The document summarizes genetic, environmental, neurobiological, and psychosocial factors related to schizophrenia. It discusses findings from family, twin, and adoption studies that suggest there is a genetic component. Prenatal and birth complications, winter birth, paternal age, and substance use are environmental risk factors. Neurobiologically, the document outlines evidence of decreased frontal lobe activity and changes in dopamine, glutamate, and GABA systems. Lower socioeconomic status, childhood trauma, and stressful life events are also discussed as psychosocial risk factors for developing schizophrenia.
2.
FAMILY STUDIES – Better research techniques yielded
estimates of an average lifetime risk of around 5-10%
among 1st degree relatives of people with schizophrenia vs
0.2-0.6% among 1st degree relatives of controls.
GENETIC FACTORS
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3.
TWIN STUDIES – Concordance rate for MZ twins is 40-
50% vs 10% for DZ twins. Among Discordant MZ twins,
the risk of schizophrenia is increased equally in children
of both the affected and unaffected twin.
ADOPTION STUDIES- children of affected mothers
separated within 3 days of birth vs control.
MODE OF INHERITANCE- Follows non-Mendelian
mode with genes acting as risk factors and not
determinants.
GENETIC FACTORS (Contd..)
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5. OBSTETRIC COMPLICATIONS - APH, DM, LBW, Birth
Asphyxia, Rh incompatibility.
MATERNAL INFLUENZA – Suggested that Influenza
infection esp in 2nd trimester . Other infections like
toxoplasmosis, HSV-2, Rubella.
MATERNAL MALNUTRITION – Children born to
mothers who experience famine early in pregnancy have
higher risk.
WINTER BIRTH
PATERNAL AGE – Increased risk of 50% for every 10 yr
increase in paternal age.
SUBSTANCE USE – Prior use of cannabis (controversial)
ENVIRONMENTAL FACTORS
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7.
NEUROPATHOLOGY
CEREBRAL BLOOD FLOW- Decreased in Frontal
lobe “HYPOFRONTALITY”.
FMRI – Decreased frontal activity esp Prefrontal
cortex during working memory tasks.
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8.
DOPAMINE – Use of PET and SPET scan to image dopamine
receptors and dopamine synthesis in brain provided evidence
of “HYPERDOPAMINERGIA” in acute schizophrenia.
Changes – a) Slight increase in D2 receptors.
b) Mainly- Increased occupancy of D2
receptors by dopamine.
GLUTAMATE – It was found that antagonists of NMDA
type of glutamate receptors(Ketamine) can induce
schizophrenia like psychosis.
NMDA Receptor Hypo functionality Model – Genetic
component involved and autoimmune anti NMDA receptor Abs
present.
NEUROCHEMICAL
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9.
NEUROCHEMICAL(Contd..)
GABA – Major inhibitory NT in brain.
a) Decrease in GAD activity in cortex.
b)Decrease in GABAergic neurons and synaptic
terminals.
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10.
EEG – Increased theta activity, fast and
paroxysmal activity.
Abnormal sensory evoked potentials and eye
tracking.
NEUROPHYSIOLOGY
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11.
OCCUPATION AND SOCIAL CLASS – Lower SE status.
PLACE OF RESIDENCE- Disadvantaged inner city areas.
MIGRATION AND ETHNICITY – Afro-Caribbean origin.
SOCIAL ISOLATION– Living alone, not married ,no friends
LIFE EVENTS – Moving house, losing job, new job.
Paykel calculated that experiencing major life events
doubles the risk of developing schizophrenia in the subsquent
6 months.
CHILDHOOD TRAUMA AND ABUSE
SOCIAL AND
PSYCHOSOCIAL FACTORS
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12. NEUROPSYCHOLOGICAL FACTORS – Model by Gray
et al suggested that positive symptoms arise from failure
to integrate stored memory with current stimuli.
FAMILY THEORY- 2 forms of abnormal family patterns
a) Marital skew- 1 parent yields to other’s eccentricities.
b) Marital schism- parents maintained contrary views
and child had divided loyalties.
PERSONALITY FACTORS- Suggested that schizophrenia
was more common in asthenic body type.
PSYCHOLOGICAL
FACTORS
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13. NEURODEVELOPMENTAL HYPOTHESIS-
Schizophrenia is a disorder of brain development at
any time of life – prenatal, adolescent or the
interaction between the two.
CURRENT ETIOLOGICAL
HYPOTHESIS
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14.
ABERRANT CONNECTIVITY HYPOTHESIS – Activities of
different brain regions / circuits is aberrant in schizophrenia.
STRESS VULNERABILITY MODEL( Syn- STRESS
DIATHESIS MODEL )
It incorporates development ,but emphasizes the
interaction of early events (genetic/biological/social) with later
stressors (substance use/ Life events).
Early factors confer vulnerability to develop Schizophrenia
, while the latter stressors explains onset and course.
CURRENT ETIOLOGICAL
HYPOTHESIS(Contd..)
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