Hyponatremia in Cerebral Disease Resulting from the Inappropriate Secretion of Antidiuretic Hormone

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Abstract
HYPONATREMIA has been observed repeatedly in patients with various brain lesions. Observations on a number of patients with cerebral hyponatremia were reported by Peters and his co-workers1 in 1950. They concluded that the etiology of the hyponatremia was an excessive urinary loss of sodium. It was postulated that the cerebral lesion diminished tubular reabsorption of sodium either indirectly by depressing adrenocortical function (decreased ACTH secretion) or directly by decreasing renal tubular reabsorption of sodium (presumably via the renal nerves). Two years later Welt and his associates2 described 2 additional patients with cerebral hyponatremia. Here, again, renal salt wastage was the . . .