A 52-year-old man from Delhi presents to the neurology clinic with a 3-month history of severe, lancinating pain in the right cheek and upper jaw. The pain is triggered by chewing, touching the face, or cold wind, and lasts 10–30 seconds per episode. Neurological examination is normal; there is no sensory loss or motor weakness. MRI brain with contrast is unremarkable. What is the most likely diagnosis?

Explanation

## Clinical Presentation **Key Point:** Trigeminal neuralgia (TN) is a disorder of the trigeminal nerve (CN V) characterized by sudden, severe, unilateral, lancinating pain in the distribution of one or more divisions of the trigeminal nerve. ## Diagnostic Criteria for Trigeminal Neuralgia | Feature | Trigeminal Neuralgia | Glossopharyngeal Neuralgia | Post-herpetic Neuralgia | | --- | --- | --- | --- | | **Distribution** | V1, V2, or V3 (CN V) | Pharynx, soft palate, ear (CN IX) | Dermatomal, follows vesicular rash | | **Pain character** | Sharp, lancinating, electric | Sharp, throat/ear pain | Burning, constant, dull | | **Trigger factors** | Touch, chewing, cold wind, talking | Swallowing, coughing, yawning | Spontaneous; minimal trigger | | **Duration** | Seconds to 2 minutes | Seconds to 2 minutes | Hours to continuous | | **Exam findings** | Normal (idiopathic) | Normal | Sensory loss in dermatomal pattern | | **MRI** | Normal or neurovascular compression | Normal | Normal | ## Why This Patient Has Trigeminal Neuralgia 1. **Distribution:** Pain is in the right V2 and V3 (cheek and upper jaw) — classic trigeminal distribution. 2. **Trigger factors:** Chewing, touch, and cold wind are pathognomonic triggers for TN. 3. **Duration:** 10–30 seconds per episode fits the brief, paroxysmal pattern of TN. 4. **Normal exam:** Idiopathic TN has a completely normal neurological examination. 5. **Normal imaging:** MRI is normal, ruling out secondary causes (tumour, demyelination). **High-Yield:** Idiopathic trigeminal neuralgia accounts for ~90% of cases; the remaining 10% are secondary to MS, tumour, or vascular compression (symptomatic TN). ## Pathophysiology **Clinical Pearl:** The leading hypothesis is **ephaptic transmission** — abnormal cross-talk between demyelinated A-delta fibres (carrying touch) and C fibres (carrying pain) in the trigeminal ganglion or root entry zone. A light touch stimulus is misinterpreted as severe pain. ## First-Line Management - **Carbamazepine** 100–200 mg BD (gold standard; ~70% response). - **Oxcarbazepine** 300–600 mg BD (better tolerability). - **Phenytoin** or **gabapentin** as alternatives. - **Surgical options** (if medical refractory): microvascular decompression, percutaneous balloon compression, radiofrequency ablation. **Mnemonic: TN-STAB** — **T**rigger factors, **N**ormal exam, **S**evere pain, **T**ransient (brief), **A**cute onset, **B**ilateral rare (unilateral ~95%).