DEMYELINATION IS the partial or total loss of the myelin sheath of nerve fibers following normal myelin development. Multiple sclerosis (MS) is the most common acquired inflammatory demyelinating disease of the central nervous system. The presumed immune-mediated nature of demyelinating diseases prompted evaluation of immunomodulatory and immunosuppressive agents for their treatment. The management of demyelinating diseases, in particular MS, has evolved significantly during the last decade. This has shifted the emphasis from treatment of acute relapses and management of symptoms to pharmacotherapy aimed at altering the natural history of the disease. Current relapse therapy, with glucocorticoids, had its origin in the 1950s and is used to accelerate recovery with no clear impact on the degree of improvement from acute neurologic dysfunction. For more than 100 years, symptom management has used unapproved or off-label uses of agents, with their expected benefit based on anecdotal reports or small case series. These interventions, although successful in improving the quality of life of patients with MS, did not alter the natural history of MS.1 The ability to favorably modify the number of relapses of MS began in 1993 when interferon beta-1b was approved by the Food and Drug Administration for the treatment of relapsing-remitting (RR) MS. Since then, additional agents such as interferon beta-1a, glatiramer acetate (previously copolymer-1), and mitoxantrone hydrochloride have become available for the treatment of patients with MS. These immunomodulatory and immunosuppressive agents, although only partially effective, are beneficial in reducing relapses, preventing disability, and stabilizing magnetic resonance imaging (MRI) changes in patients with MS.
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