An Acute, Severe Axonal Sensorimotor Polyneuropathy in the Setting of Nitrous Oxide Abuse

Abstract

Nitrous oxide, often used as an anesthetic agent, is also increasingly a drug of abuse due to its euphoric and anxiolytic effects. Frequent exposure to nitrous oxide can lead to neurologic complications, including B12 deficiency and resultant subacute myeloneuropathy, as well as direct neurotoxicity. A clinical presentation of acute sensorimotor polyneuropathy mimicking Guillain-Barré syndrome after chronic nitrous oxide abuse has been reported only rarely. Here we present a 17-year-old previously healthy girl presented with 10 days of progressive ascending sensory loss and weakness in the legs. She admitted to heavy nitrous oxide abuse over a period of a year or more. Laboratory evaluation was significant for normal vitamin B12 level with elevated homocysteine. A magnetic resonance imaging (MRI) of her spine showed abnormal signal involving the bilateral dorsal columns. Nerve conduction studies were suggestive of severe axonal sensorimotor polyneuropathy. This patient demonstrates concurrent multifactorial neurologic injury as a result of nitrous oxide abuse. She had a functional vitamin B12 deficiency as indicated by the elevated homocysteine, leading to a subacute combined degeneration that was evident on the MRI. In addition, she had evidence of direct neurotoxicity leading to axonal injury and sensorimotor polyneuropathy reminiscent of Guillain-Barré syndrome. This clinical picture is a serious but seldom reported possible complication if nitrous oxide abuse and should be considered in patients presenting with a clinical picture suspicious for Guillain-Barré syndrome or its variants.