Nitrous oxide abuse-induced subacute combined degeneration: A case report highlighting vitamin B12 metabolic dysfunction and its implications
Yixin Bao, Xiaoyun Lei, Chun Sun
Neurology Asia June 1, 2026 DOI: 10.54029/2026wvh (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case study Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | 21-year-old male with subacute combined degeneration of the spinal cord |
| Interventions | Mecobalamin Folic acid |
| Dose | 1000 µg intravenous mecobalamin daily; 5 mg oral folic acid daily |
| Key findings | A 21-year-old male with prolonged nitrous oxide inhalation developed subacute combined degeneration of the spinal cord, presenting with tetraparesis and paresthesias. Cervical MRI showed patchy T2 signal abnormalities with an inverted V-sign from C2 to C5. Treatment with daily intravenous mecobalamin and oral folic acid resulted in partial neurological recovery. |
Abstract
Subacute combined degeneration (SCD) of the spinal cord is typically caused by vitamin B₁₂ deficiency and represents a progressive neurological disorder. We report here a 21-year-old male admitted to the Neurology Department of the Second Affiliated Hospital of Jiaxing University with a 10-day history of progressive tetraparesis and paresthesias. Comprehensive investigations were conducted, including blood tests, cerebrospinal fluid analysis, and head magnetic resonance imaging (MRI), all of which yielded normal results. Electrophysiological studies demonstrated evidence of multifocal peripheral neuropathy. Imaging of the cervical spine revealed patchy long T2 signal abnormalities with an inverted V-sign extending from C2 to C5. Further detailed inquiry into his medical history disclosed a long- standing history of nitrous oxide inhalation. Based on these findings, the patient was diagnosed with SCD of the spinal cord induced by disrupted cobalamin metabolism associated with prolonged nitrous oxide inhalation. The patient was treated with daily intravenous injections of 1000 µg of mecobalamin and oral administration of 5 mg folic acid tablets. Following treatment, the patient exhibited some improvement in his symptoms. Early recognition, cessation of nitrous oxide exposure, and high-dose mecobalamin therapy led to partial neurological recovery.