Abstract
BACKGROUND AND PURPOSE: The electrophysiologic characteristics of peripheral neuropathy secondary to nitrous oxide (N(2)O) abuse remain unclear. The paper therefore aimed to summarize the electrophysiologic characteristics of N(2)O-associated peripheral neuropathy and identify the risk factors of severe nerve injury. METHODS: The electrophysiologic results and clinical data of patients with peripheral neuropathy secondary to N(2)O abuse at our hospital between 2018 and 2020 were analyzed retrospectively, and their electrophysiologic changes were summarized. RESULTS: Most patients exhibited decreased sensory and motor nerve conduction velocities (75% and 76%), decreased sensory nerve and compound motor action potentials (57% and 59%), and prolonged distal motor latency (59%), while a response was absent in 36%. These findings indicate that N(2)O abuse can result in generalized injury to sensory and motor nerves. Electrophysiologic results indicated axonal neuropathy in 37 cases (49%), demyelinating peripheral neuropathy in 4 (5%), and mixed neuropathy in 12 (16%). Peripheral nerve injury was more common in the lower limbs (72%) than in the upper limbs (42%, p<0.0001). The upper and lower limbs were primarily affected by sensory nerve demyelination (35%) and motor axonal injury (67%), respectively. Subgroup analysis indicated that longer N(2)O exposure and longer disease course were associated with more-severe motor axonal injury in the lower limbs. CONCLUSIONS: N(2)O-associated peripheral neuropathy can lead to sensory and motor nerve injury, with axonal injury being the most common. Injuries were more severe in the lower limbs. Prolonged N(2)O exposure and disease course increased the severity of motor axonal injury in the lower limbs.