PSY2003 SEMESTER 1 - WEEK 2 Flashcards

1
Q

what are copy number variants (a specific genetic factor) and what other diagnosis may they cause

A

hereditable component
also associated with ASD. may have no symptoms or meet criteria for range of diagnosis

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2
Q

where are CNV (copy number varients) found

A

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)

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3
Q

outline neuropathology in sz aside from dopamine

A

smaller cortex and hippocampus, temporal lobe degeneration, large ventricles, frontal cortex

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4
Q

where is severe loss found in early onset sz (from longitudinal MRI, Thompson 2001)

A

3-5% annually, in parietal, motor, temporal
normal pruning in grey matter frontal cortex but larger loss in sz

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5
Q

what is grey matter loss paired with for sz (especially for parietal, frontal)

A

behavioural symptoms (parietal loss leads to attentional issues, frontal loss decision-making impairment)

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6
Q

when is normal age of sz onset

A

18-25

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7
Q

where does COS (childhood onset schizophrenia) start, where does deterioration spread

A

right parietal sensorimotor cortex signif faster deterioration
visuopatial, associative thinking, then dorsolateral, prefrontal, temporal, sensorimotor, dorsolateral cortex, finishes at frontal eye fields

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8
Q

for childhood onset schizophrenia, aside from parietal lobe deterioration, what else occurs

A

overall deterioration of global functioning
failure of normal maturation in neurological tests
pre/postnatal disturbance in neuronal migration and synaptic pruning

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9
Q

in COS what does deterioration in parietal region associated with (symptoms and impairments)

A

correlate with severity of symptom and mirror neuromotor, auditory, visual search, frontal EF impairment

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10
Q

outline role of genetics in COS

A

mz twin shows environmental factors trigger deficit in pareital, motor cortex are first to develop

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11
Q

what is not seen in non-sz-psychosis (NOS) and what can this suggest

A

no temporal lobe deficit, suggests wave of disease progression into temporal cortex is specific to sz regardless of treatment, gender and IQ

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12
Q

what is faster loss in superior temporal gyri/temporal cortex associated with

A

more severe positive symptoms (hallucinations, delusions)

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13
Q

what is faster loss in frontal cortex associated with

A

severe negative symptom= flat affect, poverty of speech
consistent with physiological hypothesis of negative symptoms due to reduced dopaminergic activity in frontal

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14
Q

explain prodromal

A

period between appearance of initial symptoms and full sz development

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15
Q

what is activated less in sz in motor tasks

A

sensorimotor cortex, supplementary motor areas

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16
Q

what is easier to link to neuropathology than hallucination/delusion

A

cognitive symptoms (attention, decision-making)

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17
Q

name 2 methods of studying cognitive aspect of sz

A

eye-tracking
Wisconsin card sorting task

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18
Q

outline patterns of eye-tracking for sz

A

control has smooth-pursuit responses but sz jerks about more and more saccadic

19
Q

in sz, what does eye-tracking visual search tasks suggest about neuropathology

A

frontal cortex fastest loss area of eye fields = attentional dysfunction

20
Q

in eye-tracking of sz, explain what impairments are in exploratory eye movements

A

stare more, difficulty in top-down control of selective attention, visual search

21
Q

apply wisconsin card sorting task to sz

A

sz and frontal lobe damage patients show impairment
making perseverance error, difficulty learning the rules

22
Q

apply habituation research (orientating response) to sz

A

prepulse inhibition paradigm: habituated to stimuli
sz struggle with habituating
loud noise (stimuli) = startle response
if quieter autitory tone before then prepulse has inhibited response to less startle response

23
Q

apply theory of mind to autism, and how autism can relate to sz

A

thought to be missing in autism
struggle to see things from different POV and other peoples thought processes
comorbidity with sz, but some believe are on opposite continuum end for aspects such as ToM

24
Q

what is ToM

A

ability to recognise we have different perceptions of world, others have different thought process
eg; know someone else doesn’t know we put ball in box, if they weren’t there to see it

25
Q

apply to ToM to sz

A

overactive/distorted ToM, cause delusion, paranoia, feel everyones persecuting them, including inanimate objects, lead to hallucination

26
Q

apply low SES to sz

A

low SES more likely to have sz diagnosis

27
Q

explain social drift of SES to sz

A

people with sz have difficulty with employment so drift down SES

28
Q

explain sociogenic hypothesis of SES to sz

A

lower SES cause more stressful life events, financial strain, family dysfunciton, less educational access, worse living condition

29
Q

evaluate why low SES may not be best explanation for sz

A

parental SES at time of birth is NOT associated with increased risk and higher SES also experiences stressors

30
Q

name 4 types of influence of family on sz

A

double bind
paradoxical communication
communication deviance
expressed emotion

31
Q

what is double bind impact of family on sz

A

verbal messages contradict implied message, which invalidates both

32
Q

what is paradoxical communication in family applied to sz

A

message contradicts itself
can include presence of no choice but illusion of choice
eg; angry “you know I love you”, crying and saying “I’m very happy”

33
Q

name 5 biases of sz

A
  1. cognitive bias
  2. attentional bias
  3. reasoning bias
  4. interpretational bias
  5. attributional bias
34
Q

what is cognitive bias in sz

A

over-report confrontational interactions

35
Q

what is attentional bias of sz

A

like anxiety, over attends to negative stimuli, and those relevant to delusions

36
Q

what is reasoning bias of sz

A

jumping to conclusions

37
Q

what is interpretational bias of sz

A

hearing voices

38
Q

outline Seligmans Attributional model

A

attributions for negative event, 3 dimension
internal vs external
global vs specific
stable vs unstable
if neg event interp as internal+global+stable = depression
if neg event interp as external+global+stable=delusions

39
Q

what combination of seligman attributions dimensions leads to depression

A

internal + global + stable

40
Q

what combination of seligman attributions dimensions leads to delusions

A

external + global + stable

41
Q

name treatments of sz

A
  1. social skills training
  2. CBT
  3. personal therapy
  4. cognitive remediation training
  5. family intervention
  6. community care
  7. pharmacology
42
Q

what is social skills training - treatment for sz

A

cope with everyday life skill

43
Q

what is CBT - treatment for sz

A

reattributions therapy
change cog bias regarding delusion/hallucination and help them work out delusion is not true

44
Q

what is family therapy - treatment for sz

A

psychoeducation, supportive family management, applied family management