Psychosomatic Aspects of Vagotomy

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Abstract
There is now considerable clinical and experimental evidence that the autonomic nervous system may play an important role in the pathogenesis of gastric and duodenal ulceration. Cushing (1932) reported the development of gastric ulcers after intracranial operations, and concluded from animal experiments that parasympathetic overactivity produced changes in the gastric mucosa conducive to ulcer formation. Experimental lesions in the hypothalamus were found to give rise to gastric ulcers by Watts and Fulton (1935) and Hoff and Shehan (1935). Davey, Kaada and Fulton (1950) found that increased gastric secretion resulted from stimulation of areas of the frontal cortex in monkeys and dogs. Furthermore, clinical reports have shown that lesions in the cerebral cortex, diencephalon and midbrain have been found to be associated with gastric ulcers (Bochus, 1949).