Multiple sclerosis: a clinical neurological syndrome mediated by immune phenomenaMultiple sclerosis (MS) is the most common, disabling neurological syndrome of young adults. The etiology is idiopathic, yet most authorities agree that the immune system is crucial in the pathogenesis of the recurrent and chronic injury to the central nervous system (CNS). Nearly identical histopathological findings occur in MS and related clinical syndromes, designated as "demyelinating diseases." Clinical presentation differentiates MS from the monophasic syndromes (optic neuritis, acute transverse myelitis, and Marburg disease) and the less-common relapsing syndromes (Devic's disease, Balo's concentric sclerosis). A chronic progressive variant of MS is also well recognized.The primary pathological feature of demyelinating diseases is a focal loss of CNS myelin in the white matter, the areas of concentrated, parallel myelinated axons within the CNS. Oligodendroglia produce and maintain the myelin. This multilamellar lipid structure permits rapid, saltatory conduction of action potentials and mechanically separates CNS axons. The focal nature of demyelinating disease contrasts with the diffuse myelin loss of toxic or metabolic injuries, such as occurs in leukodystrophy, myelinolysis, radiation, and nutritional compromise. The great magnitude of myelin loss relative to the perivascular inflammatory infiltrate differentiates MS from the more cellular inflammatory response of acute disseminated encephalomyelitis.Demyelinating disease afflicts 0.2% of individuals in high prevalence areas, and incidence is increasing. MS is not associated with other immune diseases [104]. Genetic studies reveal weak associations with major histocompatibility complex (MHC) and T cell receptor (TCR) genes and only moderate concordance in monozygous twins, supporting a polygenic inheritance for susceptibility and severity, as well as environmental factors.Correspondence to: M. Rodriguez