Neuropathologic observations in electrolyte-induced myelinolysis in the rat.
A recent analysis of a group of patients with central pontine myelinolysis (CPM) disclosed that a rapid rise in serum sodium from a hyponatremic baseline preceded the clinical onset of the disorder. To test the view that electrolyte derangements may be crucial in the pathogenesis of CPM, rats were given hypertonic saline following a three-day period of hyponatremia. Symmetrical, predominantly demyelinative lesions were found the neocortex, claustrum corpus striatum, external capsule, anterior commissure, hippocampus and its fimbria, thalamus, brainstem, tegmentum, and superior vermis of the cerebellum. This report details the histopathology and topography of these lesions and compares them with human CPM. The findings support the view that rapid rise in serum sodium may be responsible for the development of CPM in man.
D000818:Animals; D001927:Brain Diseases / Q000097:blood / Q000473:pathology*; D001933:Brain Stem / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D003342:Corpus Striatum / Q000473:pathology; D003711:Demyelinating Diseases / Q000097:blood / Q000473:pathology*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000473:pathology; D007010:Hyponatremia / Q000097:blood / Q000378:metabolism / Q000473:pathology; D008297:Male; D011149:Pons / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D012964:Sodium / Q000097:blood*; D013788:Thalamus / Q000473:pathology
D012462:Saline Solution, Hypertonic; D012964:Sodium