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Nitrous Oxide Neuropathy — RACP Adult Medicine MCQ

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HardGeneral Internal MedicineNitrous Oxide NeuropathyRACP Adult Medicine

A 40-year-old man with no significant past medical history presents with a 2-week history of progressive bilateral hand paraesthesiae and difficulty with fine motor tasks. He has been using recreational nitrous oxide (nangs) heavily for the past 6 months. Serum vitamin B12 is 180 pmol/L (low-normal). MCV is 105 fL. What is the mechanism of neurological damage?

Educational content. Not a substitute for clinical judgement or local policy.

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Correct answer: A — Nitrous oxide irreversibly oxidises the cobalt ion in vitamin B12, inactivating it

Explanation lettering: B = shown as A · A = shown as B · E = shown as C · C = shown as D · D = shown as E

Nitrous oxide (N₂O) causes neurological toxicity by irreversibly oxidising the cobalt ion in cobalamin (B12) from the active Co(I) to the inactive Co(III) state, rendering B12 non-functional. This impairs methionine synthase, disrupting myelin synthesis and DNA production. Critically, serum B12 levels may be normal or only mildly reduced despite functional B12 deficiency. Elevated methylmalonic acid and homocysteine are better markers. Treatment is parenteral B12 replacement and cessation of N₂O. Neurological recovery is variable.

Reference: eTG – 2025 – Neurology; AMH – 2025 – Vitamin B12