Pathogenesisdemyelination

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Immune deficiency has been suggested. This might explain the possible persistence of a latent virus and variations in immune status could be the basis of 'relapses and remissions'. T lymphocytes and macrophages found in plaques may be sensitized to myelin antigens.

Hereditary/genetic factors appear significant. There is an increased familial incidence of multiple sclerosis. This has led to the study of histocompatibility antigens (HL-A). An association between A3, B7, B18 and DW2/ DRW2 and multiple sclerosis has been demonstrated. Concordance rate in monozygotic twins is 30% and in dizygotes 5%. Affected women transmit MS to offspring more frequently than affected men suggesting that mitochondrial genes contribute to inheritance.

Viruses may be important in the development of multiple sclerosis, infection perhaps occurring in a genetically/ immunologically susceptible host.

Elevated serum and CSF antibody titres have been found to: - varicella zoster, measles, rubella and herpes simplex during relapse.

Biochemical: No biochemical effect has been demonstrated - myelin appears normal before breakdown and the proposed excess of dietary fats or malabsorption of unsaturated fatty acids is unproven.

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