Chapter 18.Multiple Sclerosis
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Excerpt
Multiple sclerosis (MS) is a clinically and pathologically heterogeneous demyelinating disorder of the central nervous system (CNS) with inflammatory and degenerative components. Although formal proof of an autoimmune etiology remains elusive and alternative theories of MS exist, autoimmune mechanisms are strongly suspected based on the genetic association of MS with major histocompatibility complex (MHC) class II alleles, the cellular constituents of CNS infiltrates in MS patients, and similarities of MS to animal models of experimental autoimmune encephalomyelitis (Nylander and Hafler 2012). Autoimmune attack of the myelin-oligodendrocyte complex is hypothesized to originate from a breakdown of immune tolerance in susceptible individuals via activation of autoreactive myelin lymphocytes by a foreign peptide with structural homology to the myelin (molecular mimicry). Immune-mediated demyelination interferes with saltatory axonal conduction in the CNS, and diverse, paroxysmal neurological symptoms manifest from reduced or blocked conduction, spontaneous discharge, and ephaptic transmission.
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