Neurology

Trigeminal Neuralgia

삼차신경통

Electric-shock paroxysmal pain in trigeminal distribution

Written and edited by Dr. Kwang Lee, D.C., L.Ac. · Updated 2026-10-04

How common: 4–13/100k/year, female predominant
Typical age: >50 years

What is it?

Usually superior cerebellar artery compresses trigeminal root, demyelinating it; causes ephaptic transmission.

Commonly affected: V2 (maxillary) > V3 (mandibular) > V1 (ophthalmic)

How it develops

Neurovascular conflictSuperior cerebellar artery compresses trigeminal root
DemyelinationFocal demyelination at compression site
Ephaptic transmissionCross-talk between adjacent fibers
Paroxysmal painTrivial stimulus triggers explosive pain

Symptoms

Electric-shock painKnife-like or electric, lasting seconds
UnilateralOne side of face only
Trigger zonesLips, cheek, gums sensitive
Pain-free intervalsNo pain between attacks

How it is examined

Neurological examShould be normal (deficits → secondary)
Trigger avoidancePatient avoids face contact
Mandatory MRIMRI for all to exclude MS/tumor

Imaging

X-ray not useful.

N/A

Brain MRI (FIESTA/CISS) shows neurovascular conflict.

SCA-trigeminal contact
Nerve atrophy

Non-surgical care

Carbamazepine (1st)200–1200 mg/day, 70% effective
OxcarbazepineIf carbamazepine intolerant
Baclofen, lamotrigineCombination or second-line
Drug level monitoringCarbamazepine: 4–12 mg/L

Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.

When surgery is considered

Medication failure or intolerance

Procedures that may be discussed

Microvascular decompression (MVD, gold standard)
Percutaneous trigeminal RFA
Gamma knife radiosurgery

Outlook

Carbamazepine works in 70%; MVD 90% immediate response.