Nitrous oxide is clinically used as an inhaled anesthetic in surgical and dental procedures. It is also used as an inhaled recreational drug and can be incredibly addictive. It tends to irreversibly oxidize cobalamin (Vitamin B12), rendering it inactive as a coenzyme in the production of methionine. Methionine is required in myelin sheath phospholipid production, and thus overuse of this anesthetic can affect myelin formation. Furthermore, other substrates that require this coenzyme (such as methylmalonate and propionate) accumulate and get incorporated in the myelin sheath, resulting in subacute combined degeneration of the spinal cord. We present a case of a young, avid hunter with a history of polysubstance use to include inhaled nitrous-oxide abuse, prior cocaine use, current marijuana use, and tobacco abuse, who presented with ascending paresthesias without appreciable motor dysfunction. Initial labs showed isolated macrocytosis without anemia in the setting of low vitamin B12 levels. Relevant studies showed elevated methylmalonic acid, normal anti-parietal cell, and anti-intrinsic factor antibodies. Heavy metals screens were negative for high levels of lead, iron, copper, or zinc. Cervical spine MRI demonstrated dorsal cord signal abnormalities without enhancement, in a pattern consistent with vitamin B12 deficiency. The patient was diagnosed with subacute combined degenerative disease secondary to depleted vitamin B12 as a result of recreational inhaled nitrous-oxide abuse. After cessation of nitrous oxide abuse, in addition to three months of B12 replacement, he reported complete resolution of symptoms.
Keywords: neuropathy; nitrous oxide myelopathy; rare cause of vitamin b12 deficiency; subacute combined degeneration; toxic neuropathy.
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