due to … [Indicate the
General Medical Condition]
310.1 Personality Change Due to … [Indicate the AMPHETAMINE (OR AMPHETAMINE-LIKE)-
General Medical Condition] RELATED DISORDERS
Specify type: Labile Type/Disinhibited
Amphetamine Use Disorders
Type/Aggressive Type/Apathetic Type/
Paranoid Type/Other Type/Combined 304.40 Amphetamine Dependencea,b,c
Type/Unspecified Type 305.70 Amphetamine Abuse
Amphetamine-Induced Disorders 292.xx Cocaine-Induced Psychotic Disorder

.11 With DelusionsI
292.89 Amphetamine Intoxication
.12 With HallucinationsI
Specify if: With Perceptual Disturbances
292.84 Cocaine-Induced Mood DisorderI,W
292.0 Amphetamine Withdrawal
292.89 Cocaine-Induced Anxiety DisorderI,W
292.81 Amphetamine Intoxication Delirium
292.89 Cocaine-Induced Sexual DysfunctionI
292.xx Amphetamine-Induced Psychotic Disorder
292.85 Cocaine-Induced Sleep DisorderI,W
.11 With DelusionsI
292.9 Cocaine-Related Disorder NOS
292.84 Amphetamine-Induced Mood DisorderI,W
292.89 Amphetamine-Induced Anxiety DisorderI HALLUCINOGEN-RELATED DISORDERS
292.89 Amphetamine-Induced Sexual DysfunctionI
292.85 Amphetamine-Induced Sleep DisorderI,W Hallucinogen Use Disorders
292.9 Amphetamine-Related Disorder NOS 304.50 Hallucinogen Dependenceb,c
305.30 Hallucinogen Abuse
CAFFEINE-RELATED DISORDERS
Caffeine-Induced Disorders Hallucinogen-Induced Disorders
305.90 Caffeine Intoxication 292.89 Hallucinogen Intoxication
292.89 Caffeine-Induced Anxiety DisorderI 292.89 Hallucinogen Persisting Perception Disorder
292.85 Caffeine-Induced Sleep DisorderI (Flashbacks)
292.9 Caffeine-Related Disorder NOS 292.81 Hallucinogen Intoxication Delirium
292.xx Hallucinogen-Induced Psychotic Disorder
.11 With DelusionsI
CANNABIS-RELATED DISORDERS
Cannabis Use Disorders 292.84 Hallucinogen-Induced Mood DisorderI
292.89 Hallucinogen-Induced Anxiety DisorderI
304.30 Cannabis Dependencea,b,c
292.9 Hallucinogen-Related Disorder NOS
305.20 Cannabis Abuse
Cannabis-Induced Disorders INHALANT-RELATED DISORDERS

292.89 Cannabis Intoxication Inhalant Use Disorders
Specify if: With Perceptual Disturbances 304.60 Inhalant Dependenceb,c
292.81 Cannabis Intoxication Delirium 305.90 Inhalant Abuse
292.xx Cannabis-Induced Psychotic Disorder
.11 With DelusionsI
.12 With HallucinationsI Inhalant-Induced Disorders
292.89 Cannabis-Induced Anxiety DisorderI
292.9 Cannabis-Related Disorder NOS 292.89 Inhalant Intoxication
292.81 Inhalant Intoxication Delirium
292.82 Inhalant-Induced Persisting Dementia
COCAINE-RELATED DISORDERS 292.xx Inhalant-Induced Psychotic Disorder
Cocaine Use Disorders .11 With DelusionsI
304.20 Cocaine Dependencea,b,c 292.84 Inhalant-Induced Mood DisorderI
305.60 Cocaine Abuse 292.89 Inhalant-Induced Anxiety DisorderI
292.9 Inhalant-Related Disorder NOS
Cocaine-Induced Disorders
292.89 Cocaine Intoxication NICOTINE-RELATED DISORDERS
Nicotine Use Disorder
292.0 Cocaine Withdrawal
292.81 Cocaine Intoxication Delirium 305.1 Nicotine Dependencea,b
Nicotine-Induced Disorder Sedative-, Hypnotic-, or Anxiolytic-Induced

Disorders
292.0 Nicotine Withdrawal
292.9 Nicotine-Related Disorder NOS 292.89 Sedative, Hypnotic, or Anxiolytic
Intoxication
292.0 Sedative, Hypnotic, or Anxiolytic
OPIOID-RELATED DISORDERS Withdrawal
Opioid Use Disorders Specify if: With Perceptual Disturbances
292.81 Sedative, Hypnotic, or Anxiolytic
304.00 Opioid Dependencea,b,c,d Intoxication Delirium
305.50 Opioid Abuse 292.81 Sedative, Hypnotic, or Anxiolytic
Withdrawal Delirium
Opioid-Induced Disorders 292.82 Sedative-, Hypnotic-, or Anxiolytic-Induced
Persisting Dementia
292.89 Opioid Intoxication 292.83 Sedative-, Hypnotic-, or Anxiolytic-Induced
Specify if: With Perceptual Disturbances Persisting Amnestic Disorder
292.0 Opioid Withdrawal 292.xx Sedative-, Hypnotic-, or Anxiolytic-Induced
292.81 Opioid Intoxication Delirium Psychotic Disorder
292.xx Opioid-Induced Psychotic Disorder .11 With DelusionsI,W
.11 With DelusionsI .12 With HallucinationsI,W
.12 With HallucinationsI 292.84 Sedative-, Hypnotic-, or Anxiolytic-Induced
292.84 Opioid-Induced Mood DisorderI Mood DisorderI,W
292.89 Opioid-Induced Sexual DysfunctionI 292.89 Sedative-, Hypnotic-, or Anxiolytic-Induced
292.85 Opioid-Induced Sleep DisorderI,W Anxiety DisorderW
292.9 Opioid-Related Disorder NOS 292.89 Sedative-, Hypnotic-, or Anxiolytic-Induced
Sexual DysfunctionI
PHENCYCLIDINE (OR PHENCYCLIDINE-LIKE)- 292.85 Sedative-, Hypnotic-, or Anxiolytic-Induced
RELATED DISORDERS Sleep DisorderI,W
292.9 Sedative-, Hypnotic-, or Anxiolytic-Related
Phencyclidine Use Disorders Disorder NOS
304.60 Phencyclidine Dependenceb,c
305.90 Phencyclidine Abuse POLYSUBSTANCE-RELATED DISORDER
304.80 Polysubstance Dependencea,b,c,d
Phencyclidine-Induced Disorders
292.89 Phencyclidine Intoxication
OTHER (OR UNKNOWN) SUBSTANCE-
RELATED DISORDERS
292.81 Phencyclidine Intoxication Delirium
292.xx Phencyclidine-Induced Psychotic Disorder Other (or Unknown) Substance Use Disorders
.11 With DelusionsI
304.90 Other (or Unknown) Substance
Dependencea,b,c,d
292.84 Phencyclidine-Induced Mood DisorderI
305.90 Other (or Unknown) Substance Abuse
292.89 Phencyclidine-Induced Anxiety DisorderI
292.9 Phencyclidine-Related Disorder NOS
Other (or Unknown) Substance-Induced
Disorders
SEDATIVE-, HYPNOTIC-, OR ANXIOLYTIC-
RELATED DISORDERS 292.89 Other (or Unknown) Substance Intoxication
Sedative, Hypnotic, or Anxiolytic Use Disorders
292.0 Other (or Unknown) Substance Withdrawal
304.10 Sedative, Hypnotic, or Anxiolytic Specify if: With Perceptual Disturbances
Dependencea,b,c 292.81 Other (or Unknown) Substance-Induced
305.40 Sedative, Hypnotic, or Anxiolytic Abuse Delirium
292.82 Other (or Unknown) Substance-Induced 297.3 Shared Psychotic Disorder

Persisting Dementia 293.xx Psychotic Disorder Due to … [Indicate the
292.83 Other (or Unknown) Substance-Induced General Medical Condition]
Persisting Amnestic Disorder .81 With Delusions
292.xx Other (or Unknown) Substance-Induced .82 With Hallucinations
Psychotic Disorder —.— Substance-Induced Psychotic Disorder (refer
.11 With DelusionsI,W to Substance-Related Disorders for
.12 With HallucinationsI,W substance-specific codes)
292.84 Other (or Unknown) Substance-Induced Specify if: With Onset During Intoxication/
Mood DisorderI,W With Onset During Withdrawal
292.89 Other (or Unknown) Substance-Induced 298.9 Psychotic Disorder NOS
Anxiety DisorderI,W
292.89 Other (or Unknown) Substance-Induced Mood Disorders
Sexual DysfunctionI
292.85 Other (or Unknown) Substance-Induced Code current state of Major Depressive Disorder or
Sleep DisorderI,W Bipolar I Disorder in fifth digit:
292.9 Other (or Unknown) Substance-Related
Disorder NOS 1 ⫽ Mild
2 ⫽ Moderate
3 ⫽ Severe Without Psychotic Features
Schizophrenia and Other Psychotic Disorders
4 ⫽ Severe With Psychotic Features
Specify: Mood-Congruent Psychotic Features/
295.xx Schizophrenia
Mood-Incongruent Psychotic Features
The following Classification of Longitudinal Course 5 ⫽ In Partial Remission
applies to all subtypes of Schizophrenia. 6 ⫽ In Full Remission
Episodic With Interepisode Residual Symptoms 0 ⫽ Unspecified
(specify if: With Prominent Negative Symptoms)/ The following specifiers apply (for current or most
Episodic With No Interepisode Residual Symptoms/ recent episode) to Mood Disorders as noted:
Continuous (specify if: With Prominent Negative a
Severity/Psychotic/Remission Specifiers/ bChronic/
Symptoms) c
With Catatonic Features/dWith Melancholic
Single Episode In Partial Remission (specify if: With
Features/ eWith Atypical Features/f With
Prominent Negative Symptoms)/Single Episode In Full
Postpartum Onset
Remission
The following specifiers apply to Mood Disorders as
Other or Unspecified Pattern
noted:
.30 Paranoid Type
g
.10 Disorganized Type With or Without Full Interepisode Recovery/ hWith
.20 Catatonic Type Seasonal Pattern/iWith Rapid Cycling
.90 Undifferentiated Type
.60 Residual Type
DEPRESSIVE DISORDERS
295.40 Schizophreniform Disorder
Specify if: Without Good Prognostic 296.xx Major Depressive Disorder,
Features/With Good Prognostic Features .2x Single Episodea,b,c,d,e,f
295.70 Schizoaffective Disorder .3x Recurrenta,b,c,d,e,f,g,h
Specify type: Bipolar Type/Depressive Type 300.4 Dysthymic Disorder
297.1 Delusional Disorder Specify if: Early Onset/Late Onset
Specify type: Erotomanic Type/ Specify: With Atypical Features
Grandiose Type/Jealous Type/ 311 Depressive Disorder NOS
Persecutory Type/Somatic Type/
Mixed Type/Unspecified Type
BIPOLAR DISORDERS
298.8 Brief Psychotic Disorder
Specify if: With Marked Stressor(s)/Without 296.xx Bipolar I Disorder,
Marked Stressor(s)/With Postpartum Onset .0x Single Manic Episodea,c,f
Specify if: Mixed Specify if: With Generalized Anxiety/With

.40 Most Recent Episode Hypomanicg,h,i Panic Attacks/With Obsessive–Compulsive
.4x Most Recent Episode Manica,c,f,g,h,i Symptoms/With Phobic Symptoms
.6x Most Recent Episode Mixeda,c,f,g,h,i Specify if: With Onset During Intoxication/
.5x Most Recent Episode Depresseda,b,c,d,e,f,g,h,i With Onset During Withdrawal
.7 Most Recent Episode Unspecifiedg,h,i 300.00 Anxiety Disorder NOS
296.89 Bipolar II Disordera,b,c,d,e,f,g,h,i
Specify (current or most recent episode):
Hypomanic/Depressed
Somatoform Disorders
301.13 Cyclothymic Disorder
300.81 Somatization Disorder
296.80 Bipolar Disorder NOS
300.82 Undifferentiated Somatoform Disorder
293.83 Mood Disorder Due to … [Indicate the
300.11 Conversion Disorder
Specify type: With Motor Symptom or
Specify type: With Depressive Features/With
Deficit/With Sensory Symptom or Deficit/
Major Depressive-like Episode/With Manic
With Seizures or Convulsions/With Mixed
Features/With Mixed Features
Presentation
—.— Substance-Induced Mood Disorder (refer
307.xx Pain Disorder
to Substance-Related Disorders for
.80 Associated With Psychological Factors
substance-specific codes)
.89 Associated With Both Psychological Factors
Specify type: With Depressive Features/With
and a General Medical Condition
Manic Features/With Mixed Features
Specify if: Acute/Chronic
Specify if: With Onset During Intoxication/
300.7 Hypochondriasis
With Onset During Withdrawal
Specify if: With Poor Insight
296.90 Mood Disorder NOS
300.7 Body Dysmorphic Disorder
300.82 Somatoform Disorder NOS
Anxiety Disorders
Factitious Disorders
300.01 Panic Disorder Without Agoraphobia
300.21 Panic Disorder With Agoraphobia 300.xx Factitious Disorder
300.22 Agoraphobia Without History of Panic .16 With Predominantly Psychological Signs and
Disorder Symptoms
300.29 Specific Phobia .19 With Predominantly Physical Signs and
Specify type: Animal Type/Natural Symptoms
Environment Type/Blood–Injection–Injury .19 With Combined Psychological and Physical
Type/Situational Type/Other Type Signs and Symptoms
300.23 Social Phobia 300.19 Factitious Disorder NOS
Specify if: Generalized
300.3 Obsessive–Compulsive Disorder
Specify if: With Poor Insight Dissociative Disorders
309.81 Posttraumatic Stress Disorder
Specify if: Acute/Chronic 300.12 Dissociative Amnesia
Specify if: With Delayed Onset 300.13 Dissociative Fugue
308.3 Acute Stress Disorder 300.14 Dissociative Identity Disorder
300.02 Generalized Anxiety Disorder 300.6 Depersonalization Disorder
293.89 Anxiety Disorder Due to … [Indicate the 300.15 Dissociative Disorder NOS
Specify if: With Generalized Anxiety/ With
Sexual and Gender Identity Disorders
Panic Attacks/With Obsessive–Compulsive
Symptoms
SEXUAL DYSFUNCTIONS
—.— Substance-Induced Anxiety Disorder (refer
to Substance-Related Disorders for The following specifiers apply to all primary Sexual
substance-specific codes) Dysfunctions:
Lifelong Type/Acquired Type/Generalized Type/ Specify if: With Onset During Intoxication
Situational Type Due to Psychological Factors/Due to 302.70 Sexual Dysfunction NOS
Combined Factors
PARAPHILIAS
SEXUAL DESIRE DISORDERS
302.4 Exhibitionism
302.71 Hypoactive Sexual Desire Disorder 302.81 Fetishism
302.79 Sexual Aversion Disorder 302.89 Frotteurism
302.2 Pedophilia
SEXUAL AROUSAL DISORDERS Specify if: Sexually Attracted to Males/
Sexually Attracted to Females/Sexually
302.72 Female Sexual Arousal Disorder Attracted to Both
302.72 Male Erectile Disorder Specify if: Limited to Incest
Specify type: Exclusive Type/Nonexclusive
ORGASMIC DISORDERS Type
302.83 Sexual Masochism
302.73 Female Orgasmic Disorder 302.84 Sexual Sadism
302.74 Male Orgasmic Disorder 302.3 Transvestic Fetishism
302.75 Premature Ejaculation Specify if: With Gender Dysphoria
302.82 Voyeurism
SEXUAL PAIN DISORDERS 302.9 Paraphilia NOS
302.76 Dyspareunia (Not Due to a General Medical
Condition) GENDER IDENTITY DISORDERS
306.51 Vaginismus (Not Due to a General Medical
302.xx Gender Identity Disorder
Condition)
.6 in Children
.85 in Adolescents or Adults
SEXUAL DYSFUNCTION DUE TO A GENERAL Specify if: Sexually Attracted to Males/
MEDICAL CONDITION Sexually Attracted to Females/Sexually
625.8 Female Hypoactive Sexual Desire Disorder Attracted to Both/Sexually Attracted to
Due to … [Indicate the General Medical Neither
Condition] 302.6 Gender Identity Disorder NOS
608.89 Male Hypoactive Sexual Desire Disorder 302.9 Sexual Disorder NOS
Due to … [Indicate the General Medical
Condition] EATING DISORDERS
607.84 Male Erectile Disorder Due to … [Indicate
307.1 Anorexia Nervosa
the General Medical Condition]
Specify type: Restricting Type; Binge-
625.0 Female Dyspareunia Due to … [Indicate the
Eating/Purging Type
307.51 Bulimia Nervosa
608.89 Male Dyspareunia Due to … [Indicate the
Specify type: Purging Type/Nonpurging Type
307.50 Eating Disorder NOS
625.8 Other Female Sexual Dysfunction Due
to … [Indicate the General Medical
Condition] Sleep Disorders
608.89 Other Male Sexual Dysfunction Due
to … [Indicate the General Medical PRIMARY SLEEP DISORDERS
Condition]
Dyssomnias
—.— Substance-Induced Sexual Dysfunction
(refer to Substance-Related Disorders for 307.42 Primary Insomnia
substance-specific codes) 307.44 Primary Hypersomnia
Specify if: With Impaired Desire/With Specify if: Recurrent
Impaired Arousal/With Impaired Orgasm/ 347.00 Narcolepsy
With Sexual Pain 780.57 Breathing-Related Sleep Disorder
327.xx Circadian Rhythm Sleep Disorder .24 With Anxiety

.31 Delayed Sleep Phase Type .28 With Mixed Anxiety and Depressed Mood
.35 Jet Lag Type .3 With Disturbance of Conduct
.36 Shift Work Type .4 With Mixed Disturbance of Emotions and
.30 Unspecified Type Conduct
307.47 Dyssomnia NOS .9 Unspecified
Specify if: Acute/Chronic
Parasomnias
307.47 Nightmare Disorder Personality Disorders
307.46 Sleep Terror Disorder
307.46 Sleepwalking Disorder Note: These are coded on Axis II
307.47 Parasomnia NOS 301.0 Paranoid Personality Disorder
301.20 Schizoid Personality Disorder
301.22 Schizotypal Personality Disorder
SLEEP DISORDERS RELATED TO ANOTHER 301.7 Antisocial Personality Disorder
MENTAL DISORDER 301.83 Borderline Personality Disorder
327.02 Insomnia Related to … [Indicate the Axis I or 301.50 Histrionic Personality Disorder
Axis II Disorder] 301.81 Narcissistic Personality Disorder
327.15 Hypersomnia Related to … [Indicate the Axis 301.82 Avoidant Personality Disorder
I or Axis II Disorder] 301.6 Dependent Personality Disorder
301.4 Obsessive–Compulsive Personality Disorder
301.9 Personality Disorder NOS
OTHER SLEEP DISORDERS
327.xx Sleep Disorder Due to … [Indicate the Other Conditions that May Be a Focus
General Medical Condition] of Clinical Attention
.01 Insomnia Type
.14 Hypersomnia Type PSYCHOLOGICAL FACTORS AFFECTING
.44 Parasomnia Type MEDICAL CONDITION
.8 Mixed Type
—.— Substance-Induced Sleep Disorder (refer 316 … [Specified Psychological Factor]
to Substance-Related Disorders for Affecting … [Indicate the General Medical
substance-specific codes) Condition]
Specify type: Insomnia Type/Hypersomnia Choose name based on nature of factors:
Type/Parasomnia Type/ Mixed Type Mental Disorder Affecting Medical
Specify if: With Onset During Intoxication/ Condition
With Onset During Withdrawal Psychological Symptoms Affecting Medical
Condition
Personality Traits or Coping Style Affecting
Impulse Control Disorders Not Medical Condition
Elsewhere Classified Maladaptive Health Behaviors Affecting
Medical Condition
312.34 Intermittent Explosive Disorder Stress-Related Physiological Response
312.32 Kleptomania Affecting Medical Condition
312.33 Pyromania Other or Unspecified Psychological Factors
312.31 Pathological Gambling Affecting Medical Condition
312.39 Trichotillomania
312.30 Impulse-Control Disorder NOS
MEDICATION-INDUCED MOVEMENT
DISORDERS
Adjustment Disorders
332.1 Neuroleptic-Induced Parkinsonism
309.xx Adjustment Disorder 333.92 Neuroleptic Malignant Syndrome
.0 With Depressed Mood 333.7 Neuroleptic-Induced Acute Dystonia
333.99 Neuroleptic-Induced Acute Akathisia ADDITIONAL CODES

333.82 Neuroleptic-Induced Tardive Dyskinesia
300.9 Unspecified Mental Disorder (nonpsychotic)
333.1 Medication-Induced Postural Tremor
V71.09 No Diagnosis or Condition on Axis I
333.90 Medication-Induced Movement Disorder
799.9 Diagnosis or Condition Deferred on Axis I
NOS
V71.09 No Diagnosis on Axis II
799.9 Diagnosis Deferred on Axis II
OTHER MEDICATION-INDUCED DISORDER
995.2 Adverse Effects of Medication NOS
MULTIAXIAL SYSTEM
RELATIONAL PROBLEMS Axis I Clinical Disorders

Other Conditions that May Be a Focus of
V61.9 Relational Problem Related to a Mental Clinical Attention
Disorder or General Medical Condition Axis II Personality Disorders
V61.20 Parent–Child Relational Problem Mental Retardation
V61.10 Partner Relational Problem Axis III General Medical Conditions
V61.8 Sibling Relational Problem Axis IV Psychosocial and Environmental Problems
V62.81 Relational Problem NOS Axis V Global Assessment of Functioning
PROBLEMS RELATED TO ABUSE OR NEGLECT

V61.21 Physical Abuse of Child (code 995.54 if DISORDERS USUALLY FIRST DIAGNOSED IN
focus of attention is on victim) INFANCY, CHILDHOOD, OR ADOLESCENCE
V61.21 Sexual Abuse of Child (code 995.53 if focus The classification begins with disorders usually first
of attention is on victim) diagnosed in infancy, childhood, or adolescence. The
V61.21 Neglect of Child (code 995.52 if focus of provision for a separate section for so-called childhood
attention is on victim) disorders is only for convenience. Although most indi-
— . — Physical Abuse of Adult viduals with these disorders present for clinical atten-
V61.12 (if by partner) tion during childhood or adolescence, it is not uncom-
V62.83 (if by person other than partner) (code mon for some of these conditions to be diagnosed for
995.83 if focus of attention is on victim) the first time in adulthood (e.g., attention-deficit/hyper-
—.— Sexual Abuse of Adult activity disorder). Moreover, many disorders included
V61.12 (if by partner) in other sections of the DSM-IV-TR have an onset dur-
V62.83 (if by person other than partner) (code ing childhood (e.g., major depressive disorder). Thus,
995.83 if focus of attention is on victim) a clinician evaluating a child or adolescent should not
only focus on those disorders listed in this section but
ADDITIONAL CONDITIONS THAT MAY BE A also consider disorders from throughout the DSM-IV-
FOCUS OF CLINICAL ATTENTION TR. Similarly, when evaluating an adult, the clinician
should also consider the disorders in this section since
V15.81 Noncompliance With Treatment
many of them persist into adulthood (e.g., stuttering,
V65.2 Malingering
learning disorders, tic disorders).
V71.01 Adult Antisocial Behavior
The first set of disorders included in this diagnostic
V71.02 Child or Adolescent Antisocial Behavior
class—mental retardation, learning and motor skills
V62.89 Borderline Intellectual Functioning
disorders, and communication disorders—are covered
Note: This is coded on Axis II in detail in Chapters 2, 3, and 4, respectively. While
780.93 Age-Related Cognitive Decline these are not, strictly speaking, regarded as mental dis-
V62.82 Bereavement orders, they are included in the DSM-IV-TR to facili-
V62.3 Academic Problem tate differential diagnosis and to increase recognition
V62.2 Occupational Problem of these conditions among mental health professionals.
313.82 Identity Problem Autism and other pervasive developmental disorders
V62.89 Religious or Spiritual Problem are discussed in Chapter 5 and are characterized by
V62.4 Acculturation Problem gross qualitative impairment in social relatedness, in
V62.89 Phase of Life Problem language, and in repertoire of interests and activities.
Disorders covered include autistic disorder, Asperger’s functioning (e.g., language, executive functioning).
disorder, Rett’s disorder, and childhood disintegrative DSM-IV-TR includes several types of dementia based
disorder. Attention-deficit/hyperactivity disorder and on etiology, including dementia of the Alzheimer’s
other disruptive behavior disorders (Chapter 6) are type, vascular dementia, a variety of dementia due to
grouped together because they are all characterized general medical and neurological conditions (e.g., hu-
(at least in their childhood presentations) by disruptive man immunodeficiency virus infection, Parkinson’s
behavior. The chapter on feeding disorders (Chapter 7) disease), substance-induced persisting dementia, and
includes both the DSM-IV-TR categories of pica, ru- dementia due to multiple etiologies.
mination disorder, and feeding disorder of infancy and In contrast to dementia, amnestic disorder is char-
early childhood (also known as failure to thrive). Tic acterized by clinically significant memory impairment
disorders (Chapter 8) and elimination and other disor- occurring in the absence of other significant impair-
ders of infancy and early childhood (Chapters 9 and ments in cognitive functioning. DSM-IV-TR includes
10) conclude the childhood section. amnestic disorder due to a general medical condition
and substance-induced persisting amnestic disease.
DELIRIUM, DEMENTIA, AMNESTIC
DISORDER, AND OTHER COGNITIVE MENTAL DISORDERS DUE TO A GENERAL
DISORDERS MEDICAL CONDITION NOT ELSEWHERE
CLASSIFIED
In DSM-III-R, delirium, dementia, amnestic disorder,
and other cognitive disorders were included in a sec- This diagnostic class includes all of the specific men-
tion called organic mental disorders, which contained tal disorders due to a general medical condition and is
disorders that were due to either a general medical con- discussed in Chapter 12. In DSM-IV-TR, most of the
dition or substance use. In DSM-IV, the term organic mental disorders due to a general medical condition
was eliminated because of the implication that disor- have been distributed throughout the various diagnos-
ders not included in that section (e.g., schizophrenia, tic classes alongside their “nonorganic” counterparts
bipolar disorder) did not have an organic component. in the classification. For example, mood disorder due
In fact, virtually all mental disorders have both psy- to a general medical condition and substance-induced
chological and biological components, and to designate mood disorder are included in the mood disorders sec-
some disorders as organic and the remaining disorders tion of DSM-IV-TR. Two specific types of mental dis-
as nonorganic reflected a reductionistic mind–body orders due to a general medical condition (i.e., cata-
dualism that is at odds with our understanding of the tonic disorder due to a general medical condition and
multifactorial nature of the etiological underpinnings personality change due to a general medical condition)
of disorders. are physically included in this diagnostic class.
DSM-IV replaced each unitary organic mental dis-
order (e.g., organic mood disorder) with its two com-
SUBSTANCE-RELATED DISORDERS
ponent parts: mood disorder due to a general medi-
cal condition and substance-induced mood disorder. Substance-related disorders in DSM-IV-TR are more
Because of their central roles in the differential di- than just disorders related to taking drugs of abuse.
agnosis of cognitive impairment, delirium, dementia, They also include medication side effects and the
and amnestic disorder are contained within the same consequences of toxin exposure. Two types of sub-
diagnostic class in DSM-IV-TR and are discussed in stance-related disorders are included in DSM-IV-TR:
Chapter 11. substance use disorders (dependence and abuse),
Whereas both delirium and dementia are character- which describe the maladaptive nature of the pattern
ized by multiple cognitive impairments, delirium is of substance use; and substance-induced disorders,
distinguished by the presence of clouding of conscious- which cover psychopathological processes caused by
ness, which is manifested by an inability to appropri- the direct effects of substances on the central nerv-
ately maintain or shift attention. DSM-IV-TR includes ous system. Criteria sets for substance dependence,
three types of delirium: delirium due to a general medi- substance abuse, substance intoxication, and sub-
cal condition, substance-induced delirium, and delir- stance withdrawal that apply across all drug classes
ium due to multiple etiologies. are included before the substance-specific sections of
Dementia is characterized by clinically significant DSM-IV-TR. A discussion of these so-called generic
cognitive impairment in memory that is accompanied criteria that apply to all substance-related disorders
by impairment in one or more other areas of cognitive is covered in Chapter 13. Detailed discussions of
each of the DSM-IV-TR drug classes are covered in Although the term mood is broadly defined to include
Chapters 14 to 24. depression, euphoria, anger, and anxiety, the DSM-IV-
TR generally restricts mood disturbances to depressed,
elevated, or irritable mood.
SCHIZOPHRENIA AND OTHER
The mood disorders section begins with the criteria
PSYCHOTIC DISORDERS
for mood episodes (major depressive episode, manic
The title of this diagnostic class is potentially mislead- episode, hypomanic episode, mixed episode), which
ing for two reasons: (1) there are other disorders that are the building blocks for the episodic mood disor-
have psychotic features that are not included in this ders. The codable mood disorders come next and are
diagnostic class (e.g., mood disorders with psychotic divided into the depressive disorders (i.e., major de-
features, delirium) and (2) it may incorrectly imply pressive disorder and dysthymic disorder, described
that the other psychotic disorders included in this sec- in Chapter 26) and the bipolar disorders (i.e., bipolar I
tion are related in some way to schizophrenia (which is disorder, bipolar II disorder, and cyclothymic disorder,
only true for schizophreniform disorder and possibly described in Chapter 28). Finally, the many specifiers
schizoaffective disorder). Instead, what ties together all that provide important treatment-relevant information
of the disorders in this diagnostic class is the presence close this section. Several so-called subthreshold mood
of prominent psychotic symptoms. Included here are disorders (i.e., they are characterized by depression but
schizophrenia, schizophreniform disorder, schizoaf- fall short of meeting the diagnostic criteria for either
fective disorder, delusional disorder, shared psychotic major depressive disorder or dysthymic disorder) are
disorder, and brief psychotic disorder, each of which is included in DSM-IV-TR appendix B, for Criteria Sets
discussed in varying detail in Chapter 25. and Axes Provided for Further Study. These include
It should be noted that the definition of the term psy- minor depressive disorder, brief recurrent depressive
chosis has been used in different ways historically and is disorder, mixed anxiety depressive disorder, postpsy-
not even used consistently across the various categories chotic depressive disorder of schizophrenia (all briefly
in the DSM-IV-TR. The most restrictive definition of described in Chapter 26), and premenstrual dysphoric
psychosis (used in substance-induced psychotic disor- disorder (described in detail in Chapter 27).
der) requires a break in reality testing such that the per-
son has delusions or hallucinations with no insight into
ANXIETY DISORDERS
the fact that the delusions or hallucinations are caused
by taking drugs. A somewhat less restrictive definition The common element joining these disparate catego-
of psychosis (not used in DSM-IV-TR but advocated ries together is the fact that the anxiety is a prominent
by some members of the DSM-IV Psychotic Disorders part of their clinical presentation. This grouping has
Workgroup as more appropriate for substance-induced been criticized because of evidence suggesting that at
psychosis) includes hallucinations or delusions even if least some of the disorders are likely to be etiologically
the person has insight into their origin (e.g., it would distinct from the others. Most particularly, obsessive–
include an individual who was hallucinating after tak- compulsive disorder and posttraumatic stress disorder
ing phencyclidine [PCP] even if he were aware that the seem to share little in common with the other anxiety
hallucinations were due to the PCP). A much broader disorders. In fact, separate diagnostic classes for stress-
definition of psychosis (utilized in the definition of related disorders (that would also include adjustment
schizophrenia, schizophreniform, and brief psychotic disorders and perhaps dissociative disorders) and for
disorder) goes beyond delusions and hallucinations to obsessive–compulsive spectrum disorders (which
include grossly disorganized speech and catatonic or might also include trichotillomania, tic disorders, hy-
grossly disorganized behavior as evidence for psycho- pochondriasis, body dysmorphic disorder, and other
sis. Finally, the term psychosis was in the past used disorders characterized by compulsive behavior) have
most broadly to refer to any condition that caused seri- been proposed.
ous functional impairment (e.g., “affective psychosis” Detailed discussions of the various anxiety disorders
is used in ICD-9 to refer to major mood disorders). This are covered in Chapters 29 to 33 in this section of the
definition is not used in DSM-IV-TR. textbook.
MOOD DISORDERS SOMATOFORM DISORDERS

This diagnostic class includes disorders in which the This diagnostic class includes disorders in which the de-
predominant disturbance is in the individual’s mood. fining feature is a physical complaint or bodily concern
that is not better accounted for by a general medical EATING DISORDERS

condition or another mental disorder. These disorders
Although the name of this diagnostic class focuses on
(which are discussed in detail in Chapter 34) can be
the fact that the disorders in this section are charac-
divided into three groups on the basis of the focus of
terized by abnormal eating behavior (refusal to main-
the individual’s concerns: (1) focus on the physical
tain adequate body weight in the case of anorexia
symptoms themselves (somatization disorder, undif-
nervosa and discrete episodes of uncontrolled eating
ferentiated somatoform disorder, pain disorder, and
of excessively large amounts of food in the case of
conversion disorder); (2) focus on the belief that one
bulimia nervosa), of near equal importance is the in-
has a serious physical illness (hypochondriasis); and
dividual’s pathological overemphasis on body image.
(3) focus on the belief that one has a defect in physical
A third category, which is being actively researched
appearance (body dysmorphic disorder).
but has not been officially added to the DSM-IV-TR,
is binge-eating disorder (included in the appendix of
FACTITIOUS DISORDERS Criteria Sets and Axes Provided for Further Study).
Like bulimia nervosa, individuals with binge-eating
This diagnostic class contains only one disorder: facti-
disorder have frequent episodes of binge-eating. How-
tious disorder, which describes presentations in which
ever, unlike bulimia nervosa, these individuals do not
the individual intentionally produces or feigns physical
do anything significant to counteract the effects of their
or psychological symptoms in order to fulfi ll a psycho-
binge-eating (i.e., they do not purge, use laxatives or
logical need to assume the sick role. It is discussed in
diet pills, or excessively exercise). All three disorders
detail in Chapter 35. Factitious disorder should always
are described in Chapter 38.
be distinguished from malingering, in which the indi-
vidual similarly pretends to have physical or psycho-
logical symptoms. The difference is that in malinger- SLEEP DISORDERS
ing, the person’s motivation is to achieve some external
gain (e.g., disability benefits, lessening of criminal re- Sleep disorders are grouped into four sections on the
sponsibility, shelter for the night). For this reason, un- basis of presumed etiology (primary, related to another
like factitious disorder, malingering is not considered mental disorder, due to a general medical condition,
a mental disorder. and substance induced). Two types of primary sleep
disorders are included in DSM-IV-TR: dyssomnias
(problems in regulation of amount and quality of sleep)
DISSOCIATIVE DISORDERS and parasomnias (events that occur during sleep). The
The common element in this group of disorders is the dyssomnias include primary insomnia, primary hyper-
symptom of dissociation that is defined as a disruption somnia, circadian rhythm sleep disorder, narcolepsy,
in the usually integrated functions of consciousness, and breathing-related sleep disorder, whereas the para-
memory, identity, and perception. Four specific disor- somnias include nightmare disorder, sleep terror dis-
ders are included (dissociative amnesia, dissociative order, and sleepwalking disorder. Sleep disorders are
fugue, dissociative identity disorder, and depersonaliza- described in detail in Chapter 39.
tion disorder) and are discussed in detail in Chapter 36.
IMPULSE CONTROL DISORDERS
SEXUAL AND GENDER IDENTITY DISORDERS NOT ELSEWHERE CLASSIFIED
This diagnostic class contains three relatively disparate As is suggested by the title of this diagnostic grouping,
types of disorders, linked together only by virtue of no one diagnostic class in DSM-IV-TR comprehensively
their involvement in human sexuality. Sexual dysfunc- includes all of the impulse control disorders. A number
tions refer to disturbances in sexual desire or function- of disorders characterized by impulse control prob-
ing, paraphilias refer to unusual sexual preferences that lems are classified elsewhere (e.g., conduct disorder,
interfere with functioning (or in the case of preferences attention-deficit/hyperactivity disorder, oppositional-
that involve harm to others like pedophilia, merely act- defiant disorder, delirium, dementia, substance-related
ing on those preferences), and gender identity disorder disorders, schizophrenia and other psychotic disorders,
refers to a serious conflict between one’s internal iden- mood disorders, antisocial and borderline personality
tity of maleness and femaleness (gender identity) and disorders). What ties together the disorders in this class
one’s anatomical sexual characteristics. These catego- is that they present with clinically significant impul-
ries are discussed in detail in Chapter 37. sive behavior and that they are not better accounted for
by one of the mental disorders included in other parts treatment by a mental health professional. Psychologi-
of DSM-IV-TR. Five such disorders are included here: cal factors affecting medical condition are intended to
intermittent explosive disorder, pathological gambling, allow the clinician to note the presence of psychologi-
pyromania, kleptomania, and trichotillomania. These cal factors (e.g., Axis I or II disorder) that adversely af-
are discussed in Chapter 40. fect the course of a general medical condition, includ-
ing factors that interfere with treatment and factors that
constitute health risks to the individual. This condition
ADJUSTMENT DISORDERS
is described in Chapter 43.
All DSM-IV-TR categories (except NOS categories)
take priority over adjustment disorder. This category
APPENDIX CATEGORIES
is intended to apply to maladaptive reactions to psy-
chosocial stressors that do not meet the criteria for any DSM-IV-TR aims to be on the trailing edge rather
specific DSM-IV-TR disorder. These are discussed in than the cutting edge of research. A new category
Chapter 41. was considered for inclusion only if there was a
substantial research literature behind it. Although
there were proposals for more than 100 new catego-
PERSONALITY DISORDERS
ries to be introduced into DSM-IV, only a handful
This diagnostic class is for personality patterns that of new categories were added. Text and criteria for
significantly deviate from the expectations of the per- another 17 proposed categories have been included
son’s culture, are pervasive, and lead to significant im- in a DSM-IV-TR appendix, Criteria Sets and Axes
pairment or distress. Ten specific personality disorders Provided for Further Study (Table 1-2). These cri-
are included in DSM-IV-TR: paranoid personality dis- teria sets have been included to provide a common
order (pervasive distrust and suspiciousness of others), language for researchers and psychiatrists who are
schizoid personality disorder (detachment from social interested in further investigating their potential
relationships and a restricted expression of emotions), utility and validity.
schizotypal personality disorder (acute discomfort
with close relationships, perceptual distortions, and ec-
centricities of behavior), antisocial personality disorder
(disregard for the rights of others), borderline person- Criteria Sets and Axes Provided for Further
Table 1-2
Study
ality disorder (instability of personal relationships, in-
stability of self-image, and marked impulsivity), histri- Postconcussional disorder
onic personality disorder (extensive emotionality and Mild cognitive disorder
Caffeine withdrawal
attention seeking), narcissistic personality disorder Postpsychotic depression of schizophrenia
(grandiosity, need for admiration, and lack of empa- Simple deteriorative disorder
thy), avoidant personality disorder (social inhibition, Minor depressive disorder
Recurrent brief depressive disorder
feelings of inadequacy, and hypersensitivity to negative Premenstrual dysphoric disorder
evaluation), dependent personality disorder (excessive Mixed anxiety–depressive disorder
need to be taken care of), and obsessive–compulsive Factitious disorder by proxy
Dissociative trance disorder
personality disorder (preoccupation with orderliness, Binge-eating disorder
perfectionism, and mental and personal control at the Depressive personality disorder
expense of flexibility, openness, and efficiency). These Passive–aggressive personality disorder (negativistic
personality disorder)
are discussed in detail in Chapter 42. Defensive Functioning Scale
Global Assessment of Relational Functioning Scale
Social and Occupational Functioning Assessment Scale
OTHER CONDITIONS THAT MAY BE A FOCUS Source: Data from American Psychiatric Association (1994)
OF CLINICAL ATTENTION Diagnostic and Statistical Manual of Mental Disorders, 4th ed.
APA, Washington, DC.
This section of DSM-IV-TR is for problems that are not
mental disorders but that may be a focus of attention for
CHAPTER
2 Childhood Disorders:
Mental Retardation
DIAGNOSIS limitation in adaptive behavior is defined as perform-

ance of at least 2 standard deviations below the mean
Some common misconceptions about mental retarda-
on an instrument normed on the general population.
tion are that it is a specific and lifelong disorder with
The AAMR manual emphasizes the requirement for
a unique personality pattern and that comorbid mental
detailed assessment of individuals and their needs
disorders existing with mental retardation are different
in all relevant domains, including psychological and
from those encountered in other individuals. Although
emotional, and is by far the most modern and compre-
mental retardation is listed as a mental disorder in the
hensive available.
DSM-IV-TR, it is not a unique nosological entity. In-
DSM-IV-TR defines mental retardation in a manner
stead, a diagnosis of mental retardation refers to the
generally compatible with the AAMR definition. Men-
level of a person’s intellectual and adaptive functioning
tal retardation is coded on Axis II, as conceptually, it
below a cutoff point that is not even natural but is arbi-
fits more with personality disorders listed on this axis
trarily chosen in relation to the average level of func-
than with the other mental illnesses listed on Axis I. It
tioning of the population at large. Its chief function is
was also expected that placement on Axis II would en-
administrative, defining a group of persons who are in
courage clinicians to diagnose both mental retardation
need of support and educational services. Thus, mental
and mental disorders when faced with a person who has
retardation does not have a single cause, mechanism,
course, or prognosis. It has to be differentiated from
the diagnosis (if known) of the underlying medical DSM-IV-TR Criteria
condition.
The American Association on Mental Retardation 317–319 MENTAL RETARDATION
(AAMR) has published over the years 10 definitions
A. Significantly subaverage intellectual functioning: an
of mental retardation. The most recent definition pub- IQ of approximately 70 or below on an individually
lished in 2002 in the 10th edition of the manual on administered IQ test (for infants, a clinical judgment of
definition, classification, and system of supports of significantly subaverage intellectual functioning).
B. Concurrent deficits or impairments in present adaptive
the American Association on Mental Retardation is functioning (i.e., the person’s effectiveness in meeting
as follows: “Mental retardation is a disability charac- the standards expected for his or her cultural group)
in at least two of the following areas: communication,
terized by significant limitations both in intellectual self-care, home living, social/interpersonal skills, use
functioning and in adaptive behavior as expressed in of community resources, self-direction, functional ac-
conceptual, social, and practical adaptive skills. This ademic skills, work, leisure, health, and safety.
C. The onset is before age 18 years.
disability originates before age 18 years.” Signifi-
cant limitation in intellectual functioning is defi ned Severity Approximate IQ Range Code
as at least 2 standard deviations below the mean for
Mild 50–55 to approx. 70 317
the assessment instrument. The standard error of Moderate 35–40 to approx. 50–55 318
measurement for the instrument (usually between Severe 20–25 to approx. 35–40 318.1
3 and 5 points) should be taken into consideration. Profound Below 20–25 318.2
Unspecified 319
Persons with mental retardation can be classified in
various ways, such as by IQ levels, or by the inten- Reprinted with permission from the Diagnostic and Statistical
sity of supports required by them, depending on the Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
American Psychiatric Association.
purpose for which the diagnosis is used. Significant
Chapter 2 • Childhood Disorders: Mental Retardation 19
such comorbidity, rather than subsume both under the • Dimension V: Context (environments and culture).
diagnosis of mental retardation.
The clinical presentation of persons with mental re- This is a comprehensive description of the person’s
tardation is influenced by multiple factors, which can current environment: its nature, strengths, and weak-
be grossly divided into biological (such as syndromes nesses, and supports for the person’s development and
underlying the retardation), psychological (the level of well-being (including factors such as poverty, family
the person’s intellectual and adaptive functioning), and and its attitudes, availability of education, and other
environmental (such as cultural expectations and serv- services). In all aspects of the assessment, attention
ices received). should be paid both to the strengths as well as to the
The more severe the mental retardation, the earlier weaknesses and the impairments.
the child will come to medical attention, because the
developmental delay will be obvious earlier, and as- Elements of Biomedical Assessment
sociated physical impairments will be more prevalent.
Conversely, children with mild mental retardation may First Stage Workup. The scheme for assessing
not be diagnosed until they reach school age, when they the etiology of mental retardation is summarized in
fail in academic learning. If the sociocultural environ- Figure 2.1.
ment does not value and stress early academic learn-
ing and early education is not available, mild mental History. Obtaining a detailed history is most impor-
retardation might go undetected, especially if the per- tant. The family history, especially occurrence in the
son has relatively good adaptive skills. A false-positive family of similar cases, congenital anomalies, severe
diagnosis of mental retardation can also occur, espe- mental illness, and consanguinity should be explored.
cially if psychological tests are not sensitive to cultural The risk of recessively inherited diseases increases
background, and there is a language barrier between if there has been intermarriage between the parents’
the child and the tester. families in earlier generations. Drawing the family
The importance of the earliest diagnosis possible tree is helpful. The gestational, birth and neonatal, as
cannot be overstated because the prognosis will be well as developmental history is also most important.
much better if the intervention that results from the di- The presence of an appropriate relationship between
agnostic knowledge is begun as early as possible. weight, length, and head circumference at birth must
The AAMR published in 2002 a new edition of its be assessed as well as their relationship to the gesta-
manual Mental Retardation: Definition, Classification tional age to evaluate possible intrauterine growth
and Systems of Supports. Several dimensions of mental retardation, microcephaly, and so on. All events that
retardation are described, which might also serve as an may have affected CNS development during childhood
outline for its assessment: as well as developmental milestones must be recorded.
• Dimension I: Intellectual abilities. Physical Examination. This is essential and should

• Dimension II: Adaptive behavior (Conceptual, also focus on searching for physical phenotypical mani-
social, and practical skills). festations of various mental retardation-associated syn-
Assessment of the above dimensions is essentially as- dromes and dysmorphic features different from famil-
certaining that the respective criteria for the diagnosis ial phenotype. Neurological examination and growth
of mental retardation are met. The intellectual func- measurements are part of physical examination.
tioning is assessed in individual testing with one of the
standardized intelligence tests appropriate for the per- Diagnostic Studies. The Consensus Conference for
son’s cultural, linguistic, and social background, and Evaluation of Mental Retardation recommended, in ad-
communication skills. Standardized tests and scales, dition to previously mentioned history taking and phys-
such as the Vineland Adaptive Behavior Scales and the ical examination, the following: banded karyotype and
AAMR Adaptive Behavior Scales as well as history fragile X studies by DNA method for both males and
and direct observations are used. females with unexplained mental retardation. These
studies are essential if the family history is positive or
• Dimension III: Participation, interactions, and
if the physical and behavioral phenotypes are without
social roles.
major findings. Neuroimaging, preferably MRI, is to be
• Dimension IV: Health (physical health, mental
performed if the individual has neurologic symptoms,
health, etiological factors).
cranial abnormalities, microcephaly, or macrocephaly.
This is described in the following section of this After this basic workup, the probable cause or at
chapter. least timing of the injury should become apparent, thus
Figure 2-1 Diagnostic approach to mental retardation of all ages. (Source: Szymanski LS and Kaplan LC (1991) Mental retardation.
(Reprinted with permission from the Textbook of Child & Adolescent Psychiatry. Copyright 1991, American Psychiatric Press.)
allowing discussion with the family concerning possi- Prenatal Diagnosis. Prenatal diagnostic methods
ble inheritance. Sometimes the history alone might pro- are increasingly available. Amniocentesis with chro-
vide this information, but even then a detailed physical mosomal studies is usually recommended for women
examination for signs indicative of abnormal prenatal 35 years or older. Prenatal diagnostic studies should be
development is necessary. made available to everyone requesting them and should
be used if there is a known risk for a genetic or con- 3. Interventions targeted at the functional disability of
genital problem. Even if the parents do not plan a thera- the mental retardation itself: educational, habilita-
peutic abortion, if the results are positive for a certain tive, and supportive approaches depending on the
disorder, they will be able to prepare for the birth of a person’s individualized needs.
child with special needs and to marshal support.
The current approach to the services for persons
The currently available techniques include am-
with mental retardation is based on the following
niocentesis (useful in diagnosing chromosomal and
principles:
metabolic disorders), chorionic villus sampling (for
chromosomal and molecular genetic studies), and ma- • The normalization principle, which refers to mak-
ternal serum alpha-fetoprotein screening (for neural ing available to individuals with mental retardation
tube defects). Ultrasound scanning is often performed patterns and conditions of everyday life that are as
around the 20th week of gestation to screen for major close as possible to the norms and patterns of the
malformations. Carrier screening, which is increas- mainstream of society. This has largely evolved
ingly available for certain recessive disorders, should into the principle of inclusion, which is usually
be offered to all persons in high-risk populations, such interpreted as an active effort to include persons with
as Ashkenazi Jews (for Tay–Sachs disease). Careful mental retardation in all normal aspects and oppor-
counseling is necessary to help the prospective parents tunities of society’s life, through providing them with
decide on all available options if they are found to be supports necessary for success. The ultimate goal is
positive for the particular trait. to eventually end segregated services and education
and provide persons with mental retardation with the
necessary, specialized support services in regular
Differential Diagnosis educational, living, and work settings.
The diagnosis of mental retardation itself should be • The right to community living, which confers the
relatively straightforward as it reflects the current level right to live with a family, preferably one’s own or a
of intellectual and adaptive functioning. Some persons substitute one if necessary (foster or adoptive). This
with learning disorders or communication disorders includes moving individuals living in large residen-
might appear to have a low level of functioning, but ap- tial facilities to as normal a setting as possible, for
propriate psychological and communication testing will example, community residences, supervised apart-
demonstrate that the impairment is in the development ments, and foster homes. Furthermore, children are
of specific skills and is not generalized. Dementia can not to be institutionalized, regardless of the level of
be diagnosed at any age, whereas mental retardation retardation, and, generally, neither are adults. How-
is diagnosed only if the onset is before age 18 years. ever, some children are still placed in special resi-
However, both disorders might be diagnosed in persons dential schools (usually private) for specific reasons,
younger than age 18. It is often asked how one differen- typically medical or behavioral needs that require
tiates between mental retardation and autistic disorder. specialized treatment. Historically, a majority of
Actually, such a question is erroneous because these persons with mental retardation lived at home and
disorders are not mutually exclusive; in fact, most per- no more than 10% were in institutions at any point.
sons with autism also have mental retardation. An un- However, institutions played a disproportionate role
complicated mental retardation is not associated with in attitudes to their care. At their peak in 1967, there
qualitative impairment in social interaction and com- were 194,650 persons living in them: this number
munication, which is diagnostic of autistic disorder. dropped to 52,801 in 1998. In 2000, there were eight
states that closed all their large residential facilities.
In contrast, the number of persons living in small
TREATMENT (less than six persons) residences in the community
increased dramatically.
Mental retardation is a functional disability: thus, the
goal of treatment should be to reduce or eliminate the
• Education and training for all children to a maxi-
mum possible extent, regardless of their disability
disability. There are three aspects to the treatment:
and the degree of the disability, by including them
1. Treatment of the underlying disorder that is causa- full time in an age-appropriate regular classroom.
tive of mental retardation (e.g., phenylketonuria This educational program is individualized accord-
[PKU]). ing to the child’s needs. Services of special educa-
2. Treatment of the comorbid disorders that add to the tors and therapists, as necessary, are also provided
functional disability, whether physical or mental. in these programs. This has to be distinguished from
mainstreaming, which refers to placement in special medications) is used in lieu of such a program. Further-
classes in regular schools but with participation in more, medications may suppress a person’s functioning
some activities of regular classes. through side effects such as drowsiness.
• Employment of adults in the community according Psychotropic medications are used to treat a diag-
to their abilities is another aspect of inclusion. The nosed mental disorder toward the goal of maximizing a
current trend is to employ them in competitive job person’s quality of life. They should not be used merely
markets with supports, such as vocational training to suppress a single, objectionable behavior without
and supports by job coaches. However, many indi- regard to the effect on a person’s global adjustment,
viduals, especially those with severe degrees of dis- functioning, and quality of life. They cannot be used
ability, are still placed in sheltered workshops or oc- as punishment, for staff convenience (such as in un-
cupational–recreational day programs. derstaffed facilities), in lieu of appropriate habilitative
• Use of normal community services and facilities programs (if such is unavailable), or in dosages that in-
(shopping, banking, transportation, recreation) terfere with such programs and with a person’s quality
through training and ongoing supports. of life.
• Advocacy and appropriate protective measures, for These drugs are always used as part of a compre-
example, against inappropriate use of pharmacologi- hensive, treatment/habilitation program designed and
cal and behavioral measures as substitutes for active supervised by an interdisciplinary team of which the
education and treatment, inclusion in research pro- psychiatric clinician is an integral part. They should
grams without proper, truly informed consent, and not be prescribed merely in brief “psychopharmacol-
general exploitation and abuse. ogy consultation” or “medication review,” in isolation
from other aspects of the treatment.
Overall Goals of Psychiatric Treatment Review of Classes of Psychotropic Drugs

of Persons with Mental Retardation
Only issues specific to persons with mental retardation
The most common mistake made by mental health cli- are discussed here.
nicians treating persons with mental retardation is to
consider suppression (usually with medications) of sin- Neuroleptics (Antipsychotics). The use of antipsy-
gle problems (as a rule disruptive behaviors) as the only chotic drugs in persons with mental retardation is the
goal of treatment. This approach used to be the rule same as that for the general population—primarily for
in the past when people with mental retardation were the treatment of psychosis, sometimes for Tourette’s
not expected to achieve any measure of independence disorder, and as an emergency treatment of dangerous
and keeping them docile was the goal. Lately, such ap- behavior. The problem with persons with mental retar-
proaches are reemerging, partly related to the pressure dation is in making the correct diagnosis of psychosis,
from insurers to achieve a fast and inexpensive symp- especially schizophrenia. Perhaps because of the diffi-
tomatic improvement, even if short lived. Fortunately, culty (or ignorance) of making a more specific diagno-
in the past three decades, the quality of life (QOL) has sis, antipsychotic agents have been used for “off-label”
been assuming a central role as the goal of treatment indications, such as aggression, destructiveness, Self-
in the mental retardation field. More recently, the im- injurious behaviour (SIB), and any disruptive behavior.
portance of the subjective aspects of QOL have been While these medications may sometimes be effective
stressed: the individual’s subjective feeling of content- in these cases, success cannot be reliably predicted.
ment, well-being, and satisfaction with his or her own If the drug is effective in alleviating such behaviors,
life as opposed to the caregiver’s satisfaction. In other it does not necessarily mean that the individual had a
words, personal happiness of the person with mental psychotic disorder.
retardation is now stressed as a goal of habilitation as The recognition of side effects might be difficult in
well as specific treatment. persons with limited language, and extended obser-
The goal of any form of psychiatric treatment of vation by trained staff may be necessary. Drowsiness
persons with mental retardation is to contribute to this might have an adverse effect on learning and on gen-
sense of satisfaction with one’s own life, or happiness, eral level of activity. A common mistake is to confuse
in the context of a comprehensive treatment program. akathisia, especially upon withdrawal, with reemer-
Suppression of behaviors inconvenient to caregivers is gence of behavior problems and to make the disorder
not enough, especially if they are a response to an inad- worse by increasing the dose. Many adults with mental
equate habilitation program and the treatment (usually retardation have been on older antipsychotics for years,
often for no clear reason. Many of these individuals anxiety and aggression or SIB, has been suggested by
have side effects such as Parkinsonian symptoms, and one study. Benzodiazepines are still used for the treat-
tardive dyskinesia (that might appear only upon discon- ment of generalized anxiety and panic disorders, but
tinuation trial). Because of a higher tendency to cause usually only when there is no response to antidepres-
adverse effects (to which this population might be sants. There is still a fair amount of combined use of
more susceptible), these drugs (thioridazine in particu- neuroleptics and anxiolytics, especially in institution-
lar) are being discontinued and, if necessary, changed alized persons with a history of aggression. However,
to newer, second generation antipsychotics. The latter this may lead to significant CNS depression, and ben-
are, of course, not free from side effects. Weight gain, zodiazepine use might actually lead to disinhibition.
especially from olanzapine and clozapine, might be Therefore, prolonged use of anxiolytics to control un-
particularly severe and troublesome. The discontinu- desirable behaviors is generally not recommended.
ation of antipsychotic medications should be gradual As with other medications, comprehensive diagnos-
and slow to minimize side effects from withdrawal, in- tic assessment is a prerequisite to the use of anxiolytics.
cluding behavior problems such as irritability, insom- In particular, environmental anxiety-provoking factors
nia, SIB, and aggression. Clonidine might be helpful have to be ruled out and, if present, have to be dealt
for these symptoms. with in addition to pharmacological means if these are
There are case reports of successful use of clozapine used.
in persons with mental retardation and schizophrenia
or bipolar disorder who did not respond to other agents. Mood Stabilizers. The use of these agents in persons
The need for weekly blood tests may be a problem in with and without mental retardation is similar. Lithium
less than cooperative persons. carbonate, the original mood stabilizer, was shown to
be effective for bipolar disorders in persons with men-
Antidepressants. The principal uses of antidepressant tal retardation during the 1970s. However, it has con-
medications, as in the general population, include treat- siderable side effects and managing them may be dif-
ment of depression as well as anxiety, panic, and obses- ficult in persons who might be less than cooperative. It
sive–compulsive disorder (OCD). Selective serotonin has been supplanted increasingly by anticonvulsants,
reuptake inhibitors (SSRIs) are now first-line drugs including carbamazepine and valproic acid, as well
because of favorable effectiveness/side effect profile. as newer ones, like gabapentin and lamotrigine. Cur-
Tricyclic antidepressants, principally desipramine, rently, the primary use is in the treatment of mania and
were used in the treatment of ADHD if stimulants and for augmentation of antidepressants. These drugs may
clonidine were not effective, but there has been concern also be used in a therapeutic trial in some individuals
about cardiotoxic side effects. Precipitation of excite- with implusive aggressive behavior. Some clinical ex-
ment, mania, and seizures by antidepressants might periences indicate that the prognosis might be better in
be a problem, and careful prior diagnostic assessment the presence of mood lability and an abnormal electro-
and follow-up are necessary. There are a few studies, encephalogram. As seizures are frequently associated
mostly case reports, that have suggested that SSRIs with mental retardation, these drugs offer a parsimo-
might be helpful in reducing self-stimulatory, ritualis- nious way of managing both seizures and behavioral
tic, and self-injurious behaviors, although the improve- symptoms.
ment might be short lived. In some cases where antide-
pressants are effective in reducing aggressive behavior, Stimulants. As in persons without mental retardation,
there is the possibility that they actually might help the drugs such as methylphenidate and dextroamphetamine
underlying depression that has led to the aggression. are effective in the treatment of ADHD. They have been
studied primarily in children and adolescents with mild
Antianxiety Drugs. Benzodiazepines have been used mental retardation or PDD. Their effectiveness in per-
for alleviation of anxiety, but their side effects, such sons with significant retardation is less certain. Tics
as paradoxical rage reactions, adverse effects on cogni- are one side effect of methylphenidate: if the individual
tion, and serious withdrawal symptoms, argue against is engaging in self-stimulatory behaviors, videotaping
their chronic use, and a trial of an SSRI might be pref- might provide a record for later reference regarding
erable. Occasional use might be helpful in emergency whether additional tics have emerged. The diagnosis of
situations in which extreme anxiety is present as well ADHD in this population may not be easy, especially
as in preparation for anxiety-inducing medical proce- in persons with significant mental retardation, as the
dures. The usefulness of buspirone, a nonsedating anx- symptoms have to be assessed in the context of the de-
iolytic, with short half-life, in persons with combined velopmental level.
Other Psychotropic Agents. Propranolol and other and strict, current regulations. Occasional case reports
beta-adrenergic blockers have been tried extensively of its successful use can still be found in the literature.
in all kinds of aggressive behavior, often with mixed
or poor results. Depression might be a side effect of
these agents, leading to reduction in the person’s func- Psychosocial Interventions
tioning, even if the aggressive behaviors might appear Programmatic and Educational Approaches. The
to improve, because of apathy induced by the drug. goal of these interventions is to provide a proper living
They may be also effective in the treatment of anxiety, and programmatic environment. For instance, certain
especially its somatic symptoms, and for akathisia re- persons easily become overstimulated, anxious, and
lated to neuroleptic drugs. disruptive in noisy and confused large workshops; ar-
Clonidine, a presynaptic alpha-2-adrenergic agonist ranging for a smaller and quieter workroom is prefer-
also used as an antihypertensive, is commonly used in able to a prescription for a neuroleptic. The vocational
the treatment of ADHD in children without mental re- and educational program should be individualized and
tardation, and more recently for children with pervasive should focus on developing the person’s strengths and
developmental disorder (PDD); there have been case providing an opportunity for success. In turn, this
reports of its effectiveness in persons with fragile X. will lead to results such as an improvement in self-
While tics are not a side effect, drowsiness, hypoten- image. Many persons with severe mental retardation
sion, bradycardia, and skin rash (from patch) might be are placed in prevocational training indefinitely, for ex-
troublesome. It has also been reported to be effective ample, screwing or unscrewing nuts and bolts, although
in some cases of akathisia related to neuroleptic drug no one expects them to ever be employed on an assem-
withdrawal. bly line. They often engage in a struggle with caregivers
Naltrexone, an oral antagonist of endogenous opioid because of their noncompliance and may resort to ag-
receptors, has been tried in a number of studies in cases gression, which leads to removal for a “time out” and
of severe SIB, following some case reports of earlier thus avoidance of a boring task. Creating a more suitable
successes with a similar agent, naloxone, which had to task—even such as making rounds of the workshop to
be administered parenterally. It appears that it is effec- collect or deliver materials—might be more interesting
tive in 35–70% of cases, at least for a short time. and appropriate. Functional analysis of behavior is an in-
valuable guide to these interventions. As discussed previ-
Other Treatments. For many years, there have been ously, such approaches should be explored prior to resort-
reports of beneficial effects of a variety of treatments, ing to the use of medications for disruptive behaviors.
especially in children with PDDs, Down syndrome,
and fragile X syndrome. These treatments include
Psychotherapies. Psychotherapy in this population
various nutritional supplements, vitamin supplements
is not different in nature from psychotherapy in per-
(such as megavitamins, various combinations of vita-
sons with average intelligence and is similar to treat-
mins, minerals and enzymes, B6, B6 with magnesium,
ing children, inasmuch as in both cases, the techniques
folic acid, etc.), restriction diets (such as diets without
and the therapist have to adapt to the developmental
certain food additives, gluten, casein, yeast), and so on.
needs of the individual. The treatment should be driven
Often, these approaches generate considerable excite-
by the individual’s needs and responses and not by the
ment both in families and researchers. However, as a
therapist’s theoretical orientation. The indications are
rule, they are based on anecdotal reports or studies
the presence of concerns and conflicts, especially about
with methodological problems, results of which are not
oneself; impairments in interpersonal skills; or other
replicated in well-designed studies. One should bear
mental disturbances that are known to improve through
in mind that persons with developmental disabilities,
psychotherapy. The prerequisites include communica-
especially PDDs, may have very unusual eating habits
tion skills permitting a meaningful interchange with
resulting in restricted diets. Therefore, in such cases a
the therapist, an ability to develop even a minimal rela-
nutritional consultation is advisable. If a deficiency is
tionship, and the availability of a trained, experienced,
found, an appropriate supplementation and correction
and unprejudiced therapist who is comfortable working
of dietary habits is, of course, needed. One example is
in a team setting.
zinc deficiency associated with pica, which was shown
Guidelines for psychotherapy in this population in-
to disappear or decrease after treatment with 100 mg of
clude the following:
chelated zinc for 2 weeks.
Electroconvulsive therapy has fallen into disuse in 1. Appropriate goals should be set and should be rec-
this population as the result of past inappropriate uses onciled with the expectations of the caregivers, the
therapist, and the individual with mental retardation. Behavioral Treatment. Detailed functional analysis
Common goals include improvement in self-image is a prerequisite. This treatment should optimally use
and impulse control, learning to express feelings in rewards that should be age-appropriate, preferably so-
a socially appropriate manner, and understanding cial, and the frequency of rewarding should be adapted
in a constructive manner one’s own disabilities and to a person’s cognitive level, so that he or she can un-
strengths. derstand why they are given. Consistency and gener-
2. Verbal techniques should be adapted to the individ- alization among different settings are essential. Thus,
ual’s language and cognitive level, and nonverbal if such techniques are successfully used at the school,
ones should be age-appropriate. the family or other caregivers should be trained to use
3. Limits and directiveness should be used as needed: them at home as well. The focus should not be on elimi-
nondirective therapy might lead to the individual’s nation of objectionable behaviors only, but on teach-
confusion. ing appropriate replacement behaviors. Aversive tech-
4. The therapist has to be active (supportive but not niques involving active punishment (electric shocks,
paternalistic), has to use herself or himself liberally spraying of noxious substances into a person’s face) are
as a treatment tool, and has to be able to focus on not used except in a few controversial settings. There is
the immediate reality rather than just intellectual- a professional consensus that these techniques should
ize. A mix of techniques, for example, cognitive not be used at all, or used only when all other tech-
psychotherapy and behavior modification, may be niques have failed and the individual’s behavior poses
required. severe danger to herself or himself or to others (such as
5. As in all treatment modalities, the therapist should intractable SIB). Even then, these techniques should be
be involved in all aspects of the individual’s pro- used only if proved effective and for a limited time.
gram and should collaborate with other providers
and with the family.
COMPARISON OF DSM-IV-TR AND ICD-10
Group psychotherapy might be particularly effective in DIAGNOSTIC CRITERIA
helping individuals with mental retardation handle is-
The method of defining the levels of severity differ
sues related to the understanding of their own disabil-
slightly between the two systems. The ICD-10 Diag-
ity and learn social skills because of the peer support
nostic Criteria for Research define the levels using
the group offers. In general, therapy should be seen
exact cutoff scores: Mild is defined as 50 to 69, Mod-
as a cognitive learning process, using the therapist’s
erate is defined as 35 to 49, Severe is defined as 20 to
support and leading individuals to the acquisition of
34, and Profound is defined as below 20. In contrast,
understanding and necessary skills, both of concrete
DSM-IV-TR provides somewhat greater flexibility in
behaviors and of handling one’s own emotions. Group
relating severity to a given IQ score by defining sever-
psychotherapy should be differentiated from group
ity levels using overlapping scores (i.e., mild is 50 to
counseling, which is usually educational in nature, fo-
55, moderate is from 35–40 to 50–55, severe is from
cused on a specific subject (e.g., sexuality education),
20–25 to 35–40, and profound is below 20–25). Within
and does not have to be conducted by a mental health
the overlapping range, the severity is determined by the
professional with a therapeutic goal and plan.
level of adaptive functioning.
CHAPTER
3 Childhood Disorders: Learning

and Motor Skills Disorders
DIAGNOSIS measured intelligence. Thus, these conditions can be

given to children with mental retardation (MR) so long
It is important not only to understand the diagnostic
as the learning or motor skills problem is substantially
criteria used in DSM-IV-TR but also the criteria used
out of proportion to other developmental deficits asso-
by school systems. In clinical practice, the clinician
ciated with the MR. The problem must significantly in-
usually needs to help the family in getting the school
terfere with the child’s academic achievement in order
system to identify the child or adolescent as having a
to qualify for a disorder (criterion B) and, if a sensory
disability and to provide the necessary services. Thus,
deficit is present (e.g., hearing loss), the difficulties are
the clinician must know and understand the educa-
in excess of those usually associated with it. For the
tional criteria.
learning disorders, the presence of a general medical
The research of the past 30 years on neurologically
condition (e.g., neurological conditions) or sensory
based learning disorders stressed not the specific skill
deficit is noted on Axis III. In contrast, the definition
disorder but the underlying processing problems. The
of developmental coordination disorder specifically ex-
psychological and educational diagnostic tests used
cludes the diagnosis if the coordination problems are
clarify areas of learning abilities and learning disabili-
due to a general medical condition or if the criteria are
ties covering the four phases of processing (Table 3-1).
met for a pervasive developmental disorder.
Thus, although one assesses for problems with reading,
Federal guidelines for determining whether a stu-
mathematics, or writing, it is important in the diagnos-
dent in a public school is eligible for special programs
tic process also to explore the underlying processing
for learning disabilities list four criteria:
problems that result in these skill disorders.
The DSM-IV-TR criteria for each of the learning dis- 1. Documented evidence indicating that general edu-
orders require that the child’s achievement in reading, cation has been attempted and found to be ineffec-
mathematics, or writing, as measured by individually tive in meeting the student’s educational needs.
administered standardized tests, is substantially below 2. Evidence of a disorder in one or more of the basic
those expected given the individual’s chronological age psychological processes required for learning. A
and measured intelligence, and age-appropriate educa- psychological process is a set of mental operations
tion (criterion A). Developmental coordination disorder that transform, access, or manipulate information.
similarly requires that performance of daily activities The disorder is relatively enduring and limits abil-
involving motor coordination be substantially below ity to perform specific academic or developmental
that expected given the child’s chronological age and learning tasks. It may be manifested differently at
different developmental levels.
3. Evidence of academic achievement significantly be-
Areas of Psychological Processing that Affect low the student’s level of intellectual function (a dif-
Table 3-1
Learning
ference of 1.5 to 1.75 standard deviations between
Area of Processing Examples achievement and intellectual functioning is con-
sidered significant) on basic reading skills, reading
Input Visual or auditory perception
Integration Sequencing, abstracting, comprehension, mathematical calculation, math-
organization ematical reasoning, or written expression.
Memory Short-term, rote, long-term 4. Evidence that the learning problems are not due
Output Language, motor
primarily to other handicapping conditions (i.e.,
Chapter 3 • Childhood Disorders: Learning and Motor Skills Disorders 27
impairment of visual acuity or auditory acuity, in misaligned columns or rows, or decimals put in the
physical impairment, emotional handicap, mental wrong place.
retardation, cultural differences, or environmental Children who have difficulties with writing also may
deprivation). have a problem with handwriting. They grasp the pen-
cil or pen differently and tightly. They write slowly, and
The presence of a central nervous system processing their hands get tired. Often, they prefer printing rather
deficit is essential for the diagnosis of a learning dis- than cursive writing. Most also have problems with the
ability. A child might meet the discrepancy criteria, language of writing. They have difficulty with spelling,
but without central processing deficits in functions re- often spelling phonetically. They may have difficulty
quired for learning, he or she is not considered to have with grammar, punctuation, and capitalization.
a learning disability. The question of the significant Many if not most students with a learning disorder
discrepancy between potential and actual achievement also have difficulties with memory or organization. The
determines eligibility for services. child or adolescent with a memory problem has diffi-
If a child or adolescent is experiencing academic dif- culty following multistep directions or reads a chap-
ficulty, she or he would normally be referred to the spe- ter in a book but forgets what was read. Others might
cial education professionals within the school system. have sequencing problems, performing instructions out
However, the student with academic difficulties often of order. In speaking or writing, the facts may come
presents with emotional or behavior problems and is out but in the wrong sequence. Students with organiza-
more likely to be referred to a mental health profes- tional difficulties may not be able to organize their life
sional. It is critical to understand this potential refer- (notebook, locker, desk, bedroom); they forget things
ral bias. This mental health professional must clarify or lose things; they have difficulty with time planning;
whether the observed emotional, social, or family prob- or they have difficulty using parts of information from a
lems are causing the academic difficulties or whether whole concept or putting parts of information together
they are a consequence of the academic difficulties and into a whole concept.
the resulting frustrations and failures experienced by Children and adolescents with a developmental coor-
the individual, the teacher, and the parents. dination disorder may show evidence of gross motor or
The evaluation of a child or adolescent with aca- fine motor difficulties. The gross motor problems might
demic difficulties and emotional or behavior problems result in difficulty with walking, running, jumping, or
includes a comprehensive assessment of the presenting climbing. The fine motor problems may result in dif-
emotional, behavior, social, or family problems as well ficulty with buttoning, zipping, tying, holding a pencil
as a mental status examination. The clinician should or pen or crayon, arts and crafts activities, or handwrit-
obtain information from the child or adolescent, par- ing. Both gross and fine motor difficulties may result
ents, teachers, and other education professionals to help in the individual performing poorly in certain sports
clarify whether there might be a learning disorder or a activities.
motor skills disorder and whether further psychologi- The evaluation of cognitive, academic, and neuropsy-
cal or educational studies are needed. chological functioning is critical to any assessment of
Children who experience problems in reading typi- learning problems. Results of this psychoeducational
cally have difficulty in decoding the letter–sound as- assessment will indicate the parameters of the individ-
sociations involved in phonic analysis. As a result, they ual’s academic and cognitive liabilities while identify-
may read in a disjointed manner, knowing a few words ing her or his assets. If any of the clinical evaluations
on sight and stumbling across other unfamiliar words. yield results suggestive of a learning disorder, a more
If they have difficulty with visual tracking, they may involved psychoeducational assessment is needed. An
skip words or lines. If comprehension is a problem, appropriate psychoeducational evaluation will reveal
they report that they have to read material over and over the magnitude of the child’s learning difficulties as
before they understand. well as the nature of the child’s cognitive assets and
Children with mathematical difficulties may have deficits.
problems learning math concepts or retaining this in- A family evaluation must include an assessment of
formation. They may make careless mistakes when do- the parents and of the entire family. A judgment is
ing calculations. Problems with visual–spatial tasks or made on the order in which these assessments are best
with sequencing might interfere with producing on pa- done. The first clinical question is whether the family
per what is known. A problem may not be completed or is functional or dysfunctional. If the family is largely
steps skipped. They might have difficulty shifting from functional, there may be normal parenting issues that
one operation to the next and, as a result, add when they may be contributing to the child’s difficulty. If there is
should subtract. A visual–spatial difficulty might result no evidence of a psychopathological process within the
family, alternative explanations should be considered found together, when one is diagnosed, the others must
for the learning disorder, which do not relate to family be considered in the diagnostic process.
issues.
Learning problems are attributed to cognitive deficits
Differential Diagnosis
or behavior problems in the child or adolescent. Envi-
ronmental factors involving the school or community, The presenting problem is academic difficulty. The dif-
however, can also contribute to academic difficulties. ferential diagnostic process must clarify the reason for
Thus, the clinician should be aware of how social, cul- the academic difficulty. A decision tree for academic
tural, or institutional structures can influence learning. difficulties is useful for exploring all of the possible
Data collection within this context is accomplished reasons for such difficulties (see Figure 3-1). Three
through formal and informal observations of the sys- principal areas of inquiry concerning the factors con-
tem and the cultural milieu. With this understanding as tributing to the student’s learning difficulties are ex-
a backdrop, one can conduct a more direct assessment plored. The first involves considerations that are related
of how specific environmental or school considerations to the child’s or adolescent’s psychiatric, medical, or
can affect a given individual. psychoeducational status. The second area of inquiry is
Individuals with a learning disorder or a motor skills family functioning. The third area to explore involves
disorder might have other mental disorders or a related the environmental and cultural context in which the
neurological disorder. They might also have social student functions.
problems. It is not uncommon for children and adoles- Difficulties in academic performance of children
cents with learning disorders or a motor skills disorder or adolescents can be related to a range of psychiat-
to also have a diagnosable mental disorder. For many, ric, medical, or cognitive factors. To best determine the
these psychological problems are secondary to the frus- primary source of academic difficulties, the evaluation
trations and failures experienced because these disabil- should involve a comprehensive examination of these
ities were not identified or were inadequately treated. areas. The psychiatric evaluation should clarify whether
For others, these conditions may be another reflection there is a psychopathological process. If one is present,
of a dysfunctional nervous system. The presenting be- it is useful first to determine whether the problems
havioral or emotional issues might be the individual’s relate to a disruptive behavior disorder or to another
characterological style for coping with a dysfunctional mental disorder. In particular, the disruptive behavior
nervous system. disorders have high comorbidity with academic diffi-
About one-third of youths diagnosed as having a culties. A full assessment should clarify whether a dis-
conduct disorder or young adults diagnosed as having ruptive behavior disorder is causing the difficulty with
a personality disorder, especially the borderline type, academic performance or is secondary to this difficulty.
have unrecognized or recognized and poorly treated Disruptive behavior disorders can result in the student
learning disabilities (learning disorders). being unavailable for learning or being so disruptive
The learning disabilities that result in learning as to require his/her removal from traditional learn-
disorders or motor skills disorder may directly con- ing environments. The frustration and failures caused
tribute to peer problems by interfering with success by a learning disorder can be manifested by a disrup-
in doing activities required to interact with certain tive behavior disorder. In some cases, the disruptive
age groups (e.g., visual perception and visual–motor behavior disorder coexists with the learning disorder
problems interfering with ability to quickly do such and the relation is less clear. Children and adolescents
eye–hand activities as catching, hitting, or throwing with ADHD have particular difficulty maintaining at-
a ball). tention, and possibly with processing information. As a
Many children and adolescents with learning dis- result, the same variables that have an impact on their
orders have difficulty learning social skills and being attention also have an impact on their ability to learn.
socially competent. These individuals do not pick up In such instances, they may have a learning disorder
such social cues as facial expressions, tone of voice, or and ADHD.
body language and therefore do not adapt their behav- Internalizing disorders such as depression or anxi-
iors appropriately. ety may result in an uncharacteristic disinterest in or
The first neurologically based disorder recognized as avoidance of school expectations. If one of the inter-
frequently associated with a learning disability (learn- nalizing disorders is present, it is important to clarify
ing disorder) was attention-deficit/hyperactivity disor- whether it is secondary or primary to the academic
der (ADHD). Since there is a continuum of disorders difficulty. Cognitive and language deficits as well as
associated with neurological dysfunction that are often social skills deficits are often associated with learning
Difficulty with
academic performance
Preliminary screening
Child − adolescent Family

Family
Psychiatric Psycho- assessment
evaluation educational
evaluation Functional Dysfunctional
Psycho- No psycho- Normal Abnormal No Parenting Couples Family

pathology pathology pathology issues issues issues
Borderline
Disruptive Other Gifted No problem
behavioral psychiatric Mismatch Mentally Single Work Value Primary Secondary Primary Secondary
disorder disorder retarded parent schedule system
Medical
Primar y Secondary ADHD Development
evaluation
delay
General health Learning

disability
Vision ADHD
Hearing
Environmental and
Seizures cultural issues
Medications Preliminary screening
ADHD Community School

Other
Value No Special School
systems problem ser vices setting
programs
Peer
relation No problem Availability
problems of ser vices
Peers Teacher/ No problem

administrative
Competence Personality
Figure 3-1 Academic underachievement and the clinical decision-making process. ADHD, Attention-deficit/hyperactivity disorder. (Source: Reprinted from Child Adolesc Psychiatr
Clin N Am 2, Ostrander Clinical observations suggesting a learning disability, 249–263, Copyright 1993 with permission from Elsevier.)
disorders and can contribute to a dysphoric or anxious normally developing individuals. It is essential for these
presentation. students to learn compensatory skills and for the class-
The medical evaluation is necessary to explore the in- room teachers to provide essential accommodations.
fluence of health factors on the individual’s availability
and ability to learn. Problems in acquiring academic Educational Interventions for Developmental
content can be significantly affected by most visual or Coordination Disorders. The approaches for help-
hearing deficits. Generally poor health can influence ing children and adolescents with this disorder focus
the stamina, motivation, and concentration needed to on academic skills, life skills, or athletic skills. That
focus adequately on academic demands. Medications is, the focus of intervention might be on specific skills
used for any purpose might cause sedation or other needed for school (e.g., handwriting), on dressing and
side effects that may affect the child’s ability to learn. other life skills (e.g., buttoning, zipping, tying, eating),
Early developmental insults can result in global or fo- or on skills needed to do better in sports (e.g., catching,
cal deficits in neurological development. Undiagnosed hitting, throwing, running).
seizures, especially petit mal and partial complex sei-
zures, can result in difficulties in general cognitive
Psychotherapeutic Interventions
functioning, specific deficits in memory, and problems
with attention. Learning disorders affect all aspects of the child’s or ad-
olescent’s life. The same processing problems that inter-
fere with reading, writing, mathematics, and language
TREATMENT
may interfere with communicating with peers and fam-
Treatment is directed at the underlying disabilities by ily, with success in sports and activities, and with such
use of educational interventions. Psychological inter- daily life skills as dressing oneself or cutting food.
ventions are also directed at any existing emotional, Lack of success in school can lead to a poor
social, or family difficulties. In addition, social skills self-image and low self-esteem. Some individuals may
training may be helpful. become anxious or depressed, or a disruptive behavior
disorder may develop.
Genetic and family studies show that in about 40%
Somatic Treatments
of children and adolescents with learning disabilities
No medication has been found to be effective for treat- (learning disorders), there is a familial pattern. Thus,
ing the learning disorders or motor skills disorder. If from an early identification perspective, each sibling
the individual with these disorders also has ADHD, it must be considered as possibly having a learning dis-
is important that medication be used to minimize the order. Also, there is a 40% likelihood that one of the
hyperactivity, distractibility, or impulsivity so that the parents may also have a learning disorder. This parent
student can be available for learning. may not have known of this problem. If this is true,
the parent, for the first time, may be able to understand
a lifetime of difficulties or underachievement. Further,
Educational Interventions
when the psychiatrist offers suggestions for this parent,
The goal of special educational interventions is to help the parent’s areas of difficulty must be considered. Do
children and adolescents overcome or compensate for not ask a mother to be more organized when she has
their learning disorders or motor skills disorder so that been just as disorganized as her child all her life.
they can succeed in school. These efforts involve re- Some children or adolescents may need specific in-
medial and compensatory approaches and use a multi- dividual, behavioral, group, or family therapy. If so, it
sensory approach that facilitates building on all areas is critical that the therapist understands the impact that
of strength while compensating for any areas of weak- the learning disorder has had on the individual and how
ness. These efforts are to be provided in as close to a these disabilities might affect the process of therapy.
regular classroom setting as possible. It is essential that As noted earlier, many students with a learning disor-
the classroom teacher knows how to adapt the class- der have difficulties with peers and social skills prob-
room, curriculum, and teaching style to best accom- lems. Social skills training might be helpful.
modate each student’s areas of difficulty. Once the diagnosis is established, it is critical that
Learning disorders such as reading, mathematics, the clinician explains to the individual and to the par-
or writing disorders, are not cured. With appropriate ents what the problems are, focusing not only on the
interventions, children and adolescents with reading areas of learning difficulties but also on the areas of
disorders learn to read and spell at a slower rate than do learning strengths.
Chapter 3 • Childhood Disorders: Learning and Motor Skills Disorders 31
If the presenting behavior problems are not serious, it The first step in developing these skills typically re-
may be best first to provide family education and to give quires the clinician to provide verbal instructions con-
some time to see how this new knowledge affects the cerning the relevant skills (e.g., conversational skills).
family. Concurrently, the parents are taught how to advo- The skills are then modeled by the clinician. It is also
cate for the necessary services within the school system. important to discuss and emphasize positive outcomes
It may be that once the academic issues are addressed associated with these skills. In the process, the clini-
and the family begins to change, the behavior problems cian must confront and restructure thoughts that may
will diminish and no further help will be needed. inhibit the desired behaviors. The child is then required
The next step is family counseling. Parents are taught to rehearse the skills in simulated conditions, with the
how to use their knowledge of their son’s or daughter’s clinician providing reinforcement and corrective feed-
strengths and weaknesses to modify family patterns; back as warranted. Generalization is stressed through
select appropriate chores; choose appropriate activi- homework assignments whereby skills are attempted in
ties, sports, and camps; and address stresses within the the natural environment and classroom.
family. Once taught the necessary knowledge about the
child or adolescent and the concepts of intervention,
families can often move ahead, creatively working out
DIAGNOSTIC CRITERIA
their own problems.
For some children and adolescents, individual be- In ICD-10, DSM-IV-TR Reading Disorder is referred
havioral therapy or psychotherapy may be indicated to to as “Specific Reading Disorder” and DSM-IV-TR
help them develop new strategies for interacting with Mathematics Disorders as “Specific Disorder of Arith-
peers, parents, and teachers. metic Skills.” For both of these learning skills disor-
Because this form of therapy requires listening ders, the ICD-10 Diagnostic Criteria for Research sug-
and talking, it is important for the therapist to know gest that the cutoff be 2 standard deviations below the
whether the individual has a disability in these areas. If expected level of reading achievement and mathemat-
so, the therapist has to develop ways of accommodating ics achievement, respectively. In contrast, DSM-IV-TR
these problems if therapy is to progress. If a speech and does not specify a score cutoff, instead recommending
language therapist is working with the individual, she that the score be “substantially below that expected,
or he might offer suggestions. given the person’s chronological age, measured in-
The initial phases of family therapy might focus on telligence, and age-appropriate education.” Further-
helping the identified individual regain control over his more, in contrast to DSM-IV-TR, which permits both
or her behavior and helping the parents retake control to be diagnosed if present, ICD-10 Reading Disorder
of the family. A behavioral management approach is takes precedence over Mathematics Disorder so that
often the first intervention. if criteria are met for both, only Reading Disorder is
Useful interventions attempt to enhance social– diagnosed.
cognitive skills and are directed at altering specific be- ICD-10 does not include a Disorder of Written
havior patterns. Social–cognitive approaches are based Expression (as in DSM-IV-TR), but instead includes
on those cognitive processes that are related to com- a Specific Spelling Disorder. DSM-IV-TR includes
petent, prosocial behavior. Targets of intervention are spelling problems as part of the defi nition of Disor-
directed toward the underlying cognitive variables that der of Written Expression but requires writing prob-
are linked to positive peer acceptance. lems in addition to spelling in order to warrant this
The enhancement of social–cognitive skills typically diagnosis.
involves three kinds of skill development: (1) accurate Finally, DSM-IV-TR Coordination Disorder is re-
interpretation of social situations; (2) effective use of ferred to as “Specific Developmental Disorder of motor
social behaviors in interactions with others; and (3) the function” in ICD-10. Furthermore, the ICD-10 Diag-
evaluation of one’s own performance and the ability nostic Criteria for Research suggest that the cutoff be
to make adjustments, depending on the environmental two standard deviations below the expected level on a
context. standardized test of fine or gross motor coordination.
CHAPTER
Communication Disorders
The disorders of communication have traditionally setting (see Figure 4-1 for diagnostic decision tree).
been insufficiently familiar to mental health profes- The clinician should ask the parents or guardians about
sionals despite the fact that clinical practice is founded the child’s speech and language, both in terms of devel-
upon communication. A knowledge of these disorders opment and in terms of current function. Much can be
is especially of crucial importance in the care of chil- learned from even a few questions: Does the child seem
dren, since they are deeply interwoven in all aspects of to hear and understand what is being said? Does the
normal development, psychopathology, and the func- child require visual prompts? Does the child in fact use
tions of daily life. These disorders share many common spoken language to communicate? How long and com-
features, as noted in Table 4-1. Selective mutism is not plicated are his/her sentences? Does the child “make
regarded as a disorder of communication per se, and is sense” to outsiders? Can he/she be clearly understood
included among other disorders of childhood. (Refer to even by strangers? Which sounds does the child find
Chapter 9, on childhood anxiety disorders.) difficult? Does the child use unusual volume, pitch,
or nasality? Does he/she observe the rules of conver-
sation? Parent–child communication should also be
DIAGNOSIS OF COMMUNICATION
observed.
DISORDERS
Children must be assessed in an environment that
It is essential that the mental health professional see- fosters verbal communication and observed in a variety
ing children is familiar with the expected milestones of interactions because their speech and language vary
of speech and language development. This knowledge so much over time in quantity and quality. For younger
forms the basis for effective observation in a clinical children, this may best be done in the context of a play
situation. The clinician should note how well a child
can follow and draw inferences from a conversation.
Table 4-1
Features Common to All Communication “Production” refers to speech, its fluency, and intel-
Disorders ligibility. “Phonation” refers to the utterance of vocal
Inadequate development of some aspect of communication sounds produced by the larynx. “Pragmatics” are those
Absence (in developmental types) of any demonstrable aspects of language that render it useful for social com-
causes of physical disorder, neurological disorder, global
mental retardation, or severe environmental deprivation munication beyond the most concrete level. Does the
Onset in childhood child appreciate the nuances of his/her partner’s con-
Long duration versation, as for example, when they signal beginnings
Clinical features resembling the functional levels of younger
normal children and endings of conversations, topic changes, or the
Impairments in adaptive functioning, especially in school child’s turn to talk?
Tendency to occur in families Pragmatic language involves nonverbal elements.
Predisposition toward boys
Multiple presumed etiological factors Deficiencies in this area impair abstraction and may
Increased prevalence in younger age range render the individual almost “robotlike.” In all cases,
Diagnosis requiring a range of standardized techniques observations should be made in as relaxed a fashion
Tendency toward certain specific associated problems, such
as attention-deficit/hyperactivity disorder as possible, avoiding interrogation or rote exercises. If
Wide range of subtypes and severity a child fails to communicate a given item, necessary
Source: Reprinted from Psychiatric Disorders in Children and help including nonverbal prompts should be offered, so
Adolescents, Baker L, Specific communication disorders, 257–270, that the child has the experience of success. A sense of
Copyright 1990 with permission from Elsevier.
failure will stifle communication.
Chapter 4 • Childhood Disorders: Communication Disorders 33
History Clinical Interview
Is there a history of communication Do difficulties with communication

problems in home, school, or social appear in interview?
setting?
Yes No Yes No
Assess in clinical Continue standard 1. Is there evidence of No further

interview assessment, including psychiatric disorder assessment
interview such as psychosis,
affective disorder, anxiety
disorder, selective mutism?
cultural or linguistic
differences interfering
with communication?
hearing disorder?
developmental disorder?
Yes No
2. Are there difficulties

Assess further, then with symbolization,
if problems persist with comprehension,
psychiatric intervention phonation, production,
or pragmatics?
Yes No
Reassess (1), then refer

Refer to speech and
to speech and language
language pathologist
pathologist if necessary
Figure 4-1 Diagnostic decision tree.
In school settings, all of the phenomena seen in a many areas, young children receive some type of for-
clinical interview may also be pursued. Children with mal communication screening in school. Therefore,
communication disorders often feel challenged by the teacher input is essential in the evaluation of these
demands of the classroom and may limit or withdraw children.
from conversation entirely. Thus, the task-oriented Clinician should be acutely concerned with the co-
group setting of the classroom may not elicit a child’s morbidity of all communication disorders with many
best communication. It may, however, demonstrate the mental disorders. Approximately half of the children
practical effectiveness of the child’s everyday efforts. with a speech or language disorder have some other
At the same time, teachers sometimes have more in- definable Axis I clinical disorder. Similarly, among
dividual conversations with children than even their children with a psychiatric diagnosis made first, there
parents do, and their experiences may make them is a remarkably increased likelihood of speech and lan-
the first adults to detect communication problems. In guage disorders, which often go undetected.
DIAGNOSIS OF EXPRESSIVE LANGUAGE hear. The deficits may be mild or severe, and at times
DISORDER AND MIXED RECEPTIVE– deceptively subtle, since children with this disorder
EXPRESSIVE LANGUAGE DISORDER may conceal them or avoid interaction. All areas and
levels of language comprehension may be disturbed.
Expressive language disorder denotes an impairment in
Phonological disorder is especially common among
the development of expressive language. Its diagnosis
children with these disorders. In addition, many of
requires the use of one or more standardized assessment
these children may present at least some manifestations
measures that are individually administered. When
of learning disorders. Other conditions that are broadly
appropriate instruments are unavailable, as for example,
considered as neurodevelopmental are also noted in
in the case of a member of a population for which no
these children, such as motor delays, coordination dis-
instrument has been standardized, this diagnosis may
orders, and enuresis. The extent of these associations,
be made through a thorough functional investigation of
while apparently considerable, is difficult to quantify
an individual’s language ability. Individuals with this
because of methodologic variations in the literature.
disorder have expressive language scores well below
The combination of these disorders and the stress they
those obtained from measures of nonverbal intelligence
create frequently lead to adjustment disorders and so-
and of receptive language. DSM-IV-TR does not require
cial withdrawal.
any particular degree of discrepancy in scores.
The presence of a test score by itself does not define
the condition: the affected individual must have clinical Differential Diagnosis
symptoms that might include disturbances of vocabu- These disorders are distinguished from each other by
lary, grammar (e.g., tenses), or syntax (e.g., sentence the presence or absence of receptive problems. Children
length or complexity). The diagnosis of this condition with autism may have any or all of the characteristics
also requires that the individual having it experiences of the language disorders. However, they have many
social, academic, or occupational difficulties directly additional problems including the use of language in
related to the condition. The presence of a mixed re- a restricted and often stereotypic fashion rather than
ceptive–expressive language disorder (MRELD) or a for communicative purposes. They also have difficul-
pervasive developmental disorder (PDD) supersedes ties with a wider range of interactions with persons and
this diagnosis, and it is not made in their presence. objects in their environment, and exhibit a restricted
Similarly, it may not be made in the presence of mental range of behaviors. The language impairments of men-
retardation, motor or sensory deficits, or environmental retardation, oral-motor deficits, or environmental
tal observation, unless the expressive language difficul- deprivation are not diagnosed in this category unless
ties experienced are beyond what would be expected they are well in excess of what is expected. Language
for individuals with these conditions. This condition impairment due to environmental deprivation tends to
may be acquired, as from a medical condition affecting improve dramatically with environmental improve-
the central nervous system (CNS), or it may be devel- ment. Sensory deficits, especially hearing impairment,
opmental, in the sense of arising early in life without may restrict language development. Any indication of
known origin. potential hearing impairment, no matter how tenuous,
The inclusion of MRELD in DSM-IV represented should prompt a referral for an audiologic evaluation.
the most significant change from previous classification Obviously, hearing and language disorders can and do
systems, which posited the existence of receptive lan- coexist. Some children develop an acquired aphasia as
guage disorders in a solitary form. The existence of this a complication of general medical illness. This condi-
category reflects the clinical observation that receptive tion is usually temporary; only if it persists beyond the
language disorders in children seldom, if ever, can oc- acute course of the medical illness is a language disor-
cur without concurrent (and perhaps resultant) prob- der diagnosed.
lems with expression. DSM-IV-TR notes that this is in
direct contrast with such entities as Wernicke’s aphasia
DIAGNOSIS OF PHONOLOGICAL DISORDER
in adults, which affects reception alone. Children with
AND STUTTERING
these conditions have significant measurable deficits in
standardized individual assessments, of both receptive Phonological disorder was formerly known as artic-
and expressive language, compared to their similarly ulation or developmental articulation disorder. It is
assessed nonverbal intelligence. characterized by an individual’s failure to use speech
Children with MRELD may have all the problems of sounds appropriate for their developmental level and
ELD. In addition, they do not understand all that they dialect. The affected individual may substitute one
sound for another (e.g., /l/ for /r/), omit certain sounds disorder can wax and wane during childhood. By early
entirely, or exhibit other errors in organization, use, adolescence it abates spontaneously in some cases, and
or production of sounds. By definition in DSM-IV-TR from 60% to 80% of individuals eventually recover to-
these difficulties interfere with social, academic, or oc- tally or to a major extent. Stuttering may persist into
cupational functions. The symptoms may occur during adulthood, often leading to adverse social and occupa-
development without discernible cause or they may be tional consequences.
related to CNS, motor, or sensory dysfunction, or to
environmental deprivation. In the latter cases, speech
difficulties must be in excess of those usually associ-
ated with the particular problem for the diagnosis to These conditions should be distinguished from the nor-
be made. This condition ranges in severity from very mal dysfluencies that occur among young children. For
mild problems to severe disorders, which render speech example, misarticulation of some sounds, such as /l/,
totally unintelligible. /r/, /s/, /z/, /th/, and /ch/, is common among preschool-
Stuttering is one of the most commonly recognized ers and resolves with age. As with the language dis-
disorders of speech. Some occurrence of the symptoms orders, these diagnoses are given in the case of motor
of stuttering is normal in the earlier stages of devel- or sensory deficit, mental retardation, or environmental
opment, and the condition is properly diagnosed only deprivation only if the disorder is much more severe
when the symptoms are perceived to be in excess of than expected in these conditions. Problems limited to
what is developmentally expected. Similarly, since oc- voice alone are included under CDNOS.
casional symptoms appear in the speech of nearly all
persons, the diagnosis is not made unless the distur-
DIAGNOSIS OF COMMUNICATION
bances interfere with social, academic, or occupational
DISORDER NOT OTHERWISE SPECIFIED
functioning. The condition may be associated with
motoric or sensory deficits; when this is the case, the This category includes disorders that do not meet cri-
diagnosis is made only when symptoms exceed those teria for other specific communication disorders or do
expected with these problems. The characteristic symp- so incompletely. DSM-IV-TR cites voice disorders of
toms of stuttering are disturbances in fluency (such as pitch, loudness, quality, tone, or resonance, as an ex-
repetitions of sounds, syllables or words, interjections, ample. It is used to describe disorders that do not fit the
and circumlocutions) and in time patterning (sound criteria for any of the other communication disorders
prolongations, broken words, and blocking). “Clutter- and is generally used only to describe voice disorders.
ing,” the disturbance in rate and length of speech noted These are disorders of pitch, intonation, volume, or
in DSM-III-R, is subsumed in DSM-IV-TR under CD- resonance. Hyponasality is one example of a voice dis-
NOS, or ELD. order as characterized by the “adenoidal” speech that
brought many children to surgery in an earlier era.
Hypernasality, secondary to velopharyngeal insuffi-
Course
ciency, may be associated with serious voice problems.
The course of PD is much more encouraging than those Air escapes into the nasal cavity resulting in nasal air
of other communication disorders. Milder cases may emission, snorting, or a nasal grimace during speech.
not be discovered until the child starts school. These
cases often recover spontaneously, especially if the
TREATMENT OF COMMUNICATION
child does not encounter adverse psychosocial conse-
DISORDERS
quences because of his speech. Severe cases associated
with anatomic malformations may at times require Speech and language therapy, the most important ap-
surgical intervention, and its course and outcome de- proach for these disorders, typically has three major
pend upon the results of the surgery. Between these two goals: the development and improvement of commu-
extremes are children who gradually improve, often to nication skills with concurrent remediation of deficits,
the point of total remission, and whose improvement the development of alternative or augmentative com-
may be accelerated by speech therapy. munication strategies where required, and the social
Stuttering usually appears in early childhood, as habilitation of the individual in regard to commu-
early as 2 years of age and frequently has its onset nication. Thus, a very great range of approaches and
around age 5. The onset of stuttering is typically re- components must be employed in treating children
garded as gradual, with repetition of initial consonants with communication disorders. The speech and lan-
or first words or phrases heard in the beginning. The guage pathologist (SLP) plays the most direct role in
A. Is there a causative medical condition? with the therapeutic process. Nonverbal augments or
prompts should be sensitively provided to children who
need them.
The role of psychotropic medication in the manage-
Yes No
ment of communication disorders is mainly limited
to the treatment of comorbid psychiatric problems ac-
B. Is there a causative sensory or
developmental disorder?
cording to standard practices. Outcome studies of com-
munication therapy, especially for the language disor-
ders, have often been complicated by multiple theories
of language development, diagnostic and methodologic
Yes No variations, lack of standardization of therapeutic tech-
niques, and comorbidity. Thus, the literature in this
C. Is there a causative psychiatric
disorder? area is relatively sparse and not always conclusive.
Nonresponse to initial treatment may be common, re-
quiring patience and persistence. It is important to note
in assessing these issues that, even when communica-
Yes Treat No
tion therapy does not lead to apparent improvements in
or
language beyond developmental improvements, it may
D. Refer for treatment still facilitate the child’s use of extant language for en-
vironmental- and self-control.
E. Do communication problems
persist with treatment? COMPARISON OF DSM-IV-TR AND ICD-10
DIAGNOSTIC CRITERIA
Regarding expressive language disorder, the ICD-10
Yes No
Diagnostic Criteria for Research suggest specific cut-
offs for the expressive language scores: 2 standard de-
Refer to speech and language viations below the expected level and 1 standard devia-
No further
pathologist (SLP). Reconsider
treatment tion below nonverbal IQ. Furthermore, in contrast to
A,B,C above, if necessary.
DSM-IV-TR, the diagnosis cannot be made if there are
Figure 4-2 Treatment decision tree. any neurological, sensory, or physical impairments that
directly affect the use of spoken language or if there is
mental retardation.
treatment of these conditions: this role is illustrated by For DSM-IV-TR mixed receptive–expressive lan-
the diagnostic treatment tree (Figure 4-2). guage disorder, the corresponding ICD-10 disorder
The mental health professional may have a major is “receptive language disorder.” In contrast to DSM-
role in the treatment of communication disorders. IV-TR, which specifies both expressive and receptive
These children and their families may present for psy- language difficulties because these generally occur
chotherapy or other treatment for disorders based on together, the ICD-10 definition only mentions devia-
or related to communication problems. Thus, the clini- tions in language comprehension. Like with expressive
cian may, in the first place, be a case finder or a case language disorder, the ICD-10 Diagnostic Criteria for
manager, facilitating the evaluation and treatment of Research suggest a cutoff of receptive language scores
these disorders by a multidisciplinary team. The dem- of 2 standard deviations below the expected level and
onstrated psychiatric comorbidity of these disorders 1 standard deviation below nonverbal IQ. Furthermore,
will necessitate the clinician’s involvement on many in contrast to DSM-IV-TR, the diagnosis cannot be
levels, both as a clinician primarily treating a child, made if there are any neurological, sensory, or physical
and as a therapist, counselor, and agent of advice and impairments that directly affect receptive language or
support for the entire family. Psychotherapy does not if there is mental retardation.
directly address language disorders, although older As compared to DSM-IV-TR phonological disor-
literature has cited improvement in stuttering follow- der, in which no mention is made of assessment using
ing family and individual treatment. The psychothera- standardized tests, the ICD-10 Diagnostic Criteria for
pist must, in any event, be sensitive to the manner in Research suggest that articulation skills, as assessed
which communication disorders can affect or interfere on standardized tests, are 2 standard deviations below
the expected level and 1 standard deviation below Regarding stuttering, in contrast to DSM-IV-TR,
nonverbal IQ. Furthermore, in contrast to DSM-IV- which establishes clinical significance based on inter-
TR, the diagnosis cannot be made if there are any ference with academic or occupational achievement or
neurological, sensory, or physical impairments that with social communication, the ICD-10 Diagnostic Cri-
directly affect receptive language or if there is mental teria for Research establish clinical significance by re-
retardation. quiring a minimum duration of at least three months.
CHAPTER
5 Childhood Disorders: Pervasive

Developmental Disorders
DSM-IV-TR Diagnostic Criteria
The pervasive developmental disorders (PDDs) have 299.00 AUTISTIC DISORDER
been more recently conceptualized as the autism spec-
A. A total of six (or more) items from (1), (2), and (3), with
trum disorders (ASDs) in order to recognize the com- at least two from (1) and one each from (2) and (3):
monality of these conditions with the paradigmatic (1) qualitative impairment in social interaction as man-
disorder, autistic disorder. The ASDs are a group of ifested by at least two of the following:
neurodevelopmental syndromes characterized by dis- (a) marked impairment in the use of multiple non-
verbal behaviors such as eye-to-eye gaze, facial
turbances in social interactions, language and com- expression, body postures, and gestures to regu-
munication, and the presence of stereotyped behaviors late social interaction
and interests. Diagnoses subsumed under the category (b) failure to develop peer relationships appropriate
to developmental level
of the ASDs (and PDDs) include Autistic Disorder, (c) a lack of spontaneous seeking to share enjoy-
Rett’s Disorder, Childhood Disintegrative Disorder, ment, interests, or achievements with other
Asperger’s Disorder, and Pervasive Developmental people (e.g., by a lack of showing, bringing, or
pointing out objects of interest)
Disorder Not Otherwise Specified (PDDNOS). A (d) lack of social or emotional reciprocity
comparison of the definitions of the ASDs is shown (2) qualitative impairments in communication mani-
fested by at least one of the following:
in Table 5-1. (a) delay in, or total lack of, the development of
More recently, the ASDs have been conceptualized spoken language (not accompanied by an at-
as a spectrum of conditions that are related by the com- tempt to compensate through alternative modes
of communication such as gesture or mime)
mon features of the disorders: difficulties in social in- (b) in individuals with adequate speech, marked
teractions and use of language, and restricted interests impairment in the ability to initiate or sustain a
and repetitive behaviors. The term spectrum implies conversation with others
(c) stereotyped and repetitive use of language or
that there are phenomenological commonalities to idiosyncratic language
these disorders that justify that they are grouped, but (d) lack of varied, spontaneous make-believe play
that component symptoms in each syndrome vary in or social imitative play appropriate to develop-
mental level
severity. Despite the enormous heterogeneity evident (3) restricted repetitive and stereotyped patterns of be-
in this area, there is increasing evidence that concep- havior, interests, and activities, as manifested by at
tualizing these disorders as a spectrum is useful and least one of the following:
(a) encompassing preoccupation with one or more
valid. stereotyped and restricted patterns of interest
that is abnormal in either intensity or focus
(b) apparently inflexible adherence to specific,
DIAGNOSIS nonfunctional routines or rituals
(c) stereotyped and repetitive motor mannerisms
ASDs are notoriously heterogeneous in their presenta- (e.g., hand or finger flapping or twisting, or
complex whole-body movements)
tion: there may be variability in the particular symp- (d) persistent preoccupation with parts of objects
toms manifested in any individual at a given point in
B. Delays or abnormal functioning in at least one of the
time and there may be significant levels of comorbidity. following areas, with onset before age 3 years: (1) so-
Nonetheless, autism has been consistently one of the cial interaction, (2) language as used in social commu-
most reliably diagnosed disorders of childhood. Ac- nication, or (3) symbolic or imaginative play.
C. The disturbance is not better accounted for by Rett’s
curate diagnosis requires that the clinician looks for disorder or childhood disintegrative disorder.
the particular symptoms and signs that characterize Reprinted with permission from the Diagnostic and Statistical
it: peculiar and deficient modes of social interaction, Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
Chapter 5 • Childhood Disorders: Pervasive Developmental Disorders 39
demonstrating empathy or perceiving or anticipating

DSM-IV-TR Diagnostic Criteria others’ moods or responses. The child with ASD often
299.80 ASPERGER’S DISORDER
acts in a socially inappropriate manner or lacks the so-
cial responsiveness needed to succeed in social settings,
A. Qualitative impairment in social interaction, as mani- leading to difficulty in the development of close, mean-
fested by at least two of the following:
ingful relationships. Some children with ASD eventu-
(1) marked impairment in the use of multiple nonver- ally develop warm, friendly relationships with family
bal behaviors such as eye-to-eye gaze, facial ex-
pression, body postures, and gestures to regulate while their relationships with peers lag behind consider-
social interaction ably, and these deficits typically persist across time.
(2) failure to develop peer relationships appropriate to Another area of difficulty is in the acquisition and
developmental level
(3) a lack of spontaneous seeking to share enjoyment, proper use of language for communication. It is esti-
interests, or achievements with other people (e.g., mated that only about half of the children with autistic
by a lack of showing, bringing, or pointing out ob-
jects of interest to other people)
disorder develop functional speech. This is not merely
(4) lack of social or emotional reciprocity a delay in development of speech; speech patterns may
B. Restricted repetitive and stereotyped patterns of be- be deviant and idiosyncratic compared with normal
havior, interests, and activities, as manifested by at children. If autistic children do begin to speak, their
least one of the following: babble is frequently decreased in quantity and lacking
(1) encompassing preoccupation with one or more in vocal experimentation. When children with autis-
stereotyped and restricted patterns of interest that
is abnormal in either intensity or focus tic disorder do acquire some speech, it is often pecu-
(2) apparently inflexible adherence to specific, non- liar and lacking in social perspective. Some children
functional routines or rituals with autistic disorder are even loquacious, although
(3) stereotyped and repetitive motor mannerisms (e.g.,
hand or finger flapping or twisting, or complex their speech tends to be repetitious and self-directed
whole-body movements) rather than aimed at maintaining a reciprocal dialogue.
(4) persistent preoccupation with parts of objects People with autistic disorder commonly make use of
C. The disturbance causes clinically significant impair- stereotyped speech, including immediate and delayed
ment in social, occupational, or other important areas
of functioning. echolalia, pronoun reversal, and neologisms. Speech
D. There is no clinically significant general delay in lan- usage is often idiosyncratic, may consist of concrete
guage (e.g., single words used by age 2 years, com- and poorly constructed grammar, may not be used to
municative phrases used by age 3 years).
E. There is no clinically significant delay in cognitive de- convey social meaning, and is often literal, lacking in
velopment or in the development of age-appropriate inference, and lacking in imagination. The delivery of
self-help skills, adaptive behavior (other than in social speech is frequently abnormal with atypical tone, pitch,
interaction), and curiosity about the environment in
childhood. and cadence. Paradoxically, children with autistic dis-
F. Criteria are not met for another specific pervasive de- order often have echolalia, in which prosody and other
velopmental disorder or schizophrenia. aspects of speech are frequently imitated verbatim.
Reprinted with permission from the Diagnostic and Statistical Individuals with autistic disorder routinely engage in
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
American Psychiatric Association. unusual patterns of behavior. Most people with ASD
also resist or have significant difficulty with new ex-
periences or transitions. They are commonly resistant
deficits in communication, and the focused behaviors to changes in their environment. They often repeatedly
and interests. perform stereotyped motor acts such as hand clapping
Many consider the disturbance of social develop- or flapping, or peculiar finger movements. These move-
ment, including difficulty in developing meaningful ments frequently occur at the periphery of their vision
attachments and interpersonal reciprocity, to be the near their own face. Some children with autistic dis-
central impairment in ASD. There is definitely variation order engage in self-injurious behaviors including bit-
in the clinical presentation. For instance, while many ing or striking themselves or banging their heads. This
children with ASD will seem aloof and unattached to is most likely to occur with severe or profound mental
their parents, many will display age-appropriate sepa- retardation but is also seen in children with autistic dis-
ration anxiety. Typically, a child with autistic disorder order without mental retardation. Their play only oc-
has abnormal patterns of eye contact and facial expres- casionally involves traditional toys, and objects may be
sion. When compared with normal children, children used in ways other than intended (for instance, a doll
with autism fail to consistently maintain eye contact or is used as a hammer), and there is a paucity of make-
vary facial expression to establish social contact. These believe play. Individuals with autistic disorder seem to
children seem to have considerable difficulty in effec- have unusual sensitivity to some sensory experiences,
tively coordinating social cues. They have difficulty particularly, specific sounds.
Table 5-1 Comparison of Domains of Diagnostic Criteria for Pervasive Developmental Disorders
Childhood Disintegrative Pervasive Developmental

Autistic Disorder Rett’s Disorder Disorder Asperger’s Disorder Disorder NOS
Age at onset Delays or abnormal functioning in social Apparently normal prenatal Apparently normal No clinically significant Category used in cases of
interaction, language, or play by age 3 years development development for at least delay in language, pervasive impairment
Apparently normal motor the first 2 years cognitive development, in social interaction and
development for first 5 Clinically significant loss or development of communication, with
months of previously acquired age-appropriate self- presence of stereotyped
Deceleration of head growth skills before 10 years help skills, adaptive behaviors or interests
between ages 5 and 48 of age behavior, and curiosity when criteria are not met
months about the environment for a specific disorder
in childhood
Social Qualitative impairment in social interaction, as Loss of social engagement Same as autistic disorder Same as autistic disorder
interaction manifested by at least two of the following: early in the course along with loss of
• Marked impairment in the use of multiple (although often social social skills (previously
nonverbal behaviors (e.g., eye-to-eye gaze) interaction develops later) acquired)
• Failure to develop peer relationships
appropriate to developmental level
• Lack of spontaneous seeking to share
enjoyment with other people
• Lack of social or emotional reciprocity
Communication Qualitative impairments of communication as Severely impaired Same as autistic disorder No clinically significant
manifested by at least one of the following: expressive and receptive along with loss of delay in language
• Delay in, or total lack of, the development of language development expressive or receptive
spoken language and severe psychomotor language previously
• Marked impairment in initiating or sustaining retardation acquired
a conversation with others, in individuals with
adequate speech
• Stereotyped and repetitive use of language or
idiosyncratic language
• Lack of varied, spontaneous make-believe, or
imitative play
Behavior Restricted, repetitive, and stereotyped patterns Loss of previously acquired Same as autistic disorder Same as autistic disorder
of behavior, as manifested by one of the purposeful hand along with loss of bowel
following: movement. Appearance or bladder control, play,
• Preoccupation with one or more stereotyped of poorly coordinated gait motor skills previously
or restricted patterns of interest or trunk movements acquired
• Adherence to nonfunctional routines or rituals
• Stereotyped and repetitive motor mannerisms
• Persistent preoccupation with parts of objects
Exclusions Disturbance not better accounted for by Rett’s Disturbance not better Criteria are not met
disorder or childhood disintegrative disorder accounted for by for another PDD or
another PDD or schizophrenia
schizophrenia
Source: Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision, Copyright 2000. American Psychiatric Association.
Other problems in autistic disorder and other PDDs encephalitis, leukodystrophies, or other diseases. With
include impairment in “joint attention,” the sharing or the onset of childhood disintegrative disorder, the child
mutual focus on an object or event by two or more peo- loses previously mastered cognitive, language, and mo-
ple, and the ability to shift attention when the social tor skills and regresses to such a degree that there is loss
situation calls for it. Many children with ASD also have of bowel and bladder control. Children with childhood
symptoms of hyperactivity and difficulty sustaining disintegrative disorder tend to lose abilities that would
attention, but these should be distinguished from the normally allow them to take care of themselves, and
joint attentional dysfunction found in all individuals their motor activity contains fewer complex, repetitive
with autistic disorder. Examples of joint attention in- behaviors than autistic disorder. Some children with
clude social exchanges that require pointing, referential this disorder experience regression that occurs for a
gaze, and gestures showing interest. time and then becomes stable. The majority of children
Asperger’s disorder and autistic disorder, as classi- with this disorder deteriorate to a severe level of mental
cally described, share many common features, includ- retardation; a few retain selected abilities in specific
ing an unusual use of pronouns, continuous repetition areas. Differential diagnosis of childhood disintegra-
of certain words or phrases, exhaustive focus of speech tive disorder requires obtaining a particularly thorough
on particular topics, difficulty in social reciprocity, developmental history, history of course of illness, and
engaging in repetitive play, and an excessive focus on an extensive neurological evaluation and testing.
certain interests. However, children with Aspeger’s dis- PDDNOS (also known as atypical autism) should be
order speak at about the same time as other children do reserved for cases in which there are qualitative im-
and eventually gain a full complement of language and pairments in reciprocal social development, and either
syntax. Thus, the predominant differentiating feature communication or imaginative and flexible interests
between autistic disorder and Asperger’s disorder is are met, but not the full criteria for a specific PDD. It
that those with Asperger’s disorder do not have a delay is important in the education of parents, teachers, and
in general (i.e., nonsocial) language development. colleagues to be clear that PDDNOS is closely related
Rett’s disorder is a developmental disorder that pref- to autistic disorder, because many families have been
erentially strikes girls and differs substantially from given diagnoses of both autistic disorder and PDDNOS
autistic disorder past the toddler stage. Typically, a and have the mistaken impression that this represents
child with Rett’s disorder has an uneventful prenatal strong diagnostic disagreement between clinicians.
and perinatal course that continues through at least the The diagnosis of ASD first involves completing a
first 6 months. With the onset of the classic form of the comprehensive psychiatric examination (Table 5-2).
disease, there is deceleration of head growth, usually The clinician should obtain a full developmental history,
between 5 months and 4 years of age. In toddlerhood,
the manifestations can be similar to autistic disorder in
Suggested Workup for Children and Adults
which there is frequently impairment in language and Table 5-2 with Autistic Disorder or Other Pervasive
social development, along with presence of stereotyped Developmental Disorders
motor movements. In particular, there is a loss of ac- History
quired language, restricted interest in social contact or
Particular attention to:
interactions, and the start of hand-wringing, clapping, Developmental phases of language, social interactions,
or tapping in the midline of the body. This type of ac- play
tivity begins after purposeful hand movement is lost. Family history of psychiatric and neurological disease
Serious psychomotor retardation as well as receptive Physical examination
Thorough physical examination including a search for:
and expressive language impairments sets in. Between Neurological problems
the ages of 1 and 4 years, truncal apraxia and gait Cardiac problems
apraxia typically ensue. Congenital anomalies
Skin lesions or abnormalities
Childhood disintegrative disorder and autistic dis- Dysmorphology
order have some similarities in that they both involve Psychological evaluation
deficits in social interaction and communication as Autism Diagnostic Interview—Revised
well as repetitive behaviors. However, the symptoms Autism Diagnostic Observation Schedule
Cognitive testing (e.g., Differential Abilities Scales)
of childhood disintegrative disorder appear abruptly Vineland Adaptive Behavior Scales
or in the period of a few months’ time after 2 years Speech and language evaluation
or more of normal development. There is generally no Audiological evaluation
prior serious illness or insult, although a few cases have
Visual acuity evaluation
been linked to certain brain ailments such as measles,
including all information regarding pregnancy and Differential Diagnosis of Autistic Disorder
delivery. Table 5-3
and Other Pervasive Developmental Disorders
In terms of direct observation, the child with ASD
Developmental language disorder
poses some unique challenges. Because of his or her Mental retardation
dislike of novelty, the first visit to the clinician’s office Acquired epileptic aphasia (Landau–Kleffner’s syndrome)
is sometimes an anxiety-provoking undertaking. If the Fragile X syndrome
Schizophrenia
child is having difficulty, it is usually preferable, espe- Selective mutism
cially on the first visit, to allow the parents to intervene. Psychosocial deprivation
This will allow the clinician to see how (effectively) Hearing impairment
Visual impairment
the family responds to this distress, and how the child Traumatic brain injury
responds to the efforts of caregivers to soothe the child. Dementia
During observation, the clinician needs to assess social Metabolic disorders (inborn errors of metabolism, e.g.,
phenylketonuria)
interaction, communication, unusual behaviors, and
all other information in the context of developmental
level. and children with mental retardation may present with
A full physical examination should be undertaken. stereotyped movements or obsessiveness. However, the
In addition to the standard comprehensive examina- child with mental retardation and not with ASD will
tion, the clinician should observe for dysmorphic fea- have social and communicative skills commensurate
tures and unusual dermatologic lesions. The clinician with their level of overall development.
must maintain a high suspicion for seizures in this pop- Differentiating ASD from childhood schizophrenia
ulation, both when taking the history and during the is not usually difficult. The onset of psychosis in child-
examination. A full neurological examination should hood is extraordinarily rare, and hallucinations and de-
be done with an emphasis on looking at motor impair- lusions are not a part of the ASD picture. It is important
ments like hypotonia and apraxia. not to diagnose some of the atypical features in ASD as
There are no diagnostic laboratory tests for ASD. psychotic and equally important to recognize that ver-
What laboratory tests are ordered as a part of an ini- bal individuals with ASD have impaired language that
tial workup is dependent on history and examination should not be confused with schizophrenia. One should
results. also recognize that onset of symptoms before age 3 is
All children with autism require a careful language almost never consistent with schizophrenia. Selective
assessment that may include hearing testing and assess- mutism can be differentiated by the child’s ability to
ment of expressive and receptive, verbal and nonverbal interact normally in some environments.
language. Speech and language therapists trained to Children exposed to severe neglect can sometimes
work with this population are an essential part of the present with symptoms that look like ASD, but these
assessment team. symptoms will usually show dramatic improvement
Children with ASD should have a neuropsychologi- when the child is in a more appropriate environment.
cal assessment at the time of initial assessment and Perhaps the most difficult differentiation is in a child
at periodic intervals thereafter. The initial evaluation with severe obsessive–compulsive disorder (OCD)
helps establish the diagnosis and a baseline level of who also has unusual interests and is somewhat rigid in
functioning. Additionally, it can be utilized to make the terms of being inflexible to changes in routines or tran-
appropriate adjustments in the child’s educational plan. sitions to a new activity. It is even further complicated
The later evaluations serve to chart progress, evaluate if attentional problems coexist. In these cases, it is im-
the success of (pharmacological, behavioral, and aca- portant to emphasize the social difficulties of children
demic) interventions, and assess for possible regression with ASD; even if the child with OCD is difficult inter-
in particular areas. personally, his or her ability to maintain eye contact,
interpret social situations and emotions, and otherwise
interact socially is relatively preserved.
Although there may initially be some difficulty in dif-
TREATMENT
ferentiating ASD from other syndromes (Table 5-3), es-
pecially in the context of considerable comorbidity, the Developing a comprehensive individual intervention
diagnosis usually becomes clear with careful differen- program for a child with ASD is a daunting task for the
tiation. Mental retardation commonly occurs in ASD, child’s parents (Figure 5-1). Each child is unique, with
Identification of developmental delay by caretaker
Evaluation by pediatrician
Referral for specialty testing
ADOS, ADI, measures of intellectual functioning and daily functioning, full physical, history, and labs
Autism spectrum disorder established
Initiation of treatment includes:
1. Implementing changes in the child’s academic program including relevant changes in the curriculum in order to tailor it
to the child’s specific needs, as well as probable speech, occupational, and physical therapy.
2. The use of behavioral programs in order to improve social and communication difficulties as well as address negative
behaviors.
3. Examination of any symptoms that may be potential target symptoms for a pharmacological intervention.
Figure 5-1 An example of the typical progression from identification, to evaluation, to treatment of a child with ASD (ADOS, Autism
Diagnostic Observation Schedule; ADI, Autism Diagnostic Inventory).
a different set of difficulties as well as strengths. The Table 5-4 Summary of Treatment Principles
child’s primary physician must work with the parents
to help make this task less overwhelming. This usually Psychosocial Interventions
means maintaining a tempered optimism about the fu- Educational
Curricula that target communication
ture and providing encouragement without being unre- Behavioral techniques
alistic. The physician can anticipate being asked about Structured milieu
Vocational training and placement: other specialized
a wide array of alternative treatments being offered in interventions such as speech and language therapy,
the community, which vary enormously in their claims, physical therapy, and occupational therapy
in the integrity of those making the claims, and in their Social skills training
Individual psychotherapy
ultimate safety and utility. It is helpful to listen and for high-functioning
then educate the family, at a level commensurate with individuals
their sophistication, about how to analyze and interpret Medical Interventions
claims and the science underlying these treatments. Cohesive physician–patient relationship
Most parents are able to incorporate information about Supportive measures with families coping with autistic
disorder
the need for controlled studies, replication, and the Behavioral treatment
importance of information being published in peer- Pharmacotherapy to address problem signs and symptoms
reviewed journals.
Autistic disorder is recognized as a chronic disorder
with a changing course requiring a long-term course
rent cure for autistic disorder or the other ASDs goals
of treatment that includes the necessity of intervention
of treatment should encompass the short-term and
with various treatments at different times (Table 5-4).
long-term needs of the individual and his or her family
At the present time, most treatments for the ASDs are
(Table 5-5). Goals for treatment, in terms of four quin-
symptom directed. Thus, treatments of the other ASDs
tessential aims, include:
are the same as those used in autistic disorder because
similar types of symptoms are targeted for treatment 1. the advancement of normal development, particularly
in each of these disorders. Given that there is no cur- regarding cognition, language, and socialization;
Table 5-5 Goals for Treatment

repetitive actions, self-injurious behaviors, or aggres-
sion. While there is little difficulty in identifying these
Advancement of normal development, particularly regarding highly visible behaviors, what is much more difficult is
cognition, language, and socialization
Promotion of learning and problem solving (1) determining the antecedents to these behaviors and
Reduction of behaviors that impede learning (2) knowing what constitutes an appropriate reaction to
Assistance of families coping with autistic disorder these behaviors on the part of the caregiver. To deter-
Treatment of comorbid psychiatric disorders
mine the antecedent is often extraordinarily difficult,
since it is often not apparent as to what exactly hap-
pened in the environment that stimulated the behav-
2. the promotion of learning and problem solving;
ior. This is particularly true if the behavior is chronic
3. the reduction of behaviors that impede the learning
and has developed some autonomous function (i.e.,
process;
no longer a stimulus–response event). To make things
4. the assistance of families coping with autism.
more complicated, it could be internal perception or the
These goals are broad in nature; therefore, it is key meaning of what happened in a child with autism (poor
to separate these goals into immediate and long-term language and socially nonresponsive) that may have
needs for each individual with ASD. Each goal requires initiated the behavior.
a distinct scheme of its own. The key to success is a gradual shaping of the behav-
Every attempt should be made to achieve treatment ior rather than dramatic expectations and harsh con-
goals in a community-based environment since insti- sequences. One should begin intervention by evaluat-
tutionalization may hinder a child’s ability to learn ing possible underlying stimuli or predisposing factors
means of functioning and adapting in typical social for the behavior. Strategies include determining when,
settings. Community-based treatment can usually be where, and for how long an activity can take place.
maintained, except in times of extreme stress or need, Additional strategies include making environmental
during which time a child (and family) might benefit changes that reduce anxiety and even ignoring behav-
from respite care or brief hospitalization. Effective iors that do not create undue problems.
treatment often entails setting appropriate expectations Up to 50% of children with ASD will not acquire
for the child and adjusting the child’s environment to useful language. For those with some but not fully in-
foster success. tact language skills, speech therapy is an important
part of therapeutic and academic planning. An empha-
sis on the social use of language is often helpful, and
when the child can articulate some of his or her needs,
Psychological Treatments
there is often a reduction in problem behaviors.
Because the autistic individual often requires diverse Longitudinal studies indicate that children who
treatments and services simultaneously, the role of the have not acquired useful language by the age of 7 usu-
primary physician is to be the coordinator of services. ally have long-standing verbal communication diffi-
Frequent visits with the child and the child’s caretak- culties. For these children, it is often helpful to devise
ers initially allow the physician to assess the individual an alternative means of communication. Some chil-
needs of the child while establishing a therapeutic alli- dren can learn sign language, although there is great
ance. An effective approach often calls for the services variability in how much each child is able to learn,
of a number of professionals working in a multidisci- difficulties with generalizing to environments other
plinary fashion. This group may include psychiatrists, than where signs are learned, and the fact that signs
pediatricians, pediatric neurologists, psychologists, continue to be used mostly to satisfy needs rather than
special educators, speech and language therapists, so- being utilized in a spontaneous social sense. Addi-
cial workers, and other specialized therapists. tionally, it seems to be best to continue to pair signs
There is significant controversy over what particular with appropriate vocalizations, however limited. Al-
forms of therapy are best for children with ASD. Some ternatively (or additionally), the use of augmentative
of this controversy is a result of claims of children communication systems may be helpful. Irrespec-
making dramatic improvements with some of these tive of the technique used, establishing a consistent
therapies. method of communication is central to the treatment
A prerequisite to putting a behavioral plan in place of individuals with ASD.
with a child with ASD is to identify the problem be- Problems with social interactions, especially recip-
haviors. These behaviors often include interfering rocal social interactions, are common to every person
with ASD. Helping individuals with ASDs address becomes the road map of interventions for children
these challenges is difficult but also critical for enhanc- with ASD.
ing overall functioning.
Three primary techniques can be effectively
Somatic Treatments
utilized:
At this time, there are no pharmacological agents with
US Food and Drug Administration (FDA) approved la-
1. Establish proximity. Proximity refers to the
beling specific for the treatment of autistic disorder or
fact that it is very helpful to have the child with
other PDDs in either children or adults. This is all the
ASD near other children in the environment. The
more problematic because many of the symptoms com-
mere proximity increases the likelihood of in-
monly seen in autistic disorder and other PDDs (ritu-
teraction and imitation as well as positive social
als, aggressive behavior, and hyperactivity) are also
reinforcement.
commonly seen in children, adolescents, and adults
2. Use prompts and reinforcement. The use of
with mental retardation but without a PDD. Some of the
prompts relates to having specific cues to use pre-
pharmacological strategies for the treatment of autistic
viously learned behaviors in social settings (e.g.,
disorder have been extrapolated from studies of related
“Raise your hand if you have a question”). Attention
conditions, largely in adults, including attention-
to reinforcement means that even a less than fully
deficit/hyperactivity disorder and OCD. While there
competent attempt at appropriate social behavior,
may not be FDA-approved treatments, there are treat-
even if it is a response to a prompt, gets clear and
ment options available. However, clinicians and families
effective reinforcement when it occurs (e.g., calling
should be reminded before any treatment is initiated
on the child promptly when he raises his hand to
that (1) current treatments target symptoms, (2) current
ask a question and also saying “You did a good job
treatments do not target a specific etiological mecha-
when you raised your hand to ask the question”).
nism for ASD, (3) anecdotal reports do not establish
Teaching such prompting and reinforcement should
efficacy, effectiveness, or safety for any treatment, (4)
be for everyone who interacts with the individual
controlled, double-blind trials (preferably with replica-
with ASD.
tion) are the contemporary standard for determining if
3. Encourage peer initiation. It is helpful to train
a treatment is safe and appropriate, and (5) all treat-
peers who are likely to interact with the child or
ments have side effects.
adult with ASD in techniques for initiating social
Before specific pharmacological agents are dis-
contact. For many individuals, this means explain-
cussed, it must be stressed that one should not use
ing the disability and dealing with fears or biases.
psychopharmacological agents with the expectation
For others, it may mean encouraging them to per-
that they will cure children with autistic disorder.
sist in their attempts at engagement, even in the face
Although this seems obvious, one should realize that
of limited, inappropriate, or inadequate responses.
many parents and teachers of children with autistic
Persistence usually leads to familiarity and eventu-
disorder expect medication to eliminate core social,
ally to some level of social engagement.
cognitive, and communication dysfunction. There is
no pharmacological substitute for appropriate edu-
Considering the many needs of the child with ASD, cational, behavioral, psychotherapeutic, vocational,
academic resources and placement naturally emerge as and recreational programming. It is essential to re-
important components to the child’s overall treatment. member and to remind parents, teachers, and others
The reasons for this are manifold. First and foremost, that medication should always be seen as an adjunct
schools are where children go to acquire social skills to these core interventions that address the develop-
and acquaintances, as well as academic skills. Second, mental challenges associated with these disorders.
schools often have a variety of skilled professionals The clinician providing the medication should reiter-
who are trained to provide necessary services for the ate this message to the parents and others involved in
individual with ASD. And, finally, in the United States, the child’s treatment by consistently reminding them
all public schools have a statutory obligation to pro- of the specific behavioral targets of the medication,
vide all children (even those with disabilities) with a and assessing the effectiveness of the medication in
free and appropriate education in the least restrictive the context of change in these behavioral symptoms,
environment. Thus, schools often become the base and and how the pharmacotherapy facilitates the other
the requisite individualized educational plan (IEP) interventions.
Psychopharmacological Approach to
4. Medication should be selected on the basis of po-
Table 5-6 Presenting Symptoms in Pervasive tential effects on target symptoms and there should
Developmental Disorders be an established way of specifically monitoring the
Rituals, Compulsions, Irritability response to the treatment over time.
Potent serotonin transporter inhibitors 5. A careful assessment of the risk/benefit ratio must
Selective serotonin reuptake inhibitor be made before initiating treatment and, to the ex-
Fluoxetine 5–80 mg/d in a single dose
Paroxetine 2.5–50 mg/d in one or two divided doses
tent possible, the individual’s caretakers and the in-
Sertraline 25–200 mg/d in one or two divided doses dividual must understand the risks and benefits of
Fluvoxamine 25–300 mg/d in two or three divided the treatment.
doses
Citalopram 5–40 mg/d in a single or two divided doses
Tricyclic antidepressants
Clomipramine 25–250 mg/d in one or two divided Antidepressants. SSRI medications are most effective
doses when insistence on routines or rituals are present to the
Hyperactivity, Distractibility, Impulsivity point of manifest anxiety or aggression in response to
Stimulant medications interruption of the routines or rituals, or after the onset
Methylphenidate 5–60 mg/d in three to five divided of another disorder such as major depressive disorder
doses
Dextroamphetamine 5–60 mg/d in three to five divided or OCD. The common side effects associated with SS-
doses RIs are motor restlessness, insomnia, elation, irritabil-
Clonidine 0.05–0.3 mg/d in one to three divided doses or by
transdermal skin patch
ity, and decreased appetite, each of which may occur
Naltrexone 0.5–2.0 mg/kg/d in a single dose alone or, more often, together. Because many of these
Aggression, Irritability symptoms may be present in the often cyclical natural
Sympatholytics course of ASD before the medication is initiated, the
Propranolol 20–400 mg/d in three to four divided emergence of new symptoms, a different quality of the
doses
Nadolol 40–400 mg/d in a single dose symptoms, and occurrence of these symptoms in a new
Anticonvulsants cluster are clues that the symptoms are side effects of
Carbamazepine to a blood level of 4–12 ng/mL medication rather than part of the natural course of the
Valproate to a blood level of 50–100 ng/mL
Lithium to a serum level of 0.8–1.2 mEq/L disorder.
Neuroleptics
Naltrexone 0.5–2.0 mg/kg/d in a single dose
Stimulants. Small but significant reductions in inatten-
tion and hyperactivity ratings may be seen in children
The use of medications to treat autistic disorder and with autistic disorder in response to stimulants such as
other ASDs appears to have significant potential as an methylphenidate and dextroamphetamine. However,
adjunct to educational, environmental, and social inter- stereotypies may worsen, so drug trials must always be
ventions. It is a reasonable goal for the pharmacothera- assessed to determine whether the therapeutic effects
pist to adopt the judicious use of psychopharmacologi- outweigh side effects. A key distinction in assessing at-
cal agents, such as SSRIs or Clomipramine (Table 5-6) tentional problems of children with ASD is the distinc-
to assist in alleviating symptoms that have been found tion between poor sustained attention (characteristic of
to respond to pharmacological intervention. This focus children with attention-deficit/hyperactivity disorder)
on facilitating adaptation requires attention to five im- and poor joint attention (characteristic of children with
portant principles: autistic disorder). Problems in joint attention require
educational and behavioral interventions or treatment
1. Environmental manipulations, including behavioral of rituals with a potent serotonin transporter inhibitor.
treatment, may be as effective as, if not more ef- Problems in maintenance of attention of the type seen
fective than, medication for selected symptomatic in attention-deficit/hyperactivity disorder are more
treatment. likely to respond to stimulants.
2. It is essential that the living arrangement for the in-
dividual must ensure safe and consistent administra- Sympatholytics. The α2-adrenergic receptor agonist
tion and monitoring of the medication to be used. clonidine may reduce irritability as well as hyperac-
3. Individuals with autistic disorder and other ASDs tivity and impulsivity; however, tolerance developed
often have other DSM-IV-TR Axis I disorders. If a several months after initiation of the treatment in each
comorbid DSM-IV-TR Axis I disorder is present, child who was treated long-term. Tolerance was not
standard treatment for that disorder should be initi- prevented by transdermal skin patch administration of
ated first. the drug. However, tolerance may have been reduced in
several cases by administering clonidine in the morn- impulsivity, and aggression. The anticonvulsant class to
ing and then 6 to 8 hours later with a 16- to 18-hour be avoided, when possible, is the category comprising
interval between the last dose of one day and the first barbiturates (e.g., phenobarbital). Because barbiturates
dose of the next day. If tolerance does develop, the dose have been associated with hyperactivity, depression,
should not be increased because tolerance to sedation and cognitive impairment, they should be changed to
does not occur, and sedation may lead to increased ag- an alternative drug, depending on the seizure type. In
gression due to disinhibition or decreased cognitive addition, phenytoin (Dilantin) is sedating and causes
control of impulses. Adrenergic receptor antagonists, hypertrophy of the gums and hirsutism, which may
such as propranolol and nadolol, have not been tested contribute to the social challenges for people with
in double-blind trials in ASD. However, open trials autistic disorder. Carbamazepine and valproate may
have reported the use of these medications in the treat- have positive psychotropic effects, particularly when
ment of aggression and impulsivity in developmental cyclical irritability, insomnia, and hyperactivity are
disorders. present. Several children with autistic disorder were
treated with valproic acid after electroencephalograph-
Typical Neuroleptics. Reduction of fidgetiness, inter- ical abnormalities were found. These children had an
personal withdrawal, speech deviance, and stereotypies improvement in behavioral symptoms associated with
has been documented in response to Trifluoperazine, autistic disorder after valproate treatment.
thioridazine, haloperidol, and pimozide. However, in-
dividuals with autistic disorder are as vulnerable to Naltrexone. Naltrexone has little efficacy in treat-
potentially irreversible tardive dyskinesia as any other ing the core social and cognitive symptoms of autistic
group of young children with a mental disorder. Owing disorder. It may have, however, a role in the treatment
to the often earlier age at initiation of pharmacotherapy, of self-injurious behavior, although the controlled data
individuals with ASD treated with typical neuroleptics are equivocal. Potential side effects include nausea and
may be at higher risk because of the potential increased vomiting. Controlled trials in autistic disorder have not
lifetime exposure of medication. These medications shown liver dysfunction or other physical side effects.
also have significant additional side effects of varying Naltrexone may have an adverse effect on the outcome
sorts and severity that should significantly limit their of Rett’s disorder.
routine use in the care of individuals with ASD, espe-
cially as first-line treatments.
Lithium. Adolescents and adults with autistic disorder
often exhibit symptoms in a cyclic manner and so there
Atypical Neuroleptics. Because of the positive re-
is much interest in how these individuals might respond
sponse of many children with autistic disorder to typi-
to agents typically used in bipolar disorder. A single
cal neuroleptics, similar medications with reduced risk
open trial of lithium revealed no significant improve-
of tardive dyskinesia must be considered. In addition,
ment in symptoms in individuals with autistic disorder
atypical neuroleptics are often effective in treating the
without bipolar disorder.
negative symptoms of schizophrenia, which seem simi-
lar to several of the social deficits in autistic disorder.
Both risperidone and olanzapine have shown promise Anxiolytics. Benzodiazepines have not been studied
in reducing hyperactivity, impulsivity, aggressiveness, systematically in children and adolescents with autis-
and obsessive preoccupations. It seems clear that atypi- tic disorder. However, their use in reducing anxiety in
cal neuroleptics will likely play a role for the treatment short-term treatment, such as before dental procedures,
of carefully selected individuals with severe symptoms is similar to their use in management of anxiety in peo-
of ASD. ple without a PDD.
Anticonvulsants. Because 25–33% of individuals

with autistic disorder have seizures, the psychophar-
DIAGNOSTIC CRITERIA
macological management of individuals with autistic
disorder or other ASD must take into consideration The DSM-IV-TR and ICD-10 item sets and diagnostic
the past or current history of epilepsy and the potential algorithms for autistic disorder are almost identical.
role of anticonvulsants. Unfortunately, very few studies However, the ICD-10 exclusion criterion is consider-
have been undertaken in this area. In a small open trial ably more broad, requiring that a number of other dis-
of divalproex in 2001, 10 of 14 individuals responded orders should be considered instead (e.g., early onset
favorably, showing improvements in affective stability, schizophrenia, mental retardation with an associated
emotional or behavioral disorder). In ICD-10, this dis- Regarding childhood disintegrative disorder, the
order is referred to as childhood autism. DSM-IV-TR and ICD-10 item sets and diagnostic al-
The DSM-IV-TR and ICD-10 item sets and diagnos- gorithms are identical except for the C criterion, in
tic algorithms for Rett’s disorder and Asperger’s dis- which ICD-10 also allows for a “general loss of inter-
order are almost identical. In ICD-10, these disorders est in objects and the environment.” In ICD-10, this
are referred to as Rett’s syndrome and Asperger’s syn- disorder is referred to as other childhood disintegra-
drome, respectively. tive disorder.
CHAPTER
Attention-Deficit and Disruptive
Behavior Disorders
DIAGNOSIS
by the absence of any CD behaviors before 10 years
Attention-deficit/hyperactivity disorder (ADHD), of age.
conduct disorder (CD), and oppositional-defiant dis- The essential feature of ODD is a recurrent pattern
order (ODD) form the attention-deficit and disrup- of negativistic, defiant, disobedient, and hostile behav-
tive behavior disorders (AD-DBDs) in DSM-IV-TR. ior toward authority figures that persists for at least
As a group, these are the most common disorders 6 months.
of childhood. There is also an increasing recogni- The rationale for grouping ADHD, CD, and ODD
tion that these disorders continue into adulthood. In is that similar areas of difficulty are present in chil-
DSM-IV-TR, ADHD is defined as a persistent pattern dren with these disorders. Academic difficulties, poor
of inattention and/or hyperactivity–impulsivity that social skills, and overrepresentation of boys are among
is more frequently displayed and more severe than the shared characteristics. Further, the three disorders
is typically observed in individuals at a comparable demonstrate a commonality of core symptoms, with
level of development. Three subtypes of ADHD are impulsivity being prominent in all three conditions.
identified: (1) a predominantly hyperactive–impulsive Not surprisingly, there is a high degree of comorbidity
type, (2) a predominantly inattentive type, and (3) a among the three disorders.
combined type. In order to qualify for the diagnosis, The clinical evaluation of a child with possible
at least some of the symptoms must have been present AD-DBD requires a multisource, multimethod ap-
and caused impairment before age 7 years. Addition- proach. In addition to clinical interviews of parents
ally, some symptoms causing impairment in social or and children, supplemental information may be ob-
academic/occupational functioning must be evident in tained from school reports, rating scales completed by
more than one setting. ADHD can be diagnosed in in- teachers and parents, neuropsychological test data and
dividuals of all ages, although it is sometimes difficult direct observations of the child. In addition, several
to establish the childhood onset of symptoms in older structured and semistructured interviews are available,
individuals. although these tend to be used primarily in research
The essential feature of CD is a repetitive and persist- settings. Generally, adults are considered to be the best
ent pattern of behavior in which the basic rights of oth- informants of disruptive behaviors, although children
ers or major age-appropriate societal norms or rules are and adolescents may provide important data regarding
violated. Similar to ADHD, symptoms of CD are seen internalizing symptoms and some infrequent behavior
in multiple settings and cause significant impairment problems, such as antisocial acts.
in functioning. Adults with conduct problems, whose Rating scales facilitate the systematic acquisition of
behavior does not meet criteria for antisocial personal- information about the child’s behavior in different set-
ity disorder, may have symptoms that meet criteria for tings in a cost-effective manner. Most are standardized
CD and thus qualify for the diagnosis. Subtypes of CD and provide scores that are norm referenced by age and
are determined on the basis of age of onset. The child- gender. The systematic use of these instruments ensures
hood-onset subtype is diagnosed in children who show that a complete set of specific behaviors is assessed at
at least one of the behaviors before the age of 10 years, different points in time, enabling comparisons over the
while the adolescent-onset subtype is characterized course of treatment.

314.0X ATTENTION-DEFICIT/HYPERACTIVITY DISORDER
A. Either (1) or (2)

(1) Six (or more) of the following symptoms of “inattention” have persisted for at least 6 months to a degree that is maladap-
tive and inconsistent with developmental level:
Inattention
(a) often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
(b) often has difficulty sustaining attention in tasks or play activities.
(c) often does not seem to listen when spoken to directly.
(d) often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace.
(e) often has difficulty organizing tasks and activities.
(f) often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort.
(g) often loses things necessary for tasks or activities.
(h) is often easily distracted by extraneous stimuli.
(i) is often forgetful in daily activities.
(2) Six (or more) of the following symptoms of “hyperactivity–impulsivity” have persisted for at least 6 months to a degree
that is maladaptive and inconsistent with developmental level:
Hyperactivity
(a) often fidgets with hands or feet or squirms in seat.
(b) often leaves seat in classroom or in other situations in which remaining seated is expected.
(c) often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be
limited to subjective feelings of restlessness).
(d) often has difficulty playing or engaging in leisure activities quietly.
(e) is often “on the go” or often acts as if “driven by a motor.”
(f) often talks excessively.
Impulsivity
(g) often blurts out answers before questions have been completed.
(h) often has difficulty awaiting turn.
(i) often interrupts or intrudes on others.
B. Some hyperactive–impulsive or inattentive symptoms that caused impairment were present before age 7 years.
C. Some impairment from the symptoms is present in two or more settings (e.g., at school [work] and at home).
D. There must be clear evidence of clinically significant impairment in social, academic, or occupational functioning.
E. The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other
Psychotic Disorder and are not better accounted for by another mental disorder (e.g., Mood Disorder, Anxiety Disorder,
Dissociative Disorder, or a Personality Disorder).
Code based on type:
314.01 Attention-Deficit/Hyperactivity Disorder, Combined Type: if both Criteria A1 and A2 are met for the past 6
months;
314.00 Attention-Deficit/Hyperactivity Disorder, Predominantly Inattentive Type: if Criterion A1 is met but Criterion A2 is
not met for the past 6 months;
314.01 Attention-Deficit/Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type: if Criterion A2 is met but
Criterion A1 is not met for the past 6 months.
Coding note: For individuals (especially adolescents and adults) who currently have symptoms that no longer meet full crite-
ria, “In Partial Remission” should be specified.
Reprinted with permission from the Diagnostic and Statistical Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 American Psy-
chiatric Association.
There is an ever-growing number of rating scales, all symptoms of ADHD and common comorbidities,
but the most commonly used are the Conners Teach- and therefore some structured questioning is usually
ers Rating Scale—Revised (CTRS-R) and the Child required.
Behavior Checklist (CBCL), which are available in Psychological and cognitive test performance is
parent and teacher versions and possess solid norma- generally not required to determine the presence of
tive bases. Rating scales have several limitations, and an AD-DBD. Nevertheless, because the AD-DBDs
diagnoses should not be made on the bases of these are frequently associated with learning problems, neu-
data alone. Interviews with children and their parents ropsychological testing may be indicated, particularly
form the core of the clinical evaluation. In clinical when assessment of cognitive functioning is required.
practice, interviews usually follow a loosely structured Information from a neuropsychological and/or educa-
format with a flexible approach that allows for the in- tional evaluation can often be used to supplement the
depth exploration of relevant clinical information. It is clinical evaluation by providing an understanding of
essential that the interviewer directly enquires about the individual child’s level of cognitive and attentional
Chapter 6 • Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders 51

312.8X CONDUCT DISORDER
A. A repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate societal norms
or rules are violated, as manifested by the presence of three (or more) of the following criteria in the past 12 months, with
at least one criterion present in the past 6 months.
Aggression to people and animals
(1) often bullies, threatens, or intimidates others.
(2) often initiates physical fights.
(3) has used a weapon that can cause serious physical harm to others.
(4) has been physically cruel to people.
(5) has been physically cruel to animals.
(6) has stolen while confronting a victim.
(7) has forced someone into sexual activity.
Destruction of property
(1) has deliberately engaged in fire setting with the intention of causing serious damage.
(2) has deliberately destroyed others’ property.
Deceitfulness or theft
(1) has broken into someone else’s house, building or car.
(2) often lies to obtain goods or favors or to avoid obligations.
(3) has stolen items of nontrival value without confronting a victim.
Serious violations of rules
(1) often stays out at night despite parental prohibitions, beginning before age 13 years.
(2) has run away from home overnight at least twice while living in parental or parental surrogate home.
(3) is often truant from school, beginning before age 13 years.
B. The disturbance in behavior causes clinically significant impairmant in social, academic or occupational functioning.
C. If the individual is age 18 years or older, criteria are not met for Antisocial Personality Disorder.
Code based on age at onset:
312.81 Conduct Disorder, Childhood-Onset Type: onset of at least one criterion characteristic of Conduct Disorder prior to
age 10 years
312.82 Conduct Disorder, Adolescent-Onset Type: absence of any criteria characteristic of Conduct Disorder prior to age
10 years
312.89 Conduct Disorder, Unspecified Onset: age at onset is not known
Specify severity:
Mild: few if any conduct problems in excess of those required to make the diagnosis and conduct problems cause only minor
harm to others (e.g., lying, truancy, staying out after dark without permission)
Moderate: number of conduct problems and effect on others intermediate between “mild” and “severe” (e.g., stealing without
confronting a victim, vandalism)
Severe: many conduct problems in excess of those required to make the diagnosis or conduct problems cause consider-
able harm to others (e.g., forced sex, physical cruelty, use of a weapon, stealing while confronting a victim, breaking and
entering)
functioning, as well as screening for suspected mental social skills, the presence of internalizing symptoms,
retardation or learning disabilities. and response to treatment.
At the present time, there are no laboratory measures There is a high rate of comorbidity among the three
that can serve as diagnostic tools for AD-DBDs. Simi- disorders that comprise the AD-DBD group and several
larly, findings from neuroimaging studies have neither other diagnostic categories Among the AD-DBDs, ap-
been consistent enough nor specific enough to warrant proximately 90% of children with CD would also meet
their use as diagnostic tools. the criteria for ODD. Furthermore, 40% of children
Many children with AD-DBDs have impaired social with ADHD also have ODD and 40% of children with
skills and consequently experience difficulties with ODD have ADHD. In terms of the comorbidity of the
peer relationships. Information regarding social adjust- AD-DBD group with other diagnostic categories, it has
ment is crucial in treatment planning, since increased been estimated that 15–20% of children with ADHD
impairment in social and school function is predictive have comorbid mood disorders, 20–25% have anxiety
of poor outcome. Parent–child interactions also play a disorders and 6–20% have learning disabilities. Other
role in the maintenance of disruptive behaviors, poor conditions which may occur comorbidly with the
childhood cases that persist into adulthood to range

DSM-IV-TR Diagnostic Criteria from 4% to 75%. These highly variable rates may be
313.81 OPPOSITIONAL-DEFIANT DISORDER
accounted for by methodological differences. Factors
that appear to predict the persistence of ADHD into
A. A pattern of negativistic, hostile, and defiant behavior adulthood include a positive family history for ADHD
lasting at least 6 months, during which four (or more)
of the following are present: and the presence of psychiatric comorbidity, particu-
larly aggression.
(1) often loses temper.
(2) often argues with adults.
(3) often actively defies or refuses to comply with
adults’ requests or rules. Course
(4) often deliberately annoys people.
(5) often blames others for his or her mistakes or Some behaviors characteristic of the AD-DBDs are
misbehavior. observable as early as the preschool years. Hyperactiv-
(6) is often touchy or easily annoyed by others.
(7) is often angry and resentful.
ity and attentional problems emerge gradually and may
(8) is often spiteful or vindictive. overlap with the emergence of oppositional behaviors,
Note: Consider a criterion met only if the behavior occurs giving the appearance of a simultaneous, rather than
more frequently than is typically observed in individuals a sequential, onset. It is now recognized that while
of comparable age and developmental level. hyperactivity and, to a lesser extent, attentional prob-
B. The disturbance in behavior causes clinically signifi- lems show a gradual decline through adolescence and
cant impairment in social, academic, or occupational
functioning. adulthood, many individuals with ADHD continue to
C. The behaviors do not occur exclusively during the have attentional, behavioral and emotional problems
course of a Psychotic or Mood Disorder. well into adolescence and adulthood. Typically, adults
D. Criteria are not met for Conduct Disorder, and, if the
individual is age 18 years or older, criteria are not met with ADHD are less overtly overactive, although they
for Antisocial Personality Disorder may retain a subjective sense of restlessness. Impair-
Reprinted with permission from the Diagnostic and Statistical ment in these adults is more often a result of inatten-
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 tion, disorganization, and impulsive behavior.
The developmental course of oppositional behaviors
shows greater variability. When the oppositionality is
AD-DBDs include Tourette’s disorder (TD), drug and of a persistent nature and lasts beyond the preschool
alcohol abuse or dependence, and mental retardation. years, the escalation to more disruptive behaviors is
Studies examining prevalence rates of the AD-DBDs more likely. In most oppositional children, who are
in community samples are characterized by considera- usually not physically aggressive, oppositional behav-
ble variability, although rates are generally high. While iors peak around age 8 years and decline beyond that.
DSM-IV-TR estimates the prevalence rates for ADHD In a second group of children, delinquent behaviors fol-
to range from 2% to 7% in school-age children, rates low the onset of oppositional behaviors. Early physical
as high as 17.1% have been reported in community sur- aggression is a key predictor of this latter trajectory.
veys. Rates for CD have been estimated to be as low Generally, conduct problems first appear in middle
as 0.9% for school-age children but as high as 8.7% childhood. In males, the progression to more serious
in adolescents. The overall prevalence of ODD varies forms of conduct problems, such as rape or mugging,
across studies from 5.7% to 9.9%. generally emerge after age 13 years. When CD is seen
In school-age children, boys have higher rates than in adolescence for the first time, the problems tend to
girls for all three disorders. In clinic settings, the ratio diminish by adulthood.
of boys to girls is about 9 : 1, but in community sam- Considerable data indicate that a subgroup of
ples, this decreases to approximately 3 : 1. Furthermore, hyperactive children show high rates of delinquency
teachers tend to identify fewer girls than boys as hav- and substance abuse during adolescence, and this con-
ing ADHD symptoms. The combined type of ADHD is tinues into adulthood. However, it is likely because of
the most common subtype in both genders. However, the comorbidity with CD or bipolar disorder that higher
in the predominantly hyperactive–impulsive subtype rates of substance abuse are found in adolescents with
of ADHD, the male-to-female ratio is approximately ADHD
4 : 1, while in the predominantly inattentive subtype
the ratio falls to 2 : 1. In general, prevalence declines
with age, but follow-up studies of children and adoles-
cents indicate that the disorder frequently persists into Proper differential diagnosis of ADHD, CD, and ODD
adulthood. Longitudinal studies have reported rates of requires not only discrimination among the three
disorders but also from a wide range of other psychiat- symptoms of ODD and ADHD are usually not present
ric, developmental, and medical conditions. Among the during early childhood. It has been shown that children
AD-DBDs, the relationship between ADHD and CD with ODD demonstrate lower degrees of impairment
has been the most studied. It is now generally accepted and are more socially competent as compared to chil-
that the two disorders can be differentiated despite the dren with CD. Furthermore, children with CD come
high degree of overlap, both in terms of symptom pres- from less-advantaged families, and have greater con-
entation and co-occurrence within individuals. ADHD flict with school and judicial systems as compared to
can be conceptualized as a cognitive/developmental children with ODD. Family adversity scores in children
disorder, with an earlier age of onset than CD. ADHD with ODD are usually intermediate between those of
children more frequently show deficits on measures of children with CD and normal children.
attentional and cognitive function, and have increased Mood and anxiety disorders, learning disorders,
motor activity and greater neurodevelopmental abnor- mental retardation, pervasive developmental disor-
malities. In contrast, CD children tend to be character- ders, organic mental disorders, and psychotic disorders
ized by higher levels of aggression and greater familial may all present with impairment of attention, as well
dysfunction. as hyperactive/impulsive behaviors. The diagnosis of
A significant proportion of children present with ADHD in DSM-IV-TR requires that the symptoms of
symptoms of both ADHD and CD, and both condi- inattention/cognitive disorganization and impulsivity/
tions should be diagnosed when this occurs. Comorbid hyperactivity are not better accounted for by one of the
ADHD and CD are consistently reported to be more above conditions. Differentiating ADHD from bipolar
disabling than either disorder alone. These children re- disorder in childhood is complicated by the low base
tain the difficulties found in both disorders and tend rate of bipolar disorder and the variability in clinical
to show increased levels of aggressive behaviors at an presentation. Even though there are phenomenological
early age, which remain remarkably persistent. This similarities between the two disorders, there is little
is in contrast to the more typical episodic course seen evidence to suggest that most children with externaliz-
in children who have CD alone. Finally, children with ing symptoms are at risk for bipolar disorder. A positive
comorbid ADHD and CD appear to have a poorer long- family history of bipolar disorder is especially helpful
term outcome than those with either disorder alone. in diagnosing bipolar disorder in children. In addition, a
The relationship of ADHD to ODD is less well variety of medical conditions such as epilepsy, Tourette’s
studied. However, it does appear that among children disorder, thyroid disease, postinfectious and/or post-
with ADHD, those who are most hyperactive/impul- traumatic encephalopathy, and sensory impairments
sive are at greatest risk for developing ODD. Despite can present with symptoms similar to ADHD and must
the high degree of comorbidity, it is possible to dis- also be considered. Finally, many medications that are
tinguish between the two disorders. ODD symptoms, prescribed to children can mimic ADHD symptomatol-
such as “loses temper,” “actively defies,” and “swears,” ogy. Examples include anticonvulsants (e.g., phenobar-
are less characteristic of children with ADHD. In gen- bital), antihistamines, decongestants, bronchodilators
eral, the onset of ODD symptoms peaks by age 8 years (e.g., theophylline), and systemic steroids.
and shows a declining course thereafter. On the other
hand, hyperactivity and attentional problems appear at
TREATMENT
a much earlier age and often persist, although the levels
of inattentiveness and/or hyperactivity often decrease Successful treatment planning in children with
with age. AD-DBDs requires consideration of not only the core
The relationship of ODD and CD is more com- symptomatology but also of family and social factors
plex. The question has been raised as to whether these and comorbidity with other disorders. Given the het-
diagnoses constitute different levels of severity of a erogeneity of the three disorders that make up the AD-
single phenomenon, or whether they should be viewed DBDs, the wide-ranging effects of the disruptive behav-
as distinct. A diagnosis of CD supersedes ODD since iors, the high rates of comorbidity, and the presence of
approximately 90% of children with CD would also associated features such as learning disabilities, multi-
meet the criteria for ODD. Although the majority of modal treatments (i.e., psychopharmacologic and psy-
ODD children will not develop CD, in some cases ODD chosocial) are almost always warranted. Nevertheless,
appears to represent a developmental precursor of CD. good response can be achieved with either treatment
In cases where ODD precedes CD, the onset of CD is alone in certain instances (e.g., medication treatment
typically before age 10 years (childhood-onset CD). In for uncomplicated ADHD or ADHD ⫹ ODD; psy-
children who have the onset of CD after age 10 years, chosocial treatment for ADHD ⫹ anxiety disorder). A
diagnosis of ODD without any comorbid condition will Regardless of one’s view regarding the first choice
usually be responsive to behavioral intervention with- stimulant, and although the different stimulants work
out medication. One should always attempt, however, on average about as well as one another, nonresponders
to rule out the possibility that ADHD is also present. to one medication may respond well to another, since
Similarly, treatment of children with CD without co- their mechanisms of action are not identical.
morbidity usually involves psychosocial interventions Adverse effects (AE) of stimulants are generally mild,
with the possibility of augmenting treatment with one but occasionally can become problematic. The most
of several pharmacological agents. In contrast, comor- commonly observed AEs include headache, abdominal
bid ADHD ⫹ CD almost always requires medication, pain, decreased appetite (with or without weight loss),
and medication response is augmented if psychosocial and initial insomnia. There are slight increases in pulse
treatment is offered concomitantly. and BP, which are not very meaningful at the group
level, but can take on greater significance for particular
individuals. Affective changes, including blunted affect,
Somatic Treatments
irritability, and mood lability can also be seen, either at
Psychostimulants. It is well established that psychos- peak dose or when the dose wears off. Use of longer-act-
timulants are extremely effective in treating a wide range ing psychostimulants tends to minimize mood lability
of disruptive behaviors above and beyond their effects and other AEs that are often considered to be a reflec-
on ADHD. Nevertheless, ADHD remains the primary tion of the on–off effects that are more frequently seen
indication for the use of these medications. Methylphe- with IR preparations. Motor or vocal tics can develop or,
nidate (MPH), dextroamphetamine (DEX), and mixture more often, can be exacerbated, but there has been a con-
of amphetamine salts (MAS) (which is a mixture of sev- vergence of evidence that stimulant treatment does not
eral amphetamine compounds, 75% of which is DEX) necessarily exacerbate tics. There has been some con-
have all been shown to be effective in treating ADHD. cern that stimulants can precipitate psychotic symptoms
The stimulants produce significant improvement in such as hallucinations, although this is very rare and
attention, hyperactivity, impulse control, and aggres- almost always seen as a reflection of excessive dosing
siveness, leading to better organization of behavior, task or use in individuals with disorders other than ADHD
completion, and self-regulation. There is a fairly robust (e.g., psychotic disorders). The FDA has recently added
improvement in social skills, as evidenced by peer rat- a warning about the potential for psychotic symptoms
ings and parent and teacher ratings of social function. emerging with stimulant treatment.
There is also improvement in academic productivity, al-
though change in actual academic performance has been Atomoxetine. Atomoxetine (Strattera) is a medica-
more difficult to demonstrate. Although most data with tion with highly potent and selective activity to block
stimulants have been obtained in samples of school-age the noradrenergic transporter. It is structurally distinct
children with ADHD, there is increasing recognition that from both the stimulants and the tricyclic antidepres-
stimulants can be used successfully across the lifespan. sants and is the first nonstimulant medication labeled
The decision to prescribe psychostimulant medica- for the treatment of ADHD.
tion is best undertaken following a comprehensive as- Atomoxetine can be administered on either a twice-
sessment, with full consideration given to the range daily or once-daily schedule, despite the fact that its
of pharmacologic and nonpharmacologic treatment half-life in the overwhelming majority of individuals is
options that are available. Several of the rating scales 4 hours. Despite this fact, therapeutic benefit seems to
used in assessment (e.g., the Conners questionnaires) be maintained over the full day. Adverse effects with
are sensitive to medication effects and can be used to atomoxetine have been relatively mild, with decreased
monitor adequacy of dose and maintenance of medica- appetite and a small increase in pulse and blood pres-
tion effects. Prior to a trial with any of the stimulants, sure being the two most consistent findings. Because
baseline data should be obtained, including general it is not a stimulant, and because its effects are highly
medical status, and more specific evaluations of height, selective for NA and not DA, atomoxetine is thought to
weight, blood pressure, and a complete blood count. not have abuse potential.
The decision regarding which stimulant to select is
best determined by considering properties intrinsic to Tricylic Antidepressants. The noradrenergic tri-
the different medications—such as duration of activity cyclic antidepressants, principally imipramine and
and adverse effect profile—as well as the circumstances desipramine, have been the most extensively studied
of the individual (e.g., when is peak medication level and, until the mid-1990s, were the most often pre-
needed most, what is the individual’s lifestyle, etc.). scribed nonstimulant medication for individuals with
ADHD. In the case of both of these medications, car- they may be particularly useful in individuals whose
diac side effects are of concern and premedication tics worsen on a stimulant medication. These agonists
workup must include at least an EKG. Tachycardia and have also been used in combination with a stimulant.
postural hypotension are commonly seen but are not There have been, however, safety considerations in-
often problematic. Prolongation of the PR and QT involving this combination. These primarily involve the
tervals may be a greater source of concern and should possibility of additive risk of rebound hypertension of
be reviewed with a pediatric cardiologist. The deci- alpha-2 agonists with the mild increase in pulse and
sion to prescribe tricyclics for ADHD children must be blood pressure from stimulants.
made with the knowledge that several sudden deaths Clonidine has been the most often studied of the
have been reported in children taking desipramine. Al- alpha-2s, although the empirical database for both clo-
though it has been argued that data do not support the nidine and guanfacine remains quite small.
conclusion that tricyclics have a high degree of cardio- The most common side effect of the alpha-2 medica-
vascular toxicity in children, proper informed consent tions is sedation, although this tends to decrease after
should be obtained. It should also be noted that neither several weeks. Dry mouth, nausea, and photophobia
imipramine nor desipramine is FDA approved for the are among the other adverse effects reported. At high
treatment of ADHD children. doses, hypotension and dizziness are also possible.
Glucose tolerance may decrease, especially in those at
Other Antidepressants. Bupropion and venlafaxine risk for diabetes. It is important to carefully evaluate
are chemically unrelated to other known antidepres- cardiovascular function when using the alpha-2 ago-
sants. Both have been studied for their potential utility nists, especially when used in combination with stimu-
in the AD-DBDs. Bupropion in ADHD is not generally lant treatment as noted earlier. Additionally, there have
believed to be effective as stimulants. There are similar been reports of sudden death in three cases treated
but more preliminary data indicating that venlafaxine with the combination of clonidine and methylpheni-
might be useful for ADHD. date, although a review of this situation by the FDA
concluded that these unfortunate events were not attrib-
Serotonin Reuptake Inhibitors. Clomipramine, a utable to the combination. However, careful monitoring
mixed noradrenergic and serotonergic agonist, and is required. Since clonidine is not FDA approved for
fluoxetine, a selective serotonin reuptake inhibitor use in ADHD, informed consent should clearly indi-
(SSRI), have been used occasionally in the treatment cate that this is an “off-label” treatment.
of children with ADHD. Although there have been
no studies using SSRIs in ADHD and comorbid CD/ Other Agents. A variety of other pharmacotherapeu-
ODD, these medications are of some interest in light of tic agents have been utilized in the treatment of aggres-
recent findings implicating serotonergic mechanisms sion and episodic dyscontrol, although efficacy in chil-
in aggression and reported utility of fluoxetine in treat- dren with comorbid ADHD and CD has not yet been
ing adults with impulsive aggression. At present, there demonstrated. Among these medications, lithium has
are no controlled trials to support the efficacy of the been the best studied.
SSRIs for the core symptoms of ADHD, and their role Neuroleptic medications have also been used in treat-
in treating comorbid ADHD and CD/ODD is inferen- ment of the AD-DBDs, principally to treat children with
tial only. severe behavioral problems characterized by aggres-
sion and combativeness. Although older neuroleptics
Alpha-2-adrenergic Agonists. Because of their role such as chlorpromazine, thioridazine, and halperidol
in treating overarousal and aggression, the alpha-2 ago- are FDA approved for the treatment of severe behav-
nists seem to be suited for use in children with comor- ior problems in children, they are infrequently used at
bid ODD/CD/aggression. They have been effective in present. Recently, there has been more interest in the
treating individuals suffering from ADHD who either atypical neuroleptics, such as risperidone, because of
have diagnosed tic disorders, or are at increased risk their low risk of TD and other side effects.
to develop them, such as those children with a positive During the course of the last few years, there has
family history of tics. This is particularly important been a remarkable increase in the number of medica-
since as many as 40–60% of individuals with Tourette’s tions that are used in the treatment of ADHD and CD.
syndrome seen in psychiatric settings also have ADHD, It is important to keep in mind that the majority of the
and many of these individuals have significant behavior medications are not approved by the FDA for specific
problems. Although the alpha-2 agonists may be less use in ADHD and/or CD and as such their use for these
effective than stimulants in the treatment of ADHD, two disorders continues to be “off-label”. An additional
complication is that, in general, prescribing practices conducted at six performance sites across the US and
tend to vary among different settings and even among Canada, that examined the comparative response to
different physicians in the same setting. Consequently, 14 months of medication and psychosocial treatments,
less than optimal treatment is likely to result in inad- administered alone or together, in 579 seven- to nine-
equate or partial improvement. year-old children with combined subtype ADHD. The
principal objectives of the study were to determine the
Psychosocial Treatments. A variety of psychoso- relative effectiveness of the three active treatments in
cial therapies, such as behavior therapy, contingency comparison to one another, and in comparison with
management, and cognitive behavioral therapy (CBT), community standard care. The study indicated that, for
have been found to be useful for treating children with ADHD symptoms, treatments that included medica-
AD-DBD. Among the systematically studied psycho- tion performed better than other treatments in reduc-
social interventions are home-based interventions/par- ing ADHD symptoms. For non-ADHD symptoms, only
ent training, classroom-based behavior modifications, combined treatment was statistically superior to the
social skills training, and intensive summer treatment community standard care, although it was not different
programs. Since family, peer, and school interactions from the medication group.
are important in the morbidity and maintenance of
these disorders, it is important to utilize psychosocial
treatments to target each of these areas. In contrast to
DIAGNOSTIC CRITERIA
these more structured techniques, individual play ther-
apy with children is generally ineffective in decreasing For attention-deficit/hyperactivity disorder, the item set
problem behaviors of the AD-DBDs. chosen for the ICD-10 Diagnostic Criteria for Research
Despite their potential benefits, difficulties encoun- is almost identical to the items in the DSM-IV-TR cri-
tered with psychosocial interventions are that short- teria set but the algorithm is quite different, resulting in
term gains are often limited to the period that the pro- a more narrowly defined ICD-10 category. Specifically,
grams are actually in effect. Furthermore, a substantial whereas the DSM-IV-TR algorithm requires either six
number of children, particularly those with the most inattention items or six hyperactive/impulsive items,
severe presentation and with greatest psychosocial ad- the ICD-10 Diagnostic Criteria for Research requires
versity, fail to show improvement. Additional problems at least six inattention items, at least three hyperac-
in implementation include the unwillingness of many tive items, and at least one impulsive item. Instead of
teachers to use behavioral programs and the fact that subtyping the disorder on the basis of the predominant
as many as half the parents discontinue parent train- type, ICD-10 subspecifies the condition whether crite-
ing. Finally, the fact that these interventions are labor- ria are also met for a CD.
intensive and reported long-term improvements have Although formatted quite differently, the DSM-IV-
been modest, makes these therapies of limited value TR and ICD-10 item sets and diagnostic algorithms for
when used alone. These interventions are often more CD are almost identical. Although ICD-10 provides
efficacious than medication alone in children with a list of 23 items (in contrast with the 15 included in
ADHD who also have symptoms of anxiety. the DSM-IV-TR criteria for CD), only the last 15 items
count towards a diagnosis of CD. Although the first
8 items on the CD list are identical to the DSM-IV-TR
Combined Treatments
items for OD, ICD-10 ODD can be considerably more
The 1997 multimodal treatment study of children with severe because up to 2 of the items can be drawn from
ADHD (MTA) was a landmark multisite clinical trial, the 15 items that comprise the CD item set.
CHAPTER
Feeding and Eating Disorders
of Infancy or Early Childhood
Feeding Disorder of Infancy or Early Childhood Young infants who present with feeding difficulties and
growth failure dating to the postnatal period need to
DIAGNOSIS be considered for the diagnosis of a feeding disorder
of state regulation. In addition to the usual history, the
Feeding Disorder of Infancy or Early Childhood is
mother and her infant should be observed during feed-
defined in the DSM-IV-TR as a persistent failure to
ing and during play to assess the infant’s special char-
eat adequately with significant failure to gain weight
acteristics, the infant’s regulation of state and feeding
or a significant loss of weight over a period of at least
behavior, and the mother’s ability to read the infant’s
1 month. However, this general definition of feeding
signals and to respond to them in a contingent way.
disorder in DSM-IV-TR does not take into account
The information from the infant’s and the mother’s
the heterogeneity of feeding and growth problems in
histories and the observation of the mother–infant dyad
infants and its implication for treatment. Several au-
will determine which factors contribute to the difficul-
thors have used various diagnostic methods and as-
ties in the infant’s regulation of feeding. Because medi-
signed different labels to address the heterogeneity of
cal problems (e.g., cardiac or pulmonary disease) may
feeding problems associated with failure to thrive. Be-
contribute to the feeding problems, their impact on the
cause of the diversity of feeding disorders associated
feeding relationship of mother and infant needs to be
with failure to thrive and the lack of a subclassifica-
considered.
tion of feeding disorder as defined in DSM-IV-TR, this
chapter focuses on a classification of feeding disorders
proposed by Chatoor. Three developmental feeding
Feeding Disorder of Poor
disorders are described as (1) feeding disorder of state
Caregiver–Infant Reciprocity
regulation, (2) feeding disorder of poor mother–infant
reciprocity, and (3) feeding disorder of separation (in- Children with this condition show a lack of develop-
fantile anorexia). In addition, two feeding disorders are mentally appropriate signs of social reciprocity with
described that are not linked to specific developmental the primary caregiver during feeding, leading to sig-
stages: (1) sensory food aversions, a common feeding nificant growth deficiency. However, because of the
disorder that becomes evident during the introduction difficulty of assessing attachment in infants under 1
of different milks, baby food, or table food with various year of age, feeding disorder of poor caregiver–infant
tastes and consistencies, and (2) posttraumatic feeding reciprocity was chosen as diagnostic label to capture
disorder, which is characterized by an acute disruption the lack of engagement between mother and infant in
in the regulation of eating and can occur at various ages this feeding disorder.
and stages of feeding development. Most of these infants are not brought for pediatric
well-baby care but present to the emergency department
because of an acute illness, when their poor nutritional
Feeding Disorder of State Regulation
state draws the attention of pediatricians. Because of
In this condition, the infant has difficulty reaching and their severe failure to thrive, these infants frequently
maintaining a calm state of alertness for feeding, either require hospitalization. During the hospitalization, the
being too sleepy or too agitated or distressed to feed. psychiatric consultant is usually called in to assist in
the diagnosis and treatment of the infant’s growth and her childhood background, and her own eating habits and
developmental problems. attitude toward limit setting need to be explored.
Many of the mothers of affected children are elusive and
avoidant of any contact with professionals. Consequently,
Sensory Food Aversions
the observation of mother–infant interactions may have to
be obtained indirectly, through the report of other profes- In this disorder, the infant consistently refuses to eat
sionals who admitted the infant to the hospital. specific foods with specific tastes, textures, and/or
Another important part of the assessment involves smells. Sensory food aversions occur along a spectrum
the direct observation and examination of these in- of severity. Some children refuse to eat only a few types
fants. Infants with feeding disorders of poor mother– of food, making it possible for the parents to accom-
infant reciprocity characteristically feed poorly, avoid modate the child’s food preferences. Others may refuse
eye contact, and are weak in the first few days of hos- most foods, disrupt family meals, and cause serious
pitalization. When picked up, they might scissor their parental concern about the children’s nutrition. The di-
legs and hold up their arms in a surrender posture to agnosis of a feeding disorder should only be made if
balance their heads, which seem too heavy for their the food selectivity results in nutritional deficiencies,
weak bodies. They usually do not cuddle like healthy and/or has led to oral motor delay.
well-fed infants, rather they keep their legs drawn up or The evaluation of infants and young children with
appear hypotonic, like rag dolls. These infants, how- sensory food aversions should address how many foods
ever, appear to blossom under the care of a primary the child consistently refuses and how many foods he
care nurse who engages with them during feeding and or she usually accepts. A nutritional assessment needs
plays with them. They become increasingly responsive, to look not only at the anthropometric measures of the
begin to smile, feed hungrily, and gain weight. These child to rule out acute and/or chronic malnutrition, but
striking changes in behavior of these young infants needs to address whether the child may lack adequate
when they are fed and attended to by a nurturing care- intake of vitamins, zinc, iron, and/or protein. In ad-
taker are characteristic of a feeding disorder of poor dition, an oral motor assessment needs to determine
mother–infant reciprocity and differentiate these in- whether the child has fallen behind in this area of de-
fants from infants with organic problems that have re- velopment. Delayed oral motor development will limit
sulted in growth failure and developmental delays. The the kind of foods the child should be offered in order
infants with organic failure to thrive usually respond to prevent choking, and may be associated with a delay
best to their mothers and do not show the avoidance of in speech development. In addition, the parents’ food
eye contact and general withdrawal so characteristic of preferences during childhood and adulthood should be
infants with this feeding disorder. explored to assess whether the parents may be limited
in the variety of foods they offer their child.
Infantile Anorexia
Posttraumatic Feeding Disorder
In this condition, the infant refuses to eat adequate
amounts of food for at least 1 month, leading to signifi- These children refuse to eat any solid food after they
cant growth deficiency. The onset of the food refusal un- have experienced an episode of choking. This disorder
der 3 years of age is most commonly during the transi- is characterized by the infant’s consistent refusal to ei-
tion to spoon- and self-feeding. Furthermore, the infant ther drink from the bottle or to eat any solid foods, and
does not communicate hunger signals, lacks interest in in most severe cases, by the infant’s refusal to eat at
food, but shows strong interest in exploration and/or in- all. Depending on the mode of feeding that the infants
teraction with the caregiver. Infants with this infantile appear to associate with the traumatic event(s), some
anorexia are usually referred for a psychiatric evaluation refuse to eat solids, but will continue to drink from the
due to food refusal and growth failure. The infants’ food bottle; whereas others may refuse to drink from the
refusal usually becomes of concern between 6 months bottle, but are willing to eat solids. Some infants may
and 3 years, most commonly between 9 and 18 months put baby food in their mouths, but then spit out any
of age, during the transition to spoon- and self-feeding. food that has any little lumps in it. Most infants get
The diagnostic evaluation of this feeding disorder should stuck in these food patterns and may lose weight or lack
include the infant’s feeding, developmental, and health his- certain nutrients because of their limited diet.
tory, and the observation of mother and infant during feed- Reminders of the traumatic event(s) (e.g., the bottle,
ing. In addition to the infant’s history, the mother’s per- the bib, or the high chair) may cause intense distress for
ception of her infant’s temperament, her family situation, some infants, whereby they become fearful when they
Chapter 7 • Childhood Disorders: Feeding and Eating Disorders 59
are positioned for feedings and/or presented with feed- During a hospitalization, a number of infant-directed
ing utensils and food. They resist being fed by crying, interventions can be carried out while a more in-depth
arching, and refusing to open their mouths. If food is evaluation of the mother and the mother–infant rela-
placed in their mouths, they intensely resist swallow- tionship takes place. Improvement of the infant’s health
ing. They may gag or vomit, let the food drop out, ac- and affective availability can then be used to engage
tively spit the food out, or store the food in their cheeks the mother with her infant and in the treatment proc-
and spit it out later. The fear of eating seems to override ess. The mother’s ability to engage her infant and to
any awareness of hunger. Therefore, infants who refuse participate in the treatment process has to be at the core
all foods, including liquids and solids, require acute in- of the treatment plan.
tervention due to dehydration and starvation. Because the mothers frequently present with a vari-
In addition to a thorough history about the onset of ety of psychological and social disturbances, including
the infant’s food refusal and the medical and develop- a history of abuse or neglect, their problems need to
mental history, the observation of the infant and mother be explored while nutritional, emotional, and develop-
during feeding is critical for understanding this feeding mental rehabilitation goes on with the infant. In some
disorder and differentiating it from infantile anorexia situations of severe neglect or associated abuse, the
and from sensory food aversions. It is helpful to ask case needs to be reported to protective services, which
the mother to bring a variety of foods, including those at times can be instrumental in mobilizing the family
that the infant refuses and those that he or she accepts. or in finding foster care.
Infants with a posttraumatic feeding disorder charac- Discharge from the hospital is a critical time when
teristically appear engaged and comfortable with their all services need to be in place to ensure appropriate
mothers as long as the feared food is out of sight. follow-through of the treatment plan for these vulner-
able infants. Because of the complexity of the problems
involved in the etiology of this feeding disorder, a flex-
TREATMENT
ible multidisciplinary approach that is coordinated by
Treatment begins with the first contact with the infant the primary therapist is usually most effective for both
and his or her caregivers. The establishment of a thera- partners in the feeding relationship.
peutic alliance with the caregivers is critical to any suc-
cessful treatment.
Infantile Anorexia
The major goal of the treatment is to facilitate inter-
Feeding Disorder of State Regulation
nal regulation of eating by the infant. The intervention
Treatment needs to take maternal as well as infant fac- consists of three components:
tors that have interfered with feeding into consideration.
1. Assess and then explain the infant’s special tem-
Treatment can be directed toward the infant, toward the
peramental characteristics and developmental con-
mother, and toward the mother–infant interaction.
flicts to the mother to help her understand the lack
Videotaping the feeding and observing the tape to-
of expected hunger cues and the infant’s struggle for
gether with the mother can heighten her awareness of
control during the feeding situation.
the infant’s reactions during feeding and enhance her
2. Explore the mother’s upbringing and the effect it
ability to read the infant’s cues. The therapist can then
has had on the parenting of her infant to help the
engage the mother in a dialogue on how to respond
mother understand her conflicts and difficulties in
to the infant’s cues most effectively. Because of the
regard to limit setting.
complexity of the factors that may contribute to this
3. Explain the concept of internal versus external reg-
feeding disorder, the therapist needs to use a flexible
ulation of eating. Help the mother to develop meal-
approach when addressing both partners in the feeding
time routines that facilitate the infant’s awareness of
relationship.
hunger, leading to internal regulation of eating, im-
proved food intake, and growth. In addition, coach
Feeding Disorder of Poor the parents to set limits to the infant’s behaviors
Caregiver–Infant Reciprocity that interfere with eating. These feeding guidelines
include:
Because of the complexity of the issues involved in
the etiology of nonorganic failure to thrive, most a. Schedule meals and snacks at regular 3- to 4-hour
psychiatrists and researchers suggest that multiple and intervals and do not allow the infant to snack or
case-specific interventions may be required. drink from the bottle or breast in between.
b. Limit meal duration to 30 minutes. feeding, but introduce it again after a few days in a
c. Praise the infant for self-feeding but stay emo- small amount and paired with some other food that the
tionally neutral whether the infant eats little or infant likes. It is important to increase the amounts of
a lot. the new food very gradually until the infant appears
d. Do not use distracting toys or television during comfortable with it.
feedings.
e. Eliminate desserts or sweets as a reward at the
Posttraumatic Feeding Disorder
end of the meal; rather integrate them into regu-
lar meals and snacks. Because of the complexity of many of these cases, a
f. Put the infant in “time-out” for inappropriate be- multidisciplinary team is best equipped to meet all the
haviors during feeding (e.g., throwing the spoon needs of these infants and their parents.
or food, climbing out of the high chair). Before any psychiatric treatment can be successfully
initiated, the medical and nutritional needs of the in-
These three steps in the treatment are best accom- fant need to be addressed. In severe cases of total food
plished in three sessions lasting two to three hours each refusal, it is important to act quickly to maintain the
and grouped close together within a two- to three-week infant’s hydration.
period. The intensity of this brief intervention facili- The psychiatric treatment of this feeding disorder
tates a close therapeutic alliance between the therapist involves a desensitization of the infant to overcome
and the mother and gives the mother the opportunity the anticipatory anxiety about eating and return to in-
to experience the support she needs to make major ternal regulation of eating in response to hunger and
changes in her interactions with her infant. satiety. It is most important to help the parents under-
This initial intensive phase of the intervention can stand the dynamics of a posttraumatic feeding disor-
be followed up by a telephone call and by a few vis- der so that they can recognize the infant’s anticipatory
its spaced three to four weeks apart. The intervention anxiety and become active participants in the treat-
focuses primarily on the mother because in infan- ment. After identification of triggers of anticipatory
tile anorexia, the mother’s feeding relationship with anxiety (e.g., the sight of the high chair, the bottle,
the infant is seen as central. Nevertheless, the other or certain types of food), a desensitization by gradual
relationships, such as with the father, should not be exposure can be initiated or a more rapid desensitiza-
overlooked. tion through more intensive behavioral techniques can
Giving the mother the choice as to who in the family be implemented.
(or anyone else) should be included in the therapeutic With both techniques, it is important to have a pro-
process, and at what point, is part of putting the mother fessional assess the infant’s oral motor coordination
in control. Because many of the mothers have felt help- because many infants who refuse to eat for extended
less as children and ineffective as parents, the empow- periods fall behind in their oral motor development
erment of the mother is critical to the success of the due to lack of practice. Consequently, a 2-year-old may
treatment. have the oral motor skills of a 1-year-old and will not
be able to handle the chunky foods that require chew-
ing. The rapid introduction of table food to a child
Sensory Food Aversion
who has delayed oral motor skills may lead to chok-
In young infants (4–7 months of age), a few repeated ing, thereby creating a setback to the desensitization
exposures to new foods enhance the infants’ accept- process.
ance not only of that food but also of other similar As summarized in Figure 7-1, each of these five
foods. However, this changes in the second year of feeding disorders presents with specific symptom pat-
life, when the acceptance of new foods only increased terns and characteristic mother–infant interactions that
significantly after 10 or more exposures to those same help diagnose and differentiate the various feeding
foods. disorders. The correct diagnosis is critical because a
If infants show strong aversive reactions (e.g., gag- treatment that is helpful for one feeding disorder may
ging or vomiting) early on when offered a certain food, be ineffective or may even worsen another feeding dis-
it is advisable to give up on that particular food and not order. These treatments are based primarily on clinical
offer it again. If the infant shows a less severe reac- experience, and further empirical research is needed to
tion (e.g., grimaces or wants to spit out a new food), it establish which treatments are most effective for each
is also best to stop offering the new food during that feeding disorder.
Onset of Poor
Too irritable or Yes symptoms in Yes mother −infant Yes Growth Yes FEEDING DISORDER
too sleepy to feed newborn reciprocity during deficiency OF STATE REGULATION
period feeding
No
Growth failure; Yes Onset Yes Lack of Yes Yes FEEDING DISORDER
Growth
No parental concern; in first 3 caregiver−infant OF POOR CAREGIVER −
deficiency
Referral by professional years of life engagement INFANT RECIPROCITY
No
Poor appetite; Yes Onset Yes Mother−infant Yes Yes

Growth
Frequent food refusal; under 3 years conflict over INFANTILE ANOREXIA
deficiency
Poor weight gain of age infant's food refusal
No
Onset at Mother −infant

Yes Yes Yes Has specific Yes
Consistent refusal to introduction conflict over infant SENSORY FOOD
nutritional
eat specific foods of baby food not eating AVERSIONS
deficiencies
or table food specific foods
No
Has growth
Infants distressed
Consistent refusal of Yes Yes Yes deficiency Yes
Onset at when positioned POSTTRAUMATIC
either the bottle, or depending on
any age for feeding and/or FEEDING DISORDER
solids, or all foods duration of
when offered food
refusal
Figure 7-1 Diagnostic decision tree for differential diagnosis of feeding disorders of infancy or early childhood.
of it. Their rumination can be inferred only from the

Rumination Disorder
movements of their cheeks and foul oral odor because
of the frequent regurgitation.
DIAGNOSIS
In addition to taking a thorough medical history, it is
Infants with rumination disorder repeatedly regurgitate important to explore the onset of vomiting and the so-
and rechew food for a period of at least 1 month follow- cial context under which the symptoms developed. An
ing a period of normal functioning. Most frequently, acute medical illness or a stressor in the parents’ life is
infants who ruminate come to the attention of profes- frequently associated with the onset of vomiting.
sionals because of “frequent vomiting” and weight loss. Some infants ruminate only when left alone or when
Some infants ruminate primarily during the transition stressed in a relationship; others appear so “addicted”
to sleep when left alone, and their ruminatory activity to the rumination that they ruminate continuously after
might not be readily observed. However, these infants being fed, and they become distressed if interrupted
are frequently found in a puddle of vomitus, which in their ruminatory activity. In addition to assessing
should raise suspicion of rumination. Other infants the rumination in the infant, the mother–infant rela-
can be observed to posture with the back arched, to put tionship and the mother’s life circumstances need to
the thumb or whole hand into the mouth, or to suck on be evaluated because the mother’s ability to soothe
the tongue rhythmically to initiate the regurgitation of and to stimulate her infant is critical for successful
food. Most of the regurgitated food is initially vomited, intervention.
but gradually the infant appears to learn to hold more
of the food in the mouth to rechew and reswallow. “Ex-
TREATMENT
perienced” ruminators appear to be able to bring up
food through repeated tongue movements. They learn On the basis of the assumption that rumination is a
to rechew and reswallow the food without losing any learned habit reinforced by increased attention for
regurgitation, unlearning by counterconditioning has in children with accidental poisoning, with lead intoxi-
been suggested. A number of alternative procedures of cation, or with worm infestation. Young children with
punishment, such as aversive taste stimuli (lemon juice signs of malnutrition or iron deficiency should also be
or hot sauce), have been developed. There are a number considered for the diagnosis of pica.
of difficulties, however, with the use of aversive taste The assessment should include the history of the
stimuli as punishment. Frequently, the infants are out child’s development, in general, and feeding in par-
of reach of the caretakers when they ruminate; conse- ticular. Special attention should be given to other oral
quently, the use of lemon juice or hot sauce is inconsist- activities (e.g., thumb sucking or nail biting) that the
ent, and this delays learning. Some infants appear to child may use for self-soothing and relief of tension. In
become adapted to these aversive taste stimuli. Scold- addition, the home environment and the parents’ rela-
ing the infant by shouting “No,” placing the infant tionship with each other and with the child need to be
down, and leaving the room for 2 minutes immediately explored to assess the parents’ availability to nurture
on initiation of rumination by the infant have been sug- and supervise the child. Above all, mother and child
gested as more effective alternatives. If the infant is not should be observed during a meal and during play to
ruminating on the caretaker’s return, he or she is to be gain a better understanding of their relationship and
picked up, washed, and played with as a reward. how the symptoms of pica can be understood in the
It has been postulated that for some infants, the ru- context of that relationship.
mination behavior is related to social deprivation. For If the diagnosis of pica is established, it is critical that
such infants, holding the child for 10 to 15 minutes be- the child undergo a thorough physical examination to
fore, during, and after meals may be the treatment of rule out any of the complications associated with this dis-
choice. Psychodynamic approaches are based on the order, such as nutritional deficiencies (especially iron de-
assumption that rumination results from a disturbance ficiency), lead poisoning, intestinal infections (toxoplas-
in the mother–infant relationship. Mothers of ruminat- mosis or intestinal parasites), or gastrointestinal bezoars.
ing infants may be overwhelmed by their personal lives,
which make them unavailable or tense in their relation-
Course
ship with their infants. Psychotherapy for the mother and
environmental changes that produce enhanced mother- In many instances, the disorder is believed to be self-
ing have been proposed to address these problems. limited and to remit spontaneously after a few months.
Before embarking on treatment, both the child and Some children, however, are somewhat retarded in the
the child’s mother should be looked at individually. The use of their speech and show conflicts about their de-
diagnostic evaluation needs to determine whether the pendency needs and aggressive feelings. Half of the ad-
infant’s rumination is situational or pervasive, whether olescents in this group may show depression or person-
the infant has learned to ruminate because of little stim- ality disorders, or engage in other forms of disturbed
ulation and gratification from the mother, or whether the oral activities (e.g., thumb sucking, nail biting), and use
rumination serves the infant as a way of relieving ten- tobacco, alcohol, or drugs. There may be a relationship
sion in a stressed mother–infant relationship. After an between pica in childhood and symptoms of bulimia
understanding of the mother’s situation has been gained, nervosa in adolescence.
treatment is best individualized by use of a combination
of psychodynamic and behavioral interventions to en-
TREATMENT
hance the mother–infant relationship in general, and to
address the symptom of rumination in particular. In treating pica, one must consider the various factors
that appear to contribute to the development of pica as
well as its complications. It is important to treat the
Pica
child medically while addressing the psychosocial
needs of the child’s family as well. The mothers need
DIAGNOSIS
to be made aware of the dangers of pica and should
Young children with this disorder typically eat plas- be enlisted in providing a childproof environment.
ter, paper, paint, cloth, hair, insects, animal droppings, This might include removing lead from paint in old
sand, pebbles, and dirt. Because mouthing of objects substandard housing units or instituting anthelmintic
is still common in toddlers between 1 and 2 years, the therapy for family pets. A psychoeducational treatment
diagnosis of pica should be made only if the behavior approach teaching the mothers the dangers of pica
is persistent and inappropriate for the child’s develop- would also provide social support to help them become
mental level. The diagnosis of pica should be explored more available to their children. Other investigators
have used aversive and nonaversive behavioral therapy, disorders, if it is sufficiently severe to warrant inde-
physical restraints, environmental enrichment with pendent clinical attention, the ICD-10 Diagnostic
group or individual play, and time-out and overcorrec- Criteria for Research for pica exclude this diagnosis
tion to treat this disorder. in the presence of any other mental disorder (except
mental retardation). ICD-10 does not have a separate
category for rumination disorder. Instead, it includes
this DSM-IV-TR category within its defi nition of
DIAGNOSTIC CRITERIA
Feeding Disorder of Infancy and Childhood, which
In contrast to DSM-IV-TR, which allows the diagno- combines rumination with the persistent failure to eat
sis of pica to be made in the presence of other mental adequately.
CHAPTER
Tic Disorders
DIAGNOSIS etition of one’s own words (palilalia) or the words of

others (echolalia). Coprolalia (repetition of obscene
Tourette’s disorder is the most notable of the tic dis-
phrases), often incorrectly considered essential for
orders. The cardinal features of Tourette’s disorder
the diagnosis of Tourette’s disorder, is an uncommon
and the other tic disorders are motor and vocal tics.
symptom with only 2–6% of Tourette’s disorder cases
Motor tics are usually brief, rapid, and stereotyped
so affected.
movements, but can also be slower, more rhythmi-
Tics most often begin early in childhood, wax and
cal, or even dystonic in nature. Simple motor tics are
wane in severity, and change in character and quality
movements of individual muscle groups and include
over time. Tics are exacerbated by excitement and ten-
brief movements such as eye blinking, head shaking,
sion, and can attenuate during periods of focused, pro-
and shoulder shrugging. Complex motor tics involve
ductive activity and sleep. Tics are involuntary, yet be-
multiple muscle groups, such as a simultaneous eye
cause they are briefly suppressible or can be triggered
deviation, head turn, and shoulder shrug. Some com-
by environmental stimuli (e.g., mimicking another per-
plex tics appear more purposeful, such as stereotyped
son’s movement, speech, or behavior), they may appear
hopping, touching, rubbing, or obscene gestures (co-
as volitional acts. Individuals with a tic disorder de-
propraxia). Vocal tics are usually brief, staccato-like
scribe tension developing if a tic is resisted, which only
sounds, but can also be words or phrases. Simple vo-
subsides by completion of the tic. In some individuals,
cal tics, often caused by the forceful movement of air
tics are preceded or provoked by a thought or physical
through the nose and mouth, include sniffi ng, throat
sensation referred to as a premonitory urge.
clearing, grunting, or barking-type sounds. Complex
There are four diagnostic categories included in the
vocal tics usually include words, phrases, or the rep-
tic disorders section in DSM-IV-TR: Tourette’s Disor-
der, Chronic Motor or Vocal Tic Disorder (CT), Tran-
sient Tic Disorder and Tic Disorder Not Otherwise
Specified, which is a residual category for tic disorders
307.23 TOURETTES’ DISORDER not meeting the duration or age criteria of the other cat-
egories. In general, diagnostic decisions are based on
A. Both multiple motor and one or more vocal tics have whether both motor and phonic tics are present (i.e., if
been present at some time during the illness, although
not necessarily concurrently. (A tic is a sudden, rapid, both are present, the diagnosis is Tourette’s), duration
recurrent, nonrhythmic, stereotyped motor movement of time affected with tics (Tourette’s and CT persist for
or vocalization.)
B. The tics occur many times a day (usually in bouts)
at least a year whereas Transient Tic Disorder lasts at
nearly every day or intermittently throughout a period least 4 weeks but no more than 12 months), age at onset
of more than 1 year, and during this period there was (age of onset is before age 18 for all three of the specific
never a tic-free period of more than 3 consecutive
months. tic disorders), and the lack of another medical cause
C. The onset is before age 18 years. for the tics.
D. The disturbance is not due to the direct physiological Clinical assessment of the tic disorders begins with
effects of a substance (e.g., stimulants) or a general
medical condition (e.g., Huntington’s disease or post- identification of the specific movements and sounds. It
viral encephalitis). is also important to identify the severity of and impair-
Reprinted with permission from the Diagnostic and Statistical ment caused by the tics. Questioning individuals with
Manual Disorders, 4th Ed., Test Rev. Copyright 2000 American tics and their families about the presence of simple and
Psychiatric Association
complex movements in muscle groups from head to toe
Chapter 8 • Childhood Disorders: Tic Disorders 65
is a good beginning. Because vocal tics usually fol- in individuals with Tourette’s disorder so that the hi-
low the development of motor tics, questions about the erarchy of disabling conditions can be identified and
presence of simple sounds are next. Inquiring about the treatment initiated accordingly. Positive family history
presence of complex vocal tics completes the tic inven- of another mental disorder (e.g., major depressive dis-
tory. It is helpful to elucidate other aspects of tic sever- order or panic disorder) may provide clues to the pos-
ity, such as the absolute number of tics, the frequency, sible mental disorder complicating the presentation of
forcefulness, and intrusiveness of the symptoms, the an individual with Tourette’s disorder.
ability of the individual to successfully suppress the Psychosocial issues can play a role in tic severity and
tics, and how noticeable the tics are to others. It is in overall adaptation and impairment. Assessment of
also important to know whether premonitory sensory family, peer, and school support for the youngster (ad-
or cognitive experiences are a component of specific equate protection) along with assessment for the pres-
tics because these intrusive experiences may disrupt ence of opportunities to be intellectually, physically,
functioning more than the tics themselves. Although and socially challenged is important. The balance be-
the waxing and waning nature of the tics and the re- tween protection and challenge in children is critical
placement of one tic with another do not directly affect for long-term development. An environment that is too
severity, identifying the characteristic course of illness protective decreases opportunities for building skills.
is important for diagnostic confidence. An environment that is too challenging can lead to
Last, it is important to assess the impairment due to frustration, anger, and maladaptive coping.
the tics themselves. Whereas tic severity is frequently Tic assessment requires a careful evaluation of ob-
correlated with overall impairment, it is not uncom- servable tic symptoms. Interestingly, the absence of tic
mon to identify individuals in whom tic severity and symptoms during an evaluation, in spite of the parent’s
impairment are not correlated. Individuals who expe- or child’s report, is not uncommon and should not nec-
rience more impairment than their tic symptoms ap- essarily lead to clinical doubt. Occasionally, an addi-
parently warrant are a particular clinical challenge. A tional clinical observer (e.g., nurse or medical student)
number of clinical features of tics are associated with may identify tics more readily than the psychiatrist con-
impairment: ducting the evaluation. Other than the observation of
tics in the interview, there are no pathognomonic physi-
• Large, disruptive, or painful motor movements
cal examination findings. Individuals with Tourette’s
• Vocalizations that call attention to the individual
disorder have been noted to have nonfocal and non-
• Premonitory sensations or cognitions that intrude
specific subtle neurological findings (“soft” signs). If
into consciousness
tic suppression with neuroleptic agents is considered,
• Tics that are socially unacceptable.
a more structured method of documenting the complex
Whereas tic severity and impairment are often cor- movements that are part of the pretreatment baseline
related, many individuals with mild tics are most im- evaluation is useful for following the progression of the
paired by the comorbid conditions attention-deficit/hy- disease and for subsequent assessment for neuroleptic-
peractivity disorder (ADHD), obsessive–compulsive induced movements.
disorder (OCD), and learning disorders (see next sec- No specific laboratory or imaging tests are helpful in
tion). An adequate assessment of these conditions is making the diagnosis or in assessing an individual with
part of any comprehensive evaluation. Tourette’s disorder. Laboratory assessment is most often
It is standard for any evaluation to rule out all other done as part of a routine health screen or in anticipation
mental disorders. In complex cases of Tourette’s disor- of medication interventions. Currently, laboratory testing
der, the multitude of behavioral and emotional symp- for Pediatric Autoimmune Neuropsychiatric Disorders
toms can be formulated in a number of different ways. Associated with Streptococcal Infection (PANDAS) and
Behavioral and emotional problems can be seen as group A beta-hemolytic streptococcal infections (e.g.,
components of the Tourette’s disorder diathesis, as a throat culture, antistreptolysin titer, and screening for
reaction to having a chronic disorder, or as part of an antineuronal antibodies) is experimental unless there are
independent psychiatric disorder that is complicating clinical signs and symptoms of acute infection.
the clinical picture. Clinical formulations that over-
simplify and do not consider the presence of multiple
Frequently Co-occurring Symptoms
independent disorders may lead to incorrectly attribut-
and Disorders
ing unrelated symptoms to Tourette’s disorder and may
result in diagnostic imprecision and treatment failures. There is considerable evidence that there is a broad
It is important to identify all possible mental disorders array of co-occurring clinical problems in clinically
ascertained subjects with Tourette’s disorder. These Tourette’s disorder in the media. Often, these adults
co-occurring problems can be more disabling than tics have been able to function in spite of their tics. Others
and are often the reason people with tics come to clini- may have been given an incorrect diagnosis for their
cal attention. The nature and range of these problems tic disorder or may have been in treatment for co-
is broad and includes problems with mood, impulse occurring psychiatric problems without any awareness
control, obsessive–compulsive behaviors, anxiety, at- of the relationship of those problems to the tic disor-
tention and learning problems, and conduct problems. der. Even though these adults have not previously been
In some individuals, these problems reach diagnosable diagnosed with a tic disorder, most are aware of their
proportions, but in many others, they are less severe tics and may have experienced the psychosocial stigma
and do not fulfill diagnostic criteria. The most common commonly associated with a tic disorder. For these
co-occurring disorders are ADHD (50–60%) and OCD adults, a new diagnosis of Tourette’s disorder may be
(30–70%). The exact relationship of these problems to psychologically complicated. The relief provided by
Tourette’s disorder is unclear. knowing their diagnosis may be mixed with new ques-
Differences in clinical phenomenology have been tions about Tourette’s disorder and its potential impact
noted in studies of obsessions and compulsions in on their lives.
individuals with Tourette’s disorder compared with Tic disorders appear to be common ( ⬎ 1 : 100),
individuals with OCD (without Tourette’s disorder) whereas Tourette’s disorder is less common
(Table 8-1). Individuals with Tourette’s disorder have (5 : 10,000), but perhaps not as rare as previously
greater concern with physical symmetry, evenness, and thought. In general, tic disorders are more common in
exactness, which are often described as “just right” children than adults, and people with mild tic disor-
phenomena, and concerns with impulse control. In con- ders are much more common than those with severe,
trast, individuals with OCD have more frequent con- complex symptoms. Also, people with tic disorders
cerns regarding contamination and more cleaning and may present for clinical attention with tics, but tics
grooming rituals than do individuals with Tourette’s may not end up as the focus of clinical attention, as
disorder. comorbid conditions are often more impairing than
Whereas most cases of Tourette’s disorder currently the tics themselves. Given these realities, the number
presenting for care are children, there are adults who of adults with persistent and severely impairing tics
seek a clinical evaluation as a result of having a child that warrant tic-suppressing medication is probably
diagnosed with Tourette’s disorder or learning about very small and these cases may still be considered
rare. A similar pattern is seen in children, with fewer
children presenting with severe tics warranting tic
Obsessions and Compulsions Characteristic suppression than children with mild to moderate tics
Table 8-1 of Obsessive–Compulsive Disorder and
Tourette’s Disorder and comorbid psychiatric disorders. Perhaps the most
common are those children with transient tics that
Obsessive–Compulsive Tourette’s
Disorder Disorder
are not impairing and without comorbid conditions.
This last group of children may never come to clinical
Obsessions Contamination “Just right”
phenomena attention.
Dirt and germs Symmetry
Body wastes Blurting out
obscenity Course
Environmental Saying the right
thing In Tourette’s disorder, tic symptoms usually begin in
Violent images childhood; mean age at onset is 7 years. The first tic
Sexual thoughts
Embarrassment may develop during the teenage years, but this is unu-
Compulsions Cleaning Touching sual. Motor tics of the eyes and face are the most com-
Blinking mon and the earliest presenting symptoms. Vocal tics
Repeating
Self-injurious tend to follow the development of motor tics. Complex
behavior tics of both types tend to follow the development of
Hoarding simple tics. Longitudinal studies suggest that tic sever-
Counting
Ordering ity is greatest in most individuals during the latency
Source: Adapted from George MS, Trimble MR, Ring HA, et al.
and early teenage years. Most individuals experience a
(1993) Obsessions in obsessive–compulsive disorder with and decline in tic severity as they get older and only a small
without Gilles de la Tourette’s syndrome. Am J Psychiatr 150, percentage of individuals (10%) experience a severe or
93–97. Copyright 1993 American Psychiatric Association.
deteriorating course.
The course of ADHD symptoms in persons with the person turns into a hair smoothing gesture), man-
Tourette’s disorder is similar to that in children without nerism, gesture, or stereotypy. Mannerisms or gestures
Tourette’s disorder. ADHD symptoms usually begin are often not impairing; stereotypies tend to occur ex-
earlier than the tic symptoms. clusively in children and adults with developmental
Obsessive–compulsive symptoms in persons with disabilities and mental retardation.
Tourette’s disorder generally begin somewhat later It is also possible to have a tic disorder and another
than ADHD and tics, and may actually progress dif- movement disorder. For example, tic movements can
ferentially from tic symptoms. Tic symptoms tend to co-occur with dystonia. Similarly, it is not uncom-
improve into adulthood; obsessive–compulsive symp- mon in tertiary referral centers to see developmen-
toms may actually increase in severity. tally disabled children and adults with both tics and
stereotypies.
TREATMENT
Tics have many characteristics that differentiate them
from the other movement disorders (Table 8-2). Per- The initiation of treatment can be a delicate process,
haps most important to “ruling in” tics as a diagnostic given the difficulties individuals with tics and their
possibility is the childhood history of simple motor tics families experience before finding appropriate care.
in the face. Other movement disorders do not have a Most families are frightened about their child’s having
similar pattern of movement onset or location. There a neuropsychiatric disorder and envision a grim prog-
are atypical presentations of tic disorders that may re- nosis. After the evaluation is completed, often in the
semble other movement disorders, but these would be first session, general education of the individual and
unusual and would probably require a consultation with family about the course of the tic disorder is essential.
a movement disorders expert. Most children and families are relieved to hear that the
Movement disorders such as chorea and dystonia are majority of persons with tics have consistent improve-
continuous movements and can be distinguished from ment in tic severity as they move through their teenage
tics, which are intermittent. Paroxysmal dyskinesias, years and into adulthood. They are also pleased to hear
although episodic, are more often characterized by that tic symptoms are not inherently impairing. In this
choreiform and dystonic movements, which are differ- regard, it is often helpful to cite examples of sports per-
ent from tics. Myoclonic movements and exaggerated sonalities or other public figures who have identified
startle responses are also intermittent movements but themselves as having Tourette’s disorder and are doing
are usually large-muscle movements that occur in re- well both personally and professionally.
sponse to a person-specific stimulus. Complex tics can Once issues regarding the tics are discussed and clar-
be more difficult to differentiate from other complex ified, the focus shifts to the presence of comorbid con-
movements such as mannerisms, gestures, or stere- ditions. Identifying whether ADHD, LD, and OCD are
otypies. In a person with clear-cut motor tics, it may present is especially important because they are often
be difficult to differentiate a complex motor tic from a the more common impairing conditions in these chil-
“camouflaged” tic (making a simple tic appear to be a dren. Yet the transition to addressing the co-occurring
purposeful action, e.g., an upward hand movement that problems is often not easy. Individuals, families, and
mental health professionals are usually focused on the
tic symptoms. Tics are more readily apparent and rela-
Table 8-2 Differential Diagnosis of Tics tively easy to suppress with medications, whereas the
co-occurring conditions, especially if they are inter-
Simple, rapid movements
Myoclonus nalizing disorders, are easy to overlook. One of the ma-
Chorea jor pitfalls of treatment of individuals with Tourette’s
Seizures disorder is to pursue tic suppression to the exclusion of
Simple, sustained movements
Dystonia the treatment of other co-occurring conditions that are
Athetosis present and possibly more impairing.
Complex or sustained movements Creating the hierarchy of the most impairing condi-
Mannerisms
Stereotypies tions is the next major step in treatment. Most clini-
Restless legs cians, as part of their formulation, create some clinical
Source: Jankovic J (1992) Diagnosis and classification of tics and hierarchy; yet in Tourette’s disorder, with the multi-
Tourette syndrome. Adv Neurol 58, 7–14, copyright, Lipincott, tude of often complex problems, it is essential that a
Williams & Wilkins.
conscious effort be made to formulate, organize, and
create hierarchies for treatment. For example, children neuroleptics long-term may be complicated by with-
with moderate tics and separation anxiety with school drawal dyskinesias and significant tic worsening or
refusal should be considered for treatment with a selec- rebound. Withdrawal dyskinesias are choreoathetoid
tive serotonin reuptake inhibitor (SSRI) for their sepa- movements of the orofacial region, trunk, and extremi-
ration anxiety rather than neuroleptics for tic suppres- ties that appear after neuroleptic discontinuation or
sion. It is possible that with successful treatment of the dosage reduction and tend to resolve in 1 to 3 months.
anxiety disorder, the individual may also experience a Tic worsening even above pretreatment baseline level
reduction in tic severity. (i.e., rebound) can last up to 1 to 3 months after dis-
continuation or dosage reduction. Tardive dyskinesia,
which is similar in character to withdrawal dyskinesia,
Somatic Treatments
most often develops during the course of treatment or is
The goal of pharmacological treatment is the reduc- “unmasked” with dosage reductions. Rarely have cases
tion of tic severity, not necessarily the elimination of of tardive dyskinesia been reported to occur in indi-
tics. Haloperidol has been used effectively to suppress viduals with Tourette’s disorder.
motor and phonic tics for more than 30 years. Since The atypical neuroleptics appear to have replaced
that time, a number of other neuroleptic agents have the standard neuroleptics as the mainstay of treatment
also been identified as useful in tic suppression, includ- for the psychotic disorders. Given the potentially lower
ing fluphenazine and pimozide. In Europe, the substi- risk for tardive dyskinesia with these agents, their ef-
tuted benzamides, sulpiride and tiapride, and the non- ficacy has been assessed for tic suppression in individ-
neuroleptic tetrabenazine have also been shown to be uals with Tourette’s disorder. To date, there are only
useful. Preliminary results with risperidone have been small controlled or open trials to guide the clinician
mixed, whereas trials with clozapine are more uni- in the use of these agents. Clozapine does not appear
formly negative. The major drawback with neuroleptic to be effective as a tic-suppressing agent and its hema-
agents is the frequent and significant side effects, which togological side effects preclude its use. Risperidone
often preclude continued use of the medication. has been effective in reducing tic symptom severity in
There are continuing efforts to identify tic-suppress- one controlled trial and may have the added benefit of
ing agents with tolerable side effects. Most frequently augmenting SSRIs in treating tic-related OCD.
cited in this regard are the alpha-adrenergic agonists Olanzapine in low doses does not appear to have the
clonidine and guanfacine. Both of these agents were same tic-suppressing power as the typical neuroleptics.
developed as antihypertensives. These agents do not ap- The side effects, especially weight gain, have damp-
pear to be uniformly effective in tic suppression, but they ened the enthusiasm for the atypicals risperidone, olan-
can be effective for some individuals without significant zapine, and quetiapine.
side effects. Both clonidine and guanfacine also appear
to be useful for some of the symptoms of ADHD, which Clonidine and Guanfacine. There is a long history
makes these agents a reasonable first choice for those of the use of the alpha-adrenergic agonist clonidine for
individuals with both Tourette’s disorder and ADHD. suppression of tics and ADHD symptoms. Whereas
controlled trials have shown that some individuals ben-
Antipsychotics. Side effects with all neuroleptics are efit with symptom reduction, the overall effect of clo-
common and are the reason that neuroleptics are not nidine for tic suppression and ADHD is more modest
used by the majority of individuals with Tourette’s dis- than that achieved with the “gold standards” (haloperi-
order. Side effects include those traditionally seen with dol and the stimulants, respectively) for these condi-
neuroleptics, such as sedation, acute dystonic reactions, tions. Given clonidine’s mild side effect profile, it is
extrapyramidal symptoms including akathisia, weight often the first drug used for tic suppression, especially
gain, cognitive dulling, and the common anticholiner- in those children with Tourette’s disorder and ADHD.
gic side effects. There have also been reports of subtle, The onset of action is slower for tic suppression (3–6
difficult-to-recognize side effects with neuroleptics, in- weeks) than for ADHD symptoms. Side effects, in ad-
cluding clinical depression, separation anxiety, panic dition to sedation, include irritability, headaches, de-
attacks, and school avoidance. creased salivation, and hypotension and dizziness at
Dosage reduction is the most prudent response to higher doses. Interestingly, owing to clonidine’s short
side effects, although the addition of medications half-life, some individuals experience mild withdrawal
such as benztropine for the extrapyramidal symptoms symptoms between doses. More severe rebound in au-
can be useful. Dosage reduction in those children tonomic activity and tics can occur if the medication is
with Tourette’s disorder who have been administered discontinued abruptly.
Guanfacine is an alpha-2-adrenergic agonist that po- Perhaps the most useful psychosocial and educa-
tentially offers greater benefit than clonidine because of tional intervention is to make the individual aware of
differences in site of action, side effects, and duration the Tourette Syndrome Association, both national and
of action. Guanfacine may have a greater impact on at- local chapters. This and other self-help groups can be
tention without the significant sedation associated with useful as a source of support and education for individu-
the nonselective alpha-2-adrenergic agonist clonidine. als with tics, families, and mental health professionals.
Guanfacine’s long half-life offers the advantage of twice- Individual psychotherapy can be useful for support,
a-day dosing, which is more convenient than the multiple development of awareness, or for addressing personal
dosing required with clonidine. Clinically, the effect on and interpersonal problems more effectively. Family
tics is less than would be expected with neuroleptics. therapy can be useful when families have problems
adjusting, functioning, and communicating. Although
Benzodiazepines. Benzodiazepines can be useful most families do well, some families have difficulties
in decreasing comorbid anxiety in individuals with understanding the involuntary nature of tics and may
Tourette’s disorder. In addition, clonazepam appears punish their children for their tics, even after diagnosis
also to be useful in selected individuals for tic reduc- and education. Alternatively, some families have more
tion. Often, doses of 3 to 6 mg/day may be necessary behavior difficulties with their children after diagnosis
for tic reduction. Because sedation is a significant side than before. Many parents of children with Tourette’s
effect at these dosages, an extended titration phase of 3 disorder inadvertently lower general behavior expecta-
to 6 months may be necessary. Similarly, a slow taper tions because of confusion about what behaviors are tics
is required to avoid withdrawal symptoms. and what behaviors are not tics. Sometimes parents de-
crease behavior expectations for their children because
Pergolide. Agonist activity on presynaptic dopamine of the parents’ desire not to add any additional stress
neurons results in decreased dopamine release and to the youngster’s life. Also, with confusion in the field
may therefore result in decreased tic severity in people regarding the scope of problems in Tourette’s disorder,
with Tourette’s disorder. Pergolide, a mixed D1–D2–D3 some parents see all maladaptive behaviors as involun-
dopamine agonist often used for restless leg syndrome, tary and do not hold their children responsible for their
may be superior to placebo in reducing tic severity and behaviors. For children with Tourette’s disorder to do
was associated with few adverse events. Doses used are well, they need support from their family to develop
low, as higher doses may be associated with dopamine effective self-control in areas not affected by Tourette’s
agonist effects postsynaptically. disorder so that optimal adaptation can occur.
For children, active intervention at school is essen-
tial to create a supportive yet challenging academic
Psychosocial Treatments
and social environment. Efforts to educate teachers,
Published studies of behavioral approaches to tic sup- principals, and other students can result in increased
pression are few but show some promise. The behav- awareness of Tourette’s disorder and tolerance for the
ioral technique shown to be most effective is habit re- child’s symptoms.
versal training. For Tourette’s disorder, habit reversal Many young adults are finding Tourette’s disorder
training is the use of a competing muscle contraction support and social groups important for interpersonal
or behavioral response that opposes the tic movement. contact and continued adult development. Efforts to
This method is usually combined with relaxation train- keep people with Tourette’s disorder working are im-
ing, self-monitoring, awareness training, and positive portant, as are rehabilitation efforts for those who are
reinforcement. In the few published studies of habit re- not working. Finding housing and obtaining disability
versal training, there were marked overall reductions in or public assistance may be necessary for the most dis-
tic frequency. Treatment averaged 20 training sessions abled individuals with Tourette’s disorder.
during an 8- to 11-month period. Marked tic reduction
was noted at 3 to 4 months. Interestingly, urges or sen-
Treatment-Refractory Cases
sations experienced before the tic movements also de-
creased with behavioral treatment. Perhaps the most important “treatment” in individuals
There are no published systematic studies of psy- with severe incapacitating tics is a full clinical reevalu-
chosocial interventions for individuals with Tourette’s ation to assess the adequacy of previous evaluations and
disorder. Most treatment efforts are based on a com- treatment efforts. It is not uncommon for treatment-
bination of traditional psychosocial interventions and refractory individuals to have had inadequate evalua-
clinical judgment. tions and treatment trials.
When a single tic or a few tics are refractory and There have been reports in the literature and the
impairing, the injection of botulinum toxin into the media concerning the use of neurosurgical approaches
specific muscle group can be helpful. This strategy is for the treatment of refractory tics. To date, the opti-
most useful for painful, dystonic tics. Treatment has a mal size and location of the surgical treatment lesions
long duration of action, but the effect does decrease in are not known, results are variable, and thus such ap-
2 to 4 months, and repeated injections may be neces- proaches cannot be recommended at present.
sary. Specific side effects are few, other than weakness
in the affected muscle. Some individuals reported the
loss of the premonitory sensation with their botulinum
DIAGNOSTIC CRITERIA
toxin treatment. For the mental health clinician it is es-
sential to work with a neurologist experienced in using The ICD-10 and DSM-IV-TR criteria sets for the tic
botulinum toxin. disorders are almost identical.
CHAPTER
Elimination Disorders and
Childhood Anxiety Disorders
Enuresis treatment should be fully explored. Asking the child for

three wishes may help determine whether the enuresis is
DIAGNOSIS a concern to the child. This may unmask marked embar-
rassment or guilt from behind a facade of denial about
Functional enuresis is defined as the intentional or in-
the problem, and can be educational for parents who
voluntary passage of urine in bed or clothes in the ab-
believe their children could stop wetting “if only they
sence of any identified physical abnormality in children
wanted to or tried harder.” Pictures drawn by the child
older than 4 years of age. Although there is no good
that describe how the child views himself or herself when
evidence that the condition is primarily psychogenic,
enuresis is a problem and when it is not are appropriate
it is often associated with a mental disorder, and en-
for younger children, and can graphically illustrate the
uretic children are frequently referred to mental health
misery experienced by children with enuresis.
services for treatment. The DSM-IV-TR diagnosis of
All children should have a routine physical examina-
Enuresis (Not Due to a General Medical Condition) is
tion, with particular emphasis placed on the detection
made if there is repeated voiding of urine that is clini-
of congenital malformations that are possibly indicative
cally significant, as defined by either occurring at a
of urogenital abnormalities. A midstream specimen of
frequency of twice a week for at least 3 consecutive
urine should be examined for the presence of infection.
months, or else causing clinically significant impair-
Radiological or further medical investigation is indicated
ment in social, academic, or other important areas of
only in the presence of infected urine, enuresis with
functioning. Furthermore, the diagnosis is only given
symptoms suggestive of recurrent urinary tract infection
if the individual’s chronological age is at least 5 years
(UTI) (frequency, urgency, and dysuria), or polyuria.
(or equivalent developmental level).
Information on the frequency, periodicity, and dura-
tion of symptoms is needed to make the diagnosis and Course
distinguish functional enuresis from sporadic seizure- Nocturnal enuresis is as common in boys as in girls until
associated enuresis. If there is diurnal enuresis, an ad- the age of 5 years, but by age 11 years, boys outnumber
ditional treatment plan is required. A family history of girls 2 : 1. Not until the age of 8 years do boys achieve
enuresis increases the likelihood of a diagnosis of func- the same levels of nighttime continence that are seen
tional enuresis and may explain the later age at which in girls by the age of 5 years. This appears to be due to
the children are presented for treatment. Projective slower physiological maturation in boys. In addition, the
identification by the affected parent—whereby the par- increased incidence of secondary enuresis (occurring
ent does not separate their own feelings about having after an initial 1-year period of acquired continence) in
had the diagnosis with the current experience of their boys further affects the sex ratio seen in later childhood.
affected child—may further hinder treatment. For sub- Daytime enuresis occurs more commonly in girls.
jects with secondary enuresis, the precipitating factors
should be elicited, although such efforts often represent
an attempt to assign a meaning after the event.
The child’s views and any misconceptions that he The presence or absence of conditions often seen in as-
or she may have about the enuresis, its causes, and its sociation with enuresis, such as developmental delay,
? Day/night wetting
Yes
? Age at least 5 years

Yes
? Sufficient frequency
or impairment
Yes
Yes
? Associated UTI Treat
No
? Associated general Yes

medical condition Refer appropriately
(e.g., diabetes or seizure)
No
307.6 Enuresis
(specify type)
Nocturnal Diurnal Mixed noctural

and diurnal
Figure 9-1 Diagnostic decision tree for enuresis.
UTI, constipation, and comorbid psychiatric disor- fate. Practical management for nocturnal enuresis is
der, should be assessed and ruled out as appropriate presented in Table 9-1.
(Figure 9-1). Other causes of nocturnal incontinence About 10% of children have a reduction in the
should be excluded, for example, those leading to poly- number of wet nights after a single visit to a clinician in
uria (diabetes mellitus, renal disease, diabetes insip- which the only intervention was the recording of base-
idus) and, rarely, nocturnal epilepsy. line wetting frequency and simple reassurance. Such
reassurance should make clear that enuresis is a biolog-
ical condition that is made worse by stress and that may
TREATMENT OF NOCTURNAL ENURESIS
be associated in a noncausal way with other psychiat-
Questions that are useful in obtaining information for ric disorders. Younger children can be told that their
treatment planning include “Why is this a problem?” problem is shared by many others of the same age. The
and “Why does this need treatment now?” because excellent prognosis for individuals who comply with
these factors may influence the choice of treatment (is therapy should be stressed. Recording the frequency of
a rapid effect needed?) or point to other pressures or enuresis can be achieved by using a simple star chart.
restrictions on therapy. It is important to inquire about This is most effective if performed by the child, who
previous management strategies—for example, fluid records each dry night with a star. The completed chart
restriction, night lifting (getting the child out of bed to is then shown to the parents on a daily basis, and they
take to the toilet, in an often semiasleep state), rewards, can provide appropriate praise and reinforcement.
and punishments—used at home. Parents often come
with the assertion that they have tried everything and
Waking and Fluid Restriction
that nothing has helped. Examining the reasons for the
failure of simple strategies is useful for ensuring that Although systematic studies have failed to show any ef-
more sophisticated treatments do not befall the same fect of these interventions with enuretic inpatients, it may
Chapter 9 • Childhood Disorders: Elimination Disorders and Childhood Anxiety Disorders 73
Table 9-1 Practical Management of Nocturnal Enuresis Pharmacotherapy
Stage 1 Assessment Although it has been repeatedly demonstrated that

Obtain history: frequency, periodicity, and temporary suppression rather than cure of enuresis is
duration of wetting. the usual outcome of drug therapy, it remains the most
Why is this a problem? Why now?
Mental status: views and misconceptions widely prescribed treatment in the United States. Four
(parent and child). classes of drugs have principally been employed: syn-
Discover reasons for previous failure or thetic antidiuretic hormones, tricyclic antidepressants,
failures.
Perform routine physical examination (any stimulants, and anticholinergic agents. There is no
minor congenital abnormalities?). evidence that stimulants or anticholinergic agents are
Midstream specimen of urine must be effective.
obtained.
Radiology and further physical investigation
is needed only if symptoms or evidence of
urinary tract infection (dysuria and frequency Synthetic Antidiuretic Hormone. The drug is usu-
or positive culture results) or polyuria.
ally administered intranasally, although oral prepara-
Stage 2 Advice tions of equal efficacy have been developed (equiva-
Education that enuresis is common and not
deliberate. lent oral dose is 10 times the intranasal dose). It has
Aim to reduce punitive behavior. been shown that almost 50% of children are able to
Transmit optimism: however, anticipate stop wetting completely with a single nightly dose
disappointment at no instant cure.
Preview the stepwise recovery and warn of the of 20–40 mcg of DDAVP given intranasally. A fur-
possibility of relapse. ther 40% are afforded a significant reduction in the
Stage 3 Baseline frequency of enuresis with this treatment. As with
Use star chart. tricyclic antidepressants, however, when treatment is
Focus on positive achievements (be creative).
Examine the effect of simple interventions stopped, the vast majority of individuals relapse. Side
(e.g., lifting) effects of this medication include nasal pain and con-
Stage 4 Night Alarm gestion, headache, nausea, and abdominal pain. Seri-
First-line management unless important to ous problems of water intoxication, hyponatremia,
obtain rapid short-term effect.
Demonstrate night-alarm equipment in the and seizures are rare. It is important to be aware that
office. intranasal absorption is reduced when the child has a
Telephone follow-up within a few days of cold or allergic rhinitis. The mode of action of desmo-
commencing therapy.
Or pressin is unknown.
Drug Therapy
If rapid suppression of wetting is needed
(e.g., before vacation or camp, to defuse Tricyclic Antidepressants. The short-term effective-
aggressive or hostile situation between child ness of imipramine and other related antidepressants
and parents and siblings).
When family has proved incapable of using
has also been demonstrated via many randomized dou-
the equipment. ble-blind placebo-controlled trials For example imi-
After failure or multiple relapses. pramine reduces the frequency of enuresis in about 85%
Medication of choice: DDAVP,
(Desmopressin) 20–40 µg at night of bed wetters and eliminates enuresis in about 30%
of these individuals. Nighttime doses of 1–2.5 mg/kg
are usually effective, and a therapeutic effect is usu-
be that these strategies work for the majority of enuretic ally evident in the first week of treatment. Relapse after
children who are not referred for treatment. If waking does withdrawal of medication is almost inevitable, so that
appear to reduce the number of wet nights from baseline, 3 months after the cessation of tricyclic antidepressants,
a more systematic application may be indicated. nearly all children will again have enuresis at pretreat-
ment levels. Side effects are common and include dry
mouth, dizziness, postural hypotension, headache,
Surgery
and constipation. Toxicity after accidental ingestion
On the basis of the premise that enuresis is causally or overdose is a serious consideration, causing cardiac
associated with outflow-tract obstruction, various sur- effects, including arrhythmias and conduction defects,
gical procedures have been advocated. Reported posi- convulsions, hallucinations, and ataxia. Concern has
tive treatment effects are slight (no controlled studies been expressed about the possibility of sudden death
exist), and there remains a significant potential for (presumably caused by arrhythmia) in children taking
adverse effects (urinary incontinence, epididymitis, tricyclic drugs. The mode of action for tricyclic antide-
and aspermia). pressants is unclear.
Stimulant Medication. Sympathomimetic stimulants Table 9-2 Problem Solving for the Night Alarm
such as dexamphetamine have been used to reduce the
depth of sleep in children with enuresis but because Bell “does not Check position, connections, and
work” batteries.
there is no evidence that enuresis is related to abnor- If using separating sheet, check that it is
mally deep sleep, their lack of effectiveness in stopping porous.
bed-wetting is no surprise. Check that child is not turning off
equipment.
Place alarm out of easy reach.
Anticholinergic Drugs. Drugs such as propantheline, Child does not Make alarm louder.
oxybutynin, and terodiline can reduce the frequency wake
Parent should wake child.
of voiding in individuals with neurogenic bladders, re- Child does not Ensure compliance. Ensure that child
duce urgency, and increase functional bladder capacity. become dry responds promptly.
There is no evidence, however, that these anticholiner- Use adjuvant DDAVP or
dextroamphetamine.
gic drugs are effective in bed-wetting, although they Ensure that child has role (e.g., change
may have a role in diurnal enuresis. Side effects are own bedsheets) after alarm.
False alarms Ensure that separating sheet is big
frequent and include dry mouth, blurred vision, head- enough, not soiled, and will insulate.
ache, nausea, and constipation. Use thicker nightclothes.
Relapse Repeat treatment.
Consider overlearning after response to
Psychosocial Treatments re-treatment.
The original night alarm used two electrodes separated

by a device (e.g., bedding) connected to an alarm. When the somewhat remote association between the alarm
the child wet the bed, the urine completed the electrical event and a full bladder after the bladder has emptied.
circuit, sounded the alarm, and the child awoke. All Bladder-volume tracking seems to be a promising treat-
current night-alarm systems are merely refinements on ment for nocturnal enuresis in that it prevents the en-
this original design. A vibrating pad beneath the pillow uretic event, appears to facilitate a permanent cure, and
can be used instead of a bell or buzzer, or the electrodes is noninvasive. This approach uses a miniature bladder-
can be incorporated into a single unit or can be mini- volume measurement instrument during sleep.
aturized so that they can be attached to night (or day)
clothing. With treatment, full cessation of enuresis can
TREATMENT OF DIURNAL ENURESIS
be expected in 80% of cases. Reported cure rates (de-
fined as a minimum of 14 consecutive dry nights) have Daytime enuresis, although it can occur together with
ranged from 50% to 100%. nighttime enuresis, has a different pattern of associa-
The main problem with this form of enuretic treat- tions, and responds to different methods of treatment. It
ment, however, is that cure is usually achieved only is much more likely to be associated with urinary tract
within the second month of treatment. This factor abnormalities, including UTI, and to be comorbid with
may influence clinicians to prescribe pharmacological other psychiatric disorders. As a result, a more detailed
treatments that, although are more immediately grati- and focused medical and psychiatric evaluation is in-
fying, do not offer any real prospect of cure. A further dicated. Urine should be checked repeatedly for infec-
consequence of the delayed response to a night alarm tion, and the threshold for ordering ultrasonographical
is that families fail to persist with the treatment and visualization of the urological system should be low.
may abandon the treatment too soon. Relapse after suc- The history may make it apparent that the daytime wet-
cessful treatment, if it occurs, will usually take place ting is situation specific. For example, school-based
within the first 6 months after cessation of treatment. enuresis in a child who is too timid to ask to use the
It is reported that approximately one-third of children bathroom could be alleviated by the teacher tactfully
relapse; however, no clear predictors of relapse have reminding the child to go to the bathroom at regular
been identified. intervals.
Table 9-2 presents various remedies for night-alarm Observation of children with diurnal enuresis has es-
problems. tablished that they do experience an urge to pass urine
before micturition but that either this urge is ignored or
Ultrasonic Bladder Volume Alarm. The traditional the warning comes too late to be of any use because of
enuresis alarm has good potential for a permanent cure, an “irritable bladder.” Therefore, treatment strategies
but the child is mostly wet during treatment. Further- are based on establishing a pattern of toileting before
more, the moisture alarm requires that the child make the times that diurnal enuresis is likely to occur (usually
between 12 noon and 5 PM), and using positive rein- continence. As with urinary continence, girls achieve
forcement to promote regular use of the bathroom. bowel control earlier than boys do.
Unlike nocturnal enuresis, drug treatment with tri- The main efforts during the diagnostic process are to
cyclic antidepressants, such as imipramine, is ineffec- establish the presence or absence of constipation and, to
tive, whereas the use of anticholinergic agents such as a lesser extent, distinguish continuous (primary) from
oxybutynin and terodiline shows a therapeutic impact discontinuous (secondary) soiling (Figure 9-2). Three
on the frequency of daytime enuresis. types of identifiable encopresis in children have been
identified: (1) it is known that the child can control
defecation, but she or he chooses to defecate in inap-
Encopresis
propriate places; (2) there is true failure to gain bowel
control, and the child is unaware of or unable to con-
DIAGNOSIS
trol soiling; and (3) soiling is due to excessively fluid
Encopresis is usually defined as the intentional or feces, whether from constipation and overflow, physi-
involuntary passage of stool in inappropriate places cal disease, or anxiety. In practice, there is frequently
in the absence of any identified physical abnormality an overlap among types or progression from one to
in children older than 4 years. The distinction is drawn another. Unlike enuresis, fecal soiling rarely occurs at
between encopresis with constipation (retention with night or during sleep, and if present, is indicative of a
overflow) and encopresis without constipation. Other poor prognosis.
classification schemes include making a primary– In the first group, in which bowel control has been es-
secondary distinction (based on having a 1-year period tablished, the stool may be soft or normal (but different
of continence), or soiling with fluid or normal feces. from fluid-type feces seen in overflow). Soiling due to
Less than one-third of children in the United States acute stress events (e.g., the birth of a sibling, a change
have completed toilet training by the age of 2 years. of school, or parental separation) is usually brief once
Bowel control is usually achieved before bladder con- the stress has abated, given a stable home environment
trol. The age cutoff for “normality” is set at 4 years, and sensible management. In more severe pathologi-
the age at which 95% of children have acquired fecal cal family situations, including punitive management
? Soiling
Yes
? Age at least 4 years

Yes
? Sufficient frequency Treat

or impairment
Yes
No ? Associated general Yes

? Loose/fluid stool medical condition Refer appropriately
(not merely constipation)
Yes
No
? Constipated Yes
No
Yes
787.6 Encopresis 307.7 Encopresis

with constipation and without constipation and
overflow incontinence overflow incontinence
Figure 9-2 Diagnostic decision for encopresis.

or frank physical or sexual abuse, the feces may be TREATMENT

deposited in places designed to cause anger or irritation
Practical management for encopresis is presented
or there may be associated smearing of feces on furni-
in Table 9-3. The principal approach to treatment
ture and walls. Other covert aggressive antisocial acts
is predicated on the results of the evaluation and the
may be evident, with considerable denial by the child of
clinical category assigned. This differentiates between
the magnitude or seriousness of the problem.
the need to establish a regular toileting procedure in
In the second group, in which there is failure to learn
children in whom there has been a failure to learn this
bowel control, a nonfluid stool is deposited fairly ran-
social behavior and the need to address a psychiatric
domly in clothes, at home, and at school. There may
disorder, parent–child relationship difficulties, or other
be conditions such as mental retardation or specific de-
stresses in the child who exhibits loss of this previ-
velopmental delay, spina bifida, or cerebral palsy that
ously acquired skill in association with these factors.
impair the ability to recognize the need to defecate,
In both cases, analysis of the soiling behavior may
and the appropriate skills needed to defer this function
identify reinforcing factors important in maintaining
until a socially appropriate time and location. In the
absence of low IQ or pathological physical condition,
individuals with encopresis have been reported as hav-
ing associated enuresis, academic skills problems, and Table 9-3 Practical Management of Encopresis
antisocial behavior. They present to pediatricians pri-
marily, and are usually younger (age 4 to 6 years) than Stage 1 Assessment
Whether primary or secondary.
other encopretic individuals. Is there physical cause?
In the third group, excessively fluid feces are Presence or absence of constipation.
passed, which may result from conditions that cause Presence or absence of acute stress.
Presence or absence of psychiatric disorder
true diarrhea (e.g., ulcerative colitis) or, much more including phobic symptoms or smearing.
frequently, from constipation with overflow causing ABC (antecedents, behavior, consequences) of
spurious diarrhea. A history of retention, either willful encopresis including secondary gain.
Discover reasons for previous failure or
or in response to pain, is prominent in the early days failures.
of this form of encopresis, although later it may be less Stage 2 Advice
apparent because of fecal overflow. Behavior such as Education regarding diet, constipation, and
squatting on the heels to prevent defecation or marked toileting.
Aim to reduce punitive or coercive behavior.
anxiety about the prospect of using the toilet (although Transmit optimism; however, anticipate
rarely amounting to true phobic avoidance) may be disappointment at no instant cure.
described. Preview the stepwise recovery and warn of the
possibility of relapse.
Having identified the presence of encopretic behav-
Stage 3 Toileting
ior and formed some idea of the type of encopresis Baseline observation using star chart.
(primary, secondary, retentive, or a combination), the Focus on positive achievements, e.g., toileting,
remaining task is to discover the presence and extent rather than soiling.
High-fiber diet (try bran in soup, milk shakes).
of any associated conditions, both medical and psycho- Toilet after meals, 15 minutes maximum.
logical. The comprehensive assessment process should Check that adequately rising intra-abdominal
include a medical evaluation, psychiatric and family pressure is present.
Graded exposure scheme if “pot phobic.”
interviews, and a systematic behavioral recording. with
The overall prevalence of encopresis in 7- and Laxatives
8-year-old children has been shown to be 1.5%, with Indicated if physical examination or
boys (2.3%) affected more commonly than girls abdominal radiograph shows fecal loading.
Medication of choice: Senokot syrup (senna)
(0.7%). There was a steadily increasing likelihood of up to 10 mL b.i.d., lactulose syrup up to 30
continence with increasing age, until by age 16 years mL (20 mg) b.i.d.
the reported prevalence was almost zero. A retrospec- Dosage will be reduced over time; titrate with
bowel frequency.
tive study of clinic-referred encopretic children has
Enemas
shown that 40% of cases are primary (true failure to Microenema (e.g., bisacodyl, 30 mL) if the
gain control), with a mean age of 6.7 years, and 60% bowel is excessively loaded with rock-like
of cases are secondary, with a mean age of 8 years. feces.
Eighty percent of the children were constipated, with Stage 4 Biofeedback
no difference in this feature seen between primary and Consider after relapse or failure to respond to
toileting or laxatives.
secondary subtypes.
dysfunction. Detection of significant constipation will, Separation Anxiety Disorder

in addition, provide an indication for adjuvant laxative
therapy. DIAGNOSIS
Separation anxiety disorder (SAD) is typified by
Behavioral Treatments developmentally inappropriate and excessive anxi-
ety concerning separation from home or attachment
Behavioral therapy is the mainstay of treatment for
figures.
encopresis. In the younger child who has been toilet
The assessment strategy will depend upon the child’s
trained, this focuses on practical elimination skills,
age, symptom profile, the sources of available informa-
for example, visiting the toilet after each meal, stay-
tion, and the purpose of the assessment. Separation
ing there for a maximum of 15 minutes, using muscles
anxiety is normal at some ages, and is maximal around
to increase intra-abdominal pressure, and cleaning
14 months of age. The most prevalent symptoms in
oneself adequately afterward. Parents or caretakers,
or both, need to be educated in making the toilet a
pleasant place to visit and should stay with the younger
child, giving encouragement and praise for appropriate DSM-IV-TR Diagnostic Criteria
effort. Systematic recording of positive toileting be-
havior, not necessarily being clean (depending on the 309.21 SEPARATION ANXIETY DISORDER
level of baseline behavior), should be performed with a A. Developmentally inappropriate and excessive anxi-
personal star chart. ety concerning separation from home or from those
Removing the child’s and family’s attention from to whom the individual is attached, as evidenced by
three (or more) of the following:
the encopresis alone and onto noticing, recording, and
(1) recurrent excessive distress when separation from
rewarding positive behavior often defuses tension and home or major attachment figures occurs or is
hostility and provides the opportunity for therapeu- anticipated
tic improvement. Identifying and eliminating sources (2) persistent and excessive worry about losing, or
about possible harm befalling major attachment
of secondary gain, whereby soiling is reinforced by figures
parental (or other individuals’) actions and attention, (3) persistent and excessive worry that an untoward
even if negative or punitive, make positive efforts more event will lead to separation from a major attach-
ment figure (e.g., getting lost or being kidnapped)
fruitful. Formal therapy, either individual or family (4) persistent reluctance or refusal to go to school or
based, is indicated in only a minority of individuals elsewhere because of fear of separation
with an associated mental disorder, marked behavioral (5) persistently and excessively fearful or reluctant
to be alone, or without major attachment figures
disturbance (e.g., smearing, other aggressive soiling), at home, or without significant adults in other
or clear remediable family or social stresses. settings
(6) persistent reluctance or refusal to go to sleep with-
out being near a major attachment figure or to
Physical Treatments sleep away from home
(7) repeated nightmares involving the theme of
In children with retention, leading to constipation and separation
(8) repeated complaints of physical symptoms (such
overflow, medical management is nearly always reas headaches, stomach aches, nausea, or vomiting)
quired, although it is usually done with oral laxatives when separation from major attachment figures oc-
curs or is anticipated
or microenemas alone. The use of more intrusive and
invasive colonic and rectal washout or surgical dis- B. The duration of the disturbance is at least 4 weeks.
C. The onset is before age 18 years.
impaction procedures is nearly always the result of D. The disturbance causes clinically significant distress
the clinician’s impatience rather than the true clinical or impairment in social, academic (occupational), or
need. other important areas of functioning.
E. The disturbance does not occur exclusively during the
course of a pervasive developmental disorder, schizo-
phrenia, or other psychotic disorder and, in adoles-
Biofeedback Therapy cents and adults, is not better accounted for by panic
disorder with agoraphobia.
The finding that some children with treatment-resistant
retentive encopresis involuntarily contract the muscles Specify if:
of the pelvic floor and the external anal sphincter, ef- Early Onset: if onset occurs before age 6 years.
fectively impeding passage of stool has led to efforts Reprinted with permission from the Diagnostic and Statistical
to use biofeedback in such instances. Benefits are Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
unclear.
young children (aged 5–8) are worry about losing, or and comorbidity. In a 3–4-year prospective study of
about possible harm to an attachment figure, and re- subjects with anxiety disorders, 29% of children had
luctance or refusal to go to school. Children aged 9–12 separation anxiety disorder (21% had SAD as their
most frequently reported recurrent excessive distress primary diagnosis at baseline). On follow-up, 92% of
when separated from home or attachment figures, children previously diagnosed with SAD no longer had
whereas adolescents (aged 13–16 years) had physi- symptoms that met full criteria for SAD, although 25%
cal symptoms on school days. More symptoms were had developed a new disorder, most frequently a de-
reported with decreasing age. pressive disorder. Finding that 50% of adult individuals
Other anxiety disorders must be distinguished from with panic disorder had experienced separation anxiety
separation anxiety disorder. In contrast to SAD, where during childhood, it has been hypothesized that sepa-
the anxiety is focused on separation issues, in general- ration anxiety may be a childhood precursor to adult
ized anxiety disorder (GAD) the anxiety is more free panic disorder and agoraphobia. Evidence supporting
floating, less situation specific, and occurs independ- this link is uneven since most studies are retrospective,
ent of separation from the primary attachment figure. focus on separation anxiety symptoms rather than the
Children with social phobia will display a fear of social full disorder and/or fail to include an appropriate con-
situations in which they may be the object of public scru- trol group.
tiny. This anxiety may be ameliorated by the presence of
a familiar person but will not occur exclusively when the
TREATMENT
attachment figure is absent, as with separation anxiety.
School refusal has long been associated with sepa- Following a good behavioral and functional analysis,
ration anxiety disorder, though this relationship holds the most frequently employed clinical approach to the
mainly for younger children when school nonattendance treatment of separation anxiety and school refusal is
is most closely linked to fear of separation, whereas in behavioral. The principles of systematic desensitization
adolescents fear of school and social-evaluative situa- to feared objects or situations will be employed, gradu-
tions is more typical. It is important in the assessment ally increasing the amount of separation that can be
of school nonattendance, a frequent impairment associ- tolerated in a graduated fashion. Systematic desensiti-
ated with SAD, to distinguish anxiety-related school re- zation usually has three components. First, a response,
fusal from conduct disorder-related truancy. Typically incompatible with anxiety (often progressive muscular
the school-refusing child will stay at home or with par- relaxation, but can be imagery or breathing exercises)
ents, whereas the truanting child will go off with peers. is taught. The second component is the collaborative
In the presence of school refusal, a useful approach is construction of a hierarchy of feared situations. These
to attempt to categorize the behavior as fulfilling one of will range from the very mild (producing mild disquiet)
the following four functions: (1) avoidance of stimuli to the most anxiety provoking (avoided at all costs!).
provoking specific fearfulness or anxiety (e.g., separa- It is important to include a great deal of specificity
tion); (2) escape from aversive social or evaluative situ- in describing these situations, including the duration
ations (e.g., social phobia); (3) attention-getting behav- spent in the feared situation, the degree to which oth-
ior (e.g., physical complaints/tantrums); or (4) positive ers are present, the distance from home/attachment fig-
tangible reinforcement (e.g., parental collusion). ure etc. After ranking these feared situations, the final
The community prevalence of SAD is generally es- component of treatment is the regular progression of
timated to be around 4% in children and young ado- exposure to feared situations while employing anxiety
lescents; it decreases in prevalence from childhood management techniques. It is important that the child
through adolescence. Among clinically referred sub- is allowed to exercise some control over the speed with
jects (aged 5–18) with anxiety disorders, separation which the new settings are experienced. The avoidance
anxiety disorder was found to be the most frequently of reinforcement of unwanted behaviors and the promo-
occurring disorder, with a lifetime prevalence of 44.7%. tion of fear-coping strategies is similarly important.
Separation anxiety, particularly in younger samples, is In the particular example of school refusal associated
found more frequently in girls than in boys—ratio as with separation anxiety, it is important to encourage an
high as 2.5 : 1. early return to school so that secondary impairments
(academic failure and social isolation) are minimized.
Generally, if the period of absence has been less than
Course
2 months then return is very often successful; longer
The age of onset has been reported to be 4–7 years, than this is frequently associated with much greater
with earlier onset being associated with clinical status difficulty negotiating adequate attendance.
In older subjects, cognitive approaches may be more features (i.e., not talking to family members, abrupt
successful than the primary behavior strategies usually cessation of speech in one setting, absence of commu-
employed with younger children. Cognitive approaches nication in all settings) suggestive of other neurologi-
postulate that the child’s maladaptive thoughts, beliefs, cal or psychiatric disorders (e.g., pervasive develop-
and attitudes (schema) cause or maintain the experimental disorders, acquired aphasias), and any history
ence of anxiety. Treatment consists of identifying nega- of neurological insult/injury, developmental delays
tive self-statements (“I can’t ever do this”), or exter- or atypical language and/or speech. The assessment
nal beliefs (“If I’m not there my mom won’t be able to should also include the degree to which nonverbal
cope”) and replacing them with more adaptive beliefs. communication or non-face-to-face communication is
Pharmacological treatment studies of separation possible, the presence of anxiety symptoms in areas
anxiety have tended to focus on samples with school- other than speaking, social and behavioral inhibition,
refusal behavior and various comorbidities. Consider- medical history including ear infections, and hearing
ing safety and efficacy, the SSRIs appear to be the first- deficiencies. Parents will be able to give information
line treatment for separation anxiety disorder, but more on where and to whom the child will speak, the child’s
studies are needed to confirm the presently preliminary speech and language complexity at home, articulation
results. Tricyclic antidepressants and benzodiazepines problems, use of nonverbal communication (gestures
may be considered when the child has not responded to etc.), any history of speech and language delays, and
SSRIs or when adverse effects have exceeded benefits. the possible importance of bilingualism (where pri-
In practice, however, clinicians often combine drug mary language is not English). It can be useful to have
and psychosocial treatments, capitalizing on differ- the parents provide an audiotape of the child speaking
ences in dose–response and time–response parameters. at home.
There is some evidence that treatments can be additive The child evaluation can assess the presence of anxi-
(each treatment having unique benefits) or synergistic ety and social inhibition (willingness to communicate
(the benefit of the combination is greater that the addi- through gesture or drawing). Physical examination of
tive combination). Alternatively, when combining drug oral sensory and motor ability may provide evidence of
and psychosocial treatments, a lower dose of one or neurological problems (i.e., drooling, asymmetry, oro-
both may be possible, with a resultant decrease in ex- facial weakness, abnormal gag reflex, impaired sucking
pense, inconvenience, or adverse events. Drug effects or swallowing). Specialist audiometry (pure tone and
are often seen sooner than those due to exposure-based speech stimuli as well as tympanometry and acoustic
therapy, though it is hoped that the slower to emerge reflex testing) may provide evidence of hearing and/or
benefits of therapy may be more long lasting. middle ear problems that can have a significant effect
on speech and language development. Cognitive abili-
ties may be difficult to assess, but the performance sec-
Selective Mutism
tion of the WISC-R or Raven’s Progressive Matrices as
well as the Peabody Picture Vocabulary Test may be
DIAGNOSIS
useful in the nonverbal child.
The essential feature of selective mutism is the persistent The prevalence of selective mutism is usually re-
failure to speak in specific social situations (e.g., school, ported as 0.6 to 7 per 1000, with higher incidence in
or with peers) where speaking is expected, despite females rather than males. When subjects failing to
speaking in other situations (e.g., home). Previously re- speak in the first few weeks of school (a DSM-IV-TR
ferred to as Elective Mutism, in DSM-III the condition requirement) are excluded rates do not exceed 2 per
was renamed Selective Mutism, so as to be less judg- 1000. Onset is usually in the preschool years, but the
mental (doesn’t speak rather than chooses not to speak). peak age of presentation and diagnosis is between 6
Prior to making a diagnosis of selective mutism, a and 8 years. A high incidence of insidious onset of re-
comprehensive evaluation should be conducted to rule fusal to speak with anyone except family members is
out other explanations for mutism and to assess impor- reported. The other typical picture is one of acute onset
tant comorbid factors. For obvious reasons, the paren- of mutism on starting school.
tal interview will form the mainstay of evaluation, but
as discussed below, direct observation (and interview if
TREATMENT
possible) of the child can afford important diagnostic
information. Treatment has long been regarded as difficult and
It is important to obtain information about the nature prognosis poor. Approaches have included behavioral
of the onset (insidious or sudden), any uncharacteristic therapy, family therapy, speech therapy, and more
recently pharmacological agents. Unfortunately, most twice a month in children aged under 7 years and at
published studies are single case reports, with very few least once a month in children aged 7 years or more.
controlled studies. Results of pharmacotherapy use are In contrast, DSM-IV-TR requires either a frequency of
disappointing. twice a week for at least 3 consecutive months (regard-
Behavioral treatment focuses on mutism as a means less of age) or else the presence of clinically significant
of getting attention and/or escaping from anxiety. The distress or impairment. Furthermore, ICD-10 includes a
goal of a treatment program should be to decrease the very strict exclusion criterion, preventing a diagnosis of
anxiety associated with speaking while encouraging enuresis to be made if there is any evidence of another
the child to interact verbally. mental disorder. In ICD-10, this disorder is referred to
as “Nonorganic Enuresis.”
For separation anxiety disorder, the DSM-IV-TR
COMPARISON OF DSM-IV AND ICD-10
and ICD-10 symptom items are almost identical. The
DIAGNOSTIC CRITERIA
ICD-10 Diagnostic Criteria for Research are narrower
In contrast to DSM-IV-TR, which establishes a mini- in that the age of onset must be before age 6 and the
mum duration of 3 months for encopresis, the ICD-10 diagnosis cannot be made if the presentation is “part of
Diagnostic Criteria for Research has set a minimum a broader disturbance of emotions, conduct, or person-
duration of 6 months. In ICD-10, this disorder is reality.” The DSM-IV-TR criteria and ICD-10 Diagnostic
ferred to as “Nonorganic Encopresis.” Criteria for Research for selective mutism are almost
For enuresis, the ICD-10 Diagnostic Criteria for Re- identical. In ICD-10, the disorder is referred to as “elec-
search have a different frequency threshold: at least tive mutism.”
CHAPTER
10 Childhood Disorders: Reactive

Attachment Disorder of Infancy
or Early Childhood
DIAGNOSIS
DSM-IV-TR defines Reactive Attachment Disorder
(RAD) as markedly disturbed and developmentally
inappropriate social relatedness in most contexts, be-
ginning before age 5 years, as evidenced by either 313.89 REACTIVE ATTACHMENT DISORDER OF INFANCY OR EARLY
restricted or indiscriminate social interaction. The CHILDHOOD
abnormal relatedness cannot strictly be accounted for A. Markedly disturbed and developmentally inappropri-
by developmental delay or by autism. In addition, evi- ate social relatedness in most contexts, beginning be-
dence of pathogenic care such as institutionalization, fore age 5 years, as evidenced by either (1) or (2)
emotional or physical neglect, or multiple changes in (1) persistent failure to initiate or respond in a devel-
primary caregivers is evident. The diagnosis means opmentally appropriate fashion to most social in-
teractions, as manifested by excessive inhibited,
to imply that the child’s attachment relationships are hypervigilant, or highly ambivalent and contra-
impaired in reaction to “pathogenic caregiving.” The dictory responses (e.g., the child may respond to
socially aberrant behaviors are evident across social caregivers with a mixture of approach, avoidance,
and resistance to comforting, or may exhibit frozen
contexts. watchfulness).
Reactive Attachment Disorder has two subtypes: (2) diffuse attachments as manifest by indiscriminate
sociability with marked inability to exhibit appro-
the inhibited/emotionally withdrawn subtype and the priate selective attachments (e.g., excessive famili-
disinhibited/indiscriminately social subtype. The in- arity with strangers or lack of selectivity in choice
hibited subtype is marked by emotional withdrawal, of attachment figures).
failure of social and emotional reciprocity, and lack of B. The disturbance in Criterion A is not accounted for
seeking or responding to comforting when distressed. solely by developmental delay (as in Mental Retarda-
tion) and does not meet current criteria for a Pervasive
Attachment behaviors, such as seeking and accepting Developmental Disorder.
comfort, showing and responding to affection, rely- C. Pathogenic care as evidenced by at least one of the
ing on caregivers for help, and cooperating with car- following:
egivers are absent or markedly restricted. In addition, (1) persistent disregard of the child’s basic emotional
needs for comfort, stimulation, and affection
exploratory behavior is limited owing to the absence (2) persistent disregard of the child’s basic physical
of a preferred attachment figure. These children may needs
also demonstrate problems of emotion regulation that (3) repeated changes of primary caregiver that pre-
vent formation of stable attachments (e.g., frequent
range from affective blunting to withdrawal, to “fro- changes in foster care).
zen watchfulness.” This subtype has been described in D. There is a presumption that the care in Criterion C is
institutionalized children and in abused or neglected responsible for the disturbed behavior in Criterion A
children. (e.g., the disturbance in Criterion A began following
the pathogenic care in Criterion C).
The disinhibited/indiscriminately social subtype
Reprinted with permission from the Diagnostic and Statistical
is characterized by more interaction with caregivers; Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
however, there is failure to demonstrate selectivity in American Psychiatric Association.
interacting with others. Stranger wariness, which ap-
pears as early as 7 months of age and remains apparent
for several years, is absent. Children with this subtype Mental Retardation (MR). Young children with RAD
may approach strangers without expected social wari- often have significant developmental delays, and the
ness around unfamiliar adults, may seek comfort or same deprivation that causes RAD also increases risk
help from a stranger, and may demonstrate a variety for developmental delays. Infants and toddlers with
of social relatedness problems that depend upon accu- mental retardation may not develop attachments that
rately reading social cues and understanding interper- are consistent with their age, but they should be consist-
sonal boundaries. This subtype has been demonstrated ent with their developmental level. Thus, it is important
in maltreated children, institutionalized children, and to assess the cognitive level of children who appear in-
children adopted out of institutions. discriminate to be sure that they are not merely delayed
The disturbed social behavior that characterizes in the development of selectivity as evidenced by the
RAD should be evident by report or observation across absence of stranger wariness and separation anxiety.
most social contexts and relationships. Obviously, self- A developmental screen and adjustment for the child’s
report in young children is less likely to be obtained or overall mental age should suffice.
elicit relevant clinical information; therefore, caregiver
report is essential. Observation of the child in the clinic Pervasive Developmental Disorders (PDD). Al-
interacting with relative strangers as well as in natural- though deficits in reciprocal social interaction are at
istic settings is quite valuable. Specialized structured the core of autism and Pervasive Developmental Disor-
clinical interviews and semistructured observational ders (PDD) and are observed early in life, children with
assessments may be helpful in eliciting disturbances in these disorders do form selective attachments, although
sociability related to attachment. they may be deviant. Also complicating this picture is
The current diagnostic requirement is that marked that these children also have cognitive delay and stere-
disturbances in social behavior are apparent before the otypies, conditions that are frequently associated with
age of 5 years. There is no research evidence to sup- institutionalization or profound neglect (see below).
port this upper limit, although the literature on mater- If the psychosocial and caregiving environment is
nal deprivation, maltreatment, and institutionalization deemed adequate and there is no history of pathologic
suggests that earlier insults to social development and caregiving, the social disturbance is likely a social defi-
attachment result in persistent and pervasive defects in cit in the child rather than reactive to the caregiving
social competence. environment. In this case, PDD will be the most likely
A variety of impairments are associated with RAD. diagnosis. Changes in the caregiving environment will
By definition, children with the disorder are socially not result in improved social or attachment behaviors
impaired, either withdrawn and detached or socially and may worsen the child’s condition because of loss of
disinhibited and indiscriminating. Long-term impair- an attachment figure.
ments in peer relationships are associated with indis- In addition, in most cases, although cognitive and
criminate behavior at age 4 and 8 years. In addition, language delays may be apparent in both socially de-
cognitive delays often arise in the same contexts of prived children and children with PDD, there is no
deprivation that give rise to signs of RAD. reason to expect the pattern of restricted interest and
Other behavioral abnormalities that may mimic activities associated with PDD in children with RAD.
mental disorders include a quasi-autistic syndrome that Instead, one may expect children with the inhibited/
appears to arise as a result of institutionalization rather emotionally withdrawn pattern to exhibit a pervasive
than genetic or intrinsic neurobiological abnormalities. social and emotional withdrawal. Furthermore, there
Although symptomatically virtually indistinguishable is no reason to expect a selective deficit in symboliza-
from classic autism, this institutional syndrome does tion in RAD; instead, one would expect expressive and
not show male predominance, is not associated with receptive language and pretend play to be roughly at the
enlarged head circumference, and generally shows same level as overall cognitive level (e.g., as assessed
marked improvement after the child is placed with a by developmental tests such as the Bayley scores).
family.
Posttraumatic Stress Disorder (PTSD). Children
who have been abused or witnessed violence may
show fear, clinging, or withdrawal from caregivers,
Several conditions of early childhood may have symp- symptoms that may be consistent with the hyperar-
toms that overlap with RAD and cause diagnostic ousal and avoidant clusters of a toddler’s posttrau-
confusion. matic symptomatology. These symptoms overlap with
Chapter 10 • Childhood Disorders: Reactive Attachment Disorder 83
the inhibited, hypervigilant, or highly ambivalent and a persistent pattern of socially impulsive behavior.
contradictory responses defined by DSM-IV-TR cri- These behaviors must be distinguished from the im-
teria. To be certain, abuse and exposure to domestic pulsivity that characterizes ADHD. Complicating the
violence is “pathogenic caregiving,” but it is uncer- distinction is evidence that a syndrome of inatten-
tain whether these symptoms should primarily be tion and overactivity may develop in the context of
considered as Posttraumatic Stress Disorder (PTSD) institutionalization.
or RAD, inhibited/emotionally withdrawn type. If in Although ADHD and the disinhibited type of RAD
question, the clinician should inquire into and observe may be associated with social impulsivity, there is no
for reexperiencing symptoms (posttraumatic play, play reason to expect children with disinhibited RAD to
reenactment, nightmares, dissociation, distress on ex- manifest inattention or hyperactivity. If, on the other
posure), and increased arousal (sleep disturbances, hand, the child meets criteria for both disorders, both
impaired concentration, hypervigilance, and exagger- diagnoses should be assigned.
ated startle). At this point, however, there is no reason
not to diagnose both conditions if evidence for both
TREATMENT
exists.
By definition, attachment disorders are encountered in
Failure to Thrive (FTT). The DSM-III conceptualiza- children who have not experienced an opportunity to
tion of RAD included growth failure and lack of social form lasting secure relationships. Common scenarios
responsivity as central features, and confusion about include children raised in institutions, placed in mul-
this initial overlap continues in the literature. In early tiple foster care homes, or who have had extremely
infancy, lack of eye tracking or responsive smiling by disturbed experiences of care with a single caregiver.
2 months of age, and failure to reach out to be picked up Intervention, therefore, should take into account the to-
by 6 months of age should be noted as aberrant social tality of the child’s prior experience, current placement,
behaviors but not diagnosed as RAD, inhibited type. and other significant relationships.
If the child demonstrates psychosocial dwarfism and The first consideration is the child’s current health
social inhibition or indiscriminateness, both diagnoses and safety. Maltreatment of children under 4 years
would be appropriate. of age is associated with significant morbidity and
mortality; therefore, involvement of child protective
Conduct Disorder. There has been much confusion services is frequently warranted. The child should be
in older children and adolescents about RAD and assessed by a pediatrician for sequelae of malnutri-
psychopathy. In fact, it is unclear if RAD is identifi- tion, substandard health care, and abuse. Given the
able in middle childhood and adolescence, and if so, extreme comorbidity with cognitive and speech delay,
what its manifestations are. The possibilities are as the child should also be referred to early intervention
follows: (1) RAD resolves itself in early childhood or services.
soon after transition to middle childhood, (2) RAD Once these issues have been addressed, the nurtur-
has different and yet-to-be-defi ned characteristics in ing environment should be evaluated and supported to
middle childhood and adolescence, or (3) RAD is a help the current caregivers provide an appropriately
pathway into another kind of disorder, such as dis- nurturing and stimulating environment. If the child
ruptive behavior disorders. Some of the confusion ap- currently resides in a dangerous or destructive caregiv-
pears to derive from the problem that children with ing environment, an assessment of parental fitness may
disruptive behavior disorders often have troubled re- be warranted. Removal of the child is mandated if the
lationships with their caregivers, thus leading to an child has sustained life-threatening injuries or is in
assumption that symptoms and signs of aggression, imminent jeopardy. While the placement of the child
oppositionality, and anger are, in fact, disorders of in foster care necessarily disrupts the child’s relation-
attachment. In many cases, the emphasis on opposi- ship with the primary caregiver, safety must be the first
tionality, aggression, and lack of empathy suggests priority.
something other than RAD, perhaps a unique devel- After placement in care, approaches to determining
opmental path to oppositional defiant disorder or early whether reunification is possible, or whether the child
conduct disorder. should be freed for adoption should be implemented.
These approaches emphasize building new attachment
Attention-Deficit/Hyperactivity Disorder. Young relationships and helping the child transition from one
children with RAD, disinhibited type, demonstrate setting to the next gradually. Throughout, it is necessary
to maintain a focus on the child’s best interest while Pharmacotherapy

determining whether reunification or termination of
There are no reported case reports of psychopharmaco-
parental rights and adoption is indicated.
logical management of either the inhibited/emotionally
Owing to the multiple needs of children in foster
withdrawn or disinhibited/indiscriminately social sub-
care and their caregivers, coordination and integra-
types of RAD, nor is there reason to expect these signs
tion of services for the child, biological parents, and
and symptoms to respond to psychopharmacological
foster parents is critical. Appropriate mental health,
intervention.
substance use, and other supportive services programs
should be made available to the caregivers. Critical for
all caregivers is the desire to value the baby as an in- Alternative Coercive Psychosocial Treatments
dividual and the ability to appropriately respond to the
Several alternative treatments of attachment, such as
child’s bids for comfort, safety, and autonomy.
“coercive holding therapies,” “rebirthing therapies,”
Educational instruction about developmental capaci-
and similar “rage reduction therapies,” have resulted in
ties, temperamental characteristics, and appropriate
the well-publicized deaths of several children. Parents
interpretations and responses to a child’s negative emo-
of these children were following the advice of holding
tion may be indicated. Focusing on improving the par-
therapists, or allowing the therapists to coerce their
ent’s ability to respond as a “secure base” from which
children into rageful outbursts, followed by tragically
the child can explore his environment and a “safe-
misguided or frankly sadistic parental responses. It is
haven” to return to when distressed can be accom-
more than likely that these cases represent early on-
plished through focusing on the parent’s behavioral in-
set conduct disorders with a history of early pathologic
teraction with the child, the parent’s perception of the
caregiving rather than RAD. These nonconventional
child’s intentional bids, or a combination of the two.
and not recommended treatments may be called at-
Barriers to the caregiver’s emotional availability may
tachment therapies, but are not drawn from either at-
be addressed in individual therapy focused on the par-
tachment theory or research and appear to run the risk
ent’s own experience of care and its influence on their
of retraumatizing already traumatized children
own provision of care.
Long-term intervention is frequently necessary and
a successful intervention should address crisis inter- COMPARISON OF DSM-IV-TR AND ICD-10
vention, developmental guidance, and infant/toddler– DIAGNOSTIC CRITERIA
parent psychotherapy in which the child is present. If
The DSM-IV-TR Reactive Attachment Disorder has
working with parents who are providing the improved
two subtypes (inhibited type and disinhibited type)
nurturing environment—foster parents and adoptive
that roughly correspond to the two ICD-10 categories,
parents—the clinician should focus on similar aspects
reactive attachment disorder of childhood and disin-
as above and also on “goodness-of-fit” and should as-
hibited attachment disorder of childhood. The ICD-10
sess the parents’ motivation to care for this child, the
categories are probably much more inclusive because
parents’ perceptions of the child and their derivations,
they do not specify that disturbed behavior be the result
and the parent’s fears about the impact of the child’s
of pathogenic care.
early environment.
CHAPTER
11 Delirium, Dementia,
and Amnestic Disorders
This chapter reviews delirium, dementia, and amnes- its specific etiology is presented first, followed by brief
tic disorders. Traditionally, these conditions have been sections on Delirium Due to a General Medical Condi-
classified as organic brain disorders to distinguish them tion, Medication-induced Delirium, Substance Intoxi-
from such diseases as schizophrenia, mania, and major cation Delirium, Substance-Withdrawal Delirium, and
depressive disorder, the so-called functional disorders. Delirium Due to Multiple Etiologies.
With the publication of the DSM-IV, the distinction be-
tween functional and organic disorders was eliminated.
DIAGNOSIS
Significant research into the neurobiological aspects of
mental disorders and the utilization of sophisticated Delirium (also known as acute confusional state, toxic
neurodiagnostic tests such as positron emission tomo- metabolic encephalopathy) is the behavioral response
graphic scanning in individuals with schizophrenia led to widespread disturbances in cerebral metabolism.
to the inescapable conclusion that every psychiatric Like dementia, delirium is not a disease but a syn-
condition has a biological component. Thus, the term drome with many possible causes that result in a simi-
functional became obsolete and even misleading. lar constellation of symptoms (the diagnostic criteria
The conditions formerly called organic are clas- for the “syndrome” of delirium are listed as Criteria A,
sified in DSM-IV-TR into three groups: (1) delirium, B, and C).
dementia, and amnestic and other cognitive disorders; According to DSM-IV-TR, the primary feature of
(2) mental disorders due to a general medical condition delirium is a diminished clarity of awareness of the
(covered in Chapter 12 of this book); and (3) substance- environment. Symptoms of delirium are characteris-
related disorders (covered in Chapters 13–24 in this tically global, of acute onset, fluctuating, and of rela-
book). Delirium, dementia, and amnestic disorders are tively brief duration. In most cases of delirium, an often
classified as cognitive because they feature impairment overlooked prodrome of altered sleep patterns, unex-
in such parameters as memory, language, or attention
as a cardinal symptom. Each of these three major cog-
nitive disorders is subdivided into categories that as- DSM-IV-TR Diagnostic Criteria
cribe the etiology of the disorder to a general medical
condition, the persisting effects of a substance, or mul- DSM-IV-TR DIAGNOSTIC CRITERIA FOR DELIRIUM
tiple etiologies. A “not otherwise specified” category is A. Disturbance of consciousness (i.e., reduced clarity of
included for each disorder. awareness of the environment) with reduced ability to
focus, sustain, or shift attention.
B. A change in cognition (such as memory deficit, disori-
Delirium entation, language disturbance) or the development of
a perceptual disturbance that is not better accounted
for by a preexisting, established or evolving dementia.
The disorders in this section share a common symptom C. The disturbance develops over a short period of time
presentation of a disturbance in consciousness and cog- (usually hours to days) and tends to fluctuate during
the course of the day.
nition, but are differentiated (as in DSM-IV-TR) on the D. [Varies based on etiology—see specific disorders for
basis of etiology (i.e., Delirium Due to a General Medi- discussion.]
cal Condition, Substance-Induced Delirium, and Delir- Reprinted with permission from DSM-IV-TR Guidebook. Copy-
ium Due to Multiple Etiologies). Information regarding right 2004, Michael B First, Allen Frances, and Harold Alan
Pincus.
the diagnosis, and treatment of delirium regardless of
plained fatigue, fluctuating mood, sleep phobia, rest- the individual. Although auditory illusions may lead to
lessness, anxiety, and nightmares occur. A review of tactile hallucinations, the most common hallucinations
nursing notes for the days before the recognized onset in delirium are visual and auditory.
of delirium often illustrates early warning signs of the Orientation is often abnormal in delirium. Disori-
condition. entation, in particular, seems to follow a fluctuating
The clinical features of delirium can be divided into course, with individuals being unable to answer ques-
abnormalities of (1) arousal, (2) language and cognitions about orientation in the morning, yet be fully ori-
tion, (3) perception, (4) orientation, (5) mood, (6) sleep ented by the afternoon. Orientation to time, place, per-
and wakefulness, and (7) neurological functioning. son, and situation should be evaluated in the individual
The state of arousal in individuals who are deliri- who is delirious. Generally, orientation to time is the
ous may be increased or decreased. Some individu- sphere most likely impaired, with orientation to per-
als exhibit marked restlessness, heightened startle, son usually preserved. Orientation to significant people
hypervigilance, and increased alertness. This pattern (parents, children) should also be tested. Disorientation
is often seen in states of withdrawal from depressive to self is rare and indicates significant impairment. The
substances (e.g., alcohol) or intoxication by stimulants examiner should always reorient individuals who do
and hallucinogens (e.g., phencyclidine, amphetamine, not perform well in any portion of the orientation test-
lysergic acid diethylamide). Individuals with increased ing of the mental status examination, and serial testing
arousal often have such concomitant autonomic signs of orientation on subsequent days is important.
as pallor, sweating, tachycardia, mydriasis, hyperther- Individuals with delirium are susceptible to rapid
mia, piloerection, and gastrointestinal distress. These fluctuations in mood. Unprovoked anger and rage re-
individuals often require sedation with neuroleptics actions occasionally occur and may lead to attacks on
or benzodiazepines. Hypoactive arousal states such as hospital staff. Fear is a common emotion and may lead
those occasionally seen in hepatic encephalopathy and to increased vigilance and an unwillingness to sleep
hypercapnia are often initially perceived as depressed because of increased vulnerability during somnolence.
or demented states. The clinical course of delirium in Apathy, such as that seen in hepatic encephalopathy,
any particular individual may include both increased depression, use of certain medications (e.g., sulfam-
and decreased arousal states. Many such individuals ethoxazole [Bactrim]), and frontal lobe syndromes, is
display daytime sedation with nocturnal agitation and common, as is euphoria secondary to medications (e.g.,
behavioral problems (sundowning). corticosteroids, DDC, zidovudine) and drugs of abuse
Individuals with delirium frequently have abnormal (phencyclidine, inhalants).
production and comprehension of speech. Nonsensi- Sleeping patterns of individuals who are delirious
cal rambling and incoherent speech may occur. Other are usually abnormal. During the day, they can be
individuals may be completely mute. Memory may be hypersomnolent, often falling asleep in midsentence,
impaired, especially primary and secondary memory. whereas at night they are combative and restless. Sleep
Remote memory may be preserved, although the indi- is generally fragmented, and vivid nightmares are
vidual may have difficulty distinguishing the present common.
from the distant past. Neurological symptoms often occur in delirium.
Perceptual abnormalities in delirium represent an These include dysphagia as seen after a cerebrovascu-
inability to discriminate sensory stimuli and to in- lar accident (CVA), tremor, asterixis (hepatic enceph-
tegrate current perceptions with past experiences. alopathy, hypoxia, uremia), poor coordination, gait
Consequently, individuals tend to personalize events, apraxia, frontal release signs (grasp, suck), choreiform
conversations, and so forth that do not directly pertain movements, seizures, Babinski’s sign, and dysarthria.
to them, become obsessed with irrelevant stimuli, and Focal neurological signs occur less frequently.
misinterpret objects in their environment. The misin- The appropriate workup of individuals who are delir-
terpretations generally take the form of auditory and ious includes a complete physical status, mental status,
visual illusions. Individuals with auditory illusions, for and neurological examination. History taking from the
example, might hear the sound of leaves rustling and individual, any available family, previous physicians,
perceive it as someone whispering about them. This an old chart, and the individual’s current nurse is essen-
interpretation may result in paranoia and sleep phobia. tial. Previous delirious states, etiologies identified in
Typical visual illusions are that intravenous tubing is the past, and interventions that proved effective should
a snake or worm crawling into the skin, or that a res- be elucidated. Appropriate evaluation of the delirious
pirator is a truck or farm vehicle about to collide with individual is reviewed in Figure 11-1.
Chapter 11 • Delirium, Dementia, and Amnestic Disorders 87
Clues to etiology Review prescribed medications
Check for sleep−

wakefulness disturbance
Sensory deprivation
The history
Onset and duration Interview family
Review nursing notes
Previous similar episodes Review past medical record
Localizing neurological signs CT, MRI, electroencephalogram
Prominent adrenergic Investigate drug withdrawal

signs, including fever
Do a septic work-up
Indications of substance abuse Toxicology screen

The physical
examination Evidence of organ Appropriate laboratory and
disease or failure radiological studies
Overall state of Monitor intake and output

hydration and nutrition and correct imbalances
Postsurgical complications
Blood levels of
prescribed medications
Metabolic screen
The laboratory
examination Hematological screen
Endocrinological screen
Figure 11-1 Evaluation of delirium.
The overall prevalence of delirium in the commu- toms in certain populations may take weeks to resolve.
nity is low, but delirium is common among individu- The age of the individual and the period of time during
als who are hospitalized. Studies of elderly patients which the individual was delirious affect the symptom
suggest that about 40% of them admitted to general resolution time. In general, the individual has a spotty
medical wards showed signs of delirium at some point memory for events that occurred during delirium. These
during the hospitalization. Because of the increasing remembrances are reinforced by comments from the
numbers of elderly in the US and the influence of life- staff (“You’re not as confused today”), or the presence of
extending technology, the population of hospitalized a sitter, or use of wrist restraints. Such individuals should
elderly is rising, and so is the prevalence of delirium. be reassured that they were not responsible for their be-
The intensive care unit, geriatric psychiatry ward, emer- havior while delirious, and that no one hates or resents
gency department, alcohol treatment units, and oncol- them for the behavior they may have exhibited. Individu-
ogy wards have particularly high rates of delirium. als with underlying dementia show residual cognitive
impairment after resolution of delirium, and it has been
suggested that a delirium may merge into a dementia.
Course
In general, the mortality and morbidity of any serious
After elimination of the cause of the delirium, the symp- disease are doubled if delirium ensues. The risk of dying
toms gradually recede within 3 to 7 days. Some symp- after a delirious episode is greatest in the first 2 years after
the illness, with a higher risk of death from heart disease Table 11-1 Causes of Delirium
and cancer in women and from pneumonia in men. Over-
all, the 3-month mortality rate for persons who have an Medication effect or interaction
Substance intoxication or withdrawal
episode of delirium is about 28%, and the 1-year mortal- Infection
ity rate for such individuals may be as high as 50%. Head injury
Metabolic disarray
Acid–base imbalance
Differential Diagnosis Dehydration
Malnutrition
Delirium must be differentiated from dementia be- Electrolyte imbalance
Blood glucose abnormality
cause the two conditions may have different prognoses. Carbon dioxide narcosis
In contrast with the changes in dementia, those in de- Uremic encephalopathy
lirium have an acute onset. The symptoms in dementia Hepatic encephalopathy
Cerebrovascular insufficiency
tend to be relatively stable over time, whereas clinical Congestive heart failure
features of delirium display wide fluctuation with peri- Hypovolemia
Arrhythmias
ods of relative lucidity. Clouding of consciousness is an Severe anemia
essential feature of delirium, but demented individuals Transient ischemia
are usually alert. Attention and orientation are more Acute CVA
Endocrine dysfunction
commonly disturbed in delirium, although the latter Postoperative states
can become impaired in advanced dementia. Percep- Postcardiotomy delirium
tion abnormalities, alterations in the sleep–wakefulness Environmental factors
Intensive care unit psychosis
cycle, and abnormalities of speech are more common Sleep deprivation
in delirium. Most important, a delirium is more likely
to be reversible than is a dementia. Delirium and de-
mentia can occur simultaneously; in fact, the presence
Delirium Due to a General Medical Condition
of dementia is a risk factor for delirium. Some studies
suggest that about 30% of individuals who are hospital- The causes of Delirium Due to a General Medical
ized with dementia have a superimposed delirium. Condition may lie in intracranial processes, extracra-
Delirium must be differentiated from psychotic states nial ones, or a combination of the two. The most com-
related to such conditions as schizophrenia or mania mon etiological factors are described in the following
and factitious disorders with psychological symptoms subsections.
or malingering. Generally, the psychotic features of
schizophrenia are more constant and better organ- Infection Induced. Infection is a common cause of
ized than are those in delirium, and individuals with delirium among individuals who are hospitalized and
schizophrenia seldom have the clouding of conscious- typically, infected patients will display abnormalities
ness seen in delirium. The “psychosis” of individuals in hematology and serology. Bacteremic septicemia
with factitious disorder or malingering is inconsistent, (especially that caused by gram-negative bacteria),
and these persons do not exhibit many of the associated pneumonia, encephalitis, and meningitis are common
features of delirium. Apathetic and lethargic individu- offenders. The elderly are particularly susceptible to
als with delirium may occasionally resemble depressed delirium secondary to urinary tract infections.
individuals, but tests such as electroencephalogram
(EEG) distinguish between the two. The EEG demon- Metabolic and Endocrine Disturbances. Metabolic
strates diffuse slowing in most delirious states, except causes of delirium include hypoglycemia, electrolyte
for the low-amplitude, fast activity EEG pattern seen disturbances, and vitamin deficiency states. The most
in alcohol withdrawal. In contrast, the EEG in a func- common endocrine causes are hyperfunction and
tional depression or psychosis is normal. hypofunction of the thyroid, adrenal, pancreas, pitui-
Predisposing factors in the development of delirium tary, and parathyroid. Metabolic causes may involve
include old age, young age (children), previous brain consequences of diseases of particular organs, such as
damage, prior episodes of delirium, malnutrition, hepatic encephalopathy resulting from liver disease, ure-
sensory impairment (especially vision), and alcohol mic encephalopathy and postdialysis delirium resulting
dependence. from kidney dysfunction, and carbon dioxide macrosis
The specific causes of delirium are summarized in and hypoxia resulting from lung disease. The metabolic
Table 11-1. Information regarding the specific causes of disturbance or endocrinopathy must be known to induce
delirium is included in the next sections. changes in mental status and must be confirmed by lab-
oratory determinations or physical examination, and the Table 11-2 Selected Drugs Associated with Delirium
temporal course of the confusion should coincide with
the disturbance. In some individuals, particularly the Antihypertensives Indomethacin
Amphotericin B Ketamine
elderly, the brain injured, and the demented, there may Antispasmodics Levodopa
be a significant lag time between correction of meta- Antituberculous agents Lidocaine
bolic parameters and improvement in mental state. Baclofen Lithium
Barbiturates Meperidine
Cimetidine Morphine
Low-Perfusion States. Any condition that decreases Corticosteroids Procainamide
effective cerebral perfusion can cause delirium. Com- Colchicine Pentamidine
Contrast media Tricyclic antidepressants
mon offenders are hypovolemia, congestive heart fail- Digitalis Zalcitabine (DDC)
ure and other causes of decreased stroke volume such as Ephedrine Zidovudine (AZT)
arrhythmias, and anemia, which decreases oxygen bind-
ing. Maintenance of fluid balance and strict measuring
of intake and output are essential in delirious states. include such antihypertensives as methyldopa and re-
serpine, histamine (H2) receptor antagonists (cimeti-
Intracranial Causes. Intracranial causes of delirium dine), corticosteroids, antidepressants, narcotic (es-
include head trauma, especially involving loss of con- pecially opioid) and nonsteroidal analgesics, lithium
sciousness, postconcussive states, and hemorrhage; carbonate, digitalis, baclofen (Lioresal), anticonvul-
brain infections; neoplasms; and such vascular abnor- sants, antiarrhythmics, colchicine, bronchodilators,
malities as CVAs, subarachnoid hemorrhage, transient benzodiazepines, sedative-hypnotics, and anticholin-
ischemic attacks, and hypertensive encephalopathy. ergics. Of the narcotic analgesics, meperidine can pro-
duce an agitated delirium with tremors, seizures, and
Postoperative States. Postoperative causes of de- myoclonus. These features are attributed to its active
lirium may include infection, atelectasis, lingering ef- metabolite normeperidine, which has potent stimulant
fects of anesthesia, thrombotic and embolic phenom- and anticholingeric properties and accumulates with
ena, and adverse reactions to postoperative analgesia. repeated intravenous dosing. In general, adverse ef-
General surgery in an elderly patient has been reported fects of narcotics are more common in those who have
to be followed by delirium in 10–14% of cases and may never received such agents before (the narcotically
reach 50% after surgery for hip fracture. naive) or who have a history of a similar response to
narcotics.
Sensory and Environmental Changes. Many clini- Lithium-induced delirium occurs at blood levels
cians underestimate the disorienting potential of an un- greater than 1.5 mEq/L and is associated with early
familiar environment. The elderly are especially prone features of lethargy, stuttering, and muscle fascicu-
to develop environment-related confusion in the hos- lations. The delirium may take as long as 2 weeks to
pital. Individuals with preexisting dementia, who may resolve even after lithium has been discontinued, and
have learned to compensate for cognitive deficits at other neurological signs such as stupor and seizures
home, often become delirious once hospitalized. In ad- commonly occur. Maintenance of fluid and electrolyte
dition, the nature of the intensive care unit often lends balance is essential in lithium-induced delirium. Fa-
itself to periods of high sensory stimulation (as during cilitation of excretion with such agents as aminophyl-
a “code”) or low sensory input, as occurs at night. line and acetazolamide helps, but hemodialysis is often
Often, individuals use external events such as dispens- required.
ing medication, mealtimes, presence of housekeeping Principles to remember in cases of drug-induced de-
staff, and physicians’ rounds to mark the passage of lirium include the facts that (1) blood levels of possibly
time. These parameters are often absent at night, leading offending agents are helpful and should be obtained,
to increased rates of confusion during nighttime hours. but many persons can become delirious at therapeutic
Often, manipulating the individual’s environment (see levels of the drug, (2) drug-induced delirium may be
section on treatment) or removing the individual from the result of drug interactions and polypharmacy and
the intensive care unit can be therapeutic. not the result of a single agent, (3) over-the-counter
medications and preparations (e.g., agents containing
caffeine or phenylpropanolamine) should also be con-
Medication-Induced Delirium
sidered, and (4) delirium can be caused by the combi-
The list of medications that can produce the delirious nation of drugs of abuse and prescribed medications
state is extensive (Table 11-2). The more common ones (e.g., cocaine and dopaminergic antidepressants).
Substance Intoxication Delirium cases, multiple general medical conditions may impact
the central nervous system (CNS) in such a way as to
The list of drugs of abuse that can produce delirium is
lead to a delirium. For example, an individual with he-
extensive. Some such agents have enjoyed a resurgence
patic encephalopathy who falls and hits his head may
after years of declining usage. These include lysergic
develop a delirium attributable to the combined ef-
acid diethylamide, psilocybin (hallucinogenic mush-
fects of both general medical conditions. Similarly, the
rooms), heroin, and amphetamines. Other agents in-
combined effects of a medical condition coupled with
clude barbiturates, cannabis (especially dependent on
the effects of medications used to treat that condition
setting, experience of the user, and whether it is laced
may cause a delirium. In such situations, the diagnosis
with phencyclidine [“superweed”] or heroin), jimson-
Delirium Due to Multiple Etiologies is given.
weed (highly anticholingeric), and mescaline. In cases
in which intravenous use of drugs is suspected, HIV
spectrum illness must be ruled out as an etiological TREATMENT
agent for delirium.
Once delirium has been diagnosed, the etiological
The physical examination of an individual with sus-
agent must be identified and treated. For the elderly, the
pected illicit drug-induced delirium may reveal sclero-
first step generally involves discontinuing or reducing
sed veins, “pop” scars caused by subcutaneous injec-
the dosage of potentially offending medications. Some
tion of agents, pale and atrophic nasal mucosa resulting
delirious states can be immediately reversed with med-
from intranasal use of cocaine, injected conjunctiva,
ication, as in the case of physostigmine administration
and pupillary changes. Toxicological screens are help-
for anticholinergic delirium. However, most responses
ful but may not be available on an emergency basis.
are not as immediate, and attention must be directed to-
ward protecting the individual from unintentional self-
Substance-Withdrawal Delirium harm, managing agitated and psychotic behavior, and
manipulating the environment to minimize additional
Alcohol and certain sedating drugs can produce a with- impairment. Supportive therapy should include fluid
drawal delirium when their use is abruptly discontinued and electrolyte maintenance and provision of adequate
or significantly reduced. Withdrawal delirium requires nutrition. Reorienting the individual is essential and is
a history of use of a potentially addicting agent for a best accomplished in a well-lit room with a window,
sufficient amount of time to produce dependence. It is a clock, and a visible wall calendar. Familiar objects
associated with such typical physical findings as abnor- from home such as a stuffed animal, a favorite blanket,
mal vital signs, pupillary changes, tremor, diaphoresis, or a few photographs are helpful. Individuals who re-
nausea and vomiting, and diarrhea. Individuals gener- spond incorrectly to questions of orientation should be
ally complain of abdominal and leg cramps, insomnia, provided with the correct answers. Because these indi-
nightmares, chills, hallucinations (especially visual), viduals often see many consultants, physicians should
and a general feeling of “wanting to jump out of my introduce themselves and state their purpose for com-
skin.” ing at every visit. Physicians must take into account
Some varieties of drug withdrawal, although un- that impairments of vision and hearing can produce
comfortable, are not life threatening (e.g., opioid with- confusional states, and the provision of appropriate
drawal). Others such as alcohol withdrawal delirium prosthetic devices may be beneficial. Around-the-clock
are potentially fatal. Withdrawal delirium is much accompaniment by hospital-provided “sitters” or fam-
more common among individuals who are hospitalized ily members may be required (see Table 11-3).
than among individuals living in the community. The
incidence of delirium tremens, for example, is found
in 1% of all alcoholics, but in 5% of hospitalized alco- Table 11-3 Managing the Delirious Individual
hol abusers. Improvement of the delirium occurs when Identify and correct the underlying cause.
the offending agent is reintroduced or a cross-sensitive Protect the patient from unintentional self-harm.
drug (e.g., a benzodiazepine for alcohol withdrawal) is Stabilize the level of sensory input.
Reorient patient as often as possible.
employed. Employ objects from the patient’s home environment.
Provide supportive therapy (fever control, hydration).
Streamline medications.
Delirium Due to Multiple Etiologies Correct sleep deprivation.
Manage behavior with appropriate pharmacotherapy.
In many individuals with delirium, there are often Address postdelirium guilt and shame for behavior that
occurred during confusion.
multiple simultaneous causal factors involved. In some
Despite these conservative interventions, the delirious DSM-IV-TR) on the basis of etiology (i.e., Dementia of
individual often requires pharmacological intervention. the Alzheimer’s Type, Dementia Due to Pick’s Disease,
The liaison psychiatrist is the most appropriate person Dementia Due to Parkinson’s Disease, Dementia Due
to recommend such treatment in hospital settings. The to Huntington’s Disease, Vascular Dementia, Dementia
drug of choice for agitated delirious individuals has tra- Due to HIV Disease, Dementia Due to Head Trauma,
ditionally been haloperidol (Haldol). It is particularly Dementia Due to Other General Medical Conditions,
beneficial when given by the intravenous route, and Substance-Induced Persisting Dementia, and Dementia
dosages as high as 260 mg/day have been used without Due to Multiple Etiologies). Information regarding the
adverse effect. Extrapyramidal symptoms may be less diagnosis of dementia regardless of its specific etiology
common with haloperidol administered intravenously is presented first, followed by sections on the various
as opposed to oral and intramuscular administration. In specific causes of dementia.
general, doses in the range of 0.5 to 5 mg intravenously
are used, with the frequency of administration depend-
DIAGNOSIS
ing on a variety of factors, including the individual’s
age. An electrocardiogram should be obtained before Dementia is defined in DSM-IV-TR as a series of dis-
administering haloperidol. If the QT interval is greater orders characterized by the development of multiple
than 450, use of intravenous haloperidol can precipitate cognitive deficits (including memory impairment) that
an abnormal cardiac rhythm known as Torsades des are due to the direct physiological effects of a general
pointes. Lorazepam has also been proven effective in medical condition, the persisting effects of a substance,
doses of 0.5 to 2 mg intravenously. It has been suggested or multiple etiologies (e.g., the combined effects of a
that haloperidol and lorazepam act synergistically when metabolic and a degenerative disorder). (See DSM-IV-
given to the agitated individual who is delirious. If the TR diagnostic criteria A and B, page 98.) The disorders
delirium is secondary to drug or alcohol abuse, benzo- constituting the dementias share a common symptom
diazepines or clonidine should be used. For individuals presentation and are identified and classified on the ba-
who are mildly agitated or amenable to taking medica- sis of etiology. The cognitive deficits exhibited in these
tions by mouth, oral haloperidol or lorazepam is appro- disorders must be of sufficient severity to interfere
priate. Recent studies have advocated the use of newer with either occupational functioning or the individual’s
atypical antipsychotics for management of behavior and usual social activities or relationships. In addition, the
psychotic features in delirium. Such agents as quetiap- observed deficits must represent a decline from a higher
ine, olanzapine, risperdal, and ziprasidone have been level of function and not be the consequence of a de-
used successfully to treat delirium. Newer agents may lirium. A delirium can be superimposed on a dementia,
have lower incidences of dystonias and dyskinesias, but however, and both can be diagnosed if the dementia is
still carry the risk of QT interval prolongation, par- observed when the delirium is not in evidence. Demen-
ticularly in individuals with electrolyte abnormalities. tia is typically chronic and occurs in the presence of a
Quetiapine and olanzapine are quite sedating, and oc- clear sensorium. If clouding of consciousness occurs,
casionally a combination of bedtime olanzapine and “as the diagnosis of delirium should be considered. Es-
needed” haloperidol is utilized. Olanzapine may raise sential to the diagnosis of dementia is the presence of
blood glucose levels and precipitate weight gain, and cognitive deficits that include memory impairment and
is available as a Zydis preparation, which is absorbed at least one of the following abnormalities of cognition:
through the oral mucosa and can therefore be given aphasia, agnosia, apraxia, or a disturbance in executive
to individuals who are unable to take medications by function.
mouth. Parenteral forms of olanzapine and ziprasidone Memory function is divided into three compart-
are also available. Whatever antipsychotic is chosen, ments that can easily be evaluated during a mental sta-
the individual should be carefully monitored for muscle tus examination. These are immediate recall (primary
rigidity, unexplained fever, tremor, and other warning memory), recent (secondary) memory, and remote (ter-
signs of neuroleptic side effects. tiary) memory. Primary memory is characterized by a
limited capacity, rapid accessibility, and a duration of
seconds to a minute. The anatomic site of destruction
Dementia of primary memory is the reticular activating system,
and the principal activity of the primary memory is the
The disorders in this section are characterized by the registration of new information. Primary memory is
development of multiple cognitive deficits (includ- generally tested by asking the individual to repeat im-
ing memory impairment) but are differentiated (as in mediately a series of numbers in the order given. For
instance, if the examiner mentions the numbers 1-2-3, In addition to defects in memory, individuals with
the individual should be able to repeat them in the same dementia often exhibit impairments in language, rec-
order. This loss of ability to register new information ognition, object naming, and motor skills. Aphasia is
accounts in part for the confusion and frustration the an abnormality of language that often occurs in vas-
demented individual feels when confronted with unex- cular dementias involving the dominant hemisphere.
pected changes in daily routine. Because this hemisphere controls verbal, written, and
Secondary memory has a much larger capacity than sign language, these individuals may have significant
primary memory, a duration of minutes to years, and problems interacting with people in their environment.
relatively slow accessibility. The anatomic site of dys- Individuals with dementia and aphasia may exhibit
function for secondary memory is the limbic system, paucity of speech, poor articulation, and a telegraphic
and individuals with a lesion in this area may have little pattern of speech (nonfluent, Broca’s aphasia). This
difficulty repeating digits immediately, but show rapid form of aphasia generally involves the middle cer-
decay of these new memories. In minutes, the individual ebral artery with resultant paresis of the right arm
with limbic involvement may be totally unable to recall and lower face. Despite faulty communication skills,
the digits or even remember that a test has been admin- individuals having dementia with nonfluent aphasia
istered. Thus, secondary memory represents the reten- have normal comprehension and awareness of their
tion and recall of information that has been previously language impairment. As a result, such individuals
registered by primary memory. Clinically, secondary often present with significant depression, anxiety, and
memory is tested by having the individual repeat three frustration.
objects after having been distracted (usually by the ex- By contrast, individuals having dementia with fluent
aminer’s continuation of the Mental Status Examina- (Wernicke’s) aphasia may be quite verbose and articu-
tion) for 3 to 5 minutes. Like primary memory, second- late, but much of the language is nonsensical and rife
ary recall is often impaired in dementia. Often, if the with such paraphasias as neologisms and clang (rhym-
examiner gives the demented individual a clue (such ing) associations. Whereas nonfluent aphasias are usu-
as “one of the objects you missed was a color”), the ally associated with discrete lesions, fluent aphasia can
individual correctly identifies the object. If this occurs, result from such diffuse conditions as dementia of the
the memory testing should be scored as “3 out of 3 with Alzheimer type. More commonly, fluent aphasias oc-
a clue,” which is considered to be a slight impairment. cur in conjunction with vascular dementia secondary to
Giving clues to the demented individual with a primary temporal or parietal lobe CVA. Because the demented
memory loss is pointless, because the memories were individuals with fluent aphasia have impaired compre-
never registered. Wernicke–Korsakoff syndrome is an hension, they may seem apathetic and unconcerned
example of a condition in which primary memory may with their language deficits if they are, in fact, aware
be intact while secondary recall is impaired. of them at all. They do not generally display the emo-
Tertiary (remote) memory has a capacity that is tional distress of individuals with dementia and nonflu-
probably unlimited, and such memories are often per- ent aphasia (Table 11-4).
manently retained. Access to tertiary memories is slow, Individuals with dementia may also lose their ability
and the anatomical dysfunction in tertiary memory loss to recognize. Agnosia is a feature of a dominant hemi-
is in the association cortex. In the early stages of de- sphere lesion and involves altered perception in which,
mentia, tertiary memory is generally intact. It is tested despite normal sensations, intellect, and language, the
by instructing the individual to remember personal in-
formation or past material. The personal significance of Table 11-4 Classification of Aphasias
the information often influences the individual’s ability Type Language Comprehension Motor
to remember it. For example, a woman who worked
Wernicke’s Impaired Impaired Normal
for many years as a seamstress might remember many (receptive)
details related to that occupation, but could not recall Articulate
the names of past presidents or three large cities in the Paraphasias
United States. Thus, an individual’s inability to remem- Broca’s Nonfluent Intact Right
(expressive) hemiparesis
ber highly significant past material is an ominous find- Sparse
ing. Collateral data from informants is essential in the Telegraphic
proper assessment of memory function. In summary, Inarticulate
primary and secondary memories are most likely to Global Nonfluent Impaired Variable right
be impaired in dementia, with tertiary memory often hemiplegia
Mute
spared until late in the course of the disease.
individual cannot recognize objects. This is in contrast Table 11-5 Evaluation of Dementia
to aphasia, in which the individual with dementia may
not be able to name objects, but can recognize them. Medical history and physical examination
Family interview
The type of agnosia depends on the area of the sen- Routine laboratory
sory cortex that is involved. Some demented individu- Chemistry (SMA 20)
als with severe visual agnosia cannot name objects Urinalysis
Hematology (complete blood count)
presented, match them to samples, or point to objects Other routine tests
named by the examiner. Other individuals may present Chest radiography
with auditory agnosia and may be unable to localize or Electrocardiography
Specialized laboratory
distinguish such sounds as the ringing of a telephone. Thyroid functions
A minority of demented individuals may exhibit as- VDRL (fluorescent treponemal antibody screen if indicated)
tereognosis, or the inability to identify an object by Drug screen
Vitamin B12 and folate levels
palpation. Cerebrospinal fluid analysis (if indicated)
Demented individuals may also lose their ability to HIV testing (if indicated)
Other studies
carry out selected motor activities despite intact motor Computed tomography or magnetic resonance imaging
abilities, sensory function, and comprehension of the Electroencephalography
assigned task (apraxia). Affected individuals cannot
perform such activities as brushing their teeth, chew-
ing food, or waving goodbye when asked to do so. The The Mental Status Examination, in conjunction with
two most common forms of apraxia in demented in- a complete medical history from the individual and
dividuals are ideational and gait apraxia. Ideational informants and an adequate physical examination, is
apraxia is the inability to perform motor activities that essential in the evaluation and differential diagnosis
require sequential steps and results from a lesion in- of dementia (Table 11-5). The findings on the Mental
volving both frontal lobes or the complete cerebrum. Status Examination vary depending on the etiology of
Gait apraxia, often seen in such conditions as normal- the dementia. In general, symptoms seen on the Mental
pressure hydrocephalus, is the inability to perform Status Examination, whatever the etiology, are related
various motions of ambulation. It also results from con- to the location and extent of brain injury, individual
ditions that diffusely affect the cerebrum. adaptation to the dysfunction, premorbid coping skills
Impairment of executive function affects the abil- and psychopathology, and concurrent medical illness.
ity to think abstractly, plan, initiate, and end complex Disturbance of memory, especially primary and sec-
behavior. On Mental Status Examination, individu- ondary memory, is the most significant abnormality.
als with dementia display problems coping with new Confabulation may be present as the individual attempts
tasks. Activities such as subtracting serial sevens may to minimize the memory impairment. Disorientation
be impaired. and altered levels of consciousness may occur, but are
In addition to the diagnostic features already men- generally not seen in the early stages of dementia un-
tioned, individuals with dementia display other identi- complicated by delirium. Affect may be altered as in
fying features that often prove problematic. Poor insight the masked facies of Parkinson’s disease and the ex-
and judgment are common in dementia and often cause pansive affect and labile mood of pseudobulbar palsy
individuals to engage in potentially dangerous activi- after cerebral injury. The affect of individuals with he-
ties or make unrealistic and grandiose plans for the fu- patic encephalopathy is often described as blunted and
ture. Visual–spatial functioning may be impaired, and apathetic. Lack of inhibition leading to such behavior
if individuals have the ability to construct a plan and as exposing oneself is common, and some conditions
carry it out, suicide attempts can occur. More common such as tertiary syphilis and untoward effects of some
is unintentional self-harm resulting from carelessness, medication can precipitate mania.
undue familiarity with strangers, and disregard for the The physical examination may offer clues to the
accepted rules of conduct. Emotional lability, as seen etiology of the dementia; however, in the elderly, one
in pseudobulbar palsy after cerebral injury, can be par- must be aware of the normal changes associated with
ticularly frustrating for caregivers, as are occasional aging and differentiate them from signs of dementia.
psychotic features such as delusions and hallucina- Often, the specific physical examination findings in-
tions. Changes in their environment and daily routine dicate the area of the central nervous system affected
can be particularly distressing for demented individu- by the etiological process. Parietal lobe dysfunction
als, and their frustration can be manifested by violent is suggested by such symptoms as astereognosis, con-
behavior. structional apraxia, anosognosia, and problems with
two-point discrimination. The dominant hemisphere Physical Signs Associated with Dementia or
parietal lobe is also involved in Gerstmann’s syndrome, Table 11-6
Delirium
which includes agraphia, acalculia, finger agnosia, and
Physical Sign Condition
right–left confusion.
Reflex changes such as hyperactive deep tendon Myoclonus Creutzfeldt–Jakob disease
Subacute sclerosing
reflexes, Babinski’s reflex, and hyperactive jaw jerk panencephalitis
are indicative of cerebral injury. However, primitive Postanoxia
reflexes such as the palmar–mental reflex (tested by re- Alzheimer’s disease (10%)
AIDS dementia
peatedly scratching the base of the individual’s thumb, Uremia
with a positive response being slight downward move- Penicillin intoxication
Meperidine toxicity
ment of the lower lip and jaw) that occurs in 60% of Asterixis Hepatic encephalopathy
normal elderly people, and the snout reflex, seen in a Uremia
third of elderly individuals, are not diagnostically reli- Hypoxia
Chorea Huntington’s disease
able for dementia. Wilson’s disease
Ocular findings such as nystagmus (as in brain stem Hypocalcemia
Hypothyroidism
lesions), ophthalmoplegia (Wernicke–Korsakoff syn- Hepatic encephalopathy
drome), anisocoria, papilledema (hypertensive en- Oral contraceptives
cephalopathy), cortical blindness (Anton’s syndrome), Systemic lupus erythematosus
Carbon monoxide poisoning
visual field losses (CVA hemianopia), Kayser–Fleischer Toxoplasmosis
rings (Wilson’s disease), and Argyll Robertson pupils Pertussis, diphtheria
(syphilis, diabetic neuropathy) can offer valuable clues Peripheral neuropathy Wernicke–Korsakoff syndrome
Neurosyphilis
to the etiology of the cognitive deficit. Heavy metal intoxication
Movement disorders including tremors (Parkin- Organic solvent exposure
Vitamin B12 deficiency
son’s disease, drug intoxication, cerebellar dysfunc- Medications: isoniazid, phenytoin
tion, Wilson’s disease), chorea (Huntington’s disease,
other basal ganglia lesions), myoclonus (subacute
sclerosing panencephalitis, Creutzfeldt–Jakob disease, distributed among men and women, with Alzheimer’s
Alzheimer’s disease, anoxia), and asterixis (hepatic dementia (AD) much more common in women. The
disease, uremia, hypoxia, carbon dioxide retention) National Institute of Mental Health Multisite Epide-
should be noted. miological Catchment Area study revealed a 6-month
Gait disturbances, principally apraxia (normal- prevalence rate for mild dementia of 11.5% to 18.4%
pressure hydrocephalus, inhalant abuse, cerebellar for persons older than 65 years living in the commu-
dysfunction) and peripheral neuropathy (Korsakoff’s nity. The rate for severe dementia was higher for the in-
syndrome, neurosyphilis, heavy metal intoxication, stitutionalized elderly: 15% of the elderly in retirement
solvent abuse, isoniazid or phenytoin toxicity, vitamin communities, 30% of nursing home residents, and 54%
deficiencies, and HIV spectrum illnesses), are also of the elderly in state hospitals.
common in dementia. Extrapyramidal symptoms in Studies suggest that the fastest growing segment of
the absence of antipsychotics may indicate substance the US population consists of persons older than the
abuse, especially phencyclidine abuse, or basal ganglia age of 85 years, 15% of whom are demented. Half of
disease. Although the many and varied physical find- the US population currently lives to the age of 75 years
ings of dementia are too numerous to mention here in and one quarter lives to the age of 85. A study of 2000
any detail, it should be obvious that the physical exami- consecutive admissions to a general medical hospital
nation is an invaluable tool in the assessment of demen- revealed that 9% were demented and, among those,
tia (Table 11-6). 41% were also delirious on admission.
The prevalence of dementias is not precisely known.
Estimates vary depending on the age range of the Course
population studied and whether the individuals sam-
pled were in the general community, acute care fa- The course of a particular dementia is influenced by
cilities, or long-term nursing institutions. A review of its etiology. Although historically the dementias have
47 surveys of dementia conducted between 1934 and been considered progressive and irreversible, there
1985 indicated that the prevalence of dementia in- is, in fact, significant variation in the course of indi-
creased exponentially by age, doubling every 5 years vidual dementias. The disorder can be progressive,
up to age 95 years, and that this condition was equally static, or remitting. In addition to the etiology, factors
that influence the course of the dementia include (1) zil (Aricept), which acts as an inhibitor of acetylcho-
the time span between the onset and the initiation of linesterase, and galanthamine (Reminyl) may slow
prescribed treatment, (2) the degree of reversibility of down the rate of progression of the dementia.
the particular dementia, (3) the presence of comorbid
mental disorders, and (4) the level of psychosocial sup-
port. The previous distinction between treatable and
untreatable dementias has been replaced by the con- Memory impairment occurs in a variety of conditions
cepts of reversible, irreversible, and arrestable demen- including delirium, amnestic disorders, and depres-
tias. Most reversible cases of dementia are associated sion. In delirium, the onset of altered memory is acute
with shorter duration of symptoms, mild cognitive im- and the pattern typically fluctuates (waxing and wan-
pairment, and superimposed delirium. Specifically, the ing) with increased proclivity for confusion during the
dementias caused by drugs, depression, and metabolic night. Delirium is more likely to feature autonomic
disorders are most likely to be reversible. Other condi- hyperactivity and alterations in level of consciousness.
tions such as normal-pressure hydrocephalus, subdural In some cases, a dementia can have a superimposed de-
hematomas, and tertiary syphilis are more commonly lirium (Figure 11-2).
arrestable. Individuals with major depressive disorder often
Although potentially reversible dementias should complain of lapses in memory and judgment, poor
be aggressively investigated, in reality, only 8% of de- concentration, and seemingly diminished intellectual
mentias are partially reversible and about 3% are fully capacity. Often, these symptoms are mistakenly diag-
reversible. There is some evidence to suggest that early nosed as dementia, especially in elderly individuals. A
treatment of demented individuals, particularly those thorough medical history and mental status examina-
with Alzheimer’s type, with such agents as donepe- tion focusing on such symptoms as hopelessness, crying
Delirium Acute onset Dementia
Delirium Multiple cognitive deficits Dementia
Delirium Fluctuating course Dementia
Delirium Clouded sensorium Dementia
Delirium Memory deficit Dementia
Delirium Language impairment Dementia
Delirium Autonomic signs common Dementia
Most likely to
Delirium Dementia
be irreversible
Consequence of
Delirium Dementia
substance abuse
Figure 11-2 Differentiation of delirium and dementia.

episodes, and unrealistic guilt, in conjunction with

Dementia of the Alzheimer Type
a family history of depression, can be diagnostically
beneficial. The term pseudodementia has been used to
DIAGNOSIS
denote cognitive impairment secondary to a functional
mental disorder, most commonly depression. In com- The course and clinical features of Dementia of the
parison with demented individuals, those with depres- Alzheimer Type (DAT) (see diagnostic criteria for
sive pseudodementia exhibit better insight regarding Dementia of Alzheimer Type, page 98) parallel those
their cognitive dysfunction, are more likely to give “I discussed for dementia in general. Typically, the early
don’t know” answers, and may exhibit neurovegetative course of DAT is difficult to ascertain because the
signs of depression. Pharmacological treatment of the individual is usually an unreliable informant, and
depression should improve the cognitive dysfunction as the early signs may be so subtle as to go unnoticed
well. Because of the rapid onset of their antidepressant even by the individual’s closest associates. These
action, the use of psychostimulants (e.g., methylphe- early features include impaired memory, difficulty
nidate, dextroamphetamine) to differentiate between with problem solving, preoccupation with long past
dementia and pseudodementia has been advocated by events, decreased spontaneity, and an inability to re-
some authors. Some authors have proposed abandon- spond to the environment with the individual’s usual
ment of the term pseudodementia, suggesting that most speed and accuracy. Individuals with DAT may forget
individuals so diagnosed have both genuine dementia names, misplace household items, or forget what they
and a superimposed affective disorder (Figure 11-3). were about to do. Often the individuals have insight
Amnestic disorder also presents with a significant into these memory deficits and occasionally convey
memory deficit, but without the other associated fea- their concerns to family members. Such responses as
tures such as aphasia, agnosia, and apraxia. If cogni- “You’re just getting older,” and “I do that sometimes
tive impairment occurs only in the context of drug use, myself” are common from these family members and
substance intoxication or substance withdrawal is the as a result the individual becomes depressed, which
appropriate diagnosis. Although mental retardation can further affect cognitive functioning. Anomia, or
implies below-average intellect and subsequent im- difficulty with word finding, is common in this middle
pairment in other areas of function, the onset is before stage of Alzheimer’s disease. Eventually the individual
18 years of age and abnormalities of memory do not develops schemes, word associations, and excuses (“I
always occur. Mental retardation must be considered never was very good in math”) to assist in retention
in the differential diagnosis of dementias of childhood and cover up deficits. The individual may also employ
and adolescence along with such disorders as Wilson’s family members as a surrogate memory.
disease (hepatolenticular degeneration), lead intoxica- Because memory loss is usually most obvious for
tion, subacute sclerosing panencephalitis, HIV spec- newly acquired material, the individual with DAT tries
trum disorders, and substance abuse, particularly abuse to avoid unfamiliar activities. Typically, the individual is
of inhalants. If an individual develops dementia before seen by the clinician when confusion, aggression, wan-
age 18 years and has an IQ in the mentally retarded dering, or some other socially undesirable behavior en-
range (i.e., below 70), an additional diagnosis of mental sues. At that time, disorders of perception and language
retardation may be justified. may appear. The individual often turns to a spouse to
Individuals with schizophrenia may also exhibit a answer questions posed during the history taking. By
variety of cognitive abnormalities, but this condition this time, the affected individual has lost insight into his
also has an early onset, a distinctive constellation of or her dementia and abandons attempts to compensate
other symptoms (e.g., delusions, hallucinations, disor- for memory loss. Finally, in the late stage of Alzheim-
ganized speech), and does not result from a medical er’s disease, physical and cognitive effects are marked.
condition or the persisting effects of a substance. Facti- Disorders of gait, extremity paresis and paralysis, sei-
tious disorder and malingering must be distinguished zures, peripheral neuropathy, extrapyramidal signs, and
from dementia. The individual with factitious disorder urinary incontinence are seen, and the individual is of-
and psychological symptoms may have some apparent ten no longer ambulatory. The aimless wandering of the
cognitive deficits reminiscent of a dementia. middle stage has been replaced by a mute, bedridden
Dementia must also be distinguished from age- state and decorticate posture. Myoclonus occasionally
related cognitive decline (also known as benign senes- occurs. Significantly, affective disturbances remain a
cence). Only when such changes exceed the level of al- distinct possibility throughout the course of the illness.
tered function to be expected for the individual’s age is Alzheimer’s disease progresses at a slow pace for 8 to
the diagnosis of dementia warranted. 10 years to a state of complete helplessness.
Cognitive impairment Evidence of cognitive

Dementia
in depression impairment
Cognitive impairment
Precise date of onset Dementia
in depression
Rapid progression Dementia
in depression
Poor insight into deficits Dementia
in depression
"I don't know" answers Dementia
in depression
Cognitive impairment Consistently poor

Dementia
in depression performance on testing
Cognitive impairment Psychiatric

Dementia
in depression history common
At risk for suicide Dementia
in depression
Seeks treatment early Dementia
in depression
Disturbance in mood Dementia
in depression
Remote memory often spared Dementia
in depression
Usually reversible Dementia
in depression
Figure 11-3 Differential diagnosis of dementia and cognitive impairment in depression.
The role of laboratory determinations in the evalu- tex and hydrocephalus ex vacuo. MRI may show non-
ation for AD is to exclude other causes of dementia, specific alteration of white matter (leukoariosis), and
especially those that may prove reversible or arrestable. eventually EEG shows diffuse-background slowing.
Before death, AD is largely a diagnosis of exclusion. Pneumoencephalography has demonstrated enlarged
Throughout the course of this disorder, laboratory val- ventricles and widening of cortical sulci in Alzheimer’s
ues are essentially normal. Some nonspecific changes disease, and positron emission tomography in the later
may occur, but electroencephalography and lumbar stages shows decreased cerebral oxygen and glucose
puncture are not diagnostic. As the disease progresses, metabolism in the frontal lobes. At present, in the
computed tomography (CT) and magnetic resonance workup of an individual with a slowly progressive de-
imaging (MRI) may show atrophy in the cerebral cor- mentia, a good family history, physical examination,
and laboratory and radiographic tests to rule out other

DSM-IV-TR Diagnostic Criteria causes of dementia are the most effective tools in the
diagnosis of Alzheimer’s disease.
294.1X DEMENTIA OF THE ALZHEIMER TYPE Alzheimer’s disease is the most common cause of
A. The development of multiple cognitive deficits mani- dementia, accounting for 55–65% of all cases. There
fested by both were fewer than 3 million cases diagnosed in the United
(1) memory impairment (impaired ability to learn States in 1980, but the Census Bureau predicts that
new information or to recall previously learned there will be more than 10 million American citizens
information)
(2) one (or more) of the following cognitive with Alzheimer’s disease by the year 2050. Prevalence
disturbances: of the disease doubles with every 5 years between the
(a) aphasia (language disturbance) ages of 65 and 85 years.
(b) apraxia (impaired ability to carry out motor ac-
tivities despite intact motor function) Alzheimer’s disease affects women three times as of-
(c) agnosia (failure to recognize or identify objects ten as men, for unknown reasons. Furthermore, at least
despite intact sensory function) one study suggests that dementia, including Alzheimer’s,
(d) disturbance in executive functioning (i.e., plan-
ning, organizing, sequencing, abstracting) is more common in black than in white American
B. The cognitive deficits in criteria A1 and A2 each cause women. Comparison of population studies in diverse
significant impairment in social or occupational func- countries shows strikingly similar prevalence rates.
tioning and represent a significant decline from a pre-
vious level of functioning.
C. The course is characterized by gradual onset and con- TREATMENT
tinuing cognitive decline.
D. The cognitive deficits in criteria A1 and A2 are not due The two principles of management in AD are to treat
to any of the following:
what is treatable without aggravating existing symp-
(1) other central nervous system conditions that cause
progressive deficits in memory and cognition toms and to support caregivers who are also victims
(e.g., cerebrovascular disease, Parkinson’s disease, of this disease. Given the significant decrease in ACh
Huntington’s disease, subdural hematoma, normal- seen in AD, cholinesterase inhibitors which work by
pressure hydrocephalus, brain tumor)
(2) systemic conditions that are known to cause de- increasing the central nervous system concentrations
mentia (e.g., hypothyroidism, vitamin B12 or folic of ACh have shown some promise in improving cog-
acid deficiency, niacin deficiency, hypercalcemia, nitive impairments early in the course of AD. Four
neurosyphilis, HIV infection)
(3) substance-induced conditions acetylcholinesterase inhibitors (donepezil, tacrine, ri-
E. The deficits do not occur exclusively during the course
vastigmine, galantamine) have been approved for use
of a delirium. in the United States for the treatment of mild to mod-
F. The disturbance is not better accounted for by an- erate dementia. Side effects, particularly hepatic and
other Axis I disorder (e.g., major depressive disorder,
schizophrenia). cholinergic, are potentially problematic. Furthermore,
improvement in cognitive functioning is often modest
Code based on presence or absence of a clinically signifi-
cant behavioral disturbance: at best and ultimately temporary as the illness inevita-
294.10 Without Behavioral Disturbance: if the cognitive bly progresses.
disturbance is not accompanied by any clinically signifi- The N-methyl-D-aspartate (NMDA) receptor, a
cant behavioral disturbance. glutamate receptor subtype, has important effects in
294.11 With Behavioral Disturbance: if the cognitive learning and memory. Stimulation by the excitatory
disturbance is accompanied by a clinically significant be-
havioral disturbance (e.g., wandering, agitation). amino acid glutamate results in long-term potentia-
tion of neuronal activity basic to memory formation.
Specify subtype:
There appears to be a decrease in cerebral cortcial and
With Early Onset: if onset is at age 65 years or below
hippocampal NMDA receptors in Alzheimer’s dis-
With Late Onset: if onset is after age 65 years ease. Memantine is a moderate affinity noncompeti-
Coding note: Also code 331.0 Alzheimer’s disease on tive NMDA receptor antagonist approved in the US in
Axis III. Indicate other prominent clinical features re-
lated to the Alzheimer’s disease on Axis I (e.g., 293.83 2003 for the treatment of moderate to severe dementia.
Mood Disorder Due to Alzheimer’s Disease, With De- A postmarketing surveillance study conducted among
pressive Features, and 310.1 Personality Change Due to German physicians who treated dementia patients with
Alzheimer’s Disease, Aggressive Type. Code based on
type of onset and predominant features. memantine in combination with an anticholinesterase
inhibior (mainly Aricept) suggests that this combina-
tion is safe and well tolerated.
American Psychiatric Association. Depression is often associated with AD. If antide-
pressant medication is to be used, low doses (about
one-third to one-half of the usual initial dose) are doors and windows and operate appliances are helpful
advised and only agents with minimal anticholiner- and arranging for rapid dialing of essential telephone
gic activity should be employed. Appropriate choices numbers can be useful. Maintaining adequate hydra-
would be the selective serotonin reuptake inhibitors tion, nutrition, exercise, and cleanliness is essential.
such as paroxetine, fluoxetine, sertraline, citalopram, The family of the individual with Alzheimer’s dis-
and escitalopram. Although sertraline, citalopram and ease is also a victim of the disease. Family members
escitalopram are least likely to cause drug–drug inter- must watch the gradual deterioration of the individual
actions, even these agents have the potential to increase and accept that a significant part of their own lives must
confusion in Alzheimer’s individuals. Agents such as be devoted to the care of the individual. Difficult deci-
trazodone and mirtazapine have occasionally been em- sions about institutionalization and termination of life
ployed because of their sedating properties. If tricyclic support are distinct possibilities, and individuals with
antidepressants are used, the secondary amines (e.g., AD often turn their anger and paranoia toward the car-
desipramine, nortriptyline) are recommended over the egiver. Education is a valuable treatment tool for fami-
tertiary ones (e.g., amitriptyline, doxepin). Careful lies. Information about the disease and peer support are
attention to the possible side effects of these agents, available through Alzheimer’s associations, and many
particularly orthostatic hypotension, lowering of the such agencies provide family members with a compan-
seizure threshold, excessive fatigue, urinary retention, ion for the individual with AD to allow the family some
constipation, confusion, and accelerated memory im- time away. For these reasons, family members are at
pairment, is suggested. Most clinicians now feel that risk for depression, anxiety disorders, insomnia, and a
tricyclic antidepressants are inappropriate for this variety of other psychological manifestations. Should
population. these occur, they should be promptly treated.
Anxiety and psychosis, particularly paranoid delu-
sions, are common in AD. Benzodiazepines can be
Vascular Dementia
disinhibiting in such individuals and may exacerbate
confusion and should be avoided if possible. If minor
DIAGNOSIS
tranquilizers are required, agents with a shorter dura-
tion of action (e.g., lorazepam, oxazepam) are preferred. Vascular dementia usually results from multiple CVAs
Antipsychotic medications with high anticholinergic or one significant CVA. It is generally considered the
potential (e.g., thioridazine, chlorpromazine) may also second most common cause of dementia after Alzhe-
affect memory adversely. While these agents have been imer’s disease, accounting for about 10% of all cases.
favored in the past because of their tendency to produce Men are twice as likely as women to be diagnosed with
sedation, newer agents such as olanzapine (Zyprexa), this condition. Vascular dementia is characterized by
risperidone (Risperdal), quetiapine (Seroquel) ziprasi- a stepwise progression of cognitive deterioration with
done (Geodon) and aripipevazole (Abilify) have been accompanying lateralizing signs. (See DSM-IV-TR
reported to have lower incidences of neuroleptic-related diagnostic criteria, page 100) It is always associated
side effects. However, a reported increase in cerebrovas- with evidence of systemic hypertension and usually in-
cular events (e.g., stroke, TIA) in elderly patients taking volves renal and cardiac abnormalities. Risk factors for
these newer agents raises questions about their safety, the development of a vascular dementia include those
especially in patients with risk factors for vascular dis- generally associated with obstructive coronary ar-
ease. Haloperidol has less anticholinergic activity but tery disease, including obesity, hypercholesterolemia,
has a greater tendency toward extrapyramidal effects. smoking, hypertension, stress, and lack of exercise. The
The appropriate management of AD entails more actual incidence of vascular dementia has decreased
than psychopharmacological intervention. Other ele- somewhat with better standards of care, improved di-
ments of the treatment plan should include environ- agnostic techniques, and lifestyle changes.
mental manipulation and support for the family. In Vascular dementia is characterized by the early ap-
the attempt to maintain individuals with Alzheimer’s pearance of localizing neurological signs. Spasticity,
disease in their homes for as long as possible, some ad- hemiparesis, ataxia, and pseudobulbar palsy are com-
justments of their environment are important. Written mon. Pseudobulbar palsy is associated with injury to
daily reminders can be helpful in the performance of the frontal lobes and results in impairment of the cor-
daily activities. Prominent clocks, calendars, and win- ticobulbar tracts. It is characterized by extreme emo-
dows are important. An effort should be made to mini- tional lability, abnormal speech cadence, dysphagia,
mize changes in the individual’s daily activities and hyperactive jaw jerk, hyperactive deep tendon reflexes,
environment. Repeated demonstrations of how to lock and Babinski’s reflex.
TREATMENT
Primary prevention and secondary prevention are im-
290.4X VASCULAR DEMENTIA portant in the treatment of cerebrovascular disorders.
A. The development of multiple cognitive deficits mani- Lifestyle changes are effective in arresting the progress
fested by both of the disease; however, no known pharmacological
(1) memory impairment (impaired ability to learn new in- treatment can reverse the effects of a completed stroke.
formation or to recall previously learned information)
(2) one (or more) of the following cognitive disturbances: Such interventions as anticoagulants for frequent tran-
(a) aphasia (language disturbance)
sient ischemic attacks after a hemorrhagic lesion has
(b) apraxia (impaired ability to carry out motor activi- been investigated but excluded; aspirin for decreasing
ties despite intact motor function) platelet aggregation, and surgical removal of obstruct-
(c) agnosia (failure to recognize or identify objects de-
spite intact sensory function) ing plaques probably do not reverse the mental state.
(d) disturbance in executive functioning (i.e., planning, Depression occurs in 50–60% of individuals with
organizing, sequencing, abstracting) CVAs and responds to traditional antidepressants. Tri-
B. The cognitive deficits in criteria A1 and A2 each cause cyclic antidepressants, such as amitriptyline, in less
significant impairment in social or occupational func- than antidepressant doses, improve both CVA depres-
tioning and represent a significant decline from a pre-
vious level of functioning. sion and pseudobulbar palsy. Physical rehabilitation is
C. Focal neurological signs and symptoms (e.g., exag- essential and often results in an improvement in mood
geration of deep tendon reflexes, extensor plantar re-
sponse, pseudobulbar palsy, gait abnormalities, weak-
and outlook.
ness of an extremity) or laboratory evidence indicative
of cerebrovascular disease (e.g., multiple infarctions
involving cortex and underlying white matter) that are Dementia Due to HIV Disease
judged to be etiologically related to the disturbance.
D. The deficits do not occur exclusively during the course
of a delirium. DIAGNOSIS
Code based on predominant features: Acquired Immunodeficiency Syndrome (AIDS) was
290.41 With Delirium: if delirium is superimposed on first described in the United States in 1979. In the de-
the dementia veloped countries, the death rate from AIDS has been
290.42 With Delusions: if delusions are the predominant on the decline since the advent of new medication
feature
regimens utilizing traditional antiretrovirals and the
390.43 With Depressed Mood: if depressed mood (in- newer protease inhibitors. These medication cocktails
cluding presentations that meet full symptom criteria for
a major depressive episode) is the predominant feature. have also decreased the incidence of AIDS–dementia
A separate diagnosis of mood disorder due to a general complex, so that physicians are now more likely to see
medical condition is not given. AIDS-related delirium secondary to infection, meta-
209.40 Uncomplicated: if none of the above predomi- bolic disarray, and medication rather than traditional
nates in the current clinical presentation
AIDS dementia. In the truest sense, AIDS is not a
Specify if:
disease but an increased susceptibility to a variety of
With behavioral disturbance diseases caused by loss of immunocompetence due to
Coding note: Also code cerebrovascular condition on HIV infection.
Axis III.
AIDS is now best considered as part of the spectrum
of HIV infection. There are four stages of infection.
• Stage 1: Acute Infection. Most infected persons re-
member no signs or symptoms at the time of the ini-
tial infection. The acute syndrome follows infection
CT, MRI, and gross specimens show cerebral atro- by 4 to 6 weeks and is characterized by fevers, rig-
phy and infarctions, with the radiological procedures ors, muscle aches, maculopapular rash, diarrhea, and
showing multiple lucencies and the gross specimens abdominal cramps. These symptoms, often mistaken
revealing distinct white-matter lesions. The EEG is for those of influenza, resolve spontaneously after 2
abnormal but nonspecific, and positron emission to- to 3 weeks.
mography reveals hypometabolic areas. Vascular • Stage 2: Asymptomatic carrier. This stage follows
dementia is differentiated from AD on the basis of the acute infection. The infected individual is with-
its mode of progression, early appearance of neuro- out symptoms for a variable amount of time. The
logical signs, and radiographical evidence of cerebral mean symptom-free period has increased signifi-
ischemia. cantly since the disease was first identified and is
now about 10 years. Most of the estimated 2 million multifocal leukoencephalopathy. Tertiary syphilis
infected Americans are at this stage. Even though has increased significantly since the advent of AIDS,
these individuals are asymptomatic, they are carriers and neoplasms such as lymphomas, metastatic Ka-
of the disease and can infect others. posi’s sarcoma, and gliomas are also causes of AIDS
• Stage 3: Generalized adenopathy. In older terminol- dementia.
ogy, this stage was referred to as the AIDS-related Many confounding factors can increase cognitive
complex. It is characterized by palpable lymph nodes dysfunction in AIDS, including a high incidence of
that persist for longer than 3 months. These nodes drug and alcohol abuse; medications such as histamine
must be outside the inguinal area and due to no other H2 receptor antagonists (cimetidine), corticosteroids,
condition except HIV. narcotics, and antiviral drugs (e.g., zidovudine [for-
• Stage 4: Other diseases. merly azidothymidine, AZT]) that increase confusion;
and coexistent depression (Table 11-7).
– Constitutional symptoms such as lingering fever,
The CT scan shows cerebral atrophy and MRI re-
wasting syndromes, and intractable diarrhea.
veals nonspecific white-matter abnormalities. Neo-
– Secondary infections including P. carinii pneumo-
plasms and lesions such as toxoplasmosis are also
nia, cytomegalovirus retinitis, parasitic colitis, and
oral esophageal thrush.
– Secondary neoplasms such as Kaposi’s sarcoma Neuropsychiatric Effects of AIDS-related
Table 11-7
and B-cell lymphomas. Drugs
– Neurological diseases (AIDS dementia complex). Drug Use Effect
Thus, the diagnosis of AIDS is made when an infected Ketoconazole Antifungal Severe depression
individual develops either a CD4⫹ cell count of less (Nizoral)
Suicidality (rare)
than 200 or a certain condition listed in the stages. Foscarnet Cytomegalovirus Depression
Initially, the behavioral abnormalities observed in retinitis
Herpes Confusion
HIV-positive individuals were attributed to the emo- Ganciclovir Cytomegalovirus Anxiety
tional reaction to the disease. Subsequent investigations retinitis
demonstrated that neurological complications occur in Psychosis
Bactrim Pneumocystis Hallucinations
40–45% of individuals with AIDS, and in about 10% pneumonia
of cases, neurological signs are the first feature of the Depression
disease. The neurological signs present in AIDS are Apathy
Pentamidine Pneumocystis Delirium
believed to be related to both the direct effects of the pneumonia
virus on cells (such as macrophages) that enter the cen- Hallucinations
tral nervous system and the neurological conditions Interferon alpha Cancer Depression
Rifampin Tuberculosis Delirium
that opportunistically affect these individuals. Behavioral
Individuals with AIDS dementia present with changes
Isoniazid Tuberculosis Memory
impairments of cognitive, behavioral, and motor disturbance
systems. The cognitive symptoms include memory Psychosis
impairment, confusion, and poor concentration. Be- Dronabinol Appetite Wasting syndrome
(Marinol) stimulant
havioral features include apathy, reclusivity, anhedo- Nausea
nia, depression, delusions, and hallucinations. Motor Depression
symptoms include incoordination, lower extremity Anxiety
Psychosis
paresis, unsteadiness, and difficulty with fi ne motor Euphoria
movements like handwriting and buttoning clothes. Zalcitabine Antiviral Psychosis
(DDC)
As the disease progresses, parkinsonism and myo- Amnesia
clonus develop. Localizing signs such as tremors, fo- Confusion
cal seizures, abnormal reflexes, and hemiparesis can Depersonalization
Depression
result. The protozoan Toxoplasma gondii commonly Mania
infects the central nervous system and can be diag- Suicidality
nosed by CT or by increased toxoplasmosis antibody Mood swings
Didanosine Antiviral Anxiety
titers. Discrete cerebral lesions are also produced by Zidovudine Antiviral Confusion, mania
fungi such as Candida and Aspergillus, Mycobacte- (AZT)
Depression,
rium tuberculosis, and viruses such as cytomegalovi- anxiety
rus and papovavirus. Papovavirus causes progressive
visible. Lumbar puncture reveals a pleocytosis and Dementia Due to Other General
elevated protein levels, and autopsy demonstrates an Medical Conditions
atrophic brain with demyelination, multinuclear giant
cells, and gliosis of the cerebral cortex. Dementia Due to Pick’s Disease
Pick’s disease is a rare form of progressive dementia
TREATMENT clinically indistinguishable from Alzheimer’s disease.
It is about one-fifth as common as AD. Pick’s disease
The treatment of neuropsychiatric disorders in AIDS
occurs in the sixth and seventh decades of life and has
involves utilizing agents that are least likely to in-
a duration that varies from 2 to 15 years. ACh levels
terfere with other medications prescribed, or to ex-
are reduced. The pathology of Pick’s disease involves
acerbate the symptoms of the disease. AIDS-related
prominent changes (e.g., sclerosis, atrophy) in the fron-
depression has responded well to the selective sero-
tal and temporal lobes with sparing of the parietal and
tonin reuptake inhibitors (SSRIs) and to psychostim-
occipital lobes.
ulants. Some HIV drugs can have interactions with
The clinical features of Pick’s disease are quite simi-
SSRIs, and SSRIs can interact with other agents the
lar to those of Alzheimer’s disease, and since neither
individual with HIV may have been prescribed, such
condition is curable, an elaborate differential diagnosis
as antiarrhythmics, benzodiazepines, and anticonvul-
is unnecessary. Because of parietal sparing, features
sants, by inhibiting the cytochrome P-450 enzyme
such as apraxia and agnosia are less common in Pick’s
system. Some individuals have suggested that citalo-
disease, and visual–spatial ability, often impaired in
pram and escitalopram are less likely to inhibit this
Alzheimer’s disease, is preserved. Given the prominent
enzyme system. Careful attention to drug–drug inter-
changes in the frontal lobe, disinhibited behavior, loss
actions, using lower starting doses of certain psychi-
of social constraints, and lack of concern about appear-
atric drugs, and monitoring of blood levels of affected
ance and matters of personal hygiene occur relatively
medications are recommended. Among the psychos-
early in Pick’s disease. Such speech disorders as echo-
timulants, methylphenidate is preferred to dextroam-
lalia and logorrhea are common, and individuals with
phetamine because of the latter’s tendency to produce
Pick’s disease are more likely to develop Klüver–Bucy
dyskinesias. Use of stimulants for treating individu-
syndrome (orality, hyperphagia, hypersexuality, pla-
als with a history of substance abuse is not recom-
cidity) indicative of damage to the temporal lobes. Sig-
mended. Anticholingeric agents have a number of side
nificant memory impairment may occur relatively late
effects such as mydriasis, decreased gastrointestinal
in the course, and eventually the individual becomes
motility, and postural hypotension. However, low-
listless, mute, and ultimately decerebrate and coma-
dose tricyclic antidepressants are often used for their
tose. Like Alzheimer’s disease, the treatment of Pick’s
sedative, analgesic, and appetite stimulant properties.
disease is symptomatic.
Most antidepressants and some mood stabilizers and
antipsychotics can cause bone marrow suppression,
so they should be used with care, and hematologic
Dementia Due to Parkinson’s Disease
parameters should be routinely monitored. Lithium
carbonate, which produces a leukocytosis, may be Although dementia rarely occurs as an initial symptom
of benefit in recurrent unipolar and treatment-resist- of Parkinson’s disease, it is found in nearly 40% of such
ant depression, but may potentiate AIDS-related di- individuals older than 70 years of age. The prevalence
arrhea. Many of the drugs used to treat AIDS-related in persons over 60 is 1%. The disease results from loss
conditions may produce untoward psychiatric effects. of dopamine production in the basal ganglia, and can be
Depression has been well documented as a side effect idiopathic or postencephalitic. Usually, the individual
of indinavir (Crixivan), and nelfinavir (Viracept) has is 50 years of age or older, and unlike Alzheimer’s and
been associated with anxiety, depression, mood labil- Pick’s dementias, this disease occurs slightly more of-
ity, and even suicidality. St. John’s Wort may decrease ten in men. Dementia most commonly occurs in cases
the concentration of many of the protease inhibitors of Parkinson’s disease in which the decline has been
and is therefore contraindicated in individuals taking rapid and response to anticholinergics has been poor.
these agents. The clinical features of Parkinson’s disease are well
In summary, AIDS dementia is best treated by iden- described, with the cardinal triad being tremor, rigid-
tifying the associated medical condition, instituting ity, and bradykinesia. Associated features include pos-
appropriate therapy, and managing behavior in the tural instability, a festinating gait, micrographia, sebor-
interim. rhea, urinary changes, constipation, hypophonia, and
an expressionless facial countenance. The tremor in dementias, individuals with Huntington’s disease are
Parkinson’s disease has a regular rate and is most promi- often well aware of their deteriorating mentation. This
nent when the individual is sitting with arms supported; may be a factor in the high rates of suicide and alcohol-
and has been described as an intention tremor. Paranoid ism associated with this condition. Although attempts
delusions and visual hallucinations may occur, but au- have been made to increase ACh and GABA concentra-
ditory hallucinations are rare. Antipsychotics with low tions in these individuals, such pharmacological inter-
incidence of extrapyramidal symptoms such as quetiap- ventions have been unsuccessful, and the dementia is
ine, olanzapine, and ziprasidone are recommended. The untreatable. Genetic counseling is indicated.
pharmacological treatment of Parkinson’s disease in-
volves the use of a number of types of medication. These
Subacute Sclerosing Panencephalitis
include selegiline (Eldepryl), a selective monoamine
oxidase inhibitor, levodopa, other dopamine agonists Subacute sclerosing panencephalitis is an infectious
(pramipexole [Mirapex], bromocriptine, pergolide me- cause of dementia that usually appears in childhood.
sylate [Permax], amantadine), and various anticholin- The average age at onset is 10 years, and most indi-
ergic agents (e.g., benztropine). Selegiline should not viduals are male and live in rural areas. It is diagnosed
be given to individuals on antidepressant medication on the basis of periodic complexes on the EEG and an
as there is a risk that dopaminergic agents may activate elevated measles titer in the cerebrospinal fluid (CSF).
psychosis or mania. When discontinuing levodopa after The CT scan shows cerebral atrophy and dilated ventri-
a long course of treatment, the drug should be tapered cles. Myoclonus and dementia are prominent features.
so as to prevent a discontinuation syndrome similar in It has been postulated that a mutant measles virus is the
nature to the neuroleptic malignant syndrome. Some infectious agent, on the basis of the high CSF measles
medications (metoclopramide, droperidol, several an- antibody titer and the fact that the disease is virtually
tipsychotics) may produce parkinsonian features such nonexistent in children who have been vaccinated for
as masked facies, sparsity of speech, and tremor, and measles. Affected individuals show an insidious onset
in those cases, the appropriate course of treatment is to of impairment of cognition usually preceded by behav-
discontinue the offending medication. ioral problems.
Creutzfeldt–Jakob Disease
Dementia Due to Huntington’s Disease
The primary features of Creutzfeldt–Jakob disease
Dementia is also a characteristic of Huntington’s dis- are dementia, basal ganglia and cerebellar dysfunc-
ease, an autosomal, dominant, inheritable condition tion, myoclonus, upper motor neuron lesions, and rapid
localized to chromosome 4. Unfortunately, this condi- progression to stupor, coma, and death in a matter of
tion does not become apparent until age 35 to 45 years, months. The disease generally affects people 65 years
usually after childbearing has occurred. Fifty percent of age or older, with a duration of 1 month to 6 years
of offspring are affected. There is also a juvenile form and an average life span of 15 months after the onset
of the disease. Huntington’s disease affects about 4 in of the disease.
100,000 people, making it a significant cause of de- The clinical and pathological features of
mentia in middle-aged adults. Creutzfeldt–Jakob have been produced experimentally
The most noticeable clinical feature of Hunting- by injecting animals with brain tissue from affected
ton’s disease is the movement disorder, which involves adults. The agent of transmission is believed to be a
both choreiform movements (frequent movements prion-containing protein (not DNA or RNA). These pri-
that cause a jerking motion of the body) and atheto- ons have been detected in the cerebral cortex of autopsy
sis (slow writhing movements). In the juvenile form specimens of both individuals with Creutzfeldt–Jakob
of Huntington’s disease, which represents about 3% of disease and victims of kuru, a fatal disease transmit-
all cases, the chorea is replaced by dystonia, akinesia, ted by cannibalism. Slow viruses have also been impli-
and rigidity, and the course of the disease is more cated as infectious agents in kuru. Creutzfeldt–Jakob
rapid than in the adult form. In the early stages of the has been accidentally transferred to humans by corneal
disease, the chorea is not as noticeable and may be and pituitary gland transplantation, electroencephalo-
disguised by the individual by making the movements gram electrodes and ingesting meat infected with the
seem purposeful. disease (mad cow disease).
The dementia typically begins 1 year before or 1 year The memory loss in Creutzfeldt–Jakob disease in-
after the chorea and, unlike individuals with other volves all phases of memory, with recent (secondary)
memory being the most impaired. Personality changes, and dizziness. Alcohol abuse, postural hypotension,
immature behavior, and paranoia are early signs, and and gait disturbances are often associated with head
virtually every aspect of brain functioning can be in- injuries that result in dementia.
volved. Motor disorders including rigidity, incoordina-
tion, paresis, and ataxia usually follow. As with subacute
Normal-Pressure Hydrocephalus
sclerosing panencephalitis, the EEG in Creutzfeldt–
Jakob disease shows periodic complexes and biopsy Normal-pressure hydrocephalus is generally considered
specimens that reveal a characteristic spongiform en- the fifth leading cause of dementia after Alzheimer’s,
cephalopathy and occasional amyloid plaques. vascular, alcohol-related, and AIDS dementias. Long
considered reversible but often merely arrestable, nor-
mal-pressure hydrocephalus is a syndrome consisting
Neurosyphilis
of dementia, urinary incontinence, and gait apraxia. It
During the late 19th century, neurosyphilis was responsi- results from subarachnoid hemorrhage, meningitis, or
ble for a significant number of admissions to psychiatric trauma that impedes CSF absorption.
hospitals. The condition decreased in incidence after the Unlike other dementias, the dementia caused by
causative agent (Treponema pallidum) was identified and normal-pressure hydrocephalus has physical effects
penicillin treatment became readily available. The rise that often overshadow the mental effects. Psychomotor
of AIDS in the 1980s and 1990s has led to an increase in retardation, marked gait disturbances, and, in severe
the number of diagnosed cases of neurosyphilis. cases, complete incontinence of urine occur. A cister-
Dementia, secondary to neurosyphilis, produces nogram is often helpful in the diagnosis, and CT and
various physical findings in advanced cases. These may MRI show ventricular dilatation without cerebral atro-
include dysarthria, Babinski’s reflex, tremor, Argyll phy. CSF analysis reveals a normal opening pressure,
Robertson pupils, myelitis, and optic atrophy. Although and glucose and protein determinations are within the
notorious, delusions of grandeur in neurosyphilis are normal range. The hydrocephalus can be relieved by
rare. A reactive CSF VDRL result or a positive serum insertion of a shunt into the lateral ventricle to drain
fluorescent treponemal antibody result in an individual CSF into the chest or the abdominal cavity, where it
with neurological symptoms who cannot document is absorbed. Clinical improvement with shunting ap-
treatment should be treated with appropriate therapy. proaches 50% with a neurosurgical complication rate
Penicillin often improves cognitive deficits and corrects of 13–25%.
CSF abnormalities, but complete recovery is rare.
Wilson’s Disease
Dementia Due to Head Trauma
Hepatolenticular degeneration (Wilson’s disease) is
Head trauma is the leading cause of brain injury for an inherited autosomal recessive condition associated
children and young adults. Traumatic head injuries with dementia, hepatic dysfunction, and a movement
result in concussions, contusions, or open head inju- disorder. Localized to chromosome 13, this disorder
ries, and the physical examination often reveals such features copper deposits in the liver, brain, and cornea.
features as blood behind the tympanic membranes Symptoms begin in adolescence to the early twenties
(Battle’s sign), infraorbital ecchymosis, and pupillary and cases are often seen in younger children. Wilson’s
abnormalities. The psychiatric manifestations of an disease should be considered along with Huntington’s
acute brain injury are generally classified as a delirium disease, AIDS dementia, substance abuse dementia,
or an amnestic disorder; however, head trauma-induced head trauma, and subacute sclerosing panencephalitis
delirious states often merge into a chronic dementia. in the differential diagnosis of dementia that presents
Episodes of repeated head trauma, as in dementia pu- in adolescence and early adulthood. Personality, mood,
gilistica (punchdrunk syndrome), can lead to perma- and thought disorders are common, and physical find-
nent changes in cognition and thus are appropriately ings include a wing-beating tremor, rigidity, akinesia,
classified as demented states. The punchdrunk syn- dystonia, and the pathognomonic Kayser–Fleischer
drome is seen in aging boxers and includes dysarthric ring around the cornea. Wilson’s disease can mimic
speech, emotional lability, slowed thought, and impul- other conditions, including Huntington’s disease,
sivity. A single head injury may result in a postconcus- Parkinson’s disease, atypical psychosis, and neurolep-
sional syndrome with resultant memory impairment, tic-induced dystonia. Slit-lamp ocular examination,
alterations in mood and personality, hyperacusis, head- abnormal liver function tests, and markedly decreased
aches, easy fatigability, anxiety, belligerent behavior, serum ceruloplasmin levels are diagnostic. Chelating
agents such as penicillamine, if administered early, Central Nervous System Sequelae of Alcohol
can reverse central nervous system and nonneurologi- Table 11-8
Abuse
cal findings in about 50% of cases.
Blackouts
Dementia
Marchiafava–Bignami disease
Other Medical Conditions Wernicke–Korsakoff syndrome
Hepatic encephalopathy
In addition to the conditions mentioned previously, Delirium tremens
other medical illnesses can be associated with de- Withdrawal seizures
mentia. These include endocrine disorders (hypothy- Episodic dyscontrol (pathological intoxication)
Alcoholic hallucinosis
roidism, hypoparathyroidism), chronic metabolic Head injury
conditions (hypocalcemia, hypoglycemia), nutritional
deficiencies (thiamine, niacin, vitamin B12), structural
lesions (brain tumors, subdural hematomas), and mul- caused by recurrent use of alcohol and cross-sensitive
tiple sclerosis. drugs, respiratory disease related to smoking, central
nervous system hemorrhage secondary to trauma,
chronic hypoxia related to recurrent seizure activity,
Substance-Induced Persisting Dementia
folic acid deficiency, and higher rates of some neo-
plasms among those with alcoholism (Table 11-8).
DIAGNOSIS
Many other agents can produce dementia as a result
In instances in which the features of dementia result of their persisting effects. Exposure to such heavy met-
from central nervous system effects of a medication, als as mercury and bromide, chronic contact with vari-
toxin, or drug of abuse (including alcohol), the diag- ous insecticides, and use of various classes of drugs of
nosis of dementia due to the persisting effects of a abuse may produce dementia. In particular, the abuse
substance should be made. The most common demen- of organic solvents (inhalants) has been associated with
tias in this category are those associated with alcohol neurological changes (see Chapter 20). The inhalants
abuse, accounting for about 10% of all dementias. The are generally classified as anesthetics (halothane, chlo-
diagnosis of alcohol persisting dementia requires that roform, ether, nitrous oxide), solvents (gasoline, paint
the cognitive changes persist after the cessation of thinner, antifreeze, kerosene, carbon tetrachloride),
alcohol use and are not the result of changes in men- aerosols (insecticides, deodorants, hair sprays), and ni-
tation associated amnestic episodes (blackouts), or trites (amyl nitrite). The solvent category is particularly
Wernicke–Korsakoff syndrome. In addition to various toxic to the brain. In addition, acute anoxia may result
nutritional deficiencies and the toxic effects of alcohol from the common practice of inhaling a substance with
itself, alcohol abusers are more prone to develop de- a plastic bag around the head. Such neurological find-
mentia as a result of head trauma and chronic hepatic ings as peripheral neuropathy, paresis, paresthesias,
encephalopathy. areflexia, seizures, signs of cerebellar damage, and
Severe alcohol dependence is the third leading cause Babinski’s sign are common. Although the cerebellum
of dementia. Alcohol-induced dementia is a relatively is often involved, any area of the cerebral cortex may
late occurrence, generally following 15 to 20 years of be affected (Table 11-9).
heavy drinking. Dementia is more common in indi-
viduals with alcoholism who are malnourished. The
TREATMENT
CT scan shows cortical atrophy and ventricular dilata-
tion after about 10 years with neuronal loss, pigmen- The presence of dementia makes the treatment of al-
tary degeneration, and glial proliferation. The frontal coholism or other drug dependence more difficult.
lobes are the most affected, followed by parietal and Most treatment programs depend on education about
temporal areas. The amount of deterioration is related substance abuse, working the 12 steps, some degree of
to age, number of episodes of heavy drinking, and total sociability, and such relatively abstract concepts as sec-
amount of alcohol consumed over time. ondary gratification and a higher power. Such treatment
Alcohol-induced dementia, secondary to the toxic ef- programs are often reluctant to engage in the painstak-
fects of alcohol, develops insidiously and often presents ing repetition that individuals with substance-induced
initially with changes in personality. Increasing mem- persisting dementia often require. These individuals
ory loss, worsening cognitive processing, and concrete may become frustrated in peer support groups such as
thinking follow. The dementia may be affected by pe- Alcoholics Anonymous. Despite these obstacles, in-
riodic superimposed delirious states including those dividuals with alcoholism who complete a treatment
Table 11-9 Neurological Effects of Selected Inhalants DSM-IV-TR Diagnostic Criteria

Agent Use Effect
DSM-IV-TR DIAGNOSTIC CRITERIA FOR AMNESTIC DISORDER
n-Hexane Organic solvent Peripheral
neuropathy A. The development of memory impairment as mani-
Methyl butyl ketone Paint thinner Polyneuropathy fested by impairment in the ability to learn new in-
Toluene Paint thinner Cognitive formation or the inability to recall previously learned
dysfunction information.
Cerebellar ataxia B. The memory disturbance causes significant impair-
Optic neuropathy ment in social or occupational functioning and rep-
Sensorineural resents a significant decline from a previous level of
hearing loss functioning.
Dementia C. The memory disturbance does not occur exclusively
Trichloroethylene Metal Trigeminal during the course of a delirium or a dementia.
degreasing neuropathy
Extracting oils Note: Further criteria are based on etiology—see specific
Methylene chloride Paint stripping Carbon monoxide disorders for discussion.
poisoning Reprinted with permission from DSM-IV-TR Guidebook. Copy-
Aerosol right 2004, Michael B First, Allen Frances, and Harold Alan
propellant Pincus.
Hypoxic
encephalopathy
1,1,1-trichloroethane Solvent Cerebral hypoxia amnestic disorders are differentiated on the basis of the
Industrial
degreasing
etiology of the memory loss. These disorders should
not be diagnosed if the memory deficit is a feature of
a dissociative disorder, is associated with dementia, or
program and remain sober do have some improvement
occurs in the presence of clouded sensorium, as indi-
in their mental state. There is an initial improvement
viduals with amnestic disorder have impaired ability to
that peaks at 3 to 4 weeks, followed by a slow but steady
learn new information (anterograde amnesia) or cannot
improvement detected at 6 to 8 months. In general, the
remember material previously learned (retrograde am-
presence of a cognitive deficit (dementia) dictates an
nesia). Memory for the event that produced the deficit
alcohol treatment program that is behavior-based, con-
(e.g., a head injury in a motor vehicle accident) may
crete, structured, supportive, and repetitive.
also be impaired. Remote recall (tertiary memory) is
generally good, so individuals may be able to accu-
Dementia Due to Multiple Etiologies rately relate incidents that occurred during childhood
but not remember what they had for breakfast. As il-
Dementia may have more than one cause in a par- lustrated by such conditions as thiamine amnestic syn-
ticular individual. Certain types of dementia tend to drome, immediate memory is often preserved. In some
occur together, including alcohol persisting dementia instances, disorientation to time and place may occur,
and dementia caused by head trauma, vascular demen- but disorientation to person is unusual.
tia and dementia of the Alzheimer type, and alcohol The onset of the amnesia is determined by the pre-
persisting dementia and a nutritional dementia. For cipitant and may be acute as in head injury or insidious
the purpose of DSM-IV-TR diagnosis, all conditions as in poor nutritional states. DSM-IV-TR characterizes
contributing to the dementia should be diagnosed by short-duration amnestic disorder as lasting less than
coding the various types of dementia on Axis I, for 1 month and long-duration disorder lasting 1 month or
example alcohol persisting dementia and dementia due longer. Often, individuals lack insight into the memory
to head trauma. deficit and vehemently insist that their inaccurate re-
sponses on a Mental Status Examination are correct.
Amnestic Disorders The exact prevalence and incidence of the amnestic
disorders are unknown. Memory disturbances related
DIAGNOSIS to specific conditions such as alcohol dependence and
head trauma have been studied and these appear to be
The amnestic disorders are characterized by a dis- the two most common causes of amnestic disorders.
turbance in memory related to the direct effects of a
general medical condition or the persisting effects of a
substance. The impairment should interfere with social
and occupational functioning and represent a signifi- Amnestic disorders must be differentiated from the
cant decline from the previous level of functioning. The less disruptive changes in memory that occur in normal
aging, the memory impairment that is accompanied by but some individuals may continue to have blackouts
other cognitive deficits in dementia, the amnesia that for weeks even after they have stopped using alcohol.
might occur with clouded consciousness in delirium, These memory lapses are similar to blackouts experi-
the stress-induced impairment in recall seen in disso- enced while using alcohol. With continued sobriety,
ciative disorders, and the inconsistent amnestic deficits the blackouts should end, but information forgotten
seen in factitious disorder and malingering. during past blackouts is never remembered. Blackouts
The specific causes of amnestic disorders include may also be produced by agents with cross-sensitivity
(1) systemic medical conditions such as thiamine de- to alcohol, such as benzodiazepines. Blackouts should
ficiency; (2) brain conditions, including seizures, cer- not be confused with alcohol-induced dementia, which
ebral neoplasms, head injury, hypoxia, carbon mon- presents with cortical atrophy on CT scans, associ-
oxide poisoning, surgical ablation of temporal lobes, ated features of dementia, and a usually irreversible
electroconvulsive therapy, and multiple sclerosis; (3) course.
altered blood flow in the vertebral vascular system, as
in transient global amnesia; and (4) effects of a sub- Korsakoff’s Syndrome. Korsakoff’s syndrome is an
stance (drug or alcohol use and exposure to toxins). amnestic disorder caused by thiamine deficiency. Al-
Conditions that affect the temporal lobes such as her- though generally associated with alcohol abuse, it can
pes infection and Klüver–Bucy syndrome can produce occur in other malnourished states such as marasmus,
amnesia. Among drugs that can cause amnestic disor- gastric carcinoma, and HIV spectrum disease. This
ders, triazolam (Halcion) has received the most atten- syndrome is usually associated with Wernicke’s en-
tion, but all benzodiazepines can produce memory im- cephalopathy, which involves ophthalmoplegia, ataxia,
pairment, with the dose utilized being the determining and confusion. Korsakoff’s syndrome is often associ-
factor (Table 11-10). ated with a neuropathy and occurs in about 85% of un-
treated individuals with Wernicke’s disease. Complete
recovery from Korsakoff’s syndrome is rare.
Selected Amnestic Disorders
Blackouts. Blackouts are periods of amnesia for events Head Injury. Head injuries can produce a wide vari-
that occur during heavy drinking. Typically, a person ety of neurological and mental disorders even in the
awakens the morning after consumption and does not absence of radiological evidence of structural damage.
remember what happened the night before. Unlike de- Delirium, dementia, mood disturbances, behavioral
lirium tremens, which is related to chronicity of alco- disinhibition, alterations of personality, and amnestic
hol abuse, blackouts are more a measure of the amount disorders may result. Amnesia in head injury is for
of alcohol consumed at any one time. Thus, blackouts events preceding the incident and the incident itself,
are common in binge pattern drinkers and may oc- leading some clinicians to mistakenly consider these
cur the first time a person ingests a large amount of individuals as having factitious disorders or being ma-
alcohol. Blackouts are generally transient phenomena, lingerers. The eventual duration of the amnesia is re-
lated to the degree of memory recovery that occurs in
the first few days after the injury.
Table 11-10 Causes of Amnestic Disorders
Types simplex encephalopathy TREATMENT

Substance-induced (alcohol) blackouts
Wernicke–Korsakoff syndrome As in delirium and dementia, the primary goal in the
Multiple sclerosis amnestic disorders is to discover and treat the underly-
Klüver–Bucy syndrome ing cause. Because some of these causes of amnestic
Electroconvulsive therapy
Seizures disorder are associated with dangerous self-damaging
Head trauma behavior (e.g., suicide attempts by hanging, carbon
Carbon monoxide poisoning monoxide poisoning, deliberate motor vehicle acci-
Metabolic
Hypoxia dents, self-inflicted gunshot wounds to the head, and
Hypoglycemia chronic alcohol abuse), some form of psychiatric man-
Medications agement is often necessary. In the hospital, continuous
Triazolam
Barbiturates (thiopental sodium) reorientation by means of verbal redirection, clocks,
Diltiazem (Cardizem) and calendars can allay the individual’s fears. Support-
Zalcitabine (DDC) ive individual psychotherapy and family counseling are
Cerebrovascular disorders
beneficial.
Comparison of DSM-IV-TR and ICD-10

late-onset. However, in contrast to DSM-IV-TR, the
Diagnostic Criteria
ICD-10 Diagnostic Criteria for Research for these sub-
The overall construct of delirium is similar in DSM- types also specify characteristic course features and
IV-TR and ICD-10 (i.e., a disturbance in conscious- types of deficits: early-onset cases must have a “rela-
ness and cognition with an acute onset and fluctuating tively rapid onset and progression” and a characteristic
course). The ICD-10 Diagnostic Criteria for Research type of cognitive impairment (e.g., aphasia), whereas
include some additional items: impairment in short- late-onset cases have a very slow and gradual onset
term memory with intact long-term memory, disorien- with a predominance of memory impairment over other
tation, psychomotor disturbances, and problems with intellectual deficits. In ICD-10, this disorder is referred
sleep. ICD-10 does not include the DSM-IV-TR cat- to as Dementia in Alzheimer’s Disease.
egory delirium due to multiple etiologies. For vascular dementia, the ICD-10 Diagnostic Cri-
Similarly, the overall construct of dementia is simi- teria for Research are more narrowly defined than the
lar in DSM-IV-TR and ICD-10 (i.e., memory impair- DSM-IV-TR criteria in that ICD-10 specifies that the
ment plus a decline in other cognitive abilities). The deficits in higher cognitive functions are unevenly dis-
ICD-10 Diagnostic Criteria for Research are more nar- tributed and that there be both clinical and laboratory
rowly defined in several ways: the minimum duration evidence of focal brain damage. Furthermore, ICD-10
of the disturbance is 6 months as compared with DSM- subspecifies vascular dementia based on acute onset
IV-TR, which does not specify any minimum duration. and multi-infarct, subcortical, and mixed cortical and
Required cognitive deficits, in addition to memory loss, subcortical types.
are restricted to a deterioration in judgment and think- For amnestic disorder, the ICD-10 Diagnostic Cri-
ing (as opposed to DSM-IV-TR, which requires any teria for Research are more narrowly defined than the
one of aphasia, apraxia, agnosia, or disturbance in ex- criteria in DSM-IV-TR by virtue of requiring both an
ecutive functioning); and there must also be a “decline impaired ability to learn new information and a re-
in emotional control or motivation or a change in social duced ability to recall past experiences, as well as a
behavior.” requirement that immediate recall be preserved. In
Like DSM-IV-TR, ICD-10 includes two subtypes ICD-10, this disorder is referred to as Organic Amnes-
of dementia of the Alzheimer’s type: early-onset and tic Syndrome.
CHAPTER
12 Mental Disorders Due to a

General Medical Condition
This chapter describes disorders characterized by condition and could not be better accounted for by a
mental symptoms, which occur due to direct physi- primary mental disorder, then it remains to classify
ological effect of a general medical condition. In these symptoms into one of the specific types noted
evaluating individuals with mental symptoms of in Figure 12-1. There is also, at the end of the deci-
any sort, one of the fi rst questions to ask is whether sion tree, a residual category for “unspecified” mental
those symptoms are occurring as part of a primary symptoms.
mental disorder or are caused by a general medical In caring for individuals with mental disorders due
condition, and Figure 12-1 presents a decision tree to a general medical condition, the question arises as
designed to help in making this decision. The fi rst to whether symptomatic treatment for these mental
step is to review the history, physical examination, symptoms should be offered. Figure 12-2 provides a
and laboratory tests to see if there is evidence for the general treatment algorithm designed to help answer
presence of a general medical condition that could this question. First, one must determine whether the
plausibly cause the mental symptoms in question. In mental symptoms demand emergent treatment. Con-
making this determination, one looks not only for sider, for example, a postictal psychosis character-
a temporal correlation (e.g., the onset of a psycho- ized by delusions of persecution, which prompt the
sis shortly after starting or increasing the dose of individual to become assaultive: here, even though the
a medication), but also keeps in mind well-docu- condition itself will eventually resolve spontaneously,
mented associations between certain mental symp- symptomatic treatment of the psychosis is required to
toms (e.g., depression) and certain general medical protect the individual or others. In cases in which the
conditions (e.g., Cushing’s syndrome). If it appears, mental symptoms do not present an emergency, one
at this point, that the mental symptoms could indeed looks to whether the underlying general medical con-
be occurring secondary to a general medical condition is treatable or not. For example, in the case of
dition, the next step involves determining whether psychosis due to Huntington’s disease, as the underly-
these symptoms could be better accounted for by a ing condition is not treatable, one generally proceeds
primary mental disorder. For example, consider the directly to symptomatic treatment. In cases in which
case of a 45-year-old man with a history of recur- the underlying condition is treatable, one must make
rent major depressive disorder, currently euthymic, a judgment as to whether, with treatment of the un-
who begins a course of steroids for asthma and then, derlying general medical condition, the mental symp-
within a week, becomes depressed. The steroids are toms will resolve at a clinically acceptable rate. Con-
stopped but the depression continues. In this case, if sider, for example, an individual with anxiety due to
the depression had cleared shortly after stopping the hyperthyroidism who has just begun treatment with
steroids, one might make the case that the depression an antithyroid drug. In such a case, the decision as
occurred secondary to the steroid treatment; the per- to whether to offer a benzodiazepine as symptomatic
sistence of the symptoms, however, argues strongly treatment for the anxiety depends not only on the se-
that this depression represents rather a recurrence of verity and tolerability of the anxiety but also on the
the major depressive disorder. expected time required for the antithyroid drug to re-
Once it appears that the mental symptoms in ques- solve the hyperthyroidism: here, clearly, considerable
tion could directly result from a general medical clinical judgment is required.
Evidence that the mental symptoms caused

by a general medical condition
No
Yes
Symptoms better accounted for

by primary mental disorder
No Yes
Psychotic Symptoms Primary

mental
disorder
Yes No
Psychotic disorder due to a
general medical condition
Mood Symptoms
Mood disorder due to a Yes No

general medical condition,
with either depressive or
manic features
Anxiety Symptoms
Anxiety disorder due to a Yes

No
with panic attacks,
generalized anxiety,
or obsessive−
compulsive symptoms
Catatonic Symptoms
Catatonic disorder due to a Yes No

Personality Change
Yes
Personality change due to a No
Other, unspecified,
mental symptoms
Yes
Mental disorder not otherwise
specified due to a general
medical condition (e.g.,
pseudobulbar palsy,
Kluver− Bucy syndrome)
Figure 12-1 Diagnostic decision tree.

Chapter 12 • Mental Disorders Due to a General Medical Condition 111
Mental symptoms A “Laboratory Screen” for Secondary

require emergent Table 12-1
Psychosis
treatment
Serum or urine drug screen
No Testosterone level (reduced in anabolic steroid abusers)
Red blood cell mean corpuscular volume (elevated in
General medical alcoholism and many cases of B12 deficiency)
condition treatable Liver transaminases (elevated in alcoholism)
HIV testing
Yes FTA
B12 levels (or, for increased sensitivity, plasma
methylmalonic acid, and homocysteine levels)
Yes Mental symptoms ANA
resolve at a Antithyroid antibodies (present in Hashimoto’s
clinically encephalopathy)
No acceptable rate Thyroid profile with TSH
Cortisol and ACTH levels and 24-hour urine for free
Yes cortisol
Copper and ceruloplasmin levels
MRI
No EEG
Lumbar puncture
Symptomatic treatment
of mental symptoms to disclose clear evidence for another cause, a “labora-
tory screen,” as listed in Table 12-1, may be appropri-
Figure 12-2 General treatment algorithm.
ate. Clearly, one does not order all these tests at once,
but begins with those most likely, given the overall
clinical picture, to be the most informative.
Psychotic Disorder Due to a General Medical
Table 12-2 lists the various secondary causes of psy-
Condition
chosis, dividing them into those occurring secondary
to precipitants (e.g., medications), those occurring sec-
DIAGNOSIS
ondary to diseases with distinctive features (e.g., the
A psychotic disorder due to a general medical condition chorea of Huntington’s disease), and finally a group oc-
is characterized clinically by hallucinations or delusions curring secondary to miscellaneous causes (e.g., cer-
occurring in a clear sensorium, without any associated ebral tumors).
decrement in intellectual abilities. Furthermore, one Psychosis occurring secondary to precipitants is per-
must be able to demonstrate, by history, physical ex- haps the most common form of secondary psychosis.
amination, or laboratory findings, that the psychosis is Among the various possible precipitants, substances
occurring on the basis of a general medical condition. are perhaps the most common, but these are covered
Psychotic disorder due to a general medical condi- in the various chapters on specific substances known
tion is a disorder that by definition occurs in a clear to cause psychotic symptoms, like stimulants, hallu-
sensorium, without any associated decrement in intel- cinogens, phencyclidine, cannabis, and alcohol. After
lectual abilities; both delirium and dementia are com- drugs of abuse, various medications are the next most
monly accompanied by hallucinations and delusions, common precipitants, and of the medications listed in
but these conditions are clearly distinguished from Table 12-1, the most problematic are the neuroleptics
psychotic disorder due to a general medical condition themselves. It appears that in a very small minority
by the presence of confusion or significant intellectual of individuals treated chronically with neuroleptics,
deficits. When these features are present, one should a “supersensitivity psychosis” (or, as it has also been
proceed to the differential for delirium and dementia called, on analogy with tardive dyskinesia, “tardive
described in the preceding chapter of this book. psychosis”) may occur. Making such a diagnosis in the
In most cases, a thorough history and physical exam- case of individuals with schizophrenia may be diffi-
ination will disclose evidence of the underlying cause cult, as one may well say that any increase in psychotic
of the psychosis in question. In those cases, however, in symptoms, rather than evidence for a supersensitivity
which the individual’s symptomatology is atypical for psychosis, may merely represent an exacerbation of the
one of the primary causes of psychosis (e.g., schizo- schizophrenia; in the case of individuals treated with
phrenia), yet the history and physical examination fail antipsychotics for other conditions (e.g., Tourette’s
Causes of Psychosis due to a General

ing dopamine agonists as bromocriptine and lergotrile.
Table 12-2 The other medications noted in Table 12-1 very rarely
Medical Condition
cause a psychosis.
Secondary to Precipitants
Medications Of the psychoses secondary to diseases with distinc-
Neuroleptics (supersensitivity psychosis) tive features, the psychoses of epilepsy are by far the
Dopaminergic drugs most important, and these may be ictal, postictal, or
Disulfiram
Sympathomimetics interictal. Ictal psychoses represent complex partial
Bupropion seizures and are immediately suggested by their exqui-
Fluoxetine sitely paroxysmal onset. Postictal psychoses are typi-
Baclofen (upon discontinuation)
Other precipitants cally preceded by a “flurry” of grand mal or complex
Postencephalitic psychosis partial seizures and, importantly, are separated from
Posthead trauma the last of this “flurry” of seizures by a “lucid” interval
Secondary to Diseases with Distinctive Features lasting from hours to days. Interictal psychoses appear
Associated with epilepsy
Ictal psychosis in one of two forms, namely, the psychosis of forced
Postictal psychosis normalization and the chronic interictal psychosis. The
Psychosis of forced normalization psychosis of forced normalization appears when an-
Chronic interictal psychosis
Encephalitic onset ticonvulsants have not only stopped seizures but also
Herpes simplex encephalitis have essentially “normalized” the EEG; a disappear-
Encephalitis lethargica ance of the psychosis with the resumption of seizure
Infectious mononucleosis
With other specific features: activity secures the diagnosis. The chronic interictal
Huntington’s disease (chorea) psychosis, often characterized by delusions of persecu-
Sydenham’s chorea tion and of reference and auditory hallucinations, ap-
Chorea gravidarum
Manganism (parkinsonism) pears subacutely, over weeks or months, in individuals
Creutzfeldt–Jakob disease (myoclonus) with long-standing, uncontrolled grand mal or complex
Hashimoto’s encephalopathy (myoclonus)
Wilson’s disease (various abnormal involuntary
partial seizures.
movements) Encephalitic psychoses are suggested by typical “en-
AIDS (thrush, Pneumocystis pneumonia) cephalitic” features such as headache, lethargy, and fe-
Systemic lupus erythematosus (arthralgia, rash,
pericarditis, pleurisy) ver. Prompt diagnosis is critical, especially in the case
Hyperthyroidism (tremor, tachycardia) of herpes simplex encephalitis, given its treatability.
Hypothyroidism (cold intolerance, voice change, Of the miscellaneous causes capable of causing psy-
constipation, hair loss, myxedema)
Cushing’s syndrome (“Cushingoid” habitus, e.g., “moon” chosis, cerebral tumors are perhaps the most important,
facies) with psychosis being noted with tumors of the frontal
Adrenocortical insufficiency (abdominal complaints and lobe, corpus callosum, and temporal lobe. Suggestive
dizziness)
Hepatic porphyria (abdominal pain) clinical evidence for such a cause includes prominent
Autosomal dominant cerebellar ataxia headache, seizures, or certain focal signs, such as apha-
Dentatorubropallidoluysian atrophy (ataxia) sia. Cerebral infarction is likewise an important cause,
Prader–Willi syndrome (massive obesity)
and is suggested not only by accompanying focal signs
Secondary to Miscellaneous Causes
Cerebral tumors but also by its acute onset; infarction of the frontal lobe,
Cerebral infarction temporoparietal area, and thalamus have all been im-
Multiple sclerosis plicated. Neurosyphilis should never be forgotten as a
Neurosyphilis
Vitamin B12 deficiency differential possibility in cases of psychosis of obscure
Metachromatic leukodystrophy origin, and a Fluorescent Treponemal Antibody (FTA)
Subacute sclerosing panencephalitis is appropriate in such cases. Vitamin B12 deficiency,
Fahr’s syndrome
Thalamic degeneration likewise, should be borne in mind, especially as this
Velo-cardio-facial syndrome may present with psychosis without any evidence of
spinal cord or hematologic involvement. The remaining
disorders listed in Table 12-2 are extremely rare causes
syndrome), however, the appearance of a psychosis is of psychosis, and represent the “zebras” of this differ-
far more suggestive, as it could not be accounted for on ential listing. Among these “zebras,” however, one is
the basis of the disease for which the neuroleptic was of particular interest, namely, velo-cardio-facial syn-
prescribed. Dopaminergic drugs capable of causing a drome. This genetic disorder, characterized by cleft
psychosis include levodopa itself and such direct-act- palate, cardiovascular malformations, and dysmorphic
facies (micrognathia and prominent nose), and, often, Causes of Depression due to a General
mental retardation, also appears, in a substantial mi- Table 12-3
Medical Condition
nority of cases, to cause a psychosis phenotypically
very similar to that caused by schizophrenia. Medications
Propranolol
Interferon
TREATMENT ACTH
Prednisone
Treatment, if possible, is directed at the underly- Reserpine
ing cause. In those cases in which such treatment is Alpha-methyldopa
Nifedipine
unavailable or ineffective, or in which control of the Ranitidine
psychosis is emergently required, neuroleptics are in- Bismuth subsalicylate
dicated. Although conventional neuroleptics, such as Pimozide
Subdermal estrogen/progestin
haloperidol, have long been used successfully, newer Anticholinergic withdrawal (“cholinergic rebound”)
atypical agents, such as olanzapine or risperidone, may Poststroke depression
Head trauma
be better tolerated. In general, it is best to start with a Whiplash
low dose (e.g., 2.5 mg of haloperidol, 5 mg olanzapine
Secondary to Diseases with Distinctive Features
or 1 mg of risperidone) with gradual incremental in- Hypothyroidism (hair loss, dry skin, voice change)
creases, if necessary. Hyperthyroidism (weight loss with increased appetite,
tachycardia, and, in the elderly, atrial fibrillation or
congestive heart failure)
Mood Disorder Due to a General Medical Cushing’s syndrome (moon facies, hirsutism, acne, “buffalo
hump”, and abdominal striae)
Condition with Depressive Features Chronic adrenocortical insufficiency (nausea, vomiting,
abdominal pain, and postural dizziness)
DIAGNOSIS Obstructive sleep apnea (severe snoring)
Multiple sclerosis (various focal findings)
Down syndrome
A mood disorder secondary to a general medical con- Epilepsy
dition with depressive features is characterized by a Ictal depression
prominent and persistent depressed mood or loss of Chronic interictal depression
interest, and by the presence of evidence, from the Occurring as Part of Certain Neurodegenerative or
history, physical examination or laboratory tests, of Dementing Disorders
Alzheimer’s disease
a general medical condition capable of causing such Multi-infarct dementia
a disturbance. Although other depressive symptoms Diffuse Lewy body disease
(e.g., lack of energy, sleep disturbance, appetite change, Parkinson’s disease
Fahr’s syndrome
or psychomotor change) may be present, they are not Tertiary neurosyphilis
necessary for the diagnosis. Limbic encephalitis
The various secondary causes of depression are Miscellaneous or Rare Causes
listed in Table 12-3. In utilizing Table 12-3, the fi rst Cerebral tumors
Hydrocephalus
question to ask is whether the depression could be Pancreatic cancer
secondary to precipitants. Of the various possible New-variant Creutzfeldt–Jakob disease
precipitants, substances of abuse (e.g., as seen in al- Hyperparathyroidism
Systemic lupus erythematosus
coholism or during stimulant withdrawal) are very Pernicious anemia
common causes, and these are discussed in their re- Pellagra
spective chapters. Medications are particularly im- Lead encephalopathy
Hyperaldosteronism
portant; however, it must be borne in mind that most
individuals are able to take the medications listed in
Table 12-3 without untoward effect. Consequently, as benzotropine or certain tricyclic antidepressants,
before ascribing a depression to any medication, it and is characterized by depressed mood, malaise, in-
is critical to demonstrate that the depression did not somnia and gastrointestinal symptoms such as nau-
begin before the medication was begun, and, ideally, sea, vomiting, abdominal cramping, and diarrhea.
to demonstrate that the depression resolved after the Poststroke depression is not uncommon, and may be
medication was discontinued. Anticholinergic with- more likely when the anterior portion of the left fron-
drawal may occur within days after abrupt discon- tal lobe is involved; although spontaneous remission
tinuation of highly anticholinergic medications, such within a year is the rule, depressive symptoms, in the
meantime, may be quite severe. Both head trauma TREATMENT

and whiplash injuries may be followed by depressive
Treatment efforts should be directed at relieving,
symptoms in close to half of all the cases.
if possible, the underlying cause. When this is not
Depression may occur secondary to diseases with
possible, antidepressants should be considered. Con-
distinctive features, and keeping such features in mind
trolled studies have demonstrated the effectiveness
whenever evaluating depressed individuals will lead
of both nortriptyline and citalopram for poststroke
to a gratifying number of diagnostic “pick-ups.” These
depression, and nortriptyline for depression seen in
features are noted in Table 12-3, and are for the most
Parkinson’s disease. For other secondary depres-
part self-explanatory; depression associated with epi-
sions, citalopram (or escitalopram) is probably a
lepsy, however, may merit some further discussion.
good choice, given its benign side-effect profi le and
Ictal depressions are, in fact, simple partial seizures
notable lack of drug–drug interactions; nortriptyl-
whose symptomatology is for the most part restricted
ine should be used with caution in individuals with
to affective changes. The diagnosis of ictal depression
cardiac conduction defects (as it may prolong con-
is suggested by the paroxysmal onset of depression
duction time) and in those at risk for seizures as in
(literally over seconds); although such simple partial
head trauma as this agent may also lower the seizure
seizures may last only minutes, longer durations, up
threshold.
to months, have also been reported. Interictal depres-
sions, rather than occurring secondary to paroxysmal
electrical activity within the brain, occur as a result
Mood Disorder Due to a General Medical
of long-lasting changes in neuronal activity, perhaps
Condition with Manic Features
related to “kindling” within the limbic system, in in-
dividuals with chronically recurrent seizures, either
DIAGNOSIS
grand mal or, more especially, complex partial. Such
interictal depressions are of gradual onset and are Mood disorder due to a general medical condition with
chronic. manic features is characterized by a prominent and per-
Depression occurring as part of certain neurode- sistently elevated, expansive, or irritable mood which,
generative or dementing disorders is immediately on the basis of the history, physical, or laboratory ex-
suggested by the presence of other symptoms of these aminations, can be attributed to an underlying general
disorders, such as dementia or distinctive physical find- medical condition. Other manic symptoms, such as in-
ings, for example, parkinsonism. creased energy, decreased need for sleep, hyperactiv-
The miscellaneous or rare causes represent, for the ity, distractibility, pressured speech, and flight of ideas,
most part, the “zebras” in the differential for depres- may or may not be present.
sion, and should be considered when, despite a thor- As a rule, it is very rare for mania to constitute the
ough investigation, the diagnosis of a particular case of initial presentation of any of the diseases or disor-
depression remains unclear. ders listed in Table 12-4; thus, other evidence of their
presence will become evident during the routine his-
tory and physical examination. Exceptions to the rule
Course
include neurosyphilis, vitamin B12 deficiency, and
Most medication-induced depressions begin to clear Creutzfeldt–Jakob disease; however, in all these cases
within days of discontinuation of the offending medi- continued observation will eventually disclose the ap-
cation; depression as part of withdrawal from stimu- pearance of other evidence suggestive of the correct
lants or anabolic steroids clears within days or weeks, diagnosis.
and from anticholinergics, within days. Poststroke de- Table 12-4 lists secondary causes of elevated or
pression, as noted above, typically remits within a year. irritable mood, with these causes divided into cat-
The course of depression secondary to head trauma or egories designed to facilitate the task of differential
whiplash is generally prolonged, though quite vari- diagnosis. In utilizing Table 12-4, the fi rst step is to
able. Most of the other conditions or disorders in the determine whether the mania could be secondary to
list are chronic, and depression occurring secondary to precipitants. Substance-induced mood disorder re-
them likewise tends to be chronic; exceptions include lated to drugs of abuse is covered in the relevant sub-
depression in multiple sclerosis, which may have a stance-related disorders chapters in this textbook. Of
relapsing and remitting course, corresponding to the the precipitating factors listed in Table 12-4, medica-
appearance and disappearance of appropriately situ- tions are the most common offenders. However, be-
ated plaques. fore attributing the mania to one of these medications,
Causes of Mania due to a General Medical

nia, and such a syndrome occurring in “bulked up”
Table 12-4 individuals should prompt a search for other clinical
Condition
evidence of abuse, such as gynecomastia and testicu-
Medications lar atrophy. Closed head injury may be followed by
Corticosteroids or adrenocorticoptrophic hormone mania either directly upon emergence from postcoma
Levodopa delirium, or after an interval of months. Hemodialy-
Zidovudine
Oral contraceptives sis may cause mania, and in one case, mania occurred
Isoniazid as the presenting sign of an eventual dialysis demen-
Buspirone tia. Encephalitis may cause mania, as, for example,
Procyclidine
Procarbazine in postinfectious encephalomyelitis, with the correct
Propafenone diagnosis eventually being suggested by more typi-
Baclofen, upon discontinuation after long-term use cal signs such as delirium or seizures. Encephalitis
Reserpine, upon discontinuation after long-term use
Methyldopa, upon discontinuation after long-term use lethargica (Von Economo’s disease; European sleep-
Closed head injury ing sickness) may also be at fault, with the diagnosis
Hemodialysis
Encephalitis
suggested by classic signs such as sleep reversal or
Aspartame oculomotor paralyses. Aspartame taken in very high
Metrizamide dose caused mania and a seizure in one individual,
Secondary to Diseases with Distinctive Features and metrizamide myelography prompted mania in
Hyperthyroidism (proptosis, tremor, tachycardia) another. Mania occurring secondary to disease with
Cushing’s syndrome (moon facies, hirsutism, acne, “buffalo
hump”, abdominal striae) distinctive features is immediately suggested by these
Multiple sclerosis (various focal findings) features, as listed in Table 12-4. Some elaboration
Cerebral infarction (sudden onset with associated localizing may be in order regarding mania secondary to cere-
signs)
Sydenham’s chorea bral infarction. This cause, of course, is suggested by
Chorea gravidarum the sudden onset of the clinical disturbance, with the
Hepatic encephalopathy (asterixis, delirium)
Uremia (asterixis, delirium)
mania being accompanied by various other more or
Epilepsy less localizing signs; what is most remarkable here is
Ictal mania the variety of structures that, if infarcted, may be fol-
Postictal mania
lowed by mania. Thus, mania has been noted with in-
Occurring as part of Certain Neurodegenerative or farction of the midbrain, thalamus (either on the right
Dementing Diseases
Alzheimer’s disease side or bilaterally), anterior limb of the internal cap-
Neurosyphilis sule and adjacent caudate on the right, and subcortical
Huntington’s disease white matter or cortical infarction on the right in the
Creutzfeldt–Jakob disease
frontoparietal, or temporal areas. Mania associated
Miscellaneous or Rare Causes
Cerebral tumors with epilepsy may also deserve additional comment.
Systemic lupus erythematosus Ictal mania is characterized by its paroxysmal onset,
Vitamin B12 deficiency over seconds, and the diagnosis of postictal mania is
Metachromatic leukodystrophy
Adrenoleukodystrophy suggested when mania occurs shortly after a “flurry”
Tuberous sclerosis of grand mal or complex partial seizures.
Mania occurring as part of certain neurodegen-
erative or dementing diseases is suggested, in gen-
it is critical to demonstrate that the mania occurred eral, by a concurrent dementia, and in most cases the
only after initiation of that medication; ideally, one mania plays only a minor role in the overall clinical
would also want to show that the mania spontane- pictures. Neurosyphilis, however, is an exception to
ously resolved subsequent to the medication’s discon- this rule, for in individuals with general paresis of the
tinuation. Of the medications listed, corticosteroids, insane (dementia paralytica) mania may dominate the
such as prednisone, are most likely to cause mania, picture.
with the likelihood increasing in direct proportion Of the miscellaneous or rare causes of mania, cer-
to dose: in one study, 80 mg of prednisone produced ebral tumors are the most important to keep in mind,
mania within five days in 75% of subjects. Levodopa with mania being noted with tumors of the midbrain,
is the next most likely cause, and in the case of levo- tumors compressing the hypothalamus (e.g., a crani-
dopa the induced mania may be so pleasurable that opharyngioma), or a pituitary adenoma, and tumors of
some individuals have ended up abusing the drug. the right thalamus, right cingulate gyrus, or one or both
Anabolic steroid abuse may cause an irritable ma- frontal lobes.
Course Causes of Panic Attacks due to a General

Table 12-5
Medical Condition
Most cases of medication-induced mania begin to clear
in a matter of days; for other causes, the course of the Partial seizures
mania generally reflects the course of the underlying Paroxysmal atrial tachycardia
Hypoglycemia
disease. Angina or acute myocardial infarction
Pulmonary embolus
Acute asthmatic attack
TREATMENT Pheochromocytoma
Parkinson’s disease
Treatment, if possible, is directed at the underlying
cause. In cases where such etiologic treatment is not Generalized anxiety tends to be of subacute or
possible, or not rapidly effective enough, pharmaco- gradual onset, and may last for long periods of time,
logic measures are in order. Mood stabilizers, such as anywhere from days to months, depending on the un-
lithium or divalproex used in a fashion similar to that derlying cause. Here, some individuals, rather than
for the treatment of mania occurring in bipolar disor- complaining of feeling anxious per se, may complain
der, are commonly used: both lithium and divalproex of being worried, tense, or ill at ease. Autonomic symp-
are effective in the prophylaxis of mania occurring toms tend not to be as severe or prominent as those seen
secondary to prednisone; case reports also support the in panic attacks: shakiness, palpitations (or tachycar-
use of lithium for mania secondary to zidovudine and dia), and diaphoresis are perhaps most common.
divalproex for mania secondary to closed head injury. The causes of secondary panic attacks are listed in
In choosing between lithium and divalproex, in cases Table 12-5. Substance-induced anxiety disorder related
where there is a risk for seizures (e.g., head injury, to drugs of abuse (e.g., cannabis, LSD) is covered in
encephalitis, stroke, or tumors), divalproex clearly is the relevant substance-related disorders chapters in
preferable. this textbook. Partial seizures and paraoxysmal atrial
In cases where emergent treatment is required, be- tachycardia are both characterized by their exquisitely
fore lithium or divalproex could have a chance to be- paroxysmal onset, over a second or two; in addition,
come effective, oral or intramuscular lorazepam or ha- paroxysmal atrial tachycardia is distinguished by the
loperidol (in doses of 2 mg and 5 mg, respectively) may prominence of the tachycardia and by an ability, in
be utilized, again much as in the treatment of mania in many cases, to terminate the attack with a Valsalva
bipolar disorder. maneuver. Hypoglycemia is often suspected as a cause
of anxiety, but before the diagnosis is accepted, one
must demonstrate the presence of “Whipple’s triad”:
Anxiety Disorder Due to a General Medical
hypoglycemia (blood glucose ⱕ 45 mg/dL), typical
Condition with Panic Attacks or with
symptoms, and the relief of those symptoms with glu-
Generalized Anxiety
cose. Angina or acute myocardial infarction can present
with a panic attack, with the diagnosis being suggested
DIAGNOSIS
by the clinical setting, for example, multiple cardiac
Pathologic anxiety secondary to a general medical risk factors. A pulmonary embolus, at the moment of
condition may occur in the form of well-circumscribed its lodgment in a pulmonary artery, may also present
and transient panic attacks or in a generalized, more with a panic attack, and again here the correct diag-
chronic form. As the differential diagnoses for these nosis is suggested by the clinical setting, for example,
two forms of anxiety are quite different, it is critical to situations, such as prolonged immobilization, which
clearly distinguish among them. favor deep venous thrombosis. Acute asthmatic attacks
Panic attacks have an acute or paroxysmal onset, and are suggested by wheezing, and pheochromocytoma by
are characterized by typically intense anxiety or fear associated hypertension. Individuals with Parkinson’s
which is accompanied by various “autonomic” signs disease treated with levodopa may experience panic at-
and symptoms, such as tremor, diaphoresis, and palpi- tacks during “off” periods.
tations. Symptoms rapidly crescendo over seconds or The secondary causes of generalized anxiety are
minutes and in most cases the attack will clear any- listed in Table 12-6. Sympathomimetics and theophyl-
where from within minutes up to a half-hour. Although line, as used in asthma and chronic obstructive pul-
attacks tend to be similar to one another in the same in- monary disease (COPD) are frequent causes, as are
dividual, there is substantial inter-individual variability many of the antidepressants. Hyperthyroidism is sug-
in the symptoms seen. gested by heat intolerance and proptosis, and Cushing’s
Causes of Generalized Anxiety due to a Causes of Obsessions and Compulsions due

Table 12-6 Table 12-7
General Medical Condition to a General Medical Condition
Sympathomimetics Postencephalitic
Theophylline Postanoxic
Various antidepressants (tricyclics, SSRIs, etc.) Post-closed head injury
Hyperthyroidism Clozapine
Cushing’s syndrome Sydenham’s chorea
Hypocalcemia Huntington’s disease
Chronic obstructive pulmonary disease Simple partial seizures
Congestive heart failure Infarction of the basal ganglia or right parietal lobe
Poststroke Fahr’s syndrome
Post-head trauma
In the vast majority of cases, obsessions and compul-

syndrome by the typical Cushingoid habitus (i.e., moon sions occur as part of certain primary mental disorders,
facies, hirsutism, acne, “buffalo hump,” and abdomi- including obsessive–compulsive disorder, depression,
nal striae). Hypocalcemia may be suggested by a his- schizophrenia, and Tourette’s syndrome. Those rare in-
tory of seizures or tetany. Both COPD and congestive stances where obsessions and compulsions are second-
heart failure are suggested by marked dyspnea. Stroke ary to a general medical condition or medication are
and severe head trauma may be followed by chronic listed in Table 12-7.
anxiety, but this is seen in only a minority of these In most cases, these causes of secondary obsessions or
individuals. compulsions are readily discerned, as for example, a his-
tory of encephalitis, anoxia, closed head injury, or treat-
ment with clozapine. Sydenham’s chorea is immediately
TREATMENT
suggested by the appearance of chorea; however, it must
Treatment is directed at the underlying cause, and this be borne in mind that obsessions and compulsions may
is sufficient for all cases of secondary panic attacks constitute the presentation of Sydenham’s chorea, with the
and most cases of secondary generalized anxiety; ex- appearance of chorea being delayed for days. Ictal obses-
ceptions include poststroke and post-head trauma anxi- sions or compulsions, constituting the sole clinical mani-
ety, and in these cases benzodiazepines have been used festation of a simple partial seizure, may, in themselves,
with success. be indistinguishable from the obsessions and compulsions
seen in obsessive–compulsive disorder, but are suggested
by a history of other seizure types, for example, complex
Anxiety Disorder Due to a General Medical
partial or grand mal seizures. Infarction of the basal gan-
Condition with Obsessive–Compulsive
glia or parietal lobe is suggested by the subacute onset of
Symptoms
obsessions or compulsions accompanied by “neighbor-
hood” symptoms such as abnormal movements or unilat-
DIAGNOSIS
eral sensory changes. Fahr’s syndrome, unlike the forego-
Obsessions consist of unwanted, and generally anxiety- ing, may be an elusive diagnosis, only suggested perhaps
provoking, thoughts, images or ideas, which repeatedly when CT imaging incidentally reveals calcification of the
come to mind despite attempts to stop them. Allied to basal ganglia.
this are compulsions that consist of anxious urges to do
or undo things, urges which, if resisted, are followed by
Course
rapidly increasing anxiety that can often only be relieved
by giving into the compulsion to act. The acts themselves Although the course of obsessions and compulsions due
that the individuals feel compelled to perform are often to fixed lesions, such as those seen with head trauma or
linked to an apprehension on the individuals’ part that cerebral infarction, tends to be chronic, some sponta-
they have done something that they ought not to have neous recovery may be anticipated over the following
done or have left undone something that they ought to months to a year.
have done. Thus, one may feel compelled to repeatedly
subject the hands to washing to be sure that all germs
TREATMENT
have been removed, or to repeatedly go back and check
on the gas to be sure that it has been turned off. When treatment of the underlying cause is not possible,
Secondary obsessions and compulsions are relatively a trial of an SSRI, as used for obsessive–compulsive
rare. disorder, might be appropriate.
Catatonic Disorder Due to a General Medical with one arm raised high and the other stuffed inside
Condition his belt. Negativism entails a mulish, intractable, and
automatic resistance to whatever is expected, and may
DIAGNOSIS be either “passive” or “active.” Passively negativistic
individuals simply fail to do what is asked or expected:
Catatonia can develop as a result of the direct effects
if clothes are laid out they will not dress; if asked to
of a general medical condition on the central nervous
eat or take pills, their lips remain frozen shut. Active
system. Catatonia exists in two subtypes, namely, stu-
negativism manifests in doing the opposite of what
porous catatonia (also known as the akinetic or “re-
is expected: if asked to come into the office, the indi-
tarded” subtype) and excited catatonia, and each will
vidual may back into the hallway or if asked to open
be described in turn.
the eyes wide to allow for easier examination, they may
Stuporous catatonia is characterized by varying com-
cramp the eyes closed. Automatic obedience, as may
binations of mutism, immobility, and waxy flexibility;
be suspected, represents the opposite of negativism,
associated features include posturing, negativism, au-
with affected individuals doing exactly what they are
tomatic obedience, and “echo” phenomena. Mutism
told, even if this places them in danger. Echo phenom-
ranges from complete to partial: some individuals may
ena represent a kind of automatic obedience: in echo-
mumble or perhaps utter brief, often incomprehensible,
lalia individuals simply repeat what they hear and in
phrases. Immobility, likewise, ranges in severity: some
echopraxia they mimic the gestures and activity of the
individuals may lie in bed for long periods, neither
examiner. It should be noted that in negativism, auto-
moving, blinking or even swallowing; others may make
matic obedience, and echo phenomena there is nothing
brief movements, perhaps to pull at a piece of cloth-
natural or fluid about the individual’s behavior. To the
ing or to assume a different posture. Waxy flexibility,
contrary, movements are often awkward, wooden, and
also known by its Latin name cerea flexibilitas, is char-
tinged with the bizarre.
acterized by a more or less severe “lead pipe” rigidity
Excited catatonia manifests with varying degrees of
combined with a remarkable tendency for the limbs to
bizarre, frenzied, and purposeless behavior. Such indi-
stay in whatever position they are placed, regardless of
viduals typically keep to themselves: one marched in
whether the individual is asked to maintain that posi-
place, all the while chanting and gesticulating; another
tion or not. Posturing is said to occur when individuals
tore at his hair and clothing, broke plates in a corner
spontaneously assume more or less bizarre postures,
then crawled under the bed where he muttered and
which are then maintained: one individual crouched
thrashed his arms.
low with his arm wrapped over his head, another stood
Stuporous catatonia occurring in association with
epilepsy is often suggested by a history of grand mal
or complex partial seizures. Ictal catatonia is further
DSM-IV-TR Diagnostic Criteria suggested by its exquisitely paroxysmal onset, and pos-
tictal catatonia by an immediately preceding “flurry”
293.89 CATATONIC DISORDER DUE TO … [INDICATE THE
GENERAL MEDICAL CONDITION ] of grand mal or complex partial seizures. Psychosis of
forced normalization is an interictal condition distin-
A. The presence of catatonia as manifested by motoric guished by the appearance of symptoms subsequent to
immobility, excessive motor activity (that is apparently
purposeless and not influenced by external stimuli), effective control of seizures. The chronic interictal psy-
extreme negativism or mutism, peculiarities of volun- chosis is also, as suggested by the name, an interictal
tary movement, or echolalia or echopraxia. condition, which however, appears not after seizures are
B. There is evidence from the history, physical examina-
tion, or laboratory findings that the disturbance is the controlled but rather in the setting of ongoing, chronic
direct physiological consequence of a general medical uncontrolled epilepsy. Of medications capable of caus-
condition. ing catatonia, neuroleptics are by far the most common.
C. The disturbance is not better accounted for by another
mental disorder (e.g., a Manic Episode). Viral encephalitis is suggested by concurrent fever and
D. The disturbance does not occur exclusively during the headache: herpes simplex encephalitis should always
course of a delirium.
be considered in such cases, given its treatability; fur-
Coding note: Include the name of the general medical ther, it must be kept in mind that although encephali-
condition on Axis I. e.g., 293.89 Catatonic Disorder Due
to Hepatic Encephalopathy: also code the general medi- tis lethargica no longer occurs in epidemics, sporadic
cal condition on Axis III (see Appendix G for codes). cases still do occur. Focal lesions capable of causing
Reprinted with permission from the Diagnostic and Statistical catatonia are typically found in the medial or inferior
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 portions of the frontal lobes. The miscellaneous condi-
tions listed are all quite rare causes of catatonia.
Excited catatonia, in the vast majority of cases, is TREATMENT

caused by either schizophrenia or bipolar disorder
In addition to treating, if possible, the underlying cause,
(during a manic episode); only rarely is it seen because
catatonia may be symptomatically relieved by lo-
of a general medical condition, as for example, a viral
razepam given parenterally in a dose of 2 mg; in severe
encephalitis.
cases wherein lorazepam is not sufficiently effective
and the individual is at immediate risk, consideration
Differential Diagnosis should be given to emergency ECT, which is typically
dramatically effective, generally bringing relief after
Stuporous catatonia must be distinguished from aki-
but a few treatments.
netic mutism and from stupor of other causes. Akinetic
mutes appear quite similar to immobile and mute cata-
tonics; they, however, lack such signs as waxy flexibil-
Personality Change Due to a General
ity, posturing, and negativism, all of which are typi-
Medical Condition
cally seen in catatonia. Stupor of other causes is readily
distinguished from catatonic stupor by the salient fact
DIAGNOSIS
that catatonics remain alert, in stark contrast with the
somnolence or decreased level of consciousness seen in The personality of an adult represents a coalescence
all other forms of stupor. of various personality traits present in childhood and
Excited catatonia must be distinguished from mania. adolescence, and is generally quite enduring and re-
Mania is typified by hyperactivity, which at times may sistant to change. Thus, the appearance of a significant
be quite frenzied: the difference with catatonia is that change in an adult’s personality is an ominous clinical
individuals with mania want to be involved, whereas sign and indicates the presence of intracranial pathol-
those with catatonia keep to themselves. ogy. Individuals themselves may not be aware of the
Stuporous catatonia, in the majority of cases, occurs change. However, to others, who have known the in-
as part of such primary mental disorders as schizophre- dividual over time, the change is often quite obvious.
nia or a depressive episode of either major depressive Such observers often note that the individual is “not
or bipolar disorder. The causes of catatonia due to a himself” anymore.
general medical condition or medications are listed in In most cases, the change is nonspecific in nature:
Table 12-8. there may be either a gross exaggeration of hitherto
minor aspects of the individual’s personality or the ap-
pearance of a personality trait quite uncharacteristic
for the individual. Traits commonly seen in a personal-
Table 12-8
Causes of Catatonia Due to a General ity change, as noted in DSM-IV-TR, include lability,
Medical Condition disinhibition, aggressiveness, apathy, or suspiciousness
Stuporous Catatonia (see DSM-IV-TR diagnostic criteria, page 120).
Associated with epilepsy In addition to these nonspecific changes, there are
Ictal catatonia
Postictal catatonia two specific syndromes which, though not listed in
Psychosis of forced normalization DSM-IV-TR, are well described in the literature,
Chronic interictal psychosis namely, the frontal lobe syndrome and the interictal
Medication
Neuroleptics personality syndrome (also known as the “Geschwind
Disulfiram syndrome”).
Benzodiazepine withdrawal The frontal lobe syndrome is characterized by a var-
Viral encephalitis
Herpes simplex encephalitis iable mixture of disinhibition, affective changes, per-
Encephalitis lethargica severation, and abulia. Disinhibition manifests with an
Focal lesions, especially of the frontal lobes overall coarsening of behavior. Attention to manners
Miscellaneous conditions
Hepatic encephalopathy and social nuances is lost: individuals may eat with
Limbic encephalitis gluttony, make coarse and crude jokes, and may en-
Systemic lupus erythematosus gage in unwelcome and inappropriate sexual behavior,
Lyme disease, in stage III
Subacute sclerosing panencephalitis, in stage I perhaps by propositioning much younger individuals or
Tay–Sachs disease masturbating in public. Affective changes tend toward
Thrombotic thrombocytopenic purpura
a silly, noninfectious euphoria; depression, however,
Excited Catatonia may also be seen. Perseveration presents with a ten-
Viral encephalitis
dency to persist in whatever task is currently at hand,
grand mal or complex partial seizures. The cardinal

DSM-IV-TR Diagnostic Criteria characteristic of this syndrome is what is known as
310.1 PERSONALITY CHANGE DUE TO … [INDICATE THE GENERAL
“viscosity,” or, somewhat more colloquially, “sticki-
MEDICAL CONDITION ] ness.” Here, individuals seem unable to let go or di-
verge from the current emotion or train of thought:
A. A persistent personality disturbance that represents a
change from the individual’s previous characteristic existing effects persist long after the situation that oc-
personality pattern. (In children, the disturbance in- casioned them, and a given train of thought tends to
volves a marked deviation from normal development extend itself indefi nitely into a long-winded and ver-
or a significant change in the child’s usual behavior
patterns lasting at least 1 year). bose circumstantiality or tangentiality. This viscosity
B. There is evidence from the history, physical examina- of thought may also appear in written expression as
tion, or laboratory findings that the disturbance is the individuals display “hypergraphia,” producing long
direct physiological consequence of a general medical
condition. and rambling letters or diaries. The inability to “let
C. The disturbance is not better accounted for by another go” may even extend to such simple acts as shaking
mental disorder (including other Mental Disorders hands, such that others may literally have to extract
Due to a General Medical Condition).
D. The disturbance does not occur exclusively during the their hand to end the handshake. The content of the
course of a delirium. individual’s viscous speech and writing generally
E. The disturbance causes clinically significant distress or also changes, and tends toward mystical or abstruse
impairment in social, occupational, or other important
areas of functioning. philosophical speculations. Finally, there is also a
Specify type: tendency to hyposexuality, with an overall decrease
Labile Type: if the predominant feature is affective
in libido.
lability Personality change is common, and is especially fre-
Disinhibited Type: if the predominant feature is poor im- quent after closed head injury and as a prodrome to the
pulse control as evidenced by sexual indiscretions, etc.
Aggressive Type: if the predominant feature is aggressive dementia occurring with such neurodegenerative disor-
behavior ders as Pick’s disease, fronto-temporal dementia, and
Apathetic Type: if the predominant feature is marked Alzheimer’s disease.
apathy and indifference
Paranoid Type: if the predominant feature is suspicious- Personality change of the nonspecific or of the fron-
ness or paranoid ideation tal lobe type, as noted in Table 12-9, may occur second-
Other Type: if the predominant feature is not one of the ary to precipitants (e.g., closed head injury), secondary
above, e.g., personality change associated with a seizure
disorder to cerebral tumors (especially those of the frontal or
Combined Type: if more than one feature predominates temporal lobes) or as part of certain neurodegenera-
in the clinical picture tive or dementing disorders. Finally, there is a group of
Unspecified Type miscellaneous causes. In Table 12-9, those disorders or
Coding note: Include the name of the general medical
condition on Axis I, e.g., 310.1 Personality Change Due diseases that are particularly prone to cause a person-
to Temporal Lobe Epilepsy: also code the general medical ality change of the frontal lobe type are indicated by
condition on Axis III (see Appendix G for codes). an asterisk. The interictal personality syndrome occurs
Reprinted with permission from the Diagnostic and Statistical only in the setting of chronic repeated grand mal or
American Psychiatric Association. complex partial seizures, and may represent microana-
tomic changes in the limbic system which have been
“kindled” by the repeated seizures.
and individuals may repeatedly button and unbut- In the case of personality change occurring second-
ton clothing, open and close a drawer or ask the same ary to precipitants, the etiology is fairly obvious; an ex-
question again and again. Abulia is characterized by ception might be cerebral infarction, but here the acute
an absence of desires, urges, or interests, and such in- onset and the presence of “neighborhood” symptoms
dividuals, being undisturbed by such phenomena, may are suggestive. In addition to infarction of the frontal
be content to sit placidly for indefinite periods of time. lobe, personality change has also been noted with inf-
Importantly, such abulic individuals are not depressed, arction of the caudate nucleus.
nor are they incapable of activity. Indeed, with active Personality change occurring secondary to cerebral
supervision they may be able to complete tasks; how- tumors may not be accompanied by any distinctive fea-
ever, once supervision stops, so too do the individuals, tures, and indeed a personality change may be the only
as they lapse back into quietude. clinical evidence of a tumor for a prolonged period of
The interictal personality syndrome, a contro- time.
versial entity, is said to occur as a complication of Personality change occurring as part of cer-
long-standing uncontrolled epilepsy, with repeated tain neurodegenerative or dementing disorders
Causes of Personality Change of the

tween the thalamus or basal ganglia and the frontal
Table 12-9 lobe. Normal-pressure hydrocephalus is an important
Nonspecific or Frontal Lobe Type
diagnosis to keep in mind, as the condition is treata-
Closed head injury ble. Other suggestive symptoms include a broad-based
Head trauma with subdural hematoma shuffling gait and urinary urgency or incontinence.
Postviral encephalitis AIDS should be suspected whenever a personality
Gunshot wounds
Cerebral infarction change is accompanied by clinical phenomena sugges-
Secondary to Cerebral Tumors
tive of immunodeficiency, such as thrush. Neurosyphi-
Frontal lobe* lis may present with a personality change characterized
Corpus callosum* (in its anterior part) by slovenliness and disinhibition. Creutzfeldt–Jakob
Temporal lobe
disease may also present with a personality change,
Occurring as Part of Certain Neurodegenerative or and this appears particularly likely with the “new vari-
Dementing Disorders
Pick’s disease* ant” type (i.e., associated with Mad Cow disease); the
Fronto-temporal dementia* eventual appearance of myoclonus suggests the correct
Alzheimer’s disease*
Amyotrophic lateral sclerosis*
diagnosis.
Progressive supranuclear palsy* The miscellaneous causes represent the diagnos-
Cortico-basal ganglionic degeneration* tic “zebras” in the differential for personality change.
Multiple system atrophy*
Huntington’s disease Of them two deserve comment, given their treatabil-
Wilson’s disease ity: granulomatous angiitis is suggested by prominent
Lacunar syndrome* headache, and vitamin B12 deficiency by the presence of
Normal pressure hydrocephalus
AIDS macrocytosis or a sensory polyneuropathy.
Neurosyphilis
Creutzfeldt–Jakob disease
Miscellaneous Causes Course
Granulomatous angiitis
Vitamin B12 deficiency This is determined by the underlying cause; in the
Limbic encephalitis
Metachromatic leukodystrophy
case of the interictal personality syndrome, it ap-
Adrenoleukodystrophy pears that symptoms persist even if seizure control is
Mercury intoxication obtained.
Manganism
*Particularly likely to cause a frontal lobe syndrome.
deserves special mention, for in many instances the Personality change must be clearly distinguished from
underlying disorder may present with a personal- a personality disorder. The personality disorders (e.g.,
ity change—this is particularly the case with Pick’s antisocial personality disorder, borderline personality
disease, fronto-temporal dementia, and Alzheimer’s disorder), all in Chapter 42, do not represent a change
disease. The inclusion of amyotrophic lateral sclerosis in the individual’s personality but rather have been
here may be surprising to some, but it is very clear that, present in a lifelong fashion. In gathering a history of
albeit in a small minority, cerebral symptoms may not an individual with a personality change, one finds a
only dominate the early course of amyotrophic lateral more or less distinct time when the “change” occurred;
sclerosis (ALS) but may also constitute the presenta- by contrast, in evaluating an individual with a person-
tion of the disease. In the case of the other neurodegen- ality disorder, one can trace the personality traits in
erative disorders (i.e., progressive supranuclear palsy, question in a more or less seamless fashion back into
cortico-basal ganglionic degeneration, multiple system adolescence, or earlier.
atrophy, Huntington’s disease, and Wilson’s disease), a The frontal lobe syndrome, at times, may present
personality change, if present, is typically accompa- further diagnostic questions, raising the possibility of
nied by abnormal involuntary movements of one sort either mania, when euphoria is prominent, or depres-
or other, such as parkinsonism, ataxia, or chorea. The sion, when abulia is at the forefront. Mania is distin-
lacunar syndrome, occurring secondary to multiple guished by the quality of the euphoria, which tends to
lacunar infarctions affecting the thalamus, internal be full and infectious in contrast with the silly, shallow,
capsule, or basal ganglia, deserves special mention as and noninfectious euphoria of the frontal lobe syn-
it very commonly causes a personality change of the drome. Depression may be distinguished by the quality
frontal lobe type by interrupting the connections be- of the individuals’ experience: depressed individuals
definitely feel something, whether it be a depressed COMPARISON OF DSM-IV-TR AND ICD-10

mood or simply a weighty sense of oppression. By con- DIAGNOSTIC CRITERIA
trast, the individual with abulia generally feels nothing:
The DSM-IV-TR category Psychotic Disorder Due to a
the “mental horizon” is clear and undisturbed by any
General Medical Condition is referred to in ICD-10 as
dysphoria or unpleasantness. MRI scanning is diag-
“organic hallucinosis” or “organic delusional disorder”
nostic in most cases, and where this is uninformative,
depending on the type of presenting symptom.
further testing is dictated by one’s clinical suspicions
In contrast to DSM-IV-TR, which requires clinically
(e.g., HIV testing).
significant mood symptoms of any type, the ICD-10
The interictal personality syndrome must be dis-
Diagnostic Criteria for Research for Mood Disorder
tinguished from a personality change occurring
due to a General Medical Condition require that the
secondary to a slowly growing tumor of the temporal
full symptomatic and duration criteria be met for a
lobe. In some cases, very small tumors, which may
hypomanic, manic, or major depressive episode. This
escape detection by routine MRI scanning, may cause
disorder is referred in ICD-10 as “organic mood disor-
epilepsy, and then, with continued growth, also cause a
der.” Also in contrast to DSM-IV-TR, which requires
personality change. Thus, in the case of an individual
anxiety symptoms of any type, the ICD-10 Diagnos-
with epilepsy who develops a personality change, the
tic Criteria for Research for Anxiety Disorder Due to
diagnosis of the interictal personality syndrome should
a General Medical Condition require that the clinical
not be made until a tumor has been ruled out by repeat
picture meet full symptomatic and duration criteria for
MRI scanning.
panic disorder or generalized anxiety disorder.
For catatonic disorder due to a general medical con-
TREATMENT
dition, the ICD-10 Diagnostic Criteria for Research are
Treatment, if possible, is directed at the underlying more narrowly defined than the criteria in DSM-IV-TR
cause. Mood stabilizers (i.e., lithium, carbamazepine, by virtue of requiring both catatonic stupor/negativism
or divalproex) may be helpful for lability, impulsiv- and excitement and that there be a rapid alternation of
ity, and irritability; propranolol, in high dose, may stupor and excitement. In ICD-10, this disorder is re-
also have some effect on irritability. Neuroleptics ferred to as “organic catatonic disorder.”
(e.g., olanzapine, risperidone, and haloperidol) may The DSM-IV-TR category of Personality Change
be helpful when suspiciousness or disinhibition are Due to a General Medical Condition corresponds to
prominent. Antidepressants (e.g., an SSRI) may re- two ICD-10 categories: “organic personality disorder”
lieve depressive symptoms. Regardless of which agent and “organic emotionally labile disorder.” The ICD-10
is chosen, it is prudent, given the general medical con- Diagnostic Criteria for Research for Organic Personal-
dition of many of these individuals, to “start low and ity Disorder are probably more narrowly defined in that
go slow.” In many cases, some degree of supervision “at least three” features characteristic of a personality
will be required. change are required.
CHAPTER
13 Substance-Related Disorders:
General Approaches to
Substance and Polysubstance
Use Disorders/Other
Substance Use Disorders
This chapter provides an overview of the substance- maximum of 7) and by whether or not physiological
use disorders (SUDs) (those disorders that represent dependence occurs (i.e., whether there is tolerance
maladaptive pattern of substance use, i.e., substance or withdrawal), because physiological dependence is
abuse and dependence), and the substance-induced associated with a higher risk for immediate general
disorders (those disorders that represent psychiatric medical problems and a higher relapse rate (see DSM-
symptoms that result from the direct effects of a sub- IV-TR diagnostic criteria, page 125). The five criteria
stance on the central nervous system, i.e., substance indicating compulsive use alone may define substance
intoxication, substance withdrawal, and the other dependence if at least three occur at any time in the
specific substance-induced mental disorders). Many same 12-month period. Physiological dependence is
of the general principles outlined in this chapter are much more likely with some drugs, such as opioids and
elaborated on in later chapters with regard to specific alcohol, and is infrequent with other classes of drugs,
abused substances. Note that the DSM-IV-TR diag- such as hallucinogens.
nostic criteria sets included in this chapter are generic Treatment-seeking opioid users are likely to meet
in that they potentially apply across all of the classes most of the dependence syndrome criteria and there-
of substances included in DSM-IV-TR. In fact, only fore their pattern of use is at the high end of severity.
some of the generic criteria sets apply to each of the Cannabis users, in contrast, are likely to meet relatively
classes of substance (e.g., there is no Nicotine Abuse few dependence syndrome criteria and therefore their
and no Opioid-Induced Mood Disorders). Please refer pattern of use is of a lesser degree of severity. Indi-
to Table 13-1 for a cross-listing of which substance- viduals with alcohol or cocaine dependence tend to
related diagnoses apply to each class of substance. demonstrate a much wider variability in the number
Polysubstance dependence and some substances that of dependence criteria met, with the proportion of in-
do not clearly meet standards for abuse and depend- dividuals having relatively low levels of dependence
ence (e.g., steroids) are covered in this chapter. approximately equal to those having extremely high
levels of dependence. Thus, the severity of substance
dependence is variable depending on the type of drug
DIAGNOSIS abused. Some substances such as steroids are of re-
search interest but have not been clearly identified as
Substance Dependence producing the acute reinforcement or dependence and
The severity of dependence can be indicated by the withdrawal symptoms that characterize the abuse of
number of criteria met (from a minimum of 3 to a other substances. The heavy use of anabolic steroids
Table 13-1 DSM-IV-TR Substance Diagnoses Associated with Class of Substance
Intoxication Withdrawal Amnestic Psychotic Mood Anxiety Sexual Sleep

Dependence Abuse Intoxication Withdrawal Delirium Delirium Dementia Disorder Disorders Disorders Disorders Dysfunctions Disorders
Alcohol x x x x I W P P I/W I/W I/W I I/W
Amphetamines x x x x I I I/W I I I/W
Caffeine x I I
Cannabis x x x I I I
Cocaine x x x x I I I/W I/W I I/W
Hallucinogens x x x I I* I I
Inhalants x x x I P I I I
Nicotine x x
Opioids x x x x I I I I I/W
Phencyclidine x x x I I I I
Sedatives, x x x x I W P P I/W I/W W I I/W
hypnotics,
or
anxiolytics
Polysubstance x
Other x x x x I W P P I/W I/W I/W I I/W
*
Also Hallucinogen Persisting Perception Disorder (Flashbacks).
Note: X, I, W, I/W, or P indicates that the category is recognized in DSM-IV-TR. In addition, I indicates that the specifier With Onset During Intoxication may be noted for the category (except for Intoxication
Delirium); W indicates that the specifier With Onset During Withdrawal may be noted for the category (except for Withdrawal Delirium); and I/W indicates that either With Onset During Intoxication or With
Onset During Withdrawal may be noted for the category. P indicates that the disorder is persisting.
Chapter 13 • Substance-Related Disorders: General Approaches 125
DSM-IV-TR Diagnostic Criteria DSM-IV-TR Diagnostic Criteria

SUBSTANCE DEPENDENCE SUBSTANCE ABUSE
A maladaptive pattern of substance use, leading to clini- A. A maladaptive pattern of substance use leading to clin-
cally significant impairment or distress, as manifested by ically significant impairment or distress, as manifested
three (or more) of the following, occurring at any time in by one (or more) of the following, occurring within a
the same 12-month period: 12-month period:
(1) tolerance, as defined by either of the following: (1) recurrent substance use resulting in a failure to ful-
fill major role obligations at work, school, or home
(a) a need for markedly increased amounts of the
(e.g., repeated absences or poor work perform-
substance to achieve intoxication or desired effect
ance related to substance use; substance-related
(b) markedly diminished effect with continued use of
absences, suspensions, or expulsions from school;
the same amount of the substance
neglect of children or household)
(2) withdrawal, as manifested by either of the following: (2) recurrent substance use in situations in which it is
physically hazardous (e.g., driving an automobile
(a) the characteristic withdrawal syndrome for the sub-
or operating a machine when impaired by sub-
stance (refer to criteria A and B of the criteria sets
stance use)
for withdrawal from the specific substances)
(3) recurrent substance-related legal problems (e.g.,
(b) the same (or a closely related) substance is taken to
arrests for substance-related disorderly conduct)
relieve or avoid withdrawal symptoms
(4) continued substance use despite having persist-
(3) the substance is often taken in larger amounts or
ent or recurrent social or interpersonal prob-
over a longer period than was intended
lems caused or exacerbated by the effects of
(4) there is a persistent desire or unsuccessful effort to
the substance (e.g., arguments with spouse
cut down or control substance use
about consequences of intoxication, physical
(5) a great deal of time is spent in activities neces-
fights)
sary to obtain the substance (e.g., visiting multiple
doctors or driving long distances), use the sub- B. The symptoms have never met the criteria for sub-
stance (e.g., chain-smoking), or recover from its stance dependence for this class of substance.
effects Reprinted with permission from the Diagnostic and Statistical
(6) important social, occupational, or recreational Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
activities are given up or reduced because of sub- American Psychiatric Association.
stance use
(7) the substance use is continued despite knowl-
edge of having a persistent or recurrent physical or
psychological problem that is likely to have been
caused or exacerbated by the substance (e.g., cur- Substance Abuse
rent cocaine use despite recognition of cocaine-
induced depression, or continued drinking despite Substance abuse is a maladaptive pattern of substance
recognition that an ulcer was made worse by alco-
hol consumption) use leading to significant adverse consequences mani-
fested by psychosocial, medical, or legal problems or use
Specify if:
in situations in which it is physically hazardous occurring
With physiological dependence: evidence of tolerance within a 12-month period. Since a diagnosis of substance
or withdrawal (i.e., either item 1 or 2 is present)
dependence preempts a diagnosis of abuse, tolerance,
Without physiological dependence: no evidence of
tolerance or withdrawal (i.e., neither item 1 nor 2 is withdrawal, and compulsive use are generally not present
present) in individuals with a diagnosis of substance abuse.
Course specifiers (see text for definitions):
Early full remission
Early partial remission Substance Intoxication
Sustained full remission
Sustained partial remission
Substance intoxication is a reversible substance-
On agonist therapy specific syndrome with maladaptive behavioral or
In a controlled environment psychological changes developing during or shortly
Reprinted with permission from the Diagnostic and Statistical after using the substance (see DSM-IV-TR diagnostic
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 criteria, page 126). It does not apply to nicotine. Re-
cent use can be documented by history or toxicologi-
cal screening of body fluids (urine or blood). Different
substances may produce similar or identical syndromes
by body builders, with the associated possible medi- and, in polydrug users, intoxication may involve a
cal complications, has raised important public health complex mixture of disturbed perceptions, judgment,
issues, however. and behavior that can vary in severity and duration
substance. The withdrawal syndrome usually lasts

DSM-IV-TR Diagnostic Criteria several days to 2 weeks.
SUBSTANCE INTOXICATION
A. The development of a reversible substance-specific

Other Substance-Induced Disorders
syndrome due to recent ingestion of (or exposure to)
a substance. Note: Different substances may produce Not infrequently, substance intoxication and sub-
similar or identical syndromes. stance withdrawal are characterized by psychopa-
B. Clinically significant maladaptive behavioral or psy- thology that mimics the other disorders contained
chological changes that are due to the effect of the
substance on the central nervous system (e.g., bellig- in the rest of DSM-IV-TR. When this occurs, if the
erence, mood lability, cognitive impairment, impaired symptoms are in excess of those usually associated
judgment, impaired social or occupational function- with the intoxication or withdrawal syndrome, and
ing) and develop during or shortly after use of the
substance. if they are sufficiently severe to warrant independ-
C. The symptoms are not due to a general medical condi-
tion and are not better accounted for by another men-
tal disorder.
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 DSM-IV-TR Diagnostic Criteria
SUBSTANCE INDUCED DISORDER
A. Presence of the particular psychiatric symptom.

according to the setting in which the substances were B. There is evidence from the history, physical examina-
taken. Physiological intoxication is not in and of itself tion, or laboratory findings of either (1) or (2)
necessarily maladaptive and would not justify a diag- (1) the symptoms in Criterion A developed during,
or within a month of, Substance Intoxication or
nosis of the DSM-IV-TR category substance intoxica- Withdrawal
tion. For example, caffeine-induced tachycardia with (2) medication use is etiologically related to the
no maladaptive behavior does not meet the criteria for disturbance
substance intoxication. C. The disturbance is not better accounted for by a
mental disorder that is not substance-induced, Evi-
dence that the symptoms are better accounted for
by a mental disorder that is not substance-induced
Substance Withdrawal might include the following: the symptoms precede
the onset of the substance use (or medication use);
Substance withdrawal is a syndrome due to cessa- the symptoms persist for a substantial period of time
tion of, or reduction in, heavy and prolonged sub- (e.g., about a month) after the cessation of acute with-
stance use. It causes clinically significant impair- drawal or severe intoxication, or are substantially in
excess of what would be expected given the type or
ment or distress and is usually associated with amount of the substance used or the duration of use;
substance dependence. Most often, the symptoms of or there is other evidence that suggests the existence
withdrawal are the opposite of intoxication with that of an independent non-substance-induced mental
disorder (e.g., a history of recurrent non-substance-
related episodes).
Note: This diagnosis should be made instead of a
diagnosis of Substance Intoxication or Substance
Withdrawal only when the symptoms are in excess
of those usually associated with the intoxication or
DSM-IV-TR Diagnostic Criteria withdrawal syndrome and when the symptoms are
sufficiently severe to warrant independent clinical
attention.
SUBSTANCE WITHDRAWAL
Specify if:
A. The development of a substance-specific syndrome
due to the cessation of (or reduction in) substance use With Onset During Intoxication: if the criteria are met
that has been heavy and prolonged. for Intoxication with the substance and the symptoms de-
B. The substance-specific syndrome causes clinically sig- velop during the intoxication syndrome
nificant distress or impairment in social, occupational, With Onset During Withdrawal: if criteria are met for
or other important areas of functioning. Withdrawal from the substance and the symptoms de-
C. The symptoms are not due to a general medical condi- velop during, or shortly after, a withdrawal syndrome
tal disorder. Note: This is a summary of six criteria sets.
Reprinted with permission from the Diagnostic and Statistical Reprinted with permission from DSM-IV-TR Guidebook.
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 Copyright 2004, Michael B First, Allen Frances, and Harold Alan
American Psychiatric Association. Pincus.
Intoxication Recent substance use reported Withdrawal

disorder disorder
Yes
Yes Yes
No No No No
disorder Intoxicated Recurrent problems over 12 months Withdrawal
Yes No
No No No No
One or more Tolerance or withdrawal
disorder abuse criteria disorder
Yes
Yes No
Yes
Both tolerance and withdrawal Any of dependence criteria 3−7
No Yes
Fewer than three
of dependence
criteria 3−7 Yes
Any two of dependence criteria 3−7 Dependence disorder
Yes No
Yes No
Abuse disorder Any abuse criteria Withdrawal
Yes No
Withdrawal No
disorder disorder
Figure 13-1 Diagnostic decision tree for substance-use disorders.
ent clinical attention, a specific substance-induced and Substance-Induced Sleep Disorder) represent
mental disorder should be diagnosed. For example, disorders that begin during acute intoxication or
since dysphoric mood is commonly seen as a result withdrawal and subside within 4 weeks of stop-
of cocaine withdrawal, the mere presence of de- ping the substance. A specifier is available to in-
pression after stopping cocaine would not ordinar- dicate whether the substance-induced disorder
ily warrant a diagnosis of Cocaine-Induced Mood had its onset during intoxication or withdrawal
Disorder; typically a diagnosis of Cocaine With- (see Table 13-1 to determine which classes of sub-
drawal would suffice. However, if the depressed stances lead to psychopathology during intoxica-
mood is especially severe and prolonged and is as- tion versus withdrawal). To facilitate differential
sociated with suicidal ideation, then a diagnosis of diagnosis, these disorders have been placed in the
Cocaine-Induced Mood Disorder would make clini- DSM-IV-TR within the diagnostic groupings with
cal sense. which they share phenomenology (e.g., Substance-
DSM-IV-TR includes nine substance-induced Induced Anxiety Disorder is included within the
disorders (see summary of DSM-IV-TR diagnos- Anxiety Disorder section of DSM-IV-TR). Two of
tic criteria for Substance-Induced Disorders, page them (Substance-Induced Persisting Dementia and
126). Seven of these (Substance Intoxication De- Substance-Induced Persisting Amnestic Disorder)
lirium, Substance Withdrawal Delirium, Sub- represent psychopathology resulting from more or
stance-Induced Psychotic Disorder, Substance-In- less permanent damage to the central nervous sys-
duced Mood Disorder, Substance-Induced Anxiety tem, a consequence of prolonged periods of heavy
Disorder, Substance-Induced Sexual Dysfunction, substance use.
The diagnosis of substance abuse and dependence is When individuals self-report the amount of substance
made by eliciting an appropriate history, performing abused, there is a tendency to underreport the sever-
laboratory tests to confirm drug use, and observing ity and duration of abuse, particularly if the person is
the physiological manifestations of tolerance and with- being referred to treatment by an outside source such
drawal (see Figure 13-1 for a diagnostic decision tree as the family, the employer, or the legal system. In
for SUDs). general, significant others’ estimates of the amount of
The phenomenology and variations in presenta- drug use by the individual can be a good source of
tion among abused substances are related to the wide data.
range of substance-induced states as well as the con- Aberrant behaviors potentially requiring manage-
ditions under which the individual using substances is ment include intoxication, violence, suicide, impaired
brought to treatment. Many individuals who use illicit cognitive functioning, and uncontrolled affective
street drugs may not know precisely what drugs they displays. The evaluation of an intoxicated substance
have ingested and certainly will not have a good idea abuser can address only a limited number of issues.
of the precise amount. In addition, individuals who are These issues are primarily related to the safety of the
dependent on substances producing significant with- substance abuser and other individuals who may be af-
drawal syndromes, such as opioids and alcohol, may fected by his or her actions. Thus, a medical evaluation
have a mixed picture of early intoxication and overdose for signs of overdose or major cognitive impairment is
followed by an evolving withdrawal syndrome; alco- critical, with consideration of detaining the individual
hol and sedative withdrawal may produce psychiatric for several hours or even days, if severe complications
complications (e.g., hallucinations) as well as medical are evident.
complications (e.g., seizures). Temporary suicidal behavior may be encountered
The severity of withdrawal symptoms may, in part, in a variety of substance addictions, particularly those
be determined by the setting. For example, studies with alcohol and stimulants. Suicidal ideation may
of opioid-dependent individuals have shown that the be intense but may clear within hours. During the
expression of withdrawal symptoms may be substan- evaluation session, it is important to elicit the precip-
tially less when no medication treatment is available for itants that led the individual to seek treatment at this
symptom relief. As a further example of this phenom- time and to keep the evaluation focused on specific
enon, individuals with opioid addiction who have been data needed for the evaluation of substance depend-
in prison without access to opioids for several years ence, its medical complications, and any comorbid
may experience precipitous opiate withdrawal when mental disorders. Many individuals spend a great
they return to the neighborhoods where they previously deal of time detailing their drug-abusing careers,
used heroin. This conditioned withdrawal phenomenon but, in general, these stories do not provide useful
further supports the importance of setting in the pres- material for the evaluation or for future psychothera-
entation of withdrawal symptoms. peutic interventions. Similarly, the evaluation should
Finally, the issues of motivation for seeking treat- not become focused on the affective aspects of a
ment and a tendency to deny substance abuse can have individual’s recent life because affect is frequently
important influence on the individual’s presentation. used as a defense to avoid discussing issues of more
The individual who presents for treatment because immediate relevance such as precipitants or to act
of dysphoric feelings in the context of drug depend- as a pretext for obtaining benzodiazepines or other
ence is likely to articulate the severity of his or her antianxiety agents from the physician. Abused sub-
problem adequately and even exaggerate some aspects stances have generally been a way of managing af-
of present discomfort. In contrast, the automobile fect and these individuals need to develop alternative
driver forced to come to a treatment program be- coping strategies.
cause of a driving-while-intoxicated offense is likely Physical examination is critical for the assessment
to minimize her or his alcohol use or any associated of substance addiction, particularly before pharmaco-
complications. therapy is initiated. Many signs of drug withdrawal
Two special issues in the psychiatric examination of require a physical examination and cannot rely en-
substance dependence are (1) the source of informa- tirely on history. Because the general medical compli-
tion when obtaining the history of the substance abuse cations of substance addiction are also substantial, the
and (2) the management of aberrant behaviors. Infor- most clearly ill individuals must have a formal general
mation about an individual’s substance-abuse history medical evaluation. Vital signs (blood pressure, pulse,
can be provided not only by the individual but also and so on) are an essential beginning but a full ex-
by employers, family members, and school officials. amination of heart, lungs, and nervous system is min-
imally necessary. Transmissible infectious diseases terns of substance misuse and prevalence of sub-
such as AIDS, tuberculosis, and venereal diseases are stance-related disorders. Relatively high prevalence
common among illicit drug users and require screen- rates for the use of virtually every substance occur
ing for adequate detection. This screening for HIV between the ages of 18 and 24 years, with intoxi-
infection also protects health care personnel as well cation being the initial substance-related disorder,
as individuals undergoing treatment. A wide variety usually beginning in the teens. Tolerance and with-
of other infectious diseases, including hepatitis and drawal require a sustained period of use and these
endocarditis, are also associated with intravenous manifestations of physical dependence for most
drug use and require appropriate blood studies. With drugs of abuse typically begin in the twenties and
alcohol dependence, a wide range of gastrointestinal early thirties. Although most substance-related dis-
complications have been described, particularly liver orders are more common in men than in women, sex
dysfunction. ratios can vary considerably with different drugs of
Urine toxicological screens can be sensitive for abuse.
detecting drug use within 3 days of use of opiates In both the Epidemiological Catchment Area study
and cocaine. Urine screens for other abused drugs and the National Comorbidity Survey, substance
such as cannabis can remain positive for as long as abuse and dependence were the most common co-
a month in heavy users. A breathalyzer can be used morbid disorders, usually appearing in combination
for detecting alcohol use within an 8- to 12-hour with affective and anxiety disorders. In the National
period after use. Specific biological tests can also Comorbidity Survey, the lifetime rate of substance
aid in the diagnosis of dependence, for example, a abuse was 27% and the rate of comorbid depression
naloxone challenge test assesses opioid dependence among these substance abusers was 19%. Further-
by precipitating withdrawal symptoms. Associated more, 80% of these depressed substance-abusing sub-
medical fi ndings on physical examination include jects had more than one mental disorder; only 20%
track marks in intravenous drug users, nasal damage had only one mental disorder. In the Epidemiological
in intranasal drug users, and pulmonary damage in Catchment Area study, 75% of daily substance users
drug smokers. had a comorbid mental disorder. In studies of treat-
Cultural differences in the presentation of drug ment-seeking substance abusers, the rates of other
addiction can be striking. For example, the use of mental disorders are almost uniformly higher than
hallucinogens by Native Americans in religious those in community samples, but the rates of excess
ceremonies shows none of the abusive characteristics comorbidity in these abusers varies with the specific
of adolescent hallucinogen addiction in middle-class abused drug. For example, in the Epidemiological
America. Alcohol abuse can also show widely varying Catchment Area study, the lifetime rate of major
presentations based on the amount of alcohol that is depression in the community was 7%, whereas the
considered culturally acceptable in various geographi- major depression rates for substance users seeking
cal settings. treatment were 54% for opioids, 38% for alcohol, and
Wide cultural variations in attitudes toward sub- 32% for cocaine. Rates for other disorders are com-
stance consumption have led to widely varying pat- pared in Table 13-2.
Table 13-2 Lifetime diagnoses in SUD and Community Sample
Patients with New Haven

Patients with Opioid Alcoholism Cocaine Users Community
Dependence (N ⫽ 533) (N ⫽ 321) (N ⫽ 149) (N ⫽ 3058)
Major depression 53.9 38 31.5 6.7

Bipolar disorder I 0.6 2 3.4 1.1
(mania)
Schizophrenia 0.8 2 0.7 1.9
Phobia 9.6 27 11.4 7.8
Antisocial 25.5 41 34.9 2.1
personality
Alcoholism 34.5 100 63.8 11.5
Drug abuse 100 43 100 5.8
data on changing trends in substance use and its asso-

DSM-IV-TR Diagnostic Criteria ciated problems. These surveys have increasingly rec-
COURSE SPECIFIERS AVAILABLE FOR SUBSTANCE DEPENDENCE
ognized cultural differences in the course of drug use.
Thus, the natural history of substance abuse and de-
The following remission specifiers can be applied only af- pendence is determined by the type of substance used
ter no criteria for dependence or abuse have been met for
at least 1 month. Note that these specifiers do not apply and, for polysubstance dependence, can be complicated
if the individual is on agonist therapy or in a controlled by changing secular trends and epidemics lasting from
environment (see below). months to decades.
• Early Full Remission. This specifier is used if, for at least
1 month, but for less than 12 months, no criteria for
dependence or abuse have been met. Differential Diagnosis
• Early Partial Remission. This specifier is used if, for
at least 1 month, but less than 12 months, one or The differential diagnosis of substance-induced in-
more criteria for dependence or abuse have been
met (but the full criteria for dependence have not
toxication and withdrawal can involve a wide range
been met). of mental disorders. Distinguishing substance abuse
• Sustained Full Remission. This specifier is used if from these disorders is usually facilitated by a struc-
none of the criteria for dependence or abuse have
been met at any time during a period of 12 months tured interview to elicit a wide range of psychiatric
or longer. symptoms appropriately timed after the most recent
• Sustained Partial Remission. This specifier is used if full substance use. During acute intoxication in polydrug
criteria for dependence have not been met for a period
of 12 months or longer; however, one or more criteria users, the differential diagnosis might include an acute
for dependence or abuse have been met. psychotic disorder, mania, delirium, dementia, or sev-
The following specifiers apply if the individual is on ago- eral specific anxiety disorders. Among these anxi-
nist therapy or in a controlled environment: ety disorders are generalized anxiety disorder, panic
• On Agonist Therapy. This specifier is used if the indi- disorder, and obsessive–compulsive disorder. Distin-
vidual is on a prescribed agonist medication such as guishing these disorders from acute intoxication or
methadone and no criteria for dependence or abuse
have been met for that class of medication for at least withdrawal with a mixture of drugs most frequently
the past month (except tolerance to, or withdrawal requires that the clinician wait 24 to 72 hours to de-
from, the agonist). This category also applies to those termine whether the symptoms persist and, therefore,
being treated for dependence using a partial agonist or
an agonist/antagonist. whether they are independent of the drug use. A previ-
• In a Controlled Environment. This specifier is used if ous history of schizophrenia, bipolar disorder, or other
the individual is in an environment in which access to
alcohol and controlled substances is restricted, and
major psychiatric disorder that is consistent with the
no criteria for dependence or abuse have been met presenting symptoms may also be helpful in arriving at
for at least the past month. Examples of these envi- an accurate diagnosis. When individuals present with
ronments are closely supervised and substance-free
jails, therapeutic communities, or locked hospital psychotic or manic behavior during drug intoxication,
units it may be necessary to use symptomatic treatment such
Reprinted with permission from the Diagnostic and Statistical as a benzodiazepine or neuroleptic agent to conduct an
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 examination.
Antisocial and borderline personality disorders are
commonly considered in the differential diagnosis of
substance-dependent individuals. Many of the behav-
iors that characterize these personality disorders are
Course
also common to the use of illegal and illicit drugs. In
The natural history of substance dependence charac- establishing these personality disorders, particularly
teristically follows the course of a chronic relapsing antisocial personality, it is important to ascertain
disorder, although a large number of individuals who whether the behaviors are independent of the activi-
experiment with potentially abusable drugs in adoles- ties needed to obtain drugs. The symptoms of drug
cence do not go on to acquire dependence. withdrawal frequently overlap with those of depres-
The course of substance dependence is variable and sive disorders, and this differential diagnosis can be
may involve full or partial remission with six course particularly difficult. Furthermore, the syndrome of
specifiers available in the DSM-IV-TR. protracted withdrawal can include sleep and appetite
Population surveys, such as the high school senior disturbance as well as dysphoria that mimics dys-
surveys and National Institute on Drug Abuse house- thymic disorder and other affective disorders. Thus,
hold survey, have provided repeated cross-sectional conservatively, the clinician should wait 4 to 6 weeks
after acute detoxification to determine a diagnosis the substance user to treatment allies. These family
of affective disorder in these substance-dependent members need to be engaged in treatment to work as
individuals. However, waiting this long is often im- active collaborators in the therapeutic plan for the in-
practical in the clinical setting in which the mainte- dividual. Although family treatment is commonly ap-
nance of sustained abstinence may depend on relief plied to many mental disorders, it can have a particu-
of depressive symptoms using either medications or larly powerful impact with adolescent substance users
psychotherapy. to eliminate family behaviors that reinforce the drug
taking.
Psychiatric assessment is critical because of the high
rates of depression and risk of suicide in this popula-
TREATMENT
tion. A full medical assessment generally is essential
The most important goal of any treatment is absti- because of the high rates of infectious and gastroin-
nence from the abused drug. Issues of controlled use testinal diseases directly related to substance abuse
are debated by some mental health professionals, and dependence. Medical assessment is also essential
but this is usually not a realistic goal for dependent to determine whether active medical detoxification is
individuals. A critical, first treatment goal with sub- necessary. Finally, a psychotherapeutic issue early in
stance addiction is often acute treatment of overdose. treatment may be distinguishing between slips and a
A clinician must be aware of specific therapies such as full relapse. Slips are common in substance users, and
naloxone for opioid overdose and flumazenil for ben- individuals must be prepared for them and not consider
zodiazepine or other sedative overdose. The polydrug them failures that will inevitably lead to full relapse
user often has combined toxicity from drug interac- and dependence.
tions such as alcohol with barbiturates or phencyc-
lidine with cocaine. For dependence on a drug with
a significant withdrawal syndrome, such as opioids
Somatic Treatments
or alcohol, the initial treatment involves either ago-
nist stabilization, such as methadone maintenance, Pharmacotherapy can have several roles in substance
or medical detoxification when necessary. After de- dependence treatment, including treatment of over-
toxification or stabilization, prevention of relapse dose and acute intoxication (naloxone, flumazenil),
may occur through a variety of behavioral or other detoxification or withdrawal symptom relief (benzodi-
psychotherapeutic approaches. Reduction in drug use azepines, clonidine), blockage of drug reinforcement
without total abstinence using agonist maintenance (naltrexone), development of responses to the abused
(e.g., methadone) may be an early priority, together substance (disulfiram), treatment of psychiatric co-
with the provision of essential social services for legal morbidity (antidepressants), and substitution agents
problems, housing, and food. After this stabilization, to produce cross-tolerance and reduce drug craving
vocational rehabilitation and various psychotherapeu- (methadone). A key element in the treatment of many
tic issues may be addressed, including the manage- dependence-producing drugs is the need for detoxifica-
ment of affect such as depression. For individuals tion, which may last from 3 days to as long as 2 weeks.
with psychosis, inpatient treatment or interventions Detoxification is essential if antagonist pharmaco-
with medication may be required before detoxifica- therapies, such as naltrexone for opioid dependence,
tion can occur. or aversive agents, such as disulfiram for alcoholism,
Other treatment goals in longer-term management are to be employed. Conversely, agonist maintenance
include total abstinence and family involvement. A treatment, such as methadone or buprenorphine for
common treatment goal in the longer-term manage- heroin dependence, does not require detoxification
ment of individuals who abuse substances is absti- before beginning treatment. Using these agonists usu-
nence from all drugs, although the individual often ally requires regular clinic attendance by the substance
advocates for controlled use of some substances. For user and relatively prolonged treatment of 1 to 2 years,
example, alcohol use by the individual receiving meth- with some individuals continuing agonist therapy for
adone maintenance or the continued smoking of mari- up to 20 years.
juana or even tobacco by individuals formerly suffer- Figure 13-2 outlines potential roles for pharmaco-
ing from alcoholism can lead to a serious conflict in therapy and psychotherapy. The general treatment ap-
treatment goals. Another goal is to change the role of proaches, along with their indications and side effects,
family members from enablers or codependents with are seen in Table 13-3.
Recent substance use

Yes
No Yes
Withdrawal Intoxicated Overdose
Yes
No No
Yes Relapse Specific

antagonist/
general medical
support
Outpatient
Medical
drug free
detoxification
1− 2x/week
No
Suicidal
Slips or
Slips Psychotic
Yes
Antagonist Agonist Day hospital Hospitalize

maintenance maintenance 5x/week Social support
Noncompliance Noncompliance
Poor
Good
Medical Slips
detoxification
Outpatient
"dual-diagnosis"
medications
Residential
6−18 months
Figure 13-2 Treatment decision tree for substance use disorders.
Table 13-3 General Treatment Approaches: Indications and Side Effects
Treatment Indication Side Effects
Pharmacotherapy Detoxifications Dependence on Alcohol Opioids Overmedication, if not carefully monitored

Sedatives
Undermedication, leading to seizures
Antagonists Drug-free therapy failed Precipitated withdrawal
Aversive agents
Agonists Illness from use of abused drugs
Continued dependence
Psychotherapy Lower level intervention failed
Self-help
Outpatient
Day hospital
Residential
Inpatient Medical detoxification Social cost
Psychotic behavior
Suicidal behavior
Urine monitoring Outpatient treatment None
Breath alcohol
Psychosocial Treatments Other areas of medical comorbidity include vitamin

deficiencies, infectious diseases, and gastrointestinal
A wide range of psychosocial treatments are available
disorders such as cirrhosis, gastrointestinal bleeding,
in SUDs, ranging from long-term residential treatments
and peptic and duodenal ulcers. Stimulant users may
(6 to 8 months) to relatively low-intervention outpatient
experience cerebrovascular accidents. Also, dement-
medication-free treatments with once-weekly hour-long
ing disorders need particular consideration in con-
therapy. In these outpatient treatments, professional
junction with alcoholism, inhalant abuse, and sedative
interventions may be unavailable, and counseling is
dependence.
provided by nonprofessionals using group therapy.
Two clinical questions often arise: is use of ad-
These groups may be based on extensions of self-help
dictive medication flatly contraindicated in individu-
groups, such as Alcoholics Anonymous or Narcotics
als with any kind of substance-abuse history, or is
Anonymous, and use a 12-step program and the associ-
such medication prohibited only in instances of use
ated traditions of these fellowships.
of drugs of the same class (e.g., alcohol and benzo-
Behavioral treatments that have frequently been
diazepines, and methylphenidate and cocaine)? In
used include relapse prevention therapy and contin-
general, a physician should never rule out the use of
gency contracting, in which various aversive contin-
any addictive drug if there are good symptom-based
gencies are put in place for periods of up to 6 months
reasons for prescribing it. Nor should the physician
to prevent a relapse to substance abuse and potential
assume that an addicting drug of one class (e.g.,
dependence.
opiates) will be safe for an individual who abused
another class such as stimulants. However, in any
situation in which a potentially addicting drug is
Special Treatment Factors
considered for use in a remitted substance abuser,
Comorbid mental disorders, particularly depres- considerable caution and limit setting is warranted.
sive and anxiety disorders, are extremely common Finally, inpatient management may become neces-
in substance abuse, with lifetime rates approaching sary for the evaluation and use of these risky treat-
50% in individuals addicted to opioids. Although ment interventions.
the rate of major psychotic disorders among SUDs
is relatively low, the rate of substance abuse in indi-
viduals with schizophrenia or bipolar disorder may Treatment-Refractory Individuals
be as high as 50%. A variety of escalating treatment interventions can be
Splitting treatment between a mental health clinic applied to individuals with substance abuse or depend-
and substance-abuse clinic can be a significant problem ence who are refractory to treatment. If initial detoxi-
for the coordinated management of the dual-diagnosis fication with outpatient follow-up care is ineffective,
individual. A prominent problem in the management several levels of intensified interventions can be ap-
of SUDs with comorbid mental disorders is medica- plied, such as agonist maintenance with methadone for
tion management within a substance-abuse treatment individuals addicted to opioids, disulfiram treatment for
setting, because of limited psychiatric resources. In individuals with alcoholism, and perhaps antidepres-
mental health settings, the need for monitoring, us- sants for stimulant use disorders. Further interventions
ing urine toxicological screens for illicit drugs, and can include residential placement for up to 2 years to
breath testing for alcohol can pose difficult logistic enable full psychosocial rehabilitation of refractory
and boundary problems. Integrated dual-diagnosis individuals.
treatments have been developed using social skills
training combined with relapse prevention behavioral
therapies as well as pharmacological adjuncts to either Polysubstance Dependence
typical or atypical neuroleptics for individuals with
schizophrenia. Two typical patterns of drug use fall under the category
Treatment of a comorbid medical condition is es- of polysubstance dependence. In one such pattern, the
sential in SUDs because many substance users do not individual indiscriminantly uses a number of different
seek medical care and may be seen only by a mental drugs, so that he or she does not really care what drug is
health professional. The most important current co- being used, so long as a high results. The second pattern
morbid disorder in SUDs is AIDS that is spread pri- is analogous to the old concept of mixed personality dis-
marily by intravenous drug use but, increasingly, is order in which an individual would have features from
also spread through sexual activity among drug users. a number of different personality disorders but not one
would predominate the picture. In this case, one or two pressed mood, and desire to take more steroids. Other
dependence criteria are met for each of several differ- common dependence symptoms are as follows: using
ent classes of drug but full criteria for dependence are the substance more than intended, continuing to use
only met when the drug classes are grouped together as steroids despite problems worsened by its use, and the
a whole. For example, a diagnosis of polysubstance de- excessive spending of time relating to obtaining ster-
pendence applies to an individual who, during the same oids. Because few clinical laboratories are equipped to
12-month period, missed work because of his heavy conduct steroid tests and because these tests are quite
use of alcohol, continued to use marijuana despite the expensive, these signs of dependence and some com-
fact that it led to asthma attacks, and was repeatedly mon laboratory abnormalities are usually used to make
unable to stay within his self-imposed limits regard- the diagnosis.
ing his use of cocaine. In this instance, although his Anabolic steroid abuse leads to hypertrophied
problems associated with the use of any one drug were muscles, acne, oily skin, needle punctures over large
not severe enough to justify a diagnosis of dependence muscles, hirsutism in females, and gynecomastia in
on that drug, his overall use of substances significantly males. Heavy users can also develop edema and jaun-
impaired his functioning and thus warrants a diagnosis dice. Common laboratory abnormalities include ele-
of polysubstance dependence, that is, on the group of vated hemoglobin and hematocrit, elevated low-density
substances taken as a whole. lipoprotein cholesterol, elevated liver function tests,
and reduced luteinizing hormone levels.
Mental health professionals may have these individu-
Other Substance-Use Disorders: Anabolic als come to their attention because of the excessive ag-
Steroids and Nitrites gression, loss of sexual ability, or mood disturbances.
Treatment approaches are generally symptomatically
This group of substance-induced conditions most no- oriented toward controlling the depressed mood and
tably includes anabolic steroids and nitrite inhalants. the psychotic features, but longer-term interventions
Both have psychoactive effects and can have conse- such as peer counseling by former body builders and
quences for the individual and broad public health. group support may be of value for these users.
The clinical effects of anabolic steroids are related Nitrite inhalants are sometimes considered within
to a typical cycle of 4 to 18 weeks on steroids and 1 the category of inhalant abuse and produce an intoxi-
month to 1 year off. While taking the steroids, the pri- cation with mild euphoria, muscle relaxation, and a
mary effects sought by abusers are increasing muscle change in time perception. Concern has been raised
mass and strength, and not euphoria. In the context of about their impairing immune functioning, a decrease
an adequate diet and significant physical activity, these in oxygen-carrying capacity of the blood, and toxicity
individuals appear quite healthy and they are unlikely with severe headache, vomiting, and hypotension. No
to appear for treatment of their anabolic steroid abuse. physical dependence or withdrawal syndrome has been
However, some of the adverse cardiovascular, hepatic, described with these drugs.
and musculoskeletal effects of steroids as well as vi-
rilization in women may bring these users to medical
attention. Severe cases of acne can also bring some ad-
olescents to medical attention. Abuse of other psycho-
DIAGNOSTIC CRITERIA
active drugs may occur in up to a third of these steroid
users, but is generally relatively low compared to other The ICD-10 Diagnostic Criteria for Research for
substance abusers. Substance Dependence are close, but not identical,
Heavy use can increase aggression, change libido to the DSM-IV-TR criteria. ICD-10 has included all
and sexual functions, and induce mood changes with seven of the DSM-IV-TR items but condenses these
occasional psychotic features. Androgenic steroids’ into five criteria and adds a sixth item tapping drug-
tendency to provoke aggression and irritability has craving behavior. Furthermore, the method for estab-
raised concerns about violence toward family members lishing clinical significance differs in the two systems.
by abusers. Mood disturbances may be present in over DSM-IV-TR specifies that there be a maladaptive pat-
50% of body builders using anabolic steroids, as well tern of substance use leading to clinically significant
as cognitive impairment including distractibility, for- impairment or distress, whereas the ICD-10 Diagnos-
getfulness, and confusion. tic Criteria for Research indicate either a one-month
Dependence symptoms have included a withdrawal duration or repeated occurrences within a 12-month
syndrome, with common symptoms being fatigue, de- period.
The ICD-10 Diagnostic Criteria for Research corre- The ICD-10 Diagnostic Criteria for Research
sponding to Substance Abuse are less specific than the for Intoxication are nearly equivalent to the DSM-
criteria in DSM-IV-TR, requiring that there be “clear IV-TR criteria. However, in contrast to the DSM-
evidence that substance use was responsible for (or IV-TR definition of Withdrawal, which specifies
substantially contributed to) physical or psychological that the withdrawal symptoms cause clinically sig-
harm, including impaired judgment or dysfunctional nificant distress or impairment, the ICD-10 Diag-
behavior, which may lead to disability or have ad- nostic Criteria for Research for Withdrawal indi-
verse consequences for interpersonal relationships.” In cates only the presence of characteristic signs and
ICD-10, this disorder is referred to as Harmful Use. symptoms.
CHAPTER
Alcohol
DIAGNOSIS (2) increased salience of alcohol (i.e., a great deal of

time spent drinking or recovering from its effects; im-
Alcohol consumption occurs along a continuum, with
portant social, occupational, or recreational activities
considerable variability in drinking patterns among
are given up or reduced because of drinking).
individuals. There is no sharp demarcation between
Alcohol abuse is considered to be present only if
“social” or “moderate” drinking and “problem” or
the individual’s drinking pattern has never met criteria
“harmful” drinking. It is clear, however, that as aver-
for alcohol dependence and he or she demonstrates a
age alcohol consumption and frequency of intoxication
pattern of drinking that leads to clinically significant
increase, so does the incidence of medical and psycho-
impairment or distress, as evidenced by one or more
social problems.
of the four criteria in DSM-IV-TR for alcohol abuse
The most visible group of people affected by alcohol
(see generic DSM-IV-TR criteria for Substance Abuse,
problems are those who have developed a syndrome of
Chapter 13, page 125).
alcohol dependence and who are commonly referred
to as alcoholics. In this chapter, the term alcoholic is
applied specifically to those individuals with alcohol
Alcohol Intoxication
dependence. A less prominent group consists of those
persons who experience problems with their drink- A DSM-IV-TR diagnosis of alcohol intoxication is
ing but who are not dependent on alcohol. These indi- given when, shortly after alcohol consumption, there
viduals are variously termed alcohol abusers, problem are maladaptive behaviors such as aggression or inap-
drinkers, and harmful drinkers. These two “worlds” of propriate sexual behavior, or there are psychological
alcohol problems may require different approaches to changes such as labile mood and impaired judgment
diagnosis and clinical management. (see DSM-IV-TR diagnostic criteria, page 137). Clini-
cal signs indicative of alcohol intoxication include
slurred speech, lack of coordination, unsteady gait,
Alcohol Dependence and Abuse
nystagmus, impairment of attention and memory, and
The DSM-IV-TR diagnosis of alcohol dependence in the most severe cases, stupor and coma. Alcohol in-
is given when three or more of the seven criteria are toxication may also present with severe disturbances
present (see generic DSM-IV-TR criteria for Substance in consciousness and cognition (alcohol intoxication
Dependence, Chapter 13, page 125). Because physio- delirium), especially when large amounts of alcohol
logical dependence is associated with greater potential have been ingested or after alcoholic intoxication has
for acute medical problems (particularly, acute alcohol been sustained for extended periods. Usually, this con-
withdrawal), the first criteria to be considered are toler- dition subsides shortly after alcohol intoxication ends.
ance and withdrawal. The remaining criteria reflect the Physical and mental status examinations accompanied
behavioral and cognitive dimensions of alcohol depend- by analysis of blood and urine allow the clinician to
ence: (1) impaired control (i.e., alcohol is consumed in rule out general medical conditions or mental disor-
larger amounts or over a longer period of time than was ders mimicking this condition. In this regard, urine
intended; there is a persistent desire or unsuccessful ef- toxicology is a valuable tool in ruling out intoxication
forts to cut down or control drinking; the individual with benzodiazepines, barbiturates, or other sedatives
continues to drink despite knowledge of a persistent that can present with a similar clinical picture. Collat-
or recurrent physical or psychological problem), and eral information from relatives or friends confirming
Chapter 14 • Substance-Related Disorders: Alcohol 137

303.00 ALCOHOL INTOXICATION 291.81 ALCOHOL WITHDRAWAL
A. Recent ingestion of alcohol. A. Cessation of (or reduction in) alcohol use that has
B. Clinically significant maladaptive behavioral or psy- been heavy and prolonged.
chological changes (e.g., inappropriate sexual or ag- B. Two (or more) of the following, developing within sev-
gressive behavior, mood lability, impaired judgment, eral hours to a few days after Criterion A:
impaired social or occupational functioning) that de-
(1) autonomic hyperactivity (e.g., sweating or pulse
veloped during, or shortly after, alcohol ingestion.
rate greater than 100)
C. One (or more) of the following signs, developing dur-
(2) increased hand tremor
ing, or shortly after, alcohol use:
(3) insomnia
(1) slurred speech (4) nausea or vomiting
(2) incoordination (5) transient visual, tactile, or auditory hallucinations
(3) unsteady gait or illusions
(4) nystagmus (6) psychomotor agitation
(5) impairment in attention or memory (7) anxiety
(6) stupor or coma (8) grand mal seizures
D. The symptoms are not due to a general medical condi- C. The symptoms in Criterion B cause clinically signifi-
tion and are not better accounted for by another men- cant distress or impairment in social, occupational, or
tal disorder other important areas of functioning.
Reprinted with permission from the Diagnostic and Statistical D. The symptoms are not due to a general medical condi-
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 tion and are not better accounted for by another men-
American Psychiatric Association. tal disorder.
Specify if:
the ingestion of alcohol is also useful and should be With Perceptual Disturbances.
actively pursued by the clinician. Reprinted with permission from the Diagnostic and Statistical
The blood alcohol level (BAL) is frequently used as a American Psychiatric Association.
measure of alcohol intoxication, although this measure
is less reliable in persons with a high degree of tolerance
to alcohol. Euphoria, anxiolysis, and mild deficits in of alcohol withdrawal are characterized by signs and
coordination, attention, and cognition can be observed symptoms of autonomic hyperactivity, and may in-
at levels between 0.01 and 0.10%. Marked deficits in clude increased heart rate, increased blood pressure,
coordination and psychomotor skills, decreased atten- hyperthermia, diaphoresis, tremor, nausea, vomiting,
tion, ataxia, impaired judgment, slurred speech, and insomnia, and anxiety. Onset of symptoms of uncom-
mood lability can be observed at a greater BAL. Severe plicated alcohol withdrawal usually occurs between 4
intoxication, characterized by lack of coordination, and 12 hours following the last drink. Symptom se-
incoherent thoughts, confusion, nausea, and vomiting verity tends to peak around the second day, usually
can be observed at BALs between 0.20 and 0.30. How- subsiding by the fourth or fifth day of abstinence. Af-
ever, at these levels, some heavy-drinking individuals ter this period, less severe anxiety, insomnia, and au-
who have developed tolerance to the effects of alcohol tonomic symptoms may persist for a few weeks, with
may not appear intoxicated and may perform well on some individuals experiencing a protracted alcohol-
psychomotor or cognitive tasks. Stupor and loss of con- withdrawal syndrome up to 5 or 6 months after ces-
sciousness often occur when the BAL is between 0.30 sation of drinking. A small but significant number of
and 0.40. Beyond this level, coma, respiratory depres- alcohol-dependent individuals (10%) can experience
sion, and death are possible outcomes. It should also be complicated alcohol-withdrawal episodes. Alcohol-
noted that alcohol intoxication is often associated with withdrawal delirium (also known as delirium tremens)
toxicity and overdose with other drugs, particularly can occur in 5% of the cases, usually between 36 and 72
those with depressant effects on the CNS. hours following alcohol cessation. In addition to signs
of autonomic hyperactivity, this condition is charac-
terized by illusions, auditory, visual, or tactile hallu-
Alcohol Withdrawal
cinations, psychomotor agitation, fluctuating cloudi-
Alcohol withdrawal is a condition that follows a re- ness of consciousness, and disorientation. Grand mal
duction in alcohol consumption or an abrupt cessation seizures associated with alcohol withdrawal occur in
of drinking in alcohol-dependent individuals. In addi- 3–5% of the cases, typically within the fi rst 48 hours
tion to significant distress, alcohol withdrawal is also following reduction or cessation of drinking. In both
associated with impairment of social, occupational, instances of complicated alcohol withdrawal, lack or
and other areas of functioning. Uncomplicated cases delay in instituting proper treatment is associated with
an increased mortality rate. Prior history of delirium cases, memory deficits remain unchanged, and in some
tremens and/or alcohol-withdrawal seizures, older age, instances, long-term care is needed despite sobriety.
poor nutritional status, comorbid medical conditions,
and history of high tolerance to alcohol are predictors
Alcohol-Induced Psychotic Disorder
of increased severity of alcohol withdrawal.
This disorder is characterized by prominent halluci-
nations or delusions that are judged by the clinician to
Alcohol-Induced Persisting Dementia
be due to the effects of alcohol. The psychotic symp-
Continuous heavy drinking is also associated with pro- toms usually occur within a month of an alcohol in-
gressive and gradual development of multiple cognitive toxication or withdrawal episode, and the individual
deficits characterized by memory impairment, apraxia, is characteristically fully alert and oriented, lacking
agnosia, or disturbances in executive functioning. insight that these symptoms are alcohol-induced. Al-
These deficits cause serious impairment in social and though onset of psychotic symptoms can occur dur-
occupational functioning and persist beyond the dura- ing or shortly after alcohol intoxication, delirium or
tion of alcohol intoxication and alcohol withdrawal. alcohol-withdrawal delirium, alcohol-induced hallu-
History, physical examination, and laboratory tests cinations, and/or delusions do not occur exclusively
should be utilized to determine whether these deficits during the course of these conditions. Evidence that
are etiologically related to the toxic effects of alcohol hallucinations and delusions are not part of a primary
use. Other factors associated with this condition are psychotic disorder include: atypical or late age of on-
poor nutritional status and vitamin deficiencies as well set of psychotic symptoms, onset of alcohol drinking
as history of head trauma. It is believed that this con- preceding the onset of psychiatric symptoms, and re-
dition is associated with the repeated occurrence of mission of psychotic episodes during extended peri-
Wernicke’s encephalopathy. Atrophy of frontal lobes ods of abstinence. Usually, alcohol-induced psychotic
and increased ventricular size have been described in symptoms tend to subside within a few weeks of absti-
this condition. Continuous alcohol consumption ex- nence, although in a subset of individuals, psychotic
acerbates the dementia, whereas drinking cessation symptoms can become chronic, requiring long-term
is associated with improvement and even recovery of treatment with antipsychotic medication. In these
cognitive deficits. cases, clinicians are obligated to consider schizophre-
nia or delusional disorder as part of the differential
diagnosis.
Alcohol-Induced Persisting Amnestic Disorder
Continuous heavy alcohol consumption can lead to sev-
Alcohol-Induced Mood Disorder
eral neurological deficits caused by thiamine deficiency.
Among them, alcohol-induced persisting amnestic dis- Alcohol-induced mood disorder (AIMD), character-
order (AIPAD, also known as a Korsakoff’s psychosis ized by depressed mood and anhedonia, as well as
due to the fantastic confabulatory stories described by elevated, expansive, or irritable mood, frequently de-
individuals suffering this condition) is prominent. Pro- velops as a consequence of heavy drinking. Although
found deficits in anterograde memory and some deficits mood disturbances are common among alcoholic indi-
in retrograde memory characterize this condition. Indi- viduals entering treatment (occurring in up to 80% of
viduals cannot retain or learn new information and ex- individuals), alcohol-induced mood symptoms tend to
perience profound disorientation to time and place. The subside within 2 to 4 weeks following alcohol cessation.
severity of anterograde memory deficits typically leads Evidence that the mood disturbances are not better ex-
individuals suffering from Korsakoff’s psychosis, who plained by a primary mood disorder should be sought
are unaware of their deficit, to reconstruct forgotten by the clinician. Evidence suggesting a primary mood
events by confabulating. Korsakoff’s amnestic disorder disorder includes onset of mood symptoms preceding
is usually preceded by several episodes of Wernicke’s onset of alcohol abuse and persistence of mood symp-
encephalopathy, characterized by confusion, ataxia, toms after alcohol cessation or during extended periods
nystagmus, and gaze palsies. When this condition sub- of abstinence. Regardless of the primary or secondary
sides, the characteristic memory deficits of Korsakoff’s nature of mood symptoms, given the high prevalence
psychosis become prominent. of suicide among alcoholics, clinicians should closely
Cessation of drinking can lead to an improvement monitor the individual for emerging suicidal thoughts,
in memory, with approximately 20% of the cases implementing more intensive treatment (discussed
demonstrating complete recovery. However, in most later) if necessary.
Alcohol-Induced Anxiety Disorder to treatment, decisions can be made concerning the

most appropriate intensity, setting, and modality of
Although alcohol has anxiolytic properties at low doses,
treatment.
heavy alcohol consumption can induce prominent
Although denial of alcohol-related problems is legen-
anxiety symptoms. Alcohol-induced anxiety (AIA)
dary among alcoholics, there is substantial evidence that
symptoms more commonly include generalized anxi-
a valid alcohol history can be obtained, given adequate
ety symptoms, panic attacks, and phobias. An onset
assessment procedures and the right conditions. A
of drinking preceding the anxiety syndrome, and im-
complete alcohol history should include specific ques-
provement or remission of anxiety during periods of
tions concerning average alcohol consumption, maxi-
abstinence, suggest alcohol-induced anxiety disorder
mal consumption per drinking occasion, frequency of
(AIAD). Monitoring the course of these symptoms
heavy-drinking occasions, and drinking-related social
for several weeks after alcohol cessation can be use-
problems (e.g., objections raised by family members,
ful in determining their nature. Usually, a substantial
friends, or people at work), legal problems (including
improvement of anxiety will be observed during this
arrests or near-arrests for driving while intoxicated
period, suggesting a direct relationship of anxiety to
(DWI)), psychiatric symptoms (e.g., precipitation or
alcohol. In some cases, a full remission of symptoms is
exacerbation of mood or anxiety symptoms), and alco-
not observed until after 3 to 4 weeks of abstinence.
hol-related medical problems (e.g., alcoholic gastritis
or pancreatitis).
Alcohol-Induced Sleep Disorder Systematic clinical assessment often begins with
routine screening to identify active cases, as well as
Heavy alcohol consumption can be associated with a persons at risk. Perhaps the most widely used alcohol-
prominent disturbance of sleep. At intoxicating BALs, screening test is the CAGE, which contains only four
especially when BALs are declining, sedation and questions: (1) Have you ever felt you ought to cut (the
sleepiness can be observed. Alcohol intoxication in- “C” in CAGE) down on your drinking? (2) Have people
duces an increase in nonrapid eye movement (NREM) annoyed (A) you by criticizing your drinking? (3) Have
sleep, whereas rapid eye movement (REM) sleep density you ever felt bad or guilty (G) about your drinking? (4)
decreases. Subsequently, there is an increase in wake- Have you ever had a drink first thing in the morning
fulness, restless sleep, and vivid dreams or nightmares to steady your nerves or get rid of a hangover, that is,
related to a reduction in NREM sleep and a rebound in an eye opener (E)? Reliability and validity studies of
REM sleep density. During alcohol withdrawal, sleep this test have been conducted in diverse samples (e.g.,
is fragmented and discontinuous with an increase in psychiatric inpatients, ambulatory medical patients,
REM sleep. After withdrawal, individuals frequently prenatal clinics), with generally acceptable levels of
complain of sleep difficulties and may experience su- sensitivity.
perficial and fragmented sleep for months or years. The Alcohol Use Disorders Identification Test
(AUDIT), a 10-item screening instrument, may be used
as the first step in a comprehensive and sequential al-
Alcohol-Induced Sexual Dysfunction
cohol use history. The AUDIT (Table 14-1) covers the
Although small doses of alcohol in healthy individu- domains of alcohol consumption, symptoms of alcohol
als appear to enhance sexual receptivity in women and dependence, and alcohol-related consequences.
facilitate arousal to erotic stimuli in men, continuous Medical illness is a common consequence of heavy
and/or heavy drinking may cause significant sexual drinking and may be present in the absence of physi-
impairment. Alcohol-induced sexual dysfunction is cal dependence. Early in the course, individuals with
characterized by impaired desire, impaired arousal, alcoholism may show no physical or laboratory abnor-
and impaired orgasm, or sexual pain Use of other sub- malities. But as it progresses, it is widely manifested
stances, particularly those prescribed for the treatment throughout most organ systems. A thorough physical
of alcohol withdrawal such as benzodiazepines or bar- examination is indicated if, in the history, there is evi-
biturates, should be ruled out as a cause of the sexual dence of medical problems. The physical examination
dysfunction. provides essential information about the presence and
Comprehensive assessment provides the basis for an extent of end-organ damage, and should be focused
individualized plan of treatment. Depending upon the on the systems most vulnerable to developing alco-
severity of alcohol dependence, the nature of comor- hol-related pathology: the cardiovascular system, the
bid medical and psychiatric pathology, the presence gastrointestinal system, and the central and peripheral
of social supports, and evidence of previous response nervous systems. The physician should also be alert
Table 14-1 Alcohol Use Disorders Identification Test
1. How often do you have a drink containing alcohol?

(0) Never (1) Monthly or less (2) Two to four times a (3) Two or three times (4) Four or more times
month a week a week
2. *How many drinks containing alcohol do you have on a typical day when you are drinking? (Code number of standard drinks)
(0) 1 or 2 (1) 3 or 4 (2) 5 or 6 (3) 7 or 8 (4) 10 or more
3. How often do you have 6 or more drinks on one occasion?
(0) Never (1) Less than monthly (2) Monthly (3) Weekly (4) Daily or almost
daily
4. How often during the last year have you found that you were not able to stop drinking once you had started?
daily
5. How often during the last year have you failed to do what was normally expected from you because of drinking?
daily
6. How often during the last year have you needed a first drink in the morning to get yourself going after a heavy-drinking session?
daily
7. How often during the last year have you had a feeling of guilt or remorse after drinking?
daily
8. How often during the last year have you been unable to remember what happened the night before because you had been drinking
daily
9. Have you or someone else been injured as a result of your drinking?
(0) No (2) Yes, but not in the (4) Yes, during the last
last year year
10. Has a relative or friend or a physician or other health care worker been concerned about your drinking or suggested you cut down?
(0) No (2) Yes, but not in the (4) Yes, during the last
last year year
Record sum of individual item scores here .
*
In determining the response categories, it has been assumed that one “drink” contains 10 g of alcohol.
to other acute alcohol-related signs, including alcohol [GGTP], mean corpuscular volume [MCV]) of eryth-
withdrawal or delirium, intoxication or withdrawal rocytes can be used as objective indicators of heavy
from other drugs, and the acute presentation of psychi- drinking. Elevation in GGTP occurs in approximately
atric symptomatology. Other systemic or nonspecific three-fourths of alcoholics before there is clinical evi-
health problems associated with alcoholism include dence of liver disease. It is often considered to be the
malnutrition, muscle wasting, neuritis, specific vitamin earliest indication of heavy alcohol consumption and is
deficiencies, infectious diseases (such as tuberculosis, widely available clinically. GGTP levels usually return
dermatitis, pediculosis, and hepatitis), and trauma sec- to normal limits after 4 to 5 weeks of abstinence.
ondary to fights and accidents (Table 14-2). CDT is more sensitive than most routine laboratory
Several laboratory tests, particularly those related tests for the identification of heavy alcohol consump-
to hepatic function (e.g., serum transaminases, bition. In one study, CDT was found to have a sensitiv-
lirubin, prothrombin time, and partial thromboplastin ity of 91% and a specificity of 100% in distinguishing
time) have been commonly used by clinicians. Other alcoholics from light drinkers/abstainers. In contrast
laboratory tests (e.g., gamma-glutamyl transpeptidase to GGTP, CDT elevations are associated with few con-
ditions other than heavy drinking. CDT and GGTP
appear to identify two different subsets of alcoholic
Health Problems Commonly Associated with
Table 14-2 individuals. Elevations in GGTP values detect alcohol-
Alcoholism
ics with hepatic damage secondary to heavy drinking,
Malnutrition, muscle wasting, neuritis, vitamin deficiencies
Infectious diseases (e.g., tuberculosis)
whereas CDT appears to be more directly related to
Hepatitis, pancreatitis, gastritis heavy drinking. Whenever possible, CDT and GGTP
Trauma secondary to fights, accidents should be used together by classifying as a case the
Cardiovascular disease (e.g., myocardial infarction)
individuals who have elevated scores in either test.
This approach increases the likelihood of identifying and a poorer response to treatment. Greater severity
individuals experiencing alcohol use disorders. CDT of alcohol dependence has also been shown to predict
appears to detect relapse to heavy drinking among poorer treatment outcome.
individuals in alcohol treatment more accurately than While considered to be important in the development
other laboratory tests. of alcoholism, comorbid mental disorders also have
In a clinical setting where laboratory results are gen- prognostic significance. Among males, the presence of
erally not immediately available, the alcohol breath a comorbid lifetime diagnosis of ASPD, major depres-
test, which measures the amount of alcohol in expired sive disorder, or drug abuse/dependence was associated
air (providing an estimate of venous ethanol concentra- with poorer drinking outcomes. Among females, the
tion), is valuable. Although its accuracy depends on the presence of major depressive disorder predicted a bet-
individual’s cooperation (which in an intoxicated indi- ter outcome on drinking-related measures, while those
vidual is often problematic), the alcohol breath test can individuals with ASPD or drug abuse/dependence had
be a reliable and inexpensive method for assessing re- a poorer prognosis. Three-year posttreatment outcomes
cent alcohol consumption. Venous blood levels should in this group of alcoholics also showed comorbid ASPD,
be obtained if dangerously high levels of intoxication major depressive disorder, and drug abuse/dependence
are suspected, when an individual is comatose, or for to be associated with poorer outcomes, irrespective
medical–legal purposes. A BAL greater than 150 mg/dL of gender. Alcoholics with comorbid depression have
in an individual showing no signs of intoxication (i.e., greater psychiatric severity at follow-up than primary
no dysarthria, motor incoordination, gait ataxia, nys- alcoholics. Variable findings have also been reported
tagmus, or impaired attention) can be interpreted to re- concerning the prognostic significance of ASPD and
flect physiological tolerance. In nontolerant individuals, drug abuse among alcoholics.
a BAL in excess of 400 mg/dL can result in death, and
300 mg/dL indicates a need for emergency care.
TREATMENT
Another laboratory evaluation that is indicated in al-
coholics is a urine toxicology screen. To identify drug When a determination has been made that an indi-
use that the individual may not recognize or which he vidual is drinking excessively, the nature, setting, and
or she denies is a problem, the screen should include intensity of the intervention must be determined in or-
opiates, cocaine, cannabis, and benzodiazepines. Rou- der to address the specific treatment needs of the in-
tine urinalysis, blood chemistries, hepatitis profile, dividual. Among heavy drinkers without evidence of
complete blood count, and serologic test for syphilis alcohol dependence, a brief intervention aimed at the
and (for women) serum testing for pregnancy should reduction of drinking may suffice. In contrast, among
also be obtained. alcoholics, there are typically a variety of associated
disabilities, so it is necessary to address both the exces-
sive drinking and problems related to it. Consequently,
Course
alcoholism treatment is best conceived of as multimo-
A typical sequence of the symptoms of alcohol depend- dal. Table 14-3 provides an overview of the goals of
ence appears as follows: heavy drinking during the late
twenties; interference with functioning in multiple life
areas during their early thirties; loss of control, followed Table 14-3 Goals of Alcoholism Treatment
by an intensification of social- and work-related prob-
Promote complete abstinence from alcohol.
lems, and onset of medical consequences in the mid- to Stabilize acute medical (including alcohol withdrawal) and
late thirties; and severe long-term consequences by the psychiatric conditions, as needed.
late thirties and early forties. Women appear to experi- Increase motivation for recovery.
Initiate treatment for chronic medical and psychiatric
ence many of these milestones at a later age than men. conditions, as needed.
There are few effects of onset age, family history Assist the patient in locating suitable housing (e.g., moving
of alcoholism, or comorbid psychiatric diagnoses on from a setting where drinking is widespread), as needed.
Enlist social support for recovery (e.g., introduce to 12-step
the order of symptom appearance. However, other fea- programs and, when possible, help the patient to repair
tures defining the course of alcoholism, particularly damaged marital and other family relationships).
Enhance coping and relapse prevention skills (including
the response to treatment, vary as a function of vari- social skills, identification and avoidance of high-risk
ables related to the individual, including age of onset, situations).
severity of alcohol dependence, and comorbid mental Improve occupational functioning.
Promote maintenance of recovery through ongoing
disorders. There is consistent evidence that early age participation in structured treatment or self-help groups.
of onset is a predictor of greater severity of alcoholism
Initial assessment
AUDIT score 16−40 AUDIT score 8−15 AUDIT score < 8

Diagnostic Brief intervention and No intervention
evaluation and periodic reevaluation needed
treatment
intervention
Evaluate presence and

severity of physical
dependence
Physical dependence is absent or mild Physical dependence is moderate or severe
Outpatient Inpatient
Outpatient treatment detoxification detoxification
Management in psychiatrist’s office

or referral to outpatient or inpatient
rehabilitation
Inpatient rehabilitation
Aftercare including mutual

help organizations
Figure 14-1 Algorithm for the identification and management of patients with alcohol abuse and dependence.
alcoholism treatment. It should be noted that while to moderate their alcohol consumption, rather than
total abstinence is a primary goal of treatment for per- promote total abstinence with specialized treatment
sons with alcohol dependence, moderate drinking can techniques. They are simple enough to be delivered
be considered as a goal for persons with alcohol abuse. by primary care practitioners and are especially ap-
Figure 14-1 describes a process for the management propriate for individuals whose at-risk drinking meets
of individuals with alcohol abuse and dependence. The criteria for alcohol abuse rather than dependence. The
algorithm is written from the perspective of a commu- cumulative evidence shows that clinically significant
nity-based or consultation/liaison clinician who does effects on drinking behavior and related problems,
not necessarily have specialized training in addiction though not on alcohol dependence, can follow from
medicine. Following the initial assessment, using a brief interventions.
screening test such as the CAGE or AUDIT, the indi- If the individual’s screening results and diagnostic
vidual is referred to either a diagnostic evaluation with evaluation provide evidence of alcohol dependence,
a likely treatment recommendation or a brief interven- the next step is to differentiate between mild and more
tion with further monitoring. Brief interventions are severe levels of physical dependence to determine the
characterized by their low intensity and short duration. need for detoxification. If withdrawal risk is low, the in-
They are intended to provide early intervention, before dividual may be referred directly to outpatient therapy.
or soon after the onset of alcohol-related problems. If the withdrawal risk is moderate or high, outpatient or
Brief interventions seek to motivate high-risk drinkers inpatient detoxification is indicated.
There are a number of potentially life-threatening relief of discomfort, prevention or treatment of compli-
conditions for which alcoholics are at increased risk. cations, and preparation for rehabilitation. Successful
The presence of any of the following requires immedi- management of the alcohol-withdrawal syndrome pro-
ate attention: acute alcohol withdrawal (with the poten- vides a basis for subsequent efforts at rehabilitation.
tial for seizures and delirium tremens), serious medical Careful screening for concurrent medical problems
or surgical disease (e.g., acute pancreatitis, bleeding is an important element in detoxification. Administra-
esophageal varices), and serious psychiatric illness tion of thiamine (50–100 mg by mouth or IM) and mul-
(e.g., psychosis, suicidal intent). In the presence of any tivitamins is a low-cost, low-risk intervention for the
of these emergent conditions, acute stabilization should prophylaxis and treatment of alcohol-related neurologi-
be the first priority of treatment. cal disturbances. Good supportive care and treatment
The presence of complicating medical conditions of concurrent illness, including fluid and electrolyte
or mental disorders is an important determinant of repletion, are essential.
whether detoxification and rehabilitation are initiated Social detoxification, which involves the nonphar-
in an inpatient or an outpatient setting. Other consider- macological treatment of alcohol withdrawal, has been
ations are the alcoholic’s current living circumstances shown to be effective. It consists of frequent reassur-
and social support network. Women with children are ance, reality orientation, monitoring of vital signs,
sometimes unwilling to enter residential treatment un- personal attention, and general nursing care. Social
less their family needs are taken care of. Homeless detoxification is most appropriate for individuals in
people may be eager to enter residential treatment even mild-to-moderate withdrawal. The medical problems
when their medical or psychiatric condition does not commonly associated with alcoholism may substan-
warrant it. tially complicate therapy, so care must be taken to re-
In the alcoholic individual whose condition is sta- fer those individuals whose condition requires medical
bilized or in the individual without these complicat- management.
ing features, the major focus should be on the estab- Increasingly, detoxification is being done on an am-
lishment of a therapeutic alliance, which provides the bulatory basis, which is much less costly than inpatient
context within which rehabilitation can occur. The detoxification. Inpatient detoxification is indicated for
presence of a trusting relationship facilitates the in- serious medical or surgical illness, and for those indi-
dividual’s acknowledgement of alcohol-related prob- viduals with a past history of adverse withdrawal reac-
lems and encourages open consideration of different tions or with current evidence of more serious with-
treatment options. In addition to participation in struc- drawal (e.g., delirium tremens.)
tured rehabilitation treatment, the individual should Owing to their favorable side effect profile, the ben-
be made aware of the widespread availability of Alco- zodiazepines have largely supplanted all other medica-
holics Anonymous (AA) and the wide diversity of its tions for the treatment of alcohol withdrawal. Although
membership. any benzodiazepine will suppress alcohol-withdrawal
Despite treatment, some alcoholics relapse repeat- symptoms, diazepam and chlordiazepoxide are often
edly. For many emergency department personnel, the used, since they are metabolized to long-acting com-
multiple recidivist alcoholic has come to personify the pounds, which in effect are self-tapering. Because
disorder. For clinicians involved in the delivery of al- metabolism of these drugs is hepatic, impaired liver
coholism rehabilitation services, these individuals’ ap- function may complicate their use. Oxazepam and lo-
parent unresponsiveness to treatment may contribute to razepam are not oxidized to long-acting metabolites
frustration and a sense of futility. Presently, long-term and thus carry less risk of accumulation.
residential treatment appears to be the only option for Although carbamazepine appears useful as a pri-
alcoholics who do not respond to more limited efforts mary treatment of withdrawal, the liver dysfunction
at rehabilitation. Unfortunately, the availability of such that is common in alcoholics may affect its metabo-
care in many states is limited as a consequence of the lism, which makes careful blood level monitoring nec-
effort to deinstitutionalize psychiatric patients. essary. Antipsychotics are not indicated for the treat-
ment of withdrawal except in those instances where
hallucinations or severe agitation are present, in which
Management of Alcohol Withdrawal
case they should be added to a benzodiazepine. In
An important initial intervention for a substantial addition to their potential to produce extrapyramidal
number of alcohol-dependent individuals is the man- side effects, antipsychotics lower seizure threshold,
agement of alcohol withdrawal through detoxification. which may be particularly problematic during alcohol
The objectives in treating alcohol withdrawal are the withdrawal.
Psychosocial Treatments reaction when combined with alcohol. The efficacy of

such drugs in the prevention or limitation of relapse in
A variety of treatment components are delivered within
alcoholics has not been demonstrated. However, these
the context of rehabilitation services. In many programs,
drugs may be of utility in selected samples of alco-
a combination of therapeutic interventions is provided
holics with whom special efforts are made to ensure
to all individuals, based on the assumption that multiple
compliance.
components have a greater chance of meeting at least
Disulfiram (Antabuse) is the most commonly used al-
some of each individual’s needs. Therapeutic approaches
cohol-sensitizing medication and the only one approved
most often employed in both residential and outpatient
for use in the United States. When given in a single
programs include behavior therapy, group therapy, fam-
daily dose of 125–500 mg, disulfiram binds irreversibly
ily treatment, and pharmacotherapy. Regarding specific
to ALDH, permanently inactivating this enzyme.
treatment modalities, the weight of evidence suggests
When alcohol is consumed, it is metabolized to acetal-
that behavioral treatments are likely to be more effec-
dehyde, which accumulates because of inhibition of the
tive than insight-oriented or family therapies.
enzyme that metabolizes it. Elevated levels of acetalde-
Behavioral elements most frequently employed in
hyde are responsible for the aversive effects associated
treatment programs are relapse prevention, social skills
with the disulfiram–ethanol reaction (DER).
and assertiveness training, contingency management,
Although disulfiram has been used in the treatment
deep muscle relaxation, self-control training, and cog-
of alcoholism for more than 50 years, the few placebo-
nitive restructuring.
controlled studies that have been conducted have not
Behavior therapists stress the importance of teach-
shown the drug to have substantial efficacy. Given the
ing new, adaptive skills designed to alter the conditions
limited efficacy of disulfiram for the prevention of re-
that precipitate and reinforce drinking, as well as devel-
lapse, it should not be used as a first-line treatment for
oping alternative ways of coping with persons, events,
alcohol dependence. However, if an individual has not
and feelings that serve to maintain drinking. A model
responded to other pharmacological treatments and
of treatment, characterized as “relapse prevention” be-
is motivated to take disulfiram, it may be beneficial.
cause of its focus on identifying and coping with situ-
Whenever disulfiram is prescribed, individuals should
ations that represent high risk for heavy drinking, has
be warned about its hazards, including the need to avoid
been used increasingly. Individuals who received skills
over-the-counter (OTC) preparations with alcohol and
training attend aftercare more regularly and have less
drugs that interact adversely with disulfiram, as well as
severe (though no less frequent) relapses than individu-
the potential for a DER to result from alcohol used in
als in control groups.
food preparations.
The deleterious effects of alcoholism on marriages and
families have been a source of concern to both clinicians
Drugs that May Directly Reduce Alcohol
and researchers. Alcoholism creates major stress on the
Consumption. Efforts to use medications to treat ex-
family system by threatening health, interpersonal rela-
cessive drinking have increasingly focused on agents
tions, and the economic functioning of family members.
that have selective effects on specific neurotransmitter
In addition to specific treatment for alcoholic couples
systems.
or families, self-help groups for family members of al-
An extensive literature supports the role of opioider-
coholics have grown substantially. Al-Anon, although
gic neurotransmission in the pathophysiology of alco-
not formally affiliated with AA, shares the structure
hol consumption and related phenomena. In contrast,
and many of the tenets of the 12 steps of AA. Al-Anon
opioid antagonists, such as naltrexone, decrease etha-
and AA meetings are often held jointly. Alateen groups,
nol consumption and self-administration.
sponsored by Al-Anon for children of alcoholics, are
Naltrexone appears to produce a modest effect on
available as well.
drinking behavior among alcoholics. However, given
the comparatively small overall effect of the medica-
Somatic Treatments tion, a variety of other factors, including medication
compliance, the severity and chronicity of alcohol de-
In the following sections, we discuss two types of phar- pendence, and the choice of concomitant psychother-
macotherapy for alcoholics: alcohol-sensitizing drugs apy, may determine whether an effect of the medication
and medications to directly reduce drinking. is observed.
Acamprosate was approved by the FDA in 2004
Alcohol-Sensitizing Drugs. Medications such as for the maintenance of abstinence from alcohol in in-
disulfiram or calcium carbimide cause an unpleasant dividuals with alcohol dependence who are abstinent
at treatment initiation. Acamprosate, an amino acid Table 14-4 The 12 Steps of Alcoholics Anonymous
derivative, affects both gamma-aminobutyric acid
(GABA) and excitatory amino acid (i.e., glutamate) 1. We admitted we were powerless over alcohol—that our
lives had become unmanageable.
neurotransmission (the latter effect most likely being 2. Came to believe that a Power greater than ourselves
the one that is important for its therapeutic effects in al- could restore us to sanity.
coholism). Together, studies involving more than 4000 3. Made a decision to turn our will and our lives over to the
care of God as we understood Him.
individuals provide consistent evidence of the efficacy 4. Made a searching and fearless moral inventory of
of acamprosate in alcoholism rehabilitation. On the ba- ourselves.
sis of these findings, and the benign side effect profile 5. Admitted to God, to ourselves, and to another human
being the exact nature of our wrongs.
of the medication, it appears to hold considerable value 6. Were entirely ready to have God remove all these
for the treatment of alcohol dependence. defects of character.
Other drugs, including SSRIs such as fluoxetine and 7. Humbly asked Him to remove our shortcomings.
8. Made a list of all persons we had harmed, and became
citalopram, and ondansetron have been used with vari- willing to make amends to them all.
able success in reducing alcohol intake. 9. Made direct amends to such people wherever possible,
except when to do so would injure them or others.
Considerable additional research is required before 10. Continued to take personal inventory and when we were
medications are likely to play a meaningful role in the wrong, promptly admitted it.
postwithdrawal treatment of alcohol dependence. One 11. Sought through prayer and meditation to improve our
conscious contact with God as we understood Him,
currently useful strategy is the identification of comor- praying only for knowledge of His will for us and the
bid psychopathology in alcoholics, with pharmacother- power to carry that out.
apy directed toward reducing both psychiatric symp- 12. Having had a spiritual awakening as the result of these
steps, we tried to carry this message to alcoholics, and
toms and alcohol consumption. In addition, the opioid to practice these principles in all our affairs.
antagonist naltrexone, which is capable of yielding a
Source: The 12 Steps are reprinted with permission of Alcoholics
modest effect overall in reducing drinking behavior, Anonymous World Services, Inc. Permission to reprint this material
appears to be of considerable value in some individu- does not mean that AA has reviewed or approved the contents of this
publication, nor that AA agrees with the views expressed herein. AA
als. Further research is required with naltrexone to de- is a program of recovery from alcoholism. Use of the 12 Steps in
termine the optimal dosage, duration of treatment, and connection with programs and activities that are patterned after AA
but address other problems does not imply otherwise.
psychosocial treatment strategies with which to use the
medication. The question of whether the medication is
most efficacious for alcoholics with high levels of crav-
ing for alcohol remains an important one. The SSRIs drinking problems in the United States and throughout
fluoxetine, citalopram, and sertraline may be of value the world. In addition, a number of self-help organi-
in subgroups of heavy drinkers, particularly those with zations have modeled themselves after AA, basing re-
a later onset of problem drinking. In contrast, ondanset- covery from drug abuse, overeating, and other behav-
ron may be useful in alcoholics with an early onset of ioral disorders on the 12 Steps of AA (see Table 14-4).
problem drinking. Prospective replication of this sero- Unfortunately, clinicians often refer individuals to self-
tonergic matching strategy is required, however, before help groups such as AA without consideration of the
it can be recommended for general clinical use. individual’s needs and without adequate monitoring
of the individual’s response. Not all people are will-
ing to endorse the AA emphasis on spirituality and its
Alcoholics Anonymous (AA) and Mutual disease concept of alcoholism, which requires lifelong
Help Organizations abstinence as the only means to recovery. Greater fa-
Although mutual help societies composed of recover- miliarity with AA may help clinicians to identify those
ing alcoholics are not considered a formal treatment, individuals who might benefit from this approach.
they are often used as a substitute, an alternative, and Although it is regarded as one of the most use-
an adjunct to treatment. Mutual help groups based on ful resources for recovering alcoholics, the research
the Twelve Steps of AA have proliferated throughout literature supporting the efficacy of AA is limited.
the world. To the extent that AA and other mutual Attendance at AA tends to be correlated with long-
help groups are more numerous than outpatient treat- term abstinence, but this may reflect motivation for
ment, they may constitute a significant resource for recovery. The type of motivated alcoholic that persists
problem drinkers who are attempting to reduce or stop with AA might do just as well with other forms of sup-
drinking. portive therapy. In fact, the few random assignment
With an estimated 87,000 groups in 150 countries, studies that have been conducted do not indicate that
AA is by far the most widely utilized source of help for AA (or similar programs) is more effective than other
types of treatment. Personality variables do not appear perior safety profile of SSRIs, particularly in relation
to differentiate between alcoholics who affiliate with to risk of suicide by medication overdose, use of these
AA and those who do not, although there is some evi- drugs is preferable to the use of TCAs.
dence that AA is less successful among persons with
major psychiatric disorders and those of low socioeco- Treatment of Anxiety Symptoms/Disorders. While
nomic status. a number of studies have shown chlordiazepoxide to be
effective in the maintenance of alcoholics in long-term
outpatient treatment, the potential for additive CNS
Treatment of Psychiatric Comorbidity
depression produced by the concurrent use of alcohol
Comorbid mental disorders may contribute to the de- and benzodiazepines is well recognized. Furthermore,
velopment or maintenance of heavy drinking. Efforts the use of benzodiazepines may itself result in toler-
to treat the comorbidity may have beneficial effects on ance and dependence and may increase depressive
drinking outcomes. Following detoxification, many symptoms.
alcoholics complain of persistent anxiety, insomnia, Buspirone is a non-benzodiazepine anxiolytic that is
and general distress. These symptoms may last for less sedating than diazepam or clorazepate, does not
weeks or months and may be difficult to differentiate interact with alcohol to impair psychomotor skills, and
from the emergence of diagnosable mental disorders. has a low potential for abuse. When combined with ap-
Irrespective of their etiology, negative emotional states, propriate psychosocial treatment, buspirone appears
including frustration, anger, anxiety, depression, and useful in the treatment of alcoholics with persistent
boredom, have been shown to contribute to relapse in a anxiety.
substantial proportion of alcoholics. Currently, antipsychotics are indicated only in alco-
A variety of medications have been employed to treat holics with a coexistent psychotic disorder or for the
comorbid psychiatric symptoms and disorders in alco- treatment of alcoholic hallucinosis. Several placebo-
holics. Indications for the use of these medications in controlled studies have found no advantage in the use
alcoholics are similar to those for nonalcoholic popula- of phenothiazines for treatment of anxiety, tension, and
tions, but there is added potential for adverse effects depression following detoxification. Because of their
due to comorbid medical disorders and the pharmacok- capacity to lower seizure threshold, antipsychotics
inetic effects of acute and chronic alcohol consumption. should be used with caution in this population.
The use of these medications in alcoholics therefore en-
tails additional considerations that can only be arrived
at through careful psychiatric diagnosis.
DIAGNOSTIC CRITERIA
Treatment of Depressive Symptoms/Disorders. De- The ICD-10 and DSM-IV-TR criteria sets are nearly
pressive symptoms are common early in alcohol with- identical except for the following: the ICD-10 Diag-
drawal, but they often remit spontaneously with time. nostic Criteria for Research for Alcohol Intoxication
For depression that persists beyond the period of acute also lists flushed face and conjunctival injection as
withdrawal, an antidepressant is probably warranted. symptoms but does not include the DSM-IV-TR item
Although it has been argued that most instances of for impairment in attention; the ICD-10 Diagnostic
postwithdrawal depression will spontaneously remit Criteria for Research for Alcohol Withdrawal require
within a few days to several weeks, there are still a three symptoms from a list of ten, which includes
substantial number of individuals whose severe and headache and splits tachycardia and sweating into two
persistent depression requires treatment. Given the su- separate items.
CHAPTER
Amphetamine
Consistent with the schema put forward by the DSM- However, it is uncommon that those who go on to
IV-TR, this chapter defines the amphetamine-like amphetamine dependence continue to supply their
substances to include the Phenylisopropylamines habit through licit sources. Further, medically appro-
Amphetamine (AMPH), methamphetamine (METH), priate use of synthetic stimulants does not appear to
and phenylpropanolamine (PPA), the natural substances pose a significant risk for the induction of substance-
ephedrine and pseudoephedrine, and phenylethyl- use disorders. This has been most closely examined
amines including methylphenidate. While METH and for the widely prescribed methylphenidate (Ritalin)
AMPH cause the vast majority of abuse and depend- for ADHD; in this case, treatment may actually reduce
ence, use of any of these substances has been associ- the risk of developing substance abuse by controlling
ated with abuse and dependence, so as a class these ADHD, which is itself a risk factor for substance abuse.
will be referred to as amphetamine-type stimulants, or Further, methylphenidate poses a low risk for medical
ATS, in this chapter. complications. It has been postulated that the persist-
By far, the most widely abused ATS is METH, which ence of peripheral autonomic effects, as well as much
is commonly known as meth, speed, crank, CR, wire, longer half-life in the striatum, accounts for its low
and jib, and in its recrystallized smoked form, ice, crys- abuse potential relative to cocaine.
tal, or glass. Legitimate forms of METH prescribed for
attention-deficit/hyperactivity disorder (ADHD) and
DIAGNOSIS
weight control (Methedrine, Desoxyn, and Adipex)
undoubtedly represent a miniscule source of the total Consistent with the DSM-IV-TR perspective func-
amount abused each year. AMPH, most prevalent in tionally equating amphetamines with cocaine, those
Western Europe, is commonly known as amp, bennies, diagnostic categories that are included are identical
dex, or black beauties, and is prescribed as Adderall, to those for Cocaine-Related Disorders, with the sole
Dexedrine, and Dextrostat in the treatment of ADHD, exception of omitting the specifier “With Onset During
narcolepsy, weight control, and depression. Other agents Withdrawal” from the diagnostic category Ampheta-
that have been designated as Schedule II controlled mine-Induced Anxiety Disorder. For the substance use
substances by the Drug Enforcement Administration disorders, amphetamine (ATS) abuse and dependence
are methylphenidate (Ritalin, Concerta) and phenm- will be discussed below. Of the substance-induced dis-
etrazine (Preludin). On the street, Ritalin is known orders, the critical diagnoses of ATS intoxication and
as Rits or Vitamin R. A large number of Schedule III withdrawal are described. The specific complications
and IV phenylethylamines (benzphetamine, diethyl- of delirium, psychotic disorders, mood disorders, anxi-
proprion, mazindol, phendimetrazine, phenmetrazine, ety disorders, sexual dysfunctions, and sleep disorders
and phentermine) are used for weight control. There all are described under intoxication. Amphetamine-
is no specific evidence that these substances represent induced mood and sleep disorders also allow for speci-
a significant source of illicit diversion, and they are fiers of onset during withdrawal.
not further discussed in this chapter. ATS agents are
also widely available in over-the-counter (OTC) prepa-
Amphetamine Dependence
rations. PPA has been removed from the market, but
ephedrine and pseudoephedrine are still very widely ATS dependence is diagnosed when a maladaptive pat-
used as decongestants, and less so, phenylephrine and tern of use leads to clinically significant impairment or
propylhexidrine. distress, as defined by three or more of the following
that occur during the same 12-month period: (1) evi-

dence of tolerance, (2) occurrence of withdrawal, or the DSM-IV-TR Diagnostic Criteria
reuse of the substance to alleviate withdrawal, and (3) 292.89 AMPHETAMINE INTOXICATION AND 292.89 COCAINE
compulsive use of amphetamines as defined by three or INTOXICATION
more of the following: using more than intended, (4)
A. Recent use of amphetamine or a related substance
desire or efforts to reduce use, (5) occupying signifi- (e.g.,methylphenidate)/cocaine.
cant time in drug-related activities, (6) loss of social, B. Clinically significant maladaptive behavioral or psycho-
occupational, or recreational pursuits, or (7) continued logical changes (e.g., euphoria or affective blunting;
changes in sociability; hypervigilance; interpersonal
use despite known adverse, physical, or psychological sensitivity; anxiety, tension, or anger, stereotyped
consequences (see DSM-IV-TR diagnostic criteria for behaviors; impaired judgment; or impaired social
Substance Dependence in Chapter 13, page 125). or occupational functioning) that developed dur-
ing, or shortly after, use of amphetamine or a related
substance/cocaine.
C. Two (or more) of the following, developing during,
Amphetamine Abuse or shortly after, use of amphetamine or a related
substance/cocaine:
The diagnosis of ATS abuse requires a maladaptive pat-
(1) tachycardia or bradycardia
tern of use that does not meet the criteria for dependence, (2) pupillary dilation
and that results in clinically significant impairment or (3) elevated or lowered blood pressure
distress. In the preceding 12 months, recurrent sub- (4) perspiration or chills
(5) nausea or vomiting
stance use must result in one or more of the following: (6) evidence of weight loss
failure to meet major role obligations, placement of the (7) psychomotor agitation or retardation
user in physical danger, legal entanglements, or social/ (8) muscular weakness, respiratory depression, chest
pain, or cardiac arrhythmias
interpersonal problems (see DSM-IV-TR diagnostic (9) confusion, seizures, dyskinesias, dystonias, or
criteria for Substance Abuse in Chapter 13, page 125). coma
D. The symptoms are not due to a general medical condi-
Amphetamine Intoxication tal disorder.
Specific diagnostic criteria are provided for ATS in- Specify if:
toxication. These include recent use of an ATS (crite- With Perceptual Disturbances
rion A), clinically significant maladaptive behavioral Note: This is a summary of two criteria sets.
or psychological changes occurring after the use of the Reprinted with permission from DSM-IV-TR Guidebook.
ATS (criterion B), two or more specified physiological Copyright 2004, Michael B First, Allen Frances, and Harold Alan
changes after the use of the ATS (criterion C), and the Pincus.
requirement that the condition is not accounted for by

another mental or medical condition (criterion D). A
induced psychosis from psychotic states such as schizo-
specifier “with perceptual disturbances” is included.
phrenia. Nonetheless, ATS-induced psychosis shares
The specifics of criteria B and C provide a useful clin-
many features with other acute psychotic states. Of con-
ical consensus of the syndrome of ATS intoxication (see
cern, ATS-induced psychosis can sometimes persist for
Table 15-1 for a list of the maladaptive behaviors of Cri-
terion B, with comments in parentheses). Importantly,
psychosis and paranoia are experienced by approxi-
mately one-third of ATS-dependent subjects and occur Maladaptive Behaviors Listed in Criterion
Table 15-1 B of Amphetamine Intoxication, with
at a significantly greater rate than for cocaine or Ecstasy. Comments and Explications in Parentheses
With chronic use, the incidence of psychosis increases.
Euphoria or affective blunting (felt to occur in longer-term
Furthermore, the occurrence of psychotic symptoms users)
correlates with heavier use, co-use of benzodiazepines, Changes in sociability (e.g., being hypertalkative, more
and preexisting mental illness. Cognitive disturbances interactive or more withdrawn, increased libido)
Hypervigilance (with ideas of reference that can proceed to
include visual, tactile, and auditory hallucinations. frank paranoia)
Visual hallucinations often suggest an underlying “or- Interpersonal sensitivity
ganic” cause to psychosis, and formication, the feeling Anxiety, tension, or anger (agitated behavior and
altercations are common)
of “bugs crawling under the skin” is highly suggestive of Stereotyped behavior (picking at skin, grooming, pacing,
ATS or cocaine intoxication. Psychosis in the presence disassembly/reassembly of objects)
of an intact sensorium, where the subject is aware that Impaired judgment (often seen as sexual promiscuity)
Impaired social or occupational functioning
the hallucinations are not real, may differentiate ATS-
Chapter 15 • Substance-Related Disorders: Amphetamine 149
Physiological Disturbances Listed in DSM-IV-TR Diagnostic Criteria

Criterion C of Amphetamine Intoxication,
Table 15-2
with Comments and Explications in
Parentheses 292.0 AMPHETAMINE WITHDRAWAL AND 292.0 COCAINE
WITHDRAWAL
Tachycardia or reflex bradycardia
Papillary dilatation A. Cessation of (or reduction in) amphetamine (or re-
Elevated or lowered blood pressure lated substance)/cocaine use that has been heavy and
Perspiration or chills prolonged.
Nausea or vomiting B. Dysphoric mood and two (or more) of the following
Evidence of weight loss physiological changes, developing within a few hours
Psychomotor agitation or retardation (an excited delirium is to several days after Criterion A:
described as for cocaine, along with tremor) (1) fatigue
Muscle weakness, respiratory depression, chest pain, or (2) vivid, unpleasant dreams
cardiac arrhythmia (3) insomnia or hypersomnia
Confusion, seizures, dyskinesias, dystonias or coma (4) increased appetite
(Headaches and tinnitus are additional neurological (5) psychomotor retardation or agitation
symptoms that have also been described as occurring)
C. The symptoms in Criterion B cause clinically signifi-
cant distress or impairment in social, occupational, or
other important areas of functioning.
months following cessation of drug use. The physiologi- D. The symptoms are not due to a general medical condi-
cal disturbances in criterion C are listed in Table 15-2, tion and are not better accounted for by another men-
tal disorder.
again with comments in parentheses.
Note: This is a summary of two criteria sets.
Reprinted with permission from DSM-IV-TR Guidebook.
Amphetamine Withdrawal Copyright 2004, Michael B First, Allen Frances, and Harold Alan
Pincus.
While the intoxicated state is characterized as euphoric,
expansive, and activated, and often presents with agita-
tion, violence, and/or psychosis, ATS withdrawal is char- Since neurocognitive impairment occurs early in
acterized by decreased energy and mood. The clinician withdrawal, clinicians should be cognizant that instruc-
often evaluates such individuals who become suicidal tions to individuals in withdrawal be kept simple and
during the “crash.” The period of most intense withdrawal written out. Decision making, as has been known anec-
may last days, though a protracted state of depression dotally for years, appears affected. Over months, these
and low energy often persists for weeks. Resurgence of cognitive deficits may partially remit to a greater extent
craving when exposed to drug-associated environmental than in opiate abusers. Severe craving marks the early
cues probably persists for years, as is the case with other withdrawal phase, leading to high recidivism. Sleep
substance-dependence disorders. The occurrence of ATS disturbance is accompanied by increase in REM sleep.
withdrawal usually occurs in those who have progressed
from the diagnosis of abuse to dependence.
Medical Complications
The ATS withdrawal diagnosis requires cessation or
reduction of ATS use that has been heavy or prolonged For heavy users, a number of general consequences
(criterion A), dysphoric mood, and at least two physi- of ATS dependence will be obvious; malnutrition
ologic changes that occur from a few hours to days after and cachexia from sleep deprivation, exposure to the
cessation of use (i.e., fatigue; vivid, unpleasant dreams; elements and so on. Skin disorders, including infec-
insomnia and hypersomnia; increased appetite; psycho- tions and lesions from “picking” are common. More
motor retardation or agitation) which cause clinically sig- serious are ATS-related deaths due to cardiac ar-
nificant distress or impairment in social, occupational, or rhythmias, stroke, and rhabdomyolysis that have been
other important areas of functioning (criteria B and C); documented since the 1950s. These problems were
and the requirement that the condition is not accounted similar to those reported for the more widely abused
for by another mental or medical condition (criterion D). cocaine. A number of factors place ATS users at high
Both the longer half-lives of ATS relative to other psy- risk for contraction of HIV, and likely Hepatitis B and
chostimulants, as well as the broader-spectrum effects on C, infection.
nerve terminal catecholamine levels, result in prolonged Some of the medical complications result from expo-
withdrawal and abstinence states. ATS withdrawal states sure to contaminants during ATS use. The production
occur in some 87% of users. The acute phase appears methods for ATS determine what contaminants are
to last up to 5 days, with some symptoms persisting for present in illicit manufacture. Contaminants are both
weeks, possibly months, following the acute phase. toxic, as well as stimulants in their own right.
Many of the cardiovascular complications for ATS Central Nervous System. As opposed to the medical
result from peripheral catecholamine toxicity. This complications described above, which often are dis-
explains why the principal drug interactions of concerned at autopsy, CNS effects including psychosis and
cern involve the psychotropics that are meant to aug- stroke are common presenting symptoms in emergency
ment catecholamine function. Of most concern are the departments.
monoamine oxidase inhibitors, whose action can po- Seizures are one of the most common presenta-
tentiate ATS toxicity for 2 to 3 weeks following cessa- tions of ATS intoxication to emergency rooms. In as-
tion of use. Similarly, tricyclic antidepressants can po- sociation with an uncontrollable delirium, they can
tentiate effects of ATS, as well as increase absorption quickly lead to death if not controlled. Following de-
and slow hepatic metabolism creases in ATS blood levels, individuals who abuse
ATS are not left at increased risk for reoccurrence of
HIV and Immunomodulatory Effects. Intravenous seizures unless CNS lesions from prior stroke have
drug use is the fastest growing route for transmission developed.
of HIV infection. In addition, ATS use is associated Hyperthermia is related to a number of causes in
with unsafe sexual behaviors, including participation those presenting with METH intoxication. Increased
in unprotected sex and involvement with multiple motor activity, with reduced heat dissipation from pe-
sexual partners. Once HIV has been contracted, ATS ripheral vasoconstriction, is the proximate cause. It is
abuse leads to accelerated CNS and cardiovascular also likely that direct affects on hypothalamic thermal
toxicity. METH and AMPH are immunomodula- regulation exist.
tors, and in fact, may be immunotoxic to peripheral
T cells, mitogen-stimulated lymphocytes, and spleen Renal. Rhabdomyolysis is clearly the major concern
cells. for renal impairment; there does not appear to be in-
dependent toxicity to the kidney. METH, however, is
Pulmonary. In a large autopsy series of individuals an increasingly common cause of rhabdomyolysis, and
who died from ATS use, pulmonary edema was present is often associated with hyperthermia. Myoglobin and
in 70% of cases, as well as pneumonia (8.2%), and em- myoglobin breakdown products cause tubular obstruc-
physema (5.1%). Birefringent crystals at bifurcation of tion. Renal damage results from hypotension and renal
pulmonary vessels is associated with intravenous abuse ischemia secondary to metabolic derangements sec-
of crushed pills that contain insoluble fillers such as ondary to rhabdomyolysis, including phosphorus and
talc, microcrystalline cellulose, corn starch, or cotton potassium imbalance, and tubular obstruction due to
fibers. With sufficient deposition, small vessel throm- catabolic product accumulation.
bosis and granuloma formation ensues. The changes
ultimately reduce pulmonary perfusion, and increase
pulmonary vascular resistance. Effects on the Fetus. Fetal loss, developmental de-
lay, and subsequent learning disabilities are potential
Gastrointestinal. In METH-related deaths, the sum complications of ATS use during pregnancy. Most re-
of liver-related complications is second highest among cent evidence suggests a small effect of newborn birth-
organ systems. Fatty liver (16.2%), cirrhosis (9.0%), weight, and a low incidence (4%) of overt ATS with-
portal triaditis (6.1%), and hepatitis (4.1%) have been drawal in newborns of METH-dependent mothers.
detected. This may relate to the high comorbidity with
alcohol dependence, though the exact contribution is
TREATMENT
unknown.
There are few studies that specifically address the
Cardiovascular. Both cocaine and ATS cause similar treatment of ATS use disorders. This reflects the tradi-
vascular toxicity, largely related to catecholamine ex- tional focus on cocaine use disorders. Even for cocaine,
cess. Hearts of stimulant abusers develop areas of fi- effective pharmacotherapies are lacking compared to
brosis and contraction band necrosis, and usually are treatment of alcohol- and opiate-dependent individu-
increased in weight. As well, coronary artery disease is als. Behavioral treatment approaches remain the main-
accelerated. Aortic dissection is a less well known but stay of treatment of psychostimulant use disorders, and
catastrophic complication of METH use. Cardiotoxic those whose efficacy is supported in the cocaine use
effects are only partly reversible. Of note, heart failure disorders are assumed will be effective for ATS use
in children treated with Ritalin is so rare as to be at the disorders. Outcomes in psychosocial treatment cohorts
case report level. do appear to be similar.
Chapter 15 • Substance-Related Disorders: Amphetamine 151
Several unique aspects of ATS addiction must be anticholinergic effects that may worsen delirium and
addressed for treatment to be effective. Because ATS hyperthermia. If oral use of the ATS is suspected or
users begin to experience adverse consequences of confirmed, charcoal gastric lavage is indicated. Acidi-
their use later than comparable cocaine addicts, they fication of the urine with ammonium chloride solu-
appear to be more ambivalent to enter treatment, prob- tion or cranberry juice may be used to enhance ATS
ably because they reason that since they have gotten excretion, though should be avoided if rhabdomyolysis
along fairly well up to that point, why should they be- is a concern, since this would worsen dissociation and
gin the difficult process of treatment? Thus, treatment precipitation of myoglobin or where renal or hepatic
entry and retention rates are lower than those for in- dysfunction are an issue. Basic life support and initial
dividuals with cocaine dependence, and necessitates management are needed for critical conditions such as
outreach programs to enhance treatment engagement. myocardial ischemia or arrythmia, stroke or seizures,
A number of co-occurring problems, such as high HIV hyperthermia, and rhabdomyolysis. Hypertension and
and hepatitis infection rates, homelessness, and child- tachycardia, if not responsive to benzodiazepine se-
rearing difficulties, must be integrated into the treat- dation, may require treatment with an alpha-adrener-
ment approach. Further, the continued neurocognitive gic blocker, typically phentolamine. Agents with beta
deficits in METH-dependent individuals increase the blockade activity, such as propanolol and labetolol,
need to apply outreach attempts to noncompliant indi- must be avoided as alpha-adrenergic tone can increase,
viduals. Association with difficult-to-alter behaviors leading to a worsening of the clinical condition.
(sexual/social and weight loss) means those “rewards”
must be coopted by substitution of other options, such
Treatment of ATS Withdrawal
as referral to self-help groups for weight loss. As for
any addiction, the need to separate reinforcing social Emergency considerations in the withdrawal phase
contacts from the addict’s lifestyle is a difficult proc- of ATS intoxication are principally psychiatric. The
ess. Abuse by those seeking performance enhancement week following cocaine withdrawal is associated with
may be targeted through education programs and drug increased risk of silent myocardial ischemia. Because
screening programs, such as those that have been so this is hypothesized to result from coronary vasospasm,
successful in the military. this may not generalize to ATS withdrawal. Otherwise,
medical complications of ATS withdrawal, such as my-
algias, involuntary motor movements, and so on can
Treatment of ATS Intoxication
be treated symptomatically and should spontaneously
Management of acute intoxication is guided by the pre- remit.
senting medical and psychiatric symptoms. In ATS in- The use of antidepressants for 3 to 4 weeks following
toxication, there are no direct receptor targets to achieve cessation of ATS use is suggested, because depression
blockade; though dopamine receptor blockade theoreti- is a hallmark of ATS withdrawal. Often, allowing the
cally should be useful in blocking acute and or chronic individual increased time to sleep and reestablishment
affects of ATS, this has not proven to be the case. Anxi- of normal nutrition is quite helpful. Where needed,
ety and agitation are first treated by an environment the use of trazodone for sleep or short-term benzodi-
that reduces stimulation and provides orientation, with azepines for anxiety is needed along with antidepres-
staff providing reassurance and talk downs. Physical sant therapy.
restraints should be avoided, as these may worsen rhab-
domyolysis or hyperthermia. When nonpharmacologi-
Psychosocial Treatments for ATS Dependence
cal means are insufficient, benzodiazepines, typically
lorazepam or diazepam, are first-line treatments since Cognitive behavioral therapy forms the basis of many
they protect against imminent seizures. Antipsychot- treatments for psychostimulant dependence. Contin-
ics for agitation should be avoided because of the risk gency incentives, skills training, and family member
of worsening hyperthermia or rhabdomyolysis if neu- participation are helpful for maintaining ATS absti-
roleptic malignant syndrome were to occur, and their nence. An extension of such a combined approach,
ability to lower seizure threshold. However, since ben- termed the community-reinforcement-plus-vouchers
zodiazepines run the risk of disinhibiting some indi- approach, combines couples counseling, vocational
viduals, typical antipsychotics are often the preferred training and skills training, and contingency manage-
choice. ment through rewards for negative urine testing. This
For psychosis and paranoia, high potency antipsy- combined approach, developed for the treatment of
chotics, typically haloperidol, are used. This avoids the cocaine dependence, is shown to improve treatment
retention and decrease drug use and is likely to be simi- jects that those with other substance use disorders, or
larly useful for other ATS dependencies. be superior in outcome to outpatient-based programs.
Several other psychosocial treatments might be ap-
plied to individuals with ATS use disorders. Relapse
Pharmacotherapy for ATS Dependence
prevention, easily combined with widely used drug
counseling, systematically teaches individuals the As is the case with cocaine use disorders, effective
skills needed to avoid drug use through training in as- pharmacotherapies for amphetamine use disorders
sertiveness and refusal skills, how to cope with crav- are not available. The main role of pharmacotherapy
ing, how to deal with relapses, and how to recognize is acute symptomatic relief, and treatment of comorbid
patterns of behavior or thinking that lead to relapse. conditions. Behavioral treatments and self-help groups
Network therapy, meant to engage family and commu- remain the mainstay of treatment for the many indi-
nity in supporting drug-free functioning, appears well viduals suffering from ATS dependence.
suited to ATS abuse and dependence, where acquisi-
tion appears more linked to community networks than
stressful street “buys.”
DIAGNOSTIC CRITERIA
Residential treatment for pregnant women and the
homeless is likely to be of benefit for stabilization of The ICD-10 criteria sets for other stimulant intoxica-
ATS-dependent subjects, though there is no specific tion and withdrawal are almost the same as the DSM-
indication for stimulants. The prolonged nature of IV-TR criteria sets for amphetamine intoxication and
ATS-induced withdrawal, and the association with ag- withdrawal except that the ICD-10 Diagnostic Criteria
gressivity and violence, will often make inpatient psy- for Research include drug craving as an additional item.
chiatric stabilization necessary. It is unknown whether ICD-10 combines amphetamines and caffeine into a
transition to therapeutic communities or half-way single substance class, referred to as “other stimulants,
houses will be of greater benefit to ATS-dependent sub- including caffeine.”
CHAPTER
Caffeine
Caffeine is the most widely consumed psychoactive

substance in the world. In North America, it is esti- DSM-IV-TR Diagnostic Criteria
mated that more than 80% of adults and children con- 305.90 CAFFEINE INTOXICATION
sume caffeine regularly. This cultural integration of
caffeine use can make the recognition of mental disor- A. Recent consumption of caffeine, usually in excess of
250 mg (e.g., more than 2–3 cups of brewed coffee).
ders associated with caffeine use particularly difficult. B. Five (or more) of the following signs, developing dur-
It is important, however, for the clinician to recognize ing, or shortly after, caffeine use:
the role of caffeine as a psychoactive substance capable (1) restlessness
of producing a variety of psychiatric syndromes, de- (2) nervousness
spite the pervasive and well-accepted use of caffeine (3) excitement
(4) insomnia
(5) flushed face
(6) diuresis
Caffeine Intoxication (7) gastrointestinal disturbance
(8) muscle twitching
(9) rambling flow of thought and speech
DIAGNOSIS (10) tachycardia or cardiac arrhythmia
(11) periods of inexhaustibility
DSM-IV-TR defines caffeine intoxication as a set of (12) psychomotor agitation
symptoms that develop during or shortly after caffeine
use. There may be two kinds of presentation associ- cant distress or impairment in social, occupational, or
ated with caffeine intoxication. The first presentation other important areas of functioning.
is associated with the acute ingestion of a large amount tion and are not better accounted for by another men-
of caffeine and represents an acute drug overdose con- tal disorder (e.g., an anxiety disorder).
dition. The second presentation is associated with the Reprinted with permission from the Diagnostic and Statistical
chronic consumption of large amounts of caffeine and Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
results in a more complicated presentation. Caffeine
intoxication has long been recognized as a syndrome
produced by the ingestion of an excessive amount of order of frequency were frequent urination, restless-
caffeine. ness, insomnia, nervousness, and excitement (all
The primary features of caffeine intoxication can be which were at rates greater than 20%). In addition,
found in the diagnostic criteria from DSM-IV-TR. The 24% reported heart pounding in response to high
diagnostic decision tree for caffeine intoxication, caffeine- caffeine use (although this is not one of the DSM-
induced anxiety disorder, and caffeine-induced sleep IV-TR criteria).
disorder is shown in Figure 16-1. One study that uti- In a study of 124 general hospital patients, the most
lized a random-digit-dial telephone interview survey common somatic symptoms that individuals reported
of 162 users of caffeine examined the types of symp- as associated with caffeine intake (i.e., symptoms not
toms reported by persons who had experienced some specified as associated with either caffeine intoxication
features of caffeine intoxication. Results from that or caffeine withdrawal) were in descending order of
study showed that two-thirds of participants had ex- frequency: diuresis, insomnia, withdrawal headaches,
perienced at least one of the DSM-IV-TR symptoms diarrhea, anxiety, tachycardia, and tremulousness.
related to caffeine intoxication in the previous year. In addition to the characteristics of caffeine intoxica-
The most common symptoms reported in decreasing tion noted in DSM-IV-TR, there have been reports of
Heavy chronic use of caffeine

or
Acute caffeine use >normally used
No
No disorder Yes Yes
Yes
Restlessness Prominent anxiety, panic attacks

Prominent sleep disturbance
Nervousness and/or obsessions/compulsions
Excitement
Insomnia
Gastrointestinal disturbance
Rambling flow of thoughts
and speech
Periods of inexhaustibility Yes Yes
Tachycardia and/or
Psychomotor agitation
Yes
Evaluate for caffeine Evaluate for caffeine-induced Evaluate for caffeine-induced

intoxication anxiety disorder sleep disorder
Figure 16-1 Diagnostic decision tree for caffeine intoxication disorder, caffeine-induced anxiety disorder, and caffeine-induced sleep
disorder.
fever, irritability, tremors, sensory disturbances, tachyp- While many people may experience some of the
nea and headaches associated with cases of caffeine in- symptoms of caffeine intoxication at some point in
toxication. Although a wide variety of symptoms of caf- their lives, caffeine users do not generally seek out the
feine intoxication have been reported, the most common experience of caffeine intoxication (unlike many other
signs and symptoms appear to be anxiety and nervous- drugs of abuse). The symptoms of caffeine intoxica-
ness, diuresis, insomnia, gastrointestinal disturbances, tion tend to be perceived as unpleasant, and caffeine
tremors, tachycardia, and psychomotor agitation. users tend to titrate their dose of caffeine to avoid
intoxication.
Although caffeine intoxication is clearly related to
Course
caffeine ingestion, it is not simply the result of a person
In an individual who is not tolerant to caffeine, acute consuming a high dose of caffeine. Rather, caffeine in-
caffeine ingestion producing caffeine intoxication is toxication represents the relationship between the dose
a time-limited condition that will rapidly resolve with of caffeine consumed, the degree of acquired tolerance
cessation of caffeine use, consistent with the relatively to caffeine in that person, and the individual’s sensitiv-
short half-life of caffeine (3–6 hours). In an individual ity to caffeine.
who has caffeine intoxication superimposed on chronic Tolerance represents an acquired change in respon-
caffeine use, abrupt termination of all caffeine use may siveness by an individual as a result of exposure to
lead to caffeine-withdrawal symptoms (described in a drug, such that an increased amount of the drug is
detail in the section on caffeine withdrawal). Because required to produce the same effect, or a lesser effect
symptoms of caffeine withdrawal can partially overlap is produced by the same dose of the drug. In a person
with symptoms of caffeine intoxication (e.g., nervous- who regularly consumes caffeine, tolerance may occur
ness and anxiety), the time course of symptom resolu- to the acute effects of caffeine. Thus, a sensitive per-
tion can be expected to be protracted, lasting several son with no tolerance to caffeine might have signs and
days to a week or more. symptoms of caffeine intoxication in response to a rela-
Chapter 16 • Substance-Related Disorders: Caffeine 155
Typical Caffeine Content of Foods and Differential Diagnosis of Caffeine

Medications Intoxication
Substance Caffeine content Manic episode Panic disorder

Amphetamine/ Generalized anxiety disorder
Brewed coffee 100 mg/6 oz cocaine
Instant coffee 70 mg/6 oz intoxication
Espresso 40 mg/1 oz Sedative, hypnotic Medication-induced side effects (e.g.,
Decaffeinated coffee 4 mg/6 oz or anxiolytic akathisia)
Brewed tea 40 mg/6 oz withdrawal
Instant tea 30 mg/6 oz Nicotine withdrawal Sleep disorders
Canned or bottled tea 20 mg/12 oz
Caffeinated soda 40 mg/12 oz
Cocoa beverage 7 mg/6 oz the inclusion of caffeine in a differential diagnosis, and
Chocolate milk 4 mg/6 oz individuals who ingest caffeine more aware of the pos-
Dark chocolate 20 mg/1 oz
Milk chocolate 6 mg/1 oz sible role of excessive caffeine in somatic and psycho-
Caffeinated water 100 mg/16.9 oz logical symptoms.
Coffee ice cream or yogurt 50 mg/8 oz
Caffeinated gum 50 mg/stick
Several conditions should be included in the differ-
Caffeine-containing 32–65 mg/tablet ential diagnosis of caffeine intoxication (Table 16-2).
analgesics These include other substance-abuse-related disorders
Stimulants 100–200 mg/tablet
Weight-loss aids 40–100 mg/tablet
(amphetamine or cocaine intoxication; withdrawal
Sports nutrition 100 mg/tablet from sedatives, hypnotics, anxiolytics, or nicotine),
Source: Griffiths RR, Juliano LM, and Chausmer AL (2003) other psychiatric disorders (panic disorder, generalized
Caffeine pharmacology and clinical effects. In Principles of anxiety disorder, mania, and sleep disorders), medica-
Addiction Medicine, Graham AN, Schultz TK, Mayo-Smith M, et al.
(eds). ASAM, Chevy Chase, Maryland.
tion-induced side effects (e.g., akathisia), and somatic
disorders (e.g., pheochromocytoma, hyperthyroidism,
gastroesophageal reflux, and arrhythmia).
tively low dose of caffeine (such as 100 mg, the amount
found in a typical cup of brewed coffee) (Table 16-1),
whereas another person with a high daily consumption TREATMENT
of caffeine would show no evidence of intoxication The first step in evaluating an individual with a pos-
with a similar dose. sible diagnosis of caffeine intoxication is to obtain a
Although caffeine intoxication can occur in the con- careful history about all recent caffeine consumption.
text of habitual chronic consumption of high doses, The possible use of beverages and medications—both
probably most often it occurs after inadvertent over- prescription and over-the-counter (OTC) diet aids and
dosing. Examples include overdosing of intravenous energy pills—should be reviewed. Some beverages
caffeine to children in medical settings (e.g., for res- (e.g., caffeine-containing soft drinks) and medications
piratory stimulating effects), excessive caffeine con- (e.g., energy pills, aids to combat sleep, or diet pills)
sumption in tablet form by students who fail to appre- may not be recognized by the individual as contain-
ciate the dose being ingested (e.g., to study through the ing caffeine. The amount of caffeine acutely consumed
night), and the person who unknowingly consumes a should help clarify the diagnosis of caffeine intoxica-
highly concentrated form of caffeine (e.g., caffeinated tion, although it is important to determine whether the
coffee brewed with caffeine-containing water to create individual has been chronically consuming high doses
an especially high dose of caffeine in the coffee). of caffeine. If this is the case, the individual may be
tolerant and therefore less likely to be experiencing
caffeine intoxication. However, some clinicians have
reported that caffeine intoxication can occur even in
The diagnosis of caffeine intoxication is based on the the context of chronic caffeine use.
history and clinical presentation of the individual. Ide- If the individual is unable to provide an accurate
ally, the extent of caffeine exposure can also be as- history of recent caffeine consumption (e.g., because
sessed by a serum or saliva assay of the caffeine level. of delirium after a caffeine overdose), the individual
In the past, caffeine use has often been overlooked in should be evaluated on an emergency basis and medi-
individuals presenting with symptoms consistent with cally monitored.
a caffeine use disorder. However, it may be that there The primary approach to the treatment of caffeine
is presently a greater awareness of the deleterious ef- intoxication is to teach the individual about the effects
fects of caffeine, making clinicians more sensitive to of excessive caffeine consumption. In individuals who
are resistant to accepting the role of caffeine in their presence of three or more of the following five symp-
presenting symptoms, it may be useful to suggest a tom clusters: (1) headache, (2) fatigue or drowsiness,
trial-off caffeine as both a diagnostic and a potentially (3) dysphoric mood (including irritability, depression,
therapeutic probe. or anxiety), (4) difficulty concentrating or work diffi-
culty, and (5) nausea or vomiting.
The key steps in establishing a diagnosis of caffeine
Caffeine Withdrawal
withdrawal are to determine the history of the person’s
caffeine consumption from all dietary sources, and then
DIAGNOSIS
establish whether there has been a significant decrease
Like caffeine intoxication, there is a long history of in caffeine intake. The diagnostic decision tree for caf-
recognition that some people also can experience feine dependence and caffeine withdrawal is shown in
symptoms of caffeine withdrawal. The observation of Figure 16-2. Caffeine withdrawal is probably more com-
headaches associated with the cessation of caffeine mon than is generally recognized, and it seems there
use has been repeatedly observed and is now a well- is a tendency for people to attribute the symptoms of
established characteristic of caffeine withdrawal. Other caffeine withdrawal to other etiologies besides caffeine
symptoms, in roughly decreasing order of frequency, (e.g., having the flu, or a bad day). Caffeine withdrawal
are fatigue, sleepiness/drowsiness, dysphoric mood may be particularly common in medical settings where
(e.g., miserable, decreased well-being/contentedness), individuals are required to abstain from food and fluids,
difficulty concentrating, work difficulty, depression, such as before surgical procedures and certain diagnos-
anxiety, irritability, and influenza-like symptoms (e.g., tic tests. In addition, caffeine withdrawal may occur in
nausea/vomiting, muscle aches/stiffness, hot and cold settings where the use of caffeine-containing products
spells, heavy feelings in arms or legs) (Table 16-3). In is restricted or banned, such as inpatient psychiatric
addition to these symptoms, caffeine withdrawal may wards. The most common feature of caffeine with-
produce impairment in psychomotor, vigilance, and drawal is headache (Table 16-4). Caffeine-withdrawal
cognitive performances, increases in cerebral blood headache is typically described as gradual in develop-
flow, and changes in quantitative electroencephalogra- ment, diffuse, throbbing, and sometimes accompanied
phy (EEG) activity. by nausea and vomiting. Caffeine-withdrawal headache
The proposed criteria for a DSM-IV-TR research usually resolves within 2 to 4 days, although some sub-
diagnosis of caffeine withdrawal require the presence jects continue to report sporadic headaches for as long
of headache and one or more of the following: marked as 11 days after cessation of caffeine use.
fatigue or drowsiness, marked anxiety or depression, When symptoms of caffeine withdrawal occur, the
and nausea or vomiting. Problems with this approach severity can vary from mild to extreme. At its worst,
are that it does not reflect the independence of head- caffeine withdrawal has been repeatedly documented
ache and nonheadache withdrawal symptoms and it to produce clinically significant distress or impairment
excludes several withdrawal symptoms that have been in daily functioning and, on rare occasions, to be to-
repeatedly documented: difficulty concentrating, work tally incapacitating.
difficulty or feeling unmotivated, and irritable or dys- Individuals with high daily caffeine consumption or
phoric mood. individuals with a history of frequent headaches may
On the basis of expanded literature, it is proposed be at increased risk for developing caffeine withdrawal
that the diagnosis of caffeine withdrawal requires the or caffeine-withdrawal headaches.
Caffeine abstinence has been shown to contribute to
the incidence and severity of postoperative headache
Signs and Symptoms Associated with after general anesthesia. In individuals with a history of
Table 16-3
Caffeine Withdrawal
caffeine consumption who received caffeine on the day
Headache of a surgical procedure, the rate of postoperative head-
Fatigue, lethargy, sluggishness aches was lower than in those who received placebo.
Sleepiness, drowsiness
Dysphoric mood
Difficulty concentrating Table 16-4 Features of Caffeine-Withdrawal—Headache
Work difficulty, unmotivated
Depression Gradual onset between 12 and 40 hours
Anxiety Worse with exercise, Valsalva maneuver
Irritability Can be accompanied by flu-like symptoms (including
Nausea or vomiting nausea, vomiting)
Muscle aches or stiffness Diffuse, throbbing, severe
Daily caffeine use

>100 mg
No Yes Yes
No disorder
Desire or unsuccessful efforts Upon abstinence for >24 hours:
to quit or cut back Headache
Caffeine-related psychological Drowsiness
or physical problem Depression
Withdrawal Nausea and/or
Tolerance and/or Vomiting
Compulsive use
No
No Yes Yes
No disorder No disorder
Evaluate for Evaluate for

caffeine dependence caffeine withdrawal
Figure 16-2 Diagnostic decision tree for caffeine-dependence disorder and caffeine-withdrawal disorder.
Differential Diagnosis Clinicians do not typically think to inquire about caf-

feine use and about problematic use consistent with a
Caffeine withdrawal should be considered when evalu-
diagnosis of caffeine dependence. However, probing
ating individuals presenting with headaches, fatigue,
for evidence of caffeine dependence may be useful, and
sleepiness, mood disturbances, or impaired concentra-
it would be reasonable to focus upon the DSM-IV-TR
tion. The differential diagnosis of caffeine withdrawal
criteria for dependence that are more appropriate for
includes: viral illnesses; sinus conditions; other types
a substance that is widely available and generally cul-
of headaches such as migraine, tension, postanesthetic;
turally accepted. Thus, the clinician should probe for
other drug withdrawal states such as amphetamine or
evidence of tolerance, withdrawal, and continued use
cocaine withdrawal; and idiopathic drug reactions.
despite a doctor’s recommendation that the person cut
down or stop using caffeine, use despite other problems
TREATMENT associated with caffeine, often using larger amounts or
over a longer period than intended, or persistent desires
There have been few studies attempting to address the and/or difficulties in decreasing or discontinuing use.
treatment of caffeine withdrawal, although it has fre-
quently been observed that the symptoms of caffeine
withdrawal can be alleviated with the consumption of Differential Diagnosis
caffeine If the medical recommendation is made to The diagnosis of caffeine dependence includes symp-
eliminate or substantially reduce caffeine consump- toms that can also contribute to a diagnosis of caffeine
tion, then it may be useful to recommend a tapering intoxication and caffeine withdrawal, and both of these
dose schedule rather than abrupt discontinuation. conditions should be included in the differential diag-
nosis of an individual with possible caffeine depend-
ence. Since intoxication and withdrawal symptoms can
Caffeine Dependence
contribute to the diagnosis of dependence, conditions
that overlap with these caffeine-related disorders should
DIAGNOSIS
also be considered (and are reviewed above in their re-
Caffeine dependence, a diagnosis not officially included spective sections). When considering an individual for
in DSM-IV-TR, may be an unrecognized condition a possible diagnosis of caffeine dependence, the clini-
with a higher prevalence than is generally appreciated. cian should also consider other substance-dependence
syndromes—especially those related to stimulants—in A Method for Eliminating or Reducing

the differential diagnosis. Finally, the possible pres- Table 16-5
Caffeine Use
ence of other psychiatric conditions, such as depressive
Step 1: Use a daily diary to have the person identify all
and anxiety disorders, should be assessed. These disor- sources of caffeine in their diet, including different forms
ders may be more commonly found among individuals (i.e., brewed vs. instant coffee) and doses, for 1 week.
with caffeine dependence, and some of their presenting Step 2: Educate the patient about sources of caffeine. For
example, some individuals might not be aware that
features (e.g., low mood, anxiety, and disturbed sleep) caffeine is present in noncola soft drinks or analgesics.
can overlap with the symptoms of caffeine intoxication Calculate the total milligrams of caffeine consumed on a
and withdrawal, which commonly occur in caffeine daily basis.
Step 3: With the collaboration of the patient, generate a
dependence. graded dose reduction (i.e., fading schedule) of caffeine
use. Reasonable decreases would be 10% of the initial
dose every few days. Allow for individualization of the
TREATMENT caffeine fading. Rather than attempting to progressively
eliminate consumption of the preferred caffeine beverage,
Medical specialists frequently recommend that patients it may be useful to suggest that the patient substitute
decaffeinated for caffeinated beverages. In the case
reduce or eliminate caffeine for certain conditions, in- of coffee or tea, caffeine fading can be accomplished
cluding anxiety, insomnia, arrhythmias, palpitations by mixing caffeinated and decaffeinated beverages
and tachycardia, esophagitis/hiatal hernia, and fibro- together and progressively increasing the proportion
of decaffeinated beverage. It may be useful to have the
cystic disease Stopping caffeine use, however, can be patient maintain a diary throughout the time they are
difficult for some people. progressively decreasing their caffeine use, in order to
While there have been no systematic studies which monitor their progress.
Step 4: Discuss the possibility of relapse with the patient.
have examined the treatment of people with a clearly es- Discuss triggers (i.e., antecedent conditions) for caffeine
tablished diagnosis of caffeine dependence, a structured use and offer coping suggestions for high-risk relapse
caffeine reduction treatment program (i.e., caffeine fad- situations. Suggest that the patient continue to self-
monitor caffeine consumption.
ing) can be valuable in achieving substantial reductions
in caffeine consumption. These reports have generally
noted success with a combination of gradual tapering related to caffeine (see Figure 16-1 for caffeine intoxi-
of caffeine, self-monitoring of daily caffeine use, and cation, caffeine-induced anxiety disorder, and caffeine-
reinforcement for decreased use. When attempting to induced sleep disorder). Other diagnostic considera-
reduce or eliminate caffeine use, several steps may be tions besides caffeine-induced anxiety disorder include
useful (Table 16-5). Since many individuals are not caffeine intoxication and caffeine withdrawal, a pri-
knowledgeable about sources of caffeine in their diets, mary anxiety disorder, and an anxiety disorder due to
education and history taking are likely to be important a general medical condition. Caffeine-induced anxiety
components of treatment. During caffeine tapering it disorder can occur in the context of caffeine intoxica-
may be useful for the individual to consume extra non- tion or caffeine withdrawal, but the anxiety symptoms
caffeinated fluids, to avoid herbal preparations which associated with the caffeine-induced anxiety disorder
contain caffeine or other psychoactive drugs, to avoid should be excessive relative to the anxiety seen in caf-
the use of anxiolytics, and to maintain a diary through- feine intoxication or caffeine withdrawal. In addition
out the time they are progressively decreasing their to these conditions, substance-induced anxiety disor-
caffeine use in order to monitor their progress. Abrupt der can be produced by a variety of other psychoactive
cessation of caffeine should be avoided in order to mini- substances (e.g., cocaine).
mize withdrawal symptoms and increase the likelihood
of long-term compliance with the dietary change.
TREATMENT
Although there are no studies on the treatment of
Caffeine-Induced Anxiety Disorder
caffeine-induced anxiety disorder, guidelines for treat-
ment should generally follow those recommended for
DIAGNOSIS
the treatment of caffeine dependence (see Caffeine De-
In addition to the symptom of anxiety that can be a pendence). Thus, an initial, careful assessment of caf-
component of caffeine intoxication and caffeine with- feine consumption should be conducted, and a program
drawal, caffeine can also produce an anxiety disorder, of gradual decreasing caffeine use should be instituted
caffeine-induced anxiety disorder. (see Table 16-5). Abrupt cessation of caffeine use
The diagnosis of caffeine-induced anxiety disorder is should be avoided to minimize withdrawal symptoms
based on evidence of an anxiety disorder etiologically and to increase the likelihood of long-term compliance
with the dietary change. Given the etiological role of mental disorder, and a sleep disorder due to a general
caffeine in caffeine-induced anxiety disorder, the pru- medical condition. A caffeine-induced sleep disorder
dent course of treatment would avoid the use of phar- can occur in the context of caffeine intoxication or caf-
macological agents such as benzodiazepines for the feine withdrawal, but the sleep symptoms associated
treatment of the anxiety disorder until caffeine use has with the caffeine-induced sleep disorder should be ex-
been eliminated. A temporary caffeine-free trial may cessive relative to the sleep disturbance seen in caffeine
be useful in persuading skeptical individuals about the intoxication or caffeine withdrawal.
role of caffeine in their anxiety symptoms. As with caffeine-induced anxiety disorder, a trial of
caffeine abstinence may be useful in confirming the di-
agnosis and helping to convince a skeptical individual
Caffeine-Induced Sleep Disorder
about the etiological significance of caffeine in their
sleep disorder.
DIAGNOSIS
Psychoactive substances can produce sleep disorders
distinct from the sleep disturbances associated with TREATMENT
intoxication or withdrawal produced by that substance.
There are no studies on the treatment of caffeine-
It has long been recognized that caffeine-containing
induced sleep disorder. As for other conditions asso-
products can produce sleep disturbances, primarily in
ciated with caffeine use, such as caffeine dependence,
the form of insomnia
caffeine intoxication, and caffeine-induced anxiety
The primary feature of a substance-induced sleep
disorder, general guidelines for caffeine reduction can
disorder is a sleep disturbance directly related to a psy-
be recommended. These include an initial assessment
choactive substance. The form of the disorder can be in-
of total caffeine consumption followed by a program
somnia, hypersomnia, parasomnia, or mixed, although
of gradually decreasing caffeine use (see Table 16-5).
caffeine typically produces insomnia. In general, sleep
Abrupt cessation of caffeine use should be avoided
disturbance can often be a feature of substance intoxi-
to minimize withdrawal symptoms and to increase
cation or withdrawal (although sleep disturbance does
the likelihood of long-term compliance with the di-
not typically occur with caffeine withdrawal), and
etary change. Given the etiological role of caffeine in
caffeine-induced sleep disorder should be diagnosed in
caffeine-induced sleep disorder, the use of pharmaco-
individuals who are having caffeine intoxication only
logical agents or other interventions to improve sleep
if the symptoms of the sleep disturbance are excessive
should be avoided until an adequate trial-off caffeine
relative to what would typically be expected.
establishes the presence of a noncaffeine-related sleep
In addition to caffeine-induced sleep disorder, it is
disorder.
worth noting that complaints of poor sleep that are not
severe enough to qualify as a “disorder” may also be
related to caffeine use. The diagnosis of a caffeine-
induced sleep disorder is based on evidence of a
DIAGNOSTIC CRITERIA
sleep disorder etiologically related to caffeine (see
Figure 16-1 for caffeine intoxication, caffeine-induced ICD-10 includes caffeine-related disorders in its “Other
anxiety disorder, and caffeine-induced sleep disor- Stimulant” class which also includes amphetamines.
der). Other diagnostic considerations include caffeine This results in the ICD-10 Diagnostic Criteria for
intoxication and caffeine withdrawal, a primary sleep Research for Caffeine Intoxication being the same as
disorder, insomnia or hypersomnia related to another those for amphetamine intoxication.
CHAPTER
Cannabis
Cannabis preparations, derived from the female Can- group includes the following: cannabis intoxication,
nabis sativa plant, have been widely used for their psy- which is almost certainly induced by cannabis and con-
chotropic effects since the beginning of history. The sists of the common signs and symptoms that normally
drug is prepared in different ways in different parts follow cannabis use; cannabis intoxication delirium, a
of the world. The flowering tops and resin secreted degree of disturbance beyond that normally expected
by the female plant contain the highest concentrations with ordinary intoxication; cannabis-induced psychotic
of ∆-9-tetrahydrocannabinol (∆-9-THC), the primary disorder, which is subdivided into categories of psycho-
psychoactive component. Marijuana, the most com- sis with delusions and psychosis with hallucinations;
mon preparation, is made by drying and shredding and cannabis-induced anxiety disorder, which is also
the upper leaves, tops, stems, flowers, and seeds of the subdivided into several types as shown in Table 17-1.
plant. Hashish is a more potent preparation made by To diagnose any of the cannabis-related disorders, it
extracting and drying the resin and sometimes also the is important to obtain a detailed history of the individu-
compressed flowers. Hashish oil, which is even more al’s pattern of substance abuse (including abuse not only
potent, is distilled from hashish. Marijuana and hash- of cannabis but also of other substances) and to attempt
ish can be smoked either in the form of cigarettes or by to substantiate this report with toxicology screening for
using a pipe. Hashish, hashish oil, and less commonly
marijuana, can be mixed with tea or food and taken
orally. For the remainder of this chapter, we will refer Table 17-1 Cannabis-Related Disorders
to these preparations collectively as cannabis. Cannabis-Use Disorders
Intoxication occurs within minutes after smoking 304.3 Cannabis dependence
With physiological dependence
cannabis and typically persists for several hours. After Without physiological dependence
eating foods containing cannabis, intoxication occurs Early full remission
after approximately an hour and can persist for 8 to 24 Early partial remission
Sustained full remission
hours. The onset of intoxication after drinking cannabis Sustained total remission
steeped in tea is shorter, but not as rapid as after smok- In a controlled environment
ing, and has an intermediate duration of intoxication. 305.20 Cannabis abuse
Smoking is the predominant method of taking cannabis Cannabis-Induced Disorders
292.89 Cannabis intoxication
in most parts of the world including the United States. With perceptual disturbances
As with other substances of abuse, DSM-IV-TR 292.81 Cannabis intoxication delirium
distinguishes a number of different cannabis-related 292.11 Cannabis-induced psychotic disorder, with
delusions
diagnoses. These fall into two basic groups. The first With onset during intoxication
group is defined by adverse effects resulting from can- 292.12 Cannabis-induced psychotic disorder, with
nabis use; these include cannabis abuse and cannabis hallucinations
With onset during intoxication
dependence. The category of cannabis dependence in- 292.89 Cannabis-induced anxiety disorder
cludes a number of specifiers that indicate the presence With onset during intoxication
or absence of physiological dependence, type of remis- With generalized anxiety
With panic attacks
sion, and whether or not the individual has been in a With obsessive–compulsive symptoms
controlled environment. The second set of cannabis- With phobic symptoms
related disorders in DSM-IV-TR includes psychiatric 292.9 Cannabis-related disorder not otherwise
specified
syndromes presumed to be induced by cannabis. This
Chapter 17 • Substance-Related Disorders: Cannabis 161
Recent cannabis
use reported
Yes Yes
Behavioral or psychological
changes and two or more Psychosocial or
physical signs from health consequences
intoxication criteria of use
No No
Yes
No Yes
No
disorder
disorder
Cannabis
intoxication
Yes Yes
Yes
Use is frequent, regular,
long-standing, compulsive,
Anxiety Psychotic and/or there is evidence
Delirium of tolerance or withdrawal
symptoms symptoms
No
Yes
Yes Yes Yes
Cannabis
abuse
Cannabis
dependence
Cannabis-induced Cannabis-induced Cannabis-induced
anxiety disorder delirium psychotic disorder
Figure 17-1 Diagnostic decision tree for cannabis-use disorders.
drugs of abuse. Individuals who smoke cannabis regu- individuals rarely seek treatment, as they generally
larly can have substantial accumulations of THC in their do not acknowledge that they have a problem and are
fat stores. Thus, for weeks after cessation of smoking, de- unaware that treatment is available. Some individuals
tectable levels of cannabinoids may be found in the urine. with this disorder will respond to offers for treatment
However, a positive response on toxicology screening for because they realize that they are unable to stop use on
cannabinoids cannot establish any of the cannabis-related their own and because they notice the deleterious effect
diagnoses; it is useful only as an indicator that these diag- of compulsive use. Therefore, the diagnosis of canna-
noses should be considered. A diagnostic decision tree for bis dependence will most often be made in individuals
cannabis-related disorders is presented in Figure 17-1. who present with other psychiatric problems, such as
mood and anxiety disorders, and other substance-use
disorders (see generic DSM-IV-TR diagnostic crite-
Cannabis-Use Disorders ria for Substance Dependence, Chapter 13, page 125).
Another manner in which individuals with cannabis
DIAGNOSIS dependence may come to the attention of clinicians is
when they are arrested for possession of the substance
Cannabis Dependence
or some crime related to cannabis abuse, such as driv-
It is uncommon to see individuals who exhibit canna- ing under the influence of the drug. Nevertheless, can-
bis dependence as their only diagnosis because such nabis dependence is probably underdiagnosed in both
psychiatric and general medical populations because it (one or more years), and the acute problems associated
is not considered. with abuse have turned into the chronic problems as-
The diagnosis of cannabis dependence cannot be sociated with dependence.
made without obtaining a history indicating that the
cannabis use is impairing the individual’s ability to
Course
function either physically or psychologically. Areas
to inquire about include the individual’s performance About a third of those adolescents who try cannabis will
at work, ability to carry out social and family obliga- use it regularly for some period of time, whereas only
tions, and physical health. It is also important to find about 10% will go on to develop long-term dependence
out how much of the individual’s time is spent on can- lasting into adulthood. Even among these persistent
nabis-related activities and whether the individual users, the majority will stop use by age 30 years. Thus,
has tried unsuccessfully to stop or cut down on use it is possible to extrapolate from these figures that
in the past. Although it has been our experience that less than 2% of adults will exhibit cannabis depend-
people who have used cannabis daily over a period of ence during their 20s and that probably less than 1%
years almost invariably report tolerance to many of of adults will continue use into their 30s, suggesting a
the effects of cannabis and experience an unpleasant good prognosis for the majority of cannabis-dependent
withdrawal state if use is discontinued, neither toler- individuals under age 30 years. For the small minor-
ance nor withdrawal is necessary for the diagnosis of ity who continue to suffer from cannabis dependence
cannabis dependence. When this diagnosis is made, it into their 30s, most follow a chronic or relapsing course
can be described further by the following specifiers: similar to those who suffer from dependence on other
with or without physiological dependence, early full or substances
partial remission, sustained full or partial remission, or Cannabis abuse and dependence appear to pursue
in a controlled environment. These diagnostic distinc- a benign course in many individuals; many studies
tions must be based on the pattern of use reported by have suggested that individuals suffering from these
the individual. disorders do not differ in ability to function in soci-
ety from matched control subjects who are not users.
A few studies, have, however, described an “amoti-
Cannabis Abuse
vational syndrome” associated with chronic cannabis
Most individuals who are diagnosed with cannabis use, characterized by subjective reports of lack of di-
abuse have only recently started using cannabis (see rection, motivation, and ambition. This “amotivational
DSM-IV-TR diagnostic criteria for Substance Abuse in syndrome” appears to result from the effects of con-
Chapter 13 page 125). As with cannabis dependence, tinuous intoxication and likely resolves when cannabis
cannabis abuse is unlikely to be diagnosed unless some is discontinued.
additional condition or circumstance brings the indi-
vidual to medical attention. Teenagers often fall into
TREATMENT
this category because they spend time in supervised
environments like school and home where responsible Up until the last few years, the prevailing opinion
adults may intervene. Also, teenagers are more likely to was that cannabis use did not produce addiction and
have motor vehicle accidents while intoxicated because dependence and that cannabis users could discontinue
they are inexperienced drivers, and are more likely to use without the help of treatment programs. Although
be arrested for possession because they have a greater it is undeniably true that the majority of cannabis users
tendency to participate in risky behaviors of all types. are able to stop without assistance, it is also becoming
Although virtually all individuals with cannabis apparent that many cannabis-dependent individuals
dependence meet the inclusion criteria for cannabis cannot stop without help.
abuse, they cannot be given this diagnosis because the With the recognition that cannabis use produces
presence of cannabis dependence is an exclusion crite- dependence and withdrawal, and that cannabis-de-
rion. Undoubtedly, the vast majority of people with can- pendent individuals may benefit from treatment, many
nabis dependence would have been given the diagnosis substance abuse programs have started offering treat-
of cannabis abuse until they developed dependence. ment to people whose primary drug of abuse or de-
The difference between people with cannabis abuse pendence is marijuana. Unfortunately, these programs
and those with cannabis dependence is that the peo- are not generally designed specifically for cannabis
ple with dependence have been using more regularly dependence and they have not achieved high success
(one or more times per day) and for a longer duration rates. Similarly, many nonprofessional organizations
that offer support groups, such as Alcoholics Anony- the individual. These patients may or may not be suit-
mous (AA), Narcotics Anonymous (NA), and Self- able for support groups directed primarily at substance
Management and Recovery Training (SMART), have abuse because cannabis may represent a relatively mi-
also begun to welcome people whose primary drug is nor portion of the individual’s overall clinical picture.
cannabis. In addition, there is now a nonprofessional
support organization, Marijuana Anonymous (MA),
Refractory Individuals
started by and run for cannabis-dependent individuals.
The strongest predictor of successful outcome is Like alcohol, the most common problem in manag-
longer retention in treatment programs. Predictors of ing cannabis-use disorders is the high rate of relapse
dropping out of an outpatient treatment program and due to the wide availability of the drug and the large
presumably continuing use are young age, financial number of people who are users. Users are therefore
difficulties, and psychological stress. tempted to resume use soon after a period of treatment
To help an individual tolerate the 7- to 10-day with- when they find themselves in situations where they are
drawal period, practitioners should provide psychologi- surrounded by people using the substance. It is often
cal support (e.g., reassurance that the symptoms will useful for families and other people important in the
resolve in a little over a week) and in some cases, pro- individual’s life to get involved in the treatment to
vide pharmacological support. understand the role that they play in the individual’s
Decisions regarding pharmacotherapy must be influ- substance abuse. Some treaters advocate periodic ran-
enced by the fact that there is no strong evidence for pos- dom urine testing, which is an inexpensive and reli-
itive benefits. Thus, brief courses of symptom-focused able method of monitoring abstinence, because THC
treatment are most appropriate, if needed at all. remains present for a long time and can be detected
The foundation of maintenance treatment, as with with infrequent testing.
other types of substance-use disorders, is regular
attendance at groups that provide education and sup-
Cannabis-Induced Disorders
port. Since cannabis dependence, like other types of
substance abuse, is characterized by a chronic, relaps-
DIAGNOSIS
ing course, these groups provide an important function
by addressing issues around relapse prevention and Cannabis Intoxication
provide support for dealing with relapses when they do
There are four criteria necessary to make this diagnosis.
occur.
The first is that recent use of cannabis must be estab-
Several approaches that are more important to the
lished. This cannot be done with toxicology screening
treatment of cannabis dependence should be employed
because the result may be negative after a single episode
in addition to the basic, general substance abuse pro-
gram. For example, recent studies have found that both
adolescent and adult cannabis users frequently report
that they use cannabis to relax, or as a stress reduction DSM-IV-TR Diagnostic Criteria
or coping mechanism. This observation suggests that 292.89 CANNABIS INTOXICATION
treatment programs should teach healthier and more
effective coping mechanisms and cognitive behavioral A. Recent use of cannabis.
B. Clinically significant maladaptive behavioral or psy-
strategies for relaxation and stress reduction. chological changes (e.g., impaired motor coordination,
The most salient feature of cannabis abuse or euphoria, anxiety, sensation of slowed time, impaired
dependence is that it is often comorbid with other Axis judgment, social withdrawal) that developed during or
shortly after cannabis use.
I disorders as discussed earlier. Toxicology screening C. Two (or more) of the following signs, developing with
for other drugs of abuse is imperative because the most 2 hours of cannabis use:
common comorbid Axis I disorders are other types of (1) conjunctival injection
substance abuse. Even in the absence of an obvious (2) increased appetite
(3) dry mouth
Axis I diagnosis, psychological reasons for cannabis (4) tachycardia
use should be investigated.
It is a reasonable assumption that at least some in- tion and are not better accounted for by another men-
dividuals with Axis I disorders are adversely affected tal disorder.
by cannabis use even if they use the drug only occa- Reprinted with permission from the Diagnostic and Statistical
sionally. In such cases, the role of cannabis as an ex- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
acerbating factor must be assessed and discussed with
of smoking or, alternatively, may be positive even if the Psychological Effects of Cannabis
individual has not used the drug for a time much longer Table 17-3
Intoxication
than the period of intoxication. In addition, the symp-
Common and Transient
toms resulting from cannabis use must produce “clini- Euphoria
cally significant maladaptive behavioral or psychologi- Distortions in perception, including time perception
cal changes.” Third, the individual must exhibit some Enhancement of sensations
physical signs of cannabis use. DSM-IV-TR requires Uncommon and Transient
Dysphoria
the individual to have at least two of four signs—con- Anxiety, and less commonly panic reactions
junctival injection, increased appetite, dry mouth, and Restlessness
tachycardia—within 2 hours of cannabis use. Fourth, Depersonalization
Derealization
symptoms cannot be accounted for by a general medi- Paranoid ideation
cal condition or another mental disorder. There is a
specifier, “with perceptual disturbances,” that can be
used if the individual is experiencing illusions or hal- experienced psychological effects enjoyable. However,
lucinations while not delirious and while maintaining some individuals, especially women and inexperienced
intact reality testing. users in an unfamiliar environment, find them fright-
There has been extensive research on the effects of ening and experience anxiety and even have panic re-
acute cannabis intoxication. In addition to the symp- actions. Although all of these effects typically persist
toms and signs required for a DSM-IV-TR diagnosis, only for the period of acute intoxication, some reports
many psychological and physiological effects have have described individuals who report “flashbacks” of
been reported. Awareness of these may enhance the cannabis intoxication long after use, and depersonali-
clinician’s ability to recognize cannabis intoxication. zation persisting long after acute intoxication. At this
Physiological effects are listed in Table 17-2, and are time, there is insufficient evidence to ascertain whether
divided into commonly observed effects and rare these reports are attributable to cannabis itself, to con-
effects that have been described only after the use of founding factors such as the concomitant use of other
very high doses of cannabis. Cannabis has low toxic- drugs, or the presence of other Axis I disorders.
ity and no deaths from cannabis overdose have been In addition, cannabis use produces deficits in a
reported. Similarly, psychological effects are listed in number of neuropsychological functions, both during
Table 17-3, divided into commonly observed effects and acute intoxication and after up to a week or more of
uncommon effects. Most people find the commonly abstinence in chronic, long-term users. These tasks
include short-term memory, sustained or divided atten-
tion, and complex decision making. A study of chronic,
Physiological Effects of Cannabis long-term users found that these deficits were generally
Table 17-2
Intoxication
reversible after 28 days of abstinence.
Common and Transient
Tachycardia
Hypertension Cannabis Intoxication Delirium
Thirst
Increased appetite We have not located any original reports of this entity,
Constipation although it is mentioned in various reviews and is in-
Decreased intraocular pressure
Mydriasis cluded in DSM-IV-TR. Thus, if cannabis intoxication
Mild bronchoconstriction followed by bronchodilation delirium does occur in neurologically intact individuals,
Increased reaction time it is probably a rare complication. If the delirium does
Impaired coordination
Distorted time perception not resolve within 24 to 48 hours, it is almost certainly
Decreased libido a result of an underlying neurological or medical condi-
Mild analgesia tion. Therefore, in an individual with delirium, even if
Mild anti-emetic effects
recent cannabis use has been reported, a full diagnostic
Uncommon and Transient
Ataxia workup should be performed to rule out a concomitant,
Ptosis treatable neurological condition.
Miosis Cannabis-induced psychotic disorder or cannabis-in-
Drowsiness
Bradycardia duced anxiety disorder are not generally diagnosed unless
Hypotension the symptoms are in excess of those usually associated
Peripheral vasoconstriction with the intoxication or withdrawal state and are suffi-
Hypothermia
ciently severe to warrant independent clinical attention.
Cannabis-Induced Psychotic Disorder persist, other diagnoses should be considered. Simi-

larly, although there are few data regarding the course
There are two subtypes of cannabis-induced psychotic
of the other cannabis-induced disorders, it appears that
disorder: one featuring delusions, the other hallucina-
cannabis-induced psychotic and anxiety disorders as
tions. The diagnosis of this disorder is readily made in
well as cannabis intoxication delirium rarely persist
individuals who have psychotic symptoms that appear
beyond the period of acute intoxication with the drug.
immediately after ingestion of cannabis. However, a
careful history is required to establish whether the indi-
vidual has a preexisting psychotic disorder (as is often TREATMENT
the case in such situations) or whether the symptoms
arose de novo after cannabis consumption. There is lit- Uncomplicated cannabis intoxication rarely comes to
tle evidence that cannabis-induced psychotic disorders clinical attention, and if it does, it does not require
can arise in previously asymptomatic individuals. treatment other than reassurance, as it is a self-limiting
condition. Similarly, as suggested in the previous sec-
tions, symptoms of delirium, psychosis, or anxiety as-
Cannabis-Induced Anxiety Disorder sociated with cannabis use typically resolve promptly
This disorder may be further described by the follow- after the period of acute intoxication is past. Again,
ing specifiers: with generalized anxiety, with panic at- no treatment is necessary other than keeping the indi-
tacks, with obsessive–compulsive symptoms, and with vidual safe and providing reassurance that symptoms
phobic symptoms. People who experience anxiety after caused by the drug will stop, as these are also self-
using cannabis are typically inexperienced users who limiting conditions. If the symptoms continue after
react to the novel experiences of perceptual distortions more than 24 to 48 hours of abstinence from the drug,
and intensified sensations with anxiety and even panic the possibility of another Axis I diagnosis must be
reactions, rather than enjoyment. Women are more considered. In such cases, treatment should then be di-
likely than men to experience cannabis-induced anxi- rected at the primary Axis I disorder.
ety. If symptoms of severe anxiety or panic persist for
24 to 48 hours after the period of acute intoxication,
they are likely due to an underlying mental disorder
DIAGNOSTIC CRITERIA
that must be diagnosed and treated.
The ICD-10 and DSM-IV-TR criteria sets for cannabis
intoxication are virtually identical. While DSM-IV-TR
Course
does not include a category for cannabis withdrawal,
Cannabis intoxication is a self-limiting state that remits ICD-10 does include such a category (called “Cannabi-
as cannabis is metabolized and eliminated from the noid Withdrawal State”) without the inclusion of “de-
body. If symptoms suggestive of cannabis intoxication finitive diagnostic criteria.”
CHAPTER
Cocaine
Cocaine, a central nervous system stimulant produced When evaluating an individual regarding the possi-
by the coca plant, is consumed in several prepara- ble presence of a cocaine-related disorder, the initial
tions. Cocaine hydrochloride powder is usually snorted evaluation period should include the collection of a
through the nostrils, or it may be mixed in water and complete history of all substance abuse, which is es-
injected intravenously. Cocaine hydrochloride powder is sential to accurate diagnosis and appropriate treat-
also commonly heated (“cooked up”) with ammonia or ment. Figure 18-1 shows a diagnostic decision tree for
baking soda and water to remove the hydrochloride, thus cocaine-related disorders. The history includes the
forming a gel-like substance that can be smoked (“free- circumstances under which each drug was used, the
basing”). “Crack” cocaine is a precooked form of co- psychoactive effects sought and obtained, the route of
caine alkaloid that is sold on the street as small “rocks.” administration, and the frequency and amount of each
drug used. Cocaine abusers frequently abuse other
drugs and alcohol to enhance euphoria or to alleviate
DIAGNOSIS
dysphoric effects associated with cocaine abuse (agita-
The state of intense euphoria produced by cocaine in- tion, paranoia). A thorough history with diagnosis of
toxication is a powerful reinforcer and can lead to the other substance-use disorders is important to treatment
development of cocaine-use disorders in many individ- planning. Individuals may need detoxification from
uals, although only 10–16% of those who try the drug other substances prior to initiation of cocaine abuse
go on to develop these disorders. The route of admin- treatment. It is also important to monitor clinically for
istration is strongly correlated with the development relapses to any substance abuse during treatment for
of cocaine-use disorders, in that the intravenous and cocaine-use disorders because the use of other drugs
smoked routes of administration allow rapid transport and alcohol often leads to resumption of cocaine abuse.
of the drug to the brain, producing intense effects that In addition, a thorough history of current and previ-
are short-lived. Rapid tolerance to euphoria occurs and ous substance abuse is important so that treatment can
plasma concentrations are not correlated with peak eu- be individualized and individuals can be helped in de-
phoria, producing a need for frequent dosing to regain veloping coping skills that will assist them in specific
euphoric effects (binge use) that can place the cocaine situations that they identify as placing them at high risk
abuser at a risk for medical and psychiatric complica- for relapse.
tions of cocaine abuse. A careful psychiatric history with particular atten-
While the question of whether cocaine is physiologi- tion to onset of psychiatric symptoms in relation to
cally addictive is not completely clear, the psychologi- drug use is essential. The determination of a premorbid
cal addiction alone is powerful and can completely psychiatric illness is critical to providing appropriate
dominate the life of the cocaine abuser. Binge use of treatment. For persons in whom substance abuse is
cocaine may be followed by what has been described as an attempt to self-medicate an underlying mental ill-
a mild withdrawal syndrome characterized by dyspho- ness, the introduction of psychotropic medication in
ria and anhedonia. Cocaine withdrawal may resemble a conjunction with ongoing treatment for the substance
depressive disorder, in some cases requiring emergent abuse will improve both the mental disorder as well as
treatment. Some combinations of these consequences the substance-use disorder(s). Conversely, the evalu-
of cocaine abuse are usually responsible for the identi- ation of temporal onset of psychiatric symptoms may
fication and diagnosis of individuals with cocaine-use preclude erroneous use of psychotropic medication in
disorders and referral to substance-abuse treatment. cases in which the psychiatric symptoms are in fact
Chapter 18 • Substance-Related Disorders: Cocaine 167
Cocaine Recent cocaine use (by history Cocaine

intoxication or urine toxicology screen) withdrawal
Yes Yes
Yes
Intoxicated
Behavioral change, impaired No No Withdrawal
No
No cocaine Recurrent problems Recent cessation of heavy or
function, autonomic instability,
use disorder over 12 months prolonged cocaine use, dysphoria,
cognitive deficit,
abnormal movements neurovegetative symptoms
Yes
No
One or more abuse criteria
Recurrent cocaine use:
No Resulting in failure to fulfill obligations No Tolerance or No cocaine
In hazardous situations
withdrawal use disorder
With cocaine-related legal problem
Despite persistent or recurrent
psychosocial problems
Yes
No
Any of dependence criteria 3−7

e.g., (3) increasing intake, (4)
inability to cut down or control use,
Yes Yes
Both tolerance (5) increasing time spent in activities
and withdrawal necessary to obtain cocaine,
(6) important activities given up because
of cocaine use, (7) continued use despite
significant negative consequences
No
Yes
Fewer than three of Any two of Yes Cocaine

dependence criteria 3−7 dependence criteria 3−7 dependence
No
Yes Cocaine
withdrawal
Yes
Yes No No No cocaine
Cocaine abuse Any abuse criteria Withdrawal
use disorder
Figure 18-1 Diagnostic decision tree for cocaine-use disorders.

cocaine-induced and spare the individual exposure to lability, grandiosity, impaired judgment, increased
the potential side effects of these medications. psychomotor activity, hypervigilance or paranoia, and
sometimes hallucinations (visual, auditory, or tactile)
may occur. Because cocaine and amphetamines are
Cocaine Dependence
both part of the same drug class, i.e., stimulants, the
The DSM-IV-TR defines the essential features of sub- criteria set for cocaine intoxication and withdrawal are
stance dependence as a cluster of cognitive, behavioral, identical to the criteria sets for amphetamine intoxica-
and physiological symptoms indicating continued use tion and withdrawal (see DSM-IV-TR diagnostic crite-
of the substance despite significant consequences of ria, Chapter 15, page 148–149). Physical symptoms that
use (see Chapter 13, page 125 for the DSM-IV-TR di- can accompany cocaine intoxication include hyperten-
agnostic criteria for Substance Dependence). There is sion, tachycardia, hyperthermia, pupillary dilation,
a pattern of administration that usually results in toler- nausea, vomiting, tremor, diaphoresis, chest pain, ar-
ance to and compulsive self-administration of the drug rhythmia, confusion, seizures, dyskinetic movements,
and may produce a withdrawal syndrome on cessation dystonia, and, in severe cases, coma. These effects are
of drug use. Cocaine dependence can develop quickly more frequently seen in high-dose binge users of co-
after initiation of use because of the potent euphoria caine. Cardiovascular effects are probably a result of
produced by the drug. The route of administration is sympathomimetic properties of cocaine (i.e., release
related to the development of cocaine dependence; of norepinephrine and blockade of norepinephrine
smoked and intravenous routes are more highly cor- reuptake).
related with dependence than the intranasal route of
administration.
Cocaine Withdrawal
Cocaine has a short half-life requiring frequent dos-
ing to maintain the “high” (binge use). Binges may be Cocaine withdrawal develops within a few hours to a
separated by several days while the individual recovers few days after stopping or reducing cocaine use that
or attempts to obtain more money for drug purchase. has been heavy and prolonged (see DSM-IV-TR diag-
Tolerance to cocaine effects develops quickly, resulting nostic criteria, Chapter 15, page 149). The syndrome
in larger amounts of drug use with time. This is often is characterized by dysphoria and two or more physio-
associated with mental or physical complications of logical changes including fatigue, vivid and unpleasant
use, including paranoia, aggressive behavior, anxiety dreams, insomnia or hypersomnia, increased appetite,
and agitation, depression, and weight loss. Withdrawal and psychomotor agitation or retardation. Anhedonia
symptoms, most prominently dysphoric mood, may be and craving for cocaine can be part of the withdrawal
seen, but are usually short-lived and clear within sev- syndrome. Depression and suicidal ideation are the
eral days of abstinence. most serious complications and require individualized
assessment and treatment. The syndrome may last up to
several days but generally resolves without treatment.
Cocaine Abuse
Substance abuse is described by DSM-IV-TR as a
Other Cocaine-Induced Disorders
maladaptive pattern of substance use demonstrated
by recurrent and significant adverse consequences re- DSM-IV-TR also specifies additional cocaine-induced
lated to repeated use (see Chapter 13, page 125 for the disorders described in other diagnostic groupings with
DSM-IV-TR diagnostic criteria for Substance Abuse). which they share phenomenology (Table 18-1). These
The intensity and frequency of use are less in cocaine include cocaine intoxication delirium, cocaine-induced
abuse than in cocaine dependence. Episodes of abuse psychotic disorder, cocaine-induced mood disorder,
may occur around paydays or special occasions and cocaine-induced anxiety disorder, cocaine-induced
may be characterized by brief periods (hours to days) sleep disorder, and cocaine-induced sexual dysfunction.
of high-dose binge use followed by longer periods of These disorders are diagnosed instead of intoxication
abstinence or nonproblem use. or withdrawal only if symptoms are in excess of those
usually associated with cocaine intoxication or cocaine
withdrawal and warrant independent clinical attention.
Cocaine Intoxication
In addition, the clinician should pay careful attention to
The clinical effects of cocaine intoxication are charac- the temporal relationship of the psychiatric symptoms
terized initially by euphoria (referred to as “high”) and and cocaine abuse. Symptoms that are severe enough to
also include agitation, anxiety, irritability or affective warrant consideration of one of these diagnoses should
Other DSM-IV-TR Cocaine-Induced

cocaine-induced euphoria and begins to compulsively
Table 18-1 pursue this effect. These behaviors become pivotal in
Disorders
the lives of cocaine abusers, who continue drug abuse
292.89 Cocaine intoxication
Specify if: with perceptual disturbances despite the presence of increasing personal and social
292.0 Cocaine withdrawal consequences.
292.81 Cocaine intoxication delirium The psychoactive effects of cocaine are similar to
292.11 Cocaine-induced psychotic disorder, with
delusions those of amphetamine; the main difference in terms of
Specify if: with onset during intoxication abuse liability is in cocaine’s much shorter duration of
292.12 Cocaine-induced psychotic disorder, with action. Whereas the plasma elimination half-life for co-
hallucinations
Specify if: with onset during intoxication caine is approximately 90 minutes, this drug produces
292.84 Cocaine-induced mood disorder pharmacodynamic tachyphylaxis, resulting in rapidly
Specify if: with onset during intoxication/ diminishing psychoactive effects in the presence of
with onset during withdrawal
292.89 Cocaine-induced anxiety disorder continued cocaine in the plasma. This phenomenon
Specify if: with onset during intoxication/ explains the “half-life” of cocaine-induced euphoria,
with onset during withdrawal
292.89 Cocaine-induced sexual dysfunction
(which is approximately 45 minutes after intranasal use
Specify if: with onset during intoxication and 5 minutes after intravenous and smoking adminis-
292.89 Cocaine-induced sleep disorder tration), as well as characteristic binge use in which co-
Specify if: with onset during intoxication/
with onset during withdrawal caine is repetitively administered over short intervals.
292.9 Cocaine-related disorder not otherwise During binge use, the drug may be administered as fre-
specified quently as every 10 minutes, resulting in rapid mood
Source: Data Reprinted with permission from the Diagnostic and changes. Cocaine binges reportedly can last as long as
Statistical Manual of Mental Disorders, 4th ed., Text Rev. Copyright
2000 American Psychiatric Association.
7 days, although the average length is 12 hours.
Uncontrolled use of cocaine often begins with either
increased access and resultant escalating dosages and
also dissipate with continued abstinence from cocaine. frequency of administration or a change from intrana-
Symptoms that worsen after cessation of cocaine use in sal use to a route of administration with more rapid on-
a period of 1 to 4 weeks should be reevaluated and other set of effects (i.e., intravenous or smoked). These char-
Axis I or Axis III disorders considered, with modifica- acteristics are integral to the development of high-dose
tion of the treatment plan as clinically indicated. binging with cocaine. Such binges produce extreme eu-
phoria and vivid memories. These memories are later
contrasted with current dysphoria to produce intense
Course
craving, which perpetuates the binge-use pattern. Ad-
Cocaine produces a sense of intensified pleasure in dicts report that during binge use, thoughts are focused
most activities and a heightened sense of alertness exclusively on the cocaine-induced effects. Normal
and well-being. Anxiety and social inhibition are de- daily needs, including sleep and nourishment, are ne-
creased. Energy, self-esteem, and self-perception of glected. Responsibilities to family and employer and
ability are increased. There is enhancement of emotion social obligations are given up. This continues until the
and sexual feeling. Pleasurable experiences, although supply of cocaine is exhausted.
heightened, are not distorted and hallucinations are Binges are often separated by several days of absti-
usually absent. The person engaging in low-dose co- nence; cocaine-dependent individuals average one to
caine use often receives positive feedback from others three binges per week. This is in contrast to use pat-
responding to the user’s increased energy and enthu- terns for opiate and alcohol dependence, which often
siasm. This, in combination with the euphoria experi- produce physiological dependence necessitating daily
enced by the user, can be reinforcing, and cocaine use consumption to prevent withdrawal symptoms. This
is perceived as free of any adverse consequences. The differentiation is crucial to an understanding of the
duration of cocaine’s euphoric effects depends on the syndrome of cocaine dependence. Although the pre-
route of administration. The faster the drug is absorbed diction of development of cocaine-use disorders is not
and occupies receptors of the “brain rewarding region,” possible on an individual basis, it is clear that those who
the more intense the euphoric effects. progress to binge use of the drug will be significantly
Cocaine users quickly learn that higher doses are as- affected and constitute the treatment-seeking popu-
sociated with intensified and prolonged euphoria, relation. The cocaine abuser is likely to be ambivalent
sulting in increasing use of the drug and progression about the need for treatment, and the treatment drop-
to cocaine dependence. The abuser is focused on the out rate is high (ranging from 38% to 73%). Dropout
usually occurs early in treatment (during the initial the diagnosis of a comorbid primary mental disorder
evaluation process). can be challenging to make in cocaine abusers because
Newly abstinent cocaine abusers may experience a psychiatric symptoms may be the result of cocaine
triphasic abstinence pattern, although this varies by abuse or acute abstinence. When mental disorders co-
individual, that includes a period of acute abstinence, occur with cocaine-use disorders, it is important to
sometimes referred to as the “crash,” lasting several provide treatment for both disorders. Cocaine-use dis-
hours to several days consisting of dysphoria, fatigue, orders will not generally resolve with treatment of the
insomnia or hypersomnia, increased appetite, and ei- mental disorder alone, nor will substance-abuse treat-
ther psychomotor agitation or retardation, subsequent ment resolve a comorbid mental disorder.
to the more intensive “crash” phase. A more chronic
withdrawal period sometimes occurs characterized by
Medical Complications of Cocaine Abuse
minor depressive symptoms and cocaine craving last-
ing 2 to 10 weeks. This may then be followed by an Cardiac toxicity is one of the leading causes of mor-
extinction phase characterized by intermittent drug bidity and mortality associated with cocaine use. The
craving that becomes increasingly manageable with risk of myocardial infarct is well established in cocaine
continued abstinence. use and is not related to dose, route, or frequency of
Like other drug- and alcohol-use disorders, cocaine- administration. The risk of acute myocardial infarction
use disorders are chronic relapsing illnesses that present is increased 24-fold in 1 hour immediately following
substantial challenges in the treatment process. Cocaine cocaine use in persons who are otherwise at a relatively
abusers are at high risk for relapse, particularly in the low risk for such events.
first few months of treatment related to acute craving of- Cocaine use also is associated with a wide range of
ten in the context of ongoing psychosocial stressors that cardiac dysrhythmias, including sinus tachycardia, si-
result from or have been exacerbated by cocaine abuse. nus bradycardia, supraventricular and ventricular tach-
Newly abstinent cocaine abusers often lack adequate ycardia, ventricular premature contractions, ventricu-
coping skills necessary to avoid cocaine use, which lar tachycardia and fibrillation, torsades des pointes,
take time to acquire in the treatment process. Although and asystole. Life-threatening dysrhythmia caused by
the ability to cope with cocaine craving improves with cocaine in the absence of myocardial ischemia is rare.
continued abstinence, relapse to cocaine abuse or other Intranasal abuse of cocaine has been associated with
drug and alcohol abuse will continue to be a risk for a number of medical complications including chronic
those with a history of a cocaine-use disorder who re- sinusitis, septal perforation, subperiosteal abscess,
lapse to cocaine abuse. Repeated treatments may be re- pneumomediastinum, pneumothorax, and pulmonary
quired for those with cocaine-use disorders. Treatment edema. The presence of pulmonary edema in a young,
modalities include inpatient hospitalization for medical otherwise healthy individual, without predisposing risk
or psychiatric complications of cocaine abuse, partial factors, should alert the physician to the possibility of
hospital programs, self-help groups, psychotherapy cocaine abuse.
(usually group or family therapy for individuals with Cerebrovascular accidents related to cocaine use
primary cocaine-use disorders), or some combination have been well documented in the medical literature.
of these treatments according to the clinical presenta- Cerebral infarct, subarachnoid hemorrhage, intrapa-
tion of the individual (see later in the chapter). renchymal hemorrhage, and intraventricular hemor-
rhage have been observed as acute complications of
cocaine use. Seizures were one of the earliest known
Comorbidity with Other Mental Disorders
complications of cocaine abuse. Cocaine produces hy-
Comorbid conditions related to cocaine abuse are abuse perpyrexia, which in combination with its effects on
of other substances and comorbid mental disorder. Sev- neurotransmitters may contribute to the development
eral studies have documented the high rate of comorbid of seizures. Seizures may occur as a primary effect of
mental disorders in cocaine abusers entering treat- cocaine owing to its ability to lower the seizure thresh-
ment. These disorders include mood disorders (major old or may be secondary to other central nervous sys-
depressive disorder, bipolar disorders), schizophrenia, tem or cardiac events precipitated by cocaine use.
posttraumatic stress disorder, attention-deficit/hyper- Recently, acute renal failure as a result of rhabdomy-
activity disorder, anxiety disorders, and antisocial per- olysis has been recognized as an important compli-
sonality disorder. cation of cocaine abuse. Pregnancy may increase the
It is important to note that comorbid psychiatric ill- risk of rhabdomyolysis and renal failure. Renal failure
nesses are common among cocaine users. Furthermore, may progress rapidly in the context of cocaine-induced
Major Medical Complications Associated

The two primary goals of cocaine treatment are (1)
Table 18-2 the initiation of abstinence through disruption of binge
with Cocaine Abuse
cycles and (2) the prevention of relapse. Treatment
Cardiovascular
Myocardial infarct planning to achieve these goals must be considered in
Arrhythmias the context of the individual clinical presentation of
Aortic dissection the patient. Initial assessment to determine immediate
Cardiomyopathy
needs is necessary to determine the most appropriate
Respiratory
Pneumonitis (associated with smoked cocaine)
level of care (inpatient or outpatient treatment) as well
Pulmonary edema as other psychiatric and medical considerations impor-
Nasal septal perforation, chronic sinusitis (associated with tant to the development of the treatment plan.
intranasal inhalation)
The majority of those with cocaine-use disorders
Central Nervous System are most appropriately treated in an outpatient setting.
Hyperpyrexia
Seizure Outpatient treatment may vary with provider but gen-
Cerebral infarct erally includes multiple weekly contacts for the initial
Subarachnoid hemorrhage
Intraparenchymal hemorrhage
months of treatment because less frequent contact is
Intraventricular hemorrhage not effective in the initiation or maintenance of ab-
Renal stinence. These sessions consist of some combination
Renal failure secondary to rhabdomyolysis of individual drug counseling, peer support groups,
Obstetrical family or couples therapy, urine toxicology monitor-
Premature labor
Placental abruption ing, education sessions, psychotherapy, and psychiat-
Complications of Intravenous Use ric treatment that may include pharmacotherapy for
Infectious diseases (HIV, hepatitis) cocaine addiction or comorbid mental disorders. In-
Endocarditis patient treatment is reserved for those who have been
Cellulitis Abscesses
refractory to outpatient treatment, whose compulsive
Psychiatric
Depression
use of cocaine represents an imminent danger (e.g.,
Suicidality suicidality associated with cocaine toxicity or acute
Psychosis abstinence), who have other comorbid mental disor-
ders or general medical conditions, or who are depend-
ent on more than one substance and require monitored
rhabdomyolysis and dialysis may be necessary for some detoxification.
individuals. The treatment of cocaine-use disorders should be
The major medical complications of cocaine abuse undertaken in the context of a thorough understanding
are summarized in Table 18-2. of the disease (Table 18-3). One of the greatest chal-
lenges in the early stages of cocaine treatment is to
prevent an early dropout. It has been estimated that up
TREATMENT
to 80% of individuals drop out of treatment programs.
Treatments for cocaine-use disorders continue to Frequent clinical contacts especially in the early weeks
evolve and have been shown to be effective. In a large- of treatment can help establish a therapeutic alliance
outcome study, a comparison of short-term inpatient that will assist in engaging the cocaine user in the
treatment programs, outpatient drug-free programs, treatment process. Many programs offer 3 to 6 days
and long-term residential programs specifically for per week of substance-abuse treatment sessions within
those with cocaine-use disorders was undertaken. Of outpatient partial hospital programs or intensive out-
those who received any treatment, 24% relapsed to patient chemical dependency programs. Assessments
weekly cocaine use, a large decrease over the 73% re- by the program physician and counseling staff can
lapse rate in the year prior to treatment. Some required identify other areas requiring specific interventions
an additional treatment program (18%) in the year fol- (comorbid general medical condition or mental dis-
lowing treatment, which is not an uncommon scenario orders) and can expedite the initiation of appropriate
for this chronic, relapsing disorder. Those with high pharmacotherapies. These interventions will increase
levels of psychosocial, medical, or psychiatric prob- treatment retention.
lems at intake or less than 90 days of treatment had Initial treatment should include the encouragement
higher cocaine use in the follow-up period. Treatment of abstinence from all drug and alcohol use. Individu-
periods of 90 days or more were associated with better als who abuse alcohol and marijuana often do not per-
substance-abuse outcomes. ceive these drugs as problems. Education regarding the
Table 18-3 Cocaine-use Disorders: Recovery and Treatment
Parameter Acute Abstinence Withdrawal Phase Extinction Phase

Duration Several hours to four days 2 to 10 weeks 3 to 12 months
Treatment Symptomatic Initiate psychotherapy Continue psychotherapy, decrease
May need hospitalization Individual/group therapy intensity with continued
for medical or Self-help groups, other therapies, abstinence; self-help groups and
psychiatric care and e.g., family, marital, individual, as additional interventions developed
assessment needed for patients as needed
Pharmacotherapy Benzodiazepines for None approved specific for cocaine-use Unusual to initiate in this phase
anxiety, agitation, disorders Taper and discontinue
paranoia Consider disulfiram for cocaine– pharmacotherapy for cocaine
Antipsychotics (sparingly) alcohol abuse previously refractory abuse and monitor clinically
for severe psychosis or to treatment; psychotropics for
agitation comorbid psychiatric disorders
or cocaine-related disorders;
pharmacotherapies for other
substance use disorders
use of such drugs as conditioned stimuli to the use of Success with initiating and maintaining abstinence
cocaine should be emphasized. The “disease model” over several months is followed by a reduced fre-
of chemical dependency may be used to assist in the quency of contact (e.g., a decrease to weekly group or
initiation of abstinence. Emphasis is placed on the indi- individual therapy sessions). The focus should be on
viduals recognizing chemical dependency as a disease maintaining a commitment to abstinence, addressing
needing treatment to control, but one for which there renewed denial, and continued improvement of inter-
is no cure. Comprehensive drug education should also personal skills. Participation in self-help groups should
be provided in the initial treatment phase. Frequent continue to be encouraged. Self-help groups based on
contact with a drug counselor is an important part of 12-step principles encourage individuals to continue
treatment. Individual, group, and (where clinically in- to view themselves as addicts in recovery—a cogni-
dicated) family or marital therapy should be available. tive structuring that many recovering drug abusers find
Attendance at 12-step or other self-help groups is often helpful in maintaining sobriety.
a useful adjunct to treatment and can be particularly
helpful during the early stages of treatment when sup-
port for sobriety is essential.
The early recovery phase of treatment varies in dura- A variety of psychotherapeutic strategies for the treat-
tion from 3 to 12 months and is characterized by mul- ment of cocaine-use disorders have been described
tiple weekly contacts and participation in therapeutic (Table 18-4). In contrast to opiate addiction, for which
modalities with the goal of initiation and maintenance psychotherapies alone are insufficient, there appear to
of abstinence. The focus during early recovery should be at least some subpopulations of cocaine abusers for
be on relapse prevention and development of new and whom psychotherapy alone may be adequate. Behavio-
adaptive coping skills, healthy relationships, and life- ral therapies, in particular cognitive–behavioral ther-
style changes that will facilitate abstinence. apy and contingency management approaches, have
Relapses are common during early recovery. Indi- been demonstrated to be effective treatments for some
viduals often feel pleased about their progress in treat- cocaine-dependent individuals.
ment, become overly confident about their ability to
control use, and test themselves by deliberately encoun-
tering what they know to be a high-risk situation for Psychotherapies: the Mainstay of Treatment
Table 18-4
for Cocaine-use Disorders
their drug use. Individuals should be informed about
the potential for relapse from the start of the treatment Interpersonal therapy
process. Relapse should, however, also trigger a review Supportive expressive therapy
Cognitive–behavioral therapy/Relapse-prevention therapy
of the treatment plan and consideration of the need for Voucher-based treatment
additional interventions or whether a higher level of Individual and group drug counseling
care is needed to assist the individual in the recovery Systematic cue exposure
Self-help groups (e.g., Cocaine Anonymous)
process.
Although the name implies focus on the prevention of there is no effective pharmacotherapy with which to
relapse, in fact this method employs several strategies treat the disorder; therefore, the term relates to a differ-
intended to facilitate abstinence. Specific techniques ent set of occurrences in the treatment setting. Recidi-
in cocaine-addiction treatment include exploring the vism to cocaine use, treatment dropout, and multiple
positive and negative consequences of continued use, treatment experiences are common. Such problems are
self-monitoring to recognize drug cravings early on a reflection of the severity of illness and parameters of
and to identify high-risk situations for use, and devel- relative treatment refractoriness. Comorbid substance
oping strategies for coping with and avoiding high-risk use and mental disorders contribute to treatment re-
situations and the desire to use. Research indicates that fractoriness. Lack of accurate diagnosis and treatment
the skills individuals learn through relapse-prevention contributes to relapse potential in the form of continued
therapy remain after the completion of treatment. In exposure to high-risk situations and lifestyle instability
two long-term outcome studies, most people receiv- that are associated with ongoing substance abuse. Con-
ing this cognitive–behavioral approach maintained the tinued psychiatric symptoms that individuals attempt
gains they made in treatment throughout the year fol- to relieve through cocaine use contribute to poor treat-
lowing treatment and a proportion of study participants ment outcome.
continued to make gains following the termination of The psychological addiction associated with co-
the 12-week CBT treatment period. caine abuse can be disabling. Because physiologi-
Psychotherapeutic approaches are often delivered cal dependence, if it does occur, generally does not
in the context of multimodal treatment programs require pharmacotherapy, treatment referrals for in-
and nearly all substance-abuse clinicians emphasize dividuals with primary cocaine dependence but no
the importance of self-help groups such as Cocaine other acute mental disorder or general condition, are
Anonymous. generally to an outpatient drug abuse treatment clinic.
Individual and group drug counseling focuses di- Those unable to initiate and maintain sobriety in an
rectly on reducing or stopping the use of drugs. It also outpatient drug treatment program should be evalu-
addresses related areas of impaired social and oc- ated for more intensive forms of treatment. Manage-
cupational function as well as the content and struc- ment of these individuals should include consideration
ture of the patient’s individualized recovery program. of a variety of options including pharmacotherapy (see
Through its emphasis on short-term behavioral goals, the earlier section on somatic therapies for cocaine
drug counseling helps the patient develop coping strat- abuse) and programs that offer a graded increase in
egies and tools for abstaining from drug use and then structure. Such individuals may need initial detoxi-
maintaining abstinence. fication from another drug or alcohol that could re-
quire several days of inpatient treatment. Those who
are determined to need intensive outpatient treatment
Somatic Therapies
often attend these programs 5 days a week initially,
The development of pharmacological treatments for and sessions last an average of about 4 hours. There
cocaine abuse has been based on the premise that an is a gradual reduction in the number of sessions per
altered neurochemical substrate underlies the chronic, week as the period of sobriety lengthens. Such pro-
high-intensity (binge) use and acute abstinence/with- grams are of flexible duration, but a full program usu-
drawal that follows binge use. This neuroadaptation ally requires at least 12 weeks. This program can be
model has also served as a basis for a number of studies followed with resumption of the outpatient treatment
that have evaluated the clinical utility of psychotropic clinic level of care, which takes place fewer days per
agents that, based on their pharmacological profile, week and with shorter sessions. Those with comorbid
might possess anticraving properties, block euphoria, psychiatric disorders should be referred to dual diag-
or decrease cocaine abstinence symptoms. To date, nosis specialty treatment programs when available.
no medication has emerged as an accepted effective Dual diagnosis speciality programs differ from tra-
pharmacotherapy. ditional substance-abuse treatment programs in that
they have a dual diagnosis treatment orientation, with
an increased use of psychotropic medication, longer
Treatment Refractoriness
lengths of stay, and greater tolerance for relapse and
The term “treatment refractoriness” sometimes implies medication nonadherence.
a lack of response to a therapeutic trial of a pharmaco- Individuals who have failed other forms of treat-
therapy. In the case of cocaine dependence, however, ment may be referred to residential programs, although
the number of these programs is shrinking, given the tion of drug craving and acquisition of effective re-
constraints on treatment that have occurred as a result lapse-prevention skills.
of managed care and erosion of benefits provided by
health insurers for treating substance-use disorders.
Residential programs vary in length and must be tai-
DIAGNOSTIC CRITERIA
lored to the needs of the patient. Such programs can
be important to the initiation of abstinence. These The ICD-10 and DSM-IV-TR criteria sets for cocaine
programs allow sufficient time in a drug-free and intoxication and withdrawal are almost the same ex-
supportive environment so that the recovery process cept that the ICD-10 criteria set for withdrawal includes
can begin, as well as provide adequate time for reduc- drug craving as an additional item.
CHAPTER
Hallucinogens and MDMA
Human ingestion of hallucinogens can be traced back States and Europe. Within two decades it assumed cult
thousands of years. In the Americas, Europe, and status among the ministry, academics, and students,
Africa, hallucinogens were used for consecration dur- culminating in an epidemic of abuse in its third decade
ing religious ceremonies, for divination, and as tools starting in the late 1960s. Congressional reaction came
for rites of passage and shamanic healing. The major- in the form of the Drug Abuse Control Amendments of
ity of these botanicals grow in the Americas. In South 1965 and 1968, which choked off drug supplies to re-
and North America, cacti containing the hallucinogen searchers, and criminalized drug sale and use. The sci-
mescaline are still widely used by a number of Native entific impact of these laws was to retard the advance of
American tribes. In South America, boiled potions are knowledge in this field for a generation.
made from Trichocereus species, a cactus containing The development and chemical identification of ad-
about 1% mescaline. A much more potent mescaline- ditional agents causing LSD-like mental symptoms,
containing cactus, peyote (Lophophora williamsii), however, proceeded apace. This work has both clari-
grows naturally in northern Mexico and along a long fied aspects of their mechanisms of action, and created
strip of the Texas–Mexico border. The Huichol of a challenge to defining hallucinogens. Two classes of
Mexico have used peyote as a religious sacrament con- drugs appear to have more in common with LSD than
tinuously for 3000 years, as have the Native American not. These include other substituted indolealkylamines
Church (NAC) of the United States and Canada. In the (psilocybin, psilocin, ibogaine, dimethyltryptamine,
NAC, peyote is treasured as the holy sacrament from and bufotenine, inter alia) and phenethylamines (mes-
God to be ingested in all-night prayer vigils. caline, MDMA, MDA, 2CB [4-bromo-2,5-dimethoxy-
Hallucinogenic mushrooms containing psilocybin phenethylamine], and DOM [2,5-dimethoxy-4-methy-
(4-phosphoryloxy-N,N-dimethyltryptamine) and psi- lamphetamine] inter alia). Nearly 200 compounds,
locin (4-hydroxy-N,N-dimethyltryptamine), especially largely of the phenethylamine class, for hallucinogenic
from the genus Psilocybe, are found throughout the properties, have been synthesized.
Americas, Europe, and Asia. Psilocybe cubensis typi- The definition of a hallucinogenic drug has been a
cally contains 1.6 mg psilocybin per gram of dried matter of controversy. More than 90 species of hal-
mushroom; a dose of 40 µg/kg induces a 3- to 4-hour lucinogenic plants afford an anthropological defini-
intoxication. Easily grown and indigenous to many tion. Hundreds of substituted phenylethylamines and
parts of the United States, Psilocybe mushrooms are tryptamines lend themselves to chemical characteri-
commonly trafficked as hallucinogens in the illicit zation. Because few have been systematically studied
market. Dimethyltryptamine (DMT), a short-acting in humans, hallucinogens have been defined by their
hallucinogen, is also present in a wide variety of botan- botanical or chemical rubrics rather than their psy-
icals. Many tribes of the Amazon and elsewhere ingest chophysiological affects. To address the problem of
potent DMT snuffs prepared from seeds of Anadenan- classification, one may define as hallucinogenic any
thera peregrina, Anadenanthera columbrina, and other agent which has alterations in perception, cognition,
botanicals. or mood as its primary psychobiological actions in the
The dawn of modernity for hallucinogenic drugs can presence of an otherwise clear sensorium. Most com-
be placed to the moment in 1943 when Albert Hofmann, monly this includes indolealkylamines and phenethyl-
a Swiss chemist, discovered the potent psychological amines, and excludes, inter alia, the anticholinergics,
effects of LSD. Within a decade the drug was being the arylcyclohexylamine dissociative anesthetics such
tested as an agent of chemical warfare in the United as phencyclidine, stimulants such as amphetamine and
cocaine, bromism, and heavy metal intoxication (either Time Course for the Psychiatric Effects of
because changes in perception, mood, or cognition Table 19-1
LSD-like Hallucinogens
are not the primary effect or because they cloud the Time Psychiatric Effects
sensorium).
0–30 minutes Dizziness, nausea, weakness, anxiety
30–60 minutes Blurred vision, visual
Hallucinogen Intoxication pseudohallucinations and
hallucinations, afterimagery,
geometric and imagistic imagery with
DIAGNOSIS eyes closed, decreased concentration,
dissociation, depersonalization,
The DSM-IV-TR criteria for the diagnosis of acute hal- out of body sensations, reduced
lucinogen intoxication are shown below. coordination
60–240 minutes Intensified afterimagery, false
The acute effects of “tripping” on LSD-like (i.e., perceptions of movement (walls
with similar psychic effects, e.g., psilocybin or mesca- appearing to breathe or melt), loss of
line) hallucinogens are variable and profound. Subjects rectilinearity of perceptions, a rapid
flood of emotions including anxiety,
given LSD without their knowledge suffer more anxi- euphoria, and oceanic unity, loss of
ety, hypomotility, and speech disruption than those the sense of time
4–12 hours Gradual return to previous mental state,
who take it knowingly. LSD is active within 30 minutes but with continued arousal, headache,
of the ingestion of a dose of 50 to 100 µg. Physically fatigue, contemplative frame of
the drug stimulates the autonomic nervous system rap- reference, sense of profundity
idly, resulting in tachycardia, hypertension, and dilated Source: Modified from Hollister L (1984) Effects of hallucinogens
pupils, the last being present for much of the trip. The in humans. In Hallucinogens: Neurochemical, Behavioral, and
Clinical Perspectives, Jacobs B (ed). Raven Press, New York.
flood of rapidly changing perceptual, affective, and
cognitive effects are by alternate turns exhilarating,
nerve wracking, and incapacitating. Table 19-1 illus- Because chemical identification of hallucinogens in
trates a typical time course for the psychiatric effects emergency specimens with methods such as gas chro-
of LSD. matography–mass spectrometry remain costly and
time consuming, clinicians in emergency settings must
rely on a careful drug history, the information from the
DSM-IV-TR Diagnostic Criteria less drug-affected friends of the individual, the mental
status examination, and signs apparent from the physi-
292.89 HALLUCINOGEN INTOXICATION cal examination. Routes of administration other than
A. Recent use of a hallucinogen. by ingestion are rare.
B. Clinically significant maladaptive behavioral or psycho- Motor function is reduced, so that such individuals
logical changes (e.g., marked anxiety or depression, are not likely to act out aggressively. Emergency pres-
ideas of reference, fear of losing one’s mind, paranoid
ideation, impaired judgment, or impaired social or oc- entations of the proverbial “bad trip” have apparently
cupational function) that developed during, or shortly declined in recent years despite continued use by a
after, hallucinogen use. significant percentage of American youth. “Bad trips”
C. Perceptual changes occurring in a state of full wake-
fulness and alertness (e.g., subjective intensification are drug-induced panic attacks in the context of a hal-
of perceptions, depersonalization, derealization, il- lucinogenic experience, associated with prepossessing
lusions, hallucinations, synesthesias) that developed feelings of unreality, confusion, and the flooding of the
during, or shortly after, hallucinogen use.
D. Two (or more) of the following signs, developing dur- senses with unbidden imagery.
ing, or shortly after, hallucinogen use:
(1) pupillary dilation
(2) tachycardia Differential Diagnosis
(3) sweating
(4) palpitations The differential diagnosis of an acute hallucinogenic
(5) blurring of vision intoxication includes intoxication by other agents (such
(6) tremors as phencyclidine [PCP], cocaine, amphetamines, anti-
(7) incoordination
cholinergics, and inhalants, among others). It also in-
E. The symptoms are not due to a general medical condi-
tion and are not better accounted for by another men- cludes acute schizophrenia or affective disorder, panic
tal disorder. disorder, head injury, sedative, hypnotic, anxiolytic, or
Reprinted with permission from the Diagnostic and Statistical alcohol withdrawal (including gamma-hydroxybutyrate
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 [GHB]), metabolic disorders such as hypoglycemia
and hyperthyroidism, epilepsy, acute vascular events,
Chapter19 • Substance-Related Disorders: Hallucinogens and MDMA 177
release hallucinations of ophthalmologic disease, and anticholinergic drugs. Central to diagnosis is a care-
the complications of central nervous system (CNS) tu- ful premorbid history, complemented by data from
mors. Age, along with prior clinical history, the history friends and family on the individual’s recent medical
of the current event, physical examination, and toxi- history and behavior. Neurological examination, urine
cology screen for suspected nonhallucinogenic agents for toxicological screening, and computed tomography
usually reveal the diagnosis. or magnetic resonance imaging of the brain are help-
An individual presenting with a history of taking ful in ruling out treatable non-LSD-related psychotic
LSD is only correct approximately 50% of the time, disorders.
judging from analysis of street samples analyzed by
the Massachusetts Department of Public Health in the
TREATMENT
last decade. The street practice of adulteration or mis-
labeling of the drug is common. Psychosis following a Treatment for post-LSD psychoses has been described
smoked agent suggests phencyclidine. Differentiating in a number of case series. Neuroleptics, ECT, lithium,
between PCP and LSD is clinically important, since and 5-hydroxytryptophan have all been reported to be
LSD-induced panic responds well to oral benzodi- useful.
azepines, while PCP delirium requires high potency
antipsychotic medications such as haloperidol.
Hallucinogen Persisting Perception Disorder
(HPPD)
TREATMENT
DIAGNOSIS
Treatment of hallucinogen intoxication with panic is
easily managed with oral benzodiazepines (diazepam The DSM-IV-TR diagnostic criteria for hallucinogen
20 mg or lorazepam 2 mg), which bring the terror, persisting perception disorder are shown below.
as well as the trip, to an end within 30 minutes. This It is not uncommon for an individual suffering from
knowledge, along with the availability of benzodi- HPPD to consult multiple clinicians before a diag-
azepines in the environment, has reduced the need for nosis is made. Because the symptoms are primarily
psychiatric emergency interventions. perceptual, an HPPD subject may consult an ophthal-
mologist, neurologist, or psychologist before seeing
a mental health professional. Often individuals come
Hallucinogen-Induced Psychotic Disorders for help having made their own diagnoses using the
DSM-IV-TR or internet chat groups devoted to HPPD.
Among the hallucinogens, LSD has been associated
with the majority of, but not all, prolonged psychotic
reactions following acute drug use. Psychoses are ap-
parently rare with the abuse of botanical prepara- DSM-IV-TR Diagnostic Criteria
tions, in all likelihood because such agents are of low
potency, not widely abused, and often controlled by 292.89 HALLUCINOGEN PERSISTING PERCEPTION DISORDER
(FLASHBACKS)
religious sanctions.
In addition to exhibiting positive signs of schizo- A. The reexperiencing, following cessation of use of a
phrenia, individuals with post-LSD psychoses show hallucinogen, of one or more of the perceptual symp-
toms that were experienced while intoxicated with the
affective lability and the novel addition of visual hallu- hallucinogen (e.g., geometric hallucinations, false per-
cinations less common in non-drug-related psychoses. ception of movement in the peripheral visual fields,
flashes of color, intensified colors, trails of images of
moving objects, positive afterimages, halos around ob-
jects, macropsia, and micropsia).
Differential Diagnosis B. The symptoms in Criterion A cause clinically signifi-
cant distress or impairment in social, occupational, or
The differential diagnosis of posthallucinogen psycho- other important areas of functioning.
sis is the same as that for any acute psychotic disorder. C. The symptoms are not due to a general medical con-
This includes protracted psychoses following the use dition (e.g., anatomical lesions and infections of the
brain, visual epilepsies) and are not better accounted
of the dissociative anesthetics phencyclidine and keta- for by another mental disorder (e.g., delirium, demen-
mine, amphetamines, and cocaine; schizophrenia and tia, schizophrenia) or hypnopompic hallucinations.
affective disorders, migraine, deliria from CNS infec- Reprinted with permission from the Diagnostic and Statistical
tions, closed head injuries, tumors, vascular events, Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
and the toxic effects of bromine, heavy metals, and
Despite an individual’s certainty about their diagno- factors have heightened public awareness of the drug
sis, the clinician is obligated to rule out other sources and paradoxically led to an increase in use and adverse
of chronic organic hallucinosis, including other drug consequences. Emerging evidence supports the hypoth-
toxicities, strokes, CNS tumors, infections, and head esis that MDMA is a neurotoxin in humans with long-
trauma. Magnetic resonance images of the brain are lived sequelae on cognition, memory, and emotions.
usually negative. Quantitative electroencephalography
shows accelerated alpha and visual evoked potentials,
DIAGNOSIS
especially in the posterior cerebrum.
A typical MDMA user is a college student. MDMA us-
ers are more likely to use marijuana, smoke cigarettes,
TREATMENT and engage in binge alcohol consumption. While other
Treatment at the present time is palliative. Benzodi- drug use appears more common in subjects using
azepines, olanzapine, sertraline, naltrexone, and cloni- MDMA, it is of interest to note that in over a third,
dine have anecdotally been reported to help in selected their first exposure to illicit drugs is in the setting of
cases. Risperidone has been reported to exacerbate HPPD MDMA use.
symptoms. Marijuana can chronically induce an exacer- Unlike many drugs of abuse that are frequently used
bation of HPPD. Because HPPD is also exacerbated by alone, MDMA is almost always used in the company
CNS arousal, affect, stress, and stimulants, these are to of others. Most MDMA users report positive mood and
be reduced or avoided. HPPD is worse with one’s eyes emotional effects as they relate to others. In a survey of
closed, or when entering a dark environment. Thus, sun- 44 experienced MDMA users, subjects reported a greater
glasses, which serve to reduce the difference between capacity for empathy, communication, and understand-
outdoor and indoor luminance, may reduce HPPD symp- ing (Table 19-2). Subjects also reported increased self-
toms when the individual enters an interior space. esteem, high energy, relaxation, and dissociation.
Altered perceptions may be experienced by some
MDMA users as a negative consequence of the drug.
MDMA (“Ecstasy”)-Related Disorders In a double-blind, placebo-controlled study of 13
MDMA-naïve subjects, most reported anxiety, a mild
3,4-Methylenedioxymethamphetamine (MDMA, com- depersonalization or derealization, a moderate thought
monly known as “ecstasy,” and chemically N-methyl- disorder, and poor coordination. Worsening or precipi-
1-[3,4-methylene-dioxyphenyl]-2-aminopropane) is a tation of panic attacks has been reported in different
synthetic amphetamine analogue that is also similar to settings. At least 12 cases of acute psychosis associ-
mescaline. It was originally synthesized by Dr E. Merck ated with MDMA use have been reported. In most of
and patented in Germany as an appetite suppressant in these cases, there is use of concomitant substances. In
1914. It was never marketed and did not attract attention at least one case with long-term follow-up, psychotic
until the 1970s when it was studied as a hallucinogen symptoms were evident 6 months later. A wide range of
analogue. During the “psychedelic” 1970s, recreational impulsive or irrational behaviors have been associated
use of MDMA took root because of its psychological with MDMA use. Most of these reports were published
effects and the fact that it was available legally. Rec- because they resulted in a major medical problem or
reational use was partially fueled by reports of the use death. There is no a priori reason to expect that MDMA
of MDMA as a psychotherapeutic adjunct. In 1985,
guided by reports that a structurally related congener, Table 19-2
A Survey of 44 Experienced MDMA Users
3,4-methylenedioxyamphetamine (MDA), damages se- Regarding Reported Effects of Ecstasy Use
rotonergic neurons in rodents, the Drug Enforcement Reported Effect of MDMA in the % Reporting
Administration (DEA) placed MDMA on Schedule 1
Range of 50 to 700 mg 80
of controlled substances. The actions of the DEA were Increase in communication and 68
validated when subsequent reports found that MDMA empathy
is toxic to the animal and the human brain. This is Changes in cognition or mental 68
associations
not surprising since MDA is the major metabolite of Increase in euphoria or ecstasy 63
MDMA. Changes in perception* 44
The publicity that followed the scheduling of *
Illusions or hallucinations are usually associated with higher doses.
MDMA only served to increase its popularity, particu- Reprinted with permission from Cohen S (1960) Lysergic acid
larly in college campuses. Recently, the use of MDMA diethylamide: side effects and complications. J Nerv Ment Disord
130, 20–40. Copyright, Lipincott, Williams & Wilkins.
has increased and its pattern of use has changed. These
Chapter19 • Substance-Related Disorders: Hallucinogens and MDMA 179
use would produce impulsivity, but many “ecstasy” us- MDMA may also cause serotonergic hyperstimu-
ers have an increase in impulsive behaviors. lation and produce a fatal serotonin–syndrome-like
MDMA users generally limit the frequency of use of illness.
the drug. Most report limiting use of MDMA to twice
per month or less. Fridays and Saturdays are the most
Clinical Manifestations of Long-Term
common days of use because users say they need one
MDMA Neurotoxicity
day to recover after use. More frequent use is associ-
ated with a loss of the desired effect of the drug. Former chronic “ecstasy” users (an average of 527 tab-
lets) have higher self-reported depression as measured
by the Beck’s Depression Scale than non-drug-using
Physical Consequences of MDMA Use
controls. Heavy MDMA use has also been associated
Users exhibit complications that are related to both the with higher rates of psychopathology, including obses-
sympathomimetic and serotonergic properties of MDMA. sive and compulsive behaviors, anxiety, somatization,
These include nausea, vomiting, anorexia, hypertension, and loss of libido. The cause-and-effect relationship
palpitations, diaphoresis, headaches, difficulty walking, between MDMA use and these psychiatric syndromes
muscle aches and tension, hot and cold flashes, urinary is unclear, but since these syndromes involve seroton-
urgency, nystagmus, blurred vision, insomnia, and dry ergic mechanisms, additional investigation into these
mouth. The common complaints of trismus and bruxism potential long-term sequelae is warranted.
may reflect MDMA enhancement of serotonin activation MDMA users have been noted to have problems with
of the 5HT1B receptors of the trigeminal motor nuclei. memory, attention, reasoning, impulse control, and
Other frequently reported acute physical conse- sleep abnormalities in numerous studies.
quences of MDMA use are muscle tension, diaphore- All subjects exposed to MDMA, no matter how
sis, blurred vision, ataxia, hyperreflexia, tachycardia, significant the history of use, may have decreased
and hypertension. verbal fluency, decreased immediate prose recall, and
The acute motoric abnormalities have been related to decreased delayed prose recall, but no change in visual
driving impairment. recall. Most investigators agree regarding the potential
MDMA has been associated with a wide range of for neurotoxicity after even minimal use.
somatic toxic events. These include thrombotic or he-
morrhagic strokes, leukoencephalopathy, myocardial
TREATMENT
infarction, arrhythmias, and pneumothorax. The wide
range of manifestations suggests that many of these There have been no studies examining the treatment
cases are either idiosyncratic or related to impurities of MDMA use. This may be due to the rarity of pres-
remaining from the synthetic process. entation of subjects seeking treatment for MDMA
There have been cases of severe medical illness or addiction. Nonetheless, MDMA has abuse poten-
death due to electrolyte and fluid abnormalities and tial. Although not well studied, serotonin reuptake
cases of multiple organ system failure. These compli- inhibiting antidepressants may offer a possible treat-
cations may be related to the specific environment in ment for individuals who present with an MDMA
raves, where people are exposed to hot, crowded en- addiction.
vironments. In association with the increased body
temperature caused by MDMA, dehydration and its
consequences are likely. Crowding has been shown to
DIAGNOSTIC CRITERIA
increase amphetamine toxicity in animals, a phenom-
enon labeled aggregation toxicity. A similar phenom- The ICD-10 and DSM-IV-TR diagnostic criteria are
enon may occur in crowded raves in humans. nearly identical.
CHAPTER
Inhalants
The term inhalant abuse is used to describe a vari- but does not discuss the problems of the anesthetic
ety of drug-using behaviors that cannot be classified state.
by their pharmacology or toxicology but are grouped Table 20-1 enumerates the solvents (frequently noted
on the basis of their primary mode of administration. on the labels) contained in corresponding popular prod-
Although other substances can be inhaled (e.g., to- ucts currently used for recreational purposes. The term
bacco, marijuana with or without phencyclidine, and “glue sniffing” is still widely used today to describe the
even heroin or crack), this is not the primary route abuse of most of these substances. It is important to
of administration; therefore, they do not fall into keep in mind that there are many different chemicals
this classification. Several subcategories of inhalants in these different products, all of which have different
can be established on the basis of chemical classes physiological effects and toxicities as well as differ-
of products and primary abuse groups as follows: (1) ent chemical properties. Sometimes the substances are
industrial or household cleaning and paint-type sol- listed on the product label; however, many times the
vents including paint thinners or solvents, degreas- container lacks sufficient detail to identify the potential
ers or dry cleaning solvents, solvents in glues, art or toxin(s).
office supply solvents such as correction fluids, and The disorders described in this chapter are classified
solvents in magic markers (gasoline is similar to under the inhalant-related disorders section in DSM-
these products); (2) propellant gases used in house- IV-TR and are subdivided into two groups: inhalant use
hold or commercial products, such as butane in light- disorders and inhalant-induced disorders.
ers, or fluorocarbons in electronic (personal compu-
ter, office equipment) cleaners or refrigerant gases;
(3) household aerosol sprays such as paint, hair, and DIAGNOSIS
fabric protector sprays; (4) medical anesthetic gases
The practice of “sniffing,” “snorting,” “huffing,” “bag-
such as ether, chloroform, halothane, and nitrous
ging,” or inhaling to get high describes various meth-
oxide; and (5) aliphatic nitrites. Most of the fore-
ods of inhalation. These terms refer to the inhalation
going compounds affect the central nervous system
of volatile substances from (1) filled balloons, (2) bags,
(CNS) directly, whereas nitrites act on cardiovascu-
and (3) soaked rags and/or sprayed directly into oral
lar smooth muscle rather than as an anesthetic in the
orifices. Abusers can be identified by various telltale
CNS. The nitrites are also used primarily as sexual
clues such as organic odors in the breath or clothes,
enhancers rather than as mood alterants. Therefore,
stains on the clothes or around the mouth, empty spray
when discussing “inhalant abuse,” we will be refer-
paint or solvent containers, and other unusual parapher-
ring primarily to substances other than nitrites. One
nalia. These clues may enable one to identify a serious
item worthy of note: the exclusion of anesthetics from
problem of solvent abuse before it causes serious health
the inhalant-related disorders section in the DSM-IV-
problems or death.
TR is not medically correct, as almost all of the inha-
The following Inhalant-Related Disorders are in-
lants act physiologically as would any anesthetic and
cluded in DSM-IV-TR:
some, particularly the anesthetics nitrous oxide and
trichloroethylene (TCE), are abused by the primary • Inhalant Dependence. Dependence on inhalants is
inhalant abuser discussed herein. Thus, the following primarily psychological, with a less dramatic associ-
discussion includes the abuse of selected anesthetics ated physical dependence occurring in some heavy
Chapter 20 • Substance-Related Disorders: Inhalants 181
Table 20-1 Chemicals Commonly Found in Inhalants

dependence on these substances. A mild withdrawal
syndrome occurs in 10 to 24 hours after cessation
Inhalant Chemicals of use (only in those who have excessively abused
Adhesives inhalants) and lasts for several days. Symptoms in-
Airplane glue Toluene, ethyl acetate
Other glues Hexane, toluene, methyl chloride,
clude general disorientation, sleep disturbances,
acetone, methyl ethyl ketone, headaches, muscle spasms, irritability, nausea, and
methyl butyl ketone fleeting illusions. However, this is not an easily iden-
Special cements Trichloroethylene,
tetrachloroethylene tified or a characteristic withdrawal syndrome that
is useful for many practitioners in a clinical setting.
Aerosols
Paint sprays Butane, propane, fluorocarbons, The need to continue use is undeniably strong in
toluene, hydrocarbons many individuals; specific treatments for inhalant
Hair sprays Butane, propane dependence, other than the drug therapy and/or psy-
Deodorants, air Butane, propane
fresheners chotherapy used for other drug dependence, need to
Analgesic spray Fluorocarbons be developed.
Asthma spray Fluorocarbons
Fabric spray Butane, trichloroethane • Inhalant Abuse. Abuse of inhalants may lead to harm
Personal computer Dimethyl ether, hydrofluorocarbons to individuals (e.g., accidents involving automobiles,
cleaners falling from buildings when in an impaired or in-
Anesthetics toxicated state (illusionary feelings), or self-inflicted
Gaseous Nitrous oxide
Liquid Halothane, enflurane
harm such as attempted or successful suicide) (see
Local Ethyl chloride generic DSM-IV-TR diagnostic criteria, Chapter 13,
Cleaning Agents page 125). Frozen lips caused by rapidly expanding
Dry cleaners Tetrachloroethylene, trichloroethane gases or serious burns may also occur. Chronic inha-
Spot removers Xylene, petroleum distillates, lant use is often associated with familial conflict and
chlorohydrocarbons
Degreasers Tetrachloroethylene, trichloroethane, school problems.
trichloroethylene • Inhalant-Induced Disorders. The primary disor-
Solvents and der is inhalant intoxication, which is characterized
Gases by the presence of clinically significant maladaptive
Nail polish Acetone, ethyl acetate, toluene
remover behavioral or psychological changes (e.g., belliger-
Paint remover Toluene, methylene chloride, ence, assaultiveness, apathy, impaired judgment,
methanol, acetone, ethyl acetate
Paint thinners Petroleum distillates, esters, acetone
impaired social or occupational functioning) that
Correction fluids Trichloroethylene, trichloroethane develop during the intentional short-term, high-dose
and thinners exposure to volatile inhalants (see DSM-IV-TR di-
Fuel gas Butane, isopropane
Cigar or cigarette Butane, isopropane agnostic criteria for inhalant intoxication, page 182).
lighter fluid The maladaptive changes occurring after intentional
Fire extinguisher Bromochlorodifluoromethane and nonintentional exposure include disinhibition,
propellant
excitedness, light-headedness, visual disturbances
Food Products
Whipped cream Nitrous oxide
(blurred vision, nystagmus), incoordination, dysar-
aerosols thria, an unsteady gait, and euphoria. Higher doses
Whippets Nitrous oxide of inhalants may lead to depressed reflexes, stupor,
Room Odorizers coma, and death, sometimes caused by cardiac ar-
Poppers, fluids Isoamyl, isobutyl, isopropyl, or butyl rhythmia. Lethargy, generalized muscle weakness,
(Rush, Locker nitrite (now illegal) or cyclohexyl
Room) and headaches may occur some hours later depend-
ing on the dose.
users (see generic DSM-IV-TR diagnostic criteria, There is little evidence that inhalant abuse either coex-
Chapter 13, page 125). Physical tolerance of some ists with other mental disorders or leads to any such
solvents has been documented by animal studies altered state. There have been few studies of comorbid-
only under unusual conditions. The urgent need to ity in psychiatric hospital populations and almost no
continue use of inhalants has been reported among studies in other populations.
individuals with heavy use, although the nature of On the other hand, there is clinical experience which
this phenomenon is unknown. There is at least a strongly suggests that personality disorders of an anti-
psychological dependence and often a weak physical social type are common in solvent abusers.
DSM-IV-TR Diagnostic Criteria Symptoms Related to Solvent Abuse (Not

Table 20-2
All for Gases and Nitrites)
292.89 INHALANT INTOXICATION Moderate Intoxication
Dizziness
A. Recent intentional use or short-term, high-dose expo- Headache
sure to volatile inhalants (excluding anesthetic gases Lethargy
and short-acting vasodilators). Disorientation, incoherence
B. Clinically significant maladaptive behavioral or psy- Ataxia, gait (uncoordinated movement)
chological changes (e.g., belligerence, assaultiveness, Odoriferous, foul breath (solvent vapors)
apathy, impaired judgment, impaired social or occu-
pational functioning) that developed during, or shortly Strong Intoxication
after, use of or exposure to volatile inhalants. Blurred vision
C. Two (or more) of the following signs developing dur- Belligerence
ing, or shortly after, inhalant use or exposure: Nausea, vomiting
Irritability
(1) dizziness Delirium
(2) nystagmus Slurred speech
(3) incoordination
(4) slurred speech Severe (Rare)
(5) unsteady gait Seizures
(6) lethargy Violent actions
(7) depressed reflexes
(8) psychomotor retardation
(9) tremor
(10) generalized muscle weakness thousand times higher than in the occupational set-
(11) blurred vision or diplopia ting and results in numerous irreversible disease states.
(12) stupor or coma Table 20-3 describes several well-characterized disor-
(13) euphoria
ders and identifies the solvent when corroborated by
animal studies. Some substances have been strongly
tal disorder. correlated with the development of a disorder through
Reprinted with permission from the Diagnostic and Statistical numerous case studies.
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 Many organic solvents produce nonspecific effects
(e.g., encephalopathy) after exposure to extremely high
concentrations; a few produce relatively specific neu-
rological syndromes with chronic administration. Two
Toxicology of Inhalant Abuse
specific neurotoxic syndromes, a peripheral neuropathy
The majority of inhalant abusers are never seen in and an ototoxicity, are well correlated with organic sol-
a hospital or outpatient facility. Although many do vents. Most common, however, is a clinical syndrome
not need medical attention for their inhalant habit, consisting of cognitive impairment, cerebellar ataxia,
of those who do, many often die before reaching the and spasticity syndrome. In addition, a myopathy may
hospital as a result of asphyxia, cardiac arrhythmia, occur alone or in combination with any of these clinical
or related overdose effects after inhaling fluoro- syndromes.
carbons, low-molecular-weight hydrocarbon gases Most reports emphasize the cerebellar and cogni-
(butane, propane), nitrous oxide, or other solvents tive dysfunction, with most cases showing combined
including toluene during either the fi rst or a subse- impairment of cerebral and cerebellar functions as well
quent episode. Death may also occur after inhala- as pyramidal changes. Neurological abnormalities vary
tion of toluene-containing substances as a result of from mild cognitive impairment to severe dementia,
metabolic acidosis or related kidney failure if left associated with elemental neurological signs such as
untreated. Although it is not common, anesthetics cerebellar ataxia, corticospinal tract dysfunction, ocu-
abused by medical personnel or others have also lomotor abnormalities, tremor, deafness, and hypos-
been a cause of death; death related to nitrous ox- mia. Cognitive dysfunction is the most disabling and
ide use is often due to asphyxia. Some of the more frequent feature of chronic toluene toxicity and may be
common acute syndromes of the intoxicated state are the earliest sign of permanent damage. Dementia, when
listed in Table 20-2. present, is typically associated with cerebellar ataxia
and other signs.
Neurotoxic Manifestations
Ototoxicity. Sensorineural hearing loss is one of the
Chronic high-level exposure to organic solvents oc- more commonly occurring clinical neurotoxic syn-
curs in the inhalant abuse setting at levels several dromes related to inhalant abuse, along with a related
Table 20-3 Diseases Observed in Humans After Chronic Inhalant Abuse
Condition Syndrome Substance Animal Studies*

Slowly Reversible and/or Irreversible Syndromes
Encephalopathy Cognitive dysfunction “Toluene,”† other solvents —
Cerebellar syndrome Limb dysmetria “Toluene” Rat
Dysarthria —
Sensorineural optic High-frequency hearing loss TCE, toluene Rat, mouse
Sensorineural
Optic nerve Visual loss “Toluene” —
Oculomotor Oculomotor disturbances (nystagmus) Xylene, TCE Rabbits
Myeloneuropathy Sensory loss Nitrous oxide Rat, mouse
Spasticity
Axonal neuropathy Distal sensory loss, limb weakness Hexane, methyl butyl ketone Rat, monkey
Cardiotoxicity Arrhythmia Chlorofluorocarbons, butanes, propanes Mouse, rat, dog
Leukemia Myelocytic Benzene Rat, mouse
Mostly Reversible Syndromes
Trigeminal Numbness, paresthesia TCE and/or dichloroacetylene Rat
neuropathy
Renal acidosis Metabolic acidosis “Toluene” Rat
Hypokalemia —
Carboxyhemoglobin Hypoxia Methylene chloride, tobacco Human, rat
Methemoglobinemia Syncope, blue Nitrites, organic Rat
Neonatal syndrome Retarded growth, development “Toluene” Rat
Hepatotoxicity Fatty vacuoles, plasma liver enzymes Chlorohydrocarbons Rat
Immunomodulatory Loss of immune cell function Nitrites, organic Rat
*
Symptoms observed in animal studies with these solvents.
†
Quotation marks around substance indicates uncertainty about this solvent (alone) producing these symptoms.
equilibrium disorder. Neural conduction, most readily ish the olfactory responses; however, it has seldom
diagnosed by brain stem auditory evoked responses, is been studied.
often abnormal. Brain stem auditory evoked responses
may be a sensitive screening test for monitoring in- Trigeminal Neuropathy. One neurological manifes-
dividuals at risk from toluene exposure and for early tation associated with TCE intoxication is a slowly re-
detection of CNS injury. However, although specific in versible trigeminal neuropathy. Individuals developed
revealing abnormalities characteristic of CNS involve- paresthesia around the lips, which then spreads to in-
ment in chronic inhalant abuse, brain stem auditory volve the entire trigeminal distribution bilaterally. Motor
evoked responses reveal abnormalities only in a small weakness also occasionally occurred. Resolution of the
number of individuals of a chronic inhalant abuse trigeminal neuropathy occurs slowly, which is thought to
population. indicate segmental or nuclear trigeminal involvement.
High levels of nitrous oxide exposure produce a
Other Cranial Nerve Involvement. A wide variety myeloneuropathy with both central and peripheral
of neuropathic manifestations have been reported, and components, even in the presence of adequate oxygen.
all of these neuropathies can be identified with specific The symptoms include numbness and weakness in the
cranial nerves (Table 20-4). limbs, loss of dexterity, sensory loss, and loss of bal-
Anosmia is an often described syndrome of inhalant ance. The early neurological features indicate sensori-
abuse. It would be expected that solvents would dimin- motor polyneuropathy; however, with persistent abuse,
a myelopathy with severe spasticity may develop. There
is also a combined degeneration of the posterior and
Cranial Nerve Abnormalities Noted in lateral columns of the spinal cord resembling that in vi-
Table 20-4
Inhalant Abuse tamin B12 deficiency, and other neuropathic symptoms
Cranial Nerve Dysfunction resulting from spinal cord degeneration were produced
after prolonged anesthesia in vitamin B12-deficient
I Hyposmia, anosmia
II Optic neuropathy individuals. Administration of vitamin B12 (or folinic
III, IV, VI Oculomotor disorders: nystagmus, acid) dramatically aids recovery of these surgical pa-
opsoclonus, ocular dysmetria tients and may assist recovery in solvent abusers, espe-
VIII Sensorineural hearing loss
cially once the myelopathy appears.
Peripheral Neuropathy. Cases of n-hexane polyneu- various psychological assessment tools can assist not
ropathy have been reported both after occupational ex- only in evaluating the intoxication but also in following
posure and after deliberate inhalation of vapors from the progress of the treatment. Little can be done during
products containing n-hexane such as glues gasoline, this period other than to facilitate improvement of the
and naphtha. basic health of these individuals, provide supportive
Clinically and pathologically, the neuropathy occur- care, and build the individual’s self-esteem.
ring with n-hexane or MBK is that of a distal axonopa- There is no accepted treatment approach for inha-
thy. The clinical syndrome is an initially painless sen- lant abuse. It should also be emphasized that there are
sorimotor polyneuropathy, which begins after chronic various categories of solvent abusers, from those who
exposure; weight loss may be an early symptom. Sen- may use only one substance (e.g., only nitrous oxide
sory and motor disturbances are noted initially in the or butanes) to heavy users of a variety of solvents and
hands and feet, and sensory loss involves primarily gases. Many drug treatment facilities refuse treatment
small fiber sensation (i.e., light touch, pin prick, tem- of the inhalant abuser because many feel that inha-
perature) with relative sparing of large fiber sensation lant abusers are resistant to treatment or that there is
(i.e., position and vibration). no standard or accepted treatment. One facility that
Prognosis for recovery correlates directly with the focuses solely on the comprehensive treatment of in-
intensity and duration of the toxic exposure and the se- halant abusers, the International Institute on Inhalant
verity of the neuropathy. Residual neuropathy is seen Abuse based in Colorado (www.allaboutinhalants.
only in the most severely affected individuals with com), uses a three-phase model that allows longer
motor as well as sensory involvement, some of whom periods of treatment. Longer periods of treatment are
still continue to inhale despite warnings of further needed to be able to address the complex psychoso-
debilitation. cial, economic, and biophysical issues of the inhalant
abuser. When brain injury, primarily in the form of
cognitive dysfunction, is present, the rate of progres-
Nonnervous System Toxicity sion in the treatment process is even slower and as-
Most of the known adverse clinical effects of inhalant sumes a comprehensive neurological rehabilitation
abuse relate to its effects on the nervous system. There approach similar to that in individuals with traumatic
are, however, other significant adverse effects on other brain injury. As few treatment approaches with solvent
organ systems including the kidney, liver, lung, heart, abusers have been evaluated, none on a broad scale, all
and hemopoietic systems. treatments should consider several important param-
eters including the following:
TREATMENT • Culture
• Family structure
Individuals need different treatments based on the • Living environment
severity of the dependence and any medical compli- • Peer interactions
cations. Primary care physicians should address the • Individual’s ability to learn and adapt
medical issues identified earlier as well as other medi- • Establishment of self-image
cal concerns before dealing with the dependence on • Individual attitudes and behavioral characteristics
solvents and other drugs. During this period, sedatives, • Building basic life skills
neuroleptics, and other forms of pharmacotherapy are • Social bonding.
not useful in the treatment of inhalant abusers and
should be avoided in most cases as they are likely to Some of these issues may be dealt with only through
exacerbate the depressed state. Once it is determined treating these individuals separately, especially in the
that the individual is detoxified, that is, has low levels early periods of treatment.
of solvent or other depressant drug, then therapy with The inhalant abuser typically does not respond to
other drugs, such as antianxiety drugs, may be use- usual drug rehabilitation treatment modalities. Several
ful. The determination of detoxification, even in the factors may be involved, particularly for the chronic
absence of drug (solvent) administration, is not well abuser who may have significant psychosocial prob-
defined or systematic. It may take several days for the lems as well as irreversible brain injury. Treatment
major “reversible” intoxication state to be reduced to a becomes slower and progressively more difficult when
level at which coherent cognition can occur. The use of the severity of brain injury worsens as abuse progresses
through transient social use (experimenting in groups) high level of exposure to toluene commonly seen in
to chronic use in isolation. For these and other reasons, inhalant abusers. More frequently performed expired
longer therapies are necessary than are utilized in most breath analysis for toluene or other abused compounds
drug treatment facilities. Also, neurological impair- is also available. As alcohol is a common secondary
ment, the breadth of which still needs to be established, drug of abuse among inhalant abusers, alcohol abuse
may be a major complication slowing the progress of should be monitored and considered in the approach
rehabilitation. This is not as significant a problem with to treatment.
other forms of drug abuse.
Drug screening would be useful in monitoring in-
halant abusers. Routine urine screening for hippuric
DIAGNOSTIC CRITERIA
acid (the major metabolite of toluene metabolism)
performed two or three times weekly can detect the The DSM and ICD-10 criteria are nearly identical.
CHAPTER
Nicotine
Nicotine dependence is the most common substance

use disorder in the United States with about 25% of the DSM-IV-TR Diagnostic Criteria
population addicted to tobacco. Tobacco addiction has 292.0 NICOTINE WITHDRAWAL
serious health consequences for the user, family mem-
bers, and others who breathe second-hand environmen- A. Daily use of nicotine for at least several weeks.
B. Abrupt cessation of nicotine use, or reduction in the
tal tobacco smoke or are exposed during pregnancy. amount of nicotine used, followed within 24 hours by
Tobacco addiction increases morbidity and mortality. four (or more) of the following signs:
Many individuals with mental illness or other addic- (1) dysphoric or depressed mood
tions are nicotine dependent, and about half of all the (2) insomnia
cigarettes consumed in the United States are by these (3) irritability, frustration, or anger
(4) anxiety
individuals. (5) difficulty concentrating
(6) restlessness
(7) decreased heart rate
(8) increased appetite or weight gain
DIAGNOSIS
Nicotine Dependence cant distress or impairment in social, occupational, or
other important areas of functioning.
In the DSM-IV-TR, a specifier is used to designate the D. The symptoms are not due to a general medical condi-
presence or absence of physiological dependence, de- tion and are not better accounted for by another men-
tal disorder.
pending on whether tolerance or withdrawal is present or
whether both are absent (see generic DSM-IV-TR diag- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
nostic criteria for Substance Dependence in Chapter 13, American Psychiatric Association.
page 125). Further specifiers can be used to denote
course (e.g., early full remission or sustained partial
remission). Of note, the DSM distinguishes nicotine symptoms, other objective biological and physiological
from other substances by not including a diagnosis of changes are associated with nicotine withdrawal, such
nicotine abuse because most individuals transit quickly as generalized slowing of electroencephalographic ac-
and directly from use to dependence (meeting criteria tivity, decreases in catecholamine and cortisol levels,
of tolerance and withdrawal). changes in rapid eye movement, impairment on neu-
The DSM-IV-TR nicotine withdrawal syndrome ropsychological testing, and decreased metabolic rate.
describes a characteristic set of symptoms that devel- Nicotine dependence and smoking are two to three
ops after abrupt cessation or a reduction in the use of times more common in individuals with mental and
nicotine products after at least several weeks of daily other substance use disorders than in the general
use. Other symptoms that may be associated with nico- population. Smoking-related illnesses are the pri-
tine withdrawal include craving for nicotine, a factor mary cause of death among those in recovery from
thought to be significant in relapse; a desire for sweets; other substances. It is estimated that 55–90% of in-
and impaired performance on tasks requiring vigi- dividuals with mental disorders smoke versus 23% of
lance. To some extent, the degree of physiological de- the general population. The prevalence of smoking
pendence predicts severity of the withdrawal syndrome is especially high in individuals with schizophrenia
and difficulty stopping smoking. In addition to frank (70–90%), affective disorders (42–70%), and alcohol
Chapter 21 • Substance-Related Disorders: Nicotine 187
dependence (60–90%) or other substance use disor- Course

ders (70–95%). The odds ratio for “ever smoked’’ is
The National Health Interview Survey found that 70%
4.7 in persons suffering from alcohol dependence, 2.4
of smokers interviewed reported they wanted to quit
for individuals with major depressive disorder (MDD),
smoking at some point in their lifetime, and about 33%
1.8 for persons with agoraphobia, 1.6 for individuals
of smokers try to quit each year. Only about 3% of quit
with dysthymia, and 1.6 for individuals with panic
attempts without formal treatment are successful, and
disorder (PD). Conversely, there is also evidence that
in recent years, about 30% of smokers who want to quit
affective, anxiety, and substance use disorders may
are seeking treatment. Outcomes for nicotine depend-
be more common in individuals who smoke than in
ence treatment vary by the type of treatment and the
those who do not or in those who have never smoked.
intensity of treatment with specific reports ranging
Finally, there is evidence to suggest that in one study
from about 15% to 45% 1-year abstinence rates follow-
up to 75% of smokers with a history of MDD developed
ing treatment. Cessation attempts result in high relapse
depressed mood during the first week of withdrawal
rates, with the relapse curve for smoking cessation
versus only 30% of those with no depressive history,
paralleling that for opiates. Most individuals relapse
and that the withdrawal syndrome may be more severe
during the first 3 days of withdrawal and most oth-
in smokers with a history of depression. The presence
ers will relapse within the first 3 months. Withdrawal
of depressive symptoms during withdrawal is also as-
symptoms are most severe within the first 1 to 3 days
sociated with failed cessation attempts. Self-reported
of abstinence, often continue for 3 to 4 weeks, and in
depressive symptoms during adolescence also predict
some persons last for up to 6 months or longer. Current
later frequency and duration of smoking. Several stud-
depressive symptoms and a history of depression are
ies suggest a genetic predisposition to both nicotine
predictors of relapse. Weight gain may also contribute
dependence and co-occurring depression.
to relapse, particularly in women. In contrast, several
There is no simple reason why so many individu-
factors have been found to predict worse outcomes at
als with a mental disorder smoke. As with other ad-
smoking cessation (Table 21-1). Predictors include in-
dictive disorders, a combination of complex biological
dividual factors, manifestations of the addiction such
and psychosocial factors is likely. Potential biological
as severity of withdrawal, and social and environmen-
factors in this group include a greater likelihood of sus-
tal circumstances.
ceptibility to nicotine dependence, with persons expe-
Nicotine dependence, like other substance use dis-
riencing a greater sense of reward from nicotine. Other
orders, can be thought of as a chronic relapsing illness
possibilities include using nicotine to reduce the side
with a course of intermittent episodes alternating with
effects of psychiatric medications, both as a stimulant
periods of remission for most smokers. About 65% of
to counter sedation as well as a dopamine modulator
those who stop smoking relapse in 3 months and an-
that can diminish neuroleptic-induced parkinsonism.
other 10% relapse in 3 to 6 months, and with treat-
Subjectively, individuals report that using nicotine im-
ment the overall relapse rate is still about 75–80% by
proves their cognitive functioning and reduces stress,
1 year. However, these reported lower outcome rates
although research data is mixed in this regard. In indi-
do not consider the additive effects over time related to
viduals with schizophrenia, an abnormality in P50 gat-
multiple quit attempts, since about 40–50% of smokers
ing, which is believed to relate clinically to the ability
in the United States have been able to quit smoking in
to filter out distracting auditory stimuli, is reversed with
their lifetime. Less than 25% of the individuals who
nicotine. Social and behavioral factors are also impor-
have quit smoking are successful in their first attempt.
tant in understanding nicotine dependence, and psy-
chiatric and addictive comorbidity. Smoking has been
ignored and is a part of the pervasive culture in most
Factors Predicting Worse Outcomes in
mental health and substance abuse treatment centers Table 21-1
Nicotine Dependence Treatment
and residential facilities. This is beginning to change.
Historically, smoking was often used as a behavioral Physical reactivity (pulse, blood pressure, etc.) to smoking-
related cues
reward in psychiatric inpatient units and continues to Family and friends who are current smokers
serve as a social connector for many individuals with a Lack of social support from spouses, partners, family
mental disorder. Additionally, individuals coping with members, friends
Deficits in social skills and assertiveness
persistent psychiatric symptoms and reduced social Higher severity of withdrawal symptoms
and occupational functioning report smoking to fill the Limited ability to cope with effects occurring in response to
voids of boredom and disappointment. cues or triggers
Depressed mood
Repeated failures are common before successful absti- individuals receive combined medications and therapy
nence, with the average smoker attempting to quit five treatment. Most receiving treatment get medication
or six times before success. Recent prior attempts at treatments, and only about 3% of the individuals re-
quitting do increase the odds that individuals will be ceiving medication treatments will also receive psycho-
able to quit smoking on a future attempt. Relapse can social treatment despite the fact that this combination
occur even after a long time of abstinence, with about improves outcomes by 50%. Primary care treatment
33% of former smokers who are abstinent for 1 year providers tend to offer brief counseling treatment serv-
eventually relapsing 5 to 10 years after cessation. ices with follow-up visits. In addition, many individuals
Treatment of nicotine dependence with resultant ab- receive minimal formal treatment and either purchase
stinence can result in highly beneficial health effects. over-the-counter nicotine replacement patch or gum, or
Educating individuals and families about these benefits go to Nicotine Anonymous or other self-help groups in
of abstinence from smoking can be helpful. Short-term attempting to quit on their own.
effects (within 1 month) include a significant reduc- Before formal intervention is undertaken, it is ben-
tion in respiratory symptoms and respiratory infections eficial and important to perform a comprehensive
such as influenza, pneumonia, and bronchitis. Excess evaluation to determine the biological, psychological,
risk of death from coronary heart disease is reduced and social factors that are most significant in the initia-
after 1 year and continues to decline over time. In indi- tion and maintenance of nicotine use and dependence.
viduals with coronary heart disease, smoking cessation Comprehensive evaluation of the individual is outlined
decreases the risk of recurrent myocardial infarction in Table 21-3. The assessment often begins with an as-
and cardiovascular death by 50%. By 10 to 15 years of sessment of the patterns of tobacco usage (number of
abstinence, the mortality rate from all causes returns cigarettes smoked per day, times during the day, loca-
to that of a person who has never smoked. Pulmonary tion, and circumstances). In addition, the amount of
function can also return to normal if chronic obstruc- tobacco usage can be assessed through cotinine levels
tive changes have not already occurred at the time of or carbon monoxide (CO) levels. Cotinine levels can
cessation, and even with obstructive changes pulmo- be obtained from the urine, blood, or saliva to assess
nary function can improve with abstinence. the amount of nicotine ingested. The expired-air test
for a CO level is not costly and can be obtained within
a minute by any clinician with a CO meter. The CO
TREATMENT
meter is useful at intake and to monitor for relapse.
Nicotine dependence treatment targets severity of the A history of prior cessation attempts should include
problem, co-occurring disorders, and the different mo- the nature of prior treatments, length of abstinence,
tivational levels to change. Treatment is provided in a timing of relapse, and factors specifically related to
range of levels of intensity of care (self-help, brief treat- relapse (e.g., environmental or interpersonal triggers).
ment, and once or twice per week outpatient treatment) Assessing prior treatments includes assessing medica-
and may include different modalities (self-help guides, tions and psychosocial treatments. The five Food and
internet resources, medications, and individual or group
therapy). Formal treatment options have expanded rap-
idly in the past 25 years to include six FDA-approved
Assessing Nicotine Use and Nicotine
medications, and a range of effective psychosocial in- Table 21-3
Dependence
terventions including internet and phone-line services.
Current and past patterns of tobacco use
(Table 21-2). Unfortunately, most insurance plans do (include multiple sources of nicotine)
not cover nicotine dependence treatment, and only Current motivation to quit
some prescription plans will cover the medications. Few Objective measures: breath CO level or cotinine level
(saliva, blood, urine)
Assess prior quit attempts (number and what happened in
each attempt)
Effectiveness of Nicotine Dependence Why quit? How long abstinent? Why relapsed?
Table 21-2 What treatment was used (how used and for how long)
Treatment Interventions
Assess withdrawal symptoms and dependence criteria
No professional or formal intervention 5% Psychiatric and other substance use history
Physicians’ advice 10% Medical conditions
Nicotine polacrilex 15–20% Their common triggers (car, people, moods, home, phone
Nicotine patch, gum, inhaler 20–25% calls, meals, etc.)
Bupropion 25% Perceived barriers against and supports for treatment
Behavioral therapy 25–30% success
Medication and behavioral therapy 40% Preference for treatment strategy
Drug Administration (FDA)-approved medications other substance abusers start smoking earlier and are
for nicotine dependence treatment are the four nico- more physiologically dependent on nicotine. In addi-
tine replacement therapies (NRT) of the patch, gum, tion, the use of alcohol or other substances may be inti-
spray, and inhaler, and the nonnicotine pill bupropion mately linked to smoking cigarettes and can serve as a
(Zyban). Sometimes, other medications have been pre- strong trigger for craving and ultimate relapse.
scribed for nicotine dependence treatment. Assessment A careful medical history should also be obtained.
about medications includes asking about what dose of The presence of significant tobacco-related medical ill-
medications and how long it was taken, any side effects ness can sometimes serve as crucial leverage to help
that developed, and how the individual actually took the motivate the individual to attempt cessation. Current
medication (especially relevant for NRT). For exam- medications and medical conditions may also be im-
ple, the individual may report taking off the NRT patch portant considerations in determining the approach to
prior to a shower and then replacing the same patch, cessation, especially with regard to pharmacotherapy.
rendering it ineffective. Psychosocial treatments might For example, a history of seizures or an eating disorder
include group or individual treatment, American Lung is usually a contraindication to the use of bupropion/
Association and other community support groups, hyp- Zyban (nonnicotine pill medication). The individual
nosis, acupuncture, or Nicotine Anonymous. A history should be assessed for pulmonary symptoms and signs
of specific withdrawal symptoms and their severity and (cough), and if there is a long history of significant
duration is critical, as is an assessment of the smok- nicotine use, pulmonary function tests should be con-
er’s social and environmental contexts, for example, sidered. The presence of significant cardiovascular
whether other household members smoke, and avail- disease, especially a history of recent myocardial inf-
able family and social supports. arction, is especially relevant to planning psychophar-
An assessment should be made of the person’s rea- macological interventions. If the individual is already
sons for quitting, his or her motivation and commit- taking a psychiatric medication, consider it important
ment and self-efficacy (perceived ability to quit). The to realize that quitting smoking may result in an in-
individual’s stage of readiness for stopping smoking is crease in medication blood levels and side effects.
also important; that is, whether the person is not yet
seriously considering stopping smoking (precontem-
Phases of Treatment
plation), is considering attempting to quit but not for
several months (contemplation), is seriously consider- The general approach to the treatment of nicotine de-
ing quitting in the next month and has begun to think pendence considers three phases of treatment (engage-
about the necessary steps to stop smoking (prepara- ment, quitting, and relapse prevention) (Table 21-4).
tion), or is actually attempting to stop smoking (ac- Each phase of treatment includes consideration of
tion). It is also important to access the smoker’s knowl- three primary biological, psychological, and social
edge about smoking and nicotine dependence because factors affecting nicotine dependence outcomes. The
deficits in knowledge and information can have a del- biological or physiological dependence parallels the
eterious effect on smoking cessation attempts. characteristics of other physiologically addicting sub-
Assessment of the psychiatric history is also impor- stances (dose-related effects, rapid tolerance leading
tant. Numerous studies have shown the significance to increased intake and the presence of a withdrawal
of current and past depression in relation to smoking, syndrome, compulsive use). Psychological depend-
as well as the increased prevalence rates of cigarette ence involves the perceived benefits/reasons a person
smoking in individuals with a variety of mental dis- smokes, such as a perception that they are able to im-
orders, such as MDD, schizophrenia, and alcohol and prove mood and sense of well-being, to satisfy craving,
substance abuse. The presence of these comorbid disor- and to provide stimulation and relaxation. The social
ders may also make successful smoking cessation less component involves environmental and social cues
likely, especially if undiagnosed and untreated. that become associated with the behavior of smoking
Assessing the individual for a history of current cigarettes, such as the association with drinking cof-
alcohol or other substance abuse is also important, as fee or alcohol, talking on the telephone, taking a work
the prevalence of smoking in persons with alcohol de- break, or smoking at parties or social functions. The
pendence as well as in other substance abusers is much direct beneficial effects of nicotine on mood and con-
higher than in the general population. It may also be centration become highly positive reinforcements, as
more difficult for individuals with current or prior sub- do associated social context and behaviors linked with
stance abuse or dependence to stop smoking, as there smoking, which then can act as powerful triggers for
is evidence that persons with alcohol dependence and relapse during attempts at cessation.
Table 21-4 Three Phases of Nicotine Dependence Treatment
Engagement Phase
• Do a comprehensive evaluation of nicotine use and dependence
• Provide MET personalized feedback from the assessment
• Assess motivational level to quit and attempt to set a target quit date
• Explore previous quit attempts. What worked? What did not work? What triggered the return to tobacco use?
• Assess patient preference for treatment (medications, psychosocial treatments, group vs. individual, self-help, etc.) and provide
education on treatment
• Create a treatment plan
• Strengthen and renew patient’s motivation to quit smoking (MET orientation)
• Identify cues and triggers for usage
• Self-monitoring of smoking behavior (write down when use)
• Help patients gain understanding of their own tobacco use patterns
• Help increase knowledge about triggers and cues
• Help patients understand environmental influences on their smoking
• Begin education about nicotine, tobacco addiction, withdrawal symptoms, etc.
• Begin disconnecting smoking behavior and linked behaviors (no smoking while driving car, talking on phone, during meal time, etc.)
• Help them get medication evaluation and medications for the quitting phase
Quitting Phase
• Start medications on quit date (NRT) or before quit date (bupropion), sometimes begin NRT (gum, spray, inhaler, not patch) in
small amounts and reduce tobacco usage in an equivalent or greater amount
• Teach specific coping techniques for handling withdrawal symptoms, cues/triggers, and how to enhance social support
• Help patient prepare emotionally, behaviorally, and physically for the quit date and the early abstinence period
• Help identify support systems, anticipate challenges, and address ways to handle people, places, things, and mood challenges
• Address nutrition and exercise components
• Address role of family/friends in supporting or sabotaging treatment
• Continue to strengthen client’s resolve to quit
• Continue relapse prevention therapy approaches
• Assess triggers to craving and use and high-risk situations
• Coping with cravings, thoughts, and urges
• Problem solving
• Smoke refusal skills
• Planning for emergencies
• Seemingly irrelevant decisions
• Relapse analysis for slips
Relapse Prevention Phase
• Continue relapse prevention strategies for long-term abstinence
• Reinforce specific coping skills, including mood management and patient specific triggers
• Teach positive coping skills for dealing with frustration and anxiety
• Compliment success and provide encouragement
• Continue focus on maintaining motivation and commitment for abstinence
• Monitor progress
• Provide treatment within your discipline and make referrals when appropriate
• Encourage the use of peer support such as Nicotine Anonymous, help the client gain personal insight, and keep growing in their
recovery
• Manage any relapses/slips to continue the course
• Continue medications as needed
The importance of each of the biopsychosocial fac- abstinence. Before the quit date, the person should be
tors in initiating and maintaining smoking can vary encouraged to explore and organize social support for
considerably in different individuals. As a result, the self-attempt. Plans to minimize cues associated
smoking cessation interventions should be tailored to with smoking (e.g., avoiding circumstances likely to
the individual and his or her particular circumstances. contribute to relapse) are important, as is considering
This may be one reason why “one size fits all’’ generic alternative coping behaviors for situations with a higher
treatment interventions have had such a low success potential for relapse. A telephone or face-to-face fol-
rate. It must also be kept in mind that nicotine depend- low-up during the first few days after cessation is criti-
ence is as complex in its components and determinants cal because this is the time that withdrawal symptoms
as other addictions and that more comprehensive mul- are most severe, with 65% of individuals relapsing by
ticomponent treatments may be required. 1 week. A follow-up face-to-face meeting within 1 to
When a smoker is ready for a cessation attempt, a 2 weeks allows a discussion of problems that have oc-
“quit date’’ should be selected. After cessation, close curred (e.g., difficulties managing craving) and serves
monitoring should occur during the early period of as an opportunity to provide reinforcement for ongoing
abstinence. Even after the early period of abstinence, 80% of smokers. This is followed by spontaneous strat-
periodic telephone or face-to-face contacts can provide egies to handle cravings and triggers. Some smokers
continued encouragement to maintain abstinence, al- attempt to limit intake, taper the number of cigarettes
low problems with maintaining abstinence to be ad- smoked, or switch to a reduced tar or nicotine brand.
dressed, and provide feedback regarding the health Some geographical areas have Nicotine Anony-
benefits of abstinence. mous groups that are structured similar to Alcoholics
If an initial attempt at cessation using only infor- Anonymous or Narcotics Anonymous groups. These
mation and brief advice from the physician has been groups are based on the 12-Step approach to recovery
unsuccessful, pharmacotherapy may be used unless from addictions. Nicotine Anonymous is a relatively
contraindications are present or unless the person has new organization (founded in 1985) and does not have
had few or no significant withdrawal symptoms. The the extensive network that other 12-Step programs like
most common pharmacotherapy approaches are NRTs Alcoholics Anonymous or Narcotics Anonymous have
(patch, gum, spray, or inhaler) or bupropion (Zyban developed.
for nicotine dependence ⫽ Wellbutrin for depression).
Combining different types of NRT and bupropion is
Brief or Minimal Medical Professional-
becoming more common in clinical practice, includ-
Delivered Interventions/Advice
ing using these medications for at least several months
and in some cases 1 year or longer. Maintenance Even a brief face-to-face intervention by a physician or
medications are being considered in an effort of harm other medical staff can increase the likelihood of ces-
reduction in a more select group of individuals. If a de- sation two- to tenfold. The impact of physicians’ brief
toxification/quit attempt with pharmacotherapy alone advice to quit has received the most study relative to
fails, psychosocial treatments and the use of higher other disciplines such as nursing; however, clearly all
NRT dosages/multiple medications are the next pos- disciplines have opportunity to make an impact. Physi-
sible clinical steps. Psychosocial treatments are often cians can inquire about an individual’s smoking status,
available through organizations such as the American urge the individual to stop smoking, and spend a brief
Cancer Society, the American Lung Association, the time counseling the individual about cessation strate-
American Heart Association, or through local hospi- gies. Multiple follow-up interventions, even telephone
tals that provide health prevention and public education contacts by other medical staff, can further improve the
programs. If pharmacotherapy is unacceptable or con- cessation rate. Resources are available to assist physi-
traindicated, behavioral therapy (BT) alone should be cians in providing effective antismoking interventions,
provided. Failure with pharmacotherapy or BT alone which can even be used by those not highly skilled in
suggests the need for more detailed in-depth assessment counseling. Physicians’ advice appears to be most suc-
and more intensive and multimodal interventions. cessful with individuals with a serious medical problem
or specific medical reason for quitting (e.g., pregnancy
or congestive heart disease). In addition, because an
Self-Help
estimated 70% of smokers in the United States visit
Many smokers have successfully quit smoking without their physicians at least once a year, an important op-
participating in formal treatment. Although only about portunity exists for providing this type of smoking ces-
3–4% are successful during the past year, this success sation intervention.
rate improves with multiple attempts and probable self-
learning through trial and error and learning from oth-
Formal Treatment Options
ers. Eventually, about 50% of smokers are able to quit
and more than 90% of successful quitters have been There are now numerous effective psychosocial and
able to do so without the assistance of professionals or pharmacological approaches that can be used in nico-
formal programs. These numbers reflect multiple fac- tine dependence treatment. Psychosocial intervention
tors, including the limitations on access to treatment alone, pharmacotherapy alone, or combined approaches
(nonexistent health insurance coverage and limited may be used. Given individuals’ preferences and cur-
number of providers with expertise to help), the cumu- rent concerns with cost-effectiveness, less costly sin-
lative process of multiple attempts, learning from oth- gle-modality interventions are often used initially,
ers and from self-help materials, and the severity of the whereas more costly multimodal interventions are of-
nicotine dependence. The primary unassisted method ten reserved for persons for whom cessation attempts
of detoxification from nicotine dependence is precipi- have failed. This may not be the wisest strategy, but
tous cessation (cold turkey), which is used by more than it is the most common. Whether failure with unaided
or minimal intervention attempts may have a negative as-needed basis. Some studies suggest that it is also
effect on future cessation attempts is not known; how- more effective when used for longer than 3 months.
ever, some research suggests that with each repeated Tapering may be necessary after 4 to 6 months of use,
cessation attempt, the person gains additional knowl- especially for individuals using higher total daily doses
edge and experience that may contribute to success in of gum. Nicotine gum requires a highly motivated
future cessation attempts. individual and a good deal of time in instructing the
individual in proper use of the gum. Many individu-
als find the gum difficult to learn to use properly. Side
Somatic Treatments
effects and adverse effects include local irritation in the
Pharmacological interventions have become an impor- mouth, tongue, and throat, mouth ulcers, hiccups, jaw
tant component of treating nicotine dependence. Ap- ache, gastrointestinal symptoms (flatulence, indiges-
proaches used parallel other addictions in treating acute tion, nausea), anorexia, and palpitations.
withdrawal (detoxification), protracted withdrawal, The nicotine patch transdermal delivery system pro-
and even maintenance for harm reduction. The primary vides continual sustained release of nicotine, which is
medications are NRT and bupropion. All six of these absorbed through the skin. This form of nicotine re-
modalities are FDA approved and have demonstrated placement more than doubles the 1-year cessation rate.
efficacy. Other medications may have some potential; There is a dose–response relationship, with individuals
however, they are not FDA approved and have limited receiving higher doses attaining higher cessation rates.
empirical foundation to support their use (Table 21-5). The nicotine patch eliminates the conditioning of re-
NRT is the most widely used medication option and peated nicotine use, which remains present with the use
is available over the counter (patch and gum) or by pre- of other NRT products. Compliance rates are higher
scription (patch, gum, spray, and inhaler). The substi- because it involves once-daily dosing and its adminis-
tuted nicotine initially prevents significant withdrawal tration is simple and discreet. The typical starting dose
symptoms that may lead to relapse during the early pe- of NRT patch is 21 or 15 mg patch; however, in some
riod of smoking cessation. The substituted nicotine is cases multiple patches are used. Lower dose patches
then gradually tapered and discontinued. Replacement available at 7 and 14 mg are used to taper after smoking
produces a lower overall plasma level of nicotine than cessation. The nicotine patch is often used for a total
that experienced with smoking. Replacement not only of 6 to 12 weeks but can be used for much longer. The
avoids the strongly reinforcing peaks in plasma level transdermal patch does not allow for self-titrated dos-
but also prevents the emergence of withdrawal symp- ing, craving, and nicotine withdrawal symptoms like
toms by maintaining the nicotine plasma level above the other NRT routes (gum, spray, inhaler); however,
a threshold. the nicotine blood levels are significantly less than with
Nicotine gum, approved in 1984, was the first NRT smoking. The patch can be used more discreetly and
approved. It slowly releases nicotine. The NRT gum is can be used despite dental or temporomandibular joint
available in doses of 2 and 4 mg, and the recommended problems.
dosing is in the range of 9 to 16 pieces per day. Nicotine Although the nicotine patch is well tolerated, about
gum is more effective when used in conjunction with 25% of individuals have significant local skin irritation
some type of psychosocial intervention, particularly or erythema and 10% discontinue the patch because of
BT. Outcome is more positive when a definite sched- intolerable side effects. Other side effects include sleep
ule for gum use is prescribed—for example, one piece problems with the 24-hour patches. In a few cases,
of gum per hour while awake—than when used on an nicotine toxicity developed when smokers continued
their usual heavy cigarette smoking while using the
transdermal nicotine patch.
Approaches to the Pharmacological
Table 21-5
Treatment of Nicotine Dependence
The nicotine nasal spray is rapidly absorbed and
produces a higher nicotine blood level than does
Nicotine replacement or substitution (agonist transdermal nicotine or gum. It has been suggested that
administration)—FDA-approved nicotine patch, gum,
spray, lozenge, and inhaler the effective daily dose in nicotine dependent smokers
Nonnicotine pill—bupropion/Zyban—FDA approved is 15 to 20 sprays (8–10 mg) per day. Onset of action of
Combinations of nicotine replacement types and/or the spray is the most rapid of all nicotine replacements.
bupropion
Non-FDA-approved experimental options: An initial concern about the nasal spray had been the
Blockade therapy (antagonist administration) potential for abuse because it has the most rapid absorp-
Nonspecific attenuation therapy tion rate of the NRTs. It replicates repeated adminis-
Deterrent therapy
tration of nicotine in smoking, resulting in reinforcing
peaks in the plasma level of the drug. Side effects of maintained on methadone. Although long-term/main-
the spray include local airway irritation (i.e., coughing, tenance use of NRT requires further study, successful
rhinorrhea, lacrimation, nasal irritation), but tolerance maintenance in smokers who have chronic relapses
to these local effects appears to develop. Systemic ef- would potentially reduce a number of the serious health
fects include nausea, headache, dizziness, tachycardia, risks associated with smoking, in spite of individuals
and sweating. still being exposed to the effects of nicotine. Ongoing
The nicotine inhaler provides nicotine through a maintenance antidepressant treatment may also be nec-
cartridge that must be “puffed.’’ It mimics the upper essary for a time for some individuals with a history
airway stimulation experienced with smoking; how- of serious depressive illness or for those who have had
ever, absorption is primarily through the oropharyngeal significant depressive symptoms emerge on cessation
mucosa. Side effects of the inhaler and spray include that do not improve with time.
local irritation, cough, headache, nausea, dyspepsia,
the need for multiple dosing, and the impossibility of
discreet use.
Bupropion, the nonnicotine pill FDA-approved In contrast with the treatment of other substance use
medication option, is an atypical antidepressant. The disorders, psychosocial treatment is underutilized and
effects in smoking cessation appear to be unrelated to has not evolved to be the cornerstone of treatment. This
its antidepressant properties. Smoking cessation rates limited utilization of psychosocial treatments does not
appear to improve further when bupropion is combined match the very positive outcomes from either psycho-
with the nicotine patch. Adverse events have a low in- social treatments alone (25% 1-year abstinence with
cidence and include dry mouth, insomnia, nausea, and BT) or when combined with NRT or bupropion (50%
skin rash. There have been no reports of seizures in any improvement compared to NRT or bupropion alone);
smoking cessation studies to date; however, this agent however, it does match the lack of health care coverage
should not be used in individuals with a history of sei- for this service. The underutilization of psychosocial
zure disorders. treatment has become the cultural norm in nicotine
dependence treatment. This may be due to several im-
Other Antidepressants. Antidepressants have been portant considerations. These include the following: (1)
used in an attempt to attenuate withdrawal symptoms, primary care practitioners most frequently attempt to
to treat or prevent emergent depressive symptoms or address nicotine dependence and do not traditionally
episodes in the early phase of cessation, and to prevent integrate BTs; (2) nicotine dependence treatment is of-
relapse of depressive episodes in individuals with a his- ten not paid for by health care insurance companies;
tory of depression. Antidepressants may provide sig- (3) few behavioral health specialists have been for-
nificant benefits in special populations of individuals mally trained in nicotine dependence treatments; (4)
with current or prior major depressive disorder (MDD), mental health and addiction treatment programs have
dysthymic disorder, or current depressive symptoms ignored addressing tobacco in those treatment settings,
when these factors predict a poor outcome. Given that although this appears to be changing; and (5) individu-
negative affect has been shown to be the most common als are unaware of this treatment modality and its suc-
antecedent of a smoking relapse, this approach appears cess rates, and believe that medications or quitting cold
promising. If antidepressants are used, pretreatment is turkey are all that is needed.
necessary because the benefit of the medication may A great variety of psychosocial interventions have
not be apparent for 1 to 3 weeks. been developed to help in the treatment of nicotine de-
Combined NRTs/bupropion or serial pharmacother- pendence (Table 21-6). As in treating other substance
apeutic approaches may also be beneficial, especially
in more difficult to treat cases of nicotine dependence. Psychosocial Interventions for the Treatment
The combination approach offers the advantage of Table 21-6
of Nicotine Dependence
multiple neurobiological mechanisms of actions. In ad-
Self-help materials
dition, many researchers increasingly believe that peri- Brief advice from the physician
ods of pharmacotherapy should be extended, although Multiple component therapies
the issue of whether longer-term pharmacotherapy is Motivational enhancement therapy
Cognitive–behavioral therapies/relapse prevention
beneficial in improving cessation rates remains unre- Nicotine fading
solved. There may be some smokers who are unable Nicotine Anonymous
to stop smoking without ongoing nicotine replacement, Others used, but with limited empirical support: hypnosis
and acupuncture
similar to individuals dependent on heroin who must be
use disorders, the core psychotherapy approaches are the health of a developing fetus is a situation that re-
motivational enhancement therapy (MET), cognitive– quires immediate intervention. Likewise, a man with
behavioral therapy (CBT) (relapse prevention), and severe cardiac or vascular disease in whom continued
12-Step facilitation. Psychosocial interventions, partic- smoking poses a serious threat to health or life may re-
ularly BT, have been shown to increase abstinence rates quire immediate aggressive multimodal interventions.
significantly. However, only 7% of smokers attempting The skills, knowledge, and experience of a nicotine
to quit smoking are willing to participate in BT. In ad- dependence treatment specialist may be required in
dition, it is more expensive than pharmacotherapy and complex cases in which more intensive or aggressive
more labor-intensive. individualized treatment is indicated or when more
Despite the fact that there has been little controlled complex psychosocial interventions such as relapse
research examining whether psychosocial intervention prevention are tailored to the individual. Smokers who
with spouses and significant others or families can in- suffer repeated relapses may require more frequent
crease abstinence rates, overall social support for indi- monitoring as well as coordination of multiple services
viduals who are attempting to stop smoking appears to or interventions that can involve considerable expendi-
improve the outcome. Others in the smoker’s immedi- ture of clinical time. This is especially true for persons
ate family or social circle can be involved in their treat- with serious medical or psychiatric problems, or for
ment through education about appropriate supportive pregnant women who require careful coordination of
behaviors. Concerned others can also be engaged in treatment through active collaboration with medical
treatment to provide assessment information or to help caretakers. The person providing or overseeing treat-
enhance the individual’s motivation. ment for smokers who have chronic relapses must ac-
Hypnosis and acupuncture are two approaches that cept the reality of an ongoing long-term relationship
some individuals believe have helped them in their ef- that may be demanding of her or his time and attention
forts to quit smoking; however, there is limited research as well as clinical acumen if appropriate support and
support for these approaches and treatment guidelines monitoring are to be available.
still list them as potentially promising approaches. Some smokers may not be able to achieve successful
Studies suggest that hypnosis has little more than a abstinence with outpatient treatment despite intensive
weak positive effect on outcome in smoking cessation. multiple interventions. Inpatient treatment represents
Meta-analysis of studies on the effect of acupuncture a drastic intervention that should be reserved for the
shows no evidence of efficacy on the outcome of smok- most treatment-resistant individuals who have been
ing cessation. Positive effects likely represent a placebo completely unsuccessful despite repeated attempts
effect related to the individual’s expectations. and treatment with a variety of interventions. Inpatient
treatment can provide the most intensive and aggres-
sive program of treatment interventions coupled with
Combined Psychosocial and
close monitoring and prevention of access to nicotine.
Psychopharmacological Therapies
It requires a commitment of both time and money, how-
All nicotine dependence treatment practice guidelines ever, as almost no insurance policies reimburse for such
recommend the integration of nicotine dependence treatment. Inpatient nicotine dependence treatment is
treatment medications (NRT and bupropion) with be- usually 1 week in duration. Follow-up data from the
havioral and supportive psychosocial treatment ap- few programs in existence suggest that it may be effec-
proaches. Empirical evidence supports the finding that tive for some highly treatment-resistant smokers.
medications double the quit rate compared to placebo,
and face-to-face therapy can double the quit rate com-
Treatment with Co-Occurring Mental Illness
pared to minimal psychosocial intervention. Therapy
or Other Addictions
also can increase medication compliance. Integrated
treatment further increases the quit rate by another Individuals with nicotine dependence and either a
50% and triples the outcome rate. co-occurring mental illness, another addiction, or all
three are more likely to be seeking treatment and re-
quire some modifications in the traditional nicotine
Managing Repeated Relapses
treatment approach. A critical issue in the treatment
The degree of aggressiveness in treating smokers who planning is the timing of the nicotine dependence
have repeated relapses will depend in part on the imme- treatment. There is literature supporting treating all
diacy and seriousness of the consequences of continued together and also in delaying the nicotine dependence
smoking. For example, a pregnant woman endangering treatment until the other problems are stabilized.
Successful nicotine dependence treatment in persons There is a growing literature supporting that treat-
with active alcohol dependence is less likely than ment can be effective with these harder-to-treat
in individuals recovering from alcohol dependence; smokers when motivational enhancement, NRT med-
however, a few addiction treatment programs have ad- ications, psychiatric medications, and psychotherapy
dressed both problems simultaneously with success. are integrated.
Nicotine replacement appears to be especially ben-
eficial in helping smokers with co-occurring mental
illness and addiction. Appropriate treatment of the
DIAGNOSTIC CRITERIA
mental illness or other addiction is also important,
including appropriate medications and therapy ap- The DSM-IV-TR and ICD-10 symptom lists for nico-
proaches. These individuals often benefit from cli- tine withdrawal include some different items: the
nicians beginning with a motivational enhancement ICD-10 list has craving, malaise, increased cough, and
approach that enhances the smoker’s readiness to mouth ulceration and does not include the DSM-IV-TR
change and self-efficacy. decreased heart rate item.
CHAPTER
Opioids
The term opioids describes a class of substances that induced mood disorder, opioid-induced sexual dys-
acts on opioid receptors. Opioids can be naturally oc- function, and opioid-induced sleep disorder.
curring substances such as morphine, semisynthetics
such as heroin, and synthetics with morphine-like ef-
Opioid Dependence
fects such as meperidine. These drugs are prescribed as
analgesics, anesthetics, antidiarrheal agents, or cough Opioid dependence is diagnosed by the signs and
suppressants. In addition to morphine and heroin, the symptoms associated with compulsive, prolonged self-
opioids include codeine, hydromorphone, methadone, administration of opioids that are used for no legitimate
oxycodone, and fentanyl, among others. Drugs such as medical purpose, or if a medical condition exists that
buprenorphine and pentazocine, an agonist–antagonist, requires opioid treatment, are used in doses that greatly
are also included in this class because their physiologic exceed the amount needed for pain relief (see generic
and behavioral effects are mediated through opioid DSM-IV-TR diagnostic criteria for Substance Depend-
receptors (Table 22-1). ence in Chapter 13, page 125). Persons with opioid
Opioids are the most effective medications for relief dependence typically demonstrate continued use in
of severe pain and are widely used for that purpose. spite of adverse physical, behavioral, and psychological
The more potent opioids approved for medical use are consequences. Almost all persons meeting criteria for
under DEA schedule II—examples are fentanyl, hydro- opioid dependence have significant levels of tolerance
morphone, methadone, and morphine; others are under and will experience withdrawal upon abrupt discontin-
schedules III and IV. uation of opioid drugs. Persons with opioid dependence
tend to develop such regular patterns of compulsive
use that daily activities are typically planned around
DIAGNOSIS
obtaining and administering drugs. Unlike cocaine,
As with other substances, there are two general catego- hallucinogens, solvents, and other substances that do
ries of opioid-related disorders: opioid use disorders and not always produce withdrawal symptoms, opioid de-
opioid-induced disorders. Opioid use disorders include pendence is almost always accompanied by significant
opioid dependence and opioid abuse. Opioid depend- physiological tolerance and a defined withdrawal–
ence has two sets of specifiers, the first set being with abstinence syndrome.
physiologic features (i.e., tolerance and/or withdrawal), Opioids are usually purchased on the illicit market,
or without physiologic features. The second set consists but they can also be obtained by forging prescriptions,
of course specifiers: early full remission, early partial faking or exaggerating medical problems, or by receiv-
remission, sustained full remission, sustained partial ing simultaneous prescriptions from several physi-
remission, on agonist therapy, and in a controlled envi- cians. Physicians and other health care professionals
ronment. The agonist therapy specifier is used only to who are dependent will often obtain opioids by writ-
note the status of opioid dependence, and not for other ing prescriptions or by diverting opioids that have been
opioid-related disorders or substance dependencies. prescribed for their own patients.
Opioid-induced disorders include opioid intoxica-
tion, opioid withdrawal, opioid intoxication delirium
Opioid Abuse
(see the summary of DSM-IV-TR diagnostic crite-
ria for substance-induced disorders in Chapter 13, Opioid abuse is a maladaptive pattern of intermittent
page 125), opioid-induced psychotic disorder, opioid- use in hazardous situations (driving under the influence,
Chapter 22 • Substance-Related Disorders: Opioids 197
Table 22-1 Opioids*

Plasma
Active Route of Relative Half-Life Duration of
Drug Metabolite Administration Potency Medical Use (Hours) Action (Hours)
Morphine IM 1 Analgesia 2 4–6

Heroin Morphine IM 1–2 None 0.5 3–5
Codeine PO 0.05 Analgesia, 2–4 4–6
antitussive
Fentanyl IM 40–100 Analgesia 3–4 1–2
Hydromorphone IM 13 Analgesia 2–3 4–6
Oxycodone PO 0.5–1 Analgesia 4–6
Methadone PO 0.50 Analgesia, opioid 15–40 18–30
substitution
l-α-Acetylmethadol PO 0.40 Opioid substitution 14–104† 48–80
(LAAM)
Nor-LAAM 13–130†
Dinor- 97–430†
LAAM
Buprenorphine SL N/A (partial Analgesia (opioid 6–12 4–6 (for analgesia)
agonist) substitution, 12–48‡
investigational)
*
IM, intramuscular; PO, by mouth; SL, sublingual; N/A, not applicable.
†
At steady state.
‡
Appears to be dose dependent.
being intoxicated while using heavy machinery, work- slowing of gastrointestinal activity, and constipation
ing in dangerous places, etc.), or periodic use resulting are associated with both acute and chronic opioid use.
in adverse social, legal, or interpersonal problems (see Visual acuity may be impaired as a result of pupillary
generic DSM-IV-TR diagnostic criteria for Substance constriction. The magnitude of the behavioral and
Abuse in Chapter 13, page 125). All of these signs and physiologic changes depends on the dose as well as in-
symptoms can also be seen in persons who are depend- dividual characteristics of the user such as rate of ab-
ent; abuse is characterized by less regular use than de- sorption, chronicity of use, and tolerance. Symptoms
pendence (i.e., compulsive use not present) and by the
absence of significant tolerance or withdrawal. As with
other substance use disorders, opioid abuse and depend- DSM-IV-TR Diagnostic Criteria
ence are hierarchical and thus, persons diagnosed as
having opioid abuse must never have met criteria for 292.89 OPIOID INTOXICATION
opioid dependence.
A. Recent use of an opioid.
chological changes (e.g., initial euphoria followed by
apathy, dysphoria, psychomotor agitation or retarda-
Opioid Intoxication tion, impaired judgment, or impaired social or occu-
pational functioning) that developed during, or shortly
Opioid intoxication is characterized by maladaptive after, opioid use.
and clinically significant behavioral changes devel- C. Pupillary constriction (or pupillary dilation due to an-
oping within minutes to a few hours after opioid use. oxia from severe overdose) and one (or more) of the
following signs, developing during, or shortly after,
Symptoms include an initial euphoria sometimes fol- opioid use:
lowed by dysphoria or apathy. Psychomotor retarda-
1. drowsiness or coma
tion or agitation, impaired judgment, and impaired so- 2. slurred speech
cial or occupational functioning are commonly seen. 3. impairment in attention or memory
Intoxication is accompanied by pupillary constriction D. The symptoms are not due to a general medical condi-
unless there has been a severe overdose with conse- tion and are not better accounted for by another men-
tal disorder.
quent anoxia and pupillary dilatation. Persons with
intoxication are often drowsy (described as being “on Specify if:
the nod’’) or even obtunded, have slurred speech, im- With perceptual disturbances
paired memory, and demonstrate inattention to the en- Reprinted with permission from the Diagnostic and Statistical
vironment to the point of ignoring potentially harmful Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
events. Dryness of secretions in the mouth and nose,
Table 22-2 Signs and Symptoms of Opioid Intoxication

that has been heavy and prolonged. It can also be
precipitated by administration of an opioid antago-
Symptoms nist such as naloxone or naltrexone. Individuals in
Euphoria, dysphoria, or apathy
Psychomotor retardation or agitation opioid withdrawal typically demonstrate a pattern of
Impaired judgment, social, or occupational functioning signs and symptoms that are opposite from the acute
Signs agonist effects. The fi rst of these are subjective and
Pupillary constriction consist of complaints of anxiety, restlessness, and an
Drowsy or obtunded
Slurred speech, impaired memory, and inattention to
“achy feeling’’ that is often located in the back and
environment legs. These symptoms are accompanied by a wish
Dryness in mouth or nose to obtain opioids (sometimes called “craving’’) and
Slowed gastrointestinal activity and constipation
Severe intoxication can lead to coma, respiration drug-seeking behavior, along with irritability and in-
depression, pupillary dilation, unconsciousness, and creased sensitivity to pain. Additionally, individuals
death. typically demonstrate three or more of the following:
dysphoric or depressed mood, nausea or vomiting,
of opioid intoxication usually last for several hours, but diarrhea, muscle aches, lacrimation or rhinorrhea,
are dependent on the half-life of the particular opioid increased sweating, yawning, fever, insomnia, pupil-
that has been used. Severe intoxication following an lary dilatation, fever, and piloerection. Piloerection
opioid overdose can lead to coma, respiratory depres- and withdrawal-related fever are rarely seen in clini-
sion, pupillary dilatation, unconsciousness, and death cal settings (other than prison) as they are signs of ad-
(Table 22-2). vanced withdrawal in persons with a very significant
degree of physiologic dependence; opioid-dependent
persons with “habits’’ of that magnitude usually man-
Opioid Withdrawal age to obtain drugs before withdrawal becomes so far
Opioid withdrawal is a clinically significant, mala- advanced (Table 22-3).
daptive behavioral and physiological syndrome as- For short-acting drugs such as heroin, withdrawal
sociated with cessation or reduction of opioid use symptoms occur within 6 to 24 hours after the last
dose in most dependent persons, peak within 1 to
3 days, and gradually subside over a period of 5 to
DSM-IV-TR Diagnostic Criteria 7 days. Symptoms may take 2 to 4 days to emerge in
the case of longer-acting drugs such as methadone or
292.0 OPIOID WITHDRAWAL levo-alpha-acetylmethadol (LAAM). Less acute with-
A. Either of the following: drawal symptoms are sometimes present and can last
for weeks to months. These more persistent symptoms
(1) cessation of (or reduction in) opioid use that has
been heavy and prolonged (several weeks or can include anxiety, dysphoria, anhedonia, insomnia,
longer) and drug craving.
(2) administration of an opioid antagonist after a pe-
riod of opioid use
Opioid use disorders can occur at any age, includ-
ing adolescence and the geriatric years, but most af-
B. Three (or more) of the following, developing within
minutes to several days after Criterion A: fected persons are between 20 and 45 years. There
(1) dysphoric mood
(2) nausea or vomiting Table 22-3 Signs and Symptoms of Opioid Withdrawal
(3) muscle aches
(4) lacrimation or rhinorrhea Symptoms
(5) papillary dilation, piloerection, or sweating Anxiety, irritability, restlessness
(6) diarrhea Muscle aching
(7) yawning Craving for opioids
(8) fever Increased pain sensitivity
(9) insomnia
Signs
C. The symptoms in Criterion B cause clinically signifi- Dysphoric or depressed mood
cant distress or impairment in social, occupational, or Nausea/vomiting/diarrhea
other important areas of functioning. Lacrimation/rhinorrhea
D. The symptoms are not due to a general medical condi- Sweating
tion and are not better accounted for by another men- Yawning
tal disorder Insomnia
Reprinted with permission from the Diagnostic and Statistical Pupillary dilatation
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 Piloerection
American Psychiatric Association. Fever
have recently been increasing numbers of reports of chromatography/mass spectrometry. Testing for fenta-
adolescents presenting for treatment with opioid prob- nyl is not necessary in most programs, but needs to be
lems, but good data are hard to find. Neonates whose performed in assessing and treating health care profes-
mothers are addicted can also experience opioid with- sionals such as anesthesiologists who have access to
drawal. Rarely, young children are affected, with some this drug. Concomitant laboratory evidence of other
cases of dependence having been reported in persons abusable substances such as cocaine, marijuana, alco-
who are 8 to 10 years of age. Males are more com- hol, amphetamines, and benzodiazepines is common.
monly affected, with the male–female ratio typically Hepatitis screening tests are often positive, either for
being 3 or 4 to 1. hepatitis B antigen (signifying active infection) or hep-
A nonjudgmental and supportive yet firm approach atitis B and/or C antibody (signifying past infection).
to these individuals is especially important. They Mild to moderate elevations of liver function tests are
typically have engaged in antisocial or other forms common, usually as a result of chronic infection with
of problematic behavior. They are often embarrassed hepatitis C but also from toxic injury to the liver due to
or afraid to describe the extent of their behavior, and contaminants that have been mixed with injected opio-
have extremely low self-esteem. At the same time, ids, or from heavy use of other hepatotoxic drugs such
they are prone to be impulsive, manipulative, and to as alcohol. Low platelet count, anemia, or neutropenia,
act-out when frustrated. Communicating a feeling of as well as positive HIV tests or low CD-4 cell counts
nonjudgmental support in the context of setting lim- are often signs of HIV infection. HIV is commonly ac-
its, along with a clear and informed effort to provide quired via the practice of sharing injection equipment,
appropriate help, will encourage optimum therapeutic or by unprotected sexual activity that may be related
opportunities. to the substance use disorder, for example, exchanging
On physical examination, sclerosed veins (“tracks’’) sex for drugs or money to buy drugs.
and puncture marks on the lower portions of the upper
extremities are common in intravenous users. When
Course
these veins become unusable or otherwise unavailable,
persons will usually switch to veins in the legs, neck, Opioid dependence can begin at any age, but problems
or groin. Veins sometimes become so badly sclerosed associated with opioid use are most commonly first
that peripheral edema develops. When intravenous ac- observed in the late teens or early twenties. Once de-
cess is no longer possible, persons will often inject di- pendence occurs, it is usually continuous over a period
rectly into their subcutaneous tissue (“skin-popping’’) of many years even though periods of abstinence are
resulting in cellulitis, abscesses, and circular-appearing frequent. Reoccurrence is common even after many
scars from healed skin lesions. Tetanus is a relatively years of forced abstinence, such as occurs during in-
rare but extremely serious consequence of injecting carceration. Increasing age appears to be associated
into the subcutaneous tissues. Infections also occur in with a decrease in prevalence. This tendency for de-
other organ systems, including bacterial endocarditis, pendence to remit generally begins after age 40 and
hepatitis B and C, and HIV infection. has been called “maturing out.’’ Many persons, how-
Persons who “snort’’ heroin or other opioids often ever, have remained opioid dependent for 50 years or
develop irritation of the nasal mucosa. Difficulties in longer. Thus, though spontaneous remission can and
sexual function are common, as are a variety of sexu- does occur, most cases of untreated opioid dependence
ally transmitted diseases. Males often experience pre- follow a chronic, relapsing course for many years.
mature ejaculation associated with opioid withdrawal,
and impotence during intoxication or chronic use.
Females commonly have disturbances of reproductive
function and irregular menses. Individuals who are dependent on “street’’ opioids are
During dependence, routine urine toxicology tests usually easy to diagnose because of the physical signs
are often positive for opioid drugs and remain posi- of intravenous use, drug-seeking behavior, reports
tive for most opioids for 12 to 36 hours. Methadone from independent observers, the lack of medical justi-
and LAAM, because they are longer acting, can be fication for opioid use, urine test results, and the signs
identified for several days. Fentanyl is not detected by and symptoms of intoxication or withdrawal.
standard urine tests but can be identified by more spe- The signs and symptoms of opioid withdrawal are
cialized procedures. Oxycodone, hydrocodone, and hy- fairly specific, especially lacrimation and rhinorrhea,
dromorphone are often not routinely included on urine which are not associated with withdrawal from any other
toxicology tests though they can be identified by gas abusable substances. Other psychoactive substances
with sedative properties such as alcohol, hypnotics, or analog that appears to have less hypotensive and sedat-
anxiolytics can cause a clinical picture that resembles ing effects. The depot dosage form of naltrexone may
opioid intoxication. A diagnosis can usually be made increase compliance with a medication that has been
by the absence of pupillary constriction, or by the lack an effective opioid antagonist, but which has been un-
of response to a naloxone challenge. In some cases, in- derutilized because of poor acceptance by individuals.
toxication is due to opioids along with alcohol or other In almost every treatment episode using pharmacother-
sedatives. In these cases, the naloxone challenge will not apy, it is combined with some type of psychosocial or
reverse all of the sedative drug effects. behavioral treatment. Recent research has documented
Difficult diagnostic situations are seen among the value of these additional treatments and provided
persons who fabricate or exaggerate the signs and insight into the ones that are the most effective.
symptoms of a painful illness (such as kidney stones,
migraine headache, back pain, etc.). Because pain is
Detoxification: Long-Term, Short-Term, Rapid,
subjective and difficult to measure, and because some
and Ultrarapid
of these individuals can be very skillful and deceptive,
diagnosis can be difficult and time-consuming. Persons Detoxification from opioids, for most individuals, is
with opioid dependence will often present with psychi- only the first phase of a longer treatment process. Phar-
atric signs and symptoms such as depression or anxi- macological detoxification is generally ineffective in
ety. Such subjective distress often serves to motivate achieving sustained remission unless combined with
the individual to seek treatment, and thus can be thera- long-term pharmacologic, psychosocial, or behavioral
peutically useful. These symptoms can be the result of therapies. Most individuals seeking treatment have
opioid intoxication or withdrawal, or they might result been addicted to heroin or other opioids for 2 to 3 years,
from the pharmacological effects of other substances and some for 30 years or more. Thus, treatment usu-
that are also being abused such as cocaine, alcohol, or ally involves changes in individuals’ lifestyles. Though
benzodiazepines. They may also represent independ- generally ineffective in achieving sustained remission
ent, non-substance-induced psychiatric disorders that unless combined with long-term pharmacological, psy-
require long-term treatment. The correct attribution chosocial, or behavioral therapies, detoxification alone
of psychiatric symptoms that are seen in the context continues to be widely used.
of opioid dependence and abuse follows the principles The detoxification process may include use of opioid
that are outlined in the substance-related section and agonists (e.g., methadone), partial agonists (e.g., bu-
other relevant parts of DSM-IV-TR. prenorphine), antagonists (e.g., naloxone, naltrexone),
Opioids are much less likely to produce psychopa- or nonopioid alternatives such as clonidine, benzodi-
thology than most other drugs of abuse, and in some azepines, or nonsteroidal anti-inflammatory agents. In
instances, they reduce psychiatric symptoms. In these many cases, one or more medications are combined,
cases, symptoms will emerge not during opioid use, but such as naloxone with clonidine and a benzodiazepine
after it is discontinued. Examples have been observed (Table 22-4). The choice of detoxification medication
by clinicians in methadone maintenance programs, and the duration of the process depend on numerous
who occasionally see an exacerbation of symptoms of factors, including individual preference, clinician ex-
schizophrenia, posttraumatic stress disorder (PTSD), pertise and experience, type of treatment facility,
or other problems in individuals who discontinue licensing, and available resources. Ultimately, how-
chronic opioid use. ever, the goal of detoxification is the achievement (and
maintenance) of a drug-free state while minimizing
withdrawal.
TREATMENT
Opioid detoxification paradigms are frequently
There are currently a number of effective pharmaco- categorized according to their duration: long-term
logical and behavioral therapies for the treatment of
opioid dependence, with these two approaches often
Pharmacologic Agents in Opioid
combined to optimize outcome. There are also some Table 22-4
Detoxification
newer treatment options, which may take various forms.
For example, methadone maintenance is an established Opioid agonists (methadone)
Partial agonists (buprenorphine)
treatment, while the use of buprenorphine/naloxone Antagonists (naloxone, naltrexone)
in an office-based setting represents a new variation Nonopioid alternatives (clonidine, benzodiazepines,
on that theme. Clonidine has been used extensively to nonsteroidal anti-inflammatory agents)
Combinations of above medications
treat opioid withdrawal while lofexidine is a structural
(typically 180 days), short-term (up to 30 days), rapid adverse events, including sudden unexpected deaths,
(typically 3–10 days), and ultrarapid (1–2 days). These have occurred in association with this procedure and
temporal modifiers provide only a coarse description its use should probably be limited to inpatient settings
of the paradigm; they do not provide other important where monitoring by anesthesiologists and other highly
information such as the medications used or whether trained staff is available.
postdetoxification pharmacological, psychosocial, or Buprenorphine, a µ-opioid partial agonist, has also
behavioral therapy is provided. However, some general been used as a detoxification agent. Results from inpa-
guidelines typically apply. tient and outpatient studies have shown that it is safe,
The most common detoxification protocols, and well tolerated, and mitigates opioid withdrawal signs
those for which the most data are available, are the and symptoms over a range of doses and detoxification
long-term (typically 180 days) and short-term (up to schedules. Clonidine, an alpha-2-adrenergic agonist,
30 days) paradigms involving the use of methadone. has been shown to suppress many of the autonomic
Unfortunately, these strategies have not generally been signs and symptoms of opioid withdrawal. It can cause
associated with acceptable treatment response using sedation and hypotension but has been used with few
relapse to opioid use as an outcome criterion. Results problems when appropriate monitoring is available. It
from more rapid detoxification evaluations using short- does not suppress the subjective discomfort of with-
or even intermediate-term (up to 70 days) medication- drawal, and probably for that reason, is not well ac-
tapering protocols are even less encouraging and have cepted by most individuals.
an unfortunately low success rate. It should be noted, Other alpha-2-adrenergic agonists have also been
however, that provision of additional services such as evaluated in order to find agents that are as or more
counseling, behavioral therapy, treatment of underly- effective, but less sedating and hypotensive than clo-
ing psychopathologies, job skills training, and family nidine. Lofexidine, a medication that was originally
therapy to address concomitant treatment needs can promoted as an antihypertensive but was shown to
improve outcome though success rates remain low, lack clinically significant hypotensive effects, has been
even with these services. the most studied. Lofexidine is likely to be shown to
Rapid detoxification involves the use of an opioid an- be a useful opioid detoxification agent whose efficacy
tagonist, typically naltrexone or naloxone, in combina- approximates that of clonidine but with fewer side
tion with other medications (such as clonidine and ben- effects.
zodiazepines) to mitigate the precipitated withdrawal
syndrome. The procedure is intended to expedite and
Opioid Agonist Pharmacotherapy
compress withdrawal in order to minimize discomfort
and decrease treatment time. Ultrarapid detoxification Methadone maintenance has become the most com-
also utilizes other medications, along with an opioid monly used pharmacotherapy for opioid dependence.
antagonist, to moderate withdrawal effects. However, Methadone suppresses opioid withdrawal for 24 to
rather than individuals being awake as they are during 36 hours following a single oral dose, making it an
the rapid detoxification process, they are placed under ideal medication for this purpose. Another µ-opioid
general anesthesia or alternatively, deeply sedated. agonist, LAAM, received FDA approval for mainte-
A major concern regarding ultrarapid detoxification nance treatment in 1993. LAAM is a long-acting con-
is the occurrence of potentially serious adverse effects, gener of methadone, which suppresses withdrawal for
such as respiratory distress, or other pulmonary and re- 48 to 72 hours, and thus has the advantage of requiring
nal complications during or immediately following the less frequent clinic visits than methadone, which must
procedure. A high frequency of vomiting has also been be taken daily. A third medication, buprenorphine, has
reported. The degree to which serious adverse events unique properties that are likely to result in it being
occur has not yet been determined; however, there have used with fewer regulatory controls than methadone
been reports of sudden death occurring shortly after the and LAAM.
procedure, which was not caused by relapse to opioid Both methadone and LAAM are Schedule II con-
use and overdose. trolled substances and can only be used for mainte-
In spite of the emerging evidence about serious ad- nance and detoxification in programs that are licensed
verse events, ultrarapid detoxification may be appropri- and regulated by the FDA and the Drug Enforcement
ate for highly selected individuals based on considera- Administration (DEA).
tions of previous treatment history, economic factors, This combination of FDA and DEA regulations has
and individual choice. However, individuals seeking resulted in a treatment system that is separated from
this treatment must be thoroughly informed that serious the mainstream of other medical care and that consists
almost entirely of specially licensed and inspected Buprenorphine in combination with naloxone has
clinics. less potential for abuse than buprenorphine alone.
The appropriate dose of agonist medication has been The therapeutic utility of combining naloxone with
a subject of both federal and state regulations, although buprenorphine derives from the low sublingual bioa-
there has been a gradual shift toward allowing more vailability of naloxone as compared to buprenorphine.
clinical judgment in its determination. A number of Parenteral misuse of the combination by persons ad-
studies have been done during the past 25 years to de- dicted to opioids would be expected to produce an-
termine the optimal dose and, although it is clear that tagonist-like effects; thus, most persons with opioid
some individuals do well on low doses of methadone dependence would be unlikely to inject the combina-
or LAAM (about 20–50 mg), studies have consistently tion more than once. The use of the buprenorphine/
shown that most individuals need higher doses, in the naloxone combination in an office-based setting repre-
80–120 mg range, if they are to achieve maximum ben- sents an innovative alternative to the restrictive metha-
efit from agonist treatment. Clear relationships between done or LAAM maintenance paradigm described pre-
methadone blood levels and clinical response have not viously and should expand the availability of agonist
been observed consistently, suggesting that some indi- maintenance treatment with a relatively low risk for
viduals may be more sensitive to dose changes and that abuse or diversion. In addition, the partial agonist ac-
clinical response, including subjective complaints, is a tivity of buprenorphine results in a much lower risk
more important guide to adequate dosing than blood for overdose death than is the case with methadone or
levels. No controlled studies have been done examining LAAM.
doses above 120 mg; thus, the upper limits of dosing
effectiveness are not well understood.
Antagonist Maintenance
Physicians who choose to treat persons with opioid
dependence under new DEA regulations will need to Naltrexone is the prototypical opioid antagonist used
notify the Secretary of Health and Human Services in in abstinence therapy, blocking the effects of heroin
writing of their intent and show that they are qualified and other opioids through competitive receptor inhi-
to provide addiction treatment by virtue of certification bition. Naltrexone has no opioid agonist effects and
or experience. No physician will be allowed to treat is a competitive opioid antagonist. It is orally effec-
more than 30 individuals at one time without special tive and can block opioid effects for 24 hours when
approval according to the proposed legislation. administered as a single daily dose of 50 mg; doses of
This change in the regulations is especially im- 100–150 mg can block opioid effects for 48–72 hours.
portant for buprenorphine and the buprenorphine/ Despite a favorable adverse event profile (nausea is
naloxone combination, as it provides better access to typically the most common side effect), naltrexone is
treatment for persons who are unwilling or unable to generally not favored by opioid addicts because, un-
be treated in the current methadone or LAAM system. like opioid agonists and partial agonists, it produces
The overall intent of the regulatory reform is to better no positive, reinforcing effects. Furthermore, it may
integrate maintenance treatment into the mainstream be associated with the precipitation of an opioid with-
of medical care, and to make it more available and im- drawal syndrome if used too soon after opioid use
prove its quality. stops, an effect that can be minimized by administer-
The greatest advantage of buprenorphine compared ing a naloxone challenge prior to giving the first dose
to full agonists such as methadone and LAAM is the of naltrexone.
plateau effect of its agonist activity. Parenteral doses as While there is a literature spanning more than
high as 12 mg intravenously have been given to individ- 25 years on naltrexone treatment, work continues on
uals who are not tolerant to opioids with only limited increasing compliance and improving outcomes. Pres-
adverse effects (e.g., sedation, irritability, nausea, itch- ently, an individual treated with naltrexone has only to
ing). A number of large trials have confirmed the utility stop the medication for 1 to 3 days in order to experi-
of buprenorphine for agonist maintenance therapy. ence the full effects of subsequent opioid use. A depot
Buprenorphine has the potential to be abused and can dosage form of naltrexone would provide more time for
produce addiction; however, most persons who abuse individuals to overcome ambivalence about stopping
buprenorphine initiated opioid use with other drugs. opioid use and could result in more long-term success
Abuse may take the form of using greater than pre- than has currently been the case. Another variant on
scribed dosages for analgesia, using buprenorphine in antagonist treatment is nalmefene, an orally effective
place of a more desired but less available opioid, or us- but somewhat longer acting (about 48 hours at dosages
ing buprenorphine for its positive reinforcing effects. of 50–100 mg/day) opioid antagonist that has been used
for alcohol treatment and shows promise as an alterna- unless they keep appointments, and others suspend
tive to naltrexone for opioid dependence. individuals who miss appointments. For noncompli-
ant individuals, a powerful contingency is requiring
certain behaviors for individuals to remain on the pro-
gram, a procedure that is often formalized in a “treat-
As in other substance use disorders, most individu- ment contract.’’ Here, the individual is given the option
als with opioid dependence and abuse are ambivalent of stopping heroin and other drug use, keeping regular
about stopping use. This ambivalence presents a chal- counseling appointments, looking for work, or correct-
lenge as it contributes to varying levels of motivation to ing other behaviors that need improvement as a condi-
enter and remain in treatment, to early dropout, and to tion for remaining in treatment. Individuals who fail
partial or (in some cases) nontreatment response. Cli- are administratively detoxified, suspended for months
nicians must be aware of this “normal’’ ambivalence, to years, and referred to another program, although
and make reasonable efforts to resolve it in favor of the referrals are not always successful. The long-term
treatment participation and cessation of use. Sugges- effects of this form of contingency management have
tions that have been made regarding initial steps to not been well studied.
maximize the chances for engagement in treatment and
cessation of drug use include avoiding unnecessary
Addressing Comorbidity
delays in entering treatment, expressing a hopeful and
nonjudgmental attitude, performing a comprehensive Individuals seeking treatment for opioid dependence
evaluation, and developing a treatment plan that is re- are typically using one or more other substances (co-
sponsive to the individual’s self-identified goals. caine, alcohol, benzodiazepines, amphetamines, mari-
In addition to challenges related to ambivalence, in- juana, nicotine), and have additional problems in the
dividuals often have serious problems with nonopioid psychiatric, medical, family/social, employment, or
substance abuse and/or with medical, psychiatric, legal, legal areas. In fact, it is rare to find a person with only
employment, and family/social issues that preexist or opioid dependence and no other substance use, or with-
result from the addiction. Addressing these additional out a psychiatric, medical, or family/social problem.
problems can be helpful, but is complex and requires The presence of these problems, perhaps with the ex-
coordination between agonist pharmacotherapy staff, ception of nicotine dependence, tends to magnify the
and other medical and psychosocial services. severity of the opioid dependence and makes the indi-
The most common type of psychosocial treatment vidual even more difficult to treat.
in opioid agonist maintenance is individual drug coun- Among the mental disorders seen in persons with
seling. Counselors are typically persons at the masters opioid dependence, antisocial personality disorder is
level or below who deliver a behaviorally focused treat- one of the most common. Diagnostic studies of persons
ment aimed to identify specific problems, help the indi- with opioid dependence have typically found rates of
vidual access services that may not be provided in the antisocial personality disorder ranging from 20% to
clinic (e.g., medical, psychiatric, legal, family/social), 50%, as compared to less than 5% in the general popu-
stop substance use, and improve overall adjustment. lation. PTSD is also seen with increased frequency.
Functions that counselors perform include monitoring Opioid-dependent persons are especially at risk for
methadone and LAAM doses and requesting changes the development of brief depressive symptoms, and
when needed, reviewing urine test results, responding for episodes of mild to moderate depression that meet
to requests for take-home doses, assisting with family symptomatic and duration criteria for major depressive
problems, responding to crises, writing letters for court disorder or dysthymia. These syndromes represent both
or social welfare agencies, recommending inpatient substance-induced mood disorders as well as independ-
treatment when necessary, and providing support and ent depressive illnesses. Brief periods of depression are
encouragement for a drug-free lifestyle. especially common during chronic intoxication or with-
Other approaches involve group therapy, contin- drawal, or in association with psychosocial stressors
gency management techniques, self-help groups, and that are related to the dependence. Insomnia is com-
outpatient-based therapeutic community programs. mon, especially during withdrawal; sexual dysfunction,
Though counseling and other services are effective especially impotence, is common during intoxication.
enhancements of agonist treatment, compliance is of- Delirium or brief, psychotic-like symptoms are occa-
ten an issue and clinics vary in the way they respond sionally seen during opioid intoxication.
to this problem. Some remind individuals of appoint- Less than 5% of persons with opioid dependence
ments, others do not permit individuals to be medicated have psychotic disorders such as bipolar illness or
schizophrenia; however, these individuals can present more studies are needed to map out the full extent
special problems since programs typically have few of these interactions. One important interaction is
psychiatric staff. As a result, these individuals are that methadone increases plasma levels of zidovu-
sometimes excluded from methadone treatment be- dine; the associated symptoms resemble methadone
cause they cannot be effectively managed within withdrawal. There have been instances in which
the constraints of the available resources. Others are methadone doses have been increased in response to
treated with methadone, counseling, and the same complaints of withdrawal with increasing doses com-
medications used for nonaddicted individuals with pounding the problem. Another important interaction
similar disorders. Though studies evaluating the out- involves decreased methadone blood levels second-
come of combining opioid agonist treatment with an- ary to nevirapine that may result in mild to moder-
tipsychotic or antimanic medications have not been ate withdrawal. This interaction can be important if
done, there is little controversy that these medications the individual is taken off either of these two drugs
are useful for persons with opioid dependence and psy- while on methadone, since the result may be a sudden
chotic disorders. rise in methadone blood levels with signs and symp-
Women with opioid dependence can present special toms of over medication.
challenges because many have been sexually abused as As mentioned earlier, mortality is high and stud-
children, have other mental disorders, and are involved ies have found annual death rates of approximately
in difficult family/social situations. Abusive relation- 10 per 1000 or greater, which is substantially higher
ships with addicted males are common, sometimes than demographically matched samples in the general
characterized by situations in which the male exerts population. Common causes of death are overdose, ac-
control by providing drugs. These complex psychiatric cidents, injuries, and medical complications such as
and relationship issues have emphasized the need for cellulitis, hepatitis, AIDS, tuberculosis, and endocar-
comprehensive psychosocial services that include psy- ditis. The cocaine and alcohol dependence that is often
chiatric assessment and treatment, and access to other seen among opioid-dependent persons contributes to
medical, family, and social services. cirrhosis, cardiomyopathy, myocardial infarction, and
Medical comorbidity is a major problem among per- cardiac arrhythmias.
sons with opioid dependence; HIV infection, AIDS, Tuberculosis has become a particularly serious prob-
and hepatitis B and C have become some of the most lem among intravenous drug users, especially heroin
common problems. Sharing injection equipment in- addicts. In most cases, infection is asymptomatic and
cluding “cookers’’ and rinse water, or engaging in evident only by the presence of a positive tuberculin
high-risk sexual behaviors are the main routes of skin test. However, many cases of active tuberculosis
infection. Sexual transmission appears to be a more have been found, especially among those who are in-
common route of HIV transmission among females fected with HIV.
than males because the HIV virus is spread more read- Other medical complications of heroin dependence
ily from males to females than from females to males. are seen in children born to opioid-dependent women.
Females who are intravenous drug users and also en- Perhaps the most serious is premature delivery and
gage in prostitution or other forms of high-risk sex are low birth weight, a problem that can be reduced if the
at extremely high risk for HIV infection. Cocaine use mother is on methadone maintenance and receiving
has been found to be a significant risk factor as a single prenatal care. Another is physiological dependence on
drug of abuse or when used in combination with heroin opioids, seen in about half the infants born to women
or other opioids. maintained on methadone or dependent on heroin or
After rising rapidly in the late 1970s and early 1980s, other opioids. Effective treatments for neonatal with-
the incidence of new HIV infections among intravenous drawal are available and long-term adverse effects of
drug users, of whom opioid-dependent individuals con- opioid withdrawal have not been demonstrated. Ad-
stitute a large proportion, has decreased, though still verse neonatal effects associated with LAAM or bu-
a substantial source of new HIV infections. However, prenorphine have not been observed, but few studies
as a result of high levels of needle sharing and other have been done since neither medication is approved
risky behavior in the early phases of the epidemic, HIV for use in pregnancy.
infection rates are as high as 60% in some areas of the The comorbidity data have led to research that has
United States. demonstrated the positive effects of integrating psy-
Recent studies have identified several important chiatric and medical care within agonist and other sub-
interactions between methadone and drugs to treat stance abuse treatment programs. Clinical experience
HIV. Information is not complete, however, and and National Institute on Drug-Abuse demonstration
projects have shown that integration of these services individuals with schizophrenia or other major Axis
can be done, and with very positive results since in- I disorders.
dividuals are seen frequently and treatment retention
is high. Related to this line of research are studies
that have shown improved compliance with directly
DIAGNOSTIC CRITERIA
observed antituberculosis pharmacotherapy. These
fi ndings have important implications for tuberculosis The DSM-IV-TR and ICD-10 criteria sets for opioid in-
control policies in methadone programs since intrave- toxication are almost the same. The DSM-IV-TR and
nous drug users are at very high risk for tuberculosis ICD-10 symptom lists for opioid withdrawal include
infection and because maintenance programs provide some different items: the ICD-10 list has craving, ab-
settings in which directly observed therapy can be dominal cramps, and tachycardia and does not include
easily applied. Similar principles apply to adminis- the fever and dysphoric mood items from the DSM-IV-
tration of psychotropic medication in noncompliant TR criteria set.
CHAPTER
Phencyclidine
Phencyclidine (1-(1-phenylcyclohexyl)piperidine, PCP) Table 23-1 Street Names for Phencyclidine and Mixtures
was developed as a general anesthetic agent in the 1950s
Phencyclidine Phencyclidine Mixtures and Analog
under the brand name Sernyl. The drug was considered
physiologically promising because of its lack of respi- Angel dust Beam me up Scottie (crack dipped in
ratory and cardiovascular depressant effects. In fact, PCP)
Animal trank
individuals under PCP anesthesia rather than mani- Baby doll Blunt (marijuana and PCP in cigar
festing a state of relaxed sleep such as that induced by wrapper)
typical anesthetic agents appeared semiconscious with Black whack
Butt naked Love boat (marijuana dipped in PCP)
open eyes, fixed staring, flat facies, open mouth, rigid Devil’s dust Peanut butter (PCP mixed in peanut
posturing, and waxy flexibility. Because of this appar- butter)
ent sharp dissociation from the environment without Elephant
tranquilizer
true unconsciousness, PCP and the related drug keta- Embalming fluid Special K (ketamine)
mine were classified as dissociative anesthetics. Gorilla biscuits Tragic magic (crack dipped in PCP)
Approximately 50% of individuals anesthetized Heaven Wet
HogJet fuel Illy (marijuana treated with
with PCP developed behavioral syndromes including formaldehyde/formalin and PCP)
agitation and hallucinations during emergence from Mad dog Hydro
Peace pill Fry
anesthesia. A substantial number of individuals devel- Rocket fuel
oped postoperative psychotic reactions, which in some Talk to the angels
cases persisted up to 10 days. Trials of subanesthetic Yellow fever
Zombie weed
doses of PCP for treatment of chronic pain led to simi-
lar although less severe adverse reactions. As a result,
after 1965, PCP was limited to veterinary applications. level of popularity, it has remained a significant public
Ketamine remains available for human anesthesia; side health problem among certain populations and in cer-
effects are less frequent and less severe owing to the tain geographical areas. Compared to most other drugs
lower potency and shorter duration of ketamine action of abuse, PCP has more complex and potentially more
compared to PCP. harmful effects.
Illicit use of phencyclidine was first noted in 1965 in
Los Angeles. The spread of the drug from California
DIAGNOSIS
throughout the country was facilitated by its ease of
synthesis compared to other drugs. At least six syn- Physicians must be alert to the wide spectrum of PCP
thetic methods, some simple, are published in scientific effects on multiple-organ systems. Because fluctuations
journals. Surveys of street drug samples indicated that in serum levels may occur unpredictably, an individual
PCP was sold under many street names (Table 23-1) being treated for apparently selective psychiatric or be-
and frequently combined with or misrepresented as havioral complications of PCP abuse may suddenly un-
other substances. dergo radical alterations in medical status; emergency
Despite its well-documented aversive and disruptive medical intervention may become necessary to avoid
behavioral effects, PCP emerged during the 1970s as a permanent organ damage or death. Any individual
popular drug of abuse, increasing in popularity to the manifesting significant cardiovascular, respiratory,
point that in 1979, 13% of high school seniors had tried neurological, or metabolic derangement subsequent to
it. Although PCP has never regained that remarkable PCP use should be evaluated and treated in a medical
Chapter 23 • Substance-Related Disorders: Phencyclidine 207
service; the mental health professional plays a second- Nonpsychiatric Findings in Phencyclidine
ary role in diagnosis and treatment until physiological Table 23-2
Intoxication
stability has been reached and sustained.
Altered level of consciousness
PCP-intoxicated individuals may come to medical Central nervous system changes including nystagmus,
attention on the basis of alterations in mental status, hyperreflexia, and motor abnormalities
bizarre or violent behavior, injuries sustained while Hypertension
Cholinergic or anticholinergic signs
intoxicated, or medical complications, such as rhab- Hypothermia or hyperthermia
domyolysis, hyperthermia, or seizures. As illicit keta- Myoglobinuria
mine use has increased significantly as part of the “club
drug” phenomenon, it is important to remember that
ketamine can induce the same spectrum of effects and spontaneously or after an episode of bizarre or violent
complications, the chief difference from PCP being the behavior. Prolonged coma due to continued drug ab-
much shorter duration of action of ketamine. sorption from ruptured ingested packages of PCP has
The presenting symptoms may be predominantly or been described.
exclusively psychiatric, without significant alterations Nystagmus (which may be horizontal, vertical, or
in the level of consciousness, and may closely resem- rotatory) frequently has been described in individuals
ble an acute schizophrenic decompensation with con- with PCP intoxication.. Consequences of PCP-induced
crete or illogical thinking, bizarre behavior, negativism, central nervous system hyperexcitability may range
catatonic posturing, and echolalia. Subjective feelings from mildly increased deep tendon reflexes to grand
and objective signs of “drunkenness” may or may not mal seizures. Other motor signs have been observed,
be present. such as generalized rigidity, localized dystonias, facial
In PCP intoxication, the central nervous, cardiovas- grimacing, and athetosis.
cular, respiratory, and peripheral autonomic systems Hypertension is one of the most frequent physical find-
are affected to degrees ranging from mild to cata- ings, and is usually mild and self limiting, but some have
strophic (Table 23-2). had severe hypertension, and some remaine hypertensive
The level of consciousness may vary from full alert- for days. Tachycardia occurs in 30% of individuals with
ness to coma. Coma of variable duration may occur PCP intoxication. PCP-induced tachypnea can progress
to periodic breathing and respiratory arrest. Autonomic
signs seen in PCP intoxication may be cholinergic (dia-
phoresis, bronchospasm, miosis, salivation, bronchor-
DSM-IV-TR Diagnostic Criteria rhea) or anticholinergic (mydriasis, urinary retention).
Hypothermia and hyperthermia have been observed.
292.89 PHENCYCLIDINE INTOXICATION
Hyperthermia may reach malignant proportions.
A. Recent use of phencyclidine (or a related substance). Rhabdomyolysis frequently results from a combina-
B. Clinically significant maladaptive behavioral changes tion of PCP-induced muscle contractions and trauma
(e.g., belligerence, assaultiveness, impulsiveness, un-
predictability, psychomotor agitation, impaired judg- occurring in relation to injuries sustained as a result of
ment, or impaired social or occupational functioning) behavioral effects. Acute renal failure can result from
that developed during, or shortly after, phencyclidine myoglobinuria.
use.
C. Within an hour (less when smoked, “snorted,” or used The disruption of normal cognitive and memory
intravenously), two (or more) of the following signs: function by PCP frequently renders individuals inca-
(1) Vertical or horizontal nystagmus pable of giving an accurate history, including a history
(2) Hypertension or tachycardia of having used PCP. Therefore, assay of urine or blood
(3) Numbness or diminished responsiveness to pain
(4) Ataxia for drugs may be the only way to establish the diagno-
(5) Dysarthria sis. PCP is frequently taken in forms in which it has
(6) Muscle rigidity been used to adulterate other drugs, such as marijuana
(7) Seizures or coma
(8) Hyperacusis and cocaine, often without the user’s knowledge. One
of the most recent and alarming manifestations of this
tion and are not better accounted for by another men- phenomenon is a preparation known variously as illy,
tal disorder. hydro, wet, or fry, consisting of a marijuana cigarette or
Specify if: blunt containing formaldehyde/formalin (which is ad-
With perceptual disturbances vertised) and PCP (which often is not); PCP precursors
Reprinted with permission from the Diagnostic and Statistical and synthesis by-products as well as PCP have been
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 detected in toxicological screens of users who have
consumed these preparations.
By disrupting sensory pathways, PCP frequently during which the psychiatric symptoms and signs abate
renders users hypersensitive to environmental stimuli gradually and progressively. Even after complete recov-
to the extent that physical examination or psychiatric ery, flashbacks may occur if PCP sequestered in lipid
interview may cause severe agitation. If PCP intoxi- stores is mobilized. Any underlying mental disorders
cation is suspected, measures should be taken from can be detected and evaluated only after complete reso-
the outset to minimize sensory input. The individual lution of the drug-induced psychosis. Although system-
should be evaluated in a quiet, darkened room with the atic studies in humans have not been carried out, clini-
minimal necessary number of medical staff present. cal experience predicts a high likelihood of resumption
Assessments may need to be interrupted periodically. of PCP use after recovery from PCP psychosis.
Vital signs should be obtained immediately on pres-
entation. Temperature, blood pressure, and respiratory
rate are dose-dependently increased by PCP and may
be of a magnitude requiring emergency medical treat- The presence of nystagmus and hypertension with
ment to avoid the potentially fatal complications of ma- mental status changes should raise the possibility of
lignant hyperthermia, hypertensive crisis, and respira- PCP intoxication. Because of the close resemblance of
tory arrest. In all cases, monitoring of vital signs should both the acute and the prolonged forms of PCP psy-
continue at 2- to 4-hour intervals throughout treatment, chosis to schizophrenia, and the increased sensitivity
because serum PCP levels may increase spontaneously of individuals with schizophrenia to the psychotomi-
as a result of mobilization of drug from lipid stores or metic effects of the drug, an underlying schizophrenia
enterohepatic recirculation. spectrum disorder should be considered, particularly
Analgesic and behavioral changes induced by PCP if paranoia or thought disorder persists beyond 4 to
not only predispose individuals to physical injury but 6 weeks after the last use of PCP. PCP psychosis may
also mask these injuries, which may be found only with also resemble mania or other mood disorders. There-
careful physical examination. fore in all cases, a detailed psychiatric history should
On neurological examination, nystagmus and ataxia, be obtained. Robust response of psychotic symptoms
although not conclusive, are strongly suggestive of PCP to treatment with neuroleptics would favor a diagnosis
intoxication. Examination of deep tendon reflexes helps other than simple PCP psychosis.
establish the degree of nervous system hyperexcitabil- PCP psychosis is readily distinguishable from lyser-
ity. Crossed or clonic deep tendon reflexes alert the gic acid diethylamide (LSD) psychosis in normal as
physician to the possibility of subsequent seizures. well as in individuals with schizophrenia by the lack of
Because PCP is usually supplied in combination typical LSD effects, such as synesthesia. The cluster of
with other drugs and is often misrepresented, toxico- psychotic symptoms, hypertension, and stereotypy may
logical analysis of urine or blood is essential. However, be seen in both PCP psychosis and chronic ampheta-
there may be circumstances in which PCP may not be mine psychosis; in such cases, accurate histories and
detected in urine even if it is present in the body, for toxicological analysis are particularly important.
example, when the urine is alkaline. On the other hand, In cases involving prominent PCP-induced neuro-
in chronic PCP users, drug may be detected in urine up logical, cardiovascular, or metabolic derangement,
to 30 days after the last use. encephalitis, head injury, postictal state, and primary
Blood and urine samples should be sent for toxi- metabolic disorders must be ruled out. Either intoxi-
cological analysis. In addition, serum uric acid, crea- cation with or withdrawal from sedative–hypnotics
tine kinase, aspartate transaminase, and alanine may be associated with nystagmus Neuroleptic malig-
transaminase elevations are common findings in PCP nant syndrome should be ruled out in the differential
intoxication. diagnosis of PCP-induced hyperthermia and muscle
rigidity.
Course
TREATMENT
As drug levels decline, the clinical picture recedes in 5
to 21 days through periods of moderating neurological, The hierarchy of treatment goals begins with detec-
autonomic, and metabolic impairments to a stage at tion and treatment of physical manifestations of PCP
which only psychiatric impairments are apparent. Once intoxication.
the physical symptoms and signs have cleared, the pe- Equally important are measures to anticipate PCP-
riod of simple PCP psychosis may last from 1 day to induced impulsive, violent behaviors and provide ap-
6 weeks, whether or not neuroleptics are administered, propriate protection for the PCP user and others. The
Chapter 23 • Substance-Related Disorders: Phencyclidine 209
individual must then be closely observed during the pe- acidification as a measure to reduce levels of PCP in
riod of PCP-induced psychosis, which may persist for the body. However, these should be considered meas-
weeks after resolution of physical symptoms and signs. ures of last resort because of the possibility of elec-
Finally, the possibly dramatic medical and psychiatric trolyte imbalance and additional nephrotoxic effects.
presentation and its resolution must not divert the atten- Administration of activated charcoal may be useful but
tion of the clinician from full assessment and treatment is unproved.
of the individual’s drug-seeking behavior.
In contrast to psychotic states induced by drugs such
Special Features Influencing Treatment
as LSD, in which “talking the individual down” (by ac-
tively distracting the individual from his LSD-induced PCP psychosis may be clinically indistinguishable
sensory distortions and convincing the individual that from schizophrenia. It has been suggested that some
his or her distress stems from nothing more than the individuals who remain psychotic for weeks after PCP
temporary effects of a drug that soon will wear off) may ingestion may have an underlying predisposition to
be highly effective, no such effort should be made in the schizophrenia or mania. In some series, significant
case of PCP psychosis, particularly during the period of percentages of individuals suffering prolonged PCP-
acute intoxication, because of the risk of sensory over- induced psychosis are subsequently hospitalized with
load that can lead to dramatically increased agitation. nondrug-induced schizophrenic disorders. In the case
The risk of sudden and unpredictable impulsive, violent of an individual with schizophrenia, responsiveness to
behavior can also be increased by sensory stimulation. neuroleptic treatment may resume after recovery from
prolonged PCP psychosis.
Individuals with preexisting neurological, cardio-
Somatic Treatments
vascular, respiratory, or renal disorders are at increased
There is no pharmacological competitive antagonist risk for complications of PCP intoxication, such as sei-
for PCP, in contrast to opiates and benzodiazepines. zures, stroke, hypertensive crisis, respiratory arrest,
Oral or intramuscular benzodiazepines are recom- or renal failure. Abusers of more than one drug may
mended for agitation. Neuroleptics usually have little be at increased risk from the presence of other drugs
or no effect on acute or chronic PCP-induced psycho- exerting toxic effects on the same organ systems (e.g.,
sis or thought disorder. Because they lower the seizure cardiovascular effects of cocaine and amphetamine) or
threshold, neuroleptics should be used with caution. because of damage to specific organs secondary to in-
Physical restraint may be lifesaving if the individual’s fectious complications of parenteral drug use.
behavior poses an imminent threat to his or her safety
or that of others; however, such restraint risks trigger-
ing or worsening rhabdomyolysis.
DIAGNOSTIC CRITERIA
Because of the large volume of distribution of PCP,
dialysis is ineffective as a means of clearing the drug ICD-10 does not have a separate class for PCP-related
from circulation. The “trapping” of PCP in acidic body disorder and instead includes PCP in the hallucinogen
compartments suggests either gastric gavage or urinary class.
CHAPTER
Sedatives, Hypnotics,
and Anxiolytics
Sedative–hypnotics and anxiolytics include prescrip- to alleviate the side effects of cocaine and ampheta-
tion sleeping medications and most medications used mines. Individuals receiving methadone maintenance
for the treatment of anxiety. The sedative–hypnotics use benzodiazepines to boost (enhance) the effects
include a chemically diverse group of medications. of methadone. Some alcoholic individuals use benzo-
Pharmacologically alcohol is appropriately included diazepines either in combination with alcohol or as a
among sedative–hypnotics; however, it is generally second-choice intoxicant, if alcohol is unavailable. Fat-
considered separately, as it is in DSM-IV-TR and in this soluble benzodiazepines that enter the central nervous
book. The medications usually included in the category system (CNS) quickly are usually the benzodiazepines
of sedative–hypnotics are listed in Table 24-1 preferred by addicts.
The sedative–hypnotics include a chemically diverse Addicts whose urine is being monitored for ben-
group of medications. Although buspirone is marketed zodiazepines prefer benzodiazepines with high mil-
for the treatment of anxiety, its pharmacological profile ligram potency, such as alprazolam or clonazepam.
is sufficiently different that it is not usually included These benzodiazepines are excreted in urine in such
among the sedative–hypnotics. Antidepressant medi- small amounts that they are often not detected in drug
cations may also have antianxiety properties, and their screens, particularly with thin-layer chromatography.
sedative effects are often of clinical utility in sleep in-
duction; however, they too are usually excluded from
DIAGNOSIS
the sedative–hypnotic classification.
For treatment of anxiety and insomnia, the benzo- Sedative–hypnotics are among the most commonly
diazepines have largely supplanted the older sedative– prescribed medications. They are also often misused
hypnotics. The benzodiazepines have a major advantage and abused and can produce severe, life-threatening
over the older compounds. In an overdose, the older dependence. With the exception of the benzodi-
sedative–hypnotics are lethal at 10 to 15 times the usual azepines and newer hypnotics (e.g., zaleplon, zopiclone
therapeutic doses. Benzodiazepines, if taken alone, and zolpidem), overdose with sedative–hypnotics can
have a therapeutic ratio exceeding 100. In combination be lethal. Benzodiazepines and the newer hypnotics are
with alcohol or other drugs, the benzodiazepines may rarely lethal if taken alone; in combination with alco-
contribute to the lethality, but death from a benzodi- hol or other drugs, however, they can be lethal.
azepine overdose is rare. Some atavistic uses of the
older compounds remain driven primarily by economic
Sedative–Hypnotic–Anxiolytic Dependence
considerations and misguided attempts to reduce abuse
of benzodiazepines by addicts and perceived overpre- Sedative–hypnotics can produce tolerance and physi-
scription of benzodiazepines by physicians. ological dependence (see generic DSM-IV-TR diagnos-
Most people do not like the subjective effects of ben- tic criteria for Substance Dependence in Chapter 13,
zodiazepines, especially in high doses. Even among page 125). Physiological dependence can be induced
drug addicts, the benzodiazepines alone are not com- within several days with continuous infusion of anes-
mon intoxicants. They are, however, widely used by thetic doses. Individuals who are taking barbiturates
drug addicts to self-medicate opiate withdrawal and daily, for example, for a month or more above the upper
Chapter 24 • Substance-Related Disorders: Sedatives, Hypnotics, and Anxiolytics 211
Table 24-1 Medications Usually Included in the Category of Sedative–Hypnotics

Common Therapeutic-Dose
Generic Name Trade Names Therapeutic Use Range (mg/d)
Barbiturates
Amobarbital Amytal Sedative 50–150
Butabarbital Butisol Sedative 45–120
Butalbital Fiorinal, Sedapap Sedative/analgesic 100–300
Pentobarbital Nembutal Hypnotic 50–100
Secobarbital Seconal Hypnotic 50–100
Benzodiazepines
Alprazolam Xanax Antianxiety 0.75–6
Chlordiazepoxide Librium Antianxiety 15–100
Clonazepam Klonopin Anticonvulsant 0.5–4
Clorazepate Tranxene Antianxiety 15–60
Diazepam Valium Antianxiety 5–40
Estazolam ProSom Hypnotic 1–2
Flunitrazepam Rohypnol* Hypnotic 1–2
Flurazepam Dalmane Hypnotic 15–30
Halazepam Paxipam Antianxiety 60–160
Lorazepam Ativan Antianxiety 1–16
Midazolam Versed Anesthesia –
Oxazepam Serax Antianxiety 10–120
Prazepam Centrax Antianxiety 20–60
Quazepam Doral Hypnotic 15
Temazepam Restoril Hypnotic 7.5–30
Triazolam Halcion Hypnotic 0.125–0.5
Others
Chloral hydrate Noctec, Somnos Hypnotic 250–1000
Eszopiclone Lunesta Hypnotic 1–3
Ethchlorvynol Placidyl Hypnotic 200–1000
Glutethimide Doriden Hypnotic 250–500
Meprobamate Miltown, Equanil, Antianxiety 1200–1600
Equagesic
Methyprylon Noludar Hypnotic 200–400
Zaleplon Sonata (Stilnox, Hypnotic 5–20
other countries)
Zolpidem Ambien Hypnotic 5–10
*
Rohypnol is not marketed in the United States.
therapeutic range listed in Table 24-1 should be pre- in large amounts, sedative–hypnotics produce progres-
sumed to be physically dependent and in need of medi- sive respiratory depression and coma. The amount of res-
cally managed detoxification. piratory depression produced by the benzodiazepines is
much less than that produced by the barbiturates and other
Sedative–Hypnotic–Anxiolytic Abuse sedative–hypnotics. Consistent with its general approach,
the DSM-IV-TR diagnosis of intoxication requires “clini-
Abuse may occur on its own or in conjunction with cally significant maladaptive behavioral or psychologi-
use of other substances (e.g., while using high doses of cal changes” developing after drug use in addition to the
sedatives in order to “come down” from a cocaine or signs and symptoms of acute toxicity. The DSM-IV-TR
amphetamine high). Abuse of sedatives in hazardous criteria for intoxication are shown on page 126.
situations (e.g., getting “high” and then driving while
intoxicated) is among the more common reasons for
a diagnosis of Sedative–Hypnotic–Anxiolytic Abuse Sedative–Hypnotic–Anxiolytic Withdrawal
(see generic DSM-IV-TR diagnostic criteria for Sub-
The withdrawal syndrome arising from the discontinu-
stance Abuse in Chapter 13, page 125).
ation of short-acting sedative–hypnotics is similar to
that from stopping or cutting down on the use of al-
Sedative–Hypnotic–Anxiolytic Intoxication
cohol (see DSM-IV-TR diagnostic criteria, page 137).
The acute toxicity of sedative–hypnotics consists of Signs and symptoms of sedative–hypnotic withdrawal
slurred speech, incoordination, ataxia, sustained nystag- include anxiety, tremors, nightmares, insomnia, ano-
mus, impaired judgment, and mood lability. When taken rexia, nausea, vomiting, postural hypotension, seizures,
drug. With short-acting sedative–hypnotics (e.g.,

DSM-IV-TR Criteria pentobarbital, secobarbital, meprobamate, oxazepam,
292.89 SEDATIVE, HYPNOTIC, OR ANXIOLYTIC INTOXICATION
alprazolam, and triazolam), withdrawal symptoms typ-
ically begin 12 to 24 hours after the last dose and peak
A. Recent use of a sedative, hypnotic, or anxiolytic. in intensity between 24 and 72 hours (symptoms may
chological changes (e.g., inappropriate sexual or ag- develop more slowly in individuals with liver disease or
gressive behavior, mood lability, impaired judgment, in the elderly because of decreased drug metabolism).
impaired social or occupational functioning) that de- With long-acting drugs (e.g., phenobarbital, diazepam,
veloped during, or shortly after, sedative, hypnotic, or
anxiolytic use. and chlordiazepoxide), withdrawal symptoms peak on
C. One (or more) of the following signs, developing dur- the fifth to eighth day.
ing, or shortly after, sedative, hypnotic, or anxiolytic During untreated sedative–hypnotic withdrawal, the
use:
electroencephalogram (EEG) may show paroxysmal
(1) slurred speech
(2) incoordination
bursts of high-voltage, low-frequency activity that pre-
(3) unsteady gait cedes the development of seizures. The withdrawal de-
(4) nystagmus lirium may include confusion, and visual and auditory
(5) impairment in attention or memory
(6) stupor or coma. hallucinations. The delirium generally follows a period
of insomnia. Some individuals may have only delirium;
tion and are not better accounted for by another men- others only seizures; and some may have both delirium
tal disorder. and convulsions.
Reprinted with permission from the Diagnostic and Statistical Many people who have taken benzodiazepines in
therapeutic doses for months to years can abruptly dis-
continue the drug without developing withdrawal symp-
toms. But other individuals taking similar amounts of
a benzodiazepine develop symptoms ranging from
Diagnostic Criteria mild to severe when the benzodiapine is stopped or
when the dosage is substantially reduced. Character-
292.0 SEDATIVE, HYPNOTIC, OR ANXIOLYTIC WITHDRAWAL
istically, individuals tolerate a gradual tapering of the
A. Cessation of (or reduction in) sedative, hypnotic, or benzodiazepine until they are at 10–20% of their peak
anxiolytic use that has been heavy and prolonged. dose. Further reductions in benzodiazepine dose then
B. Two (or more) of the following, developing within sev-
eral hours to a few days after Criterion A: cause individuals to become increasingly symptomatic.
In addition, in medicine literature, the low-dose with-
(1) autonomic hyperactivity (e.g., sweating or pulse
rate greater than 100) drawal may be called therapeutic-dose withdrawal,
(2) increased hand tremor normal-dose withdrawal, or benzodiazepine discontin-
(3) insomnia uation syndrome. The symptoms can ultimately be cat-
(4) nausea or vomiting
(5) transient visual, tactile, or auditory hallucinations egorized as symptom reemergence, symptom rebound,
or illusions or a prolonged withdrawal syndrome.
(6) psychomotor agitation
(7) anxiety
Many individuals experience a transient increase
(8) grand mal seizures. in symptoms for 1 to 2 weeks after benzodiazepine
C. The symptoms in Criterion B cause clinically signifi- withdrawal. The symptoms are an intensified return of
cant distress or impairment in social, occupational, or the symptoms for which the benzodiazepine was pre-
other important areas of functioning. scribed. This transient form of symptoms intensifica-
tion and are not better accounted for by another mention is called symptom rebound. The term comes from
tal disorder. sleep research where rebound insomnia is commonly
Specify if:
observed after sedative–hypnotic use. Symptom re-
bound lasts a few days to weeks after discontinuation.
With Perceptual Disturbances
Symptom rebound is the most common withdrawal
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 consequence of prolonged benzodiazepine use.
American Psychiatric Association. The symptoms for which the benzodiazepine has been
taken may return to the same level as before the benzodi-
azepine therapy. This is called symptom reemergence (or
delirium, and hyperpyrexia. The syndrome is qualita- recrudescence). In other words, the individual’s symp-
tively similar for all sedative–hypnotics; however, the toms, such as anxiety, insomnia, or muscle tension, that
time course of symptoms depends on the particular had abated during benzodiazepine treatment return.
The reason for making a distinction between symp- gradually subside with continued abstinence, whereas
tom rebound and symptom reemergence is that symp- symptom reemergence and symptom sensitization do
tom reemergence suggests that the original symptoms not.
are still present and must be treated. Symptom rebound The waxing and waning of symptom intensity are
is a transient withdrawal syndrome that will disappear characteristic of the low-dose protracted benzodi-
over time. azepine withdrawal syndrome. Individuals are some-
Some drugs or medications may facilitate neuroadap- times asymptomatic for several days, and then, without
tation by increasing the affinity of benzodiazepines for apparent reason, they become acutely anxious. Often
their receptors. Prior treatment with phenobarbital has there are concomitant physiological signs (e.g., dilated
been found to increase the intensity of chlordiazepox- pupils, increased resting heart rate, and increased
ide (45 mg/day) withdrawal symptoms. Individuals at blood pressure). The intense waxing and waning of
increased risk for development of the low-dose with- symptoms are important in distinguishing low-dose
drawal syndrome are those with a family or personal withdrawal symptoms from symptom reemergence.
history of alcoholism, those who use alcohol daily, and
those who concomitantly use other sedatives. Case–
Assessment Issues
control studies suggest that individuals with a history
of addiction, particularly to other sedative–hypnotics, The individual’s drug use history is usually the first
are at high risk for low-dose benzodiazepine depend- source of information that is used in assessing sedative–
ence. The short-acting, high-milligram-potency benzo- hypnotic abuse or dependence. If the sedative–
diazepines appear to produce a more intense low-dose hypnotics were being used for treatment of insomnia
withdrawal syndrome. or anxiety, the history is often best obtained as part of
A few individuals experience a severe, protracted the history of the primary disorder and its response to
withdrawal syndrome that includes symptoms (e.g., treatment. A detailed history of use of all sedative–
paresthesia and psychosis) that were not present before. hypnotics, including alcohol, should be elicited from
This withdrawal syndrome has generated much of the the individual. When framed in terms of the presenting
concern about the long-term safety of the benzodi- disorder, individuals are generally more candid about
azepines. Protracted benzodiazepine withdrawal may their drug use and their relationship with past treating
consist of relatively mild withdrawal symptoms such as physicians.
anxiety, mood instability, and sleep disturbance similar For many reasons, individuals may minimize or ex-
to the protracted withdrawal syndrome described for aggerate their drug use and not accurately report the
alcohol and other drugs. In some individuals, the pro- behavioral consequences of their use. High doses of ben-
tracted withdrawal syndrome from benzodiazepines zodiazepines or therapeutic doses of benzodiazepines
can be severe and disabling and lasts many months. in combination with alcohol may disrupt memory. In-
There is considerable controversy surrounding even dividuals are likely to attribute impairment of function
the existence of this syndrome, which evolves primarily to the underlying disorder rather than to the medication
from the addiction medicine literature. Many symp- use. Observations of the individual’s behavior by fam-
toms are nonspecific and often mimic an obsessive– ily members can be a source of valuable information.
compulsive disorder (OCD) with psychotic features. As Whenever possible, the individual’s history should be
a practical matter, it is often difficult in the clinical set- supplemented by medical records to help piece together
ting to separate symptom reemergence from protracted as accurate a picture of drug use as possible. Pharmacy
withdrawal. New symptoms, such as increased sensi- records may be helpful in establishing and verifying
tivity to sound, light, and touch and paresthesia, are the individual’s drug use history, and urine testing can
particularly suggestive of low-dose withdrawal. be useful in verifying recent drug use history.
The protracted benzodiazepine withdrawal has no Individuals who obtain some or all of their medica-
pathognomonic signs or symptoms, and the broad tion from street sources may not know what they have
range of nonspecific symptoms produced by the pro- been taking, as deception in the street-drug market-
tracted benzodiazepine withdrawal syndrome could place is common. For example, tablets sold as meth-
also be the result of agitated depression, generalized aqualone have been found to contain phenobarbital or
anxiety disorder (GAD), panic disorder, partial com- diazepam.
plex seizures, and schizophrenia. The time course of Sustained horizontal nystagmus is a reliable indicator
symptom resolution is the primary differentiating fea- of sedative–hypnotic intoxication. Onset of tremor, ab-
ture between symptoms generated by withdrawal and normal sweating, and blood pressure or pulse increase
symptom reemergence. Symptoms from withdrawal may be produced by sedative–hypnotic withdrawal.
Urine toxicology can be useful in monitoring the barbiturates are particularly pernicious if inadvertently
individual’s use of drugs and in confirming a history injected into an artery or if the solution is injected or
of drug or medication use. The detection time var- leaked from a vein or artery into tissue surrounding the
ies widely for benzodiazepines. Diazepam or chlo- vessel. Barbiturates are irritating to the tissue, and the
rdiazepoxide may be detected for weeks following affected tissue becomes indurated and may abscess. In
chronic or high-dose use, whereas others, such as al- addition, barbiturate solution injected into an artery
prazolam or clonazepam, may not be detectable in rou- produces intense vasoconstriction and blockage of the
tine toxicology urinalysis. Because of the variability arterioles, resulting in gangrene of areas supplied by
in laboratory cut-offs and detection time, and different the artery.
drugs included in the screening panel, the analytical
laboratory should be asked about what they routinely Methaqualone. Methaqualone (Quaalude) was re-
screen for as well as the detection limits. moved from the US market in 1984 because of its
abuse. Subsequently, it has continued to be sold on
the street-drug black market. Some tablets sold on the
Patterns of Use/Abuse
black market as Quaalude contain methaqualone, ap-
Some sedative–hypnotics, such as the short-acting bar- parently diverted from countries where methaqualone
biturates, are primary drugs of abuse—that is, they are is still available; others contain diazepam, phenobarbi-
injected for the “rush” or are taken orally to produce a tal, or another sedative–hypnotic.
state of disinhibition similar to that achieved with alco-
hol. Sedative hypnotics may also be taken in combina- Benzodiazepines. Benzodiazepines are often used
tion with other primary intoxicants, such as alcohol or or misused by addicts to self-medicate opiate with-
heroin, to intensify the desired subjective effects. drawal, to intensify the CNS effects of methadone,
Drug addicts may also use sedative–hypnotics to self- or to ameliorate the adverse effects of cocaine or
medicate withdrawal of drugs such as heroin. When the methamphetamine.
avowed intent is to stop the use of drugs such as heroin, The benzodiazepine, flunitrazepam (Rohypnol,
physicians may be lured into thinking that addicts’ self- Narcozep), is singled out for additional discussion be-
administration of sedative–hypnotics is not an “abuse” cause of the media and legislative attention it received
but rather a reasonable approximation of medical use. during the 1990s, and because it is still widely abused
While on occasion this may be the case, often it is not. in Europe and other areas of the world. Flunitrazepam,
Addicts’ episodic attempts to stop using heroin by self- a potent benzodiazepine hypnotic, was never marketed
medicating opiate-withdrawal symptoms with seda- in the United States but is widely available by prescrip-
tive–hypnotics without entering drug abuse treatment tion in many other countries in 1- or 2-mg oral dosage
are rarely successful, and may result in the secondary forms and for injection.
development of sedative–hypnotic dependence. Flunitrazepam has many street names, including
Addicts may also use sedative–hypnotics to reduce rophies, ropies, roopies, roofies, ruffes, rofinol, loops,
unpleasant side effects of stimulants, particularly co- and wheels. Tablets of Rohypnol have the name of the
caine or methamphetamine. Impairment of judgment manufacturer Roche engraved on them and a number
and memory produced by the sedative–hypnotic in indicating the milligram strength (either 1 or 2). Drug
combination with wakefulness of a stimulant may re- abusers usually prefer the 2-mg tablets, which are of-
sult in unpredictable behavior. ten called “Roche dos” or just “Roche” (usually pro-
nounced “row-shay”). Although flunitrazepam is simi-
Barbiturates. During the late 1960s and early 1970s, lar in many respects to other benzodiazepines in abuse
the short-acting barbiturates, secobarbital and pentobar- potential, flunitrazepam is among the benzodiazepines
bital, were common drugs of abuse. Addicts dissolved with the highest abuse potential and has considerable
the tablets or the contents of capsules in water and in- appeal among heroin addicts.
jected the solution. The desired effect was the “rush,” In the mid-1990s, Rohypnol achieved notoriety as
a dreamy, floaty feeling lasting a few minutes after the the “date-rape drug.” Subsequently, GHB (gamma-
injection. After the rush, the addict was intoxicated, but hydroxybutyric acid), which has some properties of a
the primary appeal to injection was the rush. The intox- sedative–hypnotic, was also called a “date-rape drug.”
ication is not qualitatively different from that produced Because of the media attention, considerable public de-
by oral ingestion of a short-acting barbiturate. bate ensued and the US Congress was prompted to pass
Injection of a barbiturate is associated with the legislation increasing penalties for rape when Rohyp-
usual infectious risk of injecting street drugs, but the nol or other drugs were used to facilitate it.
Flunitrazepam and other benzodiazepines have also to return to controlled, therapeutic use of sedative–
been associated with deaths among opiate addicts tak- hypnotics. All sedative–hypnotics, including alcohol,
ing buprenorphine in France. Although buprenorphine are cross-tolerant, and physical dependence and toler-
alone or benzodiazepines alone are rarely fatal, the ance are quickly reestablished if an individual resumes
combination appears to increase the risk of overdose. use of sedative–hypnotics.
Benzodiazepines and buprenorphine may have syner- If after sedative–hypnotic withdrawal the individual
gistic action in suppressing respiration. has another mental disorder, such as GAD, panic at-
tacks, or insomnia, alternate treatment strategies other
Zolpidem. Zolpidem (Ambien) is an imidazopyridine than sedative–hypnotics should be used if possible.
hypnotic, chemically unrelated to the benzodiazepines. Definitive diagnosis of a mental disorder during early
However, it binds to a subunit of the same gamma- abstinence is often not possible because protracted
aminobutyric acid (GABA)–benzodiazepine complex withdrawal symptoms may mimic anxiety disorders,
as the benzodiazepines and its sedative effects are re- and disruption of sleep architecture for days to months
versed by the benzodiazepine antagonist flumazenil. after drug withdrawal is extremely common.
Zolpidem has been available for prescription since If the sedative–hypnotic dependence has devel-
1993 in the United States and in Europe for several oped secondary to stimulant or alcohol use, primary
years before. treatment of the chemical dependence should be a
A few case reports of abuse suggest that some in- priority. Often the symptom that was driving the seda-
dividuals increase the dosage many times above what tive–hypnotic use disappears after the individual is
is prescribed and that zolpidem produces a withdrawal drug-abstinent.
syndrome similar to that of other sedative–hypnotics.
The case histories also describe significant tolerance to
the sedative effects of zolpidem.
Zolpidem is rapidly absorbed and has a short half- The diagnosis of sedative–hypnotic abuse and depend-
life (2.2 hours). Its sedative effects are additive with ence is based primarily on drug use history and the
alcohol. DSM-IV-TR criteria of continuing behavior dysfunc-
In addition to dependence, zolpidem has produced tion caused by the drug. With dependence developing
idiosyncratic psychotic reactions. A report from Bel- from prescribed use, the practical difficulty is deter-
gium described two cases of transient psychosis after mining when the dysfunction is a result of the drug use
the first dose of 10 mg of zolpidem. Neither individual rather than the disorder for which the medication was
had a history of drug abuse or misuse nor were they prescribed.
using alcohol at the time. Both individuals experienced Long-term use of benzodiazepines can result in
a transient psychosis with visual hallucinations begin- physical dependence in nondrug-dependent medical
ning 20 to 30 minutes after 10 mg of zolpidem. Both patients. Withdrawal symptoms or return of symptoms
individuals previously used benzodiazepines without suppressed by the benzodiazepines may make discon-
difficulty and both were amnestic for the psychotic epi- tinuation difficult.
sode. Additional case reports of psychosis have been Some individuals who are physically dependent on or
reported in the United States. unable to discontinue a medication do not necessarily
have a substance use disorder. Physical dependence re-
Zaleplon. Zaleplon (Sonata) is a pyrazolopyrimidine sults from neuroadaptive changes resulting from long-
approved by the FDA as a hypnotic in 1999. Like zolpi- term exposure to a medication. Inability to discontinue
dem, it is chemically unrelated to the benzodiazepines the medication may simply mean that individuals are
and binds to the omega-1 receptor, which is a subunit unwilling to tolerate the severity of postwithdrawal
of the GABA–benzodiazepine receptor. Peak plasma symptoms that develop. In the absence of medication-
concentration occurs about 1 hour following oral inges- produced dysfunction, the continuation of the medica-
tion. It is rapidly metabolized with a half-life of about 1 tion may be an appropriate choice. Individuals who do
hour. Impairment of short-term memory may occur at not have a substance use disorder take medications in
dosages of 10 to 20 mg. the quantity prescribed. They follow their physicians’
recommendations, and they do not mix them with
drugs of abuse.
Course
Abusers of alcohol and other drugs rarely present
Once a diagnosis of sedative–hypnotic dependence is for primary treatment of sedative–hypnotic depend-
manifested, it is unlikely that an individual will be able ency. From the drug-abusing individual’s point of
view, sedative–hypnotic use is an effort to self-medi- For high-dose sedative–hypnotic dependence, the
cate anxiety or insomnia, which is often the result of pharmacological treatment strategy is the same as that
alcohol or stimulant abuse. Despite their assertion that for barbiturates. The phenobarbital conversion equiva-
the medication is being taken for symptom relief, they lents are shown in Tables 24-2 and 24-3. The dose con-
often take the medication in larger than physician-pre- versions computed using Table 24-2 and 24-3 prevent
scribed doses, combine the medication with intoxicat- the emergence of severe withdrawal of the classic seda-
ing amounts of alcohol or other drugs, and purchase tive–hypnotic type.
medications from street sources. They may also use the For treatment of protracted benzodiazepine with-
sedative–hypnotic as an intoxicant when other drugs drawal, the phenobarbital conversions based on
are not available. Tables 24-2 and 24-3 are not adequate to suppress
symptoms. For example, someone discontinuing 20 mg
of diazepam would have a computed phenobarbital con-
TREATMENT
version of 60 mg. In managing low-dose withdrawal, an
Treatment of sedative–hypnotic dependence that has approach is to begin with about 200 mg/day of phe-
developed as a result of treatment of an underlying nobarbital and then taper the phenobarbital, slowly as
mental disorder is almost always a lengthy undertaking. tolerated. If palpitations or other symptoms of auto-
The goals of the first phase of treatment are to establish nomic hyperactivity are bothersome, beta-adrenergic
the diagnosis and, to the extent possible, to delineate the blockers, such as propranolol, or alpha-2-adrenergic
comorbid psychiatric diagnoses and to establish a agonists, such as clonidine, may be useful adjuncts. Re-
therapeutic relationship with the individual. The art of ports on the use of clonidine to reduce benzodiazepine
treatment is to know when the therapeutic alliance is withdrawal severity have yielded mixed results.
sufficiently established to institute drug withdrawal, and
knowing when outpatient treatment is not progressing Stabilization Phase. The individual’s history of drug
adequately. use during the month before treatment is used to com-
pute the stabilization dose of phenobarbital. Although
many addicts exaggerate the number of pills they are
Somatic Treatments
taking, the individual’s history is the best guide to ini-
Detoxification. Three general strategies are used for tiating pharmacotherapy for withdrawal. Individuals
withdrawing individuals from sedative–hypnotics, in- who have overstated the amount of drug that they have
cluding benzodiazepines. The first is to use decreasing taken will become intoxicated during the first day or
doses of the agent of dependence. The second is to substi- two of treatment. Intoxication is easily managed by
tute phenobarbital or some other long-acting barbiturate omitting one or more doses of phenobarbital and re-
for the addicting agent, and gradually withdraw the sub- ducing the daily dose.
stitute medication. The third, used for individuals with To compute the initial daily starting dose of phe-
a dependence on both alcohol and a benzodiazepine, is nobarbital, the individual’s average daily use of each
to substitute a long-acting benzodiazepine, such as chlo- sedative–hypnotic is estimated. Next, the individual’s
rdiazepoxide, and taper it during 1 to 2 weeks. average daily sedative–hypnotic dose for each drug is
The withdrawal strategy selected depends on the converted to its phenobarbital withdrawal equivalent by
particular sedative–hypnotic, the involvement of other multiplying the average daily dose by the drug’s phe-
drugs of dependence, and the clinical setting in which nobarbital conversion constant shown in both Tables
the detoxification program takes place. The gradual re- 24-2 and 24-3. Finally, the phenobarbital withdrawal
duction of the benzodiazepine of dependence is used equivalences for each drug are added together. In any
primarily in medical settings for dependence arising case, the maximum daily phenobarbital dose is limited
from treatment of an underlying condition. The indi- to 500 mg/day. The total daily amount of phenobarbital
vidual must be cooperative, must be able to adhere to is divided into three doses per day.
dosing regimens, and must not be abusing alcohol or Before receiving each dose of phenobarbital, the
other drugs. individual is checked for signs of phenobarbital toxic-
Substitution of phenobarbital can also be used to ity: sustained nystagmus, slurred speech, or ataxia. Of
withdraw individuals who have lost control of their these, sustained nystagmus is the most reliable. If nys-
benzodiazepine use or who are polydrug-dependent. tagmus is present, the scheduled dose of phenobarbital
Phenobarbital substitution has the broadest use for all is withheld. If all three signs are present the next two
sedative–hypnotic drug dependencies and is widely doses of phenobarbital are withheld, and the daily dos-
used in drug treatment programs. age of phenobarbital for the next day is halved.
Table 24-2 Phenobarbital Withdrawal Equivalents of Benzodiazepines

Dose Equal to 30 mg Phenobarbital
Trade of Phenobarbital for Conversion
Generic Name Name Withdrawal* (mg) Constant
Alprazolam Xanax 1 30
Chlordiazepoxide Librium 25 1.2
Clonazepam Klonopin 2 15
Clorazepate Tranxene 7.5 4
Diazepam Valium 10 3
Estazolam ProSom 1 30
Flurazepam Dalmane 15 2
Halazepam Paxipam 40 0.75
Lorazepam Ativan 2 15
Oxazepam Serax 10 3
Prazepam Centrax 10 3
Quazepam Doral 15 2
Temazepam Restoril 15 2
Triazolam Halcion 0.25 120
*
Phenobarbital withdrawal conversion equivalence is not the same as therapeutic-dose
equivalence.
Table 24-3 Phenobarbital Withdrawal Equivalents of Nonbenzodiazepines

Dose Equal to 30 mg Phenobarbital
of Phenobarbital for Conversion
Generic Name Trade Name Withdrawal*(mg) Constant
Barbiturates
Amobarbital Amytal 100 0.33
Butabarbital Butisol 100 0.33
Butalbital† Fiorinal 100 0.33
Pentobarbital Nembutal 100 0.33
Secobarbital Seconal 100 0.33
Others
Chloral hydrate Noctec, Somnos 500 0.06
Ethchlorvynol Placidyl 500 0.06
Glutethimide Doriden 250 0.12
Meprobamate Miltown 1200 0.025
Methyprylon Noludar 200 0.15
Zaleplon Sonata 10 3
Zolpidem Ambien 5 6
*
Phenobarbital withdrawal conversion equivalence is not the same as therapeutic-dose
equivalence.
†
Butalbital is in combination with opiate or nonopiate analgesics.
If the individual is in acute withdrawal and has had, sedative–hypnotic withdrawal, phenobarbital is de-
or is in danger of having, withdrawal seizures, the initial creased by 30 mg/day. Should signs of phenobarbital
dose of phenobarbital is administered by intramuscular toxicity develop during withdrawal, the daily pheno-
injection. If nystagmus and other signs of intoxication barbital dose is decreased by 50% and the 30-mg/day
develop 1 to 2 hours after the intramuscular dose, the withdrawal is continued from the reduced phenobar-
individual is in no immediate danger from barbiturate bital dose. Should the individual have objective signs
withdrawal. Individuals are maintained with the initial of sedative–hypnotic withdrawal, the daily dose is in-
dosing schedule of phenobarbital for 2 days. If the indi- creased by 50% and the individual is restabilized be-
vidual has neither signs of withdrawal nor phenobarbi- fore continuing the withdrawal.
tal toxicity (slurred speech, nystagmus, unsteady gait),
phenobarbital withdrawal is begun.
Withdrawal Phase. Unless the individual devel- Psychotherapy has an important role in motivating an
ops signs and symptoms of phenobarbital toxicity or individual for primary treatment of drug dependency.
Therapists can help break down the individual’s denial a benzodiazepine or use of an antidepressant or other
of their drug dependence by helping them see how drug medications may be appropriate.
use is interfering with relationships and undermining Many abusers of alcohol or other drugs have symp-
their ability to function. In some instances, it is de- toms that would reasonably indicate treatment with ben-
sirable to continue the psychotherapeutic relationship zodiazepines or other sedatives if they were not drug
while the individual is undergoing treatment for chemi- abusers. Treating drug abusers with benzodiazepines
cal dependence. or other sedatives, while they are still abusing drugs, is,
Alcoholics Anonymous, Narcotics Anonymous, and however, generally not helpful. Such individuals are at
Cocaine Anonymous groups are important treatment high risk of misusing or abusing the medications, and
adjuncts for many people recovering from alcohol the medication may enable them to continue abuse of
and other forms of drug dependence. Although many their primary drug. Drug abusers who are symptomatic
groups are becoming more tolerant of appropriate use because of drug toxicity need hospitalization and de-
of pharmacotherapies, it is important to be aware that toxification. In individuals with drug dependence dis-
many individuals who attend 12 Step recovery meet- orders, abstinence from all abusable medications is the
ings are adamantly opposed to any form of psycho- preferred treatment goal, particularly during the first 6
tropic medication use and counsel fellow members months of abstinence. In individuals who do not have
to stop their use. Individuals with underlying mental a drug dependence disorder, return to benzodiazepine
disorders and the need for treatment with psychophar- use after detoxification may have a different implica-
macotherapeutic medications often require ongoing tion than among individuals with a drug dependence
support from their psychotherapist if they must have disorder. The term relapse could reasonably be applied
medication. to individuals who self-administer a benzodiazepine
when benzodiazepine abstinence is the agreed goal of
treatment. The term relapse, however, should not be ap-
Treatment of Individuals with Comorbid
plied to individuals without a substance abuse disorder
Disorders
who return to prescribed benzodiazepine use because
Most individuals who are being prescribed long-term emerging symptoms are not otherwise manageable.
benzodiazepine therapy have underlying major depres- Numerous studies have documented a high preva-
sive disorder, panic disorder, or GAD. The clinical lence of psychopathological conditions among alcohol
dilemma is deciding which individuals are receiving and drug abusers. Although the abuse of drugs can
appropriate maintenance therapy for a chronic mental induce a psychopathological condition, and there is
disorder. Long-term use of benzodiazepines may be ac- considerable uncertainty as to the extent to which drug
ceptable if the individual’s disabling anxiety symptoms abuse itself contributes to estimates of psychopathol-
are ameliorated. The reason for the individual’s request ogy, it is clinically apparent that some drug abusers
for benzodiazepine withdrawal from long-term, stable have severe underlying psychopathological conditions
dosing should be carefully explored. Valid reasons to that must be treated if they are to remain abstinent and
discontinue benzodiazepine treatment include: (1) functional.
breakthrough of symptoms that were previously well
controlled; (2) impairment of memory or other neuro-
cognitive functions; and (3) abuse of alcohol, cocaine,
DIAGNOSTIC CRITERIA
or other medications.
Individuals with severe underlying mental disorders The DSM-IV-TR and ICD-10 criteria sets for Sedative,
may have unrealistic hopes of becoming medication- Hypnotic, or Anxiolytic Intoxication are almost equiv-
free. Often the origin of request for benzodiazepine alent (except that ICD-10 also includes “erythematous
withdrawal comes from concerned friends or relatives. skin lesions or blisters”). The DSM-IV-TR and ICD-10
The individual’s “problems” may be reframed as the symptom lists for Sedative, Hypnotic, or Anxiolytic
use of “addictive medications” or “dependence” rather Withdrawal include some different items: the ICD-10
than the underlying psychopathology. As a practi- list has craving, postural hypotension, headache, ma-
cal matter, a trial of medication discontinuation may laise or weakness, and paranoid ideation and does not
be undertaken with the understanding that return to include the DSM-IV-TR anxiety item.
CHAPTER
25 Schizophrenia and Other

Psychotic Disorders
Schizophrenia items in criterion A. Individuals may have difficulties

maintaining employment, relationships, or academic
DIAGNOSIS achievements. If the illness presents at an early age,
rather than as a degeneration or reversal of function,
Schizophrenia is the most severe and debilitating mental
there may be a break from continued academic and so-
illness, and it has long been the focus of medical, scien-
cial gains that are developmentally appropriate so that
tific, and societal attention. The term schizophrenia is
the person never achieves what had been expected.
relatively new to our vocabulary, yet chronic psychotic
Criterion C eliminates individuals with less than
illnesses have most likely been in existence throughout
6 months of continued disturbance and again requires
civilized times. The words used historically to describe
at least 1 month of the symptoms from criterion A.
psychotic symptoms included madness, folie, insanity,
Criterion C allows prodromal and residual periods to
and dementia. They depict a constellation of symp-
include only negative symptoms or a less severely man-
toms that have been poorly understood and shrouded in
ifested version of the other symptoms of the A criteria.
mystery and fear. Even in the twenty-first century, the
Criterion D excludes individuals who have a more
layperson’s conception of schizophrenia is influenced
compelling mood aspect of their illness and there-
by these early beliefs. It is only with our modern un-
fore their symptoms might instead meet criteria for
derstanding of the pathophysiology and manifestations
schizoaffective disorder or a mood disorder. Both of
of this debilitating illness that the stigmata associated
these restrictions force a narrower view of the diagno-
with schizophrenia can be overcome.
sis of schizophrenia, which lessens the tendency of cli-
In DSM-IV-TR, criterion A of schizophrenia in-
nicians to overdiagnose schizophrenia.
cludes delusions, hallucinations, disorganized speech,
Criterion E clarifies the fact that individuals with schiz-
disorganized or catatonic behavior, and negative symp-
ophrenia are not suffering from other medical illnesses
toms (see DSM-IV-TR diagnostic criteria, page 220).
or the physiological effects of substances that might
Two or more of these symptoms are required during the
mimic the symptoms of schizophrenia. Finally, criterion
active phase of the illness. However, if the individual
F acknowledges that schizophrenia can be diagnosed in
describes bizarre delusions or auditory hallucinations
individuals with autistic disorder or developmental dis-
consisting of a voice commenting on the individual’s
order, as long as there have been prominent delusions or
behavior or voices conversing, only one of these symp-
hallucinations that have lasted at least 1 month.
toms is required to reach the diagnosis. It is important
In an attempt to describe schizophrenia in a way that
to distinguish negative symptoms, which are often dif-
was different from prevailing psychodynamic princi-
ficult to appreciate, from the myriad factors that may
ples of the day, researchers in the 1960s reported that
contribute to the severity and serious morbidity associ-
individuals with schizophrenia demonstrated profound
ated with schizophrenia. Individuals who are not moti-
deficits in selective attention. By now, it is widely ac-
vated to attend to their personal hygiene or suffer from
cepted that individuals with schizophrenia experience
alogia and a flattened affect are sadly at a disadvantage
neuropsychological deficits that can be characterized
in society. The addition of negative symptoms as a sep-
by difficulties with attention, information processing,
arate criterion in DSM-IV recognizes the prominence
executive function, learning, and memory, which leads
of these symptoms in individuals with schizophrenia.
to a generalized performance deficit. Typically, there
Criterion B addresses loss of social and occupational
is a wide variance with some aspects of performance
functioning, not exclusively because of any one of the
being more impaired then others. Interestingly, a small
In contrast, their performance is usually worse even

DSM-IV-TR Diagnostic Criteria in first-episode individuals. Usually, individuals with
295.XX SCHIZOPHRENIA
schizophrenia underperform relative to estimates of
their premorbid functioning. Cognitive impairments
A. Characteristic symptoms: Two (or more) of the follow- involving verbal learning, verbal delayed recall, work-
ing, each present for a significant portion of time dur-
ing a 1-month period (or less if successfully treated): ing memory, vigilance, and executive functioning have
a significant negative impact on social and occupational
(1) delusions
(2) hallucinations functioning. Meta-analyses of studies suggest that treat-
(3) disorganized speech (e.g., frequent derailment or ment with novel antipsychotic agents improves cogni-
incoherence) tive function compared to typical antipsychotic agents.
(4) grossly disorganized or catatonic behavior
(5) negative symptoms, i.e., affective flattening, alogia, The degree of cognitive deficit appears to be more
or avolition strongly associated with severity of negative symptoms,
Note: Only one criterion A symptom is required if delu- symptoms of disorganization, and adaptive dysfunction
sions are bizarre or hallucinations consist of a voice keep- than with positive symptoms. Verbal fluency is severely
ing up a running commentary on the person’s behavior
or thoughts, or two or more voices conversing with each impaired in individuals with psychotic disorders and
other. the use of atypical antipsychotic medications results in
B. Social/occupational dysfunction: For a significant por- significant improvement. Motor functions (e.g., reac-
tion of the time since the onset of the disturbance, one tion time, motor and graphomotor speed) improve with
or more major areas of functioning such as work, in-
terpersonal relations, or self-care are markedly below clozapine, olanzapine, and risperidone. Furthermore,
the level achieved prior to the onset (or when the on- motor functions are related to outcome, underscoring
set is in childhood or adolescence, failure to achieve the importance of this domain. The digit symbol test
expected level of interpersonal, academic, or occupa-
tional achievement). has been among the most responsive tests to atypical
C. Duration: Continuous signs of the disturbance persist antipsychotic treatment.
for at least 6 months. This 6-month period must in- In general, individuals with schizophrenia have im-
clude at least 1 month of symptoms (or less if success-
fully treated) that meet criterion A (i.e., active-phase pairments in information processing, especially when
symptoms) and may include periods of prodromal or they are exposed to increasing demands on their atten-
residual symptoms. During these prodromal or residual tional capabilities, such as under timed conditions or
periods, the signs of the disturbance may be manifested
by only negative symptoms or two or more symptoms in stressful situations. Therefore, these deficits are not
listed in criterion A present in an attenuated form (e.g., only viewed as trait linked (i.e., a manifestation of the
odd beliefs, unusual perceptual experiences).
D. Schizoaffective and mood disorder exclusion: Schizoaf-
illness itself) but may also be compounded when state
fective disorder and mood disorder with psychotic fea- linked (i.e., when there are increases in symptoms).
tures have been ruled out because either (1) no major The trait-linked disturbances in neuropsychological
depressive, manic, or mixed episodes have occurred
concurrently with the active-phase symptoms; or (2) parameters are seen in those at high risk for develop-
if mood episodes have occurred during active-phase ing schizophrenia, those who have schizophrenia, and
symptoms, their total duration has been brief relative relatives who appear clinically unaffected, which may
to the duration of the active and residual periods.
E. Substance/general medical condition exclusion: The indicate a genetic vulnerability.
disturbance is not due to the direct physiological ef- Although there are generally no consistent gross
fects of a substance (e.g., a drug of abuse, a medica- deficits of memory in individuals with schizophrenia,
tion) or a general medical condition.
F. Relationship to a pervasive developmental disorder: If close examination of certain aspects of learning and
there is a history of autistic disorder or another perva- memory has revealed striking abnormalities. Individu-
sive developmental disorder, the additional diagnosis als with schizophrenia have been shown to be poorer
of schizophrenia is made only if prominent delusions
or hallucinations are also present for at least a month in recall of word lists if the words are not grouped into
(or less if successfully treated). categories. Furthermore, unlike normal control sub-
Reprinted with permission from the Diagnostic and Statistical jects, schizophrenic individuals do not seem to show
an improvement in memory when asked to recall words
with latent positive emotional meaning. These findings
have been attributed to poor cognitive organization in
individuals with schizophrenia.
subgroup of individuals with schizophrenia have cog-
nitive functioning within the normal range. Most in-
Mental Status Examination in Schizophrenia
dividuals with schizophrenia have only modest reduc-
tions in their IQs with an average of 90 and about 0.67 There is no specific laboratory test, neuroimaging study,
standard deviation below that of the general population. or clinical presentation of an individual that yields a
Chapter 25 • Schizophrenia and Other Psychotic Disorders 221
definitive diagnosis of schizophrenia. Schizophrenia can neuroleptic exposure but have been reported in indi-
present with a wide variety of symptoms, and a longitudi- viduals even before neuroleptic use. Other behaviors or
nal history of symptoms and comorbid clinical variables movement disorders may be seen as parkinsonian fea-
such as medical illness and a history of substance abuse tures, such as a shuffling gait or a pill-rolling tremor.
must necessarily be reviewed before a diagnosis can be Psychomotor retardation may be present and may be
considered. The Mental Status Examination, much like a manifestation of catatonia or negative symptoms. On
the physical examination, is an additional clinical tool close observation, it is usually characterized, in this
that aids the clinician in generating a differential diag- group of individuals, as a lack of motor movements
nosis and appropriate treatment recommendations. rather than slowed movements.
Individuals may present with agitation, ranging from
Appearance. Although a disheveled look is not minimal to extreme. This agitation is often seen in the
pathognomonic for schizophrenia, individuals with acute state and may require immediate pharmaco-
this disorder often present, especially acutely, with a therapy. However, agitation may be secondary to neu-
disordered appearance. The description of an individu- roleptic medications, as in akathisia, which is felt as an
al’s appearance is an objective verbal sketch, much like internal restlessness making it difficult for the person
the description of a heart murmur, that can uniquely to sit still. Akathisia can manifest itself in limb shak-
identify a particular individual. ing, pacing, or frequent shifting of position. Severely
A person with schizophrenia often has difficulty at- agitated individuals may be unresponsive to verbal
tending to activities of daily living, either because of limits and may require measures to ensure their safety
negative symptoms (apathy, social withdrawal, or mo- and the safety of others around them.
tor retardation) or because of the presence of positive
symptoms, such as psychosis, disorganization, or cata- Eye Contact. Paranoid individuals may look hyper-
tonia, that interfere with the ability to maintain personal vigilant, scanning a room or glancing suspiciously at
hygiene. Also, schizophrenic individuals often present an interviewer. Psychotic individuals may make poor
with odd or inappropriate attire, such as a coat and hat eye contact, looking away, or appear to stare vacuously
worn during the summer or dark sunglasses worn dur- at the interviewer, making a conversational connec-
ing an interview. It is generally thought that the inap- tion seem distant. Characteristic responding to internal
propriate dress is a manifestation of symptoms such as stimuli is seen when a individual appears to look to-
disorganization or paranoid ideation. It should be noted ward a voice or an auditory hallucination, which the in-
that some individuals are quite neatly groomed. Thus, dividual may hear. A nystagmus may also be observed.
appearance is noted but is not diagnostic. This clinical finding has a large differential diagnosis,
including Wernicke–Korsakoff syndrome; alcohol,
Attitude. Individuals with schizophrenia may be barbiturate, or phenytoin intoxication; viral labyrinthi-
friendly and cooperative, or they may be hostile, an- tis; or brain stem syndromes including infarctions or
noyed, and defensive during an interview. The latter multiple sclerosis.
may be secondary to paranoid symptoms, which can
make individuals quite cautious and guarded in their Speech. In a mental status examination, one usually
responses to questions. comments on the rate, tone, and volume of an indi-
vidual’s speech, as well as any distinct dysarthrias that
Behavior. Schizophrenic individuals can have bizarre may be present. Pressured speech is usually thought of
mannerisms or stereotyped movements that can make in conjunction with mania; however, it can be seen in
them look unusual. Individuals with catatonia can stay schizophrenic individuals, particularly on acute pres-
in one position for weeks, even to the point of causing entation. This is often difficult to assess, as it may be
serious physical damage to their body; for example, an a normal variant or a cultural phenomenon, because
individual who stands in one place for days may de- some languages are spoken faster than others.
velop stress fractures, peripheral edema, and even pul- Tone refers to prosody, or the natural singsong qual-
monary emboli. Individuals with catatonia may have ity of speech. Negative symptoms may include a lack
waxy flexibility, maintaining a position after someone of prosody, resulting in monotonous speech. Further-
else has moved them into it. Individuals with catatonic more, odd tones may be consistent with neurological
excitement exhibit odd posturing or purposeless, repet- disorders or bizarre behavior.
itive, and often strange movements. Speech volume is important for a number of reasons.
Behaviors seen in schizophrenic individuals include Loud speech can be a measure of agitation, it can occur
choreoathetoid movements, which may be related to in conjunction with psychosis, or it could even be an
indication of hearing loss. Speech that is soft may be a particular word or phrase, such as “this and that, this
an indication of guardedness or anxiety. and that’’ (perseveration).
Dysarthrias are notable because they can be idi- Other thought disorders are part of a constellation of
opathic and long-standing, or they can be an indication negative symptoms. Examples would be thoughts that
of neurological disturbance. In individuals who have appear to stop abruptly, either because of interruption
been exposed to neuroleptics, orobuccal tardive dyski- by an auditory hallucination or because the thought is
nesia should be considered when there is evidence of lost (thought blocking); absence of thoughts (paucity of
slurred speech. thought content); and a delayed response to questions
(increased latency of response).
Mood and Affect. Affect, which is the observer’s
objective view of the individual’s emotional state, is Thought Content. Although not necessarily present
often constricted or flat in individuals with schizophre- in every individual, characteristic symptoms of schizo-
nia. In fact, this is one of the hallmark negative symp- phrenia include the belief that outside forces control a
toms. Flattened affect may also be a manifestation of person’s thoughts or actions. An individual might re-
pseudoparkinsonism, an extrapyramidal side effect of port that others can insert thoughts into her or his head
typical neuroleptics. (thought insertion), broadcast them to others (thought
Inappropriate affect is commonly seen in individu- broadcasting), or take thoughts away (thought with-
als with more predominant positive symptoms. A smile drawal). Other delusions, or fixed false beliefs, may also
or a laugh while relating a sad tale is an example. Indi- be prominent. Individuals may describe ideas of refer-
viduals with catatonic excitement or hebephrenia may ence, which is the phenomenon of feeling that some
have bizarre presentations or affective lability, laugh- external event or report relates to oneself specifically;
ing and crying out of context with the situation. Emo- for example, an individual may infer special meaning
tional reactivity must alert the clinician to the possibil- from an image seen on television or a broadcast heard
ity of neurological impairment as well, as in the case of on the radio.
pseudobulbar palsy. Paranoid ideation may be manifested as general
Mood is based on an individual’s subjective report suspiciousness or frank, well-systematized delusions.
of how he or she feels, emotionally, at the time of the The themes may be considered bizarre, such as feel-
interview. It is not uncommon for individuals with ing convinced that aliens are sending signals through
schizophrenia to be depressed (especially individuals wires in the individual’s ear, or nonbizarre, such as
with history of higher premorbid functioning who may being watched by the Central Intelligence Agency or
have some insight into the losses they are facing) or to believing that one’s spouse is having an affair. These
be indifferent, with seemingly no emotional awareness symptoms can be quite debilitating and lead to a great
of their situation. deal of personal loss, which individuals may not under-
stand because the ideas are so real to them.
Thought Process. Because actual thoughts cannot Individuals with schizophrenia commonly express
be measured, thought processes are assessed by ex- an abundance of vague somatic concerns, and a partic-
trapolation from the organization of speech. Thought ular individual might develop a delusion around a real
disorders can be more or less obvious, and a trained physiological abnormality. Therefore, somatic symp-
listener, much like a cardiologist who listens for heart toms should be evaluated appropriately in their clini-
murmurs or a neurologist who detects aphasias, is cal context without automatically dismissing them as
one who appreciates the normal logical pattern of psychotic. Preoccupations and obsessions are also seen
flow of words and ideas in speech and can thus sense commonly in this population, and certain individuals
abnormalities. have comorbid obsessive–compulsive disorder.
There are many different versions of thought disor- The mortality rate for suicide in schizophrenia
ders: lack of logical connections of ideas (looseness of is approximately 10%. It is therefore imperative to
associations); shift of the original theme because of weak evaluate an individual for both suicidal and homicidal
connections of ideas (tangentiality); overinclusiveness ideation. Individuals with mental disorders, and par-
to the point of loss of the theme (circumstantiality); use ticularly those with schizophrenia, may not sponta-
of words and phrases with no relation to grammatical neously articulate suicidal or homicidal ideation and
rules (word salad); repetition of words spoken by others must therefore be asked directly about such feelings.
(echolalia); use of sounds of other words, such as “yel- Moreover, psychotic individuals may feel compelled
low bellow, who is this fellow?’’ (clang associations); by an auditory hallucination telling them to hurt
use of made-up words (neologisms); and repetition of themselves.
Perceptions. Perceptual disturbances involve illu- Fund of Knowledge. Schizophrenia is not the equiv-
sions and hallucinations. Hallucinations may be olfac- alent of mental retardation, although these syndromes
tory, tactile, gustatory, visual, or auditory, although can coexist in some individuals. Individuals with
hallucinations of the auditory type are more typical schizophrenia generally experience a slight shift in
of schizophrenia. Hallucinations in the other sensory intellectual functioning after the onset of their illness,
modalities are more commonly seen in other medical yet they typically demonstrate a fund of knowledge
or substance-induced conditions. Auditory hallucina- consistent with their premorbid level. Schizophrenic
tions can resemble sounds, background noise, or hu- individuals manifest a characteristic discrepancy on
man voices. Auditory hallucinations that consist of standardized tests of intelligence, with the nonverbal
a running dialogue between two or more voices or a scores being lower than the verbal scores. Further-
commentary on the individual’s behavior are typical of more, some reports suggest that individuals who have
schizophrenia. These hallucinations are distinct from been chronically hospitalized or those with some cer-
verbalized thoughts that most humans experience. ebral atrophy may evidence diminished intellectual
They are often described as originating from outside function.
the individual’s head, as if they were emanating from
the walls or the radiators in the room. Less commonly, Abstraction. A classical aberration of mental function
an individual with schizophrenia describes illusions or in an individual with schizophrenia involves the ina-
misperceptions of a real stimulus, such as seeing de- bility to utilize abstract reasoning, which is similar to
mons in a shadow. metaphorical thinking, or the ability to conceptualize
ideas beyond their literal meaning. For example, when
Consciousness and Orientation. One of the obser- the individual is asked what brought him or her to the
vations that struck Kraepelin in his first descriptions hospital, a typical answer might be “an ambulance.’’
of dementia praecox was that individuals did not have On a mental status examination, this concrete thinking
clouding of consciousness. Individuals with schizo- is best elicited by asking an individual to interpret a
phrenia most likely have a clear sensorium unless there proverb or state the similarities between two objects.
is some comorbid medical illness or substance-related For example, “a rolling stone gathers no moss’’ may
phenomenon. A schizophrenic individual may be diso- mean, to the individual with schizophrenia, that “if a
riented, but this could be a result of inattentiveness to stone just stays in one place, the moss won’t be able to
details or distraction secondary to psychotic preoccu- collect.’’ More profound difficulties in abstraction and
pation. In fact, there is some literature suggesting that executive function, often seen in schizophrenia, such as
a subgroup of individuals may present as disoriented to inability to shift cognitive focus or set, may be assessed
temporal relations such as the date or their own age. by neuropsychological tests.
Attention and Concentration. Studies utilizing Judgment and Insight. Individuals suffering from
continuous performance task paradigms have demon- schizophrenia often display a lack of insight regard-
strated repeatedly that individuals with schizophre- ing their illness. Whether it is a reflection of a nega-
nia have pervasive deficits in attention in both acute tive symptom, such as apathy, or a constricted display
and residual phases. On a mental status examination, of emotion, individuals often appear to be emotionally
these deficits may present themselves as the inability disconnected from their illness and may even deny that
to perform mental exercises, such as spelling the word anything is wrong. Poor judgment, which is also char-
“earth’’ backward or serial subtractions. acteristic and may be related to lack of insight, may
lead to potentially dangerous behavior. For example, an
Memory. Careful assessment of memory in indi- individual walking barefoot in the snow because of the
viduals with schizophrenia may yield some deficits. feeling that her or his shoes could be traced by surveil-
Acquisition of new information, immediate recall, and lance cameras would be displaying both poor judgment
recent and remote memory may be impaired in some and poor insight. On a formal mental status examina-
individuals. Furthermore, answers to questions regard- tion, judgment is commonly assessed by asking indi-
ing memory may lead to idiosyncratic responses re- viduals what they would do if they saw a fire in a movie
lated to delusions, thought disorder, or other overriding theater or if they saw a stamped, addressed envelope on
symptoms of the illness. In general, individuals with the street. Insight can be ascertained by asking individ-
schizophrenia do not show gross deficits of memory uals about their understanding of why they are being
such as may be seen in individuals with dementia or evaluated by a mental health professional or why they
head trauma. are receiving a certain medication.
Physical Examination
Although there are no pathognomonic physical signs
of schizophrenia, some individuals have neurological 295.30 PARANOID TYPE
“soft’’ signs on physical examination. The neurological A type of schizophrenia in which the following criteria
deficits include nonspecific abnormalities in reflexes, are met:
coordination (as seen in gait and finger-to-nose tests), A. Preoccupation with one or more delusions or frequent
graphesthesia (recognition of patterns marked out auditory hallucinations.
B. None of the following is prominent: disorganized
on the palm), and stereognosis (recognition of three- speech, disorganized or catatonic behavior, or flat or
dimensional pictures). Other neurological findings in- inappropriate affect.
clude odd or awkward movements (possibly correlated Reprinted with permission from the Diagnostic and Statistical
with thought disorder), alterations in muscle tone, an Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
increased blink rate, a slower habituation of the blink
response to repetitive glabellar tap, and an abnormal
pupillary response.
Paranoid Type. In DSM-IV-TR, paranoid-type
The exact etiology of these abnormalities is un-
schizophrenia is marked by hallucinations or delu-
known, but they have historically been associated
sions in the presence of a clear sensorium and un-
with minimal brain dysfunction and may be more
changed cognition. Disorganized speech, disorgan-
likely in individuals with poor premorbid functioning
ized behavior, and flat or inappropriate affect are
and a chronic course. These neurological abnormali-
not present to any significant degree. The delusions
ties have been seen in neuroleptic-naive individuals
(usually of a persecutory or grandiose nature) and the
as well as those with exposure to traditional antip-
hallucinations most often revolve around a particular
sychotic medication. Overall, the literature suggests
theme or themes. Because of their delusions, these
that these findings may be associated with the disease
individuals may attempt to keep the interviewer at
itself, although further research is needed to deter-
bay, and thus they may appear hostile or angry during
mine the role of neuroleptic exposure in the manifes-
an interview. This type of schizophrenia may have a
tation of neurological signs and the extent to which
later age of onset and a better prognosis than the other
schizophrenia is itself associated with neurological
subtypes.
abnormalities.
Neuroophthalmological investigations have shown
Disorganized Type. Disorganized schizophrenia,
that individuals with schizophrenia have abnormalities
historically referred to as hebephrenic schizophrenia,
in voluntary saccadic eye movements (rapid eye move-
presents with the hallmark symptoms of disorganized
ment toward a stationary object) as well as in smooth
speech and/or behavior, along with flat or inappropri-
pursuit eye movements. The influence of attention and
ate (incongruent) affect. Any delusions or hallucina-
distraction, neuroleptic exposure, and the specificity of
tions, if present, also tend to be disorganized and are
smooth pursuit eye movements for schizophrenia have
not related to a single theme. Furthermore, these in-
raised criticisms of this area of study, and further in-
dividuals would not be classified as having catatonic
vestigation is necessary to determine its potential as a
schizophrenia. These individuals in general have more
putative genetic marker for schizophrenia.
Clinical Subtypes of Schizophrenia DSM-IV-TR Diagnostic Criteria

In DSM-IV-TR, schizophrenia has been divided into 295.10 DISORGANIZED TYPE
clinical subtypes based on the most prominent symp-
A type of schizophrenia in which the following criteria
toms, although it is acknowledged that the specific sub- are met:
type may exist simultaneously with or change over the A. All of the following are prominent:
course of the illness. DSM-IV-TR also includes an op- (1) disorganized speech
tional dimensional descriptor (included in the appendix (2) disorganized behavior
for criteria sets and axes provided for further study), (3) flat or inappropriate affect
which allows the condition to be characterized by the B. The criteria are not met for catatonic type.
presence or absence of a psychotic, disorganized, or Reprinted with permission from the Diagnostic and Statistical
negative symptom dimension over the entire course of Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
the illness.

295.20 CATATONIC TYPE 295.90 UNDIFFERENTIATED TYPE
A type of schizophrenia in which the clinical picture is A type of schizophrenia in which symptoms that meet
dominated by at least two of the following: criterion A are present, but the criteria are not met for the
paranoid, disorganized, or catatonic type.
A. motoric immobility as evidenced by catalepsy (includ-
ing waxy flexibility) or stupor Reprinted with permission from the Diagnostic and Statistical
B. excessive motor activity (that is apparently purposeless Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
and not influenced by external stimuli) American Psychiatric Association.
C. extreme negativism (an apparently motiveless resist-
ance to all instructions or maintenance of a rigid pos-
ture against attempts to be moved) or mutism
D. peculiarities of voluntary movement as evidenced by Residual Type. The diagnosis of residual schizo-
posturing (voluntary assumption of inappropriate or phrenia, according to DSM-IV-TR, is appropriately
bizarre postures), stereotyped movements, prominent used when there is a past history of an acute episode
mannerisms, or prominent grimacing
E. echolalia or echopraxia of schizophrenia but at the time of presentation, the
Reprinted with permission from the Diagnostic and Statistical individual does not manifest any of the associated
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 psychotic or positive symptoms. However, there is con-
tinued evidence of schizophrenia manifested in either
negative symptoms or low-grade symptoms of criterion
severe deficits on neuropsychological tests. According A. These may include odd behavior, some abnormali-
to DSM-IV-TR, these individuals tend to have an ear- ties of thought processes, or delusions or hallucinations
lier age at onset, an unremitting course, and a poor that exist in a minimal form. This type of schizophre-
prognosis. nia has an unpredictable, variable course.
Catatonic Type. Catatonic schizophrenia has unique Late-Onset Schizophrenia

features that distinguish it from the other subtypes of
schizophrenia. During the acute phase of this illness, The phenomenology of late-onset compared with
individuals may demonstrate marked negativism or early-onset schizophrenia may be distinct, with later-
mutism, profound psychomotor retardation or severe onset cases having a higher level of premorbid social
psychomotor agitation, echolalia (repetition of words functioning and exhibiting paranoid delusions and hal-
or phrases in a nonsensical manner), echopraxia lucinations more often than formal thought disorder,
(mimicking the behaviors of others), or bizarreness disorganization, and negative symptoms. Studies have
of voluntary movements and mannerisms. Some in- also shown a high comorbid risk of sensory deficits,
dividuals demonstrate a waxy flexibility, which is such as loss of hearing or vision, in individuals with
seen when a limb is repositioned on examination late-onset schizophrenia. Specifically, late-onset in-
and remains in that position as if the individual were dividuals are more likely to report visual, tactile, and
made of wax. Individuals with catatonic stupor must olfactory hallucinations and are less likely to display
be protected against bodily harm resulting from the
profound psychomotor retardation. They may remain
in the same position for weeks at a time. Because DSM-IV-TR Diagnostic Criteria
of extreme mutism or agitation, individuals may not
295.60 RESIDUAL TYPE
be able to report any difficulties. Some individuals
may experience extreme psychomotor agitation, with A type of schizophrenia in which the following criteria
grimacing and bizarre postures. These individuals are met:
may require careful monitoring to safeguard them A. Absence of prominent delusions, hallucinations, disor-
ganized speech, and grossly disorganized or catatonic
from injury or deterioration in nutritional status or behavior.
fluid balance. B. There is continuing evidence of the disturbance, as in-
dicated by the presence of negative symptoms or two
or more symptoms listed in criterion A for schizophre-
Undifferentiated Type. There is no hallmark symp- nia, present in an attenuated form (e.g., odd beliefs,
tom of undifferentiated schizophrenia; thus, it is the unusual perceptual experiences).
subtype that meets the criterion A for schizophrenia Reprinted with permission from the Diagnostic and Statistical
but does not fit the profile for paranoid, disorganized, Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
or catatonic schizophrenia.
affective flattening or blunting. For individuals over the ratio of prevalence of schizophrenia for men could
the age of 65, community prevalence estimates range be as high as 2 : 1
from 0.1% to 0.5%. One of the most robust findings
among the late-onset cases is the higher prevalence
Race and Ethnicity
seen in women. This does not appear to be due to sex
differences in seeking care, societal role expectations, The ECA data have shown that there is no significant
or delay between emergence of symptoms and service difference in the prevalence of schizophrenia between
contact. black and white persons when corrected for age, sex,
socioeconomic status, and marital status.. This find-
ing is significant because it refutes prior studies that
Prevalence
have shown the prevalence of schizophrenia to be much
Lifetime prevalence rates of schizophrenia, based on greater in the black population than in the white popu-
the ECA data, were approximately 1% (range across lation. Several factors have been proposed to explain
three sites, 1–1.9%). Point prevalence rates based on these discrepancies, including racial differences in
International Pilot Study of Schizophrenia data showed help-seeking behavior, research populations, commit-
no significant differences across study centers: schizo- ment status, and treatment.
phrenia was found universally with relatively equal fre-
quencies in a wide variety of cultures, with a range of
Socioeconomic Status
point prevalence between 0.6 and 8.3 cases of schizo-
phrenia per 1000 persons in the population. For many years, epidemiological studies revealed a
Interestingly, smaller studies have found specific higher incidence and prevalence of schizophrenia in
populations with either a higher or a lower prevalence groups with lower socioeconomic status. With these
of schizophrenia. For example, a higher rate of schizo- findings came the hypothesis that lower social class
phrenia has been found in a specific community in the could be considered a plausible risk factor for schizo-
north of Sweden, in northeastern Finland, in north- phrenia, possibly because of a higher risk of obstetrical
western Croatia, and in western Ireland. Lower rates of complications, poorer nutrition, increased exposure to
schizophrenia have been found in, for example, parts environmental toxins or infectious disease, or exposure
of Tonga, Papua New Guinea, Taiwan, and Micro- to greater life stressors. In the past half century, studies
nesia. In the United States, schizophrenia was almost have found that the actual incidence of schizophrenia
nonexistent in the Hutterite community, a Protestant does not vary with social class, based on first admis-
sect living in South Dakota. Epidemiologists generally sion rates, adoption studies, and a series of studies ex-
agree that these communities may represent aberrant amining the social class of the fathers of people with
findings. However, if these differences in prevalence schizophrenia.
rates are accurate, several theories have been offered When these findings did not validate the original
as explanations, including genetic preloading, differ- theory, it became clear that lower socioeconomic status
ences in diet, or even differences in factors such as was more a result than a cause of schizophrenia. This
maternal age. led to the acceptance of the downward drift hypoth-
esis, which stated that because of the nature of schizo-
phrenic symptoms, people who develop schizophrenia
Sex Differences
are unable to attain employment and positions in so-
A large body of data suggests that although men and ciety that would allow them to achieve a higher social
women have an equivalent lifetime risk, the age at on- status. Thus, these individuals drift down the socioeco-
set varies with sex. Although some sites showed dif- nomic ladder, and because of the illness itself they may
ferent prevalence rates of schizophrenia in men and become dependent on society for their well-being.
women, the overall prevalence rates, as reported in the
ECA survey, did not differ significantly between sexes.
Course
However, there is strong evidence that onset of schizo-
phrenia is on average 3.5 to 6 years earlier in men than The natural couse of schizophrenia can be divided into
in women. The WHO 10-country study observed this three phases: an early phase marked by deterioration
phenomenon in most cultures studied. Therefore, in- from premorbid levels of functioning; a middle phase
cidence and prevalence rates of schizophrenia across characterized by a prolonged period of little change
sexes may vary according to age. Interestingly, in some termed the stabilization phase; and the last period,
cultural populations (e.g., West Ireland, Micronesia), which is called the improving phase.
An enormous clinical and research effort is directed side effects. They require lower doses of medication to
internationally toward individuals in very early stages achieve therapeutic responses. The issue of treatment
of their illness and especially during their fi rst psy- adherence is of critical importance in individuals in
chotic break with a focus on early and effective inter- their first episode of psychosis. Although these individ-
vention. First episode provides a unique opportunity uals respond very well with 1-year remission rates of
to intervene early and effectively and possibly change greater than 80%, the 1-year attrition rates are as high
the course of illness. It is well known that there is a as 60%. This important issue undermines management
delay of 1 to 2 years on an average between onset of of individuals with first episode psychosis during this
psychosis and starting of treatment. This duration of critical period of their illness.
untreated psychosis (DUP) is recognized by many, The mortality rate of schizophrenia is estimated
though not all, as an important indicator of subsequent to be twice that of the general population. Approxi-
clinical outcome. Clinical deterioration appears to be mately 10% of the mortality is secondary to suicide.
correlated with the duration of psychosis and number Young men with schizophrenia are most likely to
of episodes of psychosis. The deterioration usually oc- complete suicide attempts, especially early in their
curs during the first 5 years after onset and then sta- illness. Degree of social isolation, agitation, depres-
bilizes at a level where the individual has persistent sion, a sense of hopelessness, a history of prior sui-
symptoms and is impaired in social and vocational cide attempts, and recent loss may be associated with
function. After that point, additional exacerbations increased risk of suicide among schizophrenic indi-
may occur, but they are not usually associated with viduals. There is also some evidence that an increased
further deterioration. number of relapses, rehospitalizations, and discharges
Long-term studies of schizophrenia suggest that neg- lead to an increased risk of suicide. There have been
ative symptoms tend to be less common and less severe observations that suicide rates of individuals with
in the early stages of the illness but increase in preva- schizophrenia may be increasing in the era of shorter
lence and severity in the later stages. Positive symptoms hospital stays and community treatment. However,
such as delusions and hallucinations are more common with the advent of the novel antipsychotic medications
earlier on while thought disorganization, inappropri- and especially with clozapine use, it is possible that
ate affect, and motor symptoms occur more commonly this risk of suicide may even out or decrease owing to
in the later stages of illness. A possible decline in the their possible protective effects against suicide. Other
prevalence of the hebephrenic and catatonic subtypes factors leading to increased mortality rates in schizo-
of schizophrenia may be attributed to effective treat- phrenic individuals include an increased incidence of
ment and possible arrest of the progression of illness. accidents as well as a more frequent association with
Thus with effective treatment, and with long-term com- other medical illnesses (including cardiovascular dis-
pliance, it is possible to produce favorable outcomes. ease), comorbid substance abuse, a general neglect of
Following onset of the illness, individuals experi- health, an increased rate of damaging behaviors such
ence substantial decline in cognitive functions from as smoking and poor diet, decreased access to health
their premorbid levels. However, it is unclear whether, services, and depression.
after the first episode, there is further cognitive decline
due to the illness. Some studies even suggest a slight
and gradual improvement. Increased number of epi-
sodes and the longer DUP are associated with greater Making an accurate diagnosis of schizophrenia requires
cognitive dysfunction. high levels of clinical acumen, extensive knowledge
Individuals with first-episode psychosis usually have of schizophrenia, and sophisticated application of the
excellent clinical response to antipsychotic treatment principles of differential diagnosis. It is unfortunately
early in their course of illness when compared to indi- common for individuals with psychotic disorders to be
viduals with chronic multiple episodes. Effective and misdiagnosed and consequently treated inappropri-
early intervention does help achieve clinical remission ately. The importance of accurate diagnosis is under-
and good outcome. Some suggest that atypical antipsy- lined by an emerging database indicating that early de-
chotic medication should be used preferentially in the tection and prompt pharmacological intervention may
treatment of individuals with first-episode psychosis as improve the long-term prognosis of the illness.
they are a highly treatment-responsive group, and may Possibly the most difficult diagnostic dilemma in
be best able to optimize the outcome. In addition, in- cases in which an individual has both psychotic symp-
dividuals with first-episode psychosis are sensitive to toms and affective symptoms is in the differentiation
side effects, especially extrapyramidal and weight gain between schizophrenia and schizoaffective disorder. In
DSM-IV-TR, an individual with schizoaffective disor- cial impairment or odd behavior. Moreover, individuals
der must have an uninterrupted period of illness dur- with delusional disorder do not experience hallucina-
ing which, at some time, they have symptoms that meet tions or typically have negative symptoms.
the diagnostic criteria for a major depressive episode, If the individual experiences psychotic symptoms
manic episode, or a mixed episode concurrently with solely during times when affective symptoms are
the diagnostic criteria for the active phase of schizo- present, the diagnosis is more likely to be mood dis-
phrenia (criterion A for schizophrenia). Additionally, order with psychotic features. If the mood disturbance
the individual must have had delusions or hallucina- involves both manic and depressive episodes, the di-
tions for at least 2 weeks in the absence of prominent agnosis is bipolar disorder. According to DSM-IV-TR,
mood disorder symptoms during the same period of ill- affective disorders that are seen in individuals with
ness. The mood disorder symptoms must be present for schizophrenia may fall in the category of depressive
a substantial part of the active and residual psychotic disorder not otherwise specified or bipolar disorder not
period. The essential features of schizoaffective disor- otherwise specified.
der must occur within a single uninterrupted period of Psychotic disorders, delirium, and dementia that are
illness where the “period of illness’’ refers to the period caused by substance use, in DSM-IV-TR, are distin-
of active or residual symptoms of psychotic illness, and guished from schizophrenia by virtue of the fact that
this can last for years and decades. The total dura- there is clear-cut evidence of substance use leading to
tion of psychotic symptoms must be at least 1 month symptoms. Examples of psychotomimetic properties
to meet the criterion A for schizophrenia and thus, the of substances include a phencyclidine psychosis (PCP)
minimum duration of a schizoaffective episode is also that can resemble schizophrenia clinically, chronic al-
1 month. cohol intoxication (Korsakoff’s psychosis), and chronic
The criterion for major depressive episode requires amphetamine administration, which can lead to para-
a minimum duration of 2 weeks of either depressed noid states. Therefore, individuals who have symptoms
mood or markedly diminished interest or pleasure. As that meet criterion A of schizophrenia in the presence
the symptoms of loss of pleasure or interest commonly of substance use must be reevaluated after a significant
occur in nonaffective psychotic disorders, to meet the period away from the suspected substance, and proper
criteria for schizoaffective disorder criterion A, the toxicology screens must be performed to rule out re-
major depressive episode must include pervasive de- cent substance abuse.
pressed mood. Presence of markedly diminished inter- General medical conditions ranging from vitamin
est or pleasure is not sufficient to make a diagnosis as B12 deficiency to Cushing’s syndrome have been asso-
it is possible that these symptoms may occur with other ciated with a clinical presentation resembling that of
conditions too. schizophrenia. The most common neurological dis-
The distinctions among brief psychotic disorder, order appearing clinically similar to schizophrenia is
schizophreniform disorder, and schizophrenia are epilepsy, particularly of the temporal lobe. Other medi-
based on duration of active symptoms. DSM-IV-TR has cal illnesses with symptoms similar to those of schizo-
a requirement of 6 months of active, prodromal, and/ phrenia include basal ganglia calcifications and acute
or residual symptoms for a diagnosis of schizophre- intermittent porphyria. Imbalances of endocrine func-
nia. Brief psychotic disorder is a transient psychotic tion as well as certain infectious diseases can present
state, not caused by medical conditions or substance with symptoms that mimic schizophrenic psychosis.
use, which lasts for at least 1 day and up to 1 month. Because the prognosis for the associated medical condi-
Schizophreniform disorder falls in between and re- tion is better than that for schizophrenia and the stigma
quires symptoms for at least 1 month and not exceeding attached to schizophrenia is significant, it is imperative
6 months, with no requirement for loss of functioning. to provide individuals with a thorough medical workup
If the delusions that an individual describes are not before giving a diagnosis of schizophrenia. This in-
bizarre (e.g., examples of bizarre delusions include the cludes a physical examination; laboratory analyses in-
belief that an outside force or person has taken over cluding thyroid function tests, syphilis screening, and
one’s body or that radio signals are being sent through folate and vitamin B12 levels; a CT or MRI scan; and a
the caps in one’s teeth), it is wise to consider delusional lumbar puncture when indicated in new-onset cases.
disorder in the differential diagnosis. Delusional disor-
der is usually characterized by specific types of false
TREATMENT
fixed beliefs such as erotomanic, grandiose, jealous,
persecutory, or somatic types. Delusional disorder, un- It could be argued that the successful treatment of
like schizophrenia, is not associated with a marked so- schizophrenia requires a greater level of clinical
knowledge and sophistication than the treatment of efforts to understand the mechanism of action of typi-
most other mental disorders and medical illnesses. It cal antipsychotics uncovered the intimate association
begins with the formation of a therapeutic relationship of dopamine D2 receptor blockade to the antipsychotic
between the clinician and the individual with schizo- effects. This formed the basis of the hypothesis sug-
phrenia and must combine the latest developments in gesting that symptoms of schizophrenia were possibly
pharmacological and psychosocial therapeutics and related to the hyperactivity of the (mesolimbic and
interventions. mesocortical) dopaminergic systems in the brain. An-
The relationship between the clinician and the pa- tipsychotics developed subsequent to chlorpromazine
tient is the foundation for treating individuals with such as haloperidol, thiothixene, and so on, were
schizophrenia. Because of the clinical manifestations modeled on the (misguided) belief that induction of
of the illness, the formation of this relationship is of- extrapyramidal symptoms (EPS) was an integral part
ten difficult. Paranoid delusions may lead to mistrust of having an antipsychotic efficacy. Over the years,
of the clinician. Conceptual disorganization and cogni- another belief developed that all antipsychotics were
tive impairment make it difficult for individuals with similar in their efficacy and varied only in their side
schizophrenia to attend to what the clinician is say- effects. However, clozapine challenged these beliefs by
ing and to follow even the simplest directions. Nega- being significantly superior in efficacy than the exist-
tive symptoms result in lack of emotional expression ing antipsychotics and having minimal to no EPS! This
and social withdrawal, which can be demoralizing for started the era of antipsychotic agents being referred to
the clinician who is attempting to “connect’’ with the as either typical (conventional or traditional) or atypi-
individual. cal (or novel) antipsychotic drugs. If chlorpromazine
It is important for the clinician to understand the started the first revolution in the psychopharmacologi-
ways in which the psychopathology of the illness af- cal treatment of schizophrenia, then clozapine ushered
fects the therapeutic relationship. The clinician should in the second and more profound revolution, whose im-
provide constancy to the individual with schizophre- pact is felt beyond schizophrenia and whose full extent
nia, which helps “anchor’’ individuals in their turbulent is yet to be realized. Moreover, clozapine has invigor-
world. The qualities of the relationship should include ated the psychopharmacology of schizophrenia and re-
consistency, acceptance, appropriate levels of warmth kindled one of the most ambitious searches for new an-
that respect the individual’s needs for titrating emo- tipsychotic compounds by the pharmaceutical industry.
tional intensity, nonintrusiveness, and, most important, Following approval of clozapine in 1990, FDA has al-
caring. “Old-fashioned’’ family doctors who know their ready approved five novel antipsychotics—risperidone,
patients well, are easily approachable, have a matter- olanzapine, quetiapine, ziprasidone, and aripiprazole.
of-fact style, attend to a broad range of needs, and are Though clozapine, a dibenzodiazepine compound,
available and willing to reach out during crises provide was approved for use in the US in 1990, it had been
a useful model for the relationship between the clini- available in European markets during the 1970s but
cian and the patient in the treatment of schizophrenia. had been found to be associated with agranulocytosis,
a potentially fatal side effect, which led to its removal
from clinical trials. The need for improved treatment
Psychopharmacological Treatment
of schizophrenia, particularly for individuals who do
Although chlorpromazine had been around since the not respond to traditional neuroleptics, generated inter-
late 1800s, it was not until 1952 that it was first used to est in resuming investigations of clozapine’s clinical
treat psychosis. The implementation of chlorpromazine efficacy.
became the turning point for psychopharmacology. In- Double-blind, controlled studies demonstrated the
dividuals who had been institutionalized for years were superior clinical efficacy of clozapine compared to
able to receive treatment as outpatients and live in com- standard neuroleptics, without the associated EPS. It is
munity settings. The road was paved for the deinstitu- clearly superior to traditional neuroleptics for psycho-
tionalization movement, and scientific understanding sis. A summary of the US studies of individuals with
of the pathophysiology of schizophrenia burgeoned. chronic and treatment-resistant schizophrenia suggests
The discovery of chlorpromazine led to the develop- that approximately 50% of individuals derive a better
ment of other phenothiazines and new classes of antip- response from clozapine than from traditional neu-
sychotic medications, now totaling 11 different classes roleptics. Its effect on negative symptoms is somewhat
available in the US today. The word neuroleptic, lit- controversial and has started an intense and a passion-
erally “nerve cutting,’’ was used to describe the tran- ate debate as to whether the efficacy of the medication
quilizing effects of these medications. The enormous is with primary or secondary negative symptoms or
both. There is substantial evidence that clozapine de- The risk of tardive dyskinesia at the regular therapeutic
creases relapses, improves stability in the community, doses is low.
and diminishes suicidal behavior. There have also been Olanzapine is a thienobenzodiazepine compound ap-
reports that clozapine may cause a gradual reduction in proved in 1996. It has antagonistic effects at dopamine
preexisting tardive dyskinesia. D1 through D5 receptors and serotonin 5-HT2A, 5-HT2C,
Unfortunately, clozapine is associated with agranu- and 5-HT6 receptors. The antiserotonergic activity is
locytosis, and because of this risk, it requires weekly more potent than the antidopaminergic one. It also has
white blood cell testing. Approximately 0.8% of indi- affinity for alpha-1-adrenergic, M1 muscarinic acetyl-
viduals taking clozapine and receiving weekly white cholinergic, and H1 histaminergic receptors. It differs
blood cell monitoring develop agranulocytosis. Women from clozapine by not having high affinity for the 5-
and the elderly are at higher risk than other groups. The HT7, alpha-2-adrenergic, and other cholinergic recep-
period of highest risk is the first 6 months of treatment. tors. It has significant efficacy against positive and neg-
These data have led to monitoring of white cell counts ative symptoms and also improves cognitive functions.
less frequently after the first 6 months to every other EPS is minimal when used in the therapeutic range
week if a person has a history of white cell counts with the exception of mild akathisia. As the compound
within normal range in the preceding 6 months. Cur- has a long half-life, it is used once a day and as it is well
rent guidelines state that the medication must be held tolerated, it can be started at a higher dose or rapidly ti-
back if the total white blood cell count is 3000/mm3 or trated to the most effective dose. It is available as a rap-
less or if the absolute polymorphonuclear cell count is idly disintegrating wafer form (Zyprexa Zydis), which
1500/mm3 or less. Individuals who stop clozapine treat- dissolves immediately in the mouth. An intramuscular
ment continue to require blood monitoring for at least form has also been approved by FDA for agitation. The
4 weeks after the last dose according to current guide- major side effects of olanzapine include weight gain,
lines. Other side effects of clozapine include orthostatic sedation, dry mouth, nausea, lightheadedness, ortho-
hypotension, tachycardia, sialorrhea, sedation, elevated static hypotension, dizziness, constipation, headache,
temperature, and weight gain. Furthermore, clozapine akathisia, and transient elevation of hepatic transami-
can lower the seizure threshold in a dose-dependent nases. The risk of tardive dyskinesia and neuroleptic
fashion, with a higher risk of seizures seen particularly malignant syndrome (NMS) is low. Though used as a
at doses greater than 600 mg/day. once-a-day medication, it is often administered twice a
Clozapine has an affinity for dopamine receptors day with an average dose of 15–20 mg/day. However,
(D1, D2, D3, D4, and D5), serotonin receptors (5-HT2A, 5- doses higher than 20 mg/day are often used clinically
HT2C, 5-HT6, and 5-HT7), alpha-1- and alpha-2-adren- and are thus being evaluated in clinical trials.
ergic receptors, nicotinic and muscarinic cholinergic Quetiapine, a dibenzothiazepine compound approved
receptors, and H1 histaminergic receptors. As clozap- in 1997, has a greater affinity for serotonin 5-HT2 re-
ine has a relatively shorter half-life, it is usually admin- ceptors than for dopamine D2 receptors; it has consid-
istered twice a day. erable activity at dopamine D1, D5, D3, D4, serotonin
Following clozapine, risperidone was the first novel 5-HT1A, and alpha-1-, alpha-2-adrenergic receptors.
antipsychotic medication approved by FDA in 1994. Unlike clozapine, it lacks affinity for the muscarinic
Risperidone is a benzisoxazol compound with a high cholinergic receptors. It is usually administered twice
affinity for 5-HT2A and D2 receptors and has a high a day due to a short half-life. Quetiapine is as effective
serotonin–dopamine receptor antagonism ratio. It has as typical agents and also appears to improve cognitive
high affinity for alpha-1-adrenergic and H1 histaminer- function. Among 2035 individuals enrolled in seven
gic receptors and moderate affinity for alpha-2-adren- controlled studies, quetiapine at all doses used did not
ergic receptors. Risperidone is devoid of significant have an EPS rate greater than a placebo. This is in con-
activity against the cholinergic system and the D1 re- trast to olanzapine, risperidone, and ziprasidone, where
ceptors. The efficacy of this medication is equal to that there were dose-related effects on EPS levels. The rate
of other first-line atypical antipsychotic agents, and it of treatment-emergent EPS was very low even in high
is well tolerated and can be given once or twice a day. It at-risk populations such as adolescents, parkinsonian
is available in a liquid form and as a long-acting inject- individuals with psychosis, and geriatric individuals.
able form. The most common side effects reported are There was no elevation of prolactin. Major side effects
drowsiness, orthostatic hypotension, lightheadedness, include somnolence, postural hypotension, dizziness,
anxiety, akathisia, constipation, nausea, nasal conges- agitation, dry mouth, and weight gain. Akathisia oc-
tion, prolactin elevation, and weight gain. At doses curs on rare occasions. The package insert warns about
above 6 mg/day, EPS can become a significant issue. developing lenticular opacity or cataracts and advises
periodic eye examination based on data from animal and target dose is 10–15 mg a day. The most commonly
studies. However, recent data suggest that this risk may reported adverse events from a pooled analysis of
be minimal. safety and tolerability data were headache, insomnia,
Ziprasidone, approved by FDA in 2001, has the agitation, and anxiety, but these were also the most
strongest 5-HT2A receptor binding relative to D2 bind- frequently reported events in the placebo, haloperidol,
ing among the atypical agents currently in use. Inter- and risperidone comparison groups. The incidence of
estingly, ziprasidone has 5-HT1A agonist and 5-HT1D adverse events was similar in the aripiperazole and
antagonist properties with a high affinity for 5-HT1A, placebo groups. There was also a similar incidence of
5-HT2C, and 5-HT1D receptors. As it does not interact EPS-related adverse events in the aripiperazole and pla-
with many other neurotransmitter systems, it does not cebo groups. There were also only minimal changes in
cause anticholinergic side effects and produces little mean body weight and no increases in prolactin level.
orthostatic hypotension and relatively little sedation. At present, with respect to efficacy, it does not ap-
Just like some antidepressants, ziprasidone blocks pr- pear that any one of the novel antipsychotic agents
esynaptic reuptake of serotonin and norepinephrine. (except clozapine) is better than another one in treat-
Ziprasidone has a relatively short half-life and thus ing schizophrenia. The randomized controlled trials
it should be administered twice a day and along with suggest that, on average, these antipsychotic agents are
food for best absorption. Ziprasidone is not completely each associated with 20% improvement in symptoms.
dependent on CYP3A4 system for metabolism, thus in- However, clozapine is the only new antipsychotic agent
hibitors of the cytochrome system do not significantly that is more effective than haloperidol in managing
change the blood levels. Ziprasidone at doses between treatment-resistant schizophrenia. Unfortunately, its
80 and 160 mg/day is probably the most effective for potential for treatment-emergent agranulocytosis, sei-
treating symptoms of schizophrenia. To assess the car- zures, and the new warning of myocarditis precludes
diac risk of ziprasidone and other antipsychotic agents, its use as a first-line agent for schizophrenia. A major
Pfizer and FDA designed a landmark study to evaluate difference among the newer antipsychotic agents is the
the cardiac safety of the antipsychotic agents, given at side-effect profile and its effect on the overall quality of
high doses alone and with a known metabolic inhibi- life of the individual.
tor in a randomized study involving individuals with
schizophrenia. This was done to replicate the possible Acute Treatment. Until recently, the typical antip-
worst-case scenario (overdose or dangerous combi- sychotics were the mainstay of the treatment for acute
nation treatment) in the real world. All antipsychotic episodes of psychosis. In the past few years, the use
agents studied caused some degree of QTc prolonga- of novel antipsychotics has surpassed the use of typi-
tion. Oral form of haloperidol was associated with the cal ones in the management of acute phase symptoms
least and thioridazine with the greatest change. Major of schizophrenia, except for the use of parenteral and
side effects reported with the use of ziprasidone are liquid forms of antipsychotics where typical antip-
somnolence, nausea, insomnia, dyspepsia, and prolon- sychotic agents still hold an upper hand. However,
gation of QTc interval. Dizziness, weakness, nasal dis- this trend will most likely change once the injectable
charge, orthostatic hypotension, and tachycardia occur preparations of the novel antipsychotics (olanzapine,
less commonly. ziprasidone, aripiprazole) become more widely used.
Ziprasidone should not be used in combination with The primary goal of acute treatment is the ameliora-
other drugs that cause significant prolongation of the tion of any behavioral disturbances that would put the
QTc interval. It is also contraindicated for individuals individual or others at risk of harm. Acute symptom
with a known history of significant QTc prolongation, presentation or relapses are heralded by the recurrence
recent myocardial infarction, or symptomatic heart of positive symptoms, including delusions, hallucina-
failure. Ziprasidone has low EPS potential, does not tions, disorganized speech or behavior, severe negative
elevate prolactin levels, and causes approximately 1 lb symptoms, or catatonia. Quite frequently, a relapse is
weight gain in short-term studies. a result of antipsychotic discontinuation, and resump-
Aripiprazole was approved by the FDA for the treat- tion of antipsychotic treatment aids in the resolution of
ment of schizophrenia in 2003. It has a unique phar- symptoms. There is a high degree of variability in re-
macodynamic profile compared to the other atypical sponse rates among individuals. When treatment is ini-
neuroleptics—partial agonist activity (rather than full tiated, improvement in clinical symptoms can be seen
antagonist activity) at both dopaminergic (D2) and se- over hours, days, or weeks of treatment.
rotonergic (5-HT1A) receptors and full antagonist activ- Studies have shown that although typical neurolep-
ity at (5-HT2A) receptions. The recommended starting tics are undoubtedly effective, a significant percentage
(between 20% and 40%) of individuals show only a chlorpromazine equivalents per day) have any advan-
poor or partial response to traditional agents. Further- tage over standard doses (400–600 chlorpromazine
more, there is no convincing evidence that one typical equivalents per day).
antipsychotic is more efficacious as an antipsychotic Some individuals who are extremely agitated or
than any other, although a given individual may re- aggressive may benefit from concomitant admin-
spond better to a specific drug. Once an informed istration of high-potency benzodiazepines such
choice has been made between using a novel or a typi- as lorazepam, at 1 to 2 mg, until they are stable.
cal antipsychotic medication by the patient and the Benzodiazepines rapidly decrease anxiety, calm the
clinician, selection of a specific antipsychotic agent person, and help with sedation to break the cycle of
should be based on efficacy, side-effect profile, history agitation. They also help decrease agitation due to
of prior response (or nonresponse) to a specific agent, akathisia. The use of these medications should be
or history of response of a family member to a certain limited to the acute stages of the illness to prevent
antipsychotic agent. (For a pharmacotherapy decision tachyphylaxis and dependency. Benzodiazepines
tree based on Texas Medication Algorithm Project, are quite beneficial in the treatment of catatonic or
see Figure 25-1.) Among the typical antipsychotic mute individuals but the results are only temporary,
medications, low-potency, more sedating agents, such though of enough duration to help with body func-
as chlorpromazine, were long thought to be more ef- tions and nutrition.
fective for agitated individuals, yet there are no con-
sistent data proving that high-potency agents are not Maintenance Treatment. There is by now a great
equally useful in this context. The low-potency antip- deal of evidence from long-term follow-up studies that
sychotics, however, are more associated with orthos- individuals with schizophrenia have a higher risk of
tatic hypotension and lowered seizure threshold and relapse and exacerbations if not maintained with ad-
are often not as well tolerated at higher doses. Higher equate antipsychotic regimens. Noncompliance with
potency neuroleptics, such as haloperidol and fluphen- medication, possibly because of intolerable neurolep-
azine, are safely used at higher doses and are effective tic side effects, may contribute to increased relapse
in reducing psychotic agitation and psychosis itself. rates. In a double-blind placebo-controlled study of
However, they are more likely to cause EPS than the relapse rates, 50% of patients in a research ward dem-
low-potency agents. onstrated clinically significant exacerbation of their
The efficacy of novel antipsychotic drugs on posi- symptoms within 3 weeks of stopping neuroleptic
tive and negative symptoms is comparable to or treatment. Furthermore, in a comprehensive review
even better than that of the typical antipsychotic of the literature on neuroleptic withdrawal examining
drugs. The significantly low potential to cause EPS 4365 subjects, 53.2% of individuals withdrawn from
or dystonic reaction and thus the decreased long- neuroleptics relapsed, compared with 15.6% of control
term consequences of TD has made the novel agents subjects who were maintained with neuroleptic treat-
more tolerable and acceptable in acute treatment of ment. The length of follow-up was related to the risk
schizophrenia. Other significant advantages add- of relapse. Long-term outcome studies show that per-
ing to the popularity of novel antipsychotics include sistent symptoms that do not respond to standard neu-
their beneficial impact on mood symptoms, suicidal roleptic therapy are associated with a greater risk of
risk, and cognition. Except for clozapine, which is not rehospitalization. Nonpharmacological interventions
considered fi rst-line treatment because of substantial may help decrease relapse rates.
and potentially life-threatening side effects, there is Long-term treatment of schizophrenia is a com-
no convincing data supporting the preference of one plex issue. It is clear that the majority of individuals
atypical antipsychotic over the other. However, if the require maintenance medication. Some individuals do
individual does not respond to one, a trial with an- well with stable doses of neuroleptics for years with-
other atypical antipsychotic is reasonable and may out any exacerbations. However, many individuals who
produce response. are maintained with a stable neuroleptic dose have epi-
Once the decision is made to use an antipsychotic sodic breakthroughs of their psychotic symptoms. In
agent, an appropriate dose must be selected. Initially, a 1974 study, schizophrenic individuals were followed
higher doses or repeated dosing may be helpful in up for 2 years after hospitalization and randomized to
preventing grossly psychotic and agitated individuals receive placebo alone, placebo and sociotherapy, chlo-
from doing harm. In general, there is no clear evidence rpromazine alone, or chlorpromazine and sociother-
that higher doses of neuroleptics (more than 2000 mg apy. In this study, the placebo-only group had a relapse
Stage 1
Trial of a single SGA
(OLANZAPINE, QUETIAPINE,
RISPERIDONE, or ZIPRASIDONE)
Partial or
nonresponse
Stage 2
Trial of a single SGA
(not SGA tried in Stage 1)
Partial or nonresponse Partial or nonresponse
Stage 2A Stage 3
Trial of a single agent Partial or nonresponse
FGA or SGA CLOZAPINE
(not SGA tried in Stages
1or 2)
Partial or
nonresponse
FGA = First generation AP
SGA = Second generation AP Stage 4 Clozapine
CLOZAPINE refusal
If patient is nonadherent to medication, the +
clinician may use haloperidol decanoate or (FGA, SGA or ECT)
fluphenazine decanoate at any stage, but
should carefully assess for unrecognized side Nonresponse
effects and consider a different oral AP if side
effects could be contributing to Stage 5
nonadherence. Trial of a single agent Value in
See text for discussion. Current expert FGA or SGA clozapine failures
opinion favors choice of clozapine. (not SGA tried in Stages 1, 2 or 2A ) not established
Assuming no history of failure on FGA.
Case reports,
Stage 6 no controlled
Combination therapy studies of
SGA + FGA, combination of SGAs, combinations
(FGA or SGA) +ECT, in long-term
(SGA or FGA) + mood stabilizer treatment of
schizophrenia
Side Effects Algorithms
EPS Akathisia NMS Severe TD
Tactical
Anticholinergic Propranolol
Interventions
Nonresponder Nonresponder
Stage Next stage of Next stage of Next stage of Clozapine

Change antipsychotic algorithm antipsychotic algorithm antipsychotic algorithm
Figure 25-1 Selecting antipsychotic treatment using Texas medication algorithm for schizophrenia. Choice of antipsychotic (AP) should
be guided by considering the clinical characteristics of the patient and the efficacy and side effect profiles of the medication. Any stage(s)
can be skipped depending on the clinical picture or history of antipsychotic failures. Texas Medication Algorithm Project for choosing
antipsychotic treatment, managing side effects, and coexisting symptoms. This project is a public–academic collaborative effort to
develop, implement, and evaluate medication treatment algorithms for public sector patients. For more information or to view the most
current version of the algorithm, visit www.mhmr.state.tx.us/centraloffice/medicaldirector/tmaptoc.html).
rate that was almost twice that of the chlorpromazine- suggests that the term postpsychotic depression be
treated group. Unfortunately, the difficulty in tolerating used to describe depression that occurs at any time
neuroleptic side effects often results in noncompliance after a psychotic episode of schizophrenia, even after
with medication. Furthermore, intensive case manage- a prolonged interval. The atypical antipsychotic medi-
ment and rehabilitation counseling did prevent relapse cations, with less potential to cause motor side effects
but only after a delayed period. Sociotherapy and drug and different mechanisms of action at receptor levels,
treatment were found to have additive effects in pre- themselves may contribute substantially towards a de-
venting relapse. crease in the rate of depression. Moreover, the atypi-
Given these fi ndings, it would be prudent to as- cal antipsychotic medications appear to be superior to
sess individuals for medication compliance when standard neuroleptics in treatment of negative symp-
signs of relapse are suspected. Prodromal cues may toms. The impact of clozapine on the rate of suicide
be present before an exacerbation of psychotic symp- is significantly superior compared to the conventional
toms. For example, any recent change in sleep, atten- agents. However, a large number of individuals still
tion to activities of daily living, or disorganization end up with a depression that will require treatment
may be a warning sign of an impending increase in with an antidepressant.
psychosis.
For individuals for whom compliance is a problem, Risks and Side Effects of Typical Neuroleptics. Ex-
long-acting, depot neuroleptics are available in the trapyramidal symptoms (EPS) are side effects of typi-
US for fluphenazine, haloperidol, and risperidone. cal antipsychotic medications that include dystonias,
The antipsychotic drug is is injected every 1 to 6 oculogyric crisis, pseudoparkinsonism, akinesia, and
weeks to circumvent the need for daily oral antip- akathisia. They are referred to collectively as EPS be-
sychotic medications in most cases (although some cause they are mediated at least in part by dopamin-
individuals benefit from adjuvant oral medication). ergic transmission in the extrapyramidal system.
This form of medication delivery guarantees that the Prevalence rates vary among the different types of
medication is in the system of the person taking it EPS. When present, they can be uncomfortable for the
and eliminates the need to monitor daily compliance. individual and a reason for noncompliance.
This alternative should be considered if noncompli- Dystonias are involuntary muscular spasms that
ance with oral agents has led to relapses and rehospi- can be brief or sustained, involving any muscle group.
talization. With these individuals, maintenance treat- They can occur with even a single dose of medica-
ment using long-acting preparations should begin as tion. When they develop suddenly, these spasms can
early as possible. be quite frightening to the individual and potentially
dangerous, as in the case of laryngeal dystonias. They
Depression and Schizophrenia. Symptoms of de- are more likely to be seen in young individuals. Studies
pression occur in a substantial percentage of individu- differ as to whether the prevalence is higher in males
als with schizophrenia, with a wide range of 7% to or females. Prevalence rates for dystonias secondary to
75% and a modal rate of 25%, and is associated with typical neuroleptic exposure range from 2% to 20%..
poor outcome, impaired functioning, suffering, higher Pseudoparkinsonism and akinesia are characterized by
rates of relapse or rehospitalization, and suicide. It is muscular rigidity, tremor, and bradykinesia, much as in
important to distinguish depression as a symptom or Parkinson’s disease. On examination, individuals typi-
as a syndrome when it occurs. There is an important cally have masked facies, cogwheel rigidity, slowing,
overlap of symptoms of depression with the negative and decreased arm swing with a shuffling gait. This
symptoms. Differentiating these states can sometimes condition is reported to be more prevalent than the dys-
be difficult, especially in individuals who lack the in- tonias, presenting with a frequency ranging from 15%
terpersonal communication skills to articulate their to 35%.
internal subjective states well. A link between typical Akathisia is more common, affecting more than
antipsychotic use and depression has been suggested, 20% of individuals taking neuroleptic medications.
with some considering depression to be a form of This clinical entity presents as motor restlessness or an
medication-induced akinesia. Many individuals have internal sense of restlessness. Often, individuals expe-
a reaction of disappointment, a sense of loss or pow- riencing akathisia are unable to sit still during an inter-
erlessness, or awareness of psychotic symptoms or view. Akathisia is difficult to differentiate from agita-
psychological deficits that contributes to depression. tion. The tendency to treat agitation with neuroleptics
Depression in schizophrenia is heterogeneous and may exacerbate akathisia, making treatment decisions
requires careful diagnostic clarification. DSM-IV-TR challenging.
Treatment of EPS can be difficult but usually in- Rhabdomyolysis is one of the most serious sequelae
volves administration of anticholinergic medications. of NMS; it can lead to renal failure unless individu-
Some advocate the use of prophylactic anticholinergic als are well hydrated. In some cases, dantrolene and
agents when beginning typical neuroleptic treatment bromocriptine have been reported to be effective phar-
to decrease the incidence of EPS. This option may be macological treatments. Though quite rare, NMS has
appropriate, but it should be used with caution, con- been reported even with the use of novel antipsychotic
sidering the side effects associated with anticholinergic agents. The decision to rechallenge the individual with
agents and their potential for abuse. neuroleptics after an episode of NMS must be made
Treatment of acute dystonic reactions usually in- with caution.
volves acute intramuscular administration of either an One of the major risks of neuroleptic treatment with
anticholinergic or diphenhydramine. Akathisia may the traditional antipsychotic agents is that of tardive
not respond to anticholinergic medications. Both neu- dyskinesia, a potentially irreversible syndrome of in-
roleptic dosage reduction and the use of beta-blocking voluntary choreoathetoid movements and chronic dys-
agents such as propranolol have been found to be ef- tonias associated with long-term neuroleptic exposure.
ficacious in the treatment of akathisia. These buccal, orofacial, truncal, or limb movements
Nonextrapyramidal side effects of the typical an- can be exacerbated by anxiety and disappear during
tipsychotic agents include those that are secondary to sleep. They can present with a range of severity, from
blockade of muscarinic, histaminic, and alpha-adrener- subtle tongue movements to truncal twisting and pel-
gic receptors. These side effects, which are more com- vic thrusting movements and even possible respiratory
monly seen with the low-potency neuroleptics, include dyskinesias. The prevalence rates for this syndrome
sedation, tachycardia, and anticholinergic side effects range from less than 10% to more than 50% but it is
such as urinary hesitancy or retention, blurred vision, generally accepted that the risk increases 3% to 5% per
or constipation. Other nonextrapyramidal side effects year for each year the individual is treated with typi-
include some cardiac conduction disturbances, retinal cal neuroleptics. Older age is a considerable risk factor
changes, sexual dysfunction, weight gain, lowered sei- for tardive dyskinesia, and there is some evidence that
zure threshold, and a risk of agranulocytosis. women are at increased risk for the development of this
Neuroleptic Malignant Syndrome (NMS) is a rela- condition. Of note, a withdrawal dyskinesia that resem-
tively rare but serious phenomenon seen in approxi- bles tardive dyskinesia may appear on cessation of the
mately 1% of individuals taking neuroleptics. It can be neuroleptic. The specific mechanism involved in tar-
fatal in 15% of cases if not properly recognized and dive dyskinesia remains unclear, although supersensi-
treated. Because the symptoms of NMS may reflect tivity of dopaminergic receptors has been implicated.
multiple etiologies, making diagnosis difficult, clini- All individuals receiving traditional neuroleptic
cal guidelines have been proposed. According to these treatment should be monitored regularly for any signs
guidelines, three or two major and four minor mani- of a movement disorder. If tardive dyskinesia is sus-
festations are indicative of a high probability of NMS. pected, the benefits of antipsychotic treatment must
Major manifestations of NMS comprise fever, rigid- be carefully weighed against the risk of tardive dys-
ity, and increased creatine kinase levels, and minor kinesia. This should be discussed with the individual,
manifestations include tachycardia, abnormal blood and the antipsychotic should be removed if clinically
pressure, tachypnea, altered consciousness, diaphore- feasible or at least maintained at the lowest possible
sis, and leukocytosis. Others do not subscribe to the dose that provides antipsychotic effect. This would also
major–minor manifestation distinctions. In general, be an indication to switch to the novel antipsychotic
NMS is considered to be a constellation of symptoms agents with significantly reduced risk of TD or in the
that usually develops during 1 to 3 days. Although its case of clozapine no risk of TD. In many instances,
pathogenesis is poorly understood, it has been associ- clozapine (and possibly quetiapine or olanzapine) may
ated with all antidopaminergic neuroleptic agents and be the best treatment that can be offered for the TD it-
presents at any time during treatment. It must be dis- self. Unfortunately, there is no specific treatment of tar-
tinguished from other clinical entities, including lethal dive dyskinesia, although some investigators have pro-
catatonia and malignant hyperthermia. posed the use of adrenergic agents such as clonidine,
The mainstay of treatment is cessation of neuroleptic calcium channel blockers, vitamin E, benzodiazepines,
treatment and supportive care, including intravenous valproic acid, or reserpine to reduce the spontaneous
hydration, reversal of fever with antipyretics and cool- movements.
ing blankets, and careful monitoring of vital signs be- Sudden death in individual treated with typical an-
cause of the risk of cardiac and respiratory disturbance. tipsychotic drugs has been reported for a long time.
Sudden cardiac deaths probably occur from prolonga- was among the agents with the lowest weight gain at
tion of the ventricular action potential duration repre- an average of 1 lb over the same period. Risperidone
sented as the QT interval (or QTc when corrected for and quetiapine are intermediate with approximately 5
heart rate) on the electrocardiogram, resulting in a pol- lb. Individuals with schizophrenia, independent of the
ymorphic ventricular tachycardia termed torsades des use of antipsychotic agents, are at higher risk of devel-
pointes that can degenerate into ventricular fibrillation. oping diabetes mellitus relative to the general popula-
The incidence of torsades des pointes is unknown and tion. The data from Patient Outcome Research Team
the specific duration of the QTc interval at which the (PORT) suggest that the rate of diabetes mellitus and
risk of an adverse cardiac event is greatest has not been obesity among individuals with major mental illness
established. QTc prolongation alone does not appear to was substantially higher even before the advent of the
explain torsades des pointes; several other risk factors novel antipsychotic drugs. This was more so in women
must be present simultaneously with QT prolongation and nonwhite populations. The risk of antipsychotic-
before torsades des pointes occurs. These risk factors induced weight gain and secondary diabetes with
may include hypokalemia, hypomagnesemia, hypocal- clozapine and olanzapine may result from changes in
cemia, bradycardia, preexisting cardiac diseases (life- glucose metabolism and insulin resistance induced by
threatening arrhythmias, cardiac hypertrophy, heart these agents. In approximately 40% of the cases of hy-
failure, and congenital QT syndrome), female gender, perglycemia, insulin resistance appears to occur even
advancing age, baseline QTc interval of more than in the absence of significant weight gain, raising some
460 m/s and a long list of medications. In some in- interesting questions about how these medications may
stances, torsades des pointes may be associated with interact with the insulin-glycemic control. Unfortu-
an increase in drug plasma concentrations (e.g., com- nately, in the case of clozapine, the risk of developing
bination with drugs that inhibit the cytochrome P450 abnormal glucose tolerance and diabetes mellitus ap-
systems). Thus, the increase in polypharmacy in psy- pears to be cumulative over the years. There are no ef-
chiatry is especially of concern. The frequency of ECG fective countermeasures available to help with weight
abnormalities in individuals treated with antipsychotic gain and hyperglycemia. The substantial increased risk
drugs is unclear. QTc prolongation has been reported to the health of individuals with schizophrenia due to
with virtually all antipsychotic drugs. QTc prolonga- these effects is worrisome and an important shortcom-
tion by more than 2 standard deviations was reported ing of these efficacious and important medications.
in 8% of individuals treated with antipsychotics and es- Among the novel agents, risperidone, due to its po-
pecially in those receiving thioridazine. Of the typical tent dopamine D2 blockade, removes the inhibitory
antipsychotic drugs, haloperidol, chlorpromazine, trif- dopaminergic tone in the tuberoinfundibular neurons
luoperazine, mesoridazine, prochlorperazine, droperi- resulting in significant increase in prolactin levels. This
dol, and fluphenazine have all been reported to cause increase in prolactin is significantly more than usually
QTc prolongation and torsades des pointes, but thiori- seen with the typical antipsychotic agents. It is likely
dazine may be the worst offender. Pimozide, another that the serotonin system is also involved along with
typical antipsychotic, has also been associated with dopamine in raising the prolactin levels. Clozapine and
QTc prolongation, torsades des pointes, and deaths. quetiapine, on the other hand, are less potent at the D2
A reevaluation by the FDA of the cardiac safety pa- receptors and thus are unlikely to cause prolactin eleva-
rameters of thioridazine, mesoridazine, and droperidol tions. In some individuals, these elevations of prolactin
resulted in a black box warning due to significant QTc lead to amenorrhea, galactorrhea, gynecomastia, and
prolongation. Thus, it is important to monitor QTc in- may possibly decrease bone mineral density. Ziprasi-
terval in the high-risk population to prevent this rare done and olanzapine within the therapeutic dose range
but potentially fatal side effect. do not cause significant increases in prolactin levels.
Cases of sudden death while receiving clozapine
Side Effects of Atypical Antipsychotic Agents. One therapy (in physically healthy young adults with schiz-
of the most significant advantages of the newer antip- ophrenia) from myocarditis and cardiomyopathy led to
sychotic agent is the relatively less risk of developing a black box warning from FDA.
EPS and TD. However, treatment-emergent substantial
weight gain is a harbinger for long-term health conse- Treatment Resistance and Negative Symptoms. The
quences and frequently an important reason for noncom- concept of treatment resistance has entered into com-
pliance with medication. According to a meta-analysis, mon clinical judgment with the burgeoning interest in
clozapine and olanzapine are associated with a weight atypical antipsychotics, particularly clozapine. Treat-
gain of about 10 lb over 10 weeks, and ziprasidone ment resistance was originally defined for research
purposes. Individuals who had failed to respond to of these compounds on primary negative symptoms is
or could not tolerate adequate trials of standard neu- not clear.
roleptics from three different biochemical classes and
who had a clinically significant psychopathology rat- Augmentation of Typical Neuroleptics. When an
ing based on the Brief Psychiatric Rating Scale quali- individual has shown an inadequate response to tra-
fied as treatment resistant. However, this research ditional neuroleptic agents from different classes and
definition did not necessarily encompass individuals there is a good reason for not switching to a novel an-
who, by clinical standards, would meet the definition tipsychotic drug, other strategies may be necessary to
of treatment resistance (e.g., backward schizophrenic ameliorate residual symptoms. Adding a different type
individuals, who are severely symptomatic or with se- of psychotropic medication may augment the neurolep-
vere tardive dyskinesia or EPS). One might also think tic response in some individuals. Several neuroleptic
of clinical treatment resistance as seen in individuals augmentation strategies have been studied, including
who had an early age of illness onset with subsequent the addition of beta-blockers, thyrotropin-releasing hor-
repeated hospitalizations and neuroleptic trials and mone, clonidine, and valproic acid, with mixed results.
who cannot achieve a level of social and occupational Carbamazepine was initially shown to be effective
function commensurate with their age and level of when added to neuroleptic treatment for schizophrenic
education. individuals with electroencephalographic abnormali-
The concept of treatment resistance has undergone ties and violent outbursts. Later investigation showed
significant modification in recent years. The original that carbamazepine provided adjunctive amelioration
concept of treatment refractory applied to the use of of psychotic and affective symptoms when combined
typical antipsychotic agents. With the advent of the with neuroleptics. Another study reported a significant
novel agents, which are generally more effective than antipsychotic effect of the addition of carbamazepine
the traditional ones, the individual should fail at least to neuroleptics in only one of six treatment-resistant
one novel antipsychotic agent before initiating a trial of individuals. However, the group as a whole improved
clozapine mainly to avoid its side effects. The definition significantly in terms of anxiety, withdrawal, and
of the duration of a drug trial has also evolved over the depression.
years. It is increasingly appreciated that a 4- to 6-week Lithium has been evaluated extensively for its ef-
duration of treatment with an antipsychotic agent at ficacy as an additional treatment of schizophrenia. In
therapeutic doses can be considered an adequate trial. one study, lithium seemed to improve psychotic symp-
The recommended dosing has also undergone changes. toms of individuals who had not adequately responded
The original recommendation considered a trial of to neuroleptics alone. Although lithium does not seem
1000 mg equivalent of chlorpromazine as a necessary to affect positive or negative symptoms specifically, it
minimum requirement, but this threshold has now been may be beneficial for individuals who present at the de-
reduced to 400–600 mg/day equivalent on the basis of pressed end of the spectrum.
the knowledge that these doses block enough dopamine The use of benzodiazepines as augmenting agents
D2 receptors with higher doses providing no additional in the treatment of schizophrenia has also been ex-
benefit. Thus, a 4- to 6-week trial of 400–600 mg of tensively studied. There may be some individuals who
chlorpromazine equivalent is accepted as an adequate show improvement in psychotic symptoms, and oth-
antipsychotic trial. ers who show improvement in negative symptoms. In-
In treatment-refractory individuals, typical an- terestingly, there has been a suggestion that the tria-
tipsychotic use results in less than 5% response rate. zolobenzodiazepines may be more effective than other
Clozapine is the only antipsychotic drug proven more types of benzodiazepines in augmenting the neurolep-
efficacious in rigorously defined treatment-refractory tic response.
groups. Antidepressant medications have also been consid-
Negative symptoms, such as apathy, amotivational ered in the treatment of depression associated with
syndrome, flattened affect, and alogia, are often the schizophrenia. Although there is some evidence that
most problematic for individuals with schizophrenia, typical neuroleptics themselves cause depression, there
accounting for much of the morbidity associated with undoubtedly are schizophrenic individuals who have
this illness. In addition, these symptoms are often the primary depressive symptoms. Negative symptoms
most difficult to treat and do not respond well to tradi- are often difficult to distinguish from depression (both
tional neuroleptics. The atypical antipsychotic agents have features of amotivation, apathy, and social with-
are more effective against the negative symptoms than drawal), but those that are secondary to depression
the typical agents. However, the magnitude of the effect may respond to the addition of an antidepressant to the
individual’s medication regimen. One study reported the individual’s strengths and improve his/her compe-
that fluoxetine as an adjuvant agent was effective in tencies. Ultimately, rehabilitation should focus on the
treating both positive and negative symptoms in indi- positive concept of restoring hope to those who have
viduals, although other reports of selective serotonin suffered major setbacks in functional capacity and their
reuptake inhibitors have been less encouraging. self-esteem due to major mental illness. To have this
The use of electroconvulsive therapy with concomi- hope grounded in reality, it requires promoting accept-
tant neuroleptic treatment has also been evaluated. With ance of one’s illness and the limitations that come with
electroconvulsive therapy as an adjuvant treatment, it it. While work offers the ultimate in sense of achieve-
appears that the individual may improve initially, but ment and mastery, it must be defined more broadly for
relapse is likely. However, individuals with comorbid the mentally ill and should include prevocational and
affective symptoms may have some increased benefit. nonvocational activities along with independent em-
In general, however, this option should be considered ployment. It is extremely important that work is indi-
only if the individual is not a candidate for a trial with vidualized to the talents, skills, and abilities of the indi-
an atypical antipsychotic agent and only if the individ- vidual concerned. However, psychosocial rehabilitation
ual has severe persistent symptoms. has to transcend work to encompass medical, social,
and recreational themes. Psychosocial treatment’s ba-
sic principle is to provide comprehensive care through
Nonpharmacological Treatment
active involvement of the individual in his or her own
of Schizophrenia
treatment. Thus, it is important that a holding environ-
Although psychopharmacological intervention has ment be created where individuals can safely express
proved to be the foundation on which the treatment of their wishes, aspirations, frustrations, and reservations
schizophrenia depends, other approaches to the man- such that they ultimately mold the rehabilitation plan.
agement of these individuals serve a critical function. Clearly, to achieve these goals, the intervention has to
Studies have shown repeatedly that symptoms of schiz- be ongoing.
ophrenia have not only a genetic component but also Given the chronicity of the illness, the process of
an environmental aspect, and interactions with family rehabilitation must be enduring to encounter future
and within the community can alter the course of the stresses and challenges. These goals cannot be achieved
illness. without a stable relationship between the individual
For many years, a dichotomous view of treatment and the rehabilitation counselor, which is central to an
options was tenaciously debated as dynamic psychiatry effective treatment and positive outcome. Thus, psy-
was challenged by developments in the neurosciences. chosocial rehabilitation is intimately connected to the
A more unified view is now accepted as it has become biological intervention and forms a core component of
clear that psychopharmacological treatment strategies the biopsychosocial approach to the treatment of schiz-
are most efficacious if combined with some type of ophrenia. In the real world, programs often deviate
psychosocial intervention and vice versa. It can be said from the aforementioned principles and end up putting
that because of the chronic nature of schizophrenia, excessive and unrealistic expectations on individuals,
one or more treatments may be required throughout the thus achieving exactly the opposite of the intended val-
illness and they are likely to have to be modified as ues of the program.
symptoms change over time.
Psychodynamic Approach. This psychotherapeutic
Psychosocial Rehabilitation. Psychosocial rehabili- technique held promise for many years as a potential
tation is a therapeutic approach that encourages an infor unraveling the mystery of individuals’ symptoms,
dividual with a severe mental disorder to develop his with the hope of improvement in course and symp-
or her fullest capacities through learning and environ- toms and even cure. On the basis of derivations of the
mental supports. The rehabilitation process should ap- classical analytical school, symptoms of schizophre-
preciate the unique life circumstances of each person nia were thought of in terms of conflict and defense
and respond to the individual’s special needs while mechanisms. For example, when paranoid individuals
promoting both the treatment of the illness and the believe that they are being preyed on, they are project-
reduction of its attendant disabilities. The treatment ing onto others their own internal, unconscious wish to
should be provided in the context of the individual’s kill. Thus, unconscious conflicts became manifest as
unique environment, taking into account social sup- psychotic symptoms. To the psychodynamic therapist
port network, access to transportation, housing, work then, affectively laden material elicits an increase in
opportunities, and so on. Rehabilitation should exploit thought disorder or psychotic responses, as it touches
on the individual’s unconscious feelings. These con- Schizophrenia often strikes just as a person is leav-
ceptualizations of schizophrenia influenced early work ing adolescence and entering young adulthood. The
with these individuals. higher the premorbid level of social adjustment and
Although the psychodynamic understanding of in- functioning, the more devastating and confusing the
trapsychic events has been of historical interest, the onset of symptoms becomes. Young males with a high
application of traditional psychodynamic principles level of premorbid function are at increased risk of sui-
as primary treatment modalities is not recommended. cide, presumably in part because of the tremendous loss
One of the first studies that compared outcomes be- they face. These feelings can continue for years, with
tween medication-treated individuals and psychother- schizophrenic individuals feeling isolated and robbed
apy-treated individuals was conducted at the Camarillo of a normal life. Therefore, a component of individual
State Hospital in 1968. This study found that the group work (which can also be achieved to some degree in a
of individuals who received neuroleptic medication group setting) with these individuals is a focus on the
showed greater improvement than those who received impact schizophrenia has had on their lives. Helping
psychotherapy alone. Subsequent studies have repli- individuals to grieve for these losses is an important
cated these findings even when different types of ther- process that may ultimately help them achieve a better
apy are examined. Evidence suggests that insight-ori- quality of life.
ented individual psychotherapy may not be as helpful
for individuals with schizophrenia as supportive, goal- Group Psychotherapy. Acutely psychotic individuals
directed individual therapy combined with medication do not benefit from group interaction. In fact, a quiet
treatment and social skills training. place with decreased social contact is most useful until
medications have controlled acute symptoms. It is com-
Individual Psychotherapy. Individual therapy in a mon in inpatient settings to slowly integrate individu-
nontraditional sense can begin on meeting the indi- als into the ward community only as they appear less
vidual with schizophrenia. Even the briefest of nor- agitated and are able to remain in good behavioral con-
malizing contacts with an agitated, acutely psychotic trol with improvement in psychotic symptoms. As their
individual can have therapeutic value. Psychodynamic condition improves, inpatient group therapy prepares
interpretations are not helpful during the acute stages individuals for interpersonal interactions in a control-
of the illness and may actually agitate the individual led setting. After discharge, individuals may benefit
further. The clinician using individual psychotherapy from day treatment programs and outpatient groups,
should focus on forming and maintaining a therapeutic which provide ongoing care for individuals with schiz-
alliance (which is also a necessary part of psychophar- ophrenia living in the community.
macological treatment) and providing a safe environ- Because one of the most difficult challenges of schiz-
ment in which the individual is able to discuss symp- ophrenia is the inherent deficits in relatedness, group
toms openly. A sound psychotherapist provides clear therapy is an important means of gathering individuals
structure about the therapeutic relationship and helps with schizophrenia together and providing them with a
the individual to focus on personal goals. forum for mutual support. Insight-oriented groups may
Often, an individual is not aware of or does not have be disorganizing for individuals with schizophrenia,
insight into the fact that some beliefs are part of a spe- but task-oriented, supportive groups provide structure
cific symptom. A psychotherapist helps an individual and a decreased sense of isolation for this population
to check whether his or her reality coincides with that of individuals. Keeping group focus on structured top-
of the therapist. The therapeutic intervention then be- ics, such as daily needs or getting the most out of com-
comes a frank discussion of what schizophrenia is and munity services, is useful for these individuals. In the
how symptoms may feel to the individual. This objec- era of community treatment and brief hospitalizations,
tifying of psychotic or negative symptoms can prove of many individuals are being seen in medication groups,
enormous value in allowing the individual to feel more which they attend regularly to discuss any side effects
in control of the illness. A good analogy is to diabetic or problems and to get prescriptions.
individuals, who know they have a medical illness and
are educated about the symptoms associated with ex- Psychoeducational Treatment. One of the inherent
acerbation. Just as these individuals can check blood deficits from which schizophrenic individuals suffer
glucose levels, schizophrenic individuals can discuss is an inability to engage appropriately in social or oc-
with a therapist their sleep patterns, their interpersonal cupational activities. This debilitating effect is often
relationships, and their internal thoughts, which may a lasting feature of the illness, despite adequate psy-
lead to earlier detection of relapses. chopharmacological intervention. This disability often
isolates individuals and makes it difficult for them to Additionally, impaired information processing can
advocate appropriate social support or community lead to increased susceptibility to stress and thus to an
services. Furthermore, studies have found that there is increased risk of relapse. Practice appears to improve
a correlation between poor social functioning and inci- some of the cognitive dysfunction. Remediation of cog-
dence of relapse. One of the challenges of this area of nitive dysfunctions with social skills training has been
study is the great deal of variability in each individual. reported to have positive impact. Social skills train-
However, standardized measures have been developed ing programs, cognitive training programs to improve
to ascertain objective ratings of social deficits. These neurocognitive functioning, and cognitive–behavioral
assessments have become important tools in the deter- therapy approaches are oriented toward coping with
mination of effective nonpharmacological treatment symptoms, the disorder, and everyday problems.
strategies. Cognitive adaptation training (CAT) is a novel ap-
The literature suggests that schizophrenic individu- proach to improve adaptive functioning and compen-
als can benefit from social skills training. This model is sate for the cognitive impairments associated with
based on the idea that the course of schizophrenia is, in schizophrenia. A thorough functional needs assessment
part, a product of the environment, which is inherently is done to measure current adaptive functioning. Be-
stressful because of the social deficits from which these sides measuring adaptive functioning and quantifying
individuals suffer. The hypothesis is that if individuals apathy and disinhibition, a neurocognitive assessment
are able to monitor and reduce their stress, they could using tests to measure executive function, attention,
potentially decrease their risk of relapse. verbal and visual memory, and visual organization is
For this intervention to be successful, individuals also completed. Treatment plans are adapted to the in-
must be aware of and set their own goals. Goals such dividual’s level of functioning, which includes the indi-
as medication management, activities of daily living, vidual’s level of apathy. Interventions include removal
and dealing with a roommate are achievable examples. of distracting stimuli, and use of reminders such as
Social skills and deficits can be assessed by individu- checklists, signs, and labels.
als’ self-report, observation of behavioral patterns by
trained professionals, or a measurement of physiologi- Family Therapy. A large body of the literature ex-
cal responses to specific situations (e.g., increased pulse plores the role of familial interactions and the clinical
when asking someone to dinner). Individuals can then course of schizophrenia. Many of these studies have
begin behavioral training in which appropriate social examined the outcome of schizophrenia in relation to
responses are shaped with the help of instructors. the degree of expressed emotion (EE) in family mem-
In a large number of individuals, deficits in social bers. EE is generally defined as excessive criticism
competence persist despite antipsychotic treatment. and overinvolvement of relatives. Schizophrenic indi-
These deficits can lead to social distress, whereas so- viduals have been found to have a higher risk of re-
cial competence can alleviate distress related to social lapse if their relatives have high EE levels. Clearly, an
discomfort. The “token economy’’ programs with op- individual’s disturbing symptoms at the time of relapse
erant conditioning paradigms were used in the past to may affect the level of criticism and overinvolvement of
discourage undesirable behavior. However, nowadays family members, but evidence suggests that preexisting
there are better ways to deal with these behaviors. increased EE levels in relatives predict increased risk
Paradigms using instruction, modeling, role-playing, of schizophrenic relapse and that interventions that de-
and positive reinforcement are helpful. Controlled crease EE levels can decrease relapse rates.
studies suggest that individuals with schizophrenia are Specifically, studies have demonstrated that effec-
able to acquire lasting social skills after attending such tive strategies lower the risk of relapse with the use of
programs and apply these skills to everyday life. Be- family intervention and measurements of EE levels.
sides reducing anxiety, social skills training also im- For example, in a study conducted in the early 1980s,
prove the level of social activity and foster new social 37 individuals were randomly assigned to one of two
contacts. This in turn improves the quality of life and treatment groups. One group received family therapy,
significantly shortens the duration of inpatient care. the other received individual therapy. In both groups,
However, their impact on symptom resolution and re- the individuals were maintained with appropriate neu-
lapse rates is unclear. roleptic doses. Family therapy was done in the home,
Individuals with schizophrenia generally demon- with a focus on education about schizophrenia and
strate poor performance in various aspects of infor- ways in which families could achieve lowered stress
mation processing. Cognitive dysfunction can be a levels and improved problem-solving skills. Specific
rate-limiting factor in learning and social functioning. problem-solving mechanisms were rehearsed and
modeled by trained therapists. The individual treatment the office; the caseloads are shared across clinicians
was supportive psychotherapy, which was conducted rather than individual caseloads. These are time un-
at the clinic. At the end of 9 months, family therapy limited services provided directly by the ACT team
was found to be a more effective means of preventing and not brokered out, and 24-hour coverage is pro-
relapse (1 relapsed out of 18) than individual therapy vided. Research on the ACT model confi rms that it is
(8 relapsed out of 19). Moreover, the advantages of the successful in making individuals comply with treat-
family therapy persisted after a second year of less in- ment and leads to fewer inpatient admissions. ACT
tensive follow-up also improves housing conditions (fewer homeless
A review of family interventions in 25 randomized individuals, more individuals in stable housing), em-
studies involving 1744 individuals showed that the ef- ployment, quality of life, and patient satisfaction. No
ficacy of family intervention on relapse rate is fairly clear differences between ACT and standard or in-
well supported. This efficacy was particularly evident tensive clinical case management are reported with
when contrasted with low quality or uncontrolled mental condition, social functioning, self-esteem, or
individual treatments. The addition of family inter- number of deaths.
vention to standard treatment of schizophrenia has
a positive impact on outcome to a moderate extent.
Combining Pharmacological
Family intervention effectively reduces the short-
and Psychosocial Treatments
term risk of clinical relapse after remission from an
acute episode. The elements common to most effec- The combination of pharmacological and psychosocial
tive interventions are inclusion of the individual in at interventions in schizophrenia can have complex inter-
least some phases of the treatment, long duration, and actions. For example, psychotherapies improve medica-
information and education about the illness provided tion compliance on the one hand and are more effective
within a supportive framework. There is sufficient in the presence of antipsychotic treatment on the other.
data only for males with chronic schizophrenia living Family psychoeducation has been reported to decrease
with high EE parents. Evidence is limited for recent the level of EE in the family, resulting in better social
onset individuals, women, people in different fam- adjustment and a need for lower doses of antipsychotic
ily arrangements and families with low EE. Research medications. The qualitative differences in the interac-
in family intervention is still a growing field. Thus, tions between the newer antipsychotic agents and psy-
at present it is unclear if the effect seen with family chotherapy suggest a hopeful trend of better utilization
therapy is due to family treatment or more intensive of psychosocial treatments.
care.
On the basis of these findings, it is clear that there is
Self-Directed Treatment
a significant interaction between the level of emotional
involvement and criticism of relatives of probands with Groups such as the National Alliance for Mentally Ill
schizophrenia and the outcome of their illness. Iden- (NAMI) and the Manic–Depressive Association offer
tifying the causative factors in familial stressors and tremendous resources to individuals with psychiatric
educating involved family members about schizophre- problems and their relatives. They provide newsletters,
nia lead to long-term benefits for individuals. Future neighborhood meetings, and support groups to inter-
work in this field must examine these interactions with ested persons. These nonprofessional self-help meas-
an understanding of modern sociological and biologi- ures may feel less threatening to individuals and their
cal advances in genetics, looking at trait carriers, social families and provide an important adjunct to profes-
skills assessments, positive and negative symptoms, sional settings.
and medication management with the novel antipsy- Structured self-help clubs have also been effective
chotic agents. means of bolstering individuals’ social, occupational,
and living skills. The Fountain House was the first such
Case Management. Assertive Community Treatment club aimed at social rehabilitation. Individuals who are
(ACT) is a community care model with a caseload per involved are called members of the club, giving them a
worker of 15 individuals or fewer in contrast to stand- sense of belonging to a group. They are always made to
ard case management (SCM) with a caseload of 30 feel welcome, useful, and productive members of the
to 35 individuals. Intensive clinical case management club community.
(ICCM) differs from ACT by the case manager not The clubhouse model has expanded to provide serv-
sharing the caseload. In the ACT model, most services such as transitional employment programs, apart-
ices are provided in the community rather than in ment programs, outreach programs, and medication
management and consultation services, to name a few.

A self-supportive rehabilitation program for mentally DSM-IV-TR Diagnostic Criteria
ill individuals is an important option for many schizo- 295.70 SCHIZOAFFECTIVE DISORDER
phrenic individuals who might otherwise feel isolated
and out of reach. A. An uninterrupted period of illness during which, at
some time, there is either a major depressive episode,
a manic episode, or a mixed episode concurrent with
symptoms that meet criterion A for schizophrenia.
Schizoaffective Disorder
Note: The major depressive episode must include crite-
rion A1: depressed mood.
Kraepelin’s landmark classification at the dawn of the B. During the same period of illness, there have been
twentieth century could not accurately classify those delusions or hallucinations for at least 2 weeks in the
individuals who manifested both psychotic (schizo- absence of prominent mood symptoms.
C. Symptoms that meet criteria for a mood episode are
phrenia-like) and affective symptoms and had a better present for a substantial portion of the total duration of
course of illness then schizophrenia. It was Kasanin the active and residual periods of the illness.
in 1933, who coined the term schizoaffective disorder D. The disturbance is not due to the direct physiological
effects of a substance (e.g., a drug of abuse, a medica-
to describe some of these individuals. However, over tion) or a general medical condition.
the decades, these individuals were often classified as Specify type:
having atypical schizophrenia, good prognosis schizo-
Bipolar type: if the disturbance includes a manic or a
phrenia, remitting schizophrenia, or cycloid psychosis. mixed episode (or a manic or a mixed episode and major
Inherent within these diagnoses was the implication depressive episodes)
that they shared similarities to schizophrenia and also Depressive type: if the disturbance only includes major
appeared to have a relatively better course of illness. depressive episodes
With the advent of effective treatment of bipolar dis- Reprinted with permission from the Diagnostic and Statistical
order with lithium salts, some of these individuals American Psychiatric Association.
started responding to lithium, and the term schizoaf-
fective disorder gained further momentum and evolved
in the direction of bipolar disorder. Unfortunately, this to meet the criterion A for schizophrenia and thus, the
lack of diagnostic clarity has plagued the diagnosis of minimum duration of a schizoaffective episode is also
schizoaffective disorder such that there is much that is 1 month.
unknown about the illness. The criterion for major depressive episode requires
a minimum duration of 2 weeks of either depressed
mood or markedly diminished interest or pleasure. As
DIAGNOSIS
the symptoms of loss of pleasure or interest commonly
Schizoaffective disorder criteria have evolved over occur in nonaffective psychotic disorders, to meet the
the years and undergone major changes. According criterion A for schizoaffective disorder the major de-
to the DSM-IV-TR, an individual with schizoaffective pressive episode must include pervasive depressed
disorder must have an uninterrupted period of illness mood. Presence of markedly diminished interest or
during which, at some time, they meet the diagnostic pleasure is not sufficient to make a diagnosis as it is
criteria for a major depressive episode, manic episode, possible that these symptoms may occur with other
or a mixed episode concurrently with the diagnostic conditions too.
criteria for the active phase of schizophrenia (criterion The clinical signs and symptoms of schizoaffective
A for schizophrenia). Additionally, “the individual disorder include all the signs and symptoms of schizo-
must have had delusions or hallucinations for at least phrenia, and a manic episode and/or a major depres-
2 weeks in the absence of prominent mood disorder sive episode. The schizophrenia and mood symptoms
symptoms’’ during the same period of illness. The may occur together or in an alternate sequence. The
mood disorder symptoms must be present for a subclinical course can vary from one of exacerbations and
stantial part of the active and residual psychotic pe- remissions to that of a long-term deterioration. Pres-
riod. The essential features of schizoaffective disorder ence of mood-incongruent psychotic features—where
must occur within a single uninterrupted period of ill- the psychotic content of hallucinations or delusions is
ness where the “period of illness’’ refers to the period not consistent with the prevailing mood—more likely
of active or residual symptoms of psychotic illness, indicates a poor prognosis.
and this can last for years and decades. The total dura- The DSM-IV-TR diagnosis of schizoaffective disor-
tion of psychotic symptoms must be at least 1 month der can be further classified as schizoaffective disorder
bipolar type or schizoaffective disorder depressive course similar to schizophrenia on outcome measures
type. For a person to be classified as having the bipo- such as occupational and social functioning after the
lar subtype, he/she must have a disorder that includes index episode. Regardless of the subtype, the following
a manic or mixed episode with or without a history variables are harbingers of a poor prognosis:
of major depressive episodes. Otherwise, the person
(a) a poor premorbid history
is classified as having depressive subtype having had
(b) an insidious onset
symptoms that meet the criterion for a major depres-
(c) absence of precipitating factors
sive episode with no history of having had mania or
(d) a predominance of psychotic symptoms, especially
mixed state.
deficit or negative ones
As discussed earlier, the diagnosis of schizoaffective
(e) an early age of onset
disorder has undergone numerous changes through the
(f) an unremitting course, and
decades, making it difficult to get reliable epidemiol-
(g) a family history of schizophrenia.
ogy information. When data was pooled together from
various clinical studies, approximately 2–29% of those The corollary would be that the opposite of each of
individuals diagnosed as having mental illness at the these characteristics would suggest a better prognosis.
time of the study were suffering from schizoaffective Interestingly, the presence or the absence of Schneide-
disorder, with women having a higher prevalence. This rian first-rank symptoms does not seem to predict the
could possibly be explained by a higher rate of depres- course of illness. The incidence of suicide in individu-
sion in women. Relatives of women suffering from als with schizoaffective disorder is at least 10%. Some
schizoaffective disorder have a higher rate of schizo- data indicate that the suicidal behavior may be more
phrenia and depressive disorders compared to relatives common in women then men.
of male schizoaffective subjects. The estimated life-
time prevalence of schizoaffective disorder is possibly
in the range of 0.5–0.8%. In the inpatient settings of
New York State psychiatric hospitals, approximately The possible differential diagnosis consists of bipo-
19% of 6000 individuals had a diagnosis of schizoaf- lar disorder with psychotic features, major depressive
fective disorder. disorder with psychotic features, and schizophrenia.
The depressive type of schizoaffective disorder ap- Clearly, substance-induced states and symptoms caused
pears to be more common in older people while the bi- by coexisting medical conditions should be carefully
polar type probably occurs more commonly in younger ruled out. All conditions listed in the differential di-
adults. The higher prevalence of the disorder in women agnosis of schizophrenia, bipolar disorder, and major
appears to occur particularly among those who are mar- depressive disorder should be considered including but
ried. As in schizophrenia, the age of onset for women is not limited to those individuals undergoing treatment
later than that for men. Depression tends to occur more with steroids, those abusing substances such as PCP,
commonly in women. and medical conditions such as temporal lobe epilepsy.
In circumstances where there is ambiguity, it may be
prudent to delay making a final diagnosis until the most
Course
acute symptoms of psychosis have subsided and time is
Owing to the evolving nature of the diagnosis and lim- allowed to establish a course of illness and collect col-
ited studies done thus far, much remains unknown. lateral information.
However, to the extent that this illness has symptoms
from both a major mood disorder and schizophrenia,
TREATMENT
theoretically one can confer a relatively better progno-
sis than schizophrenia and a relatively poorer prognosis With the shifting definitions of schizoaffective disor-
than bipolar disorder. In one study in which individu- der, evaluating the treatment of schizoaffective dis-
als with DSM-III and DSM-IV schizoaffective disor- order is not easy. Mood stabilizers, antidepressants,
der were followed for 8 years, the outcome of these and antipsychotic medications clearly have a role in
individuals more closely resembled schizophrenia than the management of these individuals. The presenting
mood disorder with psychosis. Some data indicate that symptoms, their duration and intensity, and the choices
individuals with a diagnosis of schizoaffective disor- of the individual need to be incorporated into deciding
der bipolar type have a 2- to 5-year course similar to what treatment(s) to choose.
that of bipolar disorder, while individuals diagnosed as Atypical antipsychotic medications are reported to
having schizoaffective disorder depressive type have a be more effective than the typical ones in the treatment
of schizoaffective disorder. They appear to have a more Depending on the level of recovery, some of the
broad-spectrum effect than the typical agents. Optimiz- individuals may need rehabilitation services to assist
ing antipsychotic treatment, especially with the novel them with either developing skills for some form of
agents, is more likely to be effective than the routine employment or assistance to maintain a job. Family
use of adjunctive antidepressants or mood stabilizers. members benefit from support groups such as NAMI
However, when indicated, the use of antidepressants or MDA groups.
is well supported in schizoaffective individuals who
present with a full depressive syndrome after stabiliza-
Brief Psychotic Disorder
tion of psychosis.
Two small open label studies suggest that valproic
DIAGNOSIS
acid is effective in treating the manic symptoms asso-
ciated with schizoaffective disorder bipolar type, with Brief psychotic disorder is defined by DSM-IV-TR as a
65.2% reduction in manic episodes in 5 individuals af- psychotic disorder that lasts more than 1 day and less
ter 29 to 51 months. than a month. Moreover, the disorder may develop in
Three double-blind, parallel-group studies exam- response to severe psychosocial stressors or group of
ined the efficacy of lithium carbonate in schizoaffec- stressors.
tive mania. One study found that chlorpromazine alone European and Scandinavian countries have tradition-
was as effective as the combination of chlorpromazine ally diagnosed this type of psychosis as psychogenic
and lithium. Another study with a small sample found psychosis, reactive psychosis, or brief reactive psycho-
that the combination of lithium and haloperidol was sis. Some have also referred to this condition as hys-
more effective than haloperidol itself in individuals
with predominantly affective symptoms compared
to those with predominantly psychotic symptoms.
Reports of carbamazepine use is sparse and difficult
to draw conclusions from. Lamotrigine was also re- 298.8 BRIEF PSYCHOTIC DISORDER
ported to be useful in three cases of schizoaffective
disorder. A. Presence of one (or more) of the following symptoms:
The novel antipsychotic agents are often effica- (1) delusions
(2) hallucinations
cious against depression in individuals who suffer (3) disorganized speech (e.g., frequent derailment or
from both depression and psychosis, negating the incoherence)
need for routine use of antidepressants. However, (4) grossly disorganized or catatonic behavior
there are individuals who remain depressed even Note: Do not include a symptom if it is a culturally sanc-
tioned response pattern.
with optimal antipsychotic and mood stabilizer
treatment. SSRIs are widely used in individuals who B. Duration of an episode of the disturbance is at least
1 day but less than 1 month, with eventual full return
present with schizoaffective disorder with depres- to premorbid level of functioning.
sion. If the SSRIs and newer antidepressants do not C. The disturbance is not better accounted for by a mood
show efficacy, tricyclic antidepressants do have a disorder with psychotic features, schizoaffective disor-
der, or schizophrenia and is not due to the direct phys-
role. Many studies suggest that addition of antide- iological effects of a substance (e.g., a drug of abuse, a
pressants helps in effective treatment of depression medication) or a general medical condition.
in schizoaffective disorder. Occasionally, antidepres- Specify if:
sants may worsen the course. For individuals suffer- With marked stressor(s) (brief reactive psychosis): if
ing from depression where they are not responding symptoms occur shortly after and apparently in response
to events that, singly or together, would be markedly
adequately and are at risk for suicide, ECT is an ef- stressful to almost anyone in similar circumstances in the
fective alternative. person’s culture
To the extent that schizoaffective disorder shares Without marked stressor(s): if psychotic symptoms do
symptoms with schizophrenia, most of the psychoso- not occur shortly after, or are not apparently in response
to events that, singly or together, would be markedly
cial treatments used in the treatment of schizophrenia stressful to almost anyone in similar circumstances in the
are likely to be useful in the treatment of schizoaf- person’s culture
fective disorder. Specifically, individuals benefit from With postpartum onset: if onset within 4 weeks
individual supportive therapy, family therapy, group postpartum
therapy, cognitive–behavioral therapy, and social Reprinted with permission from the Diagnostic and Statistical
skills training. Many individuals would be suitable Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
candidates for assertive community therapy (ACT).
terical psychosis. These terms are probably more com- psychotic disorder later display chronic mental disor-
monly used in Scandinavian countries due to Langfeldt der such as schizophrenia and bipolar disorder. Indi-
and Leonhard’s contributions to the classification of viduals with brief psychotic disorders generally have
psychosis that does not have a course like schizophre- good prognosis, and European studies indicate that
nia. In the United States, brief reactive psychosis was 50–80% of all individuals have no further major psy-
formally included as a diagnostic category in DSM-III. chiatric problems.
Subsequently, it has undergone a change in its name to The length of the acute and residual symptoms is of-
brief psychotic disorder. ten just a few days. Occasionally, depressive symptoms
The DSM-IV-TR diagnostic criteria specify the follow the resolution of the psychosis. Suicide is a con-
presence of at least one clear psychotic symptom last- cern during both the psychotic phase and the postpsy-
ing a minimum of 1 day to a maximum of 1 month. chotic depressive phase. Indicators of good prognosis
Furthermore, DSM-IV-TR allows the specification of are good premorbid adjustment, few premorbid schiz-
two additional features: the presence or the absence of oid traits, severe precipitating stressors, sudden onset of
one or more marked stressors and a postpartum onset. symptoms, confusion and perplexity during psychosis,
DSM-IV-TR describes a continuum of diagnosis for little affective blunting, short duration of symptoms,
psychotic disorder based primarily on the duration of and absence of family history of schizophrenia.
the symptoms. Once the duration criteria are met, other
conditions such as etiological medical illnesses and
substance-induced psychosis need to be excluded. In
those cases where the duration of psychosis lasts more Although the classical presentation may be short in
than 1 month, appropriate diagnoses to be considered duration and associated with stressors, a thorough and
are other psychotic conditions based on reevaluation of careful evaluation is necessary. Additional information
the clinical features, duration of psychosis, and pres- is critical to rule out other major psychotic conditions
ence of mood symptoms. as temporal association of stressors to the acute mani-
People suffering from this disorder usually present festation of symptoms may be coincidental and thus
with an acute onset, manifest at least one major symp- misleading. Other conditions to be ruled out include
tom of psychosis, and do not always include the entire psychotic disorder due to a general medical condition,
symptom constellation seen in schizophrenia. Affec- substance-induced psychosis, factitious disorder with
tive symptoms, confusion, and impaired attention may predominantly psychological signs and symptoms, and
be more common in brief psychotic disorders than in malingering. Individuals with epilepsy and delirium
chronic psychotic conditions. Some of the characteris- may also present with similar symptoms. Additional
tic symptoms include emotional lability, outlandish be- conditions to be considered are dissociative identity
havior, screaming or muteness, and impaired memory disorder and psychotic episodes associated with bor-
for recent events. Some of the symptoms suggest a di- derline and schizotypal personality disorder that may
agnosis of delirium and may warrant a more complete last for less than a day.
medical workup. The symptom patterns include acute
paranoid reactions, reactive confusions, excitations, and
TREATMENT
depressions. In French psychiatry, bouffée délirante is
similar to brief psychotic disorder. These individuals may require short-term hospitali-
The precipitating stressors most commonly encoun- zations for a comprehensive evaluation and safety.
tered are major life events that would cause any person Antipsychotic drugs are often most useful along with
significant emotional turmoil. Such events include the benzodiazepines. Long-term use of medication is often
death of a close family member or severe accidents. not necessary and should be avoided. If maintenance
Rarely, it could be accumulation of many smaller medications are necessary, the diagnosis may need to
stresses. be revised. Clearly, the newer antipsychotic agents have
a better neurological side effect profile and would be
preferred over the typical agents.
Course
Psychotherapy is necessary to help the person re-
As defined by DSM-IV-TR, the duration of the disorder integrate the experience of psychosis and possibly the
is less than 1 month. Nonetheless, the development of precipitating trauma. Individual, family, and group
such a significant mental disorder may indicate an indi- therapies may be necessary in some individuals. Many
vidual’s mental vulnerability. An unknown percentage individuals need help to cope with the loss of self-
of individuals who are first classified as having brief esteem and confidence.
Schizophreniform Disorder to resolve, or when the clinician cannot obtain a reli-

able history from an individual about the duration of
DIAGNOSIS the symptoms.
DSM-IV-TR has specifiers for the presence or ab-
Schizophreniform disorder shares a majority of the
sence of good prognostic features. These features in-
DSM-IV-TR diagnostic features with schizophrenia
clude a rapid onset (within 4 weeks) of prominent psy-
except the following two criteria: (1) the total dura-
chotic symptoms, presence of (psychogenic) confusion
tion of the illness which includes the prodrome, ac-
or perplexity at the height of the psychotic episode,
tive, and residual phases is at least 1 month but less
good premorbid adjustment as evidenced by social and
than 6 months in duration; and (2) though impair-
occupational functioning, and the absence of deficit
ment in social and occupational functioning may oc-
symptoms such as blunted or flat affect.
cur during the illness, it is not required or necessary.
Thus, the duration of more than 1 month eliminates
brief psychotic disorder as a possible diagnosis; if the Course
illness lasts or has lasted for more than 6 months, the
The course is, as anticipated, variable. The DSM-IV-
diagnosis has to be reevaluated for other possible con-
TR specifiers “with good prognostic features’’ and
ditions including schizophrenia. Therefore, the diag-
“without good prognostic features,’’ though helpful in
nosis of schizophreniform disorder is intermediate
guiding the clinician, require further validation. How-
between brief psychotic disorder and schizophrenia.
ever, confusion or perplexity at the height of the psy-
Hence, those individuals whose duration of episode
chotic episode is the feature best correlated with good
lasted more than a month and less than 6 months,
outcome. Also, the shorter the period of illness, the
and have recovered would be diagnosed as having
better the prognosis is likely to be. There is a signifi-
schizophreniform disorder. On the other hand, those
cant risk of suicide in these individuals. Postpsychotic
individuals who have not recovered from an episode,
depression is quite likely and should be addressed in
which is less than 6 months but more than one month
psychotherapy. Psychotherapy may help speed up the
in duration, and are likely to have schizophrenia
recovery and improve the prognosis. By definition,
would be diagnosed to have schizophreniform disor-
schizophreniform disorder resolves within 6 months
der until the 6 months criterion is met for schizophre-
with a return to baseline mental functioning.
nia. The diagnosis of ‘provisional’ schizophreniform
disorder is made while the clinician monitors the
evolving course of the illness, waits for the symptoms Differential Diagnosis
This is similar to schizophrenia. Psychotic disorder
caused by a general medical condition and substance-
induced psychotic disorder must be ruled out. General
295.40 SCHIZOPHRENIFORM DISORDER medical conditions to be considered are HIV infection,
temporal lobe epilepsy, CNS tumors, and cerebrovas-
A. Criteria A, D, and E of schizophrenia are met. cular disease, all of which can also be associated with
B. An episode of the disorder (including prodromal, ac-
tive, and residual phases) lasts at least 1 month but relatively short-lived psychotic episodes. The increas-
less than 6 months. (When the diagnosis must be made ing number of reports of psychosis associated with
without waiting for recovery, it should be qualified as
“provisional.”)
the use of anabolic steroids by young men who are at-
tempting to build up their muscles to perform better
Specify if:
in athletic activities require careful history. Factitious
Without good prognostic features
disorder with predominantly psychological signs and
With good prognostic features: as evidenced by two (or symptoms and malingering may need to be ruled out
more) of the following:
in some instances.
(1) onset of prominent psychotic symptoms within
4 weeks of the first noticeable change in usual behav-
ior or functioning
(2) confusion or perplexity at the height of the psychotic TREATMENT
episode
(3) good premorbid social and occupational functioning Hospitalization is often necessary and allows for effec-
(4) absence of blunted or flat affect tive assessment, treatment, and supervision of an in-
Reprinted with permission from the Diagnostic and Statistical dividual’s behavior. The psychotic symptoms, usually
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 treated with a 3- to 6-month course of antipsychotic
drugs, respond more rapidly than in individuals with
schizophrenia. One study found that 75% of the indi-

viduals with schizophreniform psychosis compared to DSM-IV-TR Diagnostic Criteria
20% of those with schizophrenia responded to antipsy- 297.10 DELUSIONAL DISORDER
chotic agents within 8 days. ECT may be indicated for
some individuals, especially those with marked cata- A. Nonbizarre delusions (i.e., involving situations that
occur in real life, such as being followed, poisoned,
tonic features or depression. If an individual has recur- infected, loved at a distance, or deceived by spouse
rent episodes, trials of lithium carbonate, valproic acid, or lover, or having a disease) of at least 1 month’s
or carbamazepine may be warranted for prophylaxis. duration.
B. Criterion A for schizophrenia has never been met.
Psychotherapy is usually necessary to help individu-
als integrate the psychotic experience into their under- Note: Tactile and olfactory hallucinations may be present
in delusional disorder if they are related to the delusional
standing of their minds, brains, and lives. theme.
C. Apart from the impact of the delusion(s) or its ramifica-
tions, functioning is not markedly impaired and behav-
Delusional Disorder ior is not obviously odd or bizarre.
D. If mood episodes have occurred concurrently with de-
DIAGNOSIS lusions, their total duration has been brief relative to
the duration of the delusional periods.
Delusional disorder refers to a group of disorders, the E. The disturbance is not due to the direct physiological
chief feature of which is the presence of nonbizarre tion) or a general medical condition.
delusions. People suffering from this illness generally Specify type (the following types are assigned based on
do not regard themselves as mentally ill and actively the predominant delusional theme):
oppose psychiatric referral. Because they may expe- Erotomanic type: delusions that another person, usually
rience little impairment, they generally remain out- of higher status, is in love with the individual
side hospital settings, appearing reclusive, eccentric, Grandiose type: delusions of inflated worth, power,
or odd, rather than ill. They are more likely to have knowledge, identity, or special relationship to a deity or
famous person
contacts with professionals such as lawyers and other
Jealous type: delusions that the individual’s sexual part-
medical specialists for health concerns. The current ner is unfaithful
shift in diagnosis from paranoid to delusional helps Persecutory type: delusions that the person (or some-
avoid the ambiguity around the term “paranoid.’’ This one to whom the person is close) is being malevolently
also emphasizes that other delusions besides the para- treated in some way
noid ones are included in this diagnosis. It is important Somatic type: delusions that the person has some physi-
to understand the definition of nonbizarre delusion so cal defect or general medical condition
as to reach an unambiguous diagnosis. Nonbizarre de- Mixed type: delusions characteristic of more than one of
the above types but no one theme predominates
lusions typically involve situations or circumstances
that can occur in real life (e.g., being followed, in- Unspecified type
fected, or deceived by a lover) and are believable. Reprinted with permission from the Diagnostic and Statistical
According to DSM-IV-TR, the diagnosis of delu- American Psychiatric Association.
sional disorder can be made when a person exhibits
nonbizarre delusions of at least 1 month’s duration
that cannot be attributed to other mental disorders.
Subtypes
Nonbizarre delusions must be about phenomena that,
although not real, are within the realm of being pos- Persecutory Type. This is the most common form of
sible. In general, the individual’s delusions are well delusional disorder. Here, the person affected believes
systematized and have been logically developed. If that he or she is being followed, spied on, poisoned or
the person experiences auditory or visual halluci- drugged, harassed, or conspired against. The person af-
nations, they are not prominent except for tactile or fected may get preoccupied by small slights that can
olfactory hallucinations where they are tied in to the become incorporated into the delusional system. These
delusion (e.g., a person who believes that he emits a individuals may resort to legal actions to remedy per-
foul odor might experience an olfactory hallucination ceived injustice. Individuals suffering from these delu-
of that odor). The person’s behavioral and emotional sions often become resentful and angry with a potential
responses to the delusions appear to be appropriate. to get violent against those believed to be against them.
Usually, the person’s functioning and personality are
well preserved and show minimal deterioration if at Jealous Type. Individuals with this subtype have the
all. delusional belief that their spouses/lovers are unfaithful.
This is often wrongly inferred from small bits of be- do sometimes to pimozide, a typical antipsychotic med-
nign evidence, which is used to justify the delusion. ication, and also to SSRIs. Usually prognosis is poor
Delusions of infidelity have also been called conjugal without treatment. It affects both sexes equally. Suicide
paranoia. The term Othello syndrome has been used to apparently motivated by anguish is not uncommon.
describe morbid jealousy. This delusion usually affects
men with no history of prior psychiatric problems. The Grandiose Type. This is also referred to as megalo-
condition is difficult to treat and may diminish only mania. In this subtype, the central theme of the delu-
on separation, divorce, or death of the spouse. Marked sion is the grandiosity of having made some important
jealousy (pathological jealousy or morbid jealousy) is discovery or having great talent. Sometimes there may
a symptom of many disorders including schizophrenia be a religious theme to the delusional thinking such that
and is not unique to delusional disorder. Jealousy is a the person believes that he or she has a special message
powerful emotion and when it occurs in delusional dis- from God.
order or as part of another condition, it can be poten-
tially dangerous and has been associated with violence, Mixed Type. This subtype is reserved for those with
including suicidal and homicidal behavior. two or more delusional themes. However, it should be
used only where it is difficult to clearly discern one
Erotomanic Type. These individuals have delusions theme of delusion.
of secret lovers. Most frequently, the individual is a
woman, though men are also susceptible to these delu- Unspecified Type. This subtype is used for cases in
sions. The individual believes that a suitor, usually more which the predominant delusion cannot be subtyped
socially prominent than herself, is in love with her. This within the above-mentioned categories. A possible
can become the central focus of the individual’s exist- example is certain delusions of misidentification, for
ence and the onset can be sudden. Erotomania is also example, Capgras’s syndrome, named after the French
referred to as de Clerambault’s syndrome. Again, these psychiatrist who described the “illusions of doubles.’’
delusions can occur as part of other disorders too. Gen- The delusion here is the belief that a familiar person
erally women (but not exclusively so), unattractive in has been replaced by an imposter. A variant of this is
appearance, working at a lower-level jobs, who lead Fregoli’s syndrome where the delusion is that the per-
withdrawn, lonely single lives with few sexual contacts secutors or familiar persons can assume the guise of
are reported to be more prone to develop this condition. strangers and the very rare delusion that familiar per-
They select lovers who are substantially different from sons could change themselves into other persons at will
them. They exhibit what has been called paradoxical (intermetamorphosis). Each disorder is not only a rare
conduct, the delusional phenomenon of interpreting all delusion but is highly associated with other conditions
denials of love no matter how clear as secret affirma- such as schizophrenia and dementia.
tions of love. Separation from the love object may be the Though the existence of delusional disorder has been
only satisfactory means of intervention. When it affects known for a long time, relatively little is known about
men, it can manifest with more aggressive and possibly the demographics, incidence, and prevalence. People
violent pursuit of love. Thus, such people are often in suffering from this illness function reasonably well in
the forensic system. The object of aggression is often the community and lack insight, resulting in minimal or
companions or protectors of the love object who are no contact with the mental health system. However, the
viewed as trying to come between the lovers. However, crude incidence is roughly 0.7 to 3.0 per 100,000 with
resentment and rage in response to an absence of reac- a more frequent occurrence in females. Some have as-
tion from all forms of love communication may escalate sociated this condition with widowhood, celibacy, and
to a point that the love object may be in danger too. history of substance abuse. In one study, 1.2% of 4144
consecutively attending subjects in an outpatient clinic
Somatic Type. Delusional disorder with somatic de- were diagnosed to have delusional disorder. Half of the
lusions has been called monosymptomatic hypochon- subjects were diagnosed to have persecutory type of de-
driacal psychosis. This disorder differs from other con- lusional disorder. Females suffering from this disorder
ditions with hypochondriacal symptoms in degree of were significantly older than males.
reality impairment. The frequency of these conditions
is low, but cases may be underdiagnosed because indi-
Course
viduals present to dermatologists, plastic surgeons, and
infectious disease specialists more often than to mental Though the onset can occur in adolescence, generally
health professionals. Individuals with these conditions it begins from middle to late adulthood with variable
patterns of course, including lifelong disorder in some anxiety and dysphoria generated because of delusional
cases. Delusional disorder does not lead to severe thinking. Cognitive therapy, when accepted and im-
impairment or change in personality, but rather to a plemented, is helpful. Confrontation of the delusional
gradual, progressive involvement with the delusional thinking usually does not work and can further alienate
concern. Suicide has often been associated with this the individual.
disorder. The base rate of spontaneous recovery may
not be as low as previously thought, especially because
Shared Psychotic Disorder
only the more severely afflicted are referred for a treat-
ment. The more chronic forms of the illness tend to
DIAGNOSIS
have their onset early in the fifth decade. Onset is acute
in nearly two-thirds of the cases and gradual in the re- Shared psychotic disorder is a rare disorder, which is
mainder. In almost half of the cases, the delusion disap- also referred to as shared paranoid disorder, induced
pears at follow-up, improves in 10%, and is unchanged psychotic disorder, folie à deux, and double insanity.
in about a third. In the more acute forms of the illness, Jules Baillarger, in 1860, first described the syndrome
the age of onset is in the fourth decade, a lasting remis- and called it folie à communiquée, while Lasegue and
sion occurs in over half of the individuals, and a pattern Falret, in 1877, first described folie à deux. In this dis-
of chronicity develops in only 10%; a relapsing course order, the transfer of delusions takes place from one
has been observed in a third. Thus, the more acute and person to another. Both persons are closely associated
earlier the onset of the illness, the more favorable the for a long time and typically live together in relative
prognosis. The presence of precipitating factors, mar- social isolation. In its more common form, folie im-
ried status, and female gender are associated with bet- posée, the individual who first has the delusion is often
ter outcome. The persistence of delusional thinking is chronically ill and typically is the influential member
most favorable for cases with persecutory delusions of the close relationship with another individual, who
and somewhat less favorable for delusions of grandeur is more suggestible and who develops the delusion too.
and jealousy. However, the outcome in terms of overall The second individual is frequently less intelligent,
functioning appears somewhat more favorable for the more gullible, more passive, or more lacking in self-es-
jealous subtype. teem than the primary case. If the two people involved
are separated, the second individual may abandon the
delusion. However, this is not seen consistently. Other
TREATMENT
forms of shared psychotic disorder reported are folie
Though generally considered resistant to treatment and simultanée, where similar delusional systems develop
interventions, the management is focused on managing independently in two closely associated people. Occa-
the morbidity of the disorder by reducing the impact sionally, more than two individuals are involved (e.g.
of the delusion on the individual’s (and family’s) life. folie à trois, quatre, cinq; also folie à famille) but such
However, in recent years, the outlook has become less cases are very rare.
pessimistic or restricted in planning effective treatment An important feature in the diagnosis is that the per-
for these conditions. An effective and therapeutic cli- son with shared psychotic disorder does not have a pre-
nician–patient relationship is important but difficult to
establish.
Overall, treatment results suggest that 80.8% of DSM-IV-TR Diagnostic Criteria
cases recover either fully or partially. Pimozide, the
most frequently reported treatment, produced full re- 297.3 SHARED PSYCHOTIC DISORDER
mission in 68.5% and partial recovery in 22.4% (N ⫽ A. A delusion develops in an individual in the context of a
143). There are reports of treatment with other typical close relationship with another person(s), who has an
antipsychotic agents with variable success in a small already-established delusion.
B. The delusion is similar in content to that of the person
number of subjects. SSRIs have been used and reported who already has the established delusion.
to be helpful. The newer atypical antipsychotic agents C. The disturbance is not better accounted for by another
have been used in a small number of cases with success Psychotic Disorder (e.g., Schizoprenia) or a Mood Dis-
order with Psychotic Features and is not due to the
but the data is anecdotal. direct physiological effects of a substance (e.g., a drug
As mentioned earlier, developing a therapeutic rela- of abuse, a medication) or a general condition.
tionship is very important and yet significantly difficult, Reprinted with permission from the Diagnostic and Statistical
and requires a frank and supportive attitude. Support- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
ive therapy is very helpful in dealing with emotions of
existing psychotic disorder. The delusions arise in the delusion may be indicated later in the course of treatment.
context of a close relationship with a person who suf- To prevent redevelopment of the syndrome, the family
fers from delusional thinking and resolve on separation may need family therapy and social support to modify
from that person. The key symptom of shared psycho- the family dynamics and to prevent redevelopment of the
sis is the unquestioning acceptance of another person’s syndrome. Steps to decrease the social isolation may also
delusions. The delusions themselves are often in the help prevent the syndrome from reemerging.
realm of possibility and usually not as bizarre as those
seen in individuals with schizophrenia. The content of
the delusion is often persecutory or hypochondriacal.
DIAGNOSTIC CRITERIA
Symptoms of a coexisting personality disorder may be
present, but signs and symptoms that meet criteria for The ICD-10 and DSM-IV-TR criteria sets for schizo-
schizophrenia, mood disorders, and delusional disorder phrenia are similar in many important ways although
are absent. The individual may have ideation about sui- not identical. The ICD-10 Diagnostic Criteria for
cide or pacts about homicide; clinicians must elicit this Research provide two ways to satisfy the criteria for
information during the interview. schizophrenia: having one Schneiderian fi rst-rank
More than 95% of all cases of shared psychotic dis- symptom or having at least two of the other charac-
order involve two members of the same family. About a teristic symptoms (hallucinations accompanied by
third of the cases involve two sisters, another one-third delusions, thought disorder, catatonic symptoms,
involve husband and wife or a mother and her child. and negative symptoms). In contrast to DSM-IV-TR,
The dominant person is usually affected by schizo- which requires 6 months of symptoms (including
phrenia or a similar psychotic disorder. In 25% of all prodromal, active, and residual phases), the ICD-10
cases, the submissive person is usually affected with defi nition of schizophrenia requires only a 1-month
physical disabilities such as deafness, cerebrovascular duration, thereby encompassing the DSM-IV-TR di-
diseases, or other disability that increases the submis- agnostic categories of both schizophrenia and schiz-
sive person’s dependence on the dominant person. This ophreniform disorder. Thus, cases of DSM-IV-TR
condition is more common in people from low socio- schizophreniform disorder are diagnosed in ICD-10
economic groups and in women. as schizophrenia.
The DSM-IV-TR and ICD-10 defi nitions of
schizoaffective disorder differ with regard to the re-
Course
lationship of the Schizoaffective Disorder category
Though separation of the submissive person from the with the category Mood Disorder with Psychotic
dominant person should resolve the psychosis, this Features. In DSM-IV-TR, the differentiation depends
probably occurs only in 10–40% of the cases. Unfor- on the temporal relationship between the mood and
tunately, when these individuals are discharged from psychotic symptoms (i.e., Mood Disorder with Psy-
hospital, they usually move back together. chotic Features is diagnosed whenever the psychotic
symptoms occur only in the presence of a mood epi-
sode, regardless of the characteristics of the psychotic
symptoms). In contrast, the ICD-10 definition of
Malingering, factitious disorder with predominantly schizoaffective disorder is much broader. It includes
psychological sign and symptoms, psychotic disorder situations in which certain specified psychotic symp-
due to a general medical condition, and substance-in- toms (i.e., thought echo, insertion, withdrawal, or
duced psychotic disorder must be considered. broadcasting; delusions of control or passivity; voices
giving a running commentary; disorganized speech,
catatonic behavior) occur even if they are confi ned to
TREATMENT
a mood episode. Therefore, many cases of DSM-IV-
The initial step in treatment is to separate the affected TR mood disorder with mood-incongruent psychotic
person from the source of the delusions, the dominant features would be considered to be schizoaffective
individual. Antipsychotic agents may be used if the disorder in ICD-10. Furthermore, the ICD-10 defi ni-
symptoms have not abated in a week after separation. tion suggests that there should be an “approximate
Psychotherapy with the nondelusional members of the in- balance between the number, severity, and duration
dividual’s family should be undertaken, and psychother- of the schizophrenic and affective symptoms.’’ For
apy with both the individual and the person sharing the delusional disorder, the ICD-10 Diagnostic Crite-
ria for Research specify a minimum 3-month dura- (i.e., whether they change rapidly or not). Further-
tion in contrast to the 1-month minimum duration in more, the maximum duration of these brief psychotic
DSM-IV-TR. episodes varies depending on the type of symptoms
In contrast to the single DSM-IV-TR category Brief (i.e., 1 month for schizophrenia-like symptoms and
Psychotic Disorder, ICD-10 has a much more complex 3 months for predominantly delusional). In contrast,
way of handling brief psychotic disorders. It includes DSM-IV-TR has a single criteria set and a maximum
criteria sets for four specific brief psychotic disorders 1-month duration.
that differ on the basis of types of symptoms (i.e., with Finally, the ICD-10 and DSM-IV-TR definitions of
or without symptoms of schizophrenia) and course shared psychotic disorder are almost identical.
CHAPTER
26 Mood Disorders:
Depressive Disorders
Major depressive disorder (MDD), dysthymic disorder requires the presence of mood disturbance or loss of
(DD), and depressive disorder not otherwise specified interest and pleasure in activities for 2 weeks or more
(DDNOS) are the group of clinical conditions in the accompanied by at least four other symptoms of de-
DSM-IV-TR characterized by depressive symptomatol- pression. There are problems in differential diagnosis
ogy. These conditions specifically exclude a history of because depressive experiences vary from individual to
manic, mixed, or hypomanic episodes, and are not due to individual. One or more depressive episodes, occurring
the physiologic effects of substances of abuse, other med- in the absence of a lifetime history of mania, hypoma-
ications, or toxins. MDD is characterized by episodes of nia, or intraepisode psychotic symptoms, warrants a
depression, each lasting at least 2 weeks. DD is character- DSM-IV-TR diagnosis of Major Depressive Disorder
ized by at least 2 years of depressed mood accompanied by (see DSM-IV-TR diagnostic criteria for Major Depres-
two or three depressive symptoms that fall short of thresh- sive Disorder, page 253). If the individual has had only
old criteria for a major depressive episode. Depressive dis- one episode, then subtype “Single Episode” is noted.
order not otherwise specified includes a set of conditions Often, however, individuals suffer from multiple major
that do not meet criteria for MDD, DD, or adjustment depressive episodes during their lifetime. If the major
disorder with depressed mood. These syndromes include depressive episodes have been recurrent, the subtype
premenstrual dysphoric disorder, minor depressive disor- “Recurrent” is noted. Remission of depression requires
der, recurrent brief depressive disorder, and postpsychotic a 2-month interval in which the full criteria are not met
depressive disorder occurring during the residual phase of for a major depressive episode.
schizophrenia. In DSM-IV-TR, two other depressive dis- The core symptoms comprising a major depressive
orders are diagnosed on the basis of etiology: mood dis- episode are illustrated in the DSM-IV-TR criteria. Each
order due to a general medical condition and substance- symptom is critical to evaluate in an individual with
induced mood disorder. depressive symptomatology since each represents one
of the essential features of a major depressive episode.
Their persistence for much of the day, nearly every day
for at least 2 weeks, is the criterion for diagnosis. The
Major Depressive Disorder
clinical syndrome is associated with significant psy-
chological distress or impairment in psychosocial or
DIAGNOSIS
work functioning.
The depressive disorders are characterized by lifelong The clinical observation of mood reveals variations
vulnerability to episodes of disease, involving depressed in presentation. An individual may have depressed
mood or loss of interest and pleasure in activities. Indi- symptomatology and experience typical sadness. An-
viduals may demonstrate ongoing potential for cycling other individual may deny sadness and experience
of mood from euthymia to depression to recovery and internal agitation and dysphoria. Another individual
sometimes to hypomania or mania. When individuals cy- with depression may experience no feelings at all, and
cle to hypomania or mania, then a diagnosis of bipolar II the depressed mood is inferred from the degree of
(in the case of hypomania) or bipolar I (in the case of ma- psychological pain that is exhibited. Some individuals
nia) is made (see Chapter 28, page 279). When the mood experience irritability, frustration, somatic preoccupa-
disorder is severe, assessment for psychosis is essential. tion, and the sensation of being numb.
The detection of major depressive episodes in both An equally important aspect of the depressive ex-
primary care settings and mental health settings perience involves loss of interest or pleasure, when an
Chapter 26 • Mood Disorders: Depressive Disorders 253

MAJOR DEPRESSIVE EPISODE
MAJOR DEPRESSIVE DISORDER
A. Five (or more) of the following symptoms have been
A. Presence of a single Major Depressive Episode (296.2x present during the same 2-week period and represent
Major Depressive Disorder, Single Episode) or two or a change from previous functioning; at least one of the
more Major Depressive Episodes (296.3x Major De- symptoms is either (1) depressed mood or (2) loss of
pressive Disorder, Recurrent). interest or pleasure.
Note: To be considered separate episodes, there must Note: Do not include symptoms that are clearly due
be an interval of at least 2 Consecutive month in which to a general medical condition, or mood-incongruent
criteria are not met for a Major Depressive Episode. delusions or hallucinations.
B. The Major Depressive Episodes are not better ac- (1) Depressed mood most of the day, as indicated by
counted for by Schizoaffective Disorder and are not either subjective report (e.g., feels sad or empty) or
superimposed on Schizophrenia, Schizophreniform observation made by others (e.g., appears tearful).
Disorder, Delusional Disorder, or Psychotic Disorder Note: In children and adolescents, can be irritable
Not Otherwise Specified. mood.
C. There has never been Manic Episode, a Mixed Epi-
sode, or a Hypomanic, Episode. (2) Markedly diminished interest or pleasure in all, or
almost all, activities most of the day, nearly every
Note: This exclusion does not apply if all of the manic- day (as indicated by either subjective account or
like, mixed-like, or hypomanic-like episodes are sub- observation made by others).
stance or treatment induced or are due to the direct (3) Significant weight loss when not dieting or weight
physiological effects of a general medical condition. gain (e.g., a change of more than 5% of body
Code in fifth digit: 1 ⫽ Mild; 2 ⫽ Moderate; 3 ⫽ Severe weight in a month), or decrease or increase in
Without Psychotic Features; 4 ⫽ Sever With Psychotic Fea- appetite nearly every day.
tures (Specify Mood-Congruent/Mood-Incongruent); 5 ⫽ In Note: In children, consider failure to make expected
Partial Remission; 6 ⫽ In Full Remission; 0 ⫽ Unspecified weight gains.
If the full criteria are currently met for a Major Depressive (4) Insomnia or hypersomnia nearly every day.
Episode, specify is current clinical status and/or features: (5) Psychomotor agitation or retardation nearly every
Mild Moderate, Severe Without Psychotic Features/ day (observable by others, not merely subjective
Severe With Psychotic Features feelings of restlessness or being slowed down).
Chronic (6) Fatigue or loss of energy nearly every day.
With Catatonic Features (7) Feelings of worthlessness or excessive or inappro-
With Melancholic Features priate guilt (which may be delusional) nearly every
With Atypical Features day (not merely self-reproach or guilt about being
With Postpartum Onset sick).
(8) Diminished ability to think or concentrate, or inde-
If the full criteria are not currently met for a Major De- cisiveness, nearly every day (either by subjective
pressive Episode, specify the current clinical status of the account or as observed by others).
Major Depressive Disorder or features of the most recent (9) Recurrent thoughts of death (not just fear of dying),
episode: recurrent suicidal ideation without a specific plan,
In Partial Remission, In Full Remission or a suicide attempt or a specific plan for commit-
Chronic ting suicide.
With Catatonic Features
With Melancholic Features B. The symptoms do not meet criteria for a mixed
With Atypical Features episode.
With Postpartum Onset C. The symptoms cause clinically significant distress or
Specify (for Major Depressive Disorder, Recurrent): areas of functioning.
Longitudinal Course Specifiers (With and Without In- D. The symptoms are not due to the direct physiologi-
terposed Recovery) cal effects of a substance (e.g., a drug of abuse, a
With Seasonal Pattern medication) or a general medical condition (e.g.,
hypothyroidism).
Note: This is a summary of two criteria sets. E. The symptoms are not better accounted for by bereave-
Reprinted with permission from DSM-IV-TR Guidebook. Copyright ment, i.e., after the loss of a loved one, the symptoms
2004, Michael B First, Allen Frances, and Harold Alan Pincus. persist for longer than 2 months or are characterized
by marked functional impairment, morbid preoccupa-
tion with worthlessness, suicidal ideation, psychotic
symptoms, or psychomotor retardation.
individual feels no sense of enjoyment in activities that
were previously considered pleasurable. There is associ- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
ated reduction in all drives including energy and alteration American Psychiatric Association.
in sleep, interest in food, and interest in sexual activity.
A common experience of insomnia or hypersom-
nia is noted in individuals with persistent depression. severe cases or alternatively significant agitation lead-
Observations of psychomotor activity include profound ing to inability to sit still and profound pacing in agi-
psychomotor retardation leading to stupor in more tated forms of depression.
The complaint of guilt or guilty preoccupation is a The assessment of MDD involves the specific iden-
common aspect of the depressive syndrome. Delusional tification of 5 of 9 criterion symptoms that would con-
forms of guilt are a common presentation of depressive stitute a diagnosis of MDD. A careful general medical
disorder with psychotic features. assessment to ascertain the presence of an etiologic
The loss of ability to concentrate, to focus atten- general medical condition is required. After the as-
tion, and to make decisions is a particularly distressing sessment for general medical conditions, one exam-
symptom for individuals. One may experience a loss ines the individual for the presence of alcohol or drug
of memory that simulates dementia. Loss of concentra- dependence. Then the clinician is required to assess
tion is reflected in an inability to perform both compli- retrospectively the occurrence of prior episodes of
cated and simple tasks. The loss of ability to perform in mood disorder, either depression or mania. It is nec-
school may be a symptom of a major depressive episode essary to examine for other comorbid mental disor-
in children, and memory difficulties in the older adult ders as well. Depressive illnesses are very common
may be mistaken for a primary dementia. In some older and recurrent, but an individual with MDD may or
adults, a depressive episode with memory difficulties may not recall prior episodes. It is therefore essential
occurs in the early phase of an evolving dementia. to interview a significant other or family member in
The most common psychiatric syndrome associated addition to the individual with depression to identify
with thoughts of death, suicidal ideation, or completed prior manic, hypomanic, or depressive episodes. Fam-
suicide is a major depressive episode. The experience ily inquiry allows one to elicit the family history of
of hopelessness is commonly associated with suicidal addiction, anxiety, depressive disorder, mania, psy-
ideation. The preoccupation with suicide in major de- chosis, trauma, or neurologic disorders in first-degree
pressive disorder requires that the assessment always relatives.
includes careful monitoring of suicidality. Suicidality is The individual who presents for outpatient or hos-
the feature of depressive disorder that poses substantial pital treatment for a primary depressive disorder will
risk of mortality in the disease. Prevention of suicide, require general medical examination, including a phys-
more than any other treatment goal, requires immedi- ical examination and laboratory testing to rule out an
ate intervention and may require hospitalization. The associated medical condition. Clinical assessment, in-
risk for subsequent completed suicide for an individual cluding the cognitive mental status examination, will
hospitalized for an episode of severe MDD is estimated direct the extent of the general medical examination.
to be 15%. To assess risk for suicide, one inquires about Traditional psychological testing may complement
the presence of active suicidal ideation in relation to the structured diagnostic instruments developed to ascer-
current episode of depression and a history of prior sui- tain the presence or absence of depressive disorders
cide attempts. The occurrence of significant life events according to DSM-IV-TR criteria. Psychological test-
such as separation, divorce, and death of significant ing such as the Rorschach Inkblot Test are sensitive to
others may precipitate the episode. It is also necessary the degree of affective lability, intensity of suicidality,
to review onsets of other medical conditions that may and impulse control in individuals with depression. In
precipitate a new episode of depression. When alcohol addition, inventories are commonly used in outpatient
or other drug use co-occurs with such significant life and inpatient settings to establish scores of clinical
events, the risk of suicidal behavior during an episode severity of depressive symptoms. Self-administered
of depression increases. The presence of a recent sui- scales include the Beck Depression Inventory. the Zung
cide attempt may suggest the need for immediate hos- Self-Rating Depression Scale, and the Inventory for
pitalization and treatment. Depressive Symptomatology (self-report). Clinician-
Familiarity with risk factors for major depressive administered scales used for assessment of depressive
disorder may help the clinician recognize or diagnose symptoms include the Hamilton Rating Scale for De-
this common and serious psychiatric illness. Accord- pression, the Montgomery Asberg Depression Rating
ingly, the following 10 primary risk factors for depres- Scale, and the Inventory for Depressive Symptomatol-
sion have been identified: (1) history of prior episodes ogy (clinician rated). It is essential to recognize that
of depression; (2) family history of depressive disor- a cross-sectional assessment is only one component
der especially in first-degree relatives; (3) history of of the total assessment. Corroborative family data and
suicide attempts; (4) female gender; (5) age of onset longitudinal assessment and reassessment of mood dis-
before age 40; (6) postpartum period; (7) comorbid order symptoms are crucial in following the natural
medical illness; (8) absence of social support; (9) neg- history and course of MDD.
ative, stressful life events; and (10) active alcohol or Laboratory studies in the management of the indi-
substance abuse. vidual with MDD includes complete blood count with
differential, electrolytes, chemical screening for renal

Subtyping of MDD
and liver function as well as thyroid function studies.
More detailed evaluation will depend upon the nature The current subtyping of MDD is based on severity,
of the clinical presentation as well as neuropsychologi- cross-sectional features, and course features.
cal examination. These studies may identify cerebral
vulnerability factors that would complicate the treat- Severity/Psychotic/Remission. The rating of severity
ment for MDD. is based on a clinical judgment of the number of cri-
When clinical signs suggest cognitive disruption or teria present, the severity of the symptomatology, and
cognitive impairment, the clinician may also consider the degree of functional distress. The ratings of current
administering neuropsychological tests or conduct- severity are classified as mild, moderate, severe without
ing more focused neurologic examination to explore psychotic features, severe with psychotic features, in
cognitive, behavioral, and neurological correlates of partial remission, or in full remission (see DSM-IV-TR
brain function. Neuropsychological assessment may diagnostic criteria, page 256). The definition of “mild”
help clarify the relative contribution of depression or refers to an episode that results in only mild impairment
another disease process to the individual’s clinical in occupational or psychosocial functioning or mild
presentation. Further, neuropsychological assessment disability. “Moderate” implies a level of severity that
will provide a functional analysis of the individual’s is intermediate between mild and severe and is associ-
cognitive and behavioral strengths and limitations. ated with moderate impairment in psychosocial func-
Neurological examination may reveal minor neurologi- tioning. The definition of “severe” describes an episode
cal abnormalities suggesting early neurodevelopmental that meets several symptoms in excess of those required
vulnerability. to make a diagnosis of major depressive episode and is
Individuals with MDD report health difficulties and associated with marked impairment in occupational or
actively use health services. Studies have indicated that psychosocial functioning and definite disability char-
as many as 23% of depressed individuals report health acterized by inability to work or perform basic social
difficulties severe enough to keep them bedridden. The functions. “Severe with psychotic features” indicates
Medical Outcomes Study examined role functioning, the presence of delusions or hallucinations, which oc-
social functioning, and number of days in bed second- cur in the context of the major depressive episode. Since
ary to poor health, and compared the degree of impact the introduction of DSM-III, the categories of mood-
of depression and other chronic medical conditions. congruent versus mood-incongruent psychotic features
Depression was associated with more impairment in are made in the context of a psychotic depressive disor-
occupational and interpersonal functioning, and more der. When the content of delusions or hallucinations is
days in bed, in comparison to several common medical consistent with depressive themes, a mood-congruent
illnesses. psychotic diagnosis is made. When the psychotic fea-
A significant relationship exists between MDD and tures are not related to depressive themes or include
mortality, characterized by suicide and accidents. symptoms such as thought insertion, broadcast, or with-
Therefore, an accurate diagnosis of MDD, early ap- drawal, the modifier of mood-incongruent psychotic
propriate intervention, and specific assessment of features is used. Mood-incongruent psychosis in MDD
suicidality is essential. Fifteen percent of individu- may be associated with a poorer prognosis. For depres-
als with MDD who require hospitalization owing to sion with psychotic features, whether they are mood-
severe depression will die by committing suicide. congruent or mood-incongruent, antipsychotic medica-
Approximately 10% of individuals with MDD who tion in combination with antidepressant medication or
attempt suicide will eventually succeed in killing electroconvulsive therapy (ECT) is required to treat the
themselves. Roughly 50% of individuals who have disorder.
successfully committed suicide carried a primary de- Partial remission indicates that the episode no longer
pressive diagnosis. Individuals with MDD who were meets full criteria for major depressive episode but that
admitted to nursing homes were found to have a 59% some symptoms are still present or the period of remis-
greater likelihood of death within the fi rst year of ad- sion has been less than 2 months. In full remission, the
mission in comparison with nondepressed admissions. individual has no significant symptoms of depression
The epidemiologic catchment area (ECA) study indi- for a period of at least 2 months.
cated that individuals with MDD 55 years of age and
older evidence a mortality rate over the next 15 months Cross-Sectional Features. The assessment of cross-
four times higher than nondepressed controls matched sectional features involves the presence or absence of
for age. catatonic, melancholic, or atypical features during an

SEVERITY/PSYCHOTIC/REMISSION SPECIFIERS WITH CATATONIC FEATURES
Note: Code in fifth digit. Mild, Moderate, Severe Without Specify if:
Psychotic Features, and Severe With Psychotic Features
With Catatonic Features (can be applied to the current
can be applied only if the criteria are currently met for
or most recent Major Depressive Episode, Manic Episode,
a Major Depressive Episode. In Partial Remission and In
or Mixed Episode in Major Depressive Disorder, Bipolar I
Full Remission can be applied to the most recent Major
Disorder, or Bipolar II Disorder)
Depressive Episode in Major Depressive Disorder and to
a Major Depressive Episode in Bipolar I or II Disorder The clinical picture is dominated by at least two of the
only if it is the most recent type of mood episode. following:
.x1—Mild: Few, if any, symptoms in excess of those re- A. Motoric immobility as evidenced by catalepsy (includ-
quired to make the diagnosis and symptoms result in only ing waxy flexibility) or stupor
minor impairment in occupational functioning or in usual B. Excessive motor activity (that is apparently purposeless
social activities or relationships with others. and not influenced by external stimuli)
C. Extreme negativism (an apparently motiveless resist-
.x2—Moderate: Symptoms or functional impairment be-
ance to all instructions or maintenance of a rigid pos-
tween “mild” and “severe.”
ture against attempts to be moved) or mutism
.x3—Severe Without Psychotic Features: Several symp- D. Peculiarities of voluntary movement as evidenced by
toms in excess of those required to make the diagnosis, posturing (voluntary assumption of inappropriate or
and symptoms markedly interfere with occupational bizarre postures), stereotyped movements, prominent
functioning or with usual social activities or relationships mannerisms, or prominent grimacing
with others. E. Echolalia or echopraxia
.x4—Severe With Psychotic Features: Delusions or hal- Reprinted with permission from the Diagnostic and Statistical
lucinations. If possible, specify whether the psychotic Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
features are mood-congruent or mood-incongruent: American Psychiatric Association.
Mood-Congruent Psychotic Features: Delusions or hal-

lucinations whose content is entirely consistent with the
typical depressive themes of personal inadequacy, guilt,
disease, death, nihilism, or deserved punishment. cation-induced movement disorder leading to catatonic
Mood-Incongruent Psychotic Features: Delusions or features, or neuroleptic malignant syndrome.
hallucinations whose content does not involve typical The specifier with melancholic features is applied
depressive themes of personal inadequacy, guilt, disease, when the depressive episode is characterized by pro-
death, nihilism, or deserved punishment. Included are
such symptoms as persecutory delusions (not directly found loss of interest or pleasure in activities and lack of
related to depressive themes), thought insertion, thought reactivity to external events as well as usual pleasurable
broadcasting, and delusions of control. stimuli (see DSM-IV-TR diagnostic criteria, page 257).
.x5—In Partial Remission: Symptoms of a Major Depres- In addition, at least three of the following melancholic
sive Episode are present but full criteria are not met, or
there is a period without any significant symptoms of a features must be present: depression is typically worse
Major Depressive Episode lasting less than 2 months fol- in the morning, early morning awakening, psychomo-
lowing the end of the Major Depressive Episode. (If the tor change with marked retardation or agitation, sig-
Major Depressive Episode was superimposed on Dys-
thymic Disorder, the diagnosis of Dysthymic Disorder nificant weight loss, or profound and excessive guilt. A
alone is given once the full criteria for a Major Depressive major depressive episode with melancholic features is
Episode are no longer met.) particularly important to diagnose because of the pre-
.x6—In Full Remission: During the past 2 months, no diction that it is more likely to respond to somatic treat-
significant signs or symptoms of the disturbance were
present. ment, including electroconvulsive therapy. Individuals
with melancholic features experience more recurrence
.x0—Unspecified.
of MDD. The findings of hypercortisolism following
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 dexamethasone as well as reduced rapid eye movement
American Psychiatric Association. (REM) latency is associated with the melancholic epi-
sodes of MDD.
Finally, the category of major depressive episode
episode of depression. The specifier with catatonic with atypical features was previously called “atypical
features is used when profound psychomotor retarda- depression.” This syndrome is characterized by promi-
tion, prominent mutism, echolalia, echopraxia, or stu- nent mood reactivity in which there is responsiveness
por dominates the clinical picture. The presentation of of the depressed mood to external events and at least
catatonia requires a differential diagnosis that includes two of the following associated features: increased ap-
schizophrenia, catatonic type, bipolar I disorder, cata- petite or weight gain, hypersomnia, leaden paralysis (a
tonic disorder due to a general medical condition, medi- feeling of profound anergia or heavy feeling), and in-

WITH MELANCHOLIC FEATURES WITH ATYPICAL FEATURES
Specify if: Specify if:

With Melancholic Features (can be applied to the cur- With Atypical Features (can be applied when these fea-
rent or most recent Major Depressive Episode in Major tures predominate during the most recent 2 weeks of a
Depressive Disorder and to a Major Depressive Episode current Major Depressive Episode in Major Depressive
in Bipolar I or Bipolar II Disorder only if it is the most Disorder or in Bipolar I or Bipolar II Disorder when a cur-
recent type of mood episode) rent Major Depressive Episode is the most recent type of
mood episode, or when these features predominate dur-
A. Either of the following, occurring during the most se-
ing the most recent 2 years of Dysthymic Disorder; if the
vere period of the current episode:
Major Depressive Episode is not current, it applies if the
(1) loss of pleasure in all, or almost all, activities feature predominates during any 2-week period)
(2) lack of reactivity to usually pleasurable stimuli
A. Mood reactivity (i.e., mood brightens in response to
(does not feel much better, even temporarily, when
actual or potential positive events)
something good happens)
B. Two (or more) of the following features:
B. Three (or more) of the following:
(1) significant weight gain or increase in appetite
(1) distinct quality of depressed mood (i.e., the de- (2) hypersomnia
pressed mood is experienced as distinctly different (3) leaden paralysis (i.e., heavy, leaden feelings in arms
from the kind of feeling experienced after the death or legs)
of a loved one) (4) long-standing pattern of interpersonal rejection
(2) depression regularly worse in the morning sensitivity (not limited to episodes of mood distur-
(3) early morning awakening (at least 2 hours before bance) that results in significant social or occupa-
usual time of awakening) tional impairment
(4) marked psychomotor retardation or agitation
C. Criteria are not met for With Melancholic Features or
(5) significant anorexia or weight loss
With Catatonic Features during the same episode.
(6) excessive or inappropriate guilt.
terpersonal hypersensitivity (rejection sensitivity). De- tum onset episodes can present either with or with-
pressive episodes with atypical features are also com- out psychosis. Postpartum psychotic episodes occur
mon in individuals with bipolar I or II disorder as well in 0.1–0.2% of deliveries. Depression in postpartum
as seasonal affective disorder. psychosis is associated with prominent guilt and may
involve individuals with a prior history of bipolar I
Course Features. MDD is diagnosed with certain disorder. If an episode of postpartum psychosis oc-
course features such as postpartum onset, seasonal curs, there is a high risk of recurrence with subse-
pattern, recurrent, chronic, and with or without full quent deliveries. Heightened attention to identifica-
interepisode recovery. Depression with postpartum tion of postpartum episodes is required because of
onset has been the subject of increasing attention potential risk of morbidity and mortality to mother
in psychiatric consultation to obstetrics and gyne- and newborn child.
cology. The specifier applies only to the current or The specifier with seasonal pattern is diagnosed
most recent major depressive episode in MDD (or when episodes of MDD occur regularly in fall and
bipolar disorder). The presence of a major depres-
sive episode may occur from 2 weeks to 12 months
after delivery, beyond the usual duration of postpar- DSM-IV-TR Diagnostic Criteria
tum “blues” (3–7 days). Postpartum blues are brief
POSTPARTUM ONSET
episodes of labile mood and tearfulness that occur in
50–80% of women within 5 days of delivery. How- Specify if:
ever, depression is seen in 10–20% of women after With Postpartum Onset (can be applied to the current
childbirth, which is higher than rates of depression or most recent Major Depressive, Manic, or Mixed Epi-
sode in Major Depressive Disorder, Bipolar I Disorder, or
found in matched controls. There is greater vulner- Bipolar II Disorder; or to Brief Psychotic Disorder)
ability in women with prior episodes of major mood Onset of episode within 4 weeks postpartum.
disorder, particularly bipolar disorder, and there is Reprinted with permission from the Diagnostic and Statistical
a high risk of recurrence with subsequent deliveries Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
after an MDD with postpartum onset. The postpar-

SEASONAL PATTERN WITH AND WITHOUT INTEREPISODE RECOVERY
Specify if: Specify if (can be applied to Recurrent Major Depressive

Disorder or Bipolar I or II Disorder):
With Seasonal Pattern (can be applied to the pattern of
Major Depressive Episodes in Bipolar I Disorder, Bipolar With Full Interepisode Recovery: if full remission is at-
II Disorder, or Major Depressive Disorder, Recurrent) tained between the two most recent Mood Episodes
Without Full Interepisode Recovery: if full remission
A. There has been a regular temporal relationship be-
is not attained between the two most recent Mood
tween the onset of Major Depressive Episodes in Bi-
Episodes
polar I or Bipolar II Disorder or Major Depressive Dis-
order, Recurrent, and a particular time of the year (e.g., Reprinted with permission from the Diagnostic and Statistical
regular appearance of the Major Depressive Episode Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
in the fall or winter). Note: Do not include cases in American Psychiatric Association.
which there is an obvious effect of season-related psy-
chosocial stressors (e.g., regularly being unemployed
every winter).
B. Full remissions (or a change from depression to mania a major depressive episode continually, satisfying full
or hypomania) also occur at a characteristic time of the MDD criteria for at least 2 years.
year (e.g., depression disappears in the spring). Across epidemiologic studies, MDD is found to be
C. In the last 2 years, two Major Depressive Episodes
have occurred that demonstrate the temporal seasonal a common psychiatric disorder. The lifetime risk for
relationships defined in Criteria A and B, and no non- MDD in community samples varies from 10% to 25%
seasonal Major Depressive Episodes have occurred for women and from 5% to 12% for men. The point
during that same period.
D. Seasonal Major Depressive Episodes (as described prevalence of MDD (proportion of the individuals that
above) substantially outnumber the nonseasonal have the disorder being studied at a designated time)
Major Depressive Episodes that may have occurred
over the individual’s lifetime.
for adults in community samples has varied from 5% to
9% for women and from 2% to 3% for men. The point
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 prevalence of MDD in primary care outpatient settings
American Psychiatric Association. ranges from 4.8% to 8.6%. In hospitalized individuals
for all medical conditions, more than 14% had MDD.
While the incidence rates of MDD in prepubertal boys
winter seasons and subsequently remit during spring and girls are equal, women over the course of their
and summer. When the pattern of onset and remission lifetime are 2 to 3 times more likely to have MDD after
occurs for the last 2 years, one diagnoses an MDD with puberty.
seasonal pattern. Often, this pattern is characterized For preschool children, the point prevalence is
by atypical features, including low energy, hypersom- thought to be 0.8%. Point prevalences of major and
nia, weight gain, and carbohydrate craving. Although minor depressive disorder of 1.8% and 2.5%, respec-
the predominant pattern is fall–winter depression, a tively, were found in a 1983 sample of 9-year-old chil-
minority of individuals show the reverse seasonal pat- dren from the general population, based upon the use
tern with spring–summer depression. Specific forms of a semistructured diagnostic instrument. A semi-
of light therapy with 2500 lux exposure has been structured diagnostic instrument was used to find a
shown to be effective in MDD with seasonal pattern. 4.7% point prevalence rate of major depressive disor-
Because seasonal depression has clinical features that der in a community sample of 150 adolescents. Those
are similar to atypical features, the risk of a possible adolescents diagnosed with MDD had symptoms that
bipolar II disorder must be considered since atypical met criteria for dysthymic disorder as well. A point
features are more common in depressive episodes oc- prevalence rate of 3.3% was found for dysthymic
curring as part of bipolar II. These individuals, when disorder.
exposed to antidepressant medication or bright light Changing rates of MDD for recent birth cohorts have
therapy, may evolve a switch into hypomanic or manic been found in North America, Puerto Rico, Western
episode. Europe, Middle East, Asia, and the Pacific Rim. Spe-
Clinical and scientific attention to the course of MDD cifically, an earlier age of onset and increased rate of
focuses upon the depiction of longitudinal course. Life depression occur in individuals born in more recent
charting of MDD involves the use of several course decades. Historical, social, economic, or biological
specifiers. Each episode is denoted with or without full events most likely account for the variability in the
recovery (see DSM-IV-TR diagnostic criteria, page •••). rate of depression noted in different countries included
The specifier chronic MDD involves the persistence of in the study. However, an overall increase in the rate
of depression has been noted across many of the geo- generations; and (5) the individual experiences hypo-
graphic locations. mania induced by antidepressant medication.
Older adults continue to manifest a higher suicide Recurrent MDD requires longitudinal observation
rate than in younger age groups. However, suicide rates because of its highly variable course. Generally, com-
have increased in younger age groups as the changing plete remission of an episode of MDD heralds a return
rate of MDD is observed in younger cohorts. In keep- to premorbid levels of social, occupational, and inter-
ing with the birth cohort effect, recurrences of MDD in personal functioning. Therefore, the goal of treatment is
late life may become a significant health concern as the in achieving full remission of depressive symptoms and
population ages. recovery. Untreated episodes of depression last 6 to 24
months. Symptom remission and a return to premorbid
level of functioning characterize approximately 66% of
Course
depressed individuals. By comparison, roughly 5–10%
The mean age of onset of major depression is 27 years of individuals continue to experience a full episode of
of age, although an individual can experience the on- depression for greater than 2 years and approximately
set of MDD at any age. New symptoms of MDD of- 20–25% of individuals experience partial recovery be-
ten develop over several days to several weeks. Early tween episodes. Furthermore, 25% of the individuals
manifestations of an episode of MDD include anxi- manifest “double depression,” characterized by the de-
ety, sleeplessness, worry, and rumination prior to the velopment of MDD superimposed upon a mild, chronic
experience of overt depression. Over a lifetime, the dysthymic disorder (DD). Individuals with double de-
presence of one major depressive episode is associated pression often demonstrate poor interepisode recovery.
with a 50% chance of a recurrent episode. A history The following four characteristics are seen in a partial
of two episodes is associated with a 70–80% risk of a remission of an episode: (1) increased likelihood of a
future episode. Three or more episodes are associated subsequent episode; (2) partial interepisode recovery
with extremely high rates of recurrence. Because the following subsequent episodes; (3) possible require-
majority of cases of MDD recur, continuation treatment of longer-term treatment; and (4) treatment with
ment and ongoing education regarding warning signs a combination of pharmacotherapy and psychotherapy
of relapse or recurrence are essential in ongoing clini- may be indicated.
cal care. Follow-up naturalistic studies have indicated that
In comparison to individuals who develop a single 40% of individuals with MDD carry the same diagno-
episode (many of whom return to premorbid function- sis 1 year later, 3% evidence DD, 17% manifest incom-
ing), individuals with recurrent episodes of depression plete recovery, and 40% do not meet criteria for MDD.
are at greater risk to manifest bipolar disorder. Indi- A significant percentage of individuals with MDD have
viduals who experience several recurrent episodes of persist chronic symptoms of MDD. A 5-year follow-up
depression may develop a hypomanic or manic episode study of MDD indicated that 50% of the individuals
requiring rediagnosis to bipolar disorder. In children showed recovery by 6 months but 12% of the sample
and adolescents, the transformation of a diagnosis of continued to be depressed for the entire 5-year period.
depression to a diagnosis of bipolar disorder is higher. The authors of this study noted that inadequate treat-
Approximately 40% of adolescents who are depressed ment may have contributed to the chronicity.
evolve into a bipolar course. Because bipolar disorder Poor outcome and likelihood of recurrent episodes
is initiated with a depressive episode in at least 4 of 5 is associated with comorbid conditions such as per-
cases, it is important to identify those individuals who sonality disorder, active substance or alcohol abuse,
are most likely to develop a bipolar disorder. Therefore, organicity, or medical illness. Recurrence and outcome
the clinician is confronted with significant diagnostic may be affected by the rapidity of clinical intervention.
and treatment challenges when called upon to evaluate Inadequate treatment (e.g., insufficient dosing or dura-
an individual, particularly an adolescent, who presents tion of pharmacotherapy) contributes to poor outcome,
with depression and has no previous history of mania. including chronic MDD. Early treatment intervention
Several risk factors have been identified which predict in an episode of MDD may be relatively more effective
when a first episode of MDD will evolve into bipolar than later intervention in an episode.
disorder: (1) the first episode of depression emerges
during adolescence; (2) the depression is severe and in-
Depression in the Medically Ill
cludes psychotic features; (3) psychomotor retardation
and hypersomnia are present; (4) a family history of Whereas a 4–5% current prevalence rate of MDD ex-
bipolar disorder exists, particularly across two to three ists in community samples, symptoms of depression are
found in 12–36% of individuals with a general medical cause depression and dementia commonly co-occur.
condition. The rate of depression may be higher in in- Treatment of co-occurring depressive features may
dividuals with a specific medical condition. MDD is relieve symptoms and improve overall quality of
identified as an independent condition and calls for life.
specific treatment when it occurs in the presence of a
general medical condition. Parkinson’s Disease. Fifty percent of individuals
Four possible relationships have been identified be- with Parkinson’s disease experience an MDD during
tween depression and a general medical condition: (1) the course of the illness. When depression occurs in
depression is biologically caused by the general medi- this context, one diagnoses mood disorder due to Par-
cal condition, (2) an individual who carries a genetic kinson’s disease. Active treatment of the depressive
vulnerability to MDD manifests the onset of depression disorder may result in improvement in the signs and
triggered by the general medical condition, (3) depres- symptoms of depression without alleviation of the in-
sion is psychologically caused by the general medical voluntary movement disorder or cognitive changes as-
condition, and (4) no causal relationship exists between sociated with subcortical brain disease. The underlying
the general medical condition and mood disorder. The etiology of associated dementia and depressive disorder
first two cases warrant initial treatment directed at the in Parkinson’s disease appears to involve physiologic
general medical condition. Treatment is advocated for changes in subcortical brain regions.
persistent depression upon stabilization of the general
medical condition. When the general medical con- Diabetes. It is estimated that the prevalence of de-
dition causes depression, specific treatment for the pression in treated individuals with diabetes is three
former condition is optimized, while psychiatric man- times as frequent than in the general population. Fur-
agement, education, and antidepressant medication are ther, there is no difference in the prevalence rate of de-
administered to treat the depression. In cases where the pression in individuals with insulin-dependent diabetes
two conditions are not etiologically related, appropriate mellitus (Type I) in comparison with individuals with
treatment is indicated for each disorder. noninsulin-dependent mellitus (Type II). The sympto-
matic presentation of MDD in individuals with diabe-
Stroke. Some poststroke patients manifest depression tes is similar to individuals without diabetes. Conse-
owing to cerebrovascular disease related to cerebral quently, full assessment of and treatment for MDD is
infarction in left frontal and left subcortical brain re- recommended in individuals who become depressed
gions. Mood disorder due to cerebrovascular disease is during the course of diabetes. The relatively high point
diagnosed when an individual manifests a recent stroke prevalence rate may be due to higher detection rate in
and has significant symptoms of depression. A point this treated population having a chronic illness as well
prevalence of mood disorder due to cerebrovascular as metabolic and endocrine factors.
disease in poststroke patients between 10% and 27%
has been documented, with an average duration of de- Coronary Artery Disease. When MDD is present,
pression lasting approximately 1 year. Case reports of increased morbidity and mortality is reported in post-
mood disorder due to cerebrovascular disease in postmyocardial infarction patients as well as in individuals
stroke individuals suggest poor treatment compliance, having coronary artery disease without myocardial inf-
irritability, and personality change. arction (MI). Therefore, treatment of MDD in individu-
als with coronary artery disease is indicated. Prevalence
Alzheimer’s Disease. According to DSM-IV-TR, estimates of MDD in postmyocardial infarction range
when symptoms of clinically significant depressed from 40% to 65%. Over a 15-month period, individu-
mood accompany dementia of the Alzheimer’s type, als 55 years or older who had mood disorder evidenced
and in the clinician’s judgment, the depression is due a mortality rate four times higher than expected, and
to the direct physiological effects of the Alzheimer’s coronary heart disease or stroke accounted for 63% of
disease, mood disorder due to Alzheimer’s disease is the deaths. Depression may promote poor adherence
diagnosed. When dementia consistent with cerebrov- to cardiac rehabilitation and worse outcome. During
ascular disease leads to prominent cognitive deficits, the first year following MI, depression is considered
focal neurological signs and symptoms, significant to be associated with a three- to fourfold increase in
impairment in functioning as well as predominant subsequent cardiovascular morbidity and mortality.
depressed mood, vascular dementia with depressed Depression in individuals with coronary artery disease
mood is diagnosed. The distinction between depres- is associated with more social problems, functional im-
sive disorders and dementia is often complicated be- pairment, and increased health care utilization.
Cancer. MDD occurs in 25% of individuals with can- Table 26-1 Medications Associated with Depression
cer at some time during the illness. MDD should be
Cardiovascular
assessed and treated as an independent disorder. The Drugs Hormones Psychotropics
intense reaction in individuals diagnosed with cancer
may lead to dysphoria and sadness without evolving a Methyldopa Oral contraceptives Benzodiazepines
Reserpine Corticotropin and Neuroleptics
full syndrome of MDD. The consulting clinician must glucocorticoids
evaluate the individual’s response to chemotherapy, side Propranolol Anabolic steroids
effects of the treatment, and medication interactions in Guanethidine
Clonidine
the overall assessment of the individual. Among indi- Thiazide
viduals with cancer, MDD is typically characterized diuretics
by heightened distress, impaired functioning, and de- Digitalis
Anticancer Anti-inflammatory Others
creased capacity to adhere to treatment. Treating co- Agents and anti-
morbid MDD with psychotherapy or pharmacotherapy infective agents
may improve the overall outcome in individuals with Cycloserine Nonsteroidal anti- Cocaine
inflammatory (withdrawal)
cancer and mitigate complications of MDD. agents
Ethambutol Amphetamines
(withdrawal)
Chronic Fatigue Syndrome. Lifetime rates of MDD Disulfiram Levodopa
in individuals with chronic fatigue syndrome range Sulfonamides Cimetidine
from 46% to 75%. Comorbid anxiety and somatization Baclofen Ranitidine
Metoclopramide
disorders are also common in individuals with chronic
fatigue. According to the Centers for Disease Control
(CDC) criteria, the diagnosis of chronic fatigue syn-
drome is excluded in individuals whose symptoms meet blockers or angiotensin converting enzyme (ACE)
criteria for a formal mental disorder, such as MDD or inhibitors.
DD. Individuals whose symptoms meet criteria for both Hormonal treatments, such as corticosteroids and
a mood disorder and a chronic fatigue syndrome should anabolic steroids, can elicit depression, mania, or psy-
be maximally treated for the mood disorder with appro- chosis. Oral contraceptives require monitoring regard-
priate pharmacotherapy and cognitive–behavioral psy- ing the possible precipitation of depressive symptoms.
chotherapy. The etiological relationship between mood Because individuals with seizure disorders and
disorder and chronic fatigue syndrome is unclear. Parkinson’s disease are at high risk for concomitant
MDD, it is difficult to establish a link between anti-
Fibromyalgia. In comparison with other general convulsant or anti-Parkinsonian treatment and the
medical conditions, little is known about the relation- precipitation of depression. Nevertheless, individuals
ship between fibromyalgia and MDD. Two studies have require close monitoring and evaluation for evolution
found higher lifetime rates of major mood disorder in of depressive symptomatology.
fibromyalgia patients in comparison with rheumatoid
arthritis patients.
Comorbid Depression with Other
Mental Disorders
Depression due to Medications
More than 40% of individuals with MDD have addi-
If MDD is judged to be a direct physiologic effect of a tional symptoms that meet criteria during their lifetime
medication, then substance-induced mood disorder is for one or more additional mental disorders. In a recent
diagnosed. Medications reported to cause depression community sample, assessing both pure and comorbid
involve several drugs from the associated groups listed MDD, the current prevalence of major depression was
in Table 26-1. 4.9%. Of the sample with current MDD, 56.3% also
Among antihypertensive treatment, beta-adrenergic had another mental disorder. The presence of a co-
blockers have been studied regarding the risk of de- morbid mental disorder may alter the course of major
pression. No significant differences are found between mood disorder in a dramatic fashion and is identified
individuals treated with beta-blockers and those treated as a primary risk factor for poor treatment response.
with other antihypertensives regarding the propensity Therefore, proper assessment, preferably with the use
to develop depressive symptoms. Lethargy is the most of a semistructured diagnostic instrument, additional
common side effect reported. No significant depres- informants, and longitudinal observation, will identify
sive complications are reported with calcium channel comorbid conditions.
Alcohol/Drug Dependence. Results of family and disorder than in cases with a single diagnosis. Lifetime
twin studies in a population-based female sample are suicide rate is twice as high for individuals with co-
consistent with a modest correlation of the liability be- morbid panic disorder and MDD than in panic disor-
tween alcohol dependence and MDD. It is common for der alone. It is imperative to assess for the presence of
individuals with alcohol dependence to evidence signs mood disorder and suicidality among individuals who
of depression or MDD, but alcoholism is not thought to present with symptoms of anxiety.
be a common consequence of mood disorder. Between
10% and 30% of individuals with alcoholism manifest Obsessive–Compulsive Disorder. The occurrence of
depression, whereas alcoholism is thought to occur in symptoms of depression is very common in individuals
under 5% of depressed individuals. with obsessive–compulsive disorder (OCD), although
Depressed women are more likely to self-medicate full symptom criteria may not be reached to warrant a
their mood disorder with alcohol than are depressed formal diagnosis of MDD. Of individuals with OCD,
men. The effect of comorbid alcoholism on the course 10–30% have mood symptoms that meet full criteria
of major mood disorder is unclear. Some evidence sug- for MDD. The relationship between OCD and schizo-
gests that remission of depression occurs within the phrenia is less clear. Individuals with OCD are at an
first month of sobriety. The effect of comorbid depres- increased risk to develop MDD but not schizophre-
sion requires further attention in relation to the course nia. It is important to distinguish between obsessive–
of drug dependence. Drug dependence is often associ- compulsive personality features that can accompany,
ated with major mood disorder and the presence of as- and can exacerbate during, an episode of depression
sociated comorbid personality disorder. and OCD itself. Symptoms of depression often dimin-
ish with successful initial treatment of OCD, since
Panic/Phobias/GAD. The co-occurrence of symp- biological treatments typically involve use of selective
toms of anxiety and depression is very common. Very serotonergic antidepressant medications such as clomi-
high genetic correlations between MDD and general- pramine, fluoxetine, or fluvoxamine.
ized anxiety disorder have been found in contrast to
only a modest overlap between phobic disorders and Posttraumatic Stress Disorder. Individuals with
MDD. Anxiety symptoms commonly appear in de- PTSD often experience co-occurring depressive dis-
pressive syndromes and MDD is frequently comorbid orders, anxiety disorders, and substance use disorders.
with anxiety disorders. From a longitudinal perspec- The range of reported rates of concurrent depressive
tive, either symptom constellation can be a precursor disorder in individuals with PTSD is 30–50%. Many of
to the development of the other disorder. The combina- the symptoms of PTSD overlap with signs and symp-
tion of anxiety and depression predicts greater severity toms of depression such that both PTSD and MDD
and impairment than the presence of each syndrome in can be considered to be the result of traumatic events.
isolation. The association of severe panic and MDD is In addition, depressive disorder may be associated
one of the predictors of suicidal risk. The clinician is with worse outcome in individuals with co-occurring
advised to assess for symptoms of each disorder and to PTSD.
obtain a thorough family history. Individuals with anx-
iety disorders often experience prior episodes of MDD Somatization Disorder. It is common for individuals
or have relatives who suffer from mood disorder. with MDD to experience somatic symptoms includ-
Of outpatients with MDD, 10–20% evidence comor- ing pain, although the intensity and frequency of the
bid panic disorder while 30–40% of depressed outpa- somatic complaints and the range of body systems af-
tients have had symptoms that met criteria for general- fected do not usually meet criteria for somatization dis-
ized anxiety disorder during the course of the mood order. Individuals who have mood symptoms that meet
disorder. In both cases, the anxiety disorder has pre- criteria for MDD evidence more complaints of pain,
ceded the major mood disorder about 50% of the time. experience more physical, interpersonal, and occupa-
The clinician is advised to evaluate three factors in tional limitations, and perceive their overall health as
order to determine treatment approaches when MDD co- worse than individuals with chronic medical illness.
occurs with panic disorder or social phobia: (1) the indi- The clinician should carefully evaluate for the pres-
vidual’s family history, (2) the constellation of symptoms ence of MDD in cases where the individual reports un-
that were first evident in the current episode, and (3) the explained pain. Typically, pain complaints are relieved
symptoms that cause the individual the most distress. upon successful treatment of the MDD. However,
Recovery is less likely and symptomatology more somatoform disorders, as outlined in DSM-IV-TR, may
severe in individuals with comorbid MDD and panic be associated with demoralization and depression.
Eating Disorders. There are little data available re- DD has more prominent changes in mood, irritability,
garding prevalence of eating disorders in individuals anger, and hopelessness. The signs and symptoms used
with MDD. However, 33–50% of individuals with ano- for diagnosis in children and adolescents are identical
rexia nervosa or bulimia nervosa experience a comor- to those used for diagnosis in adults except that irritable
bid mood disorder. Between 50% and 75% of individu- mood can substitute for depressed mood. The sequelae
als with an eating disorder have a history of an MDD of depression in children and adolescents is often char-
over a lifetime. Initial treatment is aimed at the eating acterized by disruption in school performance, social
disorder. If depression continues after proper nourish- withdrawal, increased behavioral disruption, and sub-
ment has been reestablished in anorexia nervosa, treat- stance abuse. Differential diagnosis among children
ment is directed at the primary mood disorder. and adolescents with MDD include behavioral disor-
ders such as conduct disorder, attention deficit hyper-
Personality Disorders. High rates of personality activity disorder, and bipolar disorder.
disorders are found in depressed inpatients and outpa- Later-onset MDD in adolescents is also associated
tients. Most studies report a rate of co-occurrence be- with decline in school performance, social withdrawal,
tween 30% and 40% in outpatients and between 50% or disruptive behavior. The critical differential diag-
and 60% in inpatient samples. Several studies have nostic consideration in adolescents with MDD is the
found that individuals with comorbid MDD and per- misdiagnosis of depression when the clinical presen-
sonality disorder evidence an earlier age of onset for tation will evolve into a diagnosis of bipolar disorder.
the first episode of depression, increased severity of When depression occurs during adolescence, it often
depressive symptoms, more episodes, longer duration heralds a severe disorder with recurrent course, and a
of episodes, poorer response to both pharmacotherapy family history of MDD is often noted. An additional
and psychotherapy, and increased risk for self-injury. psychosocial risk factor in later-onset depression in
adolescence is childhood sexual abuse.
Grief and Bereavement. Depressive symptoms asso-
ciated with normal grieving usually begin within 2 to
Major Depressive Disorder in the Older Adult
3 weeks of the loss and resolve spontaneously over 6 to
8 weeks. If full symptom criteria for MDD persist for Older adults with depression often experience cog-
more than 2 months beyond the death of a loved one, nitive impairment as part of the clinical syndrome.
then an episode of MDD can be diagnosed. Specific Symptoms of depression may simulate dementia with
treatment for a major depressive episode such as short- concentration difficulties, memory loss, and distract-
term psychotherapy focusing on unresolved grief or ibility. Commonly, MDD and dementia co-occur. It
pharmacotherapy is indicated. is less frequent that findings of dementia are fully ex-
plained on the basis of depression (pseudodementia).
The prevalence of MDD in older adults residing in
Depression in Children and Adolescents
nursing homes is estimated to be approximately 30%.
In prepubertal children, MDD occurs equally among MDD in the elderly often co-occurs in the presence of
boys and girls. MDD in childhood is considered to medical conditions, which complicates the treatment
have high recurrence rates with up to 70% recurrence for both the depression and the primary medical con-
in 5 years. After puberty, girls experience an increased dition. Careful evaluation of medications may also re-
rate of depression as compared to boys. There is an veal explanations for associated symptoms of depres-
increased risk of depressive disorder in children and sion. Older adults with first onset of depression must
adolescents when one or more of the parents are de- be carefully evaluated for co-occurring medical condi-
pressed. The earlier the age of onset of depression, the tions. Among the common disorders to be considered
higher the familiar loading. In addition, a number of are silent cerebral ischemic events, undiagnosed can-
childhood psychosocial risk factors have been identi- cer, or complications of metabolic conditions such as
fied to be associated with juvenile-onset MDD. These adult-onset diabetes mellitus and thyroid dysfunction.
risk factors include more perinatal insults, motor skill
abnormalities, instability in caregivers, and psychopa-
TREATMENT
thology in the first-degree relatives. Adolescent-onset
depression often takes on a more chronic course associ- The goals of treatment in MDD are full remission of
ated with dysthymic symptoms. In adolescence, MDD symptoms of depression with restoration of optimal
appears to be associated with greater fatigue, worth- work and social functioning. During the course of treat-
lessness, and more prominent vegetative signs, while ment, ongoing education of the individual and family
regarding remission, relapse, and recurrence is critical. psychotherapy, interpersonal psychotherapy, or short-
This education alerts both those affected by the illness term dynamic psychotherapy. In these forms of psy-
and their families to the early signs of relapse and can chotherapy, which have been studied to address mild
assist in prevention of recurrence. Improved social and to moderate nonbipolar depressive disorder, the focus
work functioning following an episode of depression is of the psychotherapy is very clearly explicated to the
an important associated goal of treatment. Many stud- individual before the initiation of the psychotherapy.
ies have demonstrated the benefit of depression-specific For severe depressive disorder with melancholic or
psychotherapy as an important aspect of maintaining psychotic features, these specific forms of short-term
remission and improving work and social functioning. psychotherapy may not be as effective as focused phar-
The establishment of a collaborative working relation- macotherapy. Pharmacotherapy, in these conditions, is
ship among the individual with depression, the family, associated with more rapid treatment response than is
and the clinician is an essential aspect of recovery. psychotherapy.
All treatment, whether pharmacotherapy or psy- During the acute phase of treatment for depressive
chotherapy or the integration of pharmacotherapy and disorder, the optimal treatment should result in reso-
psychotherapy, first requires a well-established diag- lution of depressive signs and symptoms any time be-
nostic formulation in order to achieve optimal response tween week 8 and week 16 of treatment. If resolution
to treatment. As the diagnostic process is undertaken, of depressive signs and symptoms does not occur dur-
an ongoing therapeutic alliance must be established. In ing the first 2 to 4 months, then the initial diagnostic
the treatment of MDD, an understanding of the clinical formulation must be reviewed and alternative treatment
history of each individual’s distress is necessary. As the strategies must be introduced. Some of the factors asso-
clinical history is elicited, the appropriate target signs ciated with lack of complete treatment response include
and symptoms of MDD are obtained and the individual the presence of co-occurring personality disorders,
is educated as to the nature of the symptom patterns concurrent alcohol or substance abuse, a poor thera-
that represent his or her unique form of depressive peutic alliance leading to lack of adherence to treat-
disorder. ment recommendations, and persistent or unfavorable
The phases of treatment include: side effects of treatment.
When acute phase treatment does lead to remission
1. An acute phase directed at reduction and elimina- of signs and symptoms, then the next phase of treatment
tion of depressive signs and symptoms, and active begins. This phase of treatment is termed continuation
restoration of psychosocial and work functioning. treatment and its goal is prevention of relapse. It is
2. A continuation phase directed at prevention of re- often necessary to maintain ongoing pharmacotherapy
lapse and reduction of recurrence through ongoing for 6 to 12 months after an acute episode of depres-
education, pharmacotherapy, and depression-spe- sion during this continuation phase, because there is
cific psychotherapy. substantial vulnerability to relapse if medication treat-
3. A maintenance phase of treatment directed at pre- ment is prematurely interrupted. During the continua-
vention of future episodes of depression based upon tion phase, ongoing psychotherapy may be particularly
the individual’s personal history of relapse and important to address residual symptoms of depression
recurrence. and to alert the individual to a depressive response to
subsequent traumatic circumstances; ongoing clinical
Acute phase treatment may involve all interventions interaction with significant others is required as well in
that are directed toward decreasing signs and symptoms order to address persisting interpersonal conflicts, and
of depression and maintaining the individual’s capacity may promote even more complete recovery from the
to work and interact with others in a manner consistent depressive episode. The continuation phase of treat-
with premorbid levels of social and work functioning. ment typically lasts 9 to 12 months to minimize the
The acute phase treatments may include supportive risk of recurrent episode. If this represents the initial
psychotherapy focusing on resolution of current dis- episode of depression, then medication treatment may
putes. A form of supportive therapy may be combined be carefully withdrawn at the end of the continuation
with recommendations for pharmacotherapy. The phase. However, if this represents a history of recur-
standard pharmacotherapies that are available for treat- rence of depression (particularly two or more episodes
ment of depression have increased dramatically in the in the preceding 3 years), maintenance treatment may
past two decades. In mild to moderate depressive disor- well be recommended. In addition, maintenance treat-
der, more depression-specific forms of psychotherapy ment is recommended if two prior episodes have oc-
have been established, including cognitive–behavioral curred within one’s lifetime.
Maintenance treatment of MDD is focused on pre- general medical condition as well as the associated
vention of future episodes of depression, after a re- mental disorder.
cent recurrence of MDD and a prior history of two or
more episodes of MDD. Often, the maintenance phase
Pharmacotherapy and Other
of treatment involves ongoing treatment with antide-
Somatic Treatment
pressants or alternatively mood-stabilizing treatment
(particularly lithium carbonate), or a combination to Treatment during the acute phase with medication is
sustain recovery from depression. When there is early highly efficacious in reducing signs and symptoms of
onset (adolescent onset) of depressive symptoms with MDD. Antidepressant medication has the most specific
associated psychosocial impairment, then ongoing effect on reduction of symptoms and is often associ-
maintenance treatment along with rehabilitative psy- ated with improved psychosocial functioning. When
chotherapy may be most critical. During maintenance symptoms of depression are mild to moderate, a course
treatment, continuing education of the individual and of depression-specific psychotherapy without medicine
family, identification of prodromal symptoms, and con- may also be effective. If symptoms of depression are
tinuing efforts at work and psychosocial rehabilitation moderate to severe, acute phase treatment with medica-
are indicated. Often, the trials of maintenance phar- tions is often indicated. A wide variety of antidepres-
macotherapy in depression demonstrate the preventive sant medications have been documented as effective in
benefit of maintenance medication. In the study quoted moderate to severe MDD.
most often, recurrence rates of 20–25% were found in The range of treatments available in the United
individuals maintained with full dose of imipramine, States has included the tricyclic antidepressants avail-
while the recurrence rate was 80–100% in those indi- able since the 1960s, MAOIs available since the late
viduals treated with placebo. The advantage of ongoing 1950s, heterocyclic antidepressants available since
maintenance medicine has also been demonstrated at the 1970s, and between 1989 and until the present,
5 to 10 years. With tricyclic antidepressants, mainte- newer SSRIs have been available. In addition, anti-
nance medication is likely more effective at full dose depressants with both serotonergic and noradrenergic
rather than lower doses. Limited data exists as to the activity or noradrenergic activity alone have become
dosing of SSRIs or other types of antidepressants in available in the 1990s. Clearly, clinical trials compar-
maintenance treatment. ing the efficacy of newer treatments with standard tri-
The site of treatment for MDD is based upon the se- cyclic antidepressants have shown equal efficacy with
verity of the acute episode and the clinician’s judgment improvement in overall tolerance to side effects with
of the individual’s potential for suicide. Individuals newer treatments.
with mild to moderate depression are often treated in Antidepressant medications that are currently
primary care or specialty office settings. Acute phase available for acute treatment of MDD are listed in
pharmacotherapy involving antidepressant medication (Table 26-2).
is often initiated by a primary care physician. How- Choice of treatment with a specific antidepressant
ever, the overall longitudinal care of MDD in primary treatment in a given clinical situation is based on prior
care is the subject of increasing attention. Typically, treatment response to medication, consideration of po-
individuals do not receive treatment for long enough tential side effects, history of response to medicines in
periods and there is limited attention to the domains of first-degree relatives, and the associated presence of
social or work functioning. The referral to a psychia- co-occurring mental disorders that may lead to a more
trist may include a request for more expertise regard- specific choice of antidepressant treatment. Table 26-3
ing medication as well as the need for depression-spe- illustrates an algorithm developed for pharmacotherapy
cific psychotherapy. In addition, there has been a lack of MDD, which includes a staged trial of newer medi-
of focused attention to the role of integrated psycho- cations (because of their superior side-effect profiles)
therapy and pharmacotherapy in primary care. Inpa- followed by treatments with older medicines available
tient treatment for depression is recommended when for the treatment of MDD. The ultimate goal of phar-
there is an immediate risk for suicide or recent suicide macotherapy is complete remission of symptoms dur-
attempt. In these settings, safety of the individual is ing a standard 6- to 12-week course of treatment.
the primary concern and often, more intensive treat-
ments including electroconvulsive therapy may be Selective Serotonin Reuptake Inhibitors. The most
initiated. When there are comorbid general medical commonly prescribed antidepressant medicines in
conditions and mental disorders, inpatient psychiatric the past 10 years are SSRIs. They are selectively ac-
hospitalization may be useful in stabilizing both the tive at serotonergic neurochemical pathways and are
Table 26-2 Antidepressant Medications Category

Category Side Effects
Hypotension
Usual (Decreased Anticholinergic Cardiac
Therapeutic Blood (i.e., Dry Mouth, (Slowed Heart
Trade Name Compound Dose (mg) Sedation Pressure) Constipation) Rate)
Tricyclics
Tertiary amines
Anafranil Clomipramine 150–300 High High High Yes
Elavil Amitriptyline 150–300 High High High Yes
Sinequan Doxepin 150–300 High Moderate Moderate Yes
Surmontil Trimipramine 150–300 High Moderate Moderate Yes
Tofranil Imipramine 150–300 Moderate High Moderate Yes
Norpramine Desipramine 100–300 Low High Low Yes
Pamelor Nortriptyline 50–150 Moderate Low Low Yes
Vivactil Protriptyline 20–60 Low Low High Yes
Monoamine
Oxidase inhibitors
Marplan Isocarboxazid 30–60 Low Moderate Low Low
Nardil Phenelzine 45–90 Low Moderate Low Low
Parnate Tranylcypromine 30–90 Low Moderate Low Low
Atypical agents
Ascendin Amoxapine 200–300 Low Moderate Low Yes
Desyrel Trazodone 300–600 High High Minimal Low
Ludiomil Maprotiline 150–200 Moderate Moderate Low Low
Wellbutrin Bupropion 150–450 Minimal Low Minimal Yes
Selective
serotonin
reuptake
inhibitors
Paxil Paroxetine 20–50 Low Minimal Minimal Low
Prozac Fluoxetine 20–100 Minimal Minimal Minimal Low
Zoloft Sertraline 50–300 Minimal Minimal Minimal Low
Luvox Fluvoxamine 150–400 Low Low Low Low
Celexa Citalopram 20–50 Minimal None None Minimal
Lexapro Escitalopram 10–30 Minimal None None Minimal
Serotonin/
norepinephrine
reuptake
inhibitors
Effexor Venlafaxine 75–450 Low None None Minimal
Cymbalta Duloxetine 30–60 Low None None Minimal
Alpha-2-
adrenergic
antagonist
Remeron Mirtazapine 30–60 Moderate Low Minimal Minimal
effective in mild to moderate nonbipolar depression. is taking other medications for primary medical con-
They may also be particularly effective in MDD with ditions or associated mental disorders. The currently
atypical features as well as DD. Often, these treatments available SSRIs in the United States include fluoxet-
are well tolerated and involve single daily dosing for ine (Prozac), paroxetine (Paxil), sertraline (Zoloft),
MDD. Because of selective serotonergic activity, these fluvoxamine, citalopram (Celexa), and escitalopram
treatments have also been demonstrated to be effec- (Lexapro).
tive with co-occurring OCD, panic disorder, general-
ized anxiety disorder, PTSD, premenstrual dysphoric Other Newer Antidepressants. In addition to SS-
disorder, bulimia nervosa, and social anxiety disorder RIs, greater attention has been brought to medicines
as well as MDD. They tend to be reasonably well tol- with dual noradrenergic and serotonergic pathways,
erated in individuals with comorbid medical condi- including venlafaxine (Effexor XR) and duloxetine
tions. There are particular medication-specific inter- (Cymbalta). In addition, an alpha-2-adrenergic agonist,
actions based on inhibition of cytochrome P-450 liver mirtazapine (Remeron) has become available. A pre-
enzyme systems that require attention if an individual dominantly noradrenergic and dopaminergic agonist,
Table 26-3 Pharmacotherapy Algorithm in Major Depressive Disorder
Major Depressive Disorder, Single or Recurrent Episode, without Psychotic Features

Begin effective monotherapy with bupropion SR, citalopram, escitalopram, fluoxetine, nefazodone, paroxetine, sertraline,
venlafaxine XR, or duloxetine (augment with lithium carbonate 600–900 mg).
or
Begin effective monotherapy with alternative antidepressant from list above (augment with bupropion SR, mirtazapine, or tricyclic
antidepressant, either nortriptyline or desipramine, recognizing important drug interactions.
If ineffective, consider tranylcypromine, augmented with lithium carbonate, if necessary, for anergic features.
or
Consider phenelzine, augmented with lithium carbonate, if necessary, for anxious, dependent, and phobic features.
Augment with atypical antipsychotics for agitation, rumination, or suspicion.
or
Offer electroconvulsive therapy to remission (ECT).
Major Depressive Disorder, Single or Recurrent Episode, with Psychotic Features
Begin typical or atypical antipsychotic to adequate doses in order to interrupt delusional features, augmented with SSRI,
venlafaxine XR, or tricyclic antidepressants, either nortriptyline or desipramine, recognizing important drug interactions.
or
Begin amoxapine as alternative.
or
Begin electroconvulsive therapy as alternative, in context of immediate suicide risk, physical deterioration, or prior response to
electroconvulsive therapy
Major Depressive Disorder with Atypical Features
Begin SSRI starting at low dose to minimize early side effects.
or
Begin MAOI, either phenelzine or tranylcypromine, to therapeutic doses.
Major Depressive Disorder with Catatonic Features
Begin lorazepam 1–3 mg/d, to interrupt catatonic symptoms; evaluate for presence of psychotic features or longitudinal history of
bipolar disorder.
Add antipsychotic medication to therapeutic doses or lithium carbonate to therapeutic doses, if bipolar or schizoaffective disorder
emerges from the longitudinal history.
bupropion (Wellbutrin), is also available in an imme- interpersonal rejection sensitivity. MAOIs continue to
diate release, sustained release (SR), and extended re- have a significant role in treatment of comorbid panic
lease (XL) preparation. disorder, social phobia, and agoraphobia if individuals
are not responsive to SSRIs. The ongoing prescription
Tricylic Antidepressants. Tricyclic antidepressants of phenelzine (Nardil) or tranylcypromine (Parnate) re-
have been best studied in individuals with MDD with quires continued education of the individual regarding
melancholic features and with psychotic features. The standard food interactions involving tyramine as well
combination of typical antipsychotic pharmacotherapy as specific drug–drug interactions involving sympatho-
in association with tricyclic antidepressants has been mimetic medications. These cautions regarding diet
recommended. The side-effect profile of tricyclic anti- and drug interaction make MAO inhibitors less attrac-
depressants has included moderate to severe sedation, tive to primary care physicians and most psychiatrists.
anticholinergic effects including constipation, and However, they continue to be effective treatments that
cardiac effects, which has made these medicines less may be useful in depression with atypical features as
popular in typical primary care or psychiatric prac- well as anergic bipolar depression.
tice. Nevertheless, the secondary amines that are me-
tabolites of imipramine and amitriptyline, specifically General Recommendations. Increasingly, a trial of
desipramine and nortriptyline, have continued to be one class of antidepressants may be associated with
useful agents in more refractory depression. incomplete response, leading to a question of augment-
ing a treatment with another medicine versus switching
Monoamine Oxidase Inhibitors. There continues from one medicine to another within the same class or
to be a role for the use of MAOIs in individuals with to a different class altogether.
MDD with atypical features. These agents may be par- All of the antidepressant medications used in the
ticularly useful in intervention in depressive episodes treatment of MDD must be prescribed in the context
with atypical features, characterized by prominent of an overall clinical relationship characterized by sup-
mood reactivity, reverse neurovegetative symptom pat- portive interaction with the individual and family and
terns (i.e., overeating and oversleeping), and marked ongoing education about the nature of the disorder and
its treatment. Clinical management optimally involves responders to responders if drug treatment is increased
careful monitoring of symptoms using standardized to full doses. This time allows for evaluation of the role
instruments and careful attention to side effects of of focused psychotherapy to address residual interper-
medication in order to promote treatment adherence. sonal disputes, loss or grief, or ongoing social deficits.
Outpatient visits, which may be scheduled weekly at the The associated augmentation strategies to standard
outset of treatment, and subsequently biweekly, encour- treatments include lithium carbonate augmentation,
age and sustain collaborative treatment relationships. tricyclic antidepressant augmentation of SSRIs, thyroid
These office consultations allow the clinician to make hormone augmentation, and bupropion augmentation
dosage adjustments as indicated, monitor side effects, of SSRIs.
and measure clinical response to treatment.
For the majority of individuals with MDD, a course Electroconvulsive Therapy. Electroconvulsive ther-
of 6 to 8 weeks of acute treatment with weekly outpa- apy (ECT) remains an effective treatment in individuals
tient visits is indicated. Subsequent office visits may be with severe MDD and those individuals with psychotic
scheduled every 2 to 4 weeks during the continuation MDD. Many individuals who have responded to ECT
phase of treatment. Appropriate adjustments of dose do not respond to pharmacotherapy. There is increased
are determined by the psychiatrist as indicated by best need for understanding the role of maintenance ECT
clinical judgments of medication effect. Optimal dos- in those individuals who respond to ECT because on-
ing ranges of SSRIs, tricyclics, and MAOIs are noted in going pharmacotherapy does not always prevent recur-
Table 26-2. Because of the early anxiety, agitation, and rence of depression after ECT is successful. ECT can
occasional insomnia associated with SSRIs, somewhat be particularly useful in interrupting acute suicidality
lower doses may be initiated early in the course before for those individuals who may require rapid resolution
achieving the typical standard therapeutic dose. of symptoms. ECT may be indicated in older adults
Incomplete response, which entails the failure to when lack of self-care and weight loss may represent
respond to acute treatment with an antidepressant medi- a greater risk. The most common side effect associated
cation at 6 to 8 weeks, requires reassessment of diagno- with ECT is amnesia for the period of treatment. There
sis and determination of adequacy of dosing. Ongoing is no consistent evidence to suggest chronic cognitive
substance abuse, associated general medical condition, or memory impairment as a result of ECT.
or concurrent mental disorder may partially explain a
lack of complete response. If substance dependence Other Somatic Treatments. Light therapy investiga-
is present, a full substance-free interval (preferably tors have continued to demonstrate benefit in individu-
4 weeks or longer) with appropriate detoxification and als with seasonal MDD by providing greater than 2500
rehabilitation may be indicated. If a reassessment dis- lux light therapy for 1 to 2 hours/day. Many of these
closes an associated mental disorder, then more specific individuals experience recurrent winter depression in
treatment of that associated disorder, whether it be bi- the context of a recurrent MDD or bipolar II disorder.
polar disorder or concurrent posttraumatic disorder, is Bright light exposure has been associated with favo-
necessary. If the reassessment suggests an associated rable response within 4 to 7 days. As with ECT, light
comorbid personality disorder, then appropriate and therapy is best prescribed by specialists who have ex-
more specialized psychotherapy may be necessary in perience in its use and can appropriately evaluate the
order to achieve a complete response to treatment. As indication for light therapy and monitor carefully the
indicated before, if the MDD has psychotic features, response to treatment.
then antipsychotic pharmacotherapy to adequate doses Ongoing investigation of alternative brain stimula-
must be initiated prior to initiating a course of stand- tion techniques have been the subject of recent investi-
ard tricyclic antidepressants or a combined serotonin gation. The use of a powerful magnet to provide tran-
norepinephrine uptake inhibitor such as venlafaxine or scranial magnetic stimulation has been the subject of
duloxetine. If MDD is associated with severe personal- several open trials. It is not yet determined whether the
ity disorder (e.g., borderline personality disorder), then repetitive transcranial magnetic stimulation demon-
adjunctive psychotherapy and low dose antipsychotic strates its effectiveness through reduction of inhibitory
medications may be necessary. If the individual has neurotransmission or other mechanisms.
severe melancholic, delusional, or catatonic features, a Vagus nerve stimulation (VNS), which has been
course of electroconvulsive therapy may be necessary found to be effective in epilepsy, has been approved by
to achieve remission of symptoms. the FDA for the treatment of recurrent MDD that has
There is also evidence that continuation of treat- not responded adequately to four or more antidepressant
ment beyond 6 to 12 weeks may convert some partial treatments. This procedure requires the implantation of
a stimulating device in the chest with the capacity to psychotherapy, and medication treatment were com-
stimulate the vagus nerve at regular intervals through parable on several outcome measures and superior to
the course of the day. The most common side effects placebo. Medication treatment was associated with the
from VNS therapy include hoarseness, a prickling feel- most rapid response and was superior to both interper-
ing on the skin, and increased coughing. These side sonal psychotherapy and cognitive–behavioral therapy
effects tend to diminish over time. Although only a in more severely depressed individuals. Continua-
third of patients responded to VNS (i.e., at least a 50% tion studies with interpersonal psychotherapy offered
improvement in their depression after a year of use), monthly as well as during maintenance treatment have
the fact that these patients responded to VNS and to no demonstrated response in prevention of recurrence,
other treatments persuaded the FDA to grant approval and was superior to placebo treatment. Those individu-
after initially rejecting the treatment. als who received ongoing interpersonal psychotherapy
and medication had the longest intervals without recur-
rence of depressive symptoms.
Psychosocial Treatment
The past decade has also led to the development of Cognitive–Behavioral Therapy. Cognitive–behavio-
more specific depression-based treatment for MDD. ral therapy for depression is a form of treatment aimed
These treatments have included supportive psychiat- at symptom reduction through the identification and
ric management techniques during pharmacotherapy, correction of cognitive distortions. These involve nega-
interpersonal psychotherapy, cognitive–behavioral tive views of the self, one’s current world, and the fu-
therapy, brief dynamic psychotherapy, and marital and ture. Several controlled studies have demonstrated the
family therapy. efficacy of cognitive therapy in resolution of MDD in
Clinical management and supportive psychotherapy adults. Cognitive–behavioral therapy as well as inter-
is the standard in office practice. The clinician focuses personal psychotherapy is generally considered to be
on establishing a positive therapeutic relationship in somewhat less effective than medication treatment in
the course of diagnosis and initiation of treatment of moderate to severe MDD. However, some investigators
depression. The clinician is attentive to all signs and have suggested a relatively equal response to cogni-
symptoms of the disorder, particularly suicidality. The tive–behavioral therapy and medication in more se-
clinician provides ongoing education, collaboration verely depressed outpatients.
with the individual, and supportive feedback to the
individual regarding ongoing response and progno- Brief Dynamic Psychotherapy. Brief dynamic psy-
sis. The supportive psychotherapeutic management of chotherapy addresses current conflicts as manifesta-
depression facilitates the ongoing pharmacologic re- tions of difficulty in early attachment and disruption of
sponse. Brief supportive psychotherapy in individuals early object relationships. Brief dynamic psychotherapy
with mild to moderate depression is indicated to im- was not specifically designed for treatment of MDD
prove medication compliance, to facilitate reduction of and is currently the subject of ongoing studies as well
active depressive signs and symptoms, and to provide as controlled clinical trials in comparison with medica-
education regarding relapse and recurrence. tion treatment. The results of these trials will allow us
to address the appropriate role of brief dynamic psy-
Interpersonal Psychotherapy. Interpersonal psycho- chotherapy in outpatients with mild to moderate de-
therapy in nonhospitalized individuals with nonbipolar pression. In addition, it will be important to understand
MDD has been demonstrated to be effective in acute whether dynamic psychotherapy may address demor-
treatment trials. Interpersonal psychotherapy of de- alization or response to traumatic circumstances.
pression addresses four areas of current interpersonal
difficulties: (1) interpersonal loss or grieving; (2) role Martial and Family Therapy. It has been difficult to
transitions; (3) interpersonal disputes; and (4) social assess the specific efficacy of marital or family therapy
deficits. This type of treatment, like other psychothera- in individuals with MDD based on current studies to
pies for depression, also involves education about the date. There is substantial evidence that marital distress
nature of MDD and the relationship between symp- is a major event associated with the development of
toms of depressive disorder and current interpersonal a depressive episode. Marital discord often will per-
difficulties. sist after the remission of depression and subsequent
Prior studies demonstrated efficacy of interper- relapses are frequently associated with disruptions
sonal psychotherapy for outpatients with depression. of marital relationships. Both acute and continuation
Interpersonal psychotherapy, cognitive–behavioral phase treatment of MDD will require ongoing attention
to marital and family issues to prevent recurrence of in particular, are unlikely to be effective in such
depression. individuals.
Severity. Individuals with mild to moderate depres-

Factors Influencing Treatment Response
sion may be effectively treated with psychotherapy,
There are a number of factors that influence ultimate pharmacotherapy, or the combination. Individuals with
treatment response in MDD, including individual severe MDD almost always require somatic interven-
characteristics, diagnostic issues, comorbidity, treat- tion with antidepressant medication or electroconvul-
ment-related complications including side effects, and sive therapy.
demographic factors. Reevaluation of diagnosis, co-
morbidity, and the clinician–patient relationship itself Recurrence. Because MDD is a recurrent disorder,
is often critical. current treatment guidelines suggest maintenance anti-
depressant treatment at full therapeutic doses if there is
Suicide Risk. Individuals with MDD are often at in- a history of more than two prior episodes of MDD.
creased risk for suicide. Suicidal risk assessment is es-
pecially indicated as individuals begin to recover from History of Hypomania or Mania. Any of the anti-
depression with increased energy and simultaneous depressant treatments including medication, ECT, light
continued despair. Persistent suicidal ideation coupled therapy, or newer somatic interventions may induce
with increased energy can often lead to impulsive sui- hypomania or mania in individuals who are vulner-
cidal acts. The careful attention to the clinician–patient able to bipolar disorder. Individuals who may have a
relationship can mediate suicidal urges through avail- family history of bipolar disorder should be carefully
ability and accessibility. Outpatients and inpatients evaluated for treatment with lithium carbonate or other
with MDD and melancholic features will often require anticonvulsant mood stabilizers before antidepressant
antidepressant therapy addressing multiple neurotrans- treatment because they are at particular risk for anti-
mitter systems, or ECT as well. depressant-induced mania. Attention to this history of
prior hypomania or mania as well as family history
Psychotic Features. MDD with psychotic features re- may promote treatment response if such individuals
quires careful assessment to rule out comorbid mental have mood-stabilizing treatment offered initially.
disorders. The combined treatment with antipsychotic
as well as antidepressant medication is indicated. Comorbidity with Alcohol or Substance Depen-
In addition, ECT is an effective intervention in psy- dence. The comorbidity of MDD and alcohol or other
chotic depression and may be considered as a first-line substance dependence requires careful attention to both
alternative. diagnoses. The first priority in treatment is abstinence
from alcohol or substance use. Co-occurring addic-
Catatonic Features. MDD with catatonic features can tion will complicate depressive disorders and increases
be associated with significant morbidity owing to the risk for suicide. If detoxification from alcohol or other
individual’s refusal to eat or drink. Active treatment substance abuse is required, this should be undertaken
with a benzodiazepine such as lorazepam 1 to 3 mg before initiation of any somatic antidepressant therapy.
daily may offer short-term treatment response. Sub- Individuals who have a family history of depression
sequent treatment with lithium alone or in association or bipolar disorder are likely to require early initia-
with antidepressants may be indicated given the possi- tion of appropriate mood disorder treatment following
ble link between catatonic features and bipolar vulner- detoxification.
ability. If psychosis is associated with catatonia, then
atypical antipsychotic medication or a course of ECT Comorbidity with Obsessive–Compulsive Disorder.
may be indicated as well. In individuals with OCD, lifetime risk of MDD ap-
proaches 70%. The use of higher dose SSRI treatment
Atypical Features. Atypical features are associated is often indicated to treat both conditions. Alternatively,
with significant comorbid anxiety disorders, reverse the tricyclic antidepressant, clomipramine (Anafranil),
neurovegetative symptoms such as hypersomnia, in- may be effective for those individuals with both OCD
creased appetite, and weight gain, as well as fatigue and MDD who do not respond to SSRIs.
and leaden paralysis. SSRIs are likely to be effective
in individuals with MDD with atypical features as Comorbidity with Panic Disorder. Lifetime risk
well as MAOIs. Conversely, tricyclic antidepressants, of MDD approaches 50% in individuals with panic
Staging Criteria for Treatment-Resistant

switching to alternative somatic treatments including
Table 26-4 ECT when indicated.
Depression
Stage Description
Refractory MDD is ameliorated in the context
of a caring and collaborative treatment relationship
1. Failure of at least one adequate trial of an based on a favorable therapeutic alliance. Sometimes,
antidepressant
2. Stage 1 resistance plus failure of adequate individuals will undermine treatment through their
trial of an antidepressant from a distinctly own persistent use of substances such as alcohol or lack
different class than in Stage 1 of adherence to specific pharmacotherapy recommen-
3. Stage 2 resistance plus failure of an adequate
trial of a tricyclic antidepressant (TCA) dations. In this context, the attention to the therapeutic
4. Stage 3 resistance plus failure of an adequate alliance is particularly critical. In assessing an individ-
trial of a monoamine oxidase inhibitor ual with refractory symptoms, pharmacologic factors,
(MAOI)
5. Stage 4 resistance plus failure of a course of including pharmacokinetic considerations, drug–drug
bilateral electroconvulsive therapy (ECT) interactions, and extreme sensitivity to antidepressant
drugs, must be considered.
Despite many alternative strategies, substantial mor-
disorder. Because many of the SSRIs and other antide- bidity and occasional mortality are associated with re-
pressants are effective treatments to treat panic as well fractory MDD. In addition, careful attention to psycho-
as depression, these treatments have gained increasing social factors associated with refractoriness is critical.
popularity. One may continue to prescribe short-term These psychosocial factors include early childhood ad-
courses of benzodiazepines, including lorazepam or versity and abuse, early family dysfunction, increased
clonazepam to alleviate acute symptoms of panic, as neuroticism, and marked disruption in the development
low doses of antidepressant treatments are introduced of a stable sense of self.
into the treatment for comorbid panic and MDD. In ad-
dition, MAOIs continue to be effective treatments for
Dysthymic Disorder
both panic and MDD.
DIAGNOSIS
Refractory Major Depressive Disorder
Dysthymic disorder is defined by the presence of
A staging system for treatment-resistant depression chronic depressive symptoms most of the day, more
(TRD) has been proposed, ranging from failure to days than not, for at least 2 years (see DSM-IV-TR di-
respond to a single agent (Stage 1) to failure of multi- agnostic criteria for Dysthymic Disorder, page 272).
ple treatments and ECT (Stage 5), and is presented in While chronic depressive conditions were traditionally
Table 26-4. The term refractory depression has been conceptualized as characterological and amenable to
proposed to describe individuals who have Stage 5 psychotherapy and resistant to pharmacotherapy, re-
TRD. cent pharmacologic trials of antidepressants as well as
Refractory MDD or Stage 5 in this table is estimated depression-specific psychotherapy have demonstrated
to occur in up to 20% of individuals. A larger percent- effectiveness in the overall treatment of DD. Both
age of individuals with MDD, up to 30%, may show focused interpersonal and variations of cognitive–
only partial improvement. The concept of treatment- behavioral psychotherapy have demonstrated response
resistant depression or refractory depression describes in dysthymia. Individuals with DD have a substantial
this lack of response to a number of clinical trials us- risk for the development of MDD. This highlights the
ing optimal dosing and duration of antidepressant importance of early assessment and treatment to mini-
medication. One must typically offer the individual a mize subsequent long-term complications.
rational series of treatment trials using optimal dos- If signs and symptoms of DD follow an MDD, then
ing and duration of each antidepressant. An individual a diagnosis of MDD, in partial remission, is made. A
is considered refractory if a course of three, four, or diagnosis of DD can be made if the individual develops
five treatments is offered without substantial clinical full remission of MDD for 6 months and subsequently
response. The standard approach to the management develops signs and symptoms of DD, which then last
of refractory depression includes increasing the antide- a minimum of 2 years. In contrast, the diagnosis of
pressant dose and monitoring for a full 8- to 12-week chronic MDD is made when an episode of MDD meets
course, augmenting the treatment with several aug- full criteria for MDD continuously for at least 2 years.
mentation strategies using an adequate combination of If DD has been present for at least 2 years in adults (or
antidepressant drug treatment and psychotherapy and 1 year in children and adolescents) and is subsequently
onset—if the onset of dysthymic symptoms occurs at

DSM-IV-TR Diagnostic Criteria age 21 or older, and With Atypical Features.
300.4 DYSTHYMIC DISORDER
Atypical features refer to a pattern of symptoms that
include mood reactivity and two of the additional atyp-
A. Depressed mood for most of the day, for more days ical symptoms (i.e., weight gain or increased appetite,
than not, as indicated either by subjective account or
by observation by others, for at least 2 years. hypersomnia, leaden paralysis, or interpersonal rejec-
tion sensitivity). Early-onset DD is usually associated
Note: In children and adolescents, mood can be irritable
and duration must be at least 1 year. with subsequent episodes of MDD. DD with atypical
B. Presence, while depressed, of two (or more) of the features may herald a bipolar I or II course.
following: The diagnosis of DD cannot be made if depressive
(1) poor appetite or overeating symptoms occur exclusively during the course of a non-
(2) insomnia or hypersomnia affective psychosis such as schizophrenia, schizoaffec-
(3) low energy or fatigue
(4) low self-esteem
tive disorder, or delusional disorder. Diagnosis of de-
(5) poor concentration or difficulty making decisions pressive disorder NOS is made if there are symptoms
(6) feelings of hopelessness that meet criteria for MDD during the residual phase of
C. During the 2-year period (1 year for children or adoles- a psychotic disorder. If DD is determined to be etiologi-
cents) of the disturbance, the person has never been cally related to a chronic medical condition, then one
without the symptoms in Criteria A and B for more
than 2 months at a time. diagnoses mood disorder due to the general medical
D. No major depressive episode has been present during condition. If substance use is judged to be the etiologic
the first 2 years of the disturbance (1 year for children
and adolescents); i.e., the disturbance is not better ac-
factor, then a substance-induced mood disorder is di-
counted for by chronic major depressive disorder or agnosed. Individuals with DD often have co-occurring
major depressive disorder, in partial remission. personality disorders and in these situations, separate
Note: There may have been a previous major depressive diagnoses on Axes I and II are made.
episode provided there was a full remission (no signifi- Ongoing studies have not completely clarified the
cant signs or symptoms for 2 months) before develop-
ment of the dysthymic disorder. In addition, after the distinction between DD and depressive personality
initial 2 years (1 year in children or adolescents) of dys- disorder. Depressive temperaments may predispose an
thymic disorder, there may be superimposed episodes of individual to a condition within the spectrum of Axis
major depressive disorder, in which case both diagnoses
may be given when the criteria are met for a major de- I mood disorders. However, it may not be specifically
pressive episode. associated with MDD. This depressive temperament
E. There has never been a manic episode, a mixed epi- may also be associated with vulnerability to bipolar
sode, or a hypomanic episode, and criteria have never disorder.
been met for cyclothymic disorder.
F. The disturbance does not occur exclusively during the Individuals with early-onset DD are at substantial
course of a chronic psychotic disorder, such as schizo- risk for development of other mental disorders, in-
phrenia or delusional disorder. cluding alcohol or substance dependence, MDD, and
G. The symptoms are not due to the direct physiologi-
cal effects of a substance (e.g., a drug of abuse, a personality disorders. Up to 15% of individuals with
medication) or a general medical condition (e.g., DD may also have a substance use pattern that meets
hypothyroidism).
H. The symptoms cause clinically significant distress or
criteria for comorbid alcohol or substance dependence
impairment in social, occupational, or other important diagnosis. The most common associated personality
areas of functioning. disorders include mixed, dependent, and borderline
Specify if: personality. Childhood and adolescent-onset DD is as-
sociated with a substantial risk for later occurrence of
Early onset: if onset is before age 21 years
Late onset: if onset is age 21 years or older both MDD and bipolar disorder.
Specify (for most recent 2 years of dysthymic disorder): A lifetime prevalence of 4.1% for women and 2.2%
With atypical features
for men has been reported for DD. In adults, DD is
more common in women than in men. In children, DD
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 occurs equally in both sexes. Across both women and
American Psychiatric Association. men, DD has a 2.5% 12-month prevalence.
followed by a superimposed MDD, then both DD and

Course
MDD are diagnosed, which is often referred to as “dou-
ble depression.” The following specifiers apply to DD Dysthymic disorder often begins in late childhood or
as noted in DSM-IV-TR: Early onset—if the onset of early adolescence and by definition takes a chronic
dysthymic symptoms occurs before age 21; and Late course. The risk for development of MDD among
children who have DD is significant because childhood items (loss of self-esteem has been separated from in-
onset of DD is an early marker for recurrent mood dis- appropriate guilt). Furthermore, ICD-10 provides sepa-
order, both recurrent MDD and bipolar disorder. rate criteria sets for each level of severity of a major
The course of DD suggests impairment in functional depressive episode: a threshold of 4 out of 10 symptoms
status, including social and occupational and physical defines mild, 6 out of 10 symptoms defines moderate,
functioning. Individuals who have both DD and MDD and 8 out of 10 symptoms defines severe. Furthermore,
have more severe functional impairment. Untreated the ICD-10 diagnostic algorithm differs by requiring
DD contributes to significant occupational and finan- that there be at least two of the following three symp-
cial burden. There is substantial reduction in activity, toms—depressed mood, loss of interest, and decreased
more days spent in bed, more complaints of poor gen- energy—for mild and moderate depressive episodes
eral medical health, and more disability days than re- and all three for severe episodes. ICD-10 episodes with
ported in the general population. psychotic features exclude first-rank symptoms and bi-
zarre delusions, which if present would shift the diag-
nosis to schizoaffective disorder.
TREATMENT
The ICD-10 Diagnostic Criteria for Research and
The treatment goals in DD are similar to those in DSM-IV-TR also differ on the threshold for defining
MDD. They include full remission of symptoms and when major depressive disorder is characterized as
full psychosocial recovery. Many individuals who have single episode versus recurrent. ICD-10 specifies that
been enrolled in clinical trials for MDD have an as- there be a period of at least two months free from any
sociated history of DD. Randomized controlled trials significant mood symptoms between mood episodes,
of pharmacotherapy and cognitive–behavior therapy whereas DSM-IV-TR requires an interval of at least
suggest a favorable response to active treatments. The two consecutive months in which full criteria for a ma-
most favorable response occurred in those individuals jor depressive episode have not been met.
treated with both active medication and specific cogni- The ICD-10 definition of dysthymic disorder speci-
tive–behavioral treatments. fies that three items from a list of 11 symptoms (which
include 5 of the 6 DSM-IV-TR items) must accompany
the depressed mood. Furthermore, ICD-10 restricts
co-occurring major depressive episodes to “none or
DIAGNOSTIC CRITERIA
very few” and specifies that dysthymic disorder may
The criteria set for a major depressive episode in ICD-10 follow a depressive episode without a period of full
contains 10 items, in contrast to the nine DSM-IV-TR remission.
CHAPTER
27 Mood Disorders: Premenstrual

Dysphoric Disorder
DIAGNOSIS
Premenstrual syndrome (PMS) is a combination of
DSM-IV-TR Research Criteria
emotional, behavioral, and physical symptoms that
occur in the premenstrual or luteal phase of the men- PREMENSTRUAL DYSPHORIC DISORDER
strual cycle. Diagnostic criteria for PMS often require
a minimum of one premenstrual symptom, such as the A. In most menstrual cycles during the past year, five
(or more) of the following symptoms were present
criteria proposed in the American College of Obstet- for most of the time during the last week of the luteal
rics and Gynecology Practice Guidelines or in the In- phase, began to remit within a few days after the onset
of the follicular phase, and were absent in the week
ternational Classification of Diseases, 10th Revision. postmenses, with at least one of the symptoms being
Approximately 80% of women report at least mild either (1), (2), (3), or (4):
premenstrual symptoms, 20–50% report moderate to (1) markedly depressed mood, feelings of hopeless-
severe premenstrual symptoms, and approximately 5% ness, or self-deprecating thoughts
of women report severe symptoms for several days with (2) marked anxiety, tension, feelings of being “keyed
up,” or “on edge”
impairment of role and social functioning. The 5% of (3) marked affective lability (e.g., feeling suddenly sad
women with the severest form of PMS generally have or tearful or increased sensitivity to rejection)
symptoms that meet the diagnostic criteria for premen- (4) persistent and marked anger or irritability or in-
creased interpersonal conflicts
strual dysphoric disorder (PMDD). (5) decreased interest in usual activities (e.g., work,
Research diagnostic criteria for PMDD are listed in school, friends, hobbies)
(6) subjective sense of difficulty in concentrating
the appendix of DSM-IV-TR. A clinician can indicate (7) lethargy, easy fatigability, or marked lack of
that a woman has symptoms that meet the diagnostic energy
criteria for PMDD by recording the DSM-IV-TR di- (8) marked change in appetite, overeating, or specific
food cravings
agnosis 311, depressive disorder not otherwise speci- (9) hypersomnia or insomnia
fied. To meet the PMDD criteria, at least five out of (10) a subjective sense of being overwhelmed or out
the eleven possible symptoms must be present in the of control
(11) other physical symptoms, such as breast tender-
premenstrual phase; these symptoms should be absent ness or swelling, headaches, joint or muscle pain,
shortly following the onset of menses; and at least one a sensation of “bloating,” weight gain
of the five symptoms must be depressed mood, anxi- B. The disturbance markedly interferes with work or
ety, lability, or irritability. The PMDD criteria require school or with usual social activities and relationships
(e.g., avoidance of social activities, decreased produc-
that role functioning be impaired as a result of the tivity and efficiency at work or school).
premenstrual symptoms. The functional impairment C. The disturbance is not merely an exacerbation of the
reported by women with PMDD is similar in severity symptoms of another disorder such as major depres-
sive disorder, panic disorder, dysthymic disorder, or a
to the impairment reported in major depressive dis- personality disorder (although it may be superimposed
order and dysthymic disorder. Unlike the functional on any of these disorders).
impairment reported in depressive disorders, women D. Criteria A, B, and C must be confirmed by prospective
daily ratings during at least two consecutive sympto-
with severe PMS and PMDD report more disruption matic cycles. (The diagnosis may be made provision-
in their relationships and parenting roles than in their ally prior to this confirmation.)
work roles. Reprinted with permission from the Diagnostic and Statistical
The PMDD criteria require that a woman prospec- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
tively rate her emotional, behavioral, and physical
Chapter 27 • Mood Disorders: Premenstrual Dysphoric Disorder 275
symptoms over two menstrual cycles to confirm the the clinician should also assess premenstrual functional
diagnosis. Several studies have reported that retro- impairment (Figure 27-1). Ratings that demonstrate fol-
spective reports of premenstrual symptoms may inac- licular symptoms with increased symptom severity in
curately identify the timing or amplify the severity of the premenstrual phase suggest “premenstrual exacerba-
symptoms compared to prospective reporting. Chart- tion” of an underlying disorder rather than PMDD. The
ing two menstrual cycles is advantageous, since some DSM-IV-TR PMDD criteria state that the premenstrual
women have variability of symptom severity from cy- symptoms should not be an exacerbation of an underly-
cle to cycle due to factors such as seasonal worsening, ing disorder, but that PMDD could be superimposed on
or a woman might have the unusual presence of follicu- another disorder, like panic disorder. No formal guide-
lar phase psychological symptoms due to a transient lines exist on how to apply this criterion clinically.
stressor. Studies of PMDD tend to utilize visual analog Irritability has been identified as the most common
scales, or Likert scale daily rating forms such as the premenstrual symptom in US and European samples.
Daily Record of Severity of Problems, with a scoring Studies have suggested some genetic liability for PMS,
method that compares the average of symptom scores but the overlap with genetic liability for major depression
during the premenstrual days to the average of symp- or personality characteristics has received mixed reports.
tom scores postmenses. Elevated lifetime prevalence of major depressive disorder
A woman presenting with PMS should ideally bring in women with PMDD has been reported in several stud-
to her clinician two cycles of an established daily rating ies, as well as an elevated lifetime prevalence of postpar-
form, or alternatively ratings of her most problematic tum depression. Even though premenstrual symptoms are
symptoms, rated with anchor points ranging from “not described in women from menarche to menopause, it is
present” to “severe.” The clinician should review the unclear if symptoms remain stable or increase in severity
daily ratings to confirm that the symptoms are in fact with age. PMS has been described in several countries
confined largely to the premenstrual phase, with the rel- and cultures and some cultures have a preponderance of
ative absence of symptoms in the follicular phase, and somatic rather than emotional symptoms.
Woman with regular menstrual cycles

presents with premenstrual symptoms
R/O Axis I psychiatric disorder

R/O medical disorder
Give daily rating forms for 2 cycles
Review daily rating forms for

timing of symptoms with cycle phase
severity of premenstrual symptoms
absence of follicular symptoms
impaired premenstrual functioning
Severe premenstrual Mild or moderate premenstrual Continuous symptoms with Symptoms not related
symptoms and impaired symptoms without follicular symptoms or without premenstrual to menstrual cycle
functioning without and no impairment of functioning exacerbation of symptoms
follicular symptoms
Reevaluate
Mild or moderate PMS Chronic psychiatric or medical
disorder with or without Consider
PMDD or severe PMS premenstrual exacerbation psychotherapy
Psychosocial treatments
Specific symptom treatment
Pharmacotherapy Pharmacotherapy Treat underlying condition first
Figure 27-1 Diagnosis and initial treatment algorithm of premenstrual symptoms.

Differential Diagnosis recommended for the treatment of major depressive

disorder (Figure 27-2). The efficacy of the continuous
Depression and anxiety disorders are the most common
(daily) dosing and intermittent dosing (SSRI admin-
Axis I mental disorders that may be concurrent and
istered during the luteal phase only from ovulation to
exacerbated premenstrually, with less clear evidence
menses) is considered to be equivalent. There have not
for bipolar disorder, eating disorders, and substance
been reports of discontinuation symptoms from doses
abuse. Since most PMDD symptoms are affective or
of fluoxetine (10 mg/day during luteal phase) and ser-
anxiety-related, “pure PMS” or PMDD is generally not
traline (50–100 mg/day during luteal phase) when they
diagnosed when an underlying depression or anxiety
were abruptly stopped from the first day of menses.
disorder is present; these women would be considered
The efficacy of intermittent dosing, as well as the find-
to have premenstrual exacerbation of their underlying
ings from most SSRI trials that efficacy is achieved by
depression or anxiety disorder. Personality disorders
the first treatment cycle, has suggested a more rapid
are not elevated in prevalence in women with PMDD,
and different mechanism of action of SSRIs in PMDD
but women with PMDD and a personality disorder
compared to its effect in major depressive disorder
may demonstrate premenstrual phase amplification
that typically takes two to six weeks. Studies have
of personality dysfunction. Schizophrenia may be an
also shown that venlafaxine, an antidepressant with
example of a disorder that does not have premenstrual
both serotonergic and noradrenergic action, reduces
exacerbation of psychotic symptoms but may have the
emotional and physical symptoms of PMDD. Efficacy
superimposition of affective and anxiety symptoms of
has also been reported with clomipramine, a tricyclic
PMDD. The prevalence of premenstrually exacerbated
antidepressant with largely serotonergic action, with
disorders is unknown, but women with these condi-
the doses of clomipramine reported to be effective for
tions present frequently to their primary care clinician
PMS (25–75 mg q.d.) lower than expected effective
or gynecologist. Since most recent treatment studies
doses for major depressive disorder (see Figure 27-2).
have been conducted on women with PMS and PMDD
Since most SSRI trials have been six months or less
without follicular symptomatology, this literature is not
in duration, long-term treatment recommendations do
particularly informative on how to treat women with
not exist. Clinically, many women note the recurrence
premenstrually exacerbated disorders. The general
of premenstrual symptoms after SSRI discontinuation
guideline is to treat the underlying disorder first and
and many clinicians treat women over a long period of
see if subsequent daily ratings suggest persistence of
time.
premenstrual symptoms that might meet the criteria for
Gonadotropin releasing hormone (GnRH) agonists
PMDD.
suppress ovulation by downregulating GnRH recep-
Several medical conditions should also be consid-
tors in the hypothalamus, leading to decreased follicle-
ered when evaluating a woman with premenstrual com-
stimulating hormone and luteinizing hormone release
plaints. Symptoms of endometriosis, polycystic ovary
from the pituitary, resulting in decreased estrogen and
disease, thyroid disorders, disorders of the adrenal sys-
progesterone levels. GnRH agonists are administered
tem, hyperprolactinemia, and panhypopituitarism may
parenterally (e.g., subcutaneous monthly injections of
mimic symptoms of PMS. Several general medical
goserelin, intramuscular monthly injections of leupro-
conditions may demonstrate a premenstrual increase
lide, and daily intranasal buserelin) (see Figure 27-2).
in symptoms without accompanying emotional symp-
GnRH agonists lead to improvement in most emotional
toms, such as migraines, asthma, epilepsy, irritable
and physical premenstrual symptoms, with possible
bowel syndrome, diabetes, allergies, and autoimmune
decreased efficacy for premenstrual dysphoria and se-
disorders. It is presumed that the menstrual cycle fluc-
vere premenstrual symptoms or for the exacerbation
tuations of gonadal hormones influence some of the
of chronic depression. After relief of PMS is achieved
symptoms of these medical conditions.
with a GnRH agonist, “add-back” hormone strategies
have been investigated due to the undesirable medi-
cal consequences of the hypoestrogenic state resulting
TREATMENT
from prolonged anovulation. The addition of estrogen
The treatment studies of SSRIs in PMDD have sug- and progesterone to goserelin and leuprolide, however,
gested a similar efficacy rate to treatment studies of may lead to the reappearance of mood and anxiety
SSRIs in major depressive disorder, with 60–70% of symptoms.
women responding to SSRIs compared to approxi- Danazol, a synthetic steroid, alleviates premenstrual
mately 30% of women responding to placebo. In gen- symptoms when administered at 200–400 mg q.d. doses
eral, the effective SSRI doses are similar to the doses that induce anovulation. A recent study with danazol
Chapter 27 • Mood Disorders: Premenstrual Dysphoric Disorder 277
Treatment of mild / moderate PMS
Vitamins, minerals, herbs Nonsomatic therapies Medications for specific symptoms
Calcium 600 mg b.i.d. Dietary changes Bromocriptine for mastalgia

Vitamin E 400 mg q.d. Exercise Spironolactone for bloating
Magnesium 200−360 mg q.d. luteally Cognitive therapy NSAID for pain, cramps
Chasteberry Relaxation
Psychoeducational groups
Treatment of PMDD and severe PMS
Serotonergic antidepressants Ovulation suppression Anxiolytics

Continuous or luteal phase
GnRH Analog
Alprazolam 0.25 mg b.i.d. luteally
Leuprolide 3.75− 7.5 mg IM monthly
Fluoxetine 20 mg q.d. Buspirone 10 mg b.i.d.
Sertraline 50 − 150 mg q.d.
Paroxetine 10 −30 mg q.d.
Citalopram 5 − 20 mg q.d. Danazol 200 −400 mg luteally
Venlafaxine 75 mg q.d. Oral contraceptives
Clomipramine 25 −75 mg q.d.
Figure 27-2 Treatment algorithm of premenstrual symptoms.
200 mg/day administered during the luteal phase only, Many lifestyle modifications and psychosocial
not causing anovulation, reported that breast tenderness treatments have been suggested for PMS. Lifestyle
but not other premenstrual symptoms were reduced. modifications are often suggested through self-help
Oophorectomy should be reserved for women with se- materials or in an individual or group psychoeduca-
vere PMS and PMDD, unresponsive to antidepressants tion format. Weekly peer support and a professional
or hormonal treatment. In addition, the small literature guidance group for four sessions has been shown to
with estrogen and progesterone administered most of reduce premenstrual symptoms. The treatment con-
the cycle has yielded mixed reports. sisted of diet and exercise regimens, self-monitor-
Even though oral contraceptives (OCs) are a com- ing and other cognitive techniques, and environment
monly prescribed treatment for PMS, there is minimal modification.
literature endorsing its efficacy. Anecdotally, women
report that OCs may benefit, worsen, or not affect their
premenstrual symptoms.
DIAGNOSTIC CRITERIA
Alprazolam (administered during the luteal phase)
may be effective for premenstrual emotional symptoms, Premenstrual Dysphoric Disorder is not included in
although it has a lower efficacy rate than SSRIs. Al- ICD-10. A related condition “premenstrual tension
prazolam should be tapered over the first few days of syndrome” is included in Chapter 14 for diseases of the
menses each cycle. genitourinary system.
CHAPTER
28 Mood Disorders:
Bipolar Disorders
DIAGNOSIS Summary of Mood Episodes and Mood

Table 28-1
Disorders
The cardinal symptoms of bipolar disorder are discrete
periods of abnormal mood and activation that define de- Episode Disorder
pressive and manic or hypomanic episodes. Diagnosis Major depressive episode Major depressive disorder,
of such episodes is based exclusively on phenomenol- single episode
ogy, the descriptive appearance of the syndrome of in- Major depressive episode ⫹ Major depressive disorder,
major depressive episode recurrent
terest. One may conceive of phenomenological data for Major depressive episode ⫹ Bipolar I disorder
the diagnosis of bipolar disorder as being of two types: manic/mixed episode
cross-sectional and longitudinal. Cross-sectional data Manic/mixed episode Bipolar I disorder
Major depressive episode ⫹ Bipolar II disorder
refer to descriptive aspects of a syndrome that occur at hypomanic episode
a particular point in time, such as the number and type Chronic subsyndromal Dysthymic disorder
depression
of depressive symptoms that occur during an episode Chronic fluctuations Cyclothymic disorder
of depression. Longitudinal data refer to the course of between subsyndromal
symptoms over time, such as the timing, duration, and depression and
hypomania
recurrence of depressive episodes. Both cross-sectional
and longitudinal data are essential for the definition of
mood disorders and the proper diagnosis of bipolar dis-
order. It is not infrequent that diagnostic errors occur period without major mood episodes are diagnosed
when longitudinal data are neglected as the clinician with cyclothymic disorder (see DSM-IV-TR diagnos-
focuses solely on cross-sectional presentation: “This tic criteria, page 279).
must be bipolar disorder because the individual appears Mood episodes are discrete periods of altered feel-
manic at the present time,” or “This cannot be bipolar ing, thought, and behavior. Typically, they have a dis-
disorder because the individual is depressed now.” tinct onset and offset, beginning over days or weeks
The DSM-based defi nition of bipolar disorder is and eventually ending gradually after several weeks or
built on the identification of individual mood epi- months. As noted earlier, bipolar disorder is defined by
sodes (Table 28-1). It is important to understand that the occurrence of depressive plus manic, hypomanic,
the diagnosis of bipolar disorder derives from the oc- or mixed episodes, or the occurrence of only manic or
currence of individual episodes over time. Persons mixed episodes.
who experience a manic, hypomanic, or mixed epi- Major depressive episodes are defined by discrete
sode, virtually all of whom also have a history of one periods of depressed or blue mood or loss of interest or
or more major depressive episodes, are diagnosed pleasure in life, which typically endures for weeks but
with bipolar disorder. Those who experience major must last for at least 2 weeks (see Chapter 26). These
depressive and manic episodes are diagnosed with symptoms are often accompanied by changes in sleep,
bipolar I disorder (see DSM-IV-TR diagnostic crite- appetite, energy, cognition, and judgment. Depressive
ria, pages 279), and those with major depressive and episodes in bipolar disorder are indistinguishable from
hypomanic (milder manic) episodes are diagnosed those in major depressive disorder. About half of persons
with bipolar II disorder (see DSM-IV-TR diagnostic with bipolar disorder experience depressive episodes
criteria, page 279). Persons who experience subsyn- characterized by decreased sleep and appetite, whereas
dromal bipolar mood fluctuations over an extended about half experience more “atypical” symptoms of in-
Chapter 28 • Mood Disorders: Bipolar Disorders 279

BIPOLAR I DISORDER, MOST RECENT EPISODE [INDICATE 296.89 BIPOLAR II DISORDER
HYPOMANIC, MANIC, MIXED, DEPRESSED, OR UNSPECIFIED]
A. Presence (or history) of one or more Major Depressive
A. Currently (or most recently) in a Hypomanic (296.40), Episodes.
Manic (296.4x), Mixed (296.6x), or Major Depressive B. Presence (or history) of at least one Hypomanic
Episode (296.5x). If the criteria except for duration are Episode.
met for one of these episodes, the episode is consid- C. There has never been a Manic Episode or a Mixed
ered unspecified (296.7). Episode.
D. The mood symptoms in Criteria A and B are not better
Note: An x in the diagnostic code indicates that a fifth
accounted for by Schizoaffective Disorder and are not
digit indicating severity is required.
superimposed on Schizophrenia, Schizophreniform
B. There has previously been at least one Manic, Mixed, Disorder, Delusional Disorder, or Psychotic Disorder
or Major Depressive Episode. Not Otherwise Specified.
C. The mood episodes in Criteria A and B are not better E. The symptoms cause clinically significant distress or
accounted for by Schizo-affective Disorder and are not impairment in social, occupational, or other important
superimposed on Schizophrenia, Schizophreni-form areas of functioning.
Disorder, Delusional Disorder, or Psychotic Disorder
Specify current or most recent episode:
Not Otherwise Specified.
Hypomanic: if currently (or most recently) in a Hypomanic
If the full criteria are currently met for a Manic or
Episode
Mixed Episode, specify its current clinical status and/or
features: Depressed: if currently (or most recently) in a Major De-
pressive Episode
Mild, Moderate, Severe Without Psychotic Features/
Severe With Psychotic If the full criteria are currently met for a Major Depres-
sive Episode, specify its current clinical status and/or
Features
features:
Mild, Moderate, Severe Without Psychotic Features/Se-
With Postpartum Onset vere With Psychotic
Reprinted with permission from DSM-IV-TR Guidebook. Copy- Features
right 2004, Michael B First, Allen Frances, and Harold Alan
Pincus. Chronic
With Melancholic Features
With Atypical Features
creased sleep and appetite. Recall that the differential With Postpartum Onset
diagnosis between major depressive and bipolar
If the full criteria are not currently met for a Hypomanic
disorders is made not by cross-sectional symptom anal- or Major Depressive Episode, specify the clinical status of
ysis but by longitudinal course. The diagnostic decision the Bipolar II Disorder and/or features of the most recent
tree for bipolar disorder is given in Figure 28-1. Major Depressive Episode (only if it is the most recent
type of mood episode):
Manic episodes are defined by discrete periods of
In Partial Remission, In Full Remission
abnormally elevated, expansive, or irritable mood ac-
companied by marked impairment in judgment and Chronic With Catatonic Features
social and occupational function. These symptoms are With Melancholic Features
frequently accompanied by unrealistic grandiosity, With Atypical Features
excess energy, and increases in goal-directed activ- With Postpartum Onset
ity that frequently have a high potential for damaging Specify:
consequences. Longitudinal Course Specifiers (With and Without In-
Hypomanic and manic symptoms may be identical, terepisode Recovery)
but hypomanic episodes are less severe (see DSM-IV- With Seasonal Pattern (applies only to the pattern of
TR diagnostic criteria for hypomanic episode, page Major Depressive Episodes)
282). A person is “promoted” from hypomania to With Rapid Cycling
mania (type II to type I bipolar disorder) by the pres- Reprinted with permission from the Diagnostic and Statistical
ence of one of three features: psychosis during the American Psychiatric Association.
episode, sufficient severity to warrant hospitalization,
or marked social or occupational role impairment.
It is important to note that the phenomenologic not as cut-and-dried as one would hope. Of the three
differentiation between hypomania and mania is characteristics by which one is “promoted” from

301.13 CYCLOTHYMIC DISORDER MANIC EPISODE
A. For at least 2 years, the presence of numerous peri- A. A distinct period of abnormally and persistently
ods with hypomanic symptoms and numerous periods elevated, expansive, or irritable mood, lasting at
with depressive symptoms that do not meet criteria for least 1 week (or any duration if hospitalization is
a major depressive episode. necessary).
B. During the period of mood disturbance, three (or
Note: In children and adolescents, the duration must be
more) of the following symptoms have persisted (four
at least 1 year.
if the mood is only irritable) and have been present to
B. During the above 2-year period (1 year in children a significant degree:
and adolescents), the person has not been without the
(1) inflated self-esteem or grandiosity
symptoms in criterion A for more than 2 months at a
(2) decreased need for sleep (e.g., feels rested after
time.
only 3 hours of sleep)
C. No major depressive episode, manic episode, or mixed
(3) more talkative than usual or pressure to keep
episode has been present during the first 2 years of the
talking
disturbance.
(4) flight of ideas or subjective experience that thoughts
D. The symptoms in criterion A are not better accounted
are racing
for by Schizoaffective Disorder and are not superim-
(5) distractibility (i.e., attention too easily drawn to un-
posed on Schizophrenia, Schizophreniform Disorder,
important or irrelevant external stimuli)
Delusional Disorder, or Psychotic Disorder Not Oth-
(6) increase in goal-directed activity (either socially,
erwise Specified.
at work or school, or sexually) or psychomotor
E. The symptoms are not due to the direct physiologi-
agitation
cal effects of a substance (e.g., a drug of abuse, a
(7) excessive involvement in pleasurable activities that
medication) or a general medical condition (e.g.,
have a high potential for painful consequences (e.g.,
hyperthyroidism).
engaging in unrestrained buying sprees, sexual in-
F. The symptoms cause clinically significant distress or
discretions, or foolish business investments)
areas of functioning. C. The symptoms do not meet criteria for a mixed
Reprinted with permission from the Diagnostic and Statistical episode.
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 D. The mood disturbance is sufficiently severe to cause
American Psychiatric Association. marked impairment in occupational functioning or in
usual social activities or relationships with others, or
to necessitate hospitalization to prevent harm to self
or others, or there are psychotic features.
E. The symptoms are not due to the direct physiological
hypomania to mania, only the presence of psychosis is effects of a substance (e.g., a drug of abuse, a medica-
firmly grounded in the characteristics of the individual. tion, or other treatment) or a general medical condition
The other two characteristics, marked social or occupa- (e.g., hyperthyroidism).
tional role impairment or hospitalization, clearly have Note: Manic-like episodes that are clearly caused by so-
matic antidepressant treatment (e.g., medication, elec-
components that are primarily external to the individ- troconvulsive therapy, light therapy) should not count
ual. If for instance, one individual has relatively mild toward a diagnosis of manic–depressive I disorder.
manic symptoms but is living with a family who is un- Reprinted with permission from the Diagnostic and Statistical
able to tolerate the behavior, he or she is more likely to Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
be hospitalized. Similarly, the comorbid presence of a
severe disorder is more likely to result in hospitaliza-
tion and a “promotion” from type II to type I disor-
der. Contrarily, limited insurance benefits, or a more of dysphoria during mania (see DSM-IV-TR diagnostic
tolerant family increase the probability that a manic criteria, page 282).
syndrome of a given severity will be managed without Rapid cycling is defined by the occurrence of four or
hospitalization and thus be diagnosed as “hypomania” more mood episodes within 12 months (see DSM-IV-
rather than “mania.” TR diagnostic criteria, page 282). It should be noted
Classically, mania has been considered to be the op- that, despite the name, the episodes are not necessar-
posite of depression: manic individuals were said to be ily or even commonly truly cyclical; the diagnosis is
cheery, optimistic, and self-confident. Hence the name based simply on episode counting. This subcategory is
bipolar disorder. However, in most descriptive stud- of significance because it predicts a relatively poorer
ies of mania, substantial proportions of hypomanic outcome and worse response to lithium and other treat-
and manic individuals actually exhibit substantial ments. Although rapid cycling has been considered
dysphoric symptoms. Mixed episodes, defined as the by some to be an “end stage” of the disorder, empiri-
simultaneous occurrence of full-blown manic and cal evidence indicates that it may have its onset at any
depressive episodes, are the most prominent example time during the disorder and may come and go during
Major depressive disorder

Depressive episode
Recurrent or single episode
Manic symptoms No Hypomanic Bipolar disorder

episode type II
Hospitalization/psychosis/severe
role dysfunction
Manic episode (probable bipolar

disorder type I)
Meet criteria for major depressive Mixed episode*

episode simultaneously
Psychosis Endures beyond Schizoaffective disorder

mood episodes
Limited to major
mood episodes
Bipolar disorder type I
Four or more episodes in 12 months Rapid cycling
Figure 28-1 Diagnostic decision tree for bipolar disorder. The building blocks for a diagnosis of bipolar disorder are individual episodes
and their characteristics, as summarized in Table 28-1. This decision tree helps the psychiatrist through the steps that lead to diagnosis of
manic–depressive disorder and identification of its subtypes. *Does not apply to hypomanic episode as per DSM-IV-TR. Reprinted with
permission of American Journal of Psychiatry, 149, 1633–1644. McElroy S, Keck P, Pope H et al (1992) Clinical and research implication
of the diagnosis of dyphoric or mixed mania or hypomania. Copyright American Psychiatric Publishing Inc.
the course of illness. Several specific risk factors may individuals with mental disorders, particularly chronic
be associated with rapid cycling, each of which may or severe illnesses, their first contact with medical care
give clues to its pathophysiology. These include fe- as an adult is during the psychiatric interview—often
male gender, antidepressant use, and prior or current under inpatient or even involuntary conditions.
hypothyroidism. The overall approach to evaluating persons with bi-
Although the diagnosis of bipolar disorder is made on polar disorder for medical problems may be general-
the basis of phenomenology, there are several reasons ized as follows. Persons with mental disorders, includ-
to conduct a thorough medical history and physical ex- ing bipolar disorder, should have regular screening for
amination. First, there are several general medical or disease detection and health maintenance purposes as
substance-related causes of mania and/or depression recommended for the general population. However,
that, if treated, may lead to the resolution of the mood it should also be kept in mind that individuals with
episode (see later). Similarly, mania may be the first bipolar disorder, by virtue of having an often severe
sign of a general medical illness that will be progres- and disabling behavioral disorder, are less likely than
sive and serious in its own right. Second, medical eval- the general population to have had adequate medical
uation is necessary before starting medications used screening and treatment. Thus, special care must be
in the treatment of bipolar disorder. Finally, for many made to ensure that health problems are not overlooked

HYPOMANIC EPISODE MIXED EPISODE
A. A distinct period of persistently elevated, expansive, A. The criteria are met both for a manic episode and for a
or irritable mood, lasting throughout at least 4 days, major depressive episode (except for duration) nearly
that is clearly different from the usual nondepressed every day during at least a 1-week period.
mood. B. The mood disturbance is sufficiently severe to cause
B. During the period of mood disturbance, three (or marked impairment in occupational functioning or in
more) of the following symptoms have persisted (four usual social activities or relationships with others, or to
if the mood is only irritable) and have been present to necessitate hospitalization to prevent harm to self or
a significant degree: others, or there are psychotic features.
C. The symptoms are not due to the direct physiological
(1) inflated self-esteem or grandiosity
(2) decreased need for sleep (e.g., feels rested after
tion, or other treatment) or a general medical condi-
only 3 hours of sleep)
tion (e.g., hyperthyroidism).
(3) more talkative than usual or pressure to keep
talking Note: Mixed-like episodes that are clearly caused by
(4) flight of ideas or subjective experience that thoughts somatic antidepressant treatment (e.g., medication, elec-
are racing troconvulsive therapy, light therapy) should not count to-
(5) distractibility (i.e., attention too easily drawn to un- ward a diagnosis of manic–depressive I disorder.
important or irrelevant external stimuli) Reprinted with permission from the Diagnostic and Statistical
(6) increase in goal-directed activity (either socially, Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
at work or school, or sexually) or psychomotor American Psychiatric Association.
agitation
(7) excessive involvement in pleasurable activities that
have a high potential for painful consequences
(e.g., the person engages in unrestrained buying general medical condition, more intensive testing is
sprees, sexual indiscretions, or foolish business
investments) warranted. A clear example of the last situation is when
C. The episode is associated with an unequivocal change a person with bipolar disorder who has extensive ex-
in functioning that is uncharacteristic of the person posure to lithium presents for treatment; such persons,
when not symptomatic. particularly the elderly, require laboratory testing for
D. The disturbance in mood and the change in function-
ing are observable by others. renal and thyroid abnormalities that can be caused by
E. The episode is not severe enough to cause marked im- lithium treatment.
pairment in social or occupational functioning, or to Alcohol and drug abuse and dependence represent
necessitate hospitalization, and there are no psychotic
features. the most consistently described and most clinically im-
F. The symptoms are not due to the direct physiological portant mental disorder comorbidities with bipolar dis-
effects of a substance (e.g., a drug of abuse, a medica- order. Whereas rates of alcohol abuse combined with
tion, or other treatment) or a general medical condi-
tion (e.g., hyperthyroidism). alcohol dependence are from 3% to 13% in the general
Note: Hypomanic-like episodes that are clearly caused population, lifetime rates for alcohol dependence from
by somatic antidepressant treatment (e.g., medication, Epidemiological Catchment Area (ECA) data indicate
electroconvulsive therapy, light therapy) should not count that they are greater than 30% in persons with bipolar I
toward a diagnosis of manic–depressive II disorder.
R APID-CYCLING SPECIFIER
and that appropriate treatment or referral is effected.
Specify if:
Unfortunately, it is the exception rather than the rule
to have well-integrated medical and mental health sys- With rapid cycling (can be applied to manic–depressive I
disorder or manic–depressive II disorder). At least four ep-
tems, so that the mental health provider can assume isodes of a mood disturbance in the previous 12 months
that some effort will need to be expended to ensure that meet criteria for a major depressive, manic, mixed, or
adequate care is delivered for individuals with bipolar hypomanic episode.
disorder. Note: Episodes are demarcated by either partial or full
remission for at least 2 months or a switch to an episode
All newly identified individuals with bipolar disor- of opposite polarity (e.g., major depressive episode to
der should undergo a history and if indicated a physi- manic episode).
cal examination. If results of the history or physical Reprinted with permission from the Diagnostic and Statistical
examination reveal abnormalities, or if the individual Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
has a mental disorder that is associated with a particular
disorder. Further, ECA lifetime rates for drug depend- prevalence rate for schizophrenia and about one-fifth
ence in individuals with bipolar I disorder are greater that for major depressive disorder. Little is known re-
than 25% and rates for any substance abuse or depend- garding the prevalence of cyclothymic disorder.
ence are above 60%. Comparable rates for alcohol, Unlike major depressive disorder, bipolar disorder
drug, or any substance abuse or dependence in major has an approximately equal gender distribution. Few
depressive disorder in ECA data are, respectively, 12%, consistent data are available regarding differences in
11%, and 27%. Thus, bipolar disorder represents an prevalence across ethnic, cultural, or rural–urban set-
enriched sample for substance use disorders, with sub- tings. However, one of the more intriguing puzzles
stantially greater rates than for the general population is the tendency of bipolar disorder to occur in higher
or even those with unipolar depression. socioeconomic strata than schizophrenia, which tends
The reasons for the co-occurrence of bipolar disor- to aggregate in lower socioeconomic strata. Although
der and substance dependence are not clear. One hy- many theories have been advanced to explain this
pothesis suggests that persons with bipolar disorder phenomenon, no certain mechanism has been iden-
self-medicate with drugs or alcohol. According to this tified. However, several issues are clear. First, the
hypothesis, individuals blunt the painful symptoms of finding is most likely not exclusively due to diagnos-
depression with drugs, similarly, they may heighten the tic bias (i.e., overdiagnosing persons of lower socio-
manic energy with stimulants. Contrarily, they may economic class with schizophrenia more frequently
also use substances to decrease manic symptoms, par- than bipolar disorder and the converse in persons of
ticularly if the symptoms are predominantly irritable higher socioeconomic class). Second, the upward
or dysphoric. Alternatively, chronic substance use may socioeconomic “drift” is not due to highly impaired
convert otherwise unipolar depression into bipolar dis- individuals “dragged” upward by higher functioning
order by inducing substance-induced manic episodes family members who are normal or who have adaptive
(according to DSM-IV-TR, such persons would not be subsyndromal bipolar spectrum characteristics; rather,
classified as having bipolar disorder but would be con- individuals themselves, at least those with type II dis-
sidered to have a substance-induced mood disorder) or order, are in many cases highly successful and occupy
by causing chronic central nervous system changes that higher socioeconomic levels. Third, the findings are
change the course of the illness irreversibly. not limited to the United States but have been repli-
Finally, it is possible that some common genetic pre- cated in European samples as well.
disposition for mood instability is associated with both Of particular interest in regard to the epidemiol-
bipolar mood phenomenology and increased craving ogy of bipolar disorder is that the incidence of bipo-
for substances, and the predominant phenotypic ex- lar disorder (and depressive disorders) appears to have
pression is then determined by other genetic or envi- increased since the 1940s. Reasons for this are not
ronmental factors. According to this hypothesis, some clear, although environmental factors, either physi-
persons possessing the gene develop bipolar disorder, ological or psychosocial, may be responsible. For in-
some develop substance dependence, and some de- stance, exposure to increasingly severe social stressors,
velop both. Regardless of the mechanism, comorbid or the breakdown of cultural supports that may buffer
substance dependence represents an important clinical stresses, may contribute; increases in exposure to puta-
challenge for clinicians treating persons with bipolar tive environmental toxins might also be considered. In
disorder. addition, in those families afflicted with bipolar disor-
Among children and adolescents, the diagnosis of der across generations, those in later generations tend
bipolar disorder is often complicated by less consistent to have earlier onset.
mood and behavior baseline than occurs in adults. Lit-
tle evidence is available regarding course and outcome
Course
in children. Available data indicate that, as with adults,
mixed or cycling episodes predict more recurrences; Outcome in bipolar disorder can be conceptualized
unlike in adults, manic and mixed presentations may according to three separate but interrelated domains:
be associated with relatively shorter episodes compared clinical outcome, functional outcome, and illness costs.
to depressive presentations. Clinical outcome consists of parameters that measure the
Estimates of the lifetime risk for bipolar I disorder illness itself, such as symptom severity, episode number,
from epidemiological studies have ranged from 0.2% and duration. Functional outcome consists of social and
to 0.9%. The ECA study found a lifetime prevalence occupational status and subjective quality of life. Illness
rate of 1.2% for combined type I and type II variants. costs consist of both direct (treatment) costs and indirect
These rates are approximately tenfold greater than the illness costs, which include lost productivity, necessary
nontreatment social supports, and nontreatment inter- perienced multiple relapses, whereas only 11% were
ventions such as jail and the legal system. episode free.
Bipolar disorder has its onset in most persons in ado- Subsyndromal affective symptoms may remain in up
lescence and young adulthood, between the ages of 15 to 13–34% and substantial interepisode morbidity may
and 30. However, prepubertal mania and first-onset dis- remain despite adequate treatment with lithium. It is
ease in the ninth decade of life also occur. Once devel- not clear whether such interepisode pathology repre-
oped, multiple episodes are the rule—the majority of sents incompletely resolved major affective episodes,
individuals with bipolar disorder have four or more epi- medication side effects, demoralization due to func-
sodes in a lifetime. Among rapid-cycling individuals, tional impairment, or a combination of these factors. It
the basis for the diagnosis is four or more episodes in a should be noted here that side effects are more than a
year with an average of more than 50 lifetime episodes. trivial issue, as they may lead to medication discontinu-
There is no typical pattern to episode recurrence, with ation in 18–53%, a figure that is greater in lower so-
some individuals having isolated manic, hypomanic, or cioeconomic classes. Thus, clinical outcome in bipolar
depressive episodes, others switching from one pole to disorder is heterogeneous, and lithium has not proved
the other in linked episodes, and still others switching to be a panacea.
continually from one pole to the other in quasi-cyclical
fashion. However, even among rapid-cycling individu-
als, episodes are rarely periodic. Rather, the pattern is
more accurately described by chaotic dynamics. Psychosis can occur in either pole of the disorder. If
Episode length typically ranges from 4 to 13 months, psychotic symptoms are limited to the major mood
with depressive episodes typically longer than manic episode, the individual is considered to have bipolar
or hypomanic episodes. Women appear to have more disorder with psychotic features. On the other hand, if
depressive relapses than manic ones, whereas men have psychotic symptoms endure significantly into periods
a more even distribution. Women predominate among of normal mood, the diagnosis of schizoaffective dis-
rapid-cycling individuals, representing 70–90% in order is made.
most studies. Secondary mania is conceptualized as mania occur-
Longitudinal studies conducted in the past three ring close on the heels of a specific known physiologi-
decades suggest an overall guarded prognosis. In early cal insult, such as general medical illness or exposure
studies conducted in the 1960s, 62% of bipolar individ- to mania-inducing pharmacological agents. Which
uals had equivocal to poor outcome and 45% of manic general medical illnesses may cause symptoms of bi-
individuals were chronically ill 6 years after hospitali- polar disorder? Most medical illnesses that affect brain
zation. Another study found only 14.3% to be “well in function have been described in case reports or small
every way.” Although these studies include data from case series to cause one or another mental disorder.
the prelithium era, more recent studies from the lithium Several general medical illnesses have been associated
era are not terribly reassuring. Approximately 20–40% with the development of bipolar disorder (Table 28-2),
of individuals with bipolar disorder do not respond well although none can be considered specific risk factors.
to lithium, and that proportion may increase to as much Furthermore, administration of medications has been
as 80% for certain subgroups such as individuals who observed frequently in clinical practice to be associated
experience rapid-cycling pattern or mixed manic and with the onset of mania, particularly in individuals with
depressive episodes. When assessed 1.5 years after in- preexisting depression. Such medications are listed in
dex hospitalization, between 7% and 32% of bipolar
individuals remain chronically ill, depending on po-
larity of index episode. Only 26% of one sample had Table 28-2
Medical Disorders Commonly Associated
good outcome after hospitalization for mania, whereas with Mania
40% had moderate and 34% had poor outcome. The Neurologic Disorders Endocrine
probabilities of remaining ill at 1, 2, 3, and 4 years af-
Stroke Hyperthyroidism (in those
ter hospitalization for mania were, respectively, 51%, with preexisting manic–
44%, 33%, and 28%. depressive disorder)
Relatively little is known regarding clinical out- Head trauma Postpartum status
Dementia
come in bipolar II individuals, although they appear to Brain tumors
be at least as impaired in terms of relapse as bipolar Infection (including HIV)
I individuals. For instance, one study found that 70% Multiple sclerosis
Huntington’s disease
of bipolar II individuals followed up for 5 years, ex-
Treatments and Drugs Commonly Treatments and Drugs Commonly Associated

Associated with Mania with Depression
Antidepressants Dopaminergic Agents High Blood Pressure Medications Hormones

Medications Levodopa Alphamethyldopa Corticosteroids
Bright visible spectrum light Clonidine Oral contraceptives
treatment Anabolic steroids
Electroconvulsant therapy Drugs of Abuse Ulcer Medications
Alcohol Cimetadine Psychotropic Agents
Adrenergic Agents Cocaine Ranitidine Benzodiazepines
Decongestants Hallucinogens Neuroleptics
Bronchodilators Amphetamines Drugs of Abuse
Stimulants Caffeine Alcohol
Other Agents Sedatives
Isoniazid Amphetamine (withdrawal)
Corticosteroids Cocaine (withdrawal)
Anabolic steroids Nicotine (withdrawal)
Disulfiram
TREATMENT
Table 28-3. Depressive symptoms may also be associ-
ated with certain medical conditions (Table 28-4) and Traditionally, treatment for bipolar disorder has been
medications or drugs (Table 28-5). categorized as acute versus prophylaxis, or mainte-
All efficacious antidepressant treatments have been nance; that is, treatment geared toward resolution of a
suspected to cause the induction of mania, with the ex- specific episode versus continued treatment to prevent
ception of lithium and the possible exception of psy- further symptoms. Treatment can also be considered
chotherapy. Occasionally, when a new antidepressant along several other lines (Table 28-6). For instance,
is developed, hope is raised that it will be the agent interventions can be categorized as somatotherapy
that will not induce mania. Clinical experience has (pharmacotherapy, ECT, and light treatment) and psy-
not borne out these early hopes. This caveat for anti- chotherapy. In addition, treatment can be categorized
depressants also includes nonpharmacological antide- according to intensity. The division into inpatient ver-
pressants such as light and electroconvulsive therapy sus outpatient treatment is becoming more and more
(ECT). The latter effect is paradoxical, as ECT is also blurred as partial or day hospital programs and inten-
used successfully to treat mania. sive ambulatory treatment coupled with night hospital
programs or respite beds become more popular.
In general, more structured treatment settings, such
as full or partial hospitalization, are indicated if indi-
viduals are likely to endanger self or others, if bipolar
Medical Disorders Commonly Associated disorder is complicated by other mental disorders or
Table 28-4
with Depression
general medical conditions that make ambulatory man-
Neurologic Disorders agement particularly dangerous, or if more aggressive
Stroke management is desired than is easily available on an am-
Head trauma
Dementia bulatory basis (e.g., intensive psychosocial intervention
Brain tumors
Infection (including HIV)
Multiple sclerosis
Parkinson’s disease Classification Schemata for Bipolar Disorder
Table 28-6
Huntington’s disease Treatment and Its Goals
Endocrine 1. Acute versus maintenance

Addison’s disease 2. Somatic versus psychotherapeutic
Cushing’s disease 3. The intensity-of-care continuum*
Hypothyroidism (a) Full hospitalization
Hyperthyroidism (b) Partial or day hospitalization
Postpartum status (c) Night hospitalization or respite beds
(d) Ambulatory care
Cancers
4. Categorization by goal
Pancreatic
(a) Improve clinical outcome
Metabolic (b) Improve functional outcome
B12, folate deficiencies (c) Improve host factors
Any medical disease that causes significant loss of function (i) Illness management skills
or self-esteem (ii) Medical and psychiatric comorbidities
or rapid dosage titration of psychotropic agents). In for mania. In contrast, not only did lithium provide an
addition, although it is frequently an afterthought in additional treatment for acute mania and depression
textbooks, social factors play an important role in the in bipolar disorder, it was also demonstrated to have
decision to hospitalize in the real world. Such reasons substantial prophylactic, or preventive, effects on both
may include lack of social support to ensure medica- manic and depressive episodes.
tion compliance during acute illness, social stresses ag- In evaluating the effectiveness of the various treat-
gravating symptoms and making treatment compliance ments for bipolar disorder, we have found it useful to
difficult (e.g., manipulative or hostile living situation), propose an explicit definition for the term “mood sta-
or lack of transportation to accommodate frequent am- bilizer” and evaluate the role of various medications
bulatory appointments during acute illness. Unfortu- against this definition. The US Food and Drug Admin-
nately, it is sometimes the case, although less frequent istration (FDA) does not formally define the term, but
in this era of managed care, that a person’s insurance it stands to reason that an agent would be optimally
plan covers inpatient but not ambulatory mental health useful for treatment of bipolar disorder if it had effi-
treatment, forcing expensive inpatient care when less cacy in four roles: (a) treatment of acute manic symp-
costly, time-limited, intensive ambulatory care would toms, (b) treatment of acute depressive symptoms, (c)
suffice. prophylaxis of manic symptoms, and (d) prophylaxis of
Finally, treatment can be categorized according to depressive symptoms. This approach leads to the con-
its goals. Treatment can be focused on improving clini- ceptual 2 ⫻ 2 table illustrated in Table 28-7. Agents
cal outcome (episodes and symptoms) or functional used in bipolar disorder can be listed in any or all of
outcome (social and occupational function and health- the four boxes in the table in which they have proven
related quality of life). Although this categorization efficacy, and according to this schema, an agent may
appears straightforward, clinical practice reveals many be categorized as a mood stabilizer if it can be listed as
subtleties. For instance, it is erroneous to assume that having efficacy in each of the four boxes.
clinical outcome is the domain of pharmacotherapy Following the FDA lead of considering an agent
and that functional outcome is the domain of psycho- to have efficacy with at least two such positive trials,
therapy. In actuality, most psychotherapies by design we have listed the agents according to the 2 ⫻ 2 table
focus on improving symptoms. Likewise, pharmaco- in Table 28-7. As can be seen, at least two placebo-
therapeutic stabilization of symptoms clearly contrib- controlled randomized controlled trials support the
utes to improved role function. Further, treatments that antimanic efficacy of lithium, carbamazepine, val-
improve one domain may cause decrements in another. proate, verapamil, olanzapine, risperidone, ziprasi-
For instance, effective maintenance treatment with done, quetiapine, and aripirazole. There are additional
lithium may come at the cost of hand tremor, which in- randomized controlled trials (nonplacebo-controlled)
terferes with work function and causes embarrassment that support efficacy for multiple older, typical neu-
in social situations. roleptics as well as the benzodiazepines, lorazepam,
Balancing the costs and benefits of various specific and clonazepam.
treatments—and every somatic and psychotherapeutic In contrast to evidence regarding acute mania, evi-
treatment has both costs and benefits—requires active dence is scarce concerning efficacy of specific agents
participation of the person with bipolar disorder and,
if available, his or her family. Compassionate psych-
oeducation and alliance building are integral goals of Summary of Efficacy Data from
each form of treatment. In analogy to infectious dis- Randomized Controlled Trials for Treating
Table 28-7
the Various Phases of Bipolar Disorder (At
ease treatment, attention to such host factors can of- Least Two Placebo-Controlled Trials)
ten make the difference between success and failure of
Mania Depression
treatment.
Acute Lithium Lithium
Carbamazepine Lamotrigine
Somatotherapy Valproate Quetiapine
Verapamil
The introduction of lithium for the treatment of bipo- Olanzapine
lar disorder in the 1960s revolutionized management of Risperidone
Ziprasidone
the illness. Before that, bipolar disorder was managed Quetiapine
with treatment targeted only toward resolution of indi- Aripiprazole
vidual episodes: antidepressants and ECT for depres- Prophylaxis Lithium Lithium
Lamotrigine Lamotrigine
sive episodes, and neuroleptics and occasionally ECT
for acute depressive episodes. Most treatment is under- is quite scanty for these agents—as it is for many other
taken primarily by extension from treatment experience agents used in clinical practice.
in unipolar depression. Efficacy data from two or more Several additional issues in prophylaxis of bipolar
randomized controlled studies exist only for lithium, disorder deserve comment. First, when is lifetime, or
lamotrigine, and quetiapine. Support for the efficacy of at least long-term, prophylaxis warranted? After one
valproate and carbamazepine in acute depressive epi- manic episode? One hypomanic episode? One depres-
sodes in bipolar disorder is notably lacking. sive episode with a strong family history of bipolar
In reviewing studies of agents for the prophylaxis disorder? There is insufficient empirical evidence with
of manic or depressive symptoms, we discovered that which to make strong recommendations. In clinical
most of the studies reported recurrence rates without practice without clear guidelines, such decisions need
distinguishing between manic and depressive symp- to take into account the capability of the individual
toms. For instance, some studies reported such statis- and family in reporting symptoms, rapidity of onset of
tics as time-to-first-episode without specifying whether episodes, episode severity, and associated morbidity.
the first episode was manic or depressed. Other stud- Clearly, the risks of a wait-and-see strategy would be
ies reported summary statistics for affective symptoms different in a person who had a psychotic manic epi-
without separating manic or depressive symptoms. sode than in a person who had mild hypomania.
We found that when studies did report specific polar- Second, can lithium ever be discontinued? Again,
ity of symptoms during recurrence, it was infrequent there are no solid data on which to base this decision.
that they reported impact of treatment on recurrence of However, if lithium discontinuation is contemplated,
depressive symptoms. Far and away, the most placebo- there is evidence that rapid discontinuation (in less than
controlled support for any prophylactic agent comes 2 weeks) is more likely to result in relapse than slow
from studies of lithium, including studies of relapse taper (2–4 weeks), with relapse rates higher in type I
prevention for depression. There is also support from individuals than in type II individuals. In type I indi-
placebo-controlled trials for lamotrigine, and some viduals, relapse rates for rapid discontinuation versus
support from controlled trials that are not placebo- slow taper were, respectively, 96% and 73%, whereas
controlled for carbamazepine. The one prophylaxis in type II individuals they were 91% and 33%. There
study of valproate showed no difference from placebo is some theoretical concern, based on a report of four
(lithium was also found to be no different from placebo individuals, that individuals in whom lithium has been
in this study, although the study was under-powered to discontinued may not be recaptured by resumption of
make definitive conclusions about this comparison). lithium but these were preliminary observations on a
Thus, in summary, this standardized evidence-based sample from the NIMH that may not be representative
review of available treatments for bipolar disorder in- of persons with bipolar disorder seen in general clini-
dicates that, to date, only lithium fulfills the stringent cal practice.
definition of a mood stabilizer. It is hoped that addi- Third, a set sequence of treatment for refractory bi-
tional agents soon take their place in the ranks based polar disorder has yet to be established. In particular,
on high quality data. persons with rapid cycling represent a treatment di-
It may be surprising that, given the paucity of data lemma. Although antidepressants may induce rapid cy-
on treatment of acute depression and prophylaxis of cling, they often leave the person in a protracted, severe
bipolar disorder, we frequently encounter many other depression. Switching from one antimanic agent to an-
medications used chronically in this illness, some- other often results in resumption of cycling. Complex
times as first-time agents, for instance, valproate and treatment strategies may be required, such as anticon-
carbamazepine. Although neuroleptics have acute vulsants plus lithium, combinations of anticonvulsants,
antimanic evidence, despite the fact that there is little or adjuvant treatment with high doses of the thyroid
evidence for prophylactic efficacy, they are often used hormone thyroxine.
chronically. This is because these agents are typically All psychotropic medications have side effects.
started during the course of an acute manic episode Some are actually desirable (e.g., sedation with some
and clinicians are loathe to stop them and switch to a antidepressants in persons with prominent insomnia),
different agent such as lithium. In addition, many indi- and specific medications are often chosen on the basis
viduals have failed or have been intolerant of treatment of desired side effects. However, side effects usually
with lithium and they are therefore treated using the represent factors that decrease an individual’s qual-
“next best thing.” This is not necessarily suboptimal ity of life and compromise compliance. Furthermore,
treatment. However, it is important that the clinician all antidepressants can cause rapid cycling and mixed
recognize that data on long-term prophylactic efficacy states in persons with bipolar disorder. These effects
Table 28-8 Side Effects of Lithium and Commonly Used Anticonvulsants I: Life-Threatening
I: Life-Threatening
At Therapeutic Levels At Toxic Levels
Idiopathic Dose-Related Dose-Related
Lithium Renal failure

Encephalopathy
CBZ Agranulocytosis*
Aplastic anemia*
Stevens–Johnson*
VPA Hepatic necrosis Thrombocytopenia Thrombocytopenia
LMT Stevens–Johnson*
II: Clinically Significant Side Effect
Lithium CBZ VPA LMT
Neurologic/muscular Lethargy Lethargy Lethargy Lethargy

Memory (anomia) Blurred vision Depression Ataxia
Tremor† Tremor† Blurred vision
Myoclonus Ataxia† Ataxia Headache
Endocrine/metabolic Weight gain† Weight gain†
Hypothyroidism
Cardiopulmonary
Hematologic Thrombocytopenia
Renal Polyuria
Hepatic Jaundice Jaundice
Gastrointestinal Nausea† Nausea† Nausea† Nausea†
Diarrhea†
Dermatologic Maculopapular rash Maculopapular rash Maculopapular rash Maculopapular rash
Psoriasis Alopecia
Acne
Other Back pain
III: Subclinical Laboratory Abnormalities
Lithium CBZ VPA LMT
Neurologic/muscular
Endocrine/metabolic Increased TSH Decreased FTI
Cardiopulmonary EKG T-wave
depression
Hematologic Leukocytosis Leukopenia Thrombocytopenia
(to 20,000) (OK ⬎ 20,000)
Renal Decreased urine
specific gravity, GFR
Hepatic Increased LFTs Increased LFTs
*Typically during fi rst 1–6 months of treatment.
†Most common reasons in our experience for noncompliance.
are not uncommonly encountered in clinical practice processes that are associated with or presage mor-
and should be watched for, even in persons taking bidity for the individual; that is, not all are clinically
mood-stabilizing agents. significant.
A brief overview of the most frequent or important Note also that the concept of the “therapeutic level”
side effects of lithium, carbamazepine, and valproic is not as straightforward as we would like to assume.
acid can be found in Table 28-8. Note that some side The lower limit is usually established by the low-
effects may be encountered at any serum level of the est level necessary for therapeutic effect, whereas the
drug, even within the therapeutic range. Some side ef- upper limit is set by the lowest level associated with
fects may be dose related even within that range and regular, significant toxicity. This range is never estab-
may respond to dosage reduction. Others are more lished with complete precision. For some medications
idiosyncratic and may need other management. Note such as lithium, the therapeutic window is actually
that not all laboratory findings represent pathological quite narrow, with toxic effects developing with some
regularity after the upper limit of the therapeutic range usually respond well to this, whereas others, such as
is surpassed and with serious toxicity developing at lithium-induced memory loss, improve less reliably.
only modestly higher serum levels. As a further compli- Second, simple changes in preparation may be help-
cation, for many persons, the minimum level of lithium ful, such as using enteric-coated lithium. Uncoated
for good response may be substantially above the 0.5 to valproic acid causes nausea so frequently that only the
0.8 mEq/L that is usually set as the lower therapeutic coated forms are routinely used; however, the pediat-
limit, but this is reached only at the cost of increased ric “sprinkle” preparation may be of some benefit in
incidence of side effects. On the other hand, experience persons with nausea even with enteric-coated valproic
with valproic acid shows that the upper limit of the acid.
therapeutic range for mood stabilization may actually Third, changing the administration schedule may
be 125 mg/dL rather than the listed range of 100 mg/dL ameliorate side effects. Commonsense strategies such
usually accepted for antiepileptic effect, and this level as taking nausea-inducing medications after a meal
may be reached without undue side effects. should not be overlooked. Single daily dosing of lith-
Thus, established therapeutic levels should be used ium, carbamazepine, or valproic acid may decrease
as important guidelines, and exceeding therapeutic lev- daytime sedation without compromising efficacy. For
els should be done only with careful monitoring. How- more obscure reasons, single daily dosing of lithium
ever, one must not be falsely reassured that reaching the appears to decrease polyuria quite effectively.
lower level of a therapeutic range is equally effective Fourth, addition of medications to counteract side ef-
for all individuals, while taking with a grain of salt the fects can sometimes be the only way to continue treat-
upper limits of the therapeutic range in drugs with a ment. Addition of beta-blockers can reduce lithium- or
wider therapeutic window. valproic acid-induced tremors. Judicious use of thi-
Another important issue to consider is drug–drug azide diuretics, often in conjunction with potassium-
interactions that may lead to side effects. Such inter- sparing diuretics or potassium supplements, can reduce
actions are often associated with increases in serum lithium-induced polyuria.
levels of the drug of interest. For example, addition of Finally, change to another drug may be the only al-
thiazide diuretics, or nonsteroidal antiinflammatory ternative. This is clearly indicated in the case of serious
agents, the latter available over the counter, is a com- allergic reactions. Polypharmacy should be avoided
mon reason for increase in lithium level and develop- wherever possible.
ment of toxicity. However, at other times the drug–drug
interactions may not be reflected in an increased serum
Psychotherapies
level if the main interaction is displacement of protein-
bound drug. Because free drug concentrations are usu- One of the fastest moving areas of research in bipo-
ally 1–10% of total serum drug, a displacement of even lar disorder has been psychotherapy. It is important to
50% of bound drug may be associated with negligible note that psychotherapy has been studied almost exclu-
if any changes in total serum level. However, since both sively in the context of ongoing medication manage-
therapeutic and toxic effects are due to free, not bound, ment, rather than as a substitute for, or alternative to,
drug, unwanted side effects may develop despite total medication treatment. Rather, psychotherapy has been
drug levels measured in the therapeutic range. utilized as an adjuvant treatment to optimize outcome
As noted previously, some side effects may be desir- in the illness. Psychotherapy has been viewed as hav-
able. However, in many cases they are impediments to ing one or more of several roles in the management of
treatment, frequently of sufficient importance to lead the disorder.
to noncompliance. As clinicians, however, we might Recall that both somatic therapies and psychothera-
reframe the noncompliance issue more appropriately pies to date have been predominantly oriented toward
as “insufficient provider–patient cost-benefit analysis.” improving clinical outcome. Under this conceptuali-
Stressing compliance when a person suffers from sig- zation, psychotherapy has been thought to directly ad-
nificant side effects is usually much less effective than dress symptoms, such as cognitive therapy for depres-
working to set appropriate expectations of the individ- sive symptoms. Less frequently has psychotherapy been
ual and to find a regimen of minimal toxicity. developed with an explicit component geared toward
Nonetheless, the astute clinician does have several addressing the functional deficits in bipolar disorder.
strategies available to improve individuals’ tolerance However, functional outcome has often been measured
of medications. First, dose reduction may be achieved in formal trials of various types of psychotherapy. A
without compromising efficacy in some individuals. third conceptualization has been to use psychotherapy as
Some side effects, such as lithium-induced nausea, a predominantly educative method to assist individuals
Basics of Education to Improve Disease

striking. Specifically, imparting education, focusing
Table 28-9 on early warning symptoms and triggers of episodes,
Management Skills
and developing detailed and individual-specific action
1. Principles
A. Gear education to educational, cultural, motivational plans are found across most of the other interventions
factors of individuals and their families. as well.
B. Include both knowledge about the disorder in general and
exploration of the individual’s specific form of illness and
how it affects their own life. Treatment of Bipolar Disorder across the
C. Pay close attention to opportunities for destigmatization
and demystification. Life Cycle
D. Emphasize the role of the person in treatment and his/her
family as comanagers of the illness, including judging Although the somatotherapeutic and psychotherapeu-
costs and benefits of specific treatment options according tic mainstays of treatment endure across the life cycle,
to the individual’s priorities. several phases of life present particular challenges.
2. Components of Psychoeducation There exist few data on treatment of bipolar disorder
A. The disorder
(1) Biological basis in childhood. Treatments are chosen by extension from
(a) Genetic factors (especially for persons of the adult literature, with the one caveat that there have
childbearing age) been rare cases of liver failure in conjunction with val-
(b) Possible brain mechanisms
(2) Environmental components
proic acid use in children younger than 10 years of age
(a) Psychosocial factors who have been exposed to multiple anticonvulsants.
(b) Physical environmental factors In pregnancy, there is some evidence that lithium
(3) Course and outcome may be teratogenic, associated with increased rates
(a) Prevalence
(b) Episode types and patterns of cardiac abnormalities, although more recent data
(c) Potential triggers for episodes indicate that this risk may be overestimated. Valproic
(d) Comorbidities and complications acid and perhaps carbamazepine have been associated
B. Treatment
(1) Somatic therapies: somatic and psychosocial with neural tube defects, leaving the neuroleptics, anti-
(a) Goals depressants, and ECT as the preferable management
(b) Side effect recognition and management strategies during pregnancy, particularly during the
(c) Costs and benefits of individual treatment options
first trimester. It should be kept in mind, however, that
(2) Coping skills
(a) Recognition of early warning signs of relapse treatment decisions are based on risk, not certainty.
(b) Avoidance/management of triggers for episodes Risk of fetal malformation, parental attitude toward
(c) Activation of adaptive coping behaviors and raising children with birth defects, severity of illness,
avoidance of maladaptive responses
and ease of management with alternative therapies all
need to be considered in conjunction with the woman
and her partner.
in participating more effectively in treatment. In this lat- Aging also presents certain treatment concerns. Tri-
ter regard, treatment is geared toward improving “host cyclic antidepressants may be associated with clinically
factors,” that is, those factors not directly due to the dis- significant cardiac conduction abnormalities, hypoten-
ease but that have an impact on its course or treatment, sion, sedation, glaucoma, and urinary retention, partic-
through education, support, and problem solving. Such ularly in the presence of prostatic hypertrophy. These
host factors include illness management skills, which are of even greater concern in the elderly. The risk of
may be improved through psychoeducation and attention sedation due to neuroleptics and benzodiazepines, and
to building the therapeutic alliance. Basics of education of hypotension due to low-potency neuroleptics can
are summarized in Table 28-9. also particularly complicate treatment of elderly per-
Five main types of psychotherapy have been studied in sons with bipolar disorder. Such side effects can cause
bipolar disorder: couples–partners, group interpersonal far-reaching and serious complications, such as hip
or psychoeducative, cognitive–behavioral, family, and fracture, which is not infrequently the initial event in a
interpersonal and social rhythms. Couples–partners, cascade of complications that can be terminal.
cognitive–behavioral, and family methods all have By contrast, lithium, carbamazepine, and valproic
some randomized clinical trials data supporting a role acid are relatively well tolerated in the elderly once
in improving clinical outcome or functional outcome or attention is given to the slower clearance of drugs in
the intermediate outcome variable of improving illness general in this population group. The risk of clinically
management skills. The degree of convergent validity significant renal toxicity with appropriately dosed
across interventions regarding agenda for disease man- lithium is not great. Although glomerular filtration rate
agement information and skills to be imparted is quite decreases with age in persons treated with lithium, the
rate of decline does not appear to be accelerated by Disorder are diagnosed as Bipolar Affective Disorder
lithium treatment. Nonetheless, careful monitoring of in ICD-10). However, ICD-10 Diagnostic Criteria for
renal function is needed in the elderly. Research does include diagnostic criteria for bipolar II
In addition, increasing age is clearly a risk factor for in its appendix, which are identical to the criteria set in
hypothyroidism, as is lithium use. Thus, elderly persons DSM-IV-TR.
taking lithium should be followed up carefully for dec- For cyclothymic disorder, the ICD-10 Diagnostic
rements in thyroid function, although hypothyroidism Criteria for Research provides list of symptoms that
is not an indication for lithium discontinuation but must be associated with the periods of depressed mood
rather simply for thyroid hormone supplementation. and hypomania, which differ from the ICD-10 item sets
for dysthymic disorder and hypomania. In contrast, the
DSM-IV-TR definition of cyclothymic disorder just re-
fers to numerous periods of hypomania and depressive
DIAGNOSTIC CRITERIA
symptoms.
The ICD-10 item set for a manic episode contains nine
items in contrast to the seven items in the DSM-IV-TR
criteria set, the two additional items being marked sex-
ual energy or indiscretions and loss of normal social DSM-IV-TR Diagnostic Criteria
inhibitions. However, the number of items required by
ICD-10 Diagnostic Criteria for Research remains the BIPOLAR I DISORDER, MOST RECENT EPISODE [INDICATE
HYPOMANIC, MANIC, MIXED, DEPRESSED, OR UNSPECIFIED]
same as the number in DSM-IV-TR (i.e., three items
if mood is euphoric, four items if mood is irritable), A. Currently (or most recently) in a Hypomanic (296.40),
which is likely to result in a more inclusive diagnosis of Manic (296.4x), Mixed (296.6x), or Major Depressive
Episode (296.5x). If the criteria except for duration are
a manic episode in ICD-10. Furthermore, the duration met for one of these episodes, the episode is consider
of mixed episodes differs, with DSM-IV-TR requiring a is considered unspecified (296.7).
duration of 1 week (as is the case for a manic episode), Note: An x in the diagnostic code indicates that a fifth
whereas the ICD-10 Diagnostic Criteria for Research digit indicating severity is required.
require a duration of at least 2 weeks. B. There has previously been at least one Manic, Mixed,
The criteria sets for hypomanic episode differ as or Major Depressive Episode.
C. The mood episodes in Criteria A and B are not better
well. The ICD-10 Diagnostic Criteria for Research con- accounted for by Schizoaffective Disorder and are not
tain several additional items (increased sexual energy superimposed on Schizophrenia, Schizophreni-form
Disorder, Delusion Disorder, or Psychotic Disorder
and increased sociability) and do not include the DSM- Not Otherwise Specified.
IV-TR items, inflated self-esteem and flight of ideas.
Furthermore, ICD-10 does not require that the change If the full criteria are currently met for a Manic or
Mixed Episode, specify its current clinical status and/or
in mood be observed by others. features:
Regarding the definition of bipolar I disorder, in
Mild, Moderate, Severe Without Psychotic Features/
addition to differences in the diagnostic criteria for a Sever With Psychotic Features
manic and major depressive episode, the ICD-10 defi- With Catatonic Features
nition of “Bipolar Affective Disorder” (i.e., any com- With Postpartum Onset
bination of hypomanic, manic, mixed, and depressive Reprinted with permission from DSM-IV-TR Guidebook. Copy-
right 2004, Michael B First, Allen Frances, and Harold Alan
episodes) does not distinguish between bipolar I and Pincus.
bipolar II disorder (i.e., cases of DSM-IV-TR Bipolar II
CHAPTER
29 Anxiety Disorders:
Panic Disorder with
and without Agoraphobia
DIAGNOSIS
According to the DSM-IV-TR, panic disorder is defined
by recurrent and unexpected panic attacks. At least one 300.01 PANIC DISORDER WITHOUT AGORAPHOBIA AND 300.21
PANIC DISORDER WITH AGORAPHOBIA
of these attacks must be followed by 1 month or more
of (1) persistent concern about having more attacks, (2) A. Both (1) and (2):
worry about the implications or consequences of the at- (1) recurrent unexpected Panic Attacks
tack, or (3) changes to typical behavioral patterns (e.g., (2) at least one of the attacks has been followed
avoidance of work or school activities) as a result of by 1 month (or more) of one (or more) of the
following:
the attack. In addition, the panic attacks must not stem
(a) persistent concern about having additional
solely from the direct effects of illicit substance use, attacks
medication, or a general medical condition (e.g., hyper- (b) worry about the implications of the attack or
thyroidism, vestibular dysfunction) and are not better its consequences (e.g., losing control, having a
heart attack, “going crazy”)
explained by another mental disorder (such as social (c) a significant change in behavior related to the
phobia for attacks that occur only in social situations). attacks
A diagnosis of panic disorder with agoraphobia is war- B. This criterion differs for Panic Disorder With and With-
ranted when the criteria for panic disorder are satisfied out Agoraphobia as follows:
and accompanied by agoraphobia. For 300.21 Panic Disorder With Agoraphobia: the
presence of Agoraphobia
Although panic attacks are a cardinal feature of For 300.01 Panic Disorder Without Agoraphobia:
panic disorder and in combination with agoraphobia absence of Agoraphobia
(i.e., anxiety about being in a place or a situation that is C. The Panic Attacks are not due to the direct physio-
not easily escaped or where help is not easily accessible logical effects of a substance (e.g., a drug of abuse,
if panic occurs) are essential to a diagnosis of panic medication) or a general medical condition (e.g.,
hyperthyroidism).
disorder with agoraphobia, the criteria sets for panic at- D. The Panic Attacks are not better accounted for by
tacks (see DSM-IV-TR diagnostic criteria for Panic At- another mental disorder, such as Social Phobia (e.g.,
tack, page 293) and for agoraphobia (see DSM-IV-TR occurring on exposure to feared social situations),
Specific Phobia (e.g., on exposure to the phobic
diagnostic criteria for Agoraphobia, page 293) are listed situation), Obsessive-Compulsive Disorder (e.g.,
separately as stand-alone, noncodable conditions that on exposure to dirt in someone with an obsession
about contamination), Posttraumatic Stress Disor-
are referred to by the diagnostic criteria for panic disorder (e.g., in response to stimuli associated with a
der and agoraphobia without history of panic disorder. severe stressor), or Separation Anxiety Disorder
Notwithstanding, accurate diagnosis is difficult without (e.g., in response to being away from home or close
relatives).
a proficient understanding of these features. While the
criteria for agoraphobia are generally straightforward, Note: This is a summary of two criteria sets.
panic attacks can be difficult to understand. Reprinted with permission from DSM-IV-TR Guidebook. Copy-
Many people report having what they consider to right 2004, Michael B First, Allen Frances, and Harold Alan
Pincus.
be a panic attack during or in association with actual
physical threat (i.e., a true alarm situation). It is, how-
ever, important to distinguish between a fear reaction
Chapter 29 • Anxiety Disorders: Panic Disorder with and without Agoraphobia 293
(i.e., almost invariably occur when exposed to a situa-

DSM-IV-TR Diagnostic Criteria tional trigger or when anticipating it), and situationally
PANIC ATTACK
predisposed (i.e., usually, but not necessarily, occur
when exposed to a situational trigger or when antici-
A panic attack is a discrete period of intense fear or pating it). The term limited symptom attacks is used to
discomfort in the absence of real danger that develops
abruptly, reaches a peak within 10 min, and is accompa- refer to panic-like episodes comprising fewer than four
nied by four (or more) of the following symptoms: symptoms.
A. palpitations, pounding heart, or accelerated heart Although unexpected panic attacks are required for
rate a diagnosis of panic disorder, not all panic attacks that
B. sweating occur in panic disorder are unexpected. The occurrence
C. trembling or shaking
D. sensations of shortness of breath or smothering of unexpected attacks can wax and wane and over the
E. feeling of choking developmental course of the disorder; they tend to be-
F. chest pain or discomfort
G. nausea or abdominal distress
come situationally bound or predisposed. Moreover,
H. feeling dizzy, unsteady, light-headed, or faint unexpected panic attacks as well as those that are situ-
I. derealization (feelings of unreality) or depersonaliza- ationally bound or predisposed can occur in the context
tion (being detached from oneself)
J. fear of losing control or going crazy of other mental disorders, including all of the other anx-
K. fear of dying iety disorders (e.g., a person with social phobia might
L. paresthesias (numbness or tingling sensations) have an occasional unexpected panic attack without the
M. chills or hot flushes
other features required to diagnose panic disorder; a
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 dog phobic might panic whenever a large dog is en-
American Psychiatric Association. countered) and some general medical conditions. A
clear understanding of the distinction between types of
panic attacks outlined in the DSM-IV-TR provides a
in response to actual threat and a panic attack. In an foundation for diagnosis and differential diagnosis.
attempt to do so, the DSM-IV-TR has clarified that Panic disorder with or without agoraphobia is associ-
panic attacks occur “in the absence of real danger” ated with impaired occupational and social function-
(page 430). Such attacks involve a paroxysmal occur- ing and poor overall quality of life. People with panic
rence of intense fear or discomfort accompanied by a disorder, compared to people in the general population,
minimum of 4 of the 13 symptoms shown in the di- report poorer physical health. Panic disorder is a lead-
agnostic criteria for Panic Attack. The DSM-IV-TR ing reason for seeking emergency department consul-
recognizes three characteristic types of panic attacks, tations and a leading cause for seeking mental health
including those that are unexpected (i.e., not associated services, surpassing both schizophrenia and mood
with an identifiable internal or external trigger and ap- disorders. Panic disorder exceeds the economic costs
pear to occur “out of the blue”), situationally bound associated with many other anxiety disorders such as
social phobia, generalized anxiety disorder, and obses-
sive–compulsive disorder. The high medical costs are
partly because individuals with panic disorder quite of-
ten present to their primary care physician or hospital
AGORAPHOBIA emergency departments, thinking they are in imminent
danger of dying or “going crazy.” In these settings, in-
A. Agoraphobia is characterized by anxiety about being dividuals may undergo a series of extensive medical
in places or situations from which escape might be
difficult (or embarrassing) or in which help may not tests before panic disorder is, if ever, finally diagnosed.
be available in the event of having an unexpected or Ruling out general medical conditions is good clini-
situationally predisposed panic attack or panic-like cal practice but the process contributes substantially
symptoms. Agoraphobic fears typically involve char-
acteristic clusters of situations, such as being outside to the costs that panic disorder places on health care
the home alone, being in a crowd, standing in a line, systems.
being on a bridge, or traveling in a motor vehicle.
B. The situations are avoided or are endured with marked
When assessing for the presence of panic disorder,
distress or worry about having a panic attack or panic- the most comprehensive and accurate diagnostic infor-
like symptoms. Confronting situations is aided by the mation emerges when the clinician uses open-ended
presence of a companion.
C. The anxiety or avoidance is not better accounted for questions and empathic listening, combined with struc-
by another mental disorder. tured inquiry about specific events and symptoms. To
Reprinted with permission from the Diagnostic and Statistical gain more detailed information on panic attacks, cli-
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 nicians and clinical researchers are increasingly in-
cluding some form of prospective monitoring in their
assessment batteries. The most widely used are the hospital emergency department where she was given a
panic attack records. The individual is provided with brief medical evaluation, reassured that she was sim-
a definition of a panic attack and then given a pad of ply experiencing anxiety and given a prescription for
panic attack records that can be readily carried in a lorazepam. In the following months, Sandra continued
purse or pocket. The individual is instructed to carry to experience unexpected panic attacks and became
the records at all times and to complete one record increasingly convinced that she was losing control
(sheet) for each full-blown or limited symptom attack, of her mind. Most of her panics occurred unexpect-
soon after the attack occurs. edly during the day, although they sometimes also oc-
Consider the application of the panic attack record to curred at night, wrenching her out of a deep sleep. An
the following case vignette. Sandra B. was a 20-year- example of how Sandra B. might complete the panic
old college student who presented to a student health attack record for one of her panic attacks is shown in
clinic reporting recurrent panic attacks. Her first at- Figure 29-1. These records are then reviewed during
tack occurred seven months earlier while smoking treatment sessions to glean information about the links
marijuana at an end-of-term party. At the time, she felt among beliefs, bodily sensations, and safety behaviors,
depersonalized, dizzy, short of breath, and her heart and to assess treatment progress.
was beating wildly. Sandra had an overwhelming fear Sandra B. reported that the panic attack summarized
that she was going crazy. Friends took her to a nearby in Figure 29-1 occurred when she was in a neighborhood
PANIC ATTACK RECORD
Sandra.B.
NAME: ____________________
Oct 2
DATE: ________ 4pm
TIME: __________ 15
DURATION (min): _________
WITH: SPOUSE ________ FRIEND ______ STRANGER ________ ALONE _______
STRESSFUL SITUATION: YES / NO EXPECTED: YES / NO
MAXIMUM ANXIETY (CIRCLE)
0 -------- 1 -------- 2 -------- 3 -------- 4 -------- 5 -------- 6 -------- 7 -------- 8

NONE M ODERATE EXTREME
SENSATIONS (CHECK):
POUNDING HEART SWEATING HOT/COLD FLASH
TIGHT/PAINFUL CHOKING ____ FEAR OF DYING ____

CHEST
BREATHLESS NAUSEA ____ FEAR OF GOING CRAZY
DIZZY UNREALITY FEAR OF LOSING CONTROL
TREMBLING ____ NUMB/TINGLE
THOUGHTS OR MENTAL IMAGES AT THE TIME (DESCRIBE):
I’m losing contact with reality

________________________________________________________________
Figure 29-1 A completed panic attack record for Sandra B.

supermarket. As she walked down the aisle, she looked alcohol abuse or dependence than those without
at the long rows of fluorescent lights and then began to agoraphobia.
feel mildly depersonalized. Upon noticing this sensa- The 1-year prevalence for any panic attack, whether
tion, she began to increasingly worry that the deper- unexpected or situationally cued, is approximately
sonalization might become so intense that she would 28%. Lifetime prevalence rates for unexpected panic
lose all contact with reality, to the point that she would attacks and agoraphobia are approximately 4% and
be permanently insane. This greatly frightened her and 9%, respectively. Investigations of unexpected panic
led to an increase in the intensity of arousal sensations. attacks in college student samples using self-report
In an effort to reduce the intensity of the feared deper- methodology have revealed similar rates, ranging from
sonalization, she averted her gaze from the lights and approximately 5% to 11%.
began studying the list of ingredients on cereal boxes. The National Comorbidity Study has reported the
This distracting safety behavior calmed her down and lifetime prevalence of panic disorder (with or without
reduced the feared depersonalization to the point that agoraphobia) in the general population to be 3.5%.
she was able to make her way to the express check- However, despite uncertainty as to the reason, this
out counter and leave with the grocery items she had rate is somewhat of an anomaly in the literature. Most
collected. epidemiological studies, including those based on Epi-
Lifetime comorbidity in panic disorder is common, demiologic Catchment Area and other data sources,
with over 90% of community-dwelling and treatment- have consistently shown lifetime rates between 1% and
seeking individuals having had symptoms meeting 2%. Despite some minor variation, lifetime prevalence
diagnostic threshold for at least one other disorder. rates are generally consistent around the world. One-
Epidemiological studies indicate that major depressive year prevalence rates in the general community also
disorder occurs in up to 65% of individuals with panic vary slightly from lifetime rates, being between 0.2%
disorder at some point in their lives. In approximately and 1.7%. In treatment-seeking individuals, the preva-
two-thirds of these cases, the symptoms of depression lence of panic disorder is considerably higher. Approx-
develop along with, or secondary to, panic disorder. imately 10% of individuals in mental health clinics and
However, since depression precedes panic disorder in between 10% and 60% in various medical specialty
the remaining third, depressive symptoms co-occurring clinics (e.g., cardiology, respiratory, vestibular) have
with panic disorder cannot be considered simply as a panic disorder. Panic disorder with agoraphobia is
demoralized response to paroxysms of anxiety. While more common than panic disorder without agoraphobia
the risk of developing secondary depression appears in clinical samples.
to be more closely associated with the severity of ago- The clinical features of panic disorder such as
raphobia than with the severity or frequency of panic number and severity of symptoms are much the same
attacks, this may be a confound of misdiagnosing of across the sexes. However, women are diagnosed with
some behavioral manifestations of depression as ago- panic disorder more than twice as often as men. Recent
raphobia. Panic disorder and depression do not appear research indicates that women are more likely to have
to be identical disorders and their co-occurrence may panic disorder with agoraphobia and that they are more
be due to a shared diathesis or mutual exacerbation of likely to have recurrence of symptoms after remission
symptoms. of their panic attacks than are men. Men, on the other
As illustrated in the case of Sandra B., panic dis- hand, are more likely to have panic disorder without
order can be precipitated by the use of psychotropic agoraphobia and are more likely to self-medicate with
drugs. Risk is higher with chronic use. Alcohol has alcohol than are women. The literature remains unclear
been identified as playing a precipitating, maintaining, as to why these sex differences exist but alludes to the
and aggravating role in panic disorder. The 6-month possible role of biological and/or socialization factors.
prevalence of alcohol abuse or dependence in panic
disorder has been reported to be 40% in men and 13%
Course
in women. These rates are higher than those observed
in people with other anxiety disorders and those with Age of onset for panic disorder is distributed bimo-
no anxiety disorder. Although alcohol problems have dally, typically developing between 15 and 19 or 25
been reported to precede panic disorder in a majority and 30 years. Panic disorder symptoms may wax
of cases, most reports indicate that alcohol problems and wane but, if left untreated, the typical course is
develop secondary to panic disorder, often as a means chronic. Data from a sample of individuals assessed
of self-medication. Those having panic disorder with and treated through the Harvard/Brown Anxiety Dis-
agoraphobia appear to be at greater risk for comorbid orders Research Program and followed prospectively
over a 5-year period indicated remission rates in both have side effects, with the most problematic being a
men and women to be 39%. In general, among those short-term increase in arousal-related sensations. To
receiving tertiary treatment, approximately 30% of overcome this problem, SSRIs can be started at a low
individuals have symptoms that are in remission, dose (e.g., 5–10 mg/d for paroxetine; 12.5–25 mg/d for
40–50% are improved but still have significant symp- sertraline) and then increased gradually (e.g., up to
toms, and 20–30% are unimproved or worse at 6 to 10 10–50 mg/d for paroxetine; up to 25–200 mg/d for ser-
years follow-up. traline). The choice of SSRI is determined on the ba-
sis of several factors, including side effects, individual
preference, and the individual’s history of responding
(or not responding) to particular agents.
A complete assessment for panic disorder includes a For drug refractory individuals, or individuals who
general medical evaluation, consisting of a medical are unable to tolerate SSRI side effects, combination
history, review of organ systems, physical examina- medications are sometimes used. For example, SSRIs
tion, and blood tests. A general medical evaluation is can be augmented with benzodiazepines. The latter are
important for identifying general medical conditions used to dampen the side effects of SSRIs. Despite some
that mimic or exacerbate panic attacks or panic-like positive preliminary reports supporting this strategy,
symptoms (e.g., seizure disorders, cardiac conditions, its value in the treatment of panic disorder remains
pheochromocytoma). These disorders should be inves- to be properly evaluated. An alternative strategy is to
tigated and treated before contemplating a course of change the individual’s medication. Some of the newer,
panic disorder treatment. It is also important to rule out non-SSRI antidepressants could be considered, such as
the other anxiety disorders and major depressive disor- venlafaxine, duloxetine, buproprion, or gabapentin. A
der as primary factors in the person’s panic attacks and concern with using these medications to treat panic dis-
avoidance prior to initiating treatment for panic disor- order is that there are fewer data to guide the clinician.
der. See Figure 29-2 for a decision tree outlining the Another approach to the drug refractory individual
differential diagnosis for a panic attack. is to use a psychosocial treatment such as cognitive–
behavioral therapy (CBT), as an alternative or adjunc-
tive intervention.
TREATMENT
There are a number of approaches that can be taken in
treating panic disorder with and without agoraphobia
(see Figure 29-3). CBT treatment packages include a number of compo-
nents, such as psychoeducation (e.g., information about
the cognitive model of panic), breathing retraining,
Somatic Treatment
cognitive restructuring, relaxation exercises, intero-
Controlled studies show that effective antipanic medi- ceptive exposure, and situational exposure. Breathing
cations include tricyclic antidepressants (e.g., imi- retraining involves teaching the individual to breathe
pramine), monoamine oxidase inhibitors (MAOIs; with the diaphragm rather than with the chest mus-
e.g., phenelzine), high-potency benzodiazepines (e.g., cles. Cognitive restructuring focuses on challenging
alprazolam), and SSRIs (e.g., fluoxetine). These treat- individual’s beliefs about the dangerousness of bodily
ments have broadly similar efficacy, although there is sensations (e.g., challenging the belief that palpitations
some evidence that SSRIs tend to be most effective. lead to heart attacks).
The classes of medication differ in their side effects Interoceptive exposure involves inducing feared
and their contraindications. Anticholinergic effects bodily sensations to further teach individuals that
(e.g., blurred vision, dry mouth) are common prob- the sensations are harmless. For example, Sandra B.’s
lems with tricyclics. They are also contraindicated in treatment involved interoceptive exposure exercises
individuals with particular comorbid cardiac disor- that induced depersonalization. Several tasks were
ders. Dietary restrictions (i.e., abstaining from foods used, including (1) staring at a ceiling fluorescent light
containing tyramine) are a limitation of many MAOIs. for 1 minute, (2) staring at her reflection in the mirror
Sedation, impaired motor coordination, and addiction for 2 minutes, and (3) staring at a spot on the wall for
are concerns with benzodiazepines. 3 minutes. Multiple tasks were used in order to promote
When efficacy and side effects are considered to- the generalization of treatment effects (i.e., to help her
gether, SSRIs emerge as the most promising drug learn that depersonalization was harmless regardless
treatments for panic disorder. However, even SSRIs of how it arises).
Panic Attacks
Yes
Are attacks due to the direct effects Anxiety Disorder Due to
of a general medical condition? a General Medical Condition
No
Are symtoms in
Yes excess of those No
Are attacks due to the direct effects
of a substance (including recreational ususally encountered Substance Intoxication;
drug, medication, or toxin)? with intoxication or Substance Withdrawal
withdrawal?
No Yes
Substance-Induced
Anxiety Disorder
Does the patient experience recurrent Yes No

unexpected panic attacks accompanied Is there evidence Panic Disorder without
by at least 1 month of concern, worry, of agoraphobia? Agoraphobia
or behaviour change?
Yes Panic Disorder with
No Agoraphobia
Yes
Is the primary trigger for panic attacks the
fear of embarrassment in social situations? Social Phobia
No
Yes
Is the primary trigger for panic attacks an
object (e.g., dogs, spiders) or situation Specific Phobia
(e.g., seeing blood, driving)?
No
Yes
Is the primary trigger for panic attacks
exposure to situations resembling prior Posttraumatic Stress
traumatic experience? Disorder
No
Is the primary trigger for panic attacks exposure to a Yes

focus of an obsessional concern (e.g., exposure to Obsessive−Compulsive
garbage in a person with contamination obsessions)? Disorder
No
Yes No
Are there clinically significant, discrete Is this anxiety in response Anxiety Disorder Not
periods of anxiety not covered above? to an identifiable stressor? Otherwise Specified
No Yes
Adjustment Disorder
Anxiety is not likely of clinical significance.
Figure 29-2 A decision tree for assessment of patients presenting with panic attacks.
Is panic disorder the primary condition in

No
need of treatment (e.g., is the patient Treat other conditions first
depressed and suicidal?)?
Yes
Does the patient have a strong preference Commence with preferred treatment
Yes
for one treatment over another (e.g., drugs (providing the patient requests an
vs CBT)? empirically supported treatment)
No
Has the patient failed to respond to a

Yes
previous course of panic treatment (e.g., Consider an alternative treatment
drugs vs CBT)?
No
Initiate treatment of panic attacks. Choose an

empirically supported treatment based on the
therapist's competency.
Medications
CBT
(e.g., SSRIs)
Refer for CBT
Implement CBT during

drug taper to reduce risk of
relapse
After panic attacks have been reduced, treat residual

problems, such as agoraphobic avoidance.
Figure 29-3 A decision tree for treating panic disorder and agoraphobic avoidance.
Situational exposure involves activities that bring imipramine at posttreatment. Preliminary evidence sug-
the individual into feared situations such as shopping gests that CBT is effective in treating individuals who
malls, bridges, or tunnels. In Sandra B.’s case, situ- have failed to respond to pharmacotherapies. Follow-up
ational and interoceptive exposure were combined. She studies suggest that CBT is effective in the long term
was asked to visit a lighting store to spend time inspect- and is likely to be more effective than short-term phar-
ing the various fluorescent lamps. Exposure exercises macological treatment. It is not known whether drug
are often framed as “behavioral experiments” to test in- treatments would be as effective as CBT if individuals
dividuals’ beliefs about the catastrophic consequences remained on their medications. Any conclusions about
of arousal-related sensations. Sandra B.’s exposure ex- the long-term efficacy of panic treatments are neces-
ercises helped her test the belief that depersonalization sarily tentative because individuals sometimes seek ad-
leads to permanent insanity. The exercises were also ditional treatment during the follow-up interval.
used to help her test the alternative, noncatastrophic be- Several other approaches have been used in the treat-
lief that depersonalization is an unpleasant but harm- ment of panic disorder, including psychodynamic psy-
less experience. chotherapies, hypnosis, Eye Movement Desensitization
A common practice in CBT is to encourage individ- and Reprocessing (EMDR), and mindfulness medita-
uals to refrain from engaging in safety behaviors. Prior tion. Support for these treatments is limited largely to
to treatment, Sandra B. typically engaged in distrac- case studies and uncontrolled trials. Controlled stud-
tion whenever she was exposed to depersonalization- ies, although few in number, indicate that hypnosis and
inducing stimuli such as fluorescent lights. The CBT EMDR are of limited value in treating panic disorder.
therapist encouraged her to refrain from distraction Interventions that look more promising are mindfulness
so she could learn that depersonalization is harmless, meditation and psychodynamic psychotherapies modi-
even when it becomes intense. Evidence suggests that fied to specifically focus on panic symptoms. However,
reducing safety behaviors improves treatment efficacy. none has been extensively evaluated as a panic treat-
Despite the advantages of exposure exercises, they are ment and none has been compared with empirically
medically contraindicated in some cases. For example, supported treatments such as CBT or SSRIs.
a hyperventilation exercise would not be used in an in-
dividual with severe asthma.
Combined Treatments
A large body of evidence shows that CBT is effective
in reducing panic attacks, agoraphobia, and associated Many clinicians believe the optimal treatment consists
symptoms such as depression. However, not all CBT of drugs combined with some form of psychosocial in-
interventions may be necessary. Interoceptive expo- tervention. This view arose from observations that even
sure, situational exposure, and cognitive restructuring the most effective drugs and the most effective psycho-
are the most widely used and supported interventions. social interventions do not eliminate panic disorder in
Several studies suggest that breathing retraining re- all cases. It was thought that combination treatments
duces panic frequency. However, recent research casts might be a way to improve treatment outcome. The
doubt about the importance of hyperventilation in available evidence provides mixed support for this
producing panic attacks. This suggests that breathing view. Evidence suggests that the efficacy of CBT is not
retraining may only be useful for a minority of indi- improved when it is combined with either diazepam
viduals, for which chest breathing or hyperventilation or alprazolam. In fact, some studies have found that
plays a role in producing panic symptoms. Breathing the efficacy of situational exposure is worsened when
retraining may be counterproductive if it prevents indi- alprazolam is added.
viduals from learning that their catastrophic beliefs are Several studies have compared CBT to CBT combined
unfounded. Given these concerns, breathing retraining with imipramine. These results have also been mixed.
should be used sparingly in the treatment of panic dis- Adding imipramine in the range of 150–300 mg/day to
order. If used at all, the clinician should ensure that either situational exposure or CBT sometimes improves
the individual understands that breathing exercises are treatment outcome in the short term, provided that in-
used to remove unpleasant but harmless sensations. dividuals are able to tolerate the dose. Any advantage
Interoceptive exposure and cognitive restructuring are of combined treatment tends to be lost at follow-up.
important for helping individuals learn that the sensa- Similarly, studies of combining CBT with SSRIs (flu-
tions are not dangerous. voxamine or paroxetine) have produced mixed results,
How effective is CBT compared to other thera- with some studies finding the combination is no better
pies? A growing literature suggests that the efficacy of than CBT alone, others finding that the combination is
CBT is equal to or greater than that of alprazolam and most effective, and yet others finding the combination
to be most effective for some symptoms but not others. set except that ICD-10 includes an additional item (i.e.,
Methodological limitations of these studies might ac- dry mouth). In contrast to the DSM-IV-TR algorithm,
count for the inconsistent findings. which does not give special weight to any particular
It remains unclear whether treatment outcome is en- symptom, the ICD-10 algorithm requires that at least
hanced by combining CBT with SSRIs. Neuroanatomi- one of the symptoms be palpitations, sweating, trem-
cal models of panic disorder with their dual emphasis bling, or dry mouth. Like DSM-IV-TR, ICD-10 requires
on cortical and serotonergic mechanisms suggest that recurrent panic attacks but, in contrast to DSM-IV-TR,
this combined treatment might be superior to CBT it does not include a criterion requiring that the panic
alone and to SSRIs alone. On the other hand, pharma- attacks be clinically significant.
cotherapies such as SSRIs might undermine the indi- The ICD-10 Diagnostic Criteria for Research for
vidual’s confidence in implementing CBT, particularly Agoraphobia differ markedly from the DSM-IV-TR
if they attribute their gains to medications rather than criteria. The ICD-10 Diagnostic Criteria for Research
to their own efforts at using the skills learned in CBT. specify that there be fear or avoidance of at least two
Large, well-designed studies are needed to explore of the following situations: crowds, public places,
these important issues. traveling alone, or traveling away from home. Further-
A more promising type of combined therapy is a more, ICD-10 requires that at least two symptoms of
sequential approach, in which individuals are treated anxiety (i.e., from the list of 14 panic symptoms) be
with pharmacotherapy during the acute phase, and then present together on at least one occasion and that these
are treated with CBT as the medication is phased out. anxiety symptoms be “restricted to, or predominate
Several studies have shown that adding CBT during in, the feared situations or contemplation of the feared
the tapering period for alprazolam and clonazepam re- situations.” In contrast, DSM-IV-TR Agoraphobia is
duces the relapse rate associated with these drugs. defined in terms of “anxiety about being in places or
situations from which escape might be difficult (or em-
barrassing) or in which help may not be available in the
event of having an unexpected or situationally predis-
DIAGNOSTIC CRITERIA
posed panic attack.” No specific avoided situations or
The ICD-10 Diagnostic Criteria for Research for a specific types of anxiety symptoms are required for a
panic attack are identical to the DSM-IV-TR criteria diagnosis.
CHAPTER
Social and Specific Phobias
DIAGNOSIS threat cues and therefore are more likely to experience

fear in the face of perceived immediate threat.
The experience of fear and the related emotion of anxi-
Fear and anxiety are not always adaptive, however.
ety are universal and familiar to everyone. Fear exists
At times, the responses can occur in the absence of any
in all cultures and appears to exist across species. Pre-
realistic threat or it may be out of proportion to the ac-
sumably, the purpose of fear is to protect an organism
tual danger. Almost everyone has situations that arouse
from immediate threat and to mobilize the body for
anxiety and fear despite the fact that the actual risk is
quick action to avoid danger. Emotion theorists con-
minimal. It is not unusual to become anxious before a
sider fear to be an alarm response that fires in the pres-
job interview or a speech. Many individuals feel fearful
ence of imminent threat or danger. The function of the
when exposed to situations such as dental visits, seeing
primarily noradrenergic-mediated fear response is to
certain animals, or being at certain heights. For some
facilitate immediate escape from threat (flight) or at-
people, these fears reach extreme levels and may cause
tack on the source of threat (fight). Therefore, fear is
significant distress or impairment in functioning. It is
often referred to as a fight-or-flight response. All the
at this point that what we typically refer to as shyness
manifestations of fear are consistent with its protective
and fearfulness might meet diagnostic criteria for so-
function. For example, heart rate and breathing rate in-
cial phobia or specific phobia, respectively.
crease to meet the increased oxygen needs of the body,
In the DSM-IV-TR, social phobia (also known as
increased perspiration helps to cool the body to facili-
social anxiety disorder) is defined as a “marked and
tate escape, and pupils dilate to enhance visual acuity.
persistent fear of one or more social or performance
Anxiety, on the other hand, is a future-oriented
situations in which the person is exposed to unfamiliar
mood state in which the individual anticipates the pos-
people or to possible scrutiny of others” (see DSM-IV-
sibility of threat and experiences a sense of uncontrol-
TR diagnostic criteria, page 302). Typical situations
lability focused on the upcoming negative event. In the
feared by individuals with social phobia include meet-
DSM-IV-TR, anxiety is defined as “the apprehensive
ing new people, interacting with others, attending par-
anticipation of future danger or misfortune accompa-
ties or meetings, speaking formally, eating or writing
nied by a feeling of dysphoria or somatic symptoms of
in front of others, dealing with people in authority, and
tension” (p. 820). If one were to put anxiety into words,
being assertive. Specific phobia is defined as a “marked
one might say, “Something bad might happen soon. I
and persistent fear that is excessive or unreasonable,
am not sure I can cope with it but I have to be ready
cued by the presence or anticipation of a specific object
to try.” Anxiety is primarily mediated by the gamma-
or situation (e.g., flying, heights, animals, receiving an
aminobutyric acid-benzodiazepine system.
injection, seeing blood)” (see DSM-IV-TR diagnostic
Despite evidence that fear and anxiety are mediated
criteria, page 302).
by different brain systems, anxiety and fear are related,
The diagnostic criteria for specific and social pho-
which makes sense ethologically. Experiencing anxi-
bias share many features. For both disorders, the pho-
ety after encountering signals of impending danger
bic situation must almost invariably lead to an anxiety
seems to lower the threshold for fear that is triggered
response (immediately, in the case of specific phobias),
when danger actually occurs (e.g., being attacked by a
which may take the form of a panic attack. In addition,
mugger or almost being hit by an automobile). Anxiety
the individual must recognize that the fear is excessive
leads to a shift in attention toward the source of danger
or unreasonable (although this feature may be absent
so that individuals become more vigilant for relevant
in children), avoid the phobic situation or endure it

300.23 SOCIAL PHOBIA (SOCIAL ANXIETY DISORDER) 300.29 SPECIFIC PHOBIA
A. A marked and persistent fear of one or more social A. Marked and persistent fear that is excessive or unrea-
or performance situations in which the person is ex- sonable, cued by the presence or anticipation of a
posed to unfamiliar people or to possible scrutiny by specific object or situation (e.g., flying, heights, ani-
others. The individual fears that he or she will act in a mals, receiving an injection, seeing blood).
way (or show anxiety symptoms) that will be humiliat- B. Exposure to the phobic stimulus almost invariably
ing or embarrassing. Note: In children, there must be provokes an immediate anxiety response, which may
evidence of the capacity for age-appropriate social retake the form of a situationally bound or situationally
lationships with familiar people and the anxiety must predisposed panic attack. Note: In children, the anxi-
occur in peer settings, not just in interactions with ety may be expressed by crying, tantrums, freezing, or
adults. clinging.
B. Exposure to the feared social situation almost invari- C. The person recognizes that the fear is excessive or
ably provokes anxiety, which may take the form of unreasonable. Note: In children, this feature may be
a situationally bound or situationally predisposed absent.
panic attack. Note: In children, the anxiety may be D. The phobic situation(s) is avoided or else is endured
expressed by crying, tantrums, freezing, or shrinking with intense anxiety or distress.
away from social situations with unfamiliar people. E. The avoidance, anxious anticipation, or distress in
C. The person recognizes that the fear is excessive or the feared situation(s) interferes significantly with the
unreasonable. Note: In children, this feature may be person’s normal routine, occupational (or academic)
absent. functioning, or social activities or relationships, or
D. The feared social or performance situations are there is marked distress about having the phobia.
avoided or else are endured with intense anxiety or F. In individuals under age 18 years, the duration is at
distress. least 6 months.
E. The avoidance, anxious anticipation, or distress in the G. The anxiety, panic attacks, and phobic avoidance as-
feared social or performance situation(s) interferes sig- sociated with the specific object or situation are not
nificantly with the person’s normal routine, occupa- better accounted for by another mental disorder, such
tional (or academic) functioning, or social activities or as obsessive–compulsive disorder (e.g., fear of dirt in
relationships, or there is marked distress about having someone with an obsession about contamination),
the phobia. posttraumatic stress disorder (e.g., avoidance of stimuli
F. In individuals under age 18 years, the duration is at associated with a severe stressor), separation-anxiety
least 6 months. disorder (e.g., avoidance of school), social phobia
G. The fear or avoidance is not due to the direct physi- (e.g., avoidance of social situations because of fear of
ological effects of a substance (e.g., a drug of abuse, embarrassment), panic disorder with agoraphobia, or
a medication) or a general medical condition and is agoraphobia without history of panic disorder.
not better accounted for by another mental disorder
(e.g., panic disorder with or without agoraphobia, Specify type:
separation-anxiety disorder, body dysmorphic disor-
Animal type
der, a pervasive developmental disorder, or schizoid
personality disorder). Natural environment type (e.g., heights, storms, water)
H. If a general medical condition or another mental dis-
Blood–injection–injury type
order is present, the fear in criterion A is unrelated to
it, for example, the fear is not of stuttering, trembling Situational type (e.g., airplanes, elevators, enclosed
in Parkinson’s disease, exhibiting abnormal eating be- places)
havior in anorexia nervosa or bulimia nervosa.
Other type (e.g., fear of choking, vomiting, or contracting
an illness; in children, fear of loud sounds or costumed
Specify if:
characters)
Generalized: if the fears include most social situations Reprinted with permission from the Diagnostic and Statistical
(also consider the additional diagnosis of avoidant per- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
sonality disorder) American Psychiatric Association.
viduals with this disability would experience, a diag-
nosis of anxiety disorder not otherwise specified may
with intense distress, and experience marked distress be appropriate.
or functional impairment as a result of the phobia. In Finally, for both disorders the fear must not be bet-
the case of social phobia, the fear must not be related ter accounted for by another problem. For example,
to another mental disorder or medical condition. For an individual with obsessive–compulsive disorder
example, if an individual develops difficulties com- who fears contamination from contact with injections
municating after suffering a stroke, the fear must be would not receive an additional diagnosis of specific
unrelated to having other people notice one’s problems phobia unless there were additional concerns about
in speaking. However, if the clinician judges that social injections that were unrelated to contamination (e.g.,
anxiety is substantially in excess of what most indi- fear of fainting during an injection, fear of pain from
Chapter 30 • Anxiety Disorders: Social and Specific Phobias 303
the needle). Each diagnosis has specifiers and sub- Perhaps the most consistent difference among spe-
types to allow for the provision of more specific di- cific phobia types is the tendency for individuals with
agnostic information. For social phobia, the clinician blood–injury–injection phobias to report a history of
can specify whether the phobia is generalized (i.e., fainting in the phobic situation. Although all phobia
includes most social situations). For specific phobias, types are associated with panic attacks in the phobic
the clinician can indicate which one of five types best situation, only individuals with blood and injection
describes the focus of the phobia: animal, natural phobias report fainting. Specifically, individuals with
environment, blood–injection–injury, situational, or blood–injury–injection phobias experience a dipha-
other. sic physiological response, which includes an initial
These specific phobia types tend to differ on a vari- increase in arousal followed by a sharp drop in heart
ety of dimensions including age at onset, sex composi- rate and blood pressure that can lead to fainting. This
tion, patterns of covariation among phobias, focus of response occurs at times in approximately 70% of peo-
apprehension, timing and predictability of the phobic ple with blood phobias and 56% of those with injection
response, and type of physiological reaction during ex- phobias and seems to be unique to situations involving
posure to the phobic situation. blood and medical procedures. In other words, people
Although anxiety about physical sensations and the who faint in these situations still show the usual type
occurrence of panic is a feature typically associated of response (i.e., increased arousal) in other situations
with panic disorder, several studies have shown that that they fear. Disgust has been identified as a potential
panic-focused and symptom-focused apprehensions mediator of faintness associated with blood–injury–
are not unique to panic disorder and agoraphobia. In- injection stimuli.
dividuals with specific phobias tend to report anxiety The different responses experienced in different
about the sensations (e.g., racing heart, breathlessness, phobias have been explained from an evolutionary
dizziness) typically associated with their fear. Also, perspective. As mentioned earlier, the typical phobic
there is evidence that in addition to fearing danger responses of fear and panic are adaptive in that the
from the phobic object (e.g., a plane crash, being bitten increased arousal facilitates escape. In contrast, the
by a dog), many individuals with specific phobias fear most adaptive response during serious injury may be
danger as a result of their reaction in the phobic situa- a drop in blood pressure to prevent excessive bleeding.
tion (e.g., having a panic attack, losing control, being It has been suggested that this response is mediated
embarrassed). Also, the few relevant studies that have by an overactive sinoaortic baroreflex that is triggered
been conducted suggest that there may be differences by heightened arousal in situations involving blood or
in sensation-focused apprehension across specific pho- needles. Of course, in people with blood and injection
bia types. phobias, the response is excessive and unwarranted, as
Data are converging to indicate that individuals there is typically no danger of excessive blood loss.
with phobias from the situational (e.g., claustrophobia) Having a phobia of one specific phobia type makes an
and blood–injury–injection types may be especially individual more likely to have additional phobias of the
internally focused on their fear. Whereas individuals same type than of other types. For example, about 70%
with situational phobias tend to fear the possible con- of individuals with blood phobias tend to have injec-
sequences of panic, those with blood-injury-injection tion phobias as well. However, the research on the clas-
phobias seem uniquely concerned about sensations that sification of specific phobia types is inconsistent. For
indicate that fainting is imminent (e.g., lightheaded- example, in several studies, height phobias tend to be
ness, hot flashes). associated with situational phobias (e.g., claustropho-
Specific phobia types may differ with respect to tim- bia), despite height phobias being listed as an example
ing and predictability of the phobic response as well. of the natural environment type in DSM-IV-TR.
One study based on retrospective self-reports found that Specific phobias tend to co-occur with other specific
individuals with phobias of driving, enclosed places, phobias. One study found that 76% of a sample of 915
and blood–injury were more likely to report that their individuals with a lifetime history of specific phobias
fear was delayed in the phobic situation than were those had one or more co-occurring specific phobias, which
with animal phobias. This suggests that delayed and is consistent with research showing that individuals
unpredictable panic attacks may be more characteristic with specific phobias often report multiple fears on a
of situational phobias than of other phobia types, con- fear survey. However, other research indicates that co-
sistent with the argument that situational phobias share morbid phobias may not be as prevalent and that num-
more features with agoraphobia than do other specific bers in previous studies may have been inflated by a
phobia types. lack of discrimination between multiple phobias and
fears of multiple situations that are accounted for by clinical interview may be especially frightening. Even
a single phobia. A recent methodologically rigorous completing self-report questionnaires in the waiting
study found that 15% of individuals with a principal di- room may be difficult for individuals who fear writ-
agnosis of specific phobia also met criteria for another ing in front of others. The clinician should be sensi-
type of specific phobia. tive to this possibility and provide reassurance when
For social phobia, DSM-IV-TR allows the clinician appropriate.
to specify whether it is “generalized,” that is, it includes Behavioral testing is an important part of any com-
most social situations. In addition, a “discrete or cir- prehensive evaluation for a phobic disorder. This is
cumscribed” subtype is often used by investigators to particularly the case if behavioral or cognitive–behav-
describe individuals with only one domain of social ioral treatment is used. Because most individuals with
anxiety, usually involving performance-related situa- phobias avoid the objects and situations that they fear,
tions (e.g., public speaking). Several studies have ex- individuals may find it difficult to describe the subtle
amined differences among these subtypes. Specifically, cues that affect their fear in the situation. In addition, it
individuals with generalized social phobias tend to be is not unusual for individuals to misjudge the amount of
younger, less educated, and less likely to be employed fear that they typically experience in the phobic situa-
than are individuals with discrete social phobias. In ad- tion. A behavioral approach test can be useful for iden-
dition, generalized social phobias are associated with tifying specific fear triggers as well as for assessing the
more depression, anxiety, general distress, and con- intensity of the individual’s fear in the actual situation.
cerns about negative evaluation from others. Discrete To conduct a behavioral approach test, individuals
social phobias appear to be associated with greater should be instructed to enter the phobic situation for
cardiac reactivity. several minutes. For example, an individual with a
As is the case with most disorders, a comprehensive snake phobia should be instructed to stand as close as
assessment is important in helping the clinician to de- possible to a live snake and note the specific cues that
cide which treatment approach is most appropriate for a affect the fear (e.g., size of snake, color, movement) and
given individual. In the case of specific and social pho- the intensity of the fear (perhaps rating it on a 0–100
bias, a thorough evaluation should include a structured point scale). Individuals should pay special attention
or semistructured interview, self-report measures, and to their physical sensations (e.g., palpitations, sweating,
a behavioral assessment. Each of these measures pro- blushing), negative thoughts (e.g., “I will fall from this
vides different types of information that may be rel- balcony”), and anxious coping strategies (e.g., escape,
evant to later treatment decisions. avoidance, distraction).
During all parts of the initial evaluation, the clinician Specific phobias tend to be more common among
should be sensitive to several issues. First, for many in- women than men. This finding seems to be strongest
dividuals with phobias, even discussing the phobic ob- for phobias from the animal type, whereas sex differ-
ject can provoke anxiety. For example, some individuals ences are smaller for height phobias and blood–injury–
with spider phobias experience panic attacks when they injection phobias. In addition, social phobia tends to
discuss spiders. Some individuals with blood phobias be slightly more prevalent among women than men, al-
faint when they discuss surgical procedures. Therefore, though these differences are relatively small. Whereas
the clinician should ask the individual whether discuss- men tend to be more fearful than women of urinating in
ing the phobic object or situation will provoke anxiety. public bathrooms and returning items to a store, women
If the interview is likely to be a source of stress, the are more likely to be fearful than men of a number of
clinician should emphasize the importance of the in- situations including talking to people in authority, pub-
formation that is being collected, as well as the poten- lic speaking, being the center of attention, expressing
tial therapeutic value of discussing the feared object. disagreement, and throwing a party.
As described later, exposure to the feared stimulus is A variety of studies have shown that specific phobias,
an essential component of the treatment of most spe- social phobia, and related conditions exist across cul-
cific phobias. Of course, the interviewer should use his tures. For example, in Japan, a condition exists called
or her judgment when deciding how much to push the taijin kyôfu in which individuals have an “obsession of
individual in the first session. For treatment to be ef- shame.” This condition has much overlap with social
fective, establishing trust in the clinician early in the phobia in that it is often accompanied by fears of blush-
course of treatment is essential. ing, having improper facial expressions in the presence
With respect to social phobia, the assessment itself of others, looking at others, shaking, and perspiring in
may be considered a phobic stimulus. Because individ- front of others. Interestingly, in some other cultures, the
uals with social phobia fear the evaluation of others, a sex ratio for phobias tends to be reversed. For example,
in studies from Saudi Arabia and India, up to 80% of Phobias are among the most common mental dis-
individuals reporting for treatment of phobias were orders. Findings based on large community samples
male. Similarly, in Japan about 60% of individuals with from five sites in the Epidemiological Catchment Area
taijin kyôfu are male. In the case of phobias in India, it (ECA) study yielded lifetime prevalence estimates of
has been suggested that traditional gender roles may ac- 11.25% for specific phobias and 2.73% for social pho-
count for the difference in treatment seeking in Indian bia. Estimates from the National Comorbidity Sur-
men and women. Specifically, Indian women are often vey (NCS) were consistent with previous findings on
discouraged from leaving the house alone or convers- specific phobias: a lifetime prevalence of 11.30% in a
ing with others without the husband’s permission. It is sample of more than 8000 individuals from across the
difficult to know how cultural expectations affect sex United States. For social phobia, data from the NCS in-
differences in phobias in other cultures. dicate a lifetime prevalence rate of 13.3%, much higher
Clinicians treating individuals from different cul- than that in the previously reported ECA study. This
tures should be aware of cultural differences in pres- difference is likely due to methodological variations
entation and response to treatment. Many cues that a across the two studies.
clinician might use to aid in the diagnosis of social Specific phobias and social phobia tend to run in
phobia in white Americans may not be useful for di- families. It appears that being a first-degree relative
agnosing the condition in other cultures. For exam- of an individual with a specific phobia puts one at a
ple, although many clinicians interpret a lack of eye greater risk for a specific phobia compared with first-
contact as indicating shyness or a lack of assertive- degree relatives of never mentally ill controls (31%
ness, avoidance of eye contact among Japanese and versus 11%). However, the particular phobia that is
Mexican-Americans is often viewed as a sign of re- transmitted is usually different from that in the rela-
spect. In contrast to white Americans, Japanese are tive, although it is often from the same general type
apparently more likely to view smiling as a sign of (e.g., animal, situational). Furthermore, relatives of
embarrassment or discomfort. Furthermore, cultural people with specific phobias are not at increased risk
differences in tone and volume of speech may lead for other types of anxiety disorders (including social
mental health professional to misinterpretations. For phobia) or subclinical fears. The heritability of blood
example, whereas white Americans often are uncom- and injection phobias may be even greater than that for
fortable with silence in a conversation, British and other phobias.
Arab individuals may be more likely to use silence Findings for individuals with social phobia and their
for privacy and other cultures use silence to indicate families show a similar pattern. In one study, 16% of
agreement among the parties or as a sign of respect. first-degree relatives of subjects with social phobia had
In addition, Asian individuals have been reported to symptoms that met criteria for social phobia, whereas
speak more quietly than white Americans, who in only 5% of first-degree relatives of never mentally ill
turn speak more quietly than those from Arab coun- control subjects had social phobia. Furthermore, there
tries. Therefore, differences in the volume of speech is no increased risk among relatives of people with so-
should not be taken to imply differences in assertive- cial phobia to develop other anxiety disorders.
ness or other indicators of social anxiety.
Among children, specific and social fears are com-
Course
mon. Because these fears may be transient, DSM-IV-
TR has included a provision that social and specific The mean age at onset of social phobia is in the mid-
phobias not be assigned in children unless they are dle teens. The age at onset of specific phobias varies
present for more than 6 months. In addition, children depending on the phobia type, with phobias of ani-
may be less likely than adults to recognize that their mals, blood, storms, and water tending to begin in early
phobia is excessive or unrealistic. The specific objects childhood, phobias of heights beginning in the teens,
feared by children are often similar to those feared by and situational phobias beginning in the late teens to
adults, although children may be more likely to fear ob- middle twenties. Although childhood fears are often
jects and situations that are not easily classified in the transient (e.g., most children outgrow fear of the dark
four main specific phobia types in DSM-IV-TR (e.g., without treatment), fears that persist into adulthood
balloons or costumed characters). In addition, children usually have a chronic course unless treated.
often report specific and social phobias having to do Although many phobias begin after a traumatic
with school. Children with social phobia tend to avoid event, many individuals do not recall the specific onset
changing for gym class in front of others, eating in the of their fear, and few empirical data have examined the
cafeteria, or speaking in front of the class. initial period after the fear onset. Clinically, however,
some individuals report a sudden onset of fear, whereas by one’s panic symptoms). In contrast, individuals with
others report a more gradual onset. Studies examining specific and social phobias are usually concerned about
the onset of phobias have tended to assess the onset of other aspects of the situation as well (e.g., being hit by
the fear rather than the onset of the phobia (i.e., the another driver, saying something foolish).
point at which the fear creates significant distress or Consider two examples in which the differential di-
functional impairment). Phobias typically began at an agnosis with panic disorder might be especially diffi-
average of 9 years after the fear onset. Anecdotally, the cult. First, individuals with claustrophobia are typically
types of factors leading to the transition from fear to extremely concerned about being unable to escape from
phobia included gradual increases in the intensity of the phobic situation as well as being unable to breathe
fear, additional traumatic events (e.g., panic attacks, in the situation. Therefore, like individuals with panic
car accidents), increased life stress, and changes in liv- disorder and agoraphobia, they usually report height-
ing situation (e.g., starting a job that requires exposure ened anxiety about the possibility of panicking. The
to heights). Similarly, it is not unusual for individuals main variable to consider in such a case is the presence
with social phobia to report having been shy as chil- of panic attacks outside of claustrophobic situations.
dren, although their anxiety may not have reached pho- If panic attacks occur exclusively in enclosed places,
bic proportions until later. a diagnosis of specific phobia might best describe the
problem. In contrast, if the individual has unexpected
or uncued panic attacks as well, a diagnosis of panic
disorder might be more appropriate.
Social anxiety is associated with a variety of DSM-IV- A second example is an individual who avoids a
TR disorders. Similarly, several disorders other than broad range of situations including shopping malls,
specific phobia are associated with fear and avoidance supermarkets, walking on busy streets, and various so-
of circumscribed stimuli. Therefore, accurate diagnosis cial situations including parties, meetings, and public
of specific and social phobias depends on a thorough speaking. Without more information, this individu-
understanding of the DSM-IV-TR criteria and knowl- al’s problem might appear to meet criteria for social
edge of how to distinguish these disorders from related phobia, panic disorder with agoraphobia, or both di-
conditions. Correct diagnosis depends on being able to agnoses. As mentioned earlier, individuals with panic
evaluate the individual’s focus of apprehension, reasons disorder often avoid social situations because of anxi-
for avoidance, and range of situations feared. ety about panicking in public. In addition, individuals
Panic disorder with agoraphobia may easily be mis- with social phobia might avoid situations that are typi-
diagnosed as social phobia or a specific phobia (es- cally avoided by individuals with agoraphobia for fear
pecially the situational type). For example, many in- of seeing someone that they know or of being observed
dividuals with panic disorder avoid a variety of social by strangers. To make the diagnosis in this case, it is
situations because of anxiety about having others no- necessary to assess the reasons for avoidance.
tice their symptoms. In addition, some individuals with It may be difficult to distinguish among types of
panic disorder may avoid circumscribed situations, such specific phobias. For example, is a bridge phobia best
as flying, despite reporting no other significant avoid- considered a situational type (i.e., driving) or a natural
ance. Four variables should be considered in making environment type (i.e., heights)? This decision should
the differential diagnosis: (1) type and number of panic be based on the context of the bridge phobia. If the in-
attacks, (2) focus of apprehension, (3) number of situa- dividual fears falling or fears other high places, a height
tions avoided, and (4) level of intercurrent anxiety. phobia may be the appropriate diagnosis. In contrast,
Individuals with panic disorder experience unex- if bridges are one of many driving-related situations
pected panic attacks and heightened anxiety outside of that the person fears, a driving phobia might be more
the phobic situation, whereas those with specific and appropriate.
social phobias typically do not. In addition, individu- Other diagnoses that should be considered before a
als with panic disorder are more likely than those with diagnosis of specific phobia is assigned include post-
specific and social phobias to report fear and avoidance traumatic stress disorder (PTSD) (if the fear follows a
of a broad range of situations typically associated with life-threatening trauma and is accompanied by other
agoraphobia (e.g., flying, enclosed places, crowds, be- PTSD symptoms such as reexperiencing the trauma),
ing alone, shopping malls). Finally, individuals with obsessive–compulsive disorder (if the fear is related
panic disorder are typically concerned only about the to an obsession, e.g., contamination), hypochondria-
possibility of panicking in the phobic situation or about sis (if the fear is related to a belief that he or she has
the consequences of panicking (e.g., being embarrassed some serious illness), separation-anxiety disorder (if
the fear is of situations that might lead to separation encounters snakes, and never even thinks about snakes
from the family, for example, traveling on an airplane would probably not be diagnosed with a specific pho-
without one’s parents), eating disorders (if the fear is of bia. In contrast, when an individual’s fear of snakes
eating certain foods but not related to a fear of chok- leads to avoidance of walking through parks, camping,
ing), and psychotic disorders (if the fear is related to a swimming, and watching certain television programs,
delusion). despite having an interest in doing these things, a diag-
Social phobia should not be diagnosed if the fear is nosis of specific phobia would be appropriate.
related entirely to another disorder. For example, if an Similar factors should be considered in deciding at
individual with obsessive–compulsive disorder avoids what point normal shyness reaches an intensity that
social situations only because of the embarrassment of warrants a diagnosis of social phobia. An individual
having others notice her or his excessive hand wash- who is somewhat quiet in groups or when meeting new
ing, a diagnosis of social phobia would not be given. people but does not avoid these situations and is not
Furthermore, individuals with depression, schizoid especially distressed by his or her shyness would prob-
personality disorder, or a pervasive developmental dis- ably not receive a diagnosis of social phobia. In con-
order may avoid social situations because of a lack of trast, an individual who frequently refuses invitations
interest in spending time with others. To be considered to socialize because of anxiety, quits a job because of
social phobia, an individual must avoid these situations anxiety about having to talk to customers, or is dis-
specifically because of anxiety about being evaluated tressed about her or his social anxiety would be likely
negatively. to receive a diagnosis of social phobia.
In the case of generalized social phobia, the diag- Diagnostic decision trees for social and specific pho-
nosis of avoidant personality disorder should be con- bias are presented in Figures 30-1 and 30-2.
sidered as well. Individuals with avoidant personality
disorder tend to display more interpersonal sensitivity
TREATMENT
and have poorer social skills than social phobic indi-
viduals without avoidant personality disorder. Further- The main goal of treatment is to decrease fear and pho-
more, most studies suggest that the differences between bic avoidance to a level that no longer causes significant
avoidant personality disorder and social phobia are distress or functional impairment. In some cases, treat-
more quantitative than qualitative and that the former ment includes strategies for improving specific skill
may simply be a more severe form of the latter. There- deficits as well. For example, individuals with social
fore, most individuals who meet criteria for avoidant phobia may lack adequate social skills and can some-
personality disorder will meet criteria for social phobia times benefit from social skills training. Likewise,
as well. some individuals with specific phobias of driving may
Finally, social and specific phobias should be dis- have poor driving skills if their fear prevented them
tinguished from normal states of fear and anxiety. from learning how to drive properly. Typically, effec-
Many individuals report mild fears of circumscribed tive treatment for social phobia lasts several months,
situations or mild shyness in certain social situations. although treatment of discrete social phobias (e.g., pub-
Others may report intense fears of public speaking or lic speaking) may take less time. Specific phobias can
heights but insist that these situations rarely arise and usually be treated relatively quickly. In fact, for cer-
that they have no interest in being in these situations. tain phobias, the vast majority of individuals are able
For the criteria for a specific or social phobia to be met, to achieve clinically significant, long-lasting improve-
the individual must report significant distress about ment in as little as one session of behavioral treatment.
having the fear or must report significant impairment Effective treatments fall into one of two main cat-
in functioning. egories: pharmacological treatment and cognitive–
A variety of factors should be considered in decid- behavioral therapy (CBT). Pharmacological treatments
ing whether an individual’s fear exceeds the threshold have been used effectively for treating social phobia,
necessary for a diagnosis of specific or social phobia. although it is generally accepted that they are of lim-
To make the differential diagnosis between normal ited utility for treating specific phobias. In contrast,
fears and clinical phobias, the clinician should consider CBT has been used with success for the treatment of
the extent of the individual’s avoidance, the frequency specific and social phobias. Despite the existence of ef-
with which the phobic stimulus is encountered, and the fective treatments, fewer than half of those who seek
degree to which the individual is bothered by having treatment in an anxiety disorders specialty clinic have
the fear. For example, an individual who fears see- previously received evidence-based treatments for their
ing snakes in the wild but who lives in the city, never social anxiety. Tables 30-1 and 30-2 summarize various
Person reports marked and persistent fear of one

or more social or performance situations that are
avoided or endured with extreme distress. Feared
social situation triggers an immediate anxiety
response (which may take the form of a
situationally bound or situationally predisposed
panic attack) and is avoided or endured with
extreme distress.
Yes
Person recognizes that fear is No

excessive or unreasonable. Consider psychotic disorder
Yes
Fear causes significant distress No

or functional impairment. Consider no mental disorder
Yes
Fear is not better accounted for by another mental

disorder (e.g., if the person reports unexpected
panic attacks, intercurrent anxiety, and the anxiety No
is not exclusively focused on the possibility of Consider alternative diagnosis
having a panic attack in the social situation, a
diagnosis of panic disorder may be appropriate).
Yes
Fear is not related to having the symptoms or No

features of a general medical condition or any Rule out social phobia
other mental disorder noticed by others.
Yes
Social phobia criteria are met. Specify if

generalized (i.e., fear includes most social
situations).
Figure 30-1 Diagnostic decision tree for social phobia.
treatments for social and specific phobias. Treatment with the research to date is that it has not taken into
decision trees for social and specific phobias are pre- account differences among specific phobia types. For
sented in Figures 30-3 and 30-4. example, claustrophobia and other phobias of the situ-
ational type appear to share more features with panic
disorder than with the other specific phobia types.
Somatic Treatments
Therefore, medications that are effective for panic dis-
Although pharmacotherapy is generally thought to be order (e.g., imipramine, alprazolam) may prove to be
ineffective for specific phobias, it is not uncommon for effective for situational phobias. Although there are
phobic individuals occasionally to be prescribed low few studies examining this hypothesis, some data sug-
dosages of benzodiazepines to be taken in the phobic gest that benzodiazepines may be helpful in the short
situation (e.g., while flying). Studies have been con- term but lead to greater relapse in the long term and
ducted that have examined the use of benzodiazepines possibly interfere with the therapeutic effects of ex-
and beta blockers alone or in combination with behav- posure across sessions. For example, one study found
ioral treatments for specific phobias and in general that CBT and providing a benzodiazepine both led to
have found that drugs do not contribute much to the fear reduction during dental surgery; however, whereas
treatment of specific phobias. However, one problem benzodiazepine treatment was associated with greater
Person reports excessive fear of a specific object

or situation. Phobic stimulus triggers an
immediate anxiety response (which may take the
form of a situationally bound or situationally
predisposed panic attack) and is avoided or
endured with extreme distress.
Yes
Person recognizes that fear is No

Consider psychotic disorder
excessive or unreasonable.
Yes
No
Fear causes significant distress
Consider no mental disorder
or functional impairment.
Yes
Fear is not better accounted for by another mental

disorder (e.g., if the person reports unexpected
panic attacks, intercurrent anxiety, and the anxiety No
Consider alternative diagnosis
is not exclusively focused on the possibility of
having a panic attack in the phobic situation, a
diagnosis of panic disorder may be appropriate).
Yes
Specific phobia criteria are met.

Specify type.
No
Fear is cued by animals Yes Specific phobia

or insects. Animal type
No
Fear is cued by storms, heights, Yes Specific phobia

water, or similar situations. Natural environment type
No
Fear is cued by the sight of blood, Yes Specific phobia

injections, or other medical
Blood-injection-injury type
procedures.
No
Fear is cued by specific situations

such as public transportation, tunnels, Yes Specific phobia
bridges, elevators, flying, driving, or Situational type
enclosed places.
No
Fear is cued by some other Yes Specific phobia

specific situation. Other type
Figure 30-2 Diagnostic decision tree for specific phobia.
relapse during follow-up, CBT was associated with fur- MAOIs such as phenelzine, and reversible inhibitors of
ther improvements. monoamine oxidase A (RIMA) such as moclobemide
In contrast to specific phobias, social phobia has and brofaromine. Numerous controlled trials across
been treated successfully with a variety of pharmaco- a range of SSRIs including sertraline, fluvoxamine,
logical interventions including SSRIs, benzodiazepines and paroxetine have demonstrated their effectiveness
such as clonazepam and alprazolam, traditional in the treatment of social phobia, such that the SSRIs
Table 30-1 Treatments for Social Phobia

Treatment Advantages Disadvantages Rating
Cognitive–behavioral therapy Good treatment response May lead to temporary increases in ⫹⫹⫹⫹
(CBT) (e.g., exposure, cognitive Brief course of treatment discomfort or fear.
restructuring, social skills Treatment gains maintained at
training, education) follow-up
Considered first line.
SSRIs (e.g., paroxetine, fluvoxamine, Good treatment response Side effects are common ⫹⫹⫹
sertraline) Early response, relative to CBT Cost is a factor
Broad spectrum efficacy for May be a risk of relapse after
comorbid disorders (i.e., discontinuation
depression)
Lack of abuse potential
Considered first line
Moclobemide Good treatment response in some Side effects common ⫹⫹
studies Does not separate from placebo in
Fewer side effects than phenelzine some studies
Considered second line Potential exists for relapse after
discontinuation
Benzodiazepines (e.g., clonazepam, Good treatment response Side effects and withdrawal occur ⫹⫹
alprazolam) Considered adjunctive or second line Potential for abuse Relapse after
discontinuation is likely. Does not
treat certain comorbid conditions
(i.e., depression)
MAOIs (e.g., phenelzine) Good treatment response Relatively high rate of adverse ⫹⫹
Early response effects
Considered third line Dietary restrictions must be
followed
Numerous drug interactions
Potential exists for relapse after
discontinuation
Gabapentin Possibly beneficial Side effects are common ⫹⫹
Considered third line More research is needed
β-blockers (e.g., atenolol) Appears to be useful for “stage Drugs are not effective for ⫹
fright” in actors, musicians, and generalized social phobia
other performers Benefits for discrete social phobias
are questionable
Side effects occur
Potential exists for relapse after
discontinuation
⫹⫹⫹⫹ First treatment of choice. Helpful for most patients, with few side effects. Good long-term benefits.
⫹⫹⫹ Helpful for most patients. Potential for relapse after treatment is discontinued.
⫹⫹ More controlled research needed, although preliminary studies suggest potential benefit OR research has been mixed.
⫹ Not especially effective for generalized social phobia.
are currently considered the first-line medication treat- study found that 78% of individuals responded to clon-
ment. Owing to their tolerability and efficacy, the SS- azepam (mean dosage, 2.4 mg/day), whereas only 20%
RIs have been referred to as “the new gold standard” in responded to placebo. Another study comparing clon-
pharmacological treatment for social phobia. Another azepam to cognitive–behavioral group therapy found
benefit of SSRIs is their broad spectrum efficacy for that individuals in both conditions improved signifi-
common comorbid disorders such as depression and cantly and no differences between treatment conditions
panic disorder. Treatment of social phobia with other were observed aside from greater improvement in the
antidepressants (e.g., imipramine, venlafaxine) has clonazepam group at 12 weeks of treatment. In addi-
also been studied in a number of uncontrolled open tri- tion, uncontrolled pilot studies have suggested that al-
als, with positive results. prazolam (mean dosage, 2.9 mg/day) may be effective
Research on the use of anxiolytics for the treat- for social phobia, although more controlled clinical tri-
ment of social phobia have focused on high potency als are needed. The findings on buspirone are mixed,
benzodiazepines (e.g., clonazepam, alprazolam) and with a number of controlled trials finding no significant
the nonbenzodiazepine buspirone. Several studies advantage of buspirone over placebo, which is in con-
have examined the utility of clonazepam for treating trast to previous uncontrolled studies that found some
social phobia. For example, one placebo-controlled benefit.
Table 30-2 Treatments for Specific Phobias

Treatment Advantages Disadvantages Rating
In vivo exposure Highly effective May lead to temporary increases in ⫹⫹⫹⫹

Early response discomfort or fear
Treatment gains maintained at follow-up
Applied tension Highly effective for individuals with Treatment is relevant for a small percentage ⫹⫹⫹
blood–injection phobias who faint of individuals with specific phobias
Early response Treatment gains maintained
at follow-up
Applied relaxation May be effective for some individuals Treatment has not been extensively ⫹⫹
researched for specific phobias
Cognitive therapy May help to reduce anxiety about conducting Treatment has not been extensively ⫹⫹
exposure exercises researched for specific phobias
Treatment is probably not effective alone
Benzodiazepines May reduce anticipatory anxiety before Treatment has not been extensively ⫹⫹
individual enters phobic situation, and researched for specific phobias
may reduce fear, particularly in situational
specific phobias
Treatment is probably not effective alone, in
many cases
Side effects (e.g., sedation) occur
Discontinuation of symptoms may
undermine benefits of treatment
SSRIs May reduce panic sensations for individuals Treatment has not been extensively
with situational phobias that are similar to researched for specific phobias
panic disorder (e.g., claustrophobia)
There are a few studies (primarily case ⫹⫹
reports) with promising results
Discontinuation of medication may result in
a return of fear
⫹⫹⫹⫹ Treatment of choice. Effective for almost all individuals.
⫹⫹⫹ Very effective for a subset of individuals.
⫹⫹ May be helpful for some individuals. More research needed.
Owing to the potentially severe side effects of MAOIs taking gabapentin had significant reductions in social
as well as the necessity for certain dietary restrictions, anxiety compared to the placebo group. However, more
they are not recommended as a first-line treatment. The research is needed to confirm this finding.
findings from more recent trials involving RIMAs have
been less encouraging than initial studies suggested. For
example, a fixed-dose study conducted over 12 weeks
found that moclobemide did not have a significant ben- Numerous studies have shown that exposure-based
efit over placebo at five dosages ranging from 75 to 900 treatments are effective for helping individuals to over-
mg/day. Discontinuation of MAOIs and RIMAs have come a variety of specific phobias, including fears of
been associated with a tendency to relapse. blood, injections, dentists, spiders, snakes, rats, en-
Research on beta blockers indicates that they are no closed places, thunder and lightning, water, flying,
better than placebo for most individuals with general- heights, choking, and balloons. Furthermore, the way
ized social phobia. Although beta blockers have been in which exposure is conducted may make a difference.
used to treat individuals from nonpatient samples with Exposure-based treatments can vary on a variety of
heightened performance anxiety (e.g., people with dimensions including the degree of therapist involve-
public speaking anxiety, musicians with stage fright), ment, duration and intensity of exposure, frequency
their efficacy for treating individuals with discrete so- and number of sessions, and the degree to which the
cial phobia has not been established. Nevertheless, beta feared situation is confronted in imagination versus in
blockers are often prescribed for discrete performance- real life. In addition, because individuals with certain
related social phobias. specific phobias often report a fear of panicking in the
Preliminary findings suggest that gabapentin, a med- feared situation, some investigators have suggested
ication typically used in the treatment of partial sei- that adding various panic management strategies (e.g.,
zures, may be effective in the treatment of social pho- cognitive restructuring, exposure to feared sensations)
bia. A placebo-controlled trial found that individuals may help increase the efficacy of behavioral treatments
Presence of marked social anxiety
Yes
Yes
Mild distress/impairment Recommend self-help readings
No
Moderate/severe distress/impairment Yes

Patient interested in CBT Initiate treatment with cognitive−
CBT available behavior therapy
No
Moderate/severe distress/impairment Yes Initiate treatment with medication

Patient uninterested in CBT (e.g., an SSRI)
CBT unavailable
No Add a secondary treatment (e.g.,

Was the initial treatment effective? add CBT to medication; add
medication to CBT)
Yes
Continue maintenance treatment (e.g.,

maintenance medications, periodic
follow-up CBT sessions)
Figure 30-3 Treatment decision tree for social phobia.
Yes
Presence of specific phobia Exposure-based treatment
Presence of vasovagal fainting response Yes

Add applied muscle tension
(e.g., in blood-injection-injury phobia)
No
Presence of sensation focused fear (e.g., Yes Add exposure to feared physical
fear of breathlessness in claustrophobia) sensations (e.g., hyperventilation)
No
Presence of cognitive distortions or Yes Add cognitive therapy or education

misinformation about feared situation about feared situation
Figure 30-4 Treatment decision tree for specific phobia.

for specific phobias. It remains to be shown whether the is important that exposure practices proceed in a pre-
addition of these strategies will improve the efficacy of dictable way, so that the individual is not surprised by
treatments that include only exposure. unexpected events. Several self-help books and manu-
Several reviews have summarized the effects of the als for treating a range of specific phobias have been
above-mentioned variables on exposure-based treat- published in the past decade and may be helpful for
ments. First, exposure seems to work best when sessions some individuals.
are spaced close together. Second, prolonged exposure Developments in technology are having an impact
seems to be more effective than exposure of shorter on the treatment of specific phobias. Videotapes are
duration. Third, during exposure sessions, individuals commonly used to show feared stimuli to individuals
should be discouraged from engaging in subtle avoid- during exposure. Computer-administered treatments
ance strategies (e.g., distraction) and overreliance on have also been used. More recent is the use of virtual
safety signals (e.g., being accompanied by one’s spouse reality to expose individuals to simulated situations
during exposure). Fourth, real-life exposure is more ef- that are more difficult to replicate in vivo such as flying
fective than exposure in imagination. Fifth, exposure and heights. Although data on the effectiveness of vir-
with some degree of therapist involvement seems to be tual reality is encouraging, other studies indicate that
more effective than exposure that is exclusively con- in vivo exposure is still superior.
ducted without the therapist present. Exposure may be Empirically validated psychosocial interventions
conducted gradually or quickly. Both approaches seem for social phobia have primarily come from a cogni-
to work equally well, although individuals may be more tive–behavioral perspective and include four main
compliant with a gradual approach. Finally, in the case types of treatment: (1) exposure-based strategies, (2)
of blood and injection phobias, the technique called ap- cognitive therapy, (3) social skills training, and (4) ap-
plied muscle tension should be considered as an alter- plied relaxation. Exposure-based treatments involve
native or addition to exposure therapy. Applied muscle repeatedly approaching fear-provoking situations until
tension involves having individuals repeatedly tense they no longer elicit fear. Through repeated exposure,
their muscles, which leads to a temporary increase in individuals learn that their fearful predictions do not
blood pressure and prevents fainting upon exposure to come true despite their having confronted the situation.
blood or medical procedures. Table 30-3 illustrates an example of an exposure hier-
Cognitive strategies have also been used either alone archy that might be used to structure an individual’s
or in conjunction with exposure for treating specific exposure practices. An exposure hierarchy is a list of
phobias. The evidence suggests that the addition of feared situations that are rank ordered by difficulty and
cognitive strategies to exposure may provide added used to guide exposure practices for phobic disorders
benefit for some individuals. including social phobia and specific phobia. The in-
Specific phobias are among the most treatable of the dividual and the therapist generate a list of situations
anxiety disorders. For example, in as little as one ses- that the individual finds anxiety provoking. Items are
sion of guided exposure lasting 2 to 3 hours, the ma- placed in descending order from most anxiety provok-
jority of individuals with animal or injection phobias ing to least anxiety provoking, and each item is rated
are judged much improved or completely recovered. with respect to how anxious the individual might be to
Moreover, exposure conducted with a parent present
was equally effective as exposure treatment conducted Exposure Hierarchy for Generalized Social
alone. However, despite how straightforward the con- Table 30-3
Phobia
cept of exposure may seem, many subtle clinical issues Fear Rating
can lead to problems in implementing exposure-based Item (0–100)
treatments. For example, although an individual might
Have a party and invite everyone from 99
be compliant with therapist-assisted exposure prac- work.
tices, he or she may refuse to attempt exposure prac- Go to work Christmas party for 1 h 90
tices alone between sessions. In such cases, involving without drinking
Invite Cindy to have dinner and see a 85
a spouse or other family member as a coach during movie.
practices at home may help. In addition, gradually in- Go for a job interview 80
creasing the distance between therapist and individual Ask boss for a day off from work 65
Ask questions in a meeting at work 65
during the therapist-assisted exposures will help the Eat lunch with coworkers 60
individual to feel comfortable when practicing alone. Talk to a stranger on the bus 50
However, to maintain the individual’s trust and to max- Talk to cousin on the telephone for 10 min 40
Ask for directions at the gas station. 35
imize the effectiveness of behavioral interventions, it
practice the item. Exposure practices are designed to treatments, individuals may avoid taking medications
help the individual become more comfortable engaging because of side effects, lack of confidence in efficacy,
in the activities from the hierarchy. Cognitive therapy or preference for an alternative type of treatment. If in-
helps individuals identify and change anxious thoughts dividuals are not compliant with medications, the cli-
(e.g., “Others will think I am stupid if I participate in nician should attempt to identify the reasons for poor
a conversation at work”) by teaching them to consider compliance and to suggest methods of increasing com-
alternative ways of interpreting situations and to exam- pliance or changing to another type of treatment.
ine the evidence for their anxious beliefs. Social skills In the case of CBT, common reasons for poor com-
training is designed to help individuals become more pliance are anxiety about conforming to treatment, lack
socially competent when they interact with others. of time, and lack of motivation to conduct the treatment
Treatment strategies may include modeling, behavioral properly. Because CBT requires individuals to confront
rehearsal, corrective feedback, social reinforcement, the situations they fear most, individuals often feel ex-
and homework assignments. Finally, applied relaxation treme anxiety about participating in the treatment. In-
involves learning to relax one’s muscles during rest, dividuals should be reassured that their anxiety is nor-
during movement, and eventually in anxiety-provoking mal and that they will never be forced to do anything
social situations. that they are unwilling to try. Furthermore, the diffi-
Although these methods are presented as four dis- culty of exposure tasks should be increased gradually
tinct treatment approaches, there is often overlap to maximize treatment compliance. If individuals do
among the various treatments. Social skills training not have the time or motivation to conduct treatment as
typically requires exposure to the phobic situation so suggested, therapists should be willing to find ways to
that new skills may be practiced (e.g., behavioral re- make the treatment more accessible to the individual.
hearsal). The same may be said of applied relaxation, For example, involvement of a friend or relative of the
which includes learning to conduct relaxation exercises individual as a coach may allow the individual to con-
in the phobic situation. In fact, most treatments for so- duct more practices without the therapist’s assistance.
cial phobia involve some type of exposure to anxiety- The therapist could also explore the possibility that the
provoking social interactions and performance-related individual consider beginning treatment later, when
tasks. Furthermore, many cognitive–behavioral thera- more time is available.
pists treat individuals using several different strategies Poor motivation can lead to poor compliance with the
delivered in a comprehensive package. treatment procedures. If an individual’s symptoms are
In summary, it seems clear that effective psychoso- not especially severe, the distress and impairment cre-
cial treatments and medications for social phobia exist. ated by the disorder may not be enough to motivate the
Although both types of treatments appear to be equally individual to take medications regularly or to confront
effective, each has advantages and disadvantages. the phobic situation in a systematic way. Furthermore,
Medication treatments may work more quickly and are as an individual improves in treatment, she or he may
less time-consuming for the individual and the thera- experience a decrease in motivation. Individuals should
pist. In contrast, improvement after CBT appears to last be encouraged to continue with treatment assignments
longer. Owing to medication side effects, CBT may be even after improvement. More complete improvements
more appropriate for some individuals. More studies may protect against a return of symptoms.
are needed to examine the efficacy of combined medi- Finally, treatment procedures may be complicated
cation and psychosocial treatments for social phobia. for some individuals. This is especially the case for
CBT. Individuals may fail to complete homework as-
signments (e.g., monitoring anxious cognitions) sim-
Treatment Nonresponse
ply because the treatment rationale and the specifics
Several variables may lead to an initially poor treat- of how to conduct the treatment procedures were not
ment response. Anticipating potential difficulties will made clear. Therefore, therapists should continually
help increase treatment efficacy. Possible reasons for assess the individual’s understanding of the treatment
a worse outcome include poor compliance, poor mo- procedures.
tivation, and poor understanding of the treatment pro-
cedures. In addition, interpersonal issues and other
possible conflicts may interfere with the successful
DIAGNOSTIC CRITERIA
treatment of specific and social phobias.
Individuals fail to comply with treatment procedures The ICD-10 Diagnostic Criteria for Research for Social
for a variety of reasons. In the case of pharmacological Phobia specify that at least two symptoms of anxiety
(i.e., from the list of 14 panic symptoms) be present particular types of anxiety symptoms nor is any restric-
together on at least one occasion along with at least one tion placed on whether anxiety can occur in situations
of the following anxiety symptoms: blushing or shak- other than social situations.
ing, fear of vomiting, and urgency or fear of micturition For specific phobia, the ICD-10 Diagnostic Criteria
or defecation. Furthermore, these anxiety symptoms for Research also specify that the anxiety symptoms be
must be “restricted to, or predominated in, the feared “restricted to, or predominated in, the feared situations
situations or contemplation of the feared situations.” In or contemplation of the feared situation.” DSM-IV-TR
contrast, the DSM-IV-TR criteria do not specify any again does not impose any such restriction.
CHAPTER
31 Anxiety Disorders: Obsessive–

Compulsive Disorder
Obsessive–Compulsive Disorder
predominantly compulsions; the remaining 96% en-
dorsed both obsessions and compulsions Individuals
DIAGNOSIS
who appear to have obsessions without compulsions
Obsessive–compulsive disorder (OCD) is an intriguing frequently have unrecognized reassurance rituals
and often debilitating syndrome characterized by the or mental compulsions, such as repetitive, ritualized
presence of two distinct phenomena: obsessions and praying, in addition to their obsessions. Pure com-
compulsions. Obsessions are intrusive, recurrent, un- pulsions are also unusual in adults, although they do
wanted ideas, thoughts, or impulses that are difficult to occur in children, especially in the young (e.g., 6 to
dismiss, despite their disturbing nature. Compulsions 8 years of age). Most people have both mental and
are repetitive behaviors, either observable or mental, behavioral compulsions; in the DSM-IV field trial,
that are intended to reduce the anxiety engendered 79.5% reported having both mental and behavioral
by obsessions. Both obsessions and compulsions have compulsions, 20.3% had behavioral compulsions only,
been described in a wide variety of mental and neu- and 0.2% had only mental compulsions.
rological disorders. However, obsessions and compul- Contamination obsessions are the most frequently
sions that clearly interfere with the functioning and/or encountered obsessions in OCD. Such obsessions are
cause significant distress are the hallmark of OCD (see usually characterized by a fear of dirt or germs. For ex-
DSM-IV-TR diagnostic criteria, page 317). ample, a 38-year-old computer programmer was exces-
OCD’s clinical presentation is characterized by phe- sively preoccupied with the thought that her apartment
nomenological subtypes based on the content of the would become dirty. She had never allowed a visitor
obsessions and corresponding compulsions. The list into her apartment or worn a coat during the winter, be-
of subtypes in the Yale-Brown Obsessive–Compulsive cause she feared that she would be unable to protect her
Scale (Y-BOCS) (Table 31-1) was generated on the apartment from dirt brought inside by either a visitor or
basis of clinical interviews with OCD patients in the a coat. Excessive washing is the compulsion most com-
1980s. The basic types of obsessions and compulsions monly associated with contamination obsessions. This
seem to be consistent across cultures. The most com- behavior usually occurs after contact with the feared
mon obsession is the fear of contamination, followed object; however, proximity to the feared stimulus is of-
by pathological doubt, a need for symmetry, and ag- ten sufficient to engender severe anxiety and washing
gressive obsessions. The most common compulsion is compulsions, even though the contaminated object has
checking, which is followed by washing, symmetry, the not been touched. Most individuals with washing com-
need to ask or confess, and counting. Children with pulsions perform these rituals in response to a fear of
OCD present most commonly with washing compul- contamination, but these behaviors occasionally occur
sions, which are followed by repeating rituals. in response to a drive for perfection or a need for sym-
Most individuals with OCD have multiple obses- metry. Some individuals, for example, repeatedly wash
sions and compulsions over time, with a particular themselves in the shower until they feel “right” or must
fear or concern dominating the clinical picture at any wash their right arm and then their left arm the same
one time. The presence of obsessions without compul- number of times.
sions, or compulsions without obsessions, is unusual. Need for symmetry is a term that describes a drive
In the DSM-IV OCD field trial of 431 individuals, to order or arrange things perfectly or to perform cer-
only 2% had predominantly obsessions and 2% had tain behaviors symmetrically or in a balanced way.
Chapter 31 • Anxiety Disorders: Obsessive–Compulsive Disorder 317
DSM-IV-TR Diagnostic Criteria Yale-Brown Obsessive–Compulsive Scale

TABLE 31-1
Symptom Checklist
300.3 OBSESSIVE –COMPULSIVE DISORDER Aggressive obsessions
Fear might harm others
A. Either obsessions or compulsions: Fear might harm self
Obsessions as defined by (1), (2), (3), and (4): Violent or horrific images
Fear of blurting out obsessions or insults
(1) recurrent and persistent thoughts, impulses, or im- Fear of doing something embarrassing
ages that are experienced, at some time during the Fear of acting on other impulses (e.g., robbing a bank,
disturbance, as intrusive and inappropriate and that stealing groceries, overeating)
cause marked anxiety or distress Fear of being responsible for things going wrong (e.g.,
(2) the thoughts, impulses, or images are not simply others will lose their job because of the patient)
excessive worries about real-life problems Fear something terrible might happen (e.g., fire, burglary)
(3) the person attempts to ignore or suppress such Other
thoughts, impulses, or images, or to neutralize Contamination obsessions
them with some other thought or action Concerns or disgust with bodily waste (e.g., urine, feces,
(4) the person recognizes that the obsessional saliva)
thoughts, impulses, or images are a product of his Concern with dirt or germs
or her own mind (not imposed from without as in Excessive concern with environmental contaminants
thought insertion) (e.g., asbestos, radiation, toxic wastes)
Compulsions as defined by (1) and (2): Excessive concern with household items (e.g., cleansers,
solvents, pets)
(1) repetitive behaviors (e.g., hand washing, order- Concerned will become ill
ing, checking) or mental acts (e.g., praying, count- Concerned will become ill (aggressive)
ing, repeating words silently) that the person feels Other
driven to perform in response to an obsession, or Sexual obsessions
according to rules that must be applied rigidly Forbidden or perverse sexual thoughts, images, or
(2) the behaviors or mental acts are aimed at prevent- impulses
ing or reducing distress or preventing some dreaded Content involves children
event or situation; however, these behaviors or Content involves animals
mental acts either are not connected in a realistic Content involves incest
way with what they are designed to neutralize or Content involves homosexuality
prevent or are clearly excessive Sexual behavior toward others (aggressive)
B. At some point during the course of the disorder, the Other
person has recognized that the obsessions or compul- Hoarding or collecting obsessions
sions are excessive or unreasonable. Note: This does Religious obsessions
not apply to children. Obsession with need for symmetry or exactness
C. The obsessions or compulsions cause marked distress, Miscellaneous obsessions
are time consuming (take more than 1 hour a day), Need to know or remember
or significantly interfere with the person’s normal rou- Fear of saying certain things
tine, occupational (or academic) functioning, or usual Fear of not saying things just right
social activities or relationships. Intrusive (neutral) images
D. If another Axis I disorder is present, the content of the Intrusive nonsense sounds, words, or music
obsessions or compulsions is not restricted to it (e.g., Other
preoccupation with food in the presence of an eat- Somatic obsession–compulsion
ing disorder; hair pulling in the presence of trichotil- Cleaning or washing compulsions
lomania; concern with appearance in the presence of Excessive or ritualized hand washing
body dysmorphic disorder (BDD); preoccupation with Excessive or ritualized showering, bathing, brushing the
drugs in the presence of a substance use disorder; pre- teeth, or grooming
occupation with having a serious illness in the pres- Involves cleaning of household items or inanimate objects
ence of hypochondriasis; preoccupation with sexual Other measures to prevent contact with contaminants
urges or fantasies in the presence of a paraphilia; or Counting compulsions
guilty ruminations in the presence of major depressive Checking compulsions
disorder). Checking that did not or will not harm others
E. The disturbance is not due to the direct physiological Checking that did not or will not harm self
effects of a substance (e.g., a drug of abuse, a medica- Checking that nothing terrible did or will happen
tion) or a general medical condition. Checking for contaminants
Other
Specify if: Repeating rituals
Ordering or arranging compulsions
With poor insight: if, for most of the time during the cur- Miscellaneous compulsions
rent episode, the person does not recognize that the ob- Mental rituals (other than checking or counting)
sessions and compulsions are excessive or unreasonable Need to tell, ask, or confess
Reprinted with permission from the Diagnostic and Statistical Need to touch
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 Measures to prevent
American Psychiatric Association. Harm to self
Harm to others
Terrible consequences
Other
Individuals describe an urge to repeat motor acts until are plagued by the concern that, as a result of their
they achieve a “just right” feeling that the act has been carelessness, they will be responsible for a dire event.
completed perfectly. Individuals with a prominent need They may worry, for example, that they will start a fire
for symmetry may have little anxiety but rather describe because they neglected to turn off the stove before leav-
feeling unsettled or uneasy if they cannot repeat actions ing the house. Although many individuals report being
or order things to their satisfaction. Individuals with a fairly certain that they performed the act in question
need for symmetry frequently present with obsessional (e.g., locking the door, unplugging the hairdryer, pay-
slowness, taking hours to perform acts such as grooming ing the correct amount on a bill), they cannot dismiss
or brushing their teeth. A 23-year-old cook spent 2 hours the nagging doubt “What if?” Excessive doubt and as-
a day brushing his teeth in a symmetrical fashion and as sociated feelings of excessive responsibility frequently
a result developed gingival erosion. He reported being lead to checking rituals. For example, individuals may
exquisitely aware of exactly how the toothbrush touched spend several hours checking their home before they
each surface of each tooth and of how he placed the leave. As with contamination obsessions, pathological
toothbrush and cup down after finishing. He was unable doubt can lead to marked avoidance behavior. Some in-
to describe any obsession or fear about not performing dividuals become housebound to avoid the responsibil-
this task adequately but rather felt unable to stop until ity of potentially leaving the house unlocked.
he had brushed completely, despite warnings from his There has been considerable interest in the role of
dentist about the harm he was causing. insight, or awareness, in OCD. An ability to recognize
Individuals with somatic obsessions are worried the senselessness of the obsessions and the ability to
about the possibility that they have or will contract an resist obsessional ideas have been considered as the
illness or disease. In the past, the most common so- fundamental components of OCD. However, research
matic obsessions consisted of fears of cancer or vene- findings during the past decade have demonstrated a
real diseases. However, a fear of developing AIDS has continuum of insight in this disorder, which ranges from
become increasingly common. Checking compulsions excellent (i.e., complete awareness of the senselessness
consisting of checking and rechecking the body part of of the content of the obsessions), through poor insight,
concern, as well as reassurance seeking, are commonly to delusional thinking (i.e., the obsessions are held with
associated with this fear. For example, a 29-year-old delusional conviction). Combining data from a number
firefighter spent 3 hours a day examining his throat in of studies, 20–25% of individuals with OCD at some
the mirror and palpating his lymph nodes to determine point during their illness are fairly convinced that their
whether he had throat cancer. obsessions are realistic and that consequences other
People with sexual or aggressive obsessions are than anxiety would occur if they did not perform their
plagued by fears that they might harm others or commit compulsions. Nonetheless, most people with OCD are
a sexually unacceptable act such as molestation. Often, aware that other people think their symptoms are un-
they are fearful not only that they will commit a dread- realistic and that the obsessions are caused by a mental
ful act in the future but also that they have already com- disorder. To reflect the fact that many individuals lack
mitted the act. Individuals are usually horrified by the insight, DSM-IV-TR includes a specifier “With Poor
content of their obsessions and are reluctant to divulge Insight” that applies to “an individual who, for most
them. It is striking that the content of these obsessions of the time in the current episode, does not recognize
tends to consist of ideas that individuals find particu- that the obsessions or compulsions are excessive or un-
larly abhorrent. A 32-year-old librarian who wanted to reasonable.” DSM-IV-TR also acknowledges that the
be a good mother had intrusive thoughts of stabbing beliefs that underlie OCD obsessions can be delusional
her daughter. Individuals with these highly distressing and notes that, in such cases, an additional diagnosis of
obsessions frequently have checking and confession or delusional disorder or psychotic disorder not otherwise
reassurance rituals. They may report themselves to the specified may be appropriate.
police or repeatedly seek out priests to confess their Women appear to develop OCD slightly more fre-
imagined crimes. For example, a 29-year-old secretary quently than do men. A predominance of males has been
constantly checked the local news to be certain that she observed in child and adolescent OCD populations.
had not murdered someone. An unsolved murder case OCD frequently occurs in association with other
caused her tremendous anxiety and led to extensive re- Axis I disorders. In a study of 100 individuals with
assurance rituals. primary OCD, 67 had a lifetime history of major de-
Pathological doubt is a common feature of individu- pressive disorder and 31 had symptoms that met criteria
als with OCD who have a variety of different obsessions for current major depressive disorder. Although it may
and compulsions. Individuals with pathological doubt be difficult to distinguish a primary from a secondary
diagnosis, some individuals with OCD view their de- 2.5%. Although the ECA survey has been criticized as
pressive symptoms as occurring secondary to the de- overestimating OCD’s prevalence, a subsequent study
moralization and hopelessness accompanying their in the United States and several epidemiological stud-
OCD and report that they would not be depressed if ies in other countries have supported its findings.
they did not have OCD. However, others view their ma-
jor depressive symptoms as occurring independently of
Course
their OCD symptoms, which may be less severe when
they cycle into an episode of major depression, because Age at onset usually refers to the age when OCD symp-
they feel too apathetic to be as concerned with their toms (obsessions and compulsions) reach a severity
obsessions and too fatigued to perform compulsions. level, wherein they lead to impaired functioning or
Conversely, OCD symptoms may intensify during de- significant distress or are time consuming (i.e., meet
pressive episodes. DSM-IV-TR criteria for the disorder). Reported age at
Although findings have varied, the generally ac- onset is usually during late adolescence. People with
cepted frequency of tic disorders in individuals with OCD, however, usually describe the onset of minor
OCD is far higher than in the general population, with symptoms in childhood, well before the onset of symp-
a rate of approximately 5–10% for Tourette’s Disorder toms meeting the full criteria for the disorder.
and 20% for any tic disorder. Conversely, individuals In several studies, earlier age at onset has been as-
with Tourette’s disorder have a high rate of comorbid sociated with an increased rate of OCD in first-degree
OCD, with 30–40% reporting obsessive–compulsive relatives. These data suggest that there is a familial
symptoms. The likelihood of childhood onset of OCD type of OCD characterized by early onset. Age at onset
is greater in this group, and the presence of tics is as- of OCD may also be a predictor of course. The vast
sociated with more severe OCD symptoms in children. majority of individuals report a gradual worsening of
There is an increased rate of both OCD and tic disor- obsessions and compulsions prior to the onset of full-
ders in the first-degree relatives of OCD probands with criteria OCD, which is followed by a chronic course.
a family lifetime history of tics and an increased fre- However, a subtype of OCD that begins before puberty
quency of tic disorders in the first-degree relatives of and is characterized by an episodic course with in-
OCD probands compared to controls. tense exacerbations has been described. Exacerbations
Studies of individuals with schizophrenia or schizoaf- of OCD symptoms in this subtype have been linked
fective disorder have found rates of OCD ranging from with Group A beta-hemolytic streptococcal infections,
8% to 46%. This strikingly large range is most likely which has led to the subtype designation of pediatric
due to the OCD criteria used (i.e., subclinical OCD autoimmune neuropsychiatric disorders associated
symptoms versus OCD symptoms severe enough to with streptococcal infections (PANDAS). In a study of
cause significant impairment or distress). Regardless, it 50 children with PANDAS, the average age of onset
is clear that a significant number of people with schizo- was 7.4 years. Whether the course of illness in indi-
phrenia have OCD symptoms that require assessment, viduals with PANDAS continues to be episodic into
and may benefit from treatment. adulthood, or, as is the case with postpubertal onset,
The relationship between OCD and personality dis- tends to be chronic, is not known.
orders, particularly obsessive–compulsive personality The course of OCD is usually waxing and waning—
disorder (OCPD), has received considerable attention. that is, once an individual acquires OCD, obsessions
Early observations noted the presence of OCPD traits or compulsions, or both, are present continuously, with
in individuals with OCD. Systematic studies, however, varying degrees of intensity over time. Relatively few
have yielded inconsistent findings. individuals have either a progressively deteriorating
Until the mid-1980s, OCD was considered extremely course or a truly episodic course.
rare. This perception was based on studies from the
1950s and 1960s that examined the frequency of men-
tal disorders in inpatient and outpatient settings. The
results of a large epidemiological study, the national OCD is sometimes difficult to distinguish from cer-
ECA survey, conducted in the United States in 1984, tain other disorders. Obsessions and compulsions may
painted a different picture of OCD’s prevalence. This appear in the context of other syndromes, which can
study found that OCD was the fourth most common raise the question whether the obsessions and compul-
mental disorder (after the phobias, substance use disor- sions are a symptom of another disorder or whether
ders, and major depressive disorder), with a prevalence both OCD and another disorder are present. A general
of 1.6% over 6 months and a lifetime prevalence of guideline is that if the content of the obsessions is not
limited to the focus of concern of another disorder (e.g., The second issue noted above—how to distinguish
an appearance concern, as in body dysmorphic disor- OCD with insight from OCD without insight—is com-
der [BDD], or food concerns, as in an eating disorder) plex. As previously discussed, insight in OCD is in-
and if the obsessions or compulsions are preoccupying creasingly being recognized as spanning a spectrum
as well as distressing or impairing, OCD should gener- from good to poor to absent. Both clinical observations
ally be diagnosed. Diagnostic dilemmas may also arise and research findings indicate that some individuals
when it is unclear whether certain thoughts are obses- hold their obsessional concerns with delusional inten-
sions or whether, instead, they are ordinary worries, sity, and believe that their concerns are reasonable. In
ruminations, overvalued ideas, or delusions. In a simi- DSM-IV-TR, delusional OCD may be double coded as
lar vein, questions may develop about whether certain both OCD and delusional disorder or as both OCD and
behaviors constitute true compulsions or whether they psychotic disorder not otherwise specified; in other
should instead be conceptualized as impulses, tics, or words, individuals with delusional OCD would receive
addictive behaviors. both diagnoses. This double coding reflects the fact that
Both OCD and the other anxiety disorders are char- it is unclear whether OCD with insight and OCD with-
acterized by the use of avoidance to manage anxiety. out insight constitute the same or different disorders.
However, OCD is distinguished from these disorders Further research using validated scales to assess insight
by the presence of compulsions. For individuals with in OCD is needed to shed light on this question.
preoccupying fears or worries but no rituals, several Differential diagnosis questions have been raised
other features may be useful in establishing the diagno- with regard to kleptomania, trichotillomania, patho-
sis of OCD. In social phobia and specific phobia, fears logical gambling, and other disorders involving im-
are circumscribed and related to specific triggers (in pulsive behaviors. Several features have been said to
specific phobia) or social situations (in social phobia). distinguish these disorders from OCD. For example,
As many as 60% of people with OCD experience full- compulsions—unlike behaviors of the impulse con-
blown panic symptoms. However, unlike panic disor- trol disorders—generally have no gratifying element,
der, in which panic attacks occur spontaneously, panic although they do diminish anxiety. In addition, the af-
symptoms occur in OCD only during exposure to spe- fective state that drives the behaviors associated with
cific feared triggers such as contaminated objects. The these disorders may differ. In OCD, fear is frequently
worries that are present in generalized anxiety disor- the underlying drive that leads to compulsions, which,
der (GAD) are more egosyntonic and involve an exag- in turn, decrease anxiety. In the impulse control dis-
geration of ordinary concerns, whereas the obsessional orders, individuals frequently describe heightened ten-
thinking of OCD is more intrusive, is limited to a spe- sion, but not fear, preceding an impulsive behavior.
cific set of concerns (e.g., contamination, blasphemy), Complex motor tics of Tourette’s disorder may be
and usually has an irrational, senseless, or unreason- difficult to distinguish from OCD compulsions. Both
able quality. tics and compulsions are preceded by an intrusive urge
One question is how to differentiate OCD from psy- and are followed by feelings of relief. However, OCD
chotic disorders such as schizophrenia and delusional compulsions are usually preceded by both anxiety and
disorder. Another question is how to distinguish OCD obsessional concerns, whereas, in Tourette’s disorder,
with insight from OCD without insight (delusional the urge to perform a tic is not preceded by an obses-
OCD). One distinguishing feature between OCD and sional fear. This distinction breaks down to some extent
the psychotic disorders is that the latter are not character- when considering the “just right” perceptions of some
ized by prominent ritualistic behaviors. If compulsions individuals with OCD. The “just right” perception re-
are present in an individual with prominent psychotic fers to the need to perform a certain motor action, such
symptoms, the possibility of a comorbid OCD diagnosis as touching, tapping, checking, ordering, arranging, or
should be considered. Furthermore, although schizo- counting, until it feels right. Determining when an action
phrenia may be characterized by obsessional thinking, has been performed enough or perfectly may depend on
other characteristic features of the disorder, such as tactile, visual, or auditory perceptions. In a study of in-
prominent hallucinations or thought disorder, are also dividuals with Tourette’s disorder and OCD symptoms,
present. With regard to delusional disorder, paranoid most individuals could distinguish between the mental
and grandiose concerns are generally not considered to urge to do something repeatedly until it felt right and
fall under the OCD rubric. However, some other types a physical urge to perform a motor tic. However, it is
of delusional disorder, such as the somatic and jealous sometimes difficult for mental health professionals to
types, seem to bear a close resemblance to OCD and are distinguish between complex tics and compulsions, es-
not always easily distinguished from it. pecially when an individual has both disorders.
Fears of illness that occur in OCD, referred to as so- is that, in contrast, OCPD features are considered ego-
matic obsessions, may be difficult to distinguish from syntonic. In addition, as previously noted, the traits of
hypochondriasis. Usually, however, individuals with restricted affect, excessive devotion to work, and rigid-
somatic obsessions have other current or past classic ity are generally characteristic of OCPD but not OCD.
OCD obsessions unrelated to illness concerns. Individ- Although useful, these guidelines are not absolute, and
uals with OCD also often engage in classic OCD rituals, some individuals defy easy categorization. Some indi-
such as checking or reassurance seeking, in an attempt viduals, for example, spend hours each day engaged in
to diminish their illness concerns. Unlike individuals egosyntonic behaviors such as excessive cleaning; such
with OCD, individuals with hypochondriasis experi- individuals may seek treatment not because they are
ence somatic and visceral sensations. BDD, a preoccu- disturbed by their behaviors but because the behaviors
pation with an imagined or slight defect in appearance cause problems in functioning or family friction. It is
(e.g., thinning hair, facial scarring, or a large nose), has unclear whether some of these individuals should be
many similarities to OCD. Individuals with BDD expe- diagnosed with OCPD or subthreshold OCD.
rience obsessional thinking about the supposed defect
and usually engage in associated repetitive ritualistic
TREATMENT
behaviors, such as mirror checking and reassurance
seeking. Preliminary evidence suggests that BDD also Both pharmacologic and behavioral therapies have
appears similar to OCD in terms of age of onset, course proved effective for OCD. The majority of control-
of illness, and other variables. Nonetheless, emerging led treatment trials have been performed with adults
data suggest that there are some important differences aged 18 to 65 years. However, these therapies have
between the two disorders and they are currently classi- been shown to be effective for individuals of all ages.
fied separately in DSM-IV-TR. Insight, for example, is In general, children and the elderly tolerate most of
more frequently impaired in BDD than in OCD. If the these medications well. For children, lower doses are
content of a individual’s obsessions involves a concern indicated because of lower body mass. For instance,
about a supposed defect in appearance, BDD, rather the recommended dose for clomipramine in children is
than OCD, is the diagnosis that should be given. up to 150 mg/day (3 mg/kg/day) versus 250 mg/day in
Obsessive–compulsive personality disorder is a life- adults. Use of lower doses should also be considered in
long maladaptive personality style characterized by the elderly because their decreased ability to metabo-
perfectionism, excessive attention to detail, indecisive- lize medications can increase the risk of side effects
ness, rigidity, excessive devotion to work, restricted af- and toxicity. Behavioral therapy has also been used
fect, lack of generosity, and hoarding. OCD and OCPD successfully in all age groups, although when treating
have historically been considered variants of the same children with this modality it is usually advisable to
disorder on a continuum of severity, with OCD viewed use a parent as a cotherapist. A flowchart that outlines
as the more severe manifestation of illness. Contrary treatment options for OCD is shown in Figure 31-1.
to this notion, studies using structured interviews to In general, the goals of treatment are to reduce the
establish diagnosis have found that not all individu- frequency and intensity of symptoms as much as pos-
als with OCD also have OCPD. One reason for the sible and to minimize the amount of interference the
perception that these disorders are linked lies in the symptoms cause. It should be noted that few individuals
frequency of several OCPD traits in individuals with experience a cure or complete remission of symptoms.
OCD. In one study, the majority of 114 individuals with Instead, OCD should be viewed as a chronic illness
OCD had perfectionism and indecisiveness (82 and 70, with a waxing and waning course. Symptoms are of-
respectively). In contrast, other OCPD traits, such as ten worse during times of psychosocial stress. Even
restricted affect, excessive devotion to work, and rigid- when on medication, individuals with OCD are often
ity, were seen infrequently. upset when they experience even a mild symptom ex-
Although perfectionism and indecisiveness are rela- acerbation, anticipating that their symptoms will revert
tively common traits in individuals with OCD, the dis- to their worst, which is rarely the case. Anticipating
tinction between OCD and OCPD is important, and sev- with the individual that stress may make the symptoms
eral guidelines may be useful in distinguishing them. worse can often be helpful in long-term treatment.
Unlike OCPD, OCD is characterized by distressing,
timeconsuming egodystonic obsessions and repetitive
Somatic Treatments
rituals aimed at diminishing the distress engendered
by obsessional thinking. One of the hallmarks that has The most extensively studied agents for OCD are medi-
been traditionally used to distinguish OCD from OCPD cations that affect the serotonin system. The principal
Treatment of OCD
Also consider
Pharmacotherapy Behavioral therapy
r
1st-line SRIs:
2nd-line SRIs: s ide Exposure with
clomipramine−−250 mg on response prevention
sertraline−−200 mg oc
fluvoxamine−−300 mg
fluoxetine−−80 mg Als
paroxetine−−60 mg
Reasons of poor response:

1. Poor compliance
Augmentors if partial response: 2. Comorbid depression
buspirone, lithium, 3. Use/abuse of CNS depressants
clonazepam, trazodone, 4. Delusions
alprazolam, liothyronine
Try a 2nd SRI/Behavior therapy
Still unresponsive
For personality disorder For severely disabled patients
1. Psychotherapy Consider neurosurgery:

2. Day program 1. After a minimum of two adequate medication
3. Halfway houses trials with augmentation
2. After behavioral treatment
3. Without severe personality disorder
Figure 31-1 Flowchart of treatment options for OCD.
pharmacologic agents used to treat OCD are the SRIs, function. Previous data have indicated that at doses of
which include clomipramine, fluoxetine, fluvoxamine, 300 mg/day or more, the risk of seizures is 2.1%, but
sertraline, paroxetine, citalopram, and escitalopram. at doses of 250 mg/day or less, the risk of seizures is
The tricyclic antidepressant clomipramine is among low (0.48%) and comparable to that of other tricyclic
the most extensively studied pharmacological agents in antidepressants. It is therefore recommended that doses
OCD. This drug is unique among the antiobsessional of 250 mg/day or less be used.
agents in that in addition to its potency as an SRI, it has Recent studies of IV clomipramine have been partic-
significant affinity for noradrenergic, dopaminergic, ularly promising because it seems to have a quicker on-
muscarinic, and histaminic receptors. The most com- set of action and fewer side effects than the oral form,
mon side effects were those typical of the tricyclic anti- and it may be effective even in individuals who do not
depressants, including dry mouth, dizziness, tremor, respond to oral clomipramine. Oral clomipramine, like
fatigue, somnolence, constipation, nausea, increased other SRIs, usually takes a minimum of 4 to 6 weeks
sweating, headache, mental cloudiness, and sexual dys- to produce a clinically significant clinical response, but
in at least one study using IV pulse dosing, individu- levels of a variety of coadministered drugs, including
als showed a response within 4.5 days. The reasons for tricyclic antidepressants (such as clomipramine), car-
this unique response are not fully understood, but it bamazepine, phenytoin, and trazodone. However, the
is postulated that the IV preparation avoids first-pass other SSRIs (with the exception of citalopram) can
hepatoenteric metabolism, leading to increased bioa- theoretically cause similar elevations, although fewer
vailability of the parent compound clomipramine. This reports on such interactions are currently available.
in turn may play a role in rapidly desensitizing sero- Some clinicians have taken advantage of these interac-
tonergic receptors or initiating changes in postsynaptic tions by carefully combining fluvoxamine with clomi-
serotonergic neurons. Although studies of IV clomipramine in order to block clomipramine’s metabolism
pramine for obsessional states date as far back as 1973, to desmethylclomipramine; this in turn favors serotonin
this preparation is still not FDA-approved for clinical reuptake inhibition provided by the parent compound
use in the United States. Cardiac monitoring is recom- rather than the norepinephrine reuptake inhibition pro-
mended during the use of IV clomipramine. vided by the metabolite. However, caution should be
Fluoxetine (as well as fluvoxamine, sertraline, par- exercised with this approach since the elevation in clo-
oxetine, citalopram and escitalopram) is often referred mipramine levels, and perhaps other compounds, can
to as a selective serotonin reuptake inhibitor (SSRI) be nonlinear and quickly lead to dangerous toxicity. At
because it has a far more potent effect on serotonergic the very least, clomipramine levels should be carefully
than on noradrenergic or other neurotransmitter sys- monitored.
tems. Despite their different chemical structures, all of All of the SSRIs are generally well tolerated, with a
the SSRIs appear to have similar efficacy in treating relatively low percentage of individuals experiencing
OCD. Fluoxetine and the other SSRIs have fewer side notable side effects or discontinuing them because of
effects than clomipramine, reflecting its more selective side effects. In addition, these compounds are unlikely
mechanism of action. The most common side effects to be lethal in overdose, except for clomipramine,
are headache, nausea, insomnia, anorexia, dry mouth, which can lead to cardiac arrhythmias and death. All
somnolence, nervousness, tremor, and diarrhea. Side these agents can cause sexual side effects, ranging from
effects occur more frequently at higher doses. Most anorgasmia to difficultly with ejaculatory function.
studies of other medications for OCD have consisted However, such symptoms are not readily volunteered
of only case reports or small samples. One small trial by the individual; thus it is important to ask. Should
suggested that venlafaxine, a medication which, like such symptoms be experienced, conservative measures
clomipramine, inhibits the reuptake of both serotonin may include dosage reduction, transient drug holidays
and norepinephrine, may hold some promise. for a special weekend or occasion, or switching to an-
The efficacy of each SSRI—clomipramine, fluox- other SSRI since individuals may not have the same
etine, fluvoxamine, sertraline, paroxetine, and citalo- degree of dysfunction with a different agent. However,
pram—is supported by existing data. During the past if the clinician feels that it is critical to continue with
10 years, at least seven head-to-head SRI comparison the same agent, various treatments have been reported
studies have been done. All of the studies found that in the literature. Usually taken within a few hours of
the agents studied were equally efficacious, although sexual activity, no one agent has been shown to work
they may have been underpowered to detect differences consistently. Among those that have been tried are
among medications. However, several meta-analyses of yohimbine, buspirone, cyproheptadine, ropinirole, bu-
OCD trials, which compared SRIs across large pla- proprion, dextroamphetamine, methylphenidate, aman-
cebo-controlled multicenter trials, lend some support tidine, and nefazodone, to name a few.
to the notion that clomipramine might be more effec- If an individual has had only a partial response to
tive than the more selective agents. However, like most an antiobsessional agent of adequate dose and dura-
meta-analyses, these studies are flawed by factors that tion, the next question is whether to change the SSRI
include variations in the study protocol, sample size, or add an augmenting agent. Current clinical practice
and the number of treatment-resistant and treatment- suggests that if there is no response at all to an SSRI,
naïve subjects. The meta-analyses do support a trial of it may be best to change to another SSRI. However, if
clomipramine in all individuals who do not respond to there has been some response to treatment, an augmen-
SRIs, even though clomipramine tends to cause more tation trial of at least 2 to 8 weeks may be warranted.
side effects. No augmentation agent has been firmly established as
It is worth noting that the SSRIs, via their effect on efficacious. Although many augmentation agents ap-
the liver cytochrome system, can inhibit the metabolism peared promising in open trials, they failed to be ef-
of certain other drugs. Fluoxetine can elevate blood fective in more systematic trials although some of the
Potential Augmenting Agents for Treatment-

Augmentation with fenfluramine (up to 60 mg/day),
Table 31-2 clonazepam (up to 5 mg/day), clonidine (0.1–0.6 mg/
Resistant Obsessive–Compulsive Disorder
Augmenting Agent Suggested Dosage Range*
day), and trazodone (100–200 mg/day), as well as the
combination of clomipramine with any of the SSRIs,
Lithium 300–600 mg/day† has had anecdotal success but has not been evaluated in
Clonazepam 1–3 mg/day
Tryptophan 2–10 g/day‡ methodologically rigorous studies. Some potential aug-
Trazodone 100–200 mg/day menting agents and their dosage ranges are presented
Buspirone 15–60 mg/day in Table 31-2.
Alprazolam 0.5–2 mg/day
Methylphenidate 10–30 mg/day Occasionally, even after receiving adequate phar-
Haloperidol 2–10 mg/day macotherapy (including augmentation), adequate
Pimozide 2–10 mg/day behavioral therapy, and a combination of behavioral
Nifedipine 10 mg t.i.d.
Liothyronine sodium 10–25 mg/day therapy and pharmacotherapy, individuals may still ex-
Clonidine 0.1–0.6 mg/day perience intractable OCD symptoms. Such individuals
Fenfluramine Up to 60 mg/day may be candidates for neurosurgery. Although criteria
*
Add these to an ongoing trial of antidepressant medication. It for who should receive neurosurgery vary, it has been
should be noted that most of these dosages have not been tested with
rigorous clinical trials but simply represent some of the reported suggested that failure to respond to at least 5 years of
doses tried in the current literature. Some would not recommend systematic treatment is a reasonable criterion. The pro-
augmentation unless the initial treatment showed some response.
†
Use with caution—there have been some reports of elevated
cedures that have been most successful interrupt tracts
lithium levels with ongoing fluoxetine treatment. involved in the serotonin system. The surgical proce-
‡
Because the use of l-tryptophan has been implicated in an dures used—anterior capsulotomy, cingulotomy, and
increased incidence of eosinophilia, the authors advise against the
prescribing and use of this agent until the issue is resolved. limbic leukotomy—all aim to interrupt the connection
Source: Jenike MA (1991) Management of patient with treatment- between the cortex and the basal ganglia and related
resistant obsessive–compulsive disorder. In Current Treatments structures. Current stereotactic surgical techniques in-
of Obsessive–Compulsive Disorder, Pato MT and Zohar J (eds).
Copyright, American Psychiatric Press, Washington DC, p. 146. volve the creation of precise lesions, which are often
only 10 to 20 mm, to specific tracts. These procedures
have often been done with radio-frequency heated elec-
trodes and more recently with gamma knife techniques.
later studies did not report response to the SRI alone, Postsurgical risks have been minimized, and in some
leaving unanswered the question of whether some cases cognitive function and personality traits improve
augmentation strategies may be effective in partial along with symptoms of OCD.
SSRI responders. Many questions about augmenta-
tion remain unanswered, including the optimal dura-
tion of augmentation, comparative efficacy of different
agents, predictors of response, and mechanism of ac- Behavioral therapy is effective for OCD both as a pri-
tion. Nonetheless, these agents do help some individu- mary treatment and as an augmentation agent. This
als significantly, and thus their systematic use should form of therapy is based on the principle of exposure
be considered (see Table 31-2). and response prevention. The individual is asked to en-
In individuals with severe symptoms or comorbid dure, in a graduated manner, the anxiety that a specific
psychosis or tic disorder, pimozide 1–3 mg/day, haldol obsessional fear provokes while refraining from com-
2–10 mg/day, and other neuroleptic agents (risperidone pulsions that allay that anxiety. The principles behind
2–8 mg/day and olanzapine 2.5–10 mg/day) have been the efficacy of behavioral treatment are explained to the
used with some success. However, the use of a neu- individual in the following way. Although compulsions,
roleptic agent should be considered carefully in light of either covert or overt, usually immediately relieve anxi-
the risk of extrapyramidal symptoms and side effects ety, this is only a short-term solution; the anxiety will
such as weight gain, lethargy, and tardive dyskinesia. ultimately return, requiring the performance of another
Thus, when a neuroleptic drug is used, target symp- compulsion. However, if the individual resists the anxi-
toms should be established before beginning treatment ety and urge to ritualize, the anxiety will eventually
and the medication discontinued within several months decrease on its own (i.e., habituation will occur), and
if target symptoms do not improve. the need to perform the ritual will eventually disappear.
The use of lithium (300–600 mg/day) and buspirone Thus, behavioral therapy helps the individual habituate
(up to 60 mg/day) as augmentation agents has also been to the anxiety and extinguish the compulsions.
explored. Both agents looked promising in open tri- Compulsions, especially overt behaviors like wash-
als but failed to be effective in more systematic trials. ing rituals, are more successfully treated by behavioral
therapy than are obsessions alone or covert rituals like powerful adjunct to pharmacotherapy. Some research
mental checking. This is because covert rituals are appears to indicate that combined treatment may be
harder to physically resist than are rituals like hand more effective than pharmacotherapy or behavioral
washing and checking a door. It has been reported that therapy alone, although these findings are still prelimi-
washing rituals are the most amenable to behavioral nary. Some studies have even suggested that adding
treatment, followed by checking rituals and then men- pharmacotherapy to behavior therapy may be particu-
tal rituals. larly helpful in reducing obsessions, while compulsions
For rituals that do not constitute overt behaviors, respond to behavior therapy. From a clinical perspec-
techniques other than exposure and response preventive, it may be useful to have individuals begin treat-
tion have been used in conjunction with exposure and ment with medication to reduce the intensity of their
response prevention. These approaches include imagi- symptoms or comorbid depressive symptoms if present;
nal flooding and thought stopping. In imaginal flood- individuals may then be more amenable to experienc-
ing, the anxiety provoked by the obsessions is evoked ing the anxiety that will be evoked by the behavioral
by continually repeating the thought, often with the challenges they perform. The data on the discontinu-
help of a continuous-loop tape or the reading of a ation of behavioral therapy are encouraging. Overall,
“script” composed by the individual and therapist, un- about 75% of individuals continue to do well at follow-
til the thought no longer provokes anxiety. In thought up, but are symptom free.
stopping, a compulsive mental ritual (e.g., continually The use of psychotherapeutic techniques of either
repeating a short prayer in one’s head) is stopped by a psychoanalytic or a supportive nature has not been
simply shouting, making a loud noise, or snapping a proved successful in treating the specific obsessions
rubber band on the wrist in an attempt to interrupt the and compulsions that are a hallmark of OCD. How-
thought. ever, the more characterological aspects that are part
In the early stages of treatment, a behavioral assess- of OCPD may be helped by a more psychoanalyti-
ment is performed. During this assessment, the con- cally oriented approach. The defense mechanisms of
tent, frequency, duration, amount of interference and reaction formation, isolation, and undoing, as well as
distress, and attempts to resist or ignore the obsessions a pervasive sense of doubt and need to be in control,
and compulsions are catalogued. An attempt is made to are hallmarks of the obsessive–compulsive character.
clarify the types of symptoms, any triggers that bring In therapy the individual must be encouraged to take
on the obsessions and compulsions, and the amount risks and learn to feel comfortable with, or at least less
and type of avoidance used to deal with the symptoms. anxious about, making mistakes and to accept anxi-
The individual, usually with the help of a therapist, ety as a natural and normal part of human experience.
then develops a hierarchy of situations according to Techniques for meeting such goals in treatment may
the amount of anxiety they provoke. During treatment, include the therapist’s being relatively active in therapy
individuals gradually engage in the anxiety-provoking to ensure that the individual focuses on the present
situations included in their hierarchy without perform- rather than getting lost in perfectly recounting the past,
ing anxiety-reducing rituals. as well as the therapist’s being willing to take risks and
Despite its efficacy, behavioral therapy has limita- present herself or himself as less than perfect.
tions. To begin with, about 15–25% of individuals
refuse to engage in behavioral treatment initially or
drop out early in treatment because it is so anxiety
DIAGNOSTIC CRITERIA
provoking. Behavioral treatment fails in another 25%
of individuals for a variety of other reasons, includ- The ICD-10 Diagnostic Criteria for Research for
ing concomitant depression; the use of central nervous Obsessive–Compulsive Disorder differentiate between
system depressants, which may inhibit the ability to obsessions and compulsions on the basis of whether
habituate to anxiety; lack of insight; poor compliance they are thoughts, ideas, or images (obsessions) or acts
with homework, resulting in inadequate exposure; and (compulsions). In contrast, DSM-IV-TR distinguishes
poor compliance on the part of the therapist in enforc- between obsessions and compulsions on the basis of
ing the behavioral paradigm. Thus, overall, 50–70% of whether the thought, idea, or image causes anxiety or
individuals are helped by this form of therapy. distress or prevents or reduces it. Thus, in DSM-IV-TR,
Behavior therapy can be used as the sole treatment of there can be cognitive compulsions that would be
OCD, particularly with individuals whose contamina- considered obsessions in ICD-10. In addition, ICD-10
tion fears or somatic obsessions make them resistant sets a minimum duration of at least 2 weeks, whereas
to taking medications. Behavioral treatment is also a DSM-IV-TR has no minimum duration.
CHAPTER
Traumatic Stress Disorders
Posttraumatic Stress Disorder Hyperarousal symptoms, somewhat similar to those

of generalized anxiety disorder, are also present in
PTSD and at least one of five of the following symp-
DIAGNOSIS toms is required: difficulty sleeping, irritability or an-
Posttraumatic stress disorder (PTSD) is defined in the ger, poor concentration, hypervigilance, and exagger-
DSM-IV-TR by six different criteria (see DSM-IV-TR ated startle response.
diagnostic criteria, page 327). The diagnosis of PTSD With regard to the symptoms as a whole, it is evi-
is based on a history of exposure to a traumatic stressor, dent that they embody features of different psychiatric
the simultaneous appearance of three different symp- disorders, including obsessive–compulsive processes,
tom clusters, a minimal duration, and the existence of generalized anxiety disorder, panic attacks, phobic
functional disturbance. To qualify as traumatic, the avoidance, dissociation, and depression. Finally, it is
event must have involved actual or threatened death or necessary for symptoms to have lasted at least 1 month
serious injury or a threat to the individual or others, and and for the disturbance to have caused clinically sig-
exposure to this event must arouse an intense affective nificant distress or impairment.
response characterized by fear, helplessness, or horror. Community-based studies conducted in the United
In children, disorganized or agitated behavior can be States have documented a lifetime prevalence rate for
seen in lieu of an intense affective response. Sympto- PTSD of approximately 8% of the adult population.
matically, there must be at least one of five possible in- General population female-to-male lifetime prevalence
trusive-reexperiencing symptoms. These have the qual- ratio is 2 : 1. The highest rates of PTSD occurrence for
ity of obsessive, recurring, intrusive, and distressing particular traumatic exposures (occurring in one-third
recollections either in the form of imagery or thoughts to three-fourths of those exposed) are among survivors
or in the form of recurrent distressing dreams. Intense of rape, military combat and captivity, graves registra-
psychological distress or physiological reactivity on tion (i.e., registering dead bodies through the morgue),
exposure to either an external reminder or an internal and ethnically or politically motivated interment and
reminder of the trauma can also occur. The flashback genocide.
experience, or reliving of the event, is less common. Epidemiological studies show that PTSD often re-
Symptom cluster C in the DSM-IV-TR criteria in mains chronic, with a significant number of people
actuality embodies two somewhat different psycho- remaining symptomatic, several years after the initial
pathologies—namely, phobic avoidance and numbing event. In support of this view are epidemiological data
or withdrawal. The phobic avoidance is expressed ei- that show that recovery does not occur frequently. For
ther in (1) efforts to avoid thoughts and feelings and example, the National Vietnam Veterans Readjustment
conversations associated with the trauma or (2) in ef- study found lifetime and current prevalence rates of
forts to avoid activities, places, or people that arouse PTSD to be, respectively, 30.9% and 15.2% in men
recollections of the trauma. (3) Psychogenic amnesia, and 26.9% and 8.5% in women. In a population of rape
a more dissociative symptom, also is in this symp- victims, lifetime prevalence of PTSD was found to be
tom grouping, followed by (4) markedly diminished 75.8% with a current prevalence rate of 39.4%. The Na-
interest, (5) feeling detached or estranged, (6) having tional Comorbidity Survey, a large epidemiological sur-
a restricted range of affect, and (7) having a sense of vey conducted in the United States in the early 1990s,
a foreshortened future. At least three of these seven documented that one-third of those diagnosed with
symptoms must be present. PTSD fail to recover even after many years. Therefore,
Chapter 32 • Anxiety Disorders: Traumatic Stress Disorders 327

309.81 POSTTRAUMATIC STRESS DISORDER
A. The person has been exposed to a traumatic event in which both of the following were present:
(1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death
or serious injury, or a threat to the physical integrity of self or others
(2) the person’s response involved intense fear, helplessness, or horror. Note: In children, this may be expressed instead by
disorganized or agitated behavior
B. The traumatic event is persistently reexperienced in one (or more) of the following ways:
(1) recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: In young
children, repetitive play may occur in which themes or aspects of the trauma are expressed
(2) recurrent distressing dreams of the event. Note: In children, there may be frightening dreams without recognizable
content
(3) acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, halluci-
nations, and dissociative flashback episodes, including those that occur on awakening or when intoxicated). Note: In
young children, trauma-specific reenactment may occur
(4) intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the trau-
matic event
(5) physiological reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic
event
C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the
trauma), as indicated by three (or more) of the following:
(1) efforts to avoid thoughts, feelings, or conversations associated with the trauma
(2) efforts to avoid activities, places, or people that arouse recollections of the trauma
(3) inability to recall an important aspect of the trauma
(4) markedly diminished interest or participation in significant activities
(5) feeling of detachment or estrangement from others
(6) restricted range of affect (e.g., unable to have loving feelings)
(7) sense of a foreshortened future (e.g., does not expect to have a career, marriage, children, or a normal life span)
D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following:
(1) difficulty falling or staying asleep
(2) irritability or outbursts of anger
(3) difficulty concentrating
(4) hypervigilance
(5) exaggerated startle response
E. Duration of the disturbance (symptoms in criteria B, C, and D) is more than 1 month.
F. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of
functioning.
Specify if:
Acute: if duration of symptoms is less than 3 months
Chronic: if duration of symptoms is 3 months or more
Specify if:
With delayed onset: if onset of symptoms is at least 6 months after the stressor
chronicity of PTSD is not limited to the more severe the symptom picture often settles into a more classic
treatment-seeking samples. PTSD presentation. After rape, for example, as many
as 90% of individuals may qualify for the diagnosis
of PTSD. Approximately 50% of people with PTSD
Course
recover, and approximately 50% develop a persistent,
Immediately following traumatic exposure, a high chronic form of the illness still present 1 year following
percentage of individuals develop a mixed symp- the traumatic event.
tom picture, which includes disorganized behavior, The longitudinal course of PTSD is variable. Perma-
dissociative symptoms, psychomotor change, and nent recovery occurs in some people, whereas others
sometimes, paranoia. The diagnosis of Acute Stress show a relatively unchanging course with only mild
Disorder accounts for many of these reactions. These fluctuation. Still others show a more obvious fluc-
reactions are generally short-lived, although by 1 month tuation with intermittent periods of well-being and
recurrences of major symptoms. In a limited number It may also develop by activation of an underlying ob-
of cases, the passage of time does not bring a resolu- sessive–compulsive disorder diathesis.
tion of symptoms, and the individual’s condition tends Autonomic hyperarousal is a cardinal part of panic
to deteriorate with age. Particular symptoms that have attack, which may indicate a diagnosis of panic disor-
been noted to increase with time in many people in- der. To distinguish between panic disorder and PTSD,
clude startle response, nightmares, irritability, and de- the therapist needs to assess whether panic attacks
pression. Clinicians during World War II also observed are related to the trauma or reminders of the same (in
that the existence of marked startle response and hy- which case they would be subsumed under a diagno-
pervigilance in the acute aftermath of exposure to com- sis of PTSD) or whether they occur unexpectedly and
bat often represented a comparatively poor prognostic spontaneously (in which case a diagnosis of panic dis-
sign. In children, PTSD can be, and often is, chronic order would be justified).
and debilitating. Depression and PTSD share a significant overlap,
General medical conditions may occur as a direct including four of the criterion C cluster symptoms and
consequence of the trauma (e.g., head injury, burns). three of the criterion D cluster symptoms. Thus, an in-
In addition, chronic PTSD may be associated with dividual who presents with reduced interest, estrange-
increased rates of adverse physical outcomes, includ- ment, numbing, impaired concentration, insomnia,
ing musculoskeletal problems and cardiovascular irritability, and sense of a foreshortened future may
morbidity manifest either disorder. PTSD may give rise to depres-
sion as well, and it is possible for the two conditions to
coexist. In a few instances, an individual with prior de-
pression may be more vulnerable to developing PTSD.
PTSD symptoms may overlap with symptoms of a Reexperiencing symptoms are present only in PTSD.
number of other disorders in the DSM-IV-TR. Both Dissociative disorders also overlap with PTSD.
PTSD and adjustment disorder are etiologically related In the early aftermath of serious trauma, the clinical
to stress exposure. PTSD may be distinguished from picture may be predominantly one of the dissociative
adjustment disorder by assessing whether the traumatic states (see the section on Acute Stress Disorder [ASD],
stress meets the severity criteria described earlier. page 332 ). ASD differs from PTSD in that the symp-
Also, if there are an insufficient number of symptoms tom pattern occurs within the first few days after expo-
to qualify for the diagnosis, a diagnosis of adjustment sure to the trauma, lasts no longer than 4 weeks, and
disorder might be merited. is typically accompanied by prominent dissociative
Specific phobias may arise after traumatic exposure. symptoms.
For example, after an automobile accident, victims may More rarely, PTSD must be distinguished from other
develop phobic avoidance of traveling, but without the disorders producing perceptual alterations, such as
intrusive or hyperarousal symptoms. In such cases, a schizophrenia and other psychotic disorders, delirium,
diagnosis of specific phobia should be given instead of substance use disorders, and general medical condi-
a diagnosis of PTSD. tions producing psychosis (e.g., brain tumors).
The criteria set for generalized anxiety disorder in- The differential diagnosis is important but, notwith-
cludes a list of six symptoms of hyperarousal, of which standing, PTSD is unlikely to occur in isolation. Psychi-
four are common to PTSD: being on edge, poor con- atric comorbidity is the rule rather than the exception,
centration, irritability, and sleep disturbance. PTSD and a number of studies have demonstrated that, in both
requires the additional symptoms as described earlier, clinical and epidemiological populations, a wide range
and the worry in PTSD is focused on concerns about of disorders is likely to occur at an increased probabil-
reexperiencing the trauma. In contrast, the worry in ity. These include major depressive disorder, all of the
generalized anxiety disorder is about a number of dif- anxiety disorders, alcohol and substance use disorders,
ferent situations and concerns. However, it is possible somatization disorder, and schizophrenia and schizo-
for the two conditions to coexist. phreniform disorder.
In obsessive–compulsive disorder, recurring and in-
trusive thoughts occur, but the individual recognizes
TREATMENT
these to be inappropriate and unrelated to any particu-
lar life experience. Obsessive–compulsive disorder is A number of goals are common to all treatments of
a common comorbid condition in PTSD and may de- PTSD and can be summarized as follows: (1) to reduce
velop with generalization (e.g., compulsive washing for intrusive symptoms; (2) to reduce avoidance symptoms;
months after a rape to reduce contamination feelings). (3) to reduce numbing and withdrawal; (4) to dampen
hyperarousal; (5) to reduce psychotic symptoms when ever, treatment by a mental health clinician (rather than
present; and (6) to improve impulse control when this a primary care clinician) is almost always indicated.
is a problem. By reducing troublesome symptoms, a The initial history taking can evoke strong affect to a
number of other important goals can also be accom- greater degree than is customarily found in other dis-
plished as follows: (1) to develop the capacity to in- orders. In fact, it may take several interviews for the
terpret events more realistically with respect to their details to emerge. A sensitive yet persistent approach is
threat content; (2) to improve interpersonal work and needed on the part of the interviewer. During treatment,
leisure functioning; (3) to promote self-esteem, trust, although the mental health care clinician will clearly
and feelings of safety; (4) to explore and clarify mean- want to impart a sense of optimism to the individual, it
ings attributed to the event; (5) to promote access to is also a reflection of reality to point out early that re-
memories that have been dissociated or repressed when covery may be a slow process and that some symptoms
judged to be clinically appropriate; (6) to strengthen (e.g., phobic avoidance, startle response) may persist. It
social support systems; and (7) to move from identifi- is important for the mental health care clinician to be
cation as a victim to that of a survivor. comfortable in hearing and tolerating unpleasant affect
The three major treatment approaches, pharma- and often horrifying stories. All these must take place
cotherapeutic, cognitive–behavioral, and psychody- in a noncritical and accepting manner. Specific treat-
namic, all emphasize different aspects of the problem. ment approaches include the use of pharmacotherapy,
Pharmacotherapy targets the underlying neurobiologi- psychotherapy, anxiety management, and attention to
cal alterations found in PTSD and attempts to control the general issues described earlier.
symptoms so that the above treatment goals can be A stepwise sequence of approaches may be used in
more effectively accomplished. Cognitive–behavioral the treatment of PTSD but it must be said that there are
treatments emphasize the phobic avoidance and coun- no definitive guidelines currently in place. As a result,
terproductive reenactments that often occur, along with the particular order in which treatments are considered
the identification of faulty beliefs that arise owing to varies on the basis of individual circumstances. Also,
the trauma, and replace them with more adaptive be- no uniform definition exists as to what constitutes a
liefs, usually in association with direct therapeutic ex- good or poor response to treatment. In general, some
posure. The psychodynamic approach emphasizes the symptoms of chronic PTSD persist, albeit at a consid-
associations that arise from the trauma experience and erably reduced level, in people who have undergone
that lead to unconscious and conscious representations. treatment.
Defense mechanisms that lead to lack of memory, and
the contributions from early development, are also
Somatic Treatments
brought into play in psychodynamic therapy.
General principles of treating PTSD involve explana- PTSD may be accompanied by enduring neurochemi-
tion and destigmatization, which can be provided both cal and psychophysiological changes and can lead to
to the individual and to family members. This often in- substantial impairment and distress. Sometimes, the
cludes a description of the symptoms of PTSD and the intensity of symptoms is severe enough to preclude the
way in which it can affect behaviors and relationships. effective use of trauma-focused psychotherapy. In these
Information can be given about general treatment situations, the use of medication should not be delayed
principles, pointing out that sometimes cure is attain- unnecessarily. Initial studies showed benefit for the tri-
able but that at other times symptom containment is cyclic antidepressant and monoamine oxidase inhibitor
a more realistic treatment goal, particularly in chronic medications. However, the selective serotonin reuptake
and severe PTSD. Regaining self-esteem and attaining inhibitors (SSRIS) have now replaced these as first-line
greater control over impulses and affect are also de- agents, based upon evidence from several placebo-
sired in many instances. Information can be provided controlled trials. The main groups of medications rel-
as to appropriate literature, local support groups and evant to the treatment of PTSD along with dose ranges
resources, and names and addresses of national advo- and chief side effects are listed in Table 32-1. A suggested
cacy organizations. If the therapist attends to these im- sequencing of treatment is outlined in Table 32-2.
portant issues early in treatment, the individual is able Several placebo-controlled trials have shown posi-
to more readily build trust and also to appreciate that tive effects for the SSRI medications, Data support pos-
the therapist shows a good understanding both of the itive effects for SSRI in men and women and in adults
condition and of the individual. who have survived all major classes of trauma (e.g.,
PTSD is sometimes comparatively straightforward combat, sexual violence, nonsexual violence, and ac-
to treat and at other times it is more complicated. How- cident). Each of these medications has broad-spectrum
Table 32-1 Medications in Posttraumatic Stress Disorder: Dose Ranges and Side Effects
Drug Category Dose Range (mg/day) Common or Problematical Side Effects
Antidepressants
Selective serotonin reuptake Gastrointestinal disturbance, sexual dysfunction, agitation
inhibitors
Fluoxetine 10–60
Fluvoxamine 50–300
Sertraline 50–200 Insomnia
Paroxetine 10–60 Tiredness
Citalopram 20–60
Tricyclic antidepressants Anticholinergic effects, cardiovascular symptoms, weight gain
Amitriptyline 50–300 Sexual dysfunction, sedation (for all tricyclic antidepressants)
Imipramine 50–300
Monoamine oxidase inhibitors
Phenelzine 15–90 Weight gain, dizziness, sleep disturbance, sexual dysfunction,
hypertensive reactions, hyperpyretic states
Anticonvulsants
Carbamazepine 200–1500 Hematological effects
Valproic acid 125–2000 Gastrointestinal disturbance, sedation
Lamotrigine 50–200 Rash, exfoliative dermatitis, Stevens–Johnson syndrome
Mood stabilizers
Lithium carbonate 300–1200 Gastrointestinal disturbance, polyuria, headache
Antiadrenergic drugs
Propranolol 20–160 Depression, hypertension, rebound hypertension
Clonidine 0.1–0.4 Memory problems, dizziness, tiredness
Prazosin 2–10 Dizziness, hypotension
Anxiolytics 0.5–6
Benzodiazepines
Clonazepam 0.5–6 Sedation, memory problems, incoordination, dependence
Alprazolam 0.25–4 Withdrawal, rebound, disinhibition (for all benzodiazepines)
Diazepam 2–40
Chlordiazepoxide 5–40
Others
Azapirones 5–60 Agitation, gastrointestinal disturbance, headaches
Buspirone
Neuroleptics
Thioridazine 25–300 Extrapyramidal symptoms
Haloperidol 0.5–4 Sedation, anticholinergic effects
Others
properties across the full symptom range of the disor-

Pharmacotherapy Steps for Posttraumatic der as well as improving function and, perhaps, resil-
Table 32-2
Stress Disorder
ience or stress coping. They also support the benefit
Step 1 of SSRI in those with and without comorbid major
Selective serotonin reuptake inhibitor (SSRI)
Adjunctive medications: depression.
If prominent hyperarousal: benzodiazepine or buspirone At this point, the indications for antipsychotic and
If prominent mood liability or explosiveness: mood-stabilizing drugs are poorly defined, but clinical
anticonvulsant or lithium
If prominent dissociation: valproic acid experience suggests that they continue to have a role in
If persistent insomnia: trazodone the pharmacologic treatment of PTSD. Antipsychotic
If psychotic: atypical antipsychotic medications can be useful in individuals with poor im-
Step 2 pulse control or in those who manifest features of border-
If no response or intolerance to SSRI:
Dual action antidepressant, e.g., mirtazapine, venlafaxine line personality disorder. Lithium and carbamazepine
Adjunctive medications as above can also be useful in such individuals but might benefit
Step 3 individuals who are subject to mood swings and angry
If no response to Step 1 or 2: or explosive outbursts. The appropriate role for the use
Monoamine oxidase inhibitor of benzodiazepines is not well defined. The antiphobic
Adjunctive medications as above
and antiarousal effects of the benzodiazepines should,
Step 4
Other useful drugs: in theory, be helpful in PTSD. However, withdrawal
Propranolol—hyperarousal from short-acting benzodiazepines may also introduce
Clonidine—startle response an additional set of problems with intense symptom re-
Neuroleptics—psychosis, poor impulse control
bound. In individuals who have a propensity to abuse
alcohol and other substances, benzodiazepines are not posure in the treatment of chronic PTSD, both treat-
recommended. ments were associated with positive improvements at
Overall, the antidepressants, mood stabilizers, posttreatment and follow-up, with no differences in
and anticonvulsants are the medication groups that outcome between treatments. However, individuals
are generally considered primary for treating PTSD; who received imaginal exposure were more likely to
beta-blockers, alpha-2-agonists, and anxiolytics have experience an increase in PTSD symptoms during the
a less clearly defined place. Often, individuals need treatment course, and those who did were more likely
a combination of drugs, but polypharmacy should be to miss treatment sessions, rate the therapy as less cred-
utilized in a carefully planned fashion. Also, since the ible, and be rated as less motivated by the therapist.
time course of response may be slow, it is advisable Other approaches have focused on efficaciously treat-
to persist with a particular course of action for at least ing one aspect of PTSD symptomatology, such as an-
8 weeks before deciding that it has been unhelpful. It ger, nightmares, or authority problems.
is possible that avoidance and numbing symptoms re-
spond more effectively to SSRI drugs.
Psychodynamic Therapy
Psychodynamically based approaches emphasize the
Cognitive and Behavioral Therapies
interpretation of the traumatic event as being a criti-
Despite theoretical differences, most schools of psycho- cal determinant of symptoms. Treatment is geared to
therapy recognize that cognitively oriented approaches alter attributions, usually by means of slow exposure
to the treatment of anxiety must include an element of and through confrontation and awareness of the nega-
exposure. Because PTSD involves aberrant and volun- tive affects that have been generated by the trauma.
tary programs for the avoidance of danger that are con- Conflictual meanings begin to appear, and it is the task
ditioned by real experience, correction of these “fear of treatment to reinterpret the experience in a more re-
structures” requires exposure to ensure habituation. alistic and adaptive fashion. During such treatment, it
Prolonged exposure depends on the fact that anxiety is important to ensure that the affect intensity is not
will be extinguished in the absence of real threat, given overwhelming or disorganizing. Obviously, support
a sufficient duration of exposure in vivo or in imagina- needs to be provided throughout, and sometimes other
tion to traumatic stimuli. In PTSD, the individual re- treatment approaches are used adjunctively. Excessive
tells the traumatic experience as if it were happening and maladaptive behaviors such as avoidance, use of
again, until doing so becomes a pedestrian exercise alcohol or work, or risk taking may occur as a means of
and anxiety decreases. Between sessions, individu- coping with the experience and these need to be identi-
als perform exposure homework, including listening fied and addressed.
to tapes of the flooding sessions and limited exposure
in vivo. However, not every individual may be a can-
Acute Stress Disorder
didate for exposure. Owing to the high anxiety and
temporarily increased symptoms associated with pro-
DIAGNOSIS
longed exposure, there are individuals who will be re-
luctant to confront traumatic reminders. Individuals in It has long been recognized that clinically significant
whom guilt or anger are primary emotional responses dissociative states are seen in the immediate aftermath
to the traumatic event (as opposed to anxiety) may not of overwhelming trauma. In addition, many individu-
profit from prolonged exposure. als may experience less clinically severe dissociative
Anxiety management techniques are designed to re- symptoms or alterations of attention and time sense.
duce anxiety by providing individuals with better skills Because such syndromes, even when short-lasting, can
for controlling worry and fear. Among such techniques produce major disruption of everyday activities, they
are muscle relaxation, thought stopping, control of may require clinical attention. During triage situa-
breathing and diaphragmatic breathing, communica- tions after a disaster, it can be important to recognize
tion skills, guided self-dialogue, and stress inoculation this clinical picture, which may require treatment in-
training (SIT). tervention and which may also be predictive of later
Further, cognitive approaches to the treatment of PTSD. As a result of these considerations, a decision
PTSD have also seen shown to be effective. A cognitive was made to include in DSM-IV a new entity, acute
approach to treatment includes training individuals in stress disorder (ASD), grouped together with PTSD in
challenging problematic cognitions such as self-blame. the anxiety disorders section. Essentially, it represents
In a comparison of cognitive therapy to imaginal ex- the clinical features of PTSD along with conspicuous
Because ASD, by definition, cannot last longer than

DSM-IV-TR Diagnostic Criteria 1 month, if the clinical picture persists, a diagnosis of
PTSD is appropriate. Some increased symptoms are
308.3 ACUTE STRESS DISORDER
expected in the great majority of subjects after expo-
A. The person has been exposed to a traumatic event in sure to major stress. These remit in most cases and
which both of the following were present: only reach the level of clinical diagnosis if they are
(1) the person experienced, witnessed, or was con- prolonged, exceed a tolerable quality, or interfere with
fronted with an event or events that involved actual
or threatened death or serious injury, or a threat to everyday function. Resolution may be more difficult if
the physical integrity of self or others there has been previous psychiatric morbidity, subse-
(2) the person’s response involved intense fear, help- quent stress, and lack of social support.
lessness, or horror
Little is known about the epidemiology of ASD as
B. Either while experiencing or after experiencing the dis-
tressing event, the individual has three (or more) of the defined in DSM-IV-TR, but after events such as rape
following dissociative symptoms: and criminal assault, the clinical picture of acute
(1) a subjective sense of numbing, detachment, or ab- PTSD is found in 70 to 90% of individuals, although
sence of emotional responsiveness the frequency of the particular dissociative symptoms
(2) a reduction in awareness of his or her surroundings
(e.g., “being in a daze”)
is unknown. One problem of most postdisaster surveys
(3) derealization is that they evaluate subjects at points several months
(4) depersonalization or years after the event. This makes any meaningful
(5) dissociative amnesia (i.e., inability to recall an im-
portant aspect of the trauma) assessment of acute stress syndromes difficult. One ex-
ception was the self-report-based assessment of mor-
C. The traumatic event is persistently reexperienced in
at least one of the following ways: recurrent images, bidity 2 months after an earthquake in Ecuador, which
thoughts, dreams, illusions, flashback episodes, or a found a 45% rate of caseness (being a clinical case),
sense of reliving the experience; or distress on expo- with the most prominent symptoms being fear, nerv-
sure to reminders of the traumatic event.
D. Marked avoidance of stimuli that arouse recollections ousness, tenseness, worry, insomnia, and fatigue.
of the trauma (e.g., thoughts, feelings, conversations,
activities, places, people).
E. Marked symptoms of anxiety or increased arousal Course
(e.g., difficulty sleeping, irritability, poor concentra-
tion, hypervigilance, exaggerated startle response, Although data do not exist on the course and natural
motor restlessness).
F. The disturbance causes clinically significant distress history of ASD as now defined, prior studies have indi-
or impairment in social, occupational, or other im- cated that dissociative and cognitive symptoms, which
portant areas of functioning or impairs the individual’s are so common in the immediate wake of trauma, im-
ability to pursue some necessary task, such as obtain-
ing necessary assistance or mobilizing personal re- prove spontaneously with time. However, it was also
sources by telling family members about the traumatic found that the likelihood of developing PTSD symp-
experience. toms at 7-month follow-up was more strongly related
G. The disturbance lasts for a minimum of 2 days and a
maximum of 4 weeks and occurs within 4 weeks of the to the occurrence of dissociative symptoms than to
traumatic event. anxiety symptoms immediately after exposure to the
H. The disturbance is not due to the direct physiological trauma.
effects of a substance (e.g., a drug of abuse, a medi-
cation) or a general medical condition, is not better
accounted for by brief psychotic disorder, and is not
merely an exacerbation of a preexisting Axis I or Axis II Differential Diagnosis
disorder.
ASD may need to be distinguished from several related
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 disorders (Figure 32-1). Brief psychotic disorder may
American Psychiatric Association. be a more appropriate diagnosis if the predominant
symptoms are psychotic. It is possible that a major de-
pressive disorder can develop posttraumatically and
that there may be some overlap with ASD, in which
dissociative symptoms, of which at least three must be case both disorders are appropriately diagnosed. When
present. The possible dissociative symptoms in ASD ASD-like symptoms are caused by direct physiological
are a subjective sense of numbing; detachment or ab- perturbation, the symptoms may be more appropriately
sence of emotional response; reduced awareness of diagnosed with reference to the etiological agent. Thus,
one’s surroundings; derealization; depersonalization; an ASD-like picture that develops secondary to head in-
and dissociative amnesia. jury is more appropriately diagnosed as mental disorder
Dissociative symptoms, No
numbing, or reduced Other disorder
awareness of surroundings
Yes
No
Traumatic event within past 29 days Other diagnosis
Yes
No Dissociative disorder or
Intrusive symptoms
adjustment disorder
Yes
Avoidance symptoms
adjustment disorder
Yes
Hyperarousal
adjustment disorder
Yes
No
Distress or impairment Anxiety NOS or V code
Yes
No Posttraumatic stress disorder

Symptoms last at least 2 days
Adjustment disorder
and less than 28 days
Anxiety NOS
Yes
Absence of direct effects from drug,

alcohol, general medical condition, brief No
psychotic disorder, or exacerbation of
preexisting Axis I or Axis II disorder
Yes
Acute stress disorder
Figure 32-1 Diagnostic decision tree for acute stress disorder.
due to a general medical condition, whereas a clinical of acute trauma is generally aimed at being brief, pro-
picture related to substance use (e.g., alcohol intoxica- vided immediately after the trauma whenever possible,
tion) is appropriately diagnosed as substance-induced administered in a centralized and coordinated fashion
disorder. Substance-related ASD is confined to the with the expectation of the person’s return to normal
period of intoxication or withdrawal. Head injury- function and as proximately as possible to the scene
induced ASD needs substantiating by evidence from of the trauma, and not directed at any uncovering or
the history, physical examination, and laboratory explorative procedures but rather at maintaining a su-
testing that the symptoms are a direct physiological perficial, reintegrating approach.
consequence of head trauma. People most highly at risk, and therefore perhaps
most in need of treatment, are as follows: survivors with
psychiatric disorders; traumatically bereaved people;
TREATMENT
children, especially when separated from their parents;
There are six general principles involved in adminis- individuals who are particularly dependent on psycho-
tering any treatment immediately after trauma. These social supports, such as the elderly, handicapped, and
include principles of brevity, immediacy, centrality, ex- mentally retarded individuals; and traumatized survi-
pectancy, proximity, and simplicity. That is, treatment vors and body handlers.
Different components of treatment include provid- management training may be effective in preventing
ing information, psychological support, crisis inter- PTSD.
vention, and emotional first aid. Providing information
about the trauma is important as it can enable the survi-
vor to fully recognize and accept all the details of what
DIAGNOSTIC CRITERIA
happened. Information needs to be given in a way that
conveys hope and the possibility that psychological The ICD-10 Diagnostic Criteria for Research for Post-
pain and threat of loss may be coped with. Unrealistic traumatic Stress Disorder provide a different stressor
hope needs to be balanced by the provision of real- criterion: a situation or event “of exceptionally threat-
istic explanations as to what happened. Psychological ening or catastrophic nature, which would be likely to
support helps to strengthen coping mechanisms and cause pervasive distress in almost everyone,” which is
promotes adaptive defenses. The survivor benefits if similar to the DSM-III-R definition of a traumatic stres-
he or she recognizes the need to take responsibility sor. DSM-IV-TR instead defines a traumatic stressor as
for a successful outcome and is as actively involved “an event or events that involved actual or threatened
with this as possible. Crisis intervention is often used death or serious injury, or a threat to the physical integ-
after disasters and acts of violence or other serious rity of self or others.” Furthermore, the ICD-10 diag-
traumas. nostic algorithm differs from that specified in DSM-IV-
There is little investigation as to whether early rec- TR in that the DSM-IV-TR criterion D (i.e., symptoms
ognition and effective treatment of acute stress reac- of increased arousal) is not required. In contrast to
tions prevent the development of PTSD, although it is DSM-IV-TR, which requires that the symptoms persist
safe to assume that they are likely to have beneficial for more than one month, the ICD-10 Diagnostic Crite-
effects in this regard. Nonetheless, as was recognized ria for Research do not specify a minimum duration.
during World War II, rapid and effective treatment For acute stress disorder, the ICD-10 Diagnostic Cri-
of acute combat stress did not always prevent vet- teria for Research differ in several ways from the DSM-
erans from developing subsequent chronicity. More IV-TR criteria: (1) primarily anxiety symptoms are in-
recently, an intervention designed to prevent the de- cluded; (2) it is required that the onset of the symptoms
velopment of PTSD and administered in the acute be within 1 hour of the stressor; and (3) the symptoms
phase, critical incident stress debriefi ng, has been must begin to diminish after not more than 8 hours (for
found to be ineffective in preventing the development transient stressors) or 48 hours (for extended stressors).
of PTSD. However, there has been an initial study In contrast to DSM-IV-TR, the ICD-10 Diagnostic Cri-
with motor vehicle accident survivors that suggested teria for Research do not require dissociative symptoms
exposure therapy, and exposure therapy with anxiety or that the event be persistently reexperienced.
CHAPTER
33 Anxiety Disorders: Generalized

Anxiety Disorder
DIAGNOSIS
Generalized Anxiety Disorder (GAD) is defined as
excessive anxiety and worry (apprehensive expecta- 300.02 GENERALIZED ANXIETY DISORDER
tion) occurring for a majority of days during at least a A. Excessive anxiety and worry (apprehensive expec-
6-month period, about a number of events or activities tation), occurring more days than not for at least
(such as work or school performance). In individuals 6 months, about a number of events or activities (such
as work or school performance).
with GAD, the anxiety and worry are accompanied by B. The person finds it difficult to control the worry.
at least three of six somatic symptoms (only one accom- C. The anxiety and worry are associated with three (or
panying symptom is required in children), which are more) of the following six symptoms (with at least some
symptoms present for more days than not for the past
restlessness or feeling keyed up or on edge, being easily 6 months). Note: Only one item is required in children.
fatigued, difficulty concentrating or mind going blank,
(1) restlessness or feeling keyed up or on edge
irritability, muscle tension, and sleep disturbance. In (2) being easily fatigued
addition, the affected individual has difficulty control- (3) difficulty concentrating or mind going blank
ling his/her worry, and the anxiety, worry, or somatic (4) irritability
(5) muscle tension
symptoms cause clinically significant distress or im- (6) sleep disturbance (difficulty falling or staying
pairment in social, occupational, and/or other impor- asleep, or restless unsatisfying sleep)
tant areas of functioning. Further, the GAD symptoms D. The focus of anxiety and worry is not confined to fea-
should not be due to the direct physiological effects of tures of an Axis I disorder, for example, the anxiety or
a substance such as drugs or alcohol or a general medi- worry is not about having a panic attack (as in panic
disorder), being embarrassed in public (as in social pho-
cal condition, and should not occur exclusively during a bia), being contaminated (as in obsessive–compulsive
mood disorder, psychotic disorder, or pervasive devel- disorder), being away from home or close relatives (as
in separation anxiety disorder), gaining weight (as in an-
opmental disorder. orexia nervosa), having multiple physical complaints (as
Worry and anxiety are part of normal human be- in somatization disorder), or having a serious illness (as
havior and it may be difficult to define a cutoff point in hypochondriasis), and the anxiety and worry do not
occur exclusively during posttraumatic stress disorder.
distinguishing normal or trait anxiety (i.e., a rela- E. The anxiety, worry, or physical symptoms cause clini-
tively stable tendency to perceive various situations cally significant distress or impairment in social, occu-
as threatening) from GAD. However, as described in pational, or other important areas of functioning.
F. The disturbance is not due to the direct physiological
the DSM-IV-TR defi nition of GAD, individuals suf- effects of a substance (e.g., a drug of abuse, a medi-
fering from a disorder exhibit significant distress and cation) or a general medical condition (e.g., hyper-
impairment in functioning as a result of their anxiety thyroidism) and does not occur exclusively during a
mood disorder, a psychotic disorder, or a pervasive
symptoms. developmental disorder.
Individuals with GAD experience chronic anxiety Reprinted with permission from the Diagnostic and Statistical
and tension. They find the worry as being uncontrol- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
lable. However, some individuals intentionally initiate
and maintain worry with an almost superstitious as-
sumption that, by doing so, they can avert a negative as making a slight social faux pas. The majority report
event. Individuals tend to worry predominantly about being anxious for at least 50% of the time during an
family, personal finances, work, and illness. They are average day. In children and adolescents, the worries
also likely to report worrying over minor matters, such often revolve around the quality of their performance
in school or other competitive area. They may also and many had undergone extensive cardiac evaluations
worry about potential catastrophic events. They are that revealed no demonstrable cardiac pathology.
concerned with their own physical or mental imperfec- Special laboratory and diagnostic evaluation of in-
tions or inadequacies, and typically require excessive dividuals with GAD may occasionally be required to
reassurance. They often appear shy, overcompliant, exclude general medical conditions that mimic symp-
perfectionistic, and frequently describe multiple physi- toms of generalized anxiety (see Differential Diagno-
cal complaints. They may have an unusually mature sis, page 335). An evaluation to identify these disorders
and serious manner and appear older than their actual includes a personal and family medical history, review
age. These children are often the eldest in small, com- of systems, and a careful physical examination includ-
petitive, achievement-oriented families. ing neurological examination. Laboratory evaluation
Individuals with GAD commonly complain of feel- should include an electrocardiogram, screening for
ing tense, jumpy, and irritable. They have difficulty abusable substances, urinalysis, complete blood count,
falling or staying asleep, and tire easily during the day. serum electrolytes, liver and thyroid function tests, cal-
Particularly distressing to such individuals is the dif- cium, phosphorus, and blood urea nitrogen.
ficulty in concentrating and collecting their thoughts. An examination of the relative frequencies of vari-
Cognitions appear to play a central role in GAD, as ous comorbid diagnoses in individuals with GAD
well as other anxiety disorders. Patterns of cognitions, obtained from the available studies reveals that other
however, appear to be disorder-specific. When the fre- anxiety and mood disorders frequently complicate the
quency of anxiety, worry, or panic attacks among in- course of GAD (see Figure 33-1). Findings from a lon-
dividuals with GAD and panic disorder, as well as the gitudinal epidemiological study in Zurich, Switzerland
severity of anxiety associated with each were exam- showed strong associations between GAD and ma-
ined, 34% of GAD individuals’ cognitions were found jor depression and between GAD and dysthymia, but
to center on interpersonal conflict or the issue of ac- found a relatively low association with panic disorder.
ceptance by others, while only 1.4% of panic disorder A high comorbidity of GAD with hypomania was also
individuals reported such concerns. While individuals found. Further, the presence of comorbidity was as-
with GAD also had exaggerated worries over relatively sociated with a high suicide attempt risk. In addition,
minor matters, panic disorder individuals reported a individuals with comorbid disorders were treated more
significantly greater frequency of cognitions concern- frequently and endorsed more work impairment than
ing physical dangers or catastrophes (e.g., accident, GAD individuals without comorbid disorders.
injury, death). Alcoholism also complicates the clinical course of
Individuals may present with complaints of mus- GAD for some individuals; however, the available lit-
cular tension, especially in their neck and shoulders. erature suggests that the diagnosis of alcohol abuse is
They may experience headaches, frequently described not as prevalent in GAD as in other anxiety disorders,
as frontal and occipital pressure or tension. They com- and the pattern of abuse is often a brief and nonper-
plain about sweaty palms, feel shaky and tremulous, sistent one. GAD onset is usually later than that of the
complain of dryness of the mouth, and experience alcohol use disorder. Personality disorders have been
palpitations and difficulty in breathing. Individuals observed to co-occur in approximately 50% of individ-
may also experience gastrointestinal symptoms such uals with GAD. For example, rates of GAD and person-
as heartburn and epigastric fullness. Approximately ality disorders in clinical populations have ranged from
30% of individuals experience severe gastrointestinal 31%–46%. Cluster C personality disorders, specifically
symptoms of irritable bowel syndrome. The physical avoidant personality disorder, dependent personality
complaints frequently lead individuals to seek medi- disorder, and obsessive–compulsive personality disor-
cal attention, and most will initially consult a primary der, are common. Interestingly, Cluster A personality
care physician. Although they frequently complain of traits, in particular, suspiciousness and mistrust, may
palpitations and breathing difficulty, studies suggest be prominent in GAD as well.
that individuals with GAD do not differ from normal Despite the shifting diagnostic criteria affecting the
comparison subjects on measures of respiration and prevalence studies, current data indicate that GAD is
heart rate. Individuals with GAD may also present probably one of the more common psychiatric dis-
complaining of chest pain. Although chest pain is more orders. A lifetime prevalence of 45% for GAD was
frequently reported by individuals with panic disorder, reported according to DSM-III diagnostic criteria.
it has been observed that 34% of individuals with GAD However, when the more stringent criteria outlined in
without panic attacks experienced chest pain. They also the DSM-III-R, which required a duration of 6 months
found that these individuals were predominantly males were used, the prevalence rate dropped dramatically to
Chapter 33 • Anxiety Disorders: Generalized Anxiety Disorder 337
Symptoms of anxiety, worry
Anxiety disorder due

Due to the effects of a Yes
to a general medical
condition
No
Due to the effects of a

Yes Substance-induced
substance (e.g., a drug of
anxiety disorder
abuse, a medication, a toxin)
No
Recurrent unexpected
Yes Panic disorder with or
panic attacks with or
without agoraphobia
without agoraphobia
No
Fear of humiliation or Yes Social phobia (social
embarrassment in social or
anxiety disorder)
performance situations
No
Major depression or Fear cued by object or Yes

dysthymia with Specific phobia
situation
prominent anxiety
symptoms No
Yes Obsessions or Yes Obsessive − compulsive

compulsions disorder
Accompanying No
symptoms
of depression Yes 6-month period of excessive
Yes Generalized anxiety
anxiety and worry plus
disorder
associated symptoms
At least 4 weeks No
of mixed anxiety No
Reexperiencing of event,
and depression Yes
Anxiety in response to a increased arousal, and avoidance
Yes severe traumatic event of stimuli associated with
traumatic event Posttraumatic
Mixed
Yes Yes stress disorder
anxiety−depressive
disorder No
Duration of 4 weeks or more
No Acute stress disorder
Anxiety develops in response Yes Adjustment disorder

to a definitive stressor with anxiety
Figure 33-1 Diagnostic decision tree for GAD.
9%. The Epidemiologic Catchment Area Study (ECA) (defined as the most recent 6-month period of anxiety),
a five-center epidemiological study of the prevalence 3.1% for 12-month GAD, and 5.1% for lifetime GAD,
of psychiatric disorders in the United States, reported with lifetime prevalence higher in females (6.6%) than
a lifetime prevalence for DSM-III-defined GAD of males (3.6%).
4.1–6.6% in the three sites that assessed for GAD. GAD appears at even higher rates in clinical set-
Prevalence rates of DSM-III-R GAD in the National tings, particularly in primary care settings. For exam-
Comoribidty Study were 1.6% for current GAD ple, prevalence rates of GAD, using DSM-III-R criteria,
reported by individuals at four primary care centers, and autonomic symptoms (e.g., respiratory or cardiac
were found to be twice as high as those reported in complaints) than depressed individuals.
community samples (i.e., 10% versus 5.1%). Similarly, Panic disorder is characterized by the presence of
a collaborative study by the World Health Organization panic attacks; that is, recurrent, discrete episodes of in-
(WHO) across 15 international sites reported preva- tense anxiety or fear associated with a cluster of somatic
lence rates of GAD at approximately 8% in primary symptoms reflecting autonomic hyperactivity such as
care settings. rapid heartbeat, dizziness, numbness or tingling, trou-
ble breathing or choking, and nausea or vomiting. In
contrast, individuals with GAD predominantly experi-
Course
ence symptoms of muscle tension and vigilance such as
GAD individuals frequently report that they have been fatigue, muscle soreness, insomnia, difficulty in con-
anxious all their lives. Typically, they were moderately centrating, restlessness, and irritability. Anxiety is also
anxious during childhood, later developing full-blown a part of the clinical picture of obsessive–compulsive
GAD when their stress levels increased through activi- disorder (OCD) and may be a central factor in initi-
ties such as attending college or starting work. Individ- ating and maintaining obsessions and compulsions.
uals with early onset of symptoms report experiencing Obsessive thoughts are described as egodystonic in-
significant anxiety and fears, social isolation, obses- trusions that often take the form of urges, impulses, or
sionality, more academic difficulties, and disturbed images. They are often senseless and are frequently ac-
home environment during their childhood. The social companied by time-consuming compulsions designed
maladjustment and emotional overreactivity persist into to reduce mounting anxiety. In contrast, the worries in
adulthood. Epidemiological studies and clinical studies GAD are about realistic concerns, such as health and
suggest that the onset of GAD typically begins between finances.
the late teens and late twenties. However, not all GAD In phobic disorders, the anxiety is characteristically
individuals have a lifelong history of excessive anxi- associated with a specific phobic object or situation that
ety. Some individuals develop their disorder at a later is frequently avoided by the individual. Such is the case
age, that is, in their thirties or later. These individu- with social anxiety disorder as well, in which the indi-
als frequently report identifiable, precipitating stress- vidual is afraid of or avoids situations in which he or
ful events, specifically unexpected, negative, important she may be the focus of potential scrutiny by others.
events in the year preceding development of GAD. Anxiety is also a characteristic part of the presenta-
Retrospective and prospective reports indicate that tion of posttraumatic stress disorder (PTSD) and acute
the typical course of GAD is chronic, nonremitting, stress disorder (ASD). However, unlike in GAD, the
and that it often persists for a decade or longer. It has principal symptoms experienced in PTSD and ASD
been reported that approximately 80% of subjects follow exposure to a traumatic event and are character-
with GAD reported substantial interference with their ized by avoidance of reminders of the event and per-
life, a high degree of professional help-seeking, and a sistent reexperiencing of the traumatic event. Finally,
high prevalence of taking medications because of their in adjustment disorders, anxiety when present occurs
GAD symptoms. The disability associated with GAD in response to a specific life stressor or stressors and
has been found to be similar to that found in individu- generally does not persist for more than 6 months.
als with panic disorder or major depression. Many general medical conditions may present with
prominent anxiety symptoms and must be considered
in the differential diagnosis of generalized anxiety
(see Table 33-1). Individuals with GAD may complain
Anxiety can be a prominent feature of many psychiatric of palpitations, skipped heartbeats, and chest pain. In
disorders and a number of disorders should be consid- addition, many GAD individuals, especially males,
ered in the differential diagnosis of GAD (Figure 33-1). fear having an acute myocardial infarction and often
Several symptom profiles discriminate between major present to the emergency room for evaluation. How-
depressive disorder or dysthymic disorder and GAD. In- ever, most individuals with GAD without a concomi-
dividuals with major depressive disorder exhibit higher tant cardiovascular disease do not experience severe
rates of dysphoric mood, psychomotor retardation, sui- chest pain. Following the controversial evidence sug-
cidal ideation, guilt, hopelessness, and helplessness, as gesting an association between mitral valve prolapse
well as more work impairment than individuals with (MVP) and panic disorder, researchers evaluated the
GAD. In contrast, individuals with GAD show higher prevalence of MVP in individuals with GAD and found
rates of somatic symptoms, specifically, muscle tension no evidence of increased prevalence in individuals with
Medical Conditions and Drugs that may

diaphoresis, tachycardia, chest pain, flushing, nausea
Table 33-1 and vomiting, headache, and significant apprehension.
Cause Anxiety
Although the clinical presentation frequently mim-
Endocrine Disorders Cardiovascular and
Addison’s disease Circulatory Disorders ics spontaneous panic attacks, pheochromocytomas
Cushing’s syndrome Anemia should also be considered in the differential diagno-
Hyperparathyroidism Congestive heart failure sis of GAD. The diagnosis of pheochromocytoma can
Hyperthyroidism Coronary insufficiency
Hypothyroidism Dysrhythmia, e.g. atrial be confirmed by increased levels of catecholamines
Carcinoid fibrillation (epinephrine and norepinephrine) or catecholamine
Pheochromocytoma Hypovolemia metabolites (metanephrines and vanillylmandelic acid)
Myocardial infarction
Drug Side Effects in a 24-hour urine collection.
Anticonvulsants Respiratory Disorders
Antidepressants Asthma Menopause is commonly referred to as the period
Antihistamines Chronic obstructive that encompasses the transition between the reproduc-
Antihypertensive agents pulmonary disease tive years and beyond the last episode of menstrual
Antiinflammatory agents Pulmonary embolism
Antiparkinsonian agents Pulmonary edema bleeding. Frequently associated with significant anxi-
Caffeine
Immunological, Collagen,
ety, menopause should be considered in the differ-
Digitalis ential diagnosis of GAD. However, other associated
and Vascular Disorders
Sympathomimetics
Systemic lupus symptoms such as vasomotor instability, atrophy of
Thyroid supplements
erythematosus
Substance Use Related Temporal arteritis urogenital epithelium and skin, and osteoporosis make
Cocaine the diagnosis of menopause probable. Another endo-
Metabolic Conditions
Hallucinogens crinologic disorder, hyperparathyroidism, can present
Acidosis
Amphetamines
Acute intermittent porphyria with anxiety symptoms, and the initial evaluation of
Withdrawal Syndromes Electrolyte abnormalities serum calcium levels may be indicated. Finally, certain
Alcohol Hypoglycemia
Narcotics neurologic conditions such as complex partial seizures,
Neurological Disorders
Sedatives–hypnotics intracranial tumors and strokes, and cerebral ischemic
Brain tumors
Gastrointestinal Cerebral syphilis attacks may be associated with symptoms typically ob-
Disorders Cerebrovascular disorders served in anxiety disorders and may require appropri-
Peptic ulcer disease Encephalopathies
Epilepsy (especially ate evaluation.
Infectious Diseases
Miscellaneous viral and
temporal lobe epilepsy) Anxiety disorders can occur frequently in asso-
Postconcussive syndrome ciation with intoxication and withdrawal from several
bacterial infections
Vertigo
Akathisia classes of substances (see Table 33-1). Excessive use
of caffeine, especially in children and adolescents,
may cause significant anxiety. Cocaine intoxication
may be associated with anxiety, agitation, and hyper-
GAD. Nevertheless, individuals with anxiety symptoms vigilance. During cocaine withdrawal, individuals
associated with unexplained chest pain should be eval- may also present with prominent anxiety, irritability,
uated for possible cardiovascular disease. insomnia, fatigue, depression, and cocaine craving.
Anxiety is a prominent feature of hyperthyroidism Adverse reaction to marijuana includes extreme anxi-
with some overlap in the symptomatology of thyro- ety that usually lasts less than 24 hours. Mild opioid
toxicosis and GAD. Symptoms such as tachycardia, withdrawal presents with symptoms of anxiety and
tremulousness, irritability, weakness, and fatigue are dysphoria. However, accompanying symptoms such as
common to both disorders. In GAD, however, the pe- elevated blood pressure, tachycardia, pupilary dilation,
ripheral manifestations of excessive concentrations rhinorrhea, piloerection, and lacrimation are rare in in-
of circulating thyroid hormones are absent, includ- dividuals with GAD.
ing symptoms such as weight loss, increased appetite, The clinical phenomenology observed both in al-
warm and moist skin, heat intolerance, and dyspnea on cohol and sedative–hypnotic drug withdrawal and in
effort. Pheochromocytomas, also known as chromaf- GAD, although variable, may be highly similar. In
fin tumors, produce, store, and secrete catecholamines. both conditions, nervousness, tachycardia, tremulous-
They are derived most often from the adrenal medulla, ness, sweating, nausea, and hyperventilation occur
as well as the sympathetic ganglia, and occasionally prominently. Additionally, the same drugs (i.e., ben-
from other sites. The clinical features of these tu- zodiazepines) can be used to treat anxiety symptoms,
mors, most commonly hypertension and hyperten- and some individuals may use alcohol in an attempt to
sive paroxysms, are predominantly due to the release alleviate anxiety. Thus, the symptoms of an underly-
of catecholamines. Individuals may also experience ing anxiety disorder may be difficult to differentiate
from the withdrawal symptoms associated with the must be considered individually according to the se-
use of benzodiazepines or alcohol. The use of many verity and chronicity of the disorder, the severity of
commonly prescribed medications may produce side somatic symptoms, the presence of stressors, and the
effects manifesting as anxiety (see Table 33-1). Such presence of specific personality traits. The clinician
medications include sympathomimetics or other bron- may also need to work with the individual to determine
chodilators such as theophylline, anticholinergics, an- how much improvement is sufficient. For example, a
tiparkinsonian preparations, corticosteroids, thyroid reduction in disability may occur without a marked
supplements, oral contraceptives, antihypertensive and change in symptoms. Symptoms may persist but occur
cardiovascular medications such as digitalis, insulin less frequently, or their intensity may be reduced. All
(secondary to hypoglycemia), and antipsychotic and these variations have important treatment implications,
antidepressant medications. Finally, heavy metals and including decisions regarding the need for long-term
toxins such as organophosphates, paint, and insecti- treatment. Individuals with milder forms of GAD may
cides may also cause anxiety symptoms. respond well to simple psychological interventions, and
require no medication treatment. In more severe forms
of GAD, it may become necessary to see the individual
TREATMENT
regularly and to provide both more specific psychologi-
Since GAD is a chronic, relapsing illness, most treat- cal and pharmacological interventions. Figure 33-2 can
ments do not cure the individual and when treatments be used as a guide to the treatment of GAD using, pri-
are discontinued, symptoms may return. Each case marily, medications.
GAD positive
First-line treatment for Monitor for

GAD includes SSRIs side effects
(e.g., paroxetine), SNRI Responder (e.g.,
(e.g., venlafaxine), or cardiovascular
nonsedating TCA (e.g., effects, sexual
imipramine, trazodone) difficulty).
TCAs monitor
plasma levels
Nonresponder
Addition of a
benzodiazepine (e.g., Begin cognitive−
alprazolam, clonazepam, Responder Monitor for behavioral therapy in
diazepam), may assist abuse or conjunction with
with acute anxiety dependence medication
reactions (not for long- management
term use)
Nonresponder
Discontinue SSRI, Monitor for side

SNRI or TCA and Responder effects (e.g.,
begin treatment with gastrointestinal
buspirone disturbances)
Nonresponder
Begin cognitive−
behavioral therapy
Figure 33-2 Generalized anxiety disorder treatment flowchart emphasizing pharmacotherapy.

During the early (acute) phase of treatment, an at- as diazepam, chlordiazepoxide, and alprazolam in the
tempt should be made to control the individual’s symp- treatment of GAD.
tomatology. It may take 3 to 6 months for an optimal The benzodiazepines have a broad spectrum of ef-
response to be achieved. However, there may be a fects including sedation, muscle relaxation, anxiety
considerable variation in the length of the initial treat- reduction, and decreased physiologic arousal (e.g.,
ment phase. For example, clinical response to benzodi- palpitations, tremulousness, etc.). Interestingly, avail-
azepines occurs early in treatment. Response to other able studies indicate that benzodiazepines have the
anxiolytic medications or to cognitive–behavioral or most pronounced effect on hypervigilance and somatic
psychodynamic treatment generally requires longer symptoms of GAD, but exhibited fewer effects on psy-
periods of time. During the maintenance phase, treat- chic symptoms such as dysphoria, interpersonal sensi-
ment gains are consolidated. Unfortunately, studies tivity, and obsessionality. The main difference between
suggesting how long treatment should be continued individual benzodiazepines is potency and elimination
are limited. Routinely, pharmacological treatment is half-life. These differences may have important treat-
continued for a total of 6 to 12 months before attempt- ment implications. For example, benzodiazepines with
ing to discontinue medications. Some studies indicate relatively short elimination half-lives such as alprazolam
that maintenance psychotherapeutic treatments such as (range of 10–14 hours) may require dosing at least three
cognitive–behavioral therapy may be helpful in main- to four times a day in order to avoid interdose symp-
taining treatment gains in individuals with anxiety dis- tom rebound. Conversely, the use of longer-acting com-
orders following the discontinuation of pharmacother- pounds such as clonazepam (range of 20–50 hours) may
apy. It is clear that many individuals may experience minimize the risk of interdose symptom recurrence.
chronic and continuous symptoms that require years of Benzodiazepines exert their therapeutic effects
long-term treatment. quickly, often after a single dose. However, concern has
The vast majority of individuals with GAD who emerged over the use of benzodiazepines, particularly,
present for treatment have been ill for many years long-term benzodiazepine use. Side effects of benzodi-
and frequently have received a variety of treatments. azepines, such as sedation, psychomotor impairment,
Some individual have been sent to mental health pro- and memory disruption, have been noted by treating
fessionals for treatment as a “last resort” in order to clinicians, and confirmed in research studies. Further,
learn how to cope with their various ill-defined so- although it was suggested that the use pattern of benzo-
matic and emotional complaints. Individuals may feel diazepines by individuals with anxiety disorders may
shame and guilt over their inability to control symp- not represent abuse, addiction, or drug dependence
toms. They are often demoralized and angry, and feel as typically understood, the chronic use of benzodi-
that their symptoms are not taken seriously. Thus, it azepines in the treatment of GAD has been increas-
is important to help the individual understand his or ingly discouraged in recent years.
her illness and to conceptualize it as a health problem When initiating treatment with benzodiazepines, it
rather than a personal weakness. Once the burden of is helpful for individuals to take an initial dose at home
perceived responsibility is lifted from the individual, in the evening to see how it affects them. Gradual titra-
and he or she believes that effective treatment is possi- tion to an effective dose allows for limiting unwanted
ble, a working alliance with the treating clinician can adverse effects. A final daily dosage of alprazolam be-
begin. The treatment plan should be outlined clearly, tween 2 and 4 mg/day, 1 and 2 mg/day for clonazepam,
and the individual cautioned that recovery may have or 15 and 20 mg/day of diazepam, is usually sufficient
a gradual, variable course. Finally, during the critical for the majority of individuals. Upon treatment discon-
early stages of treatment, the clinician should make a tinuation, it is important to consider appropriate taper
special effort to be available in person or by phone to in order to avoid withdrawal symptoms. Possible factors
answer questions and provide support. that may contribute to the severity of withdrawal and
the ultimate outcome of benzodiazepine taper include
the dosage, duration of treatment, the benzodiazepine
Somatic Therapies
elimination half-life and potency, and the rate of ben-
A number of anxiolytic agents are effective in the treat- zodiazepine taper (gradual versus abrupt). Addition-
ment of GAD (see Table 33-2). Benzodiazepines are ally, individual factors such as premorbid personality
commonly used for the treatment of GAD and are still features have been implicated. It appears that a taper
considered by some clinicians to be the first-line treat- rate of 25% per week is probably too rapid for many in-
ment for GAD. Several controlled studies have demon- dividuals. A slow benzodiazepine taper of at least 4 to
strated the efficacy of different benzodiazepines such 8 weeks, with the final 50% of the taper conducted even
Table 33-2 Anxiolytic Agents

Daily Dosage
Drug Range (mg) Advantages Disadvantages
Selective serotonin reuptake

inhibitors
Paroxetine 20–40 Efficacy with GAD Gastrointestinal side effects
Fluoxetine 20–60 Efficacy with comorbid Delayed onset
depression
Sertraline 50–200 Sexual side effects
Citalopram 20–40 Favorable side effects profile
compared with TCAs
Fluvoxamine 100–300 Easy dosing schedule
Serotonergic and noradrenergic
reuptake inhibitors
Venlafaxine extended 75–225 Efficacy with GAD Gastrointestinal side effects
release (XR)
Efficacy with comorbid Sexual side effects
depression
Potential for increased blood
pressure
Benzodiazepines
Alprazolam 2–6 Rapid onset of action Sedation
Clonazepam 1–3 Favorable side effects profile Multiple doses for shorter
acting agents
Lorazepam 4–10 Physical dependence
Diazepam 15–20 Limited antidepressant effects
Sexual side effects
Tricyclic antidepressants
Imipramine 75–300 Once-daily dosage Delayed onset
Efficacy with comorbid Need for titration
depression
Activation
Anticholinergic effects
Orthostatic hypotension
Weight gain
Toxicity in overdose
Sexual side effects
Atypical antidepressants
Trazodone 150–600 Once-daily dosage Delayed onset
Efficacy with comorbid Orthostatic hypotension
depression
Weight gain
Low anticholinergic effects Sexual side effects
Priapism (rare)
Sedation
Azapirones
Buspirone 30–60 No withdrawal symptoms Multiple doses
No physical dependence
Favorable side effects profile
more gradually, is recommended, with the individual response in the somatic and hyperarousal symptoms;
decreasing the daily dose of the benzodiazepines dur- however, imipramine and trazodone exhibited higher
ing this period by the lowest possible percentage. efficacy after 6 to 8 weeks of treatment with psychic
Clinical trials conducted in the early 1990s have con- symptoms of tension, apprehension, and worry being
firmed that tricyclic antidepressants (TCAs) may also more responsive to the antidepressants. Owing, in part,
be effective in the treatment of GAD. For example, a to their side effect profile, need for dose titration, and
placebo-controlled study which compared imipramine, importantly the emergence of new and effective agents
trazodone, and diazepam in GAD individuals without (as described below), the use of TCAs in the treatment
comorbid depression or panic disorder revealed that the of GAD has been reserved for those resistant to these
efficacy of imipramine and trazodone was comparable newer agents.
to diazepam. It should be noted that diazepam dem- Selective serotonin reuptake inhibitors (SSRIS)
onstrated greater efficacy than imipramine during the are rapidly becoming a key tool in the treatment of
first 2 weeks of treatment with the greatest degree of GAD. Several controlled double-blind studies have
demonstrated the efficacy of paroxetine in the treat- clinically significant rebound anxiety or benzodi-
ment of GAD. The most problematic side effect as- azepine withdrawal. This approach was shown to pro-
sociated with SSRI use is the interference with sexual vide clinically significant relief of anxiety symptoms
function (e.g., delayed orgasm or abnormal ejaculation) in GAD individuals previously treated with benzodi-
in women and men. azepines for 8 to 14 weeks. Perhaps the most significant
The antidepressant venlafaxine extended release problem with the use of buspirone has been that experts
(XR) is an inhibitor of both 5-HT and NE reuptake, have advocated too low a dose to produce symptom
serotonergic and noradrenergic reuptake inhibitors reduction. In order to achieve optimal response, bus-
(SNRI). Several large, placebo-controlled trials have pirone dosing in the range of at least 30–60 mg/day is
evaluated it in the treatment of individuals with DSM- currently recommended.
IV-TR-diagnosed GAD. As a result, venlafaxine XR When faced with treatment resistance, clinician
was the first antidepressant approved by the FDA for should evaluate whether an adequate treatment trial
the treatment of GAD. The adverse events for GAD in- was completed. An attempt should be made to main-
dividuals treated with venlafaxine XR resembled those tain the individual on medication for at least 6 weeks.
in depression trials. The most common adverse events Although there are no data suggesting that certain
included nausea, somnolence, dry mouth, dizziness, doses may be particularly effective in the treatment
sweating, constipation, and anorexia. of GAD, it is advisable to titrate the medication up to
Several other psychotherapeutic agents have been maximally tolerated doses prior to discontinuing the
tested in the treatment of individuals with GAD. For medication for nonresponse. It is important to inquire
example, the alpha-2-adrenoreceptor antagonist mirta- about the presence of side effects such as sedation, an-
zapine, which is also a 5-HT2, 5-HT3, and H(1) receptor ticholinergic effects, or sexual side effects, which may
antagonist, has been evaluated as a potential anxiolytic limit the attainment of a therapeutic dosage and reduce
in the treatment of individuals with major depressive compliance. Additionally, many individuals with GAD
disorder and comorbid GAD in an 8-week, open-label fear that they may become drug dependent and thus
study. Results suggest that this antidepressant may be avoid dose increases. Some estimate of the individual’s
useful in the treatment of anxiety symptoms. compliance may be helpful in determining whether a
The azapirone group of drugs was introduced in re- treatment was adequate, as indicated by blood plasma
sponse to concerns over chronic benzodiazepine use levels or pill counts. Drug plasma levels may also be
in subjects with anxiety symptoms. Buspirone hydro- useful to identify individuals who are rapid metaboliz-
chloride, the only currently marketed azapirone, was ers. A careful evaluation for the presence of psychiatric
the first nonbenzodiazepine anxiolytic agent approved comorbid conditions that may contribute to treatment
for the treatment of persistent anxiety by the FDA. refractoriness should follow. As mentioned, comorbid-
Results have been mixed about the efficacy of bus- ity which may reflect more severe loading for psycho-
pirone over placebo and benzodiazepines. For exam- pathology is often associated with increased severity of
ple, in four placebo-controlled studies that compared illness and poorer response to treatment in comparison
buspirone to a standard benzodiazepine, two showed to individuals with an uncomplicated (i.e., single) dis-
no benefit for diazepam and buspirone over placebo, order. Thus, treatment strategies in GAD individuals
and two showed no benefit for buspirone over placebo. with a concurrent disorder may differ from those in an
Benzodiazepines may also be slightly more effective uncomplicated disorder, often requiring multiple drug
than buspirone in the treatment of somatic symptoms therapy. The clinician should also be alert to the pres-
of anxiety but no significant differences appear to exist ence of underlying general medical conditions such as
between buspirone and benzodiazepines in measures hyperthyroidism, which may present with refractory
of psychic anxiety. Buspirone, however, may be more anxiety, or conditions/medications that may alter the
effective in the treatment of anger/hostility symptoms effects of treatment, such as hepatic disease or medica-
than benzodiazepines. tions (e.g., steroids) that affect hepatic clearance.
Side effects most frequently associated with bus-
pirone use included gastrointestinal system-related
Psychosocial Therapies
side effects, such as appetite disturbances and abdomi-
nal complaints, and dizziness. Prior use of benzodi- Numerous studies have shown that psychological inter-
azepines may adversely affect the therapeutic response ventions are beneficial in the comprehensive manage-
to buspirone It has been reported that a gradual 2-week ment of anxiety disorders. However, data suggesting
taper of lorazepam with a simultaneous addition of that specific psychotherapeutic techniques yield better
buspirone for 6 weeks prevents the development of results in the treatment of individuals with GAD are
inconclusive, and more evidence is needed on the com- Many individuals with milder forms of GAD will
parative efficacy and long-term effects of different psy- benefit from simple psychological interventions such
chological treatments. as supportive psychotherapy. They may experience
In recent years, specific cognitive–behavioral therapy lessening of anxiety when given the opportunity to dis-
(CBT) interventions for the treatment of individuals with cuss their difficulties with a supportive clinician and to
anxiety disorders have been developed. Components of become better informed about their illness. Thus, basic
CBT include teaching individuals to identify and label supportive techniques such as reassurance, clarification
irrational thoughts and to replace them with positive self- of individual concerns, direct suggestions, and advice
statements or modify them by challenging their verac- are often effective in reducing anxiety symptoms.
ity. The cognitive modification approaches are combined Relaxation techniques such as progressive muscle
with behavioral treatments such as exposure or relaxation relaxation and biofeedback have also been utilized in
training. There is evidence suggesting that CBT may be the treatment of individuals with anxiety symptoms.
more effective in the treatment of GAD than other psy- Biofeedback has also been found to be effective in the
chotherapeutic interventions, such as behavioral therapy treatment of individuals with GAD. It should be noted
alone or nonspecific supportive therapy. For example, a that relaxation may be associated with a paradoxical
study of CBT targeting intolerance of uncertainty, erro- increase in anxiety and tension in individuals with
neous beliefs about worry, poor problem orientation, and GAD. However, with repeated training, specifically in
cognitive avoidance demonstrated effectiveness at post- the context of CBT, this phenomenon may be used to
treatment (no change in the delayed treatment control achieve habituation and anxiety extinction.
group) 6- and 12-month follow-up, with about three quar-
ters of the treatment group no longer having symptoms
meeting criteria for a GAD diagnosis. Cognitive therapy
DIAGNOSTIC CRITERIA
was also compared to analytic psychotherapy, and was
found to be significantly more effective Overall, two- The ICD-10 Diagnostic Criteria for Research specify
thirds in the cognitive therapy group achieved clinically that four symptoms from a list of 22 be present. In con-
significant improvements, and cognitive therapy was as- trast, DSM-IV-TR requires 3 out of a list of 6 (of which
sociated with significant reductions in medication usage. 5 are included among the ICD-10 list of 22).
CHAPTER
34 Somatoform Disorders
The somatoform disorders are characterized by physi- “psychological factors affecting medical condition” is
cal symptoms suggestive of but not fully explained by not a mental disorder, but it is included in DSM-IV-TR
a general medical condition or the direct effects of a in the section for other conditions that may be a fo-
substance. In this class, symptoms are not intention- cus of clinical attention; it involves the presence of one
ally produced and are not attributable to another men- or more specific psychological or behavioral factors
tal disorder. To warrant a diagnosis, symptoms must that adversely affect a general medical condition (see
be clinically significant in terms of causing distress Chapter 41 for more information).
or impairment in important areas of functioning. The
disorders included in this class are somatization dis-
Generic Treatment Strategies
order, undifferentiated somatoform disorder, conver-
for Somatoform Disorders
sion disorder, pain disorder, hypochondriasis, body
dysmorphic disorder, and somatoform disorder not Whereas specific somatoform disorders indicate
otherwise specified (NOS). This chapter begins with specific treatment approaches, some general guide-
information about differential diagnosis and treatment lines apply to the somatoform disorders as a whole
as it applies to the diagnostic class as a whole, followed (Table 34-1). Therapeutic goals in the treatment of so-
by individual sections covering each of the somatoform matoform disorders include (1) as an overriding goal,
disorders. prevention of the adoption of the sick role and chronic
The somatoform disorders class was created for invalidism; (2) minimization of unnecessary costs and
clinical utility, not on the basis of an assumed com- complications by avoiding unwarranted hospitaliza-
mon etiology or mechanism. In DSM-IV-TR terms, it tions, diagnostic and treatment procedures, and medi-
was designed to facilitate the differential diagnosis of cations (especially those of an addictive potential); and
conditions in which the first diagnostic concern is the (3) effective treatment of comorbid mental disorders,
need to “exclude occult general medical conditions or such as depressive and anxiety syndromes. General
substance-induced etiologies for the bodily symptoms.” treatment strategies include (1) consistent treatment,
As shown in Figure 34-1, only after such explanations generally by the same physician, with careful coordi-
are reasonably excluded should somatoform disorders nation if multiple physicians are involved; (2) support-
be considered. ive office visits, scheduled at regular intervals rather
The somatoform disorder concept should be distin- than in response to symptoms; and (3) a gradual shift
guished from traditional concepts of “psychosomatic in focus from symptoms to an emphasis on personal
illness” and “somatization.” The psychosomatic ill- and interpersonal problems.
nesses involved structural or physiological changes
hypothesized as deriving from psychological factors.
Somatization Disorder
In the DSM-III, DSM-III-R, and DSM-IV somatoform
disorders, such objective changes are generally not evi-
DIAGNOSIS
dent. The “classic” psychosomatic illnesses included
bronchial asthma, ulcerative colitis, thyrotoxicosis, Somatization disorder is a polysymptomatic somato-
essential hypertension, rheumatoid arthritis, neuroder- form disorder characterized by multiple recurring
matitis, and peptic ulcer. In DSM-IV-TR, most of these pains and gastrointestinal, sexual, and pseudoneuro-
illnesses would be diagnosed as a general medical con- logical symptoms occurring for a period of years with
dition on Axis III, and in some cases with an additional onset before age 30 years (see DSM-IV-TR diagnostic
designation of psychological factors affecting medical criteria, page 347). The physical complaints are not
condition on Axis I. By definition, the diagnosis of intentionally produced and are not fully explained by
Physical symptom(s) including complaint(s) and GMC or PAIN DISORDER

preoccupation(s)/fear(s) of having a serious disease ASSOCIATED WITH A GMC
or defect(s) in appearance, leading to clinically
significant distress, treatment, or impairment in functioning
No
Yes
Yes Psychological factors Yes GMC plus PSYCHOLOGICAL

Fully explained by a GMC adversely affect FACTORS AFFECTING
the GMC MEDICAL CONDITION
No
Yes SUBSTANCE-
Fully explained as the direct
effect(s) of a substance INDUCED DISORDER
No
Yes External incentive Yes

Intentionally produced MALINGERING
present
No
No
Better accounted for by an Motivation to Yes FACTITIOUS

ANXIETY, MOOD, PSYCHOTIC, Yes assume sick role DISORDER
No
or other MENTAL DISORDER
Physical No Preoccupation(s) / fear(s) of having a ANXIETY, MOOD,

complaint(s) serious disease or defect in appearance PSYCHOTIC, or other
predominates MENTAL DISORDER
Yes
Yes
Preoccupation(s)/ Yes Yes DELUSIONAL
fear(s) of having a Delusional DISORDER,
serious disease SOMATIC TYPE
No
SEXUAL Yes Symptom(s) affecting
DYSFUNCTION sexual functioning only No HYPOCHONDRIASIS (plus
For at least Yes OBSESSIVE−COMPULSIVE
No 6 months DISORDER if also
PAIN DISORDER nonphysical concerns)
No
ASSOCIATED WITH
Yes Pain Preoccupation(s) with
PSYCHOLOGICAL FACTORS or SOMATOFORM DISORDER
WITH BOTH PSYCHOLOGICAL symptom(s) only body weight only
Yes NOT OTHERWISE
FACTORS AND A GMC SPECIFIED
No No
CONVERSION Yes Conversion Preoccupation(s) with EATING DISORDER

DISORDER symptom(s) only inappropriateness of sex
characteristics only Yes
No
GENDER IDENTITY
Begins before age 30 years, DISORDER
No
history of multiple
symptoms: at least 4 pain, No Criteria for a specific
Complaint(s), for at No
2 gastrointestinal, 1 sexual, SOMATOFORM
least 6 months DISORDER not met
1 pseudoneurologic
(conversion or dissociative), Yes
for several years Yes
BODY DYSMORPHIC DISORDER
Yes SOMATOFORM DISORDER (plus OBSESSIVE − COMPULSIVE
UNDIFFERENTIATED NOT OTHERWISE DISORDER if also nonphysical
SOMATIZATION SOMATOFORM SPECIFIED concerns; plus DELUSIONAL
DISORDER DISORDER (also includes DISORDER, SOMATIC
PSEUDOCYESIS) TYPE if delusional)
Figure 34-1 Differential diagnosis of clinically significant physical symptoms. Shadowed boxes represent diagnostic categories; GMC,
general medical condition.
Chapter 34 • Somatoform Disorders 347
consistently from interview to interview. The medical

DSM-IV-TR Diagnostic Criteria history is usually complicated, with multiple medi-
300.81 SOMATIZATION DISORDER
cal investigations, procedures, and medication trials.
If there have been symptoms for at least 6 months
A. A history of many physical complaints beginning be- but the onset is later than at age 30 years, or if the
fore age 30 years that occur over a period of several
years and result in treatment being sought or signifi- required number and distribution of symptoms are
cant impairment in social, occupational, or other im- not evident, undifferentiated somatoform disorder
portant areas of functioning. is diagnosed. If the duration has been less than 6
B. Each of the following criteria must have been met, with
individual symptoms occurring at any time during the months, a diagnosis of somatoform disorder NOS
course of the disturbance: also applies. In general, the greater the number and
(1) four pain symptoms: a history of pain related to at diversity of symptoms, and the longer they have been
least four different sites or functions (e.g., head, present without development of signs of an underly-
abdomen, back, joints, extremities, chest, rectum,
during menstruation, during sexual intercourse, or
ing general medical condition, the greater can be the
during urination) confidence that a diagnosis of somatization disorder
(2) two gastrointestinal symptoms: a history of at least is correct.
two gastrointestinal symptoms other than pain
(e.g., nausea, bloating, vomiting other than dur- In the US, somatization disorder is found predomi-
ing pregnancy, diarrhea, or intolerance of several nantly in women, with a female/male ratio of approxi-
different foods) mately 10 : 1 (see Table 34-2). This ratio is not as large
(3) one sexual symptom: a history of at least one sex-
ual or reproductive symptom other than pain (e.g., in some other cultures (e.g., in Greeks and Puerto
sexual indifference, erectile or ejaculatory dysfunc- Ricans). Thus, gender- and culture-specific rates are
tion, irregular menses, excessive menstrual bleed- more meaningful than generalized figures. The life-
ing, vomiting throughout pregnancy)
(4) one pseudoneurological symptom: a history of at time prevalence of somatization disorder in US women
least one symptom or deficit suggesting a neuro- has been estimated to be between 0.2% and 2%. The
logical condition not limited to pain (conversion magnitude of this discrepancy is attributable, at least
symptoms such as impaired coordination or bal-
ance, paralysis or localized weakness, difficulty in part, to methodological differences. The Epidemio-
swallowing or lump in throat, aphonia, urinary re- logical Catchment Area study, the most recent large-
tention, hallucinations, loss of touch or pain sensa- scale general population study in the US to include an
tion, double vision, blindness, deafness, seizures;
dissociative symptoms such as amnesia; or loss of assessment for somatization disorder, found a lifetime
consciousness other than fainting) risk of somatization disorder of only 0.2–0.3% in US
C. Either (1) or (2): women. However, this study may have underestimated
(1) After appropriate investigation, each of the symp- the prevalence of somatization disorder because non-
toms in criterion B cannot be fully explained by physician interviewers were used. It is argued that
a known general medical condition or the direct
effects of a substance (e.g., a drug of abuse, a it is difficult for lay interviewers to critically assess
medication). whether somatic symptoms are fully explained by
(2) When there is a related general medical condition, physical conditions. As a result, they may more read-
the physical complaints or resulting social or occu-
pational impairment is in excess of what would be ily accept individuals’ general medical explanations of
expected from the history, physical examination, or symptoms, resulting in fewer diagnoses of somatiza-
laboratory findings. tion disorder.
D. The symptoms are not intentionally produced or
feigned (as in factitious disorder or malingering).
Reprinted with permission from the Diagnostic and Statistical Course
American Psychiatric Association. Somatization disorder is rare in children younger than
9 years of age (see Table 34-2). Characteristic symp-
toms of somatization disorder usually begin during ad-
a general medical condition or the direct effects of a olescence, and the criteria are met by the mid-twenties.
substance. To warrant diagnosis, they must result in Somatization disorder is a chronic illness characterized
medical attention or significant impairment in social, by fluctuations in the frequency and diversity of symp-
occupational, or other important areas of functioning. toms. Full remissions occur rarely, if ever. Whereas the
Whereas criteria require the onset of symptoms most active symptomatic phase is in early adulthood,
before the age of 30 years, most individuals would aging does not appear to lead to total remission. Longi-
have had some symptoms at least by adolescence or tudinal follow-up studies have confirmed that 80–90%
early adulthood. Symptoms are often described in a of individuals initially diagnosed with somatization
dramatic yet imprecise way and may be reported in- disorder will maintain a consistent clinical picture and
Table 34-1 Treatment of DSM-IV-TR Somatoform Disorders
Somatoform Psychotherapy and Psychosocial Strategies and Pharmacological and Physical Strategies and
Disorder Treatment Goals Techniques Techniques*
Somatoform 1. Prevent adoption of the sick role and chronic invalidism 1. Consistent treatment, generally by same physician, 1. Only as clearly indicated, or as time-limited
disorders, as a 2. Minimize unnecessary costs and complications by coordinated if multiple empirical trial
group avoiding unwarranted hospitalizations, diagnostic and 2. Supportive office visits, scheduled at regular 2. Avoid drugs with abuse or addictive potential
treatment procedures, and medications intervals
3. Pharmacological control of comorbid syndromes 3. Focus gradually shifted from symptoms to personal
and social problems
Somatization 1, 2, and 3; also 1, 2, and 3; also 1 and 2, also
disorder • Instill, whenever possible, insight regarding temporal • Establish firm therapeutic alliance • Antianxiety and antidepressant drugs for
association between symptoms and personal, • Educate the individuals with somatization disorder comorbid anxiety or depressive disorders; if
interpersonal, and situational problems regarding manifestations of somatization disorder diagnosis unclear, consider empirical trial
(psychoeducative approach)
• Consistent reassurance
Undifferentiated 1, 2, and 3 1, 2, and 3 1 and 2
somatoform
disorder
Conversion 1, 2, and 3; also Acute: 1 and 2; also
disorder • Prompt removal of symptoms • Reassurance, suggestion to remove symptom • Consider narcoanalysis as an interviewing or
• Consider narcoanalysis (interview after drowsiness psychotherapy adjunct
from amobarbital or other sedative–hypnotic,
sometimes followed by methylphenidate or other
stimulant), hypnotherapy, or behavioral therapy
Chronic: 1, 2, and 3
• Exploration of various conflict areas, particularly
interpersonal relationships
• Long-term, intensive, insight-oriented dynamic
psychotherapy recommended by some
Pain disorder 1, 2, and 3; also 1, 2, and 3; also 1 and 2; also
• Acute pain: Relieve symptom • Chronic pain: Consider physical and occupational • Acute: Acetaminophen and NSAIDs alone or as
• Chronic pain: Maintain function and motility rather than therapy, operant conditioning, cognitive–behavioral adjuncts to opioids (if necessary)
focus on total pain relief therapy • Chronic: Tricyclic antidepressants,
acetaminophen, and NSAIDs; if necessary,
milder opioids or pure opioid agonists, but
these only if tied to nonpain objectives (such as
increasing activity)
• Consider acupuncture, transcutaneous electrical
nerve stimulation
Hypochondriasis 1, 2, and 3; also 1, 2, and 3; also 2; also
• Pharmacological control of central syndrome itself • Cognitive–behavioral therapy involving prevention • Attempt to decrease hypochondriacal symptoms
of checking rituals and reassurance seeking with SSRIs at higher than antidepressant doses
or clomipramine
Body 1, 2, and 3, especially avoiding corrective surgery; also 1, 2, and 3; also 2; also
dysmorphic • Pharmacological control of central syndrome itself • Cognitive–behavioral therapy involving prevention • Attempt to decrease hypochondriacal symptoms
disorder of checking rituals and reassurance seeking with SSRIs at higher than antidepressant doses
or clomipramine
Somatoform 1, 2, and 3; also 1, 2, and 3 1 and 2
disorder NOS • Evaluate carefully for alternative general medical or other
mental disorder to which the symptoms can be attributed
*
NSAIDs, Nonsteroidal antiinflammatory drugs; SSRIs, selective serotonin reuptake inhibitors.
Table 34-2 Epidemiology and Natural History of the Somatoform Disorders

Somatoform Disorder Prevalence and Incidence Age at Onset Course and Progress
Somatization disorder US women 0.2–2%; First symptoms by Chronic with fluctuations in

women/men ⫽ 10 : 1 adolescence, full criteria severity
met by mid-20s, not after Most active in early adulthood
30 year by definition Full remissions rare
Undifferentiated “Abridged somatization disorder” Variable Variable conversion disorder
somatoform disorder type estimated as 11–15% of US
adults, 20% in Puerto Rico
Preponderance of women in US
but not Puerto Rico
Conversion disorder Conversion symptoms common, as Late childhood to early Individual conversion
high as 25% adulthood, most before age symptoms generally remit
35 year within days to weeks
Treated conversion symptoms: If onset in middle or late life, Relapse within 1 year in
11–500 per 100,000 neurological or general 20–25%
5–14% of general hospital medical condition more
admissions likely
5–24% of psychiatric outpatients
1–3% of psychiatric outpatient
referrals
4% of neurological outpatient
referrals
1% of neurological admissions
Pain disorder 10–15% of US adults with work Any age Good if less than 6 months in
disability owing to back pain duration
yearly Unemployment, personality
A predominant symptom in more disorder, potential for
than half of general hospital compensation, and
admissions habituation to addictive
Present in as many as 38% of drugs associated with
psychiatric admissions, 18% of poorer prognosis
psychiatric outpatients
Hypochondriasis Perhaps 4–9% in general medical Early adulthood typical 10% recovery, two-thirds
settings, but unclear whether a chronic but fluctuating
full syndrome criteria are met course, 25% do poorly
Equal in both sexes Better prognosis if acute onset,
absence of personality
disorder, absence of
secondary gain
Body dysmorphic Not routinely screened for Adolescence or early Generally chronic, fluctuating
disorder in psychiatric or general adulthood severity
population studies Perhaps in women at In a lifetime, multiple defects
menopause perceived
Perhaps 2% of patients seeking Incapacitating: one-third
corrective cosmetic surgery house-bound
Somatoform disorder Unknown Variable Variable
NOS
be rediagnosed similarly after 6 to 8 years. Women disorder may present in a manner suggestive of multi-
with somatization disorder seen in mental health treat- ple general medical and, although too often forgotten,
ment settings are at increased risk for attempted sui- psychiatric disorders (see Table 34-3). Indeed, it can
cide, although such attempts are usually unsuccessful be said that an essential aspect of somatization disor-
and may reflect manipulative gestures more than intent der is its simulation of other syndromes. Somatization
to die. It is not clear whether such risk is true for indi- disorder is fundamentally a syndrome of apparent syn-
viduals with somatization disorder seen only in general dromes (see Table 34-3). Thus, the first task in the diag-
medical settings. nosis of somatization disorder is the exclusion of other
suggested medical and psychiatric conditions.
To help in this, three features have been identified
that generally characterize somatization disorder but
As defined in DSM-IV-TR, somatization disorder is rarely general medical disorders. Slightly restated,
characterized by multiple recurring physical symptoms these are (1) involvement of multiple organ systems, (2)
and, as will be described, often multiple psychiatric early onset and chronic course without development
complaints. Thus, it is not surprising that somatization of physical signs or structural abnormalities, and (3)
Table 34-3 Somatoform Disorders: A Syndrome of Simulated Syndromes

Examples of Simulated
Examples of Simulated Nonneurological General Examples of Simulated
Symptom Examples Neurological Conditions Medical Conditions Psychiatric Conditions
Symptoms* of somatization
disorder
Pain
Headache Migraine Temporal arteritis Pain disorder
Abdomen “Abdominal epilepsy” Peptic ulcer disease Pain disorder
Back Lumbosacral radiculopathy Ruptured disk Pain disorder
Joints or extremities Fibromyalgia Pain disorder
Chest Angina Panic disorder
Menstruation, intercourse Endometriosis Dyspareunia, vaginismus
Urination Neurogenic bladder Urinary tract infection
Gastrointestinal (nonpain)
Difficulty swallowing Myasthenia gravis Esophageal motility disorder Eating disorder
Nausea Raised intracranial pressure Ménière’s disease Eating disorder
Bloating Galactase deficiency Eating disorder
Vomiting (nonpregnancy) Raised intracranial pressure Eating disorder
Diarrhea Irritable bowel syndrome Eating disorder
Intolerance to several foods Food allergy Eating disorder
Sexual (nonpain)
Loss of interest Major depressive episode
Erectile–ejaculatory Diabetic neuropathy Antihypertensive drug effect
dysfunction
Menorrhagia Leiomyofibroma
Vomiting throughout Preeclampsia, eclampsia
pregnancy
Pseudoneurological
Conversion
Sensory Stroke (hemianesthesia) Schizophrenia/(hallucinations)
Motor Huntington’s disease Myopathy Catatonia
Seizures Epilepsy Electrolyte imbalance Catatonia
Mixed Multiple sclerosis Electrolyte imbalance Catatonia
Dissociative
Amnesia Amnestic disorder Anticholinergic drug effects Dissociative identity disorder
Loss of consciousness Coma Metabolic encephalopathy Catatonia
(nonfainting)
Symptoms* often associated
with somatization disorder
Anxiety, panic Pheochromocytoma Generalized anxiety and panic
disorders
Dysphoria, affective lability Frontal lobe syndrome Endocrinopathy Major mood disorders
Cluster B personality features Frontal lobe syndrome Acute intermittent porphyria Brief psychotic disorder
*
All of these symptoms may be reported by individuals with somatization disorder, without the clinical consistency and pathological findings to
support the diagnosis of neurological, general medical, or psychiatric conditions separate from somatization disorder.
Developed in conjunction with Sheldon H. Preskorn.
absence of laboratory abnormalities characteristic of infections such as brucellosis and trypanosomiasis,

the suggested physical disorders (Table 34-4). Another myopathies, and vasculitides. In general, such condi-
way of characterizing the distinction is the “reverse tions begin with disseminated, nonspecific subjective
funnel effect.” With most general medical conditions, symptoms and transient or equivocal physical signs or
the process of investigation “funnels down” to fewer laboratory abnormalities.
and fewer specific diagnostic possibilities; in somatiza- Somatization disorder is characterized by excessive
tion disorder, the more extensive the investigation, the psychiatric as well as physical complaints. Thus, other
greater the number of suggested disorders. mental disorders, including anxiety and mood disor-
Several general medical conditions may also fit ders and schizophrenia, may be suggested. Although
this pattern and may be confused with somatiza- no specific exclusion criteria regarding other mental
tion disorder. These include multiple sclerosis, other disorders are given, one must be careful in accepting
neuropathies, systemic lupus erythematosus, acute in- “comorbidity” and critically evaluate whether sug-
termittent porphyria, other hepatic and hematopoietic gested syndromes are truly additional syndromes or
porphyrias, hypercalcemia, certain chronic systemic simply manifestations of somatization disorder.
Discrimination of Somatization Disorder

symptoms. Interestingly, somatization disorder indi-
Table 34-4 viduals complaining of depression have been found to
from General Medical Conditions
Features Suggesting Features Suggesting a
proffer greater depressive symptoms than individuals
Somatization Disorder General Medical Condition with major depression. As in anxiety disorders, ma-
jor depressive episodes may occur in individuals with
Involvement of multiple Involvement of single or few
organ systems organ systems somatization disorder and must be differentiated from
Early onset and chronic If early onset and chronic the tendency to have multiple complaints, which is
course without course, development characteristic of somatization disorder. As with anxiety
development of physical of physical signs and
signs or structural structural abnormalities disorders, in considering comorbidity with a depressive
abnormalities disorder, the individual’s reports should be corrobo-
Absence of laboratory Laboratory abnormalities rated by collateral information or by direct observation.
abnormalities evident
characteristic of the Thus, the veracity of the self-report of overwhelming
suggested general depression and suicidal ideation should be doubted if
medical condition the individual appears cheerful and charming, at least
Source: Martin RL and Yutzy SH (1994) Somatoform disorders. In at times, when interviewed, or if the individual is re-
The American Psychiatric Press Textbook of Psychiatry, 2nd ed.,
Hales RE, Yudofsky SC, and Talbott JA (eds). American Psychiatric ported to be actively involved in social activities on an
Press, Washington, DC, p. 600. inpatient psychiatric service.
Schizophrenia may present with generally single but
occasionally multiple unexplained somatic complaints.
The overlap between somatization disorder and anxi- The assessment interview usually uncovers psychotic
ety disorders may be a particular problem. Individuals symptoms such as delusions, hallucinations, or disor-
with somatization disorder frequently complain of many ganized thought. In some cases, the underlying psycho-
of the same somatic symptoms as individuals with anxi- sis cannot be identified initially, but in time, schizophre-
ety disorders, such as increased muscle tension, features nia will become manifest. Hallucinations are included
of autonomic hyperactivity, and even discrete panic as examples of conversion symptoms in DSM-IV-TR
attacks. Likewise, individuals with anxiety disorder which may lead to diagnostic problems. As discussed
may report irrational disease concerns and such somatic in the conversion disorder section, careful analysis of
complaints as those involving gastrointestinal function this symptom is warranted so that a misdiagnosis is not
that are commonly seen in somatization disorder. How- made, relegating an individual to long-term neuroleptic
ever, individuals with anxiety disorders neither typically treatment on the basis of conversion hallucinations.
report sexual and menstrual complaints or conversion or Individuals with histrionic, borderline, and antiso-
dissociative symptoms as in somatization disorder, nor cial personality disorders frequently have an excess of
do they have the associated histrionic presentation and somatic complaints, at times presenting with somati-
personal, marital, and social maladjustment common in zation disorder. Antisocial personality disorder and
individuals with somatization disorder. somatization disorder appear to cluster in individuals
Mood disorders (in particular, depression) frequently and within families and may share common causes. Dis-
present with multiple somatic complaints, especially in sociative phenomena, in particular dissociative identity
certain cultures such as in India, where somatic but disorder, are commonly associated with somatization
not mental complaints are acceptable. A longitudinal disorder. Because dissociative symptoms are included
history identifying age at onset and course of illness in the diagnostic criteria for somatization, a separate
may facilitate discrimination of a mood disorder from diagnosis of a dissociative disorder is not made if such
somatization disorder. In mood disorders, the age at symptoms occur only in the course of somatization
onset of the somatic symptoms is generally later than disorder.
in somatization disorder; their first appearance gener- Unlike that in hypochondriasis and body dysmorphic
ally correlates with the onset of mood symptoms, and disorder, in which preoccupations and fears concerning
a lengthy pattern of multiple recurring somatic com- the interpretation of symptoms predominate, the focus
plaints is not seen. Also, resolution of the underlying in somatization disorder is on the physical complaints
mood disorder will generally result in disappearance themselves. Unlike that in pain disorder and conver-
of the somatic complaints. sion disorder, multiple complaints of different types are
From the other perspective, individuals with somati- reported; by definition, in DSM-IV-TR, the history is
zation disorder often present with depressive complaints. of pain in at least four sites or functions (e.g., pain with
In somatization disorder, a thorough investigation will intercourse, pain in swallowing), at least two nonpain
reveal a multitude of somatic as well as “depressive” gastrointestinal symptoms, at least one nonpain sexual
or reproductive symptom, and at least one conversion general medical condition and to obtain a fuller picture
or dissociative (i.e., pseudoneurological) symptom. of psychosocial difficulties that may relate temporally
to somatic symptoms.
Only after the diagnosis has been clearly established
TREATMENT
and the therapeutic alliance is firmly in place can the
First, a “management” rather than a “curative” strategy clinician confidently limit diagnostic evaluations and
is recommended for somatization disorder. With the therapies to those performed on the basis of objective
current absence of an identified definitive treatment, a findings as opposed to merely subjective complaints.
modest, practical, empirical approach should be taken. Of course, the clinician should remain aware that indi-
This should include efforts to minimize distress and viduals with somatization disorder are still at risk for
functional impairments associated with the multiple development of general medical illnesses so that a vigi-
somatic complaints; to avoid unwarranted diagnostic lant perspective should always be maintained.
and therapeutic procedures and medications; and to The second component is education. This involves
prevent potential complications including chronic inva- advising individuals that they suffer from a “medically
lidism and drug dependence. sanctioned illness,” that is, a condition recognized by
The individual should be encouraged to see a single the medical community and one about which a good
physician with an understanding of and, preferably, expe- deal is known. Ultimately, it may be possible to intro-
rience in treating somatization disorder. This helps limit duce the concept of somatization disorder, which can
the number of unnecessary evaluations and treatments. be described in a positive light (i.e., the individual does
Routine, brief, supportive office visits scheduled at regu- not have a progressive, deteriorating, or potentially
lar intervals to provide reassurance and prevent individu- fatal medical disorder, and the individual is not “going
als from “needing to develop” symptoms to obtain care crazy” but has a condition by which many symptoms
and attention have been advocated. This “medical” man- will be experienced). A realistic discussion of progno-
agement can well be provided by a primary care physi- sis and treatment options can then follow.
cian, perhaps in consultation with a mental health profes- The third component is reassurance. Individuals with
sional. Studies have demonstrated that such a regimen led somatization disorder often have control and insecurity
to markedly decreased health care costs, with no appar- issues, which often come to the forefront when they
ent decrements in health or satisfaction of individuals. perceive that a particular physical complaint is not be-
Three interrelated components have been proposed ing adequately addressed. Explicit reassurance should
for the treatment of somatization disorder: (1) estab- be given that the appropriate inquiries and investiga-
lishment of a strong relationship or bond between the tions are being performed and that the possibility of
clinician and the individual; (2) education of the indian underlying physical disorder as the explanation for
vidual regarding the nature of somatization disorder; symptoms is being reasonably considered.
and (3) provision of support and reassurance. In time, it may be appropriate to gradually shift em-
The first component, establishing a strong therapeutic phasis away from somatic symptoms to consideration of
bond, is especially important in the treatment of soma- personal and interpersonal issues. In some individuals,
tization disorder. Without it, it will be difficult for the it may be appropriate to posit a causal theory between
individual to overcome skepticism deriving from past somatic symptoms and “stress,” that is, that there may
experience with many physicians and other therapists be a temporal association between symptoms and per-
who “never seemed to help.” In addition, trust must be sonal, interpersonal, and even occupational problems.
strong enough to withstand the stress of withholding In individuals for whom such “insight” is difficult, be-
unwarranted diagnostic and therapeutic procedures that havioral techniques may be useful.
the individual may feel are indicated. The cornerstone Even following such therapeutic guidelines, indi-
of establishing a therapeutic relationship is laid when viduals with somatization disorder are often difficult
the clinician indicates an understanding of the individ- to treat. Attention-seeking behavior, demands, and ma-
ual’s pain and suffering, legitimizing the symptoms as nipulation are common, necessitating firm limits and
real. This demonstrates a willingness to provide direct careful attention to boundary issues. This, again, is a
compassionate assistance. A full investigation of the management rather than a curative approach. Thus,
medical and psychosocial histories, including extensive such behaviors should generally be dealt with directly
record review, will illustrate to individuals the willing- rather than interpreted to the individual.
ness of the clinician to gain the fullest understanding No effective somatic treatments for somatization
of them and their plight. This also provides another op- disorder itself have been identified. Individuals with
portunity to evaluate for the presence of an underlying somatization disorder may complain of anxiety and
depression, suggesting readily treatable comorbid men- other hand, it is a less residual category than somato-
tal disorders. As previously discussed, it is often dif- form disorder NOS, in that the disturbance must last
ficult to distinguish actual comorbid conditions from at least 6 months (see Figure 34-1). Virtually any un-
aspects of somatoform disorder itself. Pharmacological intentional, medically unexplained physical symptoms
interventions are likely to be helpful in the former but causing clinically significant distress or impairment
not in the latter. At times, such discrimination will be can be considered. In effect, this category serves to
impossible, and an empirical trial of such treatments capture syndromes that resemble somatization disorder
may be indicated. Individuals with somatization dis- but do not meet full criteria.
order are often inconsistent and erratic in their use The term undifferentiated somatoform disorder was
of medications. They will often report unusual side introduced in 1987 with DSM-III-R, replacing the
effects that may not be explained pharmacologically. atypical somatoform disorder of DSM-III. However,
This makes evaluation of treatment response difficult. the category has not been well used, not only by mental
In addition, drug dependence and suicide gestures and health professionals but also by primary care physi-
attempts are not uncommon. cians for whom identification of such a syndrome could
be useful. Terms that have been used in a similar man-
ner include subsyndromal, forme fruste, or abridged
Undifferentiated Somatoform Disorder somatization disorder.
In addition to the range of symptoms specified in
DIAGNOSIS the other somatoform disorders, individuals with un-
As defined in DSM-IV-TR, this category includes dis- differentiated somatoform disorder, complaining pri-
turbances of at least 6 months’ duration, with one or marily of fatigue (chronic fatigue syndrome), bowel
more unintentional, clinically significant, medically problems (irritable bowel syndrome), or multiple mus-
unexplained physical complaints. In a sense, it is a re- cle aches/weakness (fibromyalgia), can be considered
sidual category, subsuming syndromes with somatic for undifferentiated somatoform disorder. Substantial
complaints that do not meet criteria for any of the “dif- controversy exists regarding the etiology of such syn-
ferentiated” somatoform disorders, yet are not better dromes. Even if an explanation on the basis of a known
accounted for by any other mental disorder. On the pathophysiological mechanism cannot be established,
many argue that the syndromes should be considered
general medical conditions. However, for the time be-
ing, these syndromes could be considered in a highly
tentative manner under the undifferentiated somato-
300.81 UNDIFFERENTIATED SOMATOFORM DISORDER form disorder rubric. Careful reconsideration of the
undifferentiated somatoform label should be under-
A. One or more physical complaints (e.g., fatigue, loss of taken at regular intervals if the symptoms persist. The
appetite, gastrointestinal or urinary complaints).
B. Either (1) or (2): clinician should remain ever vigilant to the emergence
(1) After appropriate investigation, the symptoms can- of another general medical condition or mental disor-
not be fully explained by a known general medical der. When individuals are diagnosed with chronic fa-
condition or the direct effects of a substance (e.g., tigue syndrome, careful evaluation procedures should
a drug of abuse, a medication).
(2) When there is a related general medical condition, be followed.
the physical complaints or resulting social or occu- Some have argued that undifferentiated somatoform
pational impairment is in excess of what would be disorder is the most common somatoform disorder. A
expected from the history, physical examination, or
laboratory findings. 1991 study using an abridged somatization disorder
C. The symptoms cause clinically significant distress or construct requiring six somatic symptoms for women
impairment in social, occupational, or other important and four for men, reported that 11% of non-Hispanic
areas of functioning. US whites and Hispanics, 15% of US blacks, and 20%
D. Duration of the disturbance is at least 6 months.
E. The disturbance is not better accounted for by another of Puerto Ricans in Puerto Rico fulfilled criteria. A
mental disorder (e.g., another somatoform disorder, preponderance of women was evident in all groups ex-
sexual dysfunction, mood disorder, anxiety disorder, cept the Puerto Rican sample (see Table 34-2).
sleep disorder, or psychotic disorder).
F. The symptom is not intentionally produced or feigned
(as in factitious disorder or malingering).
Course
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 As shown in Table 34-2, it appears that the course and
prognosis of undifferentiated somatoform disorder
are highly variable. This is not surprising, because pseudoneurological symptoms, and the specific cri-
the definition of this disorder allows a great deal of teria for a sexual dysfunction, pain disorder, and/or
heterogeneity. conversion disorder are met, the specific disorder or
disorders should be diagnosed. If other types of symp-
toms or symptoms of more than one of these disorders
have been present for at least 6 months, yet criteria
In comparison to the situation when the full criteria for somatization disorder are not met, undifferentiated
for the well-validated somatization disorder are met, somatoform disorder should be diagnosed. By defini-
exclusion of an as-yet-undiscovered general medical or tion, undifferentiated somatoform disorder requires
substance-induced explanation for physical symptoms a duration of 6 months. If this criterion is not met,
is far less certain when the less stringent criteria for a diagnosis of somatoform disorder NOS should be
undifferentiated somatoform disorder are met. Thus, considered.
the diagnosis of undifferentiated somatoform disorder Individuals with an apparent undifferentiated
should remain tentative, and new symptoms should be somatoform disorder should be carefully evaluated
carefully investigated. for somatization disorder. Typically, individuals with
Because undifferentiated somatoform disorder rep- somatization disorder are inconsistent historians, at one
resents a somewhat residual category, the major diag- evaluation reporting a large number of symptoms ful-
nostic process, once occult general medical conditions filling criteria for the full syndrome and at another time
and substance-induced explanations have been con- endorsing fewer symptoms. In addition, with follow-up,
sidered, is one of exclusion. As shown in Figure 34-1, additional symptoms may become evident, and criteria
whether the somatic symptoms are intentionally pro- for somatization disorder will be satisfied. Individuals
duced as in malingering and factitious disorder must with multiple somatic complaints not diagnosed with
be addressed. Here, motivation for external rewards somatization disorder because of a reported onset later
(for malingering) and a pervasive intent to assume than 30 years of age may be inaccurately reporting a
the sick role (for factitious disorder) must be assessed. later age at onset. If the late age at onset is accurate, the
The next consideration is whether the somatic symp- individual should be carefully scrutinized for an occult
toms are the manifestation of another mental disorder. general medical condition.
Anxiety and mood disorders commonly present with
somatic symptoms; high rates of anxiety and major
TREATMENT
depressive disorders are reported in individuals with
somatic complaints attending family medicine clinics. In view of the broad inclusion and minimal exclusion
Of course, undifferentiated somatoform disorder could criteria for undifferentiated somatoform disorder, it is
be diagnosed in addition to one of these disorders, so difficult to make treatment recommendations beyond
long as the symptoms are not accounted for by the the generic strategies discussed in the beginning of
other mental disorder. Crucial in this determination is this chapter. A substantial proportion of individuals
whether the symptoms are present during periods in with undifferentiated somatoform disorders improve or
which the anxiety or mood disorders are not actively recover with no formal therapy. However, appropriate
present. psychotherapy and pharmacological intervention may
Next, other somatoform disorders must be con- accelerate the process.
sidered. In general, undifferentiated somatoform Recommendations have been proposed for indi-
disorders are characterized by unexplained somatic viduals with symptoms of headache, fibromyalgia, and
complaints, the most common being female reproduc- chronic fatigue syndrome, conditions that some would
tive symptoms, excessive gas, abdominal pain, chest include under undifferentiated somatoform disorder.
pain, joint pain, palpitations, and fainting, rather than Generally recommended are brief psychotherapy of a
preoccupations or fears as in hypochondriasis or body supportive and educative nature. As with somatization
dysmorphic disorder. However, an individual with disorder, the physician–patient relationship is of great
some manifestations of these two disorders but not importance. Judicious use of pharmacotherapy may be
meeting full criteria could conceivably receive a di- of benefit also, particularly if the somatoform syndrome
agnosis of undifferentiated somatoform disorder. An is intertwined with an anxiety or depressive syndrome.
example is an individual with recurrent yet shifting Here, usual antianxiety and antidepressant medications
hypochondriacal concerns that do respond to medi- are recommended. Individuals with unexplained pains
cal reassurance. If symptoms are restricted to those may benefit from pain management strategies as out-
affecting the domains of sexual dysfunction, pain, or lined in the pain disorder section.
Conversion Disorder impaired coordination or balance, paralysis or local-

ized weakness, difficulty swallowing or lump in throat,
DIAGNOSIS aphonia, and urinary retention); with sensory symptom
or deficit (e.g., loss of touch or pain sensation, double
As defi ned in DSM-IV-TR, conversion disorders
vision, blindness, deafness, and hallucinations); with
are characterized by symptoms or deficits affecting
seizures or convulsions; and with mixed presentation
voluntary motor or sensory function that are sugges-
(i.e., has symptoms of more than one of the other sub-
tive of, yet are not fully explained by, a neurological
types). The list of examples is also contained among
or other general medical condition or the direct ef-
the pseudoneurological symptoms listed in the diag-
fects of a substance. The diagnosis is not made if the
nostic criteria for somatization disorder. Although
presentation is explained as a culturally sanctioned
determination is highly subjective and of questionable
behavior or experience, such as bizarre behaviors
reliability and validity, association with psychological
resembling a seizure during a religious ceremony.
factors is required.
Symptoms are not intentionally produced or feigned,
The relationship of conversion disorder to the disso-
that is, the person does not consciously contrive a
ciative disorders warrants comment. Long recognized
symptom for external rewards, as in malingering,
as related, they were subsumed as subtypes of hysteri-
or for the intrapsychic rewards of assuming the sick
cal neurosis in DSM-II: conversion involving voluntary
role, as in factitious disorder.
motor and sensory functioning, and dissociation affect-
Four subtypes with specific examples of symp-
ing memory and identity. They are unified in one cat-
toms are defined: with motor symptom or deficit (e.g.,
egory in ICD-10: dissociative (conversion) disorders.
Although DSM-IV-TR classifies conversion disorder
DSM-IV-TR Diagnostic Criteria with the somatoform disorders; the DSM-IV-TR text
acknowledges the symptomatic, epidemiological, and
300.11 CONVERSION DISORDER probable pathogenetic similarities between conversion
A. One or more symptoms or deficits affecting voluntary and dissociative symptoms. Such symptoms have been
motor or sensory function that suggest a neurological attributed to similar psychological mechanisms, and
or other general medical condition. they often occur in the same individual, sometimes
B. Psychological factors are judged to be associated with
the symptom or deficit because the initiation or ex- during the same episode of illness. DSM-IV-TR does
acerbation of the symptom or deficit is preceded by suggest that individuals with conversion disorder be
conflicts or other stressors.
C. The symptom or deficit is not intentionally produced
carefully scrutinized for dissociative symptoms.
or feigned (as in factitious disorder or malingering). Hallucinations are included among the sensory nerv-
D. The symptom or deficit cannot, after appropriate in- ous symptoms in DSM-IV-TR. Inclusion of hallucina-
vestigation, be fully explained by a general medical
condition, or by the direct effects of a substance, or as tions as a conversion symptom is supported by the
a culturally sanctioned behavior or experience. DSM-IV somatization disorder field trial, in which one
E. The symptom or deficit causes clinically significant third of a large sample of nonpsychotic women with
distress or impairment in social, occupational, or other
important areas of functioning or warrants medical evidence of unexplained somatic complaints reported
evaluation. a history of hallucinations. Among the 40% who had
F. The symptom or deficit is not limited to pain or sexual symptoms that met criteria for somatization disorder,
dysfunction, does not occur exclusively during the
course of somatization disorder, and is not better ac- more than half reported hallucinations. Women with
counted for by another mental disorder. other conversion symptoms were more likely to report
hallucinations than were those with no other conver-
Specify type of symptom or deficit:
sion symptoms.
With motor symptom or deficit (e.g., impaired coordi-
nation or balance, paralysis or localized weakness, dif- In general, conversion hallucinations (referred to
ficulty swallowing or lump in throat, aphonia, and urinary by some as pseudohallucinations) differ in several
retention) ways from those in psychotic conditions. Conversion
With sensory symptom or deficit (e.g., loss of touch or
pain sensation, double vision, blindness, deafness, and hallucinations typically occur in the absence of other
hallucinations) psychotic symptoms, insight that the hallucinations are
With seizures or convulsions (includes seizures or con- not real may be retained, and they often involve more
vulsions with voluntary sensory components)
With mixed presentation (if symptoms of more than one than one sensory modality, whereas hallucinations in
category are evident). psychoses generally involve a single sensory modal-
Reprinted with permission from the Diagnostic and Statistical ity, usually auditory. Conversion hallucinations also
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 often have a naive, fantastic, or childish content, as if
they are part of a fairy tale, and are described eagerly,
sometimes even provocatively, as an interesting story longitudinally. Factors associated with good prognosis
(e.g., “I was driving downtown and a flying saucer flew include acute onset, clearly identifiable precipitants, a
over my car and I saw you [the psychiatrist] in a win- short interval between onset and institution of treat-
dow and I heard your voice calling to me”). They often ment, and good intelligence. Conversion blindness,
bear some understandable psychological purpose, al- aphonia, and paralysis are associated with relatively
though the individual may not be aware of intent. In the good prognosis, whereas individuals with seizures and
example given, the “sighting” was reported at the time tremor do more poorly. Some individuals diagnosed in-
that no further sessions were scheduled. itially with conversion disorder will have a presentation
Conversion symptoms themselves may be common; that meets the criteria for somatization disorder when
it has been reported that 25% of normal postpartum they are observed longitudinally.
and medically ill women had a history of conversion Individual conversion symptoms are generally self-
symptoms at some time during their life, yet in some limited and do not lead to physical changes or dis-
instances, there may have been no resulting clinically abilities. Rarely, physical sequelae such as atrophy
significant distress or impairment. Lifetime prevalence may occur. Marital and occupational problems are not
rates of treated conversion symptoms in general popu- as frequent in individuals with conversion disorder as
lations are much more modest, ranging from 11 to 500 they are in those with somatization disorder.
per 100,000 (see Table 34-2). About 5–24% of psychi-
atric outpatients, 5–14% of general hospital patients,
and 1–3% of outpatient psychiatric referrals reported a
history of conversion symptoms, although their current As shown in Figure 34-1, the first consideration is
treatment was not necessarily for conversion symptoms. whether the conversion symptoms are explained on the
A rate of nearly 4% of outpatient neurological referrals basis of a general medical condition. Because conver-
and 1% of neurological admissions have involved con- sion symptoms by definition affect voluntary motor or
version disorder. In virtually all studies, an excess (to sensory function (thus pseudoneurological), neurologi-
the extent of 2 : 1 to 10 : 1) of women reported conver- cal conditions are usually suggested, but other general
sion symptoms relative to men. In part, this may relate medical conditions may be implicated as well. Neu-
to the simple fact that women seek medical evaluation rologists are generally first consulted by primary care
more often than men do, but it is unlikely that this fully physicians for conversion symptoms; mental health
accounts for the sex difference. There is a predilec- clinicians become involved only after neurological or
tion for lower socioeconomic status; less educated, less general medical conditions have been reasonably ex-
psychologically sophisticated, and rural populations cluded. Nonetheless, the mental health clinician should
are overrepresented. Consistent with this, higher rates have a good appreciation of the process of making such
(nearly 10%) of outpatient psychiatric referrals are for exclusions. More than one eighth of actual neurological
conversion symptoms in “developing” countries. As cases are diagnosed as functional before the elucidation
countries develop, there may be a declining incidence of a neurological illness. Even after referral, vigilance
in time, which may relate to increasing levels of educa- for an emerging general medical condition should con-
tion, and medical and psychological sophistication. tinue. A significant percentage–21% to 50%—of indi-
viduals diagnosed with conversion symptoms are found
to have neurological illness on follow-up.
Course
Apparent conversion symptoms mandate a thorough
Age at onset is typically from late childhood to early evaluation for possible underlying physical explana-
adulthood. Onset is rare before the age of 10 and after tion. This evaluation must include a thorough medical
35, but cases with an onset as late as the ninth dec- history, physical (especially neurological) examina-
ade have been reported. The likelihood of a neurologi- tion, and radiographical, blood, urine, and other tests
cal or other medical condition is increased when the as clinically indicated. Reliance should not be placed
age at onset is in middle or late life. Development is on determination of whether psychological factors
generally acute, but symptoms may develop gradually explain the symptom. Such determinations are un-
as well. The course of individual conversion symptoms reliable except, perhaps, in cases in which there is a
is generally short; half to nearly all symptoms remit clear and immediate temporal relationship between a
by the time of hospital discharge. However, symptoms psychosocial stressor and the symptom, or in cases in
relapse within one year in one-fifth to one-fourth of in- which similar situations led to conversion symptoms
dividuals. Typically, one symptom is present in a single in the past. A history of previous conversion or other
episode, but multiple symptoms are generally involved unexplained symptoms, particularly if somatization
disorder is diagnosable, lessens the probability that an excluded. If the conversion symptom cannot be fully
occult medical condition will be identified. Although accounted for by the other mental disorders, conver-
conversion symptoms may occur at any age, symptoms sion disorder should be diagnosed in addition to the
are most often first manifested in late adolescence or other disorder if it meets criteria (e.g., an episode of
early adulthood. Conversion symptoms first occurring unexplained blindness in an individual with a major
in middle age or later should increase suspicion of an depressive episode). In hypochondriasis, neurological
occult physical illness. illness may be feared (“I have strange feelings in my
Symptoms of many neurological illnesses may ap- head; it must be a brain tumor”), but the focus here is
pear inconsistent with known neurophysiological or on preoccupation with fear of having the illness rather
neuropathological processes, suggesting conversion than on the symptom itself as in conversion disorder.
and posing diagnostic problems. These illnesses in- By definition, if symptoms are limited to sexual dys-
clude multiple sclerosis, in which blindness due to function or pain, conversion disorder is not diagnosed.
optic neuritis may initially present with normal fundi, Criteria for somatization disorder require multiple
myasthenia gravis, periodic paralysis, myoglobinuric symptoms in multiple organ systems and functions,
myopathy, polymyositis, and other acquired myopa- including symptoms affecting motor or sensory func-
thies, in which marked weakness in the presence of tion (conversion symptoms) or memory or identity (dis-
normal deep tendon reflexes may occur, and Guillain– sociative symptoms). Thus, it would be superfluous to
Barré syndrome, in which early extremity weakness make an additional diagnosis of conversion disorder in
may be inconsistent. the context of a somatization disorder.
Complicating diagnosis is the fact that physical ill- A last consideration is whether the symptom is a
ness and conversion or other apparent psychiatric over- culturally sanctioned behavior or experience. Conver-
lay are not mutually exclusive. Individuals with physical sion disorder should not be diagnosed if symptoms are
illnesses that are incapacitating and frightening may clearly sanctioned or even expected, are appropriate to
appear to be exaggerating symptoms. Also, individuals the sociocultural context, and are not associated with
with actual neurological illness will also have “pseudo” distress or impairment. Seizure-like episodes, such as
symptoms. For example, individuals with actual seizures those that occur in conjunction with certain religious
may have pseudoseizures as well. Considering these ob- ceremonies, and culturally expected responses, such as
servations, mental health clinicians should avoid a rash women “swooning” in response to excitement in Victo-
and hasty diagnosis of conversion disorder when faced rian times, qualify as examples of these symptoms.
with symptoms that are difficult to interpret.
As with the other somatoform disorders, symptoms
TREATMENT
of conversion disorder are not intentionally produced,
in distinction to malingering or factitious disorder. Reports of the treatment of conversion disorder date
To a large part, this determination is based on assess- from those of Charcot, which generally involved symp-
ment of the motivation for external rewards (as in ma- tom removal by suggestion or hypnosis. Breuer and
lingering) or for the assumption of the sick role (as in Freud, using such psychoanalytic techniques as free
factitious disorder). The setting is often an important association and abreaction of repressed affects, had
consideration. For example, conversion-like symptoms more ambitious objectives in their treatment of Anna
are frequent in military or forensic settings, in which O., including the resolution of unconscious conflicts.
obvious potential rewards make malingering a serious To date, whereas some recommend long-term, inten-
consideration. sive, insight-oriented psychodynamic psychotherapy in
A diagnosis of conversion disorder should not be pursuit of such goals, most mental health clinicians ad-
made if a conversion symptom is fully accounted for by vocate a more pragmatic approach, especially for acute
a mood disorder or by schizophrenia (e.g., disordered cases.
motility as part of a catatonic syndrome of a psychotic Therapeutic approaches vary according to whether
mood disorder or schizophrenia). If the symptom is the conversion symptom is acute or chronic. Whichever
a hallucination, it must be remembered that the de- the case, direct confrontation is not recommended.
scriptors differentiating conversion from psychotic Such a communication may cause an individual to feel
hallucinations should be seen only as rules of thumb. even more isolated. An undiscovered physical illness
Differentiation should be based on a comprehensive may also underlie the presentation.
assessment of the illness. In the case of hallucinations, In acute cases, the most frequent initial aim is re-
posttraumatic stress disorder and dissociative identity moval of the symptom. The pressure behind accom-
disorder (multiple personality disorder) must also be plishing this depends on the distress and disability
associated with the symptom. If the individual is not influence such as a “toxin” or even a “spell,” experi-
in great distress and the need to regain function is not ence similar symptoms that do not appear to have any
immediate, a conservative approach of reassurance, organic basis. Often, the epidemic can be contained if
relaxation, and suggestion is recommended. With this affected individuals are segregated. Simple announce-
technique, the individual is reassured that on the basis ments that no such factor has been identified and that
of evaluation the symptom will disappear completely symptoms experienced by the group have been linked
and, in fact, is already beginning to do so. The indi- to mass hysteria have been effective.
vidual can then be encouraged to ventilate about recent Thus far, this discussion has centered on acute treat-
events and feelings, without any causal relationships ment primarily for symptom removal. Longer-term
being suggested. This is in contrast to attempts at ab- approaches include strategies previously discussed for
reaction, by which repressed material, particularly re- somatization disorder—a pragmatic, conservative ap-
garding a painful experience or a conflict, is brought proach involving support and exploration of various
back to consciousness. conflict areas, particularly of interpersonal relation-
If symptoms do not resolve with such conservative ships. A certain degree of insight may be attained, at
approaches, a number of other techniques for symp- least in terms of appreciating relationships between
tom resolution may be instituted. It does appear that various conflicts and stressors and the development
prompt resolution of conversion symptoms is impor- of symptoms. Others advocate long-term, intensive,
tant because the duration of conversion symptoms is insight-oriented, dynamic psychotherapy.
associated with a greater risk of recurrence and chronic
disability. The other techniques include narcoanalysis
Pain Disorder
(e.g., amobarbital interview), hypnosis, and behavio-
ral therapy. In narcoanalysis, amobarbital or another
DIAGNOSIS
sedative–hypnotic medication such as lorazepam is
given intravenously to the point of drowsiness. Some- As defined in DSM-IV-TR, the essential feature of pain
times this is followed by administration of a stimulant disorder is pain with which psychological factors “have
medication, such as methamphetamine. The individual an important role in the onset, severity, exacerbation,
is then encouraged to discuss stressors and conflicts. or maintenance” (see Table 34-2 and DSM-IV-TR diag-
This technique may be effective acutely, leading to at nostic criteria, page 359). Pain disorder is subtyped as
least temporary symptom relief as well as expansion of pain disorder associated with psychological factors and
the information known about the individual. This tech- pain disorder associated with both psychological factors
nique has not been shown to be especially effective with and a general medical condition. The third possibility,
more chronic conversion symptoms. In hypnotherapy, pain disorder associated with a general medical condi-
symptoms may be removed with the suggestion that the tion, is not considered to be a mental disorder, because
symptoms will gradually improve posthypnotically. the requirement is not met that psychological factors
Information regarding stressors and conflicts may be play an important role. It should be noted that the focus
explored as well. Formal behavioral therapy, includ- of the Pain Disorder diagnosis in DSM-IV-TR is placed
ing relaxation training and even aversive therapy, has on the presence of psychological factors rather than the
been proposed and reported by some to be effective. exasperating determination of whether the pain is at-
In addition, simply manipulating the environment to tributable to organic disease.
interrupt reinforcement of the conversion symptom is A diagnosis of pain disorder requires that the pain
recommended. be of sufficient severity to warrant clinical attention,
Anecdotally, somatic treatments including pheno- that is, it causes clinically significant distress or im-
thiazines, lithium, and electroconvulsive therapy have pairment. A number of instruments have been devel-
been reported effective. However, in many cases, this oped to assess the degree of distress associated with
may be attributable to simple suggestion. In other cases, the pain, including the McGill Pain Questionnaire,
resolution of another psychiatric disorder, such as a and the West Haven–Yale Multidimensional Pain
psychotic disorder or a mood disorder, may have led to Inventory.
the symptom’s removal. It is also likely that in various DSM-IV-TR includes a number of exclusionary con-
rituals, such as exorcism and other religious ceremo- ventions. By definition, if pain is restricted to pain with
nies, immediate “cures” are based on suggestion. Sug- sexual intercourse, the sexual disorder, dyspareunia,
gestion seems to play a major role in the resolution of not pain disorder, is diagnosed. If pain occurs in the
“mass hysteria,” in which a group of individuals who context of a mood, anxiety, or psychotic disorder, pain
believe that they have been exposed to some noxious disorder is diagnosed only if it is an independent focus
because pain symptoms are part of the criteria for so-

DSM-IV-TR Diagnostic Criteria matization disorder and are thereby subsumed under
307.XX PAIN DISORDER
the more comprehensive diagnosis. Because somati-
zation disorder is virtually a lifelong condition, this
A. Pain in one or more anatomical sites is the predomi- exclusion generally applies in someone with somatiza-
nant focus of the clinical presentation and is of suf-
ficient severity to warrant clinical attention. tion disorder by history. Important here is that in ad-
B. The pain causes clinically significant distress or impair- dition to pain, somatization disorder involves multiple
ment in social, occupational, or other important areas symptoms of the gastrointestinal system, the reproduc-
of functioning.
C. Psychological factors are judged to have an important tive system, and the central and peripheral nervous
role in the onset, severity, exacerbation, or mainte- systems, whereas in pain disorder, the focus is on pain
nance of the pain. symptoms only.
D. The symptom or deficit is not intentionally produced
or feigned (as in factitious disorder or malingering). Specification of acute versus chronic pain disor-
E. The pain is not better accounted for by a mood, anxi- der on the basis of whether the duration is less than
ety, or psychotic disorder and does not meet criteria or greater than 6 months is an important distinction.
for dyspareunia.
Whereas acute pain, in most cases, will be linked with
Code as follows: physical disorders, when pain remains unexplained af-
307.80 Pain Disorder Associated with Psychological Fac- ter 6 months, psychological factors are often involved.
tors: Psychological factors are judged to have the major However, the clinician must remember that a signifi-
role in the onset, severity, exacerbation, or maintenance of
the pain. (If a general medical condition is present, it does cant minority (in one study 19%) of individuals with
not have a major role in the onset, severity, exacerbation, or chronic pain of no apparent physical origin will ulti-
maintenance of the pain.) This type of pain disorder is not mately be found to have occult organic disease.
diagnosed if criteria are also met for somatization disorder.
In individuals with unexplained pelvic pain, clini-
Specify if:
cians should be warned about cavalier conclusions
Acute: Duration of less than 6 months regarding the absence of physical disease. With lapar-
Chronic: Duration of 6 months or longer
307.89 Pain Disorder Associated with both Psychologi- oscopy, a high frequency of occult organic disease has
cal Factors and a General Medical Condition: Both psy- been identified in several studies. Thus, laparoscopy
chological factors and a general medical condition are may be indicated in individuals with pelvic pain. Elec-
judged to have important roles in the onset, severity, ex-
acerbation, or maintenance of the pain. The associated tromyography may be helpful in distinguishing muscle
general medical condition or anatomical site of the pain contraction headaches. Failure to show coronary artery
(see below) is coded on Axis III.
spasm with provocative procedures and failure to re-
Specify if: spond to nitroglycerin may be useful in distinguishing
Acute: Duration of less than 6 months individuals with pain disorder from those in whom the
Chronic: Duration of 6 months or longer
Note: The following is not considered to be a mental disor- pain is attributable to coronary artery disease.
der and is included here to facilitate differential diagnosis. Given the fact that diagnostic criteria for pain have
Pain Disorder Associated with a General Medical Condi- significantly changed across the various editions of the
tion: A general medical condition has a major role in the
onset, severity, exacerbation, or maintenance of the pain. DSMs, only estimates can be made for the epidemio-
(If psychological factors are present, they are not judged logical parameters of pain disorder. As to pain itself,
to have a major role in the onset, severity, exacerbation, some empirical studies suggest that it is common. Per-
or maintenance of the pain.) The diagnostic code for the
pain is selected based on the associated general medical haps as indirect evidence of this is the proliferation of
condition if one has been established or on the anatomi- pain clinics nationally. Of course, many individuals
cal location of the pain if the underlying general medi- attending these clinics fall into the category of pain
cal condition is not yet clearly established—for example,
low back (724.2), sciatic (724.3), pelvic (625.9), head- disorder associated with a general medical condition,
ache (784.0), facial (784.0), chest (786.50), joint (719.4), but undoubtedly, some also have involvement of psy-
bone (733.90), abdominal (789.0), breast (611.71), renal chological factors as required for a diagnosis of pain
(788.0), ear (388.70), eye (379.91), throat (784.1), tooth
(525.9), and urinary (788.0). disorder as a mental disorder. The same would apply to
Reprinted with permission from the Diagnostic and Statistical the 10–15% of adults in the United States in any given
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 year who have work disability because of back pain.
Pain has been found to be a predominant symptom
in 75% of consecutive general medical patients, with
of clinical attention and is not better accounted for by 75% of these (thus 50% overall) judged as having no
the other disorder, a highly subjective judgment. identifiable physical cause. Whereas primary care and
If pain occurs exclusively during the course of other nonpsychiatric physicians probably see most pain
somatization disorder, pain disorder is not diagnosed patients, up to 40% of psychiatric inpatient admissions
and 20% attending a psychiatric outpatient clinic re- depending on whether external incentives or assumption
port pain as a significant problem. of the sick role is the motivation. Evidence of malinger-
ing includes consideration of external rewards relative
to the chronology of the development and maintenance
Course
of the pain. In factitious disorder, a pattern of succes-
Given the heterogeneity of conditions subsumed under sive hospitalizations and medical evaluations is evident.
the pain disorder rubric, course and prognosis vary Inconsistency in presentation, lack of correspondence
widely. The subtyping at 6 months is of significance. to known anatomical pathways or disease patterns, and
The prognosis for total remission is good for pain disor- lack of associated sensory or motor function changes
ders of less than 6 months’ duration. However, for syn- suggest malingering or factitious disorder, but pain dis-
dromes of greater than 6 months’ duration, chronicity order associated with psychological factors may show
is common. The site of the pain may be another factor. this pattern as well. The key question is whether the in-
Certain anatomically differentiated pain syndromes dividual is experiencing rather than feigning the pain.
can be distinguished, and each has its own characteris- Determination of the relative contributions of psy-
tic pattern. These include syndromes characterized pri- chological and general medical factors is difficult. Of
marily by headache, facial pain, chest pain, abdominal course, careful assessment of the nature and severity of
pain, and pelvic pain. In such syndromes, symptoms the potential underlying medical condition and the na-
tend to be recurrent, with relapses occurring in asso- ture and degree of pain that would be expected should
ciation with stress. A high rate of depression has been be made. Traditionally, the so-called conversion V or
observed among individuals with unexplained facial neurotic triad (consisting of elevation of the hypochon-
pain. Facial pain is often alleviated by antidepressant driasis and hysteria scales with a lower score on the de-
medication. This effect has been observed in both indi- pression scale) on the Minnesota Multiphasic Personal-
viduals with depressive symptoms and those without. ity Inventory has been purported to indicate emotional
Other factors affecting course and prognosis include indifference to the somatic concerns as might be ex-
associated mental disorders and external reinforce- pected if the symptom is attributable to psychological
ment. Employment at the outset of treatment predicts factors rather than organic disease. However, evidence
improvement. Chronicity is more likely in the presence indicates that this configuration may also occur as an
of certain personality diagnoses or traits, such as pro- adjustment to chronic illness.
nounced passivity and dependency. External reinforce-
ment includes litigation involving potential financial
TREATMENT
compensation for disability. Continuation of the pain
disorder may prove more lucrative than its resolution An overriding guideline in the treatment of pain is that
and return to work. Level of activity, which is generally the clinician not do anything that will actually perpetu-
associated with improvement, is discouraged by fears ate and even promote “pain-related behavior.” Thus, a
of losing compensation. Thus, although outright malin- major goal is to encourage activity. Other guidelines
gering may be rare, pain behaviors are often reinforced include avoidance of sedative–antianxiety drugs, judi-
and maintained. Habituation with addictive drugs is as- cious use of analgesics on a fixed interval schedule so
sociated with greater chronicity. as not to reinforce pain-related behaviors, avoidance of
opioids, and consideration of alternative treatment ap-
proaches such as relaxation therapy. Depression should
be treated with appropriate antidepressant drugs, not
As shown in Figure 34-1, the differential diagnosis sedative–antianxiety medications. The difficulties in
begins with an assessment of whether the presentation managing individuals with pain disorder have resulted
is fully explained by a general medical condition. If in the establishment of many clinics and programs es-
not, it may be assumed that psychological factors play pecially designed for pain. Referral to such a service
a major role. If it is judged that psychological factors may be indicated. Intervention should best be provided
do not play a major role, a diagnosis of pain disorder early in the course of the syndrome, before pain-related
associated with a general medical condition may apply. behaviors become entrenched. Once continuing dis-
As previously mentioned, this does not have a mental ability compensation is established, therapeutic efforts
disorder code. become much more difficult.
If psychological factors are involved, the first con- The preceding general guidelines apply whether or
sideration is whether the pain is feigned. If so, ei- not a general medical basis for the pain is involved.
ther malingering or factitious disorder is diagnosed, Of course, if only pain disorder associated with
psychological factors is involved, psychological man- opioids if possible. Agents to be tried first include
agement will be the mainstay. For individuals with antidepressants, acetaminophen, NSAIDs (including
pain associated with general medical factors (not a aspirin), and anticonvulsants such as carbamazepine.
mental disorder) in which psychological factors do not Antidepressants seem particularly useful for neu-
play a major role, efforts should be made to prevent ropathic pain, headache, facial pain, fibrositis, and
the development of psychological problems in response arthritis (including rheumatoid arthritis). Analge-
to the resulting distress, isolation and loss of function, sic action seems to be independent of antidepressant
and iatrogenic effects such as exposure to potentially effects. Most work has been done with the tricyclic
addicting drugs. antidepressants; other classes, such as the monoam-
In acute pain, the major goal is to relieve the pain. ine oxidase inhibitors (MAOIS) and the selective
Thus, pharmacological agents generally play a more serotonin reuptake inhibitors (SSRIS), may be effec-
significant role than in chronic syndromes. Whereas tive as well. Although it was thought that the action
the risk of developing opioid dependence appears to is mediated by serotoninergic effects, agents such as
be surprisingly low (4 per 12,000) among individu- desipramine with predominantly noradrenergic activ-
als without a prior history of dependence, nonopioid ity seem to be effective as well. NSAIDs, of which
agents should be used whenever they can be expected aspirin, ibuprofen, naproxen, and piroxicam are com-
to be effective. These include, in particular, acetami- monly used examples, may alleviate pain through
nophen and the nonsteroidal antiinflammatory drugs inhibition of prostaglandin synthesis. Unfortunately,
(NSAIDS), of which aspirin is considered a member. this effect may also contribute to side effects, such as
Even if an opioid analgesic is employed, these drugs aggravation of peptic or duodenal ulcers and interfer-
should be continued as adjuncts; often, they lessen the ence with renal function. For individuals unable to tol-
required dose of the opioid. erate NSAIDs, acetaminophen should be tried.
It is with the chronic syndromes that proper manage- If opioid analgesics are used, it is recommended
ment is crucial to ease distress and prevent the devel- that use be tied to objectives such as increasing level
opment of additional problems. The overriding goal is of activity rather than simply pain alleviation. Milder
to maintain function, because total relief of the pain opioids, such as codeine, oxycodone, and hydrocodone,
may not be possible. Physical and occupational therapy should be implemented first. The once widely used pro-
may play a major role. There may be resistance to the poxyphene has less analgesic effect than these drugs; it
involvement of a mental health professional as an indi- is not devoid of abuse potential as once thought and is
cation that the pain is not seen as real. Such issues must not recommended. Pure opioid agonists such as mor-
first be resolved. An attempt should be made to ascer- phine, methadone, and hydromorphone should be tried
tain the roles that psychological and general medical next. Meperidine, also in this class, is contraindicated
factors play in the maintenance of the pain. for prolonged use because accumulation of the toxic
A large variety of psychotherapies including individ- metabolite, normeperidine, a cerebral irritant, may re-
ual, group, and family strategies have been employed. sult in anxiety, psychosis, or seizures. Meperidine may
Two techniques that warrant special attention are op- also have a lethal interaction with MAOIs. There are no
erant conditioning and cognitive–behavioral therapy. advantages to mixed opioid agonist–antagonists. The
In operant conditioning, the pattern of reinforcement commonly used pentazocine should be avoided because
of pain behavior by medication, attention, and excuse it has abuse potential and psychotomimetic effects in
from responsibilities is to be interrupted and reinforce- some individuals. It remains to be seen whether newer
ment shifted to usual daily activities. To assess the role agents (buprenorphine, butonphanol, and nalbuphine)
of operant conditioning, it may be necessary to have have lower abuse potential as claimed. Above all, clini-
individuals keep a diary and to interview family mem- cians should be judicious in the use of opioid analge-
bers to identify any conditioning patterns. In cogni- sics, considering not only their abuse potential but their
tive–behavioral therapies, the goal is the identification large number of side effects including constipation,
and correction of attitudes, beliefs, and expectations. nausea and vomiting, excessive sedation, and, in higher
Biofeedback and relaxation techniques may be used doses, respiratory depression that may be fatal.
to minimize muscle tension that may aggravate if not In addition to pharmacotherapy, a number of other
cause pain. Hypnosis may also be used to achieve mus- “physical” techniques have been used, such as acu-
cle relaxation and to help the individual “dissociate” puncture and transcutaneous electrical nerve stimula-
from the pain. tion. These carry little risk of adverse effects or ag-
Pharmacological intervention may also be useful gravation of the pain disorder. Other procedures such
in chronic syndromes. Effort should be made to avoid as trigger point injections, nerve blocks, and surgical
ablation may be recommended if specifically indicated Some degree of preoccupation with disease is appar-
by an underlying general medical disorder. ently common. In a 1991 study, 10–20% of “normal”
and 45% of “neurotic” persons were reported to have
intermittent unfounded worries about illness, with 9%
Hypochondriasis of individuals doubting reassurances given by physi-
cians. Many individuals manifest some hypochon-
DIAGNOSIS driacal symptoms as part of other mental disorders,
As defined in DSM-IV-TR, the essential feature in hy- and others have transient hypochondriacal symptoms
pochondriasis is preoccupation with fears or the idea in response to stresses such as serious physical illness
of having a serious disease based on the “misinter- yet never fulfill the inclusion criteria for DSM-IV-TR
pretation of bodily symptoms”. This is in contrast to hypochondriasis. Assessment of the incidence and
somatization disorder, conversion disorder, and pain prevalence of hypochondriasis undoubtedly requires
disorder, in which the symptoms themselves are the study of general or primary care rather than psychiatric
predominant focus (see Table 34-2). Bodily symptoms populations, because individuals with hypochondriasis
may be interpreted broadly to include misinterpreta- are convinced that they suffer from some physical ill-
tion of normal body functions. In hypochondriasis, the ness. To date, study of such populations suggests that
preoccupation persists despite reassurance from physi- 4–9% of individuals in general medical settings suffer
cians and the accumulation of evidence to the contrary. from hypochondriasis.
As in the other somatoform disorders, symptoms must It does appear that hypochondriasis is equally com-
result in clinically significant distress or impairment in mon in males and females. Data concerning socioeco-
important areas of functioning. The duration must be nomic class are conflicting.
at least 6 months. Hypochondriasis is not diagnosed if
the hypochondriacal concerns are better accounted for Course
by another mental disorder, such as major depressive
episodes or various psychotic disorders with somatic Data are conflicting, but it appears that the most com-
delusions. mon age at onset is in early adulthood. Available data
suggest that approximately 25% of individuals with a
diagnosis of hypochondriasis do poorly, 65% show a
chronic but fluctuating course, and 10% recover. This
DSM-IV-TR Diagnostic Criteria pertains to the full syndrome. A much more variable
course is seen in individuals with just some hypochon-
300.7 HYPOCHONDRIASIS driacal concerns. It appears that acute onset, absence of
A. Preoccupation with fears of having, or the idea that a personality disorder, and absence of secondary gain
one has, a serious disease based on the person’s mis- are favorable prognostically.
interpretation of bodily symptoms.
B. The preoccupation persists despite appropriate medi-
cal evaluation and reassurance. Differential Diagnosis
C. The belief in criterion A is not of delusional intensity
(as in delusional disorder, somatic type) and is not re- As shown in Figure 34-1, the first step in approaching
stricted to a circumscribed concern about appearance
(as in body dysmorphic disorder). individuals with distressing or impairing preoccupation
D. The preoccupation causes clinically significant distress with or fears of having a serious disease is to exclude
or impairment in social, occupational, or other impor- the possibility of explanation on the basis of a general
tant areas of functioning.
E. The duration of the disturbance is at least 6 months. medical condition. Fears that may seem excessive may
F. The preoccupation is not better accounted for by gen- also occur in individuals with general medical condi-
eralized anxiety disorder, obsessive–compulsive disor- tions with vague and subjective symptoms early in their
der, panic disorder, a major depressive episode, sepa-
ration anxiety, or another somatoform disorder. disease course. These include neurological diseases,
such as myasthenia gravis and multiple sclerosis, en-
Specify if:
docrine diseases, systemic diseases that affect several
With poor insight: If, for most of the time during the organ systems, such as systemic lupus erythematosus,
current episode, the person does not recognize that the
concern about having a serious illness is excessive or and occult malignant neoplasms. The disease convic-
unreasonable tion of hypochondriasis may actually be less amenable
Reprinted with permission from the Diagnostic and Statistical to medical reassurance than the fears of individuals
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 with general medical illnesses, who may at least tem-
porally accept such encouragement. Hypochondriacal
complaints are not often intentionally produced such also be seen (e.g., “I’m trying not to defecate because
that differentiation from malingering and factitious it will cause my brain to turn to jelly”). Schizophrenic
disorder is seldom a problem. individuals may also show improvement with neurolep-
Exclusion is made if the preoccupation is better tic treatment, at least in the “active” symptoms of their
accounted for by another mental disorder. DSM-IV- illness, under which somatic delusions are included.
TR lists generalized anxiety disorder, obsessive– Differentiation from delusional disorder, somatic
compulsive disorder, panic disorder, a major depressive type, may be more difficult. It is often a thin line be-
episode, separation anxiety, or another somatoform tween preoccupation and fear that is a conviction and
disorder as candidates. Chronology will be of utmost that which is a delusion. Often, the distinction is made
importance in such discriminations. Hypochondria- on the basis of whether the individual can consider the
cal concerns occurring exclusively during episodes of possibility that the conviction is erroneous. Yet, individ-
another disturbance, such as an anxiety or depressive uals with hypochondriasis vary in the extent to which
disorder, do not warrant an additional diagnosis of hy- they can do this. DSM-IV-TR acknowledges this by its
pochondriasis. The presence of symptoms of another inclusion of the specifier “with poor insight.” In the past,
mental disorder will also be helpful. For example, an some argued that differentiation could be made on the
individual with hypochondriacal complaints as part of basis of response to neuroleptics, especially pimozide;
a major depressive episode will show other symptoms individuals with delusional disorder, but not hypochon-
of depression, such as sleep and appetite disturbance, driasis, respond. Interestingly, there is at least one report
feelings of worthlessness, and self-reproach, although of successful treatment of a syndrome corresponding to
depressed elderly individuals may deny sadness or other delusional disorder, somatic type, in a nondepressed in-
expressions of depressed mood. A confounding factor dividual with the SSRI paroxetine. As with hypochon-
is that individuals with hypochondriasis often have co- driasis, response was obtained only when the dose was
morbid anxiety or depressive syndromes. Again, char- raised beyond an antidepressant dose (to 60 mg/day).
acterizing the symptoms by chronology will be useful. If it is concluded that the preoccupations are not
Treatment trials may also have diagnostic significance. delusional, the next consideration is whether the du-
Depressed individuals who are hypochondriacal may ration requirement of 6 months has been met (see
respond to non-SSRI antidepressant medications or Figure 34-1). Syndromes of less than 6 months’ dura-
electroconvulsive therapy (often necessary to reverse tion are diagnosed under either somatoform disorder
a depressive state of sufficient severity to lead to such NOS or adjustment disorder if the symptoms are an
profound symptoms), with resolution of the hypochon- abnormal response to a stressful life event. The rea-
driacal as well as the depressive symptoms. son to make such a distinction is to distinguish hypo-
Hypochondriasis is differentiated from other chondriasis from transient syndromes, the longitudinal
somatoform disorders such as pain, conversion, and course of which have been shown to be more variable,
somatization disorders by its predominant feature of suggesting heterogeneity.
preoccupation with and fears of having an underlying Other diagnostic considerations include whether the
illness based on the misinterpretation of body symp- preoccupations or fears are restricted to preoccupations
toms, rather than the physical symptoms themselves. with being overweight, as in anorexia nervosa; with the
Individuals with these other somatoform disorders at inappropriateness of one’s sex characteristics, as in a
times are concerned with the possibility of underlying gender identity disorder; or with defects in appearance,
illness, but this will generally be overshadowed by a as in body dysmorphic disorder. The preoccupations of
focus on the symptoms themselves. hypochondriasis resemble the obsessions, and the health
The next consideration is whether the belief is of de- checking and efforts to obtain reassurance resemble the
lusional proportions. Individuals with hypochondriasis, compulsions of obsessive–compulsive disorder. How-
although preoccupied, generally acknowledge the pos- ever, if such manifestations are health centered only,
sibility that their concerns are unfounded. Delusional obsessive–compulsive disorder is not diagnosed. If, on
individuals do not. Somatic delusions of serious illness the other hand, nonhealth related obsessions and com-
are seen in some cases of schizophrenia and in delu- pulsions are present, obsessive–compulsive disorder
sional disorder, somatic type. In general, individuals may be diagnosed in addition to hypochondriasis.
with schizophrenia who have such delusions also show
other signs of schizophrenia, such as disorganized
TREATMENT
speech, peculiarities of thought and behavior, halluci-
nations, and other delusions. Belief that an underlying Individuals with hypochondriasis generally present
illness is being caused by some bizarre process may initially to nonpsychiatric physicians and are often
reluctant to see a mental health clinician. Referral

should be done sensitively, with the referring physi- DSM-IV-TR Diagnostic Criteria
cian stressing to the individual that his or her distress 300.7 BODY DYSMORPHIC DISORDER
is real and that psychiatric evaluation will be a sup-
plement to, not a replacement for, continued medical A. Preoccupation with an imagined defect in appear-
ance. If a slight physical anomaly is present, the per-
care. son’s concern is markedly excessive.
Initially, the generic strategies outlined for somato- B. The preoccupation causes clinically significant distress
form disorders (see page 353) should be followed. or impairment in social, occupational, or other impor-
tant areas of functioning.
However, it has not been demonstrated that a specific C. The preoccupation is not better accounted for by an-
psychotherapy for hypochondriasis is particularly ef- other mental disorder (e.g., dissatisfaction with body
fective. Dynamic psychotherapy appears to be of shape and size in anorexia nervosa).
minimal effectiveness; supportive–educative psycho- Reprinted with permission from the Diagnostic and Statistical
therapy is only somewhat helpful and primarily for American Psychiatric Association.
those with syndromes of less than 3 years’ duration;
and cognitive–behavioral therapy, especially response
prevention of checking rituals and reassurance seek- toms are limited to preoccupation with body weight, as
ing, is of only moderate effectiveness at best. All of in anorexia nervosa or bulimia nervosa, or to perceived
these techniques seem to lack definitive effects on hy- inappropriateness of sex characteristics, as in gender
pochondriasis itself. identity disorder.
Until recently, this could be said of pharmacologi- Preoccupations most often involve the nose, ears,
cal approaches also. Pharmacotherapy of comorbid face, or sexual organs. Common complaints include a
depressive or anxiety syndromes was often effective, diversity of imagined flaws of the face or head, includ-
and control of such syndromes aided in general man- ing defects in the hair (e.g., too much or too little), skin
agement, yet hypochondriasis itself was not amelio- (e.g., blemishes), and shape or symmetry of the face or
rated. Although controlled trials are lacking, anecdo- facial features (e.g., nose is too large and deformed).
tal and open-label studies suggest that serotoninergic However, any body part may be the focus, including
agents such as clomipramine and the SSRI fluoxetine genitals, breasts, buttocks, extremities, shoulders, and
may be effective in ameliorating hypochondriasis. even overall body size.
Similar effects are expected from the other SSRIs. In terms of its relationship to the psychotic disorders,
Response to fluoxetine has been reported with doses a continuum exists from clearly nondelusional preoc-
recommended for obsessive–compulsive disorder, cupations to unequivocal delusions such that defining
rather than usual antidepressant doses (i.e., 60–80 mg a discrete boundary between the two ends of the spec-
rather than 20–40 mg/day). Such pharmacotherapy is trum would be artificial. Furthermore, some individu-
best combined with the generic psychotherapy rec- als seem to move back and forth along this continuum.
ommendations for somatoform disorders, as well as Perhaps as a reflection of the state of knowledge at this
with cognitive–behavioral techniques to disrupt the point, both body dysmorphic disorder and delusional
counterproductive checking and reassurance-seeking disorder, somatic type, can be diagnosed on the basis
behaviors. of the same symptoms, in the same individual, at the
same time. Thus, the definition of body dysmorphic
disorder differs from hypochondriasis, which is not di-
Body Dysmorphic Disorder
agnosed if hypochondriacal concerns are determined
to be delusional.
DIAGNOSIS
Individuals with body dysmorphic disorder gener-
As defined in DSM-IV-TR, the essential feature of this ally first present to nonpsychiatric physicians such as
disorder is preoccupation with an imagined defect in plastic surgeons, dermatologists, and internists be-
appearance or a markedly excessive concern with a mi- cause of the nature of their complaints and are not seen
nor anomaly. In body dysmorphic disorder, a person psychiatrically until they are referred. Many resist or
can be preoccupied with an imagined defect while she refuse referral because they do not see their problem
or he actually has some other anomaly and is not ap- as psychiatric; thus, study of psychiatric clinic popula-
pearing normal. To exclude conditions with trivial or tions may underestimate the prevalence of the disorder.
minor symptoms, the preoccupation must cause clini- It has been estimated that 2% of individuals seeking
cally significant distress or impairment. By definition, corrective cosmetic surgery suffer from this disorder.
body dysmorphic disorder is not diagnosed if symp- Although women outnumber men in this population, it
is not known whether this sex distribution holds true in unamenable to reassurance from friends or family or
the general population. consultation with physicians, cosmetologists, or other
professionals.
Next, the possibility of an explanation by a general
Course
medical condition must be considered (see Figure 34-1).
Age at onset appears to peak in adolescence or early As mentioned, individuals with this disorder often fi rst
adulthood. Body dysmorphic disorder is generally a present to plastic surgeons, oral surgeons, and others,
chronic condition, with a waxing and waning of in- seeking correction of defects. By the time a mental
tensity but rarely full remission. In a lifetime, multiple health professional is consulted, it has generally been
preoccupations are typical; in one study, the average ascertained that there is no physical basis for the degree
was four. In some, the same preoccupation remains un- of concern. As with other syndromes involving somatic
changed. In others, new perceived defects are added to preoccupations (or delusions), such as olfactory ref-
the original ones. In still others, symptoms remit, only to erence syndrome and delusional parasitosis (both in-
be replaced by others. The disorder is often highly inca- cluded under delusional disorder, somatic type), occult
pacitating, with many individuals showing marked im- medical disorders, such as an endocrine disturbance or
pairment in social and occupational activities. Perhaps a a brain tumor, must be excluded.
third becomes housebound. Most attribute their limita- In terms of explanation on the basis of another men-
tions to embarrassment concerning their perceived de- tal disorder, there is little likelihood that symptoms of
fect, but the attention and time-consuming nature of the body dysmorphic disorder will be intentionally pro-
preoccupations and attempts to investigate and rectify duced as in malingering or factitious disorder. Unlike
defects also contribute. The extent to which individu- in other somatoform disorders, such as pain, conver-
als with body dysmorphic disorder receive surgery or sion, and somatization disorders, preoccupation with
medical treatments is unknown. Superimposed depres- appearance predominates. Somatic preoccupations may
sive episodes are common, as are suicidal ideation and occur as part of an anxiety or mood disorder. However,
suicide attempts. Actual suicide risk is unknown. these preoccupations are generally not the predominant
In view of the nature of the defects with which indi- focus and lack the specificity of dysmorphic symptoms.
viduals are preoccupied, it is not surprising that they Because individuals with body dysmorphic disorder of-
are found most commonly among individuals seeking ten become isolative, social phobia may be suspected.
cosmetic surgery. Preoccupations persist despite reas- However, in social phobia, the person may feel self-
surance that there is no defect to surgically correct. Sur- conscious generally but will not focus on a specific im-
gery or other corrective procedures rarely if ever lead to agined defect. Indeed, the two conditions may coexist,
satisfaction and may even lead to greater distress with warranting both diagnoses. Diagnostic problems may
the perception of new defects attributed to the surgery. present with the mood-congruent ruminations of major
depression, which sometimes involve concern with an
unattractive appearance in association with poor self-
esteem. Such preoccupations generally lack the focus
The preoccupations of body dysmorphic disorder must on a particular body part that is seen in body dysmor-
first be differentiated from usual concerns with groom- phic disorder. On the other hand, individuals with body
ing and appearance. Attention to appearance and dysmorphic disorder commonly have dysphoric affects
grooming is universal and socially sanctioned. However, described by them variously as anxiety or depression. In
diagnosis of body dysmorphic disorder requires that the some cases, these affects can be subsumed under body
preoccupation cause clinically significant distress or dysmorphic disorder; but in other instances, comorbid
impairment. In addition, in body dysmorphic disorder, diagnoses of anxiety or mood disorders are warranted.
concerns focus on an imaginary or exaggerated defect, Differentiation from schizophrenia must also be
often of something, such as a small blemish, that would made. At times, a dysmorphic concern will seem so
warrant scant attention even if it were present. Persons unusual that such a psychosis may be considered. Fur-
with histrionic personality disorder may be vain and thermore, individuals with this disorder may show ideas
excessively concerned with appearance. However, the of reference in regard to defects in their appearance,
focus in this disorder is on maintaining a good or even which may lead to the consideration of schizophrenia.
exceptional appearance, rather than preoccupation with However, other bizarre delusions, particularly of perse-
a defect. Such concerns are probably unrelated to body cution or grandiosity, and prominent hallucinations are
dysmorphic disorder. In addition, by nature, the preoc- not seen in body dysmorphic disorder. From the other
cupations in body dysmorphic disorder are essentially perspective, schizophrenia with somatic delusions
generally lacks the focus on a particular body part and the preoccupations do not extinguish as would be ex-
defect. Also in schizophrenia, bizarre interpretations pected with phobias. A cognitive–behavioral approach
and explanations for symptoms are often present, such similar to what was recommended for hypochondriasis
as “this blemish was a sign from Jesus that I am to may be more effective. This includes response preven-
protect the world from Satan.” Other signs of schizo- tion techniques whereby the individual is not permitted
phrenia, such as hallucinations and disorganization of to repetitively check the perceived defect in mirrors. In
thought, are also absent in body dysmorphic disorder. addition, individuals are advised not to seek reassur-
As previously mentioned, the preoccupations in body ance from family and friends, and these persons are
dysmorphic disorder appear to be on a continuum from instructed not to respond to such inquiries. Some indi-
full insight to delusional intensity whereby the individ- viduals adopt such behaviors spontaneously, avoiding
ual cannot even consider the possibility that the preoc- mirrors and other reflecting surfaces, refusing even to
cupation is groundless. In such instances, both body allude to their perceived defects to others. Such “self-
dysmorphic disorder and delusional disorder, somatic techniques” may be encouraged and refined.
type, are to be diagnosed. Biological treatments have long been used but until
Body dysmorphic disorder is not to be diagnosed if recently were of limited benefit to individuals with body
the concern with appearance is better accounted for by dysmorphic disorder. Approaches have included elec-
another mental disorder. Anorexia nervosa, in which troconvulsive therapy, tricyclic and MAOI antidepres-
there is dissatisfaction with body shape and size, is sants, and neuroleptics (particularly pimozide). In most
specifically mentioned in the criteria as an example reports of positive response to tricyclic or MAOI antide-
of such an exclusion. Although not specifically men- pressant drugs, it is unclear whether response was truly
tioned in DSM-IV-TR, if a preoccupation is limited to in terms of the dysmorphic syndrome or simply repre-
discomfort or a sense of inappropriateness of one’s pri- sented improvement in comorbid depressive or anxiety
mary and secondary sex characteristics, coupled with a syndromes. Response to neuroleptic treatment has been
strong and persistent cross-gender identification, body suggested as a diagnostic test to distinguish body dys-
dysmorphic disorder is not diagnosed. morphic disorder from delusional disorder, somatic type.
The preoccupations of body dysmorphic disorder The delusional syndromes often respond to neuroleptics;
may resemble obsessions and ruminations as seen in body dysmorphic disorders, even when the body preoc-
obsessive–compulsive disorder. Unlike the obsessions cupations are psychotic, generally do not. Pimozide has
of obsessive–compulsive disorder, the preoccupations been singled out as a neuroleptic with specific effective-
of body dysmorphic disorder focus on concerns with ness for somatic delusions, but this specificity does not
appearance. Compulsions are limited to checking appear to apply to body dysmorphic disorder.
and investigating the perceived physical defect and An exception to this uninspiring picture is the obser-
attempting to obtain reassurance from others regard- vation of a possible preferential response to antidepres-
ing it. Still, the phenomenology is similar, and the two sant drugs with serotonin reuptake blocking effects,
disorders are often comorbid. If additional obsessions such as clomipramine, or SSRIs, such as fluoxetine and
and compulsions not related to the defect are present, fluvoxamine. It has been reported that more than 50%
obsessive–compulsive disorder can be diagnosed in ad- of individuals with body dysmorphic disorder showed a
dition to body dysmorphic disorder. partial or complete remission with either clomipramine
or fluoxetine, a response not predicted on the basis of
coexisting major depressive or obsessive–compulsive
TREATMENT
disorder. As with hypochondriasis, effectiveness is gen-
First, the generic treatment strategies outlined for the erally achieved at levels recommended for obsessive–
somatoform disorders overall (see page 353) should compulsive disorder rather than for depression (e.g.,
be instituted. These are beneficial in interrupting an 60–80 mg rather than 20–40 mg/day of fluoxetine).
unending procession of repeated evaluations and the The SSRIs appear to ameliorate delusional as well as
possibility of needless surgery, which may lead to ad- nondelusional dysmorphic preoccupations. Successful
ditional perceptions that surgery has resulted in further augmentation of clomipramine or SSRI therapy has
disfigurement. been suggested with buspirone, another drug with sero-
Traditional insight-oriented therapies have not gen- toninergic effects. Neuroleptics, particularly pimozide,
erally proved to be effective. Results with traditional may also be helpful adjuncts, particularly if delusions
behavioral techniques, such as systematic desensitiza- of reference are present. Little seems to be gained with
tion and exposure therapy, have been mixed. At least the addition of anticonvulsants or benzodiazepines to
without amelioration with effective pharmacotherapy, the SSRI therapy.
Somatoform Disorder Not Otherwise Specified COMPARISON OF DSM-IV-TR AND ICD-10

DIAGNOSTIC CRITERIA
Somatoform disorder NOS is the true residual cat-
The ICD-10 Diagnostic Criteria for Research for So-
egory for this diagnostic class. By definition, disorders
matization Disorder have both a different item set and
considered under this category are characterized by
algorithm. Six symptoms are required out of a list
somatic symptoms, but criteria for any of the specific
of fourteen symptoms, which are broken down into
somatoform disorders are not met. Several examples
the following groups: six gastrointestinal symptoms,
are given, but syndromes potentially included under
two cardiovascular symptoms, three genitourinary
this category are not limited to these. Unlike for undif-
symptoms, and three “skin and pain” symptoms. It
ferentiated somatoform disorder, no minimal duration
is specified that the symptoms occur in at least two
is required. DSM-IV-TR lists as examples pseudocye-
groups. In contrast, DSM-IV-TR requires four pain
sis, disorders involving hypochondriacal complaints
symptoms, two gastrointestinal symptoms, one sexual
but of less than 6 months’ duration, and disorders
symptom, and one pseudoneurological symptom. Fur-
involving unexplained physical complaints, such as
thermore, the ICD-10 Diagnostic Criteria for Research
fatigue or body weakness not due to another mental
specify that there must be “persistent refusal to accept
disorder and again of less than 6 months’ duration.
medical reassurance that there is no adequate physical
This last syndrome would seem to resemble neuras-
cause for the physical symptoms.” DSM-IV-TR only
thenia of short duration, a syndrome with a long his-
requires that the symptoms result in treatment being
torical tradition with inclusion in DSM-II, ICD-9, and
sought or significant impairment in social, occupa-
ICD-10. Neurasthenia was considered for inclusion as
tional, or other important areas of functioning and that
a separate DSM-IV somatoform disorder but was not
the symptoms cannot be fully explained by a known
included because of difficulties in delineating it from
general medical condition or substance. For Undiffer-
depressive and anxiety disorders and from other so-
entiated Somatoform Disorder, the ICD-10 Diagnostic
matoform disorders. If included, neurasthenia could
Criteria for Research and the DSM-IV-TR criteria are
have become a clinical “wastebasket” that could facili-
almost identical.
tate premature closure of diagnostic inquiry, such that
Regarding conversion disorder, ICD-10 considers
underlying general medical conditions as well as other
conversion a type of dissociative disorder and includes
mental disorders would more likely be overlooked.
separate criteria sets for dissociative motor disorders,
Inclusion of pseudocyesis as an example of Somato-
dissociative convulsions, and dissociative anesthesia
form Disorder NOS deserves special mention. This
and sensory loss in a section that also includes disso-
syndrome was included in DSM-III and DSM-III-R as
ciative amnesia and dissociative fugue.
an example of a conversion symptom under the broad-
For pain disorder, the ICD-10 Diagnostic Criteria for
ened definition of conversion, on the basis that it repre-
Research require that the pain last at least 6 months
sented a somatic expression of a psychological conflict
and that it not be “explained adequately by evidence
or need, in this case involving ambivalence toward
of a physiological process or a physical disorder.” In
pregnancy. The resulting conflict was resolved somati-
contrast, DSM-IV-TR does not force the clinician to
cally as a false pregnancy, lessening anxiety (primary
make this inherently impossible judgment and instead
gain) and leading to unconsciously needed environ-
requires the contribution of psychological factors.
mental support (secondary gain). With the restriction
Furthermore, DSM-IV-TR includes both acute (dura-
of conversion in DSM-IV to include only symptoms
tion less than 6 months) and chronic pain (more than
affecting voluntary motor and sensory function, pseu-
6 months). This disorder is referred to in ICD-10 as
docyesis was excluded from the conversion disorder
“Persistent Somatoform Pain Disorder.”
definition. In a sense, it is placed in the somatoform
ICD-10 provides a single criteria set that applies to
disorder NOS category for lack of a more appropriate
both the DSM-IV-TR categories of hypochondriasis
place. It could also be described as a psychophysiologi-
and body dysmorphic disorder. The ICD-10 Diagnostic
cal endocrine disorder since, in many cases, a neuroen-
Criteria for Research for Hypochondriasis specify that
docrine change accompanies and at times may antedate
the belief is of a “maximum of two serious physical
the false belief of pregnancy. However, in most in-
diseases” and requires that at least one be specifi-
stances, a discrete general medical condition (such as a
cally named by the individual with the disorder. The
hormone-secreting tumor) cannot be identified.
DSM-IV-TR has no such requirement.
CHAPTER
35 Factitious Disorders
DIAGNOSIS
referring to the Baron von Munchausen, a character
An individual with a factitious disorder consciously in- in German literature who was known for greatly ex-
duces or feigns illness in order to obtain a psychologi- aggerating the tales of his exploits. Asher described
cal benefit by being in the sick role. It is the conscious Munchausen’s syndrome as a severe, chronic factitious
awareness of the production of symptoms that differ- disorder combined with antisocial behavior including
entiates factitious disorder from the somatoform dis- wandering from hospital to hospital (peregrination).
orders in which the individual unconsciously produces However, his memorable term has often been used
symptoms for an unconscious psychological benefit. interchangeably with “factitious disorder” and incor-
It is the underlying motivation to produce symptoms rectly applied to individuals with less severe forms of
that separates factitious disorders from malingering. the disease.
Individuals who malinger consciously feign or induce Individuals have been known to create or feign
illness in order to obtain some external benefit such numerous illnesses, both acute and chronic, in all of
as money, narcotics, or excuse from duties. While the the medical specialties. These illnesses can be either
distinctions among these disorders appear satisfyingly physical or psychological. It appears that the only limit
clear, in practice, individuals often blur the bounda- is the creativity and knowledge of a given individual.
ries. Individuals with somatoform disorders will some- Individuals with a factitious disorder are often quite
times consciously exaggerate symptoms that they have medically sophisticated. Even though acquired im-
unconsciously produced, and it is a rare individual who mune deficiency syndrome was not described until the
consciously creates illness and yet receives no external early 1980s, the first factitious cases followed shortly
gain at all, be it disability benefits, excuse from work, thereafter, at least as early as 1986.
or even food and shelter. For a diagnosis of factitious disorder (see DSM-IV-
Individuals with factitious disorders seek, often des- TR diagnostic criteria, page 369) to be justified, a per-
perately, the sick role. They usually have little insight son must be intentionally producing an illness; his or
into the motivations of their behaviors but are still pow- her motivation is to occupy the sick role, and there must
erfully driven to appear ill to others. In many cases, not be external incentives for the behavior. The diag-
they endanger their own health and life in search of nosis is further subclassified, depending on whether
this role. Individuals with this disorder will often in- the factitious symptoms are predominantly physical,
duce serious illness or undergo numerous unnecessary, psychological, or a combination of both. Individuals
invasive procedures. As most people avoid sickness, who readily admit to inducing symptoms, such as self-
the actions of these individuals appear to run counter mutilating individuals, are not diagnosed with facti-
to human nature. Also, since entry into the “sick role” tious disorder as they are not using their symptoms to
requires that the sick person should try to get better, occupy the sick role.
individuals with factitious disorders must conceal the Individuals with Factitious Disorder with Predomi-
voluntary origin of their symptoms. The inexplicability nantly Physical Signs and Symptoms present with phys-
of their actions combined with their deceptive behavior ical signs and symptoms. The three main methods that
stir up both intense interest and intense (usually nega- individuals use to create illness are (1) giving a false
tive) countertransference in health care providers. history, (2) faking clinical and laboratory findings, and
While physicians have known about the feigning of (3) inducing illness (e.g., by surreptitious medication
illness since the time of ancient Greece, it is likely that use, inducing infection, or preventing wound healing).
Richard Asher’s 1951 article in Lancet brought the con- There are reports of factitious illnesses in all of the
cept of factitious illness into general medical knowl- medical specialties. Particularly common presentations
edge. Asher coined the term Munchausen’s syndrome include fever, self-induced infection, gastrointestinal
Chapter 35 • Factitious Disorders 369
psychological symptoms who also have some of the key

DSM-IV-TR Diagnostic Criteria features of Munchausen’s (pathological lying, wander-
FACTITIOUS DISORDER
ing, and recurrent hospitalizations).
Numerous reports in the literature describe two dif-
A. Intentional production or feigning of physical or psy- ferent subclasses of factitious individuals. The first type
chological signs or symptoms.
B. The motivation for the behavior is to assume the sick fits with the classic Munchausen’s syndrome diagnosis:
role. they have chronic factitious symptoms associated with
C. External incentives for the behavior (such as economic antisocial traits, pathological lying, minimal social
gain, avoiding legal responsibility, or improving physi-
cal well-being, as in malingering) are absent. supports, wandering from hospital to hospital, and very
poor work and relationship functioning. They are of-
Code based on type ten very familiar with hospital procedure and use this
300.16 With Predominantly Psychological Signs and
Symptoms: if psychological signs and symptoms pre- knowledge to present dramatically during off-hours or
dominate in the clinical presentation at house-officer transition times when the factitious na-
300.19 With Predominantly Physical Signs and Symp- ture of their symptoms is least likely to be discovered.
toms: if physical signs and symptoms predominate in the
clinical presentation Males comprise the majority of these cases. Individu-
300.19 With Combined Psychological and Physical als with Munchausen’s syndrome appear to have an ex-
Signs and Symptoms: if both psychological and physi- tremely poor prognosis. Fortunately, this most severe
cal signs and symptoms are present and neither predomi-
nates in the clinical presentation. class of individuals makes up the minority of factitious
Reprinted with permission from the Diagnostic and Statistical individuals, probably fewer than 10%.
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 The second, and more typical, type of individual
does not display pathological lying or wandering. Their
recurrent presentations are usually within the same
community, and they become well-known within the
symptoms, impaired wound healing, cancer, renal dis- local health care system. They often have stable social
ease (especially hematuria and nephrolithiasis), endo- supports and employment, and a history of a medically
crine diseases, anemia, bleeding disorders, and epilepsy. related job. This larger class of factitious individuals
True Munchausen’s syndrome fits within this subclass is mostly made up of women, and is more likely to ac-
and is the most severe form of the illness. According to cept psychiatric treatment and to show improvement.
the DSM-IV-TR, individuals with Munchausen’s syn- Finally, there are individuals who may have an episode
drome have a chronic factitious disorder with physical of factitious disorder in reaction to a life stressor, but
signs and symptoms, and in addition, have a history of may return to premorbid functioning after the stressor
recurrent hospitalization, peregrination, and pseudolo- is resolved.
gia fantastica—dramatic, untrue, and extremely im- All types of factitious disease show a strong asso-
probable tales of their past experiences. ciation with substance abuse, as well as borderline and
Another subtype of factitious disorder includes in- narcissistic personality disorders. Factitious individu-
dividuals who present feigning psychological illness. als span a broad age range. Reports in the literature
They both report and mimic psychiatric symptoms. show individuals ranging from 4 to 85 years.
These individuals can be particularly difficult to diag- The diagnosis of factitious disorder is made in sev-
nose as psychiatric diagnosis depends greatly on the eral ways (see Figure 35-1). Factitious disorder is oc-
individual’s report. There are reports of factitious psy- casionally diagnosed accidentally when the individual
chosis, posttraumatic stress disorder, and bereavement. is discovered in the act of creating symptoms. A history
In addition, there are reports of psychological distress of inconsistent or unexplainable signs and symptoms or
due to false claims of being a victim of stalking, rape, or failure to respond to appropriate treatment can prompt
sexual harassment, and these cases are often diagnosed health care providers to probe for evidence of the dis-
with a factitious psychological disorder such as post- order, as can evidence of peregrination or pathological
traumatic stress disorder. While individuals with facti- lying. In some cases, it is a diagnosis of exclusion in an
tious psychological symptoms feign psychiatric illness, otherwise inexplicable case.
they also often suffer from true comorbid psychiatric If there is suspicion of a factitious disorder, confir-
disorders, particularly Axis II disorders and substance mation can be difficult. Laboratory examination can
abuse. Case reports suggest that individuals with psy- confirm some factitious diagnoses such as exogenous
chological factitious disorder have a high rate of suicide insulin or thyroid hormone administration. Collateral
and a poor prognosis. While Munchausen’s syndrome information from family members or previous health
is considered a subset of physical factitious disorder, care providers can also be extremely helpful. Factitious
there are case reports of individuals presenting with disorder with psychological signs and symptoms can be
Usually, the victim is a preverbal child. While numer-

Unexplained physical or
psychiatric symptom
ous symptoms have been reported, common presen-
tations include apnea, seizures, and gastrointestinal
problems. The mothers appear extremely caring and
attentive when observed, but appear indifferent to the
child when they are not aware of being observed.
The diagnosis of factitious disorder by proxy is usu-
Genuine medical or No Complete medical
and/or psychiatric ally made by having an index of suspicion in a child
psychiatric cause
excluded? workup with unexplained illnesses. The diagnosis is supported
if symptoms occur only in the parent’s presence and
Yes resolve with separation. Covert video surveillance has
been used to diagnose this condition, though it raises
questions of invasion of privacy. In general, it has been
Does symptom appear No Diagnosis: Somatoform felt that the welfare of the child overrides the parent’s
to be consciously disorder
produced? right to privacy.
As counterintuitive as it is to comprehend why any-
one would induce illness in oneself, it can be even more
Yes difficult to understand inducing illness in one’s own
child. The perpetrator in factitious disorder by proxy
appears to seek not the “sick role” but the “parent to the
Secondary gain Diagnosis:
What is the basis sick child” role. This role is similar to the sick role in
of the conscious Malingering that it provides structure, attention from others, caring,
motivation?
and relief from usual responsibilities. The parent also
receives some psychological benefit from inducing ill-
Patient role ness in his or her child. On the basis of case reports, the
parent often has a comorbid personality disorder and a
Diagnosis: Factitious history of family dysfunction.
disorder The nature of factitious disorder makes it difficult
to determine how common it is within the population.
Figure 35-1 Diagnostic decision tree for factitious disorder. Individuals attempt to conceal themselves, thereby ar-
tificially lowering the prevalence. The tendency of indi-
viduals to present themselves several times at different
particularly difficult to diagnose, as so much of psychi- facilities, however, may artificially raise the prevalence.
atric diagnosis relies on the individual’s report. Most estimates of the prevalence of the disease, there-
The course of untreated factitious disorder is vari- fore, rely on the number of factitious individuals within
able. While individuals with factitious disorder com- a given inpatient population. Such attempts have gener-
monly suffer a great deal of morbidity, fatal cases ap- ated estimates that 0.5–3% of medical and psychiatric
pear to be less common. One survey of 41 cases noted inpatients suffer from factitious disorder. There are few
only one fatality, though many of the other cases were data about the prevalence of factitious disorder in an
life-threatening. However, individuals with psychologi- outpatient population. Because factitious individuals
cal signs and symptoms are reported to have a high rate do not readily identify themselves in large community
of suicide and a poor prognosis. surveys, it is not currently possible to determine the
In factitious disorder by proxy, one person creates or prevalence of the disorder in the general population.
feigns illness in another person, usually a child, though As in factitious disorder, the exact prevalence of facti-
occasionally the victim is an elder or developmentally tious disorder by proxy is unknown. Factitious disorder
delayed adult. The veterinary literature even reports by proxy appears to have a much higher mortality rate
cases of factitious disorder by proxy in which the than self-inflicted factitious disorder.
victim is a pet. Factitious disorder by proxy is not de-
fined as a specific disorder in DSM-IV-TR, but instead
is listed under the “not otherwise specified” heading
with research criteria included. While rare instances of The differential diagnosis of factitious disorder in-
fathers perpetrating factitious disorder by proxy have cludes rare or complex physical illness, somatoform
been reported, the perpetrator is usually the mother. disorders, malingering, other psychiatric disorders,
Chapter 35 • Factitious Disorders 371
and substance abuse. It is especially important to rule her boyfriend proposed marriage that she might feel
out genuine physical illness since individuals with a a need to punish herself when good things happened
factitious disorder often induce real physical illness. to her. She agreed, and soon after, admitted that she
Furthermore, it is always important to remember that had injected a contaminant intravenously. The second
individuals with factitious disorders are certainly not technique is the therapeutic double-bind. The clinician
immune to the physical illnesses that plague the gen- presents the individual with a new medical intervention
eral population. to treat his or her illness. The individual is told that
one possibility is that the individual’s illness has a fac-
titious origin, and that, if so, the treatment would not be
TREATMENT
expected to work while, if the illness is biological, the
The goals in treating individuals with a factitious disor- treatment will work and the individual will improve.
der are twofold; first to minimize the damage done by The individual must decide to give up the factitious
the disorder to both the individual’s own health and the illness or admit it. A third technique is to provide the
health care system. The second goal is to help individu- individual with a face-saving way, such as hypnosis or
als recover, at least partially, from the disorder. These biofeedback, of giving up his or her symptoms without
goals are furthered by treating comorbid medical ill- admitting that they are not genuine. In emergent situa-
nesses, avoiding unnecessary procedures, encouraging tions, however, there may not be time for nonconfron-
individuals to seek psychiatric treatment, and provid- tational techniques, and more directly confrontational
ing support for health care clinicians. Because the lit- means may be necessary.
erature is based exclusively on case reports and series, Another important component in the treatment of in-
determining treatment effectiveness is difficult. As dividuals with factitious disorder is the coordination of
mentioned before, individuals with true Munchausen’s health care among all clinicians. This allows for fewer
syndrome (including antisocial traits, pathological ly- unnecessary interventions, minimizes splitting among
ing, wandering, and poor social support) are felt to be the health care team, and allows the health care team
refractory to treatment. While factitious disorder is ex- to vent and process the strong emotions that arise when
tremely difficult to cure, effective techniques exist to caring for factitious individuals. This decreases both
minimize morbidity, and some individuals are able to the negative impact on the clinicians and the chance
benefit greatly from psychiatric intervention. that anger will be acted out on the individual.
Soon after Asher’s 1951 article was published, many While many individuals with factitious disorder
individuals with a factitious disorder were vigorously are hesitant to pursue mental health treatment, there
confronted once the nature of their illness was discov- are numerous case reports of successful treatment of
ered. Unfortunately, most individuals would deny their the disorder with long-term psychotherapy. In many
involvement and seek another clinician who was una- of these cases, the therapy lasted several years, in-
ware of their diagnosis. In addition, the idea of “black- cluding one individual who received treatment while
lists” was proposed in order to aid detection of these imprisoned for over 10 years. These case reports sup-
individuals. However, issues regarding an individual’s port the idea that treatment of individuals with facti-
confidentiality as well as concerns about cursory medi- tious disorder is not impossible, and these individuals
cal evaluations that might miss genuine physical ill- can improve. However, expectations must be realistic
ness prevented this idea from being adopted. Although as improvement in the disorder itself can take several
aggressive confrontation is usually unsuccessful, years. Techniques that target short-term reduction in
supportive, nonpunitive confrontation may be help- the production of factitious symptoms can be effective
ful for some. In one case series, 33 individuals were more quickly. See Figure 35-2 for a treatment flowchart
confronted with the factitious nature of their illness. for factitious disorder.
While only 13 admitted feigning illness, most of the Treating individuals with factitious disorder often
individuals’ illnesses subsequently improved, at least raises ethical questions including those regarding con-
in the short term. fidentiality, privacy, and medical decision-making, and
Three alternatives to confrontation have been found it is important to be alert to these issues. Often, indi-
to be effective. First is inexact interpretation, in which viduals with factious disorder will want to keep their
the clinician interprets the psychodynamics thought to diagnosis confidential, even when to do so may harm
be underlying the individual’s behavior without explic- the individual or others. For example, although a con-
itly identifying the factitious behavior. For example, a sulting clinician may diagnose an individual with fac-
consultant suggested to an individual suspected of hav- titious disorder, the individual may refuse consent to
ing factitious disorder who developed septicemia after reveal this information to the referring physician. If the
Factitious
regarding the individual’s privacy also arise with facti-
diagnosis tious individuals. For example, hospital room searches
could often help clarify the diagnosis or remove mate-
rials the individual is using to harm himself, but these
searches also violate the individual’s privacy. Dilem-
Treat comorbid mas surrounding medical decision-making can arise
medical when an individual with factitious disorder refuses
conditions
treatment or requests potentially harmful treatments.
It can often be difficult to resolve these ethical dilem-
mas. In general, even though the factitious individual is
deceptive within the relationship between the clinician
Coordinate health and the individual, the clinician is not released from his
care among all
providers or her responsibilities within that relationship, and the
individual retains his or her rights of confidentiality,
privacy, and autonomy. As with all such individuals,
emergency situations require different ethical guide-
Avoid unnecessary lines. Often, an ethics consultation can be very helpful
procedures in sorting through the difficult issues of care of the in-
dividual in the setting of factitious disorder.
Owing to the high morbidity and mortality, treat-
ment of Factitious Disorder By Proxy requires at least
Consider temporary separation from the parent and notification
Nonpunitive confrontation of local child protective agencies. The perpetrators
Inexact interpretation often face criminal charges of child abuse. There is
Therapeutic double blind
high psychiatric morbidity in the children—many go
Face-saving techniques
on to develop factitious disorder or other psychiatric
illnesses themselves. Psychiatric intervention is neces-
sary to ameliorate this morbidity as much as possible
Encourage psychiatric in these children. In this disorder, there are some case
treatment reports of successful psychotherapeutic treatments of
the parents.
Figure 35-2 Treatment flowchart for factitious disorder.
COMPARISON OF DSM-IV AND ICD-10

consultant does inform the referring physician, she has
DIAGNOSTIC CRITERIA
violated the individual’s confidentiality, but if she does
not, the referring physician is likely to continue to treat The ICD-10 Diagnostic Criteria for Research and the
the individual for the incorrect diagnosis. Dilemmas DSM-IV-TR criteria sets are almost identical.
CHAPTER
36 Dissociative Disorders
Dissociative phenomena are best understood through three primary characteristics: first, the memory loss
the term désagrégation (disaggregation) originally is episodic, with first-person recollection of certain
given by Janet in 1920. Events normally experienced as events, rather than knowledge of procedures, being
connected to one another on a smooth continuum are lost. Second, the memory loss is for one or more dis-
isolated from the other mental processes with which crete time periods, ranging from minutes to years. It
they would ordinarily be associated. The dissocia- is not vagueness or inefficient retrieval of memories
tive disorders are a disturbance in the organization of but rather a dense unavailability of memories that were
identity, memory, perception, or consciousness. When encoded and stored. Unlike the situation in amnestic
memories are separated from access to consciousness, disorders, for example, resulting from damage to the
the disorder is dissociative amnesia. Fragmentation of medial temporal lobe in surgery there is usually no
identity results in dissociative fugue or dissociative difficulty in learning new episodic information. Thus,
identity disorder (DID; formerly multiple personality the amnesia of dissociative disorders is typically retro-
disorder). Disintegrated perception is characteris- grade rather than anterograde. Third, the memory loss
tic of depersonalization disorder. Dissociation of as- is usually for events of a traumatic or stressful nature.
pects of consciousness produces acute stress disorder Although the majority of cases involved child abuse
and various dissociative trance and possession states. (60%) in one study, disavowed behaviors such as mari-
Numbing and amnesia are diagnostic components of tal problems, sexual activity, suicide attempts, crimi-
posttraumatic stress disorder (PTSD), both of which nal activity, and the death of a relative have also been
are described in Chapter 32. These dissociative and re- reported as precipitants.
lated disorders are more a disturbance in the organiza- Dissociative amnesia most frequently occurs af-
tion or structure of mental contents than in the contents ter an episode of trauma, and its onset may be grad-
themselves. Memories in dissociative amnesia are not ual or sudden. It occurs most often in the third and
so much distorted or bizarre as they are segregated from fourth decades of life. Although it usually involves
one another. The identities lost in dissociative fugue or one episode, multiple periods of lost memory are not
fragmented in DID are two-dimensional aspects of an uncommon.
overall personality structure. In this sense, individuals Individuals with dissociative amnesia may not ini-
with DID suffer not from having more than one per- tially be aware of the memory loss; that is, they do not
sonality but rather from having less than one personal- remember that they do not remember. They often report
ity. The problem involves information processing: the being told that they have done or said things that they
failure of integration of elements rather than the con- cannot remember. Some individuals do suffer from
tents of the fragments. episodes of selective amnesia, usually for specific trau-
matic incidents, which may be interwoven with periods
of intact memory. In these cases, the amnesia is for a
Dissociative Amnesia
type of material remembered rather than for a discrete
time period.
DIAGNOSIS
Although information is kept out of consciousness in
This is the classical functional disorder of episodic dissociative amnesia, it may well exert an influence on
memory. It does not involve procedural memory consciousness: out of sight does not mean out of mind.
or problems in memory storage, as in Wernicke– For example, a rape victim with no conscious recollec-
Korsakoff syndrome. Furthermore, unlike dement- tion of an assault nonetheless behaves like someone
ing illnesses, dissociative amnesia is reversible, for who has been sexually victimized. Such individuals
example, by using hypnosis or narcoanalysis. It has often suffer detachment and demoralization, are unable
to enjoy intimate relationships, and show hyperarousal The screen can be employed to facilitate cognitive re-
to stimuli reminiscent of the trauma. structuring of the traumatic memory, for example, by
Individuals with dissociative amnesia generally do picturing on the left side of the screen some component
not suffer disturbances of identity, except to the ex- of the traumatic experience, and on the right side some-
tent that their identity is influenced by the warded-off thing they did to protect themselves or someone else
memory. It is not uncommon for such individuals to during it. This makes the memory both more complex
develop depressive symptoms as well, especially when and more bearable.
the amnesia occurs in the wake of a traumatic stres- A particularly useful feature of this technique is
sor. Comorbidity with conversion disorder, bulimia that it allows for the recollection of traumatic events
nervosa, and alcohol abuse are also common, and Axis without triggering an uncontrolled reliving of the
II diagnoses of histrionic, dependent, or borderline trauma, as is the case of traumatic flashbacks. The
personality disorders occur in a substantial minority of screen technique provides a “controlled dissocia-
such individuals. tion” between the psychological and somatic aspects
of memory retrieval. Individuals can be put into self-
hypnosis and instructed to get their body into a state
TREATMENT
of floating comfort and safety. They can do this by
Often, individuals suffering from dissociative amne- imagining that they are somewhere safe and comfort-
sia experience spontaneous recovery when they are able: “Imagine that you are floating in a bath, a lake, a
removed from the stressful or threatening situation, hot tub, or just floating in space.” They are reminded
when they feel safe, and/or when exposed to personal that no matter what they see on the screen their bod-
cues from their past (i.e., home, pets, family members). ies are safe and comfortable: “Do the work on your
For cases in which exposure to a safe environment is imaginary screen, not in your body.” In this way, the
not enough to restore normal memory functioning, tendency for physiological arousal to accompany and
pharmacologically facilitated interviews may prove intensify the working through of traumatic memories
useful. can be controlled, facilitating the psychotherapeutic
Most individuals with dissociative disorders are work.
highly hypnotizable on formal testing and are therefore The psychotherapy of dissociative amnesia involves
easily able to make use of hypnotic techniques such as accessing the dissociated memories, working through
age regression. Hypnosis can enable such individuals affectively loaded aspects of these memories, and sup-
to reorient temporally and therefore achieve access to porting the individual through the process of integrat-
otherwise dissociated and unavailable memories. ing these memories into consciousness.
If there is traumatic content to the warded-off mem-
ory, individuals may abreact, that is, express strong
Dissociative Fugue
emotion as these memories are elicited. Such abreac-
tions are rarely damaging in themselves but are not in-
DIAGNOSIS
trinsically therapeutic either. They may be experienced
by the individual as a reinflicting of the traumatic stres- Dissociative fugue combines failure of integration of
sor. Such individuals need psychotherapeutic help in certain aspects of personal memory with loss of cus-
integrating these warded-off memories and the associ- tomary identity and automatisms of motor behavior. It
ated affect into consciousness, thereby gaining a sense involves one or more episodes of sudden, unexpected,
of mastery over them. purposeful travel away from home, coupled with an
One technique that can help bring such memories into inability to recall portions or all of one’s past, and a
consciousness while modulating the affective response loss of identity or the assumption of a new identity. The
to them is a projective technique known as “the screen onset is usually sudden, and it frequently occurs after
technique.” While using hypnosis, such individuals a traumatic experience or bereavement. A single epi-
are taught to recall the traumatic event as if they were sode is not uncommon, and spontaneous remission of
watching it on an imaginary movie or television screen. symptoms can occur without treatment. It was origi-
This technique is often helpful for individuals who are nally thought that the assumption of a new identity was
unable to remember the event as if it were occurring in typical of dissociative fugue. However, in the majority
the present, either because for some highly hypnotiz- of cases there is loss of personal identity but no clear
able individuals that approach is too emotionally tax- assumption of a new identity.
ing or because others are not sufficiently hypnotizable Many cases of dissociative fugue remit spontane-
to be able to engage in such hypnotic age regression. ously. Again, hypnosis can be useful in accessing
Chapter 36 • Dissociative Disorders 375
dissociated material. Not infrequently, fugue episodes nosis is used, individuals are trained on self-hypnotic
represent dissociated but purposeful activity. techniques, promoting the use of hypnosis instead of
spontaneous dissociation. This enhances the individu-
als’ level of control while enhancing a sense of mastery
TREATMENT
and self-control.
Hypnosis can be helpful in treating dissociative fugue
by accessing otherwise unavailable components of
Depersonalization Disorder
memory and identity. The approach used is similar to
that for dissociative amnesia. Hypnotic age regression
DIAGNOSIS
can be used as the framework for accessing informa-
tion available at a previous time. Demonstrating to This dissociative disorder involves lack of integration
individuals that such information can be made avail- of one or more components of perception. The essen-
able to consciousness enhances their sense of control tial feature of depersonalization disorder is the occur-
over this material and facilitates therapeutic working rence of persistent feelings of unreality, detachment, or
through of emotionally laden aspects of it. estrangement from oneself or one’s body, usually with
Once reorientation is established and the overt iden- the feeling that one is an outside observer of one’s own
tity and memory loss of the fugue have been resolved, mental processes. Individuals suffering depersonaliza-
it is important to work through interpersonal or intra- tion are distressed by it. They are aware of some dis-
psychic issues that underlie the dissociative defenses. tortion in their perceptual experience and therefore are
Such individuals are often relatively unaware of their not hallucinating or delusional. Affected individuals
reactions to stress because they can so effectively dis- often fear that they are “going crazy.” The symptom is
sociate them. Thus, effective psychotherapy is antici- not infrequently transient.
patory, helping individuals to recognize and modify Derealization, in which affected individuals notice
their tendency to set aside their own feelings in favor an altered perception of their surroundings, resulting
of those of others. Individuals with dissociative fugue in the world seeming unreal or dream-like, frequently
may be helped with a psychotherapeutic approach occurs as well. Such individuals often ruminate anx-
that facilitates conscious integration of dissociated iously about this symptom and are preoccupied with
memories and motivations for behavior previously ex- their own somatic and mental functioning.
perienced as automatic and unwilled. It is often help- Depersonalization frequently co-occurs with a va-
ful to address current psychosocial stressors, such as riety of other symptoms, especially anxiety, panic, or
marital conflict, with the involved individuals. To the phobic symptoms. It is often a symptom of PTSD and
extent that current psychosocial stress triggers fugue, also occurs as a symptom of alcohol and drug abuse, as
resolution of that stress can help resolve it and reduce
the likelihood of recurrence. Highly hypnotizable in-
dividuals prone to these extreme dissociative symp-
toms often have great difficulty in asserting their own DSM-IV-TR Diagnostic Criteria
point of view in a personal relationship. Rather, they 300.6 DEPERSONALIZATION DISORDER
interact with others as though they were undergoing
a spontaneous trance experience. One such individual A. Persistent or recurrent experiences of feeling detached
from, and as if one is an outside observer of, one’s
described herself as a “disciple in search of a teacher.” mental processes or body (e.g., feeling like one is in
Psychotherapy can help such individuals recognize a dream).
and modify their tendency to unthinking compliance B. During the depersonalization experience, reality test-
ing remains intact.
with others, and extreme sensitivity to rejection and C. The depersonalization causes clinically significant dis-
disapproval. tress or impairment in social, occupational, or other
In the past, medication-facilitated interviews were important areas of functioning.
D. The depersonalization experience does not occur ex-
used to reverse dissociative amnesia or fugue. How- clusively during the course of another mental disorder,
ever, such techniques offer no advantage over hypno- such as schizophrenia, panic disorder, acute stress dis-
sis and are not especially effective. Not infrequently, order, or another dissociative disorder, and is not due
to the direct physiological effects of a substance (e.g.,
the ceremony of injecting the drug elicits spontaneous a drug of abuse, a medication) or a general medical
hypnotic phenomena before the pharmacological effect condition (e.g., temporal lobe epilepsy).
is felt, and sedation, respiratory depression, and other Reprinted with permission from the Diagnostic and Statistical
side effects can be troublesome. It also promotes de- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
pendency on the therapist. On the contrary, when hyp-
a side effect of the use of prescription medication, and or phobic disorders or of antipsychotic medications for
during stress and sensory deprivation. The symptom of psychotic disorders is often beneficial in conditions in
depersonalization is also commonly seen in the course which there is contributory comorbidity.
of a number of other neurological and psychiatric dis-
orders. It is considered a disorder when it is a persistent
Dissociative Identity Disorder (Multiple
and predominant symptom. The phenomenology of the
Personality Disorder)
disorder involves both the initial symptoms themselves
and the reactive anxiety caused by them.
DIAGNOSIS
Dissociative identity disorder (DID) is a rare but real
TREATMENT
disorder that is the most widely discussed of the dis-
Depersonalization is most often transient and may re- sociative disorders. It involves the presence of two
mit without formal treatment. Recurrent or persistent or more distinct identities or personality states (each
depersonalization should be thought of both as a symp- with its own relatively enduring pattern of perceiv-
tom in itself and as a component of other syndromes ing, relating to, and thinking about the environment
requiring treatment, such as anxiety disorders and and self). The diagnostic criteria also require that “At
schizophrenia. least two of these identities or personality states re-
The symptom itself may respond to training in self- currently take control of the person’s behavior” and
hypnosis. Paradoxically, induction or deliberate wors- that there be amnesia (i.e., “Inability to recall impor-
ening of symptoms may provide relief by teaching a tant personal information that is too extensive to be
method of controlling them. For example, a hypnotic explained by ordinary forgetfulness”). It is a failure of
induction may induce transient depersonalization integration of various aspects of identity and person-
symptoms, such as a sense of detachment from part of ality structure. Often different relationship styles (de-
the body, in such individuals. This is a useful exercise, pendent versus assertive/aggressive) and mood states
in that by having a structure for inducing the symp- (depressed versus hostile) segregate with different
toms, one provides the individual with a context for un- identities and personal memories. Such individuals
derstanding and controlling them. They are presented may be mystified by events that occurred in another
as a spontaneous form of hypnotic dissociation that can “state,” or by responses of others to them for behavior
be modified. Such individuals can be taught to induce a that occurred in a different “state.” This fragmenta-
pleasant sense of floating lightness or heaviness in place tion of personality often occurs in response to trauma
of the anxiety-related somatic detachment. The use of in childhood, and is perceived by the individual as
an imaginary screen to picture problems in a way that protective, allowing him or her to tolerate and par-
detaches them from the typical somatic response is also
helpful. Other relaxation techniques such as systematic
desensitization, progressive muscle relaxation, and bio-
feedback may also be of help. Psychotherapy aimed at DSM-IV-TR Diagnostic Criteria
working through emotional responses to any traumatic 308.14 DISSOCIATIVE IDENTITY DISORDER
or other stressors that tend to elicit the depersonaliza-
tion is also helpful. A. The presence of two or more distinct identities or per-
sonality states (each with its own relatively enduring
Pharmacological approaches involve balancing pattern of perceiving, relating to, and thinking about
therapeutic benefit and risk. Antianxiety medications the environment and self).
are most commonly used and may be helpful in reduc- B. At least two of these identities or personality states re-
currently take control of the person’s behavior.
ing the amplification of depersonalization caused by C. Inability to recall important personal information
anxiety. However, depersonalization and derealiza- that is too extensive to be explained by ordinary
tion are also side effects of antianxiety drugs, so their forgetfulness.
D. The disturbance is not due to the direct physiological
use should be carefully monitored. Increasing dosage, effects of a substance (e.g., blackouts or chaotic be-
a standard technique when there is lack of therapeu- havior during alcohol intoxication) or a general medi-
tic response, may also increase symptoms, leading to cal condition (e.g., complex partial seizures).
a spiral of increasing symptoms and drug dosage but Note: In children, the symptoms are not attributable to
without therapeutic benefit. imaginary playmates or other fantasy play.
However, appropriate pharmacological treatment for Reprinted with permission from the Diagnostic and Statistical
comorbid disorders is an important part of treatment. Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
Use of antianxiety medications for generalized anxiety
tially evade chronic abuse. These individuals thus diagnostic criteria starting with DSM-III, and (3) re-
view treatment ambivalently as an attempt to deprive duced misdiagnosis of DID as schizophrenia or border-
them of a defense against attack. They also tend to see line personality disorder.
others as irrational and unfair, since response to one Other authors attribute the increase in reported cases
aspect of their personality frequently reflects experi- to social contagion, hypnotic suggestion, and misdiag-
ence with other aspects. One DID individual (prior to nosis. Proponents of this point of view argue that these
diagnosis) reported puzzlement about accusations by individuals are highly hypnotizable and therefore quite
friends and acquaintances that she had made hostile suggestible. They would therefore be especially vulner-
comments for which she had no memory. She would able to direct or implicit hypnotic suggestion. They note
find people angry at her for no reason. Thus, their that not infrequently a few specialist clinicians make
personality fragmentation renders them vulnerable to the vast majority of diagnoses. However, it has been
interpersonal problems, yet gives them the belief that observed that the symptoms of individuals diagnosed
they are relatively protected from them. by specialists in dissociation do not differ from those of
The diagnosis can be facilitated by psychological individuals diagnosed by psychiatrists, psychologists,
testing. Scales of trait dissociation have been devel- and physicians in more general practice who diagnose
oped, and individuals with DID score extremely high one or two cases a year. Nonetheless, because these in-
on these scales, in contrast to normal populations and dividuals are indeed highly hypnotizable and therefore
other groups of individuals. Those with DID score far suggestible, care must be taken in the manner in which
higher than normal individuals on standard measures the illness is presented to them.
of hypnotizability, whereas schizophrenic individuals The major comorbid mental disorders are the de-
tend to have lower than normal scores or the absence of pressive disorders, substance use disorders, and bor-
high hypnotizability. Thus, there is comparatively lit- derline personality disorder. Sexual, eating, and sleep
tle overlap in the hypnotizability scores of individuals disorders co-occur less commonly. Such individuals
with schizophrenia and those with DID. frequently display self-mutilative behavior, impulsive-
DID is more frequently recognized during childhood ness, and overvaluing and devaluing of relationships.
but typically emerges between adolescence and the Indeed, approximately a third of individuals with DID
third decade of life; it rarely presents as a new disorder have symptoms that fit criteria for borderline person-
after age 40 years, but there is often considerable delay ality disorder as well. Such individuals are also more
between initial symptom presentation and diagnosis. frequently depressed. Conversely, research shows dis-
Untreated, it is a chronic and recurrent disorder. It sociative symptoms in many individuals with border-
rarely remits spontaneously, but the symptoms may line personality disorder, especially those who report
not be evident for certain time periods. DID has been histories of physical and sexual abuse. Indeed, the
called a disease of hiddenness. The dissociation it- impulsiveness, splitting, hostility, and fear of abandon-
self hampers self-monitoring and accurate reporting ment, frequently seen in certain personality states, are
of symptoms and history. Many individuals with the similar to the presentation of many individuals with
disorder are not fully aware of the extent of their dis- borderline personality disorder. Many such individuals
sociative symptoms. They may be reluctant to bring up also have symptoms that meet criteria for PTSD, with
symptoms because of confusion or shame about the ill- intrusive flashbacks, recurrent dreams of physical and
ness or because they encountered previous skepticism. sexual abuse, avoidance of and loss of pleasure in usu-
Furthermore, because the majority of individuals really pleasurable activities, and symptoms of hyperar-
port histories of sexual and physical abuse, the shame ousal, especially when exposed to reminders of child-
associated with that and fear of retribution may inhibit hood trauma.
reporting of symptoms as well. Thus, comorbidity is a complex issue. In addition,
There are no convincing studies of the absolute these individuals are not infrequently misdiagnosed as
prevalence of DID, although there is widespread agree- having schizophrenia. This diagnostic confusion is un-
ment that the number of diagnosed cases has increased derstandable in that they have an apparent delusion that
considerably in the United States and some European their bodies are occupied by more than one person. In
countries in the past two decades. Two studies have addition, they frequently have auditory hallucinations
estimated the prevalence as approximately 1% of psy- when one personality state speaks to or comments
chiatric inpatients. Factors that may account for the in- on the activities of another. When misdiagnosed as
crease in the number of true reported cases include (1) schizophrenic, individuals with DID are frequently
more general awareness of the diagnosis among men- given neuroleptics, which results in a poor therapeutic
tal health professionals, (2) the availability of specific response and a flattening of affect that tends to confirm
the misdiagnosis (since flat affect is characteristic of This then becomes a means of teaching such an indi-
schizophrenia). vidual how to control the dissociative process.
Alternatively, entering the state of hypnosis may
make it possible simply to address and elicit differ-
TREATMENT ent identities or personality states. Individuals can be
taught a simple self-hypnosis exercise for this purpose.
Psychosocial Treatment
For example, the individual can be told to count to her-
It is possible to help individuals with DID gain con- self or himself from one to three. After some formal
trol over the dissociative process underlying their exercises such as this, it is often possible to ask the in-
symptoms in several ways. The fundamental psycho- dividual to speak with a given alter personality, without
therapeutic stance should involve meeting persons the formal use of hypnosis. Merely asking to talk with a
undergoing treatment halfway, a form of structured given identity usually suffices after a while.
empathy in which their experience of themselves as Because the loss of memory in DID is complex
fragmented is acknowledged while the reality that the and chronic, its retrieval is likewise a more extended
fundamental problem is a failure of integration of dis- and integral part of the psychotherapeutic process.
parate memories and aspects of the self is kept in view. The therapy becomes an integrating experience of
In this sense, such individuals suffer from having less information sharing among disparate personality ele-
than one personality rather than more than one. There- ments. Conceptualizing DID as a chronic PTSD, the
fore, the goal in therapy is to facilitate integration of psychotherapeutic strategy involves a focus on working
disparate elements. This can be done in a variety of through traumatic memories in addition to controlling
ways. the dissociation.
Secrets are frequently a problem with such individu- Controlled access to memories greatly facilitates
als, who attempt to use the clinician to reinforce a dis- psychotherapy. As with dissociative amnesia, a vari-
sociative strategy of withholding relevant information ety of strategies can be employed to help individuals
from certain personality states. Such individuals often with DID break down amnesic barriers. Eliciting vari-
like to confide in the clinician with the idea that the ous identities or personality states can facilitate access
information is to be kept from other parts of the self, to memories previously unavailable to consciousness.
for example, traumatic memories or plans for self- While so-called pseudomemories can occur, previously
destructive activities. dissociated traumatic memories are often accurate.
Clear limit setting and commitment on the part of Once these memories of earlier traumatic experience
the clinician to helping all portions of the individual’s have been brought into consciousness, it is crucial to
personality structure learn about warded-off informa- help the individual work through the painful affect,
tion are important. It is wise to clarify explicitly that the inappropriate self-blame, and other reactions to these
clinician will not become involved in secret collusion. memories. It may be useful to have individuals visual-
Furthermore, when important agreements are negoti- ize the memories rather than relive them as a means
ated, such as commitments on the part of individuals to of making their intensity more manageable. It can also
seek medical help before acting on a thought to harm be useful to have individuals divide the memories, for
themselves or others, it is useful to discuss with the in- example, picturing on one side of an imaginary screen
dividuals that this is an “all-points bulletin,” requiring something an abuser did to them and on the other side
attention from all the relevant personality states. The how they tried to protect themselves from the abuse.
excuse that certain personality states were “not aware” Such techniques can help make the traumatic memo-
of the agreement should not be accepted. ries more bearable by placing them in a broader per-
Hypnosis can be helpful in facilitating psychother- spective, one in which trauma victims can also identify
apy as well as establishing the diagnosis. First of all, adaptive aspects of their response to the trauma.
the simple structure of hypnotic induction may elicit This and similar approaches can help these individu-
dissociative phenomena. Hypnosis can be particularly als work through traumatic memories, enabling them
helpful in facilitating access to dissociated personali- to bear them in consciousness and therefore reducing
ties. They may simply occur spontaneously during hyp- the need for dissociation as a means of keeping such
notic induction. An alternative strategy is to hypnotize memories and associated painful affect out of con-
the individual and use age regression to reorient to a sciousness. Although these techniques can be helpful
time when a different personality state was manifest. and often result in reduced fragmentation and integra-
An instruction later to change times back to the present tion, a number of complications can occur in the psy-
usually elicits a return to the other personality state. chotherapy of these individuals.
The therapeutic process can be thought of as a kind uncaring family figure who knew that abuse was oc-
of grief work in which information retrieved from curring but did little or nothing to stop it. It is important
memory is reviewed, traumatic memories are put into in managing the therapy to keep these issues in mind
perspective, and emotional expression is encouraged and make them frequent topics of discussion. This can
and worked through, thereby making it more possible diffuse, if not eliminate, such traumatic transference
to endure and disseminate the information as widely as distortions of the therapeutic relationship.
possible among various parts of the individual’s per- The ultimate goal of psychotherapy is integration of
sonality structure. Instructions to other alter personali- the individual’s multiple ego states. It is often the case
ties to listen while a given one is talking and reviewing that one or more of the personality states may exert
previously dissociated material can be helpful. considerable resistance to the process of integration,
The psychotherapy of DID can be a time-consuming particularly early in the process of therapy. Also, in-
and emotionally taxing process. The rule of thirds is a dividuals may experience efforts of integration as an
helpful guideline. Spend the first third of the psycho- attempt on the part of the therapist to “kill” personali-
therapy session assessing the individual’s current men- ties. These fears must be worked through and the in-
tal state and life problems and defining a problem area dividual needs to understand that the goal is to learn
that might benefit from retrieval into conscious mem- how to control the episodes of dissociation. This gives
ory and working through. Spend the second third of the individuals a sense of gradually being able to control
session accessing and working through this memory. their dissociative processes in order to work through
Allow a final third for helping the individual assimilate the traumatic memories. In order to enhance mastery
the information, regulate and modulate emotional re- and control, the process of the psychotherapy must help
sponses, and discuss any responses to the clinician and individuals minimize rather than reinforce the content
plans for the immediate future. The clinician may re- of traumatic memories, which often involves reexperi-
sist doing this because the intense abreactive materials encing a sense of helplessness in a symbolic reenact-
are often so compelling and interesting. The individual ment of the trauma.
may also resist sharing information across personali- At the same time, the dissociative defense repre-
ties. Nonetheless, the clinician can be helpful in impos- sents an internalization of the abusive people in the
ing structure on often chaotic memories and identity individual’s past, a kind of identification with the ag-
states. gressor, which makes the individual feel powerful
Given the intensity of the material that often emerges rather than helpless. Setting aside the defense also
involving memories of sexual and physical abuse and means acknowledging and bearing the helplessness of
sudden shifts in mental state accompanied by amnesia, having been victimized and working through the irra-
the clinician is called on to take a clear and structured tional self-blame that gave such individuals a fantasy
role in managing the psychotherapy. Appropriate limits of control over events during which they were help-
must be set concerning self-destructive or threatening less. Yet, difficult as it is, ultimately the goal of psy-
behavior, agreements must be made regarding physi- chotherapy is mastery over the dissociative process,
cal safety and treatment compliance, and other matters controlled access to dissociative states, integration
must be presented to the individual in such a way that of warded-off painful memories and material, and a
dissociative ignorance is not an acceptable explanation more integrated continuum of identity, memory, and
for failure to live up to the agreements. consciousness. The stages of therapy are presented in
Transference applies with special meaning to indi- Table 36-1.
viduals who have been physically and sexually abused,
especially in childhood. They have experienced indi-
Somatic Treatment
viduals who are presumed to be caretakers acting in-
stead in an exploitative and sometimes sadistic fash- As with other dissociative disorders, there is little evi-
ion. They thus expect similar betrayal from mental dence that psychoactive drugs are of great help in re-
health clinicians. Although their reality testing is good versing dissociative symptoms. In the past, short-acting
enough that they can perceive genuine caring, they barbiturates such as sodium amobarbital were used in-
often unconsciously expect mental health professionals travenously to reverse functional amnesia, but this tech-
to exploit them. They may experience working through nique is no longer employed, largely because of poor
of traumatic memories as a reinflicting of the trauma, results. Research data provide no evidence suggesting
with the clinician taking sadistic pleasure in their suf- that any medication regimen has any significant thera-
fering. They may expect excessive passivity on the part peutic effect on the dissociative process manifested by
of the clinician, identifying the clinician with some DID individuals. To date, pharmacological treatment
Table 36-1 Stages of Therapy

as the impulsiveness associated with personality disor-
ders and brain injury. Also, despite their effectiveness,
Stage Technique
these agents produce less amnestic side effects than the
Establishing treatment Education, atmosphere of benzodiazepines and thus may be preferred. On the
safety, instill confidence other hand, the need for closer monitoring due to po-
Preliminary interventions Confirm diagnosis, set
limits, access dissociation tential toxicity, particularly in overdoses, makes their
with hypnosis use less desirable than the newer SSRIs.
History gathering Explore components of Of all pharmacological agents available, antipsy-
dissociative structure
Working through trauma Grief work chotics may be the least desirable. First, they are rarely
Move toward integration Enhance communication useful in reducing dissociative symptoms. In fact, there
across dissociative states have been reports of increased levels of dissociation
Integration–resolution Encourage development of
integrated self and an increased incidence of side effects when used in
Learning coping skills Help with life decisions and individuals suffering from dissociative disorders.
relationships
Solidification of gains Transference examination
Follow-up Maintenance Dissociative Trance Disorder
Source: Kluft RP (1991) Multiple personality disorder. In American
Psychiatric Press Review of Psychiatry, Vol. 10, Tasman A and
Goldfinger SM (eds). Copyright, American Psychiatric Press, DIAGNOSIS
Washington, DC.
Dissociative-like phenomena have been described in
virtually every culture. Yet they appear to be more
has been limited to symptom control or the manage- prevalent in the less-heavily industrialized Second
ment of comorbid conditions (e.g., depression). and Third World countries. Studies on the prevalence
Of all available classes of psychotropic agents, anti- of dissociative disorders in India have suggested that
depressants are the most useful class for the treatment the 1-year prevalence of dissociative trance disorder is
of individuals with DID. That is because individu- approximately 3.5% of all psychiatric hospitalizations,
als suffering from dissociation frequently experience making it a highly frequent mental disorder. Trance
comorbid dysthymic or major depressive disorder. and possession syndromes are by far the most common
Selective serotonin reuptake inhibitors (SSRIs) are type of dissociative disorders seen around the world.
particularly useful, given their high level of effective- On the other hand, DID, which is relatively more com-
ness, low side effect profile, and even lower danger in mon in the United States, is virtually never diagnosed
overdose, compared to tricyclic antidepressants and in underdeveloped countries. This difference in preva-
monoamine oxidase inhibitors. Nevertheless, medica- lence and distribution of dissociative disorder across
tion compliance may be a problem with dissociative different populations may be mediated by cultural,
individuals because dissociated personality states may as well as biological factors. For example, Eastern
interfere with medication taking or may take the medi- culture is far more sociocentric than Western culture.
cation in an overdose attempt. Thus, being “possessed” by an outside entity would be
Benzodiazepines have mostly been used to facili- more culturally comprehensible and acceptable in the
tate recall by controlling secondary anxiety associated East. On the other hand, an apparent proliferation of
with retrieval of traumatic memories (i.e., medication- individual identities would fit better with the Western
facilitated interviews). Nevertheless, despite their preoccupation with individualism. Nonetheless, the
short-term usefulness, CNS-depressant agents may underlying dissociative mechanism inhibiting integra-
cause sudden mental state transitions, which may in tion of perception, memory, and identity may suggest a
turn increase rather than decrease amnesic barriers. common underlying mechanism among these dissocia-
Therefore, as useful as they could be on a short-term tive syndromes.
basis (i.e., acute management of a panic attack), the Trance and possession episodes are usually under-
long-term use of these agents may, in fact, contribute stood as an idiom of distress and yet they are not viewed
to rather than treat dissociative episodes. as normal. That is, they are not a generally accepted
There are several uses for anticonvulsant agents. Sei- part of cultural and religious practice, which often does
zures disorders have a high rate of comorbidity with involve normal trance phenomena, such as trance danc-
DID. Thus, anticonvulsant agents may help control the ing in the Balinese Hindu culture. Trance dancers en-
dissociation associated with epileptogenic activity. On joy the remarkable privilege of being the only portion
the other hand, anticonvulsant agents have proven to be of this socially rigid society able to elevate their social
effective in the management of mood disorders, as well status. The way they are able to do that is by developing
the ability to enter trance states. During these altered possession trance victims often exhibit rather complex
states of consciousness, which usually occur within behavior. During these episodes, subjects may, for ex-
the context of a socially acceptable ceremony setting, ample, express otherwise forbidden thoughts or needs,
they dance over hot coals, hold a sword at their throat, engage in unusual and uncharacteristic aggressive be-
or in other ways exhibit supernormal powers of con- havior (e.g., verbal or physical expressions of aggres-
centration and physical prowess. The mechanism me- sion), or may attempt to negotiate for change in family
diating these phenomena is not fully understood, but or social status. Also, in contrast to dissociative trance
there is evidence of elevations in plasma noradrenaline, episodes, possession trance episodes are often followed
dopamine, and beta-endorphin among Balinese trance by dense amnesia for a large portion of the episode dur-
dancers during trance states. This form of trance is ing which the spirit identity was in control of the sub-
considered socially normal and even exalted. ject’s behavior.
By contrast, disordered trance and possession trance
are viewed by the local community as an aberrant form
of behavior that requires intervention. Such symptoms TREATMENT
often arise in the context of family or social distress,
Treatment of these disorders varies from culture to
for example, discomfort in a new family environment.
culture. Rubbing the body with special potions, ne-
Thus, cultural informants make it clear that people with
gotiating to change the affected person’s social cir-
dissociative trance disorder are abnormal.
cumstances, and physical restraint are often used.
Dissociative trance disorder has been divided into
Ceremonies to remove or appease the invading spirit
two broad categories, dissociative trance and posses-
are also employed.
sion trance. Dissociative trance phenomena are char-
acterized by a sudden alteration in consciousness, not
accompanied by distinct alternative identities. In this
form, the dissociative symptom involves an alteration
DIAGNOSTIC CRITERIA
in consciousness rather than identity. Also, in dis-
sociative trance, the activities performed are rather The ICD-10 Diagnostic Criteria for Research for dis-
simple, usually involving sudden collapse, immobi- sociative amnesia specify that there be a “convincing
lization, dizziness, shrieking, screaming, or crying. association in time between the onset of symptoms of
Memory is rarely affected, and if there is amnesia, it the disorder and stressful events, problems, or needs.”
is fragmented. In DSM-IV-TR, the criteria set notes that the forgot-
Dissociative trance phenomena frequently involve ten information is usually of a stressful or traumatic
sudden, extreme changes in sensory and motor control. nature.
A classic example is the ataque de nervios, prevalent in For dissociative fugue, in contrast to DSM-IV-TR,
Latin-American countries. For example, this phenom- the ICD-10 Diagnostic Criteria for Research specify
enon is estimated to have a 12% lifetime prevalence “amnesia for the journey.” Furthermore, in contrast to
rate in Puerto Rico. A typical episode involves a sud- DSM-IV-TR, the ICD-10 Diagnostic Criteria for Re-
den feeling of anxiety, followed by total body shakes, search do not indicate that there be an inability to recall
which may mimic convulsions. This is then followed one’s past during the fugue or that there be confusion
by hyperventilation, unintelligible screaming, agita- about personal identity.
tion, and often violent bodily movements. Often, this is Dissociative identity disorder is included in ICD-10
followed by collapse and probably transient loss of con- as an example of an “other dissociative (conversion)
sciousness. After the episode is over, subjects complain disorder” under the rubric “multiple personality disor-
of fatigue and having been confused, although this be- der.” The ICD-10 Diagnostic Criteria for Research and
havior is dramatically different from classic postictal the DSM-IV-TR criteria are almost identical.
states. Some subjects may experience amnesia at least Finally, ICD-10 has a single category “depersonali-
to some aspects of the event. zation–derealization syndrome” for presentations char-
In contrast to dissociative trance episodes, possession acterized by either depersonalization or derealization.
trance involves the assumption of a distinct alternative In contrast, the DSM-IV-TR category includes only
identity. The new identity is presumed to be that of a depersonalization and mentions derealization as an
deity, ancestor, or spirit who has transiently taken pos- associated feature. Furthermore, unlike DSM-IV-TR,
session of the subject’s mind and body. Different from which includes this category in the dissociative disor-
dissociative trance episodes, which are characterized ders section, ICD-10 includes the category within the
by rather crude, simplistic, regressive-like behaviors, “other neurotic disorders” grouping.
CHAPTER
37 Sexual Disorders
An adult’s sexuality has seven components—gender a particular dysfunction, for instance male erectile
identity, orientation, intention (what one wants to do disorder, to attempts to estimate the prevalence of a
with a partner’s body and have done with one’s body series of separate dysfunction—for example, desire,
during sexual behavior), desire, arousal, orgasm, and arousal, and orgasmic disorders of women. All such
emotional satisfaction. The first three components con- efforts quickly confront methodological influences of
stitute our sexual identity. The second three comprise sampling, means of obtaining the information, defi-
our sexual function. The seventh, emotional satisfac- nition of each dysfunction, purpose of the study, and
tion, is based on our personal reflections on the first perspective of its authors. These data not surprisingly,
six. The DSM-IV-TR designates impairments of five of therefore, demonstrate a range of prevalence depend-
these components as pathologies. Variations in orienta- ing on the problem studied. Gender identity disorders
tion and the failure to find ordinary sexual experience are relatively rare (⬍1–2%). Lifelong sexual desire
emotionally satisfying, although problems for some, are disorders among women may involve 15% but are less
not designated as disorders (see Figure 37-1 for a diag- frequent among men. Acquired desire disorders among
nostic decision tree covering the sexual disorders). older individuals are probably three times as common.
Perhaps more than half of women at age 55 years have
recognized a deterioration in their sexual function.
Sexual Dysfunctions
Perhaps 25% of women in their twenties have diffi-
culty having orgasm and 33% of men less than age 40
DSM-IV-TR specifies three criteria for each sexual
claim to ejaculate too rapidly. The majority of men by
dysfunction. The first criterion describes the psycho-
age 70 years are likely to be having erection problems.
physiologic impairment—for example, absence of sex-
A careful epidemiologic study from 1994, designed by
ual desire, arousal, or orgasm. The second and third
sociologists, successfully generated a representative
criteria are the same for each impairment: the dysfunc-
sample of the US. They interviewed men and women
tion causes marked distress or interpersonal difficulty
between age 18 and 59 years and found that sexual dys-
and the dysfunction is not better accounted for by an-
function is common, particularly among young women
other Axis I diagnosis or not due exclusively to the di-
and older men. This is noteworthy for psychiatrists
rect physiological effects of a substance (e.g., a drug
because our studies of sexual dysfunction caused by
of abuse, a medication) or a general medical condition.
medications or acquired psychiatric disorders tend to
Table 37-1 lists the first criterion of each of the 12 sex-
assume that individuals are generally functionally in-
ual dysfunction diagnoses. DSM-IV-TR gives the clini-
tact prior to becoming ill or taking medications. This
cian additional latitude for deciding when a person who
assumption is not tenable on the basis of a generation
meets the first criterion qualifies for a disorder. The cli-
of epidemiologic studies.
nician is asked to consider the effects of the individu-
al’s age, experience, ethnicity and cultural background,
the degree of subjective distress, adequacy of sexual
Problems of Sexual Desire
stimulation, and symptom frequency. No instructions
are provided about how to exercise this judgment. In
DIAGNOSIS
this way, DSM-IV-TR makes it clear that understand-
ing sexual life requires more than counting symptoms; Sexual desire manifestations are diverse: erotic fan-
it requires judgment. tasies, sexual dreams, initiation of sexual behavior,
Numerous attempts to describe the prevalence of receptivity to partner-initiated sexual behavior, mas-
sexual dysfunction have been made in the past 25 years. turbation, genital sensations, heightened responsivity
These range from attempts to define the frequency of to erotic environmental cues, and sincere statements
Chapter 37 • Sexual Disorders 383
SEXUAL DISORDERS
Lack of emotional satisfaction from Sexual identify

Sexual dysfunctional symptoms
sexual behavior difficulties
Psychogenic etiology Organic etiology Sexual disorder See sexual See sexual
not otherwise specified identity difficulties dysfunctions
1. Sexual desire disorders 1. Substance abuse
a. Hypoactive sexual sexual dysfunction (may
desire disorder involve any of the
b. Sexual aversion symptoms under
disorder psychogenic etiology)
2. Arousal disorders 2. Sexual dysfunction Gender identity Homosexualities−−not Unusual intentions
a. Female arousal due to a general medical struggles typically given a 1. Paraphilias that
disorder condition 1. Gender identity psychiatric diagnosis, are sexual crimes
b. Male erectile disorder 3. Sexual dysfunction due disorder of childhood, but, occasionally are a. Pedophilia
3. Orgasmic disorder to combined factors adolescence, 1. Sexual disorder not b. Voyeurism
a. Female orgasmic (psychogenic and organic) or adulthood otherwise specified c. Exhibitionism
disorder 2. Gender identity d. Rape (sadism)
b. Male disorders disorder not e. Frotteurism
(1) Premature otherwise specified 2. Paraphilias that are
ejaculation not sexual crimes
(2) Male orgasmic a. Masochism
disorder b. Transvestic
4. Sexual pain disorder fetishism
a. Dyspareunia c. Fetishism
b. Vaginismus 3. Paraphilia not
5. Sexual dysfunction otherwise specified
not otherwise specified (confusing, mixed,
or other forms)
Figure 37-1 Diagnostic decision tree for sexual disorders.
Table 37-1 Delineating Criteria of 12 Sexual Dysfunction Diagnoses
Sexual Desire Disorders Sexual Arousal Disorders Orgasmic Disorders Sexual Pain Disorders
Hypoactive sexual desire Female sexual arousal Female orgasmic disorder: Dyspareunia:
disorder: disorder: persistent or recurrent delay recurrent or persistent
persistently or recurrently persistent or recurrent in, or absence of, orgasm genital pain associated
deficient (or absent) inability to attain, after a normal sexual with sexual intercourse in
sexual fantasies and or to maintain until excitement phase either a male or a female
desire for sexual completion of the sexual Male orgasmic disorder: Vaginismus:
activity activity, an adequate persistent or recurrent delay recurrent or persistent
Sexual aversion disorder: lubrication–swelling in, or absence of, orgasm involuntary spasm of the
persistent or recurrent response of sexual after a normal sexual musculature of the outer
extreme aversion to, excitement excitement phase during third of the vagina that
and avoidance of, all Male erectile disorder: sexual activity interferes with sexual
(or almost all) genital persistent or recurrent Premature ejaculation: intercourse
sexual contact with a inability to attain, persistent or recurrent
sexual partner or to maintain until ejaculation with minimal
completion of the sexual sexual stimulation before,
activity, an adequate on, or shortly after
erection penetration and before the
person wishes it
Sexual Dysfunction Due Substance-Induced Sexual Sexual Dysfunction Not
to a General Medical Dysfunction Otherwise Specified
Condition
Any of the above-mentioned A sexual dysfunction that For problems that do not meet
diagnoses must be judged is fully explained by the categories just described
to be exclusively due to substance use in that it
the direct physiological develops within a month
effects of a medical of substance intoxication
condition
Three Interactive Components of Sexual

When the clinician concludes that the individual’s
Table 37-2 acquired generalized HSDD is either due to a medical
Desire
condition, a medication, or a substance of abuse, the
Sexual Drive—Biological Component
Evolves over time, decreasing with increasing age diagnosis is further elaborated to sexual dysfunction
Diminished by many psychotropic and antihypertensive due to general medical condition (for instance, HSDD
medications due to multiple sclerosis). The frequency of the spe-
Manifested by the internally stimulated genital sensations
and thoughts of sexual behavior that occur within a cific etiologies are heavily dependent on the clinical
person’s privacy setting. In oncology settings, medical causes occur
Sexual Motivation—Psychological Component in high frequency; in drug rehabilitation programs,
Highly contextual in terms of relationship status methadone maintenance will be a common cause. In
The most socially and psychologically responsive of the
three components marital therapy clinics, anger and loss of respect for
Evolves over time but not predictably the partner, hidden incompatibility of sexual identity
Manifested by a person’s willingness to bring his or her between the self and the partner because of covert
body to a specific person for sexual behavior
homosexuality or paraphilia, an affair, or childhood
Sexual Wish—Social Component
Expectations for sexual behavior based on membership
sexual abuse will commonly be the basis. In general
in various subcultural groups such as family, religion, mental health settings, medication side effects will
gender, region, and nation often be the top layer of several causes. When a ma-
These expectations begin as cognitions of what is right and
wrong and what a person is entitled to sexually and are jor depression disorder is diagnosed, for instance, the
influenced by what people think others in their cohort are desire disorder is often assumed to be a symptom of
experiencing the depression. This usually is incorrect. The desire
Often clinically difficult to distinguish from motivation,
which wishes influence disorder often preceded the decompensation into
depression.
Sexual aversion should strongly suggest three pos-
about wanting to behave sexually. For most of the twen- sibilities to the clinician: (1) that a remote traumatic ex-
tieth century, these have been referred to as manifes- perience is being relived by the partner’s expression of
tations of libido. Psychiatrists spoke of libido as if it interest in sexual behavior; (2) that without the symp-
was a homogeneous instinctive force. Clinicians will tom the individual feels powerless to say “no” to sexual
find it far more useful to conceptualize that the diverse advances; or (3) that the individual feels guilty about
and changeable desire manifestations are produced by her own sexual behavior with another person.
the intersection of three mental forces: drive (biology), The clinician’s attention should focus on the indi-
motive (psychology), and wish (culture). vidual’s sexual development as a child, adolescent,
The appearance and disappearance of sexual desire and young adult when the aversion is lifelong, whereas
is often enigmatic to an individual, but its ebb and flow when it is acquired, the focus of the history should
result from the ever-changing intensities of its com- be on the period immediately prior to the onset of the
ponents, biological drive, psychological motive, and symptom.
socially acquired concepts, wish (Table 37-2). Desire disorders require the clinician to think both
Two diagnoses are given to men and women whose in terms of development and personal meanings of sex
desires for partner sexual behavior are deficient: hy- to the individuals under their care (Table 37-3). Be-
poactive sexual desire disorder (HSDD) and sexual cause all explanations are speculative, they should at
aversion disorder (SAD). The differences between least make compelling sense of the individuals’ life
the two revolve around the emotional intensity with experiences.
which the individual avoids sexual behavior. When
visceral anxiety, fear, or disgust is routinely felt as
TREATMENT
sexual behavior becomes a possibility, sexual aver-
sion is diagnosed. HSDD is far more frequently Most sexual desire disorders are difficult to quickly
encountered. It is present in at least twice as many overcome. Brief treatment generally should not be
women than men; female to male ratio for aversion undertaken. Serious individual or couple issues fre-
is far higher. Like all sexual dysfunctions, the desire quently underlie these diagnoses. They have to be
diagnoses may be lifelong or may have been acquired afforded time to emerge and to be worked through.
after a period of ordinary fluctuations of sexual However, clinicians need not be pessimistic about
desire. Acquired disorders may be partner specific all of these conditions. For example, helping a cou-
(situational) or may occur with all subsequent part- ple resolve a marital dispute may return them to their
ners (generalized). usual normal sexual desire manifestations. For many
Obstacles to Discovering the Psychological Problems with Arousal

Table 37-3
Contributants to a Sexual Desire Disorder
DIAGNOSIS
Obstacles that Reside in the patient
The patient may not tell the psychiatrist the truth about life Female Sexual Arousal Disorder
circumstances
The patient may have strong defenses against knowing the
truth Female sexual arousal disorder implies that drive and mo-
The patient may be unable to tell the truth in front of the tivation are relatively intact although arousal is difficult.
partner
The patient may not actually know what is occurring in the The disorder is usually an acquired diagnosis. Premeno-
partner’s life, although she or he is reactive to it pausal women who have this disorder focus on the lack of
Obstacles that Reside in the Psychiatrist moisture in the vagina or their failure to be excited by the
The psychiatrist may not realize the psychological factors behaviors that previously reliably brought pleasure. They
that usually cause these problems
The psychiatrist may not believe that developmental have drive and motive and wish, but enigmatically are
influences can organize an adult sexual function such as unable to sustain arousal. Some mental factor arises to
sexual motivation distract them from their excitement during lovemaking.
The psychiatrist may not like to deal with the murky
complexity of nonbiological developmental and Therapy is focused, therefore, on the meaning of what
interpersonal issues when thinking about etiology preoccupies them. This often involves the dynamics of
their current individual or partnered life or the influence
of their past relationships on their present. With therapy,
individuals and couples, therapy assists the couple to the diagnosis often is changed to an HSDD.
more calmly accept the profound implications of con- In peri- and postmenopausal women, arousal problems
tinuing marital discord, infidelity, homosexuality, or are more often focused on the body as a whole rather
other contributing factors. Some treatment failures than just genital moisture deficiencies. Skin insensitivity,
lead to divorce and the creation of a relationship with often a euphemism for decreased pleasure in response
a new partner. There is then no further sign of the de- to oral and manual nipple, breast, and vulvar stimula-
sire problem. Problems rooted in early developmen- tion, is often initially treated as a symptom of “estrogen”
tal experiences are particularly difficult to overcome. deficiency. Early in the menopause, a small minority of
While DSM-IV-TR asks the clinician to make many women have an increase in drive due to changing testo-
distinctions among the desire disorders, no follow-up sterone–estrogen ratios. Yet, they may still subjectively
study has been published in which either the subtypes experience arousal as different than it used to be. Ther-
(lifelong, acquired, situational, and generalized) or apy often focuses on the women’s concerns about estro-
etiologic organizers (relationship deterioration with gen replacement and the consequences of menopause in
and without extramarital affairs, sexual identity in- terms of body image, attractiveness, fears of partner infi-
compatibilities, parental, and medical) are separated delity, loss of health and vigor, and aging.
into good and poor prognosis categories.
Developmental and identity matters are typically Male Erectile Disorder
approached in long-term individual psychotherapy. In
these sessions, women often discuss the development The mechanisms of erection–the sequestering and
of their femininity from adolescence to young woman- maintaining of arterial blood within the corpora
hood, focusing on issues of body image, beauty, social cavernosa–are being elucidated by urological research.
worth to others, moral sensibilities, social awkward- This research has led to a diminishing emphasis on “psy-
ness, and whether they consider themselves deserving chogenic impotence” diagnosis. Urologists may refer to
of personal physical pleasure. Men often discuss simi- male erectile disorders (ED) of a psychogenic origin
lar issues in terms of masculinity. as “adrenergic” ED, a reference to the preponderance
Anger, loss of respect, marital discord, and extra- of sympathetic tone on the corporal mechanisms that
marital affairs may be approached in either individual maintain flaccidity. Adrenergic dominance of the pe-
or conjoint formats. In either setting, individuals often nile arterial tone is created by a mind that perceives the
formulate the etiology as having fallen out of love with sexual context as dangerous, frightening, or unwanted.
the partner. Those whose cultural backgrounds limit At every age, selectivity of erectile failure is the sin-
their ease in being a sexual person are often encour- gle most important diagnostic feature of primary erec-
aged in educational and cultural experiences that might tile dysfunction. Clinicians should inquire about the
help them outgrow their earliest notions about what is relative firmness and duration of erections under each
proper sexual behavior. of these circumstances: masturbation, sex other than
intercourse, sex with other female or male partners, What the Clinician Should Expect to
upon stimulation with explicit media materials, in the Encounter Among Men Who Have Never
Table 37-4
middle of the night, and upon awakening. If under some Been Able to Have Intercourse with a
Woman
circumstances the erection is firm and lasting, the clini-
cian can usually assume that the man’s neural, endo- Unconventional Sexual Identity
crine, and vascular physiology is sufficiently normal and Gender identity problem
Wish to be a woman
that the problem is psychogenic in origin. This is true A history of cross-dressing in women’s clothing in
even for men in their fifties and older. Clinicians often private and/or public
feel more certain about this diagnosis when no diseases Suspected by psychiatrist but information initially
withheld
thought to lead to erectile dysfunction are present. Homoeroticism
Without sexual behavior with men
With sexual behavior with men but not known to the
TREATMENT female partner
With sexual behavior with men and known to the female
Lifelong male ED typically is psychogenic and involves partner
Paraphilia
either a sexual identity dilemma—such as transvestism, One or more of a wide range of paraphilic patterns
gender identity disorder, a homoerotic orientation, a Preference for prepubertal or young adolescents often
paraphilia, or another diagnosis that expresses the indi- initially denied unless thoroughly, systematically, and
nonjudgmentally questioned
vidual’s fear of being sexually close to a partner. Sexual Compulsivity with or without obvious paraphilic imagery
identity problems are often initially denied unless the confined to masturbation with the help of pornographic
clinician is nonjudgmental and thorough during the in- images for stimulation
quiry. However, obsessive–compulsive disorder, schiz- Serious Character Disorders (Men Have Strong Fear of
oid personality, a psychotic disorder, or severe character Closeness to Women)
Obsessive–compulsive
disorders may be present. Occasionally, a reasonably Schizotypal
normal young man with an unusually persistent fear of Schizoid
Avoidant
sexual intercourse seeks attention. These good progno- Past history of psychotic decompensation
sis cases are sometimes informally referred to as anx-
Anxious Beginners
ious beginners (Table 37-4). With that exception, men Psychiatrically normal young men with inordinate anxiety
with lifelong male arousal disorder (MAD), when taken and shyness that quickly respond to psychiatrist’s
into individual therapy, are usually perceived as having encouragement and optimism and partner warmth and
patience
a strong motive to avoid sexual behavior and while dys-
functional with a partner during much of their therapy,
might equally be diagnosed as having HSDD with nor- relationship with their partner. Many of these therapies
mal drive but a motive to avoid partner sex. The progno- become focused on resentments that have not been
sis with older men with lifelong erectile dysfunction is identified, discussed, and worked through by the cou-
poor even with modern erectogenic agents. Long-term ple. Such distressed couples are most efficiently helped
therapy, even if it does not enable regular intercourse,
may enable more emotional and sexual closeness to a Apparent Precipitants of Recently Acquired
Table 37-5 Psychogenic Erectile Disorder and Their
partner. Some reasonably masculine-appearing men Associated Private Emotions*
with mild gender identity problems can quickly become
Deterioration of marital relationship: anger, guilt, disdain,
potent if they can reveal their need during sexual rela- sadness
tionship to cross-dress (use a fetish article of clothing) Divorce: abandonment, anger, guilt, sadness, shame
to a partner who calmly accepts his requirement. How- Deterioration of personal or spousal health: sadness,
anxiety, anger, shame
ever, most of these men have inordinate fears of sexu- Death of spouse (widower’s impotence): sadness, longing,
ally bonding to any woman, and, in therapy, become guilt
preoccupied with basic developmental issues. Some of Threat of or actual unemployment: anxiety, worthlessness,
guilt, anger, shame
them marry and form companionate relationships that Financial reversal: shame, guilt, anxiety
are rarely or never consummated. Surreptitious extramarital affair: guilt
In dramatic contrast, men with long-established good Reunited marriage after extramarital affair: shame, anxiety
potency who have recently lost their erectile capacities *
These short lists of simple emotions are a mere introduction to
what transpires within the man’s mind as a result of the meanings
with their partner—acquired psychogenic ED—have a that the sexual behavior has for him. Although incomplete and
far better prognosis (Table 37-5). They may be treated oversimplified, they are listed to remind the psychiatrist that what
in individual or couples format, depending on the pre- the man feels about his life competes with sexual arousal during
sexual behavior to generate the psychogenic erectile dysfunction.
cipitants of the sexual problem and the status of their
in a conjoint format. When extramarital affairs are levels of a substance called cyclic guanosine mono-
part of the relationship deterioration and cannot be dis- phosphate (cGMP) and that is the key to getting and
cussed, most clinicians simply work with one spouse. sustaining an erection for intercourse. All three medica-
Potency is frequently lost following a separation or ditions block the enzyme PDE5, which is responsible for
vorce. Impaired potency after a spouse’s death is either the neutralization of cGMP. PDE5 blockers generally
about unresolved grief or problems that existed prior to will not cause erections at inappropriate times because
the wife’s terminal illness. Men also often get worried they only block degradation of cGMP produced in re-
about their potency when their financial or vocational action to sexual stimulation. In the absence of sexual
lives crumble, when they have a serious new physical stimuation, there is no cGMP to protect, so the drugs
illness such as a myocardial infarction or stroke, or remains in the background. The three medications dif-
when their wives become seriously ill. The esthetics fer primarily in terms of duration of action: Cialis lasts
of lovemaking require a context of reasonable physi- from 30 to 100 hours, Levitra lasts up to 24 hours, and
cal health; when one spouse becomes chronically ill or Viagra lasts from 4-6 hours. These drugs must not be
disfigured by illness or surgery, either one of the couple used when any organic nitrate is being taken because
may lose their willingness to be sexual. This may be it dangerously potentiates the hypotensive effect of the
reflected in impaired erections or sexual avoidance. nitrates, risking brain and myocardial infarction. Be-
Regardless of the precipitating factors, men with cause the PDE5 inhibitors’ rate of improving erections
arousal disorders have performance anxiety. They an- is significantly higher than the restoration of a mutually
ticipate erectile failure before sex begins and vigilantly satisfactory sexual equilibrium (approximately 44%),
monitor their state of tumescence during sex. Perform- psychological ED that persists after medication should
ance anxiety is present in almost all impotent men. be treated by a mental health professional.
Performance anxiety is efficiently therapeutically ad-
dressed by identifying it to the individual and asking
Problems With Orgasm
him to make love without trying intercourse on several
occasions to demonstrate to himself how different love-
Female Orgasmic Disorder
making can feel for him when he is not risking failure.
This enables many to relax, concentrate on sensation,
DIAGNOSIS
and return to previous states of sensual abandon dur-
ing lovemaking. This technique is known as sensate The attainment of reasonably regular orgasms with a
focus. partner is a crucial personal developmental step for
The psychological treatment of acquired arousal young women. This task of adult sexual development
disorders is often highly satisfying for the professional rests upon a subtle interplay of physiology, individual
because many of the men are anxious for help. Moti- psychology, and culture. Orgasm is the reflexive culmi-
vation to behave sexually is often present, fear can be nation of arousal. It is manifested by rhythmic vaginal
allayed, and men can learn to appreciate the emotional wall contractions and the release of muscular tension
complexity of their lives. They can be shown how their and pelvic vasocongestion, accompanied by varying
minds prevented intercourse until they could acknowl- degrees of pleasurable body sensations. Its accomplish-
edge what has been transpiring within and around ment requires: (1) the physiologic apparatus to augment
them. Many recently separated men, for example, are and sustain arousal; (2) the psychological willingness
grieving, angry, guilty, uncertain, and worried about to be swept away by excitement; and (3) tenacious focus
their finances. Yet, they may propel themselves into a on the required physical work of augmenting arousal.
new relationship. Two characteristics seem to predis- The diagnosis of female orgasmic disorder (FOD) is
pose to erectile problems at key life transitions: (1) the made when the woman’s psychology persistently in-
pursuit of the masculine standard that men ought to be terferes with her body’s natural progression through
able to perform intercourse with anyone, anywhere, un- arousal.
der any circumstances; (2) the inability to readily grasp While assessing for the presence of this disorder, the
the nature and significance of his inner experiences. doctor should determine the answers to the following
The introduction of phosphodiesterase-5 (PDE5) in- questions. Does the individual have orgasms under any
hibitors in 1998 revolutionized the treatment of erectile of the following sexual circumstances: solitary mastur-
dysfunction. Sildenafil (Viagra) was introduced first, bation, partner manual genital stimulation, oral–genital
followed by Vardenafil (Levitra) and Tadalafil (Cialis). stimulation, vibratory stimulation, any other means?
When a man gets sexually stimulated, a chain reaction Does she have orgasms with a partner different than
occurs in the tissue of the penis that results in elevated her significant other? How are they stimulated? Does
a particular fantasy make orgasmic attainment easier active pursuit of orgasm, have enabled many women
or possible? Under what conditions has she ever been to grow more comfortable and competent in sexual
orgasmic? Has she had an orgasm during her sleep? expression.
The lifelong generalized variety of the disorder is
recognized when a woman has never been able to attain
orgasm alone or with a partner by any means, although Male Orgasmic Disorder
she regularly is aroused. When a woman can only read-
ily attain orgasm during masturbation, she is diagnosed When a man can readily attain a lasting erection with
as having a lifelong situational type. Women with any a partner, yet is consistently unable to attain orgasm
form of lifelong FOD more clearly have conflicts about in the body of the partner, he is diagnosed with male
personal sexual expression due to fear, guilt, ignorance, orgasmic disorder (MOD). The disorder has three levels
or obedience to tradition than those with the acquired of severity: (1) the most common form is characterized
variety. Women who can masturbate to orgasm often by the ability to attain orgasm with a partner outside of
feel fear and embarrassment about sharing their private her or his body, either through oral, manual, or personal
arousal with any other person. masturbation; (2) the more severe form is characterized
The acquired varieties of this disorder are more com- by the man’s inability to ejaculate in his partner’s pres-
mon and are characterized by both complete anorgas- ence; and (3) the rarest form is characterized by the in-
mia, too-infrequent orgasms, and too-difficult orgasmic ability to ejaculate when awake. The disorder is usually
attainment. The most common cause of this problem lifelong and not partner specific. Some of these men get
are serotonergic compounds. Prospective studies of better with psychotherapy, others improve spontane-
various antidepressants have demonstrated up to 70% ously with time, and, for others, the dysfunction leads
incidence of this disorder among those treated with se- to the cessation of the aspiration for sex with a part-
rotonergic antidepressants. Bupropion and nefazodone ner. One controlled study of individuals with numerous
do not cause this problem. When medications are not sexual dysfunctions suggested that bupropion 300–450
the cause of an acquired FOD, the clinician needs to mg/day may improve the capacity to ejaculate in a mi-
carefully assess the meaning of the changes in her life nority of individuals.
prior to the onset of the disorder.
Premature Ejaculation
TREATMENT
DIAGNOSIS
The ideal era to begin treatment is young adulthood.
Four formats are known to be of help. Individual ther- Premature ejaculation is a high-prevalence (25–40%)
apy is the most commonly employed. In lifelong va- disorder seen primarily in heterosexuals characterized
rieties of the disorder, therapy focuses on the cultural by a very low threshold for the reflex sequence of or-
sources of sexual inhibition and how and when they gasm. The problem, a physiological efficiency of sperm
impacted upon the individual. In the situational varie- delivery, causes social and psychological distress. The
ties, the therapist focuses on the meaning of the life range of intravaginal containment times among self-
changes that preceded the onset of the disorder. Group diagnosed individuals extends from immediately be-
therapy is highly effective in helping women reliably fore or upon vaginal entry (rare), to less than a minute
masturbate to orgasm and be moderately effective in (usual), to less than the man and his partner desire
overcoming partner inhibition. It is typically done with (not infrequent). Time alone is a misleading indicator,
college and graduate students in campus settings, not however. The essence of the self-diagnosis is an emo-
older women. Couple therapy may be useful to assist tionally unsatisfying sexual equilibrium apparently
the couple with the subtleties of their sexual equi- due to the man’s inability to temper his arousal. Most
librium. The personal and interpersonal dimensions men sometimes ejaculate before they wish to, but not
of orgasmic attainment can be stressed. Often, other persistently.
issues then come to the fore that initially seemed to The history should clarify the answers to follow-
have little to do with orgasmic attainment. The most ing questions: why is he seeking therapy now? Is
cost-effective treatment is bibliotherapy. Female orgas- the individual a sexual beginner or a beginner with
mic attainment has been widely written about in the a particular partner? Does he have inordinately high
popular press for several decades. It is widely believed expectations for intravaginal containment time for a
that these articles and books, which strongly encourage man his age and experience? Is he desperate about
knowledge of her genital anatomy, masturbation, and losing the partner because of the rapid ejaculation? Is
the relationship in jeopardy for another reason? Does Sexual Pain Disorders
his partner have a sexual dysfunction? Does she have
orgasms with him other than through intercourse? Is The clinician needs to consider a series of questions
he requesting help in order to cover his infidelity? Is when dealing with a woman who reports painful in-
his partner now blaming the man’s sexual inadequacy tercourse. Does she have a known gynecologic abnor-
for her infidelity? Is his new symptom a reflection of mality that is generally associated with pain? Is there
his fear about having a serious physical problem dur- anything about her complaint of pain that indicates a
ing sex such as angina, a stroke, or another myocardial remarkably low pain threshold? Does she now have an
infarction? The answers will enable the clinician to aversion to sexual intercourse? At what level of physi-
classify the rapid ejaculation into an acquired or life- cal discomfort did she develop the aversion? Does her
long and specific or general pattern, to sense the larger private view of her current relationship affect her will-
context in which his sexual behavior is conducted, and ingness to be sexual and her experience of pain? Does
to plan treatment. her partner’s sexual style cause her physical or mental
discomfort—for example, is he overly aggressive or
does he stimulate memories of former abuse? What has
TREATMENT
been the partner’s response to her pain? What role does
There are three efficient approaches to this dysfunc- her anticipation of pain play in her experience of pain?
tion. The fi rst is simply to refuse to confirm the in- These clinical questions are typical biopsychosocial
dividual’s self-diagnosis. Some anxious beginners, ones. Sex-limiting pain often is the result of the subtle
men with reasonable intravaginal containment times interplay of personal and relational, cognitive and af-
of 2 or more minutes, and those with exaggerated no- fective, and fundamental biological processes that are
tions of sexual performance can be reassured with a inherent in other human sexual struggles that operate
few visits. When they no longer think of themselves to produce these confusing disorders.
as dysfunctional, their intravaginal containment The DSM-IV-TR presents dyspareunia and vagin-
times improve. The second is the use of serotonergic ismus as distinct entities. However, they have been
medications. Numerous reports testify to the fact that viewed as inextricably connected in much of the mod-
various serotonergic reuptake inhibitors can signifi- ern sexuality literature—vaginismus is known to cre-
cantly lengthen the duration of intercourse. Clinicians ate dyspareunia and dyspareunia has been known to
need to determine with each individual whether the create vaginismus.
medication can be taken within hours or days of an-
ticipated intercourse. Improvement is not sustained
Dyspareunia
after medication is stopped. Serotonergic medications
are the most common treatment of rapid ejaculation
DIAGNOSIS
because they are so quickly effective in over 90% of
men. The third approach is behaviorally oriented sex Recurrent uncomfortable or painful intercourse in ei-
therapy that trains the man to focus his attention on ther gender is known as dyspareunia. Women’s dys-
his penile sensations during vaginal containment and pareunia varies from discomfort at intromission, to
to signal his partner to cease movement or to apply a severe unsparing pain during penile thrusting, to vagi-
firm squeeze of the glans/shaft area to interrupt the nal irritation following intercourse. In both sexes, re-
escalation of arousal. This requires an increase in curring coital pain leads to inhibited arousal and sexual
communication and full cooperation of the partner, avoidance. Dyspareunia is used as both a symptom and
which in themselves can go a long way in improving a diagnosis. When coital pain is caused solely by de-
their sexual equilibrium. fined physical pathology, dyspareunia due to a medi-
The advantages of costlier couple psychotherapy are cal condition is diagnosed. When coital pain is due to
to allow the man and his partner to understand their vaginismus, insufficient lubrication, or other presuma-
lives better, to address both of their sexual anxieties, bly psychogenic factors, dyspareunia not due to a medi-
and to deal with other important nonsexual issues in cal condition diagnosis is made.
their relationship. Effective psychotherapy allows the Because the symptom dyspareunia is produced by
man to become positioned to continue the usual bio- numerous organic conditions, the clinician should be
logical evolution that occurs during the life cycle from certain that the individual has had a pelvic examina-
rapid ejaculation, which is true for many young men, tion by a person equipped to assess a broad range of
to occasional difficulty in ejaculating, which is true for regional pathology. Vulvovestibulitis is diagnosed by
many men in their sixties. pain in response to cotton swab touching in a normal
appearing vulvar vestibule. In these individuals and TREATMENT OF DYSPAREUNIA

some others, the pain cannot be classified with cer- AND VAGINISMUS
tainty as a symptom or a disorder. Pain upon penile
While vaginismus has the reputation of being readily
or digital insertion may be due to an intact hymen
treatable by gynecologists by pairing relaxation tech-
or remnants of the hymenal ring, vaginitis, cervici-
niques with progressively larger vaginal dilators, the
tis, episiotomy scars, endometriosis, fibroids, ovarian
mental health professional typically approaches the
cysts, and so on. Postcoital dyspareunia often begins
problem differently. The psychological approach to both
at orgasm when uterine contractions occur. Fibroids,
vaginismus and dyspareunia is attuned to the role that
endometriosis, and pelvic inflammatory disease should
her symptom plays in her life. The therapy, therefore,
be considered. Postmenopausal pain, particularly if the
does not begin with a one dimensional attempt to re-
woman has had many years without intercourse, is of-
move the symptom, which only frightens some individ-
ten a result of thinning of the vaginal mucosa, loss of
uals. Rather, it begins with a patient exploration of the
elasticity of the labia and vaginal outlet, and decreased
developmental and interpersonal meanings of the need
lubrication. Normal menopause, however, is often as-
for the symptom. “I wonder how this problem originally
sociated with mild pain due to inadequate lubrication
got started? Can you tell me a bit more about your life?”
(in both partners).
In the course of assisting women with these problems, a
Dyspareunia in men is usually due to a medical con-
variety of techniques may be utilized including relaxa-
dition. Herpes, gonorrhea, prostatitis, and Peyronie’s
tion techniques, sensate focus, dilatation, marital ther-
disease cause pain during intercourse. Remote trauma
apy, and medication. Short-term therapies should not be
to the penis may cause penile chordee or bowing which
expected to have lasting good results because once the
makes intercourse mechanically difficult and some-
symptom is relieved, other problematic aspects of the
times painful. Pain experienced upon ejaculation can
individual’s sexual equilibrium and nonsexual relation-
be a side effect of trazodone.
ship often come into focus. Clinicians have developed
an impression that women with a diagnosis of dyspare-
Vaginismus unia are particularly difficult to help permanently. This,
however, is a largely unstudied topic.
DIAGNOSIS
Vaginismus is an involuntary spasm of the musculature Sexual Dysfunction Due to a General
of the outer third layer of the vagina, which makes pe- Medical Condition
nile penetration difficult or impossible. The diagnosis
is not made if an organic cause is known. Although Many general medical conditions can cause sexual dys-
a woman with vaginismus may wish to have inter- function, including neurological conditions (e.g., multi-
course, her symptom prevents the penis from enter- ple sclerosis, spinal cord lesions, neuropathy, temporal
ing her body. In lifelong vaginismus, the anticipation lobe lesions), endocrine conditions (e.g., diabetes melli-
of pain at the first intercourse causes muscle spasm. tus, hypothyroidism, hyper- and hypoadrenocorticism,
Pain reinforces the fear and on occasion, the partner’s hyperprolactinemia, hypogonadal states, pituitary
response gives her good reason to dread a second op- dysfunction), vascular conditions, and genitourinary
portunity to have intercourse. Early episodic vaginis- conditions (e.g., testicular disease, Peyronie’s disease,
mus may be common among women, but most of the urethral infections, postprostatectomy complications,
cases that are brought to medical attention are chronic. genital injury, atrophic vaginitis, infections of the
Lifelong vaginismus is relatively rare. The clinician vagina and external genitalia, postsurgical complica-
needs to focus attention on what may have made the tions such as episiotomy scars, shortened vagina, cys-
idea of intercourse so overwhelming to her: parental titis, endometriosis, uterine prolapse, pelvic infections,
intrusiveness, sexual trauma, childhood genital injury, neoplasms).
illnesses whose therapy involved orifice penetration, The diagnosis of Sexual Dysfunction due to a Gen-
and surgery. eral Medical Condition applies when the sexual dys-
The woman with lifelong vaginismus not only has a function is judged to be exclusively due to the direct
history of unsuccessful attempts at penetration but dis- physiological effects of the general medical condition.
plays an avoidance of finger and tampon penetration. This determination is based on history (e.g., impaired
The most dramatic aspect of her history, however, is erectile functioning during masturbation), physical ex-
her inability to endure a speculum examination of her amination (e.g., evidence of neuropathy), and labora-
vagina. Vaginismus is a phobia of vaginal entrance. tory findings (e.g., nocturnal penile tumescence, pulse
wave assessments, ultrasound studies, intracorporeal Gender Identity Disorder

pharmacological testing or angiography). If both a pri-
mary sexual dysfunction and a general medical condi- The organization of a stable gender identity is the first
tion are present, then the primary diagnosis with the component of sexual identity to emerge during child-
subtype “With Combined Factors” should be used (e.g., hood. The processes that enable this accomplishment
Male Erectile Dysfunction With Combined Factors). are so subtle that when a daughter consistently acts
as though she realizes that “I am a girl and that is all
right,” or when a son’s behavior announces that “I am a
Substance-Induced Sexual Dysfunction boy and that is all right,” families rarely even remember
their children’s confusion and behaviors to the contrary.
The diagnosis of Substance-Induced Sexual Dysfunc- Adolescent and adult gender problems are not rare.
tion applies when a clinically significant sexual dys- They are, however, commonly hidden from social view,
function is judged to be exclusively due to the direct sometimes long enough to developmentally evolve into
physiological effects of a medication or drug of abuse. other less dramatic forms of sexual identity.
Sexual dysfunctions can occur in association with in-
toxication with the following classes of substances:
alcohol, amphetamines and related substances, co- Early Forms: Extremely Feminine Young Boys
caine, opioids, sedatives, hypnotics, and anxiolytics.
Although occasionally the parents of a feminine son
Acute intoxication with or chronic abuse of substances
have a convincing anecdote about persistent feminine
of abuse has been reported to decrease sexual interest
interests dating from early in the second year of life,
and cause arousal problems in both sexes. A decrease
boyhood femininity is more typically only apparent
in sexual interest, arousal disorders, and orgasmic dis-
by the third year. By the fourth year, playmate prefer-
orders may also be caused by prescribed medications,
ences become obvious. Same-sex playmate preference
including antihypertensives, histamine H2 receptor
is a typical characteristic of young children. Cross-
antagonists, antidepressants, neuroleptics, anxiolytics,
gender-identified children consistently demonstrate
anabolic steroids, and antiepileptics. Painful orgasm
the opposite sex playmate preference. The avoidance
has been reported with the use of fluphenazine, thiori-
of other boys has serious consequences in terms of
dazine, and amoxapine. Priapism has been reported
social rejection and loneliness throughout the school
with use of chlorpromazine, trazodone, closapine, and
years. The peer problems of feminine boys cause some
following penile injections of papaverine or prostaglan-
of their behavioral and emotional problems, which are
din. Serotonin reuptake inhibitors may cause decreased
in evidence by middle-to-late childhood. However,
sexual desire, arousal, or orgasmic disorders.
psychometric studies support clinical impressions that
feminine boys have emotional problems even before
peer relationships become a factor—that is, something
Sexual Dysfunction Not Otherwise
more basic about being cross-gender-identified cre-
Specified (NOS)
ates problems. Young feminine boys have been shown
to be depressed and have difficulties with separation
This diagnosis is reserved for circumstances that leave
anxiety.
the clinician uncertain as to how to diagnose the in-
dividual. This may occur when the individual has too
many fluctuating dysfunctional symptoms without a
Early Forms: Masculine Girls (Tomboys)
clear pattern of prominence of anyone of them. Some-
times, the clinician is unable to determine whether the The masculinity of girls may become apparent as early
dysfunction is the basic complaint or whether the sex- as age 2 years. The number of girls brought to clinical
ual complaints are secondary to marital dysfunction. attention for cross-gendered behaviors, self-statements,
At other times the etiology is the uncertain: psycho- and aspirations is consistently less than boys by a factor
genic, due to a general medical condition, or substance of 1 : 5 at any age of childhood in most Western coun-
induced. When the individual does not emphasize the tries. It is not known whether this reflects a genuine
dysfunction as the problem but emphasizes instead the difference in incidence of childhood gender disorders,
lack of emotional satisfaction from sex, the psychiatrist cultural perceptions of femininity as a negative in boys
may temporarily provide this not otherwise specified versus the neutral-to-positive perception of boy-like
(NOS) diagnosis. It is usually possible to find a better behaviors in girls, the broader range of cross-gender
dysfunction diagnosis after therapy begins. expression permitted to girls but not to boys, or an
intuitive understanding that cross-gender identity more

accurately predicts homosexuality in boys than girls. DSM-IV-TR Diagnostic Criteria
The distinction between tomboys and gender- GENDER IDENTITY DISORDER
disordered girls is often difficult to make. Tomboys
are thought of as not as deeply unhappy about their A. A strong and persistent cross-gender identification (not
merely a desire for any perceived cultural advantages
femaleness, not as impossible to occasionally dress in of being the other sex). In children, the disturbance is
stereotypic female clothing, and not thought to have manifested by four (or more) of the following:
a profound aversion to their girlish and future wom- (1) repeatedly stated desire to be, or insistence that he
anly physiologic transformations. Tomboys are able to or she is, the other sex
enjoy some feminine activities along with their obvi- (2) in boys, preference for cross-dressing or simulating
female attire; in girls, insistence on wearing only
ous pleasures in masculine-identified toys and games stereotypical masculine clothing
and the company of boys. Girls who are diagnosed as (3) strong and persistent preferences for cross-sex roles
in make-believe play or persistent fantasies of be-
gender-disordered generally seem to have a relentless ing the other sex
intensity about their masculine preoccupations and an (4) intense desire to participate in the stereotypical
insistence about their future. The onset of their cross- games and pastimes of the other sex
(5) strong preference for playmates of the other sex
gendered identifications is early in life. Although most
lesbians have a history of tomboyish behaviors, most In adolescents and adults, the disturbance is mani-
fested by symptoms such as a stated desire to be the
tomboys develop a heterosexual orientation. other sex, frequent passing as the other sex, desire to live
or be treated as the other sex, or the conviction that he
or she has the typical feelings and reactions of the other
DIAGNOSIS sex. Persistent discomfort with his or her sex or sense of
inappropriateness in the gender role of that sex.
Adults who permanently change their bodies to deal In children, the disturbance is manifested by any of
the following: in boys, assertion that his penis or tes-
with their gender dilemmas represent the far end of tes are disgusting or will disappear or assertion that
the spectrum of adaptations to gender problems. Even it would be better not to have a penis, or aversion
the lives of those who reject bodily change, however, toward rough-and-tumble play and rejection of male
stereotypical toys, games, and activities; in girls, rejec-
have considerable pain because the images of a bet- tion of urinating in a sitting position, assertion that she
ter gendered self may recur throughout life, becom- has or will grow a penis, or assertion that she does not
ing more powerful whenever life becomes strained or want to grow breasts or menstruate, or marked aver-
sion toward normative feminine clothing.
disappointing.
B. In adolescents and adults, the disturbance is manifested
The diagnosis of the extreme end of the gender iden- by symptoms such as preoccupation with getting rid of
tity disorder spectrum is clinically obvious. The chal- primary and secondary sex characteristics (e.g., request
lenging diagnostic task for clinicians is to suspect a for hormones, surgery, or other procedures to physi-
cally alter sexual characteristics to simulate the other
gender problem and inquire about gender identity and sex) or belief that he or she was born the wrong sex.
its evolution in those whose manner suggests a unisexed C. The disturbance is not concurrent with a physical in-
or cross-gendered appearance, those with dissociative tersex condition.
D. The disturbance causes clinically significant distress or
gender identity disorder (GID), severe forms of char- impairment in social, occupational, or other important
acter pathology, and those who seem unusual in some areas of functioning.
undefinable manner.
Code based on current age:
DSM-IV-TR provides the clinician with two Axis
302.6 Gender identity disorder in children
I gender diagnoses: Gender Identity Disorder, and 302.85 Gender identity disorder in adolescents or
Gender Identity Disorder Not Otherwise Specified adults
(GIDNOS). To qualify for GID, an individual of any Specify (for sexually mature individuals):
age must meet four criteria. Sexually attracted to males
Children, teenagers, and adults exist who rue the Sexually attracted to females
day they were born to their biological sex and who Sexually attracted to both
Sexually attracted to neither
long for the opportunity to simply live their lives in
a manner befitting the other gender. They repudiate Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
the possibility of finding happiness within the broad American Psychiatric Association.
framework of roles given to members of their sex
by their society. Their repudiation is not motivated
by an intellectual attack on sexism, homophobia, or her body, repudiates the self in that body, and rejects
any other injustice imbedded in cultural mores. A performing roles expected of people with that body.
gender-disordered person literally repudiates his or It is a subtle, usually self-contained rebellion against
the need of others to designate them in terms of their (former fetishistic transvestites) who are evolving
biological sex. toward GID, socially isolated men who want to be-
By mid-adolescence, the extremely gender-disor- come a woman shortly after their wives or mothers
dered have often envisioned the solution for their para- die (secondary transvestites) but express considerable
lyzing self-consciousness: to live as a member of the ambivalence about the very matter they passionately
opposite gender, to transform their bodies to the extent desired at their last visit, extremely feminized homo-
possible by modern medicine, and to be accepted by sexuals including those with careers as “drag queens”
all others as the opposite sex. Most people with these who seem to want to change their sex when depressed,
cross-gender preoccupations, however, do not go be- and so on. GIDNOS would also capture men who want
yond the fantasy or private cross-dressing. Those that to be rid of their genitals without being feminized,
do, may often come to psychiatric attention. When a unisexual females who imagine themselves as males
clinician is called in, the family has one set of hopes, but who are terrified of any social expression of their
the individual another. The clinician has many tasks, masculine gender identity, hypermasculine lesbians in
one of which is to mediate between the ambitions of the periodic turmoil over their gender, and those women
gender-disordered person and society and see what can who strongly identify with both male and female who
be done to help the individual. lately want mastectomies. In using gender identity di-
The usual clarity of distinctions between heterosex- agnoses, clinicians need to remember that extremely
ual, bisexual, and homosexual orientations rests upon masculine women or extremely feminine men are not
the assumption that the biological sex and psychologi- to be dismissed as homosexual. “Lesbian” or “gay” is
cal gender of the person and the partner are known. only a description of orientation. They are more aptly
A woman who designates herself as a lesbian is un- described as also cross-gendered.
derstood to mean she is erotically attracted to other
women. Lesbian loses its meaning if the woman says
TREATMENT
she feels she is a man and lives as one. She insists, “I
am a heterosexual man; men are attracted to women The treatment of these conditions, although not as
as am I!” DSM-IV-TR suggests that adults with GIDs well based on scientific evidence as some psychiatric
should be subgrouped according to which sex the indi- disorders, has been carefully scrutinized by multidis-
vidual is currently sexually attracted: males, females, ciplinary committees of specialists within the Harry
both, or neither. This makes sense for most individu- Benjamin International Gender Dysphoria Association
als with GID because it is their gender identity that is for over 20 years. The treatment of any GID begins af-
most important to them. Some are rigid about the sex ter a careful evaluation, including parents, other family
of those to whom they are attracted because it supports members, spouses, psychometric testing, and occasion-
their idea about their gender, others are bierotic and ally physical and laboratory examination. The details
are not too concerned with their orientation, still oth- will depend on the age of the individual. It is possible,
ers have not had enough experiences to overcome their of course, to have a GID as well as mental retardation,
uncertainty about their orientation. a psychosis, dysthymia, severe character pathology, or
If an accurate community-based study of the gen- any other psychiatric diagnosis (Table 37-6).
der impaired could be conducted, most cases would be
diagnosed as Gender Identity Disorder Not Otherwise
Psychotherapy
Specified (GIDNOS). The diagnostician needs to un-
derstand that gender identity development is a dynamic No one knows how to “cure” an adult’s gender problem.
evolutionary process and clinicians get to see people at People who have long lived with profound cross-gender
crisis points in their lives. At any given time, although identifications do not get insight—either behaviorally
it is clear that the individual has some form of GID, it modified or medicated—and find that they subsequently
may not be that which is described in DSM-IV-TR as have a conventional gender identity. Psychotherapy is
GID. useful, nonetheless. If the individual is able to trust a
GIDNOS is a large category designed to be inclu- therapist, there can be much to talk about—family rela-
sive of those with unusual genders who do not clearly tionships are often painful, barriers to relationship in-
fit the criteria of GID. There is no implication that if timacy are profound, work poses many difficult issues,
an individual is labeled GIDNOS that his or her label and the individual has to make monumental decisions.
cannot change in the future. GIDNOS would contain The central one is, “How am I going to live my life?
the many forms of transvestism—masculine-appearing Should I go through with cross-gender living, hormone
boys and teenagers with persistent cross-dressing therapy, mastectomy, or genital surgery?” The therapist
Steps in Evaluation of the Profoundly

mental health team dealing with gender problems.
Table 37-6 The effects of administration of estrogen to a biologi-
Gender Disordered
cal male are breast development, testicular atrophy,
Formal evaluation and diagnosis—gender identity disorder
or gender identity disorder NOS. Can the patient be decreased sexual drive, decreased semen volume and
referred to a gender program? Is another treatable fertility, softening of skin, fat redistribution in a female
psychiatric or physical disorder present? pattern, and decrease in spontaneous erections. Breast
Individual psychotherapy within the gender program or
with an interested professional. Do the diagnoses remain development is often the highest concern to the indi-
the same? If yes, does the patient consistently want to: vidual. Because hair growth is not affected by estro-
Discuss his (or her) situation but make no changes? gens, electrolysis is often used to remove beard growth.
Increase cross-dressing toward crossliving?
Prepare the family for the real-life test? Side effects within recommended doses are minimal
Obtain permission to proceed with hormones? but hypertension, hyperglycemia, lipid abnormalities,
Approval for hormones from a gender committee or on thrombophlebitis, and hepatic dysfunction have been
written recommendation from the psychiatrist to an
endocrinologist. Individual or group psychotherapy described. The most dramatic effect of hormones is
should continue. on the sense of well-being. Individuals report feeling
Real-life test of living and working full time in the aspired-
to gender role for at least 1 year.
calmer and happier knowing that their bodies are being
Does the patient want to continue to surgery? demasculinized and feminized. All results derive from
Gender committee approval for surgery. Many patients have open-labeled studies.
cosmetic surgery other than that listed with only ordinary
patient–surgeon consent. This most often involves The administration of androgen to females results
breast augmentation but may include numerous other in an increased sexual drive, clitoral tingling and
attempts to improve ability to pass as opposite sex and be growth, weight gain, and amenorrhea and hoarseness.
attractive.
Men—genital reconstruction An increase in muscle mass may be apparent if weight
Women—mastectomy, hysterectomy, genital training is undertaken simultaneously. Hair growth de-
reconstruction; Most patients will not complete all of pends on the individual’s genetic potential. Androgens
these steps.
are administrated intramuscularly 200–300 mg/month
and are generally safe. It is prudent, however, to peri-
odically monitor hepatic, lipid, and thyroid function-
can help the individual recognize the drawbacks and ing. Most individuals are delighted with their bodily
advantages of the various available options and to re- changes, although some are disappointed that they re-
spect the initially unrecognized or unstated ambiva- main short, wide-hipped, relatively hairless men with
lence. Completion of the gender transformation process breasts that do not significantly regress.
usually takes longer than the individual desires, and the
therapist can be an important source of support during
Surgical Therapy
and after these changes.
Surgical intervention is the final and obviously irrevers-
ible external step. It should not occur without a mental
Group Therapy
health professional’s input, even when the individual
Group therapy for gender-disordered people has the ad- provides a heartfelt convincing set of reasons to bypass
vantages of allowing individuals to know others with the real-life test, hormones, and therapeutic relation-
gender problems, of decreasing their social isolation, ship. Genital surgery is expensive, time consuming,
and of being among people who do not experience their at times painful, and has frequent anatomic complica-
cross-gender aspirations and their past behaviors as tions and functional disappointments. Surgery can be
weird. Group members can provide help with groom- expected to add further improvements in the lives of
ing and more convincing public appearances. The suc- some individuals—more social activities with friends
cess of these groups depends on the therapist’s skills in and family, more activity in sports, more partner sexual
selection of the individuals and using the group proc- activity, and improved vocational status.
ess. Groups are generally only available in a few spe-
cialized treatment programs.
The Paraphilias
Hormone Therapy DIAGNOSIS

Ideally, hormones should be administered by endo- A paraphilia is a disorder of intention, the final com-
crinologists who have a working relationship with a ponent of sexual identity to develop in children and
adolescents. Intention refers to what individuals want Paraphilic images are usually devoid of any pretense of
to do with a sexual partner and what they want the part- caring or human attachment. The hatred, anger, fear,
ner to do with them during sexual behavior. Normally, vengeance, or worthlessness expressed in them require
the images and the behaviors of intention fall within no familiarity with the partner. Paraphilic images are
ranges of peaceable mutuality. The disorders of inten- conscious—clearly known to the individual. They
tion are recognized by unusual eroticism (images) and should not be confused with speculations about “un-
often socially destructive behaviors such as sex with conscious” aggression or sadomasochism that some as-
children, rape, exhibitionism, voyeurism, masochism, sume are part of all sexual behavior. Clinicians should
obscene phone calling, or sexual touching of strangers. expect to occasionally see paraphilic individuals whose
While 5% of the diagnoses of paraphilia are given to preoccupations are not hostile to others.
women, most etiologic speculations refer to male sexual An individual’s paraphilic themes often change in
identity development gone awry. This raises the impor- intensity or seem to change in content from time to
tant question about what happens to girls who have the time. The stimuli for these changes often remain un-
same developmental misfortunes that are speculated to clear. In most instances, it is reasonable to consider that
create male paraphilia. paraphilia is a basic developmental disorder in which
Now it is apparent that paraphilias occur among particular erotic and sexual manifestations are shaped
individuals of all orientations and among those with by the individuality of the person’s history. To make a
conventional and unconventional gender identities. diagnosis of paraphilia, the individual must evidence
A homosexual sadist is paraphilic only on the basis at least 6 months of the unusual erotic preoccupation.
of sexual cruelty. A transsexual who desires to be Duration is usually not in question, even among adoles-
beaten during arousal is paraphilic only on the basis cents, however.
of masochism. To be paraphilic means that the erotic imagery ex-
Erotic intentions that are not longstanding, unusual, erts a pressure to play out the often imagined scene. In
and highly arousing may be problematic in some way its milder forms, the pressure results merely in a pre-
but they are not clearly paraphilic. The sine qua non occupation with a behavior. For instance, a man who
of the diagnosis of paraphilia is unusual, often hostile, prefers to be spoken to harshly and dominated by his
dehumanized eroticism that has preoccupied the indi- wife during sex thinks about his masochistic images
vidual for most of his adolescent and adult life. The primarily around their sexual behaviors. He does not
paraphilic fantasy is often associated with this preoc- spend hours daydreaming of his erotic preferences. In
cupying arousal when it occurs in daydreams and mas- their more intense forms, paraphilias create a driven-
turbation reveries or is encountered in explicit films ness to act out the fantasy in sexual behavior—usually
or magazines. The specific imagery varies from one in masturbation. Frequent masturbation, often more
paraphilic individual to the next, but both the imagined than once daily, continues long after adolescence. In
behavior and its implied relationship to the partner are the most severe situations, the need to attend to the
unusual in that they are preoccupied with aggression. fantasy and masturbate is so overpowering that life’s
Images of rape, obscene phone calling, exhibitionism, ordinary activities cannot efficiently occur. Masturba-
and touching of strangers, for example, are rehearsals tion and sometimes partner-seeking behavior is expe-
of victimization. In masochistic images, the aggression rienced as driven. The individual reports either that he
is directed at the self—for instance, autoerotic stran- cannot control his behavior or he controls it with such
gulation, slavery, torture, and spanking. In others, the great effort that his work, study, parenting, and rela-
aggression is well disguised as love of children or teen- tionships are disrupted.
agers. In some, such as simple clothing fetishism, the Two other conditions, compulsive sexual behav-
aggression may be absent. Aggression is so apparent ior and sexual addiction, not part of the DSM-IV-TR,
in most paraphilic content, however, that when none are informally and synonymously used to refer to het-
seems to exist, the clinician needs to wonder whether erosexual and homosexual men and women who dis-
it is actually absent or being hidden from the doctor. play an intense drivenness to behave sexually without
Paraphilic fantasies often rely heavily upon the image paraphilic imagery. The personal, interpersonal, and
of a partner who does not possess “personhood.” Some medical consequences of paraphilic and nonparaphilic
imagery in fact has no pretense of a human partner at sexual compulsivity seem indistinguishable as do their
all; clothing, animals, or excretory products are the usual psychiatric comorbidities: depression, anxi-
focus. Other themes, such as preoccupation with feet ety disorders, substance abuse, and attention deficit
or hair, combine both human and inanimate interests. disorders.
Criminal Sex-Offending Behaviors for this purpose. Some of these crimes result in rape
or nonsexual violence, but many are motivated by pure
Exhibitionism voyeuristic intent (which is subtly aggressive).
Exhibitionism generally involves teenagers and men

Sexual Sadism
displaying their penises so that the witness will be
shocked or (in the paraphilic’s fantasy) sexually in-
While rape is an extreme variety of sadism, paraphilic
terested. They may or may not masturbate during or
sadism is present only in a minority of rapists. It is
immediately following this act of victimization. This
defined by the rapist’s prior use of erotic scripts that
diagnosis is not usually made when a man is arrested
involve a partner’s fear, pain, humiliation, and suffer-
for “public indecency” and his penile exposures are
ing. Rapists are highly dangerous men whose antisocial
motivated to arrange homosexual contact in a public
behaviors are generally thought to be unresponsive to
place generally unseen by heterosexuals. Penile display
ordinary psychiatric methods. Their violence poten-
in parks is one way to make anonymous contact. The
tial often makes psychiatric therapy outside of institu-
presence or absence of exhibitionistic imagery allows
tions imprudent. Noncriminal paraphilic sadism—that
the clinician to make the distinction between paraphilia
is, arousal to images of harming another that has not
and homosexual courting.
crossed into the behavioral realm—can be treated in
outpatient settings.
Pedophilia
Frotteurism
Pedophilia is the most widely and intensely socially
repudiated of the paraphilias. Pedophiles are men who
Frotteurism, the need to touch and rub against noncon-
erotically and romantically prefer children or young
senting persons, although delineated as a criminal act, is
adolescents. They are grouped into categories depending
probably better understood as a less malignant form of
upon their erotic preferences for boys or girls and for in-
paraphilic sadism. Frotteurism often occurs in socially
fant, young, or pubertal children. Some pedophiles have
isolated men who become sexually driven to act out.
highly age- and sex-specific tastes, others are less dis-
They often are unaware of how frightening they can be.
criminating. Since the diagnosis of pedophilia requires,
over a period of at least 6 months, recurrent, intense sexu-
ally arousing fantasies, sexual urges, or behaviors involv- Noncriminal Forms of Paraphilia
ing sexual activity with a prepubescent child or children
the disorder should not be expected to be present in every Because the individual manifestations of paraphilia
person who is guilty of child molestation. Some intrafa- depend on the particular individual life history of the
milial child abuse occurs over a shorter time interval and affected, over 40 paraphilic categories have been iden-
results from combinations of deteriorated marriages, sex- tified, although only a few are listed in the DSM-IV-TR.
ual deprivation, sociopathy, and substance abuse. Child Most of these are unusual means of attaining arousal
molestation, whether paraphilic or not, is a crime, how- during masturbation or consenting partner behaviors.
ever. Child molesters show several patterns of erectile Each of the themes identified below demonstrates a
responses to visual stimulation in the laboratory. Some wide range of manifestations from the bizarre to the
have their largest arousal to children of a specific age more “reasonable” and from the common to the unique.
and others respond to both children and adults. Others They often subtly combine elements of more than one
respond with their greatest arousal to aggressive cues. paraphilia.
Voyeurism Fetishism/Transvestic Fetishism
Men whose sexual life consists of watching homo- Fetishism, the pairing of arousal with wearing or hold-
sexual or heterosexual videos in sexual book stores ing an article of clothing or inanimate object such as
occasionally come to psychiatric attention after being an inflatable doll, has a range of manifestations, from
charged with a crime following a police raid. They may infantilism in which a person dresses up in diapers to
or may not qualify for this diagnosis. The voyeurs who pretend he is a baby to the far more common use of a
are more problematic for society are those who watch female undergarment for arousal purposes. Fetishism
women through windows or break into their dwellings when confined to one garment for decades is classified
as a paraphilia, but many cases involve more complex out. Well-described cognitive–behavioral interventions
varieties of cross-dressing and overlap with gender exist for interrupting paraphilic arousal via pairing
identity disorders, usually GIDNOS. Fetishistic trans- masturbatory excitement with either aversive imagery
vestism is the diagnosis used when it is apparent that or aversive stimuli. Comprehensive behavioral treat-
the urges to use the clothing of the opposite sex are part ment involves social skills training, assertiveness train-
of a larger mental preoccupation with that sex. ing, and confrontation with the rationalizations that are
used to minimize awareness of the victims of sexual
crimes, and marital therapy. The self-help movement
Sexual Masochism
has created 12-step programs for sexual addictions to
which many individuals now belong. Group psycho-
Sexual masochism is diagnosed over a range of behav-
therapy is offered by trained therapists as well. When
iors from the sometimes fatal need to nearly asphyxi-
the lives of paraphilics are illuminated in various thera-
ate oneself to the request to be spanked by the partner
pies, it becomes apparent that the emotional pain of the
in order to be excited. Masochism may be the most
individuals is thought to be great; the sexual acting out
commonly reported or acknowledged form of female
is often perceived as a defense against recurrent un-
paraphilia, although it is more common among men.
pleasant emotions from any source. These often, how-
Sadists and masochists sometimes find one another and
ever, involve self-esteem and primitive anxiety.
work out an arrangement to act out their fantasies and
In the early 1980s, depo-medroxyprogesterone
occasionally reverse roles.
(Provera) was first used to treat those who were con-
stantly masturbating, seeking out personally dangerous
Paraphilia Not Otherwise Specified sexual outlets, or committing sex crimes. The weekly
400- to 600-mg injections often led to the men being
Paraphilia not otherwise specified is a DSM-IV-TR cat- able to work, study, or participate in activities that were
egory for other endpoints of abnormal sexual develop- previously beyond them because of concentration or
ment that lead to preoccupations with amputated body attention difficulties. In the late 1980s, the use of oral
parts, feces, urine, sexualized enemas, and sex with Provera, 20–120 mg/day led to similar results: the drug
animals. enabled these men to leave their former state in which
their sexual needs took priority over other life de-
mands—and they did not have depo-Provera’s side ef-
TREATMENT
fect profile: weight gain, hypertension, muscle cramps,
Four general approaches are employed to treat the and gynecomastia. Today, gonadotrophin-releasing
paraphilias: evaluation only, psychotherapy, medica- blockers are occasionally used for this purpose. The
tions, and external controls. The treatments are not possible side effects are similar to oral Provera. De-
mutually exclusive; rather, they are often multimodal spite the fact that the clinical results are among the
in application. most powerful effected by any psychopharmacologic
Evaluation only is often selected when the evalua- treatment, many clinicians cannot overcome their dis-
tor concludes that the paraphilia is benign in terms of inclination about giving a “female” hormone to a man
society, and the individual will be resistant to the other or working with individuals who victimize others sexu-
approaches, and does not suffer greatly in terms of so- ally. Serotonergic agents are now more commonly used
cial and vocational functioning in ways that might be as a first line of treatment. While these studies are not
improved. Often, these are isolated men with private as methodologically sophisticated as they need to be,
paraphilic sexual pleasures, such as telephone sex with the SSRIs are in widespread use for compulsive sexual
a masochistic scenario. behaviors and sexual obsessions. Their efficacy is the
What constitutes psychotherapy for paraphilia source of the speculation that some of the paraphilias
heavily depends on the therapist training rather than may be an obsessive–compulsive spectrum disorder.
strident declarations of treatment of choice. Little opti- Sexual advantage-taking, whether it be by a paraphilic
mism exists that any form of therapy can permanently clinician with the individuals under his care, by a pedo-
change the nature of a long-established paraphilic philic mentally retarded man in the neighborhood, or of
erotic script, even among teenage sex offenders. In- a grandfather who has abused several generations of his
dividual psychodynamic psychotherapy can be highly offspring, can often be stopped by making it impossible
useful in diminishing paraphilic intensifications and for these behaviors to be unknown to most people in his
gradually teaching the individual better management life. The clinician’s staff can be told, the neighbors can
techniques of the situations that have triggered acting know, the family can meet to discuss the current crisis
and review who has been abused over the years and plan criteria are essentially identical except that ICD-10
to never allow the grandfather alone with any child in specifies a minimum duration of at least 6 months
or outside the family. The concept of external control is (DSM-IV-TR has no minimum duration).
taken over by the judicial system when sex crimes are The ICD-10 Diagnostic Criteria for Research for Sex-
highly repugnant or heinous. The offender is removed ual Aversion Disorder differ from the DSM-IV-TR cri-
from society for punishment and the protection of the teria in several ways. In contrast to DSM-IV-TR, which
public. Increasing pressure exists to criminalize sexual restricts the condition to the aversion to, and avoidance
advantage-taking by clinicians who are even more sus- of, sexual genital contact, ICD-10 also includes pres-
ceptible to losing their licenses at least for several years. entations characterized by sexual activity resulting in
Clinicians need to be realistic about the limitations of “strong negative feelings and an inability to experience
various therapeutic ventures. Sexual acting out may read- any pleasure.” Furthermore, ICD-10 excludes cases
ily continue during therapy beyond the awareness of the in which the aversion is due to performance anxiety.
therapist. The more violent and destructive the paraphilic Finally, ICD-10 specifies a minimum duration of at
behavior to others, the less the therapist should risk am- least 6 month whereas DSM-IV-TR does not specify
bulatory treatment. Since paraphilia occurs in individu- any minimum duration.
als with other mental disorders, the clinician needs to For female sexual arousal disorder and male erectile
remain vigilant that the treatment program is comprehen- disorder, the ICD-10 Diagnostic Criteria for Research
sive and does not lose sight of the paraphilia just because and the DSM-IV-TR criteria are essentially equivalent
the depressive or compulsive symptoms are improved. except that ICD-10 specifies a minimum duration of
Paraphilia may be improved by medications and psycho- at least 6 months. ICD-10 includes a single category
therapy, but the clinician should expect that the intention (“Failure of Genital Response”) with two separate cri-
disorder is the individual’s lasting vulnerability. teria sets by gender. In contrast, DSM-IV-TR includes
two separate categories.
For female and male orgasmic disorders, the ICD-10
Sexual Disorder Not Otherwise Specified Diagnostic Criteria for Research and the DSM-IV-TR
criteria are essentially equivalent except that ICD-10
If the clinician is uncertain about how to categorize specifies a minimum duration of at least 6 months. In
a person’s problem, it is more reasonable to use this contrast to DSM-IV-TR, which has male and female
diagnosis than one that does not encompass the range versions defined separately, ICD-10 has a single cat-
of the individual’s suffering. Sexual disorder not other- egory that applies to both genders.
wise specified can be used when the therapist perceives For premature ejaculation, the ICD-10 Diagnostic
a dramatic interplay between issues of sexual identity Criteria for Research and the DSM-IV-TR criteria are
and sexual dysfunction, or when “everything” seems to essentially equivalent except that ICD-10 specifies a
be amiss. DSM-IV-TR, however, encourages the clini- minimum duration of at least 6 months. Similarly,
cian to make multiple sexual diagnoses involving, for the ICD-10 Diagnostic Criteria for Research and the
instance, a gender identity disorder, a desire disorder, DSM-IV-TR criteria for Dyspareunia and Vaginis-
erectile, and orgasmic disorder. mus are essentially equivalent except that ICD-10
DSM-IV-TR provides two examples when it would be specifies a minimum duration of at least 6 months.
appropriate to use the diagnosis sexual disorder NOS: Furthermore, these conditions are referred to in
(1) nonparaphilic compulsive sexual behaviors—that ICD-10 as “Nonorganic Dyspareunia” and “Nonor-
is, relentless pursuit of masturbatory or heterosexual ganic Vaginismus.”
or homosexual partner experiences without evidence The definition of a paraphilia is essentially the same
of paraphilic imagery; (2) complicated or exaggerated in DSM-IV-TR and ICD-10. However, ICD-10 does not
struggles to manage homosexual urges. include a separate category for Frotteurism and has a
combined “Sadomasochism” category.
For gender identity disorder, ICD-10 defines three
separate disorders: “Gender Identity Disorder of
DIAGNOSTIC CRITERIA
Childhood,” “Dual-role Transvestism,” and “Trans-
For hypoactive sexual desire disorder, the ICD-10 Di- sexualism,” all of which are included under the single
agnostic Criteria for Research and the DSM-IV-TR DSM-IV-TR category Gender Identity Disorder.
CHAPTER
38 Eating Disorders
In the current diagnostic nomenclature DSM-IV-TR, social stigmatization and its psychological sequelae.
eating disorders consist of two clearly defined syn- The widely held assumption that obesity is the result of
dromes: anorexia nervosa and bulimia nervosa. Many a psychiatric disorder in which eating is used as a cop-
individuals presenting for treatment of an eating disor- ing mechanism for depression or anxiety has not been
der fail to meet the formal criteria for either anorexia substantiated by empirical research.
nervosa or bulimia nervosa, which raises an important
theoretical and practical question: what is an eating
Anorexia Nervosa
disorder? Although this topic has received surprisingly
little attention, it has been suggested that a working
DIAGNOSIS
definition of an eating disorder might be “a persistent
disturbance of eating behavior or behavior intended to The DSM-IV-TR criteria for Anorexia Nervosa re-
control weight, which significantly impairs physical quire the individual to be significantly underweight
health or psychosocial functioning.” This definition for age and height. Although it is not possible to set
provides a basis for viewing eating disorders as clini- a single weight-loss standard that applies equally to
cally significant problems that do not meet criteria for
anorexia nervosa or bulimia nervosa. The term atypi- DSM-IV-TR Diagnostic Criteria
cal eating disorder is often applied to such problems,
even though the number of individuals suffering from 307.1 ANOREXIA NERVOSA
them may well outnumber those with “typical” eating A. Refusal to maintain body weight at or above a mini-
disorders. One example of an atypical eating disorder mally normal weight for age and height (e.g., weight
is that of women who are overly concerned about their loss leading to maintenance of body weight less than
85% of that expected; or failure to make expected
weight, have dieted to a below-normal weight, but have weight gain during period of growth, leading to body
not ceased menstruating and, therefore, do not meet weight less than 85% of that expected).
full criteria for anorexia nervosa. Another is that of B. Intense fear of gaining weight or becoming fat, even
though underweight.
individuals who binge and vomit regularly, but at less C. Disturbance in the way in which one’s body weight or
than the twice-a-week frequency required for bulimia shape is experienced, undue influence of body weight
nervosa. or shape on self-evaluation, or denial of the serious-
ness of the current low body weight.
An additional example of a clinically important D. In postmenarcheal females, amenorrhea, i.e., the ab-
atypical eating disorder is the occurrence of frequent sence of at least three consecutive menstrual cycles.
binge-eating that is not followed by the self-induced (A woman is considered to have amenorrhea if her
periods occur only following hormone, e.g., estrogen,
vomiting or other inappropriate attempts to compen- administration.)
sate that are characteristic of bulimia nervosa. This
disturbance is a common behavioral pattern among Specify type:
obese individuals who present for treatment at weight- Restricting type: during the current episode of anorexia
nervosa, the person has not regularly engaged in binge-
loss clinics. eating or purging behavior (i.e., self-induced vomiting or
At present, obesity is not formally considered an the misuse of laxatives, diuretics, or enemas).
eating disorder. Obesity refers to an excess of body fat Binge-eating/purging type: during the current episode
of anorexia nervosa, the person has regularly engaged in
and is viewed as a general medical, not a psychiatric, binge-eating or purging behavior (i.e., self-induced vom-
condition. At this stage of our knowledge, obesity is iting or the misuse of laxatives, diuretics, or enemas).
conceived as an etiologically heterogeneous condition. Reprinted with permission from the Diagnostic and Statistical
Obese individuals are at increased risk for a number of Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
serious medical problems and are subject to significant
all individuals, DSM-IV-TR provides a benchmark Medical Problems Commonly Associated

of 85% of the weight considered normal for age and Table 38-1
with Anorexia Nervosa
height as a guideline. Despite being of an abnormally
Skin
low body weight, individuals with anorexia nervosa Lanugo
are intensely afraid of gaining weight and becoming Cardiovascular system
fat, and remarkably, this fear typically intensifies as Hypotension
Bradycardia
the weight falls. Arrhythmias
DSM-IV-TR criterion C requires a disturbance in the Hematopoietic system
person’s judgment about his or her weight or shape. For Normochromic, normocytic anemia
Leukopenia
example, despite being underweight, individuals with Diminished polymorphonuclear leukocytes
anorexia nervosa often view themselves or a part of Fluid and electrolyte balance
their body as being too heavy. Typically, they deny the Elevated blood urea nitrogen and creatinine concentrations
Hypokalemia
grave medical risks engendered by their semistarva- Hyponatremia
tion and place enormous psychological importance on Hypochloremia
Alkalosis
whether they have gained or lost weight. For example, Gastrointestinal system
someone with anorexia nervosa may feel intensely dis- Elevated serum concentration of liver enzymes
tressed if her or his weight increases by half a pound. Delayed gastric emptying
Constipation
DSM-IV-TR suggests that individuals with anorexia Endocrine system
nervosa be classed as having one of two variants, either Diminished thyroxine level with normal thyroid-
the binge-eating/purging type or the restricting type. stimulating hormone level
Elevated plasma cortisol level
Individuals with the restricting type of anorexia ner- Diminished secretion of luteinizing hormone, follicle-
vosa do not engage regularly in either binge-eating or stimulating hormone, estrogen, or testosterone
purging, and compared with individuals with the binge- Bone
Osteoporosis
eating/purging form of the disorder, are not as likely to
abuse alcohol and other drugs, exhibit less mood labil-
ity, and are less active sexually. There are also indica-
tions that the two subtypes may differ in their response is clearly affected. Computed tomography has dem-
to pharmacological intervention. onstrated that individuals with anorexia nervosa have
In assessing individuals who may have anorexia ner- enlarged ventricles, an abnormality that improves with
vosa, it is important to obtain a weight history includ- weight gain. The cerebrospinal fluid concentrations of
ing the individual’s highest and lowest weights and the a variety of neurotransmitters and their metabolites are
weight he or she would like to be now. For women, it is altered in underweight individuals with anorexia ner-
useful to know the weight at which menstruation last oc- vosa and tend to normalize as weight is restored.
curred, because it provides an indication of what weight Some of the most striking physiological alterations
is normal for that individual. Probably the greatest in anorexia nervosa are those of the hypothalamic–
problem in the assessment of individuals with anorexia pituitary–gonadal axis. In women, estrogen secretion
nervosa is their denial of the illness and their reluctance from the ovaries is markedly reduced, accounting for
to participate in an evaluation. A straightforward but the occurrence of amenorrhea. In analogous fashion,
supportive and nonconfrontational style is probably the testosterone production is diminished in men with ano-
most useful approach, but it is likely that the individual rexia nervosa.
will not acknowledge significant difficulties in eating or In an adult with anorexia nervosa, the status of the
with weight and will rationalize unusual eating or exer- hypothalamic–pituitary–gonadal axis resembles that of
cise habits. It is therefore helpful to obtain information a pubertal or prepubertal child–the secretion of estro-
from other sources such as the individual’s family. gen or testosterone, of luteinizing hormone and follicle-
An impressive array of physical disturbances has stimulating hormone, and of gonadotropin-releasing
been documented in anorexia nervosa, and the physio- hormone is reduced.
logical bases of many are understood (Table 38-1). Most The functioning of other hormonal systems is also
of these physical disturbances appear to be secondary disrupted in anorexia nervosa, although typically not
consequences of starvation, and it is not clear whether as profoundly as is the reproductive axis. Presum-
or how the physiological disturbances described here ably as part of the metabolic response to semistar-
contribute to the development and maintenance of the vation, the activity of the thyroid gland is reduced.
psychological and behavioral abnormalities character- Plasma thyroxine levels are somewhat diminished,
istic of anorexia nervosa. The central nervous system but the plasma levels of the pituitary hormone and
Chapter 38 • Eating Disorders 401
thyroid-stimulating hormone are not elevated. The The motility of the gastrointestinal tract is dimin-
activity of the hypothalamic–pituitary–adrenal axis ished, leading to delayed gastric emptying and con-
is increased, as indicated by elevated plasma levels tributing to complaints of bloating and constipation.
of cortisol and by resistance to dexamethasone sup- Rare cases of acute gastric dilatation or gastric rupture,
pression. The regulation of vasopressin (antidiuretic which is often fatal, have been reported in individuals
hormone) secretion from the posterior pituitary is with anorexia nervosa who consumed large amounts of
disturbed, contributing to the development of partial food when binge-eating.
diabetes insipidus in some individuals. Anorexia nervosa is a relatively rare illness. Even
Anorexia nervosa is often associated with the devel- among high-risk groups, such as adolescent girls and
opment of leukopenia and of a normochromic, normo- young women, the prevalence of strictly defined ano-
cytic anemia of mild to moderate severity. Surprisingly, rexia nervosa is only about 0.5%. The prevalence rates
leukopenia does not appear to result in a high vulner- of partial syndromes are substantially higher, however.
ability to infectious illnesses. Serum levels of liver en- Despite the infrequent occurrence of anorexia nervosa,
zymes are sometimes elevated, particularly during the most studies suggest that its incidence has increased
early phases of refeeding, but the synthetic function of significantly during the past 50 years, a phenomenon
the liver is rarely seriously impaired so that the serum usually attributed to changes in cultural norms regard-
albumin concentration and the prothrombin time are ing desirable body shape and weight.
usually within normal limits. Serum cholesterol levels Anorexia nervosa usually affects women; the ra-
are sometimes elevated in anorexia nervosa, although tio of men to women is approximately 1 : 10 to 1 : 20.
the basis of this abnormality remains obscure. In some Anorexia nervosa occurs primarily in industrialized
individuals, self-imposed fluid restriction and exces- and affluent countries and some data suggest that even
sive exercise produce dehydration and elevations of within those countries, anorexia nervosa is more com-
serum creatinine and blood urea nitrogen. In others, mon among the higher socioeconomic classes. Some
water loading may lead to hyponatremia. The status of occupations, such as ballet dancing and fashion mod-
serum electrolytes is a reflection of the individual’s salt eling, appear to confer a particularly high risk for the
and water intake and the nature and the severity of the development of anorexia nervosa. Thus, anorexia ner-
purging behavior. A common pattern is hypokalemia, vosa appears more likely to develop in an environment
hypochloremia, and mild alkalosis resulting from fre- in which food is readily available but in which, for
quent and persistent self-induced vomiting. women, being thin is somehow equated with higher or
It has become clear that individuals with anorexia special achievement.
nervosa have decreased bone density compared with
age- and sex-matched peers and, as a result, are at in-
Course
creased risk for fractures. Low levels of estrogen, high
levels of cortisol, and poor nutrition have been cited as Anorexia nervosa often begins innocently. Typically,
risk factors for the development of reduced bone den- an adolescent girl or young woman who is of normal
sity in anorexia nervosa. Theoretically, estrogen treat- weight or, perhaps, a few pounds overweight decides to
ment might reduce the risk of osteoporosis in women diet. This decision may be prompted by an important but
who are chronically amenorrheic because of anorexia not extraordinary life event, such as leaving home for
nervosa, but controlled studies indicate that this inter- camp, attending a new school, or a casual unflattering
vention is of limited, if any, benefit. remark by a friend or family member. Initially, the diet-
Abnormalities of cardiac function include bradycar- ing seems no different from that pursued by many young
dia and hypotension, which are rarely symptomatic. women, but as weight falls, the dieting intensifies. The
The pump function of the heart is compromised, and restrictions become broader and more rigid; for exam-
congestive heart failure occasionally develops in in- ple, desserts may first be eliminated, then meat, then any
dividuals during overly rapid refeeding. The electro- food that is thought to contain fat. The person becomes
cardiogram shows sinus bradycardia and a number of increasingly uncomfortable if she is seen eating and
nonspecific abnormalities. Arrhythmias may develop, avoids meals with others. Food seems to assume a moral
often in association with fluid and electrolyte distur- quality so that, for example, vegetables are viewed as
bances. It has been suggested that significant prolon- “good” and anything with fat is “bad.” The individual
gation of the QT interval may be a harbinger of life- has idiosyncratic rules about how much exercise she
threatening arrhythmias in some individuals with must do, and when, where, and how she can eat.
anorexia nervosa, but this has not been conclusively Food avoidance and weight loss are accompanied by
demonstrated. a deep and reassuring sense of accomplishment, and
weight gain is viewed as a failure and a sign of weak- minimize their symptoms and suggest that the con-
ness. Physical activity, such as running or aerobic ex- cerns of the family and friends, who have often been
ercise, often increases as the dieting and weight loss instrumental in arranging the consultation, are greatly
develop. Inactivity and complaints of weakness usually exaggerated. It is helpful to identify a problem that the
occur only when emaciation has become extreme. The individual can acknowledge, such as weakness, irrita-
person becomes more serious and devotes little effort to bility, difficulty concentrating, or trouble with binge-
anything but work, dieting, and exercise. She may be- eating. The clinician may then attempt to educate the
come depressed and emotionally labile, socially with- individual regarding the pervasive physical and psy-
drawn, and secretive, and she may lie about her eating chological effects of semistarvation and about the need
and her weight. Despite the profound disturbances in for weight gain if the acknowledged problem is to be
her view of her weight and of her calorie needs, reality successfully addressed.
testing in other spheres is intact, and the person may A second goal of treatment is to assess and address
continue to function well in school or at work. Symp- acute medical problems, such as fluid and electrolyte
toms usually persist for months or years until, typically disturbances and cardiac arrhythmias. Depending on
at the insistence of friends or family, the person reluc- the severity of illness, this may require the involvement
tantly agrees to see a physician. of a general medical physician. The additional but most
difficult and time-consuming goals are the restoration
of normal body weight, the normalization of eating,
and the resolution of the associated psychological dis-
Although depression, schizophrenia, and obsessive– turbances. The final goal is the prevention of relapse.
compulsive disorder may be associated with disturbed As already noted, virtually all of the physiological
eating and weight loss, it is rarely difficult to differenti- abnormalities described in individuals with anorexia
ate these disorders from anorexia nervosa. Individuals nervosa are also seen in other forms of starvation, and
with major depression may lose significant amounts of most improve or disappear as weight returns to normal.
weight but do not exhibit the relentless drive for thin- Therefore, weight restoration is essential for physi-
ness characteristic of anorexia nervosa. In schizophre- ological recovery. Weight restoration also is believed
nia, starvation may occur because of delusions about to be essential for psychological recovery as well. Ac-
food, for example, that it is poisoned. Individuals with counts of human starvation amply document the pro-
obsessive–compulsive disorder may describe irrational found impact of starvation on mental health. Starving
concerns about food and develop rituals related to meal individuals lose their sense of humor, their interest in
preparation and eating but do not describe the intense friends and family fades, and mood generally becomes
fear of gaining weight and the pervasive wish to be thin depressed. They may develop peculiar behavior simi-
that characterize anorexia nervosa. lar to that of individuals with anorexia nervosa, such
A wide variety of medical problems cause seri- as hoarding food or concocting bizarre food combina-
ous weight loss in young people and may at times be tions. If starvation disrupts psychological and behav-
confused with anorexia nervosa. Examples of such ioral functioning in normal individuals, it presumably
problems include gastric outlet obstruction, Crohn’s does so as well in those with anorexia nervosa. Thus,
disease, and brain tumors. Individuals whose weight correction of starvation is a prerequisite for the restora-
loss is due to a general medical illness generally do not tion of both physical and psychological health.
show the drive for thinness, the fear of gaining weight, A common major impediment to the treatment of in-
and the increased physical activity characteristic of an- dividuals with anorexia nervosa is their disagreement
orexia nervosa. However, the clinician is well advised with the goals of treatment; many of the features of
to consider any chronic medical illness associated with their illness are simply not viewed by these individu-
weight loss, especially when evaluating individuals als as a problem. In addition, this may be compounded
with unusual clinical presentations such as late age at by a variety of concerns of the individual, such as ba-
onset or prominent physical complaints, for example, sic mistrust of relationships, feelings of vulnerability
pain and gastrointestinal cramping while eating. and inferiority, and sensitivity to perceived coercion.
Such concerns may be expressed through considerable
resistance, defiance, or pseudocompliance with the
TREATMENT
clinician’s interventions, and contribute to the power
The first goal of treatment is to engage the individual struggles that often characterize the treatment proc-
and her or his family. For most individuals with ano- ess. The clinician must try to avoid colluding with the
rexia nervosa, this is challenging. Individuals usually individual’s attempts to minimize problems but at the
Weight < 65% Yes During this phase of treatment, it is necessary to

of expected? monitor individuals carefully; many will resort to
Hospitalization throwing food away or vomiting after meals. Careful
No supervision is also required to obtain accurate weights;
individuals may consume large amounts of fluid be-
Weight < 75%
of expected? fore being weighed or hide heavy articles under their
clothing.
Day program or
During the weight restoration phase of treatment,
No
intensive outpatient individuals require substantial emotional support. It is
program probably best to address fears of weight gain with edu-
Medically or Yes
psychologically
cation about the dangers of semistarvation and with the
unstable (e.g., reassurance that individuals will not be allowed to gain
suicidal)? “too much” weight. Most eating-disorder units impose
behavioral restrictions, such as limits on physical ac-
No tivity, during the early phase of treatment. Some units
use an explicit behavior modification regimen in which
Yes Individual outpatient
Over 18
treatment & medical weight gain is tied to increased privileges and failure to
years old?
management gain weight results in bed rest.
No A consistent and structured treatment approach, with
or without an explicit behavior modification program, is
generally successful in promoting weight recovery but
Structured family requires substantial energy and coordination to main-
treatment & medical tain a supportive and nonpunitive treatment environ-
management
ment. In most experienced treatment units, parenteral
methods of nutrition, such as nasogastric feeding or
intravenous hyperalimentation, are only rarely needed.
Figure 38-1 Algorithm for choice of initial treatment of
anorexia nervosa.
Nutritional counseling and behavioral approaches can
also be effective in helping individuals expand their di-
etary repertoire to include foods they have been fright-
same time allow the individual enough independence ened of consuming.
to maintain the alliance. Dealing with such dilemmas As weight increases, individual, group, and family
is challenging and requires an active approach on the psychotherapy can begin to address other issues in ad-
part of the clinician. In most instances, it is possible dition to the distress engendered by gaining weight.
to preserve the alliance while nonetheless adhering to For example, it is typically important for individuals
established limits and the need for change. to recognize that they have come to base much of their
The initial stage of treatment should be aimed at self-esteem on dieting and weight control and are likely
reversing the nutritional and behavioral abnormalities to judge themselves according to harsh and unforgiv-
(Figure 38-1). The intensity of the treatment required ing standards. Similarly, individuals should be helped
and the need for partial or full hospitalization should to see how the eating disorder has interfered with
be determined by the current weight, the rapidity of the achievement of personal goals such as education,
weight loss, and the severity of associated medical and sports, or making friends.
behavioral problems and of other symptoms such as de- There is, at present, no general agreement about the
pression. In general, individuals whose weights are less most useful type of psychotherapy or the specific top-
than 75% of the expected weight should be viewed as ics that need to be addressed. Most eating disorders
medically precarious and require intensive treatment, programs employ a variety of psychotherapeutic inter-
such as hospitalization. ventions. A number of experts recommend the use of
Most inpatient or day treatment units experienced individual and group psychotherapy using cognitive–
in the care of individuals with anorexia nervosa use a behavioral techniques to modify the irrational overem-
structured treatment approach that relies heavily on su- phasis on weight. Although most authorities see little
pervision of calorie intake by the staff. After the initial role for traditional psychoanalytic therapy, individual
medical assessment has been completed and weight has and group psychodynamic therapy can address such
stabilized, calorie intake is gradually increased to an problems as insecure attachment, separation and indi-
amount necessary to gain 2 to 5 lb/week. viduation, sexual relationships, and other interpersonal
concerns. There is good evidence supporting the in-

volvement of the family in the treatment of younger DSM-IV-TR Diagnostic Criteria
individuals with anorexia nervosa. Family therapy can 307.51 BULIMIA NERVOSA
be helpful in addressing family members’ fears about
the illness; interventions typically emphasize parental A. Recurrent episodes of binge-eating. An episode of
binge-eating is characterized by both of the following:
cooperation, mutual support and consistency, and es-
tablishing boundaries regarding the individual’s symp- (1) eating, in a discrete period of time (e.g., within any
2-hour period), an amount of food that is definitely
toms and other aspects of his or her life. larger than most people would eat during a similar
Despite the multiple physiological disturbances as- period of time and under similar circumstances.
sociated with anorexia nervosa, there is no clearly es- (2) a sense of lack of control over eating during the
episode (e.g., a feeling that one cannot stop eating
tablished role for medication. or control what or how much one is eating).
A large percentage of individuals with anorexia ner- B. Recurrent inappropriate compensatory behavior in or-
vosa remain chronically ill; 30–50% of individuals der to prevent weight gain, such as self-induced vom-
successfully treated in the hospital require rehospitali- iting; misuse of laxatives, diuretics, enemas, or other
medications; fasting; or excessive exercise.
zation within 1 year of discharge. Therefore, posthos- C. The binge-eating and inappropriate compensatory be-
pitalization outpatient treatments are recommended to haviors both occur, on average, at least twice a week
prevent relapse and improve overall short- and long- for 3 months.
D. Self-evaluation is unduly influenced by body shape
term functioning. Several studies have attempted to and weight.
evaluate the efficacy of various outpatient treatments E. The disturbance does not occur exclusively during epi-
sodes of anorexia nervosa.
for anorexia nervosa including behavioral, cognitive–
behavioral, and supportive psychotherapy, as well as Specify type:
a variety of nutritional counseling interventions. Al- Purging type: during the current episode of bulimia ner-
though most of these treatments seem to be helpful, the vosa, the person has regularly engaged in self-induced
clearest findings to date support two interventions. For vomiting or the misuse of laxatives, diuretics, or enemas.
Nonpurging type: during the current episode of bulimia
individuals whose anorexia nervosa started before age nervosa, the person has used other inappropriate com-
18 years and who have had the disorder for less than 3 pensatory behaviors, such as fasting or excessive exer-
years, family therapy is effective, and for adult indi- cise, but has not regularly engaged in self-induced vomit-
ing or the misuse of laxatives, diuretics, or enemas.
viduals, cognitive–behavioral therapy reduces the rate
of relapse. Preliminary information suggests that fluox- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
etine treatment may reduce the risk of relapse among American Psychiatric Association.
individuals with anorexia nervosa who have gained
weight, but additional controlled data are required to
document the usefulness of this intervention. vosa do indeed consume larger than normal amounts
of food.
Episodes of binge-eating are associated, by defini-
Bulimia Nervosa
tion, with a sense of loss of control. Once the eating
has begun, the individual feels unable to stop until an
DIAGNOSIS
excessive amount has been consumed. This loss of con-
The salient behavioral disturbance of bulimia nervosa trol is only subjective, in that most individuals with
is the occurrence of episodes of binge-eating. During bulimia nervosa will abruptly stop eating in the midst
these episodes, the individual consumes an amount of of a binge episode if interrupted, for example, by the
food that is unusually large considering the circum- unexpected arrival of a roommate.
stances under which it was eaten. Although this is a After overeating, individuals with bulimia nervosa
useful definition and conceptually reasonably clear, engage in some form of inappropriate behavior in an
it can be operationally difficult to distinguish normal attempt to avoid weight gain. Most individuals who
overeating from a small episode of binge-eating. In- present to eating disorders clinics with this syndrome
deed, the available data do not suggest that there is a report self-induced vomiting or the abuse of laxatives.
sharp dividing line between the size of binge-eating Other methods include misusing diuretics, fasting for
episodes and the size of other meals. On the other hand, long periods, and exercising extensively after eating
while the border between normal and abnormal eating binges.
may not be a sharp one, both individual reports and In the DSM-IV-TR nomenclature, the diagnosis of
laboratory studies of eating behavior clearly indicate bulimia nervosa is not given to individuals with ano-
that, when binge-eating, individuals with bulimia ner- rexia nervosa. Individuals with anorexia nervosa who
recurrently engage in binge-eating or purging behav- number of ingested calories. The weight loss associated
ior should be given the diagnosis of anorexia nervosa, with the misuse of laxatives and diuretics is primarily
binge-eating/purging subtype, rather than an additional due to the loss of fluid and electrolytes, not calories.
diagnosis of bulimia nervosa. When not binge-eating, individuals with bulimia
In DSM-IV-TR, a subtyping scheme was introduced nervosa tend to restrict their calorie intake and to
for bulimia nervosa in which individuals are classed avoid the foods usually consumed during episodes of
as having either the purging or the nonpurging type of binge-eating. Although there is some phenomenologi-
bulimia nervosa. This scheme was introduced for sev- cal resemblance between binge-eating and substance
eral reasons. First, those individuals who purge are at abuse, there is no evidence that physiological addiction
greater risk for the development of fluid and electro- plays any role in bulimia nervosa.
lyte disturbances such as hypokalemia. Second, data Among individuals with bulimia nervosa who are
suggest that individuals with the nonpurging type of seen at eating disorders clinics, there is an increased
bulimia nervosa weigh more and have fewer mental frequency of anxiety and mood disorders, especially
disorders compared with those with the purging type. major depressive disorder and dysthymic disorder, of
Finally, most of the published literature on the treat- drug and alcohol abuse, and of personality disorders. It
ment of bulimia nervosa has been based on studies of is not certain whether this comorbidity is also observed
individuals with the purging type of this disorder. in community samples or whether it is a characteristic
Bulimia nervosa typically begins after a young of individuals who seek treatment.
woman who sees herself as somewhat overweight starts In a small fraction of individuals, bulimia nervosa is
a diet and, after some initial success, begins to over- associated with the development of fluid and electrolyte
eat. Distressed by her lack of control and by her fear abnormalities that result from the self-induced vomit-
of gaining weight, she decides to compensate for the ing or the misuse of laxatives or diuretics. The most
overeating by inducing vomiting or taking laxatives, common electrolyte disturbances are hypokalemia, hy-
methods she has heard about from friends or seen in ponatremia, and hypochloremia. Individuals who lose
media reports about eating disorders. After discovering substantial amounts of stomach acid through vomiting
that she can successfully purge, the individual may, for may become slightly alkalotic; those who abuse laxa-
a time, feel pleased in that she can eat large amounts tives may become slightly acidotic.
of food and not gain weight. However, the episodes of There is an increased frequency of menstrual dis-
binge-eating usually increase in size and in frequency turbances such as oligomenorrhea among women with
and occur after a variety of stimuli, such as transient bulimia nervosa. Several studies suggest that the hy-
depression or anxiety or a sense that she has begun pothalamic–pituitary–gonadal axis is subject to the
to overeat. Individuals often describe themselves as same type of disruption as is seen in anorexia nervosa
“numb” while they are binge-eating, suggesting that but that the abnormalities are much less frequent and
the eating may serve to avoid uncomfortable emotional severe.
states. Individuals usually feel intensely ashamed of Individuals who induce vomiting for many years
their “disgusting” habit and may become depressed by may develop dental erosion, especially of the upper
their lack of control over their eating. front teeth. The mechanism appears to be that stom-
The binge-eating tends to occur in the late afternoon ach acid softens the enamel, which in time gradually
or evening and almost always while the individual is disappears so that the teeth chip more easily and can
alone. The typical individual presenting to eating dis- become reduced in size. Some individuals develop
orders clinics has been binge-eating and inducing vom- painless salivary gland enlargement, which is thought
iting 5 to 10 times weekly for 3 to 10 years. Although to represent hypertrophy resulting from the repeated
there is substantial variation, binges tend to contain episodes of binge-eating and vomiting. The serum level
1000 or more calories and to consist of sweet, high- of amylase is sometimes mildly elevated in individuals
fat foods that are normally consumed as dessert, such with bulimia nervosa because of increased amounts of
as ice cream, cookies, and cake. Although individuals salivary amylase.
complain of “carbohydrate craving,” they only rarely Most individuals with bulimia nervosa have surpris-
binge-eat foods that are pure carbohydrates, such as ingly few gastrointestinal abnormalities. Potentially
fruits. Individuals usually induce vomiting or use their life-threatening complications such as an esophageal
characteristic compensatory behavior immediately after tear or gastric rupture occur, but fortunately, rarely. The
the binge and feel substantial relief that the calories are long-standing use of syrup of ipecac to induce vomit-
“gone.” In reality, it appears that vomiting is the only ing can lead to absorption of some of the alkaloids and
purging method capable of disposing of a significant cause permanent damage to nerve and muscle.
Over time, the symptoms of bulimia nervosa tend to they view as a binge does not contain an abnormally
improve although a substantial fraction of individuals large amount of food. Individuals with these charac-
continue to engage in binge-eating and purging. On teristics fall into the broad and heterogeneous category
the other hand, some controlled clinical trials have re- of atypical eating disorders. Binge-eating disorder (see
ported that structured forms of psychotherapy have the section on Binge-Eating Disorder, page 407), a cate-
potential to yield substantial and sustained recovery gory currently included in the DSM-IV-TR Appendix
in a significant fraction of individuals who complete B for categories that need additional research, is char-
treatment. It is not clear what factors are most predic- acterized by recurrent binge-eating similar to that seen
tive of good outcome, but those individuals who cease in bulimia nervosa but without the regular occurrence
binge-eating and purging completely during treatment of inappropriate compensatory behavior.
are least likely to relapse.
Soon after bulimia nervosa was recognized as a
TREATMENT
distinct disorder, surveys indicated that many young
women reported problems with binge-eating, and it was The power struggles that often complicate the treat-
suggested that the syndrome of bulimia nervosa was ment process in anorexia nervosa occur much less fre-
occurring in epidemic proportions. Later careful stud- quently in the treatment of individuals with bulimia
ies have found that although binge-eating is frequent, nervosa. This is largely because the critical behavioral
the full-blown disorder of bulimia nervosa is much less disturbances, binge-eating and purging, are less ego-
common, probably affecting 1–2% of young women in syntonic and are more distressing to these individuals.
the United States. Although sufficient research data do Most bulimia nervosa individuals who pursue treat-
not exist to pinpoint specific epidemiological trends in ment agree with the primary treatment goals, and wish
the occurrence of bulimia nervosa, research suggests to give up the core behavioral features of their illness.
that women born after 1960 have a higher risk for the As with anorexia nervosa, the first treatment consid-
illness than those born before 1960. eration is whether the individual is so medically or psy-
Bulimia nervosa primarily affects women; the ratio chologically unstable so as to require hospitalization or
of men to women is approximately 1 : 10. It also occurs a day treatment program (see Figure 38-2). If the indi-
more frequently in certain occupations (e.g., modeling) vidual is relatively stable, the next decision is whether
and sports (e.g., wrestling, running). to choose psychotherapy or medication.
The form of psychotherapy that has been examined
most intensively for the treatment of bulimia nervosa is
cognitive–behavioral therapy, modeled on the therapy
Bulimia nervosa is not difficult to recognize if a of the same type for depression. Cognitive–behavioral
full history is available. The binge-eating/purging therapy for bulimia nervosa concentrates on the dis-
type of anorexia nervosa has much in common with torted ideas about weight and shape, on the rigid rules
bulimia nervosa, but is distinguished by the charac- regarding food consumption and the pressure to diet,
teristic low body weight and, in women, amenorrhea. and on the events that trigger episodes of binge-eating.
Some individuals with atypical forms of depression The therapy is focused and highly structured and is
overeat when depressed; if the overeating meets the usually conducted in 3 to 6 months. Approximately
definition of a binge described previously (i.e., a large 25–50% of individuals with bulimia nervosa achieve
amount of food is consumed with a sense of loss of abstinence from binge-eating and purging during a
control), and if the binge-eating is followed by inap- course of cognitive–behavioral therapy, and in most,
propriate compensatory behavior, occurs sufficiently this improvement appears to be sustained. The most
frequently, and is associated with overconcern regard- common mode of cognitive–behavioral therapy is in-
ing body shape and weight, an additional diagnosis of dividual treatment, although it can be given in either
bulimia nervosa may be warranted. Some individu- individual or group format. The effect of cognitive–
als become nauseated and vomit when upset; this and behavioral therapy is greater than that of supportive
similar problems are probably not closely related to psychotherapy and of interpersonal therapy, indicating
bulimia nervosa and should be viewed as a somato- that cognitive–behavioral therapy should be the treat-
form disorder. ment of choice for bulimia nervosa.
Many individuals who believe they have bulimia The other commonly used mode of treatment that
nervosa have a symptom pattern that fails to meet has been examined in bulimia nervosa is the use of
full diagnostic criteria because the frequency of their antidepressant medication. This intervention was ini-
binge-eating is less than twice a week or because what tially prompted by the high rates of depression among
Medically or
psychologically Yes Hospitalization, day
unstable program, or intensive
(e.g., outpatient program
suicidal)?
No
Therapist
experienced Course of
in CBT Yes individual CBT
available?
No
Course of SSRI
treatment (e.g.,
fluoxetine, 60 mg/day)
Figure 38-2 Algorithm for choice of initial treatment of bulimia nervosa.
individuals with bulimia nervosa and has now been A major factor influencing the treatment of bulimia
tested in more than a dozen double-blind, placebo-con- nervosa is the presence of other significant psychiatric
trolled studies using a wide variety of antidepressant or medical illness. For example, it can be difficult for
medications. Active medication has been consistently individuals who are currently abusing drugs or alco-
found to be superior to placebo, and although there hol to use the treatment methods described, and many
have been no large “head-to-head” comparisons be- experts suggest that the substance abuse needs to be
tween different antidepressants, most antidepressants addressed before the eating disorder can be effectively
appear to possess roughly similar antibulimic potency treated. Other examples include the treatment of indi-
(Figure 38-3). Fluoxetine at a dose of 60 mg/day is viduals with bulimia nervosa and serious personality
favored by many investigators because it has been disturbance and those with insulin-dependent diabe-
studied in several large trials and appears to be at least tes mellitus who “purge” by omitting insulin doses.
as effective as, and better tolerated than, most other al- In treating such individuals, the clinician must decide
ternatives. It is notable that it has not been possible to which of the multiple problems must be first addressed,
link the effectiveness of antidepressant treatment for and may elect to tolerate a significant level of eating
bulimia nervosa to the pretreatment level of depres- disorder to confront more pressing disturbances.
sion. Depressed and nondepressed individuals with
bulimia nervosa respond equally well in terms of their
Binge-Eating Disorder
eating behavior to antidepressant medication.
Although antidepressant medication is clearly su-
DIAGNOSIS
perior to placebo in the treatment of bulimia nervosa,
several studies suggest that a course of a single anti- As noted earlier, binge-eating disorder is a proposed
depressant medication is generally inferior to a course diagnostic category related to, but quite distinct from,
of cognitive–behavioral therapy. However, individuals bulimia nervosa. The phenomenon of binge-eating
who fail to respond adequately to, or who relapse fol- without purging among the obese was clearly described
lowing a trial of psychotherapy, may still respond to 20 years before bulimia nervosa was recognized. Yet
antidepressant medication. binge-eating disorder has been the focus of sustained
% Reduction in binge frequency

−25 0 25 50 75 100
Imipramine*
Amitriptyline
Desipramine*
Imipramine*
Bupropion*
Phenelzine*
Trazodone*
Imipramine*
60 mg
Fluoxetine* 20 mg
Desipramine*
Fluoxetine*
Brofaromine
Drug
Imipramine
Placebo
Figure 38-3 Results of controlled trials of antidepressants in bulimia nervosa. (*indicates a statistically significant difference between
the active medication and placebo; Source: Reprinted from Child Adolesc Psychiatr Clin N Am 4, Walsh BT and Devlin MJ, Eating
disorders, 343–357, Copyright 1995 with permission from Elsevier.)
attention only in the past decade. Suggested diagnostic but it is not clear whether such behavior is best viewed
criteria for binge-eating disorder are included in an ap- as binge-eating.
pendix of DSM-IV-TR, which provides criteria sets for Individuals who meet the proposed definition of
further study. binge-eating disorder clearly have increased complaints
In theory, binge-eating disorder should be easy to of depression and anxiety compared to individuals of
recognize on the basis of individual self-report: the in- similar weight without binge-eating disorder.
dividual describes the frequent consumption of large Individuals with binge-eating disorder who are
amounts of food in a discrete period of time about obese should be followed by a primary care physician
which he or she feels distressed and unable to control. for assessment and treatment of the complications of
Difficulties arise, however, because of uncertainty obesity. There is no evidence suggesting that the be-
about what precisely constitutes a “large amount of havioral disturbances characteristic of binge-eating
food,” especially for an obese individual, and regard- disorder add to the physical risks of obesity. Whether
ing what constitutes a discrete period of time. Many in- the presence of binge-eating disorder affects the natu-
dividuals describe eating continuously during the day ral history of obesity is an intriguing but unanswered
or evening, thereby consuming a large amount of food, question.
Differential Diagnosis of more psychologically oriented treatments, such as

CBT.
As noted above, the most difficult issue in the diagnos-
tic assessment of binge-eating disorder is determining
whether the eating pattern of concern to the individual
meets the proposed definition of binge-eating. There
DIAGNOSTIC CRITERIA
are numerous varieties of unhealthy eating, such as
the consumption of high-fat foods, and the nosology The ICD-10 Diagnostic Criteria for Research and the
of these patterns of eating is poorly worked out. Some DSM-IV-TR criteria for anorexia nervosa differ in sev-
individuals with atypical depression binge-eat when eral ways. ICD-10 specifically requires that the weight
depressed; if the individual meets criteria for both loss be self-induced by the avoidance of “fattening
binge-eating disorder and an atypical depression, both foods” and that in men there be a loss of sexual interest
diagnoses should be made. and potency (corresponding to the amenorrhea require-
ment in women). Finally, in contrast to DSM-IV-TR,
which gives anorexia nervosa precedence over bulimia
TREATMENT
nervosa, ICD-10 excludes a diagnosis of anorexia ner-
For most individuals with binge-eating disorder, there vosa if regular binge-eating has been present.
are three related goals. One is behavioral, to cease For bulimia nervosa, the ICD-10 Diagnostic Criteria
binge-eating. A second focuses on improving symp- for Research and the DSM-IV-TR criteria for bulimia
toms of mood and anxiety disturbance, which are fre- nervosa are similar except that ICD-10 requires a “per-
quently associated with binge-eating disorder. The third sistent preoccupation with eating and a strong desire
is weight loss for individuals who are also obese. or sense of compulsion to eat.” Furthermore, whereas
Treatment approaches to binge-eating disorder are the ICD-10 definition requires a self-perception of be-
currently under active study. There is good evidence ing too fat (identical to an item in anorexia nervosa),
that psychological (e.g., CBT) and pharmacological the DSM-IV-TR criteria set requires instead that “self-
(e.g., SSRI) interventions that are effective for bulimia evaluation is unduly influenced by body shape and
nervosa are also useful in reducing the binge frequency weight.”
of individuals with binge-eating disorder and in al- Both DSM-IV-TR and ICD-10 include categories
leviating mood disturbance. However, it is not clear unique to their systems. DSM-IV-TR has a category for
how helpful these approaches are in facilitating weight “Binge-Eating Disorder” in its appendix of research
loss. Standard behavioral weight-loss interventions categories whereas ICD-10 has categories for “Overeat-
employing caloric restriction appear useful in helping associated with other psychological disturbances”
ing individuals control binge-eating, but the benefits and “Vomiting associated with other psychological
of such treatment have not been compared to those disturbances.”
CHAPTER
39 Sleep and Sleep–Wake

Disorders
Sleep disorders can be divided into four major categories or change in medications. Chronic sleep disorders, on
based on the type of sleep disturbance: (1) insomnias, the other hand, are often multidetermined and multi-
disorders associated with complaints of insufficient, faceted. (2) Does the individual suffer from any preex-
disturbed, or nonrestorative sleep; (2) hypersomnias, isting or comorbid disorders? Does another condition
disorders of excessive sleepiness; (3) disturbances of cause the sleep complaint, modify a sleep complaint,
the circadian sleep–wake cycle; and (4) parasomnias, or affect possible treatments? In general, because
abnormal behaviors or abnormal physiological events common sleep disorders are frequently secondary to
in sleep. By definition, the DSM-IV-TR limits itself to underlying causes, treatment should be directed at un-
chronic disorders (at least 1 month in duration). On the derlying medical, mental, pharmacological, psychoso-
other hand, the International Classification of Sleep cial, or other disorders.
Disorders includes sleep disorders of short-term and A detailed history of the complaint and attendant
intermediate duration, which in fact are more common symptoms must be obtained (Table 39-1). Special atten-
than chronic disorders. tion should be given to the timing of sleep and wakeful-
Sleep disorders can also be categorized according to ness; qualitative and quantitative subjective measures
presumed etiology. According to DSM-IV-TR, primary of sleep and wakefulness; abnormal sleep-related be-
sleep disorders are presumed to arise from endogenous haviors; respiratory difficulties; medications or other
abnormalities in sleep–wake-generating mechanisms, substances affecting sleep, wakefulness or arousal; ex-
timing mechanisms, sleep hygiene, or conditioning, pectations, concerns, attitudes about sleep, and efforts
rather than occurring secondary to medical or psychi- used by the individual to control symptoms; and the
atric disorders. Two types of primary sleep disorders sleep–wake environment. The clinician must be alert
are defined: dyssomnias (abnormalities in the amount, to the possibility that sleep complaints are somatic
quality, or timing of sleep) and parasomnias (abnormal symptoms, which reflect individual ways of experienc-
behaviors associated with sleep, such as nightmares or ing, expressing, and coping with psychosocial distress,
sleepwalking). Three other etiologic types of sleep stress, or psychiatric disorders.
disorders are included in DSM-IV-TR: sleep disorders Sleep disorders vary with age and gender and, pos-
related to other mental disorders, sleep disorders due sibly, with culture and social class. As mentioned previ-
to a general medical condition, and substance-induced ously, the circadian timing of rest–activity, duration of
sleep disorders. sleep at night, and daytime napping and sleepiness vary
with age and gender. In addition, parasomnias are most
common in boys, Kleine–Levin syndrome in adoles-
DIAGNOSIS
cent boys, delayed sleep phase syndrome in adolescents
To assist the individual with a sleep complaint, one and young adults, insomnia in middle-aged and elderly
needs to have a diagnostic framework with which one women, REM sleep behavior disorder and sleep-related
can obtain the information needed about both the in- breathing disorders in middle-aged men, and advanced
dividual as a person and his or her disorder. Two is- sleep phase syndrome in the elderly. Sleep–wake pat-
sues are particularly important: (1) How long has the terns are also influenced by cultural or geographical
individual had the sleep complaint? Transient insomnia factors, such as the siesta and late bedtime commonly
and short-term insomnia, for example, usually occur in associated with tropical climates, or the winter hyper-
persons undergoing acute stress or other disruptions, somnia and summer hyposomnia said to occur near the
such as admission to a hospital, jet lag, bereavement, arctic circle. Insomnia is more common in lower than
Chapter 39 • Sleep and Sleep–Wake Disorders 411
Office Evaluation of Chronic Sleep

necessary, arrange for sleep laboratory or ambulatory
Table 39-1 diagnostic procedures (see Table 39-2 for definitions of
Complaints
terms associated with clinical sleep laboratory studies).
A detailed history and review of the sleep complaint:
predisposing, precipitating, and perpetuating factors One of the most important and common laboratory
Review of difficulties falling asleep, maintaining sleep, and examinations is all-night polysomnography, which typ-
awakening early ically records the EEG activity’s eye movements with
The timing of sleep and wakefulness in the 24-hour day
Evidence of excessive daytime sleepiness and fatigue the electrooculogram, and muscle tone with the elec-
Bedtime routines, sleep setting, physical security, tromyogram from the chin (submental) muscles. These
preoccupations, anxiety, beliefs about sleep and sleep measures are used to determine sleep stages visually
loss, fears about consequences of sleep loss
Medical and neurological history and examination, routine scored as 20- or 30-second epochs by a sleep techni-
laboratory examinations: look for obesity, short fat neck, cian. To evaluate sleep-related respiration and cardio-
enlarged tonsils, narrow upper oral airway, foreshortened vascular function, measures are made of nasal and oral
jaw (retrognathia), and hypertension
Psychiatric history and present symptomatology air flow with a thermistor; of sounds of breathing and
Use of prescription and nonprescription medications, snoring with a small microphone near the mouth; of
alcohol, stimulants, toxins, insecticides, and other
substances
respiratory movements of the chest and abdominal
Evidence of sleep-related breathing disorders: snoring, walls; of heart rate with the electrocardiogram; and of
orthopnea, dyspnea, headaches, falling out of bed, blood-oxygen saturation with finger oximetry. To eval-
nocturia
Abnormal movements or behaviors associated with sleep uate PLMS, an electromyogram from the shin (ante-
disorders: “jerky legs,” leg movements, myoclonus, rior tibial) muscles is obtained. Other more specialized
restless legs, leg cramps, cold feet, nightmares, enuresis, tests include intraesophageal pressures, which increase
sleepwalking, epilepsy, bruxism, sleep paralysis,
hypnagogic hallucinations, cataplexy, night sweats, and during the upper airway resistance syndrome if respi-
so on ration is impeded, nocturnal penile tumescence in the
Social and occupational history, marital status, living evaluation of impotence, and core body temperature
conditions, financial and security concerns, physical
activity (usually rectal or tympanic membrane).
Sleep–wake diary for 2 weeks Daytime sleepiness can be evaluated in the sleep
Interview with bed partners or persons who observe laboratory with the Multiple Sleep Latency Test, which
individual during sleep
Tape-recording of respiratory sounds during sleep to screen measures sleep latency during opportunities for nap-
for sleep apnea ping during the day. In addition, subjective sleepiness
can be assessed by a questionnaire, the Stanford Sleep-
iness Scale, in which the subject rates sleepiness on a
in middle and upper socioeconomic classes, perhaps 7-point scale at set intervals throughout the day.
reflecting the stress of poverty, crowding and lack of
privacy, poor medical care, drugs and alcohol, lack of
Dyssomnias
physical security, and so forth.
One approach to the differential diagnosis of per-
Primary Insomnia
sistent sleep disorders is suggested in the algorithm in
Figure 39-1. First, determine whether the sleep com-
DIAGNOSIS
plaint is due to another medical, psychiatric, or sub-
stance abuse disorder. Second, consider the role of Primary insomnia is a subjective complaint of poor,
circadian rhythm disturbances and sleep disorders as- insufficient, or nonrestorative sleep lasting more than
sociated with abnormal events predominantly during a month; associated with significant distress or impair-
sleep. Finally, evaluate in greater detail the complaints ment; and without obvious relationships to another
of insomnia (difficulty initiating or maintaining sleep) sleep, medical or mental disorder, or physiological ef-
and excessive sleepiness. fects of a substance (see DSM-IV-TR diagnostic cri-
Clinicians can usually diagnose most sleep disorders teria, page 413). Primary insomnia is similar to some
by traditional, simple but systematic clinical methods. insomnia diagnoses in the International Classification
Referral to a specialized sleep disorders center, however, of Sleep Disorders, including psychophysiological in-
should be considered in individuals suspected of having somnia, which is often ascribed to conditioned arousal
severe intractable insomnia, persistent excessive daytime factors; sleep state misperception, in which the mag-
sleepiness, and sleep disorders due to a general medi- nitude of the subjective complaint often exceeds that
cal condition (such as narcolepsy, REM sleep behavior of the objective abnormality; and idiopathic insomnia,
disorder, sleep apnea, periodic limb movements in sleep with a childhood onset and lifelong course.
[PLMS], or sleep-related epilepsy). Specialists in sleep Diagnosis and treatment of chronic insomnia are
disorders medicine will evaluate the individual and, if often challenging and difficult. Both the clinician and
A. Sleep disorder due to a general

Step 1: Consider the role of medical condition
general medical conditions, Yes B. Breathing-related sleep disorder
substance use, and other C. Substance-induced sleep disorder
mental disorders D. Other mental disorders and/or
insomnia related to a mental disorder
No
A. Circadian rhythm sleep disorder

Step 2: If the individual B. Sleep−wake schedule disorder
suffers from the sleep C. Delayed sleep phase
involved in shift work, Yes
D. Advanced sleep phase
frequently crosses over E. Shift work
time zones, or has F. Jet lag
abnormal timing of sleep G. Non-24-h day
No
A. Nightmare disorder
Step 3: Are the symptoms B. Sleep terror disorder
predominantly events during Yes C. Sleepwalking disorder
sleep (i.e., abrupt awakening, D. Periodic limb movements or
frightening dreams, walking restless legs syndrome
about while sleeping) E. Nocturnal panic attacks
No
A. Primary insomnia (if symptoms
Step 4: If the primary persist for more than 1 mo)
complaint is insomnia Yes
B. Dyssomnia not otherwise
(i.e., difficulty initiating or specified (symptoms persist
maintaining sleep) for less than 1 mo)
No A. Narcolepsy (sleep attacks)

B. Primary hypersomnia
(prolonged sleep episodes, regular
daytime sleep episodes)
Step 5: If the primary Yes C. Dyssomnia not otherwise specified
complaint is excessive D. Breathing-related sleep disorder
sleepiness or hypersomnia (see Step 1A)
E. Kleine−Levin syndrome
No F. Menstrual cycle-associated
hypersomnia
G. Atypical or winter depression
Step 6: If clinically significant
criteria are not met for a
previously described specific
disorder, or if one wants to Yes
Dyssomnia not otherwise specified
note symptoms as a more
complete evaluation is being
conducted
Figure 39-1 An algorithm for the differential diagnosis of persistent sleep disorder complaints.
the individual must be forbearing and realistic as they insomnia during a period of intense stress in her busi-
jointly explore the evolution, causes, manifestations, ness, but it continued long after the stress had been
and ramifications of the sleep complaint. In part, the satisfactorily resolved. Factors that contributed to
diagnosis of primary insomnia is reached by exclusion chronicity included her lifelong somewhat obsessive,
after a careful differential diagnosis of other causes. anxious personality structure and after the onset of
Simple answers and simple solutions are rare. Even her insomnia, her gradually escalating concerns about
if insomnia is initially precipitated by a single event her insomnia; these resulted in advanced sleep phase
or condition, chronic insomnia is usually maintained as she tried to spend more time in bed for “rest” and
by various predisposing and perpetuating factors. For the use of wine and sleeping pills at bedtime to sleep.
example, a business woman in her early thirties had If all these factors can be properly sorted out and dealt
Selected Disorders and Terms Used in DSM-IV-TR Diagnostic Criteria

Table 39-2
Clinical Sleep Disorders Medicine
Term Definition 307.42 PRIMARY INSOMNIA
Apnea index Number of apneic events per hour A. The predominant complaint is difficulty initiating or
of sleep; usually is considered maintaining sleep, or nonrestorative sleep, for at least
pathological if ⱖ5. 1 month.
Cataplexy Sudden, brief loss of muscle tone in B. The sleep disturbance (or associated daytime fatigue)
the waking stage, usually triggered causes clinically significant distress or impairment
by emotional arousal (laughing, in social, occupational, or other important areas of
anger, surprise), involving either a functioning.
few muscle groups (i.e., facial) or C. The sleep disturbance does not occur exclusively
most of major antigravity muscles during the course of narcolepsy, breathing-related
of the body; may be related to sleep disorder, circadian rhythm sleep disorder, or a
muscle atonia normally occurring parasomnia.
during REM sleep; is associated D. The disturbance does not occur exclusively during
with narcolepsy. the course of another mental disorder (e.g., major
Hypopnea 50% or more reduction in respiratory depressive disorder, generalized anxiety disorder, a
depth for 10 seconds or more delirium).
during sleep. E. The disturbance is not due to the direct physiological
Multiple sleep An objective method for determining effects of a substance (e.g., a drug of abuse, a medica-
latency test daytime sleepiness; sleep latency tion) or a general medical condition.
and REM latency are determined
for four or five naps (i.e., a 20-min Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
opportunity to sleep every 2 hours American Psychiatric Association.
between 10 a.m. and 6 p.m.);
normal mean values are above
15 minutes.
Periodic limb Number of leg kicks per hour of sleep;
movements in usually is considered pathological their apprehensions: “If I don’t get to sleep right now,
sleep index if ⱖ5. I’ll make a bad impression tomorrow.” Cognitive–
Polysomnography Describes detailed, sleep laboratory- behavioral therapy (CBT) therefore is very effective
based, clinical evaluation of
individual with sleep disorder; may Clinical management is often multidimensional, in-
include electroencephalographical volving psychosocial, behavioral, and pharmacological
measures, eye movements, approaches. The relationship with the treating clinician
muscle tone at chin and limbs,
respiratory movements of chest can often be important since many insomniac individu-
and abdomen, oxygen saturation, als are skeptical that they can be helped overtly. They
electrocardiogram, nocturnal are focused on the symptom rather than the underlying
penile tumescence, esophageal pH,
as indicated. causes, and are not psychologically minded. Behavio-
Respiratory Number of apneas and hypopneas per ral treatments, in combination with addressing sleep
disturbance hour of sleep. hygiene, may be helpful in treating psychophysiologi-
index
Sleep apnea Sleep-related breathing disorder cal and other insomnias. Relaxation training (progres-
characterized by at least five sive relaxation, autogenic training, meditation, deep
episodes of apnea per hour of sleep,
each longer than 10 seconds in
breathing) can be effective if overtaught to become
duration. automatic. Two other behavioral therapies have been
shown to be effective for insomnia: stimulus control
and sleep restriction therapy.
with, both the clinician and the individual will be The aim of stimulus control therapy is to break the
gratified. negative associations of being in bed unable to sleep
(Table 39-3). It is especially helpful for individuals
with sleep-onset insomnia and prolonged awakenings.
TREATMENT
Sleep restriction therapy (Table 39-4) is based on the
Treatment of insomnia should, insofar as possible, be observation that more time spent in bed leads to more
directed at identifiable causes, or those factors that fragmented sleep. Both therapies may take 3 to 4 weeks
perpetuate the disorders, such as temperament and or longer to be effective.
lifestyle, ineffective coping and defense mechanisms, A wide variety of sedating medications have com-
inappropriate use of alcohol or other substances, mala- monly been used as sleeping pills including benzodi-
daptive sleep–wake schedules, and excessive worry azepines, imidazopyridines (zolpidem), pyrazolopy-
about poor sleep. The harder these individuals try to rimidines (zaleplon), chloral hydrate, antihistamines
sleep, the worse it is. They keep themselves awake by (diphenhydramine, hydroxyzine, doxylamine), certain
Table 39-3 Sleep Hygiene and Stimulus Control Rules Comparison of Long and Short Half-Life
Table 39-6
Hypnotics
Curtail time spent awake while in bed.
Go to bed only when sleepy. Half-Life
Do not remain in bed for more than 20–30 minutes while
awake. Measure Short Long
Get up at the same time each day.
Avoid looking at the bedroom clock. Sedative hangover effects ⫹ ⫹⫹⫹⫹
Avoid caffeine, alcohol, and tobacco near bedtime. Accumulation with 0 ⫹⫹⫹
Exercise during the morning or afternoon. consecutive nightly use
Eat a light snack before bed. Tolerance ⫹⫹⫹ ⫹
Adjust sleeping environment for optimal temperature, Withdrawal insomnia ⫹⫹⫹ ⫹
sound, and darkness. Anxiolytic effects next day 0 ⫹⫹⫹
Do not worry right before and in bed. Use the bed for Amnesia ⫹⫹⫹ ⫹⫹
sleeping. Full benefits the first night ⫹⫹⫹ ⫹⫹
Do not nap during the day. Note: Although zaleplon is short acting, research suggests that it
does not have some of the problems of other short-acting hypnotics,
such as tolerance or withdrawal insomnia.
Table 39-4 Sleep Restriction Therapy
Stay in bed for the amount of time you think you sleep each ideal sleeping pill would shorten latency to sleep; main-
night, plus 15 minutes. tain normal physiological sleep all night without block-
Get up at the same time each day. ing normal behavioral responses to the crying baby or
Do not nap during the day.
When sleep efficiency is 85% (i.e., sleeping for 85% of the the alarm clock; leave neither hangover nor withdrawal
time in bed), go to bed 15 minutes earlier. effects the next day; and be devoid of tolerance and side
Repeat this process until you are sleeping for 8 hours or the
desired amount of time.
effects such as impairment of breathing, cognition, am-
Example: if you report sleeping only 5 hours a night and bulation, and coordination. Furthermore, sleeping pills
you normally get up at 6 a.m., you are allowed to be in should not be habit-forming or addictive. Unfortunately,
bed from 12:45 a.m. until 6 a.m.
the ideal sleeping pill has not yet been found. Sleep-
ing pills, if given in appropriate doses, are effective
antidepressants (amitriptyline, doxepin, trimipramine, compared to placebo at least from a few days to a few
and trazodone), barbiturates, and over-the-counter weeks. The duration of action of these medications is
medications. However, they do vary in their pharma- important for several reasons (Table 39-6). Drugs with
cokinetic properties and side effects (Table 39-5). The long half-life metabolites may have next-day hangover
Table 39-5 Clinical Characteristics of Sedative–Hypnotics

Active
Name Dose (mg) Absorption Metabolite Half-Life
Chlordiazepoxide 5–10 Intermediate Yes 2–4 d

(Librium)
Diazepam (Valium) 2–10 Fast Yes 2–4 d
Estazolam (ProSom)* 0.5–2.0 Intermediate Yes 17 h
Flurazepam 7.5–30 Intermediate to fast Yes 2–4 d
(Dalmane)*
Clorazepate 7.5–15 Fast Yes 2–4 d
(Tranxene)
Clonazepam 0.5–1.0 Intermediate Yes 2–3 d
(Klonopin)
Quazepam (Doral)* 7.5–15 Intermediate Yes 2–4 d
Oxazepam (Serax) 10–15 Slow No 8–12 h
Lorazepam (Ativan) 0.5–4.0 Intermediate No 10–20 h
Temazepam 7.5–15 Slow No 10–20 h
(Restoril)*
Alprazolam (Xanax) 0.25–2 Intermediate No 14 h
Zoplicone† 7.5–15 Fast Yes 4–6.5 h
Triazolam (Halcion)* 0.125–0.5 Intermediate No 2–5 h
Zolpidem (Ambien)* 5–10 Fast No 2–5 h
Zaleplon (Sonata)* 5–10 Fast No 1h
*
Marketed as a sleeping pill in the United States.
†
Not yet marketed in the United States.
effects and tend to accumulate with repeated nightly maintain sleep when administered to normal subjects
administration, especially in the elderly, who metabo- or, in a few studies, to individuals with insomnia, jet
lize and excrete the drugs more slowly than the young lag, or other circadian rhythm disturbances. In addition,
do. In addition, long half-life metabolites may act ad- it is possible that melatonin administration can shift the
dictively or synergistically the next day with alcohol, phase position of the underlying biological clock. The
with drugs with sedative side effects, or during peri- entraining effects of a dose of 0.5 mg melatonin act
ods of decreased alertness, such as the afternoon dip in like a “dark pulse,” that is, the phase–response curve is
arousal levels. Because the elderly are more sensitive nearly opposite that of light. Future research is needed
to both the benefits and the side effects at a given dose to fulfill the promise that melatonin can be used to pre-
than are younger individuals, a dose for the elderly and vent or treat some forms of insomnia or other sleep dis-
debilitated individual should normally be about half of orders, especially in the elderly, or in cases associated
that for young and middle-aged individuals. with circadian rhythm disorders (jet lag, shift work, the
Short half-life hypnotics usually produce less day- non-24-hour-day syndrome, phase displacement), neu-
time sedation than long half-life drugs, but they often rological disorders, or psychiatric disorders.
result in more rebound insomnia when they are discon- Melatonin is currently treated by the US Food and
tinued. Whereas nearly all hypnotics and sedatives can Drug Administration as a nutritional supplement rather
produce amnesia, the problem may be more common than a medication. Therefore, purity of the product,
with some short half-life drugs, especially for material safety, efficacy, and claims by manufacturers are not
that is learned during the periods of peak concentra- carefully regulated in the United States. Physicians are
tions of drugs, for example, if the subject is awakened advised to maintain a watchful eye at this time and to
during the middle of the night. Administration of za- be prudently cautious about recommendations to indi-
leplon 4 hours or more before arising in the morning viduals and the public about the uses and benefits of
does not appear to be associated with impairment in melatonin.
motor performance.
Individuals should be educated about the anticipated
Primary Hypersomnia
benefits and limitations of sleeping pills, side effects,
and appropriate use, and should be followed up by of-
DIAGNOSIS
fice visits or phone calls regularly if prescriptions are
renewed. Although hypnotics are usually prescribed A specific diagnostic category for primary hypersomnia
for relatively short periods of time (2–6 weeks at most), exists in DSM-IV-TR, defining a disorder characterized
about 0.5–1% of the population uses a hypnotic nearly by clinically significant excessive sleepiness of at least
every night for months or years. Whether this practice 1 month’s duration, with significant distress or impair-
is good, useless, or bad remains controversial. Treat- ment (see DSM-IV-TR diagnostic criteria, page 416).
ment of these individuals should focus on the lowest Previously called non-REM narcolepsy, this rela-
possible effective dose—intermittently if possible—for tively rare disorder is represented by perhaps 5–10%
the treatment of insomnia. of individuals presenting to sleep disorders centers
Hypnotics are relatively contraindicated in individu- for evaluation of hypersomnia. The diagnosis must be
als with sleep-disordered breathing; during pregnancy; made on the basis of polysomnographic confirmation
in substance abusers, particularly alcohol abusers; and of hypersomnia; subjective complaints of excessive
in those individuals who may need to be alert during sleepiness are not adequate. A family history of exces-
their sleep period (e.g., physicians on call). In addition, sive sleepiness may be present.
caution should be used in prescribing hypnotics to in- Although usually seen as a persistent complaint,
dividuals who snore loudly, to individuals who have re- primary hypersomnia includes recurrent forms, well
nal, hepatic, or pulmonary disease, and to the elderly. defined with periods of excessive sleepiness of at least
The limited database available suggests that mela- 3 days’ duration occurring several times a year for
tonin may eventually have a role in the prevention and at least 2 years. Among the recurrent or intermittent
treatment of circadian and sleep disturbances. Some hypersomnia disorders are Kleine–Levin syndrome,
evidence suggests that it has intrinsic hypnotic effects. usually seen in adolescent boys, and menstrual cycle–
Laboratory studies suggest that people are more likely associated hypersomnia syndrome. In addition to hy-
to sleep during the period of endogenous melatonin persomnia (up to 18 hours per day), individuals with
secretion than during periods of the day without mela- Kleine–Levin syndrome often demonstrate aggres-
tonin secretion. Furthermore, some, but not all, studies sive or inappropriate sexuality, compulsive overeating,
suggest that melatonin (0.3–10.0 mg) may induce and and other bizarre behaviors. The rare nature of this
no significant therapeutic effects. For individuals intol-

DSM-IV-TR Diagnostic Criteria erant of, or insensitive to, stimulants, some success has
307.44 PRIMARY HYPERSOMNIA
been obtained with the use of stimulating antidepres-
sants, both of the MAOI and the selective serotonin
A. The predominant complaint is excessive sleepiness for reuptake inhibitor (SSRI) classes. Methysergide, a se-
at least 1 month (or less if recurrent) as evidenced by
either prolonged sleep episodes or daytime sleep epi- rotonin receptor antagonist, may be effective in some
sodes that occur almost daily. treatment-resistant cases but must be used with caution
B. The excessive sleepiness causes clinically significant in view of the possibility of pleural and retroperitoneal
distress or impairment in social, occupational, or other
important areas of functioning. fibrosis with persistent, uninterrupted use. Careful
C. The excessive sleepiness is not better accounted for documentation should be maintained of interruption of
by insomnia and does not occur exclusively during drug use at regular intervals and of physical examina-
the course of another sleep disorder (e.g., narcolepsy,
breathing-related sleep disorder, circadian rhythm tions that find the absence of obvious side effects of
sleep disorder, or a parasomnia) and cannot be ac- any sort.
counted for by an inadequate amount of sleep.
D. The disturbance does not occur exclusively during the
course of another mental disorder. Narcolepsy
E. The disturbance is not due to the direct physiological
tion) or a general medical condition. DIAGNOSIS
Specify if: Narcolepsy is associated with a pentad of symptoms:
Recurrent: if there are periods of excessive sleepiness (1) excessive daytime sleepiness, characterized by ir-
that last at least 3 days occurring several times a year for resistible “attacks” of sleep in inappropriate situations
at least 2 years
such as driving a car, talking to a supervisor, or social
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 events; (2) cataplexy, which is sudden bilateral loss of
American Psychiatric Association. muscle tone, usually lasting seconds to minutes, gen-
erally precipitated by strong emotions such as laugh-
ter, anger, or surprise; (3) poor or disturbed nocturnal
syndrome and its unusual behaviors may be mistaken sleep; (4) hypnagogic hallucinations, varied dreams at
for psychosis, malingering, or a personality disorder. sleep onset; and (5) sleep paralysis, a brief period of
Another syndrome, idiopathic recurring stupor, has paralysis associated with the transitions into, and out
been described and may be confused with hypersom- of, sleep.
nia. Individuals experience attacks of stupor or coma Narcolepsy is lifelong. The first symptom is usually
as infrequently as once or twice a year to as often as excessive sleepiness, typically developing during the
once a week. The duration of each episode varies from late teens and early twenties. The full syndrome of cat-
2 hours to 4 days. Unlike individuals with hypersom- aplexy and other symptoms unfolds in several years.
nia, these individuals are in a stuporous coma-like state Observers may mistake classic sleepiness in its mild
and cannot be easily aroused or awakened. form as withdrawal, poor motivation, negativism, and
Aside from associated general medical conditions hostility. The hypnagogic imagery and sleep paralysis
and mental disorders, the frequency and importance symptoms, alone and in combination, may resemble bi-
of hypersomnia and daytime sleepiness in otherwise zarre psychiatric illness. Like many medical disorders,
healthy individuals have been increasingly recognized. narcolepsy presents a wide range of severity, from mild
Sleepiness, for example, as a result of sleep depriva- to cases so severe that employment is functionally im-
tion, disrupted sleep, or circadian dyssynchronization, possible. Partial remissions and exacerbations occur.
probably plays a major role in mistakes and accidents Sleep paralysis and hypnagogic imagery may be seen
in sleepy drivers, interns and medical staff, and indus- without cataplexy; cataplexy may present in isolation
trial workers. without other REM-associated phenomena. The pres-
ence of REM sleep onset at night or during daytime
naps, an important sleep laboratory parameter, re-
TREATMENT
mains the most valid and reliable method available for
Clinical management is controversial owing to the lack diagnosing narcolepsy. Because of the seriousness of
of controlled studies. As in narcolepsy, the stimulant the disorder and likelihood that amphetamine or other
compounds are the most widely used and most often stimulants will be used to treat the individual at some
successful of the treatment options available. However, time, it is important that the diagnosis of narcolepsy be
some individuals are intolerant of stimulants or report objectively verified as soon as possible. Furthermore,
stimulant abusers have been known to feign symptoms motivation and performance, and inappropriate and
of narcolepsy to obtain prescriptions. inadvertent attacks of sleep. Sometimes the individu-
als do not realize they have fallen asleep until they
awaken.
TREATMENT
The second complaint is loud snoring, sometimes
The major goals of treatment of narcolepsy include (a) noisy enough to be heard throughout or even outside
to improve quality of life, (b) to reduce excessive day- the house. Often the wife has complained for years
time sleepiness (EDS), and (c) to prevent cataplectic about the snoring and has threatened to sleep elsewhere
attacks. The major wake-promoting medications are if she has not moved out already. Bed partners describe
modafinil, amphetamine, dextroamphetamine, and a characteristic pattern of loud snoring interrupted by
methylphenidate. Modafinil is preferred on grounds periods of silence, which are then terminated by snort-
of efficacy, safety, availability, and low risk of abuse ing sounds. Snoring results from a partial narrowing
and diversion. The pharmacological treatment of cata- of the airway caused by multiple factors, such as in-
plexy, sleep paralysis, and hypnagogic hallucinations adequate muscle tone, large tonsils and adenoids, long
includes administration of activating SSRIs such as soft palate, flaccid tissue, acromegaly, hypothyroidism,
fluoxetine and tricyclic antidepressants such as prot- or congenital narrowing of the oral pharynx. Snoring
riptyline. Another new drug, sodium oxybate xyrem, has been implicated not only in sleep apnea but also
appears to be well tolerated and beneficial for the treat- in angina pectoris, stroke, ischemic heart disease,
ment of cataplexy, daytime sleepiness, and inadvertent and cerebral infarction, even in the absence of com-
sleep attacks. plete sleep apneas. Because the prevalence of snoring
increases with age, especially in women, and because
snoring can have serious medical consequences, the
Breathing-Related Sleep Disorder
psychiatrist must give serious attention to complaints
of loud snoring. Snoring is not always a symptom of
DIAGNOSIS
BRSD. Approximately 25% of men and 15% of women
The essential feature of breathing-related sleep disor- are habitual snorers.
der (BRSD) is sleep disruption resulting from sleep ap- Other symptoms of BRSD include unexplained
nea or alveolar hypoventilation, leading to complaints morning headaches, nocturnal confusion, automatic
of insomnia or, more commonly, excessive sleepiness. behavior, dysfunction of the autonomic nervous system,
The disorder is not accounted for by other medical or night sweats. The severity of BRSD will depend on
or psychiatric disorders or by medications or other the severity of the cardiac arrhythmias, hypertension,
substances. excessive daytime sleepiness, respiratory disturbance
Sleep apnea is characterized by repetitive episodes index, amount of sleep fragmentation, and amount of
of upper airway obstruction that occur during sleep, oxygen desaturation.
resulting in numerous interruptions of sleep continu- Mild to moderate sleep-related breathing distur-
ity, hypoxemia, hypercapnia, bradytachycardia, and bances increase with age, even in elderly subjects with-
pulmonary and systemic hypertension. It may be as- out major complaints about their sleep. The frequency
sociated with snoring, morning headaches, dry mouth is higher in men than in women, at least until the age
on awakening, excessive movements during the night, of menopause, after which the rate in women increases
falling out of bed, enuresis, cognitive decline and per- and may approach that of men. With use of the apnea
sonality changes, and complaints of either insomnia index of 5 or more apneic episodes per hour as a cutoff
or, more frequently, hypersomnia and excessive day- criterion, prevalence rates range from 27% to 75% for
time sleepiness. The typical individual with clinical older men and from 0% to 32% for older women. In
sleep apnea is a middle-aged man who is overweight general, the severity of apnea in these older persons is
or who has anatomical conditions narrowing his upper mild (an average apnea index of about 13) compared
airway. with that seen in individuals with clinical sleep apnea.
The most common symptoms of BRSD include ex- However, older men and women with mild apnea have
cessive daytime sleepiness and snoring. The excessive been reported to fall asleep at inappropriate times sig-
daytime sleepiness probably results from sleep frag- nificantly more often than older persons without apnea.
mentation caused by the frequent nocturnal arousals Furthermore, the frequency of sleep apnea and other
occurring at the end of the apneas, and possibly from BRSDs is higher in individuals with hypertension,
hypoxemia. The excessive daytime sleepiness is as- congestive heart failure, obesity, dementia, and other
sociated with lethargy, poor concentration, decreased medical conditions.
The diagnosis of BRSD must be differentiated from sleep phase, shift work, jet lag, and a non-24-hour-day
other disorders of excessive sleepiness such as nar- syndrome.
colepsy. Individuals with BRSD will not have cataplexy, The diagnosis of circadian rhythm sleep disorder
sleep-onset paralysis, or sleep-onset hallucination. is based on a careful review of the history and circa-
Narcolepsy is not usually associated with loud snoring dian patterns of sleep–wakefulness, napping, alertness,
or sleep apneas. In laboratory recordings, individuals and behavior. The diagnosis of circadian rhythm sleep
with BRSD do not usually have sleep-onset REM peri- disorder requires significant social or occupational im-
ods either at night or in multiple naps on the Multiple pairment or marked distress related to the sleep distur-
Sleep Latency Test. However, one must be aware that bance. It is often useful for individuals with chronic
both BRSD and narcolepsy can be found in the same complaints to keep a sleep–wake diary covering the en-
individual. BRSD must also be distinguished from tire 24-hour day each day for several weeks. If possible,
other hypersomnias, such as those related to major de- an ambulatory device that measures rest–activity, such
pressive disorder or circadian rhythm disturbances. as a wrist actigraph, might supplement the sleep–wake
diary. Wrist actigraphs record acceleration of the wrist
at frequent intervals, such as every minute, and save
TREATMENT it for later display. Because the wrist is mostly at rest
Sleep apnea is sometimes alleviated by weight loss, during sleep, the record of wrist rest–activity provides
avoidance of sedatives, use of tongue-retaining devices, a fairly accurate estimate of the timing and duration
and breathing air under positive pressure through a face of sleep–wakefulness. In addition, some commercial
mask (continuous positive airway pressure [CPAP]). wrist activity devices have a built-in photometer, which
Oxygen breathed at night may alleviate insomnia asso- provides a record of ambient light–darkness against
ciated with apnea that is not accompanied by impeded which the rest–activity pattern can be compared.
inspiration. Surgery may be helpful, for example, to The prevalence of circadian rhythm disturbances
correct enlarged tonsils, a long uvula, a short mandi- has not been established. Approximately two-thirds
ble, or morbid obesity. Pharyngoplasty, which tightens of shift workers have difficulty with their schedules.
the pharyngeal mucosa and may also reduce the size Circadian rhythm disturbances must be differentiated
of the uvula, or the use of a cervical collar to extend from sleep-onset insomnia due to other causes (such as
the neck, may relieve heavy snoring. Although tricyclic pain, caffeine consumption), early morning insomnia
antidepressants are sometimes used in the treatment of due to depression or alcohol use, and changes in sleep
clinical sleep apnea in young adults, they may cause patterns due to lifestyle or lifestyle changes.
considerable toxic effects in older people. The newer
shorter-acting nonbenzodiazepine hypnotics seem to Delayed Sleep Phase Type
be safer in these individuals and may be considered in
those individuals who snore. DIAGNOSIS
In the delayed sleep phase type, there is a delay in the
Circadian Rhythm Sleep Disorder (Sleep–Wake circadian rhythm in the sleep–wake cycle. These in-
Schedule Disorders) dividuals are generally not sleepy until several hours
after “normal” bedtime (i.e., 2–3 a.m.). If allowed to
Circadian rhythm disturbances result from a mismatch sleep undisturbed, they will sleep for 7 or 8 hours,
between the internal or endogenous circadian sleep– which means they awaken around 10 to 11 a.m. Peo-
wake system and the external or exogenous demands ple with delayed sleep phase are considered extreme
on the sleep–wake system. The individual’s tendency “owls.” They may or may not complain of sleep-onset
to sleep–wakefulness does not match that of her or insomnia. They usually enjoy their alertness in the
his social circumstances or of the light–dark cycle. evening and night and have little desire to sleep begin-
Although some individuals do not find this mismatch ning at 10 p.m. or midnight. Their problem is trying to
to be a problem, for others the circadian rhythm dis- wake up at normal times (i.e., 6–7 a.m.). In essence,
turbance interferes with the ability to function prop- their rhythm is shifted to a later clock time relative to
erly at times when alertness or sleepiness is desired conventional rest–activity patterns.
or required. For those individuals, insomnia, hyper- Individuals with delayed sleep phase often choose
somnia, sleepiness, and fatigue result in significant careers that allow them to set their own schedules, such
discomfort and impairment. The circadian rhythm as freelance writers. Delayed sleep phase occurs com-
disturbances include delayed sleep phase, advanced monly in late adolescence and young adulthood, such
as in college students. As many of these individuals of the endogenous circadian oscillator to the imposed
age, however, their endogenous sleep–wake rhythm ad- sleep–wake cycle is necessary.
vances and they eventually are able to conform them-
selves to a normal rest period at night.
TREATMENT
For others, however, this phase shift of the endog-
enous oscillator may lead at a later age to the advanced No totally satisfactory methods currently exist for man-
sleep phase. In this condition, individuals become aging shift-work problems. Because people vary in their
sleepy earlier in the evening (e.g., 7–8 p.m.). They will ability to adjust to these schedules, self-selection may
also sleep for 7 to 8 hours, but that means they awaken be involved for those who can find other employment
around 2 to 3 a.m. These individuals are “larks,” be- or work schedules. Older individuals appear to be less
ing most alert in the morning. They complain of sleep flexible than younger persons in adjusting to shift work.
maintenance insomnia, that is, they cannot stay asleep Some experiments suggest that the principles of chrono-
all night long. This condition is more prevalent in the biology may be useful in reducing the human costs of
elderly than in the young. shift work. For example, because the endogenous pace-
maker has a cycle length (tau) longer than 24 hours, rotat-
ing shift workers do better when their schedules move in
TREATMENT
a clockwise direction (i.e., morning to evening to night)
Clinical management includes chronobiological strat- rather than in the other direction. Appropriate exposure
egies to shift the phase position of the endogenous to bright lights and darkness may push the circadian
circadian oscillator in the appropriate direction. For pacemaker in the correct direction and help stabilize its
example, exposure to bright light in the morning ad- phase position, especially in association with the use of
vances the delayed sleep phase, that is, individuals dark glasses outside and blackout curtains at home to
will become sleepy earlier in the evening. On the other maintain darkness at the appropriate times for promo-
hand, administration of bright light in the evening acts tion of sleep and shifting of the circadian pacemaker.
to delay the circadian rhythm, that is, individuals will Naps may also be useful in reducing sleep loss. Modest
get sleepy later in the evening. Light is usually admin- amounts of coffee may maintain alertness early in the
istered in doses of 2500 lux for a period of 2 hours per shift but should be avoided near the end of the shift.
day, although the ideal intensity and duration are yet to
be determined. For some individuals, spending more
Jet Lag Type
time outdoors in bright sunlight may be sufficient to
treat the sleep phase. For example, individuals with
DIAGNOSIS
delayed sleep phase should be encouraged to remove
blinds and curtains from their windows, which would Jet lag occurs when individuals travel across several
allow the sunlight to pour into their bedrooms in the time zones. Traveling east advances the sleep–wake
morning when they should arise. In addition, gradual cycle and is typically more difficult than traveling west
adjustments of the timing of the sleep–wake cycle may (which delays the cycle). Jet lag may be associated with
be used to readjust the phase position of the circadian difficulty initiating or maintaining sleep or with day-
oscillator. For example, individuals with delayed phase time sleepiness, impaired performance, and gastroin-
disorder can be advised to delay the onset of sleep by testinal disturbance after rapid transmeridian flights.
2 to 3 hours each day (i.e., from 4 to 7 to 10 a.m., and Individuals older than 50 years appear to be more vul-
so on) until the appropriate bedtime. After that, they nerable to jet lag than are younger persons.
should maintain regular sleep–wake patterns, with ex-
posure to bright light in the morning.
TREATMENT
Considerable research and theorizing are under way to
Shift-Work Type
better prevent and manage the problems associated with
jet lag. Some efforts before departure may be useful to
DIAGNOSIS
prevent or ameliorate these problems. For persons who
Shift-work problems occur when the circadian sleep– plan to readjust their circadian clock to the new location,
wake rhythm is in conflict with the rest–activity cycle it may be possible to move the sleep–wake and light–
imposed by the externally determined work schedule. dark schedules appropriately before departure. In addi-
Rotating work schedules, particularly rapidly shifting tion, good sleep hygiene principles should be respected
schedules, are difficult because constant readjustment before, during, and after the trip. For example, many
people are sleep deprived or in alcohol withdrawal when or hot feet, disrupted and torn bedclothes, unrefreshing
they step on the plane because of last-minute prepara- sleep, insomnia, or excessive daytime sleepiness. Indi-
tions or farewell parties. Whereas adequate fluid intake viduals may be unaware of these pathological leg move-
on the plane is necessary to avoid dehydration, alcohol ments or arousals, although their bed partners may be
consumption should be avoided or minimized because all too aware of the kicking, frequent movements, and
it causes diuresis and may disrupt sleep maintenance. restlessness. If these disorders are strongly suspected,
On arriving at the destination, it may be preferable to the individual should probably be referred to a sleep
try to maintain a schedule coinciding with actual home disorders laboratory for evaluation and an overnight
time if the trip is going to be short. For example, the indi- polysomnogram with tibial electromyograms.
vidual should try to sleep at times that correspond to the A related disturbance, restless legs syndrome, is as-
usual bedtime or with the normal midafternoon dip in sociated with disagreeable sensations in the lower legs,
alertness. If, on the other hand, the trip will be longer and feet, or thighs that occur in a recumbent or resting posi-
it is desirable to synchronize the biological clock with lo- tion and cause an almost irresistible urge to move the
cal time, exposure to appropriate schedules of bright light legs. Whereas almost all individuals with restless legs
and darkness may be helpful, at least theoretically. Unfor- syndrome have PLMS, not all individuals with PLMS
tunately, the exact protocols have not been established in have restless legs syndrome. Restless legs syndrome
all instances yet and require further research and experi- may be frequent in individuals with uremia and rheu-
mentation. In addition, some of these protocols require matoid arthritis or in pregnant women.
avoidance of bright light at certain times, necessitating
wearing dark goggles, for example, when traveling.
In addition to synchronizing the clock with the new TREATMENT
environment, sleep and rest should be promoted by Because the pathogenesis of PLMS is usually unknown,
good sleep hygiene principles, by avoidance of exces- treatment is often symptomatic (Table 39-8). At the
sive caffeine and alcohol, and, possibly, by administra- present time, dopaminergic agents such as levodopa
tion of short-duration hypnotics. Care should be taken, (L-dopa), pergolide, or pramipexole generally provide
however, to avoid hangover effects or amnesia associ- the most effective treatment for both PLMS and restless
ated with hypnotics. Because individual responses to legs syndrome. Opiates, such as oxycodone and pro-
sleeping pills vary considerably from person to person, poxyphene, have also been demonstrated to be effective
it is often helpful to develop experience with specific in the treatment of PLMS and restless legs syndrome.
compounds and doses before departure. Anticonvulsants, such as carbamazepine and gabap-
entin, have been shown to be effective in treatment of
Periodic Limb Movements in Sleep restless legs syndrome. Clonazepam, a benzodiazepine
anticonvulsant, is effective in the treatment of PLMS
DIAGNOSIS and possibly for restless legs syndrome. Other benzodi-
azepines have also been used to treat these conditions,
Periodic limb movements in sleep (PLMS), previously as they will decrease some of the awakenings but may
called nocturnal myoclonus, is a disorder in which re- have no effect on the number of leg movements.
petitive, brief, and stereotyped limb movements occur
during sleep, usually about every 20 to 40 seconds.
Dorsiflexions of the big toe, ankle, knee, and some- Parasomnias
times the hip are involved (Table 39-7 )
Questioning of the individual or bed partner often The parasomnias are a group of disorders character-
yields reports of restlessness, kicking, unusually cold ized by disturbances of either physiological processes
or behavior associated with sleep, but not necessarily
Features of Periodic Limb Movements in causing disturbances of sleep or wakefulness.
Table 39-7
Sleep
Leg kicks every 20–40 seconds Nightmare Disorder

Duration of 0.5–5 seconds
Complaints of:
Insomnia DIAGNOSIS
Excessive sleepiness
Restless legs The essential feature of this disorder is the repeated
Very cold or hot feet occurrence of frightening dreams that lead to full
Uncomfortable sensations in legs
awakenings from sleep. The dreams or awakenings
Table 39-8 Pharmacologic Treatment Options in RLS/PLMS

Medication Dosage Range Side Effects Advantages Disadvantages
L-dopa/carbidopa 25/100–100/400/D Dyskinesia Low cost Breakthrough

restlessness
Nausea Loss of efficacy
Hallucinations
Pergolide 0.05–1 mg Dyskinesia High rate of Frequent side effects
response
Nausea
Rhinitis
Dizziness
Pramipexole 0.25–0.875 mg Orthostasis High rate of Expense
response
Dizziness Good tolerance
Sedation
Anticonvulsants Variable Sedation Low cost Variable response
Sleep promotion
Opiates Variable Nausea Low cost Variable response
Constipation Abuse potential
Clonazepam 0.5–2 mg Sedation Sleep promotion Variable response
Dizziness Abuse potential
cause the individual significant distress or dysfunc- TREATMENT

tion. By definition, the disorder is excluded if the
Nocturnal administration of benzodiazepines has been
nightmare occurs in the course of another mental or
reported to be beneficial, perhaps because these drugs
medical disorder or as a direct result of a medication
suppress delta sleep, the stage of sleep during which
or substance
sleep terrors typically occur.
Whereas more than half of the adult population prob-
ably experiences an occasional nightmare, nightmares
start more commonly in children between the ages of 3 Sleepwalking Disorder
and 6 years. The exact prevalence is unknown.
DIAGNOSIS
TREATMENT This disorder is characterized by repeated episodes
The disorder is usually self-limited in children but can of motor behavior initiated in sleep, usually during
be helped sometimes with psychotherapy, desensitiza- delta sleep in the fi rst third of the night. While sleep-
tion, or rehearsal instructions. Secondary nightmares, walking, the individual has a blank staring face, is
as in posttraumatic stress disorder (PTSD), can be dif- relatively unresponsive to others, and may be con-
ficult to treat. fused or disoriented initially on being aroused from
the episode. Although the person may be alert after
several minutes of awakening, complete amnesia for
Sleep Terror Disorder the episode is common the next day. Adult onset of
sleepwalking should prompt the search for possible
DIAGNOSIS medical, neurological, psychiatric, pharmacologi-
This disorder is defined as repeated abrupt awaken- cal, or other underlying causes, such as nocturnal
ings from sleep characterized by intense fear, panicky epilepsy.
screams, autonomic arousal (tachycardia, rapid breath-
ing, and sweating), absence of detailed dream recall,
TREATMENT
amnesia for the episode, and relative unresponsiveness
to attempts to comfort the person. Sleep terrors oc- No treatment for sleepwalking is established, but some
cur primarily during the first third of the night. These individuals respond to administration of benzodi-
episodes may cause distress or impairment, especially azepines or sedating antidepressants at bedtime. The
for caretakers who witness the event. Sleep terrors major concern should be the safety of the sleepwalker,
may also be called night terrors, pavor nocturnus, or who may injure herself or himself or someone else dur-
incubus. ing an episode.
REM Sleep Behavior Disorder Sleep-Related Epilepsy
DIAGNOSIS Some forms of epilepsy occur more commonly dur-

ing sleep than during wakefulness and may be asso-
First described in 1986, this disorder, like sleepwalk-
ciated with parasomnia disorders. Nocturnal seizures
ing, is associated with complicated behaviors during
may at times be confused with sleep terror, REM sleep
sleep such as walking, running, singing, and talking.
behavior disorder, paroxysmal hypnogenic dystonia,
In contrast to sleepwalking, which occurs during the
or nocturnal panic attacks. They may take the form
first third of the night during delta sleep, REM sleep
of generalized convulsions or may be partial seizures
behavior disorder usually occurs during the second
with complex symptoms. Nocturnal seizures are most
half of the night during REM sleep. Also, in contrast to
common at two times: the first 2 hours of sleep, and
sleepwalking, memory for the dream content is usually
around 4 to 6 a.m. They are more common in children
good. Furthermore, the idiopathic form typically oc-
than in adults. The chief complaint may be only dis-
curs in men during the sixth or seventh decade of life.
turbed sleep, torn up bedsheets and blankets, morning
The cause or causes remain unknown. It has been re-
drowsiness (a postictal state), and muscle aches. Some
ported in a variety of neurological disorders and during
individuals never realize that they suffer from noctur-
withdrawal from sedatives or alcohol; during treatment
nal epilepsy until they share a bedroom or bed with
with tricyclic antidepressants or biperiden (Akineton);
someone who observes a convulsion.
and in various neurological disorders including demen-
tia, subarachnoid hemorrhage, and degenerative neuro-
logical disorders. Sleep Disturbances Related to Other
Mental Disorders
TREATMENT DIAGNOSIS
Nocturnal administration of clonazepam, 0.5 to 1 mg, Subjective and objective disturbances of sleep are com-
is usually remarkably successful in controlling the mon features of many mental disorders. General ab-
symptoms of this disorder. Individuals and their fami- normalities include dyssomnias (such as insomnia and
lies should be educated about the nature of the disorder hypersomnia), parasomnias (such as nightmares, night
and warned to take precautions about injuring them- terrors, and nocturnal panic attacks), and circadian
selves or others. rhythm disturbances (early morning awakening). Before
assuming that a significant sleep complaint invariably
signals a diagnosis of a mental disorder mental health
Nocturnal Panic Attacks specialists should go through a careful differential diag-
nostic procedure to rule out medical, pharmacological,
The typical daytime panic attack, as bizarre and or other causes. Even if the sleep complaint is primarily
frightening as it may seem to the individual experienc- related to an underlying mental disorder, sleep disorders
ing it, is often fairly obvious to the assessing clinician. in the mentally ill may be exacerbated by many other fac-
When these symptoms occur at night, the task of the tors, such as increasing age; comorbid mental, sleep, and
assessing clinician is greatly complicated. The indi- medical diagnoses; alcohol and substance abuse; effects
vidual may assume that the cause is a nightmare or a of psychotropic or other medications; use of caffeinated
night terror and may be resistant to the diagnosis of beverages, nicotine, or other substances; lifestyle; past
an anxiety disorder, particularly if the symptoms are episodes of psychiatric illness (persisting “scars”); and
absent or mild during the daytime. Individuals with cognitive, conditioned, and coping characteristics such
panic disorder often have not only disturbed subjec- as anticipatory anxiety about sleep as bedtime nears.
tive sleep but also panic attacks during sleep. Clini- Some features of these sleep disorders may persist dur-
cian should remember that panic attacks could occur ing periods of clinical remission of the mental disorder
exclusively during sleep, without daytime symptoms, and may be influenced by genetic factors. Finally, even
in some individuals. if the sleep complaint is precipitated by a nonpsychiatric
Conversely, a report of “awakening in a state of factor, psychiatric and psychosocial skills may be useful
panic” may be associated with a variety of other disor- in ferreting out predisposing and perpetuating factors
ders including obstructive sleep apnea, gastroesopha- involved in chronic sleep complaints.
geal reflux, nocturnal angina, orthopnea, nightmares, Although signs and symptoms of sleep distur-
night terrors, and others. bance are common in most mental disorders, an
Table 39-9 Generalized Polygraphic Sleep Features of Individuals with Mental Disorders*
Total Sleep Sleep Sleep REM REM
Disorder Time Efficiency Latency Latency Delta % REM % Density
Depression ↓↓ ↓↓ ↑↑ ↓↓ ↓↓ ↓↓ ↑
Alcoholism ↓ ↓ /⫽ ↑ ⫽ ↓ ↑ ↑⫽
Panic disorder ↓ /⫽ ↓↓ ↑↑ ⫽ ⫽ ⫽ ⫽
Generalized anxiety disorder ⫽ ⫽ ↑ ⫽ ⫽ ⫽ ⫽
Posttraumatic stress disorder ↓↓ ↓↓ ⫽ ↑ /⫽ ⫽ ↓↑ ↑ /⫽
Borderline disorder ↓ /⫽ ↓ /⫽ ↑ /⫽ ↓ /⫽ ⫽ ⫽ ⫽
Eating disorders ↓ /⫽ ↓ /⫽ ⫽ ↓ /⫽ ⫽ ⫽ ↓ /⫽
Schizophrenia ↓↓ ↓↓ ↑↑ ↓↓ ↓ /⫽ ⫽ ↓
Insomnia ↓↓ ↓↓ ↑↑ ⫽ ↓↓ ⫽ ⫽
Narcolepsy ⫽ ↓ ↓↓ ↓↓ ⫽ ⫽ ⫽
*
Two arrows (↑↑ or ↓↓) signify predominance of evidence; one arrow (↑ or ↓) signifies weak evidence, and (⫺) signifies weak evidence; equal sign
(⫽) means no difference; ↓/⫽ or ↑/⫽ means mixed results.
Reprinted from Dow BM, Kelsoe JRJ, and Gillin JC (1996) Sleep and Dreams in Vietnam and Depression. Biological Psychiarty 39: 42–50,
Copyright 1996, Society of Biological Psychiatry.
additional diagnosis of insomnia or hypersomnia re- improve sleep during the first week of antidepressant
lated to another mental disorder is made according to therapy, a low dose of zolpidem, zaleplon, trazodone,
DSM-IV-TR criteria only when the sleep disturbance or any other sedating antidepressant at night in addition
is a predominant complaint and is sufficiently severe to the antidepressant may be less likely to produce tol-
to warrant independent clinical attention. Many of the erance and may have additive antidepressant benefits.
individuals with this type of sleep disorder diagnosis Antipsychotic medications should not be administered
focus on the sleep complaints to the exclusion of other as sleeping aids unless the individual is psychotic or
symptoms related to the primary mental disorder. As otherwise unresponsive to other medications.
summarized in Table 39-9, no single measure or con-
stellation of measures has yet been found to be diag-
Sleep Disorder Due to a General
nostically pathognomonic for any specific disorder.
Medical Condition
Most diagnostic disorders are associated with insom-
nia, characterized by increased sleep latency and re-
A sleep disorder due to a general medical condition is
duced total sleep, sleep efficiency, and delta sleep.
defined in DSM-IV-TR as a prominent disturbance in
sleep severe enough to warrant independent clinical
TREATMENT attention. Subtypes include insomnia, hypersomnia,
parasomnia, and mixed types.
The sleep complaint in the individual with an apparent
As a general rule, any disease or disorder that causes
mental disorder deserves the same careful diagnostic
pain, discomfort, or a heightened state of arousal in the
and therapeutic attention that it does in any individual.
waking state is capable of disrupting or interfering with
Just because an individual is depressed does not mean
sleep. Examples of this phenomenon include pain syn-
that the complaint of insomnia or hypersomnia can be
dromes of any sort, arthritic and other rheumatologi-
explained away as a symptom of depression. Too many
cal disorders, prostatism and other causes of urinary
individuals with depression have been found to have
frequency or urgency, chronic obstructive lung disease,
a BRSD; too many individuals with panic disorder to
and other pulmonary conditions. Many of these condi-
have insomnia secondary to caffeinism. Chronic sleep
tions increase in prevalence with advancing age, sug-
complaints are multidetermined and multifaceted, even
gesting at least one reason that sleep disorders are more
in many individuals with mental disorder. Differential
likely to be seen in senior populations.
diagnosis remains the first obligation of the clinician
before definitive treatment, which should be aimed at
the underlying cause or causes. Substance-Induced Sleep Disorder
Sleeping pills should be prescribed reluctantly to indi-
viduals who receive adequate doses of antidepressants. An important aspect of the evaluation of any individual,
Although coadministration of a benzodiazepine may particularly those with sleep disorders, is the review of
medications and other substances (including prescrip- Alcohol, nicotine, amphetamines, caffeine, opiates,
tion, over-the-counter and recreational drugs, as well sedatives, and anxiolytics can cause or exacerbate
as alcohol, stimulants, narcotics, coffee and caffeine, sleep problems. Many medications produce sleep dis-
and nicotine) and exposure to toxins, or heavy metals. turbance, including those with central or autonomic
These substances may affect sleep and wakefulness nervous system effects, like adrenergic agonists and
during either ingestion or withdrawal, causing most antagonists, dopamine agonists and antagonists,
commonly insomnia, hypersomnia, or, less frequently, cholinergic agonists and antagonists, antihistamines,
parasomnia or mixed types of difficulties. On the ba- and steroids. Among the prescription drugs associated
sis of DSM-IV-TR criteria, a diagnosis of substance- frequently with sleep disorders are the SSRIs, which
induced sleep disorder may be made if the disturbance have been connected with overarousal and insomnia
of sleep is sufficiently severe to warrant independent in some individuals and, more commonly, sedation
clinical attention and is judged to result from the direct in other individuals. Coadministration of trazodone
physiological effects of a substance. Substance-induced at night has been shown, to be effective in managing
sleep disorder cannot result from mental disorder or oc- fluoxetine-induced insomnia in depressed individuals.
cur during delirium. If appropriate, the context for the Additional sleep-related disturbances occasionally as-
development of sleep symptoms may be indicated by sociated with the SSRIs include sleepwalking, REM
specifying with onset during intoxication or with onset sleep behavior disorder, and rapid eye movements dur-
during withdrawal. ing non-REM sleep.
The recognition of substance-related sleep distur-
bances usually depends on active searching by the
clinician, beginning with a careful history, physical
DIAGNOSTIC CRITERIA
examination, laboratory and toxicological testing, and
information (with permission) from former health care For primary insomnia, the ICD-10 Diagnostic Criteria
providers or friends and relatives. Individuals may not for Research and the DSM-IV-TR criteria are almost
know what prescription medications they are taking or identical except that ICD-10 requires a frequency of at
the doses, and may forget to mention over-the-counter least three times a week for at least a month, whereas
medications, coffee, occupational or environmental DSM-IV-TR does not specify a required frequency. For
toxins, and so forth. In the case of alcohol and drugs of primary hypersomnia, the ICD-10 Diagnostic Criteria
abuse, they may deny to themselves and others their use, for Research and the DSM-IV-TR criteria are almost
or quantity, or frequency of use. Substance dependence identical except that ICD-10 also counts sleep drunk-
and abuse is often associated with other psychiatric di- enness as a presenting symptom. Furthermore, ICD-10
agnoses or symptoms. When comorbidity does exist, it requires that the problems occur nearly every day for
is important to establish, if possible, whether the sleep at least 1 month (or recurrently for shorter periods of
disturbance is primary or secondary; that is, whether time).
the sleep disturbance is substance-induced (second- Since narcolepsy and breathing-related sleep disor-
ary) or whether the substance use functions as a form der are included in Chapter VI (Diseases of the Nerv-
of “self-medication” for sleep disturbance, in which the ous System) in ICD-10, there are no diagnostic criteria
sleep disturbance would be considered primary. Many provided for these conditions.
individuals with alcoholism experience secondary de- For circadian rhythm sleep disorder, the ICD-10 Di-
pression during the first few weeks of withdrawal from agnostic Criteria for Research and the DSM-IV-TR cri-
alcohol and exhibit short REM latency and other sleep teria are almost identical except that ICD-10 specifies
changes similar to those reported in primary depres- that the problems occur nearly every day for at least
sion. This secondary depression usually remits sponta- 1 month (or recurrently for shorter periods of time)
neously. Likewise, about one-third of individuals with (DSM-IV-TR has no specified duration). This condi-
unipolar depression and about three-fifths of individu- tion is referred to in ICD-10 as “Nonorganic disorder of
als with bipolar disorder, manic type, have a substance the sleep–wake cycle.”
use pattern that meets diagnostic criteria for alcoholism The ICD-10 Diagnostic Criteria for Research and the
or substance abuse at some point. Prognosis and treat- DSM-IV-TR criteria for nightmare disorder and sleep-
ment may be altered in comorbid states, depending on walking disorder are essentially identical. The ICD-10
whether the sleep disturbance is primary or secondary. Diagnostic Criteria for Research and the DSM-IV-TR
In general, treatment should be aimed at the primary criteria sets for sleep terror disorder are almost identi-
diagnosis after management of any acute withdrawal cal except that ICD-10 explicitly limits the duration of
condition that may exist. the episode to less than 10 minutes.
CHAPTER
40 Impulse Control Disorders
Although dissimilar in behavioral expressions, the dis-

orders in this chapter share the feature of impulse dy- DSM-IV-TR Diagnostic Criteria
scontrol. Individuals who experience such dyscontrol 312.34 INTERMITTENT EXPLOSIVE DISORDER
are overwhelmed by the urge to commit certain acts
that are often apparently illogical or harmful. The out- A. Several discrete episodes of failure to resist aggressive
impulses that result in serious assaultive acts or de-
come of each of these behaviors is often harmful, either struction of property.
for the afflicted individual (trichotillomania, patho- B. The degree of aggressiveness expressed during the epi-
logical gambling) or for others (intermittent explosive sodes is grossly out of proportion to any precipitating
psychosocial stressors.
disorder, pyromania, kleptomania). Trichotillomania, C. The aggressive episodes are not better accounted for
pyromania, and pathological gambling may involve by another mental disorder (e.g., antisocial personality
episodes in which a sudden desire to commit the act disorder, borderline personality disorder, a psychotic
disorder, a manic episode, conduct disorder, or atten-
of hair-pulling, fire-setting, or gambling is followed by tion-deficit/hyperactivity disorder) and are not due to
rapid expression of the behavior. But in these condi- the direct physiological effects of a substance (e.g., a
tions, the individual may spend considerable amounts drug of abuse, a medication) or a general medical con-
dition (e.g., head trauma, Alzheimer’s disease).
of time fighting off the urge, trying not to carry out
the impulse. The inability to resist the impulse is the Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
common core of these disorders, rather than the rapid American Psychiatric Association.
transduction of thought to action.
Because of the limited body of systematically col-
lected data, the following sections largely reflect accu- behavior have been ruled out. The individual may de-
mulated clinical experience. Therefore, the practicing scribe the aggressive episodes as “spells” or “attacks.”
psychiatrist should be particularly careful to consider The symptoms appear within minutes to hours and,
the exigencies of individual subjects in applying treat- regardless of the duration of the episode, may remit al-
ment recommendations. most as quickly. As in other impulse control disorders,
the explosive behavior may be preceded by a sense of
tension or arousal and is followed immediately by a
Intermittent Explosive Disorder
sense of relief or release of tension.
Episodes of violent behavior appear in several com-
DIAGNOSIS
mon psychiatric disorders such as antisocial person-
Individuals with intermittent explosive disorder have a ality disorder, borderline personality disorder, and
significant problem with their temper. This definition substance use disorders and need to be distinguished
highlights the centrality of impulsive aggression in from the violent episodes of individuals with intermit-
intermittent explosive disorder. Impulsive aggression, tent explosive disorder, which are apparently rare.
however, is not specific to intermittent explosive disor- Although not explicitly stated in the DSM-IV-TR
der. It is a key feature of several mental disorders and definition of intermittent explosive disorder, impulsive
nonpsychiatric conditions, and may emerge during the aggressive behavior may have many motivations that
course of other mental disorders. Therefore, the defini- are not meant to be included within this diagnosis. In-
tion of intermittent explosive disorder as formulated in termittent explosive disorder should not be diagnosed
the DSM-IV-TR is essentially a diagnosis of exclusion. when the purpose of the aggression is monetary gain,
As described in criterion C, a diagnosis of intermit- vengeance, self-defense, social dominance, or express-
tent explosive disorder is made only after other mental ing a political statement or when it occurs as a part of
disorders that might account for episodes of aggressive gang behavior. Typically, the aggressive behavior is
egodystonic to individuals with intermittent explosive The small literature on the comorbidity of impulsive
disorder, who feel genuinely upset, remorseful, regret- aggressive episodes suggests that it often occurs with
ful, bewildered, or embarrassed about their impulsive three classes of disorders:
aggressive acts.
1. Personality disorders, especially antisocial person-
The physical and laboratory findings relevant to the
ality disorder and borderline personality disorder.
diagnosis of intermittent explosive disorder and the
By definition, antisocial personality disorder and
differential diagnosis of impulsive aggression may
borderline personality disorder are chronic and in-
be divided into two main groups: those associated
clude impulsive aggression as an essential feature.
with episodic impulsive aggression but not diagnos-
Therefore, their diagnosis effectively excludes the
tic of a particular disorder and those that suggest the
diagnosis of intermittent explosive disorder.
diagnosis of a psychiatric or medical disorder other
2. A history of substance-use disorders, especially al-
than intermittent explosive disorder. No laboratory or
cohol abuse. A concurrent diagnosis of substance
physical findings are specific for intermittent explosive
intoxication excludes the diagnosis of intermittent
disorder.
explosive disorder. However, many individuals with
The first group of findings that are associated with
intermittent explosive disorder report past or fam-
impulsive aggression across a spectrum of disorders
ily histories of substance abuse, and in particular
includes soft neurological signs such as subtle im-
alcohol abuse. Therefore, when there is evidence
pairments in hand–eye coordination and minor reflex
suggesting that alcohol abuse may be present, a sys-
asymmetries. These signs may be elicited by a com-
tematic evaluation of intermittent explosive disorder
prehensive neurological examination and simple pen-
is warranted, and vice versa.
cil-and-paper tests such as parts A and B of the Trail
3. Neurological disorders, especially severe head
Making Test. Measures of central serotonergic function
trauma, partial complex seizures, dementias, and
such as CSF 5-HIAA levels, the fenfluramine challenge
inborn errors of metabolism. Intermittent explosive
test, and positron emission tomography of prefrontal
disorder is not diagnosed if the aggressive episodes
metabolism also belong to this group. Although these
are a direct physiological consequence of a general
measures advanced our neurobiological understanding
medical condition. Such cases would be diagnosed
of impulsive aggression, their utility in the diagnosis of
as personality change due to a general medical con-
individual cases of intermittent explosive disorder and
dition, delirium, or dementia.
other disorders with impulsive aggression is yet to be
demonstrated. Some children with Tourette’s disorder may be prone
The second group of physical and laboratory find- to rage attacks. The clinical manifestation of these rage
ings is useful in the diagnosis of causes of impul- attacks is similar to intermittent explosive disorder
sive aggression other than intermittent explosive (IED) and may be more common among children with
disorder. The smell of alcohol in an individual’s Tourette’s who have comorbid mood disorders. On the
breath or a positive alcohol reading with a breath- basis of these observations, the rage attacks of these
alyzer may help reveal alcohol intoxication. Blood children may flow from an underlying dysregulation of
and urine toxicology screens may reveal the use of brain function.
other substances, and track marks on the forearms
may suggest intravenous drug use. Partial complex
seizures and focal brain lesions may be evaluated by
use of the EEG and brain imaging. In cases without The DSM-IV-TR diagnosis of intermittent explosive
a grossly abnormal neurological examination, mag- disorder is essentially a diagnosis of exclusion, and
netic resonance imaging may be more useful than the clinician should evaluate and carefully rule out
computed tomography of the head. Magnetic reso- more common diagnoses that are associated with im-
nance imaging can reveal mesiotemporal scarring, pulsive violence. The lifelong nonremitting history of
which may be the only evidence for a latent seizure impulsive aggression associated with antisocial per-
disorder, sometimes in the presence of a normal or sonality disorder and borderline personality disorder,
inconclusive EEG. Diffuse slowing on the EEG is a together with other features of antisocial behavior (in
nonspecific fi nding that is probably more common antisocial personality disorder) or impulsive behav-
in, but not diagnostic of, individuals with impulsive iors in other spheres (in borderline personality disor-
aggression. Hypoglycemia, a rare cause of impul- der) may distinguish them from intermittent explosive
sive aggression, may be detected by blood chemistry disorder, in which baseline behavior and functioning
screens. are in marked contrast to the violent outbursts. Other
Chapter 40 • Impulse Control Disorders 427
features of borderline personality disorder such as un- to hallucinations or delusions. Impulsive aggression
stable and intense interpersonal relationships, frantic may also appear in variants of obsessive–compulsive
efforts to avoid abandonment, and identity disturbance disorder (OCD), which may present with concurrent
may also be elicited by a careful history. More than impulsive and compulsive symptoms.
in most psychiatric diagnoses, collateral informa- A special problem in the differential diagnosis of
tion from an independent historian may be extremely impulsive aggression, which may arise in forensic
helpful. This is especially true in forensic settings. Of settings, is that it may represent purposeful behavior.
note, individuals with intermittent explosive disorder Purposeful behavior is distinguished from intermit-
are usually genuinely distressed by their impulsive tent explosive disorder by the presence of motivation
aggressive outbursts and may voluntarily seek psy- and gain in the aggressive act, such as monetary gain,
chiatric help to control hem. In contrast, individuals vengeance, or social dominance. Another diagnostic
with antisocial personality disorder do not feel true problem in forensic settings is malingering, in which
remorse for their actions and view them as a problem individuals may claim to have intermittent explosive
only insofar as they suffer their consequences, such disorder to avoid legal responsibility for their acts.
as incarceration and fi nes. Although individuals with Common disorders that should be excluded before
borderline personality disorder, like individuals with intermittent explosive disorder is diagnosed and fea-
intermittent explosive disorder, are often distressed tures that may be helpful in the differential diagnosis
by their impulsive actions, the rapid development of are summarized in Table 40.1.
intense and unstable transference toward the clinician
during the evaluation period of individuals with bor-
TREATMENT
derline personality disorder may be helpful in distin-
guishing it from intermittent explosive disorder. Given the rarity of pure intermittent explosive disorder,
Other causes of episodic impulsive aggression are it is not surprising that few systematic data are avail-
substance-use disorders, in particular alcohol abuse able on its response to treatment and that some of the
and intoxication. When the episodic impulsive aggres- recommended treatment approaches to intermittent
sion is associated only with intoxication, intermittent
explosive disorder is ruled out. However, as discussed
earlier, intermittent explosive disorder and alcohol Table 40-1
Differential Diagnosis of Intermittent
abuse may be related, and the diagnosis of one should Explosive Disorder
lead the clinician to search for the other. Intermittent Explosive In Contrast to
Neurological conditions such as dementias, focal Disorder Must Be Intermittent Explosive
Differentiated from Disorder, the Other
frontal lesions, partial complex seizures, and post- Aggressive Behavior in Condition
concussion syndrome after recent head trauma may
Substance intoxication or Is due to the direct
all present as episodic impulsive aggression and need withdrawal physiological effects of a
to be differentiated from intermittent explosive disor- substance
der. Other neurological causes of impulsive aggression Delirium or dementia Includes characteristic
(substance induced or symptoms (e.g., memory
include encephalitis, brain abscess, normal-pressure due to a general medical impairment, impaired
hydrocephalus, subarachnoid hemorrhage, and stroke. condition) attention)
In these instances, the diagnosis would be personality Requires the presence of
an etiological general
change due to a general medical condition, aggressive medical condition or
type, and it may be made with a careful history and the substance use
characteristic physical and laboratory findings. Personality change due Requires presence of
to a general medical an etiological general
Chronic impulsivity and aggression may occur as condition, aggressive type medical condition
part of disorders first diagnosed during childhood and Conduct disorder or Is characterized by more
adolescence such as conduct disorder, oppositional de- antisocial personality general pattern of
disorder antisocial behavior
fiant disorder, attention-deficit/hyperactivity disorder, Other mental disorders Includes the characteristic
and mental retardation. In addition, impulsive aggres- (schizophrenia, manic symptoms of the other
episode, oppositional mental disorder
sion may appear during the course of a mood disorder, defiant disorder,
especially during a manic episode, which precludes the borderline personality
diagnosis of intermittent explosive disorder, and dur- disorder)
ing the course of an agitated depressive episode. Im- Source: First M and Frances A (eds) (1995) DSM-IV Handbook of
pulsive aggression may also be an associated feature Differential Diagnosis. Copyright, American Psychiatric Press,
Washington, DC, p. 200.
of schizophrenia, in which it may occur in response
explosive disorder are based on treatment studies of the best approach may be to tailor the psychopharma-
impulsivity and aggression in the setting of other men- cological agent to coexisting psychiatric comorbidity.
tal disorders and general medical conditions. Thus, no In the absence of comorbid disorders, carbamazepine,
standard regimen for the treatment of intermittent ex- titrated to antiepileptic blood levels, may be used
plosive disorder can be recommended at this time. Both empirically.
psychological and somatic therapies have been utilized
in the treatment of intermittent explosive disorder. A
Kleptomania
prerequisite for both modalities is the willingness of
the individual to acknowledge some responsibility for
DIAGNOSIS
the behavior and participate in attempts to control it.
Kleptomania shares with all other impulse control dis-
orders the recurrent failure to resist impulses, in this
case, the impulse to steal. Unfortunately, in the absence
The major psychotherapeutic task of teaching indi- of epidemiological studies, little is known about klepto-
viduals with intermittent explosive disorder is how to mania. There are no established treatments of choice.
recognize their own feeling states and especially the Generally, the diagnosis of kleptomania is not a com-
affective state of rage. Lack of awareness of their own plicated one to make. However, kleptomania may fre-
mounting anger is presumed to lead to the buildup of quently go undetected because the individual may not
intolerable rage that is then discharged suddenly and mention it spontaneously and the clinician may fail to
inappropriately in a temper outburst. Individuals with inquire about it as part of the routine history. The index
intermittent explosive disorder are therefore taught of suspicion should rise in the presence of commonly
how to first recognize and then verbalize their anger associated symptoms such as chronic depression, other
appropriately. In addition, during the course of insight- impulsive or compulsive behaviors, tumultuous back-
oriented psychotherapy, they are encouraged to iden- grounds, or unexplained legal troubles. It could convinc-
tify and express the fantasies surrounding their rage. ingly be argued that a cursory review of compulsivity
Group psychotherapy for temper-prone individuals has and impulsivity, citing multiple examples for the indi-
also been described. The cognitive–behavioral model vidual, should be a part of any thorough and complete
of psychological treatment may be usefully applied to mental health evaluation. In addition, it is important to
problems with anger and rage management. do a careful differential diagnosis and pay attention to
the various exclusion criteria before diagnosing theft
as kleptomania. Possible diagnoses of sociopathy, ma-
Somatic Treatments
nia, or psychosis should be carefully considered. In this
Several classes of medications have been used to treat regard, the clinician must inquire about the affective
intermittent explosive disorder. The same medications state of the individual during the episodes, the presence
have also been used to treat impulsive aggression in
the context of other disorders. These included beta-
blockers (propranolol and metoprolol), anticonvul-
sants (carbamazepine and valproic acid), lithium, DSM-IV-TR Diagnostic Criteria
antidepressants (tricyclic antidepressants and serot-
312.32 KLEPTOMANIA
onin reuptake inhibitors), and antianxiety agents (lo-
razepam, alprazolam, and buspirone). Carbamazepine A. Recurrent failure to resist impulses to steal objects that
may be more effective in individuals with intermittent are not needed for personal use or for their monetary
value.
explosive disorder and propranolol may be more effec- B. Increasing sense of tension immediately before com-
tive in individuals with attention-deficit/hyperactivity mitting the theft.
disorder. A substantial body of evidence supports the C. Pleasure, gratification, or relief at the time of commit-
ting the theft.
use of propranolol–often in high doses–for impulsive D. The stealing is not committed to express anger or
aggression in individuals with chronic psychotic disor- vengeance and is not in response to a delusion or a
ders and mental retardation. Lithium has been shown hallucination.
E. The stealing is not better accounted for by conduct
to have antiaggressive properties and may be used to disorder, a manic episode, or antisocial personality
control temper outbursts. In individuals with comor- disorder.
bid major depressive disorder, OCD, or cluster B and Reprinted with permission from the Diagnostic and Statistical
C personality disorders, SSRIs may be useful. Over- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
all, in the absence of more controlled clinical trials,
of delusions or hallucinations associated with the occur-

rence of the behavior, the motivation behind the steal- DSM-IV-TR Diagnostic Criteria
ing, and the fate and subsequent use of the objects. 312.33 PYROMANIA
A. Deliberate and purposeful fire-setting on more than

TREATMENT one occasion.
B. Tension or affective arousal before the act.
The general goal of treatment is the eradication of C. Fascination with, interest in, curiosity about, or attrac-
kleptomanic behavior. Treatment typically occurs in tion to fire and its situational contexts (e.g., parapher-
nalia, uses, consequences).
the outpatient setting, unless comorbid conditions such D. Pleasure, gratification, or relief when setting fires, or
as severe depression, eating disturbances, or more dan- when witnessing or participating in their aftermath.
gerous impulsive behaviors dictate hospitalization. In E. The fire-setting is not done for monetary gain, as an
expression of sociopathic ideology, to conceal crimi-
the acute treatment phase, the aim is to decrease signal activity, to express anger or vengeance, to improve
nificantly or, ideally, eradicate episodes of stealing dur- one’s living circumstances, in response to a delusion
ing a period of weeks to months. Concurrent conditions or hallucination, or as a result of impaired judgment
(e.g., in dementia, mental retardation, substance
may compound the problem and require independently intoxication).
targeted treatment. F. The fire-setting is not better accounted for by conduct
The acute treatment of kleptomania has not been, to disorder, a manic episode, or antisocial personality
disorder
date, systematically investigated. Recommendations
are based on retrospective reviews, case reports, and Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
small case series. Maintenance treatment for kleptoma- American Psychiatric Association.
nia has not been investigated either, and only anecdotal
data exist for individuals who have been followed up
for significant periods after initial remission. The diagnosis of pyromania emphasizes the affective
No treatments have been systematically shown arousal, thrill, or tension preceding the act, as well as
to be effective for kleptomania. In general, based on the feeling of tension relief or pleasure in witnessing the
case reports and retrospective reviews, it appears that outcome. This is useful in distinguishing between py-
thymoleptic medications and behavioral therapy may romania and fire-setting elicited by other motives (i.e.,
be the most efficacious treatments for the short term, financial gain, concealment of other crimes, political,
whereas long-term psychodynamic psychotherapy arson related to other mental illness, revenge, attention
may be indicated and have good results for selected seeking, erotic pleasure, part of conduct disorder).
individuals. The onset of pyromania has been reported to occur
as early as age 3 years, but the condition may initially
present in adulthood. Because of the legal implications
Pyromania and Fire-Setting Behavior
of fire-setting, individuals may not admit previous
events, which may result in biased perceptions of the
DIAGNOSIS
common age at onset. Men greatly outnumber women
The primary characteristics of pyromania are recur- with the disorder.
rent, deliberate fire-setting, the experience of tension In children and adolescents, the most common el-
or affective arousal before the fire-setting, an attraction ements are excitation caused by fires, enjoyment pro-
or fascination with fire and its contexts, and a feeling duced by fires, relief of frustration by fire-setting, and
of gratification or relief associated with the setting of a expression of anger through fire-setting.
fire or its aftermath.
True pyromania is present in only a small subset of
fire-setters. Multiple motivations are cited as causes
for fire-setting behavior. These include arson for profit, Other causes of fi re-setting must be ruled out. Fire-
crime concealment, revenge, vandalism, and political setting behavior may be motivated by circumstances
expression. In addition, fire-setting may be associated unrelated to mental disorders. Such motivations in-
with other psychiatric diagnoses. Fire-setting behavior clude profit, crime concealment, revenge, vandalism,
may be a focus of clinical attention, even when criteria and political statement or action. Furthermore, fi re-
for pyromania are not present. Because the large ma- setting may be a part of ritual, cultural, or religious
jority of fire-setting events are not associated with true practices in some cultures.
pyromania, this section also addresses fire-setting be- Fire-setting may occur in the presence of other men-
havior in general. tal disorders. A diagnosis of fire-setting is not made
when the behavior occurs as a part of conduct disorder, gambling behavior as indicated by five (or more) of
antisocial personality disorder, or a manic episode or the following.” This defi nition of pathological gam-
if it occurs in response to a delusion or hallucination. bling differs from some other defi nitions of impulse
The diagnosis is also not given if the individual suffers control disorders not elsewhere classified, which are
from impaired judgment associated with mental retar- worded as “Failure to resist an impulse to.” This dif-
dation, dementia, or substance intoxication. ference implies that neither gambling behavior nor
failure to resist an impulse to engage in it is viewed
as pathological in and of itself. Rather, the maladap-
TREATMENT
tive nature of the gambling behavior is the essential
Because of the danger inherent in fire-setting behavior, feature of pathological gambling and defi nes it as a
the primary goal is elimination of the behavior. The disorder.
treatment literature does not distinguish between pyro- It is not difficult to diagnose pathological gambling
mania and fire-setting behavior of other causes. once one has the facts. It is much more of a challenge to
Much of the literature is focused on controlling fire- elicit the facts, because the vast majority of individuals
setting behavior in children and adolescents. with pathological gambling view their gambling behav-
ior and gambling impulses as egosyntonic, and may of-
ten lie about the extent of their gambling (criterion A7).
Pharmacotherapy
Individuals with pathological gambling may first seek
There are no reports of pharmacological treatment of medical or psychological attention because of comor-
pyromania. Because fire-setting may be frequently bid disorders. Given the high prevalence of addictive
embedded in the context of other mental disorders, disorders in pathological gambling and the increased
therapeutic attention may be directed primarily to the prevalence of pathological gambling in those with al-
underlying disorder. coholism and other substance abuse, an investigation
It has been estimated that up to 60% of childhood fire-
setting is motivated by curiosity. Such behavior often 312.31 PATHOLOGICAL GAMBLING
responds to direct educational efforts. In children and A. Persistent and recurrent maladaptive gambling behav-
adolescents, focus on interpersonal problems in the ior as indicated by five (or more) of the following:
family and clarification of events preceding the be- (1) is preoccupied with gambling (e.g., preoccupied
havior may help control the behavior. The treatments with reliving past gambling experiences, handi-
capping or planning the next venture, or thinking
described as more helpful for fire-setting are largely of ways to get money with which to gamble)
behavioral or focused on intervening in family or in- (2) needs to gamble with increasing amounts of
trapersonal stresses that may precipitate the episode of money in order to achieve the desired excitement
(3) has repeated unsuccessful efforts to control, cut
fire-setting. back, or stop gambling
Relaxation training may be used (or added to graph- (4) is restless or irritable when attempting to cut down
ing techniques) to assist in the development of alterna- or stop gambling
(5) gambles as a way of escaping from problems or of
tive modes of dealing with the stress that may precede relieving a dysphoric mood (e.g., feelings of help-
fire-setting. Principles of cognitive–behavioral therapy lessness, guilt, anxiety, depression)
have been recently applied to childhood fire-setting. (6) after losing money gambling, often returns an-
other day to get even (“chasing” one’s losses)
(7) lies to family members, therapist, or others to con-
ceal the extent of involvement with gambling
Pathological Gambling (8) has committed illegal acts such as forgery, fraud,
theft, or embezzlement to finance gambling
DIAGNOSIS (9) has jeopardized or lost a significant relationship,
job, or educational or career opportunity because
of gambling
Gambling as a behavior is common. Current estimates (10) relies on others to provide money to relieve a des-
suggest that approximately 80% of the adult popula- perate financial situation caused by gambling
tion in the United States gamble. DSM-IV-TR, like B. The gambling behavior is not better accounted for by
DSM-III-R before it, covertly recognized the ubiq- a manic episode.
uity of gambling behavior and the desire to gamble Reprinted with permission from the Diagnostic and Statistical
by the careful wording of criterion A for pathologi- Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
cal gambling: “Persistent and recurrent maladaptive
of gambling patterns and their consequences is war- Differential Diagnosis

ranted for any individual who presents with a substance
The differential diagnosis of pathological gam-
abuse problem. Likewise, the high rates of comorbidity
bling is relatively straightforward. Pathological
with mood disorders suggest the utility of investigating
gambling should be differentiated from profes-
gambling patterns of individuals presenting with an af-
sional gambling, social gambling, and a manic epi-
fective episode.
sode. A diagnosis of pathological gambling should
The spouses and the significant others of individuals
be given only if a history of maladaptive gam-
with pathological gambling deserve special attention.
bling behavior exists at times other than during
Individuals with pathological gambling usually feel en-
a manic episode. Problems with gambling may also
titled to their behavior and often rely on their families
occur in individuals with antisocial personality disor-
to bail them out (criterion A10). As a consequence, it
der. If criteria are met for both disorders, both can be
is often the spouse of the individual with pathologi-
diagnosed.
cal gambling who first realizes the need for treatment
and who bears the consequences of the disorder. The
spouse may be a valuable and motivated informant who
TREATMENT
should be questioned about the individual’s behavior,
and second, spouses should be specifically asked about The goals of treatment of an individual with pathologi-
the effects of the individual’s illness on their own well- cal gambling are the achievement of abstinence from
being and functioning and about suicidal ideation and gambling, rehabilitation of the damaged family and
attempts and the control of their own impulsivity. work roles and relationships, treatment of comorbid
Overall, individuals with pathological gambling have disorders, and relapse prevention. This approach ech-
high rates of comorbidity with several other psychiat- oes the goals of treatment of an individual with sub-
ric disorders and conditions. Individuals presenting for stance dependence. There are many similarities and
clinical treatment of pathological gambling apparently several important differences between the treatment of
have impressive rates of comorbidity, including alcohol pathological gambling and the treatment of substance
disorders, depression, and bipolar disorder. dependence. For most individuals without severe acute
psychiatric comorbidity, such as major depressive dis-
order with suicidal ideation or alcohol dependence with
Course
a history of delirium tremens, treatment may be given
Pathological gambling usually begins in adolescence in on an outpatient basis. Inpatient treatment in special-
men and later in life in women. The onset is usually in- ized programs may be considered if the gambler is un-
sidious, although some individuals may be “hooked” by able to stop gambling, lacks significant family or peer
their first bet. There may be years of social gambling support, or is suicidal, acutely depressed, multiply ad-
with minimal or no impairment followed by an abrupt dicted, or contemplating some dangerous activity.
onset of pathological gambling that may be precipi- No standard treatment of pathological gambling has
tated by greater exposure to gambling or by a psycho- emerged. Despite many reports of behavioral and cog-
social stressor. The gambling pattern may be regular nitive interventions for pathological gambling, there are
or episodic, and the course of the disorder tends to be minimal data available from well-designed or clearly
chronic. Over time, there is usually a progression in detailed treatment studies. Pharmacologic treatments
the frequency of gambling, the amounts wagered, and offer promise, but research-guided approaches are still
the preoccupation with gambling and with obtaining insufficient to offer a standardized approach. There-
money with which to gamble. The urge to gamble and fore, general approaches, based in clinical experience
gambling activity generally increase during periods of and available resources (such as Gamblers Anonymous
stress or depression, as an attempted escape or relief or other support groups) should be considered.
(criterion A5). The treatment of pathological gambling may consist
Without treatment, the prognosis of pathological of participation in Gamblers Anonymous, individual
gambling is poor. It tends to run a chronic course with therapy, family therapy, treatment of comorbid dis-
increasing morbidity and comorbidity, gradual disrup- orders, and medication treatment. As is the case for
tion of family and work roles and relationships, deple- substance dependence, the gambler needs to be absti-
tion of financial reserves, entanglement with criminals nent to be accessible to any or all of these treatment
and the criminal justice system, and, often, suicide modalities. For many gamblers, participation in Gam-
attempts. In the hands of an experienced psychiatrist, blers Anonymous is sufficient, and it is an essential
treatment is associated with a favorable prognosis. part of most treatment plans. Gamblers Anonymous is
a 12-step group built on the same principles as Alco-

holics Anonymous. It utilizes empathic confrontation DSM-IV-TR Diagnostic Criteria
by peers who struggle with the same impulses and a 312.39 TRICHOTILLOMANIA
group approach. Gam-Anon is a peer support group
for family members of individuals with pathologi- A. Recurrent pulling out of one’s hair resulting in notice-
able hair loss.
cal gambling. Extensive data are lacking, but overall, B. An increasing sense of tension immediately before
Gamblers Anonymous appears somewhat less effec- pulling out the hair or when attempting to resist the
tive than Alcoholics Anonymous in achieving and behavior.
C. Pleasure, gratification, or relief when pulling out the
maintaining abstinence. hair.
The greatest differences between the treatment of D. The disturbance is not better accounted for by another
pathological gambling and other addictions are in the mental disorder and is not due to a general medical
condition (e.g., a dermatological condition).
area of family therapy. Because relapse may be diffi- E. The disturbance causes clinically significant distress or
cult to detect (there is no substance to be smelled on impairment in social, occupational, or other important
the individual’s breath, no dilated or constricted pupils, areas of functioning.
no slurred speech or staggered gait) and because of a Reprinted with permission from the Diagnostic and Statistical
long history of exploitative behavior by the individual, American Psychiatric Association.
the spouse and the other family members tend to be
more suspicious of, and angry at, the individual with
pathological gambling compared with families of al- in the behavior, but attempts to resist the urge result
coholic individuals. Frequent family sessions are often in great tension. Thus, hair-pulling is motivated by a
essential to offer the gambler an opportunity to make desire to reduce this dysphoric state. In some cases, the
amends, learn communication skills, and deal with hair-pulling results in a pleasurable sensation, in addi-
preexisting intimacy problems. In addition, the spouse tion to the relief of tension. Tension may precede the
and other family members have often acquired their act or may occur when attempting to stop. Distress over
own psychiatric illnesses during the course of the in- the symptom and the resultant hair loss may be severe.
dividual’s pathological gambling and need individual- Typically, the person complaining of unwanted hair-
ized treatment to recover. pulling is a young adult or the parent of a child who
Although research reports of the pharmacological has been seen pulling out hair. Hair-pulling tends to
treatment of pathological gambling have begun to occur in small bursts that may last minutes to hours.
emerge, there are still as yet insufficient data to come Hair-pulling is most commonly limited to the eyebrows
to any conclusions about the utility of medication. and eyelashes. The scalp is the next most frequently af-
The effectiveness of selective serotonin reuptake inflicted site. However, hairs in any location of the body
hibitors has been examined in a limited number of may be the focus of hair-pulling urges, including facial,
double-blind trials, but do show promise. The opi- axillary, chest, pubic, and even perineal hairs.
ate antagonist, naltrexone, has also shown prelimi- Anxiety is almost always associated with the act of
nary evidence of efficacy. Doses at the higher end of hair-pulling. Such anxiety may occur in advance of
the usual treatment range should be considered with the hair-pulling behavior. A state of tension may oc-
both these classes of agents. The use of mood sta- cur spontaneously—driving the person to pull out hair
bilizers (lithium and carbamazepine) has been the in an attempt to reduce dysphoric feelings. Varying
subject of a limited number of reports. At this time, lengths of time must pass before the tension abates.
no clear guidelines for pharmacologic treatment have Consequently, the amount of hair that may be extracted
emerged. in an episode varies from episode to episode and from
person to person. Frequently, hair-pulling begins au-
tomatically and without conscious awareness. In such
Trichotillomania circumstances, individuals discover themselves pulling
out hairs after some have already been pulled out. In
DIAGNOSIS these situations, dysphoric tension is associated with
The essential feature of trichotillomania is the recur- the attempt to stop the behavior.
rent failure to resist impulses to pull out one’s own hair. Circumstances that seem to predispose to epi-
Resulting hair loss may range in severity from mild sodes of hair-pulling include both states of stress and,
(hair loss may be negligible) to severe (complete bald- paradoxically, moments of particular relaxation. Fre-
ness and involving multiple sites on the scalp or body). quently, hair-pulling occurs when at-risk individu-
Individuals with this condition do not want to engage als are engaged in a relaxing activity that promotes
distraction and ease (e.g., watching television, reading, may be empty or contain a deeply pigmented keratinous
talking on the phone). material. The absence of inflammation distinguishes
Patterns of hair-pulling behavior among children trichotillomania-induced alopecia from alopecia areata,
are less well described. Usually, the parent observes a the principal condition in the differential diagnosis.
child pulling out hair and may note patches of hair loss.
Children may sometimes be unaware of the behavior or
Course
may, at times, deny it. Childhood trichotillomania has
been reported to be frequently associated with thumb The age at onset typically ranges from early childhood
sucking or nail biting. It has been suggested that tri- to young adulthood. Peak ages at presentation may be
chotillomania with onset in early childhood may occur bimodal, with an earlier peak about age 5 to 8 years
frequently with spontaneous remissions. Consequently, among children in whom it has a self-limited course,
some have recommended that trichotillomania in early whereas among individuals who present to clinicians
childhood may be considered a benign habit with a self- in adulthood, the mean age at onset is approximately
limited course. However, many individuals who present 13 years. Initial onset after young adulthood is appar-
with chronic trichotillomania in adulthood report onset ently uncommon.
in early childhood. Trichotillomania may be one of the earliest occurring
Individuals with trichotillomania have increased conditions in psychiatry. Some parents insist that their
risk for mood disorders (major depressive disorder, child began pulling hair before 1 year of age. When tri-
dysthymic disorder) and anxiety symptoms. The fre- chotillomania begins before age 6 years, it tends to be a
quency of specific anxiety disorders (such as general- milder condition. It often responds to simple interven-
ized anxiety disorder and panic disorders as well as tions and may be self-limited, with a duration of several
OCD) may be increased as well. weeks to several months, even if not treated. It often
In general, the diagnosis of trichotillomania is not occurs in association with thumb sucking. In some
complicated. The essential symptom—recurrently cases, it remits spontaneously when therapeutic atten-
pulling out hair in response to unwanted urges—is eas- tion is directed at concurrent, severe thumb sucking. It
ily described by the individual. When the individual has been suggested that trichotillomania in childhood
acknowledges the hair-pulling behavior and areas of may be associated with severe intrapsychic or familial
patchy hair loss are evident, the diagnosis is not usu- mental disorder. But there is no reliable evidence that
ally in doubt. Problems in diagnosis may arise when supports such a conclusion. Indeed, some have sug-
the diagnosis is suspected but the individual denies gested that because it may be common and frequently
it. Such denial may occur in younger individuals and self-limiting, it should be considered a normal behavior
some adults. When the problem is suspected but denied among young children.
by the individual, a skin biopsy from the affected area Some individuals have continuous symptoms for
may aid in making the diagnosis. decades. For others, the disorder may come and go for
Despite the hair loss, most individuals with this con- weeks, months, or years at a time. Sites of hair-pulling
dition have no overtly unusual appearance on cursory may vary over time. Circumscribed periods of hair-
inspection. If the hair loss is not covered by clothing or pulling (weeks to months) followed by complete remis-
accessories, artful combing of hair or use of eyeliner sion are reported among children.
and false eyelashes may easily hide it. The ease with Progression of the condition appears to be unpre-
which the condition may often be hidden may explain dictable. Waxing and waning of the severity of hair-
the general underappreciation of its apparent frequency pulling and number of hair-pulling sites occur in most
and potential associated distress. individuals. It is not known which factors may predict
Histological findings are considered characteristic a protracted and unremitting course.
and may aid diagnosis when it is suspected despite de-
nial by the individual. Biopsy samples from involved ar-
TREATMENT
eas may have the following features. Short and broken
hairs are present. The surface of the scalp usually shows Treatment of trichotillomania typically occurs in an
no evidence of excoriation. On histological examination, outpatient setting. Eradication of hair-pulling behavior
normal and damaged follicles are found in the same is the general focus of treatment. Distress, avoidant
area, as well as an increased number of catagen (i.e., behaviors, and cosmetic impairment are secondary to
nongrowing) hairs. Inflammation is usually minimal or the hair-pulling behavior and would be likely to remit
absent. Some hair follicles may show signs of trauma if the hair-pulling behavior were controlled. However,
(wrinkling of the outer root sheath). Involved follicles if sufficient control of hair-pulling cannot be attained,
treatment goals should emphasize these associated which the individual is taught to lower the arm and
problems as well. Even if hair-pulling persists, thera- extend the muscles of the hand. As with behavioral
peutic interventions may be targeted at reducing sec- techniques in general, these interventions are most
ondary avoidance and diminishing distress. successful when the individual is strongly motivated
Treatment may be considered in three phases: and compliant. In addition, the treating psychiatrist
should be experienced in the use of such techniques.
• Initial Contact. The diagnosis is made and the in-
If necessary, a referral should be made to such an ex-
dividual and clinician agree on a strategy that may
perienced individual. Modified behavioral approaches
incorporate both pharmacological and psychologi-
have been described for children and adolescents.
cal interventions. If distress is severe, supportive
Cognitive–behavioral therapy (CBT) has been de-
interventions should be immediately considered in
veloped for, and applied to, individuals with trichotil-
anticipation of incomplete treatment response or of
lomania. At this time, the potential for the efficacy of
a delay of weeks to months before interventions may
this treatment approach appears good.
be beneficial.
Self-help groups for individuals with trichotilloma-
• Acute Treatment. Even when treatment of hair-pull-
nia have appeared. Some are based in the structure
ing behavior is optimally successful, there may be
of other 12-step programs. Some individuals appear
a delay of several weeks to months before adequate
to experience meaningful reduction in hair-pulling
control is attained. Therefore, the acute treatment
symptoms after beginning participation in such a
phase may be prolonged.
group. Although the efficacy of such groups in reduc-
• Maintenance. It is not known how long individuals
ing symptoms remains to be established, most indi-
must maintain active treatment interventions to pre-
viduals with trichotillomania can benefit from meeting
vent relapse. It should be anticipated that a substan-
other individuals with similar symptoms. Because of
tial number of individuals require ongoing treatment
the lack of general awareness of trichotillomania, these
for an extended time. Pharmacological treatments
individuals frequently believe that they are “oddball”
may need to be maintained for open-ended periods.
individuals with a behavior that is unique. Many have
Behavioral or hypnotic intervention may require
experienced parental condemnation for the behavior
periodic “booster shots” to support continuation of
and have been frequently castigated for a “habit” that
benefits.
may be viewed by others as under their voluntary con-
A variety of treatment approaches have been advocated trol. The experience of meeting others with the condi-
for trichotillomania. However, there have, as yet, been tion is extremely supportive for such individuals and
few controlled studies of the efficacy of any treatment may help reduce the attendant stress while supporting
approach. A number of investigations of the use of self-esteem. Where programs specifically oriented to-
antidepressants with specific inhibition of serotonin reward trichotillomania may not be generally available,
uptake (i.e., fluoxetine and clomipramine) have yielded these individuals may benefit from groups oriented to-
mixed results A multimodal approach, simultaneously ward OCD.
utilizing several complementary treatment options,
may turn out to be the most effective approach for most
individuals.
DIAGNOSTIC CRITERIA
While a number of treatment options can be currently
offered to individuals with trichotillomania, the dura- The ICD-10 Diagnostic Criteria for Research do not
bility of long-term outcomes is unclear. Among those include diagnostic criteria for intermittent explosive
who have had a response to treatment, improvements disorder. It is included in ICD-10 as an “other habit and
were often lost over time, and persistent treatment and Impulse Control Disorder.”
ongoing treatment was common over the course of sev- The ICD-10 Diagnostic Criteria for Research and the
eral years. DSM-IV-TR criteria for kleptomania, pyromania, and
trichotillomania are essentially equivalent.
Finally, the ICD-10 Diagnostic Criteria for Research
for pathological gambling are monothetic (i.e., A plus
The most successful technique, habit reversal, is B plus C plus D are required) whereas the DSM-IV-
based on designing competitive behaviors that should TR criteria set is polythetic (i.e., 5 out of 10 required)
inhibit the behavior of hair-pulling. For example, if with different items. Furthermore, the ICD-10 criteria
hair-pulling requires raising the arm to the scalp and specify “two or more episodes of gambling over a pe-
contracting the muscles of the hand to grasp a hair, riod of at least 1 year,” whereas DSM-IV-TR does not
the behaviorist may design a behavioral program in specify a duration.
CHAPTER
41 Adjustment Disorders
DIAGNOSIS
The essential feature of adjustment disorder (AD) is
the development of clinically significant emotional or 309.XX ADJUSTMENT DISORDERS
behavioral symptoms in response to an identifiable A. The development of emotional or behavioral symp-
psychosocial stressor. The symptoms must develop toms in response to an identifiable stressor(s) occur-
within 3 months after the onset of the stressor (cri- ring within 3 months of the onset of the stressor(s).
B. These symptoms or behaviors are clinically significant
terion A). The clinical significance of the reaction is as evidenced by either of the following:
indicated either by marked distress that is in excess of (1) marked distress that is in excess of what would be
what would be expected given the nature of the stressor expected from exposure to the stressor
or by significant impairment in social or occupational (2) significant impairment in social or occupational
(academic) functioning
(academic) functioning (criterion B). This disorder
should not be used if the emotional and cognitive dis- C. The stress-related disturbance does not meet the cri-
teria for another specific Axis I disorder and is not
turbances meet the criteria for another specific Axis I merely an exacerbation of a preexisting Axis I or
disorder (e.g., a specific anxiety or mood disorder) or Axis II disorder.
are merely an exacerbation of a preexisting Axis I or D. The symptoms do not represent bereavement.
E. Once the stressor (or its consequences) has termi-
Axis II disorder (criterion C). AD may be diagnosed if nated, the symptoms do not persist for more than an
other Axis I or II disorders are present, but do not ac- additional 6 months.
count for the pattern of symptoms that have occurred Specify if:
in response to the stressor. The diagnosis of AD does
Acute: if the disturbance lasts less than 6 months
not apply when the symptoms represent bereavement Chronic: if the disturbance lasts for 6 months or longer
(criterion D). By definition, AD must resolve within Adjustment disorders are coded based on the sub-
6 months of the termination of the stressor or its type, which is selected according to the predominant
symptoms. The specific stressor(s) can be specified on
consequences (criterion E). However, the symptoms Axis IV.
may persist for a prolonged period (i.e., longer than 6 309.0 With Depressed Mood
309.24 With Anxiety
months) if they occur in response to a chronic stressor 309.28 With Mixed Anxiety and Depressed Mood
(e.g., a chronic, disabling general medical condition) 309.3 With Disturbance of Conduct
or to a stressor that has enduring consequences (e.g., 309.4 With Mixed Disturbance of Emotions and
Conduct
the financial and emotional difficulties resulting from 309.9 Unspecified
a divorce). Reprinted with permission from the Diagnostic and Statistical
The symptoms of AD are defined in terms of their Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
being a maladaptive response to a psychosocial stres- American Psychiatric Association.
sor. There are, in fact, no specific symptoms of AD;

any combination of behavioral or emotional symptoms
that occur in association with a stressor may qualify. this diagnosis having insufficient specificity. However,
The nature of the symptomatology is described by a va- it is this lack of specificity, which permits the clinician
riety of possible “subtypes”, including With Depressed to have a “diagnosis” to use when the individual is pre-
Mood, With Mixed Anxiety and Depressed Mood, senting with early, vague, nonconcrete symptomatol-
With Disturbance of Conduct, With Mixed Distur- ogy, which should be noted, identified, and followed.
bance of Emotions and Conduct, and Unspecified. This is similar to the situation with early fever, or fever
Although this diagnosis lacks rigorous specificity, of unknown origin, which, by the way, may never go
its treatment is no less challenging or less important. on to a specific medical diagnosis, but be at discharge
AD’s lack of a designated symptom profile results in simply diagnosed as a “fever of unknown origin.”
According to DSM-IV-TR, even if a specific and pre- the clinical course is required to ascertain whether the
sumably causal stressor is identified, if enough symp- AD is a transitory remitting event, the prodromal state
toms develop so that diagnostic criteria are met for a of a more serious and developing disorder, or an in-
specific disorder, then that diagnosis should be made termittent chronic state of a low-level mood disorder.
instead of a diagnosis of AD. Therefore, the presence There is considerable evidence indicating that major
of stressors does not automatically signify a diagnosis depressive disorder is a highly recurrent, often chronic
of AD, and conversely, a diagnosis of a specific disor- condition that is frequently associated with low-grade
der (e.g., major depressive or anxiety disorder) does not symptoms prior to, and between, major episodes. Thus,
imply the absence of concomitant or concurrent stress- the differential diagnoses of depressed mood must
ful events. be linked to ongoing assessment, not cross-sectional
Although the diagnosis of AD requires evidence evaluation, which is so often the case; it is essential to
of maladaption, it is notable that no specific require- maintain a longitudinal view of the subthreshold dis-
ment for functional impairment has been included (e.g., orders to know their place in an individual’s affective
there is no requirement for a certain decrement in the history.
Global Assessment of Functioning Scale score in order
to make the diagnosis). The clinician needs to exam-
Course
ine the individual’s behavior to see whether it is beyond
what is expected in a particular situation, and for that There appear to be important differences in adoles-
individual. In order to do this, the clinician needs to cents and adults with regard to prognosis, according
take into account the individual’s cultural beliefs and to a 5-year follow-up study of adults and adolescents
practices, his or her developmental age, and the tran- with AD. Although the prognosis was favorable and
sient nature of the behavior. If the behavior lasts a few most adult individuals with AD were symptom free
moments or is an impulsive outburst, it would not qual- at 5 years (71% were completely well, 8% had an in-
ify for a maladaptive response to justify the diagnosis tervening problem, and 21% had a major depressive
of AD. The behavior in question should be maladaptive disorder or alcoholism), adolescents had a far different
for that individual, in his/her culture, and sufficiently outcome. A 5-year follow-up study of adolescents indi-
persistent to qualify for the maladaptation attribute of cated that 43% had a major psychiatric disorder (e.g.,
the AD diagnosis. schizophrenia, schizoaffective disorder, major depres-
Several studies reported an association of suicidal sive disorder, substance abuse disorder, and personality
behavior in adolescents and young adults with AD. One disorder); 13% had an intervening mental disorder; and
study found that 56% of those hospitalized for suicidal 44% had no mental disorder. In adolescents, behavio-
behavior in an urban hospital setting met the DSM-II ral symptoms and the chronicity of the morbidity were
criteria for transient situational disturbance (an earlier the major predictors for psychopathological disorders
diagnostic label for what came to be called AD). A ret- at the 5-year follow-up. This was not so with the adults
rospective review of 325 consecutive hospital admis- in the study, and raises the question of whether these
sions for deliberate self-poisoning revealed that 58% of adolescents were diagnosed as having AD as part of a
all cases met criteria for AD with depressed mood, the prodrome of another more serious disorder.
majority of whom were women aged 15 to 24 years.
These studies underscore the seriousness of AD in a
TREATMENT
subset of individuals and suggest that although the di-
agnosis may be subthreshold, its morbidity can be seri- Appropriate and timely treatment is essential for indi-
ous and at times even fatal. viduals with AD so that their symptoms do not worsen,
The issue of boundaries between the specific mood do not further impair their important relationships, and
and anxiety disorders, depressive disorder or anxiety do not compromise their capacity to work, study, or be
disorder NOS, and AD remains problematic. The spe- active in their interpersonal pursuits. Treatment must
cific mood and anxiety disorders are often associated attempt to forestall further erosion of the individual’s
with, and even precipitated by, stress. Therefore, it is capacity to function that could ultimately have grave
not always possible to say one group of diagnoses is and untoward consequences.
accompanied by stress (the AD) and another (e.g., ma- There are two approaches to treatment. One is based
jor depressive disorder) is not. Stress may accompany on the understanding that this disorder emanates from a
many of the mental disorders but it is not an essential psychological reaction to a stressor. The stressor needs
component to make certain diagnoses (e.g., major de- to be identified, described, and shared with the individ-
pressive disorder). Serial and ongoing observation of ual; plans must be made to mitigate it, if possible. The
Chapter 41 • Adjustment Disorders 437
abnormal response may be attenuated if the stressor stressor and enhance coping. Drugs and alcohol are to
can be eliminated or reduced. It has been shown that be discouraged.
in the medically ill, the most common stressor is the Psychotherapy, medical crisis counseling, crisis in-
medical illness itself, and the AD may remit when the tervention, family therapy, group treatment, cognitive–
medical illness improves or a new level of adaptation is behavioral treatment, and interpersonal therapy all
reached. The other approach to treatment is to provide encourage the individual to express affects, fears,
intervention for the symptomatic presentation, despite anxiety, rage, helplessness, and hopelessness to the
the fact that it does not reach the threshold level for a stressors imposed. They also assist the individual to
specific disorder, on the premise that it is associated reassess reality in the service of adaptation. Following
with impairment and that treatments that are effective the example given above, the loss of a leg is not the loss
for more pronounced presentations of similar pathol- of one’s life. But it is a major loss. Brief psychotherapy
ogy are likely to be effective. This may include psy- should attempt to reframe the meaning of the stressor,
chotherapy, pharmacotherapy, or a combination of the find ways to minimize it, and diminish the psychologi-
two. cal deficit due to its occurrence. The treatment should
expose the concerns and conflicts that the individual is
experiencing, help the individual gain perspective on
the adversity, and encourage the individual to establish
Psychotherapeutic intervention in AD is intended to relationships and to attend support groups or self-help
reduce the effects of the stressor, enhance coping to groups for assistance in the management of the stressor
the stressor that cannot be reduced or removed, and and the self.
establish a mental state and support system to maxi- Interpersonal psychotherapy was applied to de-
mize adaptation. Psychotherapy can involve any one pressed outpatients with human immunodeficiency
of several approaches: cognitive–behavioral treat- virus (HIV) infection and was found to be useful.
ment, interpersonal therapy, psychodynamic efforts, Some of the attributes of interpersonal psychotherapy
or counseling. are psychoeducation regarding the sick role, using a
The first goal of these psychotherapies is to analyze here-and-now framework, formulation of the problems
the nature of the stressors affecting the individual to from an interpersonal perspective, exploration of op-
see whether they may be avoided or minimized. It is tions for changing dysfunctional behavior patterns,
necessary to clarify and interpret the meaning of the and identification of focused interpersonal problem
stressor for the individual. For example, an amputation areas.
of the leg may have devastated an individual’s feelings Support groups have been demonstrated to help in-
about himself or herself, especially if the individual dividuals adjust and enhance their coping mechanisms,
was a runner. It is necessary to clarify that the indi- and they may prolong life as well. For example, a 1989
vidual still has enormous residual capacity; that he or study showed that women with stage IV breast cancer
she can engage in much meaningful work, does not lived longer after ongoing group therapy than those
have to lose valued relationships, and can still be sexu- with standard cancer care. However, these findings on
ally active; and that it does not necessarily mean that group psychological intervention and mortality have
further body parts will be lost. (However, it will also not been confirmed in at least two replication trials.
involve redirecting the physical activity to another pas-
time.) Otherwise, the individual’s pernicious fantasies
Pharmacological Treatments
(“all is lost”) may take over in response to the stressor
(i.e., amputation), make the individual dysfunctional Given the potential effectiveness of psychopharma-
(at work, sex), and precipitate a painful dysphoria or cological interventions for the treatment of minor de-
anxiety reaction. pression, such measures may also be helpful for other
Some stressors may elicit an overreaction (e.g., the subthreshold disorders. It has been recommended that
individual’s attempted suicide or homicide after aban- antidepressant therapy be considered if there is no
donment by a lover). In such instances of overreaction benefit from 3 months of psychotherapy or other sup-
with feelings, emotions, or behaviors, the therapist portive measures. Although psychotherapy is the first
would help the individual put his or her feelings and choice treatment, psychotherapy combined with ben-
rage into words rather than into destructive actions zodiazepines may also be helpful, especially for in-
and gain some perspective. The role of verbalization dividuals with severe life stress(es) and a significant
and the joining of affects and conflicts cannot be over- anxious component. Tricyclic antidepressants or bus-
estimated in an attempt to reduce the pressure of the pirone are recommended in place of benzodiazepines
for individuals with current or past heavy alcohol use employed to assist the individual in optimally adapt-
because of the greater risk of dependence in these ing to the stressor.
individuals.
Those individuals who do not respond to coun-
seling or the various modes of psychotherapy that
DIAGNOSTIC CRITERIA
have been outlined and to a trial of antidepressant or
anxiolytic medications should be regarded as treat- In contrast to DSM-IV-TR (which requires the onset
ment nonresponders. It is essential to reevaluate the of symptoms within 3 months of the stressor), the
individual to ensure that the diagnostic impression ICD-10 Diagnostic Criteria for Research specify an
has not altered and, in particular, that the individual onset within 1 month. Furthermore, ICD-10 excludes
has not developed a major mental disorder, which stressors of “unusual or catastrophic type.” In con-
would require a more aggressive treatment, often trast, DSM-IV-TR allows extreme stressors so long
biological. The clinician must also consider that an as the criteria are not met for posttraumatic or acute
Axis II disorder might be interfering with the indi- stress disorder. ICD-10 also provides for several dif-
vidual’s resolution of the AD. Finally, if the stressor ferent subtypes, including “brief depressive reaction”
continues and cannot be removed (e.g., the continu- (depressive state lasting 1 month or less) and “pro-
ation of a seriously impairing chronic illness), addi- longed depressive reaction” (depressive state lasting
tional support and management strategies need to be up to 2 years).
CHAPTER
42 Personality Disorders
Everybody has a personality, or a characteristic manner

of thinking, feeling, behaving, and relating to others. DSM-IV-TR General Diagnostic Criteria
Some persons are typically introverted and withdrawn, PERSONALITY DISORDER
others are more extraverted and outgoing. Some per-
sons are invariably conscientious and efficient, whereas A. An enduring pattern of inner experience and behavior
that deviates markedly from the expectations of the in-
other persons might be consistently undependable and dividual’s culture. This pattern is manifested in two (or
negligent. Some persons are characteristically anxious more) of the following areas:
and apprehensive, whereas others are typically relaxed (1) cognition (i.e., ways of perceiving and interpreting
and unconcerned. These personality traits are often self, other people, and events)
felt to be integral to each person’s sense of self, as they (2) affectivity (i.e., the range, intensity, lability, and ap-
propriateness of emotional response)
involve what persons value, what they do, and their in- (3) interpersonal functioning
nate tendencies and preferences. (4) impulse control
It is when personality traits are inflexible and mala- B. The enduring pattern is inflexible and pervasive across
daptive and cause significant functional impairment a broad range of personal and social situations.
C. The enduring pattern leads to clinically significant dis-
or subjective distress that they constitute a Personal- tress or impairment in social, occupational, or other
ity Disorder. The DSM-IV-TR provides the diagnostic important areas of functioning.
criteria for 10 personality disorders. This chapter be- D. The pattern is stable and of long duration and its onset
can be traced back at least to adolescence or early
gins with a discussion of the diagnosis and treatment of adulthood.
personality disorders in general, followed by a discus- E. The enduring pattern is not better accounted for as
a manifestation or consequence of another mental
sion of these issues for the 10 individual personality disorder.
disorders. F. The enduring pattern is not due to the direct physi-
ological effects of a substance (e.g., a drug of abuse, a
medication) or a general medical condition (e.g., head
Personality Disorder trauma).
DIAGNOSIS American Psychiatric Association.
A personality disorder is defi ned in DSM-IV-TR as

“an enduring pattern of inner experience and behav-
ior that deviates markedly from the expectations of the criteria set for one of the 10 specific personality
the individual’s culture, is pervasive and inflexible, disorders. A general definition of what is meant by a
has an onset in adolescence or early adulthood, is sta- personality disorder is therefore helpful when deter-
ble over time, and leads to distress or impairment” mining whether the NOS diagnosis should in fact be
(page 686). provided.
Personality disorder is the only class of mental Gender and cultural biases are one potential source
disorders in DSM-IV-TR for which an explicit defi- of inaccurate personality disorder diagnosis that are
nition and criteria set are provided. A general defini- worth noting in particular. One of the general diagnos-
tion and criteria set can be useful to clinicians because tic criteria for personality disorder is that the personal-
the most common personality disorder diagnosis in ity trait must deviate markedly from the expectations
clinical practice is often the diagnosis “not otherwise of a person’s culture. The purpose of this cultural de-
specified” (NOS). Clinicians provide the NOS diag- viation requirement is to compel clinicians to consider
nosis when they determine that a personality disor- the cultural background of the individual. A behavior
der is present but the symptomatology fails to meet pattern that appears to be aberrant from the perspective
of one’s own culture (e.g., submissiveness or emotion- Diagnostic categories provide clear, vivid descriptions
ality) could be quite normative and adaptive within of discrete personality types, but the personality struc-
another culture. The cultural expectations or norms of ture of actual individuals might be more accurately de-
the clinician might not be relevant or applicable to an scribed by a constellation of maladaptive personality
individual from a different cultural background. How- traits.
ever, one should not infer from this requirement that a Personality disorders must be evident since ado-
personality disorder is primarily or simply a deviation lescence or young adulthood and have been rela-
from a cultural norm. Deviation from the expectations tively chronic and stable throughout adult life (see
of one’s culture is not necessarily maladaptive, nor is DSM-IV-TR general diagnostic criteria for personal-
conformity to one’s culture necessarily healthy. Many ity disorder, page 439). A 75-year-old man can be di-
of the personality disorders may even represent (in part) agnosed with a DSM-IV-TR DPD, but the symptoms
extreme or excessive variants of behavior patterns that must have been present throughout the duration of his
are valued or encouraged within a particular culture. adulthood (e.g., since the age of 18 years), unless the
For example, it is usually adaptive to be confident but dependent behavior was a direct, explicit expression of
not to be arrogant, to be agreeable but not to be submis- a neurochemical disease or lesion.
sive, or to be conscientious but not to be perfectionistic. The requirement that a personality disorder be evi-
Gender and cultural biases of particular relevance to dent since late adolescence and be relatively chronic
individual personality disorders will be discussed fur- thereafter has been a traditional means by which to
ther in the chapter. distinguish a personality disorder from an Axis I dis-
Estimates of the prevalence of personality disorder order. Mood, anxiety, psychotic, sexual, and other
within clinical settings are typically above 50%. As mental disorders have traditionally been conceptual-
many as 60% of inpatients within some clinical set- ized as conditions that arise at some point during a
tings would be diagnosed with borderline personality person’s life and that are relatively limited or circum-
disorder (BPD) and as many as 50% of inmates within scribed in their expression and duration. Personality
a correctional setting could be diagnosed with antiso- disorders, in contrast, are conditions that are evident
cial personality disorder (ASPD). Although the comor- as early as late adolescence (and in some instances
bid presence of a personality disorder is likely to have prior to that time), are evident in everyday function-
an important impact on the course and treatment of an ing, and are stable throughout adulthood. However,
Axis I disorder, the prevalence of personality disorder the consistency of this distinction across disorders in
is generally underestimated in clinical practice owing the classification has been decreasing with each edi-
in part to the failure to provide systematic or compre- tion of the DSM, as early-onset and chronic variants
hensive assessments of personality disorder symptoma- of Axis I disorders are being added to the diagnostic
tology and perhaps as well to the lack of funding for the manual (e.g., early-onset dysthymia and generalized
treatment of personality disorders. social phobia).
According to the best available estimates, approxi-
mately 10–15% of the general population would be
TREATMENT
diagnosed with one of the 10 DSM-IV-TR personality
disorders, excluding personality disorder not otherwise One of the mistaken assumptions or expectations of
specified (PDNOS). Prevalence rates for individual Axis II is that personality disorders are untreatable. In
personality disorders will be discussed later in this fact, maladaptive personality traits are often the focus
chapter. of clinical treatment. Personality disorders are among
There is also considerable personality disorder di- the more difficult of mental disorders to treat as they
agnostic co-occurrence. Individuals who meet the involve entrenched behavior patterns, some of which
DSM-IV-TR diagnostic criteria for one personality will be integral to an individual’s self-image. Never-
disorder are likely to meet the diagnostic criteria for theless, there is compelling empirical support to indi-
another. DSM-IV-TR instructs clinicians that all diag- cate that meaningful responsivity to psychosocial and
noses should be recorded because it can be important to pharmacologic treatment does occur. Treatment of a
consider, for example, the presence of antisocial traits personality disorder is unlikely to result in the develop-
in someone with a BPD or the presence of paranoid ment of a fully healthy or ideal personality structure,
traits in someone with a dependent personality disor- but clinically and socially meaningful change to per-
der (DPD). However, the extent of diagnostic co-oc- sonality structure and functioning does occur. In fact,
currence is at times so extensive that most researchers given the considerable social, occupational, medical,
prefer a more dimensional description of personality. and other costs that are engendered by such person-
Chapter 42 • Personality Disorders 441
ality disorders as the antisocial and borderline, even

marginal reductions in symptomatology can represent DSM-IV-TR Diagnostic Criteria
quite significant and meaningful public health care, so- 301.0 PARANOID PERSONALITY DISORDER
cial, and clinical benefits.
A. A pervasive distrust and suspiciousness of others
such that their motives are interpreted as malevolent,
beginning by early adulthood, and present in a vari-
Specific DSM-IV-TR Personality Disorders ety of contexts, as indicated by four (or more) of the
following:
DSM-IV-TR includes 10 individual personality disor-
der diagnoses that are organized into three clusters: (a) (1) suspects, without sufficient basis, that others are
exploiting, harming, or deceiving him or her
paranoid, schizoid, and schizotypal (placed within an (2) is preoccupied with unjustified doubts about the
odd–eccentric cluster); (b) antisocial, borderline, his- loyalty or trustworthiness of friends or associates
(3) is reluctant to confide in others because of unwar-
trionic, and narcissistic (dramatic–emotional–erratic ranted fear that the information will be used mali-
cluster); and (c) avoidant, dependent, and obsessive– ciously against him or her
compulsive (anxious–fearful cluster). Each of these (4) reads hidden demeaning or threatening meanings
into benign remarks or events
personality disorders will be discussed in turn. (5) persistently bears grudges, i.e. is unforgiving of in-
sults, injuries, or slights
(6) perceives attacks on his or her character or reputa-
Paranoid Personality Disorder tion that are not apparent to others and is quick to
react angrily or to counterattack
DIAGNOSIS (7) has recurrent suspicions, without justification, re-
garding fidelity of spouse or sexual partner.
Paranoid personality disorder (PPD) involves a per- B. Does not occur exclusively during the course of schiz-
vasive and continuous distrust and suspiciousness of ophrenia, a mood disorder with psychotic features, or
the motives of others, but the disorder is more than another psychotic disorder, and is not due to the direct
physiological effects of a general medical condition.
just suspiciousness. Persons with this disorder are also
hypersensitive to criticism, they respond with anger Note: if criteria are met prior to the onset of schizophre-
to threats to their autonomy, they incessantly seek out nia, add “premorbid,” e.g., paranoid personality disorder
(premorbid).
confirmations of their suspicions, and they tend to be
quite rigid in their beliefs and perceptions of others. Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
The presence of PPD is indicated by four or more of the American Psychiatric Association.
seven diagnostic criteria presented in the DSM-IV-TR
criteria for PPD.
Trust versus mistrust is a fundamental personality poor with respect to interpersonal relationships. They
trait along which all persons vary. Thirteen percent may become socially isolated or fanatic members of
of the adult male population and 6% of the adult fe- groups that encourage or at least accept their paranoid
male population may be characteristically mistrustful ideation. They might maintain a steady employment
of others. However, only 0.5–2.5% of the population but are difficult coworkers, as they tend to be rigid,
are likely to meet the DSM-IV-TR diagnostic criteria controlling, critical, blaming, and prejudicial. They are
for a PPD. It is suggested in DSM-IV-TR that approxi- likely to become involved in lengthy, acrimonious, and
mately 10–30% of persons within inpatient settings litigious disputes that are difficult, if not impossible,
and 2–10% within outpatient settings have this, but to resolve.
the lower end of these rates may represent the more ac-
curate estimate. It does appear that more males than
females have the disorder.
PPD paranoid ideation is inconsistent with reality and
is resistant to contrary evidence, but the ideation is not
Course
psychotic, absurd, inconceivable, or bizarre. PPD also
Premorbid traits of PPD may be evident prior to ado- lacks other features of psychotic and delusional dis-
lescence in the form of social isolation, hypersensitiv- orders (e.g., hallucinations) and is evident since early
ity, hypervigilance, social anxiety, peculiar thoughts, adulthood, whereas a psychotic disorder becomes evi-
angry hostility, and idiosyncratic fantasies. As chil- dent later within a person’s life or remits after a much
dren, individuals may appear odd and peculiar to their briefer period of time. Persons with PPD can develop
peers and they may not have achieved to their capac- psychotic disorders but to diagnose PPD in such cases,
ity in school. Their adjustment as adults is particularly the paranoid personality traits must be evident prior to
and persist after the psychotic episode. If PPD precedes is preferable to be especially forthright and precise with
the onset of schizophrenia, then it should be noted that paranoid individuals. Details that are inconsequential
it is premorbid to the schizophrenia. However, it may and of no interest to most individuals can be important
not be meaningful to diagnose a person with both PPD to provide to persons with PPD so that they are assured
and schizophrenia, as the premorbid paranoid traits that nothing is being withheld or hidden from them.
may in some cases have simply represented a prodro- Clinicians agree on several general principles in
mal phase of the schizophrenic pathology. the treatment of paranoid personality traits. It is usu-
Paranoid personality traits are evident in other per- ally pointless and often harmful to confront (or argue
sonality disorders. Persons with avoidant personal- with) the paranoid beliefs. Such efforts may only alien-
ity disorder are socially withdrawn and apprehensive ate the individual and confirm his or her suspicions.
of others; borderline, antisocial, and narcissistic per- The therapist should maintain a sincere and consistent
sons may be impatient, irritable, and antagonistic; and respect for the individual’s autonomy and for his or her
schizotypal persons may display paranoid ideation. right to make his or her own decisions. However, one
The diagnosis of PPD often co-occurs with these other should not attempt to ingratiate oneself by being overly
personality disorder diagnoses. Persons with PPD are acquiescent and compliant. This can appear to be ob-
prone to develop a variety of Axis I disorders, includ- viously patronizing, insincere, or manipulative. The
ing substance-related, obsessive–compulsive, anxiety, goal is to develop, in a nonthreatening way, more self-
agoraphobia, and depressive disorders. reflection and self-awareness (e.g., recognition of the
contribution of the paranoid traits and behaviors to the
difficulties he or she has been experiencing). A useful
TREATMENT
approach can be to communicate a sincere and respect-
Persons with PPD rarely seek treatment for their feel- ful willingness to explore the implications, logic, and
ings of suspiciousness and distrust. They experience reality of the suspicions. Whenever one appears to be
these traits as simply accurate perceptions of a ma- endangering rapport by moving too quickly, one should
levolent and dangerous world (i.e., egosyntonic). They retreat to a more neutral and accepting position.
may not consider the paranoid attributions to be at all One must also be careful to avoid defensive reactions
problematic, disruptive, or maladaptive. They are not to the inevitable accusations. Any one of the conflicts
delusional but they also fail to be reflective, insight- they have had with others can develop within the thera-
ful, or self-critical. They may recognize only that they peutic relationship and persons with PPD have a ten-
have difficulty controlling their anger and getting along dency to be contentious, rigid, accusatory, suspicious,
with others. They might be in treatment for an anxi- and litigious, which can tax the empathy and patience
ety, mood, or substance-related disorder or for various of the therapist. One must attempt to maintain an em-
marital, familial, occupational, or social (or legal) con- pathic concern for their feelings of betrayal, and reas-
flicts that are secondary to their personality disorder, sure them in an understanding, forthright manner that
but they also externalize the responsibility for their is neither patronizing nor disrespectful. Termination
problems and have substantial difficulty recognizing of treatment may at times be necessary if continuation
their own contribution to their internal dysphoria and would only result in further acrimony.
external conflicts. They consider their problems to be The suspicions, accusations, and acrimony often
due to what others are doing to them, not to how they makes the person with PPD a poor candidate for group
perceive, react, or relate to others. therapies. There is the potential to learn much about
The presence of paranoid personality traits compli- themselves within a group, but it is usually very dif-
cates the treatment of an Axis I disorder or a relation- ficult for them to develop the feelings of trust, respect,
ship problem. Trust is central to the development of an and security that are necessary for successful group
adequate therapeutic alliance, yet it is precisely the ab- therapy. Their propensity to make unfair hostile accu-
sence of trust that is central to this disorder. It can be sations alienates them from other group members, and
tempting to be less than forthright and open in the treat- they may quickly become a scapegoat for difficulties
ment of excessively suspicious persons because they and conflicts that develop within the group.
distort, exaggerate, or escalate minor errors, misunder- There have been a variety of studies on the pharma-
standings, or inconsistent statements. However, thera- cologic treatment of psychotic paranoid ideation and of
pists find that they weave an increasingly tangled web schizotypal personality disorder (which often includes
as they walk gingerly around the truth. Also, persons paranoid personality traits) but little to no research on
with PPD seize upon any kernel of deception to confirm the pharmacologic responsivity of the nonpsychotic
their suspicion that the therapist is not to be trusted. It suspiciousness and egosyntonic paranoid ideation of
PPD. Persons with PPD may also perceive the use of

a medication to represent an effort to simply suppress DSM-IV-TR Diagnostic Criteria
or control their accusations and suspicions rather than 301.20 SCHIZOID PERSONALITY DISORDER
to respectfully consider and address them. However,
they may be receptive and responsive to the benefits A. A pervasive pattern of detachment from social relation-
ships and a restricted range of expression of emotions
of a medication to help control feelings of anxiousness in interpersonal settings, beginning by early adulthood
or depression that are secondary to their personality and present in a variety of contexts, as indicated by
disorder. four (or more) of the following:
(1) neither desires nor enjoys close relationships, in-
cluding being part of a family
Schizoid Personality Disorder (2) almost always chooses solitary activities
(3) has little, if any, interest in having sexual experi-
ences with another person
DIAGNOSIS (4) takes pleasure in few, if any, activities
(5) lacks close friends or confidants other than first-
The schizoid personality disorder (SZPD) is a pervasive degree relatives
pattern of social detachment and restricted emotional (6) appears indifferent to the praise or criticism of
others
expression. Introversion (versus extraversion) is one (7) emotional coldness, detachment, or flattened
of the fundamental dimensions of general personality affectivity
functioning. Facets of introversion include low warmth B. Does not occur exclusively during the course of schiz-
(e.g., cold, detached, impersonal), low gregariousness ophrenia, a mood disorder with psychotic features, an-
other psychotic disorder, or a pervasive developmen-
(socially isolated, withdrawn), and low positive emo- tal disorder, and is not due to the direct physiological
tions (reserved, constricted or flat affect, anhedonic), effects of a general medical condition.
which define well the central symptoms of SZPD. The
Note: if criteria are met prior to the onset of schizophre-
presence of SZPD is indicated by four or more of the nia, add “premorbid,” e.g., schizoid personality disorder
seven diagnostic criteria presented in the DSM-IV-TR (premorbid).
criteria for SZPD. Reprinted with permission from the Diagnostic and Statistical
Approximately half of the general population will Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
exhibit an introversion within the normal range of func-
tioning. However, only a small minority of the popula-
tion would be diagnosed with an SZPD. Estimates of
the prevalence of SZPD within the general population that is relatively comfortable, but they could also drift
have been less than 1%, and SZPD is among the least from one job to another and remain isolated throughout
frequently diagnosed personality disorders within clin- much of their life. If they do eventually become a par-
ical settings. Many of the persons who were diagnosed ent, they have considerable difficulty providing warmth
with SZPD prior to DSM-III are probably now diag- and emotional support, and they may appear neglect-
nosed with either the avoidant or the schizotypal per- ful, detached, and disinterested.
sonality disorders, and prototypic (pure) cases of SZPD
are likely to be quite rare within the population.
SZPD can be confused with the schizotypal and avoid-
Course
ant personality disorders as both involve social isola-
Persons with SZPD would have been socially isolated tion and withdrawal. Schizotypal personality disorder,
and withdrawn as children. They may not have been however, also includes an intense social anxiety and
accepted well by their peers, and may have even borne cognitive–perceptual aberrations. The major distinction
the brunt of some ostracism. As adults, they have few with avoidant personality disorder is the absence of an
friendships. The friendships that do occur are likely to intense desire for intimate social relationships. Avoid-
be initiated by their peers or colleagues. They have few ant persons will also exhibit substantial insecurity and
sexual relationships and may never marry. Relation- inhibition, whereas the schizoid person is largely indif-
ships fail to the extent to which the other person desires ferent toward the reactions or opinions of others.
or needs emotional support, warmth, and intimacy. The presence of premorbid schizoid traits can have
Persons with SZPD may do well and even excel within prognostic significance for the course and treatment
an occupation, as long as substantial social interaction of schizophrenia, but more importantly, it might not
is not required. They prefer to work in isolation. They be meaningful to suggest that a person has an SZPD
may eventually find employment and a relationship that is independent of or unrelated to a comorbid
schizophrenia. The negative, prodromal, and residual group is patient and accepting, they can benefit from
symptoms of schizophrenia resemble closely the fea- the experience.
tures of SZPD. Once a person develops schizophrenia, There have been many studies on the pharmaco-
a diagnosis of SZPD can become rather pointless as all logic treatment of the schizotypal PD but no compa-
of the schizoid symptoms can then be understood as rable studies on SZPD. The schizotypal and schizoid
(prodromal or residual) symptoms of schizophrenia. PDs share many features, but the responsivity of the
schizotypal PD to pharmacotherapy will usually reflect
schizotypal social anxiety and cognitive–perceptual
TREATMENT
aberrations that are not seen in prototypic, pure cases
Prototypic cases of SZPD rarely present for treatment, of SZPD.
whether it is for their schizoid traits or a concomitant
Axis I disorder. They feel little need for treatment, as
Schizotypal Personality Disorder
their isolation is often egosyntonic. Their social isola-
tion is of more concern to their relatives, colleagues,
DIAGNOSIS
or friends than to themselves. Their disinterest in and
withdrawal from intimate or intense interpersonal con- Schizotypal PD (STPD) is a pervasive pattern of
tact is also a substantial barrier to treatment. They at interpersonal deficits, cognitive and perceptual aber-
times appear depressed but one must be careful not to rations, and eccentricities of behavior. The interper-
confuse their anhedonic detachment, withdrawal, and sonal deficits are characterized in large part by an
flat affect with symptoms of depression. acute discomfort with and reduced capacity for close
If persons with SZPD are seen for treatment for a relationships. The symptomatology of STPD has been
concomitant Axis I disorder (e.g., a sexual arousal differentiated further into components of positive
disorder or a substance dependence), it is advisable to (cognitive, perceptual aberrations) and negative (so-
work within the confines and limitations of the schizoid cial aversion and withdrawal) symptoms comparable
personality traits. Charismatic, engaging, emotional, or to the distinctions made for schizophrenia. The pres-
intimate therapists can be very uncomfortable, foreign, ence of STPD is indicated by five or more of the nine
and even threatening to persons with SZPD. A more diagnostic criteria listed in the DSM-IV-TR criteria for
business-like approach can be more successful. STPD (see page 445).
It is also important not to presume that persons with STPD may occur in as much as 3% of the general
SZPD are simply inhibited, shy, or insecure. Such population although most studies with semistructured
persons are more appropriately diagnosed with the interviews have suggested a somewhat lower percent.
avoidant personality disorder. Persons with SZPD are STPD might occur somewhat more often in males.
perhaps best treated with a supportive psychotherapy STPD co-occurs most often with the schizoid, bor-
that emphasizes education and feedback concerning in- derline, avoidant, and paranoid personality disorders.
terpersonal skills and communication. One may not be Common Axis I disorders are major depressive disor-
able to increase the desire for social involvements but der, brief psychotic disorder, and generalized social
one can increase the ability to relate to, communicate phobia.
with, and get along with others. Persons with SZPD
may not want to develop intimate relationships but they
Course
will often want to interact and relate more effectively
and comfortably with others. The use of role playing STPD is classified within the same diagnostic group-
and videotaped interactions can at times be useful in ing as schizophrenia in ICD-10 because of its close
this respect. Persons with SZPD can have tremendous relationship in phenomenology, etiology, and pathol-
difficulty understanding how they are perceived by ogy. However, it is classified as a personality disorder
others or how their behavior is unresponsive to and in DSM-IV-TR because its course and phenomenol-
perceived as rejecting by others. ogy are more consistent with a disorder of personal-
Group therapy is often useful as a setting in which ity (i.e., early onset, evident in everyday functioning,
the individual can gradually develop self-disclosure, characteristic of long-term functioning, and egosyn-
experience the interest of others, and practice social tonic). Persons with STPD are likely to be rather iso-
interactions with immediate and supportive feedback. lated in childhood. They may have appeared peculiar
However, persons with SZPD are prone to being re- and odd to their peers, and may have been teased or
jected by a group because of their detachment, flat ostracized. Achievement in school is usually impaired,
affect, and indifference to the feelings of others. If the and they may have been heavily involved in esoteric
anxiety of STPD does not diminish with familiarity,

DSM-IV-TR Diagnostic Criteria whereas the anxiety of avoidant personality disorder
301.22 SCHIZOTYPAL PERSONALITY DISORDER
(AVPD) is concerned primarily with the initiation of a
relationship. STPD is also a more severe disorder that
A. A pervasive pattern of social and interpersonal deficits includes a variety of cognitive and perceptual aberra-
marked by acute discomfort with, and reduced capac-
ity for, close relationships as well as by cognitive or tions that are not seen in persons with AVPD.
perceptual distortions and eccentricities of behavior, An initial concern of many clinicians when con-
beginning by early adulthood, and present in a vari- fronted with a person with STPD is whether the more
ety of contexts, as indicated by five (or more) of the
following: appropriate diagnosis is schizophrenia. Persons with
(1) ideas of reference (excluding delusions of
STPD closely resemble persons within the prodromal
reference) or residual phases of schizophrenia. This differentia-
(2) odd beliefs or magical thinking that influences be- tion is determined largely by the absence of a deteri-
havior and is inconsistent with subcultural norms
(e.g., superstitiousness, belief in clairvoyance, te-
oration in functioning. It is indicated in DSM-IV-TR
lepathy, or “sixth sense”; in children and adoles- that one should note that STPD is “premorbid” if the
cents, bizarre fantasies or preoccupations) schizotypal symptoms were present prior to the onset of
(3) unusual perceptual experiences, including bodily
illusions schizophrenia. Premorbid schizotypal traits will have
(4) odd thinking and speech (e.g., vague, circumstan- prognostic significance for the course and treatment
tial, metaphorical, overelaborate, or stereotyped) of schizophrenia and such traits should then be noted.
(5) suspiciousness or paranoid ideation
(6) inappropriate or constricted affect However, as discussed for SZPD, in most of these cases
(7) behavior or appearance that is odd, eccentric, or the schizotypal PD symptoms could then be readily un-
peculiar derstood as prodromal symptoms of schizophrenia.
(8) lacks close friends or confidants other than first-
degree relatives
(9) excessive social anxiety that does not diminish with
familiarity and tends to be associated with paranoid TREATMENT
fears rather than negative judgments about self
Persons with STPD may seek treatment for their feel-
B. Does not occur exclusively during the course of schiz-
ophrenia, a mood disorder with psychotic features, ings of anxiousness, perceptual disturbances, or de-
another psychotic disorder, or a pervasive develop- pression. Treatment of persons with STPD should be
mental disorder. cognitive, behavioral, supportive, and/or pharmaco-
Note: if criteria are met prior to the onset of schizophre- logic, as they will often find the intimacy and emo-
nia, add “premorbid,” e.g., schizotypal personality disor- tionality of reflective, exploratory psychotherapy to be
der (premorbid). too stressful and they have the potential for psychotic
Reprinted with permission from the Diagnostic and Statistical decompensation.
American Psychiatric Association. Persons with STPD will often fail to consider their
social isolation and aberrant cognitions and percep-
tions to be particularly problematic or maladaptive.
fantasies and peculiar interests, particularly those that They may consider themselves to be simply eccentric,
do not involve peers. As adults, they may drift toward creative, or nonconformist. Rapport can be difficult to
esoteric–fringe groups that support their magical think- develop as increasing familiarity and intimacy may
ing and aberrant beliefs. These activities can provide only increase their level of discomfort and anxiety.
structure for some persons with STPD, but they can They are unlikely to be responsive to informality or
also contribute to a further loosening and deterioration playful humor. The sessions should be well-structured
if there is an encouragement of aberrant experiences. to avoid loose and tangential ideation.
Only a small proportion of persons with STPD develop Practical advice is usually helpful and often neces-
schizophrenia. The symptomatology of STPD does not sary. The therapist should serve as the individual’s
appear to remit with age. The course appears to be rela- counselor, guide, or “auxiliary ego” to more adaptive
tively stable, with some proportion of schizotypal per- decisions with respect to everyday problems (e.g.,
sons remaining marginally employed, withdrawn, and fi nding an apartment, interviewing for a job, and
transient throughout their lives. personal appearance). Persons with STPD should
also receive social skills training directed at their
awkward and odd behavior, mannerisms, dress, and
speech. Specific, concrete discussions on what to ex-
Avoidant personality disorder and STPD share the fea- pect and do in various social situations (e.g., formal
tures of social anxiety and introversion, but the social meetings, casual encounters, and dates) should be
provided. The rate of progress will tend to be slow,

and it is helpful if there remains a continuity in the DSM-IV-TR Diagnostic Criteria
therapeutic relationship. 301.7 ANTISOCIAL PERSONALITY DISORDER
Most of the systematic empirical research on the
treatment of STPD has been confined to pharmacologic A. There is a pervasive pattern of disregard for and vi-
olation of the rights of others (occurring since age
interventions. Low doses of neuroleptic medications 15 years), as indicated by three (or more) of the
(e.g., thiothixene) have shown some effectiveness in following:
the treatment of schizotypal symptoms, particularly the (1) failure to conform to social norms with respect to
perceptual aberrations and social anxiousness. Group lawful behaviors as indicated by repeatedly per-
therapy has also been recommended for persons with forming acts that are grounds for arrest
(2) deceitfulness, as indicated by repeated lying, use
STPD but only when the group is highly structured of aliases, or conning others for personal profit or
and supportive. The emotional intensity and intimacy pleasure
(3) impulsivity or failure to plan ahead
of unstructured groups will usually be too stressful. (4) irritability and aggressiveness, as indicated by re-
Schizotypal individuals with predominant paranoid peated physical fights or assaults
symptoms may even have difficulty in highly struc- (5) reckless disregard for safety of self or others
(6) consistent irresponsibility, as indicated by repeated
tured groups. failure to sustain consistent work behavior or honor
financial obligations
(7) lack of remorse, as indicated by being indifferent
to or rationalizing having hurt, mistreated, or stolen
Antisocial Personality Disorder from another
DIAGNOSIS B. The individual is at least age 18 years.
C. Evidence of conduct disorder with onset before age
Antisocial personality disorder (ASPD) is a pervasive 15 years.
D. The occurrence of antisocial behavior is not exclu-
pattern of disregard for and violation of the rights of sively during the course of schizophrenia or a manic
others. Persons with ASPD will also be irresponsible episode.
and exploitative in their sexual relationships, and irre- Reprinted with permission from the Diagnostic and Statistical
sponsible as employees and parents. They may display a Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000
lack of empathy, an inflated or arrogant self-appraisal, a
callous, cynical, and contemptuous response to the suf-
fering of others, and a glib, superficial charm. This dis-
order has also been referred to as psychopathy, socio- the persons within these settings. More specific criteria
pathy, or dissocial personality disorder. The presence for psychopathy provide a more conservative estimate
of ASPD is indicated by the occurrence of a conduct of 20–30% of male prisoners with ASPD.
disorder prior to age 15 years and by three of the seven ASPD is much more common in males than in
adult diagnostic criteria presented in DSM-IV-TR Cri- females. A sociobiological explanation for the dif-
teria for ASPD. ferential sex prevalence is the presence of a genetic
Persons with ASPD are at a high risk for developing advantage for social irresponsibility, infidelity, su-
substance-related and impulse dyscontrol disorders. perficial charm, and deceit in males that contrib-
They are also likely to display borderline, narcissistic, utes to a higher likelihood of developing features of
and paranoid personality traits. Females with ASPD ASPD. It has also been suggested that ASPD and his-
will also display histrionic personality traits. trionic personality disorder (HPD) share a biogenetic
The National Institute of Mental Health Epidemio- disposition (perhaps towards impulsivity or sensa-
logic Catchment Area (ECA) study indicated that ap- tion-seeking) that is mediated by gender-specific
proximately 3% of males and 1% of females have biogenetic and sociological factors toward respective
ASPD. This rate has been replicated in subsequent stud- gender variants.
ies, but it has also been suggested that the ECA finding
may have underestimated the prevalence in males be-
Course
cause of the failure to consider the full range of ASPD
features. Other estimates have been as high as 6% in ASPD is evident in childhood in the form of a conduct
males. The rate of ASPD within prison and forensic disorder. Evidence of a conduct disorder prior to the age
settings has been estimated at 50% but the ASPD cri- of 15 years is in fact required for a DSM-IV-TR ASPD
teria may exaggerate the rate within such settings be- diagnosis. The continuation into adulthood is particu-
cause of the emphasis given to overt acts of criminality, larly likely to occur if multiple delinquent behaviors are
delinquency, and irresponsibility that are common to evident prior to the age of 10 years. As adults, persons
with ASPD are unlikely to maintain steady employ- a lack of empathy, glib and superficial charm, and ar-
ment and they may even become impoverished, home- rogant self-appraisal.
less, or spend years within penal institutions. However,
some persons with ASPD characterized by high rather
TREATMENT
than low levels of conscientiousness may express their
psychopathic tendencies within a socially acceptable or The presence of ASPD is important to recognize in the
at least legitimate profession. They may in fact be quite treatment of any Axis I disorder, as their tendency to
successful as long as their tendency to bend or violate be manipulative, dishonest, exploitative, aggressive,
the norms or rules of their profession and exploit, de- and irresponsible will often disrupt and sabotage treat-
ceive, and manipulate others, contribute to a career ad- ment. It is also very easy to be seduced by psychopathic
vancement. Their success, however, may at some point charm. Persons with ASPD can be seductive in their
unravel when their psychopathic behaviors become engaging friendliness, expressions of remorse, avowed
problematic or evident to others. The same pattern commitment to change, and apparent response to or
may also occur within sexual and marital relationships. even fascination with the success, skills, and talents of
They may at first appear to be charming, engaging, and the therapist, none of which will be sincere or reliable.
sincere, but most relationships will end because of a The extent to which ASPD is untreatable has at
lack of empathy, responsibility, and fidelity. times been overstated and exaggerated. Nevertheless,
There does tend to be a gradual remission of an- ASPD is the most difficult personality disorder to treat.
tisocial behaviors, particularly overt criminal acts, Persons with ASPD will often lack a motivation or
as the person ages. Persons with ASPD, however, commitment to change. They might see only the ad-
are more likely than the general population to have vantages of their antisocial traits and not the costs (e.g.,
died prematurely by violent means (e.g., accidents or risks of arrest and failure to sustain lasting or meaning-
homicides) and to engage in quite dangerous, high- ful relationships). They are prone to manipulate, abuse,
risk behavior. or exploit their fellow individuals and the staff. The
immediate motivation for treatment is often provided
by an external source, such as a court order or the de-
mands of an employer or relative. Motivation may last
ASPD will at times be difficult to differentiate from a only as long as an external pressure remains.
substance use disorder in young adults because many The most effective treatment is likely to be preven-
persons with ASPD develop a substance-related dis- tion through an identification and intervention early
order and many persons with substance dependence in childhood. In adulthood, the most effective treat-
engage in antisocial acts. The requirement that the ment may at times be simply some form of sustained
ASPD features be evident prior to the age of 15 years incarceration (e.g., imprisonment), as many antisocial
will usually assure the onset of ASPD prior to the on- behaviors do tend to dissipate (or burn out) with time.
set of a substance-related disorder. If both are evident The tendency to rationalize irresponsibility, minimize
prior to the age of 15 years, then it is likely that both the consequences of acts, and manipulate others needs
disorders are in fact present and both diagnoses should to be confronted on a daily and immediate basis. Com-
then be made. ASPD and substance dependence will munity residential or wilderness programs that provide
often interact, exacerbating and escalating each other’s a firm structure, close supervision, and intense con-
development. frontation by peers have been recommended. The in-
Antisocial acts will also be evident in the histrionic volvement of family members in the treatment has been
and borderline personality disorders, as persons with shown to be helpful, but there are also data to suggest
these disorders will display impulsivity, sensation- that interventions with little professional input are less
seeking, self-centeredness, manipulativeness, and a successful and are at times counterproductive.
low frustration tolerance. Females with ASPD are of- There is some research to suggest that the ability to
ten misdiagnosed with HPD. Prototypic cases of ASPD form a therapeutic alliance is an important indicator
might be distinguished from other personality disorders of treatment success. Factors to consider are the de-
by the presence of the childhood history of conduct dis- mographic similarity of the therapist and individual,
order and the cold, calculated exploitation, abuse, and the quality of the individual’s past relationships, and
aggression. Persons with narcissistic personality disor- the therapist’s positive regard for the individual. Many
der (NPD) are also characterized by a lack of empathy clinicians may also experience strong feelings of ani-
and may often exploit and use others. In fact, many of mosity and distaste for antisocial persons who have
the traits of NPD are evident in psychopathy, including a history of abusive and exploitative acts. Rational,
utilitarian approaches that help the person consider

the long-term consequences of behavior can be help- DSM-IV-TR Diagnostic Criteria
ful. This approach does not attempt to develop a sense 301.83 BORDERLINE PERSONALITY DISORDER
of conscience, guilt, or even regret for past actions,
but focuses instead on the material value and future A. A pervasive pattern of instability of interpersonal rela-
tionships, self-image, and affects, and marked impul-
advantages to be gained by a more prosocial behavior sivity beginning by early adulthood and present in a
pattern. There are data to suggest the use of pharmaco- variety of contexts, as indicated by five (or more) of
therapy in the treatment of impulsive aggression but it the following:
is unclear whether these findings would generalize to (1) frantic efforts to avoid real or imagined abandon-
the full spectrum of ASPD psychopathology. ment. Note: do not include suicidal or self-mutilat-
ing behavior covered in criterion 5
(2) a pattern of unstable and intense interpersonal re-
lationships characterized by alternating between
Borderline Personality Disorder extremes of idealization and devaluation
(3) identity disturbance: markedly and persistently un-
stable self-image or sense of self
DIAGNOSIS (4) impulsivity in at least two areas that are poten-
tially self-damaging (e.g., spending, sex, substance
Borderline personality disorder (BPD) is a pervasive abuse, reckless driving, binge eating). Note: do not
pattern of impulsivity and instability in interpersonal include suicidal or self-mutilating behavior covered
relationships and self-image. A broad domain of gen- in criterion 5
(5) recurrent suicidal behavior, gestures, or threats, or
eral personality functioning is neuroticism (or emo- self-mutilating behavior
tional instability) characterized by facets of angry (6) affective instability due to a marked reactivity of
hostility, anxiousness, depressiveness, impulsivity, mood (e.g., intense episodic dysphoria, irritabil-
ity, or anxiety usually lasting a few hours and only
and vulnerability; BPD is essentially the most extreme rarely more than a few days)
and highly maladaptive variant of emotional instabil- (7) chronic feelings of emptiness
ity. This disorder is indicated by the presence of five (8) inappropriate, intense anger or difficulty control-
ling anger (e.g., frequent displays of temper, con-
or more of the nine diagnostic criteria presented in the stant anger, recurrent physical fights)
DSM-IV-TR criteria for BPD. (9) transient, stress-related paranoid ideation or severe
Axis I disorders are commonly comorbid with BPD. dissociative symptoms.
The range of potential Axis I comorbid psychopathol- Reprinted with permission from the Diagnostic and Statistical
ogy includes mood (major depressive disorder), anxi- American Psychiatric Association.
ety (posttraumatic stress disorder), eating (bulimia
nervosa), substance (alcohol dependence), dissociative
(dissociative identity disorder), and psychotic (brief 75% of persons with BPD will be female. Persons
psychotic) disorders. Persons with BPD also meet with BPD often meet DSM-IV-TR criteria for at least
DSM-IV-TR criteria for at least one other personality one Axis I disorder.
disorder, particularly histrionic, dependent, antiso-
cial, or schizotypal. Researchers and clinicians have at
Course
times responded to this extensive co-occurrence by im-
posing a diagnostic hierarchy whereby other disorders As children, persons with BPD are likely to have been
are not diagnosed in the presence of BPD because BPD emotionally unstable, impulsive, and angry or hostile.
is generally the most severely dysfunctional disorder. A Their chaotic impulsivity and intense affectivity may
potential limitation of this approach is that it resolves contribute to involvement within rebellious groups as
the complexity of personality by largely ignoring it. a child or adolescent, along with a variety of Axis I
This approach may fail to recognize the presence of disorders, including eating, substance use, and mood
maladaptive personality traits that could be important disorders. BPD is often diagnosed in children and ado-
for understanding an individual’s dysfunctions and for lescents, but considerable caution should be used when
developing an optimal treatment plan. doing so as some of the symptoms of BPD (e.g., iden-
Approximately 1–2% of the general population tity disturbance and unstable relationships) could be
would meet the DSM-IV-TR criteria for BPD. BPD is confused with a normal adolescent rebellion or identity
the most prevalent personality disorder within hospi- crisis. As adults, persons with BPD may require nu-
tal clinical settings. Approximately 15% of all inpa- merous hospitalizations due to their affect and impulse
tients (51% of inpatients with a personality disorder) dyscontrol, psychotic-like and dissociative symptoma-
and 8% of all outpatients (27% of outpatients with tology, and risk of suicide. Minor problems quickly be-
a personality disorder) have a BPD. Approximately come crises as the intensity of affect and impulsivity
result in disastrous decisions. They are at a high risk for be explicitly addressed. Suicidal behavior should be
developing depressive, substance-related, bulimic, and confronted and contained, by hospitalization when
posttraumatic stress disorders. The potential for suicide necessary. Individuals with BPD can be very difficult
increases with a comorbid mood and substance-related to treat because the focus of the individual’s love and
disorder. Approximately 3–10% commit suicide by the wrath will often be shifted toward the therapist, and
age of 30 years. Relationships tend to be very unstable the treatment may itself become the individual’s latest
and explosive, and employment history is poor. Affec- unstable, intense relationship. Immediate and ongoing
tivity and impulsivity, however, may begin to dimin- consultation with colleagues is often necessary, as it is
ish as the person reaches the age of 30 years, or earlier not unusual for therapists to be unaware of the extent
if the person becomes involved with a supportive and to which they are developing or expressing feelings of
patient sexual partner. Some, however, may obtain sta- anger, attraction, annoyance, or intolerance toward the
bility by abandoning the effort to obtain a relationship, individual with BPD.
opting instead for a lonelier but less volatile life. The A particular form of cognitive–behavioral therapy,
mellowing of the symptomatology, however, can be dialectical behavior therapy, has been shown empiri-
easily disrupted by the occurrence of a severe stressor cally to be effective in the treatment of BPD. Part of
(e.g., divorce or death of a significant other) that results the strategy entails keeping individuals focused ini-
in a brief psychotic, dissociative, or mood disorder tially on the priorities of reducing suicidal threats and
episode. gestures, behaviors that can disrupt or resist treatment,
and behaviors that affect the immediate quality of life
(e.g., bulimia, substance abuse, or unemployment).
Once these goals are achieved, the focus can then shift
Most persons with BPD develop mood disorders and it to a mastery of new coping skills, management of reac-
is at times difficult to differentiate BPD from a mood tions to stress, and other individualized goals. Individ-
disorder if the assessment is confined to the current ual therapy is augmented by skills-training groups that
symptomatology. A diagnosis of BPD requires that the may be highly structured (e.g., comparable to a class-
borderline symptomatology be evident since adoles- room format). Individuals are taught skills for coping
cence, which should differentiate BPD from a mood with identity diffusion, tolerating distress, improving
disorder in all cases other than a chronic mood disorder. interpersonal relationships, controlling emotions, and
If there is a chronic mood disorder, then the additional resolving interpersonal crises. Individuals are given
features of transient, stress-related paranoid ideation, homework assignments to practice these skills, which
dissociative experiences, impulsivity, and anger dys- are further addressed and reinforced within individual
control that are evident in BPD should be emphasized sessions. Negative affect is also addressed through a
in the diagnosis. mindful meditation that contributes to an acceptance
and tolerance of past abusive experiences and current
stress. The dialectical component of the therapy is that
TREATMENT
the dialectical therapist helps the individual achieve
Persons with BPD often develop intense, dependent, synthesis of oppositions, rather than focusing on veri-
hostile, unstable, and manipulative relationships with fying either side of an oppositional argument. An il-
their therapists as they do with their peers. At one time lustrative list of dialectical strategies is presented in
they might be very compliant, responsive, and even Table 42-1.
idealizing, but later angry, accusatory, and devaluing. Dialectical behavior therapy (DBT), however, also
Their tendency to be manipulatively as well as impul- includes more general principles of treatment that are
sively self-destructive is often very stressful and dif- important to emphasize in all forms of therapy for
ficult to treat. BPD, some of which are presented in Table 42-2. For
Persons with BPD are often highly motivated for example, exasperated therapists may unjustly experi-
treatment. Psychotherapeutic approaches tend to be ence and even accuse borderline individuals of being
both supportive and exploratory. Therapists should unmotivated or unwilling to work. It is important to
provide a safe, secure environment in which anger can appreciate that they do want to improve and are do-
be expressed and actively addressed without destroy- ing the best that they can. One should not make the
ing the therapeutic relationship. The historical roots of therapy personal, but instead identify the sources of the
current bitterness, anger, and depression within past inhibition or interference to their motivation to change.
familial relationships should eventually be explored, One should take seriously their complaints that their
but immediate, current issues and conflicts must also lives are indeed unbearable but not absolve them of
Table 42-1 Dialectical Behavior Therapy Strategies

need to honestly recognize their own limitations. All
therapists have their own flaws and limits, and individ-
Alternate between acceptance and change strategies uals with BPD invariably strain and overwhelm these
Balance nurturing with demands for self-help
Balance persistence and stability with flexibility limits. Therapists need to be open and receptive to out-
Balance capabilities with limitations and deficits side support, advice, and criticism.
Move with speed, keeping the patient slightly off balance Pharmacologic treatment of individuals with BPD
Take positions whole-heartedly
Look for what is not included in patient’s own points of is varied, as it depends primarily on the predominant
view Axis I symptomatology. Persons with BPD can display
Provide developmental descriptions of change a wide variety of Axis I symptoms, including anxiety,
Question intransigence of boundary conditions of the
problem depression, hallucinations, delusions, and dissociations.
Highlight importance of interrelationships in identity It is important in their pharmacologic treatment not
Advocate a middle path to be unduly influenced by transient symptoms or by
Highlight paradoxical contradictions in the patient’s own
behavior, in the therapeutic process, and in life in general symptoms that are readily addressed through explora-
Speak in metaphors and tell parables and stories tory or supportive techniques. On the other hand, it is
Play the devil’s advocate
Extend the seriousness or implications of the patient’s
equally important to be flexible in the use of medica-
statements tions and not to be unduly resistant to their use. Relying
Add intuitive knowing to emotional experience and logical solely upon one’s own psychotherapeutic skills can be
analysis
Turn problems into assets unnecessary and even irresponsible.
Allow natural changes in therapy
Assess the individual, therapist, and process dialectically
Histrionic Personality Disorder
Source: Reprinted from Cognitive–Behavioral Treatment of
Borderline Personality Disorder, Linehan MM, Basic Propositions
of BPD Treatment from DBT, 206, Copyright (1993) with DIAGNOSIS
permission from Guilford Press.
Histrionic personality disorder (HPD) is a pervasive
pattern of excessive emotionality and attention-seek-
their responsibility to solve their own problems. They ing. Histrionic persons tend to be emotionally manipu-
are unlikely to change simply through a passive recep- lative and intolerant of delayed gratification. HPD is
tion of insight, nurturance, support, and medication. indicated by the presence of five or more of the eight
They will need to actively work on changing their lives. diagnostic criteria presented in DSM-IV-TR criteria for
Therapists will often be tempted to rescue the individu- HPD (see page 451).
als under their care, particularly when they are within Approximately 1–3% of the general population may
a crisis. However, it is precisely at such times that there be diagnosed with HPD. A controversial issue is its
will be the best opportunity to develop and learn new differential sex prevalence. It is stated in DSM-IV-TR
coping strategies. Failures can occur, and it is a failure that the sex ratio for HPD is “not significantly differ-
of the therapy that should be conscientiously and ef- ent than the sex ratio of females within the respective
fectively addressed by the therapist. Finally, therapists clinical setting” (p. 712). However, this should not be
interpreted as indicating that the prevalence is the same
for males and females. It has typically been found that
Basic Propositions of BPD Treatment from
Table 42-2 at least two-thirds of persons with HPD are female, al-
DBT
though there have been a few exceptions. Whether or
1. Patients are doing the best they can. not the rate will be significantly higher than the rate
2. Patients want to improve.
3. Patients need to do better, try harder, and be more of women within a particular clinical setting depends
motivated to change. upon many factors that are independent of the differen-
4. Patients may not have caused all of their own problems, tial sex prevalence for HPD.
but they have to solve them anyway.
5. The lives of suicidal, borderline individuals are
unbearable as they are currently being lived.
6. Patients must learn new behaviors in all relevant contexts. Course
7. Patients cannot fail in therapy.
8. Therapists treating patients with BPD need support. Little is known about the premorbid behavior pattern of
Source: Reprinted from Cognitive–Behavioral Treatment of
persons with HPD. During adolescence, they are likely
Borderline Personality Disorder, Linehan MM, Basic Propositions to be flamboyant, flirtatious, and attention-seeking. As
of BPD Treatment from DBT, 106–108, Copyright (1993) with adults, persons with HPD readily form new relation-
permission from Guilford Press.
ships but have difficulty sustaining them. They may
diagnostic criteria when confronted with histrionic

DSM-IV-TR Diagnostic Criteria and antisocial symptoms in females.
301.50 HISTRIONIC PERSONALITY DISORDER
Persons with HPD will often have borderline, de-
pendent, or narcissistic personality traits. Prototypic
A pervasive pattern of excessive emotionality and cases of HPD can be distinguished from other person-
attention-seeking, beginning by early adulthood and
present in a variety of contexts, as indicated by five (or ality disorders. For example, the prototypic narcissis-
more) of the following: tic person ultimately desires admiration whereas the
A. is uncomfortable in situations in which he or she is histrionic person desires whatever attention, interest,
not the center of attention or concern can be obtained. As a result, the histrionic
B. interaction with others is often characterized by person will at times seek attention through melodra-
inappropriate sexually seductive or provocative
behavior matic helplessness and emotional outbursts that could
C. displays rapidly shifting and shallow expression of be experienced as denigrating and humiliating to the
emotions
D. consistently uses physical appearance to draw atten-
narcissistic person. However, most cases will not be
tion to self prototypic and the most accurate description of an indi-
F. has a style of speech that is excessively impression- vidual’s constellation of maladaptive personality traits
istic and lacking in detail
G. shows self-dramatization, theatricality, and exagger- will be the provision of multiple diagnoses.
ated expression of emotion
H. is suggestible, i.e. easily influenced by others or
circumstances TREATMENT
I. considers relationships to be more intimate than
they actually are. Persons with HPD readily develop rapport but it is of-
Reprinted with permission from the Diagnostic and Statistical ten superficial and unreliable. Therapists may also fail
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 to appreciate the extent of influence they can have on
the highly suggestible individual with HPD. Persons
with HPD can readily become converts to whatever the
fall in love quite quickly, but just as rapidly become therapist may suggest or encourage. The transforma-
attracted to another person. They are unlikely to be re- tion to the theoretical model or belief system of the cli-
liable or responsible. Relationships with persons of the nician is unlikely to be sustained.
same sexual orientation are often strained because of A key task in treating the individual with HPD is
their competitive sexual flirtatiousness. Employment countering their global and diffuse cognitive style by
history is likely to be erratic, and may be complicated insisting on attending to structure and detail within
by the tendency to become romantically or sexually sessions and to the practical, immediate problems en-
involved with colleagues, by their affective instability, countered in daily life. It is also important to explore
and by their suggestibility. Persons with HPD may be- within treatment the historical source for their needs
come devoted converts to faddish belief systems. They for attention and involvement. Persons with HPD are
have a tendency to make impulsive decisions that will prone to superficial and transient insights but they will
have a dramatic (or melodramatic) effect on their lives. benefit from a carefully reasoned and documented ex-
The severity of the symptomatology may diminish ploration of their current and past relationships.
somewhat as the person ages. Many clinicians recommend the use of group ther-
apy for persons with HPD. It is quite easy for them to
become involved within a group, which may then be
very useful in helping them recognize and explore their
HPD involves to some extent maladaptive variants of attention-seeking, suggestibility, and manipulation, as
stereotypically feminine traits. The DSM-IV-TR diag- well as develop alternative ways to develop more mean-
nostic criteria for HPD are sufficiently stringent that a ingful and sustained relationships. However, it is also
normal woman would not meet these criteria, but stud- important to closely monitor their involvements within
ies have indicated that clinicians will at times diagnose the group, as they are prone to dominate and control
HPD in females who in fact have antisocial traits. Both sessions and they may escalate their attention-seeking
of these disorders can involve impulsivity, sensation- to the point of suicidal gestures. The intense affectivity
seeking, low frustration tolerance, and manipulative- of persons with HPD may also be responsive to antide-
ness, and the presence of a female gender may at times pressant treatment, particularly those individuals with
contribute to a false presumption of HPD. It is there- substantial mood reactivity, hypersomnia, and rejec-
fore important to adhere closely to the DSM-IV-TR tion sensitivity.
Narcissistic Personality Disorder narcissism. NPD is observed within clinical settings

(approximately 2–20% of individuals) although it is
DIAGNOSIS also among the least frequently diagnosed personality
disorders.
Narcissistic personality disorder (NPD) is a pervasive
pattern of grandiosity, need for admiration, and lack of
empathy. Persons with NPD can be very vulnerable to Course
threats to their self-esteem. They may react defensively
Little is known about the premorbid behavior pattern
with rage, disdain, or indifference but are in fact strug-
of NPD, other than through retrospective reports of
gling with feelings of shock, humiliation, and shame.
persons diagnosed when adults. As adolescents, per-
NPD is indicated by the presence of five or more of the
sons with NPD are likely to be self-centered, assertive,
nine diagnostic criteria presented in the DSM-IV-TR
gregarious, dominant, and perhaps arrogant. They
Criteria for NPD.
may have achieved well in school or within some other
Persons with NPD are considered to be prone to
activity. As adults, many persons with NPD will have
mood disorders, as well as anorexia and substance-
experienced high levels of achievement. However,
related disorders, especially cocaine. Persons with NPD
their relationships with colleagues, peers, and staff
are likely to have comorbid antisocial (psychopathic),
will eventually become strained as their exploitative
histrionic, paranoid, and borderline personality traits.
use of others and self-centered egotism become evi-
Approximately 18% of males and 6% of females
dent. Success may also be impaired by their difficulty
may be characterized as being excessively immod-
in acknowledging or resolving criticism, deficits, and
est (i.e., arrogant or conceited), but only a small per-
setbacks. Interpersonal and sexual relationships are
cent of these persons would be diagnosed with NPD.
usually easy for them to develop but difficult to sus-
In fact, the median prevalence rate obtained across
tain owing to their low empathy, self-centeredness,
10 community data collections was zero. The absence
and need for admiration. Persons who are deferential
of any cases within community studies, however, may
and obsequious, or who share a mutual need for sta-
reflect inadequacies within the diagnostic criteria or
tus and recognition, may help sustain a relationship.
limitations of semistructured interview assessments of
As parents, persons with NPD may attempt to live
through their children, valuing them as long as they
are a source of pride. Their personal sense of adjust-
ment may be fine for as long as they continue to expe-
301.81 NARCISSISTIC PERSONALITY DISORDER rience or anticipate success. Some may not recognize
the maladaptivity of their narcissism until middle-age,
A pervasive pattern of grandiosity (in fantasy or behavior),
need for admiration, and lack of empathy, beginning by when the emphasis given to achievement and status
early adulthood and present in a variety of contexts, as may begin to wane.
indicated by five (or more) of the following:
A. has a grandiose sense of self-importance (e.g. ex-
aggerates achievements and talents, expects to Differential Diagnosis
be recognized as superior without commensurate
achievements) Individuals with NPD may often appear relatively high
B. is preoccupied with fantasies of unlimited success, functioning. Exaggerated self-confidence may in fact
power, brilliance, beauty, or ideal love
C. believes that he or she is “special” and unique and
contribute to success in a variety of professions and
can only be understood by, or should associate with, narcissistic traits will at times be seen in highly suc-
other special or high-status people (or institutions) cessful persons. A diagnosis of NPD requires the ad-
D. requires excessive admiration
E. has a sense of entitlement, i.e. unreasonable expec- ditional presence of interpersonal exploitation, lack of
tations of especially favorable treatment or auto- empathy, a sense of entitlement, and other symptoms
matic compliance with his or her expectations beyond simply arrogance and grandiosity.
F. is interpersonally exploitative, i.e., takes advantage
of others to achieve his or her own ends Both narcissistic and antisocial persons may exploit,
G. lacks empathy: is unwilling to recognize or identify deceive, and manipulate others for personal gain, and
with the feelings and needs of others both may demonstrate a lack of empathy or remorse. As
H. is often envious of others or believes that others are
envious of him or her indicated above, many of the traits of narcissism, such
I. shows arrogant, haughty behaviors or attitudes. as arrogance and glib charm, are seen in psychopathic
Reprinted with permission from the Diagnostic and Statistical persons. Prototypic cases can be distinguished, as the
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 motivation for the narcissistic person will be for recog-
nition, status, and other signs of success, whereas the
prototypic antisocial person would be motivated more awareness of the impact of narcissistic behaviors and
for material gain or for the subjugation of others. An- statements on interpersonal relationships. The ideali-
tisocial persons will also display an impulsivity, reck- zation and devaluation can be responsive to role play-
lessness, and lax irresponsibility that may not be seen ing and rational introspection, an intellectual approach
in narcissistic persons. that may itself be valued by some persons with NPD.
However, therapists must be careful not to become em-
broiled within intellectual conflicts (or competitions).
TREATMENT
This approach may not work well with the narcissis-
Persons with narcissistic personality traits seek treat- tic person who is motivated to defeat or humiliate the
ment for feelings of depression, substance-related dis- therapist.
orders, and occupational or relational problems that are Group therapy can be useful for increasing aware-
secondary to their narcissism. Their self-centeredness ness of the grandiosity, lack of empathy, and devalua-
and lack of empathy are particularly problematic within tion of others. However, these traits not only interfere
marital, occupational, and other social relationships, with the narcissistic person’s ability to sustain mem-
and they usually lack an appreciation of the contribu- bership within groups (and within individual therapy)
tion of their conflicts regarding self-esteem, status, and but also may become quite harmful and destructive
recognition. It is difficult for them even to admit that to the rapport of the entire group. There is no ac-
they have a psychological problem or that they need cepted pharmacologic approach to the treatment of
help, as this admission is itself an injury to their self- narcissism.
esteem. In addition, one of the characteristics of NPD is
the belief that they can only be understood by persons
of a comparably high social status or recognition. They Avoidant Personality Disorder
may be unable to accept advice or insight from persons DIAGNOSIS
they consider less intelligent, talented, or insightful than
themselves, which may eventually effectively eliminate Avoidant personality disorder (AVPD) is a pervasive
most other persons. pattern of timidity, inhibition, inadequacy, and social
When they are involved in treatment, persons with hypersensitivity. Persons with AVPD may have a strong
NPD will often require some indication that their desire to develop close, personal relationships but feel
therapist is among the best or at least worth their time. too insecure to approach others or to express their feel-
They are prone to idealizing their therapists (to affirm ings. AVPD is indicated by the presence of four or more
that he or she is indeed of sufficient status or quality) of the seven diagnostic criteria presented in the DSM
or to devalue them (to affirm that they are of greater criteria for AVPD (see page 454).
intelligence, capacity, or quality than their therapist, to Timidity, shyness, and social insecurity are not
reject the insights that they have failed to identify, and uncommon problems and AVPD is one of the more
to indicate that they warrant or deserve an even better prevalent personality disorders within clinical settings,
therapist). How best to respond is often unclear. It may occurring in 5–25% of all individuals presenting with
at times be preferable to simply accept the praise or personality disorders. However, AVPD may be diag-
criticism, particularly when exploration will likely be nosed in only 1–2% of the general population. It ap-
unsuccessful, whereas at other times it is preferable to pears to occur equally among males and females, with
confront and discuss the motivation for the devaluation some studies reporting more males and others report-
(or the idealization). ing more females.
Psychodynamic approaches to the treatment of NPD
vary in the extent to which emphasis is given to an in-
Course
terpretation of underlying anger and bitterness, or to
the provision of empathy and a reflection (or mirroring) Persons with AVPD are shy, timid, and anxious as chil-
of a positive regard and self-esteem. It does appear to dren. Many are diagnosed with a social phobia during
be important to identify the current extent and histori- childhood. Adolescence is a particularly difficult de-
cal source of the conflicts and sensitivities regarding velopmental period due to the importance at this time
self-esteem. Active confrontation may at times be use- of attractiveness, dating, and popularity. Occupational
ful, particularly when the therapeutic alliance is strong, success may not be significantly impaired, as long as
but at other times the vulnerability of the individual there is little demand for public performance. Persons
may require a more unconditional support. Cognitive– with AVPD may in fact find considerable gratification
behavior approaches to NPD emphasize increasing and esteem through a job or career that they are unable
needs for reassurance, and hypersensitivity to criticism

DSM-IV-TR Diagnostic Criteria and neglect (i.e., abnormally high levels of anxious-
301.82 AVOIDANT PERSONALITY DISORDER
ness, self-consciousness, and vulnerability). A distinc-
tion between AVPD and DPD is best made when the
A pervasive pattern of social inhibition, feelings of inad- person is seeking a relationship. Avoidant persons tend
equacy, and hypersensitivity to negative evaluation, be-
ginning by early adulthood and present in a variety of to be very shy, inhibited, and timid (and are therefore
contexts, as indicated by four (or more) of the following: slow to get involved with someone) whereas dependent
A. avoids occupational activities that involve significant persons urgently seek another relationship as soon as
interpersonal contact, because of fears of criticism, one ends (i.e., avoidant persons are high in introversion
disapproval, or rejection whereas dependent persons are high in extraversion).
B. is unwilling to get involved with people unless cer-
tain of being liked Avoidant persons may also be reluctant to express their
C. shows restraint within intimate relationships because feelings whereas dependent persons can drive others
of the fear of being shamed or ridiculed
D. is preoccupied with thoughts of being criticized or
away by continuous expressions of neediness. The dif-
rejected in social situations ferentiation of AVPD from the schizoid, paranoid, and
E. is inhibited in new interpersonal situations because schizotypal personality disorders was discussed in pre-
of feelings of inadequacy
F. views self as socially inept, personally unappealing, vious sections.
or inferior to others
G. is unusually reluctant to take personal risks or to en-
gage in any new activities because they may prove TREATMENT
embarrassing
Persons with AVPD seek treatment for their avoidant
Manual of Mental Disorders, 4th ed., Text Rev. Copyright 2000 personality traits, although many initially seek treat-
American Psychiatric Association. ment for symptoms of anxiety, particularly social
phobia (generalized subtype). It is important in such
cases to recognize that the shyness is not due simply to
to find within their relationships. The job may serve a dysregulation or dyscontrol of anxiousness. There is
as a distraction from intense feelings of loneliness. instead a more pervasive and fundamental psychopa-
Their avoidance of social situations will impair their thology, involving feelings of interpersonal insecurity,
ability to develop adequate social skills, and this will low self-esteem, and inadequacy.
then further handicap any eventual efforts to develop Social skills training, systematic desensitization,
relationships. As parents, they may be very responsible, and a graded hierarchy of in vivo exposure to feared
empathic, and affectionate, but may unwittingly impart social situations have been shown to be useful in the
feelings of social anxiousness and awkwardness. Se- treatment of AVPD. However, it is also important to
verity of the AVPD symptomatology diminishes as the discuss the underlying fears and insecurities regard-
person becomes older. ing attractiveness, desirability, rejection, or intimacy.
Persons with AVPD are at times reluctant to discuss
Differential Diagnosis such feelings, as they may feel embarrassed, they may
fear being ridiculed, or they may not want to “waste the
The most difficult differential diagnosis for AVPD is time” of the therapist with such “foolish” insecurities.
with generalized social phobia. Both involve an avoid- They may prefer a less revealing or involved form of
ance of social situations, social anxiety, and timidity, treatment. It is important to be understanding, patient,
and both may be evident since late childhood or ado- and accepting, and to proceed at a pace that is com-
lescence. Many persons with AVPD in fact seek treat- fortable for the individual. Insecurities and fears can
ment for a social phobia. To the extent that the behavior at times be addressed through cognitive techniques as
pattern pervades the person’s everyday functioning and the irrationality is usually readily apparent. It remains
has been evident since childhood, the diagnosis of a useful though to identify the historical source of their
personality disorder would be more descriptive. development, as this understanding will help the in-
Many persons with AVPD may also meet the criteria dividual appreciate the irrationality or irrelevance of
for DPD. This might at first glance seem unusual, given their expectations and perceptions for their current
that AVPD involves social withdrawal whereas DPD relationships.
involves excessive social attachment. However, once a Persons with AVPD often find group therapies to be
person with AVPD is able to obtain a relationship, he or helpful. Exploratory and supportive groups can provide
she will often cling to this relationship in a dependent them with an understanding environment in which to
manner. Both disorders include feelings of inadequacy, discuss their social insecurities, to explore and practice
more assertive behaviors, and to develop an increased

self-confidence in approaching others and developing DSM-IV-TR Diagnostic Criteria
relationships outside of the group. Focused and special- 301.6 DEPENDENT PERSONALITY DISORDER
ized social skills-training groups would be preferable
to unstructured groups that might be predominated by A pervasive and excessive need to be taken care of that
leads to submissive and clinging behavior and fears of
much more assertive and extraverted members. separation, beginning by early adulthood and present in
Many persons with AVPD will respond to anxiolytic a variety of contexts, as indicated by five (or more) of the
medications, and at times to antidepressants, particu- following:
larly monoamine oxidase inhibitors such as phenelzine. A. has difficulty making everyday decisions without an
Normal and abnormal feelings of anxiousness can be excessive amount of advice and reassurance from
others.
suppressed or diminished through pharmacologic in- B. needs others to assume responsibility for most major
terventions. This approach may in fact be necessary areas of his or her life.
C. has difficulty expressing disagreement with others
to overcome initial feelings of intense social anxiety because of fear of loss of support or approval (Note:
that are markedly disruptive to current functioning Do not include realistic fears of retribution).
(e.g., inability to give required presentations at work or D. has difficulty initiating projects or doing things on
his or her own (because of a lack of self-confidence
to talk to new acquaintances). However, it is also im- in judgment or abilities rather than to a lack of mo-
portant to monitor closely a reliance on medications. tivation or energy).
Persons with AVPD could be prone to rely excessively E. goes to excessive lengths to obtain nurturance and
support from others, to the point of volunteering to
on substances to control their feelings of anxious- do things that are unpleasant.
ness, whereas their more general feelings of insecurity F. feels uncomfortable or helpless when alone, be-
and inadequacy would require a more comprehensive cause of exaggerated fears of being unable to care
for himself or herself.
treatment. G. urgently seeks another relationship as a source of
care and support when a close relationship ends.
H. is unrealistically preoccupied with fears of being left
Dependent Personality Disorder to take care of himself or herself.
DIAGNOSIS American Psychiatric Association.
Dependent personality disorder (DPD) involves a per-
vasive and excessive need to be taken care of, which
leads to submissiveness, clinging, and fears of separa- to be by themselves, as their sense of self-worth, value,
tion. Persons with DPD will also have low self-esteem, or meaning is obtained by or through the presence of
and will often be self-critical and self-denigrating. a relationship. They have few other sources of self-
DPD is indicated by the presence of five or more of esteem. Along with the need for emotional support
the eight diagnostic criteria presented in DSM-IV-TR are perpetual doubts and insecurities regarding the
Criteria for DPD. current source of support. Persons with DPD con-
DPD is among the most prevalent of the personality stantly require reassurance and reaffirmation that any
disorders, occurring in 5–30% of individuals present- particular relationship will continue, because they
ing with personality disorders and 2–4% of the general anticipate or fear that at some point they may again
community. A controversial issue is its differential sex be alone. Because of their intense fear of being alone,
prevalence. DPD is diagnosed more frequently in fe- they may become quickly attached to persons who are
males but there is some concern that there might be a unreliable, unempathic, and even exploitative or abu-
failure to recognize adequately the extent of dependent sive. More desirable or reliable partners are at times
personality traits within males. driven away by their excessive clinging and continued
demands for reassurance. Occupational functioning is
impaired to the extent that independent responsibil-
Course
ity and initiative are required. Persons with DPD are
Persons with DPD are likely to have been excessively prone to mood disorders, particularly major depres-
submissive as children and adolescents, and some sive disorder and dysthymic disorder, and to anxiety
may have had a chronic physical illness or a separa- disorders, particularly agoraphobia, social phobia, and
tion anxiety disorder during childhood. Persons with perhaps panic disorder. However, the severity of the
DPD fear intensely a loss of concern, care, and sup- symptomatology tends to decrease with age, particu-
port from others, particularly the person with whom larly if the person has obtained a reliable, dependable,
they have an emotional attachment. They are unable and empathic partner.
Differential Diagnosis the opposite error of rejecting and abandoning them to

be rid of their needy and clinging dependency. Such re-
Excessive dependency will often be seen in persons
sponses are common in the interpersonal (marital and
who have developed debilitating mental and general
sexual) history of persons with DPD, and are at times
medical conditions such as agoraphobia, schizophre-
experienced as well within therapeutic relationships.
nia, mental retardation, severe injuries, and dementia.
Persons with DPD tend to have unrealistic expectations
However, a diagnosis of DPD requires the presence
regarding their therapist. They may attempt to have the
of the dependent traits since late childhood or adoles-
therapist take control of their lives, and may make un-
cence. One can diagnose the presence of a personality
realistic requests or demands for their therapist’s time,
disorder at any age during a person’s lifetime, but if,
involvement, and availability.
for example, a DPD diagnosis is given to a person at
Exploration of the breadth and source of the need for
the age of 75 years, this presumes that the dependent
care and support is often an important component of
behavior was evident since the age of approximately
treatment. Persons with DPD often have a history of
18 years (i.e., predates the onset of a comorbid mental
exploitative, rejecting, and perhaps even abusive rela-
or physical disorder).
tionships that have contributed to their current feelings
Deference, politeness, and passivity will also vary
of insecurity and inadequacy. Cognitive–behavioral
substantially across cultural groups. It is important not
techniques are useful in addressing the feelings of inad-
to confuse differences in personality that are due to
equacy, incompetence, and helplessness. Social skills,
different cultural norms with the presence of a person-
problem-solving, and assertiveness training also makes
ality disorder. The diagnosis of DPD requires that the
important contributions.
dependent behavior be maladaptive, resulting in clini-
Persons with DPD may also benefit from group
cally significant functional impairment or distress.
therapy. A supportive group is useful in diffusing the
Many persons with DPD will also meet the criteria
feelings of dependency onto a variety of persons, in
for HPD and BPD. Persons with DPD and HPD may
providing feedback regarding their manner of relating
both display strong needs for reassurance, attention,
to others, and in providing practice and role models for
and approval. However, persons with DPD tend to
more assertive and autonomous interpersonal function-
be more self-effacing, docile, and altruistic, whereas
ing. There is no known pharmacologic treatment for
persons with HPD tend to be more flamboyant, as-
DPD.
sertive, and self-centered, and persons with BPD will
tend to be much more dysfunctional and emotionally
dysregulated. Obsessive–Compulsive Personality Disorder
DIAGNOSIS
TREATMENT
Obsessive–compulsive personality disorder (OCPD)
Persons with DPD are often in treatment for one or includes a preoccupation with orderliness, perfection-
more Axis I disorders, particularly a mood (depressive) ism, and mental and interpersonal control. OCPD is
or an anxiety disorder. They tend to be very agree- indicated by the presence of four or more of the eight
able, compliant, and grateful individuals, at times to diagnostic criteria presented in DSM criteria for OCPD
excess. An important issue in the treatment of persons (see page 457).
with DPD is not letting the relationship with the thera- Conscientiousness is one of the fundamental dimen-
pist become an end in itself. Many persons with DPD sions of personality, characterized by the tendency to
find the therapeutic relationship satisfying their need emphasize duty, order, deliberation, discipline, compe-
for support, concern, and involvement. The therapist tence, and achievement. Persons who are excessively
can be perceived as a nurturing, caring, and depend- organized, ordered, deliberate, dutiful, and disciplined
able partner who is always available for as long as the would be characterized as having OCPD. Only 1–2%
individual desires. Successful treatment can in fact be of the general community may meet the diagnostic cri-
feared because it suggests the termination of the re- teria for the disorder, but this could be an underestima-
lationship, an outcome that is at times avoided at all tion. Up to 10% of the population has been estimated
costs. As a result, they may be excessively compliant, to be maladaptively stubborn, 4% excessively devoted
submissive, agreeable, and cooperative in order to be to work, and 8% excessively perfectionistic. OCPD is
the individual that the therapist would want to retain. one of the less frequently diagnosed personality dis-
Therapists need to be careful not to unwittingly en- orders within inpatient settings, occurring in approxi-
courage or exploit this submissiveness, nor to commit mately 3–10% of individuals, but its prevalence may
are secondary to their worrying, indecision, and stress.

DSM-IV-TR Diagnostic Criteria Those with concomitant traits of angry hostility and
301.4 OBSESSIVE –COMPULSIVE PERSONALITY DISORDER
competitiveness may be prone to cardiovascular disor-
ders. Mood disorders may not develop until the person
A pervasive pattern of preoccupation with orderliness, recognizes the sacrifices that have been made by their
perfectionism, and mental and interpersonal control at
the expense of flexibility, openness, and efficiency, be- devotion to work and productivity, which may at times
ginning by early adulthood and present in a variety of not occur until middle age. However, most will experi-
contexts, as indicated by four (or more) of the following: ence early employment or career difficulties, or even
A. is preoccupied with details, rules, lists, order, or- failures that may result in depression.
ganization, or schedules to the extent that the major
point of the activity is lost
B. shows perfectionism that interferes with task com-
pletion (e.g., is unable to complete a project because
his or her own overly strict standards are not met)
C. excessive devotion to work and productivity to the
Devotion to work and productivity will vary substan-
exclusion of leisure activities and friendships (not tially across cultural groups. One should be careful not
accounted for by obvious economic necessity) to confuse normal cultural variation in conscientious-
D. is overconscientious, scrupulous, and inflexible
about matters of morality, ethics, or values (not ac- ness with the presence of this personality disorder. A
counted for by cultural or religious identification) diagnosis of OCPD requires that the devotion to work
E. is unable to discard worn-out or worthless objects be maladaptive or to the exclusion of leisure activities
even when they have no sentimental value
F. is reluctant to delegate tasks or to work with others and friendships.
unless they submit to exactly his or her way of do- OCPD resembles to some extent the obsessive–
ing things compulsive disorder (OCD). However, many persons
G. adopts a miserly spending style toward both self and
others; money is viewed as something to be hoarded with OCPD fail to develop OCD, and vice versa. OCD
for future catastrophes involves intrusive obsessions or circumscribed and
H. shows rigidity and stubbornness. repetitively performed rituals whose purpose is to re-
Reprinted with permission from the Diagnostic and Statistical duce or control feelings of anxiety. OCPD, in contrast,
American Psychiatric Association. involves rigid, inhibited, and authoritarian behavior
patterns that are more egosyntonic. If both behavior
patterns are present, both diagnoses should be given as
be much higher within private practice settings. This these disorders are sufficiently distinct that it is likely
disorder does appear to occur more often in males than that in such cases two different disorders are in fact
in females but exceptions to this finding have been present.
reported. OCPD may at times resemble narcissistic PD, as
both disorders can involve assertiveness, domination,
achievement, and a professed perfectionism. However,
Course
the emphasis in OCPD will be on work for its own sake,
As children, some persons with OCPD may have ap- whereas narcissistic persons will work only to achieve
peared to be relatively well-behaved, responsible, and status and recognition. Persons with OCPD will also
conscientious. However, they may have also been overly be troubled by doubts, worries, and self-criticism,
serious, rigid, and constrained. As adults, many will whereas the narcissistic person will tend to be overly
obtain good to excellent success within a job or career. self-assured.
They can be excellent workers to the point of excess,
sacrificing their social and leisure activities, marriage,
TREATMENT
and family for their job. Relationships with spouse and
children are likely to be strained because of their ten- Persons with OCPD may fail to seek treatment for the
dency to be detached and uninvolved, yet authoritarian OCPD symptomatology. They may seek treatment in-
and domineering with respect to decisions. A spouse stead for disorders and problems that are secondary to
may complain of a lack of affection, tenderness, and their OCPD traits, including anxiety disorders, health
warmth. Relationships with colleagues at work may problems (e.g., cardiovascular disorders), and problems
be equally strained by the excessive perfectionism, within various relationships (e.g., marital, familial,
domination, indecision, worrying, and anger. Jobs that and occupational). Treatment will be complicated by
require flexibility, openness, creativity, or diplomacy their inability to appreciate the contribution of their
may be particularly difficult. Persons with OCPD may personality to these problems and disorders. It is not
be prone to various anxiety and physical disorders that unusual for persons with OCPD to perceive themselves
as being simply conscientious, dutiful, moral, and re- (PDNOS), for persons with a personality disorder who
sponsible, rather than perfectionistic, stubborn, rigid, do not meet the diagnostic criteria for any one of the
domineering, and unavailable. Their understanding is 10 officially recognized diagnoses. PDNOS has in fact
complicated further by the contribution of their traits been the single most commonly used personality dis-
to various achievements and successes (e.g., career ad- order diagnosis in almost every study in which it has
vancement) and to the control of negative affect (e.g., been considered. It would not, of course, be possible to
ability to control feelings of dysphoria during a crisis). discuss the etiology, pathology, course, or treatment of
The OCPD traits are not invariably or always maladap- the PDNOS disorder as the diagnosis refers to a wide
tive, and persons with this disorder may not appreciate variety of personality types. However, one usage of
the disorder’s cost to their physical health, psychologi- PDNOS is for the two personality disorders presented
cal well-being, and personal relationships. in the appendix to DSM-IV-TR for criterion sets pro-
Cognitive–behavioral techniques that address the ir- vided for further study, the passive–aggressive and the
rationality of excessive conscientiousness, moralism, depressive.
perfectionism, devotion to work, and stubbornness can
be effective in the treatment of OCPD. Persons with
OCPD may in fact appreciate the rational approach to COMPARISON OF DSM-IV-TR AND ICD-10
treatment provided by cognitive–behavioral therapy. A DIAGNOSTIC CRITERIA
common difficulty though is the tendency to drift into
The items sets for paranoid, schizoid, schizotypal,
lengthy and unproductive ruminations and intellectual-
antisocial, histrionic, avoidant, dependent, and obses-
ized speculations. Therapeutic techniques that empha-
sive–compulsive personality disorders in the ICD-10
size the acknowledgment, recognition, and acceptance
Diagnostic Criteria for Research and the DSM-IV-TR
of feelings will therefore be useful. Gestalt techniques
criteria differ but define essentially the same condi-
that focus upon and confront feeling states will often
tion. Furthermore, ICD-10 does not consider schizo-
feel threatening to persons with OCPD, but precisely
typal to be a personality disorder and instead includes
for this reason, they can also be quite revealing and
this condition in the section containing schizophre-
useful. Persons with OCPD will attempt to control
nia and other psychotic disorders. ICD-10 also refers
therapeutic sessions, and techniques that encourage
to several of the DSM-IV-TR disorders by different
uncontrolled, freely expressed associations to explore
names: antisocial is called “dissocial,” borderline is
historical motivations for control, perfectionism, and
called “emotionally unstable personality disorder,
workaholism are often helpful.
borderline type,” and obsessive–compulsive is called
Persons with OCPD can be problematic in groups.
“anankastic.”
They will tend to be domineering, constricted, and
ICD-10 includes an “emotionally unstable person-
judgmental. There is no accepted pharmacologic treat-
ality disorder” with two subtypes: impulsive type
ment for OCPD. Some persons with OCPD will benefit
and borderline type; criteria are provided for each
from anxiolytic or antidepressant medications, but this
subtype but not for emotionally unstable personal-
will typically reflect the presence of associated features
ity disorder. Neither of these subtypes by themselves
or comorbid disorders. The core traits of OCPD might
correspond to the DSM-IV-TR BPD, which includes
not be affected by pharmacologic interventions.
some items from each of these subtypes. Narcissistic
personality disorder in DSM-IV-TR is not included
Personality Disorder Not Otherwise Specified in ICD-10 as a specific personality disorder, although
the DSM-IV-TR criteria set is included in Annex I
As indicated earlier, DSM-IV-TR includes a diagnostic of ICD-10 (i.e., “provisional criteria for selected
category, personality disorder not otherwise specified disorders”).
CHAPTER
43 Psychological Factors Affecting

Medical Condition
DIAGNOSIS
This diagnostic category recognizes the variety of
ways in which specific psychological or behavioral 316. PSYCHOLOGICAL FACTORS AFFECTING MEDICAL CONDITION
factors can adversely affect medical illnesses. Such
A. General medical condition (coded on Axis III) is
factors may contribute to the initiation or the exac- present.
erbation of the illness, interfere with treatment and B. Psychological factors adversely affect the general med-
rehabilitation, or contribute to morbidity and mortal- ical condition in one of the following ways:
ity. Psychological factors may themselves constitute (1) the factors have influenced the course of the gen-
eral medical condition as shown by a close tempo-
risks for medical diseases, or they may magnify the ral association between the psychological factors
effects of nonpsychological risk factors. The effects and the development or exacerbation of, or delayed
may be mediated directly at a pathophysiological recovery from, the general medical condition
(2) the factors interfere with the treatment of the gen-
level (e.g., psychological stress inducing myocardial eral medical condition
ischemia) or through the individual’s behavior (e.g., (3) the factors constitute additional health risks for the
noncompliance). individual
(4) stress-related physiological responses precipitate
The subject of psychological factors affecting medi- or exacerbate symptoms of the general medical
cal condition (PFAMC) has become the focus of intense condition.
research because of the illumination it may provide of Choose name based on the nature of the psychological
basic disease mechanisms (e.g., psychoneuroimmunol- factors (if more than one factor is present, indicate the
most prominent):
ogy) and because of the deep interest in improving both
the outcomes and the efficiency of health care delivery. Mental disorder affecting . . . [indicate the general medi-
cal condition] (e.g., an Axis I disorder such as major de-
In epidemiological studies, several mental disorders pressive disorder delaying recovery from a myocardial
increase the likelihood of mortality, especially depres- infarction)
sion, bipolar disorder, schizophrenia, and alcohol abuse Psychological symptoms affecting . . . [indicate the gen-
eral medical condition] (e.g., depressive symptoms
or dependence. Psychiatric disorders or symptoms in delaying recovery from surgery; anxiety exacerbating
individuals with medical illness may increase their use asthma)
Personality traits or coping style affecting . . . [indicate
of health care services, particularly the length of costly the general medical condition] (e.g., pathological denial
hospital stays. Interest has been further increased by of the need for surgery in a patient with cancer; hos-
intervention trials aimed at psychological factors or tile, pressured behavior contributing to cardiovascular
disease)
disorders that have demonstrated improvements in Maladaptive health behaviors affecting . . . [indicate the
medical outcomes and in quality of life in individuals general medical condition] (e.g., overeating; lack of ex-
with serious medical disorders. ercise; unsafe sex)
Stress-related physiological response affecting . . . [indi-
It should be evident that this diagnosis is not really cate the general medical condition] (e.g., stress-related
a discrete diagnostic category but rather a label for the exacerbations of ulcer, hypertension, arrhythmia, or ten-
interactive effects of psyche on soma. Mind–body in- sion headache)
Other or unspecified psychological factors affect-
teractions have long been a focus of interest, both in ing . . . [indicate the general medical condition] (e.g.,
health and in disease. Mental disorder and medical interpersonal, cultural, or religious factors)
disease frequently coexist. Mental health professionals Reprinted with permission from the Diagnostic and Statistical
and investigators of past eras were misled by this fre- Manual of Mental Disorders, 4th ed.,Text Rev. Copyright 2000
quent comorbidity into premature conclusions that the
psychological factors were preeminent in the causation always include significant interactions between them.
of the medical disorders, and these were designated To make the diagnosis of PFAMC, either the factors
psychosomatic. A more modern approach has been must have influenced the course of the medical con-
to recognize that all medical illnesses are potentially dition, interfered with its treatment, contributed to
affected by many different factors in the biological, health risks, or physiologically aggravated the medical
psychological, and social realms. The earlier designa- condition.
tion of certain disorders as psychosomatic (e.g., peptic Let us consider each of these four ways of making
ulcer disease) overvalued the contribution of psycho- the diagnosis of PFAMC in more detail. The psycho-
logical factors to those disorders and undervalued their logical factor’s influence on the course of a general
contribution to other medical disorders (e.g., cancer). medical condition can be inferred from a close tempo-
Furthermore, whereas labeling medical illnesses as ral relationship between the factor and the development
psychosomatic drew attention to the importance of or exacerbation of the medical condition (or delayed
mind–body interactions, it unfortunately and falsely recovery). For example, a 45-year-old male executive
implied to many individuals undergoing treatment and reports symptoms sounding like typical angina, but oc-
physicians that the illness was basically psychogenic, curring only on weekends. Further questioning reveals
that the symptoms were not “real,” and that the illness that he is depressed over deterioration in his marriage.
was somehow the individual’s fault. During the week he works late and has limited contact
The diagnosis of PFAMC focuses attention on one with his family, but he spends the weekend at home.
causal direction in the interactions between psyche and The symptoms began after he and his wife started ar-
soma, that is, the effects of psychological factors on the guing every weekend. The temporal link between onset
medical condition (Figure 43-1). This represents a heu- and recurrence of angina and marital arguments sup-
ristic simplification, highlighting a particular process ports a diagnosis of PFAMC.
for further exploration, understanding, and interven- PFAMC can also be diagnosed when the psycho-
tion. In most individuals, there are effects in the other logical factor interferes with treatment, including not
direction as well (i.e., the effects of general medical seeking medical care, not following up, nonadherence
illness on psychological function). Furthermore, both to prescribed drugs or other treatment, or maladaptive
mind and body interact with social and environmental modifications in treatment made by the individual or
factors, both dramatic (e.g., poverty, racism, war) and family. The executive with angina rejected his physi-
more subtle (e.g., employment status, neighborhood), cian’s recommendations for further assessment and
that affect the incidence and outcome of medical ill- treatment. He said, “I do get upset at home but I feel
ness. Diagnosing PFAMC may help the mental health just fine at the office, so there couldn’t be anything re-
professional and the individual address an important ally wrong with me.” The individual is able to acknowl-
dimension of care, but the other “arrows” of Figure 43- edge marital discord, but the defense of denial clouds
1 often warrant attention too. his perception of his physical health and blocks appro-
The diagnosis of PFAMC differs from the diagnosis priate medical care. This is another form of PFAMC.
of most other mental disorders in its focus on the in- PFAMC can also be diagnosed when the psychologi-
teraction between the mental and medical realms. As cal factor contributes to health risks, exemplified by the
noted, the criteria require more than that the individual executive increasing his smoking and drinking despite
has both a medical illness and contemporaneous psy- his physician’s warnings (“Its the only way I can cope
chological factors, because their coexistence does not with my wife.”). Finally, PFAMC is an appropriate di-
agnosis when there are stress-related physiological re-
sponses precipitating or exacerbating symptoms of the
PFAMC medical condition. The same man observes that angina
is most likely to occur after marital arguments during
Mind (psyche) Body (soma)
Axis I, II Axis III which he becomes irate, yells, slams doors, and throws
things.
When a person’s medical illness is faring worse
than expected and not responding well to standard
Social factors treatment, clinicians should and often do consider
Axis IV whether a psychological factor may be responsible for
Figure 43-1 Psychological factors affecting medical condition the poorer-than-expected outcome. This is a far from
(PFAMC): interaction between psyche and soma. Social factors trivial task. To ignore the possibility of PFAMC may
warrant attention as well. miss the crucial barrier to the individual’s recovery. On
Chapter 43 • Psychological Factors Affecting Medical Condition 461
the other hand, premature or facile attribution to psy- Examples include anxiety that aggravates irritable
chological factors may lead the clinician to overlook bowel syndrome, depressed mood that hinders recov-
medical or social explanations for “treatment-resistant ery from hip replacement surgery, and anger that inter-
disease” and unfairly blame the individual, with result- feres with rehabilitation after spinal cord injury.
ant further deterioration in health outcomes and the
clinician–patient relationship. Personality Traits or Coping Style Affecting a
To illustrate, a common clinical problem is the brit- General Medical Condition. This may include per-
tle diabetic adolescent with labile blood glucose levels sonality traits or coping styles that do not meet criteria
and frequent episodes of ketoacidosis and hypoglyc- for an Axis II disorder and other patterns of response
emia, despite vigorous attempts by the physician to im- considered to be maladaptive because they may pose a
prove diabetic management and glucose control. The risk for particular medical illnesses. An example is the
considerable difficulty in controlling such persons’ competitive hostility component of the type A behav-
diabetes is often attributed to adolescents’ dislike of ior pattern, and its impact on coronary artery disease.
lifestyle restrictions, their tendency to act out and rebel Maladaptive personality traits or coping styles are par-
against authority figures, their denial of vulnerability, ticularly likely to interfere with the physician–patient
their ambivalence about their need for nurturance, and relationship as well as the relationships which the indi-
their wish to be “normal.” There are many adolescent viduals have with other caregivers.
(and some adult) diabetics for whom these psychologi-
cal issues do play an important role in undermining Maladaptive Health Behaviors Affecting a General
diabetes management through noncompliance regard- Medical Condition. Many maladaptive health behav-
ing medication, diet, visits to the physician, substance iors have significant effects on the course and treat-
use, and activity limitations. However, psychological ment of many medical conditions. Examples include
factors do not always account for brittleness and are sedentary lifestyle, smoking, abuse of alcohol or other
sometimes incorrectly suspected. It has been demon- substances, and unsafe sexual practices. If the mala-
strated that much of the difficulty in achieving stable daptive behaviors can be better accounted for by an
glucose control in adolescent diabetics is the result of Axis I or Axis II disorder, the first subcategory (mental
the dramatically labile patterns of hormone secretion disorder affecting a medical condition) should be used
(cortisol, growth hormone) typical of adolescence, in- instead.
dependent of psychological status.
PFAMC has descriptive names for subcategories de- Stress-Related Physiological Response Affecting
scribed as follows. a General Medical Condition. Examples of stress-
related physiological responses affecting a medical
Mental Disorder Affecting a General Medical condition include the precipitation by psychological
Condition. If the individual has a mental disorder stress of angina, cardiac arrhythmia, migraine, or
meeting criteria for an Axis I or Axis II diagnosis, the attack of colitis in medically vulnerable individuals.
diagnostic name is mental disorder affecting medical In such cases, stress is not the cause of the illness or
condition, with the particular medical condition speci- symptoms; the individual has a medical condition that
fied. In addition to coding PFAMC, the specific mental etiologically accounts for the symptoms (e.g., coronary
disorder is also coded on Axis I or Axis II. Examples artery disease, migraine, or ulcerative colitis), and the
include major depressive disorder that reduces energy stressor instead represents a precipitating or aggravat-
and compliance in an individual with hemodialysis, ing factor.
panic disorder that makes an asthmatic hypersensitive
to dyspnea, and schizophrenia in an individual with re- Other or Unspecified Psychological Factors
current ventricular tachycardia who refuses placement Affecting a General Medical Condition. There are
of an automatic implantable defibrillator because he other psychological phenomena that may not fit within
fears it will control his mind. one of these subcategories. An interpersonal example is
marital dysfunction. A cultural example is the extreme
Psychological Symptoms Affecting a General discomfort women from some cultures may experience
Medical Condition. Individuals who have psycho- being alone with a male physician, even while they are
logical symptoms that do not meet the threshold for an fully dressed. A religious example is a Jehovah’s Wit-
Axis I diagnosis may still experience important effects ness who ambivalently refuses blood transfusion. These
on their medical illness, and the diagnosis would be fall under the residual category of other or unspecified
psychological symptoms affecting a medical condition. psychological factors affecting a medical condition.
Course and PFAMC (mental disorder affecting end stage re-

nal disease).
Given the wide range of mental disorders and psycho-
Individuals with somatoform disorders (e.g., somati-
logical factors that may affect medical illness and the
zation disorder, hypochondriasis) present with physical
large number of different general medical conditions
complaints that may mimic a medical illness, but the
that may be influenced, there are no general rules about
somatic symptoms are actually accounted for by the
the course of the PFAMC interaction. Psychological
psychiatric disorder. In principle, it might seem that
factors may have minor or major effects at a particular
somatoform disorders are easily distinguished from
point or throughout the course of a medical illness. We
PFAMC because PFAMC requires the presence of a di-
do know in general that individuals with general medi-
agnosable medical condition. The distinction in prac-
cal conditions who also have significant psychological
tice is sometimes difficult because the individual may
symptoms have poorer outcomes and higher medical
have both a somatoform disorder and one or more med-
care costs than those individuals with the same general
ical disorders. For example, an individual with seizures
medical conditions but without psychological distress.
regularly precipitated by emotional stress might have
A number of studies now document that psychological
true epilepsy aggravated by stress (PFAMC), pseudo-
or psychiatric problems (particularly cognitive disor-
seizures (conversion disorder), or both.
der, depression, and anxiety) in general medical inpa-
tients are associated with significant increases in length
of hospital stay. Psychosocial interventions have been TREATMENT
able to improve outcomes in medical illness, some-
Management of psychological factors affecting the in-
times with an attendant saving in health care costs.
dividual’s medical condition should be tailored both to
the particular psychological factor of relevance and to
the medical outcome of concern. Some general guide-
lines, however, can be helpful. The physician, whether
As noted before, the close temporal association be- in primary care or a specialty, should not ignore ap-
tween psychiatric symptoms and a medical condi- parent psychiatric illness. Unfortunately, this occurs all
tion does not always reflect PFAMC. If the two are too often because of discomfort, stigma, lack of train-
considered merely coincidental, then separate men- ing, or disinterest. Referring the individual to a mental
tal disorder and general medical condition diagnoses health specialist for evaluation is certainly better than
should be made. In some cases of coincident mental ignoring the psychological problem but should not be
disorders and general medical conditions, the mental regarded as “disposing” of it, because the physician
symptoms are actually the result of the medical condi- must still attend to its potential impact on the individu-
tion (i.e., the causality is in a direction opposite from al’s medical illness. Similarly, psychiatrists and other
that of PFAMC). When a medical condition is judged mental health practitioners should not ignore coinci-
to be pathophysiologically causing the mental disorder dent medical disease and should not assume that refer-
(e.g., hypothyroidism causing depression), the correct ral to a nonpsychiatric physician absolves them of all
diagnosis is the appropriate mental disorder due to a responsibility for the individual’s medical problem.
general medical condition (e.g., mood disorder due to
hypothyroidism, with depressive features). In PFAMC, Mental Disorder Affecting a Medical Condition. If
the psychological or behavioral factors are judged to the individual has a treatable Axis I disorder, treatment
precipitate or aggravate the medical condition. for it should be provided. Whereas this is obviously jus-
Substance use disorders may adversely affect many tified on the basis of providing relief from the Axis I
medical conditions, and this can be described through disorder, mental treatment is further supported by the
PFAMC. However, in some individuals, all of the myriad ways in which the mental disorder may cur-
psychiatric and medical symptoms are direct conse- rently or in future adversely affect the medical illness.
quences of substance abuse, and it is usually parsimo- The same psychopharmacological and psychothera-
nious to use just the substance-use disorder diagnosis. peutic treatments used for Axis I mental disorders are
For example, an individual with delirium tremens normally appropriate when an affected medical con-
after alcohol withdrawal would receive a diagnosis dition is also present. However, even well-established
of alcohol withdrawal delirium, not PFAMC, but an psychiatric treatments supported by randomized con-
individual with alcohol dependence who repeatedly trolled trials have seldom been validated in the medi-
missed hemodialysis treatments because of intoxica- cally ill, who are typically excluded from the controlled
tion would receive diagnoses of alcohol dependence trials. Thus, psychiatric treatments may not always be
Chapter 43 • Psychological Factors Affecting Medical Condition 463
directly generalizable to, and often must be modified example, if the clinician wrongly presumes to know
for, the medically ill. why a particular individual seems anxious without
When prescribing psychiatric medications for indi- asking, the individual is likely to feel misunderstood.
viduals with significant medical comorbidity, the clini- Facile, nonspecific reassurance can undermine the
cian should keep in mind potential adverse effects on clinician–patient relationship because the individual
impaired organ systems (e.g., anticholinergic exacerba- is likely to feel that the clinician is out of touch with
tion of postoperative ileus; tricyclic antidepressant caus- and not really interested in the individual’s experience.
ing completion of heart block), changes in pharmacok- It is especially important with depressed individuals
inetics (absorption, protein binding, metabolism, and that clinicians avoid premature or unrealistic reassur-
excretion), and drug–drug interactions. Psychotherapy ance or an overly cheerful attitude; this tends to alien-
may also require modification in individuals with co- ate depressed individuals, who feel that their clinician
morbid medical illness, including greater flexibility re- is insensitive and either does not understand or does
garding the length and frequency of appointments, and not want to hear about their sadness. Clinicians should
deviations from standard therapeutic abstinence and provide specific and realistic reassurance, emphasize
neutrality. Psychotherapists treating individuals with on a constructive treatment plan, and mobilize the in-
PFAMC should usually be much more active in com- dividual’s support system.
municating with other health care professionals caring
for the individual (with the individual’s consent), than Personality Traits or Coping Style Affecting a
is usually the case in psychotherapy. General Medical Condition. As with Axis II disor-
If the individual has an Axis II personality disorder or ders affecting a medical condition, clinicians should be
other prominent personality or coping style, the mental aware of the personality style’s effects on the therapeu-
health clinician should modify the individual treatment tic relationship and modify management to better fit
accordingly, which is usually more easily accomplished the individual. For example, with type A “time urgent”
than trying to change the individual’s personality. For individuals, clinicians may need to be more sensitive
example, individuals who tend to be paranoid or mis- to issues of appointment scheduling and waiting times.
trustful should receive more careful explanations, par- Group therapy interventions can enhance active coping
ticularly before invasive or anxiety-provoking proce- with serious medical illnesses like cancer, heart dis-
dures. With narcissistic individuals, the clinician should ease, and renal failure but to date have usually been
avoid relating in ways that may seem excessively pater- designed to be broadly generalizable rather than tar-
nalistic or authoritarian to the individual. With some geted to one particular trait or style (with the exception
dependent individuals, it may be advisable to be more of type A behavior).
directive, without overdoing it and fostering excessive Another general guideline is not to attack or interfere
dependency. with a individual’s defensive style unless the defense is
having an adverse impact on the medical illness or its
Psychological Symptoms Affecting a General management. Clinicians are particularly tempted to in-
Medical Condition. In some instances, psychiatric tervene when the defense is dramatic, breaks with real-
symptoms not meeting the threshold for an Axis I di- ity, or makes the clinician uncomfortable.
agnosis will respond positively to the same treatments For example, denial is a defense mechanism that
used for the analogous Axis I mental disorder, with ap- reduces anxiety and conflict by blocking conscious
propriate modifications as noted before. There is not a awareness of thoughts, feelings, or facts that an indi-
great amount of treatment research on subsyndromal vidual cannot face. Denial is common in the medically
psychiatric symptoms, and even less in individuals ill but varies in its timing, strength, and adaptive value.
with comorbid medical illness, so this area of practice Some individuals are aware of what is wrong with them
remains less evidence-based. Some psychiatric symp- but consciously suppress this knowledge by avoiding
toms affecting a medical condition may be amenable to thinking about or discussing it. Others cope with the
stress management and other behavioral techniques as threat of being overwhelmed by their illness by uncon-
well as appropriate reassurance. sciously repressing it and thereby remain unaware of
Any intervention directed by the mental health cli- their illness. Marked denial, in which the individual
nician at a particular individual’s psychological symp- emphatically refuses to accept the existence or signifi-
toms or behavior should be grounded in exploratory cance of obvious symptoms and signs of the disease,
discussion with the individual. Interventions without may be seen by the clinician as an indication that the
such grounding tend to seem at best superficial and individual is “crazy” because the individual seems im-
artificial, and at worst are entirely off the mark. For pervious to rational persuasion. In the absence of signs
of another major mental disorder (e.g., paranoid delu- Maladaptive Health Behavior Affecting a General
sions), such denial is not often a sign of psychosis but Medical Condition. This is an area of research with
rather represents a defense against overwhelming fear. many promising approaches. To achieve smoking cessa-
The adaptive value of denial may vary, depending tion, bupropion, nicotine replacement, behavioral ther-
on the nature or stage of illness. When an individual’s apies, and other pharmacological strategies all warrant
denial does not preclude cooperation with treatment, consideration. Behavioral strategies are also useful in
the clinician should leave it alone. The clinician does promoting better dietary practices, sleep hygiene, safe
have an ethical and professional obligation to ensure sex, and exercise. For some individuals, change can be
that the individual has been informed about the ill- achieved efficiently through support groups, whereas
ness and treatment. After that, if the individual accepts others change more effectively through a one-to-one
treatment but persists with an irrationally optimistic relationship with a health care professional.
outlook, the clinician should respect the individual’s
need to use denial to cope. For some, the denial is frag- Stress-Related Physiological Response Affecting
ile, and the clinician must decide whether the defense a Medical Condition. Biofeedback, relaxation tech-
should be supported and strengthened, or if the indi- niques, hypnosis, and other stress management inter-
vidual had better give up the denial to discuss fears di- ventions have been helpful in reducing stress-induced
rectly and receive reassurance from the clinician. The exacerbations of medical illness including cardiac, gas-
clinician should not support denial by giving the in- trointestinal, headache, and other symptoms. Pharma-
dividual false information, but rather encourage hope cological interventions have also been useful (e.g., the
and optimism. When denial is extreme, individuals widespread practice of prescribing benzodiazepines
may refuse vital treatment or threaten to leave against during acute myocardial infarction to prevent stress-
medical advice. Here, the clinician must try to help re- induced increase in myocardial work).
duce denial but not by directly assaulting the individu-
al’s defenses. Because such desperate denial of reality
usually reflects intense underlying anxiety, trying to
DIAGNOSTIC CRITERIA
scare the individual into cooperation will intensify de-
nial and the impulse to flight. A better strategy for the Although the corresponding ICD-10 category (“Psy-
clinician is to avoid directly challenging the individu- chological and behavioral factors associated with dis-
al’s claims while simultaneously reinforcing concern orders or diseases classified elsewhere”) does not have
for the individual and maximizing the individual’s specified diagnostic criteria, it is defined in essentially
sense of control. the same way as DSM-IV-TR.
Index
A eating disorders 57 Alcohol-induced sleep disorder 139

12-step programs 105, 146, 147, 193 generalized anxiety disorder 335 Alcohol intoxication 136, 137, 138
AAMR See American Association on major depressive disorder 267 assessment 139, 142
Mental Retardation opioid use disorders 196 comorbidity with psychiatric
AB-DBDs See Attention-deficit and reactive attachment disorder 81 disorders 146
disruptive behavior disorders separation anxiety disorder 77 course 141
Abridged somatization disorder See somatization disorder 345–346 diagnosis 136, 138, 141, 146
Undifferentiated somatoform disorder substance-related disorders 125, 129 etiology 146
Abstinence 171 Adoption studies pharmacotherapy 144, 145
Abstraction 225 bipolar disorder 286 treatment 141–145
Abulia 119 major depressive disorder 252 Alcohol-sensitizing drugs 144
Abuse See Child abuse; Substance-related schizophrenia 219 Alcohol use disorders See Alcohol abuse;
disorders; individual substances Aerosols 181 Alcohol dependence
Abusive relationships 206 Aggression 51 Alcohol withdrawal
Academic difficulty 27–28 Agitation 221 diagnosis 136
See also Learning… Agnosia 98, 100 DSM-IV-TR diagnostic criteria 137
Acquired Immunodeficiency Syndrome Agonist therapy 125, 131, 133, 196 management 143, 144
See AIDS Agoraphobia Alpha-adrenergic agonists 55, 201
ACT See Assertive Community Treatment See also Panic disorder Alprazolam 277
Acupuncture 191, 195–196 anxiety disorders 292–300 Alveolar hypoventilation 417
Acute abstinence 172 DSM-IV-TR diagnostic Alzheimer’s disease (AD)
Acute confusional state See Delirium criteria 292–293 dementia of the Alzheimer type 96,
Acute renal failure 200 Agranulocytosis 229 98, 106
Acute stress disorder (ASD) 328, 331–334 AIDS (Acquired Immunodeficiency etiology 85, 106
course 332 Syndrome) 100 major depressive disorder 263
diagnosis 327–328, 331 Akathisia 234 risk factors 99
differential diagnosis 328, 332 Akinesia 234 treatment 98, 100, 102, 105
DSM-IV-TR diagnostic criteria 327, Alcohol Ambien See Zolpidem
332 sleep disturbance 424 American Association on Mental
DSM-IV-TR/ICD-10 diagnostic criteria Alcohol abuse Retardation (AAMR) 18
comparison 336 diagnosis 136 Amnesia
epidemiology 332 substance-induced persisting dissociative amnesia 373–375,
treatment 327, 332 dementia 105 1031–1034
AD See Adjustment disorders treatment 141 dissociative fugue 374, 375, 381
Adaptive behavior 19 Alcohol dependence dissociative identity disorder 376, 381
Adhesives 181 bipolar disorder comorbidity 281 dissociative trance disorder 380,
Adjustment disorders (AD) 436 caffeine dependence relationship 157, 381
course 436 159 Amnestic disorders
diagnosis 435–436 diagnosis 136 diagnosis 106
DSM-IV-TR classification 4 major depressive disorder differential diagnosis 88, 95, 106
DSM-IV-TR diagnostic criteria 435 comorbidity 252, 263 DSM-IV-TR classification 4
DSM-IV-TR/ICD-10 diagnostic criteria mutual help organizations 142, 145 DSM-IV-TR diagnostic criteria 85, 98,
comparison 440 pharmacotherapy 144, 145 100, 106
pharmacological treatments 437 psychosocial treatments 144 Amphetamines
studies 436 treatment 141–145 See also MDMA
treatment 436 women 139, 141, 143 sleep disturbance 422
Adolescents Alcoholics Anonymous (AA) 145 Amphetamine-type stimulants (ATS)
See also Childhood disorders Alcohol-induced anxiety disorder 139 abuse 148
bipolar disorder 290 Alcohol-induced mood disorder 138 CNS effects 150
cannabis abuse 162 Alcohol-induced persisting amnestic dependence 147, 151, 152
conduct disorder 51 disorder 138 drug interactions 150
disorders usually first diagnosed Alcohol-induced persisting dementia 138 immunomodulatory effects 150
in infancy, childhood or Alcohol-induced psychotic disorder 138 intoxication 148, 149, 151
adolescence 4 Alcohol-induced sexual dysfunction 139 withdrawal 149, 151
466 Index
Amphetamine-type stimulants (ATS)- cannabis use relationship 162, 163–165 Attention, schizophrenia 219, 220,
related disorders 147 Anxiety disorder due to a general medical 223–224
diagnosis 147 condition with obsessive-compulsive Attention-deficit and disruptive behavior
DSM-IV-TR diagnostic criteria 148, symptoms disorders (AD-DBDs) 49–56
149 course 117 combined treatments 56
maladaptive behaviors 148 diagnosis 117 comorbidity 53–54
medical complications 149, 151 etiology 117 course 52
pharmacotherapy 152 treatment 117 diagnosis 49–52
physiological disturbances 148, 149 Anxiety disorder due to a general medical differential diagnosis 52
psychosocial treatments 151, 152 condition with panic attacks or with DSM-IV-TR diagnostic criteria 50–52
treatment 150 generalized anxiety DSM-IV-TR/ICD-10 diagnostic criteria
Anabolic steroids 114 diagnosis 116 comparison 56
Anadenanthera columbrina 175 Anxiety disorders psychosocial treatments 56
Analgesics 360–361 See also Generalized anxiety disorder; psychostimulants 54
Anesthetics 180, 181 Panic disorder; Social phobia; treatment 53–56
Anorexia nervosa 399, 400 Specific phobias Attention-deficit/hyperactivity disorder
body dysmorphic disorder acute stress disorder 331–332 (ADHD)
distinction 364, 366 caffeine-induced anxiety disorder 158 combined treatments 56
course 401 diagnosis 301–307 diagnosis 49–52
diagnosis 399, 402 hypochondriasis relationship 362, 363 DSM-IV-TR diagnostic criteria 50–52
differential diagnosis 402 obsessive–compulsive disorder 317–325 DSM-IV-TR/ICD-10 diagnostic criteria
DSM-IV-TR diagnostic criteria 399, panic disorder 292–300 comparison 56
404 phobias 301–315 learning disorders relationship 27–30
DSM-IV-TR/ICD-10 diagnostic criteria posttraumatic stress disorder 326–330 medication 53–55
comparison 409 sedative-, hypnotic-, or anxiolytic- psychotropic drugs 22–23
major depressive disorder 252, 253, related disorders 214 rating scales 49
263, 271 selective mutism 79–80 reactive attachment disorder
treatment 402, 406, 409 separation anxiety disorder 77–80 relationship 81–83
zolpidem 215 social phobias 301–315 tic disorder relationship 64–70
Anosmia 183 somatization disorder relationship 351 Attitude, schizophrenia 221
Antagonist maintenance, opioid 202 specific phobias 301–315 Atypical autism See Pervasive
Antenatal See also Pregnancy substance-induced anxiety developmental disorders
Antianxiety drugs See Anxiolytics disorder 126 Atypical neuroleptics 47, 68
Anticonvulsants 46, 47 traumatic stress disorders 326–334 Auditory hallucinations 223
Antidepressants Anxiolytics Augmentation
attention-deficit and disruptive behavior See also Sedative-, hypnotic-, or major depressive disorder 267
disorders 49, 50 anxiolytic-related disorders obsessive–compulsive disorder 324
bipolar disorder 278, 279, 286, 290 autism spectrum disorders 47 schizophrenia 237–238
bulimia nervosa 404 mental retardation 23 Autism spectrum disorders (ASDs) 38–47
dissociative identity disorder 376, 381 sleep disturbance 422 Asperger’s disorder 39–44
generalized anxiety disorder 335, 340 somatization disorder 352 autistic disorder 38–47
major depressive disorder 252, 253, 263 Aphasia 92 childhood disintegrative
mental retardation 18, 22 See also Mixed receptive–expressive disorder 38–42
nicotine dependence treatment 187, 190 language disorder diagnosis 38–42
pain disorder 358–359 Apnea 417–418 differential diagnosis 41–42
schizoaffective disorder 242 Appearance, schizophrenia 221 DSM-IV-TR diagnostic criteria 38–39
schizophrenia 219, 224, 238 Appendix categories, DSM-IV-TR 17 DSM-IV-TR/ICD-10 diagnostic criteria
Antidiuretic hormones 73 Apprehensive expectation See Generalized comparison 47
Antipsychotics anxiety disorder language disorders relationship 34
See also Neuroleptics Apraxia 93 pervasive development disorder not
risks and side effects 234 ARBDs See Alcohol-related birth defects otherwise specified 40–42
schizoaffective disorder 219–225, 227, Arithmetic skills disorders See psychological treatments 44–45
228, 242, 243, 250 Mathematics disorders; Specific Rett’s disorder 38–41
schizophrenia 239 disorder of arithmetic skills somatic treatments 45
Texas Medication Algorithm Arson See Pyromania treatment 43–47
Project 232, 233 Articulation disorders See Phonological Automatic obedience 118
Antisocial personality disorder (ASPD) 446 disorder Avoidance personality disorder
course 446 ASD See Acute stress disorder (AVPD) 445, 453–455
diagnosis 446 ASDs See Autism spectrum disorders course 441
differential diagnosis 447 ASPD See Antisocial personality disorder diagnosis 439–440
DSM-IV-TR diagnostic criteria 446 Asperger’s disorder 38–41 differential diagnosis 441–457
opioid dependence 203 Assertive Community Treatment DSM-IV-TR diagnostic criteria 457
treatment 447 (ACT) 241 DSM-IV-TR/ICD-10 diagnostic criteria
Antisocial traits 181 Ataxia 208 comparison 458
Anxiety Atomoxetine (strattera) 54 treatment 457–458
attention-deficit/hyperactivity disorder ATS See Amphetamine-type stimulants Axes, DSM-IV-TR multiaxial system 1–4
comorbidity 56 Attachment 57 Azapirones 342
Index 467
B antidepressants 290 epidemiology 349

Babies See Infants children 280, 283, 290 etiology 353
‘Bad trips’ 176 clinical outcome 283 medication 352, 363
Bagging, inhalant-related disorders 180 course 283 treatment 366
BAL See Blood alcohol level cyclothymic disorder 280, 283 Borderline personality disorder
Barbiturates 210, 211, 214–217 diagnosis 278–288 (BPD) 448, 450
Behavior diagnostic decision tree 281 course 448
See also Attention-deficit and disruptive differential diagnosis 284–285 diagnosis 448
behavior disorders; Conduct disorder; drug dependence comorbidity 283 dialectical behavior therapy 449, 450
Disruptive behavior disorders DSM-IV-TR classification 4 differential diagnosis 449
autism spectrum disorders 38, 43 DSM-IV-TR/ICD-10 diagnostic criteria dissociative identity disorder
learning/motor disorder comparison 291 relationship 376, 381
relationship 27–28 education 290 DSM-IV-TR diagnostic criteria 448
mental retardation treatment 22–23 elderly persons treatment 291 DSM-IV-TR/ICD-10 diagnostic criteria
phencyclidine intoxication 207 episode lengths 284 comparison 458
schizophrenia 219–234 functional outcome 283, 289–290 etiology 444, 458
Behavioral therapy gender 283 major depressive disorder
approach tests 304 general medical conditions 280, 282, comorbidity 263
attention-deficit and disruptive behavior 285 treatment 449
disorders 49–56 genetic hypotheses 283, 290 Botulinum toxin 70
autism spectrum disorders 43 hypomanic episode 279, 284 Bowel control See Encopresis
encopresis 76–77 illness costs 283 BPD See Borderline personality disorder
mental retardation 25 incidence increase since 1940s 283 BPRS See Brief Psychiatric Rating
nicotine dependence 192–194 lithium 286–291 Brain injury 104
posttraumatic stress disorder 330 manic episode 278–281, 287, 291 Breathing-related sleep disorder (BRSD)
selective mutism 79–80 medical disorders associated with diagnosis 417
separation anxiety disorder 77 mania 284 treatment 418
Benzodiazepines medical evaluation 281 Brief dynamic psychotherapy 269
See also Sedative-, hypnotic-, or mixed episode 278–280, 282 Brief Psychiatric Rating Scale
anxiolytic-related disorders mood stabilizers 286 (BPRS) 237
alcohol withdrawal 143 occupational function 279–280, 282 Brief psychotic disorder 244, 245, 246
cocaine-related disorders 172 onset 283 course 245
drug addicts 210 physical examinations 281 diagnosis 244, 245
generalized anxiety disorder 339–340 pregnancy 290 differential diagnosis 245
LSD intoxication 177 psychotherapies 286, 289 DSM-IV-TR diagnostic criteria 244
medications available 211 rapid cycling specifiers 282 DSM-IV-TR/ICD-10 diagnostic criteria
mental retardation 23 refractory bipolar disorder 287–288 comparison 250
overdose 210 schizoaffective disorder differential epidemiology 243
periodic limb movements in sleep/ diagnosis 242–245, 250 schizophrenia differential diagnosis 219
restless legs syndrome 420 socioeconomic class 283 treatment 245
REM sleep behavior disorder 422 somatotherapy 286–289 Brief reactive psychosis See Brief
restless legs syndrome 420 stress 285 psychotic disorder
schizophrenia 233 substance dependence comorbidity 283 Briquet’s syndrome See Somatization
sleep terror disorder 421 treatment 285–286 disorder
tic disorders 64–70 Bipolar I disorder BRSD See Breathing-related sleep
use/abuse patterns 214 DSM-IV-TR/ICD-10 diagnostic criteria disorder
withdrawal 211–212 comparison 291 BT See Behavioral therapy
Beta-blockers most recent episode… 279, 291 Bulimia nervosa 404–406
mental retardation 18–25 Bipolar II disorder See also Binge-eating disorder
Binge behavior DSM-IV-TR diagnostic criteria 291 body dysmorphic disorder
See also Bulimia nervosa DSM-IV-TR/ICD-10 diagnostic criteria distinction 364
cocaine 167–169, 172 comparison 291 diagnosis 404
food 405–406 Bipolar type schizoaffective disorder 242 differential diagnosis 406
Binge-eating disorder 407–409 Birth DSM-IV-TR diagnostic criteria 404
See also Bulimia nervosa postpartum blues 257 DSM-IV-TR/ICD-10 diagnostic criteria
diagnosis 407–408 Blackouts 105, 107 comparison 409
differential diagnosis 409 Bladder control See Enuresis major depressive disorder 263
DSM-IV-TR/ICD-10 diagnostic criteria Blood alcohol level (BAL) 137 treatment 406, 409
comparison 409 Blurred vision 176, 179 Buprenorphine 201, 202, 204
treatment 409 Body dysmorphic disorder Bupropion 193
Biofeedback, encopresis 177 See also Somatic type delusional disorder
Biological rhythms course 365
See also Circadian rhythms diagnosis 364 C
major depressive disorder 271 differential diagnosis 365 Caffeine dependence
Bipolar disorder 278–291 DSM-IV-TR diagnostic criteria 364 diagnosis 157
adolescents 283 DSM-IV-TR/ICD-10 diagnostic criteria differential diagnosis 157
alcohol dependence comorbidity 282 comparison 367 treatment 158
468 Index
Caffeine-induced anxiety disorder inhalant abuse 181 disorders of written expression 31

diagnosis 158 CAT See Cognitive adaptation training eating disorders 57–63
treatment 158 Catatonia elimination disorders 71–79
Caffeine-induced sleep disorder excited 118, 119 encopresis 75–77
diagnosis 159 major depressive disorder 256, 271 enuresis 71–76, 80
treatment 159 phencyclidine intoxication 207 expressive language disorder 34–36
Caffeine intoxication schizophrenia 221 feeding disorders of infancy or early
course 154 Catatonic disorder due to a general childhood 61
differential diagnosis 153, 155 medical condition learning and motor skills
DSM-IV-TR diagnostic criteria 153 diagnosis 118–119 disorders 26–31
treatment 155 differential diagnosis 119 mathematics disorders 31
Caffeine-related disorders 157, 159 DSM-IV-TR diagnostic criteria 120 mental retardation 18–25
caffeine consumption 155, 156, 157, treatment 119 motor skills disorders 26–31
158 CBCL See Child behavior checklist pediatric autoimmune neuropsychiatric
caffeine dependence 157–159 CBT See Cognitive–behavioral therapy disorders 65
caffeine-induced anxiety disorder 158, CCTS See Collaborative Cocaine phonological disorders 34–36
159 Treatment Study pica 62–63
caffeine-induced sleep disorder 159 CD See Conduct disorder reactive attachment disorder 81, 83
caffeine intoxication 153–155 Central nervous system reading disorders 31
caffeine withdrawal 156 malformations 21 rumination disorder 61, 63
Caffeine withdrawal phencyclidine intoxication 207 selective mutism 79–80
diagnosis 156 Cerebellar syndrome 183 separation anxiety disorder 77–80
differential diagnosis 157 Cerebral tumors stuttering 34–37
treatment 157 mood disorder due to a general medical tic disorders 64–69
Calcium, premenstrual dysphoric condition with manic features 114 Children
disorder 274 personality change due to a general See also Adolescents; Child… ; Infants
Cancer medical condition 119 bipolar disorder 278–291
major depressive disorder 263 pseudobulbar palsy 109, 110 generalized anxiety disorder 335–344
nicotine dependence 186 Cerebrovascular accidents (CVAs) major depressive disorder 252–253, 269
Cannabis-induced disorders cocaine abuse 166 phencyclidine intoxication 207
cannabis-induced anxiety disorder 165 major depressive disorder 263 phobias 301–315
cannabis-induced psychotic Chemical dependency disease Chlordiazepoxide 212
disorder 165 model 171–172 Chlorohydrocarbons 181, 183
cannabis intoxication 163 Child abuse Chlorpromazine 229, 232, 234
cannabis intoxication delirium 164, 165 conversion disorder 354–355 Choking 58
Cannabis-induced psychotic disorder 165 dissociative disorders 373, 380 phencyclidine intoxication 207
Cannabis intoxication major depressive disorder 252, 267 Chorea
course 165 opioid dependence 203 Choreoathetoid movements 221
delirium 164, 165 pedophilia 396 Chronic fatigue syndrome 261
diagnosis 163 posttraumatic stress disorder 82 Chronic motor or vocal tic disorder (CT)
DSM-IV-TR diagnostic criteria 163 reactive attachment disorder of infancy diagnosis 64
physiological effects 164 or early childhood 83, 84 DSM-IV-TR diagnostic criteria 64
psychological effects 164 Childbirth See Antenatal infections; Birth; motor skills disorder relationship 27
treatment 165 Neonatal effects; Pregnancy Chronobiology 419
Cannabis-related disorders 160, 161 Childhood See also Circadian rhythm…
abuse 162 gender identity disorder 11, 391–392 Cigarette smoking See Nicotine…
cannabis-induced anxiety disorder 165 neglect 59, 81–82 Circadian rhythms
cannabis-induced psychotic pathogenic caregiving 81, 83 See also Biological rhythms
disorder 165 posttraumatic stress disorder 82 bipolar disorder 278, 290
cannabis intoxication 163 Childhood disintegrative disorder 38, major depressive disorder 263
cannabis intoxication delirium 164, 165 41, 48 premenstrual dysphoric disorder 274,
dependence 161, 162, 163 Childhood disorders 277
pharmacotherapy 163 anxiety disorders 77–80 sleep and wakefulness 410, 411
phencyclidine intoxication 207 attention-deficit and disruptive behavior Circadian rhythm sleep disorder (sleep–
withdrawal 162–163 disorders 49 wake schedule disorders) 418
Cannabis-use disorders autism spectrum disorders/pervasive delayed sleep phase type 418
abuse 161, 163 development disorders 39, 43 jet lag type 419
course 162–165 autistic disorder 38, 47 shift-work type 419
dependence 160–163 childhood disintegrative disorder 38, Citalopram 145
diagnosis 161–165 40, 41 Classification
treatment 162–163 coercive psychosocial treatments 84 See also Diagnostic and Statistical
CAPD See Central auditory processing communication disorders 32–37 Manual of Mental Disorders
disorder developmental coordination Clomipramine
Carbamazepine 237, 286–287 disorder 26, 31 body dysmorphic disorder 364
Carboxyhemoglobin 183 disorders usually first diagnosed obsessive–compulsive disorder 316
Cardiotoxicity in infancy, childhood or premenstrual dysphoric disorder 274,
cocaine 170–174 adolescence 4, 13 275
Index 469
Clonidine comorbidity 33, 36 Cranial nerve abnormalities 183

attention-deficit and disruptive behavior diagnostic decision tree 33 ‘Crash’ phase, cocaine abstinence 170
disorders 49 diagnostic treatment tree 36 Creutzfeldt–Jakob disease 94, 103
mental retardation 18, 22 differential diagnosis 34, 35 Criminal sex-offending behaviors 396
tic disorders 64, 66 DSM-IV-TR/ICD-10 diagnostic criteria Criteria Sets and Axes provided for
Clozapine comparison 36 Further Study 517
agranulocytosis 229, 230 expressive language disorder 34, 36 CT See Chronic motor or vocal tic
diabetes mellitus 236 mixed receptive–expressive language disorder
prolactin levels 231 disorder 34, 36 CTRS-R See Conners Teacher Rating
schizoaffective disorder 242 stuttering 34–37 Scale–Revised
schizophrenia 219, 220, 221 treatment 35, 36 Culture
weight gain 227, 236 types 32 dissociative disorders 380–381
CO See Carbon monoxide Community living, mental retardation 21 drinking behavior 142, 144–145
Cocaine Comorbidity personality disorder 439–440
sleep disturbance 422 adjustment disorders 435, 437 specific phobias 304
Cocaine-related disorders 166, 172 cocaine abuse 170 substance-related disorders 129
abuse 168, 170, 171 nicotine dependence 187, 188 CVAs See Cerebrovascular accidents
comorbidity with other psychiatric opioid-related disorders 196 Cyclothymic disorder 280, 291
disorders 170 psychological factors affecting medical
course 169 condition 459
diagnosis 166 Compulsive sexual behavior 395 D
intoxication 168 COMT See Catechol-o-methyl transferase Daily living, schizophrenia 221
medical complications 170–171 Concentration Daily ratings, premenstrual dysphoric
psychoactive effects 166, 169 major depressive disorder 253 disorder 274
psychosocial treatments 172 schizophrenia 222–223 Daily rhythms See Circadian…
refractory 171, 172 Conduct disorder (CD) Danazol 276
treatment 171–172 diagnosis 49 Darkness See Light and darkness
withdrawal 168, 169, 172 DSM-IV-TR diagnostic criteria 51 DAT See Dementia of the Alzheimer type;
Coercive psychosocial treatments 84 DSM-IV-TR/ICD-10 diagnostic criteria Dopamine transporter protein
Cognition comparison 56 Date-rape drug See Flunitrazepam
communication disorders 32, 35 learning/motor disorder DBH See Dopamine beta-hydroxylase
depression 95, 97, 100 relationship 28 De Clerambault’s syndrome 248
panic disorder 292, 296 reactive attachment disorder Degenerative disorders See individual
phencyclidine intoxication 207 relationship 81 disorders
schizophrenia 219, 220, 224, 225 treatment 53, 56 Delayed sleep phase type circadian
Cognitive adaptation training (CAT) 240 Congestive heart failure 417 rhythm sleep disorder 418
Cognitive–behavioral theories Conners Parent Rating Scale–Revised Delinquency 52
generalized anxiety disorder 335 (CPRS-R) 50 Delirium
major depressive disorder 263 Conners Teacher Rating Scale–Revised course 87–88
Cognitive–behavioral therapy (CBT) (CTRS-R) 50 diagnosis 85–86
alcohol dependence 144 Consciousness 207 differential diagnosis 88, 95–97
attention-deficit and disruptive behavior See also Dissociative trance disorder DSM-IV-TR diagnostic criteria 85,
disorders 158 Constipation 76, 77 98–100, 106
cannabis dependence 161, 163 Contamination obsessions 317, 318 DSM-IV-TR/ICD-10 diagnostic criteria
cocaine-related disorders 169, 172 See also Obsessive–compulsive disorder comparison 108
generalized anxiety disorder 335 Continuation treatment, major depressive due to a general medical
major depressive disorder 271 disorder 264 condition 88–89
nicotine dependence 188, 191 Control, dissociative identity disorder 379 treatment 107
panic disorder treatment packages 296 Conversion disorder Delirium tremens 90
primary insomnia 411, 413 course 365 Delusional disorder 247–248
social phobia 302, 307, 310 diagnosis 364 body dysmorphic disorder
Cognitive disorders, DSM-IV-TR differential diagnosis 365 relationship 364
classification 5, 6, 14 DSM-IV-TR diagnostic criteria 355 course 248
Cognitive therapy DSM-IV-TR/ICD-10 diagnostic criteria diagnosis 247
posttraumatic stress disorder 326, 327, comparison 367 DSM-IV-TR diagnostic criteria 247
330 treatment 357 DSM-IV-TR/ICD-10 diagnostic criteria
premenstrual dysphoric disorder 274 Conversion symptoms 357–358 comparison 250
separation anxiety disorder 77 Convulsions 367 hypochondriasis distinction 362–363
Coma, phencyclidine intoxication 207 Coping style 461, 463 schizophrenia differential
Communication disorder not otherwise Coprolalia 64 diagnosis 227–228
specified 35 Copropraxia 64 subtypes 247
Communication disorders Coronary artery disease 260 treatment 249
See also Selective mutism; Speech and Cotinine 188 Dementia
language problems Counseling 201, 203–204 course 94–95
assessment 33, 34, 36 CPRS-R See Conners Parent Rating diagnosis 85–87
autism spectrum disorders Scale–Revised differential diagnosis 88, 95–96
relationship 38 ‘Crack’ See Cocaine DSM-IV-TR classification 4–13
470 Index
Dementia (continued) DSM-IV-TR/ICD-10 diagnostic criteria DRSC See Developmentally Reduced

DSM-IV-TR diagnostic criteria 85, 98, comparison 458 Synaptic Connectivity
100, 106 Depressive type schizoaffective Drugs See Medication; Substance…
DSM-IV-TR/ICD-10 diagnostic criteria disorder 242, 243 DSM… See Diagnostic and Statistical
comparison 108 Derealization 381 Manual of Mental Disorders…
Dementia of the Alzheimer type (DAT) Desmopressin 73 Duration of untreated psychosis
diagnosis 96–97 sedative-, hypnotic-, or anxiolytic- (DUP) 227
DSM-IV-TR diagnostic criteria 98 related disorders 211 Dysarthrias 221
DSM-IV-TR/ICD-10 diagnostic criteria Development 131, 132 See also Body dysmorphic disorder
comparison 108 Tourette’s disorder 21 Dyspareunia 389–400
treatment 98 Developmental articulation disorders See diagnosis 389–400
Dementia due to HIV disease 100–102 Phonological disorder DSM-IV-TR diagnostic criteria 392
Dementia due to multiple etiologies 106 Developmental coordination disorder 30 DSM-IV-TR/ICD-10 diagnostic criteria
Dementia due to other general medical Dextroamphetamine (DEX) 54 comparison 398
conditions 102 major depressive disorder 253 etiology 383
Dementia pugilistica (punchdrunk novel antipsychotic agents 231 symptoms 392
syndrome) 104 schizophrenia 231 treatment 384
Dependence See Substance dependence; Diagnosis 1–49 Dyssomnias 411
individual substances See also individual disorders breathing-related sleep disorder 417
Dependent personality disorder history 3, 8 DSM-IV-TR classification 4
(DPD) 455 multiaxial system 13 narcolepsy 416–418
course 455 Diagnostic and Statistical Manual of primary hypersomnia 415–416
diagnosis 455–456 Mental Disorders Third Edition primary insomnia 411–413
differential diagnosis 456 (DSM-III) 2–5 Dysthymic disorder 271–273
DSM-IV-TR diagnostic criteria 455 multiaxial system 13 diagnosis 271–273
DSM-IV-TR/ICD-10 diagnostic criteria Dialectical behavior therapy (DBT) 449 diagnostic criteria comparison 273
comparison 458 Diarrhea 76 DSM-IV-TR diagnostic criteria 272
treatment 456 Diazepam 212 Dystonias 234
Depersonalization disorder mental retardation 18
diagnosis 375–376 premenstrual dysphoric disorder 275
DSM-IV-TR diagnostic criteria 375 Differential diagnosis See individual E
DSM-IV-TR/ICD-10 diagnostic criteria disorders Eating disorders 399–409
comparison 381 Disruptive behavior disorders 28 anorexia nervosa 399–404
treatment 376 Dissociative amnesia binge-eating disorder 407–409
Depression diagnosis 373–374 bulimia nervosa 404–407
Alzheimer’s disease 98 DSM-IV-TR diagnostic criteria 375 childhood 58–63
cannabis use relationship 162–165 DSM-IV-TR/ICD-10 diagnostic criteria DSM-IV-TR classification 4
differential diagnosis 95 comparison 381 feeding disorders of infancy and early
due to a general medical condition 116 treatment 374 childhood 57–63
MDMA use 179 Dissociative disorders 374 major depressive disorder
medical disorders associated with depersonalization disorder 373 comorbidity 263
depression 285 dissociative amnesia 373 pica 62–63
medications associated with dissociative fugue 375 rumination disorder 61–62
depression 261 dissociative identity disorder 376 sleep-related characteristics 422
mood disorder due to a general dissociative trance disorder 380 ‘Ecstasy’ See MDMA
medical condition with depressive Dissociative fugue ECT See Electroconvulsive therapy
features 114 diagnosis 374 ED See Erectile disorder
schizoaffective disorder 244 DSM-IV-TR diagnostic criteria 375 Education
schizophrenia 234 treatment 376 bipolar disorder 278–291
treatments/medications associated with DSM-IV-TR diagnostic criteria 375 learning/motor skills disorders 26–31
depression 285 Dissociative trance disorder 380 mental retardation 18, 22
vascular dementia 100 DLMO See Dim light melatonin onset EE See Expressed emotion
Depressive disorders 253–273 method Ejaculation, premature 388–389
DSM-IV-TR classification 9 L-dopa 420 ELD See Expressive language disorder
dysthymic disorder 271–272 bipolar disorder 279 Elderly people
generalized anxiety disorder caffeine 153 alcohol-related disorders 139–143
relationship 338 cocaine 168 bipolar disorder treatment 278–291
hypochondriasis relationship 362 nicotine 186 delirium 88
major depressive disorder 252 social phobia 301 dementia 91
minor depressive disorder 258 substance-related disorders 124 major depressive disorder 252, 263,
premenstrual dysphoric Double depression 259 267
disorder 274–277 Down Syndrome 24 substance-related disorders 125
somatization disorder relationship 345, Downward drift hypothesis 226 Elective mutism See Selective mutism
351 Drinking behavior 142 Electroconvulsive therapy (ECT)
substance-related disorder Drive, sexual 382 major depressive disorder 254–263
relationship 129 Driving impairment 179 schizophrenia 221
Index 471
Elimination disorders See Encopresis; F obsessive–compulsive disorder 324

Enuresis Factitious disorders schizophrenia 237–238
Emotional withdrawal 81, 82 comorbid psychiatric disorders 369 Fluphenazine decanoate 234
Encephalitic psychoses 112 diagnosis 368–372 FOD See Female orgasmic disorder
Encephalitis lethargica (von Economo’s differential diagnosis 370 Food products 181
disease) 112 DSM-IV-TR classification 10, 16 Foster care 81, 83
Encopresis DSM-IV-TR diagnostic criteria 369 Frontal lobe syndrome 119, 121
with constipation 75–76 factitious disorder by proxy 370, 372 Frotteurism 396
diagnosis 75–76 somatoform disorder relationship 10, FTQ See Fagerstrom Tolerance
treatment 76 15, 345, 353 Questionnaire
Endocrine disturbances 88 treatment 371–372 FTT See Failure to thrive
Engagement phase, nicotine dependence Failure to thrive (FTT) 57, 83 Functioning
treatment 190 False pregnancy (pseudocyesis) 367 evaluation Axis V 4
Enuresis Families
alarms 73–74 Alzheimer’s disease 96
diagnosis 71 learning/motor skills disorders 28, G
diurnal 71–72, 74 30 GAD See Generalized anxiety disorder
medication 73–74, 76 nicotine dependence treatment 187, GAF Scale See Global Assessment of
treatment 72–73 188, 191 Functioning Scale
Ephedrine misuse 147 posttraumatic stress disorder 332 Gambling See Pathological gambling
Epidemiology See individual disorders schizophrenia 226–227 Gamma-aminobutyric acid See
Epilepsy Family therapy GABAergic neurotransmission
catatonic disorder due to a general learning/motor skills disorders 30 Gender
medical condition 119 major depressive disorder 269 autism spectrum disorders 44
mood disorder due to a general schizophrenia 240 bipolar disorder 283
medical condition with depressive FAS See Fetal alcohol syndrome communication disorders 33, 34
features 113 Fear 301 dissociative disorders 380
mood disorder due to a general See also Anxiety disorders encopresis 75, 76
medical condition with manic specific 305 enuresis 71–72
features 114 Feeding disorders of infancy or early factitious disorders 369, 370
psychoses secondary to diseases with childhood 57–63 learning/motor skills disorders 30
distinctive features 112 See also Eating disorders major depressive disorder 258
schizophrenia differential course 62 personality disorder 439
diagnosis 228 decision tree 61 schizophrenia 226
sleep-related 422 diagnosis 57, 61 separation anxiety disorder 78
Episode lengths, bipolar disorder disorder of poor caregiver–infant somatization disorder 347
284 reciprocity 57 Gender identity disorder 391–394
Episodic memory 374 disorder of state regulation 57, 59 body dysmorphic disorder
EPS See Extrapyramidal symptoms DSM-IV-TR/ICD-10 diagnostic criteria distinction 364, 365
Erectile disorder (ED) 385–386 comparison 63 boys 391
Erotomanic type delusional disorder etiology 59 diagnosis 392–394
248 infantile anorexia 58, 59, 61 DSM-IV-TR classification 16
ERPs See Event-related potentials posttraumatic feeding disorder 58, 60 DSM-IV-TR diagnostic criteria 392
Estrogen 276 sensory food aversion 58, 60 DSM-IV-TR/ICD-10 diagnostic criteria
Ethical considerations 371 treatment 60 comparison 398
Ethnicity Female orgasmic disorder (FOD) 387 early forms 391
major depressive disorder 258 diagnosis 387 feminine young boys 391
schizophrenia 226 DSM-IV-TR/ICD-10 diagnostic criteria girls 391
Euphoria 162, 168–169, 173 comparison 398 group therapy 394
Evaluation See Psychiatric evaluation treatment 388 hormone therapy 394
Excited catatonia 118–119 Females masculine girls 391
Exercise 277 abusive relationships 204 psychotherapy 393
Exhibitionism 396 pathological gambling 430 surgical therapy 394
Expressed emotion (EE) 240 Female sexual arousal disorder 385 treatment 393
Expressive language disorder (ELD) Feminine young boys 391 Gender identity disorder not otherwise
diagnosis 34–35 Fentanyl See Opioid… specified (GIDNOS) 393
differential diagnosis 35 Fetishism 396–397 General medical conditions
treatment 35–36 Fetuses bipolar disorder 281, 284
Expressive writing disorders See Written inhalant abuse 184 body dysmorphic disorder
expression disorders Fibromyalgia 261 relationship 364–365
Extinction phase, cocaine-related Fire-setting behavior See Pyromania conversion disorder distinction 354–355
disorders 172 Flashbacks 177 dementia due to 5
Extrapyramidal symptoms (EPS), Fluent aphasia 92 encopresis 75–77
neuroleptics 234 Flunitrazepam 215 enuresis 71–75
Eye contact 221 Fluoxetine generalized anxiety disorder
Eye movements 224 body dysmorphic disorder 366 relationship 336, 338, 339
472 Index
General medical conditions (continued) Hashish See Cannabis Hypochondriasis

giving rise to sexual Headaches 156–157 See also Monosymptomatic
dysfunctions 390–391 Head injuries 107 hypochondriacal psychosis
hypochondriasis relationship 363 Head trauma 104 course 360
learning disorders relationship 28 Hearing 34, 182–183 diagnosis 360
major depressive disorder 260 See also Mixed receptive–expressive differential diagnosis 360
medication-induced disorders 13 language disorder DSM-IV-TR diagnostic criteria 360
mental conditions due to a general Hepatitis 199, 204 DSM-IV-TR/ICD-10 diagnostic criteria
medical condition not elsewhere Hepatolenticular degeneration See comparison 365
classified 6, 14 Wilson’s disease somatic type delusional disorder 246
mental disorders due to 109–122 Heroin Hypoglycemia 116, 424
opioid dependence comorbidity 204 See also Opioid… Hypomania 277, 278, 279
pain disorder relationship 358–360 HHMA See Hypothalamic–pituitary–adrenal axis 398
psychological factors affecting 12 3,4-Dihydroxymethamphetamine Hypothalamic–pituitary–gonadal
schizophrenia differential 5-HIAA See 5-hydroxyindoleacetic axis 398
diagnosis 228 acid Hypothermia 205
sexual dysfunction 10–11 History Hypoxia
somatization disorder 347, 351, 352 hallucinogen use 175–176 Hysteria See Somatization disorder
somatoform disorder 343, 346 MDMA 178 Hysterical psychosis See Brief psychotic
Generalized anxiety disorder mental retardation 19–21 disorder
(GAD) 335–344 Histrionic personality disorder
comorbidity 336 (HPD) 450–451
course 338 course 452 I
diagnosis 335–338 diagnosis 450 ICD See International Classification of
differential diagnosis 338–340 differential diagnosis 451 Diseases…
DSM-IV-TR 335 DSM-IV-TR diagnostic criteria 451 Ideation 220
DSM-IV-TR/ICD-10 diagnostic criteria DSM-IV-TR/ICD-10 diagnostic criteria Identity 372, 374, 376, 377
comparison 344 comparison 458 Illusions 221
major depressive disorder treatment 451 Immobility 118
comorbidity 261 HIV (human immunodeficiency virus) Impotence See Male erectile disorder;
medication 343 dementia due to HIV disease 100 Psychogenic impotence
physical symptoms 335 opioid dependence 204 Impulse control disorders 423, 425, 427,
psychosocial therapies 943 opioid use disorders 198 428, 429, 431
separation anxiety disorder distinction 78 HMMA See 4-Hydroxy-3- intermittent explosive disorder 423–426
somatic therapies 341 methoxymethamphetamine kleptomania 428–429
treatment 340 Hofmann, Albert 175 pathological gambling 430–432
Geriatric population See Elderly people Homicidal ideation 222 pyromania (and fire-setting
Geschwind syndrome See Interictal Hopelessness 272 behavior) 429–430
personality syndrome Hormone therapy, gender identity trichotillomania 432–434
GIDNOS See Gender identity disorder not disorder 394 Impulsivity See Attention-deficit/
otherwise specified Hospitalization 270 hyperactivity disorder
Giles de la Tourette syndrome See See also Peregrination See also Attention-deficit/hyperactivity
Tourette’s disorder HPD See Histrionic personality disorder
Girls, gender identity disorder 391 disorder Inclusion principle 21
Global Assessment of Functioning (GAF) HPPD See Hallucinogen persisting Incontinence
Scale 3–4 perception disorder See also Encopresis; Enuresis
GnRH See Gonadotropin releasing HPT See Hypothalamic–pituitary–thyroid Incubus See Sleep terror disorder
hormone HSDD See Hypoactive sexual desire Indiscriminate sociability 81
Gonadotropin releasing hormone (GnRH) disorder Individual psychotherapy 239
agonists 276 Huffing 178 Indolealkylamines 175
Grandiose type delusional disorder 248 Human immunodeficiency virus Induced illness See Factitious disorders;
Grief 263 See HIV Malingering; Munchausen’s
Group therapy 239, 394 Huntington’s disease 103 syndrome
Guanfacine 55 Hyperactivity See Attention-deficit/ Infantile anorexia 58, 59, 61
Guilt 254 hyperactivity disorder Infants
Hyperglycemia 234 See also Children; Feeding disorders of
Hypernyctohemeral syndrome See infancy or early childhood
H Non-24-hour-day syndrome disorders usually first diagnosed
Hair pulling See Trichotillomania Hypertension 205–206 in infancy, childhood or
Hallucinations 223, 355, 357 Hyperthermia 205–206 adolescence 4, 5, 13
Hallucinogen-induced psychotic Hypnosis failure to thrive 57
disorders 177 dissociative fugue 373 rumination disorder 61, 63
Hallucinogens 175–178 nicotine dependence treatment 192 sleep–wakefulness 424
Haloperidol Hypnotic-related disorders See Infections
delirium treatment 90 Sedative-, hypnotic-, or anxiolytic- delirium 85
schizoaffective disorder 244 related disorders Streptococcal 65
schizophrenia 231–233 Hypnotics 413 Information processing 219–220, 240
Index 473
Inhalant abuse 181 J bipolar disorder 283

See also Inhalant-related disorders Jealous type delusional disorder 295 delirium induction 89
nitrites 135 Jet lag type circadian rhythm sleep schizoaffective disorder 244
substance-induced persisting disorder 417 schizophrenia 237
dementia 105 Judgment, schizophrenia 221 side effects 288, 289
toxicology 181 trichotillomania 425
Inhalant dependence 180 Lofexidine 201
Inhalant-induced disorders 180 Lophophora williamsii 176
K
Inhalant intoxication 181–182 Lorazepam 91
Ketamine 205
Inhalant-related disorders 180 Love 247–248
Kleine–Levin syndrome 412
abusers 183–185 LSD (lysergic acid diethylamide)
Kleptomania 426
abuse toxicology 181 intoxication
course 431
cardiotoxicity 183 benzodiazepines 177
diagnosis 426–427
chemicals 180–181 differential diagnosis 176
differential diagnosis 424–429
comorbidity 181 effects 176
DSM-IV-TR diagnostic
cranial nerve abnormalities 183 flashbacks 177
criteria 426–427
diagnosis 180 signs 176–177
psychosocial treatments 432
DSM-IV-TTR/ICD-10 diagnostic Luteinizing hormone (LH)
somatic treatments 426
criteria comparison 185 secretion 400
treatment 431–432
encephalopathy 182–183 Lying, pathological 369, 371
Knowledge fund, schizophrenia 221
inhalant abuse 183 Lysergic acid diethylamide See LSD
Kraepelinian model 657–658
inhalant intoxication 182 (lysergic acid diethylamide)
Kuru 103
irreversible syndromes 183
myeloneuropathy 183
neonatal syndrome 183 M
ototoxicity 182 L Magnetic stimulation 268
peripheral neuropathy 183 LAAM See Levo-alpha-acetylmethodol Maintenance treatment
treatment 184–185 Laboratory testing generalized anxiety disorder 340–341
trigeminal neuropathy 183 mental retardation 19, 20, 21 major depressive disorder 265–266
Inhibited reactive attachment disorder 81, Language See Communication disorders; schizophrenia 233–234
84 Speech and language problems Major depressive disorder
Insight 223 Learning disabilities 26, 28 (MDD) 254–273
Insomnia Learning disorders acute phase treatment 264, 265
See also Primary insomnia related to ADHD relationship 28, 29, 30 adolescents 263
other psychiatric disorders 422 communication disorder age 254, 255, 258
Institutionalized children 81, 82 relationship 33, 35 alcohol dependence comorbidity 270
Intellectual functioning 18, 19 diagnosis 26–28 Alzheimer’s disease 260
Interictal personality syndrome 120 differential diagnosis 28 antidepressants 265–267
Intermetamorphosis 248 disruptive behavior disorders atypical features 270
Intermittent explosive disorder 425–428 relationship 28, 30 augmentation strategies 268
diagnosis 425–426 psychoeducational assessment 27 bereavement 263
differential diagnosis 426–427 psychotherapeutic interventions 30 borderline personality disorder
DSM-IV-TR diagnostic criteria 425 treatment 30 comorbidity 268
hypoglycemia 426 Learning and motor skills cancer 261
obsessive–compulsive disorder 427 disorders 26–31 catatonic features 256, 257, 270
psychosocial treatments 428 Leukemia 183 children 263
somatic treatments 428 Levo-alpha-acetylmethodol (LAAM) 198 chronic fatigue syndrome 261
treatment 427 LH See Luteinizing hormone… comorbidity 270
International Classification of Diseases, Life cycle, bipolar disorder treatment 290 continuation treatment 264
Ninth Revision, Clinical Modification Life events coronary artery disease 260
(ICD-9-CM) 4 major depressive disorder 263 course 259
International Classification of Diseases, Lifestyle alterations cross-sectional features 255
Ninth Revision (ICD-9) 4 nicotine dependence treatment 194 depression due to medications 261
Intoxication premenstrual dysphoric disorder 277 diabetes mellitus 260
See also Substance intoxication; Light and darkness, circadian diagnosis 252, 263
individual substances rhythms 419 diagnostic criteria comparison 273
cocaine 166 Light therapy differential diagnosis 95
delirium 85–87 delayed sleep phase type circadian double depression 259
hallucinogen intoxication 173–176 rhythm sleep disorder 418 drug dependence comorbidity 262
inhalants 178–180 major depressive disorder 271 DSM-IV-TR diagnostic criteria 253,
sedative-, hypnotic-, or anxiolytic- non-24-hour-day syndrome 415 256, 257, 258, 272
related disorders 209–211 premenstrual dysphoric disorder 277 eating disorders comorbidity 263
Intravenous drug users 202 sleep disturbances in dementia 422 electroconvulsive therapy 268
I/O syndrome See Inattention/overactivity Lithium etiology 260
syndrome attention-deficit and disruptive behavior general medical condition 260
IPT See Interpersonal psychotherapy disorders 49 generalized anxiety disorder
IQ 218 autism spectrum disorders 44 comorbidity 266
474 Index
Major depressive disorder MAS See Mixture of amphetamine salts mood disorder due to a general
(MDD) (continued) Masculine girls 391 medical condition with depressive
grief 263 Masochism 397 features 113–114
hypomania history 270 Maternal care sleep disturbance 422–424
interepisode recovery 257 mental retardation 22 Megalomania 248
light therapy 268 nonorganic failure to thrive 59 Melatonin 415
maintenance treatment 265 Maternal–infant relationship Memory
melancholic features 257 feeding disorders 60 See also Amnesia; Amnestic disorders
monoamine oxidase inhibitors 267 reactive attachment disorder 81–84 dissociative disorders 373, 375, 380
mortality 255 rumination disorder 61, 63 learning disorders 26, 28, 30
obsessive–compulsive disorder Mathematics disorders phencyclidine intoxication 207
comorbidity 262, 270 DSM-IV-TR diagnostic criteria 31 schizophrenia 219–227
older adults 263 educational interventions 30 Menstrual cycle-associated hypersomnia
onset 263 MBK See Methyl butyl ketone syndrome 373, 376, 380
panic disorder comorbidity 262, 270 MDD See Major depressive disorder Menstrual cycles See also Premenstrual
Parkinson’s disease 260 MDMA (ecstasy)-related disorders 178 dysphoric disorder; Premensrual
personality disorders comorbidity 263 depression 176, 179 Syndrome
pharmacotherapy 264, 265, 268 diagnosis 176–178 Mental disorder not otherwise
phobic disorders comorbidity 262 treatment 177–179 specified due to a general medical
postpartum onset 257 Mechanistic views, psychopathology 50 condition 110, 117
posttraumatic stress disorder Medical complications Mental retardation
comorbidity 262 cocaine abuse 168, 170 assessment 18–25
primary risk factors 254 MDMA use 178–179 autism spectrum disorders
psychological testing 254 Medical conditions See General medical relationship 38
psychosocial treatment 269 conditions; Psychological factors biomedical assessment 19
psychotic features 270 affecting medical condition course 18, 23, 24
refractory 271 Medical management, somatization diagnosis 18, 21–23
remission specifiers 256 disorder 335 differential diagnosis 21
seasonal pattern 253, 258 Medication dimensions 19
somatic treatments 268, 271 abuse 125, 128, 131 etiology 19
somatization disorder comorbidity 262 AIDS-related drugs 101 medication 22–23
stroke 260 amphetamine dependence 147 psychosocial interventions 24
suicide 253–255, 259, 265 amphetamine psychotropic drugs 22, 24
treatment 263–273 intoxication/withdrawal 152 quality of life 22
tricyclic antidepressants 265, 267, 269 attention-deficit and disruptive behavior treatment 22–24
vagus nerve stimulation 268 disorders 53–54 Mescaline 175, 176, 178, 220–223
Maladaptive behaviors 148 autism spectrum disorders 43 Metabolic disturbances
Male erectile disorder 385–387 body dysmorphic disorder 364–366 delirium 88
Male orgasmic disorder (MOD) 388 caffeine containing 155 Methadone 196, 198, 201, 202
DSM-IV-TR diagnostic criteria 392 communication disorders 33 Methamphetamine (METH) 147
DSM-IV-TR/ICD-10 diagnostic criteria conversion disorder 353 Methaqualone 213–214
comparison 398 dissociative disorders 375, 379–380 Methemoglobinemia 183
premature ejaculation 388–389 drug interaction 150 Methyl butyl ketone (MBK) 184
Malingering encopresis 75, 76 3,4-Methylenedioxymethamphetamine See
factitious disorders distinction 368–371 enuresis 71, 72 MDMA
somatoform disorder distinction 345, generalized anxiety disorder 335 Methylphenidate (MPH)
353, 367 hypochondriasis 362 attention-deficit and disruptive behavior
Malnutrition mental retardation 22–25 disorders 54
See also Eating disorders; Feeding mood disorder due to a general mental retardation 18–24
disorders medical condition with depressive Minor depressive disorder 252, 258
reactive attachment disorder 81, 84 features 113–114 Minority groups 34
Mania posttraumatic stress disorder 326, 327, Mixed receptive-expressive language
due to general medical 330 disorder (MRELD)
condition 114–116 primary insomnia 411–413, 424 course 34
major depressive disorder 253–259 selective mutism 79, 80 diagnosis 32–36
phencyclidine intoxication 207 separation anxiety disorder 77–80 differential diagnosis 34–35
Manic episode sleep disturbances related to other treatment 35–36
bipolar disorder 228, 242, 244 psychiatric disorders 410, 415, 417 Mixed type delusional disorder 247
caffeine intoxication 153 somatization disorder 345, 347, 349, MOD See Male orgasmic disorder
DSM-IV-TR diagnostic 352, 559, 562, 563 Molestation 318
criteria 278–282 tic disorders 64, 68 Monosymptomatic hypochondriacal
DSM-IV-TR/ICD-10 diagnostic criteria Medication-induced conditions psychosis 248
comparison 291 delirium 89 Mood disorders 272
MAOIs See Monoamine oxidase inhibitors depression 256, 261, 267 bipolar disorder 257, 259, 263, 267,
Marijuana See Cannabis generalized anxiety disorder 270, 272, 273
Marital therapy 269 symptoms 335 cocaine abuse comorbidity 167–173
Index 475
depressive disorder not otherwise Narcissistic personality disorder Nicotine

specified 252, 254–258, 262–263, (NPD) 452–453, fading treatment 193
267, 268–272 course 452 gum 188–189
depressive disorders 252–256, 262, diagnosis 452 inhalers 193
267, 272 differential diagnosis 452–453 nasal sprays 192–193
DSM-IV-TR classification 4 DSM-IV-TR diagnostic criteria patches 192
dysthymic disorder 252, 256–257, 452 replacement therapy 189–195
271–273 treatment 453 sleep disturbance 424
major depressive disorder 252, Narcoanalysis 358 Nicotine Anonymous groups 191
256–258, 263, 268, 271–273 Narcolepsy Nicotine dependence
premenstrual dysphoric disorder 252, diagnosis 416–417 caffeine dependence relationship 157
266 treatment 417 combined psychosocial/
somatoform disorder distinction 345– Narcozep See Flunitrazepam pharmacological treatments 194
347, 349, 352–367 Nasal spray nicotine 192 comorbidity 187
Mood disorders due to a general medical National Alliance for Mentally Ill course 187–188
condition (NAMI) 241 diagnosis 186
course 114, 116, 117, 120, 121, Negativism DSM-IV-TR diagnostic criteria 188
with depressive features 113 catatonic disorder due to a general formal treatment options 191–192
diagnosis 111, 113, 118, 117–120 medical condition 118 mental illness comorbidity 194–195
etiology 120 major depressive disorder 256 other addiction comorbidity 194–195
Mood episodes 278–279, 280 phencyclidine intoxication 207 pharmacological treatments 192–194
Mood stabilizers 23 schizophrenia 225 professional interventions/advice 191
Mortality Negativistic personality disorder See psychosocial treatments 193–194
major depressive disorder 255 Passive-aggressive personality repeated relapse management
schizophrenia 227 disorder 194–195
Mothers See Maternal… ; Pregnancy Neonatal effects self-help treatment 191
Motivational enhancement therapy caffeine withdrawal 156 somatic treatments 192
(MET) opioid dependence 203–204 tobacco usage assessment 188–191
cannabis dependence 163 Nervous system processing deficit 27 treatment 188–189
nicotine dependence 193–194 Neurasthenia 367 Nicotine-related disorders 186–195
Motive, sexual 384 Neurodegenerative disorders diagnosis 186–187
Motor activities mood disorder due to a general medical DSM-IV-TR/ICD-10 diagnostic criteria
conversion disorder 355 condition 114 comparison 195
Motor skills disorders personality change due to a general treatment 188–189
diagnosis 26, 27 medical condition 119, 120 Nicotine withdrawal
educational interventions 30 Neurodevelopment diagnostic criteria 186
Movement disorders, language disorders 34 DSM-IV-TR diagnostic criteria 186
medication-induced 235 Neuroimaging studies 177 DSM-IV-TR/ICD-10 diagnostic criteria
MPH See Methylphenidate Neuroleptic malignant syndrome comparison 195
MRELD See Mixed receptive–expressive (NMS) 234 symptoms 187–188
language disorder Neuroleptics NIDA See National Institute of Drug
MRI See Magnetic resonance imaging attention-deficit and disruptive behavior Abuse
Multiaxial system, DSM-IV-TR 1, 2–4, 13 disorders 55–56 Night alarms, enuresis 72, 74–75
Multimodal treatment See Integrated augmentation strategies 237–238 Nightmare disorder
treatment autism spectrum disorders 46–47 diagnosis 383
Multiple disorder assessment 65–66 extrapyramidal symptoms 234 DSM-IV-TR diagnostic criteria 382
Multiple personality disorder See mental retardation 23 DSM-IV-TR diagnostic criteria
Dissociative identity disorder risks/side effects 234–236 comparison 424
Multiple Sleep Latency Test 411 supersensitivity psychosis 111–112 treatment 421
Munchausen’s syndrome 368, 369, 371 tic disorders 68 Nightmares, posttraumatic stress
See also Factitious disorders 179 Neurological dysfunction disorder 421
Mushrooms, Psilocybe 175 learning/motor skills disorders 27 Night terrors See Sleep terror disorder
Mutism schizophrenia 223–224 NIP See Neuroleptic-induced
akinetic 119 Neuroophthalmology 224 parkinsonism
catatonic disorder due to a general Neurosurgery, tic disorders 69–70 Nitrates, aliphatic 180
medical condition 118 Neurosyphilis 104, 112 Nitrite inhalants 134
selective mutism 79–80 Neurotoxicity 179, 182–185 Nitrous oxide 181
Myeloneuropathy 183 Neurotransmitter systems NMDA See N-methyl-D -aspartate
Myocardial infarct 170, 171 See also individual neurotransmitter NMS See Neuroleptic malignant
Myoglobinuria 207 systems syndrome
alcohol effects 138–141 Nocturnal, See also Sleep…
alcohol-related disorders 139 Nocturnal myoclonus See Periodic limb
N obsessive–compulsive movements in sleep
Naloxone 200, 202 disorder 316–317 Nocturnal panic attacks 422
NAMI See National Alliance for Mentally NHSDA See National Household Survey Nonbizarre delusions 247
Ill on Drug Abuse Nonnicotine pill 193
476 Index
Nonorganic disorder of the sleep–wake differential diagnosis 457 DSM-IV-TR/ICD-10 diagnostic criteria
cycle See Circadian rhythm sleep DSM-IV-TR diagnostic criteria 457 comparison 56
disorder DSM-IV-TR/ICD-10 diagnostic criteria epidemiology
Nonorganic failure to thrive 56, 59 comparison 458 etiology
Non-rapid eye movement (non-REM) treatment 457–458 treatment 53–56
narcolepsy See Primary hypersomnia Obstructive sleep apnea 422 Optical neuropathy 183
Non-rapid eye movement (non-REM) OCD See Obsessive–compulsive disorder Oral contraceptives (OCs) 277
sleep 410 OCPD See Obsessive–compulsive Orgasm problems 387–389
Nonsteroidal antiinflammatory drugs personality disorder Orientation 86, 223
(NSAIDs) 361–362 OCs See Oral contraceptives Othello syndrome 247
Nonverbal learning disabilities 28 Oculomotor dysfunction 182, 183 Ototoxicity 182–183
Norepinephrine system ODD See Oppositional defiant Overdoses 131
cocaine effects 168 disorder 224
Normalization principle 21 Odorizers 181
Normal-pressure hydrocephalus 104 Olanzapine P
Novel antipsychotic agents 236, 244 diabetes mellitus 236 Pain disorder
NPD See Narcissistic personality disorder schizoaffective disorder 243 course 360
NSAIDs See Nonsteroidal schizophrenia 229–231, 232, 234, 236 differential diagnosis 362–363
antiinflammatory drugs treatment-refractory groups 237 DSM-IV-TR diagnostic criteria 359
Nutritional supplements 24 weight gain 236 DSM-IV-TR/ICD-10 diagnostic criteria
Nystagmus 207–208, 221 Older adults See Elderly people comparison 367
Olfactory reference syndrome 248 Palilalia 64
Olfactory responses to inhalant PANDAS See Pediatric autoimmune
O abuse 183 neuropsychiatric disorders associated
Obesity 236 Ondansetron 145 with streptococcal infection
See also Weight gain Onset age Panencephalitis, subacute
Obsessive-compulsive disorder major depressive disorder 263, 271 sclerosing 103
(OCD) 316–325 schizophrenia 225 Panic attacks
anxiety disorder due to a general Onset season, schizophrenia See also Panic disorder
medical condition with obsessive– Oophorectomy 277 anxiety disorder due to a general
compulsive symptoms 117 Opiodergic neurotransmission medical condition with panic
augmenting agents 324 Opioid agonist pharmacotherapy 200, 201 attacks or with generalized
body dysmorphic disorder Opioid dependence anxiety 117
relationship 365–366 course 199 assessment tree 297
clomipramine 322–323 diagnosis 196, 197 DSM-IV-TR diagnostic criteria 293
contamination obsessions 316 differential diagnosis 199–200 DSM-IV-TR/ICD-10 diagnostic criteria
course 319 medical comorbidity 204–205 comparison 300
diagnosis 316–319 Opioid-induced disorders 196, 197–198 nocturnal 1155–1156
differential diagnosis 319–321 Opioid intoxication record 293–294
DSM-IV-TR diagnostic criteria 316 diagnosis 196, 197–198 Panic disorder
DSM-IV-TR/ICD-10 diagnostic criteria diagnostic criteria 197 agoraphobia 292
comparison 325 differential diagnosis 199 CBT treatment 296
fluoxetine 323 DSM-IV-TR/ICD-10 diagnostic criteria combined treatments 299
generalized anxiety disorder comparison 205 course 295
relationship 337–338 Opioid-related disorders 196–205 decision tree 298
hypochondriasis relationship 351 comorbidity 203–204 diagnosis 292–295
intermittent explosive disorder 426 course 199 differential diagnosis 296
learning/motor disorder relationship 28 detoxification 200–201 DSM-IV-TR/ICD-10 diagnostic criteria
major depressive disorder diagnosis 196–200 comparison 300
comorbidity 262, 270 differential diagnosis 199–200 generalized anxiety disorder
medication 321–324 DSM-IV-TR/ICD-10 diagnostic criteria relationship 338–339
molestation 318 comparison 205 major depressive disorder
options flowchart of treatments 322 psychosocial treatments 203 comorbidity 261
psychosocial treatments 324–325 treatment 200 psychosocial treatments 296
schizophrenia relationship 319 Opioid therapy record 294
somatic treatments 321–324 pain disorder 354 separation anxiety disorder
symptom checklist 317 sleep disturbance 423–424 relationship 78
tic disorder relationship 64–67 Opioid use disorders 196–203 somatic treatment 296
treatment 321–325 Opioid withdrawal treatments 296–299
Yale–Brown Scale symptom diagnosis 196–205 PANSS See Positive and Negative
checklist 317 differential diagnosis 194–200 Syndrome Scale
Obsessive–compulsive pathology, DSM-IV-TR/ICD-10 diagnostic criteria PAPD See Passive-aggressive personality
kleptomania 428 comparison 205 disorder
Obsessive–compulsive personality Oppositional defiant disorder (ODD) Paradoxical conduct 248
disorder (OCPD) 452–458 comorbidity 51 Paranoid ideation 222
course 457 diagnosis 49–52 Paranoid personality disorder
diagnosis 456–457 differential diagnosis 52–53 (PPD) 441–444
Index 477
course 441 Periodic limb movements in sleep opioid agonist 201–202, 204
diagnosis 441 (PLMS) 420–421 posttraumatic stress disorder 330
differential diagnosis 441 Peripheral neuropathy 184 pyromania 430
DSM-IV-TR diagnostic criteria 441 Persecutory type delusional disorder 247 schizophrenia, 229–242, 248–250
DSM-IV-TR/ICD-10 diagnostic criteria Personal hygiene 221 side effects 22, 288, 289
comparison 458 Personality change due to a general Texas Medication Algorithm
treatment 442–443 medical condition Project 232, 233
Paranoid type schizophrenia 224–225 course 121 trichotillomania 430–432
Paraphilias 394–395 diagnosis 119 Phencyclidine-related
criminal sex-offending behaviors 396 differential diagnosis 121 disorders 206–209
diagnosis 394–395 DSM-IV-TR diagnostic criteria 120 course 208
DSM-IV-TR classification 11 DSM-IV-TR/ICD-10 diagnostic criteria diagnosis 206
DSM-IV-TR/ICD-10 diagnostic criteria comparison 122 differential diagnosis 176, 208
comparison 398 Personality disorders 439–441 DSM-IV-TR diagnostic criteria 207
noncriminal forms 396 antisocial personality disorder 446–451 DSM-IV-TR/ICD-10 diagnostic criteria
not otherwise specified 397, 398 avoidance personality disorder 453–454 comparison 209
specific 1087–1094 borderline personality street names for phencyclidine 206
treatment 397–398 disorder 448–451 treatment 208–209
Parasites, delusional parasitosis 714 cluster A 441–446 Phenobarbital 213, 216, 217
Parasomnias cluster B 446–453 1-(-1-Phenylcyclohexyl)piperidine See
DSM-IV-TR classification 39 cluster C 453–458 Phencyclidine
nightmare disorder, 420–421 course 441 Phenylethylamines 147, 176
nocturnal panic attacks 422 cultural bias 439–440 Phenylisopropylamines 148
REM sleep behavior disorder 422 dependent personality disorder 455 Phenylpropanolamine (PPA), misuse 148
sleep-related epilepsy 422 diagnosis 439–441 Phobias 301–315
sleep terror disorder 421 DSM-IV-TR classification 13, 17 See also Social phobia; Specific
sleepwalking disorder 421 DSM-IV-TR diagnostic criteria 440, phobias
Parkinson’s disease 441 course 305
dementia 102 evaluation Axis II 1–2 diagnosis 301–302
major depressive disorder 263 gender 439–440 major depressive disorder
Patches, nicotine 192 generalized anxiety disorder comorbidity 261
Pathogenic caregiving relationship 336 treatment 307, 314
feeding disorder 57, 58 histrionic personality disorder 450–451 Phonological disorder (PD)
posttraumatic stress disorder in inhalant abuse 181 comorbidity 33, 36
children 82–83 learning/motor disorder course 35
reactive attachment disorder 81, 84 relationship 28–29 diagnosis 34
Pathological gambling 430–432 major depressive disorder differential diagnosis 34
course 431 comorbidity 254 Physical symptoms
diagnosis 430–431 narcissistic personality disorder 452 generalized anxiety disorder 335
differential diagnosis 431 not otherwise specified 458 schizophrenia 223
DSM-IV-TR diagnostic criteria 430 obsessive–compulsive personality Physical withdrawal, phencyclidine
DSM-IV-TR/ICD-10 diagnostic criteria disorder 456–457 intoxication 207
comparison 434 paranoid personality disorder 441, 444 Physiological dependence, substance-use
losing 430 personality disorder 439–441 disorders 125
treatment 431 schizoid personality disorder 443 Pica 62
Pathological lying 369 schizotypal personality disorder 444– course 62
Pavor nocturnus See Sleep terror disorder 445, 454 diagnosis 62
PCP See Phencyclidine substance-related disorder treatment 62
PD See Phonological disorder relationship 130 Pick’s disease
PDDs See Pervasive developmental treatment 440 KlÜver–Bucy syndrome 110
disorders WHO 440 Pimozide 68, 249
Pediatric autoimmune neuropsychiatric Personality states 376–379 PKU See Phenylketonuria
disorders associated with Personality traits 461, 463 PLMS See Periodic limb movements in
streptococcal infection Pervasive developmental disorders sleep
(PANDAS) 65 (PDDs) 34, 38, 41, 82 PMDD See Premenstrual dysphoric
Pediatric onset disorders See Childhood See also Autism spectrum disorders disorder
disorders PFAMC See Psychological factors PMS See Premenstrual syndrome
Pedophilia 396 affecting medical condition Polysomnography 413
Peer relationship problems 28 Pharmacotherapy Polysubstance dependence 133
Pemoline See also Medication Possession trances 380, 381
Perception adjustment disorders 438 Postpartum blues 257
communication disorders 121 communication disorders 36 Postpartum onset, major depressive
delirium 85, 86 discontinuation 23 disorder 257
schizophrenia 222–223 dosages 22 Posttraumatic feeding disorder 58–60
Peregrination 368, 369 major depressive disorder 267, 272 Posttraumatic stress disorder
Pergolide 69 mental retardation 22–25 (PTSD) 326
Perimenopausal period 385 nicotine dependence 192–195 behavioral therapy 331
478 Index
Posttraumatic stress disorder Propellant gases 180 mental retardation 24–25

(PTSD) (continued) Pseudobulbar palsy 109 nicotine dependence 193
cognitive therapy 331 Pseudocyesis 367 obsessive–compulsive disorder 325–326
course 327 Pseudodementia 96 opioid-related disorders 203
diagnosis 326–331 Pseudoephedrine 147 panic disorder 296–297
differential diagnosis 328 Pseudoparkinsonism 234 premenstrual dysphoric disorder 277
drug doses/side effects 330 Psilocybe mushrooms 175 schizophrenia 238–241
DSM-IV-TR diagnostic criteria 327 Psyche 460 sedative-, hypnotic-, or anxiolytic-
DSM-IV-TR/ICD-10 diagnostic criteria Psychiatric disorders related disorders, 217
comparison 334 communication disorders comorbidity specific phobia 311–313
epidemiology 326 learning/motor disorder tic disorders 69
major depressive disorder relationship 28, 30 Psychosomatic illness, somatoform
comorbidity 262 nicotine dependence comorbidity 186 disorder distinction, 345
pharmacotherapy steps 330 opioid dependence 203 Psychostimulants
psychodynamic therapy 331 Psychic blindness See Agnosia See also Amphetamine-type stimulants;
reactive attachment disorder Psychodynamic theories 238 Cocaine
relationship 82–83 Psychodynamic therapy 331 attention-deficit and disruptive behavior
somatic treatments 329 Psychoeducational treatment 239 disorders 53–54
treatment 328–334 Psychogenic impotence 385–389 Psychotherapy
Potent Serotonin Transporter Psychological factors affecting medical bipolar disorder 289–290
Inhibitors 46 condition (PFAMC) 459–461 communication disorders 36
See also Selective serotonin reuptake comorbidity 459 factitious disorders 371–372
inhibitors coping style 461, 463 gender identity disorder 394
PPA See Phenylpropanolamine course 462 group 239
PPD See Paranoid personality disorder diagnosis 459–461 individual 239
Pragmatic language 33 differential diagnosis 462 learning/motor skills disorders 30
Pregnancy DSM-IV-TR diagnostic criteria 459 mental retardation 24
amphetamine-type stimulants 147 DSM-IV-TR/ICD-10 diagnostic criteria sedative-, hypnotic-, or anxiolytic-
bipolar disorder 290 comparison 469 related disorders, 217
opioid dependence 203 maladaptive health behavior 461 therapist role 36
prenatal diagnosis of mental mental disorder affecting medical Psychotic disorder due to a general
retardation 20 condition 461 medical condition
schizophrenia 223–226 personality traits 461, 463 diagnosis 111
solvent abuse 181 psyche–soma interaction 460 DSM-IV-TR/ICD-10 diagnostic criteria
substance-related disorders 129 psychological symptoms 461, 463 comparison 122
Premature ejaculation 388 stress-related physiological treatment 113
diagnosis 388 responses 461 Psychotic disorders
DSM-IV-TR/ICD-10 diagnostic criteria treatment 462–464 DSM-IV-TR classification 9, 15
comparison 398 unspecified psychological factors 461 hallucinogen-induced 177
treatment 389 Psychological symptoms opioid dependence 204
Premenstrual dysphoric disorder See also Factitious disorders schizophrenia differential
(PMDD) 252, 274–277 affecting general medical diagnosis 228
diagnosis 274 condition 463 somatoform disorder distinction 345
diet 277 Psychological testing 254 Psychotropic drugs See Pharmacotherapy
differential diagnosis 276 Psychological treatments 44 PSYN See Presynaptic group secretory
DSM-IV-TR/ICD-10 diagnostic criteria Psychomotor retardation 221 function
comparison 277 Psychosis PTSD See Posttraumatic stress disorder
DSM-IV-TR research criteria 274 due to a general medical Pulmonary conditions
exercise 277 condition 109–122 cocaine abuse 171
lifestyle modifications 277 lysergic acid diethylamide 208 nicotine dependence 187
medical conditions 276 major depressive disorder 256 Punchdrunk syndrome 104
psychosocial treatments 277 mental retardation 21 Pyromania (and fire-setting behavior) 429
treatment 276 phencyclidine intoxication 207 diagnosis 429–430
Premenstrual syndrome (PMS) 274 zolpidem 215 differential diagnosis 429
Premonitory experiences 64, 65 Psychosocial factors DSM-IV-TR diagnostic criteria 429
Primary hypersomnia evaluation Axis IV 2 pharmacotherapy 430
diagnosis 415 major depressive disorder 269 psychosocial treatments 430
DSM-IV-TR diagnostic criteria 416 Psychosocial treatments treatment 430
DSM-IV-TR diagnostic criteria adjustment disorders 437
comparison 424 amphetamine dependence 151
treatment 416 cocaine-related disorders 172–173 Q
Primary insomnia dissociative identity disorder 378 QOL See Quality of life
diagnosis 411 enuresis 74 QTc interval 231, 236
DSM-IV-TR diagnostic criteria 413 generalized anxiety disorder 343–344 Quaalude 214
treatment 413–414 intermittent explosive disorder 428 Quality of life (QOL) 22
Privacy rights 370 kleptomania 434 Quetiapine
Progesterone 276 major depressive disorder 269 prolactin levels 238
Index 479
schizophrenia 233–234, 238–239 diagnosis 61 extrapyramidal symptoms 229

weight gain 238 treatment 61–62 family therapy 240–241
Quitting phase, nicotine dependence fluoxetine 238
treatment 192 fluphenazine 233
S fluphenazine decanoate 234
Saccadic eye movements 224 gender differences 226
R SAD See Separation anxiety general medical conditions 228
Race See Ethnicity disorder;Sexual aversion disorder group psychotherapy 239
Rapid cycling specifiers, bipolar Sadism 396 hypochondriasis relationship 363
disorder 284 Scalp See Trichotillomania individual psychotherapy 239–240
Rapid eye movement (REM) sleep Schizoaffective disorder 242–244 late-onset 225–226
behavior disorder 424 course 243 lithium 237
Rapid eye movement (REM) sleep depression 244 maintenance treatment 232–234
narcolepsy 418 diagnosis 242–243 Mental Status Examination 220
Reactive attachment disorder (RAD) differential diagnosis 227–228, 243 mood 222
diagnosis 81–82 DSM-IV-TR diagnostic criteria 242 neuroleptics 234–235, 237
differential diagnosis 82–83 DSM-IV-TR/ICD-10 diagnostic criteria nonpharmacological treatments 238,
DSM-IV-TR diagnostic criteria 81 comparison 250–251 240
treatment 83–84 epidemiology 243 novel antipsychotic agents side
Reactive psychosis See Brief psychotic treatment 243–244 effects 236–237
disorder Schizoid personality disorder obesity 236
Reading disorders (SZPD) 443–444 obsessive–compulsive disorder 319
educational interventions 30 course 443 olanzapine 230, 235–236
Receptive language disorder 36 diagnosis 443 paranoid type 224
See also Mixed receptive–expressive differential diagnosis 443–444 pharmacological treatments 229, 235
language disorder DSM-IV-TR diagnostic criteria 443 phencyclidine intoxication 207
Recurrent major depressive disorder 255 DSM-IV-TR/ICD-10 diagnostic criteria physical examinations 224
Refractory bipolar disorder 289 comparison 458 postpsychotic depressive disorder 246
Refractory major depressive disorder 273 treatment 444 prevalence rates 226
Regurgitation, rumination disorder 61–62 Schizophrenia 219–242 psychoeducational treatment 239–240
Relapse acute treatment 231–232 psychopharmacological
cocaine-related disorders 170, 172 affect 222 treatments 229–230
nicotine dependence 187–188, 190 antidepressant medications 237 psychosocial treatments 238
REM See Rapid eye movement… antipsychotic medication 227 quetiapine 230–236
Remission Assertive Community Treatment 241 race 226
major depressive disorder 256 benzodiazepines 232, 237 relapse 232
substance-related disorders 131 body dysmorphic disorder residual type 225
Renal conditions distinction 365 resistance to treatment 236–237
cocaine abuse 170–171 cannabis use relationship 162, 163 risperidone 230–231
inhalant abuse 184 carbamazepine 237 self-directed treatment 241
Repetitive behavior case management 241 social skills training 240–241
See also Obsessive–compulsive catatonic type 225 socioeconomic status 226
disorder; Tic disorders chlorpromazine 229, 232 sociotherapy 232–233
autism spectrum disorders 38, 39, 41, clinical subtypes 224–225 somatization disorder
43, 44 clozapine 229, 235, 236 relationship 351
Residual type schizophrenia 225 cognitive adaptation training 240 subtypes (clinical) 224–225
Respiratory conditions See Pulmonary cognitive dysfunction 240 suicide 227
conditions course 226–227 treatment 228–229
Restless legs syndrome (RLS) 420 depression 234, 237 treatment-refractory
Rett’s disorder 40, 41 diabetes mellitus 236 individuals 236–237
Rhabdomyolysis diagnosis 220–249 undifferentiated type 225
cocaine abuse 170–171 differential diagnosis 88, 96, 227, 243 weight gain 236–237
inhalant abuse 184 disorganized type 224 ziprasidone 232, 236
phencyclidine intoxication 207 dissociative identity disorder Schizophreniform disorder 246
Rights, mental retardation 21–22 relationship 376 course 246
Rigidity dopamine 232–234 diagnosis 245
Risperidone dosage (maintenance) requirements 235 differential diagnosis 245
prolactin levels 236 DSM-IV-TR classification 9–10, 14, 15 DSM-IV-TR diagnostic criteria 246
schizoaffective disorder 242–244 DSM-IV-TR diagnostic criteria 220, DSM-IV-TR/ICD-10 diagnostic criteria
schizophrenia 232, 236–237 224, 225, 242, 244, 246 comparison 250
treatment-refractory groups 237 DSM-IV-TR/ICD-10 diagnostic criteria schizophrenia differential
weight gain 236 comparison 250 diagnosis 227–228
Rituals, autism spectrum disorders 45 electroconvulsive therapy 238 treatment 246–247
RLS See Restless legs syndrome ethnicity 226 Schizotypal personality disorder
‘Rocks’ See Cocaine etiology 224 (STPD) 444
Rohypnol See Flunitrazepam expressed emotion (family diagnosis 444–445
Rumination disorder 61–62 members) 240 differential diagnosis 445
480 Index
Schizotypal personality disorder generalized anxiety disorder 336, 338 Shared psychotic disorder 249–251
(STPD) (continued) major depressive disorder 252–259 course 250
DSM-IV-TR diagnostic criteria 445 MDMA 178–179 diagnosis 249
DSM-IV-TR/ICD-10 diagnostic criteria obsessive–compulsive differential diagnosis 250
comparison 458 disorder 316–325 DSM-IV-TR diagnostic criteria 249
treatment 445 premenstrual dysphoric disorder 274 DSM-IV-TR/ICD-10 diagnostic criteria
School Serotonin comparison 250
communication disorder assessment 32 bipolar disorder 290 treatment 250
separation anxiety disorder 77 cocaine effects 168 Shift-work type circadian rhythm sleep
Sclerosed veins 199 MDMA 178 disorder 419
SCN See Suprachiasmatic nucleus schizophrenia 219–220 Sick role, factitious disorders 368–369
Screen technique, dissociative Sex-offending behaviors 396 Skin popping 199
amnesia 374 Sexual abuse Sleep apnea 417
Seasonality See also Child abuse Sleep disorders 410
major depressive disorder 257 conversion disorder See also Circadian rhythm sleep
Sedative-, hypnotic-, or anxiolytic-related Sexual addiction 395, 397 disorder
disorders 210–218 Sexual arousal 385 caffeine-induced sleep disorder 159
abuse 211 Sexual aversion disorder (SAD) 383 differential diagnosis 411–412
assessment issues 213 Sexual desire disorder 393, 398 DSM-IV-TR classification 11, 16
barbiturates 211–214 diagnoses 384 Sleep disorder due to a general medical
benzodiazepines 210–215, 217 interactive components 384 condition 423
comorbidity treatment 218 Sexual differences See Gender Sleep disturbances related to other
course 215 Sexual disorders 382–397 psychiatric disorders
dependence 210 not otherwise specified 398 diagnosis 422–423
diagnosis 210 sexual dysfunctions 382 treatment 423
differential diagnosis 215 substance-induced sexual Sleep hygiene 413, 414
DSM-IV-TR/ICD-10 diagnostic criteria dysfunction 127 Sleep-related epilepsy 422
comparison 218 Sexual drive 384 Sleep restriction therapy 413–414
intoxication 211 Sexual dysfunctions 382 Sleep terror disorder
methaqualone 214 addiction 395, 397 diagnosis 421
somatic treatments 216 arousal 387–389 DSM-IV-TR diagnostic criteria
treatment 216 compulsive sexual behavior 395, 398 comparison 424
use/abuse patterns 214 criminal sex-offending behaviors 396 treatment 421
withdrawal 211 decision tree 383 Sleep-wake schedule disorders See
zaleplon 215 drive 386 Circadian rhythm sleep disorder
zolpidem 215 DSM-IV-TR diagnostic criteria 385 Sleepwalking disorder
Seizures DSM-IV-TR/ICD-10 diagnostic criteria diagnosis 421–422
cocaine abuse 170 comparison 398 DSM-IV-TR diagnostic criteria
conversion disorder 355 due to general medical comparison 424
Selective attention deficits 219 conditions 390–391 treatment 422
Selective mutism dyspareunia 389–390 Smoking
diagnosis 79 exhibitionism 396 See also Cannabis; Nicotine…
Selective serotonin reuptake inhibitors female orgasmic disorder 387–388 Snoring, breathing-related sleep
(SSRIs) female sexual arousal disorder 417
body dysmorphic disorder 366 disorder 385–387 Snorting
major depressive disorder 267 fetishism 396 inhalant-related disorders 180
schizoaffective disorder 244 frotteurism 396 opioid use disorders 198
Self-directed schizophrenia treatment 241 gender identity disorder 391 Social anxiety disorder See Social phobia
Self-harm male erectile disorder 385 Social phobia 301–315
dementia 91 male orgasmic disorder 387–388 children 305
factitious disorder 368–369 masochism 397 cognitive–behavioral therapy 314
Self-help motive 384, 386 course 305
alcoholics 145–146 not otherwise specified 383 diagnosis 301–305
nicotine dependence treatment 187–188 orgasm problems 387–388 differential diagnosis 306, 307
schizophrenia 219 pain disorders 389 DSM-IV-TR diagnostic criteria 302
Self-hypnosis, dissociative disorders 378 paraphilias 394–395 DSM-IV-TR/ICD-10 diagnostic criteria
Sensorineural hearing loss 182–183 pedophilia 396 comparison 314
Sensory food aversion in childhood 57–60 premature ejaculation 388–389 exposure hierarchy 313
Separation anxiety disorder (SAD) sadism 396 separation anxiety disorder
diagnosis 77–79 substance-induced 391 distinction 78
DSM-IV-TR diagnostic criteria 77 transvestic fetishism 396 treatment 308, 310
treatment 78 vaginismus 390 Social skills
Sernyl See Phencyclidine voyeurism 396 learning/motor skills disorders 28, 30
Serotonergic neurotransmission wish 383–386 schizophrenia 239–240
See also Selective serotonin reuptake Sexual identity disorder See Gender Socioeconomic status (SES)
inhibitors identity disorder bipolar disorder 283–284
alcohol 141–142 Sexual pain disorders 389 major depressive disorder 258
Index 481
Sociotherapy 226 children 305 DSM-IV-TR diagnostic criteria 125

Soiling See Encopresis cultural differences 305 DSM-IV-TR/ICD-10 diagnostic criteria
Solvent abuse diagnosis 301 comparison 134
See also Inhalant-related disorders diagnostic decision tree 308 major depressive disorder
substance-induced persisting differential diagnosis 307 comorbidity 270
dementia 105 DSM-IV-TR diagnostic Substance-induced anxiety disorder 126
Soma, psyche interaction 460 criteria 302–303 Substance-induced disorders 126–130
Somatic symptoms See Physical symptoms DSM-IV-TR/ICD-10 diagnostic criteria diagnosis 126–130
Somatic treatments comparison 315 DSM-IV-TR/ICD-10 diagnostic criteria
See also Medication post traumatic stress disorder 306–307 comparison 134
autism spectrum disorders 47 psychosocial treatments intoxication 125–126
bipolar disorder 286–288 somatic treatments 311–314 withdrawal 126, 128, 131
cocaine-related disorders 173 treatment 311–314 Substance-induced persisting dementia
kleptomania 428–429 types 303 diagnosis 105
major depressive disorder 267 Specific reading disorder 31 treatment 105
nicotine dependence 192–193 See also Reading disorders Substance-induced sexual
obsessive–compulsive disorder 321–324 Specific spelling disorder 31 dysfunctions 391
panic disorder 296 Speech and language problems Substance-induced sleep
phencyclidine intoxication 209 See also Communication disorders disorder 423–424
posttraumatic stress disorder 329–331 delirium 85 Substance intoxication
sedative-, hypnotic-, or anxiolytic- reactive attachment disorder 81–82 delirium 85, 90
related disorders 216–217 schizophrenia 221–222 DSM-IV-TR diagnostic criteria 126
specific phobia 308–311 selective mutism 79–80 Substance-related disorders
tic disorders 68–69, 69–70 Spelling 27, 31 alcohol 136–146
Somatic type delusional disorder 248 Spirit possession 381 amphetamine-type stimulants 147–152
Somatization concept 345 Sprays, nicotine nasal 192 anabolic steroids 134
Somatization disorder 349–352 SSRIs See Selective serotonin reuptake anxiolytics 210–218
comorbidity inhibitors caffeine 153–159
course 347 Stereotyped behavior cannabis 147–152
diagnosis 345–347 See also Obsessive–compulsive cocaine 166–174
differential diagnosis 349–352 disorder; Tic disorders comorbidity 133
DSM-IV-TR diagnostic criteria 347 autism spectrum disorders 38, 39, 41, course 130
DSM-IV-TR/ICD-10 diagnostic criteria 43, 44 diagnosis 123–129
comparison 367 Stickiness (viscosity) 120 differential diagnosis 130–131
major depressive disorder Stimulants drug counseling 203
comorbidity 262 See also Amphetamine-type stimulants; DSM-IV-TR classification 6–9, 14–15
medication 352–353 Cocaine DSM-IV-TR diagnoses recognition 124
subsyndromal/forme fruste/abridged autism spectrum disorders 46 hallucinogen-induced psychotic
See Undifferentiated somatoform enuresis 73 disorders 177
disorder mental retardation 23–24 hallucinogen intoxication 176–177
Somatoform disorders 345–367 Stimulus control therapy 413–414 hallucinogen persisting perception
body dysmorphic disorder 364–366 STPD See Schizotypal personality disorder 177–178
comorbidity 350–351 disorder hypnotics 210–218
conversion disorder 355–358 Strattera 54 inhalants 180–185
decision tree 345 Streptococcal infections 65 MDMA-related disorders 178–179
differential diagnosis 349–350 Stress medical complications 128
DSM-IV-TR diagnostic criteria 345– dissociative fugue 375 nicotine 186–195
346, 353, 355, 358–359, 362, 364 general medical conditions 461, 463 opioids 196–205
DSM-IV-TR/ICD-10 diagnostic criteria trichotillomania 434 pharmacotherapy 131, 133
comparison 367 Stroke See Cerebrovascular accidents phencyclidine 206–209
hypochondriasis 362–364 Stuperous catatonia 118, 119 physical examination 128
pain disorder 358–362 Stuttering polysubstance dependence 133–134
somatization disorder 345–353 course 35 psychiatric examination 128–129
somatoform disorder not otherwise diagnosis 34–35 psychosocial treatments 133
specified 367 differential diagnosis 35 sedatives 210–218
treatment 348 Subacute sclerosing panencephalitis 103 somatic treatments 131
undifferentiated somatoform Substance abuse substance-induced disorders 123,
disorder 353–354 attention-deficit and disruptive behavior 126–129
Sonata See Zaleplon disorders 52 substance-use disorders 123–133
Specific developmental disorder of motor diagnosis 125, 127 treatment 131–133
function 31 DSM-IV-TR diagnostic criteria 125 Substance-use disorders (SUDs) 123
See also Developmental coordination DSM-IV-TR/ICD-10 diagnostic criteria abuse 125, 128
disorder comparison 134–135 dependence 125, 128–130
Specific disorder of arithmetic skills 31 Substance dependence diagnostic decision tree 127
See also Mathematics disorders bipolar disorder comorbidity 283 DSM-IV-TR classification 6–9, 14–15
Specific phobias 301–315 course specifiers 130 DSM-IV-TR/ICD-10 diagnostic criteria
behavioral approach test 304 diagnosis 123–125, 127–128 comparison 134–135
482 Index
Substance-use disorders adults 66, 67, 69 Tricyclic antidepressants (TCAs)

(SUDs) (continued) chronic tic disorder 64 attention-deficit and disruptive behavior
generalized anxiety disorder comorbid conditions 65–67 disorders 54
relationship 339–340 course 66 enuresis 73
Substance withdrawal diagnosis 64–66 generalized anxiety disorder
alcohol 143 differential diagnosis 67 340–343
cocaine 166, 167, 168, 172 DSM-IV-TR diagnostic criteria 64 major depressive disorder 267
delirium 90 medication 68 Trigeminal neuropathy 183
diagnosis 126, 128 neurosurgical approaches 70 Truancy 51, 78
DSM-IV-TR diagnostic criteria 126 protection–challenge balance 65 Trust of therapists See Physician-patient
DSM-IV-TR/ICD-10 diagnostic criteria psychosocial treatments 69 relationship
comparison 134–135 treatment 67–70 TSH See Thyroid-stimulating hormone
pharmacotherapy 131 TLE See Temporal lobe epilepsy Tuberculosis 204
sedative-, hypnotic-, or Tobacco addiction See Nicotine… 12-Step programs 105, 144, 145
anxiolytic-related 211–213 Token economy 240 Twin studies
Subsyndromal somatization disorder See Tolerance bipolar disorder 286
Undifferentiated somatoform disorder See also Substance dependence major depressive disorder 267
Sudden deaths, antipsychotic caffeine 155 schizophrenia 228
drugs 235–236 phencyclidine intoxication 207
SUDs See Substance-use disorders Toluene 182
Suggestibility 377 Tomboys 391 U
Suicide Torsades de pointes 236 Ultrasonic bladder volume alarms 74
major depressive disorder 253, 270 Tourette’s disorder Undifferentiated somatoform disorder
schizophrenia 222 See also Tic disorders course 353
Supersensitivity psychosis 111, 112 adults 66 diagnosis 353
Support organizations comorbid disorders 65 differential diagnosis 354
Alcoholics Anonymous 143, 145–146 diagnosis 64–68 DSM-IV-TR diagnostic criteria 353
Surgery DSM-IV-TR diagnostic criteria 64 DSM-IV-TR/ICD-10 diagnostic criteria
breathing-related sleep disorder 418 learning/motor disorder relationship 28 comparison 367
enuresis 73 obsessive-compulsive symptoms treatment 354
gender identity disorder 394 psychosocial and developmental factors Undifferentiated type schizophrenia
tic disorders 69–70 treatment 67–68 225
Sympatholytics 46–47 Toxic metabolic encephalopathy See Urinary incontinence See Enuresis
Sympathomimetic activation 179 Delirium Urine tests
Symptomatic treatment 109–111 Toxicology, inhalant abuse 122 opioids 198
Symptomology See Diagnosis Toxic substances phencyclidine intoxication 207
Symptom rebound/reemergence, learning disorders 30 sedative-, hypnotic-, or anxiolytic-
benzodiazepines withdrawal 212–213 Tracks, opioid use disorders 199 related disorders 213
Syndrome simulation 349–350 Trail Making Test 426 USA federal learning disability
Synthetic antidiuretic hormone Trance states 381 guidelines 26–27
(desmopressin) 73 Transference 379–380
Syphilis 104 Transient tic disorder 64
SZPD See Schizoid personality disorder Transsexualism See Gender identity V
disorder Vaginismus 389, 390
Transvestic fetishism 396 diagnosis 390
T Trauma, dissociative disorders 374, 379, DSM-IV-TR/ICD-10 diagnostic criteria
Tachycardia 207, 236 380 comparison 398
Tardive dyskinesia See Neuroleptic- Traumatic stress disorders treatment 390
induced tardive dyskinesia See also Posttraumatic stress disorder Vagus nerve stimulation (VNS) 269
Tardive psychosis See Supersensitivity acute stress disorder 331–334 Valproic acid 237, 289
psychosis Travel, dissociative fugue 374 Vascular dementia
TCE See Trichloroethylene Treatment resistance 236–237 diagnosis 99
TD See Neuroleptic-induced tardive Treatment-resistant depression DSM-IV-TR diagnostic criteria
dyskinesia (TRD) 271 100
Temporal lobe 228 Tremor DSM-IV-TR/ICD-10 diagnostic criteria
Temporal lobe epilepsy (TLE) 431 Triangulation, erotomanic type delusional comparison 108
Tetrahydrocannabinol See Cannabis… disorder 247 treatment 100
Texas Medication Algorithm Project 232, Trichloroethylene (TCE) 180–81 Venereal disease research laboratory
233 Trichotillomania 432–434 (VDRL) test 104
Therapeutic bond See Physician–patient course 433 Venlafaxine 276, 342, 343
relationship diagnosis 432 Ventricular tachycardia 236
Therapeutic community programs 203 DSM-IV-TR diagnostic criteria 432 Viscosity (stickiness) 120
Therapeutic levels of DSM-IV-TR/ICD-10 diagnostic criteria Vital signs monitoring 208
medications 288–289 comparison 434 VNS See Vagus nerve stimulation
Thiamine 105–107 maintenance 434 Voice disorders
Tic disorders psychosocial treatments 434 See also Speech and language
See also Tourette’s disorder treatment 433 problems
Index 483
communication disorder not otherwise nicotine dependence treatment 193 Y

specified 35 novel antipsychotic agents 235 Yale-Brown Obsessive-Compulsive Scale
Vomiting, rumination disorder 62–63 schizophrenia 236 (Y-BOCS) 314
Von Economo’s disease (encephalitis Wernicke’s aphasia 92
lethargica) 112 WHO See World Health Organization Z
Voucher-based treatment 172 Wilson’s disease 104 Zaleplon 215
Voyeurism 396 Wish, sexual 384 Ziprasidone
Withdrawal See Emotional withdrawal; schizoaffective disorder 243
Substance withdrawal schizophrenia 231, 232, 236
W Women See Female… tic disorders 68
Weight gain Worry See Generalized anxiety disorder weight gain 236
breathing-related sleep disorder 417 Written expression disorders 31 Zolpidem 215

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CLINICAL GUIDE TO THE

DIAGNOSIS AND TREATMENT

With love and thanks to my family, in particular to my

Chapter 1 Psychiatric Diagnosis 1

Chapter 3 Childhood Disorders: Learning and Motor Skills Disorders 26

Chapter 4 Childhood Disorders: Communication Disorders 32

Chapter 5 Childhood Disorders: Pervasive Developmental Disorders 38

Chapter 6 Childhood Disorders: Attention-Deficit and Disruptive Behavior Disorders 49

Chapter 8 Childhood Disorders: Tic Disorders 64

Chapter 9 Childhood Disorders: Elimination Disorders and Childhood Anxiety Disorders 71

Chapter 10 Childhood Disorders: Reactive Attachment Disorder of Infancy or Early Childhood 81

Chapter 11 Delirium, Dementia, and Amnestic Disorders 85

Chapter 12 Mental Disorders Due to a General Medical Condition 109

Chapter 13 Substance-Related Disorders: General Approaches to Substance and Polysubstance Use

Chapter 14 Substance-Related Disorders: Alcohol 136

Chapter 15 Substance-Related Disorders: Amphetamine 147

Chapter 16 Substance-Related Disorders: Caffeine 153

Chapter 17 Substance-Related Disorders: Cannabis 160

Chapter 18 Substance-Related Disorders: Cocaine 166

Chapter 19 Substance-Related Disorders: Hallucinogens and MDMA 175

Chapter 20 Substance-Related Disorders: Inhalants 180

Chapter 21 Substance-Related Disorders: Nicotine 186

Chapter 22 Substance-Related Disorders: Opioids 196

Chapter 24 Substance-Related Disorders: Sedatives, Hypnotics, and Anxiolytics 210

Chapter 25 Schizophrenia and Other Psychotic Disorders 219

Chapter 26 Mood Disorders: Depressive Disorders 252

Chapter 27 Mood Disorders: Premenstrual Dysphoric Disorder 274

Chapter 28 Mood Disorders: Bipolar Disorders 278

Chapter 31 Anxiety Disorders: Obsessive–Compulsive Disorder 316

Binge-Eating Disorder 407

Chapter 39 Sleep and Sleep–Wake Disorders 410

Comparison of DSM-IV-TR and ICD-10 Diagnostic Criteria 424

Chapter 40 Impulse Control Disorders 425

Chapter 41 Adjustment Disorders 435

Chapter 42 Personality Disorders 439

Dependent Personality Disorder 455

Henry David Abraham Substance Abuse: Hallucinogen- and MDMA-Related Disorders

Global Assessment of Functioning (GAF) Scale

Code (Note: Use intermediate codes when appropriate, e.g., 45,68,72.)

Example of DSM-IV-TR Multiaxial DSM-IV-TR Classification

DSM-IV-TR CLASSIFICATION If criteria are no longer met, one of the following

PERVASIVE DEVELOPMENTAL DISORDERS OTHER DISORDERS OF INFANCY,

AMNESTIC DISORDERS Alcohol-Induced Disorders

Amphetamine-Induced Disorders 292.xx Cocaine-Induced Psychotic Disorder

Cannabis-Induced Disorders INHALANT-RELATED DISORDERS

Nicotine-Induced Disorder Sedative-, Hypnotic-, or Anxiolytic-Induced

292.82 Other (or Unknown) Substance-Induced 297.3 Shared Psychotic Disorder

Specify if: Mixed Specify if: With Generalized Anxiety/With

327.xx Circadian Rhythm Sleep Disorder .24 With Anxiety

333.99 Neuroleptic-Induced Acute Akathisia ADDITIONAL CODES

RELATIONAL PROBLEMS Axis I Clinical Disorders

PROBLEMS RELATED TO ABUSE OR NEGLECT

MOOD DISORDERS SOMATOFORM DISORDERS

that is not better accounted for by a general medical EATING DISORDERS

DIAGNOSIS limitation in adaptive behavior is defined as perform-

• Dimension I: Intellectual abilities. Physical Examination. This is essential and should

Overall Goals of Psychiatric Treatment Review of Classes of Psychotropic Drugs

3 Childhood Disorders: Learning

DIAGNOSIS measured intelligence. Thus, these conditions can be

Child − adolescent Family

Psycho- No psycho- Normal Abnormal No Parenting Couples Family

General health Learning

ADHD Community School