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| Multiple sclerosis | ||
| Etiology •Multiple sclerosis is a demyelinating disease (see loss of myelin with relative preservation of neurons and axons) characterized by remissions and exacerbations which is due to an inborn error of immune reaction to an environmental agent, probably a virus. | ||
| Pathogenesis •T and B cells through immunological mechanisms still unknown influence macrophages to strip myelin off axons in random areas of the white matter during periods of active disease. •Oligodendroglia are not primarily affected and may even multiply to remyelinate the periphery of the lesion the first time. •Although with time oligodendroglia and remyelination decreases and astrocytes proliferate to form glial "scar" tissue., | ||
| Epidemiology •MS is seen in approximately 1 in 1000 persons in the US. •However, its prevalance varies with latitude being higher the farther from the Equator one lives. •It is related to exposure to the agent before 15 years of age. People who migrate from a high to low before 15 take on the low prevalance whereas, those that migrate from a high to low area after 15 maintain the high prevalence. •The concordance in monozygotic twins is 25%. •Women develop the disease approximately twice as often as men. •The onset of the disease is between 20 and 40 years of age. | ||
| General Gross Description •The lesions appear as greyish plaques randomly distributed throughout the nervous system. •Most commonly they are found periventricularly but can be seen anywhere including predominately grey matter. •Examples: | ||
| General Microscopic Description •Acute MS plaques appear as areas with many macrophages filled with lipid and a few perivascular lymphocytes as well as lymphocytes in the tissue. •As time passes, the macrophage reaction decrease and there is proliferation of reactive astrocytes forming fibers throughout the plaque. •Perivascular and tissue lymphocytes remain for months. •With time oligodendroglia and axons decrease in number throughout the plaque for reasons that are not well understood. •Examples: | ||
| Clinical Correlation •With the onset of active disease, acute exacerbation, the patient develops neurological symptoms and signs such as optic neuritis with unilateral or partial blindness, hemiparesis, ataxia, and hemisensory defects depending on where the lesions are in the brain. •Over weeks the symptoms remit although there is often permanent damage. •The remission is thought to be due to decreased edema, remyelination and some ability of unmyelinated fibers to conduct signals. •A chronic progressive form of MS is also known. | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1328. • Poirer J et.al. Manual of basic neuropathology. Philadelphia: Saunders, 1990, pp.128-129. Please be patient during transfer. Medline will open in a new window. To return, close the Medline Window Multiple sclerosis
| Synopsis by: ML Grunnet, MD (TX2000D88710)[587]
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