Acute nitrous oxide‐induced neuropathy mimicking <scp>Guillain‐Barré</scp> syndrome
Xing Qin, Li Kang, Xiao Liu, Jiaoting Jin, Fangfang Hu, Wenhui Lu, Yongning Deng, Qiao Yi Chen, Jingxia Dang
Abstract
Abstract The early clinical features of nitrous oxide (N 2 O)‐induced neuropathy were mimicking that of Guillain‐Barré syndrome (GBS). We aimed to explore clinical and laboratory characteristics of N 2 O‐induced neuropathy in comparison with GBS. We retrospectively reviewed data of 15 patients with N 2 O‐induced neuropathy and compared them with 15 GBS patients. The age of the N 2 O‐induced neuropathy group was significantly younger than that in the GBS group (22 ± 5 vs 45 ± 17). Paresthesia was more common in N 2 O‐induced neuropathy group (100% vs 53.3%). The proportion of distal upper limbs weakness was lower than that in GBS group (20.0% vs 93.3%). There was no significant difference in the distal weakness of the lower limbs (100% vs 80.0%). The incidence of motor conduction block and compound muscle action potential amplitude reduction in upper limbs was lower than that in GBS group (6.7% vs 60.0%; 26.7% vs 80.0%). The sensory nerve action potential amplitude drop in the lower limbs was more severe than that in GBS group (53.3% vs 0). The increase of Mean corpuscular volume (MCV) was more pronounced compared to GBS group (96.97 ± 6.00 vs 88.55 ± 5.41). High homocysteine levels were more common in N 2 O‐related group [29.80(11.60, 70.50) vs 14.35(9.22, 19.30)]. Typical clinical features of the acute N 2 O neuropathy appears to be a myeloneuropathy, affecting the lower limbs more than the upper limbs, mixed axonal‐demyelinating electrophysiological performance, higher homocysteine level, and larger MCV and common posterior spinal cord involvement in cervical segment.