A hypothesis of osmotic endothelial injury. A pathogenetic mechanism in central pontine myelinolysis.
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.
D001696:Biomechanical Phenomena; D001808:Blood Vessels / Q000293:injuries*; D001927:Brain Diseases / Q000209:etiology / Q000473:pathology; D002908:Chronic Disease; D003711:Demyelinating Diseases / Q000209:etiology* / Q000473:pathology; D004727:Endothelium; D006801:Humans; D007010:Hyponatremia / Q000150:complications; D008108:Liver Diseases, Alcoholic / Q000150:complications; D009995:Osmosis; D011149:Pons / Q000473:pathology