schizophrenia paper 3

Schizophrenia

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This topic is one of three options for section C in A-level Paper 3 for AQA Psychology.

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Example Answers for Section C Schizophrenia Topic Paper 3 June 2018 (AQA)

Last updated 13 Aug 2018

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Here are a series of suggested answers for the Schizophrenia topic questions in AQA A Level Psychology Paper 3 (Section B) in June 2018.

Question 22 : (2 marks)

Comorbidity is when the same person has two or more disorders at the same time. For example, about 50% of people with schizophrenia are also diagnosed with depression.

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Question 23 : (2 marks)

System overlap refers to the way that disorders have shared symptoms. For example hallucinations are a symptom of both schizophrenia and bipolar disorder. This can lead to problems with reliability of diagnosis as one doctor might diagnose the person as having schizophrenia while another might diagnose bipolar disorder.

Question 24: (4 marks)

Group A’s scores suggest a normal distributed as the mean, median and mode are all almost the same (22). However, group B’s scores suggest a positively skewed distribution as the mean (26) is higher than both the median (22.5) and the mode (16).

Question 25 : (16 marks)

One biological explanation for schizophrenia is that it is passed on through the genes. Gottesman reports that while the rate of schizophrenia in the general population is 1%, if one parent has schizophrenia there is a 12% likelihood their child will develop it and if both parents have schizophrenia, it increases to 40%. Schizophrenia seems to be polygenic, as a number of genes have been implicated. It also seems to be aetiologically heterogeneous as different studies have identified different candidate genes. For example, Ripke et al. found 108 separate genetic variations were associated with increased risk of schizophrenia.

Evidence to support the genetic explanation comes from Gottesman and Shields, who found a concordance rate of 42% for MZ and 9% for DZ. MZ twins share 100% of their genes, compared to DZ twins who only share 50% of their genes, so this suggests that genes must have some influence on the development of schizophrenia. However, the concordance rate for MZ twins is not 100% which suggests that other factors must also be involved. It is also important to note that two-thirds of people with schizophrenia have no relative with a similar diagnosis and therefore have no one to inherit it from. However, one explanation for this is mutation in parental DNA.

The dopamine hypothesis is another biological explanation for schizophrenia. The original version suggested it was due to high levels or activity of dopamine in the subcortex (hyperdopaminergia). For example, an excess of dopamine receptors in Broca’s area might be responsible for poverty of speech and auditory hallucinations. More recent versions have included hypodopaminergia, where low levels of dopamine in the prefrontal cortex are believed to be responsible for some of the negative symptoms of schizophrenia.

Research evidence from autopsies has shown that schizophrenia sufferers have more dopamine receptors, which may lead to more neural firing and therefore an over production of messages. Further support comes from the fact that dopamine agonists (e.g. amphetamines) can produce-schizophrenia like symptoms in non-sufferers. Conversely, antipsychotic drugs work by binding to dopamine receptors and reduce symptoms. However, the newer antipsychotic drugs affect other neurotransmitters such as serotonin and glutamate as well as dopamine. Therefore it appears that several neurotransmitters may be involved in the development of schizophrenia, meaning the dopamine hypothesis is too simplistic. Biological explanations for schizophrenia can be criticised for being biologically reductionist. By oversimplifying schizophrenia in terms of genes and neurotransmitters, the social context within which it develops has not been considered. In order to explain schizophrenia effectively it would be better to take an interactionist approach, such as the diathesis stress model. This suggests that biological factors predispose someone to schizophrenia, but this has to be ‘triggered’ by some sort of experience or stressor. Evidence to support this view comes from the prospective adoption study by Tienari et al. Although this study showed that children with a biological parent were still at greater risk even if they had been adopted into families with no history of schizophrenia, all reported cases of schizophrenia occurred in families rated as ‘disturbed’. When the families were rated as ‘healthy’, the likelihood of developing schizophrenia for those with a biological mother with schizophrenia fell to below 1%. However, biological factors must have had a role to play as none of the adoptees with no family history of schizophrenia from ‘disturbed’ families developed schizophrenia

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