Schizophrenia is a generic name for a group of psychiatric disorders, which are usually associated with disturbances in thinking, behavior, social conduct and emotional response.
It is a disabling mental illness, which runs a protracted course that often results in personality change. However, it should not be confused with Multiple Personality Disorder, which refers to a genuine separation between two sets of behavior (Marcovitch, 2005). The term was first coined by the Swiss psychiatrist Eugen Bleuler, who suggested including a wide array of mental illnesses (which were previously described as dementia praecox, or “premature dementia”) under the general term schizophrenia (“split-mind”). The reason for this choice was Bleuler’s assumption that schizophrenia represents a split between a person’s emotional life and faculty of reasoning.
With the development of early psychotherapy, Meduna (1935) assumed that epilepsy and schizophrenia and depression are antagonistic and suggested that patients with schizophrenia should be treated with metrazol shock (convulsion). Generally speaking, Meduna’s approach to schizophrenia, which was widely accepted by American psychiatrists during the 1940s, tried to find pharmacological and explanations to the phenomenon. His shock therapy was based on few accidental results and his work categorically ignored the developmental and/or biological underpinnings of schizophrenia.
Later observations did not find systematical effectiveness of the metrazol shock on schizophrenia. The treatment was still used for depressed patients, and was ultimately replaced with electroconvulsive treatment (ECT). Nevertheless, Meduna and others ask only questions that could be answered with the scientific methods of their times. These methods were based on experiments with animals and patients, often without having justifications for what they observed.
In sharp contrast to this symptom-based methodology, modern psychiatry tends not to accept suggestions to treatment without clear, evidence-based referral to the pathology of the disease. Recent advancements in neuroimaging and psychopathology enable researchers to locate abnormalities among patients who show symptoms of one of the known subtypes of schizophrenia, and then to compare the results with others who have similar symptoms. This can be done, for example, with fMRI maps (functional MRI scans, which are based on oxygenation levels of brain tissues), which can locate the exact location of the abnormality. Instead of speaking in general anatomical terms such as lobes and hemispheres, today’s scientists measure changes in specific tissues of living patients.
Furthermore, schizophrenia can be now linked to the functions of specific transmitters and receptors in brain cells, and try to develop medications that can influence those tiny elements of the brain. Speculations are still part of this process, but the jargon has changed dramatically.
Meduna, for example, tried to find evidences for “the unconfirmed notion that there existed a ‘biological antagonism’ between epilepsy and schizophrenia,” (Lehmann, & Ban, 1997). In the poor terminology and biological understanding of time, an early suggestion of his was that the blood of patients with epilepsy should be infused to schizophrenias. As mentioned earlier, depression was later suggested as the “antagonist” for schizophrenia.
Lieberman et al. (2005), who studied the effect of antipsychotic drugs on schizophrenia, were also looking for antagonists. In sharp contrast, however, they are looking for “high-affinity antagonists of dopamine D2 receptors” as well as for “other neuroreceptors, including those for serotonin […] and norepinephrine” in specific regions of the cerebral cortex. This change, given only as one example, can be linked not only to technological developments, but also to a new wing in psychiatry. In simple words, researchers do no ask themselves anymore “what will reduce the symptoms?” but “what can decrease the quantity of proteins that bring about the disease?”
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Marcovitch, H. (2005). Black’s Medical Dictionary (41st edition). London: A&C Black.
Meduna, L. V. (1935). Versuche über die biologische Beeinflussung des Ablaufes der Schizophrenie [Experiments on biological influences on the course of schizophrenia]. Zeitschrift für die Gesamte Neurologie und Psychiatrie, 152, pp. 235–262. English Review in Lehmann, H. E. & Ban, T. A. (1997). The history of the psychopharmacology of schizophrenia. Canadian Journal of Psychiatry, 42, pp. 152–162. Retrieved August 11, 2009 from <https://ww1.cpa-apc.org/Publications/Archives/PDF/1997/Mar/lehmann.pdf>
Lieberman, J. A., Stroup, T. S., McEvoy, J. P., Swartz, M. S., Rosenheck, R. A., Perkins, D. O., et al. (2005). Effectiveness of antipsychotic drugs in patients with chronic schizophrenia. The New England Journal of Medicine, 353(12), pp. 1209-1223. Retrieved August 11, 2009 from <https://www.mhafc.org/pdf/CATIE-Study.pdf>