INTERMITTENT flaccid paralysis of the extremities, and to a lesser extent of other body musculature, is a syndrome that has been recognized for about one hundred years. Although the therapeutic value of K salts was empirically discovered at the turn of this century (Singer and Goodbody, 1901; Buzzard, 1901; Mitchell, Flexner and Edsall, 1902), such treatment was not applied with any degree of regularity during the next four decades even though Kramer in 1908 had discovered that high carbohydrate intake was capable of precipitating attacks. The actual occurrence of a decline in serum K levels during attacks of paralysis was not noted until 1934 by Biemond and Daniels. Soon, Aitken et al.(1937), Allott and McArdle (1938) and then many others since them (Grob, Johns, and Liljestrand, 1957; Zierler and Andres, 1957; Shy, Wanko, Rowley and Engel, 1961) investigated the role that K plays in this syndrome.

As metabolic studies have extended and become more refined, it came to light that the level of serum K does not always drop during attacks of paralysis. In some persons, the K levels may remain within the normal range, or in fact they may actually rise during attacks. This knowledge has led to the division of" potassium periodic paralysis" into at least three categories:(a) hypokalsemic (familial) periodic paralysis (Hypo PP), which is by far the most common (Talbott, 1941; Bekeny, Hasznos and Solti, 1961);(b) normokalaemic periodic paralysis (Normo PP), which has only been reported sporadically (Tyler, Stephens, Gunn and Perkoff, 1951; Poskanzer and Kerr, 1961); and (c) hyperkalaemic periodic paralysis (Hyper PP), also called adynamia episodica hereditana (Gamstorp, 1956, 1957; Bekeny, Hasznos and Solti, 19616; Creutzfeldt, 1961; McArdle, 1962), which has been recognized as a distinct disorder only