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

Arch Neurol. 1983 Feb;40(2):66-9. doi: 10.1001/archneur.1983.04050020028004.


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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Biomechanical Phenomena
  • Blood Vessels / injuries*
  • Brain Diseases / etiology
  • Brain Diseases / pathology
  • Chronic Disease
  • Demyelinating Diseases / etiology*
  • Demyelinating Diseases / pathology
  • Endothelium
  • Humans
  • Hyponatremia / complications
  • Liver Diseases, Alcoholic / complications
  • Osmosis*
  • Pons* / pathology