Trigeminal Neuralgia
Lightning-like facial pain — one of the most distinctive and often most disabling neurological pain syndromes. Specialist diagnosis and medical/surgical treatment pathway at Sydney Headache Centre, Bondi Junction.
Book a ConsultationWhat is Trigeminal Neuralgia?
Trigeminal neuralgia is a disorder of the trigeminal nerve — the fifth cranial nerve, which carries sensation from the face. It produces recurrent attacks of severe, brief, lightning-like or electric-shock pain on one side of the face. Attacks last seconds to minutes and are typically triggered by ordinary actions: light touch, chewing, talking, brushing teeth, shaving, washing the face, or a breath of cold air. Between attacks there is often complete relief, though many patients also describe a background ache.
The pain follows the territory of the trigeminal nerve — most commonly the maxillary (cheek) or mandibular (jaw) branches, less often the ophthalmic (forehead) branch. The most attributable cause is microvascular compression of the trigeminal nerve as it emerges from the brainstem by a small artery or vein — what's called classical trigeminal neuralgia. Secondary causes (multiple sclerosis, posterior fossa tumour, vascular malformation) make up a small but important minority.
The Distinctive Features
Brief and severe
Each attack lasts seconds to up to 2 minutes. Pain reaches maximum intensity within seconds — often described as a stab, jolt, electric shock or lightning bolt.
Trigger zones
Very light touch to specific facial areas reliably triggers attacks. Trigger zones often include a small area near the corner of the mouth, nostril, gum, or cheek.
Strictly one-sided
Almost always one side at a time. Bilateral trigeminal neuralgia is rare and should prompt thorough investigation for an underlying cause (especially multiple sclerosis).
Nerve territory
Pain follows trigeminal nerve branches — most commonly the maxillary (V2) or mandibular (V3). Pure V1 (ophthalmic) trigeminal neuralgia is uncommon.
Refractory period
After an attack, there is often a brief period when triggers don't fire. This refractory period is characteristic of trigeminal neuralgia.
Avoidance behaviours
Patients commonly stop eating on the affected side, wear scarves to avoid cold air, defer dental work, lose weight, and become socially withdrawn. Quality-of-life impact is profound.
Diagnosis
Trigeminal neuralgia is fundamentally a clinical diagnosis — the pattern is so distinctive that an experienced clinician can usually recognise it immediately. The neurological examination is typically normal in classical trigeminal neuralgia. Abnormal findings (sensory loss, weakness, brainstem signs) raise the possibility of a secondary cause.
MRI is recommended in all new cases
MRI of the brain — including dedicated thin-slice sequences through the trigeminal nerve root entry zones — is recommended in all new presentations. The role is twofold: to exclude a secondary cause (multiple sclerosis, posterior fossa tumour, vascular malformation), and to assess for vascular compression of the trigeminal nerve, which may inform surgical planning down the line.
Medical Treatment — First Line
For most patients, medical treatment is the starting point. Response can be dramatic — sometimes effectively pain-free within 24–48 hours of starting carbamazepine.
| Medication | Role / starting dose | Notes |
|---|---|---|
| Carbamazepine | First-line. 100 mg twice daily, titrating up to 200–400 mg three times daily as tolerated | Most effective single agent. Side effects include sedation, dizziness, ataxia, nausea, rash, hyponatraemia, and bone marrow suppression (rare). Drug interactions are common. |
| Oxcarbazepine | Alternative first-line. 300 mg twice daily, titrating up to 1200–1800 mg/day | Often better tolerated than carbamazepine, particularly in older patients. Similar efficacy. Watch for hyponatraemia. |
| Lamotrigine | Second-line or adjunct. Slow titration starting 25 mg/day | Slow titration mandatory to avoid Stevens-Johnson syndrome. Often combined with carbamazepine. |
| Baclofen | Adjunct. 5 mg three times daily, titrating up | Particularly useful in multiple-sclerosis-related TN. Can cause weakness. |
| Gabapentin / pregabalin | Adjunct or alternative | Less consistent benefit than carbamazepine but better tolerated. Useful when carbamazepine is contraindicated. |
When Medication Isn't Enough — Surgical Options
Around 30% of patients eventually fail medical treatment due to either inadequate pain control or intolerable side effects. At this point, neurosurgical or interventional options should be considered. Dr Granot facilitates referral to neurosurgeons with specific trigeminal neuralgia experience.
| Procedure | How it works | Considerations |
|---|---|---|
| Microvascular decompression (MVD) | Open neurosurgery — small craniotomy behind the ear; sponge placed between the offending blood vessel and the trigeminal nerve | Highest durable pain-free rate (70–80% at 10 years). Surgical risks include hearing loss, facial weakness, CSF leak. Generally preferred in younger fitter patients. |
| Gamma Knife stereotactic radiosurgery | Focused radiation targeted at the trigeminal nerve root | Non-invasive. Slower onset (weeks to months). Good for patients unfit for surgery. Some loss of facial sensation common. |
| Percutaneous balloon compression | Needle through cheek to compress the trigeminal ganglion with a small balloon | Day procedure. Repeatable. Some sensory loss expected. |
| Percutaneous radiofrequency lesioning | Selective thermal injury of trigeminal nerve fibres at the ganglion | Day procedure. Repeatable. Higher risk of unpleasant sensory loss / anaesthesia dolorosa. |
| Glycerol rhizolysis | Glycerol injected into Meckel's cave to damage nerve fibres | Less commonly used now. Repeatable. |
Frequently Asked Questions
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