Central pontine myelinolysis. An ultrastructural and elemental study.
Central pontine myelinolysis (CPM) has been classified as a unique disease of myelin with a peculiar localization in the central pons. Although its etiology and pathogenesis are unknown, some have compared its histopathology to that of multiple sclerosis. Ultrastructural studies of suitably preserved tissue have been lacking. We have recently studied 3 cases of CPM, selectively immunostaining 2 cases and examining the fine structure and elemental composition of the third case obtained shortly after death. IgG could not be demonstrated within or around the lesions. The findings of an increased Na/K ratio and of intramyelinic vocuoles at the periphery of the lesion sjggest that the pathogenesis of CPM might include a phase of intramyelinic edema with subsequent rupture of the distended myelin sheaths. An increase in the permeability of the blood-brain barrier might represent a complicating factor. The spheroids in our case are primarily reactive in type and do not support pior light-microscopic interpretations of concomitant neuroaxonal dystrophy. The unexplained presence of tin within the lesion indicates a need for further study of this element in CPM.
D000328:Adult; D002857:Chromium / Q000378:metabolism; D003711:Demyelinating Diseases / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007074:Immunoglobulin G; D008297:Male; D008875:Middle Aged; D011149:Pons / Q000378:metabolism / Q000648:ultrastructure; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D014001:Tin / Q000378:metabolism
D007074:Immunoglobulin G; D002857:Chromium; D014001:Tin; D012964:Sodium; D011188:Potassium