Severe neurologic deficit after nitrous oxide anesthesia

The interaction of nitrous oxide and vitamin B₁₂ is well known from experimental studies in animals and anecdotal clinical reports. Nitrous oxide oxidizes cobalamin in vitamin B₁₂ and disrupts several pathways involved in one-carbon chemistry. The result is an irreversible inactivation of the enzyme methionine synthase, which requires vitamin B₁₂ in the +1 oxidation state to act as its coenzyme. The clinical syndrome associated with oxidation of vitamin B₁₂ develops after prolonged exposure to nitrous oxide and consists of megaloblastic erythropoiesis and subacute combined degeneration of the spinal cord. We present the case of a patient who developed a severe neurologic deficit 6 weeks after anesthesia with nitrous oxide.