Autor: |
Brunt TM; Amsterdam UMC, Department of Psychiatry, University of Amsterdam, Amsterdam, The Netherlands., van den Brink W; Amsterdam UMC, Department of Psychiatry, University of Amsterdam, Amsterdam, The Netherlands., van Amsterdam J; Amsterdam UMC, Department of Psychiatry, University of Amsterdam, Amsterdam, The Netherlands. |
Jazyk: |
angličtina |
Zdroj: |
Addiction (Abingdon, England) [Addiction] 2024 Dec 23. Date of Electronic Publication: 2024 Dec 23. |
DOI: |
10.1111/add.16753 |
Abstrakt: |
Nitrous oxide (N 2 O), 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, N 2 O is proven to be neurotoxic, especially with prolonged, heavy use, which is often unexpected for users. The neurotoxicological mechanism underlying N 2 O-induced neurotoxicity involves inactivation of vitamin B 12 (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 2 O-induced peripheral neuropathy is largely unknown, although some research suggests it is not uncommon. Treatment includes immediate cessation of N 2 O use and vitamin B 12 supplementation. Although this treatment often reverses damage, residual symptoms such as limb weakness may persist. Additionally, genetic and dietary factors, such as vitamin B 12 deficiency, may heighten individual vulnerability for N 2 O's detrimental effects. (© 2024 The Author(s). Addiction published by John Wiley & Sons Ltd on behalf of Society for the Study of Addiction.) |
Databáze: |
MEDLINE |
Externí odkaz: |
|