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Psychology: Schizophrenia > Biological And psychological > Flashcards

Biological And psychological Flashcards

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1
Q

Genetic basis of SZ

A
  1. SZ runs in famailies
  2. Strong relationship between genetic similarity and likelihood of developing SZ
  3. 48% identical twins
  4. 17% non-identical
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2
Q

Candidate genes

A
  1. Appears to be aetiologically heterogenous (different combos lead to SZ)
  2. Genes include those that code for a number of neurotransmitters
  3. Ripke
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3
Q

Describe Ripkes study into candidate genes

A
  1. Genome wide study
  2. Genetic make up of 37,000 patients compared with 113,000 controls
  3. 108 genes associated with SZ
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4
Q

Dopamine hypothesis

A

Dopamine Systems seem to be faulty

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5
Q

What is the original hypothesis

A
  1. Hyperdopaminergia in the sub cortex
  2. Possible high levels of dopamine
  3. Such as high numbers of dopamine receptors in Broca’s area may be associated with speech poverty
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6
Q

What is the updated hypothesis

A
  1. Hypodopaminergia in the cortex
  2. Low levels of domapine identified in the prefrontal cortex (decision making) could cause the negative symptoms
  3. Could be that both are correct
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7
Q

Neural correlates

A

These are measurements of structure and function of the brain that correlate with experience

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8
Q

Neural correlates of negative

A
  1. Avolition is loss of motivation
  2. Ventral striatum inloved In reward system
  3. Lower levels of activity in striatum in SZ than in controls
  4. Moreover a negative correlation between levels of activity and severity of overall negative symptoms
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9
Q

Neural correlates of positive symptoms

A
  1. Brain scans of those who experience auditory hallucinations and compared to control
  2. Had to identify pre-recorded speech as their own of others
  3. Lower activity in the superior temporal gyrus were found in hallucination group
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10
Q

Multiple sources of evidence for genetic susceptibility

A
  1. Gottesman: showed relationship between shared genes and genetic vulnerability
  2. Adoption studies
  3. Ripke et al into candidate genes
  4. All these studies genetic susceptibility is important
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11
Q

Describe the concordance rates in Gottesmans study

A

Identical: 48%, 100% genes
Non-identical: 17%, 50% genes
Children: 13%

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12
Q

evidence for dopamine hypothesis

A
  1. Inflammatory response
  2. Dopamine agonists such as amphetimans can produce SZ like symptoms
  3. Antipsychotics work by reducing dopamine
  4. Radioactive tags on chemicals needed to make dopamine taken up faster than in controls
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13
Q

Evidence against dopamine hypothesis

A
  1. Some genes identified don’t code for dopamine
  2. New focus on glutamate neurotransmitter
  3. So there is mixed evidence for hypothesis
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14
Q

Correlation-causation problem

A
  1. Number of neural correlates for SZ
  2. Is it these areas cause the symptoms or is there a 3rd factor that causes both
  3. For instance reduced activity in striatum may inhibit it’s development
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15
Q

What are the 3 family dysfunction explanations

A
  1. Schizophrenigenic mother
  2. Double-bind
  3. Expressed emotion
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16
Q

Outline SZgenic mother

A
  1. Psychodynamic Explanation based on accounts of early childhood from patients
  2. Lots spoke of a particular parent type
  3. Cold, rejecting and controlling
  4. Creates a climate of tension and secrecy
  5. Leads to distrust that develops into paranoid delusions and then SZ
17
Q

Outline double bind

A
  1. Emphasis on communication style within the family
  2. Child receives mixed messages
  3. Punished with withdrawal of love
  4. Leaves them with feeling the world is confusing and dangerous which turns into disorganised thinking and paranoid delusions
  5. Suggested this was just a risk factor
18
Q

Expressed emotion

A

Several elements involved

19
Q

Outline expressed emotion

A
  1. Verbal criticism of patient
  2. Hostility, inc anger and rejection
  3. Emotional over involvement in life of patient (needless self-sacrifice)
    All of these cause stress to patient which can cause a relapse
    OR can cause of there is a genetic vulnerability
20
Q

What is a cognitive explanation

A

Anything that focuses on the role of mental processes

21
Q

What two areas have reduced processing

A

Negative symptoms: ventral striatum
Positive: temporal and cingulate gyri
These suggest cognition is impaired

22
Q

What are the two kinds of dysnfctional thought processing

A
  1. Metarepresentation

2. Central control

23
Q

Describe metarepresnation

A
  1. This is the cognitive ability to reflect on thoughts and behaviours
  2. Allows us insight into our own and others intentions
  3. Faulty MR would affect our ability to be able to identify our thoughts as our owns rather than someone else’s
24
Q

Describe central control

A
  1. Ability to be able to suppress automatic responses

2. Disorganised speech and thought could be an inability to suppress things

25
Q

Evidence to support family dysfunction as a risk factor

A
  1. Study reviewed 46 studies of child abuse and SZ
  2. Concluded that 69% of adult women patients had a history of physical and/or sexual abuse in childhood
  3. For men the figure is 59%
  4. Men with ‘insecure attachment’ also more likely to have SZ
26
Q

Problem with validity into evidence for family dysfunction

A
  1. Information about childhood gathered after development of symptoms
  2. SZ may have distorted recall
  3. Although there is some evidence collected before symptoms but is quite weak
27
Q

Weak evidence for SZ mother or Double bind

A
  1. Both these theories based on clinical observations
  2. Personality of mothers assessed by ‘crazy-making charactisrics’
  3. Leads to parent blaming which can be psychologically damaging
28
Q

Strong evidence for dysfunctional informational processing

A
  1. 30 SZ compared with 18 non-SZ controls
  2. Given a rage of cognitive tasks such as stroop test SZ took twice as longer
  3. Patients struggled to suppress saying the colour the word spelt suggesting central control dysfunction
29
Q

What’s the problem with cognitive explanations of SZ

A

Can explain causes of symptoms but tell us very little about the causes

30
Q

Describe anti-psychotics

A
  1. Tablet, syrup or injection (2-4 weeks)
  2. Short or long term (for life)
  3. Divided into typical and atypical
31
Q

Describe typical antipsychotics

A
  1. Associates with dopamine hypsies
  2. Act as antagonists in dopamine system
  3. Reduced activity of dopamine by blocking receptors
  4. Initially dopamine builds up but then levels out
  5. Aims to normalise transmission in key areas of the brain
  6. Used for sedative propoties
32
Q

What’s the main typical antipsychotic

A

Chlorpromazine

33
Q

Name 2 atypical antipsychotics

A

Clozapine

Risperidone

34
Q

Describe Clozapine

A
  1. Used when other treatments fail
  2. Can give blood poisoning so regular blood tests required
  3. Binds to receptors of domaine as well as serotonin and glutamate
  4. Improved mood and cognitive function
  5. Good for the 50% of patients who are suicide
35
Q

Describe Disperidone

A
  1. Same as Clozapine but without the dangerous side effects

2. Binds in same way as clozapine but more strongly to dopamine so need less

36
Q

Evidence for effectiveness of typical antipsychotics

A
  1. Throley et al compared studies with Chlorpromazine and placebos
  2. Data from 13 trials with a total of 1121 patients
  3. Chlorpromazine was associated with better functioning and reduced symptom severity
  4. Data from 3 trials with 512 patients showed release rate was lower with Chlorpromazine
37
Q

Evidence for effectiveness of atypical antipsychotics

A
  1. Clozapine more effective than both typical and other atypical ones
  2. Effective in 30-50% of treatment resistant cases where typical had no effect
38
Q

Serious side effects

A

Typical:

  1. Insomnia
  2. Weight gain
  3. Tarditve dyskinesia: dopamine supersentivity (involuntarily facial movements)
  4. Dopamine blocking in hypothalamus can cause NMS which can cause a coma
  5. Atypical have less side effects

Psychology: Schizophrenia (6 decks)

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