Abstract Introduction Nitrous oxide (N₂O) misuse is an underrecognized and increasingly prevalent cause of neurologic injury. Stigma surrounding substance use, mistrust of healthcare providers, and limited awareness of N₂O’s harms can delay disclosure, hinder diagnosis, and complicate treatment. This case highlights how these factors contributed to a challenging diagnosis of subacute combined degeneration due to N₂O-induced vitamin B₁₂ inactivation. Case presentation A 49-year-old man with ankylosing spondylitis presented with rapidly progressive weakness, numbness, and gait instability following a fall. Neurologic examination revealed lower extremity hyperreflexia, sensory ataxia, and impaired proprioception. MRI spine showed longitudinal T2 hyperintensity of the dorsal columns. On direct questioning, the patient disclosed chronic N₂O use with a recent binge. He initially withheld this information due to embarrassment, mistrust, and the belief that N₂O was harmless. Laboratory testing revealed vitamin B₁₂ deficiency with elevated methylmalonic acid and homocysteine. He was treated with intramuscular vitamin B₁₂ and substance use counseling, with significant neurologic improvement. Conclusion N₂O misuse is an emerging, preventable cause of neurologic morbidity that remains underrecognized by both clinicians and the public. Greater education, awareness, and public health policy efforts are needed to mitigate harm. Addressing stigma and mistrust related to substance use is equally critical. Creating a nonjudgmental environment that fosters honest disclosure can support timely diagnosis, improve outcomes, and strengthen trust between patients and healthcare providers.
Ramagiri et al. (Sat,) studied this question.