What are the basic defects in patients with familial periodic paralysis, and where are these defects located? It has become increasingly clear that hypokalemia in itself is not the primary factor in this disease. Cases have been reported without alteration in serum potassium, and the onset, severity, and remission of attacks are not necessarily related to the degree of hypopotassemia. Solomon,1 reported in the July issue of the Archives of Neurology, has considered the diencephalic factors which might be present. His study was prompted by the case of a patient who presented features of both periodic paralysis and cataplexy.
The diencephalon as a pathophysiological site common to both periodic paralysis and the narcolepsy-cataplexy syndrome is suggested by the similarity of incidence, precipitating factors, and clinical features of the paralysis in the two conditions. Solomon's theory of a central-nervous-system defect in periodic paralysis is supported by the following facts and
PERIODIC PARALYSIS. JAMA. 1963;186(4):422–423. doi:10.1001/jama.1963.03710040148014