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Arch Neurol. 1998;55:1487.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Twenty point mutations have been identified in the gene encoding a-subunit of skeletal muscle sodium channel (SCN4A) in patients with hyperkalemic periodic paralysis (HYPP) and myotonic disorders^1-4; however, no information on the normokalemic periodic paralysis (NOPP) has been well documented. We encountered an interesting case of congenital adrenal hyperplasia (CAH) accompanying NOPP. Soon after birth, the patient exhibited salt-wasting symptoms. Her mother had noticed abnormalities of the infant's external genitalia since the birth, and she was diagnosed as having CAH due to 21-hydroxylase deficiency by the findings of 46XX chromosomes, the gynecologic laparoscopy, and increased plasma 17a-hydroxyprogesterone and urinary 17-ketosteroid levels. The patient had been treated with glucocorticoid replacement since the diagnosis of CAH, and the dosage had been increased as she grew up. Nevertheless, she began to experience occasional paralytic episodes at 12 years old. The paralysis tended to appear first in the legs, and then spread to . . . [Full Text of this Article]