Neurological disorders induced by nitrous oxide abuse: analysis of 57 clinical cases
N.N. Turovets, D.A. Grishina, N.A. Suponeva
S.S. Korsakov Journal of Neurology and Psychiatry April 15, 2026 DOI: 10.17116/jnevro202612603125 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Observational cohort Peer reviewed |
|---|---|
| Sample size | 57 |
| Population | Patients aged 18 to 55 years with a history of nitrous oxide abuse and neurological complications |
| Key findings | Neurological complications from nitrous oxide abuse in this cohort most commonly presented as sensory ataxia (79%) and polyneuritic disorders (63%), with vitamin B12 deficiency in 65% and hyperhomocysteinemia in 93%. Treatment for B12 deficiency, given parenterally in 91% of patients, was followed by improvement and normalization of vitamin B12 and homocysteine levels regardless of administration route; the authors report that oral vitamin B12 supplementation was effective. |
Abstract
Objective. To analyze neurological disorders induced by nitrous oxide use and to evaluate the effectiveness of various pathogenetic therapy regimens. Material and methods. Clinical and paraclinical data from 57 patients (45 men and 12 women), aged 18 to 55 years (median 26 years [LQ 21; UQ 33]), with a history of nitrous oxide abuse were analyzed. Results. This study represents the first large-scale analysis of neurological complications induced by nitrous oxide use in the Russian population (n=57). In 52% of patients (n=30), symptoms developed acutely or subacutely, whereas in 47% (n=27), they developed gradually over more than 8 weeks. The predominant clinical syndromes were sensory ataxia (n=45; 79%) and polyneuritic disorders (n=36; 63%). Vitamin B12 deficiency was confirmed in 65% of cases, and hyperhomocysteinemia was observed in 93%. Neurophysiological examination revealed nonspecific peripheral nerve changes in 61% of cases, and spinal cord subacute degeneration was confirmed by MRI in 33%. All patients received treatment for B12 deficiency. Two primary treatment regimens were implemented: parenteral (n=52; 91%) and oral (n=3) therapy. Follow-up demonstrated improvement and normalization of vitamin B12 and homocysteine levels, regardless of the route of administration. Conclusion. Enhanced awareness of the harmful effects of nitrous oxide may facilitate early diagnosis of related complications and timely initiation of pathogenetic therapy targeting vitamin B12 deficiency. The effectiveness of oral vitamin B12 supplementation in patients abusing nitrous oxide has been demonstrated.