Peripheral Neuropathy Linked to Recreational Nitrous Oxide Use: A Case Report.

BACKGROUND Nitrous oxide (N₂O) deactivates vitamin B12 and, when inhaled regularly, can lead to vitamin B12 deficiency, resulting in temporary or permanent peripheral neuropathy. This case report describes a young adult with N₂O-induced B12 deficiency, whose neurological symptoms were initially misattributed to a distracting traumatic injury from a motor vehicle collision (MVC). CASE REPORT We present a case of a previously healthy 24-year-old man who presented with low back pain and bilateral leg paresthesia that began 2 days after being a passenger in an MVC. There was no head trauma, loss of consciousness, or bowel or bladder dysfunction. Examination revealed an apraxic gait with a positive Romberg sign, while motor strength and sensation remained intact. Laboratory tests showed severely low vitamin B12 level. Diagnostic challenges included misattributing the symptoms to trauma from the MVC. MRI of the lumbar spine and CT scans of the head and spine were unremarkable. Follow-up questioning revealed recreational N₂O inhalation, which was sporadic over the preceding year and most recently occurred on the same night following the MVC. Intramuscular B12 provided rapid improvement in gait and paresthesias, thereby also offering support for a diagnosis of vitamin B12 deficiency secondary to N2O use rather than the initially presumed traumatic etiology. The patient was discharged within 24 hours without requiring admission. CONCLUSIONS This case underscores the importance of considering N₂O use in patients with unexplained neurological deficits, along with obtaining directed social history and serum B12 levels when this differential diagnosis is plausible. Early recognition, supplementation, and counseling can prevent lasting deficits.