Schizophrenia and Other Psychotic

Disorders

A.Jayalangkara Tanra MD,Ph.D.

Department of Psychiatry, Faculty of Medicine,

Hasanuddin University, Makassar
 What is Psychosis?
• Generic term
• “Break with Reality”
• Symptom, not an illness
• Caused by a variety of conditions that affect
the functioning of the brain.
• Includes hallucinations, delusions and thought
disorder
 P
Mood disorders S
Y Substance
C induced
“organic”
H mental
“Functional” O disorders
disorders S Delirium
Schizophrenia
“spectrum” I Dementia
disorders S Amnestic d/o
 Differential Diagnoses: (Cont)
• Personality disorders
Schizoid
• Miscellaneous
PTSD
Schizotypal
Dissociative disorders
Paranoid Malingering
Borderline Culturally specific phenomena:
Antisocial
Religious experiences
Meditative states
Belief in UFO’s, etc
SKIZOFRENIA
 SKIZOFRENIA
GGN BERAT DLM BIDANG : PIKIRAN, PERASAAN, PERBUATAN,
PERSEPSI, KEINGINAN, DORONGAN KEHENDAK &
PENGENDALIAN

ONSET SULIT DITENTUKAN,BIASANYA DI DAHULUI FASE

PRODROMAL (GEJALA RINGAN & TDK KONSISTEN)

GEJALA PSIKOLOGIK MAJEMUK : DISTORSI PIKIRAN & PERSEPSI

→ WAHAM & HALUSINASI YG KHAS, AFEK TDK WAJAR /
TUMPUL, SIKAP/PERILAKU ANEH, PERASAAN & PIKIRAN
DIKETAHUI ORANG ATAU DIKENDALIKAN KEKUATAN GAIB DARI
LUAR

PERJALANAN PENY SULIT DITENTUKAN, KRONIS, DETERIORASI

TERGANTUNG : GENETIK, FISIK & SOSIAL BUDAYA.
 Schizophrenia

• Schizophrenia occurs with regular frequency nearly

everywhere in the world in 1 % of population and
begins mainly in young age (mostly around 16 to 25
years).

• Schizophrenia is defined by
– a group of characteristic positive and negative symptoms
– deterioration in social, occupational, or interpersonal
relationships
– continuous signs of the disturbance for at least 6 months
 History
• Emil Kraepelin: This illness develops relatively early in life, and
its course is likely deteriorating and chronic; deterioration
reminded dementia („Dementia praecox“), but was not
followed by any organic changes of the brain, detectable at that
time.
• Eugen Bleuler: He renamed Kraepelin’s dementia praecox as
schizophrenia (1911); he recognized the cognitive impairment
in this illness, which he named as a „splitting“ of mind.
• Kurt Schneider: He emphasized the role of psychotic symptoms,
as hallucinations, delusions and gave them the privilege of „the
first rank symptoms” even in the concept of the diagnosis of
schizophrenia.
 4 A (Bleuler)
• Bleuler maintained, that for the diagnosis of schizophrenia are
most important the following four fundamental symptoms:
– affective blunting
– disturbance of association (fragmented thinking)
– autism
– ambivalence (fragmented emotional response)
• These groups of symptoms, are called „four A’ s” and Bleuler
thought, that they are „primary” for this diagnosis.
• The other known symptoms, hallucinations, delusions, which are
appearing in schizophrenia very often also, he used to call as a
“secondary symptoms”, because they could be seen in any other
psychotic disease, which are caused by quite different factors —
from intoxication to infection or other disease entities.
 Course of Illness

• Course of schizophrenia:
– continuous without temporary improvement
– episodic with progressive or stable deficit
– episodic with complete or incomplete remission

• Typical stages of schizophrenia:

– prodromal phase
– active phase
– residual phase
 PEDOMAN DIAGNOSTIK UMUM

I. PALING KURANG 1 GEJALA

1. a. THOUGHT ECHO
b. THOUGHT INSERTION OR WITHDRAWAL
c. THOUGHT BROADCASTING

2. a. DELUSION OF CONTROL (WAHAM DIKENDALIKAN)

b. DELUSION OF INFLUENCE (WAHAM PENGARUH)
c. DELUSION OF PASSIVITY
d. DELUSION OF PERCEPTION
3. HALUSINASI PENDENGARAN
a. SUARA BERKOMENTAR TENTANG
PERILAKUNYA
b. SUARA-SUARA SALING BERBICARA /
BERDISKUSI TENTANG HAL IHWALNYA
c. SUARA LAIN DARI SALAH SATU BAGIAN
TUBUHNYA

4. WAHAM MENETAP LAIN YG MENURUT

BUDAYA SETEMPAT DIANGGAP TDK WAJAR /
MUSTAHIL
II. PALING KURANG 2 GEJALA
5. HALUSINASI MENETAP DARI PANCA INDERA APA
SAJA, BISA DISERTAI WAHAM TANPA KANDUNGAN AFEKTIF
YG JELAS, ATAU IDE BERLEBIHAN YG MENETAP ATAU BILA
TERJADI SETIAP HARI SELAMA BERMINGGU2 / BERBLN
TERUS-MENERUS.

6. ARUS PIKIRAN TERPUTUS ATAU MENGALAMI SISIPAN

→ INKOHERENSI, IRRELEVANSI ATAU NEOLOGISME.

7. PERILAKU KATATONIK : GADUH GELISAH, POSTURING,

FLEKSIBILITAS CEREA, NEGATIVISME, MUTISME, STUPOR.
8. GEJALA NEGATIF : APATIS, BICARA JARANG,
RESPONS EMOSIONAL YG TUMPUL / TDK WAJAR,
PENARIKAN DIRI DARI PERGAULAN SOSIAL,
MENURUNNYA KINERJA SOSIAL (BUKAN OLEH
DEPRESI ATAU REAKSI NEUROLEPTIKA)

9. SUDAH BERLANGSUNG 1 BULAN (DI LUAR FASE

PRODROMAL)

10. PERUBAHAN KONSISTEN BERMAKNA ASPEK

PERILAKU → HILANGNYA MINAT, HIDUP TAK
BERTUJUAN, TDK BERBUAT SESUATU, LARUT DLM
DIRI SENDIRI & PENARIKAN DIRI SECARA SOSIAL.
 Positive and Negative Symptoms

Negative Positive
Alogia Hallucinations
Affective flattening Delusions
Avolition-apathy Bizarre behaviour
Anhedonia-asociality Positive formal thought
disorder
Attentional impairment

Andreasen N.C., Roy M.-A., Flaum M.: Positive and negative symptoms. In: Schizophrenia,
Hirsch S.R. and Weinberger D.R., eds., Blackwell Science, pp. 28-45, 1995
 I. SKIZOFRENIA PARANOID
• PALING SERING DITEMUKAN
• PEDOMAN DIAGNOSTIK
1. PED DIAGNOSTIK UMUM
2. HALUSINASI DAN / ATAU WAHAM HARUS MENONJOL :
a. SUARA MENGANCAM / MEMERINTAH, BUNYI
PLUIT, MENDENGUNG ATAU TAWA
b. PEMBAUAN / PENGECAP RASA. PERABAAN YG
BERSIFAT SEKSUAL, JARANG VISUAL
c. WAHAM HAMPIR SETIAP JENIS, TETAPI PALING
KHAS ADALAH DIKENDALIKAN, DIPENGARUHI,
PASSIVITY DAN DIKEJAR-KEJAR
 II. SKIZOFRENIA HEBEFRENIK
• ONSET BIASA PD UMUR < MUDA
• PEDOMAN DIAGNOSTIK
1. PED DIAGNOSTIK UMUM
2. DIAGNOSTIK PERTAMA KALI PD USIA REMAJA ATAU DEWASA
MUDA (15-25 THN)
3. KEPRIBADIAN PREMORBID CIRI KHAS : PEMALU, SENANG
MENYENDIRI
4. UTK DIAGNOSIS DIPERLUKAN PENGAMATAN KONTINU 2-3 BLN
a. MANNERISME, CENDERUNG MENYENDIRI, HAMPA
TUJUAN / PERASAAN
b. AFEK DANGKAL & TDK WAJAR, CEKIKIKAN, RASA
PUAS DIRI, SENYUM SENDIRI, TAWA
MENYERINGAI, UNGKAPAN KATA DI ULANG-ULANG
c. PROSE PIKIR DISORGANISASI, PEMBICARAAN TDK
MENENTU, INKOHERENSI
5. DORONGAN KEHENDAK HILANG, TDK ADA MINAT, KADANG
INGIN BERBUAT SESUATU TAPI SEGERA DITINGGALKAN,
PREOKUPASI YG DANGKAL DGN TEMA ANEH → SULIT
MEMAHAMI JALAN PIKIRAN
 III. SKIZOFRENIA KATATONIK
• YG MENONJOL GAMBARAN PSIKOMOTOR : HIPEKINESIS,
STUPOR, OTOMATISME & NEGATIVISME

• PEDOMAN DIAGNOSTIK
1. PED DIAGNOSTIK UMUM
2. > 1 PERILAKU MENDOMINASI GAMBARAN KLINISNYA
a. STUPOR ATAU MUTISME
b. GADUH GELISAH
c. POSTURING (TDK WAJAR & ANEH)
d. NEGATIVISME
e. RIGIDITAS
f. FLEKSIBILITAS CEREA
g. GEJALA LAIN : COMMAND AUTOMATISM,
VERBIGERASI, EKOLALI & EKOPRAKSI
 IV. SKIZOFRENIA SIMPLEKS
• SULIT DIBUAT
• PEDOMAN DIAGNOSTIK
GEJALA KRONIK PROGRESIF DARI :
a. GEJALA NEGATIF SKIZOFRENIA
RESIDUAL TANPA DIDAHULUI GEJALA
POSITIF
b. PERUBAHAN PERILAKU PRIBADI,
HILANG MINAT, TDK BERBUAT
SESUATU, TANPA TUJUAN HIDUP &
PENARIKAN DIRI SECARA SOSIAL
 GANGGUAN SKIZO AFEKTIF
• TERDPT GGN AFEKTIF & GEJALA SKIZOFRENIA PD SAAT
BERSAMAAN
• PEDOMAN DIAGNOSTIK UMUM :
1. TERDPT GEJALA2 SKIZOFRENIA & GGN
AFEKTIF SAMA MENONJOL PD SAAT
BERSAMAAN
2. TDK BOLEH ADA GEJALA SKIZOFRENIA &
GGN AFEKTIF DLM EPISODE PENYAKIT YG
TERPISAH
3. BILA SEORANG SKIZOFRENIA MENUNJUKKAN
GEJALA2 DEPRESIF SETELAH MENGALAMI
SUATU EPISODE PSIKOTIK DIBERI
DIAGNOSIS DEPRESI PASCA SKIZOFRENIA
 I. GGN SKIZO AFEKTIF TIPE MANIK
PEDOMAN DIAGNOSTIK :

1. PED DIAGNOSTIK UMUM

2. ADA EPISODE SKIZOAFEKTIF MANIK YG TUNGGAL
MAUPUN BERULANG DGN SEBAGIAN BESAR TIPE
MANIK.
3. AFEK HRS MENINGKAT SECARA MENONJOL ATAU TAK
BEGITU MENONJOL TETAPI DISERTAI IRITABILITAS
ATAU KEGELISAHAN YG MEMUNCAK.
4. DLM EPISODE YG SAMA HRS JELAS ADA SATU ATAU
LEBIH BAIK LAGI KALAU DUA GEJALA SKIZOFRENIA YG
KHAS.
 II. GGN SKIZOAFEKTIF TIPE DEPRESIF
PEDOMAN DIAGNOSTIK
1. PED DIAGNOSTIK UMUM
2. ADA EPISODE SKIZOAFEKTIF TIPE DEPRESIF YG
TUNGGAL MAUPUN BERULANG DGN SEBAGIAN BESAR
TIPE DEPRESIF
3. AFEK DEPRESIF HRS MENONJOL DISERTAI OLEH
SEDIKITNYA DUA GEJALA KHAS, BAIK DEPRESIF
MAUPUN KELAINAN PERILAKU TERKAIT SEPERTI
TERCANTUM DLM URAIAN UTK KRITERIA EPISODE
DEPRESIF
4. DLM EPISODE YG SAMA HRS JELAS ADA SEDIKITNYA
SATU ATAU LEBIH LAGI KALAU DUA GEJALA KHAS
SKIZOFRENIA
III. GGN SKIZOAFEKTIF TIPE CAMPURAN

• GGN DGN GEJALA2 SKIZOFRENIA BERADA

SECARA BERSAMA-SAMA DGN GEJALA-GEJALA
AFEKTIF BIPOLAR CAMPURAN
 Prognosis contd.
• Some of the predictors of outcome are the
consequence of a less severe illness

• Predicting risk of suicide

» Acute exacerbation of psychosis
» Depressive symptoms
» History of attempted suicide
 Genetics of Schizophrenia

• Many psychiatric disorders are multifactorial (caused

by the interaction of external and genetic factors)
and from the genetic point of view very often
polygenically determined.

• Relative risk for schizophrenia is around:

– 1% for normal population
– 5.6% for parents
– 10.1% for siblings
– 12.8% for children
 Etiology of Schizophrenia

• The etiology and pathogenesis of

schizophrenia is not known

• It is accepted, that schizophrenia is „the group

of schizophrenias“ which origin is
multifactorial:
– internal factors – genetic, inborn, biochemical
– external factors – trauma, infection of CNS, stress
 Etiology of Schizophrenia - Dopamine
Hypothesis
• The most influential and plausible are the hypotheses, based on
the supposed disorder of neurotransmission in the brain, derived
mainly from
1. the effects of antipsychotic drugs that have in common the ability to
inhibit the dopaminergic system by blocking action of dopamine in the
brain
2. dopamine-releasing drugs (amphetamine, mescaline, diethyl amide of
lysergic acid - LSD) that can induce state closely resembling paranoid
schizophrenia

• Classical dopamine hypothesis of schizophrenia: Psychotic

symptoms are related to dopaminergic hyperactivity in the brain.
Hyperactivity of dopaminergic systems during schizophrenia is
result of increased sensitivity and density of dopamine D2
receptors in the different parts of the brain.
 Etiology of Schizophrenia -
Contemporary Models
• Dopamine hypothesis revisited: various neurotransmitter
systems probably takes place in the etiology of schizophrenia
(norepinephric, serotonergic, glutamatergic, some peptidergic
systems); based on effects of atypical antipsychotics
especially.

• Contemporary models of schizophrenia conceptualize it as a

neurocognitive disorder, with the various signs and symptoms
reflecting the downstream effects of a more fundamental
cognitive deficit:
– the symptoms of schizophrenia arise from “cognitive dysmetria”
(Nancy C. Andreasen)
– concept of schizophrenia as a neurodevelopmental disorder (Daniel R.
Weinberger)
 Etiology of Schizophrenia -
Neurodevelopmental Model
• Neurodevelopmental model supposes in schizophrenia the
presence of “silent lesion” in the brain, mostly in the parts,
important for the development of integration (frontal, parietal
and temporal), which is caused by different factors (genetic,
inborn, infection, trauma...) during very early development of
the brain in prenatal or early postnatal period of life.
• It does not interfere too much with the basic brain functioning
in early years, but expresses itself in the time, when the
subject is stressed by demands of growing needs for
integration, during formative years in adolescence and young
adulthood.
 More modern approaches emphasize other transmitter systems, too

“1-Dopamine adjusts
the volume—Blocked
by antipsychotics

2-Acetycholine and
GABA filter signal
from noise

3-Glutamate imprints
new memories”

33
Robert Freedman
 Treatment of Schizophrenia
• The acute psychotic schizophrenic patients will respond usually
to antipsychotic medication.
• According to current consensus we use in the first line therapy
the newer atypical antipsychotics, because their use is not
complicated by appearance of extrapyramidal side-effects, or
these are much lower than with classical antipsychotics.

chlorpromazine, chlorprotixene, clopenthixole,

conventional levopromazine, periciazine, thioridazine
antipsychotics droperidole, flupentixol, fluphenazine, fluspirilene,
(classical haloperidol, melperone, oxyprothepine, penfluridol,
neuroleptics) perphenazine, pimozide, prochlorperazine,
trifluoperazine
atypical amisulpiride, clozapine, olanzapine, quetiapine,
antipsychotics risperidone, sertindole, sulpiride
 Psychosocial Factors
• Expressed emotion
• Stressful life events
• Low socioeconomic class
• Limited social network
 Some factors rejected as causal

• “Schizophrenogenic Mother”

• “Skewed” family structure

 Genetic factors:
(The evidence mounts…)
• Monozygotic twins (31%-78%) vs dizygotic
twins
• 4-9% risk in first degree relatives of
schizophrenics
• Adoption studies
• Linkage, molecular studies
 Genetics of Schizophrenia:
The take-home message
• Vulnerability to schizophrenia is likely
inherited
• “Heritability” is probably 60-90%
• Schizophrenia probably involves dysfunction
of many genes
 Typical Neuroleptics
• Low potency: • High potency:
– Chlorpromazine – Haloperidol
– Thioridazine – Fluphenazine
– Mesoridazine – Thiothixene
– Loxapine (mid)
 Neuroleptic (typicals):
side effects
• Acute dystonia
• Parkinsonian side effects (EPS)
• Akathisia
• Tardive dyskinesia
• Sedation, orthostasis, QTC prolongation,
anticholinergic, lower seizure threshold,
increased prolactin
 Atypical Antipsychotics:
• Risperidone
• Olanzapine
• Quetiapine
• Clozapine
• Ziprasidone
• Aripiprazole (new-partial DA agonist)
 Atypical Antipsychotics: Side Effects
• Sedation
• Hyperglycemia, new-onset diabetes
• Anticholinergic effects
• Less prolactin elevation
• QTC prolongation
• Some EPS
• Increased lipids
 Neuroleptic (typicals):
side effects
• Acute dystonia
• Parkinsonian side effects (EPS)
• Akathisia
• Tardive dyskinesia
• Sedation, orthostasis, QTC prolongation,
anticholinergic, lower seizure threshold,
increased prolactin
 Atypical Antipsychotics:
• Risperidone
• Olanzapine
• Quetiapine
• Clozapine
• Ziprasidone
• Aripiprazole (new-partial DA agonist)
 Atypical Antipsychotics: Side Effects
• Sedation
• Hyperglycemia, new-onset diabetes
• Anticholinergic effects
• Less prolactin elevation
• QTC prolongation
• Some EPS
• Increased lipids
 Treatment
• May require admission if acutely disturbed or
present a risk to self or others
• Admission may be useful in assessment
• Essential to assess suicide risk as there is a
mortality of about 10% from suicide in SCZ
• May require involuntary detention in some
cases
 Treatment contd.
• Antipsychotic drugs are mainstay of treatment
• Generally atypicals are first-line treatment eg
olanzapine, respiridone, amisulpiride
• May require depot injection
• Side effects of typicals can be stigmatising
• Side effects of atypicals – screen for DM
 Treatment contd.
• Atypicals have fewer extra-pyramidal side
effects and tend to be better for negative
symptoms that typicals
• Initial management may include use of
sedative medication such as lorazepam
• IM medication may be required in a very
disturbed, involuntary patient
 Treatment contd.
• Maintenance treatment – generally
maintenance on one medication
• Compliance may be a significant problem
because of long-term nature of treatment and
lack of insight
 Treatment contd.
• Psychosocial treatment
» Education of patient and carers
» Reduction of high expressed emotion – shown to affect
relapse rates
» Cognitive behavioural therapy – controversial
» Rehabilitation
» Self –help – Schizophrenia Ireland
 Prognosis
• 22% have one episode and no residual
impairment
• 35% have recurrent episodes and no residual
impairment
• 8% have recurrent epsiodes and develop
significant non-progressive impairment
• 35% have recurrent episodes and develop
significant progressive impairment
 Prognosis contd.
• The majority therefore do not recover fully
• Suicide rate is up to 13%
• Little evidence that anitpsychotic have altered
the course of illness for most patients
• However, evidence that prolonged psychosis
which is untreated has a bad prognosis
 Prognosis contd.
• Good outcome is associated with:
– Female
– Older age of onset
– Married
– Higher SEG
– Living in a developing (as opposed to developed) country
– Good premorbid personality
– No previous psych history
– Good education and employment record
– Acute onset, affective symptoms, good compliance with meds
 Prognosis contd.
• Some of the predictors of outcome are the
consequence of a less severe illness

• Predicting risk of suicide

» Acute exacerbation of psychosis
» Depressive symptoms
» History of attempted suicide
“He saw the world in a way no one could have imagined.”

55
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