clinical psychology schizophrenia 5 essays on explanations and treatments
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Course
Unit 5 - Clinical psychology
Institution
PEARSON (PEARSON)
5 sample essays on 5 extended response questions ranging from 8 to 20 marks on schizophrenia (a compulsory mental disorder to learn in clinical psychology)
evaluation of biological and non-biological explanations and treatments for schizophrenia
Dopamine hypothesis
Evaluate 1 bio explanation of schizophrenia (20)
One strength of the dopamine hypothesis is that it has supporting evidence.
Excess dopamine is produced by overactive dopaminergic neurons, which leads to
symptoms seen in schizophrenia. This is because patients overreact to the presence of
dopamine in their brains, which leads to hallucinations as the brain is too active.
Lieberman et al. (1987) found that 75% of patients with schizophrenia have an increase
in psychosis after taking amphetamine which is known to increase dopamine activity
and lead to “cocaine psychosis”. This means that dopamine may be the chemical
responsible for the psychotic symptoms seen in schizophrenia. This is a strength as it
provides objective evidence for the dopamine hypothesis as a scientifically credible
explanation for schizophrenia. However, in Lieberman’s study, only a small proportion of
regular users of amphetamine continued to have psychotic symptoms. This suggests
that there must be a different factor as to how brains react to the presence of dopamine
and how this leads to symptoms of schizophrenia since the dopamine hypothesis
would predict the regular users to keep having psychotic symptoms as amphetamine
increases dopamine activity, but they did not.
One weakness of the dopamine hypothesis is that it may be reductionist. This
explanation explains schizophrenia, a disorder that has many complex features, by the
imbalance of a single neurotransmitter (dopamine). For example, it would suggest that
schizophrenia may result from high levels of dopamine in the brain or a greater number
of D2 receptors in the brain which have a higher affinity to dopamine and are more likely
to bind to it. This leads to hypersensitivity of D2 dopamine receptors. As a result though,
this explanation ignores other environmental factors that may contribute to the onset of
schizophrenia. For example, Brown and Birley (1968) found that 50% of patients with
schizophrenia reported a major life event 3 weeks prior to relapse. This implies that
social conditions may be involved in triggering relapse in schizophrenic patients. This is
a weakness as the complex interrelationship between neurotransmitter levels and other
biological, physiological and social factors is ignored, but this may be a more valid
, 2
explanation of why schizophrenia may develop in the first place, instead of just
explaining it with high levels of dopamine in the brain. However, since there is a 50% risk
rate of substance misuse in patients with schizophrenia, it may be clear that
neurotransmitters do have a role in the development of schizophrenia since drugs are
known to increase dopamine levels. Therefore, there is support for the dopamine
hypothesis to an extent, but other factors should be considered as well to obtain a more
holistic explanation of schizophrenia.
One strength of the dopamine hypothesis is that it successfully explains
symptoms of schizophrenia. Davis et al. (1991) proposed that hyperdopaminergia in the
mesolimbic pathway may lead to positive symptoms of schizophrenia, and
hypodopaminergia in the mesocortical pathway may lead to negative symptoms. This
may be credible since the mesocortical pathway links to the reward pathway, meaning
that low levels of dopamine do not motivate the person to repeat certain behaviours to
increase the sensation of pleasure. Therefore, this results in the negative symptoms of
schizophrenia such as flattened affect, avolition and a depressed mood state. There is a
50% risk rate of depression in patients with schizophrenia, as both disorders have
similar symptoms such as asociality, avolition, and alogia. This means that the
dopamine explanation may be a scientifically credible explanation of schizophrenia.
This is a strength as it increases the validity of the theory. However, one of the most
effective antipsychotics -clozapine, affects serotonin activity and not only dopamine.
This suggests that other neurotransmitters must be linked to schizophrenia and not just
dopamine as correcting serotonin levels through clozapine has led to improvements in
symptoms of schizophrenia.
One weakness of the dopamine hypothesis is that there are other more suitable
explanations for explaining schizophrenia. The dopamine hypothesis explains
schizophrenia in terms of a high number of dopamine receptors in the brain which
account for 6% increase in dopamine than normal. The Glutamate hypothesis explains
schizophrenia in terms of low glutamate levels in the brain, which is linked to abnormal
dopamine levels since glutamate regulated dopamine. This means that glutamate may
be the main neurotransmitter responsible for the development of schizophrenia as it
affects the levels of dopamine, which subsequently influences the probability of
developing schizophrenia. This is a weakness as this disproves the dopamine
hypothesis in proposing that glutamate levels determine whether or not the somebody
develops schizophrenia. On the other hand, Wong (1987) found through PET scans, that
brains of patients with schizophrenia have twice as many dopamine receptors
compared to controls without schizophrenia. This supports the dopamine hypothesis in
there being a higher than usual number of dopamine receptors which account for the
increased dopamine in the brain which results in symptoms of schizophrenia.
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