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January 1924

STUDIES OF THE METABOLISM IN EPILEPSY: I. THE NONPROTEIN NITROGENOUS CONSTITUENTS OF THE BLOOD

Author Affiliations

Fellow in Medicine of the National Research Council; BOSTON; PALMER, MASS.

From the laboratories of the Department of Neuropathology, Medical School of Harvard University, and the Monson State Hospital. This research was made possible through a grant by the Committee on Epilepsy, New York City. This paper is No. 6 of a series of studies in metabolism from the Harvard Medical School and allied hospitals. The expenses have been defrayed in part by a grant from the Proctor Fund of the Harvard Medical School for the study of chronic diseases.

Arch NeurPsych. 1924;11(1):54-63. doi:10.1001/archneurpsyc.1924.02190310060004
Abstract

Many physicians believe that defects of protein metabolism are of etiologic importance in epilepsy. This belief finds expression in the low protein diet which these clinicians prescribe for epileptic patients. The basis of such a belief is partly the result of therapeutic test and partly the result of laboratory experiment. Many writers have reported the beneficial effect of low protein, or of purin-free diets, though this favorable testimony is not unanimous. Cuneo,1 for example, states that improvement is more marked with a high protein than with a carbohydrate diet. Weeks2 et al. find no relation between diet and convulsions. The experimental evidence for faulty protein metabolism is found in the work of numerous investigators, mostly French, English and German, who have reported variations in the amounts of urinary uric acid, urea, ammonia or total nitrogen in the periods preceding or following convulsions. An analysis of these published data

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