Abstract

Our working hypothesis, over the past decade, has been that the limbic system modulates stress ulcer susceptibility1,2. It was largely based on early reports in the literature that linked (in a vague kind of way) this system of interconnected brain structures to the development of so-called “psychosomatic” disorders. In 1949 MacLean3, elaborating on the Papez4 theory of emotions, proposed that the limbic system might represent a primitive “visceral brain”, responsible for the development of psychosomatic diseases. Much of the evidence was based on case reports from patients with temporal lobe epilepsies. Patients with so-called uncinate fits were described, whose feelings of terror were also sometimes associated with visceral auras, i.e., various gastric and intestinal symptoms, ranging from epigastric uneasiness, chewing movements and grinding of the teeth, to feelings of hunger and frequent defecation and urination. Correspondingly, the data from early animal studies indicated that parts of the limbic system might be involved in emotional behavior. Kluver and Bucy5 had reported that monkeys with bilateral temporal lobectomies became tame and docile, showed a collection of symptoms which were labelled “psychic blindness”, displayed various “oral tendencies”, and engaged in bizarre sexual activities. It appeared that the monkeys could no longer discriminate between potentially dangerous objects and objects that might be useful to them. One interpretation of these studies is that the brain lesions had disconnected sensory inputs from the appropriate, adaptive behaviors. Later experiments showed that many of the effects of these radical lobectomies could be traced to damage in the amygdala6. These findings lead to the proposal that the amygdala connects sensory inputs with emotional and visceral responses, based on the recognition that a particular situation may be threatening to the organism7.

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