Schizophrenia

Kristian Liaury MD, Ph.D, Psych.

Department of Psychiatry, Faculty of
Medicine, Hasanuddin University,
Makassar
Schizophrenia /
psychotic??
Schizophrenia /
psychotic??
What is Psychosis?
• Tanda gejala, bukan gangguan
• Hendaya berat dalam menilai
realita
• Tanda utama: halusinasi dan atau
waham
• Gejala hendaya berat lainnya juga
termasuk
Mood disorders
“Functional” disorders
Schizophrenia “spectrum” disorders

Scope of psychosis
PSYCHOSIS
Substance induced
Delirium Dementia Amnestic d/o
“organic” mental disorders

SKIZOFRENIA
SKIZOFRENIA
GGN PERSEPSI, PENGENDALIAN
BERAT KEINGINAN, DLM BIDANG
DORONGAN : PIKIRAN, KEHENDAK
PERASAAN, &
PERBUATAN,
ONSET PRODROMAL SULIT
DITENTUKAN,BIASANYA (GEJALA
RINGAN & TDK DI KONSISTEN)
DAHULUI FASE
GEJALA → TUMPUL, DIKETAHUI LUAR
WAHAM PSIKOLOGIK SIKAP/PERILAKU
ORANG & HALUSINASI ATAU MAJEMUK
DIKENDALIKAN ANEH, YG KHAS, :
DISTORSI PERASAAN AFEK KEKUATAN
PIKIRAN TDK & WAJAR PIKIRAN
& GAIB PERSEPSI
/
DARI
PERJALANAN TERGANTUNG PENY :
GENETIK, SULIT DITENTUKAN, FISIK &
SOSIAL KRONIS, BUDAYA.
DETERIORASI

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 1 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.
ENRON'S DIRTY LAUNDRY • THE TROUBLE WITH
POP MUSIC
Newsweek
Starch 11, 2002
Newsweekshc.cam

The Mystery of
SCHIZOPHRENIA
From Andrea Yates to A Beautiful Mind
The Faces Of a Tragic Disease
KOL
$3.95 US/$4.95 Canada
O
Course of Illness
Typical stages of schizophrenia:
– prodromal phase – active phase – residual
phase

Dimensi Disabilitas
Skizofrenia
Gejala Positif Waham Halusinasi Kekacauan pembicaraan Katatonia

Gejala Interpersonal
Negatif Ekspresi Perawatan datar

diri
Kehilangan minat

Kontak Sosial
Gejala
ide motivasi

Pekerjaan
Kognitif
Pemanfaatan Konsentrasi Gangguan

akses
 Kemampuan Memori
Perencanaan
Gejala Perasaan Pikiran Ketidaknyamanan
Putus Bunuh Kesejahteraan
Asa
psikologis
Diri
Hervita Diatri, 2013

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.
PERILAKUKATATONIK:GADUHGELISAH,
POSTURING,
FLEKSIBILITAS CEREA, NEGATIVISME,
MUTISME, STUPOR.
8. GEJALA NEGATIF : APATIS,
BICARA JARANG, RESPONS
EMOSIONALYGTUMPUL/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.
Alogia
Affective flattening
Avolition
Anhedonia
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

Positive and Negative

Symptoms
-
apathy
Negative
-
asociality
Hallucinations
Delusions
Bizarre behaviour
Positive formal thought
disorder
Positive
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.
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
b.
c.
MANNERISME, TUJUAN / PERASAAN
CENDERUNG MENYENDIRI, HAMPA
AFEK PUAS MENYERINGAI, DANGKAL DIRI,
SENYUM & UNGKAPAN TDK SENDIRI, WAJAR,
KATA CEKIKIKAN, TAWA
DI ULANG
RASA
PROSE PIKIR DISORGANISASI, PEMBICARAAN
TDK
-
ULANG

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
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

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 -
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.
Dopamine Pathways
Serotonin Pathways
Frontal cortex
Striatum
Substantia nigra
23737

Functions
• Mood
• Memory processing Sleep
• Cognition
Functions
Nucleus - Reward (motivation) accumbens -
Pleasure, euphoria
• Motor function (fine tuning)
Compulsion - Perseveration
VTA
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Hippocampus
Raphe nucleus
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”
Robert Freedman
29

Neurocircuitry of reward
meso-limbic dopaminergic system
AMYG
Cocaine
ανήκος, Cumbinadoplanes
O
battles
DA
Nicole
VTA

Psychosocial Factors
• Expressed emotion
• Stressful life events
• Low socioeconomic class
• Limited social network
Treatment Goal of
Schizophrenia
Recovery
Productivity
Subjective
(school, earning Quality of
Life
money or being a volunterary worker) GAF > 65 Harding, dkk 1987
Symtoms (Free of symtoms & without medicine,2 yrs) Lieberman, et all, 2002

Goals of Pharmacotherapy for Schizophrenia

Recovery
Remission Symtoms & function
Remisssion (symtoms mild or less for 6 months) Cognitive & Insight
Functionality Resolusion (symtoms ↓↓ → no time limit)
Response
Acute Episode
Efficacy
Negative Positive Hostility, Smooth IM symptom aggression
to PO transition
relief
Control Behavior (agitation)
Improve Cognitive depressive mood symptom improvement symptoms
and
relief
Relapse Prevention 1-3 days
7-14 days 6+ months Acute Sedation Orthostasis QTc prolongation
dystonia
EPS Drug-drug QTc prolongation
interactions
TD Hyperprolactinemia Weight Hyperglycemia QTc prolongation
gain

Safety

The Continuum of Care

Recovery

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)
chlorpromazine, chlorprotixene, clopenthixole,
levopromazine, periciazine, thioridazine droperidole,
flupentixol, fluphenazine, fluspirilene, haloperidol,
melperone, oxyprothepine, penfluridol,
perphenazine, pimozide, prochlorperazine,
trifluoperazine atypical antipsychotics
amisulpiride, clozapine, olanzapine, quetiapine,
risperidone, sertindole, sulpiride

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
Pedoman Penatalaksanaan Gangguan
Skizofrenia
- Kondisi emergensi
(gaduh gelisah):
Bila sulit tidur:
Lorazepam 0.5-2 mg (malam)
Bila sulit tidur: - Lorazepam 0.5-2 mg
(malam)
- Injeksi Haloperidol 5
mg (IM), boleh diulangi setiap 30 menit, dosis maks
30 mg/hari - Rujuk ke PPK 2/PPK
Non farmakologik - Psikoedukasi - Psikoterapi
Non farmakologik - Psikoedukasi - Psikoterapi
Fase akut (dengan indikasi rawat)
Fase akut (dengan indikasi rawat)
Terapi pemeliharaan /lanjutan setelah penanganan di PPK
2/PPK 3: - sesuai terapi anjuran
dr. SpK) - konsultasi kembali
ke PPK 2/PPK 3 setiap 3-6 bulan
- Bila gaduh gelisah (min.
salah satu item PANSS EC 4-5) - Injeksi Haloperidol 5
mg (IM) boleh
diulangi setiap 30 menit, dosis maks 30
mg/hari atau - Olanzapin 10mg (IM)
- Bila gaduh gelisah (min.
salah satu item PANSS EC 4-5) - Injeksi Haloperidol 5
mg (IM) boleh
diulangi setiap 30 menit, dosis maks 30 mg/hari atau - Olanzapin
10mg (IM)

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
Predictors of treatment
outcome
Modifiable factors
43
Longer duration of untreated psychosis
Poor premorbid adjustment
Early age of onset
Inherent refractoriness
Robinson et al. Am J Psychiatry 2004;161:473–479; Emsley et al. J Clin Psychiatry 2006;67:1707–1712

POOR OUTCOME
Cognitive impairment
Male sex
Reduced brain volume
Poor medication adherence

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.”
46

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
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 NON-
ORGANIK LAINNYA