Abstract
Multiple sclerosis (MS) afflicts approximately 250,000 to 350,000 individuals in the United States and is the most common autoimmune disease involving the nervous system. Multifocal immune-mediated destruction of the myelin sheath and secondary axonal damage in the central nervous system (CNS) results in variable neurological dysfunction, most commonly altered vision, incoordination, gait ataxia, paralysis, and sensory disturbances (1). Relapsing-remitting MS (RRMS), where patients have attacks of neurological dysfunction lasting days to weeks followed by complete to near complete recovery, accounts for approximately 85% of patients with MS. After approximately 10 years, the majority of patients with RRMS have entered secondary-progressive MS (SPMS), where there is gradual accumulation of neurological dysfunction without recovery. This may represent a neurodegenerative phase of the disease that results from axon transfection and neuronal loss (2,3). Primary-progressive MS (PPMS), accounting for approximately 15% of patients with MS, is similar to SPMS, except that these patients do not have a preceding relapsing-remitting phase.
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Demetriou, M. (2005). Multiple Sclerosis, Genetics, and Autoimmunity. In: Olek, M.J. (eds) Multiple Sclerosis. Current Clinical Neurology. Humana Press. https://doi.org/10.1385/1-59259-855-2:103
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DOI: https://doi.org/10.1385/1-59259-855-2:103
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