Your SlideShare is downloading. ×
Trigeminal neuralgia
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.


Introducing the official SlideShare app

Stunning, full-screen experience for iPhone and Android

Text the download link to your phone

Standard text messaging rates apply

Trigeminal neuralgia


Published on

Published in: Health & Medicine

  • Be the first to comment

No Downloads
Total Views
On Slideshare
From Embeds
Number of Embeds
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

No notes for slide


  • 1. Trigeminal Neuralgia Yury Khelemsky, MD Assistant Professor Anesthesiology and Pain Medicine The Mount Sinai Medical Center
  • 2. Introduction
    • Common cause of facial pain
    • Sudden, usually unilateral, severe, brief, stabbing/lancinating, recurrent episodes of pain in one or more branches of the 5 th cranial nerve.
  • 3. Anatomy
    • Sensory supply to face and sensory and motor to muscles of mastication
    • 3 major divisions: V1 (ophthalmic), V2 (Maxillary), V3 (Mandibular)
    • Nerve starts at midlateral surface of pons, sensory ganglion ( gasserian ganglion resides in Meckel ’s cave in the floor of the middle cranial fossa
  • 4. Epidemiology
    • Annual incidence 4-13/100k
    • 15k new cases per year in US
    • Incidence increases with age (as with PHN).
    • Male:Female 1:1.5
    • Rare familial cases. Most sporadic.
  • 5. Etiology
    • Classic : Most cases (80-90%) due to compression of trigeminal nerve root by aberrant loop of artery or vein. Usually within a few mm of entry into pons. Primary TN also includes idiopathic cases
    • Secondary: acoustic neuroma, meningioma, AVN, saccular aneurysm, multiple sclerosis.
  • 6. Pathogenesis
    • Mechanism: demyelination in area around vascular compression. Ephaptic (occurring without neurotransmitters) crosstalk between light touch and pain fibers.
    • Central pain/sensitization develops
  • 7. Classification
    • International Headache Society (IHS)
    • Classic: idiopathic (since most do not have surgery most of these are likely vascular) and vascular
    • Secondary: all structural lesions other than vascular compression
  • 8. Clinical Features 1
    • Sudden, unilateral, severe, brief, stabbing, electric
    • Maximal at or near onset
    • May have facial muscle spasm (tix douloureux)
    • Refractory period is common
    • Typically does not awaken patient
    • Unilateral, may be bilateral, but not simultaneously
  • 9. Clinical Features 2
    • Mostly V2/3. V1<5%.
    • Trigger zones: in distribution of affected nerve, closer to midline, patient protect these areas, may demonstrate on physical exam
    • Other triggers: chewing, talking, brushing teeth, cold air, smiling, grimacing
    • Pretrigeminal neuralgia – dull aching continuous pain evolving into TN
    • May be precipitated by dental procedures
  • 10. Course
    • Variable
    • Episodes may last weeks – months, followed by pain free intervals.
    • Recurrence common, some patients have continuous pain
    • Most often, TN waxes and wanes in severity and frequency of exacerbations
  • 11. Diagnosis
    • International Headache Society (IHS)
    • Classic:
    • Paroxysmal pain in one or more division of CNV
    • Pain has at least one: intense, sharp, superficial, or stabbing; precipitated from trigger areas or by trigger factors
    • Attacks are stereotyped in the individual patient
    • No clinically significant neurologic deficit
    • Not attributable to another disorder
    • Secondary: demonstrable structure other than vascular compression
  • 12. Neuroimaging
    • Some obtain MRI in all TN pts
    • Some only in: young patients, bilateral sx, trigeminal sensory loss
    • American Academy of Neurology (AAN) and European Federation of Neurologic Societies (EFNS) review
    • Routine imaging identified secondary cause in 15% of patients
    • Insufficient evidence to support or refute utility of MRI to identify neurovascular compression or indicate most reliable MRI technique.
  • 13. Electrophysiologic Testing
    • Trigeminal Reflex Tests: Blink Reflex and Masseter Inhibitor Reflex. 2008 AAN/EFNS: high sensitivity (94%) and specificity (87%) for distinguishing between secondary and classic TN
    • Trigeminal Evoked Potentials: not clinically useful
  • 14. DDx
    • Short-Lasting Unilateral Neuralgiform Headache with Conjunctival Injection and Tearing (SUNCT)
    • Cluster-tic syndrome
    • Jabs and jolts syndrome
    • Other neuralgias
  • 15. Treatment: Medical
    • Carbamazepine - complete or near complete pain control attained in 58 to 100 percent of patients, compared with 0 to 40 percent of patients on placebo
    • NNT <2
    • sometimes poorly tolerated, with numbers needed to harm for minor and severe adverse events of 3 and 24 respectively.
  • 16. Treatment: Medical Carbamazepine
    • The usual starting dose 100 to 200 mg Q12h.
    • Increase by 200 mg daily as tolerated until sufficient pain relief is attained.
    • The typical maintenance dose is 600 to 800 mg/day, given in two divided doses for tablets and extended release capsules, or four divided doses when for oral suspension.
    • The maximum suggested total dose is 1200 mg daily.
  • 17. Treatment: Medical Carbamazepine
    • Adverse effects carbamazepine: drowsiness, dizziness, nausea and vomiting; slow titration may minimize these effects.
    • Carbamazepine-induced leukopenia is not uncommon, but it is usually benign; aplastic anemia is a rare side effect.
  • 18. Treatment: Medical Carbamazepine
    • The HLA-B*1502 allele is a genetic susceptibility marker in Asians that is associated with an increased risk of developing Stevens-Johnson syndrome and/or toxic epidermal necrolysis.
    • For most patients of Asian ancestry, genetic testing for the presence of this marker is recommended by the manufacturer prior to initiation
  • 19. Treatment: Medical: Oxcarbazepine
    • equally effective as carb., decreased SE, with a >50 percent reduction of attacks achieved by 88 percent or more of patients in both treatment groups.
    • started at a total dose of 600 mg daily, given in two divided doses.
    • The dose can be increased as tolerated in 300 mg increments every third day to a total dose of 1200 to 1800 mg daily.
  • 20. Treatment: Medical Baclofen
    • Limited evidence from a small double-blind crossover trial
    • Treatment with baclofen 40 to 80 mg daily resulted in a reduction in paroxysms in 7/10 patients with typical TN, compared with 1/10 placebo.
    • The starting dose 15 mg daily given in three divided doses, with gradual titration to a maintenance dose of 50 to 60 mg per day.
    • drug should be discontinued slowly since seizures and hallucinations have been reported with upon withdrawal.
  • 21. Treatment: Medical Opioids
    • no controlled data regarding the efficacy of opioids in TN
    • may help make the pain bearable while other, more effective and long-term, treatments take effect.
    • may be effective at lower doses when combined with neuropathic agents
  • 22. Treatment: Medical Other treatments
    • Small open label studies have suggested benefit with a number of medications used for TN: phenytoin, valproic acid, gabapentin, pregabalin, clonazepam, topiramate, misoprostol (with MS)
    • Lidocaine IV – 100-300mg over 30 minutes.
    • No controlled trial comparing monotherapy with combination therapy
  • 23. Treatment: Interventional Overview
    • Microvascular decompression
    • Ablative procedures, including:
    • Rhizotomy with either radiofrequency thermocoagulation, mechanical balloon compression, or chemical (glycerol) injection
    • Gamma knife radiosurgery
    • Peripheral neurectomy and nerve block
  • 24. Treatment: Interventional Microvascular Decompression
    • Craniotomy
    • Initial pain relief 90%, 1 yr. (80%, 3 yr. (75%), 5 yr. (73%)
    • 0.2% mortality
    • 4% major adverse events: CSF leak, infarction, hematoma
    • 11% aseptic meningitis
    • 10% long term hearing loss
    • 7% sensory loss
  • 25. Treatment: Interventional Rhizotomy
    • Percutaneous procedures via foramen ovale
    • RF thermocoagulation, mechanical balloon compression, chemical neurolysis (0.1-0.4% glycerol)
    • 2008 AAN/EFNS: initial pain relief 90%, 1 yr. (68-85%), 3 yr. (54-64%), 5 yr. (50%)
    • 0.2% aseptic meningitis
    • 12 % dysesthesia (burning, aching, heavy)
    • 50% sensory loss
    • 4% anesthesia dolorosa
    • 4% corneal numbness with risk of keratitis
  • 26. Treatment: Gasserian Ganglion Block Submental oblique image of foramen ovale Yin W. Radiofrequency gasserian rhizotomy: The Role of RF Lesioning in the Management of Facial Pain. Techniques in Regional Anesthesia and Pain Management 2004; 8(1): 30-34.
  • 27. Treatment: Interventional Gamma Knife Radiosurgery
    • Beams aimed at proximal trigeminal root causing axonal degeneration and necrosis
    • Pain relief lags by a month
    • 1 yr. (69%), 3 yr. (52%)
    • 9-37% new or worsened facial sensory impairment
    • Anesthesia dolorosa very rare
    • May be more effective as a first intervention rather than second
  • 28. Treatment: Interventional Peripheral Neurectomy
    • Branches of trigeminal – supraorbital, infraorbital, alveolar, lingual.
    • Incision, alcohol, RF, cryotherapy
    • AAN/EFNS – evidence is negative or inconclusive
  • 29. Treatment Algorithm
  • 30. References
    • UpToDate 2010: Trigeminal Neuralgia
    • Han I, Shin D, Chang J, Kim K, Chang J, Huh R, Chung Effect of Various Surgical Modalities in Recurrent or Persistent Trigeminal Neuralgia. Stereotact Funct Neurosurg 2010;88:156-162