Progressive multifocal leukoencephalopathy pathophysiology: Difference between revisions
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Latest revision as of 18:48, 18 September 2017
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Progressive multifocal leukoencephalopathy Microchapters |
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Differentiating Progressive multifocal leukoencephalopathy from other Diseases |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
PML is a demyelinating disease, in which the myelin sheath covering the axons of nerve cells is gradually destroyed, impairing the transmission of nerve impulses. It affects the white matter, which is mostly composed of axons from the outermost parts of the brain (cortex). Symptoms include weakness or paralysis, vision loss, impaired speech, and cognitive deterioration. PML is similar to another demyelinating disease, multiple sclerosis, but since it destroys the cells that produce myelin (unlike MS, in which myelin itself is attacked but can be replaced), it progresses much more quickly. Most patients die within four months of onset. PML destroys oligodendrocytes and produces intranuclear inclusions.