Elucidating Unique Axonal Dysfunction Between Nitrous Oxide Abuse and Vitamin B12 Deficiency
Jowy Tani1,2,3, Hsing-Yu Weng1,4, Hung-Ju Chen1
1Department of Neurology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan.
Frontiers in Neurology
|July 30, 2019
Summary
Nitrous oxide (N2O) abuse causes unique myeloneuropathy distinct from vitamin B12 deficiency. This inhalant abuse may lead to axonal dysfunction through methionine metabolism interference and direct toxicity to nerve paranodal regions.
Area of Science:
- Neurology
- Toxicology
- Metabolic Disorders
Background:
- Nitrous oxide (N2O) abuse is a growing global health concern.
- N2O abuse can lead to myeloneuropathy, often linked to vitamin B12 deficiency.
- The exact pathophysiology of N2O-induced myeloneuropathy requires further elucidation.
Purpose of the Study:
- To investigate the underlying pathophysiology of myeloneuropathy in nitrous oxide (N2O) abuse.
- To compare the neurophysiological changes in N2O abuse with those in vitamin B12 deficiency.
- To differentiate the axonal damage patterns between N2O abuse and vitamin B12 deficiency.
Main Methods:
- Recruited 18 patients with N2O abuse or vitamin B12 deficiency.
- Performed comprehensive neuro-diagnostic tests, including whole spine MRI and quantitative sensory testing (QST).
- Utilized paired motor and sensory nerve excitability tests to assess sensorimotor axonal damage.
Main Results:
- N2O abuse patients exhibited significant motor nerve excitability alterations, including increased superexcitability and decreased accommodation.
- Vitamin B12 deficiency patients showed distinct changes, primarily decreased accommodation in motor nerves and specific sensory nerve alterations.
- MRI revealed T2 hyperintensity in a higher percentage of N2O abuse patients (87.5%) compared to vitamin B12 deficiency patients (50%).
Conclusions:
- Nitrous oxide (N2O) abuse induces a unique pattern of sensorimotor axonal dysfunction.
- Prominent motor superexcitability changes in N2O abuse suggest a pathological process distinct from vitamin B12 deficiency.
- N2O toxicity may involve direct effects on the paranodal region in addition to vitamin B12 metabolism disruption.
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