National Multiple Sclerosis Society
MS overview, disease courses, epidemiology and theories of causation
Multiple sclerosis (MS) is a chronic, inflammatory disease of unknown etiology that involves an immune-mediated attack on the central nervous system. Central myelin and the oligodendrocytes that form central myelin appear to be the primary targets of the inflammatory attack, although the axons themselves are also damaged. The inflammatory attack on CNS white matter is associated with TH-1 and TH-17 cells and the loss of function of regulatory T cells. Gray matter lesions also occur early in the disease, and may even precede damage to the white matter (Popescu & Lucchinetti, 2012; Lucchinetti et al., 2011) in some individuals. The collective damage to white and gray matter results in a broad spectrum of clinical signs and symptoms.
The disease is thought to be precipitated by a combination of one or more environmental triggers acting in a genetically susceptible individual.
In most patients, MS begins with a relapsing-remitting course (RRMS) that eventually transitions to a more steadily progressive course -- secondary-progressive MS (SPMS). The onset of SPMS appears to be a dominant determinant of long-term disease prognosis (Scalfari et al., 2010). Male sex, older age at disease onset, and a higher number of early relapses are associated with a higher probability of progressive disease and shorter time to SPMS (Scalfari et al., 2013). A prediction model based on age, cortical lesion load, and cerebellar cortical volume has been offered to explain the probability of evolving to SPMS, with gray matter damage appearing to play a pivotal role (Calabrese et al., 2013). Preventing the onset of SPMS is a primary target of treatment at this time (Scalfari et al., 2013). In a much smaller percentage of patients, the disease is progressive from onset (primary-progressive MS).
There are four disease courses that have been identified in MS
Multiple sclerosis is an inflammatory demyelinating disease that most often appears in young adulthood, with the incidence peaking around age 30
Because of ongoing research in the areas of genetics and environmental factors, we are able to provide more information than ever before
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