Posters
Presenting Author Academic/Professional Position
Bhargavi Akkineni
Academic Level (Author 1)
Medical Student
Discipline/Specialty (Author 1)
Internal Medicine
Discipline Track
Patient Care
Abstract Type
Research/Clinical
Abstract
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. He initially denied it, but later admitted to inhaling nitrous oxide on a daily basis and that he last used inhaled it 6 months ago.
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. Although in our case, the patient presented with a vitamin B12 deficit, serum B12 levels may be normal or even elevated, since nitrous oxide is reported to inhibit the activation of vitamin B12, but not reduce the levels of this essential vitamin. 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.
Presentation Type
Poster
Recommended Citation
Akkineni, Bhargavi, "Vitamin B12 Deficiency and Subacute Combined Degeneration" (2025). Research Colloquium. 64.
https://scholarworks.utrgv.edu/colloquium/presentation/poster/64
Included in
Vitamin B12 Deficiency and Subacute Combined Degeneration
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. He initially denied it, but later admitted to inhaling nitrous oxide on a daily basis and that he last used inhaled it 6 months ago.
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. Although in our case, the patient presented with a vitamin B12 deficit, serum B12 levels may be normal or even elevated, since nitrous oxide is reported to inhibit the activation of vitamin B12, but not reduce the levels of this essential vitamin. 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.
