Disorders of Magnesium Metabolism in Epilepsy.

Clinical observations in man (Griffiths, 1947; Randall, Rossmeisl, and Bleifer, 1959; Hanna, Harrison, Maclntyre, and Fraser, 1960; Vallee, Wacker, and Ulmer, 1960) and experimental investigations in animals (Kruse, Orent, and McCollum, 1932) have shown that magnesium (Mg) depletion causes a marked irritability of the nervous system, eventually resulting in epileptic seizures. The possibility that convulsions may occur in Mg deficiency led some investigators to study the metabolism of this metal in the epilepsies, and a trend to low blood concentrations was usually found (Denis and Talbot, 1921; Blumgarten and Rohdenburg, 1927; Hirschfelder and Haury, 1934, 1935; Haury, 1942; Suter and Klingman, 1955). In successive studies, Hirschfelder and Haury (1935, 1938) found a lowering of Mg and a rise of potassium in the blood of epileptic patients, leading to a definite increase in the K/Mg ratio, proportional to the severity of the disease. Concerning the metabolism of magnesium in the cerebrospinal fluid, Cohen (1927), McCance and Watchorn (1931), and Greenberg and Aird (1938) found in epilepsy the same range of magnesium levels as in other nervous diseases. Hirschfelder and Haury (1938) found low concentrations of Mg in the cerebrospinal fluid of epileptic patients, though the levels were higher than in the blood. These findings, associated with the fact that Mg is a known depressor of the central nervous system and is involved in several enzymatic processes, including the synthesis of acetylcholine, were not appreciated by some authorities in the field of epilepsy, even when the neurochemistry of this disease was analysed (Tower, 1960).