Our training in psychiatry during the early 1960s was at a time of intense controversy regarding the origins of schizophrenia. Rather comprehensive explanatory theory for psychopathology was postulated at the level of genetics/biology or psychology or social theory. These perspectives competed for dominance more often than seeking integration although the biopsychosocial medical model, espoused by Engel,1 integrated these perspectives in a general systems framework. At that time the Danish adoption studies confirmed that inherited genes conveyed familial risk for schizophrenia, but were often interpreted as not only establishing schizophrenia as a genetic disease but also as falsifying psychological and social theories of etiology.2 At the time of our early research concerning schizophrenia, there was the view that a careful diagnosis based on stringent criteria would identify persons with a disease entity that sharply reduced the heterogeneity observed in development and course of illness in cohorts based on a broad concept of schizophrenia. Schneider viewed symptoms of first rank as distinguished nuclear schizophrenia and Langfeldt separated true from pseudo schizophrenia with criteria including first rank symptoms. The view that a broad concept of schizophrenia without stringent criteria in the United States led to over-inclusion, and hence heterogeneity, suggested a solution partly based on first rank symptoms. Our understanding of the data including our analyses in the context of the International Pilot Study of Schizophrenia (IPSS)3 led to a very different interpretation. We had found that criteria specified by Schneider and Langfeldt were not associated with course of illness and did not reduce heterogeneity when applied to a broadly defined cohort.4 We also documented that these special symptom criteria were observed in other disorders with psychotic symptoms.5,6 We concluded that schizophrenia was a clinical syndrome, a poor target for discovery, and called attention to separable psychopathological targets within the syndrome as meaningful targets for investigation.7 We also found that components of developmental history predicted future course of the same component independent of positive psychotic symptoms including those of first rank.8 As a footnote on the role of ideology over science, note that of the 9 IPSS centers only the Washington center collected development based prognostic data and follow-up data related to heterogeneity. Also note that DSM-III allowed a single first rank symptom to be sufficient to meet the A criteria (corrected in DSM-5), omitted negative symptoms from the A criteria, and imposed a duration of illness criteria to assure chronicity. In the 1981 book, Schizophrenia,9 we introduced the developmental interactive concept of schizophrenia. Now, with 36 years of research in the field, how so we view this conceptual framework? The essential elements in the developmental interactive model of schizophrenia are:
原文链接
分享
引用
