Hypernatraemia in cerebral disorders

Abstract

SYNOPSIS Six patients are described in whom cerebral damage was associated with raised plasma sodium and chloride concentrations and with extremely low urinary outputs of sodium and chloride. The patients were not clinically dehydrated and direct determinations showed that the blood and plasma volumes, the endogenous creatinine clearance, and the urinary output of antidiuretic hormone were normal. For these and other reasons it is concluded that the metabolic picture results not from diminished circulatory volume, water deficiency, sodium deficiency, undetected diabetes insipidus or osmotic diuresis, but from the cerebral damage itself.In these and other cited cases, the cerebral damage was localized chiefly in the frontal lobes, hypothalamus or lower brain-stem, thus suggesting a descending pathway, the relationship of which to the pineal area controlling aldosterone secretion requires clarification.Allott (1939) first reported the occurrence of hypernatraemia and hyperchloraemia, associated with an abnormally low urinary excretion of sodium and chloride, in patients suffering from cerebral disease in whom there was no renal disease, and Higgins, Lewin, O'Brien, andTaylor (1951, 1954) described a total of 14 patients in coma after severe head injury in whom the same features were found. Cooper and MacCarty (1951) also described this syndrome in three patients suffering from different intracranial disorders. Subsequently, there have been reports of essentially similar cases (Persson, 1953;Anthonisen, Hilden, and Thomsen, 1954;Elliot, 1955; Allott, 1957; Petit-Dutaillis and BernardWeil, 1958). These authors have, in general, taken the view that the hypernatraemia that they have observed could not be adequately explained without postulating a direct and primary connexion, other than diabetes insipidus, between the cerebral disorder and the metabolic effect.Hypernatraemia

Pineal Enlargement, with Hypernatraemia, Hypokalaemic Alkalosis, and Thyrotoxicosis

“…8, 1962644 SmFP. 8, 1962 PINEAL ENLARGEMENT Hypernatraemia with hyponatruria has been described on several occasions in association with cerebral disease (for references see Taylor, 1962). The sites of brain damage are most usually the orbital surface of the frontal lobes, the hypothalamus, and the brain-stem.…”

Trichophytic Granuloma Simulating Bazin's Disease

“…Such patients resemble ours in sometimes having a .severe degree of hypernatraemia but only a moderately raised aldosterone output (Allott, 1957;Taylor, 1962). They differ in not showing hypokalaemia or alkalosis.…”

“…Hypernatraemia with hyponatruria has been described on several occasions in association with cerebral disease (for references see Taylor, 1962). The sites of brain damage are most usually the orbital surface of the frontal lobes, the hypothalamus, and the brain-stem.…”

Neurogenic hypernatraemia

“…In 1952 Cooper and Crevier described neurogenic hypernatraemia related to intracranial lesions in a patient with adipsia and plasma hypertonicity, without clinical signs of dehydration. The concept of neurogenic hypernatraemia was then developed by Taylor (1962), who observed a few cases of hypernatraemia sub-sequent to head injury. He concluded that it may be due to alterations of neural organization subserving the regulation of sodium excretion by the kidney.…”