Nitrous oxide (N₂O) misuse is a growing cause of neurologic morbidity in young adults. N₂O oxidizes and inactivates vitamin B12, disrupting myelin synthesis and resulting in subacute combined degeneration (SCD) of the spinal cord. Clinical features often mimic traumatic or compressive myelopathies, delaying recognition. 

We report the case of a 21-year-old man with a history of polysubstance use and anabolic steroid injections who presented with progressive weakness and sensory ataxia following heavy lifting. His symptoms included ascending numbness, paresthesias, gait instability, and impaired coordination, without bowel/bladder dysfunction or cognitive changes. He reported heavy recreational nitrous oxide use (15–16 liters per week over 8 months), along with use of marijuana, opioids, stimulants, ketamine, and benzodiazepines.

Neurologic examination revealed impaired proprioception, mild distal weakness, ataxic gait, and areflexia, consistent with dorsal column dysfunction. MRI of the cervical spine showed T2 hyperintensities in the dorsal columns from C1–C7 with the classic inverted V sign, and associated ligamentous injury. Laboratory evaluation revealed vitamin B12 deficiency (191 pg/mL), markedly elevated homocysteine (67 µmol/L), and methylmalonic acid (2832 nmol/L). CSF analysis was largely unremarkable except for mildly elevated myelin basic protein. Brain and thoracic spine MRI were normal. Patient was started on Vitamin B12 1000 mcg sub q injections daily for 1 week. Patient consistently reported marked improvement in gait and dorsal/palmar sensation, and gait improved to ability to walk without front wheeled walker which he initially required for balance.

This case highlights nitrous oxide-induced functional B12 deficiency leading to subacute combined degeneration of the spinal cord. Recognition of this potentially reversible condition is critical, especially in young patients with recreational nitrous oxide use.