Recovery from acute experimental allergic encephalomyelitis in the Lewis rat. Early restoration of nerve conduction and repair by Schwann cells and oligodendrocytes

Abstract

Light and electron microscopic histological studies and electrophysiological studies were performed on Lewis rats with acute experimental allergic encephalomyelitis (EAE) induced by whole spinal cord or myelin basic protein to determine the mechanism of clinical recovery. In these animals, total clinical recovery from complete paraplegia may occur as early as 4 days after the onset of hindlimb weakness. These studies indicate that this recovery occurs at a time when there is restoration of nerve conduction in the peripheral nervous system (PNS) and central nervous system (CNS) and when most demyelinated fibres have been invested, and some partially remyelinated, by Schwann cells or oligodendrocytes in the PNS and CNS, respectively. These findings support the hypothesis that the neurological signs of acute EAE are due to demyelination in the PNS and CNS.