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While its reinforcing and addictive potential remains debated, N<jats:sub>2<\/jats:sub>O is proven to be neurotoxic, especially with prolonged, heavy use, which is often unexpected for users. The neurotoxicological mechanism underlying N<jats:sub>2<\/jats:sub>O\u2010induced neurotoxicity involves inactivation of vitamin B<jats:sub>12<\/jats:sub> (cobalamin), which disrupts methionine synthesis, essential for maintaining the myelin sheath. This can result in demyelinating diseases, including generalized demyelinating polyneuropathy (GDP). Clinical incidence of N<jats:sub>2<\/jats:sub>O\u2010induced peripheral neuropathy is largely unknown, although some research suggests it is not uncommon. Treatment includes immediate cessation of N<jats:sub>2<\/jats:sub>O use and vitamin B<jats:sub>12<\/jats:sub> supplementation. Although this treatment often reverses damage, residual symptoms such as limb weakness may persist. Additionally, genetic and dietary factors, such as vitamin B<jats:sub>12<\/jats:sub> deficiency, may heighten individual vulnerability for N<jats:sub>2<\/jats:sub>O's detrimental effects.<\/jats:p>","DOI":"10.1111\/add.16753","type":"journal-article","created":{"date-parts":[[2024,12,23]],"date-time":"2024-12-23T08:13:38Z","timestamp":1734941618000},"page":"1046-1050","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Rare but relevant: Nitrous oxide and peripheral neurotoxicity, what do we know?"],"prefix":"10.1111","volume":"120","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5337-9649","authenticated-orcid":false,"given":"Tibor M.","family":"Brunt","sequence":"first","affiliation":[{"name":"Amsterdam UMC, Department of Psychiatry University of Amsterdam  Amsterdam The 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