A 38-year-old woman from rural Maharashtra presents with a 6-month history of progressive weakness, numbness in her feet, and difficulty walking. On examination, she has a stocking-glove distribution of sensory loss, absent ankle reflexes, and a positive Romberg sign. Her diet consists mainly of polished rice and minimal protein intake. Hemoglobin is 9.2 g/dL. Serum vitamin B12 level is normal. Which vitamin deficiency is most likely responsible for her neurological manifestations?

Explanation

## Clinical Presentation Analysis This patient presents with a classic peripheral neuropathy pattern characterized by: - Stocking-glove sensory loss (distal, symmetrical) - Absent ankle reflexes (lower limb predominance) - Positive Romberg sign (proprioceptive/posterior column involvement) - Progressive weakness and difficulty walking - **Key risk factor: polished rice diet** — polishing removes the bran layer, which is the primary source of thiamine (Vitamin B1) - Normal serum B12 level (excludes subacute combined degeneration) ## Why Thiamine (B1) Deficiency — Dry Beriberi? **Key Point:** The combination of a polished rice–based diet with peripheral neuropathy (stocking-glove sensory loss, absent ankle reflexes, Romberg sign, and progressive weakness) is the **classic textbook presentation of dry beriberi**, caused by thiamine (Vitamin B1) deficiency. This is one of the highest-yield associations in PSM/Community Medicine (Park's Textbook of Preventive and Social Medicine). **High-Yield:** Beriberi has two major forms: - **Dry beriberi** — predominantly neurological: peripheral neuropathy with sensory and motor involvement, absent reflexes, wasting - **Wet beriberi** — predominantly cardiovascular: high-output cardiac failure, edema The neurological manifestations of dry beriberi result from thiamine's essential role as a cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase — enzymes critical for oxidative metabolism in neurons. Deficiency leads to axonal degeneration and demyelination of peripheral nerves. **Clinical Pearl:** Polished rice removes thiamine-rich bran; populations subsisting on polished rice (South and Southeast Asia, rural India) are at highest risk. This is a classic PSM exam scenario (Park, 24th edition). ## Differential Considerations | Feature | B1 (Thiamine) | B3 (Niacin) | B6 (Pyridoxine) | B12 | |---------|---|---|---|---| | **Classic syndrome** | Dry/Wet Beriberi, Wernicke-Korsakoff | Pellagra (3 Ds) | Sensory neuropathy (INH-induced) | Subacute combined degeneration | | **Neuropathy type** | Peripheral (motor + sensory) | Rare neuropathy | Sensory predominant | Posterior + lateral column | | **Reflexes** | **Absent (early sign)** | Normal | Absent | Hyperactive (UMN) | | **Risk factor** | **Polished rice diet** | Corn-based diet | INH therapy, alcoholism | Pernicious anemia, veganism | | **B12 level** | Normal | Normal | Normal | **Low** | **Key Point:** The normal B12 level excludes subacute combined degeneration. Pyridoxine (B6) deficiency neuropathy is predominantly sensory and is classically associated with INH therapy or excess B6 supplementation — not a polished rice diet. Niacin deficiency (pellagra) presents with the triad of dermatitis, diarrhea, and dementia — not peripheral neuropathy. **Mnemonic: Dry Beriberi = THIAMINE NEUROPATHY** - **T**hiamine deficiency - **H**yporeflexia/absent ankle jerks - **I**nsidious onset - **A**xonal degeneration - **M**ainly peripheral nerves (stocking-glove) - **I**ndia — polished rice diet - **N**umbness and weakness (distal) - **E**ndemic in rice-eating populations