Nitrous Oxide “Whippet” Induced Subacute Combined Degeneration of the Spinal Cord: A Case Report
Joshua Kern, Carolyn Shanks
Clinical Practice and Cases in Emergency Medicine October 31, 2026 DOI: 10.5811/cpcem.64776 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | A patient presenting to the emergency department with progressive neurologic symptoms after recreational nitrous oxide use |
| Interventions | Intramuscular vitamin B12 replacement cessation of nitrous oxide exposure |
| Key findings | The authors report a case of subacute combined degeneration of the spinal cord associated with recreational nitrous oxide use and argue that nitrous oxide-induced SCD should be considered in patients with subacute weakness, paresthesia, and ataxia, particularly with a history of recreational inhalant use. They contend that early recognition and treatment with intramuscular vitamin B12 replacement, together with cessation of nitrous oxide exposure, are essential to optimize neurologic recovery. |
Abstract
Introduction: Subacute combined degeneration (SCD) is an uncommon neurologic complication of vitamin B12 deficiency characterized by demyelination of the dorsal and lateral columns of the spinal cord, resulting in weakness, paresthesias, sensory deficits, and gait ataxia. Recreational nitrous oxide inhalation has emerged as an important cause of functional vitamin B12 deficiency and may precipitate SCD, particularly in otherwise healthy individuals. Case Report: We report a case of nitrous oxide-associated SCD in a patient who presented to the emergency department with progressive neurologic symptoms. This case illustrates a rare but increasingly recognized complication of recreational nitrous oxide use.
Conclusion: Nitrous oxide-induced SCD should be considered in patients presenting with subacute weakness, paresthesia, and ataxia, particularly when there is a history of recreational inhalant use. Early recognition and treatment with intramuscular vitamin B12 replacement, together with cessation of nitrous oxide exposure, are essential to optimize neurologic recovery.