Trigeminal neuralgia

Trigeminal neuralgia (TN), also called tic douloureux, is the most common craniofacial pain syndrome. It is characterised by sudden, severe, brief episodes of electric-shock-like or stabbing pain in the face, along the distribution of the trigeminal nerve (cranial nerve V) — the large sensory nerve that supplies sensation to the face, scalp, teeth, gums, sinuses, and parts of the mouth.

It occurs predominantly in adults over 50, with an incidence of approximately 4 per 100,000 per year, and is more common in women. Because of its severity and the way pain can be triggered by entirely ordinary activities, trigeminal neuralgia profoundly affects quality of life.

**Cause:** In most cases, the underlying mechanism is vascular compression — typically an arterial loop (superior cerebellar artery, basilar artery, or a vein) pressing against the trigeminal nerve root near the brainstem. Over time, this pulsatile compression damages the myelin sheath around the nerve, disrupting its electrical insulation and causing spontaneous, inappropriate firing. Less commonly, TN is caused by a tumour near the trigeminal nerve or by demyelination from multiple sclerosis.

**Three branches of the trigeminal nerve** are each associated with a distribution of pain: - **V1 (ophthalmic)** — forehead, scalp, upper eyelid, nose - **V2 (maxillary)** — cheek, upper lip, upper teeth, gums, side of nose - **V3 (mandibular)** — lower jaw, lower teeth, gums, chin, lower lip

Most cases involve V2, V3, or both. Bilateral cases are rare and may suggest multiple sclerosis.

**Symptoms:** Pain attacks are typically: - Sudden and severe — described as electric shock, stabbing, or lancinating - Brief — lasting a fraction of a second to 2 seconds, though repetitive volleys may feel continuous - Unilateral — strictly on one side of the face - Triggered by: touch to a "trigger zone" (upper lip, lower teeth, eyebrow), eating, talking, chewing, cold wind, tooth brushing, or even the light touch of clothing - Followed by a refractory period in which triggers do not produce pain

Between attacks, most patients have completely normal sensation and no pain. In advanced cases, attacks become more frequent, the pain may become more constant, and the refractory period disappears.

**Diagnosis** is clinical, based on the characteristic history. High-resolution MRI can demonstrate the compressing vessel or, in atypical cases, a tumour or demyelinating plaque.

**Treatment** is staged: 1. *Pharmacological:* Carbamazepine (Tegretol®) or oxcarbazepine are first-line and provide initial relief in most patients. Side effects (sedation, unsteadiness, blood count changes) often limit long-term use. 2. *Interventional:* When medications fail or cause intolerable effects, percutaneous procedures (radiofrequency rhizotomy, glycerol injection, balloon compression), Botox injection, or Gamma Knife radiosurgery offer effective alternatives. 3. *Surgical:* Microvascular decompression (MVD) — removing or repositioning the offending blood vessel — has the highest long-term success rates and is the preferred option for suitable, younger, medically fit patients.