The EPPIC researchers decided to interpret the low transition rate of their patients as indicating that a substantial fraction were false positives.[19] They promptly began a new prospective study of at-risk individuals using updated diagnostic criteria. The same sixteen to thirty years age group was targeted, with the same division of the subjects into three groups. This time, however, the DSM-III-R prodromal symptoms were replaced with DSM-IV symptoms for Schizotypal Personality Disorder. This switch to using the symptoms of a personality disorder, which psychiatrists think of as a milder form of deviance than a psychosis, was necessary because the newer fourth revision of the DSM had dropped the prodromal symptoms of schizophrenia from its specifications.
DSM-IV specifies nine symptoms for Schizotypal Personality Disorder: (1) ideas of reference; (2) odd beliefs or magical thinking; (3) unusual perceptual experiences; (4) odd thinking and speech; (5) suspiciousness or paranoid ideation; (6) inappropriate or constricted affect; (7) behaviour or appearance that is odd, eccentric, or peculiar; (8) lack of close friends or confidantes other than first degree relatives; (9) excessive social anxiety. A diagnosis normally requires the presence of five or more. But the researchers at the PACE clinic decided that only one symptom would be sufficient to indicate the presence of the schizophrenia prodrome. This assumption was in defiance of the DSM-IV view that ‘Schizotypal Personality Disorder has a relatively stable course, with only a small proportion of individuals going on to develop Schizophrenia or another Psychotic Disorder’.[20] If this is true about people who meet the normal diagnostic criteria for Schizotypal Personality Disorder by having five or more symptoms, what is to be assumed about the real risk of psychosis for people who met the PACE diagnostic criteria by only having one symptom? It should be noted that magical thinking is once again on the list so we know that over 50 per cent of the adolescent population would be identified by this method.
Defying expectations, the PACE research found that 48 per cent of the people inducted into the programme using the diluted schizotypal indicators became psychotic within twelve months. The transition rate to psychosis at six months was 40 per cent. But these results still raised ethical questions about treatment of the non-psychotic majority: ‘because over 50% of cases do not develop psychosis within twelve months routine treatment of this group would result in many young people being subject to unnecessary treatment and labelling’.[21]
These claims of having calculated a precise rate of transition into psychosis suggest that the threshold of psychosis is a well-defined boundary and that non-psychotic people can be easily distinguished from psychotic people. But this is not the case. In a recent publication, the EPPIC researchers admitted that psychosis has no precise definition and that ‘[t]he point of onset is difficult to define prospectively and has to be defined arbitrarily’.[22]
When the point of psychotic onset is determined retrospectively, which is the usual way of making a determination, it can be simply pegged to the point in time at which a psychiatrist judged that a person’s behaviour required urgent psychiatric treatment. But psychiatric treatment was given to the people in the PACE study while they were still in an acknowledged pre-psychotic state. This blurred the distinction and made it impossible to tell with any certainty when the psychotic threshold had been crossed.
The whole purpose of the research was to follow the progress of supposedly pre-psychotic patients and determine whether they crossed the threshold into psychosis. But the threshold is an arbitrarily defined boundary, as the researchers admitted, so the significance of their findings must be called into question. If the criteria for determining psychosis is arbitrary then, arguably, the researchers could contrive whatever results suited their purpose. These doubts are compounded by the apparent lack of control groups in the design of the research.
It should be noted here that a serious gap exists in the material published about the efficacy of pre-psychotic treatment programmes. No convincing evidence has been provided to support claims that a particular type of prophylactic treatment can help to prevent psychosis. Nor is there evidence that a lack of treatment will lead to psychosis. It is quite possible, from the anecdotal evidence provided so far, that attempts to apply prophylactic treatments might actually exacerbate symptoms, rather than ameliorate them, and thereby induce psychosis.
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[19] Yung et al., ‘Monitoring and care of young people at incipient risk of psychosis’, p. 299.
[20] American Psychiatric Association, op. cit., 1994, p. 643.
[21] A. R. Yung, et al., ‘Can we predict the onset of first-episode psychosis in a high-risk group?’, p. 28.
[22] Ibid., p. 26.