Multiple sclerosis. Current etiological concepts.

An animal model for acute multiple sclerosis (ms) is experimental allergic encephalomyelitis (eae). eae is produced by intradermal injection of a protein component of central nervous system (cns) myelin. Ultrastructural studies of eae and of a peripheral nerve analog, experimental allergic neuritis (ean), have revealed an orderly sequence of cellular events leading to the destruction and removal of myelin with sparing of axons (primary demyelination). Acute ms has not been studied electron microscopically, but the ultrastructural similarities between ean and a case of acute Landry-Guillain-Barré syndrome, a primary demyelinating disease of the peripheral nervous system, suggest that a similar sequence of events might be found in acute ms. While the pathological findings support a cellmediated or delayed hypersensitivity response, there is also evidence for the pathogenetic role of circulating antibodies. Among such evidence is included the finding that sera from animals with eae and humans with acute ms rapidly produce a reversible block of complex (polysynaptic) electrical activity when applied to cns tissue cultures, which suggests a possible mechanism for transient symptoms in ms. Epidemiological and other studies link ms with a viral cause, although no direct evidence that ms is caused by a virus exists. Viral and immunological mechanisms are not mutually exclusive in considering pathogenetic possibilities for ms, for it can be postulated that a viral infection of the central nervous system acts as a triggering agent for a series of immune responses, including production of a bioelectric blocking antibody and demyelination mediated by sensitized cells, the combination of which ultimately produces the total clinical picture of ms.