Abnormalities of serum sodium levels and salt excretion in patients with cerebral disease have attracted considerable attention in recent years.1-7 Persistent, excessive sodium loss in the urine with hyponatremia and even circulatory collapse is a rare syndrome which has been described in detail.6 Hypernatremia is much more common, may be complicated by azotemia, and occurs with particular frequency in patients with damage to the frontal lobes and/or hypothalamus.1,7 It has been postulated that these latter cases are due to chronic dehydration, related in all probability to dulling of the sensation of thirst, with or without an associated diabetes insipidus.8-10 However, such an explanation has not found universal acceptance.In experimental animals, Lewy and Gassman11 found hyperchloremia and hypochloruria following passage of coagulating currents into the "paroptic" region of the hypothalamus, while Keeler12 observed sodium diuresis in the first 24 hours after paraventricular lesions.
GANONG WF, YUEN VS, STEVENSON RS, DAILY WJR, DAVIDSON JM. Diencephalic and Frontal Lobe Lesions: Effect on Sodium Metabolism in Dogs. Arch Neurol. 1961;4(2):182–189. doi:10.1001/archneur.1961.00450080064007
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