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Howard L. Weiner, MD

Arch Neurol. 2004;61:1613-1615.

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

The etiology and pathogenesis of multiple sclerosis (MS) have been much debated during the past 50 years. It is now recognized that MS is a complex disease with different clinical and pathological phenotypes, perhaps reflecting different pathways to tissue injury. Thus, MS may not be a single disease entity. Nonetheless, with recent advances in immunology and magnetic resonance imaging and the demonstration that immunomodulatory treatment can have an ameliorating effect on the disease process, it is now clear that the core process in MS is inflammatory, with T cells and their mediators triggering injury of axons and their myelin sheaths through a complex sequence of events. The T- cell–mediated inflammation is driven by an autoimmune process, which in turn can trigger a degenerative phase that is immune independent. As described below, a large body of evidence suggests there is a Th1-type bias in MS (interferon [IFN] . . . [Full Text of this Article]

PATHOLOGIC FEATURES


AUTOIMMUNITY DIRECTED AGAINST MYELIN COMPONENTS

MAJOR HISTOCOMPATIBILITY COMPLEX ASSOCIATION

RESPONSE TO THERAPY

INTERFERON BETA

GLATIRAMER ACETATE

NATALIZUMAB

IMMUNOSUPPRESSION

PREGNANCY

ASSOCIATION WITH OTHER AUTOIMMUNE DISEASES

CORRELATIONS BETWEEN CLINICAL FEATURES AND BIOMARKERS

RELATIONSHIP OF MS TO EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

PROGRESSIVE MS

CONCLUSIONS

AUTHOR INFORMATION
Author Affiliations: Partners Multiple Sclerosis Center and Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

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