Byron E. Leach

BRAIN RECORDINGS WITH SCHIZOPHRENIC BEHAVIOR: SOME METABOLIC FACTORS RESPONSIBLE FOR PHYSIOLOGICAL ALTERATIONS *

Our studies in schizophrenia began with the intensive clinical investigation of patients with this disease. The clinical observations have been the primary determinant of the direction our program has followed through the years. There have been no convincing data gathered in our studies to suggest that the basic nature of schizophrenia is primarily a consequence of faulty learning experience, that is, environmentally determined. While continuing to stress the importance of sound clinical observations in all of our investigations, we are convinced, on the basis of accumulated evidence, that the disease is fundamentally a disorder of some biological mechanism with the clinical picture representing symptoms of the process. The evolution of our investigative program directed toward correlating brain activity with behavior has been described in a number of publications.’e2J We therefore give only brief mention to the highlights of our principal developments as background for presenting data concerning our current studies. Our studies, throughout, have focused 011 the brain as the organ of behavior. A detailed description of the clinical picture of the disease schizophrenia is not necessary here. In summary, however, the outstanding and consistent manifestation of the disease is the lowered level of psychological awareness of patients afflicted with the disease. The patient’s conception of reality is distorted; his mental function, particularly during the overt, psychotic state, resembles in some aspects that of a “normal” person during a dream. The schizophrenic patient’s conceptualization of himself as a distinct entity is vague. His machinery for emotional expression and feeling is deficient; this is most marked in regard to his inability to experience pleasurable feelings. We currently consider these psychological phenomena to be manifestations of disordered brain function brought about by a metabolic aberration that, in the light of genetic and epidemiological studies, appears to be inherited. Numerous cortical ablation studies with humans carried out in the Columbia Greystone Project4 in 1948, as well as numerous animal studies, indicated to us that basic affectivity, that is, the effector mechanism for expression of emotion, did not require an intact cortex. With extensive removal of cortical tissue, the patients often had an alteration of affect associated with memory, but their basic effector machinery for expression of feeling and emotion was unchanged. We therefore evolved techniques for studying the relationship between physiological activity of other anatomical regions of the brain and affect ivity. Our studies suggested that specific parts of the olfactory brain were important in the expression of emotion. Stimulation of the septa1 region, an area