PSY2003 SEMESTER 1 - WEEK 2 Flashcards
what are copy number variants (a specific genetic factor) and what other diagnosis may they cause
hereditable component
also associated with ASD. may have no symptoms or meet criteria for range of diagnosis
where are CNV (copy number varients) found
16p11.2 section of chromosome contain genes importantly associating with brain development
CNV here means deletion or duplication of this section of chromosome
if deleted or duplicated, individual has similar effect. need midpoint (just right)
outline neuropathology in sz aside from dopamine
smaller cortex and hippocampus, temporal lobe degeneration, large ventricles, frontal cortex
where is severe loss found in early onset sz (from longitudinal MRI, Thompson 2001)
3-5% annually, in parietal, motor, temporal
normal pruning in grey matter frontal cortex but larger loss in sz
what is grey matter loss paired with for sz (especially for parietal, frontal)
behavioural symptoms (parietal loss leads to attentional issues, frontal loss decision-making impairment)
when is normal age of sz onset
18-25
where does COS (childhood onset schizophrenia) start, where does deterioration spread
right parietal sensorimotor cortex signif faster deterioration
visuopatial, associative thinking, then dorsolateral, prefrontal, temporal, sensorimotor, dorsolateral cortex, finishes at frontal eye fields
for childhood onset schizophrenia, aside from parietal lobe deterioration, what else occurs
overall deterioration of global functioning
failure of normal maturation in neurological tests
pre/postnatal disturbance in neuronal migration and synaptic pruning
in COS what does deterioration in parietal region associated with (symptoms and impairments)
correlate with severity of symptom and mirror neuromotor, auditory, visual search, frontal EF impairment
outline role of genetics in COS
mz twin shows environmental factors trigger deficit in pareital, motor cortex are first to develop
what is not seen in non-sz-psychosis (NOS) and what can this suggest
no temporal lobe deficit, suggests wave of disease progression into temporal cortex is specific to sz regardless of treatment, gender and IQ
what is faster loss in superior temporal gyri/temporal cortex associated with
more severe positive symptoms (hallucinations, delusions)
what is faster loss in frontal cortex associated with
severe negative symptom= flat affect, poverty of speech
consistent with physiological hypothesis of negative symptoms due to reduced dopaminergic activity in frontal
explain prodromal
period between appearance of initial symptoms and full sz development
what is activated less in sz in motor tasks
sensorimotor cortex, supplementary motor areas
what is easier to link to neuropathology than hallucination/delusion
cognitive symptoms (attention, decision-making)
name 2 methods of studying cognitive aspect of sz
eye-tracking
Wisconsin card sorting task