Early schizophrenia concepts

Key points
- There has been no time since attempts at classification began when controversy about the nature of 'schizophrenia' was absent.
- It was not until the publication of the fifth edition of Kraepelin's textbook (1896/1987) that a firm line of demarcation was drawn between dementia praecox and affective psychosis and a sort of consensus again achieved.
- The term 'schizophrenia' stems from Eugen Bleuler (1911/1950), who acknowledged in his preface his indebtedness to Kraepelin for 'grouping and description of the separate symptoms' and to Freud, whose ideas Bleuler used to 'advance and enlarge the concepts of psychopathology'.
- However, there have been periods when a sort of orthodoxy was accepted.
Griesinger
There has been no time since attempts at classification began when controversy about the nature of 'schizophrenia' was absent. However, there have been periods when a sort of orthodoxy was accepted. One of these was based on Griesinger's teaching that only what we would now call affective and schizoaffective disorders constituted a 'primary' disease process (Griesinger 1861). What we now call chronic schizophrenic impairments could develop secondarily, but only after earlier affective episodes. Griesinger eventually came to agree that there could be a primary psychosis, even in the absence of these preliminaries, and thus 'abandoned the classification system of mental disorders hitherto traditional for him and his time' (Janzarik 1987). Thirty years of confusion about the relationships between a multiplicity of syndromes followed.
Kraepelin
It was not until the publication of the fifth edition of Kraepelin's textbook (1896/1987) that a firm line of demarcation was drawn between dementia praecox and affective psychosis and a sort of consensus again achieved. Both Griesinger's and Kraepelin's concepts were couched in terms of 'disease entities', following the lines of successful developments in medicine at that time. The discovery of the anatomical and physiological concomitants of clinically identified syndromes, often with a 'natural' history and a pathology, and sometimes with what appeared to be a single causal agent such as the tubercle bacillus or the cholera vibrio, proved irresistible to the neuropsychiatrists who were also carving more specific syndromes out of the global concepts of dementia, delirium and insanity that preceded them.
Kraepelin introduced a simple distinction between conditions characterized by mental deterioration such as the catatonia and hebephrenia of his contemporary Kahlbaum (1874/1973), which with paranoid deterioration became subdivisions of the disease, and more periodic forms of mania and melancholia, such as the folie circulaire of Falret (1854). His follow-up data suggested a mental state profile recognizable at the time of presentation and a 'generally regular and progressive' course.
Emil Kraepelin, a German psychiatrist, provided the first characterization of schizophrenia, in the late nineteenth century. He believed that the disorder was caused by irreversible physical damage to the brain. National Library of Medicine Because cause was unknown, although variously postulated, classification depended largely on the course and outcome of groups of symptoms.
The chief symptoms were auditory and tactile hallucinations, delusions, thought disorder, incoherence, blunted affect, negativism, stereotypies and lack of insight. The phenomena were expressed as psychological rather than physical abnormalities, with catatonic symptoms, for example, being described in terms of disorders of the will. Paranoia was regarded as a separate disorder, characterized by incorrigible delusions often circumscribed in topic, a general absence of hallucinations, and a chronic but non-deteriorating course. Kraepelin also adopted Kahlbaum's model – general paralysis of the insane – as his prototype for a disease based on unity of cause, course and outcome. The nature of the disease was obscure although probably related to 'a tangible morbid process in the brain'.
Written and revised by
David Cohen, M.D.
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