Abstract
Background Nitrous oxide misuse causes severe neurotoxicity due primarily to functional vitamin B12 (cobalamin) deficiency. Peripheral neuropathy is a less frequent presentation than subacute combined degeneration of the cord (SCDC).
Methods Review of a patient with severe axonal neuropathy secondary to nitrous oxide misuse.
Results An 18-year-old Chinese male presented with subacute bilateral foot drop, distal numbness and neuropathic pain. There was transient finger weakness and no proximal weakness, symptoms of CNS dysfunction or constitutional symptoms. He was misusing nitrous oxide over several months and self-initiated oral cobalamin supplementation.
On examination, there was mild abductor pollicis brevis weakness bilaterally and bilateral foot drop (2/5 power on dorsiflexion, ankle eversion and great toe extension). Ankle jerks were absent. Plantar responses were flexor. Coordination was normal. Sensation was reduced distally. Gait was high-stepping and tandem was unsteady. Romberg’s could not be performed.
Nerve conduction studies demonstrated severe axonal motor neuropathy with active denervation change on electromyography. MR spine showed subtle T2/FLAIR dorsal column hyperintensity. Somatosensory evoked potentials revealed abnormal large-fibre sensory conduction rostral to the cauda equina. Bloodwork demonstrated mild macrocytosis, low red-cell folate and normal cobalamin. Neuropathy/vasculitic screens and CSF analysis were unremarkable.
He received high-dose parenteral cobalamin and supportive care. He did not return for follow-up.
Conclusions Nitrous oxide misuse can cause severe axonal neuropathy, in addition to the more frequent SCDC, and can be the predominant clinical phenotype, even in the setting of oral supplementation. This syndrome is profoundly disabling but potentially reversible with abstinence and high-dose cobalamin replacement.
