Neurology· Topic 10.3 Headache and facial pain· 10.3.6

Trigeminal neuralgia

Trigeminal neuralgia causes brief, unilateral, electric shock-like facial pain in the maxillary or mandibular trigeminal distribution, often triggered by light touch, most commonly from neurovascular compression of the nerve; contrast-enhanced brain MRI evaluates for a structural or demyelinating cause, and first-line treatment is carbamazepine, with microvascular decompression or ablative procedures for medically refractory disease.

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What this article covers

  • Overview

    Definition: trigeminal neuralgia is the most common and most intense cranial neuralgia, characterized by brief, severe, electric shock-like or stabbing facial pain confined to one or more divisions of the trigeminal nerve (cranial nerve V).

  • Epidemiology

    Age distribution: incidence increases with advancing age, with most cases occurring after age 50; onset before age 50, or bilateral symptoms, should raise suspicion for a secondary cause, particularly multiple sclerosis.

  • Risk factors

    Advancing age: the dominant risk factor, likely reflecting age-related vascular tortuosity and greater likelihood of neurovascular contact.

  • Pathophysiology

    Neurovascular compression: in most patients, a vessel, classically a loop of the superior cerebellar artery, pulsates against the trigeminal root as it exits the brainstem, producing focal demyelination at the contact point.

  • Clinical features

    Pain quality: sudden, brief, unilateral episodes of severe, electric shock-like or stabbing pain, lasting seconds to at most a couple of minutes per paroxysm.

  • Differential diagnosis

    Dental or temporomandibular joint pain: more constant and related to jaw movement or a visible dental source on examination, lacking the brief shock-like, trigger-refractory pattern of trigeminal neuralgia.

  • Diagnosis

    Establishing basis: the diagnosis is made clinically from the characteristic history of brief, unilateral, electric shock-like facial pain in a trigeminal distribution, often trigger-evoked, together…

  • Management

    First step: begin carbamazepine 100 mg PO twice daily, increasing by 200 mg per day as needed and tolerated to 400–800 mg per day in divided doses, maximum 1200 mg per day, as first-line…

  • Complications

    Chronic disabling pain and reduced quality of life: severe, recurrent, unpredictable pain can lead to anxiety around eating, speaking, and grooming (due to fear of triggering an attack), sometimes…

  • Prognosis

    Response to first-line medical therapy: most patients achieve meaningful pain relief with carbamazepine, particularly early in the disease course.

  • Prevention

    No established primary prevention: because the dominant mechanism is anatomic neurovascular contact or an unpredictable demyelinating event, there is no proven strategy to prevent a first episode.

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