Demyelination refers to a pathologic process that causes the destruction of myelin sheaths without injury to axons. According to etiology, the demyelinating diseases can be classified into genetic, nutritional, toxic, allergic, or virus-induced disorders. Clues to etiology are found by observing early ultrastructural alterations that may affect either myelin lamellae or the myelin supporting cells, i.e., oligodendrocytes or Schwann cells in the central or peripheral nervous system, respectively. Metabolic changes induced by nutritional deficiencies or intoxications may initially manifest themselves in the most distal extensions of the cytoplasm of the myelin-supporting cells, i.e., at nodes of Ranvier or at the inner glial loops of myelin sheaths (Fig. 1). In other conditions, myelin lamellae are primarily affected resulting in wide lamellar separation as seen in intoxications with hexachlorophene or triethyltin . Early lysis of myelin lamellae without damage to the myelin-supporting cells is seen in allergic neuritis  and presumably also occurs in autoimmune encephalomyelitis in which the myelin lamellae rather than the myelin-supporting oligodendrocytes are the target of the allergic reaction. This review is concerned with virus infections of the central nervous system that cause demyelination by different mechanisms such as direct virus-induced lysis of oligodendrocytes, immune-mediated destruction of persistently infected cells, “bystander” demyelination accompanying nonspecific inflammatory reactions, and autoimmune demyelination occurring after virus-induced sensitization to myelin.
KeywordsPermeability Hepatitis Lymphoma Leukemia Neurol
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