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An Experimental Study

Oscar E. Espinas, MD; Charles M. Poser, MD

Arch Neurol. 1969;20(2):182-186.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 . . . [Full Text PDF of this Article]

Author Affiliations
Kansas City, Mo

From the Division of Neurology, University of Missouri School of Medicine, Kansas City General Hospital and Medical Center, Kansas City, Mo. Dr. Espina is presently with the Montreal Neurological Institute. Dr. Poser is presently with the College of Medicine, University of Vermont, Burlington, Vt.

Footnotes
Submitted for publication Sept 16, 1968; accepted Sept 26.

Reprint requests to Department of Neurology, Mary Fletcher Hospital, Burlington, Vt (Dr. Poser).

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