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IRVINE MCQUARRIE, A. E. HANSEN, M. R. ZIEGLER, Studies on the Convulsive Mechanism in Idiopathic Hypoparathyroidism, The Journal of Clinical Endocrinology & Metabolism, Volume 1, Issue 10, 1 October 1941, Pages 789–798, https://doi.org/10.1210/jcem-1-10-789
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Abstract
THE LACK OF AGREEMENT not infrequently observed between the level of serum calcium and the occurrence of generalised convulsions in the ‘low-calcium’ types of tetany indicates the need for further information regarding other factors involved in the convulsive mechanism in such disorders. That a disturbance in the metabolism of calcium and phosphorus is primarily responsible for the initial development of the neuromuscular hyperexcitability characterizing parathyreoprivic tetany, as well as tetany associated with calcium deprivation or vitamin D deficiency, can no longer be gainsaid. Neither the milder symptoms of active tetany nor generalized convulsions occur in these clinical disorders without a marked decrease in the calcium of the blood plasma and other extracellular body fluids. Furthermore, all available evidence indicates that the ionized fraction of the calcium plays the chief role in this respect. That occurring in the combined or undissociated phase (either with protein or as colloidal calcium phosphate) appears to be physiologically inactive. The parathyroid glands have been shown to play a decisive rôle in the regulation of the Ca++ concentration (1, 2). In hypoparathyroidism the Ca++ is below normal; in hyperparathyroidism, it is above.
