Substantial advances have occurred in the understanding of someof the central mechanisms underlying the inflammation, demyelination,and neurodegeneration that occur in multiple sclerosis sincethe topic was last reviewed in the Journal.1 Accordingly, theavailable clinical strategies for the management of the diseasehave widened (Table 1).2 However, the treatment options forthe disease are most effective during the relapsingremittingphase (relapsingremitting multiple sclerosis), whichis characterized by clinical exacerbations, inflammation, andevidence of plaques within the brain and spinal cord on magneticresonance imaging (MRI). Less understood are factors that promotethe transition from relapsingremitting . . . [Full Text of this Article]
Evolution of the Multiple Sclerosis Plaque
Cells Involved in the Pathogenesis of the Multiple Sclerosis Plaque
T Cells
B Cells
Other Immune Cells
Disease Initiation and Pathogenesis
Pathogenesis of Multiple Sclerosis Lesions Revisited
Neuropathology
Classification of Lesions Stages or Types?
Axonal Dysfunction and Channelopathy
Excitatory Amino Acid Receptors and Neurodegeneration
Growth Factors
The Enigma of Remyelination
A Role for Oligodendrocyte Apoptosis?
The Plaque Edge A Fine Line
Radiographic Measures of the Lesion's Pathological Character
Prospects for Characterizing the Evolution and Progression of Multiple Sclerosis
Source Information
From the Departments of Neurology and Ophthalmology (E.M.F.), and the Department of Neurology and the Center for Immunology (M.K.R.), University of Texas Southwestern Medical Center at Dallas, Dallas; and the Division of Neuropathology, the Department of Pathology and Neurology, Albert Einstein College of Medicine, Bronx, N.Y. (C.S.R.).
Address reprint requests to Dr. Frohman at the Department of Neurology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390, or at elliot.frohman@utsouthwestern.edu.
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