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April 1, 1939


Author Affiliations


From the Division of Psychiatry, Bellevue Hospital, and the Department of Psychiatry, New York University Medical College.

JAMA. 1939;112(13):1217-1219. doi:10.1001/jama.1939.02800130001001

Beyond the fact that delirium tremens occurs in habitually severe and chronic alcoholism and that it frequently follows injuries, operations and acute infections, little is known of the actual etiologic factors at play. Since this syndrome was adequately and accurately described as long ago as 1813,1 it seems remarkable that no real attempt has been made to study the physiologic and chemical changes which accompany it. The more recent therapies,2 which have included various means of dehydration and repeated spinal drainage, are all based on the observation that at autopsy persons with delirium tremens frequently show cerebral edema. Such therapy, however, takes no account of the generalized dehydration and manifest toxicity which all these patients show and, furthermore, ignores many pathophysiologic phenomena which not only exist in these patients but are probably of at least equal importance.

In the prodromal period of delirium tremens the patient often experiences