Case Presentation: A 23 year old male with no pertinent past medical history presented to ED with acute worsening ataxia and paresthesia of upper and lower extremities with an onset of 5 days. Patient denied recent vaccinations, respiratory or GI illness, prior episodes of ataxia or paresthesia, bowel or urinary incontinence, and camping or tick bites. On physical exam, patient exhibited hyporeflexia in upper and lower extremities, along with impaired proprioception and detection of light touch and vibration, but patient’s motor strength was preserved. MRI of brain revealed no abnormalities. MRI of C-spine demonstrated an abnormal T2 signal within the cervical spinal cord extending from level of C2 to C6, in addition to spinal canal narrowing at C4 to C5 and evidence of degenerative intervertebral disc disease, most prominent at C4-C5. Upon evaluation of basic laboratory tests, B12 was staggeringly low, but there was no evidence of megaloblastic anemia. The following day, patient was started on vitamin B12 1000mcg daily, in addition to Solu-Medrol 1g daily due to suspicions of Guillain-Barre syndrome and MS. Within three days of initiating the therapy, patient regained reflexes (+2) in upper and lower extremities. He also reported subjectively feeling better as his stay in the hospital progressed. However, the workup for vitamin B12 deficiency turned out negative, and the patient was then asked about nitrous oxide use. The patient initially denied it, but then admitted to inhaling nitrous oxide on a daily basis, but that he quit 6 months ago.
Discussion: Nitrous oxide, commonly known as “laughing gas”, is becoming notorious for substance abuse. It inactivates vitamin B12, which then cannot participate in the metabolic pathways involving methionine synthase and methymalonyl-CoA mutase. As a result, patients can present with symptoms mimicking a vitamin B12 deficiency. Hence, it is imperative physicians are aware of the neurological effects of nitrous oxide use and specifically ask about its use in patients suspected of such symptoms, since past literature suggests nitrous oxide related neuropathy can persist, to some extent, even after treatment.
Conclusions: We present a case of nitrous oxide induced B12 deficiency and subsequent subacute combined degeneration in a healthy, young adult male with symptoms developing 6 months after reported use.