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SEYMOUR SOLOMON, MD

Arch Neurol. 1963;9(1):55-63.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

In the literature of the first three decades of this century, the central origin of periodic paralysis was postulated. As it became clear that periodic paralysis was associated with hypopotassemia, the possible role of the central nervous system in this condition was summarily discounted.

That hypopotassemia in itself is not the basic factor in periodic paralysis is supported by the following facts. Cases of familial periodic paralysis have been reported without alteration in serum potassium during an attack.^1-5 (Some of these cases, for example Wolf's,¹ may have been unrecognized hyperpotassemic paralysis). The onset, severity, and remission of attacks are not necessarily related to the degree of hypokalemia.^2,6,7,8-10

Attacks may occur at levels of serum potassium that do not cause paralysis in normal individuals. Conversely, decrease of serum potassium in patients with familial periodic paralysis does not necessarily produce weakness, whereas strength may begin to improve while . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Division of Neurology, Montefiore Hospital.

Footnotes
Submitted for publication Feb 16, 1963; accepted March 12.

Assistant Clinical Professor of Neurology, College of Physicians and Surgeons, Columbia University.

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