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PS2028 - Mental Health & Clinical Psychology > schizophrenia > Flashcards

schizophrenia Flashcards

1
Q

how was SZ diagnosed in the 1800s?

A
  • neurodegenerative disorder in the young
  • cognitive impairment central to the concept
  • “madness” can be divided into small number of “diseases” with different types of brain pathology and different aetiologies
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2
Q

when was SZ coined and what did it mean?

A
  • 1908
  • a splitting of the mind, not personalities
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3
Q

what are positive symptoms of SZ?

A
  • additional to normal experience and behaviour
  • describe psychosis and include delusions, hallucinations and thought disorders
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4
Q

what are negative symptoms of SZ?

A
  • lack or decline in normal experience or behaviour
  • describe inappropriate or non-present emotion, poverty of speech and lack of motivation
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5
Q

what does factor analysis do in regards to SZ symptoms?

A
  • into 3 semi-independent factors
  • hallucinations and delusions
  • negative symptoms
  • disorganised
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6
Q

what are hallucinations and delusions?

A
  • reality distortions- can occur in any modality
  • typically auditory
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7
Q

PP,FA

what are negative symptoms (+ affect type)?

A
  • psychomotor poverty
  • flattened affect
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8
Q

DB,IA

what are disorganised symptoms (+ affect type)?

A
  • disorganised behaviour
  • inappropriate affect
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9
Q

how to be diagnosed with SZ using DSM-5?

A
  • have at least 2 or more of characteristic symptoms, each present for sig. amount of time (e.g., delusions, hallucinations, negative symptoms)
  • must have social/occupational dysfunction for sig. amount of time in 1 or more areas of functioning (e.g., work, self-care)
  • duration = at least 6 months of symptoms
  • substance exclusion
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10
Q

how are pp’s asked to rate severity of symptoms in DSm-5?

A
  • each of the five characteristic symptoms, DSM-5 gives guidelines as to how to rate their severity
    from 0-5 (highest severity)
  • also asked to rate depression and mania
  • to help clinicians out
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11
Q

what are some limitations of using DSm-5 to diagnose SZ?

A
  • ignores cognitive symptoms even though they are highly present in SZ
  • lack of clear distinctions between the various subtypes
  • subtypes have poor diagnostic stability over-time
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12
Q

risk factors for SZ: gender?

A

males lower age at first episode (24.5 vs 28)

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13
Q

risk factors for SZ: social class?

A

highest rates in lowest socioeconomic class and found in inner city areas

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14
Q

risk factors for SZ: urbanisation?

A
  • prevalence of SZ in Chicago
  • rates increase closer to city centre
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15
Q

risk factors for SZ: immigrant groups?

A
  • unusually high rates of SZ found in variety of groups
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16
Q

what are some perinatal risk factors of SZ?

A
  • linked with winter births
  • stress in pregnancy
  • low birth weight
  • pregnancy complications
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17
Q

what might a family environment look like that could provoke onset of SZ?

A
  • lots of critical comments
  • hostility
  • over-concern
  • over-protectiveness
  • high expressed emotion = higher relapse rates
  • childhood trauma may play causal role in development of SZ
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18
Q

what did studies find regarding the neurodevelopmental perspective of SZ acquisition?

A
  • more neuromotor problems, less positive facial expressions, odd hand positions
  • fewer than 2 friends; prefer socialising in small groups; more sensitive than other people; no
    steady girlfriend; ever used drugs (incl. cannabis); low IQ
  • deficits in social function, low IQ, lack of organisation ability
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19
Q

how does recreational drug use affect SZ onset?

A
  • cannabis linked to higher SZ risk
  • heavy use by age 18 associated with risk increase x6
  • issue of causality = those at risk may be more likely to use cannabis
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20
Q

what do adoption studies find about SZ?

A
  • adopted cases admitted for SZ versus control group of adoptees not admitted
  • significantly higher rates of psychotic admissions in biological parents than adopted parent
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21
Q

what was the first risk gene of SZ and what developments have been made in identifying genetics in SZ?

A
  • neuregulin 1
  • new candidate genes still emerging
  • ‘SZ gene’ findings are not well replicated and a complex POLYGENIC picture is emerging
  • increasing notion that genetic risk not specific for SZ, but for other psychiatric disorders as well – e.g. autism spectrum disorder, ADHD
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22
Q

what are some broad conclusions from the psychiatric genomics revolution?

A
  • psychiatric disorders are polygenic i.e. many
    genes involved
  • extensive pleiotropy at level of clinical
    diagnosis
  • increasing evidence for convergence onto
    plausible biological systems, e.g,. glutamate
    neurotransmission
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23
Q

psychiatric genomics revolution: what is pleiotropy?

A
  • occurs when one gene influences multiple, seemingly unrelated phenotypic traits
  • an example being phenylketonuria, which is a human disease that affects multiple systems but is caused by one gene defect
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24
Q

what do GWAS implicate regarding SZ?

A
  • many alleles of small effect in SZ
  • many hundreds of genetic variants contribute to risk
25
Q

how do genes operate across diagnostic categories?

A
  • common alleles (polygenes)
  • rare alleles (CNVs mainly so far)
  • increasing evidence for familial overlap including impairments of cognition, developmental delay, motor abnormalities and significant co-morbidity
  • genes are not specific for conditions
  • more CNVs someone has = greater risk of SZ episode or diagnosis
26
Q

genes & diagnostic categories suggest a need for … ?

A

greater phenotypic specificity

27
Q

how do CNVs relates to SZ?

A
  • specific, recurrent but rare CNVs confer relatively high risk of SZ
  • CNV can be addition or deletion of sections of DNA
28
Q

what evidence has been presented to support the polygenic model?

A
  • papers strongly supporting the polygenic model – need to reach threshold with common
    alleles of small effect
  • found a polygenic burden
    primarily arising from rare mutations distributed across many genes (cluster on synaptic plasticity/transmission)
  • convergence onto synaptic networks - glutamate hypothesis
29
Q

what is the link between the introduction of drugs and mental hospital attendance?

A
  • neuroleptic drugs were introduced in 1950s
  • decline of people being admitted to mental hospital is correlated with drugs introduced
  • along with social pressures, better understanding and better community care (80/90s)
  • drugs primarily treat positive symptoms but awful side effects
30
Q

what are the effects of anti-psychotic drugs?

A
  • drugs not targeted at specific brain regions, act generally
  • affect dopaminergic and glutamate NTs
  • many people improve after using drugs but some people also just get better from taking placebo
31
Q

what is the dopamine hypothesis and what are the observations it is based on?

A
  • based on 3 primary observations
  • pharmacology (chlorpromazine found to be helpful for SZ and block dopamine receptors)
  • amphetamines (linked to excess dopamine, can lead to psychosis including paranoia)
  • Parkison’s disease (less dopamine in basal ganglia, drug L-Dopa used to increase dopamine side-effects but side effects = psychotic episode in people with PD)
  • it is a bit dated (1960s)
  • dopamine receptors = 5 subtypes and an increase in D2 receptors
32
Q

domaine hypothesis: why is it hard to use post-morterm studies?

A
  • hard to interpret findings
  • people may have been taking medication
33
Q

how is COMT involved in the dopamine hypothesis?

A
  • candidate gene for SZ
  • located on chromosome 22
  • involved in metabolism of dopamine
  • helps maintain appropriate levels of neurotransmitters in the PFC
34
Q

what is the glutamate hypothesis?

A
  • increasing evidence for other NTs
  • ketamine is a glutamate antagonist which induces hallucinations and cognitive changes consistent with SZ
  • DA receptors inhibit release of glutamate leading to under-activity of glutamate receptors
35
Q

why are enlarged ventricles important in SZ people?

A
  • they are an indicator of a reduction in the amount of brain tissue
  • enlarged ventricles imply that the brain areas that border the ventricles have shrunk/decreased in volume
  • enlarged ventricles not found in all people with SZ, also found in AD, Huntington’s
36
Q

how do SZ people perform on neuropsychological tests?

A
  • poor performance on range of tests
  • attention problems on continuous performance tests and eye tracking dysfunction
  • similar deficits observed in 1st degree relatives
37
Q

how did 1st episode patients perform on neuropsychological tests vs controls and what are the implications of this?

A
  • first episode SZ compared to IQ matched controls
  • multiple deficits in executive function, processing speed and verbal memory
  • increasing impetus to the idea that cognitive changes (which form no part of DSM) maybe integral to aetiology of SZ
38
Q

how does white matter in brain link to SZ people?

A
  • nerve fibers are covered in myelin
    sheath-acts as an insulator & increase speed/efficiency of conduction btw nerve cells (brain connectivity)
  • SZ = reduction in white matter volume found in 1st episode and at risk people
  • white matter changes in temporal area predict later social functioning
  • also reduction of white matter in children of SZ people
39
Q

where is the structural damage in SZ people in the brain?

A
  • amygdala (emotion), hippocampus (memory), thalamus (sensory input) and frontal lobes
  • reduction in amygdala
40
Q

are structural brain alterations unique for SZ people only?

A
  • NO
  • alteration in brain regions for SZ also implicated in other disorders (severe mood disorder, PTSD)
41
Q

what do PET scans show about wide spread brain abnormalities in SZ people?

A
  • show hypoactivity in brain of a person with SZ
  • prefrontal hypoactivity in SZ twin (under-activity)
42
Q

what can we seen in the frontal cortex in SZ people regarding wide spread brain abnormalities?

A
  • reduced blood in frontal cortex during Wisconsin card sorting task
  • impaired functioning of frontal lobes during cognitive tasks and in pp’s in early stage of disorder and at high risk of SZ
43
Q

what are some critiques of the brain abnormalities theory?

A
  • pharmacology more effective for positive than negative symptoms
  • 1/3 patients don’t respond to treatment
  • not all studies find differences in DA receptors and/or alternations in brain functioning
  • dopamine abnormalities may be due in part to the brain’s response to trauma
  • bi-directional influence between brain / chemicals and the environment
44
Q

what did the Finish adoptive study of SZ find?

A
  • followed up adoptive children of women hospitalised for SZ between 1960-79 vs. adoptive children without a diagnosis of SZ
  • studied degree of adversity in adoptive family environment
  • only adoptive children who were raised in dysfunctional families AND had high risk of SZ went on to develop SZ
45
Q

what did gene x environment interaction find in regards to SZ?

A
  • children at high genetic risk in healthy family environment similar to controls
  • concordance in MZ twins limited to 50% therefore also role of environment
  • epigenetics – MZ twins who are discordant for SZ show differences in gene expression
  • only people had a parent with SZ AND had birth complications showed brain abnormalities (enlarged ventricles)—deficits worse if both parents had SZ
  • genetic risk for SZ associated with smaller brain volume—those who develop SZ suffer additional brain abnormalities that aren’t genetic
46
Q

what is the diathesis stress model of SZ?

A
  • diathesis = genetic vulnerability leading to brain abnormalities and/or disturbed NT functioning
  • PLUS potential stress factor = (prenatal trauma, birth complications, harsh family environment, stressful life environment)
  • linked with potential protective factors = (healthy communicative style within family, nurturing family environment, low level of life stress)
  • EQUALS SZ
47
Q

what are the assumptions about the course and outcomes of SZ?

A
  • assumption that a diagnosis of a “psychotic illness” means a lifetime of illness and
    disability but the course and outcome are highly variable
  • “social recovery” occurs in 40-45% of cases
  • outcome generally better in developing countries than in the west due to greater social inclusion, quicker return to valued roles, less stigmatisation, increased optimism, community involvement etc.
48
Q

what are the cognitive factors of SZ?

A
  • negative symptoms of SZ associated with
    lower self-esteem and negative self-concept about interpersonal abilities
  • psychotic disorders appear to reflect low self- esteem and that this might make people feel they ‘deserve’ to be persecuted
49
Q

what are the cognitive processes seen in people with SZ?

A
  • study showing people with diagnosis of
    SZ appear to have a bias against disconfirmatory evidence
  • meta-analysis showing people with psychosis require less information to make decisions (‘jumping to conclusions bias’)
50
Q

what is the aim of the cognitive model of SZ?

A
  • aim to develop model of cognitive processes that lead to positive symptoms and to integrate with social factors
  • incorporates disruption in automatic cognitive processes and maladaptive conscious appraisals
  • covers delusions and hallucinations and posits a central role for emotion
51
Q

what is the background of the cognitive model of SZ?

A
  • occurs in people of vulnerable disposition & typically follows adverse event/illicit drugs/isolation
  • social isolation contributes to psychotic appraisal
  • disruptions in attention, perception, judgement
  • at onset most prominent symptoms = delusional beliefs and hallucinations
  • trigger→disruption cognitive processes (weakening of influences of stored memory on current perception + difficulties with self-monitoring of intentions and actions)→emotional changes→search for explanation of cause
  • trigger→disturbed affect→activates biased appraisal processes and maladaptive schema
52
Q

how does CBT help people with SZ?

A
  • CBT encourages people to make links between thoughts, feelings and behaviours and helps to re-evaluate perceptions, beliefs and reasoning about targeted symptoms
  • gathering data to understand more about someone’s experiences
  • helping to explore the origins of one’s worldview (e.g., that others are out to get me)
  • helping access social support
  • learning tools for reducing the impact of voices (e.g., listening to music)
53
Q

what does Garety’s cognitive model of SZ help to explain?

A

explaining the development and maintenance of positive symptoms

54
Q

what does Morrison cognitive model of SZ help to explain?

A

explaining how people interpret anamalous experiences and how this ultimately maintains these experiences

55
Q

what does Freeman’s cognitive model of SZ help to explain?

A

explaining persecutory delusions

56
Q

what are the family interventions for SZ?

A
  • FI should be available to families who are living with someone with psychosis or who are in close contact with them
  • high levels of ‘expressed emotion’ (EE) within a family has been shown to be an effective predictor of relapse in SZ
  • high EE is harmful when it is associated with critical and hostile comments and emotional over- involvement towards the person with SZ
  • aim to change communication between the person with ‘schizophrenia’ and their close relatives e.g. reduce EE and ‘double bind’/deviant communication patterns
57
Q

why are psychological interventions an essential part of treatment?

A

for both relapse prevention and symptom reduction

58
Q

how to combat hearing voices in SZ?

A
  • voice identity
  • voice characteristics
  • triggers for the voices
  • history of the voices
  • person’s life history

PS2028 - Mental Health & Clinical Psychology (13 decks)

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