Compston Alastair
School of Clinical Medicine, University of Cambridge Neurology, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.
Clin Neurol Neurosurg. 2004 Jun;106(3):246-8. doi: 10.1016/j.clineuro.2004.02.007.
The central concept underlying ideas on the pathogenesis of multiple sclerosis is that inflammatory events cause acute injury of axons and myelin. The phases of symptom onset, recovery, persistence and progression in multiple sclerosis can be summarized as functional impairment with intact structure due to direct effects of inflammatory mediators, demyelination and axonal injury with recovery through plasticity and remyelination, and chronic axonal loss due to failure of enduring remyelination from loss of trophic support for axons normally provided by cells of the oligodendrocyte lineage.
多发性硬化症发病机制相关观点的核心概念是,炎症事件会导致轴突和髓鞘的急性损伤。多发性硬化症症状的发作、恢复、持续和进展阶段可概括为:由于炎症介质的直接作用,结构完整但功能受损;脱髓鞘和轴突损伤,通过可塑性和再髓鞘化实现恢复;以及由于少突胶质细胞谱系细胞通常为轴突提供的营养支持丧失,持久的再髓鞘化失败导致慢性轴突丢失。