Biological explanations for schizophrenia Flashcards

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1
Q

What are the two types of twins?

A
  • Identical (monozygotic)

- Fraternal (dizgotic)

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2
Q

What needs to be done in order to form identical twins?

A

One fertilised egg splits and develops two babies with the same genetic information

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3
Q

What did Gottesman (1991) find about MZ twins?

A

They have a 48% risk of getting schizophrenia
whereas
Fraternal twins have a 17% risk

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4
Q

What does the evidence from Gottesman’s study show?

A

That the higher the degree of genetic relativeness, the higher the risk of getting schizophrenia

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5
Q

What dod Benzel et al. (2007) find?

A

Three genese that have all been associated with excess dopemine in specifc D2 receptors

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6
Q

What are the three genes thay Benzel et al found?

A

COMT
DRD4
AKT1

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7
Q

What are the effects of the excess of specific D2 receptors?

A
  • Acute episodes
  • Positive symptoms
    > hallucinations
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8
Q

What did Miyakawa research?

A

DNA from human families affected by schizophrenia

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9
Q

What did Miyakawa find?

A

that those with the disease were more likely to have a defective version of a gene, called PPP3CC which is associated with the production of calcineurin which regulates the immune system

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10
Q

What has research by Sherrington et al. found?

A

a gene located on chromosome 5 which has been linked in a small number of extended families where they have the disorder

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11
Q

What does evidence suggest about the biological relationship and schizophrenia?

A

that the closer the biological relationship, the greater the risk of developing schizophrenia

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12
Q

What has Kendler (1985) shown?

A

That first degree relatives of those with schizophrenia are 18 times more at risk that the general population

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13
Q

What is a weakness of the genetic explanation of schizophrenia?

A

Methodological problems
Family, twin and adoption studies must be considered cautiously because they are retrospective, and diagnosis may be biased by knowledge that other family members who may have been diagnosed. This suggests that there may be problems of demand characteristics.

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14
Q

What is the issue with nature and nurture and schizophrenia?

A

It is very difficult to separate out the influence of nature-v-nurture
The fact that the concordance rates are not 100% means that schizophrenia cannot wholly be explained by genes and it could be that the individual has a pre-disposition to schizophrenia and simply makes the individual more at risk of developing the disorder. This suggests that the biological account cannot give a full explanation of the disorder.

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15
Q

What is an issue of the genetic explanation of schizophrenia?

A

biologically reductionist
The Genome Project has increased understanding of the complexity of the gene. Given that a much lower number of genes exist than anticipated, it is now recognised that genes have multiple functions and that many genes behavior. Schizophrenia is a multi-factorial trait as it is the result of multiple genes and environmental factors. This suggests that the research into gene mapping is oversimplistic as schizophrenia is not due to a single gene.

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16
Q

What is dopamine?

A

A neurotransmitter

17
Q

What does dopamine cause to happen in the brain?

A

Neurons to fire

18
Q

What did the orginal dopamine hypothesis state?

A

that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages.

19
Q

What does high dopamine activity lead to?

A

acute episodes, and positive symptoms which include: delusions, hallucinations, confused thinking.

20
Q

What is evidence for the dopamine hypothesis?

A

Large doses of amphetamine given to people with no history of psychological disorders produce behavior which is very similar to paranoid schizophrenia. Small doses given to people already suffering from schizophrenia tend to worsen their symptoms.

21
Q

What do amphetamines increase?

A

The amount of dopamine

22
Q

What does the second explanation suggest?

A

That it is not excessive dopamine but the fact that there are more dopemine receptors

23
Q

What does the increase in receptors mean?

A

That there is more firing and an over production of messages

24
Q

What have autopsies found?

A

found that there are generally a large number of dopamine receptors (Owen et al., 1987)

25
Q

What is a criticism of the dopamine hypothesis?

A

there is a problem with the chicken and egg. Is the raised dopamine levels the cause of the schizophrenia, or is it the raised dopamine level the result of schizophrenia? It is not clear which comes first. This suggests that one needs to be careful when establishing cause and effect relationships in schizophrenic patients.

26
Q

What does Farde et al criticise about the dopamine hypothesis?

A

no difference between schizophrenics’ levels of dopamine compared with ‘healthy’ individuals in 1990.

27
Q

What are neural correlates?

A

Patterns of structure or activity in the brain that occur in conjunction with schizophrenia

28
Q

What has been shown about people with schizophrenia’s brain?

A

abnormally large ventricles in the brain

29
Q

What are ventricles?

A

fluid filled cavities (i.e. holes) in the brain that supply nutrients and remove waste

30
Q

What is a strength of the research into enlarged ventricles and neurotransmitter levels?

A

High reliability
the research is carried out in highly controlled environments, which specialist, high tech equipment such as MRI and PET scans. These machines take accurate readings of brain regions such as the frontal and pre-frontal cortex, the basil ganglia, the hippocampus and the amygdale. This suggests that if this research was tested and re-tested the same results would be achieved.

31
Q

What is weakness of neuroanatomical explanations?

A

Biologically deterministic
The reason for this is because if the individual does have large ventricles then does it really mean that they will develop schizophrenia? This suggests that the dopamine hypothesis does not account for freewill.