Nitrous oxide (N2O) misuse creates a diagnostic dilemma due to its clinical presentation, difficulty in identification, and toxicity related to its chronic abuse, with resultant morbidity and mortality. Chronic abuse can lead to myeloneuropathy and subacute combined degeneration in otherwise healthy individuals. Health professionals should be aware of the commercial availability and abuse of N2O by the public, and N2O toxicity should be included in the differential diagnosis in patients presenting with myelopathy of unknown etiology. A case report was conducted on a 38-year-old female at approximately 30 weeks of gestation who presented to the emergency department with worsening bilateral lower extremity numbness, tingling, and weakness. The patient admitted to nitrous oxide inhalation during the two months prior to admission. She reported using four cans of whippets per week (approximately 8 g of N2O per whippet) up to 50 cans per day (400 g N2O) prior to the onset of symptoms. An MRI of the cervical spine was performed, showing T2 hyperintensity from C2 to C6 involving dorsal columns indicative of subacute combined degeneration. The patient was treated with intravenous vitamin B12 due to the clinical and radiographic evidence of nitrous oxide-induced myelopathy. The pathophysiology of N2O toxicity involves the oxidation of the cobalt atom of cobalamin (vitamin B12) from its reduced active 1+ valent state to its oxidized inactive 3+ valent state. This oxidation inactivates the enzyme methionine synthetase. B12 is an essential cofactor for downstream DNA synthesis. Consequently, excess N2O creates functional B12 deficiency leading to irreversible nerve damage if left undiagnosed and untreated.