There is supporting evidence for this hypothesis; for example, in the 1950s a selection of drugs known as anti-psychotics, were developed, which worked by reducing levels of dopamine in the brain. These drugs were very successful, and brought about substantial improvement in eighty per cent of schizophrenic patients, (those with positive symptoms).
The problems with these drugs include the fact that they do not work in twenty per cent of schizophrenics; those experiencing negative symptoms. However newer drugs, such as clozapine, have proved more successful in treating the disorder, (class notes). Anti-psychotic drugs have an effect on neurotransmitters other than dopamine as well; therefore it is unlikely that high dopamine levels alone cause schizophrenia. Another criticism of the dopamine hypothesis is that dopamine is not necessarily a ‘cause’ of schizophrenia, but rather it could be an ‘effect’, or symptom of the disorder.
The ‘diathesis stress model’ explains how genetic and psychological factors may interact in the formation of schizophrenia. Some individuals are born with a genetic ‘pre-disposition’ to developing the illness, however the disorder will only present itself should it be ‘triggered’ by environmental factors that cause significant stress. This would help to explain why schizophrenia normally develops in the teens and early twenties; as this is usually a very stressful time for people.
Further biological explanations of schizophrenia include brain abnormalities; for example studies using computed tomography (CT) and magnetic resonance imaging (MRI) have shown that, in comparison with healthy people, those with schizophrenia have smaller brains and larger cerebral ventricles, (Stirling and Hellewell, 1999). Such abnormalities may be the result of poor brain development, or some sort of damage; such problems, it is believed, may lead to the onset of schizophrenia.
A criticism of this theory is quite simply that not enough is known about the way in which the brain works. In addition there is the question of cause and effect; these types of abnormalities may be a symptom of schizophrenia rather than a cause. Furthermore such abnormalities may exist in many healthy individuals; however we would not know this for sure as perfectly healthy people tend not to have brain scans as there is no need to.
Certain viral infections, (that may occur before birth), are also believed to play a role in the development of schizophrenia. There is some evidence to back up this theory; Torrey (2000) found that a high percentage of schizophrenics are born during winter, when exposure to viruses is high. Mothers of schizophrenics are more likely to have been exposed to illnesses (such as the flu virus) during pregnancy, than the mothers of those without the disorder. It is believed that the effects of the virus on the child may remain dormant until activated by hormonal changes at puberty which bring about schizophrenia, (Gherardelli, 1992, cited in class notes).
This would help to explain why some children display unusual behaviour, (such as withdrawal), before they reach their teens or early twenties, when they develop symptoms of schizophrenia. A further strength of this theory is that it explains why schizophrenia can, and often does, appear in individuals who do not have relatives with the disorder, and therefore no genetic pre-disposition to developing it. However there is no evidence to suggest that all schizophrenics have been exposed to viruses before birth, (class notes).
More psychological approaches to explaining schizophrenia include Freud`s psychodynamic perspective, that the symptoms of schizophrenia arose due to ‘inner conflicts’. Freud believed that an individual may have a wish or urge to do something that is in some way unacceptable to them, and so they unconsciously, (and therefore unknowingly) project these thoughts or views on to another person; and behaves as if the wish or view originated from that individual and was directed towards them. In this way, Freud reasoned that rather than accepting their own views or urges, they might develop ‘paranoid’ ideas about other people and their intentions. This would explain some of the delusional or paranoid behaviour of schizophrenic patients; but unfortunately, like most psychodynamic explanations, supporting evidence is absent, (Stirling and Hellewell, 1999).
Other psychologists have suggested that schizophrenia may be a way of thinking and behaving acquired in childhood, due to the attitudes, communication and behaviour of parents, (Stirling and Hellewell, 1999). Fromm-Reichman (1948) described such a parent as a ‘schizophrenogenic mother’, and believed that such mothers who are domineering, cold, rejecting and guilt-producing, drive their children to develop the illness, (class notes). However this theory fails to explain why only some children, rather than all the children of such parents develop schizophrenia.
Another theory, by Bateson et al (1956), argued that schizophrenia develops as the result of frequent exposure to what he described as the ‘double bind’. By this term he was describing communications that are inherently contradictory or conflicting, and which put the child in a ‘no win’ situation, (Stirling and Hellewell, 1999). It is argued that children who experience double binds may begin to lose their grip on reality and not think that their own feelings, thoughts and perceptions are accurate indicators of it, (class notes), and thus go on to develop schizophrenia. However this theory also lacks empirical evidence.
There is however a theory of family interactions known as ‘expressed emotion’, which has provided some supporting evidence. Expressed emotion, according to Vaughn and Leff (1976), is the criticism and negative feelings that are sometimes expressed by the families of schizophrenic patients towards the ill person. Stirling et al (1993) stated that people recovering from schizophrenia who live in high expressed emotion households tend to relapse more frequently than those living in low expressed emotion households, (Stirling and Hellewell, 1999). However evidence from ‘intervention studies’ shows that the risk of relapse in high expressed emotion households can be reduced through family therapy; such therapy includes practical help and information, and stress-reduction methods, (Stirling and Hellewell, 1999).
There is also a behavioural approach to explaining how schizophrenia may develop; through conditioning and observational learning. According to Ullman and Krasner (1969, cited in class notes), people show schizophrenic behaviour when it is more likely than normal behaviour to be ‘reinforced’. For example, in psychiatric institutions professionals are more likely to pay attention to those displaying unusual behaviour such as schizophrenic symptoms; this in turn may reinforce the behaviour and cause it to continue, despite treatment. Patients may also see certain behaviours by other patients receiving attention; and so learn to behave more in such a way themselves as a result.
Unfortunately this theory does not account for how schizophrenic behaviours start, but only how they may be reinforced once they are already there. It also fails to explain why some patients genuinely experience symptoms such as hallucinations, and withdrawal, (in which case a patient would not want to receive attention). For such reasons it is generally accepted that the behavioural model contributes little to the understanding of the causes of schizophrenia, (Freud, 1998, cited in class notes).
In conclusion, it is the biological explanations of the causes of schizophrenia that seem to receive most support; however the fact that the concordance rate in twin studies does not match up completely shows that other factors must be involved. This idea is backed up by the diathesis stress model, which shows the importance of stressful life events in contributing to the illness. Furthermore the fact that patients living in households high in expressed emotion suffer more relapses shows that stress does appear to be a significant factor also. Psychodynamic and behavioural explanations of the illness have received little support and are largely lacking in empirical evidence; therefore they have contributed little to our knowledge of schizophrenia.
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References
Class Notes (2008)
Stirling, J. Hellewell, J. (1999) Psychopathology. Routledge. 11 New Fetter Lane, London.
