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December 1952


Author Affiliations


Markle Scholar in Medical Sciences (Dr. Jenkins).; Associate Professor of Medicine and Pediatrics, University of California, in San Francisco; formerly Associate in Medicine, Peter Bent Brigham Hospital, and Instructor in Medicine, Harvard Medical School (Dr. Forsham).; Hersey Professor of the Theory and Practice of Physic, Harvard Medical School, and Physician-in-Chief, Peter Bent Brigham Hospital (Dr. Thorn).; From the Department of Medicine, Harvard Medical School, and the Medical Clinic, Peter Bent Brigham Hospital.

AMA Arch NeurPsych. 1952;68(6):776-782. doi:10.1001/archneurpsyc.1952.02320240051004

THE ETIOLOGY of multiple sclerosis remains obscure. The extensive experimental studies pertaining to the role of hypersensitivity phenomena as a possible underlying mechanism in the development of demyelinating diseases in general, and of multiple sclerosis in particular, has recently been reviewed by Hurst.1 Although the allergic causation of multiple sclerosis is far from being established, there is no doubt about the apparently spontaneous remissions and exacerbations which mark the course of this chronic, progressive disease. The tendency of multiple sclerosis to follow this particular clinical pattern leads one to investigate those nonspecific factors in human metabolism which are capable of altering tissue reaction. It is well established that an antibody-antigen reaction, as well as other types of inflammatory action, may be modified significantly by an alteration in the level of circulating adrenocortical steroids. It was only logical, therefore, that the status of spontaneous adrenocortical activity, as well as the

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