EPIDEMIOLOGY 1
ETIOPATHOPHYSIOLOGY 1
CLINICAL FEATURES & DIAGNOSIS 2
Psychological testing 4
Neuroimaging 4
Laboratory studies 4
SCHIZOPHRENIA SUBTYPES 4
COURSE 4
DIFFERENTIAL DIAGNOSIS 5
TREATMENT 5
GROUP THERAPY 6
INDIVIDUAL PSYCHOTHERAPY 6
FAMILY THERAPY 6
COMMUNITY TREATMENT 6
SELF-HELP PROGRAMS 6
NEUROLEPTICS 6
ELECTROCONVULSIVE THERAPY (ECT) 7
PROGNOSIS 7
Mortality 7
Quality of life 7
PEDIATRIC ASPECTS 7
,EPIDEMIOLOGY
INCIDENCE - 0.11-0.70 per 1000.
PREVALENCE:
Point prevalence (i.e. number of cases at one moment in time) ≈ 1% (0.6-8.3%).
Lifetime prevalence in USA ≈ 1.3% (i.e. ≈ as of diabetes mellitus).
N.B. schizophrenic patients in developing countries tend to recover from their illness at higher rate (than
do schizophrenic patients in industrialized nations) → lower prevalence rates!
Gender
Western world: men ≈ women; men tend to develop earlier and more severe disease* (→ men with
schizophrenia tend never to have been married; affected women tend to be divorced or separated).
*may be because of antidopaminergic influence of estrogen.
Developing countries: men >> women.
Role of socioeconomic status
- PREVALENCE and INCIDENCE as well as DISEASE COURSE correlate with socioeconomic status.
in USA highest rates are found in lower socioeconomic classes (schizophrenic patients tend to drift
downward in socioeconomic status [drift hypothesis]; parents of schizophrenics have social class
distribution similar to that of general population).
,in India, highest rates occur in upper castes (social stress on class of people, rather than drift, may be
major factor in precipitating schizophrenia).
in cities with populations > 100,000, INCIDENCE increases in proportion to size of city.
Premorbid personality
- research has not demonstrated specific personality features that reliably predict development of
schizophrenia.
ETIOPATHOPHYSIOLOGY
- complex and yet undetermined.
NEURODEVELOPMENTAL VULNERABILITY to schizophrenia (genetic predisposition;
intrauterine, perinatal complications) + triggering (biochemical* or social**)
*e.g. substance abuse (esp. marijuana) **e.g. leaving home for college, breaking off romantic
relationship
No evidence that schizophrenia is caused by poor parenting!
A. Genetic predisposition theories
, genetic factors clearly play role, but actual manner of genetic transmission of schizophrenia is
complicated (simple single gene transmission is no longer plausible; schizophrenia transmission in
families does not fit any known pattern of pure genetic transmission; polygenic transmission is likely).
risk of schizophrenia is elevated in biological relatives but not in adopted relatives. studies show high
rates of mental illness* in relatives of patients with schizophrenia.
*not necessarily schizophrenia.
monozygotic twins have ≈ 53% risk (risk higher if twins are raised together); dizygotic twins ≈
10-14%.
if individual has 1st-degree relative with schizophrenia, his risk ≈ 10% (vs. ≈ 1% in general population).
B. Developmental (perinatal) insult theories
developmental factors play major role (schizophrenia is neurodevelopmental disorder, perhaps
sometimes beginning in utero or at birth).
season of birth - schizophrenia risk is greatest for individuals born in late winter ÷ early spring (prenatal
exposure to virus such as influenza is implicated).
prenatal malnutrition, low birth weight are also associated with increased risk. preeclampsia → ninefold
increased risk.
C. Psychological theories
- no longer play etiologic role:
1. Family interaction theories:
a. mistakes in mothering by so-called “schizophrenogenic mother”.