Citation

Pino S, Vega E, Fragoso M, Salazar G. Cureus 2024; 16(6): e63003.

Copyright

(Copyright © 2024, Curēus)

DOI

10.7759/cureus.63003

PMID

38915835

PMCID

PMC11194535

Abstract

Recreational use of nitrous oxide (N(2)O), commonly known as laughing gas, has increased in the last few years, bringing an increase in the number of reported cases of toxicity due to this gas. Subacute combined degeneration (SCD) of the spinal cord is the most frequently reported neurological disorder due to the use of N(2)O, as well as polyneuropathy and even psychiatric symptoms. All of these disorders are consequences of a functional deficit of vitamin B(12). We are reporting the cases of two patients with a history of N(2)O abusive use presenting to the emergency department with progressive symptoms of paresthesia, ascending symmetric paraparesis, and gait ataxia, emulating the clinical characteristics of Guillain-Barré Syndrome (GBS). In both cases, magnetic resonance imaging (MRI) showed findings compatible with transverse myelitis of the cervical spinal cord, and electrodiagnosis studies reported the presence of polyneuropathy with a mixed mechanism. All these findings together pointed to the presence of myeloneuropathy due to a vitamin B(12) deficit induced by the prolonged use of N(2)O. Symptoms improved gradually with vitamin B(12) supplementation and abstinence from N(2)O. It is important to acknowledge the clinical characteristics of complications due to neurotoxicity induced by N(2)O. Such complications are potentially reversible if they are treated appropriately and quickly. Considering the increase in N2O abuse, it should be considered a probable cause when treating patients with myelopathy and/or neuropathy of an unusual etiology.

Language: en

Keywords

myeloneuropathy; nitrous oxide; polyneuropathy; subacute combined degeneration; vitamin b12