Badria Munir 1, Caitlin Montgomery 1, Azzouz Mouhannad1, Benjamin Paserba1
1Neurology, West Virginia University
Objective:
Nitrous Oxide is a potent analgesic. It is known commonly as “laughing gas” due to feelings of euphoria experienced on inhalation with a rapid onset of action and short duration, which has made it an increasingly popular recreational drug. Routine drug screens do not test for this, so patient history is crucial in the assessment of exposure. Nitrous oxide toxicity can mimic neuropathy but is reversible with high levels of vitamin B12 supplementation when identified early.
Background:
32-year-old male seen in clinic for numbness and tingling of the upper and lower extremities for four days. His symptoms had sudden onset paresthesias on his palms and soles bilaterally, which progressed to decreased sensation on the back of his hands, decreased sensation up to L3, impaired proprioception and reduced vibration without motor weakness On further exploration he endorsed use of nitrous oxide during a party. MRI C-spine showed non-enhancing cord signal involving the dorsal column from C2-C5. Blood work revealed low normal B12 of 200 pg/mL and MCH 32.6 pg. Other relevant blood values and CSF from were unremarkable. H
Design/Methods:
Retrospective review of medical records.
Results:
He was started on B12 supplementation (1000 mcg injection daily for 14 days), and discharged home with subsequent improvement on follow up visits
Conclusions:
This case illustrates the need for a targeted drug use history in the setting of acute neuropathy in young adults. Nitrous oxide induced neuropathy affects in dose dependent manner with higher doses causing significant neurological toxicity. While normal vitamin b12 levels could be normal, serum levels do not correlate to symptoms. Other neurologic abnormalities seen including myelopathy, encephalopathy, pancytopenia, venous thromboembolic events and rashes. This highlights the need for clinicians to enquire about N2O use in medical histories (which may not be volunteered) and be aware of the pathophysiology and management of acute N2O toxicity.