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Acute inflammatory demyelination in reperfusion nerve injury
Author(s) -
Nukada Hitoshi,
McMorran P. Denise,
Shimizu Jun
Publication year - 2000
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/1531-8249(200001)47:1<71::aid-ana12>3.0.co;2-p
Subject(s) - myelin , inflammation , pathology , medicine , pathological , lesion , sciatic nerve , ischemia , macrophage , reperfusion injury , schwann cell , immunology , central nervous system , anatomy , biology , cardiology , in vitro , biochemistry
We investigated the pathological appearance of acute inflammation and its role in the development of demyelination in reperfused rat sciatic, tibial, and peroneal nerves after a 5‐hour period of near‐complete ischemia. Polymorphonuclear neutrophil migration was seen early in the endoneurial lesion. After 18 hours of reperfusion, there was maximal intercellular adhesion molecule‐1 expression on endoneurial vessels, and polymorphonuclear neutrophil accumulation was then prominent, reaching a peak 24 hours after reperfusion. Endoneurial mononuclear macrophages increased nearly fourfold after 48 to 72 hours of reperfusion. Macrophages were observed invading Schwann cells and myelin lamellae with associated demyelination. Thus, this study provides evidence of macrophage‐associated demyelination after reperfusion similar to that seen in inflammatory neuropathies. Ann Neurol 2000; 47:71–79