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of hypokalemia When the myotonia is more troublesome than the weakness, mexiletine 200 mg tid is perhaps the best alternative, since it prevents both cold- and exercise-induced myotonia, but it does not in uence frequency of acute attacks Some additional bene t may be gained by adding beta-adrenergic agonists such as albuterol or salbutamol Some studies suggest that clenbuterol may have a direct effect in blocking the sodium channel, independent of its activation of adrenergic receptors Procainamide or the lidocaine derivative tocainide, in doses of 400 to 1200 mg daily, are also useful for the myotonia (the last carries a small risk of agranulocytosis) For the treatment of an acute and severe episode, intravenous calcium gluconate (1 to 2 g) often restores power If, after a few minutes, this treatment is unsuccessful, intravenous glucose or glucose and insulin and hydrochlorothiazide should be tried in order to reduce serum potassium concentration Other Sodium Channel Disorders Several other clinical presentations of hereditary periodic paralysis have been linked to mutations of the gene encoding the alpha subunit of the skeletal muscle sodium channel and probably represent variants of the disease just described One of these, described by Ricker and colleagues, has been designated myotonia uctuans, because muscle stiffness uctuated in severity from day to day In other respects the clinical features resembled those of myotonia congenita, including provocation of attacks of myotonia by exercise The muscle stiffness was only slightly sensitive to cold but was markedly aggravated by the ingestion of potassium and, interestingly, never progressed to muscular weakness or paralysis Myotonia permanens is the name given to a severe, persistent myotonia and marked hypertrophy of muscles, particularly of the neck and shoulders The EMG discloses continuous muscle activity This disease was discovered in the course of genotyping a patient who earlier had been reported by Spaans and associates as an example of myogenic SchwartzJampel syndrome, but it affects the same chloride channel as in hyperkalemic periodic paralysis Trudell and colleagues studied 14 patients from a large kindred with autosomal dominant myotonia, the main feature of which was periodic worsening of myotonia accompanied by muscle pain and stiffness, most severe in the face and hands The symptoms were enhanced by cold (suggesting paramyotonia), and severe stiffness and palpable rigidity followed within 15 min of the ingestion of potassium Neither of these measures provoked muscle weakness Muscle biopsy disclosed a normal ratio of types 1, 2A, and 2B bers, further distinguishing this disorder from typical myotonia congenita, where 2B bers may be reduced in number All patients in this family who were treated with the carbonic anhydrase inhibitor acetazolamide had a dramatic resolution of symptoms within 24 h hence the name acetazolamide-responsive myotonia This disorder has now been linked to the same molecular alteration of the sodium channel gene as occurs in hyperkalemic periodic paralysis (Ptacek et al) Rosenfeld and coworkers have described yet another form of painful congenital myotonia attributable to a novel mutation in the sodium channel alpha-subunit gene (SCN4A) Affected members of this family experienced debilitating pain, particularly severe in the intercostal muscles Also, the pain was resistant to treatment with acetazolamide and other antimyotonic drugs (mexiletine and tocainamide) and could not be provoked by ingestion of potassiumrich foods differing in these ways from the patients described by Trudell and Ptacek and their associates.

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Finally, in regard to disorders of the sodium channel, it should be mentioned that the marine toxins (ciguatoxin, tetrodotoxin, saxitoxin), discussed in Chap 43, produce their effects on the peripheral and central nerves by blocking sodium channels, but they have little obvious effect on muscle function

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