Japanese Journal of Psychosomatic Medicine
Online ISSN : 2189-5996
Print ISSN : 0385-0307
ISSN-L : 0385-0307
Neurophysiological Study of Anorexia Nervosa
Shin-ichiro IshibashiHiroyuki Suematsu
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JOURNAL FREE ACCESS

1978 Volume 18 Issue 3 Pages 223-230

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Abstract

Up until the present, very little is known about the pathophysiology of anorexia nervosa, one of the most typical psychosomatic diseases, which creates a disturbance in the food intake together with a variety of psychological symptoms. A biological change in the brain may be suggetsted from the fasts that it often appears in adolescent women, that it accompanies endocrinological disturbances, and that it usually has a certain character tendency and behavior pattern. It would be of great use in understanding the pathology of anorexia nervosa, to take synthetically the clinical data and the food intake regulation system, which has been substantiated recently in animal experiments.Animals have their delicate food intake regulation system in the hypothalamus which is regulated by humoral factors such as glucose and FFA, as main substances, together with growth hormone, insuline, glucagon, ACTH, corticosteroid, sex hormones and so on. These humoral factors in anorexia nervosa change very little in the direction of strengthening food intake. This fact is a result of long periods of starvation and cannnot explain the diturbance in food intake as the result of the change in humofal factors. The pathological state of the food intake system in the hypothalamus must now be considered. It would appear, from the facts, that a disturbance of food intake is influenced by psychological factors and it is reversible, that it is a functional change. First of all, an abnormal condition of a neurotransmitter in the brain is considered to account for the pathological state of anorexia nervosa. Until the present, no definitive evidence for the role of monoamine in the feeding behavior has been completed. It would appear, according to electrophoretic experiments, that noradrenaline and dopamine create an inhibitory effect to the feeding center. To explain the pathophysiology of anorexia nervosa, the hypothesis that dopamine may be increased in the hypothalamus may be accountable for an anorexia and psychological systems such as hyperactivety etc. But from the standpoint that psychological factors are closely related to onset and clinical course of this disease, it is necessary to consider changes in the higher central nervous system. Recent studies have demonstrated the existence of an inhibitory pathway in monkeys that goes directry from the orbitofrontal cortex, a part of the frontal cortex, to the feeding center. Thus, in anorexia nervosa patient, it would be of interest in understanding this disease to assume that a pathway exists from the cerebral cortex via the orbitofrontal cortex through which psychological factors inhibit the feeding center.

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© 1978 Japanese Society of Psychosomatic Medicine
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