Biological explanations for schizophrenia Flashcards

1
Q

What is genetic explanation of schizophrenia?

A

We can inherit schizophrenia from our parents.

  • there are particular gene alleles associated with schizophrenia.
  • it doesn’t suggest that there are single gene allele that causes schizophrenia there are alleles of multiple genes that are associated with risk of developing schizophrenia.

-these alleles are called genetic risk alleles.
- the more genetic risk allele that a person carries the more likely that they will develop schizophrenia

  • according to genetic explanation if your mother, father or uncle has schizophrenia then your more likely to inherit it but if you carry a gene allele doesn’t mean you definitely get it because it depends on other genes you carry and environmental factors.
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2
Q

What is evidence supporting genetic explanation?

what is weakness of this study?

A

twin studies

  • gottersman and shields conducted a twin study looking at concordance rate for schizophrenia in monozygotic and dizygotic
  • concordance for mz= 74%
    concordance rate for dz= 24%
  • there large difference between concordance rate between mono and dio indicates that genetic contributes to schizophrenia.
  • but since concordance rate for mono isn’t 100% shows that environment must also play role in schizophrenia.

evaluation:
one weakness of twin study is that it assumes mz and dz twins have similar amount of shared environment. but this might not be true as identical twins are more likely to be treated the same than dizygotic twins. this shows that high concordance rate might be caused by shared environmental factors

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3
Q

what is neural correlates explanations of schizophrenia?

what is support for neural studies?

what is 2 limitation?

A

they say that schizophrenia is caused by abnormal brain structure for e.g people with schizophrenia have larger ventricles than normal and have smaller frontal cortex.

in 2002, Torrey looked a mri scans of brain of schizophrenics. he compared their brains to healthy control group who didn’t have schizophrenia.
- he found participants with schizophrenia had 15% larger ventricles than average compared to control group

limitation: correlation between schizophrenia and brain abnormalities such as enlarged ventricles doesn’t necessarily mean brain abnormalities cause schizophrenia for instance the enlarged ventricles might be a side effect in taking medications.

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4
Q

dopamine hypothesis?

what is dopamine?

A

dopamine IS neurotransmitter that plays a role in attention and processing reward.

  • people with schizophrenia have high level of dopamine than normal. these dopamine are located in basal ganglia as well surrounding brain regions.
  • these brain region are mesolimbic system.
  • dopamine has excitatory affect meaning that neurones will generate more electrical activity than normal and this causes overactivity in mesolimbic system
  • overactivity causes people to experience hallucinations and delusions.
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5
Q

what does revise dopamine hypothesis say ?

A

says that there are high levels of dopamine in mesolimbic PATHWAY causing overactivity in this region.
- this lead to positive symptom of schizo

  • there are also low levels of dopamine in frontal cortex leading to underactivity in this region and this leads to negative symptoms
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6
Q

what is strength of dopamine hypothesis?

A

support from drug studies
- drug studies show that drugs that increase dopamine like amphetamines cause hallucinations and delusions and drugs that reduce dopamine reduce likelihood delusions and hallucinations in patients with schizophrenia.

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7
Q

what is biological treatment for schizophrenia?

how does it work?

A

antipsychotic drugs = decreases dopamine levels

antipsychotic drugs bind to post synaptic dopamine receptors but don’t allow electrical charge.

this prevents dopamine from binding to receptors which reduces overactivity of neurones and thus reduce overactivity causing positive symptoms

limitation: causes side effects. the drugs cause extra pyramidal symptoms which involves a loss of control in movement to stiff jerky movements and causes other problems such as increased heart problems, obesity and diabetes.

limitation: don’t treat negative symptoms because negative symptoms is caused by low level of dopamine in frontal cortex therefore antipsychotic drugs reduce dopamine and don’t increase it.

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8
Q

difference between typical and atypical antipsychotic drugs?

what is support for atypical antipsychotic drugs ?

A

typical = bind to post synaptic dopamine receptors for a very long time

atypical = newer antipsychotic drugs that bind to post synaptic dopamine receptors for a short period.
- fewer side effects and might also help to treat negative symptoms.

leucht conducted a meta analysis of 65 studies into the effectiveness of antipsychotic drugs and compared them to placebo found that antipsychotic drugs were more effective in treating schizophrenia than placebo pills and patients taking drugs were less likely to relapse.

  • Crossley conducted a meta analysis of 15 studies comparing typical and atypical drugs and found no difference however atypical had significantly fewer side effects than typical psychotics as there were no extra pyramidal symptoms
  • patients are likely to relapse if they stop taking drugs so might not be treating the underlying cause of schizophrenia they may just be blocking the symptoms
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