Synopsis
Identify the distinctive paroxysmal facial-pain syndrome, detect secondary causes and dangerous mimics, and use carbamazepine and neurosurgical referral safely within current specialist pathways.
- Trigeminal neuralgia causes recurrent unilateral electric-shock, stabbing or shooting pain in one or more trigeminal divisions, most often maxillary or mandibular, lasting a fraction of a second to about two minutes.
- Innocuous triggers such as light touch, talking, chewing, tooth brushing, shaving or a breeze are characteristic; patients may identify a small trigger zone and pause during attacks.
- Classical disease is associated with neurovascular compression that produces morphological change of the trigeminal root; secondary disease arises from multiple sclerosis, tumour or another structural lesion.
- A normal examination is usual in classical disease. Objective sensory loss, bilateral symptoms, prominent hearing change or another cranial-nerve sign increases concern for a secondary cause.
- Persistent aching can coexist between paroxysms, but continuous pain without brief triggered shocks should prompt reconsideration of dental, temporomandibular, neuropathic or trigeminal-autonomic diagnoses.
- MRI of the brain and trigeminal pathways is indicated through specialist pathways, especially in younger people, atypical presentations, sensory signs or when an intervention is being considered.
- Carbamazepine is the standard initial medicine in UK guidance; introduce and titrate it deliberately, checking interactions, pregnancy potential, baseline blood count, liver tests, sodium and relevant ancestry-related genetic risk.
- Oxcarbazepine is commonly used by specialists when carbamazepine is ineffective or poorly tolerated, but hyponatraemia and off-label or local formulary status require explicit review.
- Opioids and ordinary analgesics rarely control the momentary discharges and can add harm; early expert help is preferable during severe flares that prevent oral intake.
- Microvascular decompression offers durable relief when neurovascular compression is suitable and the person accepts craniotomy; ablative procedures and stereotactic radiosurgery trade different onset, recurrence and sensory-loss risks.
Key red flags
Repeated triggers can make swallowing, drinking and oral hygiene impossible, causing dehydration, weight loss and psychological crisis despite a normal examination.
Investigation priorities
Test the syndrome against recognised diagnostic features and common mimics.
Management branches
A patient reports recurrent unilateral episodes of severe facial pain.
- Characterise each attack's quality, duration, distribution and triggers, then ask about rash, vision, dental symptoms, jaw pain, temporal tenderness and cranial autonomic features.
- Examine oral structures, temporomandibular joints, trigeminal sensation and the remaining cranial nerves, escalating infection, ocular disease, vasculitis or neurological deficit appropriately.
- Make a working clinical diagnosis when brief shock-like triggered attacks fit, but arrange imaging or specialist review rather than using medicine response as proof.
Adequately titrated first-line therapy fails, toxicity occurs or nutrition is threatened.
- Check diagnosis, adherence, interactions and whether a continuous pain syndrome or dental pathology has been misclassified before simply increasing the dose.
- Seek neurology or specialist facial-pain advice about oxcarbazepine or other add-on options, making off-label status and laboratory monitoring clear.
- Use urgent hospital or specialist pathways when attacks prevent fluids, oral medicines or sleep, avoiding reflex opioid escalation that does not target the mechanism.