Beginning with a case report of nitrous oxide (N2O)-induced B12 deficiency myelopathy, this article reviews
the clinical biochemistry of vitamin B12, and examines the pathogenetic mechanisms by which B12 deficiency
leads to neurologic damage, and how this damage is potentiated by N2O exposure. The article systematically
examines the available experimental data relating to the two main coenzyme mechanisms that are usually
suggested in clinical articles, particularly the deficient methylation hypothesis. The article demonstrates that
neither of these mechanisms is fully consistent with the available data. The article then presents a novel
mechanism based on new data from the neuroimmunology basic science literature which suggests that the
pathogenesis of B12 deficiency myelopathy may not be related to its role as a coenzyme, but rather to newly
discovered functions of B12 in regulating cytokines and growth factors.