Deficit and Nondeficit Schizophrenias: Some Neurobiological Correlates and more than 25 Years of Follow-Through Results

Abstract

Characteristic deficit features that become manifest in the realm of terminal states of schizophrenia have long been regarded, and still remain, as unique of the schizophrenia (Leonhard 1966; Mitsuda 1975, 1979; Fukuda 1979, 1997, 2000). In contrast, the atypical (nondeficit) schizophrenia, estimated to comprise about one-third of contemporary classification systems, e.g., DSM-IV or ICD-10 (Leonhard 1986; Hayashi et al. 1991, 1998; Suga et al. 1994), has been repeatedly shown to differ beyond doubt: the two phenotypes at issue are distinct one from the other not only at clinicogenetic (Mitsuda 1942, 1968) but also at pathogenetic levels. Thus, the differential imbalance of the central autonomic functions, including the limbic system, was shown in our earlier work (Fukuda and Matsuda 1969). Further, differential brain structure-functions have been shown by brain imaging techniques such as CT, SPECT, and MRI (Hayashi et al. 1992, 1993, 2000). Although the precise cerebral sites or circuits involved await further investigation, recent moves toward prospective longitudinal studies by a few groups as well as the proposal of a paradigm shift to deficit-nondeficit schizophrenia (Carpenter et al. 1999) are promising research approaches in line with those of the present authors and are only welcome and encouraged. The result of more than 25 years in-person follow-through, showing various subtypes of deficit exclusively in the typical group, argues strongly that our typical versus atypical designation could equate with deficit versus non deficit distinction. It is tempting to conceive of clinical identification of such distinction as early as at the onset of illness, if not even earlier. Impact of the distinction is obvious, as our results indicate.