罕见但相关:氧化和外围神经毒性,我们知道什么?
Tibor M Brunt1, Wim van den Brink1, Jan van Amsterdam1
1Amsterdam UMC, Department of Psychiatry, University of Amsterdam, Amsterdam, The Netherlands.
Addiction (Abingdon, England)
|December 23, 2024
概括
娱乐性氧化 (N2O) 的使用可以通过非活化维生素B12导致神经损伤,从而导致意外的神经毒性. 早期停止和B12治疗可以帮助,但有些效果可能会持续.
科学领域:
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
- 神经学 神经学
背景情况:
- 氧化 (N2O) 越来越多地用于娱乐用途,其麻醉应用之外存在风险.
- 用户通常没有意识到N2O的神经毒性潜力,特别是在长时间或大量使用时.
- 神经毒性影响与维生素B12的不活化有关,破坏了必不可少的代谢途径.
研究的目的:
- 为了阐明娱乐性氧化的神经毒理学机制.
- 为了突出与N2O使用相关的脱髓化疾病的风险.
- 告知潜在的治疗方法和个人的弱点.
主要方法:
- 对N2O神经毒性现有文献的综述.
- 涉及维生素B12和 metionin合成的生化途径的分析.
- 临床观察N2O诱导的外围神经病变.
主要成果:
- 氧化会使维生素B12 (可巴胺) 失活,从而抑制 metionin 的合成.
- 这种干扰会损害髓膜的维护,可能导致泛化脱髓化多神经病变 (GDP).
- N2O诱导的神经病变的临床发病率报告不足,但可能显著.
结论:
- 立即停止使用N2O和补充维生素B12对于治疗至关重要.
- 虽然治疗可以扭转损伤,但残留症状,如四肢疲软可能会持续存在.
- 遗传和饮食因素,如先前存在的维生素B12缺乏症,可以增加对N2O神经毒性的敏感性.
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