Nitrous Oxide-Induced Myelopathy: A Case From French-Speaking Switzerland

Recreational nitrous oxide (N₂O) use has increased worldwide, driven by its accessibility, low cost, and perception as a harmless “party drug.” Chronic or heavy use can cause neurological complications through functional vitamin B₁₂ deficiency. Despite its growing prevalence, such cases remain rarely documented in French-speaking Switzerland. Our patient is a 27-year-old man of Cape Verdean origin who presented with rapidly progressive paresthesia and gait ataxia following heavy N₂O inhalation. Neurological examination revealed profound sensory ataxia and loss of vibration sense in the lower limbs. Laboratory tests showed low serum vitamin B₁₂ with markedly elevated methylmalonic acid and homocysteine levels. Cervical MRI demonstrated a T2-weighted hyperintensity of the dorsal columns (C1-C5) with the characteristic “inverted V” sign, consistent with posterior column myelopathy. Nerve conduction studies were normal, excluding polyneuropathy. Treatment with hydroxocobalamin and methionine supplementation was initiated; folate was started concomitantly rather than after vitamin B₁₂ normalization. At the three-month follow-up, the patient had discontinued vitamin therapy and resumed N₂O use, with persistent sensory deficits and ataxic gait. This case illustrates a typical presentation of N₂O-induced dorsal myelopathy due to functional vitamin B₁₂ deficiency. It represents a rare and probably underreported occurrence in French-speaking Switzerland. Clinicians should maintain high suspicion for N₂O toxicity in young adults presenting with unexplained sensory ataxia. Early recognition, sustained abstinence, and appropriate vitamin B₁₂ replacement are crucial to prevent irreversible neurological damage.