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Previous Volume 346:199-200 January 17, 2002 Number 3 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The complex pathogenesis of multiple sclerosis includes inflammation and potentially disabling focal lesions that are associated with heterogeneous, often destructive pathologic changes disseminated throughout the white matter of the central nervous system.¹ The usual pathologic changes include demyelination, some remyelination, axonal damage, and scar formation (gliosis). In recent years, researchers have refocused attention on axonal injury and its causes. Axons are damaged by bouts of autoimmune inflammation, the target of which seems to be myelin or the oligodendrocytes that form myelin.² In addition, chronically demyelinated axons may become structurally and metabolically abnormal and vulnerable to other types of damage; gradually, . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Daumer, M, Griffith, L M, Meister, W, Nash, R A, Wolinsky, J S (2006). Survival, and time to an advanced disease state or progression, of untreated patients with moderately severe multiple sclerosis in a multicenter observational database: relevance for design of a clinical trial for high dose immunosuppressive therapy with autologous hematopoietic stem cell transplantation. Mult Scler 12: 174-179 [Abstract]  
• Battistini, L., Piccio, L., Rossi, B., Bach, S., Galgani, S., Gasperini, C., Ottoboni, L., Ciabini, D., Caramia, M. D., Bernardi, G., Laudanna, C., Scarpini, E., McEver, R. P., Butcher, E. C., Borsellino, G., Constantin, G. (2003). CD8+ T cells from patients with acute multiple sclerosis display selective increase of adhesiveness in brain venules: a critical role for P-selectin glycoprotein ligand-1. Blood 101: 4775-4782 [Abstract] [Full Text]