Disinhibitory psychopathology: A new perspective and a model for research.

TLDR

Disinhibitory psychopathology encompasses psychopathy, hysteria, hyperactivity, antisocial and impulsive personality, and alcoholism, and its physiological basis is debated, with limbic system dysfunction proposed but evidence largely indirect. The authors propose that these categories are separate manifestations of a single genetic diathesis and that the septal syndrome in animals can serve as a valid model of its behavioral aspects. They outline a program of experiments using the septal lesion animal model to investigate this diathesis.

Abstract

The produced by lesion of the septum in animals can serve as a functional research model of human disinhibitory psychopathology. Disinhibitory psychopathology appears to span several traditionally separate psychological categories—psychopathy, hysteria, hyperactivity, antisocial and impulsive personality, and alcoholism. It is proposed that these categories are separate manifestations of the same genetic diathesis and that the septal syndrome may constitute a valid model of behavioral aspects of this diathesis. A program of experimentati on utilizing this animal model is outlined. The quest for a physiological explanation of syndromes of disinhibition or dyscontrol, especially psychopathy, is a current preoccupation among theoreticians of impulsive behavior (see Mawson & Mawson, 1977; Syndulko, 1978). One line of speculation in particular has focused on the limbic system as a possible site of central nervous system (CNS) dysfunction responsible for behavioral disinhibition (Gray, 1972; Hare, 1970). Evidence bearing on this hypothesis, however, is rather indirect, consisting mainly of psychophysiological anomalies open to a variety of interpretations. Among findings enumerated as possibly implicating limbic dysfunction are the electroencephalogram abnormalities discovered in psychopaths and impulsive children (Arthurs & Cahoon, 1964; Ehrlich & Keough, 1956; Knott, Platt, Ashby, & Gottlieb, 1953), including temporal lobe slow-wave activity (Bay-Rakal, 1965; Hill, 1952). Also cited are the abnormal positive spikes localized in the temporal lobe that have been observed in human syndromes of extreme violence, aggres