Severe motor neuropathy or neuronopathy due to nitrous oxide toxicity after correction of vitamin B12 deficiency

Abstract

Introduction: Nitrous oxide (N₂O) toxicity can cause a sensory predominant myeloneuropathy identical to subacute combined degeneration caused by vitamin B12 deficiency. We describe a patient with a typical vitamin B12 deficiency syndrome after N₂O abuse who recovered and then developed a severe lower motor neuron syndrome following vitamin B12 correction. This suggests N₂O toxicity independent of functional vitamin B12 deficiency. Methods: Electrophysiological, serological, and clinical evaluations were undertaken in the evaluation of this patient. Results: A 22‐year‐old man abused N₂O and presented with a dorsal column syndrome with low vitamin B12 and high homocysteine serum levels. He recovered with treatment but presented later with profound motor axonal degeneration and normal vitamin B12, homocysteine, and methlymalonic acid levels. Conclusions: This case illustrates that N₂O‐associated severe motor neuropathy or neuronopathy can develop separately from typical vitamin B12 deficiency dorsal column myelopathy. This syndrome can present when functional measures of vitamin B12 deficiency have normalized.