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

Mood disorders

Functional
disorders
Schizophrenia
spectrum
disorders

P
S
Y
C
H
O
S
I
S

Substance
induced

Delirium
Dementia
Amnestic d/o

organic
mental
disorders

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 Kraepelins 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.
b.
c.
d.

DELUSION OF CONTROL (WAHAM DIKENDALIKAN)

DELUSION OF INFLUENCE (WAHAM PENGARUH)
DELUSION OF PASSIVITY
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

Alogia
Affective flattening
Avolition-apathy
Anhedonia-asociality

Positive

Hallucinations
Delusions
Bizarre behaviour
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.
2.
3.
4.

5.

PED DIAGNOSTIK UMUM

DIAGNOSTIK PERTAMA KALI PD USIA REMAJA ATAU
DEWASA MUDA (15-25 THN)
KEPRIBADIAN PREMORBID CIRI KHAS : PEMALU,
SENANG MENYENDIRI
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
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.
b.
c.
d.
e.
f.
g.

STUPOR ATAU MUTISME

GADUH GELISAH
POSTURING (TDK WAJAR & ANEH)
NEGATIVISME
RIGIDITAS
FLEKSIBILITAS CEREA
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
PED DIAGNOSTIK UMUM
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
1.
2.

III. GGN SKIZOAFEKTIF TIPE

CAMPURAN
GGN DGN GEJALA2 SKIZOFRENIA
BERADA SECARA BERSAMA-SAMA
DGN GEJALA-GEJALA AFEKTIF
BIPOLAR CAMPURAN

GGN WAHAM MENETAP

WAHAM BERLANGSUNG LAMA SBG SATU2NYA
GEJALA KLINIS YG PALING MENONJOL
MUNGKIN ADA GEJALA DEPRESIF, AGRESIF
SEMENTARA/INTERMITTEN & SERASI DGN ISI
WAHAM

RAGAM WAHAM
EROTOMANIK
KEBESARAN (GRANDIOSE)
KECEMBURUAN
KEJARAN ATAU CURIGA
SOMATIK
ONSET : USIA PERTENGAHAN, KADANG DEWASA
MUDA (WAHAM SOMATIK)

PED DIAGNOSTIK
1. WAHAM2 MERUPAKAN SATU2NYA CIRI KHAS KLINIS
ATAU GEJALA YG PALING MENONJOL, BERSIFAT
KHAS PRIBADI & BUKAN BUDAYA SETEMPAT SERTA
SUDAH ADA SEDIKITNYA 3 BLN LAMANYA
2. GEJALA DEPRESI MUNGKIN ADA ATAU BAHKAN
SUATU EPISODE DEPRESI LENGKAP SECARA
INTERMITTEN TETAPI WAHAM MENETAP TERUS ADA PD
SAAT2 TDK TERDPT GEJALA AFEKTIF
3. TAK ADA BUKTI TENTANG ADANYA PENYAKIT OTAK
ATAU PENGGUNAAN ZAT
4. TAK ADA HALUSINASI DENGAR ATAU HANYA KADANG2
& SIFATNYA SEMENTARA
5. TAK ADA RIWAYAT GEJALA2 SKIZOFRENIA (WAHAM
DIKENDALIKAN, SIAR PIKIRAN, PENUMPULAN AFEK,
dsb)

BILA ADA WAHAM TAPI < 3 BLN & BKN

SKIZOFRENIA ATAU PENYEBAB ORGANIK GGN
PSIKOTIK AKUT DGN PREDOMINAN WAHAM.

GGN WAHAM TERINDUKSI

JARANG TERJADI
DIALAMI > 2 ORANG MEMPUNYAI HUB
EMOSIONAL ERAT
HANYA SEORANG YG GGN PSIKOTIK
(DOMINAN), LAINNYA WAHAM TERINDUKSI
PSIKOSIS INDIVIDU YG DOMINAN : PALING
SERING SKIZOFRENIA
SIFATNYA KRONIS, ISINYA SERINGKALI
KEBESARAN ATAU KEJARAN

PEDOMAN DIAGNOSTIK
1. DUA ORANG ATAU LEBIH MENGALAMI WAHAM YG SAMA
& SALING MENDUKUNG DLM KEYAKINAN ITU
2. MEREKA MEMPUNYAI HUBUNGAN YG LUAR BIASA
DEKATNYA
3. ADA BUKTI DLM KONTEKS WAKTU ATAU LAINNYA
BAHWA WAHAM ITU DIINDUKSI MELALUI KONTAK
ANTARA ORANG YG DOMINAN DGN YG PASIF

JIKA ADA ALASAN UTK PERCAYA BAHWA

DUA ORANG YG TINGGAL BERSAMA
MEMPUNYAI GGN PSIKOTIK YG TERPISAH
MAKA DIAGNOSIS GGN INI TDK DIBUAT
MESKIPUN TERDPT WAHAM YG DIYAKINI
BERSAMA.
NAMA LAIN : FOLIE A DEUX, GGN PARANOID
BERSAMA, PSIKOSIS SIMBIOTIK

GGN PSIKOTIK AKUT & SEMENTARA

ONSET AKUT ; YAITU PERUBAHAN DARI KEADAAN
TANPA GEJALA PSIKOTIK KE KEADAAN PSIKOSIK YG
TERJADI DLM WAKTU 2 MINGGU ATAU KURANG
SEBAGAI CIRI KHAS YG MENENTUKAN SELURUH KLP
ADANYA SINDROM YG KHAS ; YG DIPILIH PERTAMA
IALAH KEADAAN YG BERANEKA RAGAM SERTA
BERUBAH CEPAT YG DINAMAKAN POLIMORFIK,
SEDANG YG KEDUA IALAH ADANYA GEJALA2
SKIZOFRENIA YG KHAS
TERDPTNYA STRES AKUT TERKAIT, YG DIANGGAP
SECARA LAZIM BERHUBUNGAN DGN TIMBULNYA
PSIKOSIS AKUT.
LAMANYA BERLANGSUNG SULIT DIPASTIKAN,
SERINGKALI DLM BEBERAPA MINGGU ATAU BAHKAN
DLM BEBERAPA HARI TETAPI KADANGKALA DLM 2-3.

DAHULU DISEBUT : PSIKOSIS REAKTIF SINGKAT

PEDOMAN DIAGNOSTIK :
ADANYA CIRI2 UTAMA TERPILIH DARI GGN INI
DLM URUTAN PRIORITAS SBB :
1. ONSET AKUT ; DLM JANGKA WAKTU 2 MGG ATAU
KURANG, GEJALA2 PSIKOTIK SDH NYATA &
MENGGANGGU SEDIKITNYA BBRP ASPEK
KEHIDUPAN & PEKERJAAN SEHARI2.
2. ADA SINDROM KHAS BERUPA POLIMORFIK
ARTINYA ADA ANEKA RAGAM GEJALA & BERUBAH
CEPAT ATAU GEJALA SKIZOFRENIA YG KHAS.
3. ADA STRES AKUT TERKAIT, NAMUN TAK PERLU
SELALU ADA

TDK MEMENUHI KRITERIA EPISODE MANIK ATAU

DEPRESIF, WALAUPUN PERUBAHAN EMOSIONAL
& GEJALA2 AFEKTIF DPT MENONJOL DARI WAKTU
KE WAKTU.
TDK ADA PENYEBAB ORGANIK ATAU INTOKSIKASI
AKIBAT PENGGUNAAN ZAT.

I.

GGN PSIKOTIK POLIMARFIK AKUT

TANPA GEJALA SKIZOFRENIA

PEDOMAN DIAGNOSTIK
1. PEDOMAN DIAGNOSTIK UMUM
2. HALUSINASI ATAU WAHAM YG BERUBAH DLM JENIS
& INTENSITASNYA
3. KEKALUTAN EMOSIONAL YG ANEKA RAGAM & LEBIH
SERING SENANG, SEDIH, CEMAS ATAU MARAH
4. GEJALA YG ANEKA RAGAM ITU TAK SATUPUN
SECARA CUKUP KONSISTEN DPT MEMENUHI KRITERIA
SKIZOFRENIA, EPISODE MANIK ATAU DEPRESIF

DISEBUT JUGA BOUFFEE DELIRANTE, PSIKOSIS

SIKLOID TANPA GEJALA SKIZOFRENIA

II. GGN PSIKOTIK POLIMARFIK AKUT

DGN GEJALA SKIZOFRENIA
PEDOMAN DIAGNOSTIK
1. MEMENUHI KRITERIA 1, 2, & 3 GGN
PSIKOTIK POLIMORFIK AKUT TANPA
GEJALA SKIZOFRENIA
2. DISERTAI GEJALA2 YG MEMENUHI
KRITERIA D/ SKIZOFRENIA YG SUDAH
HRS ADA UTK SEBAGIAN BESAR WAKTU
SEJAK
MUNCULNYA GAMBARAN KLINIS
PSIKOSIS
ITU SECARA JELAS.
3. JIKA GEJALA SKIZOFRENIA MENETAP
LEBIH DARI 1 BLN MAKA DIAGNOSIS HRS
DIRUBAH SKIZOFRENIA

III. GGN PSIKOTIK LIR-SKIZOFRENIA

AKUT
PEDOMAN DIAGNOSTIK
1. PEDOMAN DIAGNOSTIK UMUM
2. GEJALA2 YG MEMENUHI KRITERIA UTK SKIZOFRENIA
YG HRS SDH ADA UTK SEBAGIAN BESAR WAKTU SEJAK
MUNCULNYA GAMBARAN PSIKOTIK YG JELAS
3. TAK ADA ATAU KALAU ADA GEJALA LAIN SANGAT
MINIM RAGAMNYA, SANGAT SEMENTARA &
INTENSITASNYA RINGAN
4. JIKA GEJALA SKIZOFRENIA MENETAP LEBIH DARI 1
BLN MAKA DIAGNOSIS HRS DIRUBAH SKIZOFRENIA

DAHULU JENIS INI DISEBUT :

1. SKIZOFRENIA AKUT ATAU REAKSI SKIZOFRENIA
2. GGN ATAU PSIKOSIS SKIZOFRENIFORM SINGKAT
3. ONEIROFRENIA

IV.

GGN PSIKOTIK AKUT

PREDOMINAN WAHAM

UNTUK D/ PASTI:
ONSET GEJALA PSIKOTIK HRS AKUT
WAHAM & HALUSINASI HRS SUDAH ADA DLM
SEBAGIAN BESAR WKT SEJAK
BERKEMBANGNYA KEADAAN PSIKOTIK YG
JELAS
TDK MEMENUHI KRITERIA SKIZOFRENIA
MAUPUN PSIKOTIK POLIMORFIK AKUT

KALAU WAHAM MENETAP > 3 BLN GGN

WAHAM MENETAP, KALAU HALUSINASI
MENETAP > 3 BLN GGN PSKOTIK NONORGANIK LAINNYA

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.

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.
conventional
antipsychotics
(classical
neuroleptics)
atypical
antipsychotics

chlorpromazine, chlorprotixene, clopenthixole,

levopromazine, periciazine, thioridazine
droperidole, flupentixol, fluphenazine, fluspirilene,
haloperidol, melperone, oxyprothepine, penfluridol,
perphenazine, pimozide, prochlorperazine,
trifluoperazine
amisulpiride, clozapine, olanzapine, quetiapine,
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:
Chlorpromazine
Thioridazine
Mesoridazine

High potency:

Haloperidol
Fluphenazine
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