When schizophrenia was in its primary stages of definition, it was presented as a novel form of a neuro-degenerative disorder, similar to that which had been previously seen amongst sufferers of Alzheimer’s or Huntington’s diseases (Woods, 1998, p. 1661). Emil Kraepelin (1904) was the first to propose that schizophrenia could be considered as a disease. Recent years have shown alternative views to what schizophrenia actually is as opposed to its primary presenting forms. Contradictory findings amongst researchers have created an overabundance of explanations and ideas surrounding the disorder from the neurological through to the social learning approach. At the time of writing, Woods noted that there was no firm understanding about the causation of schizophrenia and as such, those involved were unable to define schizophrenia in terms of a mental disorder or in fact, disease. Over 100 years of investigation have still failed to find a definitive cause through either genetics or the environment. This has resulted in the eclectic approach of genetic predisposition with an environmental ‘push’ (Jablensky, 1997, p. 111).
The reality of schizophrenia is that it is treatable, be that with pharmacological or psychological treatment. Science based upon intervention has shown through numerous rigorous research projects that interventions are an effective method of dealing with such a disabling condition (Drake & Essock, 2009, p. 677). However, although advances in science have come a long way since the first methodical investigations began, authors note that there is still a lack of a basic understanding of the disorder. This causes restrictions on treatment ability and furthermore, suitability (Lehman, 2009, p. 659). However, some of the most successful treatments for schizophrenia have come from the pharmacological world with regard to anti-psychotic medications; yet the cost is high both in monetary terms and the possible side effects. Meta-analysis of second generation antipsychotic treatments showed that when medication was tailored to the individual patient, many of the medications were efficacious and were able to limit the symptoms (both positive and negative) of schizophrenia (Leucht et al., 2009, p. 152). Here, support for the disease model of schizophrenia is found, in the sense that the medical model is able to provide treatment in the form of antipsychotics and treat the condition. Further support for the medical model comes from research into the effect of phencyclidine and ketamine on individuals. Research has shown that the intravenous administration of the drugs leads to symptomology which matches that of schizophrenia and not only supports the hypoglutamatergic hypothesis of schizophrenia but also the dopamine hypothesis (Jentsch & Roth, 1999, p. 201). If we are able to chemically manipulate the symptoms of schizophrenia, then a disease model is the proposed model of acceptance.
In an approach which differs from that of the medical/disease model, is that proposed by J.D. Laing. In his book, The Divided Self, Laing describes schizophrenics as individuals divorcing themselves from their bodies as being as one is a painful endurance for the individual. Interestingly, his evaluation of a young lady who attempted suicide as part of her schizophrenic illness, was that it was not that she was incapable of making rational decisions and was perceived to have harmed herself, but rather that she had made the choice to kill herself rather than to be killed by her illness (Laing, 1959, p. 161). It appears as though the individual has severed her ‘mental’ self from her ‘actual’ self and in doing so has been left with a schizoid disorder (Ibid, p.162). Here we are able to question the idea of mental illness as a disease. Laing has ideas which route themselves to mental capabilities and the capacity for rational thought and also quotes the aforementioned schizophrenic as being aware of when she was in a catatonic state, in that it was intentional (Ibid, p. 176). In this instance, Laing is not referring to schizophrenia as a disease per se, but as a disorder of the mind, one for which he feels there is therapy. However, general findings into cognitive behavioural therapies (CBT), based upon psychological and learning models for schizophrenia have shown disappointing results. Turkington, Kingdon, & Chadwick, (2003, P. 98) noted that a meta-analysis of the effectiveness of CBT indicated that many programmes showed poor efficacy through inadequate programme deliverance.
Cultural differences have also led to issues in the understanding of the epistemology of schizophrenia. It has been noted amongst psychiatrists based in the developing countries that there is a more favourable prognosis for schizophrenia than in Western populations. It was found that individuals with schizophrenia in Asia and African were more likely to have a favourable prognosis than individuals living in the UK (Murphy & Raman, 1971, p. 489). The World Health Organisation (WHO) realised there was a need for individual projects to concentrate on why the prognosis was improved in different civilisations and in particular among those with less medical advancement. Interestingly, there were similar findings with other major psychiatric disorders (Leff et al., 1992). This would be more supportive of a psychological approach to schizophrenia than that of the disease model. With little or no access to psychotropic medication, yet with improved prognoses, one questions the validity of medications and their effectiveness. It is also interesting to note that the severity of symptoms appear less problematic where the medications are less available. At this point, cross-cultural research into the effects of medication is suggested; the idea that medication may be worsening the disorder can be investigated.
The overall impression that such a small investigation into the true epistemology of schizophrenia has allowed for, and as such its standing on, the disease/disorder/mental disability debate is that, yes, schizophrenia is in fact a disease; a disease that with the right pharmacological intervention and correct management can be treated, allowing individuals with the disorder to lead fairly normal lives. As with any major psychological disorder, further investigation is always needed to allow the science of psychology to take the understanding of schizophrenia to a deeper level and thus provide more effective treatments.
Drake, R. E., & Essock, S. M. (2009). The Science-to-Service Gap in Real-World Schizophrenia Treatment: The 95% Problem. Schizophrenia Bulletin, 35(4), 677 -678.
Jablensky, A. (1997). The 100-year epidemiology of schizophrenia. Schizophrenia Research, 28(2-3), 111-125.
Jentsch, J. D., & Roth, R. H. (1999). The Neuropsychopharmacology of Phencyclidine: From NMDA Receptor Hypofunction to the Dopamine Hypothesis of Schizophrenia. Neuropsychopharmacology, 20(3), 201-225.
Kraepelin, E. (1904) Lectures on Clinical Psychiatry. New York: Hafner, 1968.
Laing, R. D. (1959). The Divided Self. London: Tavistock.
Leff, J., Sartorius, N., Jablensky, A., Korten, A., Emberg, G. (1992). The International Pilot Study of Schizophrenia: five – year follow up findings. Psychological Medicine. 22: 131 -145.
Lehman, A. F. (2009). Leaping Tall Buildings—The Science-to-Service Gap in Schizophrenia Treatment. Schizophrenia Bulletin, 35(4), 659 -660.
Leucht, S., Komossa, K., Rummel-Kluge, C., Corves, C., Hunger, H., Schmid, F., Asenjo Lobos, C., et al. (2009). A Meta-Analysis of Head-to-Head Comparisons of Second-Generation Antipsychotics in the Treatment of Schizophrenia. Am J Psychiatry, 166(2), 152-163.
Murphy, H. B. M., & Raman, A. C. (1971). The Chronicity of Schizophrenia in Indigenous Tropical Peoples: Results of a Twelve-Year Follow-up Survey in Mauritius. The British Journal of Psychiatry, 118(546), 489-497.
Turkington, D., Kingdon, D., & Chadwick, P. (2003). Cognitive-behavioural therapy for schizophrenia: filling the therapeutic vacuum. The British Journal of Psychiatry, 183(2), 98-99.
Woods, B. T. (1998). Is Schizophrenia a Progressive Neurodevelopmental Disorder? Toward a Unitary Pathogenetic Mechanism. Am J Psychiatry, 155(12), 1661-1670.