August 28, 2004
Early intervention and Schizophrenia
Early intervention, or as I prefer to view it, prevention (a very important distinction-for this term does not imply an already present putative genetic diathesis or premorbid condition), in schizophrenia is a contemporary issue needing more research and open discussion in our field. Early intervention implies that there already exists a reified premorbid, sub-syndromal condition (genotype?) awaiting full phenotypic emergence. However, we know from various research bases (see Chris Harrop & Peter Trower 2003 “Why Does Schizophrenia Develop at Late Adolescence?: A Cognitive-Developmental Approach to Psychosis” published by Wiley), that the prevalence of ‘prodromal’ symptoms of a putative psychotic process is actually quite high in ‘normal’ adolescent populations. Therefore the risk of false positives is significant in this field, not to mention the risk of a self-fulfilling expectancy leading to increasing levels of anxiety and psychosomatic symptomatology (similar to the cognitive research in panic disorder in which researchers have identified catastrophic interpretations of normal somatic events as etiologic, not secondary epiphenomena, in the initiation of panic attacks). Many researchers, including some within the our ISPS organization, have advocated for the early use of atypical antipsychotic agents in ‘high-risk’ populations.
Anthony David (2004- “Is early intervention a waste of valuable resources?” in “Schizophrenia: Challenging the Orthodox” edited by C. McDonald et al for Taylor & Fancis), Professor of Cognitive Neuropsychiatry from the Institute of Psychiatry in London, has suggested that early intervention, much advocated by the pharmaceutical industry, may actually be a waste of valuable resources which could be better and more effectively used in providing needed continuous services to already identified patients who tend to be under-served, particularly the older more chronic population which many clinicians may give up on due to the stubborn persistence of symptoms (perhaps leading to narcissistic injuries in treaters and ‘burn-out’), non-collaboration with treatment, economic status, etc. After noting that the concept of early intervention is hard to argue with, David raises the issues of high false positives, questionable effective treatment with minimal side effects, unknown benefits of early treatment and cost effectiveness, etc.
He reported on a Swedish conscript survey which illustrates the pitfalls of an early, broadly based targeted intervention strategy. The males who were most likely to develop schizophrenia 15 years later were those who had fewer than two friends, preferred to socialize in small groups, were more sensitive and did not have a steady romantic partner. The odds ratio if all of these risk factors were present is 30, a factor similar to having both parents with schizophrenia or an identical twin with schizophrenia. This is a powerful social risk factor and it has been adjusted for social history. If early intervention was directed at these social factors, the risk of later development of schizophrenia would be substantially lowered. However, with no support from powerful pharmaceutical companies, this kind of research is rare. Yet, the implications of this research is consistent with actual research findings in social treatment studies of already diagnosed patients with schizophrenia conducted at Yale University recently by Larry Davidson and colleagues and reported in his excellent volume “Living Outside Mental Illness: Qualitative Studies of Recovery in Schizophrenia” published in 2003 by New York University Press.
David suggested that although early intervention sounds good, in practice there are enough established cases of psychosis that need, in a triage model, our attention first. He noted: “After all of the experimental interventions have been done (with or without effect), and all of the new monies are spent, and after all of the reports have been written and published [most with economic backing of pharmaceutical companies-the latter like it because it has great potential to massively increase their markets] when patients are 35 years they are no longer of interest to early interventionists and the generic services have to take over” (p. 109).
David notes that this is when medical truisms must not be ignored:
1) continuity of care
2) follow medical precedent (i.e., if it does not work in breast cancer-figures for screening for breast cancer with mammography published in 2001 by the Cochrane Collaboration, which remains very controversial, is it really going to work in schizophrenia?)
3) first, do no harm
4) triage, treat the sickest first
David concluded his review with the following comments: “From a dispassionate appraisal of the research literature on the treatment of schizophrenia, the most obvious and evidence-based target for interventions in schizophrenia is to prevent premature discontinuation of treatment and not early intervention...If an early intervention service is to be useful, it should be at the population level, free of side effects and inexpensive, and should not undermine clinical practice. On the basis of the Swedish data [Malmberg et al British Journal of Psychiatry 1998; 172: 308-313], we might consider a befriending scheme [this is consistent with known effectiveness of treatment as exemplified in research by Davidson and colleagues 2003]. As it stands there is only one possible conclusion: early intervention in schizophrenia is a waste of valuable resources” (p. 111).
I believe that this is an area that needs further research and reflection, as well as participation of a broad range of ISPS members, not just those who are advocating early use of atypical antipsychotics and CBT. We also need research on social psychiatric interventions, as well as psychotherapy. There are many roads to Rome.
Brian Koehler PhD
New York University
80 East 11th Street #339
New York NY 10003