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 reject feedback from those around them and develop delusional beliefs that they are being manipulated and persecuted by others. An alternative explanation is that stressful life events cause the onset of schizophrenia. Events such as death of a close relative act as a trigger. The individual may have a biological predisposition for schizophrenia but only some people with such a predisposition will develop this disorder – those who experience stressors.
Brown and Birley found that, prior to a schizophrenic episode, patients reported twice as many stressful life events compared to a healthy control group, who reported a low and unchanging level of stressful life events over the same period. This illustrates the link between stressors and the onset of schizophrenia. There is biological evidence to support the cognitive explanation. Meyer-Linderberg et al found a link between excess levels of dopamine in the prefrontal cortex and dysfunctions of working memory. Working memory dysfunction is associated with the cognitive disorganisation typically found in schizophrenics.
This supports the idea that biological factors underlie some of the early symptoms of schizophrenia. The cognitive approach has real-world applications as the basis for a form of therapy. Yellowlees et al have trialled a machine that can deliver ‘virtual’ auditory and visual hallucinations, such as hearing the TV tell you to kill yourself, or one person’s face morphing into another. 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 vents 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 relationship between stressful life events and schizophrenia. It could be that the early symptoms of the disorder (e. . erratic behaviour) were the cause of major life events (e. g. divorce, loss of job). As a result, it is possible that the stressful major life events that are evident in the lives of some schizophrenics might be the consequence rather than the cause of this disorder. In general the biological explanations probably have better research support than psychological ones. There is a large body of evidence, for example, supporting the role of genetic factors, such as research by Gottesman which showed that the greater the degree of genetic relatedness, the greater the risk of schizophrenia.
However, the best solution is probably the diathesis stress model which combines both biological and psychological approaches. The diathesis stress model suggests that people have vulnerability for schizophrenia (diathesis) but the disorder only manifests itself when triggered by life events (a stressor). The same model can be applied to the cognitive explanation where a biological diathesis only turns into schizophrenia if a person misinterprets other people’s behaviour (a kind of stressor).