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This is the best-known form of periodic paralysis The history of the disease is dif cult to trace, but the rst unmistakable account was probably that of Hartwig in 1874, followed by the accounts of Westphal (1885) and Oppenheim (1891) Gold am (in 1895) rst called attention to the remarkable vacuolization of the muscle bers that is characteristic of the process In 1937, Aitken and associates described the occurrence of low serum potassium during attacks of paralysis and reversal of the paralysis by the administration of potassium, thus setting the stage for subsequent differentiation of the hyperkalemic forms of periodic paralysis For English-speaking readers, Talbott s monograph serves as the best historical review of the subject and includes all cases that had been reported prior to 1941; the more recent reviews by Layzer and by Lehmann-Horn and Engel and their associates bring the subject largely up to date The usual pattern of inheritance is autosomal dominant with reduced penetrance in women (male-to-female ratio of 3 or 4 to 1) Fontaine and Ptacek and their coworkers have localized the disease to chromosome 1q in a region containing the gene that encodes the alpha subunit of the calcium channel of skeletal muscle The subunit, which is part of the dihydropyridine receptor complex, is located in the transverse tubular system This region is believed to act both as a voltage sensor that controls calcium release from the sarcoplasmic reticulum, thus mediating muscle excitationcontraction coupling, and as a calcium-conducting pore How the reduced calcium channel function relates to hypokalemia-induced attacks of muscle weakness is not known Clinical Manifestations In our experience, this disease has become clinically apparent after adolescence and has been much more severe in males We note, however, that in Talbott s review of 152 cases, there were 40 in which symptoms began before the 10th year of life and 92 before the 16th year The typical attack comes on during the second half of the night or the early morning hours, after.

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a day of unusually strenuous exercise; a meal rich in carbohydrates favors its development Excessive hunger or thirst, dry mouth, palpitation, sweating, diarrhea, nervousness, and a sense of weariness or fatigue are mentioned as prodromata but do not necessarily precede an attack Usually the patient awakens to discover a mild or severe weakness of the limbs However, diurnal attacks also occur, especially after a nap that follows a large meal The attack evolves over minutes to several hours; at its peak, it may render the patient so helpless as to be unable to call for assistance Once established, the weakness lasts a few hours if mild or several days if severe The distribution of the paralysis varies Limbs are affected earlier and often more severely than trunk muscles, and proximal muscles are possibly more susceptible than distal ones The legs are often weakened before the arms, but exceptionally the order is reversed The muscles most likely to escape are those of the eyes, face, tongue, pharynx, larynx, diaphragm, and sphincters, but on occasion even these may be involved When the attack is at its peak, tendon re exes are reduced or abolished and cutaneous re exes may also disappear Sensation is preserved As the attack subsides, strength generally returns rst to the muscles that were last to be affected Headache, exhaustion, diuresis, and occasionally diarrhea may follow the attack Myotonia is not seen; indeed, clinical or EMG evidence of myotonia essentially excludes the diagnosis of hypokalemic periodic paralysis Attacks of paralysis tend to occur every few weeks and tend to lessen in frequency with advancing age Rarely, death may occur from respiratory paralysis or derangements of the conducting system of the heart Mainly, such fatal cases were reported in the era before modern intensive care Atypical forms include weakness of one limb or certain groups of muscles, bibrachial palsy (inability to lift one s arms or to comb one s hair), and transient weakness during accustomed activities Earlier descriptions in the literature of daily brief attacks, some associated with exposure to cold or coupled with muscular hypertrophy or exophthalmic goiter, preceded recognition of the other types of periodic paralysis and cannot be evaluated Some of our patients had a talipes deformity from early life During middle adult life, a number of patients have developed a slowly progressive proximal myopathy, with vacuolated and degenerated bers and myopathic action potentials, in some instances long after attacks of periodic paralysis had ceased Laboratory Findings The attacks are accompanied by reduction in serum K levels, as low as 18 meq/L, but usually at levels that would not be associated with muscle weakness in normal subjects The fall in serum K is associated with little or no increase in urinary K excretion Presumably, large quantities of K enter the muscle bers during an attack, but this explanation may not be complete Some episodes occur with near-normal levels of K, and weakness persists for a time after the serum level has been restored The serum K levels return to normal during recovery Although the shifts in K are of undoubted importance in the pathogenesis of muscle weakness, the marked sensitivity to small reductions of serum K suggests that other factors are also operative and that the fall in K may be a secondary phenomenon As in hyperkalemic paralysis, the muscular weakness in this disease is associated with a decrease in the amplitude, and eventual loss, of muscle action potentials and there is failure of excitation by supramaximal stimulation of peripheral nerve or by strong voluntary effort A decline in strength precedes loss of motor unit potentials and the failure of propagation of action potentials over the surface of the ber The polarization potentials of muscle bers.

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