Describe Two or More Psychological Explanations of Schizophrenia

725 Words May 20th, 2013 3 Pages
Describe two or more psychological explanations of schizophrenia
8+16 marks
A01 A02 Sociocultural AO2 Cognitive Introducing Biology

The cognitive explanation acknowledges the role of biological factors in schizophrenia, suggesting that the basis of the condition is abnormal brain activity producing visual and auditory hallucinations. Further features of the disorder emerge as people try to make sense of the hallucinations.
When schizophrenics first experience voices and other worrying sensory experiences, they turn to others to confirm the validity of what they are experiencing. Other people fail to confirm the reality of these experiences, so the schizophrenic comes to believe that others must be hiding the truth. They begin to
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The intention is to show schizophrenics that their hallucinations are not real. As yet, however, there is no evidence that this will provide a successful treatment.
The research by Brown and Birley was a retrospective study where data is collected after events have occurred. In other words, once a person had developed schizophrenia they were asked about events leading up to the onset. It is quite likely that recall would be negatively affected by the events surrounding the onset of schizophrenia so such evidence may be unreliable.
Prospective studies are preferable, where people are studied after the onset of the disorder. Hirsch et al followed 71 schizophrenic patients over a 48-week period. It was clear that life events made a significant cumulative (increasing) contribution in the 12 months preceding relapse rather than immediately prior to the schizophrenic episode. This does support the retrospective research.
However, not all research supports the importance of life stressors. For example, Van Os et al reported no link between life events and the onset of schizophrenia. In the prospective part of the study, patients who had experienced a major life event went on to have a lower incidence of relapse rather than an increased risk as predicted.
One criticism of this research is that it is correlational. Therefore, we cannot infer a causal
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