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.
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