A hypothesis of osmotic endothelial injury. A pathogenetic mechanism in central pontine myelinolysis

Research output: Contribution to journalArticle

103 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)66-69
Number of pages4
JournalArchives of Neurology
Volume40
Issue number2
StatePublished - Jan 1 1983
Externally publishedYes

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Central Pontine Myelinolysis
Sodium
Osmotic Pressure
Wounds and Injuries
Demyelinating Diseases
Myelin Sheath
Serum
Endothelium
Blood Vessels
Edema
Chronic Disease
White Matter
Experimental Study
Person
Lesion
Arrangement
Bundle
Causes

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

A hypothesis of osmotic endothelial injury. A pathogenetic mechanism in central pontine myelinolysis. / Norenberg, Michael D.

In: Archives of Neurology, Vol. 40, No. 2, 01.01.1983, p. 66-69.

Research output: Contribution to journalArticle

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