Lancet 2002 Apr 6;359(9313):1221-31
Compston A, Coles A.
Neurology Unit, University of Cambridge Clinical School, Addenbrooke's Hospital, CB2 2QQ, Cambridge, UK
Multiple sclerosis is the prototype inflammatory autoimmune disorder of the central nervous system and, with a lifetime risk of one in 400, potentially the most common cause of neurological disability in young adults.
As with all complex traits, the disorder results from an interplay between as yet unidentified environmental factors and susceptibility genes.
Together, these factors trigger a cascade of events, involving engagement of the immune system, acute inflammatory injury of axons and glia, recovery of function and structural repair, post-inflammatory gliosis, and neurodegeneration.
The sequential involvement of these processes underlies the clinical course characterised by episodes with recovery, episodes leaving persistent deficits, and secondary progression.
The aim of treatment is to reduce the frequency, and limit the lasting effects, of relapses, relieve symptoms, prevent disability arising from disease progression, and promote tissue repair.
Despite limited success in each of these categories, everyone touched by multiple sclerosis looks for a better dividend from applying an improved understanding of the pathogenesis to clinical management.