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The concept of schizophrenia is contentious. Although most psychiatrists accept without question the notion that schizophrenia is a disease - a psychiatric disorder brought about by changes in brain function, scepticism reigns outside the profession, especially in many of those to whom the label is attached. So-called ‘schizophrenics’ may choose a variety of non-medical ways to understand and explain the nature of their experiences, and this leads us to the heart of a conflict in which the subject’s explanation of his or her experiences lies at odds with the psychiatrists. Inevitably it is the psychiatrist’s account which will turn out to be the most powerful, as can be seen in the famous case of Judge Daniel Schreber (see, for example Leudar & Thomas 1999). But it need not always be this way. In this paper, I shall try to demonstrate some of the shortcomings of the way in which psychiatrists interpret the Kraepelinian concept of schizophrenia, especially the relationship between the acute ‘symptoms’ of the condition and outcome. I shall then challenge the way this interpretation is used to justify the use of long-term neuroleptic medication, with the conclusion that psychiatrists must jettison the medical model when working with people in acute psychoses, in favour of humanistic models which recognise the importance of the relationship between the individual and the experience of psychosis. But first, we must consider the origins of the concept of schizophrenia.
and Dementia Praecox
Early psychiatrists, influenced by Griesinger, believed that medical science would reveal the cause of all forms of insanity. But basic clinical sciences such as pathology, physiology and anatomy, which had been so successful in revealing the cause of neuro-syphilis, failed to reveal the cause of dementia praecox so Kraepelin had to rely on systematic clinical observation. Hoenig (1983) has described Kraepelin’s katamnestic method, which relied on the detailed description of individual cases, in an attempt to delineate the specific symptoms and signs of dementia praecox, in the hope that such an approach would confirm that dementia praecox was a disease entity with a specific anatomical basis and pathology. The issue here concerns the extent to which he succeeded in describing a single disease, dementia praecox with poor outcome?
point concerns the great variability of symptoms to be found in
schizophrenia. Even Kraepelin (1913) admitted this, going so far as
Kraepelin failed to provide a “pathognomonic” symptom for schizophrenia, and, in lieu of this, he chose to emphasise the importance of the course of the illness. This position has been immensely influential. After Kraepelin, psychiatrists believed that a deteriorating course was a cardinal feature of schizophrenia. Deterioration here refers to the “changes which develop in the course of the illness” in the quotation from Kraepelin above. It is this that forms the basis of the belief that schizophrenia is a poor prognosis illness. Furthermore, there is an implicit assumption that deterioration is related to the putative disease process.
is that Kraepelin not only found it difficult to be prescriptive
symptoms required to diagnose schizophrenia and thus predict outcome,
he was also unable to show that all of the 127 cases of schizophrenia
studied in detail actually turned out to have poor outcome and
deteriorating course. Kraepelin himself found that complete recovery
possible in 12.5% of cases (Vol. II, p. 865, quoted in Hoenig, 1983).
Bleuler remained unconvinced that the condition was a single disease
entity, because of the diversity of symptoms and variation in outcome
(Kraepelin) is the sole, flawed, authority for this extraordinary but
This forces us to the conclusion that there is little evidence to support the Kraepelinian model of schizophrenia. There is neither the evidence to support biological models of the condition, nor the evidence to justify the existence of the condition as a diagnostic category, characterised by specific acute symptoms which predict outcome. I want to make one final point concerning poor outcome. Ciompi found that in two thirds of cases social outcome was either intermediate or poor. His figures suggest that the main field of impairment in schizophrenia is not symptoms, but social functioning. But in view of the fact that all the patients studied had been institutionalised for decades, this is hardly surprising, and may have little to do with the progress of an illness. Zubin et al (1983; see chapter two, p. 38) have suggested that over the last fifty years schizophrenia has become a less severe condition with a better outcome. Over this period the management of the condition has changed profoundly. People who have the condition are no longer incarcerated in institutions for years as was the case when Kraepelin wrote about dementia praecox. This raises the possibility that the poor outcome described by Kraepelin was an artefact of institutionalisation.
Efficacy of neuroleptics
Neuroleptics and long-term course
Freeman (1994) have reviewed the advantages and drawbacks of
treatment. First, they make the point that a number of authorities
doubted whether neuroleptics have a beneficial effect on
Karl Leonhard (1980) argued that psychiatrists should only consider using long term therapy once it was established without doubt that the condition from which the individual was suffering was a phasic disorder, that is a condition characterised by recurrent episodes of positive, or other acute psychotic symptoms. This was based on his view that such a symptom pattern tended to respond to neuroleptics, whereas the defect state did not. Schooler (1991) in her study of dose reduction commented that the results of naturalistic long-term follow up studies in schizophrenia show clearly the great diversity of outcomes of the condition. Despite long term medication, some people appear to have a very poor outcome. On the other hand some people do very well with little or no medication. The word naturalistic is very important here. Most of the accepted evidence in support of the value of neuroleptics in the short-term and long-term management of schizophrenia comes from drug trials, which are special studies resourced and supported by the pharmacological industry. Such studies can hardly be described as independent. In addition, they are performed under ideal conditions which are hardly representative of the circumstances under which these drugs are used by psychiatrists in the daily work. In this sense, the ecological validity of these studies must be called into question.
The most naturalistic study in this sense was undertaken by Johnstone et al (1986) working at Northwick Park in London. Patients were under the care of forty psychiatrists working within a thirty five mile radius of Harrow. Over 460 patients met the criteria for inclusion in the study over a period of almost two and a half years, yet 14% of these patients could not be assessed for a number of reasons. These included refusal of either patient or consultant to consent to study, self-discharge before assessment could be made, administrative problems such as patient not admitted, or ‘conversation’ barriers. These problems are typical of those commonly encountered by psychiatrists in their day to day work. Of the patients who could be assessed, only 120 could be entered into a randomised placebo-controlled drug trial of maintenance neuroleptic medication (Crow et al, 1986). They found surprisingly high rates of relapse in the two years following discharge both in the placebo group and, surprisingly, the group who received active medication. Although 70 percent of patients on placebo relapsed, 58 percent of those taking active medication did so over the same period. Overall these results suggest that at best, the benefits of neuroleptic medication in preventing relapse are marginal.
is summarised well by another quote from Kane and Freeman
- drug discontinuation or illness?
There is evidence that this indeed may be the case. A few years ago, Chouinard and Jones (1980) published a paper in the American Journal of Psychiatry, which, in its day, was widely quoted as evidence in support of the dopamine theory of schizophrenia. In it, they described in detail the drug treatment histories of ten patients treated with neuroleptic drugs. In each case a recurrence of psychotic symptoms was noticed almost immediately following reduction or discontinuation of medication. This runs contrary to expectation. There is nothing in our knowledge of the course of schizophrenia that would lead us to expect a sudden reappearance of symptoms on discontinuing medication. All the subjects had had lengthy periods of exposure to neuroleptic, and in addition, most had evidence of tardive dyskinesia. The dyskinesia became more apparent on discontinuation of medication, and with the appearance of psychotic symptoms. The authors note that:
implication of neuroleptic-induced mesolimbic supersensitivity is
tendency toward psychotic relapse in such patients is determined by
than just the normal course of the illness.’
Further evidence in support of the supersensitivity psychosis comes from one of the most thorough reviews of neuroleptic withdrawal ever made. Gilbert et al (1995) reviewed 66 studies of neuroleptic withdrawal in schizophrenia involving over 4,000 patients. She found that amongst other things ‘relapse’ was more likely to occur in people who had been taking higher doses of neuroleptic medication prior to discontinuation, or in people who had experienced rapid discontinuation (over two weeks) as opposed to gradual discontinuation (over eight weeks). These are exactly the features we might expect to find in a disturbance that occurs simply as part of a drug withdrawal state.
Of course, no research study has seriously addressed the possibility that symptom recurrence in schizophrenia on stopping neuroleptics is effectively a drug withdrawal syndrome. To examine this possibility you would have to examine the symptoms of a large number of people in their first episodes of schizophrenia, and then compare these symptoms in great detail with those seen in the same people after discontinuing neuroleptics. Such a study has yet to be performed. It is interesting to note how the drug withdrawal explanation for ‘relapse’ has been overwhelmingly neglected in the psychiatric literature. Descriptions of drug withdrawal states dominate clinical accounts of the effects of psychoactive drugs and substances. All doctors are familiar with the phenomenon of drug withdrawal syndrome, and although Chouinard’s work has been in the literature for 16 years, this explanation for the link between relapse and medication has been glossed over. The implications of this are too frightening for psychiatry to contemplate. It means that for many patients ‘relapse’ may be iatrogenic, a consequence of drug treatment and not an inevitable part of the process of a disease.
There are enormous difficulties in undertaking a study such as this. For example, there are different ways of defining relapse. For some people relapse is defined simply as the reappearance of psychotic symptoms. For others it is necessary for you to be readmitted to hospital. This makes it very difficult to compare the outcome in different studies.
© Asylum Magazine 2002