WHAT IS multiple sclerosis (MS)? Virtually every text book of neurology lists MS among the "demyelinating" diseases, and it has classically been regarded as a prototype of these disorders. Descriptions of the neuropathological abnormalities in MS emphasize the loss of myelin, and its diagnosis rests in part on the demonstration, via imaging and/or evoked potentials, of evidence of demyelination.
Demyelination of axons that maintain their structural integrity and the response of neurons to demyelination of axons appear to provide at least a partial basis for the remissions that are commonly observed in MS. In the relapsing-remitting type of MS, exacerbations are followed (usually within weeks to a few months) by remissions in which there is clinical recovery. Clinical deficits in MS are, in part, a result of interruption of conduction in demyelinated axons. Clinical recovery appears to reflect the restoration of secure impulse conduction in some demyelinated axons that acquire a higher-than-normal number of sodium channels.1-3 This molecular remodeling of demyelinated axons provides an instructive example of adaptive neuronal plasticity. By understanding the molecular mechanisms involved in this type of neuronal plasticity, it is conceivable that, in the future, it may be possible to induce, or enhance, remissions.
Waxman SG. Multiple Sclerosis as a Neuronal Disease. Arch Neurol. 2000;57(1):22–24. doi:10.1001/archneur.57.1.22
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