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Predictors of functional disability in nitrous oxide induced myeloneuropathy: an observational study
Ignacio Lopera-Rodríguez1, Alicia Silva-Cátedra2, Alexandra Rincón-Valencia3
1Neuromuscular Disorders Unit, Department of Neurology, Hospital Universitario Virgen del Rocío/Instituto de Biomedicina de Sevilla (IBiS)/CSIC/Universidad de Sevilla, Seville, Spain.
None:
Recreational nitrous oxide (N₂O) use is an emerging cause of severe neurotoxicity due to vitamin B12 inactivation. This study analyzes the relationship between initial clinical, biochemical and neuroimaging findings and functional disability at discharge in a cohort of 10 patients recruited between 2024 and 2025. All patients presented with hyperhomocysteinemia, while only 40% showed vitamin B12 hypovitaminosis, confirming hyperhomocysteinemia as a more sensitive diagnostic marker. The most common clinical manifestations were acroparesthesia (90%) and unstable gait (80%). Electrodiagnostic testing revealed pure motor axonal or mixed polyneuropathy in the lower limbs in all analyzed cases. Spinal Magnetic Resonance Imaging (MRI) showed posterior column hyperintensity in 60% of patients. In this series, patients with a poor functional status at discharge (mRS ≥ 2), tended to present with radiological signs of myelopathy, a higher number of affected spinal segments on MRIand combined cervical and thoracic involvement. These findings suggest that the anatomical extent of spinal cord damage on MRI is the primary predictor of functional outcome in N₂O-induced myeloneuropathy after discharge.
