A 34-year-old woman from Bangalore presents with progressive weakness of both lower limbs over 3 weeks, with preserved pain and temperature sensation but loss of vibration sense and proprioception in the feet bilaterally. Examination shows hyperreflexia, positive Romberg sign, and a sensory level at T8. MRI shows a T2-hyperintense lesion in the dorsal columns spanning T6–T10. What is the most appropriate next step in management?

Explanation

## Clinical Presentation Analysis This patient presents with a **dorsal column syndrome** — selective damage to the fasciculus gracilis and cuneatus with preservation of spinothalamic tracts. ### Anatomical Correlation **Key Point:** Dorsal column pathology produces a characteristic pattern: loss of vibration and proprioception (dorsal columns) with **preserved** pain and temperature sensation (spinothalamic tract intact). | Dorsal Column | Function | Clinical Finding | |---------------|----------|------------------| | **Fasciculus gracilis** | Proprioception & vibration from lower limbs | Loss of vibration/proprioception in feet | | **Fasciculus cuneatus** | Proprioception & vibration from upper limbs | Preserved in this case (lower limb predominance) | | **Spinocerebellar tracts** | Coordination | Ataxia (positive Romberg sign) | ### Differential Diagnosis for Dorsal Column Lesions **Mnemonic: VITAMIN-D** (Dorsal column disease) - **V**itamin B12 deficiency (subacute combined degeneration) ← **MOST COMMON** - **I**nfection (syphilis, TB) - **T**rauma - **A**utoimmmune (MS, NMO) - **M**etabolic (copper deficiency) - **I**diopathic - **N**eoplasm - **D**egenerative (Friedreich ataxia) ### Why Vitamin B12 Deficiency Is Most Likely **High-Yield:** Subacute combined degeneration (SCD) from B12 deficiency is the **most common reversible cause** of dorsal column disease in India, particularly in vegetarian populations. **Clinical Pearl:** The triad of SCD includes: 1. Dorsal column signs (vibration/proprioception loss, Romberg +) 2. Corticospinal tract signs (hyperreflexia, Babinski) 3. Peripheral neuropathy (paresthesias) This patient has all three elements. ### Management Strategy **Key Point:** B12 deficiency is **reversible if caught early**. Delayed diagnosis leads to permanent neurological damage. 1. **Immediate serum B12 level** — confirms deficiency 2. **Methylmalonic acid (MMA) assay** — functional marker of B12 status (elevated in B12 deficiency) 3. **Empirical cyanocobalamin** — start immediately while awaiting confirmatory tests (no harm if B12 is normal; prevents further demyelination if deficient) 4. **Intranasal or parenteral B12** — preferred route (oral absorption impaired in pernicious anemia) **Warning:** Do NOT delay treatment awaiting test results. Neurological damage becomes irreversible after 6–12 months of B12 deficiency.