Thiamine and B12 deficiency in the CNS
- Lesion
Lack of thiamine damages memory and eye-movement centres; lack of B12 damages the back and side columns of the spinal cord.
What it is
Two vitamin deficiencies cause classic CNS lesions. Thiamine (B1) deficiency, common in alcohol use disorder, malnutrition and prolonged vomiting, causes Wernicke encephalopathy: confusion, ophthalmoplegia and ataxia, with hemorrhagic lesions in the mammillary bodies and around the third ventricle and aqueduct. If untreated it leaves Korsakoff amnesia. Vitamin B12 deficiency causes subacute combined degeneration of the dorsal and lateral columns of the spinal cord, often with megaloblastic anemia.
Step by step
- Thiamine stores, small to begin with, run out within weeks of poor intake.
- Thiamine-dependent enzymes of glucose metabolism fail in active brain regions.
- Energy failure and lactic acidosis injure neurons and vessels around the third ventricle.
- Petechial bleeds and necrosis form in the mammillary bodies.
- Untreated lesions leave permanent amnesia (Korsakoff).
Thiamine vs vitamin B12 deficiency in the CNS
| Feature | Thiamine (B1) | Vitamin B12 |
|---|---|---|
| Main causes | Alcohol, malnutrition, hyperemesis, bariatric surgery | Pernicious anemia, gastrectomy, strict vegan diet, metformin, ileal disease |
| Biochemical role | Cofactor of pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase | Methionine synthase and methylmalonyl-CoA mutase |
| Lesion | Mammillary bodies, periventricular grey matter | Dorsal and lateral spinal columns |
| Clinical | Confusion, ophthalmoplegia, ataxia; amnesia | Lost position and vibration sense, spastic weakness, Romberg sign |
| Blood | Usually normal | Megaloblastic anemia, high methylmalonic acid and homocysteine |
Clinical notes
- Thiamine is given early in any patient at risk with confusion, before glucose.
- B12 replacement stops progression of subacute combined degeneration; recovery depends on how long the deficit lasted.
Test yourself
Think of the answer, then tap the question to see it.
Which structures show lesions in Wernicke encephalopathy?
The mammillary bodies, walls of the third ventricle and periaqueductal grey matter, with acute petechial hemorrhage.
Which spinal cord tracts degenerate in vitamin B12 deficiency?
The dorsal columns and lateral corticospinal tracts (subacute combined degeneration).
Why should thiamine be given before glucose in a malnourished, confused patient?
Glucose metabolism uses up the remaining thiamine and can precipitate or worsen Wernicke encephalopathy.
Elsewhere in DurgiPedia
- Absorption of iron, calcium and vitamin B12
- Spinal cord syndromes: complete, Brown-Séquard, central, anterior
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Wernicke-Korsakoff syndrome: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Vitamin B12 deficiency anemia: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026).
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Representative model, for educational purposes only.