Thyrotoxic periodic paralysis in western countries.
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A case is reported of sporadic hypokalemic form of periodic paralysis, calling attention to the presence of certain rare signs, that is bilateral facial palsy and speech disturbances. The most modern reports on the aetiology and pathogenesis of periodic paralysis are discussed.
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Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism mainly seen in patients of Oriental origin and is rarely encountered in Western countries. TPP clinically resembles familial periodic paralysis with recurrent episodes of weakness or flaccid paralysis of especially the legs. Transient hypokalaemia is regularly observed during attacks and remission can be achieved by administration of potassium salts. The definitive treatment of TPP is to restore euthyroidism. This case describes a thyrotoxic patient who initially presented with periodic paralysis.
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An in vivo study of skeletal muscle paralysis induced by intravenous barium chloride has been made in curarized and non-curarized rats. The influence of potassium and calcium chlorides, propranolol, ouabain, and prior adrenalectomy on the paralysis has also been studied. Paralysis is found to be due to a direct effect on skeletal muscle, and to correlate well with the development of hypokalaemia. Possible mechanisms of action of barium are discussed, and attention is drawn to the similarity between barium poisoning and hypokalaemic familial periodic paralysis.
A rare complication of hyperthyroidism consists of sudden diffuse muscle weakness associated with severe hypokalemia. The clinical presentation is similar in most respects to familial periodic paralysis; however, the therapies proven to be effective differ in the two syndromes. A case of thyrotoxic hypokalemic periodic paralysis is presented and the literature is reviewed.
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Lateral gastrocnemius muscle biopsies from a 26-year-old man with hyperkalemic periodic paralysis and a 23-year-old man with hypokalemic periodic paralysis were studied. Both patients came from families in which older relatives had developed a vacuolar myopathy in association with their periodic paralysis. Muscle fibers were chemically skinned, and individual fibers were studied with a low-compliance strain gauge. The tension generated by fibers was studied in baths with calcium concentrations from 10(-8) mol/L to 2.5 x 10(-5) mol/L. The Ca-tension relationships and maximal tensions (normalized to fiber cross-sectional area) of fast and slow twitch fibers were indistinguishable from those found in fibers from 5 normal subjects. The results reinforce earlier findings which suggested that loss of Ca-induced myofibril contraction was not the cause of paralysis in periodic paralysis.
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