eMedicine Specialties > Ophthalmology > Neurologic Disorders

Trigeminal Neuralgia: Treatment & Medication

Author: Marc E Lenaerts, MD, Clerkship Director, Assistant Professor, Department of Neurology, University of Oklahoma
Coauthor(s): James R Couch, MD, PhD, FACP, Professor of Neurology, University of Oklahoma Health Sciences Center
Contributor Information and Disclosures

Updated: Mar 17, 2006

Treatment

Medical Care

Treatment can be subdivided into pharmacologic therapy, percutaneous procedures, surgery, and radiation therapy. Adequate pharmacologic trials should always precede the contemplation of a more invasive approach. Most patients respond well to initial therapy, but some are resistant to any type of treatment. Treatment must be tailored individually, based on the patient's age and general condition. In the case of secondary trigeminal neuralgia, adequate treatment is that of its cause, the detail of which is out of the scope of this article.

  • Carbamazepine (Tegretol, Carbatrol) was introduced in the 1960s and has proven its efficacy in numerous studies. It remains the criterion standard of treatment for this condition.
  • Phenytoin (Dilantin) has a lower rate of success, but a patient occasionally responds to it and not to carbamazepine. The dose varies greatly among patients.
  • Baclofen has shown its efficacy in the literature.
  • Clonazepam (Klonopin) has moderate efficacy but is not recommended because of its adverse effects (eg, sedation) and dependence.
  • Amitriptyline (Elavil) can be tried, but the success rate is low.
  • Gabapentin (Neurontin) seems to be effective, but as of yet no controlled study is available.
  • Lamotrigine (Lamictal) has been proven more effective than placebo. The dosage should be increased slowly for better tolerance (eg, 25 mg daily dose each week; up to 250 mg twice a day).

Surgical Care

The success rate varies according to the experience of the surgeon or the anesthesiologist and, therefore, should be performed only by experienced surgeons. Surgical therapy can be divided into external or percutaneous procedures (usually performed by pain management specialists) and open skull surgery (also called microvascular decompression). The latter has an overall better success rate, but the former may be more cost-effective. The former may also be more accessible to elderly patients who are at high surgical risk.

  • Jannetta pioneered microvascular decompression (MVD). This procedure consists of opening a keyhole in the mastoid area and freeing the trigeminal nerve from the compression/pulsating artery; then, a piece of Teflon is placed between them. Large series have been published, and the initial efficacy is more than 80%. Recurrence rates are among the lowest compared with other invasive treatments. Usually, it requires the demonstration of true contact and compression by the artery on the nerve, but series are published that show an almost equally effective result without any demonstrated abnormality on imaging or even frank compression shown preoperatively. See Image 3.
  • Alcohol injection of the trigeminus can be performed at various locations along the nerve and is aimed at destroying selective pain fibers. Although it is an easy procedure, the success rate is low, in part because of a low selectivity of effect on the fiber type with this substance.
  • Glycerol injection of the gasserian ganglion to selectively destroy the pain-transmitting fibers has been used for a long time. This injection has a higher efficacy rate and a lower recurrence rate than the alcohol injection. It is easy to perform, and anesthesia is not needed.
  • Percutaneous radiofrequency rhizotomy and percutaneous microcompression with balloon inflation are relatively inexpensive accessible techniques and less invasive than surgery, with a lower (long-term) efficacy-to-recurrence ratio. The result is highly dependent on the surgeon's skill. General anesthesia is required.
  • Recently introduced, gamma-knife treatment consists of multiple rays (over 200) of high-energy photons concentrated with high accuracy on the target (ie, trigeminal nerve root). This treatment destroys specific components of the nerve. Of those treated, 60% of patients are pain-free immediately, and more than 75% of patients have greater than 50% relief after 1.5 years. This treatment can be used after a patient's failure to respond to any of the above-mentioned procedures, including this one. The device contains a stable source of radiation (60-Co) that frees this technique from requiring an external source of radioactivity (eg, cyclotron). See Image 2.
  • Pulsed radiofrequency on the trigeminal ganglion appears promising in reports. Likewise, linear-accelerated particle radiation appears to be a valid alternative.

Diet

No specific diet is recommended.

Activity

Other than avoiding the triggers, the activity of the patient should remain normal.

Medication

Treatment of trigeminal neuralgia is prophylactic. Indeed no abortive therapy could be conceived for this very short-lived pain condition. Carbamazepine remains the criterion standard, but a number of other drugs have been used for a long time and with fair success. They 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. Duration of treatment depends on clinical evolution but usually is long-term, often lasting years. Refer to Physician's Desk Reference (PDR) for details on medications mentioned.

Anticonvulsants

Reduce firing of nerve potentials in the trigeminal nerve.


Carbamazepine (Tegretol, Carbatrol)

Criterion standard in the medical management of trigeminal neuralgia, its efficacy has been demonstrated in multiple clinical trials. As of yet, a controlled trial has not occurred on oxcarbazepine (Trileptal), another carbamate close to carbamazepine. Slow-release forms now available allow a bid dosage. Titrating slowly improves tolerance.

Adult

200 mg PO tid (range 400-1600 mg/d, fractionated over the day); titrate slowly by 200 mg q3d

Pediatric

Not established

Serum levels may increase significantly within 30 d of danazol coadministration (avoid whenever possible); do not coadminister with MAOIs; cimetidine may increase toxicity, especially if taken in first 4 wk of therapy; carbamazepine may decrease primidone and phenobarbital levels (coadministration may increase carbamazepine levels)

Documented hypersensitivity; history of bone marrow depression; administration of MAOIs within last 14 d

Pregnancy

D - Unsafe in pregnancy

Precautions

Most frequent adverse effects are dizziness, ataxia, diplopia, hyponatremia, vertigo, sedation, and skin rash (rare); all are dose dependent; bone marrow suppression is rare but necessitates monitoring; monitor CBC (bone marrow suppression) and sodium (hyponatremia) levels monthly for at least 3 mo; monitor blood levels in case of toxicity or suspected noncompliance but not as routine; because of an autoinduction of its metabolism, carbamazepine levels tend to decrease after a few weeks of treatment, and dosage may need to be adjusted


Phenytoin (Dilantin)

Not as efficient as carbamazepine; use is based on same potential mechanisms.

Adult

300 mg PO qhs (range 100-400 mg/d qd/bid)

Pediatric

Not established

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, fluconazole, isoniazid, metronidazole, miconazole, phenylbutazone, succinimides, sulfonamides, omeprazole, phenacemide, disulfiram, ethanol (acute ingestion), trimethoprim, and valproic acid may increase phenytoin toxicity; phenytoin effects may decrease when taken concurrently with barbiturates, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, carbamazepine, theophylline, and sucralfate; phenytoin may decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, quinidine, theophylline, methadone, metyrapone, mexiletine, oral contraceptives, and valproic acid

Pregnancy

D - Unsafe in pregnancy

Precautions

Monitor blood levels in case of potential toxicity but not as routine; adverse effects are dizziness, ataxia, somnolence, and diplopia (rare at usual therapeutic dosages)


Lamotrigine (Lamictal)

A few controlled studies document its efficacy. The adverse event to prevent is a skin rash, sometimes severe and life threatening, mostly if titration is too rapid.

Adult

25 mg PO qd initially, increase q2wk by 25 mg bid; increase until efficacy or adverse effects, up to 250 mg PO bid

Pediatric

Not established

Acetaminophen increases renal clearance of medication, decreasing effects; similarly, phenobarbital and phenytoin increase lamotrigine metabolism causing a decrease in lamotrigine levels; administration of valproic acid with lamotrigine increases half-life

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Monitor for rash and inform patient; other adverse effects are headache, anorexia, nausea, vomiting, and dizziness (infrequent)


Gabapentin (Neurontin)

Same mechanism of action is supposed to play a role here. This drug is more expensive than the other drugs but has a very low adverse effect profile. No controlled study has been completed, but several open trials have reported an improvement on this drug. As for other indications, the 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. It is given in 4 divided doses a day.

Adult

1200-3600 mg/d PO tid/qid
300 mg PO qd initially, then titrate 300 mg/d

Pediatric

Not established

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in impaired renal or hepatic function

GABA-agonists

GABA-agonist effect reduces the central projection of painful afferent impulses.


Baclofen (Lioresal)

Not as often efficient as carbamazepine. Has been demonstrated to be useful by well-conducted clinical studies.

Adult

10 mg PO tid, up to 30 mg PO tid, depending on response and tolerance
5 mg PO bid initially, gradually increase by 5 mg q2-3d

Pediatric

Not established

Opiate analgesics, benzodiazepines, alcohol, tricyclic antidepressants, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase baclofen effects

Pregnancy

D - Unsafe in pregnancy

Precautions

Caution in patients with history of autonomic dysreflexia and when spasticity is used to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication

Tricyclic antidepressants

A complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission. They block the active re-uptake of norepinephrine and serotonin.


Amitriptyline (Elavil)

A minority of patients might respond to this drug. The anticholinergic adverse effects will be the limitation.

Adult

25-75 mg/d PO qhs

Pediatric

Not established

Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme system inhibitors (eg, cimetidine, quinidine) may increase amitriptyline levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; patient has taken MAOIs in past 14 d; has history of seizures, cardiac arrhythmias, glaucoma, and urinary retention

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in cardiac conduction disturbances, history of hyperthyroidism, and renal or hepatic impairment; avoid using in elderly patients

Toxin

Appears to potentially decrease painful afferents, but mechanism of action remains unclear.


Botulinum toxin (BOTOX®)

Subcutaneous injections have been beneficial in a pilot study, but these results await confirmation.

Adult

100 U in the zygomatic arch

Pediatric

Not established

Myasthenia; documented hypersensitivity

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Excessive dosages can cause dysphagia or diplopia

More on Trigeminal Neuralgia

Overview: Trigeminal Neuralgia
Differential Diagnoses & Workup: Trigeminal Neuralgia
Treatment & Medication: Trigeminal Neuralgia
Follow-up: Trigeminal Neuralgia
Multimedia: Trigeminal Neuralgia
References

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Further Reading

Keywords

tic douloureux

Contributor Information and Disclosures

Author

Marc E Lenaerts, MD, Clerkship Director, Assistant Professor, Department of Neurology, University of Oklahoma
Marc E Lenaerts, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Merck and OrthoMcNeil Neurologics Honoraria Speaking and teaching

Coauthor(s)

James R Couch, MD, PhD, FACP, Professor of Neurology, University of Oklahoma Health Sciences Center
James R Couch, MD, PhD, FACP is a member of the following medical societies: American Academy of Neurology, American Geriatrics Society, American Headache Society, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, American Stroke Association, and United Council of Neurologic Subspecialties, Certification in Headache Medicine
Disclosure: Nothing to disclose.

Medical Editor

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.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
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.

Managing Editor

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.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

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.

 
 
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