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Nitrous Oxide Use Leading to Lower Extremity Paresthesias Secondary to Vitamin B12 Deficiency: A Case Report

Kathy Plavnik, DO (NYU School of Medicine Physical Medicine and Rehabilitation Program, United States); Afua Asante, MD; Renat Sukhov, MD; Amy L Tenaglia, MD

Meeting: AAPM&R Annual Assembly 2019

Session Information

Date: Saturday, November 16, 2019

Session Title: Section Info: Annual Assembly Posters (Non Presentations)

Session Time: 11:15am-12:45pm

Location: Research Hub - Kiosk 8

Disclosures: Kathy Plavnik, DO: Nothing to disclose

Case Description: The patient presented with ascending numbness and difficulty walking for 3 weeks. He denied any recent travel history or illness. He reported daily nitrous oxide inhalation via ‘whippets’ for the past 6 months. Neurological examination revealed reduced vibration and proprioception in bilateral lower extremities, an ataxic gait and bilateral foot drop. The remainder of the examination was normal.

Setting: Acute inpatient rehabilitation

Patient: 17-year-old patient with numbness in bilateral feet for 3 weeks.

Assessment/Results: Laboratory workup revealed an elevated methylmalonic acid level consistent with Vitamin B12 deficiency. EMG revealed moderate acute motor axonal polyneuropathy. An MRI of the spinal cord was refused by the patient. He was treated with intramuscular vitamin B12 replacement, followed by oral vitamin B12 for 3-6 months. He was admitted to acute inpatient rehabilitation where he received multidisciplinary treatment from physical therapy, occupational therapy, cognitive rehabilitation and psychological support. Patient was advised to discontinue nitrous oxide use and referred to an addiction counseling center. Upon discharge, patient ambulated with modified independence and bilateral ankle-foot orthoses due to foot drop.

Discussion: Nitrous oxide is an increasingly popular recreational drug used amongst young adults. The typical mode of inhalation involves small pressurized canisters of nitrous oxide in whipped cream dispensers. Nitrous oxide irreversibly inactivates vitamin B12, eventually leading to deficiency. Vitamin B12 depletion causes demyelination and gliosis within the dorsal cord of the spinal cord and peripheral nerves. In addition, cognitive impairment and optic atrophy may occur. The common neurological presentation of toxicity includes paresthesias and gait disturbance, which improve over time with high dose vitamin B12 replacement.

Conclusion: Nitrous oxide-induced vitamin B12 deficiency leading to neuropathy is a rare diagnosis seen in the acute rehabilitation setting that physiatrists should be able to recognize. Children and adults with neurological symptoms should have a thorough illicit drug history screen during history taking.

Level of Evidence: Level V

To cite this abstract in AMA style:

Plavnik K, Asante A, Sukhov R, Tenaglia AL. Nitrous Oxide Use Leading to Lower Extremity Paresthesias Secondary to Vitamin B12 Deficiency: A Case Report [abstract]. PM R. 2019; 11(S2)(suppl 2). https://pmrjabstracts.org/abstract/nitrous-oxide-use-leading-to-lower-extremity-paresthesias-secondary-to-vitamin-b12-deficiency-a-case-report/. Accessed May 15, 2025.
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