Neurological damage from recreational nitrous oxide use: Two distinct electroclinical profiles in a retrospective cohort

Abstract

The recreational nitrous oxide (N₂O) use is increasingly recognized as a cause of serious neurological disorders, particularly among young individuals. This retrospective multicenter study aimed to describe the clinical, biological, and electrophysiological features of 41 patients with neurological impairments linked to recreational N₂O use. Most patients presented myeloneuropathy and motor-dominant, length-dependent, axonal neuropathy involving the lower limbs. Notably, two distinct electroclinical patterns emerged from nerve conduction studies and electromyography: a predominant sensorimotor axonal neuropathy (78.4% of cases) and a pure motor neuropathy (13.5%), both primarily involving the lower limbs. Despite normal serum B12 levels in most cases, elevated homocysteine and methylmalonic acid levels confirmed a functional vitamin B12 deficiency. These findings highlight the characteristic electrophysiological profiles associated with recreational N₂O use and underscore the importance of early detection and targeted management to prevent long-term disability.