Remyelination in demyelinating diseases of the central nervous system

It is well accepted that a thorough understanding of pathogenetic mechanisms involved in demyelination and remyelination of the central nervous system (CNS) is fundamental to a better understanding of the etiology and pathogenesis of clinical demyelinating disease. In this review, experimental and clinical models of demyelination are discussed in an attempt to elucidate the mechanism by which they cause breakdown of the myelin sheath and/or damage to the oligodendrocyte. An attempt is made to determine whether mechanisms operating during experimental diseases may be applicable to the human situation. In a similar fashion, the occurrence of remyelination within the CNS in experimental animals and its relationship to the potential for remyelination following not only demyelinating disease but also remyelination following trauma and other destructive lesions are explored. The evidence for meaningful remyelination in the clinical situation is assessed, and the importance of such theoretical factors as the ability of oligodendrocytes to proliferate and migrate is evaluated.