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B12 deficiency and subacute combined degeneration of the cord
Vitamin B12 deficiency damages the posterior columns and lateral tracts of the spinal cord, the peripheral nerves and the brain — and it can cause permanent neurological damage even without anaemia, so treatment is early and full-dose.
Why it matters in the exam
Questions present a patient with tingling feet, an unsteady gait worse in the dark, loss of vibration and position sense, a positive Romberg, and sometimes an extensor plantar with absent ankle jerks — a mix of upper motor neuron signs and neuropathy. They test the causes (pernicious anaemia, metformin, proton pump inhibitors, a vegan diet, gastric or bowel surgery, and nitrous oxide "laughing gas" use), the tests when the level is borderline (methylmalonic acid and homocysteine), and treatment. A classic distractor is giving folic acid alone, which corrects the anaemia but not the nerve damage. Another point: neurological damage can appear with a normal blood count and normal cell volume. The MRI sign is high signal in the posterior columns in an "inverted V" shape. An important mimic is copper deficiency after bariatric surgery or with zinc excess. The earlier treatment starts, the better the chance of neurological recovery.
Key points
- B12 deficiency damages the posterior columns and lateral tracts, the nerves and the brain.
- Neurological damage can occur without anaemia or macrocytosis.
- With a borderline level, check methylmalonic acid and homocysteine.
- Treatment: hydroxocobalamin 1 mg intramuscularly on alternate days until no improvement, then every 2 months.
- Folic acid alone is dangerous; nitrous oxide and copper deficiency are important mimics.
Summary table
| Aspect | Finding | Note |
|---|---|---|
| Clinical picture | Tingling, loss of vibration and position, sensory ataxia, spasticity with absent ankle jerks, Babinski, cognitive change | Sometimes optic nerve involvement too |
| Causes | Pernicious anaemia (intrinsic factor antibodies), metformin, proton pump inhibitors, veganism, gastrectomy or terminal ileal resection, nitrous oxide | Nitrous oxide inactivates B12 even when the blood level is normal |
| Tests | Low B12; if borderline — raised methylmalonic acid and homocysteine | Anaemia and macrocytosis are not required |
| Imaging | MRI: high signal in the posterior columns, "inverted V" | Supports the diagnosis, not required |
| Treatment | Hydroxocobalamin 1 mg intramuscularly on alternate days until no further improvement, then every 2 months for life in pernicious anaemia | Never folic acid alone; nitrous oxide — stop use |
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Sources
- BSH Guidelines for the Diagnosis and Treatment of Cobalamin and Folate Disorders, 2014 — Diagnosis and treatment with neurological involvement
- British National Formulary — Hydroxocobalamin, 2025 — Dosing with neurological involvement
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.