Abstract
In 1896 Emil Kraepelin distinguished “dementia praecox” from the affective psychoses. Shortly afterwards, Bleuler proposed the name “schizophrenia”, and since that time, the beginning of modern biological psychiatry, studies have been performed with the aim of understanding the basic mechanisms of these somatic disturbances (Kraepelin 1919; Bleuler 1923). While genetic factors have indicated a hereditary contribution to the aetiology of schizophrenia (Tsuang 1976), the search for distinct pathophysiological associations with this disease has, until very recently, proved disappointing. Nevertheless, the results of some investigations, particularly in the fields of biochemistry and pharmacology, have provided us with a pointer to the changes at the level of brain chemistry which may underly this disease. This progress has been made with three overlapping approaches:
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1.
The model psychoses
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2.
The pharmacology of the antipsychotic drugs
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3.
Human postmortem brain studies.
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Riederer, P., Reynolds, G.P. (1985). Brain Biochemistry in Schizophrenia: An Assessment. In: Beckmann, H., Riederer, P. (eds) Pathochemical Markers in Major Psychoses. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69743-2_4
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DOI: https://doi.org/10.1007/978-3-642-69743-2_4
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