ABSTRACT
The history of research in schizophrenia could be written as a history of dichotomies – process versus reactive, good premorbid versus poor premorbid, acute versus chronic, and nonparanoid versus paranoid. Although such a history would include many inconsistent results, it would also contain meaningful information about valid approaches to characterizing differences among schizophrenic patients. But as Houlihan (1977) has noted, even though these distinctions have been successful in forming more homogeneous subgroups in schizophrenia research, their contribution may have reached a plateau. The dimensions of chronicity, paranoid status, and premorbid adjustment account for only a portion of the variance in research on schizophrenia, and it is possible that “more statistically powerful, perhaps more central, independent variables may be available” (Houlihan, 1977, p. 256). The distinction between positive symptoms (e.g., delusions, hallucinations) and negative symptoms (e.g., apathy, blunted affect) may be one such “independent variable.” Originally introduced in neurology by Reynolds and Hughlings Jackson (Berrios, 1985), this distinction owes its current appeal among schizophrenia researchers to Strauss, Carpenter, and Bartko (1974), Crow (1980a), and Andreasen (Andreasen, 1982a; Andreasen & Olsen, 1982). The distinction between positive and negative symptoms figures prominently in recent discussions of the diagnosis and pathogenesis of schizophrenia (e.g., Abrams & Taylor, 1978; Andreasen, 1979b, 1985; Bowers, 1980, 1983; Crow, 1980a, 1980b, 1982, 1985; J. S. Strauss, 1985). Crow (1980a) has proposed that there may be at least two syndromes in schizophrenia, one characterized by florid positive symptoms and disturbances in dopaminergic transmission, and the other characterized by enduring negative symptoms and structural abnormalities in the brain. A variety of data are consistent with the suggestion that these two groups of symptoms reflect different pathophysiological processes. For example, negative symptoms have been found to be associated with ventricular enlargement and other neuropathologic abnormalities (Andreasen et al., 1986; Andreasen, Olsen, Dennert, & Smith, 1982; Stevens, 1982), neurological signs (Owens & Johnstone, 1980), genetic influences (Dworkin & Lenzenweger, 1984), and cognitive impairment (Andreasen & Olsen, 1982; Cornblatt, Lenzenweger, Dworkin, & Erlenmeyer-Kimling, 1985; Frith, 1977; Green & Walker, 1985, 1986; Johnstone, Crow, Frith, Stevens, et al., 1978; Lenzenweger, 1986; Owens & Johnstone, 1980). In addition, negative symptoms generally do not respond to treatment with neuroleptics, whereas positive symptoms often do (Angrist, Rotrosen, & Gershon, 1980; Johnstone, Crow, Frith, Carney, & Price, 1978).
