Trigeminal Neuralgia Medication

  • Author: Manish K Singh, MD; Chief Editor: Robert A Egan, MD   more...
 
Updated: Apr 5, 2012
 

Medication Summary

Carbamazepine remains the criterion standard, but a number of other drugs have been used for a long time and with fair success in trigeminal neuralgia (TN). These agents should be considered successively in case of resistance. Rarely, combination therapy can be provided, but it should remain exceptional for tolerance reasons and because a synergistic effect rarely occurs.[43] Duration of treatment depends on clinical evolution but usually is long term, often lasting years. Topical analgesics have failed in patients with ophthalmologic manifestations of trigeminal neuralgia.[64]

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Anticonvulsant Agents

Class Summary

Anticonvulsant drugs reduce the excitability of gasserian ganglion neurons, preventing anomalous discharges and related lancinating volleys of pain. Thus, these agents may help control paroxysmal pain by limiting the aberrant transmission of nerve impulses and reducing the firing of nerve potentials in the trigeminal nerve.

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Carbamazepine (Tegretol)

 

Carbamazepine is the criterion standard in the medical management of trigeminal neuralgia. A 100-mg tablet may produce significant and complete relief within 2 hours, and, for this reason, a 100 mg twice a day (bid) prescription is suitable to start. If this initial dose fails, one may push the dose to 1200 mg daily (qd), as the patient will tolerate, for initial relief; maintenance doses generally are lower, 100-800 mg daily bid. If using the extended-release caplet, begin with 200 mg qd and increase as needed to a maximum dose of 1200 mg/d bid. Titrating slowly improves tolerance.

So immediate, predictable, and powerful is the relief that if the patient does not respond at least partially to carbamazepine, one should reconsider the diagnosis of idiopathic trigeminal neuralgia. Note, however, that 15% of patients do not benefit from carbamazepine, forcing trials of other medications.

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Gabapentin (Neurontin)

 

Small, uncontrolled studies have indicated possible effectiveness of gabapentin in patients whose pain has become refractory to carbamazepine. This agent is often better tolerated than carbamazepine by elderly patients. No placebo-controlled studies have been published, but several open trials have reported an improvement on this drug.

As for other indications, an adequate dosage seems to vary greatly, and a trial should include raising the dose (eg, 3600 mg/d) as long as no efficacy is yet encountered, before stopping it.

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Lamotrigine (Lamictal, Lamictal ODT, Lamictal XR)

 

Lamotrigine provided sustained relief in 2 small prospective studies. In an open-label design by Lunardi et al, all 5 patients with symptomatic trigeminal neuralgia associated with multiple sclerosis (MS) and 10 of 15 patients with idiopathic disease gained complete relief when followed for 3-8 months.[37] Doses varied widely from 100-400 mg/d.

In a double-blind, placebo-controlled, crossover study, Zakrzewska et al found 400 mg of lamotrigine relieved the pain in 7 of 13 patients with trigeminal neuralgia compared with only 1 of 14 on placebo.[38]

The adverse event to prevent is a rash, sometimes severe and life threatening, mostly if titration is too rapid.

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Phenytoin (Dilantin, Phenytek)

 

Phenytoin has a similar mechanism of action to carbamazepine but is probably less effective. Phenytoin may provide relief as an add-on drug when carbamazepine monotherapy wanes, as commonly happens after 1 or several years. This drug has several common adverse effects, which are often troublesome in older patients, and drug levels do not always correlate with efficacy.

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Topiramate (Topamax)

 

This therapy is experimental. In a pilot study of 3 patients enrolled in a National Institutes of Health (NIH)–sponsored trial, investigators could not confirm the benefits of topiramate.[65] However, it may be a reasonable second-line agent.

Zvartau-Hind et al reported success in an uncontrolled, open-label trial of 200-300 mg daily in 6 patients with multiple sclerosis (MS), prescribed as monotherapy (in 5 of the 6 individuals) over a 6-month interval.[66] All 6 patients reported complete relief and appeared to tolerate the drug well. Solaro et al found 150-300 mg total daily doses relieved all trigeminal neuralgia pains in a case series of 4 patients, 2 with multiple sclerosis, 1 with idiopathic trigeminal neuralgia, and 1 with previous arteriovascular malformation resection, when followed for 6 months. Carbamazepine and gabapentin had previously failed in all patients.

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Oxcarbazepine (Trileptal)

 

Oxcarbazepine is a close cousin of carbamazepine and presumably works on similar mechanisms. This agent offers a better tolerance and is easier to manage. Studies are limited, as opposed to the large body of high-level evidence with carbamazepine.

Daily maintenance doses of oxcarbazepine 400-2400 mg/d were effective in several small uncontrolled studies.[67] Three small, multicenter, double-blind randomized trials found it as efficacious as carbamazepine in newly diagnosed or refractory trigeminal neuralgia and to be better tolerated.[68]

The recommended starting dose is 300 mg bid. Note that this drug has not yet been approved by the US Food and Drug Administration (FDA) for trigeminal neuralgia.

This drug has not yet been approved by the FDA for trigeminal neuralgia (TN).

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Skeletal Muscle Relaxants

Class Summary

Several small, uncontrolled studies in the 1970s and 1980s, including those by Parekh et al and Fromm et al, demonstrated effectiveness of baclofen, particularly when added to an existing regimen of carbamazepine that is not providing adequate pain control. Once baclofen is added to an anticonvulsant, the dosage of the anticonvulsant often can be reduced.

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Baclofen (Lioresal, Gablofen)

 

Baclofen is the only medication in this class with published data to support efficacy. This drug may induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at the spinal level.

Baclofen is most often used after therapy with carbamazepine has been initiated, and its effects may be synergistic with those of carbamazepine.

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Tricyclic Antidepressants

Class Summary

Tricyclic antidepressants are a complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission and block the active reuptake of norepinephrine and serotonin.

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Amitriptyline

 

A minority of patients might respond to amitriptyline. Anticholinergic adverse effects are the limitation.

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Toxins

Class Summary

Toxins are a relatively recent experimental approach to management of trigeminal neuralgia and have been mentioned to respond to patient inquiries. These agents are not recommended because of scant evidence of efficacy. The mechanism of action of these agents remains unclear, but they appear to potentially decrease painful afferents.[69]

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Botulinum toxin (BOTOX)

 

Subcutaneous injections of botulinum toxin have been beneficial in a pilot study of patients with ophthalmologic manifestations of trigeminal neuralgia, but these results await confirmation.

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Contributor Information and Disclosures
Author

Manish K Singh, MD  Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience

Manish K Singh, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American Association of Physicians of Indian Origin, American Headache Society, American Medical Association, and American Society of Regional Anesthesia and Pain Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Gordon H Campbell, MSN, FNP-BC  Neuroscience Nurse Practitioner, Neurology Service, Portland Veterans Affairs Medical Center; Primary Faculty, Clinical Instructor, and Guest Lecturer, Family Nursing Department, Oregon Health Sciences University School of Nursing

Gordon H Campbell, MSN, FNP-BC is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Siddharth Gautam, MBBS  Resident Physician, Jersey Neuroscience Institute

Disclosure: Nothing to disclose.

Helmi L Lutsep, MD  Professor and Vice Chair, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Chief Editor

Robert A Egan, MD  Director of Neuro-Ophthalmology, St Helena Hospital

Robert A Egan, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, North American Neuro-Ophthalmology Society, and Oregon Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Jane W Chan, MD Professor of Neurology/Neuro-ophthalmology, Department of Medicine, Division of Neurology, University of Nevada School of Medicine

Jane W Chan, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Ophthalmology, American Medical Association, North American Neuro-Ophthalmology Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

James R Couch, MD, PhD, FACP Professor of Neurology, University of Oklahoma Health Sciences Center

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Simon K Law, MD, PharmD Associate Professor of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Andrew W Lawton, MD Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center

Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association

Disclosure: Nothing to disclose.

Marc E Lenaerts, MD, FAHS Staff Neurologist, Mercy Medical Group; Associate Clinical Professor of Neurology, Department of Neurology, University of California, Davis, School of Medicine

Marc E Lenaerts, MD, FAHS is a member of the following medical societies: American Academy of Neurology, American Headache Society, and International Headache Society

Disclosure: Nothing to disclose.

Jorge E Mendizabal, MD Consulting Staff, Corpus Christi Neurology

Jorge E Mendizabal, MD is a member of the following medical societies: American Academy of Neurology, American Headache Society, National Stroke Association, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Hampton Roy Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Tom Scaletta, MD Chair, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine

Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Brian R Younge, MD Professor of Ophthalmology, Mayo Clinic School of Medicine

Brian R Younge, MD is a member of the following medical societies: American Medical Association, American Ophthalmological Society, and North American Neuro-Ophthalmology Society

Disclosure: Nothing to disclose.

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Illustration depicting the trigeminal nerve with its 3 main branches
Microscopic demonstration of demyelination in primary trigeminal neuralgia. A tortuous axon is surrounded by abnormally discontinuous myelin. (Electron microscope; 3300×).
Magnetic resonance image (MRI) with high resolution on the pons demonstrating the trigeminal nerve root. In this case, the patient with trigeminal neuralgia has undergone gamma-knife therapy, and the left-sided treated nerve (arrow) is enhanced by gadolinium.
Microvascular decompression (Jannetta procedure) used to treat trigeminal neuralgia. The anteroinferior cerebellar artery and the trigeminal nerve are in direct contact. Courtesy of PT Dang, CH Luxembourg
Table 1. Characteristic Features of 3 Common Craniofacial Pains
ConditionMale:Female RatioAge of onset, yLocalizationAccompanying SymptomsAttack DurationCyclesProvocation
Trigeminal neuralgia1:2>50UnilateralNoneSecondsMonth intervalsTrigger zones
Cluster headache31:130-40Always unilateralHorner syndrome, conjunctival infection, epiphora15-180 minutesClusters with weeks to months intervalsNocturnal attacks
Migraine1:110-20VariablePhotophobia, phonophobia, gastrointestinal symptoms4-72 hoursDays to weeks intervalsVariable
Table 2. Distinguishing Features Between Trigeminal Neuralgia and Atypical Facial Pain
FeatureTrigeminal NeuralgiaAtypical Facial Pain
PrevalenceRareCommon
Main locationTrigeminal areaFace, neck, ear
Pain durationSeconds to 2 minutesHours to days
CharacterElectric jerks, stabbingThrobbing, dull
Pain intensitySevereMild to moderate
Provoking factorsLight touch, washing, shaving, eating, talkingStress, cold
Associated symptomsNoneSensory abnormalities
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