Best Student Essay: Chloe Parkinson



Best Student Essay: Chloe Parkinson

Score: 11/12

Feedback from Miss Earl: In order to ensure that you are always in the top mark band ensure that you always have thorough (i.e. detailed) discussion. You should work towards immediate evaluation of any A01 points rather than leaving it until the end of a section so that your A02 runs throughout.

Outline and evaluate the biological explanation of schizophrenia (12 marks)

The biological explanation of schizophrenia is also known as the ‘medical model’. This approach sees mental disorders as having physical causes. A number of biological explanations for schizophrenia have emerged including genetic, neurochemical and neuro-anatomical explanations.

The genetic explanation of schizophrenia says that the disorder tends to run in families, studies have shown the closer the generic relatedness; the higher is the likelihood of schizophrenia. The risk of schizophrenia in the general population is 1%. Gottesman and Shields carried out early familial studies and gave % likelihood rates for various relatives. For example, if you have a parent with schizophrenia, the life-time risk of schizophrenia for you is 5.6%. Family studies have confirmed that the disorder does tend to run in families; however it is not clear whether this is due to genetics or environmental factors. Twin and adoption studies have been carried out to investigate this. As monozygotic twins have 100% of genes in common, it is suggested that the concordance rate for them is greater then dizygotic twins. Gottesman and Shields confirmed that the average concordance rate for monozygotic twins is 46% whereas is it only 14% in dizygotic twins. These averages were worked out from five studies that they conducted. Adoption studies can separate the environment from genes. An early adoption study by Heston in 1966 of 47 mothers with schizophrenia whose children were adopted within days by psychiatrically well mothers, found the incidence of schizophrenia in the children to be 16% (well above the 1% chance level). To evaluate, the 46% concordance rate for monozygotic twins suggests a major contribution of genotype. It is also about three times that of dizygotic twins, however, although it is high, there is still a discordance rate of about 40%. More studies into this discordant group have shown that about half of the group will develop a schizoid which makes the monozygotic concordance rate even higher. Owing to the rare incidence of both twins and schizophrenia in the general population, twin studies have only provided small samples (teacher note: why is this important?). Evidence from Lytton, 1977, suggests that monozygotic twins are reared in a more similar environment than dizygotic twins and therefore nurture might partly explain the higher concordance rate found in monozygotic twins. Finally, findings from adoption studies suggest that inheritance does play a part in schizophrenia and that there may be a genetic predisposition to the disorder.

Neurochemical explanations of schizophrenia have carried out investigations of neurotransmitters in three ways: by looking for evidence of metabolites in urine and blood, through the examination of post-mortem brain tissue and, more recently, through the use of neuro-imaging techniques. The activity of neurotransmitters, for example, dopamine and the enzyme responsible for its metabolism, has been investigated in the search for a neurochemical explanation for schizophrenia. At first, the dopamine hypothesis thought that excessive dopamine activity in the brain was the cause of schizophrenic symptoms. Evidence for this theory came from a number of areas: when taken by healthy individuals, drugs that increase dopaminergic activity in the brain result in psychotic symptoms like those experienced by people with schizophrenia, such drugs also exacerbate psychotic symptoms in people with the disorder and neuroleptic drugs that block the dopaminergic neurons reduce psychotic symptoms. However, post-mortem studies didn’t provide consistent evidence for an increase dopamine level in the brains of people with schizophrenia. This led to the theory that the cause was not an increase in dopamine; it was the heightened sensitivity of the receptors for dopamine in the brain that led to an abundance of the chemical and to schizophrenic symptoms. Evidence for this comes from a number of areas: post-mortem studies have show that there are many more dopamine receptors in the brains of people with schizophrenia than there are in normal brains, studies using PET scans have reported a substantial increase in dopamine receptors in patients with schizophrenia and, Seeman et al (1993) again, using PET scans, found six times the density of receptors similar to dopamine ones, in the brains of people with schizophrenia. To evaluate, it is not clear whether the increase in dopamine receptors found in the brains of people with schizophrenia at post-mortem is the cause of the pathology or an effect of the neuroleptic drug taken, as it is known that such drugs are attracted to this particular receptor. However, the neuro-imaging studies by Pearlson et al (1993) were carried out on patients who had not been exposed to neuroleptic drugs, thus ruling out the cause and effect problem found with post-mortem studies. Finally, although it is widely accepted that the majority of anti-psychotic drugs block dopamine receptors, to infer from this that dopamine hyper-activity is the major cause of schizophrenia is to oversimplify. It is now clear that the neurotransmitter systems interact and that the mapping of these cortical pathways is only just being explored.

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