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Nitrous oxide misuse and vitamin B12 deficiency
Thomas H Massey1, Trevor T Pickersgill2, Kathryn J Peall1
1Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University, Cardiff, UK.
BMJ Case Reports
|June 2, 2016
Summary
Habitual nitrous oxide (N2O) inhalation can cause severe vitamin B12 deficiency, leading to neurological damage like sensory ataxia. Prompt treatment with vitamin B12 injections can reverse these debilitating effects.
Area of Science:
- Neurology
- Toxicology
- Nutritional Science
Background:
- Nitrous oxide (N2O) is known to inactivate vitamin B12.
- Chronic N2O abuse can lead to severe vitamin B12 deficiency and neurological complications.
- This case highlights the potential neurotoxic effects of recreational N2O use.
Observation:
- A 36-year-old man presented with a 5-week history of progressive sensory disturbances and balance issues.
- Neurological examination revealed sensory ataxia, pseudoathetosis, and reduced vibration sensation.
- Investigations showed low serum vitamin B12, macrocytosis, and elevated homocysteine.
Findings:
- Spinal cord MRI revealed a longitudinal myelitis from C1 to T11.
- The patient was diagnosed with myeloneuropathy secondary to vitamin B12 deficiency caused by N2O inhalation.
- This demonstrates a direct link between N2O abuse and severe neurological impairment.
Implications:
- Early recognition of N2O abuse is crucial in patients with unexplained neurological symptoms.
- Vitamin B12 supplementation is essential for managing N2O-induced myeloneuropathy.
- This case underscores the importance of patient history in diagnosing toxicological neurological syndromes.