Publisher's Synopsis
Multiple sclerosis (MS), the most common disabling neurologic disease of young people, afflicts approximately a quarter of a million Americans. The symptoms of MS result from recurrent attacks of inflammation in the central nervous system, which probably occur through an autoimmune mechanism. The target of the immune attack is myelin, the lipoprotein sheath that surrounds the axons and insulates them, and enhances nerve conduction. The white matter of the brain takes its name from the glistening white appearance of this lipid wrapping, which contains most of the pathways, tracts and axonal projections of the central nervous system. (The gray matter contains primarily the cell bodies of the neurons themselves.) Myelin is made by cells called oligodendrocytes and when it is inflamed and damaged, nerve conduction is disrupted and nerves thus lose function, thereby producing the neurologic symptoms of MS.The cause of MS is unknown and its pathophysiology remains poorly understood. Patients are not born with MS, but rather some environmental factor apparently acts on genetically susceptible individuals to produce the disease; but the nature of that factor (such as whether or not it is a virus) remains elusive. The best accepted explanation postulates that macrophages present myelin antigens to appropriate T-cells, thereby activating the T-cells to proliferate. They then cross the blood-brain barrier through interactions with intercellular adhesion molecules and once inside the central nervous system, they release cytokines that further damage myelin and that perpetuate the immune response. The details of this process, including the nature of the triggering antigen, are still subject to speculation but there is strong evidence that MS is a T-cell mediated autoimmune attack on the central nervous system. Concomitant with the myelin destruction, there is also damage to the underlying axon, which leads to further disability.Among the unanswered questions is whether MS is a single disease. It could be that different antigens are involved in different patients, different T-cells are activated, or the mechanisms of cell damage are different.
