The concepts of “process” and “reactive” schizophrenia currently receive much attention in the literature. The former term implies an inherent biological process which eventuates in a schizophrenic outcome, regardless of life stress; the latter implies that schizophrenia is to be seen as a reaction to severe and usually psychological stress. “Process” schizophrenia is associated, therefore, with a poor outcome; “reactive” schizophrenia with a good one. It is unfortunate that the idea of a dichotomy, or a continuum, with “process” at one pole and “reactive” at the other, is used as it is, for it implies a unitary or uni-dimensional base on which to judge patients. In fact, if one reads current descriptions of the typical “process” 1 or “reactive” 2 patient, it becomes apparent that there are several parameters concealed in these apparently unitary concepts. The six most important parameters are shown in Table 1. Where then do we put the patient who had good premorbid adjustment (characteristic of the “reactive” patient), for whom no precipitating event was observable (characteristic of the “process” patient), whose primary symptomatology demonstrated aggression, intact social awareness and sensorial impairment (characteristic again for the “reactive” patient)? The process-reactive distinction would serve better if fewer parameters were buried implicit within it, but it has come into usage with its several parameters. Subtle implications about etiology contaminate the usage of these terms, ranging from one extreme of seeing the schizophrenic “process” as the manifestation of a monogenically determined, biochemical defect, to the opposite extreme of seeing it solely as a “reaction” to early and contemporary life stress. Such usages are of limited usefulness at best; the truth lies somewhere in between, and a more sophisticated model of etiology must be employed. 3 In this study, we have chosen to avoid the controversies and contradictions inherent in the concepts of “process” and “reactive” and their etiological implications and to deal instead with some of the observable and relatively objective parameters cited in Table 1. In particular, we have studied the interrelationships of the four following factors: premorbid adjustment, nature of onset, diagnostic category, and response to treatment (including intellectual functioning).