Evaluation of Explanations of Schizophrenia

Evaluation of the Explanations of Schizophrenia Explain why the psychodynamic approach provides an interesting alternative to the dominant biological explanations? The psychodynamic approach provides an interesting alternative to the dominant biological approaches, as it brings psychologists' attention to the impact of early childhood experiences on later mental health. Therefore, this explanation of schizophrenia has good face validity because the belief that early childhood experiences can have a significant impact on our later mental health is a plausible idea. As there is a lack of empirical evidence to support the psychodynamic explanation, what does this suggest? There is a significant lack of empirical evidence to support the psychodynamic explanation of schizophrenia, this suggests that this explanation lacks external validity, as it is difficult to apply to people who suffer from schizophrenia. Explain how the findings of the Mednick et al (1984) study support the idea that a dysfunctional family and, in particular, the mother, can cause schizophrenia. The findings of Mednick et al's study suggest that the mother's behaviour and living in a dysfunctional family could cause a child to develop schizophrenia, as it was found that out of a group of 207 children who were identified as being at  a high risk of developing schizophrenia due to having a mother with a schizophrenogenic personality (cold, domineering, over-protective, rigid, and moralistic about sex), 17 developed schizophrenia compared to one child developing the disorder in a control group of 107 children. Some critics would argue that the mother's behaviour may be the result of having to look after a child with schizophrenia rather than causing the disorder in their child. Explain what this would mean for this explanation is it was an effect rather than a cause. Some critics of this explanation of schizophrenia argue that the mother’s “schizophrenogenic” behaviour may be a result of having to care for a child with schizophrenia, rather than being the cause of their child’s disorder. This viewpoint suggests that the cause and effect of this explanation cannot be established, as the child’s disorder may have caused their mother’s cold, domineering and over-protective behaviour rather than the mother’s behaviour causing the child’s disorder. Explain the ethical issue that may arise from accepting the schizophrenogenic mother as a valid explanation for the disorder, as we now have objective scientific explanations and schizophrenia is clearly caused by biological factors and/or a complex interaction of biological and psychological factors. One ethical issue that may arise from accepting the schizophrenogenic mother as a valid explanation of schizophrenia is deception. The British Psychological Society states in its ethical guidelines that an individual should not be purposely misled without strong scientific justification. Due to the extensive research that has been undertaken with regards to the cause of schizophrenia and the wealth of evidence that strongly suggests that there are other factors that can contribute to the development of schizophrenia in an individual, it would be ethically unacceptable to tell a mother of a child with schizophrenia that she has caused her child’s disorder. This point also raises another ethical issue, which is protecting people from harm. Allowing a mother to believe that she has caused her child’s disorder could lead to her feeling extremely guilty and could possibly affect her mental health. How does Rosenhan’s research demonstrate how the label “schizophrenic” can become a self-fulfilling prophecy? Rosenhan’s research demonstrates how the label of “schizophrenic” can become a self-fulfilling prophecy, as even though the pseudopatients displayed no further characteristics of schizophrenia after being admitted to the hospital, the hospital staff interpreted their behaviour as being typical of the disorder, spent little time interacting with them, answered questions abruptly, were very authoritarian in manner and often acted as though the patients were invisible. Explain why the labelling theory is a flawed explanation for the cause of schizophrenia. The labelling theory is a flawed explanation of the cause of schizophrenia as it does not consider any biological factors that could contribute to the development of the disorder. Therefore, this explanation is extremely over-simplified and reductionist. Another reason why the labelling theory is a flawed explanation of the cause of schizophrenia is that the cause and effect cannot be established. For a person to be labelled as “schizophrenic,” they must have been displaying characteristics of the disorder prior to be labelled. Therefore, in theory, it should not be surprising to see the individual displaying characteristics of the disorder after being given a label. However, it can be argued that giving an individual a label does not help in the recovery of the disorder and it may encourage characteristic behaviour of the disorder as it is what is expected of them by others. It takes 2-3 weeks for the anti-psychotic drugs to reduce the symptoms of schizophrenia, however they reduce an individual’s dopamine levels almost immediately. What does this imply about the dopamine hypothesis? The fact that it takes two to three weeks for anti-psychotic drugs to reduce the symptoms of schizophrenia even though the level of dopamine in an individual’s brain is reduced almost immediately greatly discredits the validity of the dopamine hypothesis. If the dopamine hypothesis was completely correct, then the symptoms of schizophrenia would be reduced as soon as the levels of dopamine were reduced, due to the dopamine hypothesis believing that too much or too little dopamine in the brain causes schizophrenia. Therefore, there must be other factors that cause schizophrenic symptoms, such as a complex combination of neurotransmitters. This suggests that the dopamine hypothesis is far too oversimplified and extremely reductionist. How does the effects of the Parkinson’s drug L-Dopa provide supporting evidence for the dopamine hypothesis? The dopamine hypothesis is the theory that too much or too little of the neurotransmitter dopamine in the brain can cause schizophrenia. L-Dopa is a drug given to people who have Parkinson’s disease which increases the level of dopamine in the brain. An overdose of L-Dopa in a person with Parkinson’s disease can produce symptoms similar to those of schizophrenia, such as hallucinations and delusions. Giving L-Dopa to a person suffering from schizophrenia can worsen their symptoms. These findings support the dopamine hypothesis, as increasing the amount of dopamine in the brain of a person who does not suffer from schizophrenia can produce schizophrenic symptoms, which suggests that high levels of dopamine can cause schizophrenia. It has been suggested that there is a problem with cause and effect with the dopamine hypothesis. What does this mean? This means that it cannot be confirmed whether an imbalance of the neurotransmitter dopamine in the brain causes symptoms of schizophrenia, or whether the symptoms of schizophrenia cause an imbalance of dopamine in the brain. What percentage of DNA do identical (MZ) twins share? Monozygotic twins share 100% of their DNA. What concordance rate would you therefore expect to see if schizophrenia did have a genetic basis? If schizophrenia did have a genetic basis, it would be expected that there would be a 100% concordance rate of having schizophrenia for monozygotic twins, due to the fact that they share 100% of their DNA. Can you think of any alternative reasons as to why the concordance rates may be higher in twins? The concordance rates for schizophrenia may be higher in twins, as twins are often brought up in the same environment and share the same experiences. This supports the behavioural approach which believes that every person is born as a blank slate and that all behaviours are learned. Research by Tienari (1991) found that in a study of 155 adopted children whose biological mothers had schizophrenia and compared these with 185 adopted children whose biological mother had no mental disorder, 10.3% of children with schizophrenic mothers had developed schizophrenia by adulthood compared to 1.1% of the control group. What does this suggest? These findings suggest that schizophrenia does have a genetic basis, as even though the children whose mothers had schizophrenia were adopted and raised away from them, 10.3% of the children had developed schizophrenia by adulthood compared to only 1.1% of the control group. This eliminates any extraneous variables such as being brought up in environment with a mother who has schizophrenia, which gives the study good external validity. What would be a reasonable conclusion to draw regarding the genetic basis for schizophrenia? A reasonable conclusion regarding the genetic basis for schizophrenia could be that the absolute genetic theory, which believes that only genes can cause schizophrenia, is incorrect. This is due to findings from Tienari’s study which show that only 10.3% of children who had mothers with schizophrenia developed the disorder. If the absolute genetic theory was correct, then 100% of the children would have developed the disorder. Twin studies also show that the conconrdance rate of schizophrenia in monozygotic twins who share 100% of their DNA is only 40-50%. It would be expected that the concordance rate would be 100% if the absolute genetic theory was correct. The genetic predisposition theory, which believes that maladaptive genes can be inherited which raise the likelihood of the individual developing schizophrenia, but that the disorder will only develop if other factors are present, is much more plausible. The findings from Tienari’s study support this theory, as the children whose mothers had schizophrenia may have inherited the maladaptive gene which increases the likelihood of the individual developing the disorder, and as only 10.3% of these children developed schizophrenia, these children may have experienced other factors that could have contributed to the development of the disorder that the other 89.7% of the group did not experience. .

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