Neurotoxicity Linked to Nitrous Oxide (Galaxy Gas) Recreation: An Overview of Clinical Evidence

Nitrous oxide (N2O), known as laughing gas, is a colorless, low-volume gas that has become commonly used in busy maternity wards, emergency rooms, and dental offices. It provides an introduction to the principles and practices of anesthesia, sedation, and analgesia. This review examines the recreational use and prolonged exposure to nitrous oxide (N2O), both of which are associated with neurological, psychiatric, and cardiovascular complications. A comprehensive search was conducted in databases including Medline, PubMed, PMC, Google Scholar, Web of Science, and Scopus, with additional references identified through citation lists. The focus was on the recreational use of nitrous oxide and its associated neurological consequences. In China and other regions, nitrous oxide use has become increasingly prevalent among young individuals. The temptation to misuse it is driven by its affordability, easy accessibility, the absence of legal chains, and a deceptive cloak of safety. Multiple studies and case reports have documented the neurotoxic effects associated with prolonged nitrous oxide use. As nitrous oxide misuse increases, reports of its association with neurotoxicity, particularly related to vitamin B12 deficiency, have also risen. Nitrous oxide disrupts vitamin B12 metabolism, increases oxidative stress, and inhibits NMDA receptor activity, contributing to nervous system dysfunction. Timely intervention is critical to prevent permanent nerve damage, as prolonged exposure can result in persistent sensory deficits, muscle weakness, and gait disturbances. This review emphasizes the need for standardized treatment protocols and further research, particularly randomized controlled trials, to determine the most effective strategies for managing N2O-induced neurotoxicity.