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Studies over the past decade have demonstrated that a sustained sodium influx through voltage-gated sodium channels can trigger reverse sodium–calcium exchange which imports damaging levels of calcium into axons after they are exposed to insults such as anoxia, thereby activating injurious calcium-mediated processes (Stys et al., 1992a). Persistent sodium currents have, in fact, been demonstrated along the trunks of axons within the CNS (Stys et al., 1993) and PNS (Tokuno et al., 2003), and sodium channel blockers have been shown to have a protective effect, preventing axonal degeneration when axons are exposed to anoxia (Stys et al., 1992b). A link to neuroinflammation was provided by Smith and colleagues, who demonstrated that nitric oxide (NO, which is present at high concentrations within the lesions of GBS and multiple sclerosis; see Smith and Lassmann 2002) can, possibly via mitochondrial injury which leads in turn to energy deficiency, trigger axonal degeneration (Smith et al., 2001). These investigators further showed that NO-induced axonal degeneration can be prevented by pharmacological blockade of sodium channels (Kapoor et al., 2003).