Multiple sclerosis (MS) is a chronic, inflammatory disease of unknown etiology that involves an immune-mediated attack on the central nervous system. Targets of the immune attack include the myelin coating around nerve fiber axons, the axons themselves, and the oligodendrocytes that produce myelin. 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 that eventually transitions to a more steadily progressive course. 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 diagnosis of MS is a clinical one, requiring evidence from the medical history, neurologic exam, and supporting laboratory findings, of multiple lesions that have occurred in different locations and at different points in time (dissemination in space and time) and that cannot be explained by other disease entities [Polman et al., 2011]. Click here for the 2010 McDonald MS Diagnostic Criteria.