Ludwin S K
Crit Rev Neurobiol. 1987;3(1):1-28.
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.
人们普遍认为，深入了解中枢神经系统（CNS）脱髓鞘和再髓鞘化所涉及的发病机制，对于更好地理解临床脱髓鞘疾病的病因和发病机制至关重要。在这篇综述中，我们讨论了脱髓鞘的实验模型和临床模型，试图阐明它们导致髓鞘破坏和/或少突胶质细胞损伤的机制。我们还试图确定实验性疾病中起作用的机制是否适用于人类情况。以类似的方式，我们探讨了实验动物中枢神经系统内再髓鞘化的发生情况，以及它与脱髓鞘疾病后再髓鞘化潜力的关系，以及创伤和其他破坏性病变后的再髓鞘化情况。我们评估了临床情况下有意义的再髓鞘化的证据，并评估了少突胶质细胞增殖和迁移能力等理论因素的重要性。
