Disease as entity or as deviation from normal functioning

Kendell (1987) has pointed out that none of the four types of psychosis – schizophrenic, affective, good prognosis acute and chronic paranoid – discussed above has been clearly demonstrated to be a disease entity. Does it matterf? Kraepelin and Bleuler thought it did. But even so well ‘validated’ a disease as tuberculosis cannot be said to be an ‘entity’ in the sense that everyone with the bacillus in the bloodstream has the same (or any) symptoms, let alone the same course or outcome.

Cohen (1961) argued that the concept of disease that ‘still dominates our textbook descriptions, as illustrated by the socalled classical pictures of typhoid fever, influenza, disseminated sclerosis and the rest, is little more helpful in diagnosis than would be a composite portrait of a football team in revealing whether any one individual is a member’.

Throughout medicine,  but particularly during the past 50 years, rigid disease categories have been replaced by more useful concepts that are constantly evolving in the light of the experimental evidence. As disease concepts evolve in the light of the successes and failures of hypothesis testing, it becomes obvious that some diseases previously thought to be ‘entities’ are actually linked and that the fundamental processes involve deviations or blockages in the functioning of normal homeostatic cycles. Hypertension, diabetes and coronary heart disease are obvious examples, but so, increasingly, are most well-known diseases. Different defining formulae that use the same name have to fight against each other for survival. Which is more successful at any one time depends on the weight of evidence its protagonists can provide.

The   evidence   must   also   include   the   epidemiology   of schizophrenia: the genetics, age and sex distribution, excess of births in the winter months and the possibility that the course and even the incidence varies both geographically and over time.

Hierarchy in psychiatric disorders

Some sense can be made of the relationships between psychiatric disorders if dimensional as well as categorical concepts are borne in mind. Both are useful so long as it is recognized that it is essential to move easily between them. The ancient hierarchies divided mental faculties into conative, cognitive and affective. If brain function is profoundly impaired, there can be no or only negligible function of will. Movement, thought and emotion will then be absent or distorted.

It is possible that each of the three faculties can be impaired independently of the others and that the conventional hierarchical system of diagnosis would have more than just practical use if based on three or four dimensions (the extra one representing motor functions). Positive and negative aspects would then be represented at every level.

At the moment, in practice, diagnoses tend to be made as follows:

•   At the top are disorders such as dementia, which, at least in the early stages, can be associated with any other type of problem. For example, ‘schizophrenic symptoms’ occurring in the course of Huntington’s disease or temporal lobe epilepsy or severe learning disability tend to be discounted for the purpose of diagnosis.
• Similarly, disorders in the autistic spectrum, if diagnosed on the developmental history and the spectrum, should not be given a primary diagnosis of schizophrenia.
• In general,  schizophrenic symptoms,  in the absence of ‘organic’  disorder,  take precedence in diagnosis and for treatment over bipolar psychoses if both are present.
• Affective psychoses in turn take precedence over unipolar depression and the anxiety that is so commonly associated with all the above disorders.
• Symptoms such as fatigue, worry and muscular tension are regarded as non-specific.

The hierarchy is generally non-reflexive, i.e. each disorder tends to manifest the symptoms of those lower down (Foulds 1965; Sturt 1981) but not those of disorders higher up. By the same token, all disorders can be seen in cross-section as well as longitudinally, manifesting a complex of symptoms, some negative and some positive, and many ‘non-specific’ for the ‘diagnosis’.
Both perspectives are legitimate for different purposes (Wing 1978).

Other types of theory

A review of the history of concepts of schizophrenia would not be complete without a reference to theories of ‘not-schizophrenia’,  although these tend to be logically self-destructive.  Most are variants of those by Goffman (1961), Laing and Esterson (1964), Scheff (1966) and Szasz (1971), which have been dealt with elsewhere (Wing 1978).

This is far from saying that there are no other components to the aetiology of schizophrenia than those that involve purely biological elements. In fact, from the time of Kraepelin, concepts of disordered attention or arousal have suggested that environmental events may influence symptoms for better or worse.

Certainly, some sufferers have learned for themselves how to cope with symptoms without losing control, and many carers have found, without help from professionals, how to provide an optimal environment (Creer &  Wing 1974;  Wing 1975).

Interactive biosocial theories that suggest how environmental over- and understimulation may act to improve or exacerbate the positive and negative impairments (Wing 1978) cannot be taken seriously by those who reject any deviation from a purely biological approach. Thus, an absolute biologism is as limiting and ultimately sterile as an absolute rejection of biology.

The value of cognitive–behaviour therapy for the enhancement, in some cases, of the effects of the new medications during recovery from an attack of schizophrenia, and the acquisition of a degree of control over symptoms during convalescence and between attacks, is not only a success of the past decade but a pointer to the future.  Tools for assessing claims of efficacy for such treatment methods are available, and must be applied according to strict rules by disinterested investigators.

Excluding clinical concepts that cannot be expressed clearly and numerically does not mean they are clinically valueless.

Some may in time prove to be significant, but they have to wait until someone with the clinical intuition of Alzheimer, Asperger, Kanner or Kurt Schneider clarifies them.

Some critics of formulations such as schizophrenia (e.g. Bentall et al. 1988) have suggested that there is no need to do more than study symptoms, pointing to evidence that symptombased therapies can provide relief and greater autonomy to sufferers and their families. It has yet to be demonstrated how far control of one symptom will generalize to others, how long relief lasts and what proportion of sufferers can benefit. A more specific disadvantage is that concentrating on single symptoms, instead of – rather than as well as – syndromes, may divert attention from the clinical context of the symptoms,  with a resulting detriment to problems that are multifaceted and interconnected.

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 London, UK

Daniel R. Weinberger MD
Chief, Clinical Brain Disorders Branch Intramural Research Program National Institute of Mental Health Bethesda MD 20982, USA

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