Trigeminal Neuralgia and Bell Palsy
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Direct answer
Trigeminal neuralgia and Bell palsy are two common cranial nerve disorders with very different mechanisms. Trigeminal neuralgia is brief, electric-shock pain in the trigeminal territory, most often caused by neurovascular compression at the root entry zone, and carbamazepine is the first-line drug. Bell palsy is an acute, idiopathic lower motor neuron facial palsy, thought to be viral, and oral prednisolone started within 72 hours is the standard treatment.
What you must remember
- Trigeminal pain: brief, stabbing episodes lasting seconds in the V2 or V3 territory, often triggered by touch, chewing or speaking.
- Commonest cause: neurovascular compression at the trigeminal root entry zone, most often by the superior cerebellar artery.
- Carbamazepine: first-line; screen for HLA-B1502 before starting in people of Asian ancestry because of the risk of severe skin reactions.
- Red flags: bilateral pain, onset before 40 years, constant burning pain or sensory loss, which need MRI for multiple sclerosis or a posterior fossa lesion.
- Surgical options: microvascular decompression for drug-refractory pain, with percutaneous procedures or radiosurgery when surgery is unsuitable.
- Bell palsy: acute lower motor neuron facial weakness involving forehead, eye and mouth, with recovery over weeks to months in most patients.
- Steroid timing: oral prednisolone is started within 72 hours of onset; the added value of antivirals is uncertain outside severe cases.
- Eye protection: incomplete eyelid closure risks exposure keratitis, so lubricating drops by day and ointment with taping or patching at night are standard.
Two faces, two pathways
A 56-year-old woman describes electric-shock pain on the right cheek lasting about ten seconds, triggered by brushing her teeth, with a normal neurological examination between attacks. The diagnosis is trigeminal neuralgia, but the red flags are checked first, and MRI with contrast is obtained to exclude a lesion. HLA-B1502 is tested before carbamazepine is started at a low dose and titrated, with blood counts and sodium monitored, because carbamazepine can cause agranulocytosis and hyponatraemia. If the response is poor or the drug is not tolerated, oxcarbazepine, lamotrigine or baclofen are alternatives, and surgical referral follows drug failure.
A 42-year-old man wakes with a drooping right face and cannot close his right eye. Forehead weakness confirms a lower motor neuron lesion, and the examiner looks for vesicles in the ear canal or palate, which would indicate Ramsay Hunt syndrome. In idiopathic Bell palsy, oral prednisolone is started within 72 hours of onset, and blood sugar and HIV status are checked. Eye care begins on the first visit, because exposure keratitis is the main preventable complication. Reassessment over the following weeks shows the expected recovery.
Where the examiner separates facial pain and facial palsy
Trigeminal neuralgia is confused with atypical facial pain, which is constant, burning and rarely responds to carbamazepine, so the examiner expects the pattern of pain to decide the diagnosis. In Bell palsy, the trap is the forehead, which is spared in a central stroke but involved in Bell palsy. Students also miss Ramsay Hunt syndrome, which causes a more severe facial palsy with a poorer recovery and needs aciclovir. The HLA-B1502 link is a favourite, as is the reminder that carbamazepine can cause hyponatraemia and bone marrow suppression, so the drug must be monitored rather than simply prescribed.
Frequently asked questions
Why is carbamazepine used first for trigeminal neuralgia?
Carbamazepine is the first-line drug for trigeminal neuralgia because it reduces the abnormal paroxysmal firing of the trigeminal nerve, giving relief in most patients. Oxcarbazepine, lamotrigine and baclofen are alternatives when carbamazepine is not tolerated.
Why is HLA-B1502 testing done before carbamazepine?
HLA-B1502 testing is done before carbamazepine because carrying this allele greatly increases the risk of Stevens-Johnson syndrome and toxic epidermal necrolysis. The test is especially relevant in people of Asian ancestry, and carbamazepine is avoided in carriers.
When should Bell palsy be treated with steroids?
Bell palsy is treated with oral prednisolone when it is started within 72 hours of onset, as steroids reduce nerve oedema and improve the chance of recovery. Treatment should not wait for electrophysiology, and eye care must begin at the same time.
How does Ramsay Hunt syndrome differ from Bell palsy?
Ramsay Hunt syndrome is facial palsy caused by varicella zoster virus reactivation in the geniculate ganglion, usually with painful vesicles in the ear canal or palate. It needs antiviral treatment such as aciclovir and tends to recover less well than idiopathic Bell palsy.