PT - JOURNAL ARTICLE AU - Taylor, W. H. TI - Hypernatraemia in cerebral disorders AID - 10.1136/jcp.15.3.211 DP - 1962 May 01 TA - Journal of Clinical Pathology PG - 211--220 VI - 15 IP - 3 4099 - http://jcp.bmj.com/content/15/3/211.short 4100 - http://jcp.bmj.com/content/15/3/211.full SO - J Clin Pathol1962 May 01; 15 AB - 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.