THE interaction of nitrous oxide and vitamin B-12 is well known from e
xperimental studies in animals and anecdotal clinical reports.(1-4) Ni
trous oxide oxidizes cobalamin in vitamin B-12 and disrupts several pa
thways involved in one-carbon chemistry. The result is an irreversible
inactivation of the enzyme methionine synthase, which requires vitami
n B-12 in the +1 oxidation state to act as its coenzyme. The clinical
syndrome associated with oxidation of vitamin B-12 develops after prol
onged exposure to nitrous oxide and consists of megaloblastic erythrop
oiesis and subacute combined degeneration of the spinal cord.(2-4) We
present the case of a patient who developed a severe neurologic defici
t 6 weeks after anesthesia with nitrous oxide.