To describe a case of nitrous oxide induced subacute combined degeneration (SCD) of spinal cord.

Nitrous oxide (NO) is a weak anesthetic, increasingly being among young adults for recreational use. It interferes with the metabolism of Vitamin B12 which can lead to adverse neurological effects such as SCD.

A 29-year-old male with no significant past medical history presented with chief complaint of difficulty ambulating for 3 weeks.  Patient reported increased unsteadiness with inability to maintain his balance. Patient denied any bowel or bladder dysfunction. Patient endorsed using inhaled NO daily for a week prior to the onset of the symptoms. Prior to that he reported only occasional use of 1-2 times per week.  

Physical exam was notable for significantly impaired proprioception and vibration sensation in bilateral lower extremities. Strength was normal. Knee and ankle reflexes were absent bilaterally. Sensations were preserved for light touch and temperature. Patient had ataxic gait with positive Romberg’s test. Memory and cognitive function were intact. Laboratory testing was remarkable for normal Vitamin B12 level with elevated homocysteine and MMA levels. HIV and Syphilis testing was negative. MRI of the spine showed subtle T2 hyperintensity in dorsal column from T8-T11 in a characteristic "inverted V-shape" consistent with NO myelopathy. Patient was treated with parenteral B12 therapy with 1000ug intramuscular injections daily for 5 days and discharged on oral supplementation.

NO interferes with vitamin B12 metabolism by inactivating the enzyme methionine synthetase. Patients can also present with functional Vitamin B12 deficiency with normal serum levels. High levels of MMA and homocysteine can be used as a marker for functional B12 deficiency in such patients. There is also reported a strong dose dependent risk of neurological complication which was also noted in our patient.