biological explanations for schizophrenia Flashcards

1
Q

concordance rate

A

refers to the extent to which a pair of twins share similar characteristics/traits

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2
Q

gottesman (1991)- meta anaylsis of family studies
- Procedure

A

12 studies, across 8 countries, ranging over 60 years with approx 2000 pairs of twins

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3
Q

gottesman (1991)
- Findings

A
  • if a parent suffers from schizophrenia, there there’s a 6% of developing it (compared to 1% of general population)
  • concordance rates for schizophrenia was 48% for MZ twins compared to 17% in DZ twins
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4
Q

gottesman (1991)
- Conclusions

A
  • genetics play a significant role in explaining schizophrenia
  • however, as MZ concordance rates are not 100%, there are clearly environmental factors as well
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5
Q

strengths of gottesman

A
  • the meta-analysis is large-scale and longitudinal, both contributing to validity
  • many other studies shown a genetic link e.g Tienari et al (2004), Ripke (2014)
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6
Q

weaknesses of gottesman

A
  • higher concordance rate between MZ twins could be explained by greater environmental similarity rather than genetic similarity,,, MZ twins elicit more similar treatment than DZ twins,,, always an issue with twin studies
  • studies in gottesman’s meta-analysis were from 1920s onwards, and had wide range of different methods for measuring twins and schizophrenia - questions both reliability and validity
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7
Q

candidate genes

A

genes that have been implicated in the development of schizophrenia

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8
Q

polygenic

A

schizophrenia is thought to be polygenic - its development is not determined by a single gene but a few (maybe as many as 108)

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9
Q

aetiologically heterogeneous

A

schizophrenia can be caused by a different combination of genes

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10
Q

the dopamine hypothesis

A

an imbalance or disregulation of dopamine has been implicated in the development of schizophrenia

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11
Q

hyperdopaminergia

A
  • excess levels of dopamine in the subcortex (central area of brain)
  • e,g brocas area
  • associated with disorganised speech and auditory hallucinations (positive symptoms)
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12
Q

hypodopaminergia

A
  • low levels of dopamine in prefrontal cortex
  • resulting in negative symptoms e.g avoliton
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13
Q

evidence: amphetamines and cocaine

A
  • dopamine agonists (increase)
  • large doses of these drugs cause hallucinations and delusions in non-schizophrenics and make schizophrenics worse
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14
Q

antipsychotic drugs

A
  • dopamine anatgonists (reduce)
  • eliminate hallucinations and delusions
  • by alleviating many of the symptoms of schizoprenia, antipsychotic drugs strengthen the case for dopamine being a significant contributory factor
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15
Q

evaluation of dopamine hypothesis

A
  • post mortems have revealed higher than normal levels of D2 dopamine receptors in the brain of schizophrenics
  • PET scans of schizophrenics have found similar results
  • dopamine hypothesis is simplistic as there are many more neurotransmitters involved - such as glutamate
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16
Q

neural correlates

A

refers to finding areas or circuits of the brain that are related to a specific behaviour or condition

17
Q

neural correlates of negative symptoms

A
  • lower levels of activity in the ventral striatum has been linked to the development of avoliton
  • ventral striatum: involved in the anticipation of a reward for certain actions
  • therefore, if there is abnormality in areas, such as the ventral striatum, then this would result in a lack of motivation (avolition)
18
Q

neural correlates of positive symptoms

A

reduced activity in the superior temporal gyrus and anterior cingulate gyrus have been linked to the development of auditory hallucinations

19
Q

evaluation summary

A
  • there is no conclusive explanation that account for all schizophrenics- research is difficult to interpret and there have been contradictory findings
  • difficult to establish cause and effect- as many participant studies have suffered from schizophrenia for a while and have been undergoing treatment
  • biological explanations are reductionist in attempting to explain a complex multi-faceted disorder at the level of cells, genes, and chemicals - diathesis stress model