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Neurological Rehabilitation

Not a Laughing Matter: A Case Report of Progressive Lower Extremity Weakness and Sensory Loss Secondary to Nitrous Oxide Abuse

Saturday, October 25, 2025
8:00 AM - 9:15 AM MT
Location: Kiosk 6

    Poster Presenter(s)

  • Brian Abarbanel, MD

    Resident Physician
    McGaw Medical Center of Northwestern University (SRAL) PM&R Program
    Chicago, Illinois

    • Co-Author(s)

  • Ifeolu Akinnola, MD,PhD

    Resident Physician
    McGaw Medical Center of Northwestern University (SRAL) PM&R Program
    Chicago, Illinois

  • Gayle R. Spill, MD

    Attending MD
    Shirley Ryan Ability Lab
    Chicago, Illinois

  • Samman Shahpar, MD

    Associate Professor, Attending Physician
    Shirley Ryan AbilityLab
    Chicago, Illinois

Disclosure(s):
Brian Abarbanel, MD: No financial relationships to disclose
Ifeolu Akinnola, MD,PhD: No financial relationships to disclose
Gayle R. Spill, MD: No financial relationships to disclose
Samman Shahpar, MD: No financial relationships to disclose
Case Diagnosis: 64 year-old male with history of alcohol abuse with acute on chronic bilateral lower extremity weakness, sensory loss, and neuropathic pain caused by excessive nitrous oxide use.

Case Description or Program Description: Patient presented to acute care with weakness, numbness, neuropathic pain, and gait instability leading to an inability to walk at home. He had severe vibratory and proprioceptive loss in his bilateral lower extremities on examination, as well as cognitive deficits. Laboratory studies were significant for unremarkable vitamin B12 levels, with elevated homocysteine and methylmalonic acid levels, consistent with a functional B12 deficiency. MRI of the patient’s cervical, thoracic, and lumbar spine were negative for dorsal column disease. Patient was given intramuscular cyanocobalamin supplementation, and was discharged to an inpatient rehabilitation facility (IRF).

Setting: Acute care hospital, IRF

Assessment/Results: On discharge from IRF, patient improved from moderate/maximum assistance to independent for dressing, toileting, and bed to chair transfers. Patient showed no improvement in his cognitive deficits, requiring moderate assistance for memory at discharge.

Discussion (relevance): Nitrous oxide abuse can cause inactivation of vitamin B12, leading to a functional vitamin B12 deficiency. This can lead to subacute combined degeneration of the spinal cord and peripheral neuropathy. The inactivation of vitamin B12 can lead to impaired enzymatic activity despite having normal vitamin B12 levels, causing elevated homocysteine and methylmalonic acid levels. Treatment of this disease involves intensive therapies and high dose cyanocobalamin supplementation.

Conclusions: Our case highlights a rare complication of excessive nitrous oxide use. This case is particularly noteworthy given the patient’s history of alcohol abuse, cognitive deficits that did not improve with therapies, and the MRI spine without signs of dorsal column disease. Intensive inpatient therapies were effective in providing functional improvements in this patient.