Psychological Explanations for Schizophrenia

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Psychological Explanations for Schizophrenia

There are two psychological explanations for Schizophrenia.

  • Family Models (Expressed Emotion)
  • Cognitive Explanations

In questions regarding explanations for Schizophrenia in general the Diathesis-Stress Model can also be implemented. If not then the Diathesis Stress model can be used in evaluation.

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Family Models: Expressed Emotion

Brown showed in his research that schizophrenics are more likely to relapse if they return to a family with high levels of Expressed Emotion. Such families frequently express criticism, disapproval and hostility and are highly intrusive and overly concerned

Vaughn and Leff suggest that the extent of Expressed Emotion within a family is a strong predictor of relapse rates amongst discharged patients. In their study 51% of those in high-EE homes relapsed whilst only 13% did so in low-EE homes. They also found that relapse rates increased the longer the patient spent in face-to-face contact with their high-EE relatives.

Nowadays Expressed Emotion is a well-established maintenance model of schizophrenia and it has become so well accepted that treatment programmes for schizophrenia usually include the education and training of family members in controlling levels of EE.

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Evaluation of Family Models: Expressed Emotion

  • Direction of causality is not clear in studies of EE. One possibility is that EE does cause relapses however another possibility is that individuals in poor emotional shape are more likely to provoke EE from family members.
  • High EE patterns have been found in families of patients with other disorders besides schizophrenia suggesting that high EE may provide the psychological trigger that interacts with a variety of genetic vulnerabilities (diathesis-stress). It may also suggest however that high EE is a result of living with the stress of having a family member with mental health issues.
  • It has been found that high EE is less common in families of first-episode patients in comparison to those with frequent readmissions. This suggest high EE develops as a result of living with somebody with Sz.
  • Prospective studies of children though to be at risk of developing schizophrenia have found that high risk children who do actually develop the disorder were more likely to have come from families characterised by negative relationships.
  • Weisman et al found that relatives are more likely to attribute postive symptoms of Sz to the disorder and do not lay blame on the patient whereas they are often critical of their negative symptoms and do blame the patient. This may explain why those with negative symptoms are more likely to relapse.
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Cognitive Explanations of Schizophrenia

Frith explains schizophrenia in terms of difficulties in information processing. Specifically he was interested in two cognitive abilities.

  • Meta-Representation (the ability to reflect on our thoughts, behaviour and experience. It is the mental ability that allows us self-awareness of our own intentions and goals and allows us to interpret other people's action. Problems with this would result in difficulty distinguishing between our own actions and the actions of others)
  • Central Control (the ability to suppress our automatic responses to stimuli whilst we perform actions which reflect our wishes and intentions)

Positive symptoms are easily explained by issues with metarepresentatin. Schizophrenics have problems distinguising between the thoughts they have in their own heads and the spoken words of others, explaining hallucinations. Delusions about being persecuted are also explained as problems with metarepresentation means we are unable to interpret the actions of others.

The disorganised thinking and behaviour is a result of issues with central control as schizophrenics are unable to suppress stimulus-driven actions.

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Evaluation of Cognitive Explanations

  • Supporting evidence for Frith's model comes from Bentall's study. His study involved asking participants to either read out category words or think of category items themselves. One group were Sz diagnosed whilst the control had no Sz diagnosis. A week later the pps were given a list of words and asked to identify those they had read, which were new and which they had thought of themselves. The Sz group did significantly worse suggesting that they struggled to distinguish between words they had come up with and those they had heard. This supports the idea of an issue with metarepresentation as those with normal metarepresentation would be able to spot the words they had thought of themselves.
  • Cognitive theories may not be able to offer a full explanation of Sz but they may help to explain the origins of particular symptoms in terms of cognitive deficits. However the approach is criticised as it does not explain where these deficits come from and so it does not provide a complete explanation of the disorder as the biological theories do. This may mean it is viewed as reductionist.
  • Cognitive deficits are usually identified by tests that measure cognitive skills. Based on these tests few differences have been found between people with bi-polar and people with Sz, suggesting that cognitive deficits do not fully explain the behaviour of those diagnosed with Sz.
  • Frith's work has provided a comprehensive framework for explaining many of the symptoms of Sz. Research however is far from conclusive and so the theory is still speculative.
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Diathesis-Stress Model

Zubin and Spring first suggested that stressful life events might act as a trigger for schizophrenia in individuals who are already biologically vulnerable to developing the disorder. This model suggests the following:

Predisposing Factors         +         Trigger                   = Outcome

  • Predisposing Factors = genetic predisposition, increased sensitivity to psychosocial factors, birth complications, viral infections
  • Trigger = adverse family circumstance, major life event, traumatic experience

Mednick took a group of 297 at-risk children and compared them with children with no family background of mental illness, matching them on sex, age, father's occupation and educational level. They used tests and interviews and monitored the children over a twenty five year period. 15 of the children in the high risk group developed Sz whilst none of the control group did. These 15 also seemed to have environmental triggers such as separation from mother at an early age and having fathers who were more likely to be hospitalised for things such as alcoholism.

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Evaluation of Diathesis-Stress Model

  • Offers an explanation of why concordance rates for MZ twins are never 100% as the genetic vulnerability needs environmental triggers.
  • In a Finnish Adoption Study by Tienari he found that all reported cases of Sz occurred in families rated as disturbed and when the family environment was rated as healthy even in the high risk sample occurence of Sz was well below the general population rate of 1%. However the environment was not the sole cause as the low risk children from disturbed families did not develop Sz. This research provides strong evidence for the proposal that Sz is best explained by looking at the interaction between genetic inheritance and environmental trigger.
  • The Israeli High Risk Study showed that all the reported cases of Sz had poor parental rating however all these cases also showed sighns of neuropsychological abnormalities thirteen years earlier at initial assessment so perhaps these abnormalities influenced the parent child interaction.
  • In evaluation of the above studies all of them are ongoing and not all children have passed through the critical period for onset of Sz. Evidence to date however does strongly support the model.
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