The pathophysiology of multiple sclerosis

Abstract

Multiple sclerosis is on inflammatory autoimmune disease with the autoimmunity directed against myelin proteins of the CNS. A genetic predisposition and environmental factors are important in the etiology of the disease. The initial event is probably an activation of antigen-specific T-cells, followed by an inflammatory cascade involving T- and B-lymphocytes, macrophages, microglial cells, and astrocytes leading to a functional nerve conduction block and to a demyelination of the inflammatory area in the CNS. Although reparative mechanisms exist, the loss of oligodendrocytes and axons and the astrocytic gliosis may produce a permanent impairment of neurological functions.