Kapoor Raju
National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N3BG, UK.
J Neurol Sci. 2008 Nov 15;274(1-2):54-6. doi: 10.1016/j.jns.2008.03.019. Epub 2008 May 19.
Neurodegeneration is a major cause of disability in multiple sclerosis, and it is therefore important to understand its mechanisms in order to develop rational neuroprotective therapy. Recent work on the toxicity of nitric oxide to axons has suggested that damage can occur from the combined effects of energy failure and axonal sodium overload. Partial blockade of axonal sodium channels should therefore be protective, and this has been confirmed in several models of inflammatory axonal injury. Clinical trials of neuroprotection using blockers of sodium channels are now under way. There is no agreement yet on several aspects of trial design, but the situation should become clearer once the results of these trials are reported.
神经退行性变是多发性硬化症导致残疾的主要原因，因此了解其机制对于开发合理的神经保护疗法至关重要。最近关于一氧化氮对轴突毒性的研究表明，能量衰竭和轴突钠超载的联合作用可导致损伤。因此，部分阻断轴突钠通道应具有保护作用，这已在几种炎性轴突损伤模型中得到证实。目前正在进行使用钠通道阻滞剂进行神经保护的临床试验。在试验设计的几个方面尚未达成共识，但一旦报告这些试验的结果，情况应该会变得更加清晰。
