EpistemisTrigeminal neuralgia
Specialty: Neurology.
Why it occurs
- Microvascular compression of the trigeminal nerve in its entry area to the brainstem by an arterial branch (frequently the superior cerebellar artery)
- Multiple sclerosis (demyelinating plaque in the trigeminal nucleus in the pons, common in young patients with bilateral involvement)
- Tumor of the cerebellopontine angle (meningioma, acoustic neuroma) that mechanically compresses the nerve
- Post-traumatic or postsurgical trigeminal neuropathy (iatrogenic damage in dental or maxillofacial procedures)
- Herpes zoster virus infection (acute trigeminal neuralgia in the eruptive or postherpetic phase)
Initial workup
Detailed exploration of the sensitivity of the three trigeminal branches (ophthalmic V1, maxillary V2, mandibular V3) and the corneal reflex; 3 Tesla brain MRI with specific high-resolution sequences (FIESTA type, CISS or 3D-T2) to assess the presence of neurovascular conflict in the cerebellopontine angle or demyelinating plaques.
red flags
Recent-onset trigeminal neuralgia associated with objective facial anesthesia or hypoesthesia, abolition of the corneal reflex, weakness of the masticatory muscles (pterygoid, masseter) or ipsilateral hearing loss. These data suggest a structural expansive process in the posterior fossa or brainstem involvement.
Standard management
- Carbamazepine — first-line medical treatment, start with 100 mg every 12 hours and gradually increase up to 600-1200 mg/day in divided doses, monitoring blood count and transaminases for risk of bone marrow aplasia or hyponatremia
- Oxcarbazepine — 300-1800 mg/day, better tolerance profile
- Baclofen — 10-40 mg/day
- Surgical microvascular decompression (Janetta technique) in cases of neurovascular conflict proven refractory to pharmacological treatment.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Neurology
- Listed causes
- 5
- Treatment options
- 4