How to distinguish Guillain‐Barré syndrome from nitrous oxide‐induced neuropathy: A 2‐year, multicentric, retrospective study

Abstract

Abstract Background Recreational use of nitrous oxide (N 2 O) has dramatically increased in recent years, resulting in numerous cases of acute sensorimotor tetraparesis secondary to nitrous oxide‐induced neuropathy (N 2 On). Challenging clinical features can mimic Guillain‐Barré syndrome (GBS), the main differential diagnosis upon admission. The most sensitive biomarkers for distinguishing between these two conditions remain to be determined. Methods Fifty‐eight N 2 On patients from three referral centers were retrospectively included over a 2‐year period and compared to GBS patients hospitalized during the same timeframe (47 patients). Collected demographic, clinical, biological, and electrophysiological data were compared between the two groups. Results The typical N 2 On clinical pattern included distal sensorimotor deficit in lower limbs with absent reflexes, proprioceptive ataxia, and no cranial involvement (56.7% of our cohort). Misleading GBS‐like presentations were found in 14 N 2 On patients (24.1%), and 13 patients (22.4%) did not report N 2 O use during initial interview. Only half the N 2 On patients presented with reduced vitamin B12 serum levels upon admission. A slightly increased cut‐off (<200 pmol/L) demonstrated 85.1% sensitivity and 84.5% specificity in distinguishing N 2 On from GBS. Only 6.9% of N 2 On patients met the criteria for primary demyelination ( p < 0.01), with only one presenting conduction blocks. A diagnostic algorithm combining these two biomarkers successfully classified all GBS‐like N 2 On patients. Conclusions Vitamin B12 serum level < 200 pmol/L cut‐off and conduction blocks in initial electrophysiological study are the two most sensitive biomarkers for rapidly distinguishing N 2 On from GBS patients. These two parameters are particularly useful in clinically atypical N 2 On with GBS‐like presentation.

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