How to distinguish Guillain-Barré syndrome from nitrous oxide-induced neuropathy: A 2-year, multicentric,...

Recreational use of nitrous oxide (N₂ O) has dramatically increased in recent years, resulting in numerous cases of acute sensorimotor tetraparesis secondary to nitrous oxide-induced neuropathy (N₂ 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.

Fifty-eight N₂ 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.

The typical N₂ 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 N₂ On patients (24.1%), and 13 patients (22.4%) did not report N₂ O use during initial interview. Only half the N₂ 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 N₂ On from GBS. Only 6.9% of N₂ 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 N₂ On patients.

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 N₂ On from GBS patients. These two parameters are particularly useful in clinically atypical N₂ On with GBS-like presentation.