schizophrenia

Question 1

what are the 3 categories of SZ symptoms?

Answer 1

positive, negative and cognitive

Question 2

describe the difference between the different categories of SZ symptoms?

Answer 2

positive = emerges after 3 years, extra behaviours, thought disorders, delusions (persecution, grandeur or control), hallucinations
negative = 1st to emerge, absence of regular behaviours, social withdrawal, poverty of speech, flattened emotional response
cognitive = 2nd to emerge, difficulty sustaining attention, poor problem solving and abstract thinking

Question 3

what are sensory motor gating deficits, and describe a study which supports it as a cognitive symptom of SZ?

Answer 3

difficulty screening out irrelevant stimuli and focusing on salient ones
p50 signal in ERPs (event related potentials) - 2 auditory stimuli presented 500ms apart. healthy response = p50 wave to 2nd stimulus is 80% diminished, sz = there is no change

Question 4

describe structural difference in sz patients

Answer 4

weinberger and wyatt 1982
ct scans of 80 sz patients and 66 healthy controls of the same age
ventricle size of sz was 2x as big as healthy
sz had reduced brain volume(less grey matter) in temporal and frontal lobes and hippocampus
sz has faulty cellular arrangement in cortex and hippocampus

Question 5

what is the evidence of heritability in sz?

Answer 5

DISC1 = very rare and not unique to sz, but its presence increases chance of sz by 50x
paternal age = children with older fathers are more likely to develop sz

Question 6

describe the early neurodevelopmental model

Answer 6

events in prenatal life cause deviations from normal neurodevelopment which lie dormant until the brain matures and begins using the affected systems

Question 7

describe the late neurodevelopmental model

Answer 7

sz may result from deviation from normality in adolescence when synaptic pruning takes place

Question 8

what is the two-hit model?

Answer 8

combines the early and late neurodevelopmental model

atypical development in sz takes place in two critical time periods: early brain development and adolescence

Question 9

what is the evidence that dopamine is involved in the development of sz?

Answer 9

overactivity in mesolimbic systems = positive symptoms
underactivity in mesocortical systems = negative and cognitive symptoms
DA agonists induce psychosis

Question 10

what are the problems with the DA hypothesis of sz?

Answer 10

it only explains part of sz - positive but not negative symptoms

Question 11

how do new atypical antipsychotics work?

Answer 11

work in treatment resistant patients

have a low affinity for d2 receptors so there are no parkinsonian side effects

Question 12

describe clozapine?

Answer 12

the first atypical antipsychotic drug, is highly effective but not widely used, is the only antipsychotic to reduce suicide rates in sz, has many side effects including neutropenia

Question 13

what is the glutamate hypothesis of sz?

Answer 13

sz is caused by a NMDA receptor dysfunction.
evidence = pcp and ket can cause positive, negative and cognitive symptoms - both are nmda receptor antagonists
can explain why there are so many treatment resistant cases, why onset is in early adulthood, why sz is associated with structural changes and cognitive deficits

Question 14

what is the neuroinflammatory hypothesis of sz?

Answer 14

the brain’s immune cells (microglia) are hyperactive in people who are at risk of developing sz
symptoms are reversed with treatment with antipsychotics or antibiotics that reduce microglial activation
supports the evidence showing that prenatal or perinatal infections increase the risk for sz