Brunt Tibor M, van den Brink Wim, van Amsterdam Jan
Amsterdam UMC, Department of Psychiatry, University of Amsterdam, Amsterdam, The Netherlands.
Addiction. 2025 May;120(5):1046-1050. doi: 10.1111/add.16753. Epub 2024 Dec 23.
Nitrous oxide (NO), used medically as an anaesthetic, has gained popularity as a recreational drug, with rising prevalence particularly among young adults. While its reinforcing and addictive potential remains debated, NO is proven to be neurotoxic, especially with prolonged, heavy use, which is often unexpected for users. The neurotoxicological mechanism underlying NO-induced neurotoxicity involves inactivation of vitamin B (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 NO-induced peripheral neuropathy is largely unknown, although some research suggests it is not uncommon. Treatment includes immediate cessation of NO use and vitamin B supplementation. Although this treatment often reverses damage, residual symptoms such as limb weakness may persist. Additionally, genetic and dietary factors, such as vitamin B deficiency, may heighten individual vulnerability for NO's detrimental effects.
一氧化二氮（NO）在医学上用作麻醉剂，作为一种消遣性药物越来越受欢迎，其流行率不断上升，尤其是在年轻人中。虽然其强化和成瘾潜力仍存在争议，但NO已被证明具有神经毒性，尤其是长期大量使用时，而使用者往往对此并不知情。NO诱导神经毒性的神经毒理学机制涉及维生素B（钴胺素）失活，这会干扰维持髓鞘所必需的蛋氨酸合成。这可能导致脱髓鞘疾病，包括全身性脱髓鞘性多发性神经病（GDP）。虽然一些研究表明NO诱导的周围神经病变并不罕见，但其临床发病率在很大程度上尚不清楚。治疗包括立即停止使用NO并补充维生素B。虽然这种治疗通常能逆转损伤，但肢体无力等残留症状可能会持续存在。此外，遗传和饮食因素，如维生素B缺乏，可能会增加个体对NO有害影响的易感性。
