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Article
April 14, 1906

THE METABOLIC FACTOR IN THE ETIOLOGY OF THE PAROXYSMAL NEUROSES.

JAMA. 1906;XLVI(15):1115-1116. doi:10.1001/jama.1906.02510420045011
Abstract

Migraine, asthma and epilepsy, in addition to their periodicity of recurrence and a certain interchangeability, have in common the peculiarity that the paroxysm is not infrequently preceded by phenomena of functional derangement of one sort or other, which disappears with the attack, suggesting the possibility of some disturbance in the body chemistry as the exciting factor. These phenomena, in the opinion of Dr. Francis Hare,1 are dependent on variations in the intake and output of carbon dioxid. The disorders mentioned also exhibit certain relations to acute articular gout. Accordingly, Hare formulates the hypothesis that all the affections named are due primarily to an accumulation of unoxidized or imperfectly oxidized carbonaceous material in the blood, the paroxysm being a conservative measure adapted to the dispersion of such an accumulation. To this condition he gives the name hyperpyremia, and from a series of observations he develops the generalization that whatever tends

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