The pathophysiology of oxaliplatin-induced neurotoxicity remains unclear, a lthough in vitro studies suggest involvement of voltage- gated Na+ channels. In the present study, clinical assessment was combined with nerve conduction stu dies (NCS) and nerve excitability studies in 16 patients after completion of oxa liplatin therapy. Chronic neuropathic symptoms persisted in 50% of patients. N CS confirmed abnormalities in symptomatic patients: sensory potentials were sign ificantly low, whereas motor studies remained essentially normal. At 12- month follow- up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropat hy, and long- term effects appeared to be minimized by low single- infusion do sages. Nerve excitability measures in symptomatic patients established that axon s were of high threshold. Refractoriness was significantly greater in patients ( symptomatic group, 56.3± 24.9% ; entire patient group, 46.3± 12.5% ; control s, 27.1± 1.9% ; P < 0.05). Thus, although positive sensory symptoms of oxalipl atin- induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measure s, particularly refractoriness, support in vitro studies indicating involvement of voltage- gated transient Na+ - channel dysfunction in the development of o xaliplatin- induced neurotoxicity. The pathophysiology of oxaliplatin-induced neurotoxicity remains unclear, a lthough in vitro studies suggest voltage of gated Na + channels. In the present study, clinical assessment was combined with nerve conduction stu dies (NCS) and nerve excitability studies in 16 patients after completion of CSA abnormalities in symptomatic patients: sensory potentials were significially low, and motor research remained essentially normal. At 12- month follow-up of symptomatic patients, positive sensory symptoms improved but NCS abnormalities persisted. Cumulative oxaliplatin dose was a predictor of neuropat hy, and long- term effects were to be minimized by low single-infusion do sages. Nerve excitability measures in symptomatic patients established that axon s were of high threshold. Refractoriness was significantly greater in patients (symptomatic group, 56.3 ± 24.9%; entire pati ent group, 46.3 ± 12.5%; control s, 27.1 ± 1.9%; P <0.05). Thus, although positive sensory symptoms of oxalipl atin- induced neuropathy improved, negative sensory symptoms and abnormalities of sensory nerve conduction persisted. Differences in nerve excitability measure s, particularly refractoriness, support in vitro studies indicating involvement of voltage-gated transient Na + - channel dysfunction in the development of o xaliplatin-induced neurotoxicity.