Nitrous oxide abuse-induced subacute combined degeneration: A case report highlighting vitamin B12 metabolic dysfunction and its implications

Authors

  • Yixin Bao The second affiliated hospital of Jiaxing University
  • Xiaoyun Lei
  • Chun Sun

DOI:

https://doi.org/10.54029/2026wvh

Keywords:

Subacute combined degeneration, Vitamin B₁₂ deficiency, nitrous oxide (laughing gas), hyperhomocysteinemia, methylmalonic acid

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.

Published

2026-06-07

Issue

Section

Case Report