Professional Documents
Culture Documents
AND
NEUROLOGY]
Extrapyramidal
Examinations in Psychiatry
by RICHARD D. SANDERS, MD, and PAULETTE MARIE GILLIG, MD, PhD
Dr. Sanders is Associate Professor, Departments of Psychiatry and Neurology, Boonshoft School of
Medicine, Wright State University, and Dayton VA Medical Center, Dayton, Ohio; and Dr. Gillig is
Professor of Psychiatry and Faculty of the Graduate School, Department of Psychiatry, Boonshoft
School of Medicine, Wright State University, Dayton, Ohio.
SERIES EDITOR: Paulette M. Gillig, MD,
PhD, Professor, Department of Psychiatry,
Boonshoft School of Medicine, Wright State
University, Dayton, Ohio
FUNDING: No funding was received for the
development of this article.
FINANCIAL DISCLOSURES: The authors have
no conflicts of interest relevant to the content
of this article.
ADDRESS CORRESPONDENCE TO: Paulette
Gillig, MD, Professor, Dept. of Psychiatry,
Boonshoft School of Medicine, Wright
State University, 627 S. Edwin C. Moses
Blvd., Dayton, OH 45408-1461; E-mail:
paulette.gillig@wright.edu
KEY WORDS: Extrapyramidal signs,
parkinsonian signs, tremor, rigidity, motor
retardation, neurologic examination
ABSTRACT
Extrapyramidal signs include
increased motor tone, changes in the
amount and velocity of movement,
and involuntary motor activity. They
include two groups of signs and
related disorders: hypokinetic
(similar to Parkinsons disease) and
hyperkinetic (similar to Huntingtons
disease). This article covers some of
the neuroscience behind
extrapyramidal disorders, the
relevance of extrapyramidal signs in
the major psychiatric disorders, the
major extrapyramidal movement
disorders, and how to elicit
extrapyramidal signs.
INTRODUCTION
Of all the parts of a neurologic
examination, nothing is more
essential to daily psychiatric practice
than extrapyramidal motor
functioning. Extrapyramidal function
can affect many aspects of the
mental status examination, such as
speech, affect, and spontaneous
motor activity. Extrapyramidal
disorders (both iatrogenic and
idiopathic) are common in
psychiatric patients, and psychiatric
syndromes are quite common in
patients with extrapyramidal
disorders. Accordingly, the central
10
9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
[ V O L U M E 9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
11
obsessive-compulsive disorder; in
fact, some consider tics to be a form
of compulsion. They are a feature of
pediatric autoimmune
neuropsychiatric disorder associated
with streptococcal infection
(PANDAS).22 They also tend to be
found in attention deficit
hyperactivity disorder, even without
exposure to stimulants. Stimulants
can precipitate tics, which may or
may not remit after the stimulants
are stopped.23
9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
DEPRESSION AND
PARKINSONISM
Depression and parkinsonism are
statistically related and share clinical
features. Depression affects nearly
half of those with Parkinsons
disease.18 Also, idiopathic major
depression and parkinsonism share
certain signs and symptoms, such as
psychomotor retardation/
bradykinesia, blunted
affect/abulia/hypomimia, sleep
disturbances, and apathy. Patients
with melancholic40 or catatonic41
depression in particular may have
parkinsonian signs. Sometimes these
patients are in an early phase of
idiopathic parkinsonism, but often
the parkinsonism resolves with the
depressive episode.
DRUG-INDUCED MOVEMENT
DISORDERS
Dopamine-blocking drugs, such as
the antipsychotics (both typical and
atypical) and some anti-emetic
drugs, are the most recognized
causes of secondary extrapyramidal
movement disorders. Parkinsonian
side effects almost always arise
within one week of reaching the
necessary dose or concentration of
the drug, are reversible, and can
include any of the motor signs and
symptoms of Parkinsons disease.
When parkinsonian side effects are
caused or aggravated by dopamine
blocking drugs, dyskinesia rarely
emerges before four months on the
drug, but the effects often persist
after dopamine blocking drugs have
been discontinued. Tremor and
postural instability are less
prominent in drug-induced
parkinsonism than in Parkinsons
disease.42 Dopamine-depleting drugs,
such as reserpine and tetrabenazine,
can have the same side effects.
Stimulant drugs, such as cocaine
and amphetamines, also can have
similar effects, but via opposing
mechanisms. In acute withdrawal, a
stimulant user can have a
parkinsonian presentation,
presumably caused by dopamine
EXAMINATION METHODS
Poverty of movement may present
to simple observation as diminished
gesturing, diminished arm swing
while walking, or diminished facial
expression (blunted affect or
hypomimia, which is a reduced
degree of facial expression).
Hypophonia (soft, thin speech)
also shows itself in the interview. If
asked to speak louder, the patient
usually does so only temporarily. Of
course, patients sometimes
deliberately speak softly, but the
distinction is almost always obvious.
Micrographia is evident in almost
any writing sample. It becomes more
pronounced after the first few
letters, so very brief samples may fail
to capture the effect.48,49 Some
healthy people are habitually
micrographic, but in parkinsonism
[ V O L U M E 9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
13
9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
MOVEMENT DISORDER
ASSESSMENT SCALES
Movement disorder assessment
scales are widely available and often
used in clinical as well as research
settings. For hypokinetic or
parkinsonian signs, these include the
Unified Parkinsons Disease Rating
Scale motor exam section,56 and the
Simpson-Angus scale.57 For
hyperkinetic or tardive-like signs,
these include the Unified
Huntingtons Disease Rating Scale58
and Abnormal Involuntary Movement
Scale.53 The Extrapyramidal
Symptoms Rating Scale59 attempts to
cover both hyperkinetic and
hypokinetic signs.
These assessments can be
sharpened with the use of some
fairly simple instruments. Tremor
measurement can be facilitated with
an iPhone app.60 Scaling of movement
velocity exploits the fact that healthy
people moving between two targets
have a maximal velocity
proportionate to the distance
between the targets, but that in
parkinsonism there is no such
relationship.61 Several aspects of
parkinsonism can be assessed using a
windows-based system.62 Writing on a
12.
13.
CONCLUSION
The extrapyramidal examination,
which consists of observation and
very simple tests, is important in
understanding the mental status,
making psychiatric diagnosis,
selecting medication, and monitoring
of the effects of medications.
14.
15.
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
16.
17.
18.
19.
20.
21.
22.
23.
in schizophrenia: dopamine
connections and anomalies. J
Neurochem. 2010;113:287302.
Lozano AM, Snyder BJ, Hamani C,
et al. Basal ganglia physiology and
deep brain stimulation. Mov
Disord. 2010;25 Suppl 1:S71S75.
Bronstein JM, Tagliati M, Alterman
RL, et al. Deep brain stimulation
for Parkinsons disease: an expert
consensus and review of key
issues. Arch Neurol. 2011;68:165.
Weiner WJ. A differential diagnosis
of parkinsonism. Rev Neurol Dis.
2005;2:124131.
Handley A, Medcalf P, Hellier K,
Dutta D. Movement disorders after
stroke. Age Ageing.
2009;38:260266.
Kobayashi S, Maki T, Kunimoto M.
Clinical symptoms of bilateral
anterior cerebral artery territory
infarction. J Clin Neurosci.
2011;18:218222.
Ferrer I, Martinez A, Blanco R, et
al. Neuropathology of sporadic
Parkinsons disease before the
appearance of parkinsonism:
preclinical Parkinsons disease. J
Neural Transm.
2011;118:821839.
Jankovic J. Parkinsons disease:
clinical features and diagnosis. J
Neurol Neurosurg Psychiatry.
2008;79:368376.
Phukan J, Albanese A, Gasser T,
Warner T. Primary dystonia and
dystonia-plus syndromes: clinical
characteristics, diagnosis, and
pathogenesis. Lancet Neurol.
2011;10:10741085.
Hyde TM, Hotson JR, Kleinman JE.
Differential diagnosis of choreiform
tardive dyskinesia. J
Neuropsychiatry Clin Neurosci.
1991;3:255268.
Walker RH. Differential diagnosis of
chorea. Curr Neurol Neurosci
Rep. 2011;11:385395.
Pavone P, Parano E, Rizzo R,
Trifiletti RR. Autoimmune
neuropsychiatric disorders
associated with streptococcal
infection: Sydenham chorea,
PANDAS, and PANDAS variants. J
Child Neurol. 2006;21:727736.
Swain JE, Leckman JF. Tourette
syndrome and tic disorders:
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
[ V O L U M E 9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
15
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
16
45.
46.
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
2010;22:148156.
Meara J. Serotonin and the
extrapyramidal system: a
neurological perspective. Hum
Psychopharmacol.
1996;11:s95s102.
Pasternak B, Svanstrm H, Nielsen
NM, et al. Use of calcium channel
blockers and Parkinsons disease.
Am J Epidemiol.
2012;175(7):627635.
Garcia-Ruiz PJ, Javier JimnezJimnez F, Garcia de Ybenes J.
Calcium channel blocker-induced
parkinsonism: clinical features and
comparisons with Parkinsons
disease. Parkinsonism Relat
Disord. 1998;4:211214.
Angus JW, Simpson GM.
Handwriting changes and response
to drugs--a controlled study. Acta
Psychiatr Scand Suppl.
1970;212:2837.
Caligiuri MP, Teulings HL, Dean
CE, et al. Handwriting movement
kinematics for quantifying
extrapyramidal side effects in
patients treated with atypical
antipsychotics. Psychiatry Res.
2010;177:7783.
Kowall NW, Berman SA. Primitive
reflexes in psychiatry and
neurology. In: Joseph AB, Young
RR (eds). Movement Disorders in
Neurology and Neuropsychiatry.
New York: Blackwell;1999.
Borroni B, Broli M, Costanzi C, et
al. Primitive reflex evaluation in
the clinical assessment of
extrapyramidal syndromes. Eur J
Neurol. 2006;13:10261028.
Karson CN. Spontaneous eye-blink
rates and dopaminergic systems.
Brain. 1983;106:643653.
Munetz MR, Benjamin S. How to
examine patients using the
Abnormal Involuntary Movement
Scale. Hosp Comm Psychiatry.
1988;39:11721177.
Marcus D, Kurlan R. Tic and its
disorders. Neurol Clin.
2001;19:735758.
Grandas F. Hemiballismus. Handb
Clin Neurol. 2011;100:249260.
Fahn S, Elton RL, UPDRS
Development Committee. Unified
Parkinsons disease rating scale. In:
Fahn S, Marsden CD, Goldstein M,
9 , N U M B E R 7 8 , J U LY A U G U S T 2 0 1 2 ]
57.
58.
59.
60.
61.
62.
63.