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.
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’.
A sympathetic and illuminating account of the development of Kraepelin’s ideas up to 1913 has been provided by Berrios and Hauser (1988). They point out that his concept was neither as simple nor as rigid as is generally assumed and that it continued to develop. Indeed, Kraepelin (1920) eventually came to agree that dementia praecox and manic-depressive psychosis could coexist and, thus, that a unitary psychosis could not be ruled out.
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’. He retained the separation from manic-depressive psychosis while pointing out that affective symptoms could coexist. His concept was based on an assumption that the manifold external clinical manifestations masked an inner clinical unity that ‘clearly marked [them] off from other types of disease’. Moreover, he argued that ‘each case nevertheless reveals some significant residual symptoms common to all’. The end results were identical, ‘not quantitatively but qualitatively’.
Eugen Bleuler, a contemporary of Emil Kraepelin, believed that schizophrenia was caused by psychological trauma sustained early in life. National Library of Medicine. Bleuler’s primary symptom was cognitive: a form of ‘thought disorder’, loosening of the associations. It provided links to Kraepelin’s ‘dementia’ and to the biological origins of the disease, but also, through ‘psychic complexes’, to disorders of affectivity, ambivalence, autism, attention and will. These essential symptoms could be observed in every case. Catatonia, delusions, hallucinations and behavioural problems he regarded as accessory psychological reactions, not caused by the biological process or processes.
A substantial subgroup was designated ‘simple schizophrenia’, in which no accessory symptoms (the most easy to recognize) need be present. Diem (1903/1987), who worked with Bleuler, gave a description of two cases that he thought were caused by simple dementing forms of dementia praecox.
Both were apparently normal as children, but as young men they began inexplicably to lose volition and purpose, ending as vagrants. Delusions and hallucinations were absent. Although no early developmental history was provided, these two people certainly became severely impaired in psychological and personal functioning and fitted Bleuler’s severe version of simple schizophrenia. Bleuler’s own examples are less easy to recognize. Among the lower classes, they ‘vegetate as day labourers, peddlars, even as servants’. At higher levels, ‘the most common type is the wife . . . , who is unbearable, constantly scolding, nagging, always making demands but never recognizing duties’. Beyond this ‘simple’ form of the disease, the largest subgroup was labelled ‘latent schizophrenia’: ‘irritable, odd, moody, withdrawn or exaggeratedly punctual people’. Bleuler thought it ‘not necessary to give a detailed description’ of the manifestations in this group but there is a clear merger with subsequent concepts of schizoid and schizotypal personality (e.g. Kendler 1985).
This is in contrast to Kraepelin, whose account even of the ‘mild’ form of the course sounds severe. Thus, although Bleuler separated those with the disease from those without, the concept was in effect dimensional. Although accepting much of Kraepelin’s formulation, Bleuler substantially widened the concept, while continuing to describe his concept as a disease entity.
The simple and latent forms, whose vaguely defined primary symptoms could be elaborated through ‘psychic complexes’, were thus able to carry the weight, power and putative severity of a widely recognized diagnosis. Under the influence of contrasting types of theory – one psychoanalytical, the other biological – Bleuler’s least differentiated subgroups came to exert an undue influence on the way that the diagnosis of schizophrenia was made and used in the USA and USSR during the 1970s (Wing 1978).
J.K. Wing and N. Agrawal
Edited by Steven R. Hirsch MD FRCP FRCPsych
Professor of Psychiatry Emeritus, Division of Neuroscience and Psychological Medicine Imperial College Faculty of Medicine and Director of Teaching Governance, West London Mental Health NHS Trust
Daniel R. Weinberger MD Chief, Clinical Brain Disorders Branch
Intramural Research Program
National Institute of Mental Health
MD 20982, USA
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