## Thiamine Deficiency and Wernicke-Korsakoff Syndrome **Key Point:** Thiamine (vitamin B1) deficiency is the most common cause of the classic triad of peripheral neuropathy, ataxia, and ophthalmoplegia (Wernicke encephalopathy), particularly in alcoholics and malnourished populations. ### Mechanism of Thiamine Deficiency Thiamine is a coenzyme for: 1. Pyruvate dehydrogenase (carbohydrate metabolism) 2. α-ketoglutarate dehydrogenase (TCA cycle) 3. Transketolase (pentose phosphate pathway) Deficiency leads to impaired energy metabolism in high-demand tissues (brain, peripheral nerves). ### Clinical Presentation of Wernicke Encephalopathy | Feature | Mechanism | |---------|----------| | Ophthalmoplegia (CN III, IV, VI palsies) | Midbrain and pons involvement | | Ataxia | Cerebellar dysfunction | | Peripheral neuropathy | Demyelination of peripheral nerves | | Confusion/memory loss | Mammillary body and medial thalamus damage | **High-Yield:** The classic triad is ophthalmoplegia + ataxia + confusion; peripheral neuropathy is also common but not part of the "classic triad" of Wernicke encephalopathy proper. ### Why Thiamine Deficiency is Most Common in India - Chronic alcoholism with poor nutritional intake - Polished rice consumption (thiamine removed during milling) - Low dietary diversity in economically disadvantaged populations - Thiamine is water-soluble and not stored in body; deficiency develops rapidly with malnutrition **Clinical Pearl:** Thiamine must be given BEFORE glucose in suspected Wernicke encephalopathy, because glucose metabolism requires thiamine; giving glucose without thiamine can precipitate acute encephalopathy. **Mnemonic:** **WERNICK** — **W**ernicke encephalopathy, **E**ye palsies, **R**ecent alcohol/malnutrition, **N**europathy, **I**nataxia, **C**onfusion, **K**orsakoff (memory loss).
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