Schwartz Gwen, Fehlings Michael G
Toronto Western Research Institute, Division of Cell and Molecular Biology, Division of Neurosurgery, University of Toronto, Toronto, Canada.
Prog Brain Res. 2002;137:177-90. doi: 10.1016/s0079-6123(02)37016-x.
Traumatic spinal cord injury is a consequence of a primary mechanical insult and a sequence of progressive secondary pathophysiological events that confound efforts to mitigate neurological deficits. Pharmacotherapy aimed at reducing the secondary injury is limited by a narrow therapeutic window. Thus, novel drug strategies must target early pathological mechanisms in order to realize the promise of efficacy for this form of neurotrauma. Research has shown that an accumulation of intracellular sodium as a result of trauma-induced perturbation of voltage-sensitive sodium channel activity is a key early mechanism in the secondary injury cascade. As such, voltage-sensitive sodium channels are an important therapeutic target for the treatment of spinal cord trauma. This review describes the evolution of acute spinal cord injury and provides a rationale for the clinical utility of sodium channel blockers, particularly riluzole, in the management of spinal cord trauma.
创伤性脊髓损伤是原发性机械性损伤以及一系列渐进性继发性病理生理事件的结果，这些事件使得减轻神经功能缺损的努力变得复杂。旨在减轻继发性损伤的药物治疗受到狭窄治疗窗的限制。因此，新型药物策略必须针对早期病理机制，以实现这种神经创伤形式的疗效前景。研究表明，创伤引起的电压敏感性钠通道活性紊乱导致细胞内钠积累是继发性损伤级联反应中的关键早期机制。因此，电压敏感性钠通道是治疗脊髓创伤的重要治疗靶点。本综述描述了急性脊髓损伤的演变，并为钠通道阻滞剂，特别是利鲁唑在脊髓创伤管理中的临床应用提供了理论依据。
