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February 1984

Hypermagnesemic Paralysis, Digitalis, and Acetylcholine Release

Author Affiliations

Consultation d'Endocrinologie-Nutrition Sce du Pr J Guerre Chu Cochin F 75674 Paris Cédex 14 France

Arch Neurol. 1984;41(2):134-135. doi:10.1001/archneur.1984.04050140032007

To the Editor.  —I read with interest the report of a case of hypermagnesemic periodic paralysis1 in the Archives.This paralysis, similar to hypokalemic paralysis, is associated with elevated serum magnesium levels and low urinary magnesium excretion. Emser thinks that this hypermagnesemic paralysis is due to a genetic disorder of renal magnesium absorption. An increased active ion transport causes hypermagnesemia, which itself induces paralysis. The mechanism of the preventive effects of the hypermagnesemic attacks by digoxin therapy seems, according to Emser, to be due to the blocking of active electrolyte tubular resorption. However, in this case, this treatment should have accompanied an increase in magnesium excretion. Emser did not observe such an increase.Therefore, I suggest another reason for the beneficial therapeutic effect of cardiac glucoside.The main mechanism of paralysis induced by magnesium excess is the blocking of neuromuscular transmission due to the magnesium-indiced inhibition of acetylcholine release

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