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

organic mental disorders

Delirium Dementia Amnestic d/o

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 Positive

Alogia Affective flattening Avolition-apathy Anhedonia-asociality

Attentional impairment

Hallucinations Delusions Bizarre behaviour Positive formal thought disorder

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. 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

5.

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.
2.

PED DIAGNOSTIK UMUM

ADA EPISODE SKIZOAFEKTIF MANIK YG TUNGGAL MAUPUN BERULANG DGN SEBAGIAN BESAR TIPE MANIK. AFEK HRS MENINGKAT SECARA MENONJOL ATAU TAK BEGITU MENONJOL TETAPI DISERTAI IRITABILITAS ATAU KEGELISAHAN YG MEMUNCAK. DLM EPISODE YG SAMA HRS JELAS ADA SATU ATAU LEBIH BAIK LAGI KALAU DUA GEJALA SKIZOFRENIA YG KHAS.

3.

4.

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