Visual Evoked Potentials and Pathology in Relapsing Experimental Allergic Encephalomyelitis
Guinea pigs with chronically implanted skull electrodes were repeatedly tested for flash evoked responses, in the awake state, before and up to ten months, following a single sensitization with homologous spinal cord in Freund’s adjuvant. This method of sensitization leads to chronic relapsing EAE, which has been characterized by Lassmann and Wisniewski (1978 Acta Neuropath.), and proposed as a model of human demyelinating disease — particularly multiple sclerosis. In the present study R-EAE affected the visual systems in a pilot group of animals, with plaque formations in optic nerves, tracts, and white matter of occipital lobes. Changes in amplitudes and latencies of early evoked response components, PI, Nl and P2, from occipital-frontal leads, were found to precede or vary with clinical ratings of disease, and with observations of demyelination. Amplitude reductions in the Pl-Nl component generally preceded lengthening of latencies or appearance of clinical changes in the intact animals. Reliable latency delays were usually confined to a severe first attack or more generally to subsequent relapses.One case, with recovery of latencies to preinoculation levels during a clinical relapse, showed up to 50% remyelination in optic nerve fibers near the disc. Work in progress will explore the effects of age at sensitization, and relative contributions of central inflammation reactions, parenchyma infiltration, and extent of demyelination on various components of the visual evoked responses.
KeywordsMultiple Sclerosis Optic Nerve Occipital Lobe Visual Evoke Potential Amplitude Reduction
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