Subacute combined degeneration (SCD) is caused by demyelination of spinal cord white matter secondary to vitamin B12 (cobalamin) deficiency leading to core symptoms of spastic paresis and vibratory and proprioceptive deficits. Most common causes of B12 deficiency revolve around malabsorption and pernicious anemia; however, nitrous oxide (N2O) can also indirectly cause B12 deficiency by inactivating its biologically active form. We report a case of a patient who took advantage of the unregulated N2O market and presented with signs and symptoms of SCD secondary to N2O abuse. Prior to symptom onset, the patient reported approximately 3,000g of N2O inhalation within five days prior to symptom onset in addition to daily use three weeks prior. Work up revealed laboratory and imaging abnormalities consistent with SCD, although B12 levels were normal intrinsic-factor-blocking (IFB) antibodies were present. Appropriate treatment was undertaken, and the patient was followed up at one week and one month with noticeable clinical improvements. Similarities of this patient to literature include the classic presenting symptoms of SCD and the gradual symptomatic improvement with B12 injections and N2O abstinence. This case is remarkable due to SCD occurrence after recreational N2O abuse, objective quantification of N2O intake over a specified time period to induce SCD, occurrence secondary to N2O inhalation, positive IFB antibodies, and symptomatic presentation with B12 values within normal limits. This report highlights the dangers associated with N2O abuse and moving forward awareness of this case can be referenced to aid in educating members of our communities at risk for substance abuse.