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Arch Neurol. 2001;58:37-39.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

THE PAST FEW YEARS have brought significant progress in the field of multiple sclerosis (MS) research. New findings and insights, built upon a foundation of previous knowledge, have emerged into a preliminary understanding of many aspects of the disease. For example, genetics and susceptibility, identification of myelin antigens, inflammation, the roles of T cells and macrophages, mechanisms of demyelination, and reactive astrogliosis have all been studied. Drugs such as interferon beta and glatiramer acetate exert documented, albeit modest, effects during relapsing-remitting MS and are now widely available.

In addition, renewed interest in axonal injury in MS has suggested new directions to approach the understanding and treatment of this disorder. Although MS is primarily an inflammatory demyelinating disease, it has become evident that axonal degeneration plays an important role in the pathogenesis of disability for patients with MS.^{1, 2, 3} While axonal pathology was elegantly and precisely described in classic MS neuropathology studies . . . [Full Text of this Article]

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