Nicholas Morris1, Karen Lynch, Steven A Greenberg. 1. Partners Neurology Residency, Brigham and Women's Hospital, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Abstract
INTRODUCTION: Nitrous 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. METHODS: Electrophysiological, serological, and clinical evaluations were undertaken in the evaluation of this patient. RESULTS: A 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. CONCLUSIONS: This 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.
INTRODUCTION:Nitrous 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 B12deficiency syndrome after N2 O abuse who recovered and then developed a severe lower motor neuron syndrome following vitamin B12 correction. This suggests N2 Otoxicity 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 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. CONCLUSIONS: This case illustrates that N2 O-associated severe motor neuropathy or neuronopathy can develop separately from typical vitamin B12deficiency dorsal column myelopathy. This syndrome can present when functional measures of vitamin B12 deficiency have normalized.
Authors: Stephen Keddie; Ashok Adams; Andrew R C Kelso; Benjamin Turner; Klaus Schmierer; Sharmilee Gnanapavan; Andrea Malaspina; Gavin Giovannoni; Ian Basnett; Alastair J Noyce Journal: J Neurol Date: 2018-03-03 Impact factor: 4.849
Authors: Bruce H R Wolffenbuttel; Hanneke J C M Wouters; M Rebecca Heiner-Fokkema; Melanie M van der Klauw Journal: Mayo Clin Proc Innov Qual Outcomes Date: 2019-05-27