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Article
February 1983

A Hypothesis of Osmotic Endothelial Injury: A Pathogenetic Mechanism in Central Pontine Myelinolysis

Author Affiliations

From the Laboratory of Neuropathology, Denver Veterans Administration Medical Center, and Department of Pathology, University of Colorado Health Sciences Center, Denver.

Arch Neurol. 1983;40(2):66-69. doi:10.1001/archneur.1983.04050020028004
Abstract

• Central pontine myelinolysis (CPM) is a demyelinative disorder of unknown origin. Recent clinical and experimental studies have indicated an association of CPM with a rise in the serum sodium level. I propose that the rapid rise in the serum sodium level causes an osmotic injury to the endothelium resulting in the release of myelinotoxic factors and/or the production of vasogenic edema. The latter factors may lead to demyelination. The patient at risk, viz, a chronically ill, alcoholic, cirrhotic person, may be the one least able to generate protective cerebral mechanisms against the osmotic stress. The location of lesions may be explained by a suitable anatomic arrangement consisting of an extensive admixture of gray and white matter; thus, myelinotoxic factors derived from the richly vascular gray are able to interact with adjacent bundles of myelin-containing white matter.

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