Experimental allergic neuritis induced by galactocerebroside

Abstract

Experimental allergic neuritis (EAN), an animal model of human demyelinative neuritis, was induced by sensitization with galactocerebroside, a glycolipid hapten common in central and peripheral nervous system myelin. Between two months and one year after the initial sensitization, 11 of 24 rabbits immunized repeatedly with bovine brain galactocerebroside (GC) in complete Freund's adjuvant developed a neurological disorder manifested by flaccid quadriparesis, limb hypesthesia, and respiratory paralysis. Seventeen of 20 autopsied rabbits, including all those with clinical illness, had small multiple perivascular foci of demyelinative lesions in roots, dorsal root ganglia, proximal peripheral nerves adjacent to ganglia, and, less frequently, in distal nerves. No change was found in the central nervous system. Demyelination started around venules, with splitting and vesiculation of the outer myelin sheaths of adjacent fibers, and later progressed to form confluent lesions. The lesions were associated with infiltration of phagocytic mononuclear cells, mostly macrophages, which insinuated themselves between myelin lamellae, phagocytized myelin, and subsequently denuded axons. Perivenular infiltration of small lymphocytes, comparable to that seen in whole nerve– induced EAN, was not encountered. The distribution of demyelinative lesions seems to correspond to areas known to have a defective blood-nerve barrier.