Clinical Evidence Handbook
A Publication of BMJ Publishing Group
Am Fam Physician. 2016 Jul 15;94(2):133-135.
Author disclosure: Joanna M. Zakrzewska and Mark E. Linskey are authors of references cited in this review.
Trigeminal neuralgia is a sudden, unilateral, brief, stabbing, recurrent pain in the distribution of one or more branches of the fifth cranial nerve. The diagnosis is made using the history alone, based on characteristic features of the pain.
Pain occurs in paroxysms, which can last from a few seconds to several minutes. The frequency of the paroxysms ranges from a few to hundreds of attacks per day.
Periods of remission can last for months to years, but tend to get shorter over time.
The condition can impair activities of daily living and lead to depression.
The annual incidence in the United Kingdom (based on physician practice lists and rather liberal diagnostic criteria) has been reported to be 26.8 per 100,000. However, studies in other countries with stricter definitions, such as the United States and the Netherlands, have reported much lower incidence rates ranging between 5.9 and 12.6 per 100,000.
Experts find that symptoms worsen over time and become less responsive to medication, despite dose increases and adding further agents.
Treatment success is defined differently in studies of medical and surgical therapies for trigeminal neuralgia.
Treatment success in medical studies is usually defined as at least 50% pain relief from baseline. However, complete pain relief is the measure of treatment success in surgical studies.
Carbamazepine is considered the first-line medication for the initial medical treatment of trigeminal neuralgia symptoms.
Carbamazepine has been shown to increase pain relief compared with placebo, but also increases adverse effects, such as drowsiness, dizziness, rash, liver damage, and ataxia.
Studies evaluating durability of response with carbamazepine are lacking, but consensus expert opinion suggests that it may have a greater than 50% failure rate for long-term (five to 10 years) pain control.
Based on the strength of published evidence, carbamazepine remains the best-supported standard medical treatment for trigeminal neuralgia.
There is consensus that oxcarbazepine is an effective treatment in persons with trigeminal neuralgia and may have fewer adverse effects than carbamazepine, although there is a lack of data from randomized controlled trials (RCTs) to confirm this.
Oxcarbazepine rarely provides complete or long-term pain relief, although studies evaluating durability of response with this drug are lacking.
We found no sufficient evidence to judge the effectiveness of baclofen or lamotrigine.
Lamotrigine is often used in persons who cannot tolerate carbamazepine, but the dose must be increased slowly to avoid rashes, thus making it unsuitable for acute use.
There is consensus that baclofen may be useful for persons with multiple sclerosis who develop trigeminal neuralgia.
We found no evidence comparing gabapentin vs. placebo/no treatment or other treatments covered in this review in persons with trigeminal neuralgia.
Gabapentin does have support for use in treating other neuropathic pain conditions, particularly multiple sclerosis.
Despite a lack of RCT data, observational evidence supports the use of microvascular decompression to relieve symptoms of trigeminal neuralgia.
Microvascular decompression has been shown in at least two prospective comparative cohort trials to have superiority over stereotactic radiosurgery for complete pain relief, durability of response (up to five years), and preservation of trigeminal sensation.
However, microvascular decompression requires general anesthesia and is rarely associated with surgical complications, of which a less than 5% risk of ipsilateral hearing loss appears to be the most common.
Well-conducted observational studies have demonstrated that microvascular decompression has a greater magnitude of therapeutic effect than any medical and surgical therapy for trigeminal neuralgia. As such, this procedure
This is one in a series of chapters excerpted from the Clinical Evidence Handbook, published by the BMJ Publishing Group, London, U.K. The medical information contained herein is the most accurate available at the date of publication. More updated and comprehensive information on this topic may be available in future print editions of the Clinical Evidence Handbook, as well as online at http://www.clinicalevidence.bmj.com (subscription required).
This series is coordinated by Kenny Lin, MD, MPH, Associate Deputy Editor for AFP Online.
A collection of Clinical Evidence Handbook published in AFP is available at http://www.aafp.org/afp/bmj.
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