• Nicholas Morris, Karen Lynch, and Steven A Greenberg.
• Partners Neurology Residency, Brigham and Women's Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
• Muscle Nerve. 2015 Apr 1; 51 (4): 614-6.

IntroductionNitrous oxide (N2 O) 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 N2 O abuse who recovered and then developed a severe lower motor neuron syndrome following vitamin B12 correction. This suggests N2 O toxicity independent of functional vitamin B12 deficiency.MethodsElectrophysiological, serological, and clinical evaluations were undertaken in the evaluation of this patient.ResultsA 22-year-old man abused N2 O 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.ConclusionsThis case illustrates that N2 O-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.© 2014 Wiley Periodicals, Inc.

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