Abstract
Purpose To evaluate the differences in the electrophysiological profile of patients with neuropathy due to Nitrous oxide (N2O) misuse in comparison to primary vitamin B12 deficiency as both may present with reduced serum B12 levels. N2O misuse impairs methionine metabolism and is also hypothesised to cause direct axonal toxicity.
Methods A retrospective analysis of clinical, laboratory and neurophysiological [nerve conduction studies (NCS) and somatosensory evoked potentials (SSEPs)] parameters was undertaken in 19 patients, (B12 = 6, N2O = 13).
Results The N2O group was younger (26 vs 59 years, p=0.008). All patients had neurophysiological evidence of length-dependent axonal sensorimotor neuropathy.
Tibial CMAP was attenuated in 77% of N2O (10/13, absent in 4) and 33% of B12 patients (2/6). Common peroneal (CP) compound motor action potential (CMAP) was attenuated in 92% (11/12, absent in 3) of N2O patients. The N2O group had lower tibial and CP CMAP amplitudes than the B12 group (Tibial 1.26 vs 6.47 mV, p = 0.034; CP 0.72 vs 3.14 mV, p <0.0001).
Sural SNAP was attenuated in 77% of N2O (10/13) and 83% (5/6, absent in 4) of B12 patients.
Ulnar SNAP was attenuated in 12% (1/8) N2O and 50% (2/4) B12 patients. Conduction block, temporal dispersion, or F-wave latency prolongation were not noted in either group.
Conclusion Electrophysiological findings of a motor-predominant sensorimotor axonal neuropathy in B12 deficient patients is suggestive of N2O misuse. N2O misuse leads to a motor-predominant axonal neuropathy, in contrast to a sensory-predominant neuropathy in primary B12 deficiency.
