Case report demonstrates spinal cord degeneration from nitrous oxide misuse despite low-normal vitamin B12 levels, indicating the critical diagnostic value of spine MRI.
Nitrous oxide misuse is an increasingly recognized cause of functional vitamin B12 deficiency and subacute combined degeneration (SCD) of the spinal cord. We present the case of a 37-year-old man with progressive bilateral extremity weakness, sensory deficits, gait instability, and worsening neuropathic symptoms. Initial laboratory evaluation revealed a low-normal serum vitamin B12 level of 224 pg/mL, which could have delayed recognition of the underlying diagnosis. Magnetic resonance imaging of the cervical and thoracic spine demonstrated longitudinally extensive symmetric dorsal column T2 hyperintensity with the characteristic “inverted V sign,” findings highly suggestive of SCD. Subsequent history revealed recent recreational nitrous oxide exposure. Treatment with parenteral vitamin B12 supplementation resulted in gradual neurologic improvement. This case highlights the limitations of serum vitamin B12 measurements in identifying functional deficiency and emphasizes the diagnostic value of characteristic MRI findings in patients with nitrous oxide–associated myelopathy. Early recognition and treatment are essential to prevent permanent neurologic injury.
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Mustaquim et al. (2026) studied this question.
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