Schizophrenia: topic 3 ‘biological explanations of SZ’ Flashcards

1
Q

what is the genetic explanation of SZ

A
  • SZ is passed on from one generation to the next through genetic inheritance
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2
Q

who has an increased chance of developing SZ from genetics

A
  • closer degree family members to the schizophrenic = higher chance of developing the disorder
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3
Q

what gene is thought to be responsible for the development of schizophrenia?

A
  • no one gene is thought to be responsible for the development, it is more likely that different combinations of genes make individuals more vulnerable
  • believed to be polygenic
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4
Q

where does much of the evidence for this explanation come from? what are they used for?

A
  • twin, family and adoption studies
  • these studies are used to establish a concordance rate (or the degree to which relatives share the same disorder)
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5
Q

example of how a twin study can be used for schizophrenia

A
  • identical (monozygotic) and non-identical (dizygotic) twins where one of each twin pair has SZ can be compared to see how often the other twin also shows the illness
  • if SZ is genetic then it is argued that monozygotic twins should have higher concordance rates for the disorder than dizygotic twins
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6
Q

evidence to support genetic explanation from family studies + HOWEVER

A
  • varma found that 16% of the first degree relatives of schizophrenics developed SZ compared to only 7% of the controls
  • this supports the genetic explanation because it suggests that the more genetically related you are to someone with schizophrenia, the more likely you are to develop the disorder, supporting that SZ is inherited
  • it could be argued that the increased rate of SZ amongst those with parents with SZ was due to environmental rather than genetic influence
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7
Q

evidence to support genetic explanation from twin studies + HOWEVER

A
  • joseph found a concordance rate of 40% for MZ twins compared to just over 7% for DZ twins
  • this suggests SZ may be in part genetic
  • however the concordance rate for MZ twins is not 100% therefore there must be other possible explanations for development of SZ
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8
Q

evidence to support genetic explanation from adoption studies + HOWEVER

A
  • tienari compared adopted children whose biological mother had SZ compared to a control group with no genetic risk
  • found much higher rate of SZ amongst those whose biological mothers had SZ
  • this suggests that even when the environmental influence of the biological mother was removed, the genetic risk was still evident
  • however, it was found that a ‘healthy’ adopted family could protect against those with a high genetic risk developing SZ suggesting the environment does play a role in SZ onset as well
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9
Q

what is the neural correlates explanation of schizophrenia

A
  • the idea that the experience of a mental illness is associated (or correlated) with abnormalities to structure or function of the brain
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10
Q

what did early research find about the brain structure of schizophrenics?

A
  • enlarged ventricles (the fluid-filled gaps between brain areas)
  • enlarged ventricles are especially associated with damage to central brain areas and the prefrontal cortex, which recent scanning studies have also linked to the disorder
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11
Q

what is the dopamine hypothesis?

A
  • a neural correlate explanation of schizophrenia
  • suggests that the positive symptoms of schizophrenia are the result of overactive transmission of the neurotransmitter dopamine
  • schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing
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12
Q

what do dopamine neurons do? what happens if there is a disturbance in this process?

A
  • play a key role in guiding attention, so disturbances in this process may well lead to the problems relating to attention, perception and thought found in people with SZ
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13
Q

What is the revised dopamine hypothesis? who revised it?

A
  • Davis and Kahn
  • proposed that the positive symptoms of SZ are caused by an excess of dopamine in the sub cortical areas of the brain (mesolimbic pathway)
  • negative symptoms are thought to arise from a deficit of dopamine in areas of the pre frontal cortex (mesocortical pathway)
  • suggests that dopamine has an important but complex role in the development of SZ
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14
Q

evidence for dopamine hypothesis from drug research (2)

A
  • amphetamine drugs are dopamine agonists which means that they stimulate neurons containing dopamine, causing the synapse to be flooded with this neurotransmitter
  • it has been found that large doses of these drugs cause hallucinations and delusions similar to the symptoms seen in SZ
  • similarly, research has shown that L-dopa, a drug used to treat Parkinson’s disease which also works by raising levels of dopamine, can also result in symptoms similar to positive symptoms of SZ
  • this suggests that an excess of dopamine in the brain could explain the onset of some of the positive symptoms of SZ
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15
Q

support for the dopamine hypothesis - practical applications + HOWEVER

A
  • practical applications in developing treatments for schizophrenia
  • typical antipsychotic drugs used to treat SZ are all dopamine antagonists
  • reduces stimulation of neurons containing dopamine by blocking D2 receptors and therefore reducing positive symptoms such as hallucinations and delusions
  • this is positive as it shows the dopamine has been useful in developing treatments that benefit people’s lives and also supports the theory that dopamine overactivity is a key in explaining SZ because reducing levels reduces symptoms
  • however, newer antipsychotic drugs called atypical antipsychotics only temporarily block dopamine receptors whilst also acting in serotonin receptors and these drugs have been shown to be more effective than the typical antipsychotics in reducing SZ symptoms
  • this seems to suggest that the dopamine hypothesis is too simplistic as other neurotransmitters nay also be implicated in the development of SZ and they may interact to cause symptoms
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16
Q

problem with neurocorrelates explanation

A
  • the cause and effect is unclear
  • brain abnormalities could be the effect rather than the cause of SZ
  • for example, it could be the symptoms that cause changes in the brain function
  • this is a problem as we do not fully understand the role of these neural correlates in the development of schizophrenia
17
Q

evaluation of all overall biological explanations of schizophrenia being determinist (positive and negative)

A
  • overall, all biological explanations of SZ could be said to be determinist, this means that SZ is caused by factors (neural correlates or genes) outside of a sufferers control
  • this could be viewed both positively and negatively
  • on the one hand, biological explanations could be said to be more humane because it removes the blame from the patient for developing the disorder
  • on the other hand, a biologically determinist explanation could have a negative impact because if an individual feels that they have no control over developing the disorder, they may engage in risk taking behaviours (eg substance abuse) which could in turn trigger the onset of SZ
18
Q

evaluation of all overall biological explanations of schizophrenia being reductionist

A
  • they focus wholly on internal factors (eg genes and neurochemistry) and ignore environmental factors
  • there are psychological explanations of SZ such as family explanations which argue that the way parents treat their child is the main influence on SZ onset
  • as a result, biology alone may not explain all aspects of SZ