To the Editor: In a recent issue of the Journal, Shitij Kapur, M.D., Ph.D., F.R.C.P.C., described the linkage between biology, phenomenology, and pharmacology in schizophrenia (1). Two articles in the British literature from 1961 (2) and 1966 (3) seem to dovetail nicely with Dr. Kapur’s elegantly crafted framework.

The British authors argued against Federn’s 1953 theoretical model of psychosis (4) as an impairment of ego functions and suggested that the breakdown in interpersonal difficulties was a reaction to a primary cognitive disturbance in the field of attention and perception and that all schizophrenia symptom profiles could be interpreted as reactions to this basic disorder. Their methods consisted of meticulously recording clinical interviews with schizophrenia patients. They were not aware of the central role of dopamine in reward and reinforcement. Thus, they were not able to describe the reported abnormalities of perception in terms of aberrant salience rather than as phenomenological entities alone.

Dr. Kapur’s convincing hypothesis presents strong experimental, pharmacological, and neurobiological data to help one understand the mass of schizophrenia phenomenology previously described and ascribed to varying, now presumably incorrect, hypotheses.