THE ROLE that systemic blood hyperosmolality may play in causing neurologic disease has been called in question by the clinical description of hyperosmolal, hyperglycemic nonketotic coma. This condition, which occurs mostly in elderly persons with early diabetes mellitus, consists of coma, dehydration, elevation in blood sugar, hyperosomolality, and various neurologic deficits. There is a good clinical response to insulin and hypotonic fluids. Since the first report by Sament and Schwartz in 19571 the syndrome has been described in other disturbances such as severe burns, during peritoneal dialysis, and during the course of steroid therapy.2-4 Recently, Maccario et al5 have recorded seven cases presenting focal neurologic deficits in association with the above syndrome.
In order to explain the occurrence of the clinical manifestations such factors as hyperosmolality, intracellular dehydration, and a direct toxic effect of glucose upon the nervous system, acting singly or in combination, have been
Espinas OE, Poser CM. Blood Hyperosmolality and Neurologic Deficit: An Experimental Study. Arch Neurol. 1969;20(2):182–186. doi:10.1001/archneur.1969.00480080082009
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