The conventional distinction between schizophrenia and manic depression has received little objective support from recent studies of phenomenol-ogy, outcome, or familial homotypy. Instead, much clinical, epidemiologi-cal, and morphological evidence sug-gests that within the broad range of Schneiderian schizophrenia there ex-ists one form (congenital schizo-phrenia) that can be distinguished from other types, the manifestations of which are confined to adult life. We hypothesize that congenital schizophrenia is a consequence of aberrant brain development during fetal and neonatal life. Such patients show structural brain changes and cognitive impairment, and in their male predominance, early onset, and poor outcome, they reflect Kraepe-lin's original description of dementia praecox. We contend that adult-onset schizophrenia is itself heterogeneous. One important component is a re-lapsing and remitting disorder that is more frequent in females than in males, exhibits positive but not nega-tive symptoms, and has much in common etiologically with affective psychosis. There also exists a very-late-onset group in which degenera-tive brain disorder is implicated. In 1985 we put forward the view that it would soon be possible for psychiatry to move beyond the syn-dromal diagnosis of the psychoses (Murray et al. 1985a). In particular, we emphasized the value of distin-guishing between genetic and envi-ronmental causes, and we suggested that the structural brain abnormalities found in a portion of sporadic cases of schizophrenia were consequences of environmental hazards operating during fetal or neonatal life. Since that time, neuropathologic and neuroimaging research into schizophrenia has continued apace, and it is now commonplace to inter-pret the findings in neurodevelop-mental terms (Feinberg 1983; Wein
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