Demyelination and Nerve Conduction Abnormalities in Acute and Chronic Experimental Allergic Encephalomyelitis in the Lewis Rat

We have been using histological and electrophysiological techniques to compare the pathology and pathophysiology in different forms of experimental allergic encephalomyelitis (EAE) in the Lewis rat. In acute EAE induced by sensitization to myelin basic protein (MBP) or by the passive transfer of MBPspecific lymphocytes, there is inflammation and demyelination in the ventral and dorsal spinal roots and inflammation and limited demyelination in the spinal cord. More extensive spinal cord demyelination as well as demyelination in the spinal roots and ganglia is observed in acute EAE induced by inoculation with whole central nervous system (CNS) tissue. In chronic relapsing EAE induced by inoculation with whole CNS tissue and treatment with low dose cyclosporin A, large plaques of spinal cord demyelination occur in rats with clinical episodes >28 days after inoculation. In rats with clinical disease <25 days after inoculation there is prominent demyelination in the spinal roots and ganglia as well as in the spinal cord. In all 4 forms of EAE, peripheral nervous system (PNS) remyelination by Schwann cells and CNS remyelination by oligodendrocytes occurs during clinical recovery. Electrophysiological studies revealed PNS and CNS nerve conduction abnormalities during clinical episodes, with improvement during remissions.