Introduction
The possibility of a correlation between peptic ulceration and intracranial disease processes was postulated as early as 1841 by Schiff and 1845 by Rokitansky.43,46,47 Both described a peculiar kind of gelatinous gastromalacia associated with intracranial lesions in newborn infants. Rokitansky extended these observations to include a similar malacia seen in agonal states which characteristically involved the stomach and distal esophagus. He also noted a relationship between third ventricular tumors and discrete gastric ulcers.43 In spite of these observations the preeminence of Virchow and his theory of local vascular disease as the prime factor in peptic ulceration obscured the importance of the central influences for nearly 80 years.54 Harvey Cushing in the Balfour Lecture of 1932 redirected attention to the neurologic aspects of the problem. He presented data concerning 11 neurosurgical patients with intracranial disease, associated gastric ulceration or malacia, and postulated diencephalic centers for the control