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. Myelin and the oligodendrocytes that form 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 T lymphocyte activity (Th-1 and Th-17), impairment of regulatory T cell function and B lymphocyte activity (antibody and complement). Gray and white matter are targeted by the abnormal immune response. 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 approximately 85 percent of patients, MS begins with a relapsing-remitting course (RRMS). In a much smaller percentage of patients, the disease is progressive from onset (primary-progressive MS). Most people with RRMS have fewer relapses and less inflammatory activity over time, eventually transitioning to a more progressive course -- secondary-progressive MS (SPMS). The onset of SPMS appears to be a dominant determinant of long-term disease prognosis (Scalfari et al., 2014). 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., 2014, Alroughani et al., 2015). A prediction model based on age, cortical lesion load, and cerebellar cortical volume has been offered to explain the probability of evolving to SPMS (Calabrese et al., 2013). There is growing evidence that gray matter damage plays a pivotal role in MS disease progression (Calabrese et al., 2013, Herranz et al., 2016, Lavorgna et al, 2014 & Tortorella, 2014). Preventing the onset of SPMS is a primary target of treatment at this time (Scalfari et al., 2013).
Much of the CNS damage in MS is believed to result from an immune-mediated process that includes components of the innate immune system as well as adaptive immune system activation of certain lymphocyte populations in peripheral lymphoid organs.
There are four disease courses that have been identified in MS
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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