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Trigeminal Neuralgia Treatment & Management

  • Author: Manish K Singh, MD; Chief Editor: Robert A Egan, MD  more...
Updated: Oct 22, 2015

Approach Considerations

Trigeminal neuralgia is treated on an outpatient basis, unless neurosurgical intervention is required. Management of this condition must be tailored individually, based on the patient's age and general condition. In the case of symptomatic trigeminal neuralgia, adequate treatment is that of its cause, the details of which are out of the scope of this article.

Because most patients incur trigeminal neuralgia when older than 60 years, medical management is the logical initial therapy. Medical therapy is often sufficient and effective, allowing surgical consideration only if pharmacologic treatment fails. Medical therapy alone is adequate treatment for 75% of patients.

Patients may find immediate and satisfying relief with one medication, typically carbamazepine. However, because this disorder may remit spontaneously after 6-12 months, patients may elect to discontinue their medication in the first year following the diagnosis. Most must restart medication in the future. Furthermore, over the years, they may require a second or third drug to control breakthrough episodes and finally may need surgical intervention.

Simpler, less invasive procedures are well tolerated but usually provide only short-term relief. At this point, further and perhaps more invasive operations may be required, and with these procedures the risk of the disabling adverse effect of anesthesia dolorosa increases.

Thus, 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.

Transcranial magnetic stimulation appears promising, but results are still scarce.[26]

Adjunct Treatments

Adjunct treatments such as mechanical, electrical, and thermal stimuli sometimes modify pain with fewer adverse effects than medication. Self-adhesive bandages may also be used.

Depression is often seen in patients with trigeminal neuralgia; thus, this underlying depression should be adequately treated. Tricyclic antidepressants (eg, amitriptyline, nortriptyline), as well as sodium valproate or pregabalin, have not been well studied. Amitriptyline (Elavil) can be tried, but the success rate is low.


Overview of Antiepileptic Drugs

Antiepileptic drugs (AEDs) work well for trigeminal neuralgia (TN) and have been known to do so since a study was completed with phenytoin (PHE) in 1942 (Bergouignan) and another with carbamazepine (CBZ) in 1962 (Blom).[27] With 3 placebo-controlled crossover studies validating its efficacy in trigeminal neuralgia, providing relief by roughly 75% versus only 25% in the placebo arms (Killian, Nicol, Campbell), carbamazepine is the best studied drug for this disorder and the only one with US Food and Drug Administration (FDA) approval in this setting.

Since the carbamazepine studies, however, newer second- and third-generation AEDs have expanded the choice of AED in trigeminal neuralgia, having demonstrated their efficacy in a variety of neuropathic pain syndromes, including trigeminal neuralgia, as well as in painful diabetic polyneuropathy and postherpetic neuralgia.

Other anticonvulsant agents possibly useful in the treatment of this disorder include sodium valproate and clonazepam (Klonopin). Clonazepam has moderate efficacy but is not recommended because of a low level of evidence and its adverse effects (eg, sedation) and dependence. The National Institutes of Health (NIH) currently is sponsoring studies of topiramate.

Also see Antiepileptic Drugs.


Because patients with trigeminal neuralgia will be using medications for years, perhaps decades, their cost is relevant. Generic carbamazepine is the cheapest; costs vary widely for the other agents, depending on the source, but approach a 4-fold increase for generic gabapentin (GBP), 8-fold for lamotrigine (LTG), 10-fold for topiramate (TPM), and 20-fold for oxcarbazepine (OCB) in moderate daily doses.

To justify these hugely higher costs, providers can point to the promise of improved tolerability of the new agents, often a determining factor in a person with multiple sclerosis or with advanced age. Some drugs do not affect serious idiosyncratic hepatic and hematopoietic reactions, eliminating the burden and cost of routine laboratory monitoring. Some agents offer more linear pharmacokinetics and fewer drug-drug interactions, facilitating combination therapy. Some pose less long-term risk for osteoporosis. Furthermore, some drugs do not autoinduce their metabolism, simplifying dose titration and adjustment.


Most of the literature on medications for trigeminal neuralgia consists of case series, uncontrolled studies with less than a dozen subjects, or small randomized clinical trials, so the apparent efficacy of the drugs requires confirmation through well-designed, large, phase III trials. The controlled data published for lamotrigine and baclofen (BCF) is promising but derives from studies with only 14 and 10 subjects, respectively.

No controlled data exist for the use of phenytoin, clonazepam, sodium valproate, oxcarbazepine, gabapentin, or mexiletine in trigeminal neuralgia; similarly, no controlled data exist for the common practice of adding a second drug when the first fails, except for the addition of lamotrigine to carbamazepine. No head-to-head comparison studies of these agents exists, and only one surgery versus medication study has been published, limited to refractory trigeminal neuralgia, a small (n = 15) trial. Only one Cochran review of medications for trigeminal neuralgia exists, and it looks only at carbamazepine, the traditional favorite. Confusion arises over outcome measures, as some researchers accept only complete relief of pain, whereas others accept partial relief.


Serum levels of the anticonvulsants in ranges appropriate for epilepsy may be necessary, at least to control the initial symptoms of trigeminal neuralgia; a much smaller maintenance dosage may be adequate thereafter. Because this disorder may remit spontaneously after 6-12 months, patients may elect to discontinue medication, only to restart it when the pain recurs. Once a patient experiences breakthrough pain on a single agent, a second and even third additional medication may be required to restore relief, at which point, many seek a surgical solution. Resistance develops anywhere from 2 months to 10 years after treatment begins with the most studied and successful drug, carbamazepine.


According to Dalessio, medications work by interrupting the temporal summation of afferent impulses that precipitate the attack.[28]

Anticonvulsant medications pose risks of sedation and ataxia, particularly in elderly patients, which may make driving or operating machinery hazardous. They also may pose risks to the liver and the hematologic system. Thus, documentation of patient education about these potential risks is important.

Patients also need to understand that medications for trigeminal neuralgia are only palliative and often are of limited and temporary value. They also must be informed thoroughly of the risks involved with neurosurgical interventions, including anesthesia dolorosa.


Carbamazepine Therapy

Carbamazepine and oxcarbazepine are considered first-line therapy in trigeminal neuralgia (TN).[29, 30] Lamotrigine and baclofen are second-line therapy. Other treatments are third line and the evidence for their efficacy is scant.

Carbamazepine acts by inhibiting the neuronal sodium channel activity, thereby reducing the excitability of neurons. A 100-mg tablet may produce significant and complete relief within 2 hours, and for this reason, it is a suitable agent for initial trial, although the effective dose ranges from 600-1200 mg/d, with serum concentrations between 40-100 mcg/mL. Indeed, serum levels of carbamazepine (but not necessarily phenytoin) in ranges appropriate for epilepsy may be necessary, at least to control initial symptoms, although a much smaller maintenance dosage may be adequate thereafter.

So predictable and powerful is the relief that if the patient does not respond at least partially to carbamazepine, reconsider the diagnosis of idiopathic trigeminal neuralgia.

Once a patient experiences breakthrough pain on a single agent, a second and even third additional medication may be required to restore relief. If this dosage does not relieve the discomfort adequately, administer a higher dose.

Many adverse central nervous system (CNS) effects (eg, vertigo, sedation, ataxia, diplopia) are associated with carbamazepine, which may make it difficult to use in elderly patients. The dose may be tapered once pain is controlled, since remission may occur.

Oxcarbazepine (Trileptal) has not been studied as extensively as carbamazepine, but efficacy outcomes are similar. Better tolerability can be considered an advantage over carbamazepine.[31]


Gabapentin Therapy

Gabapentin has demonstrated effectiveness in trigeminal neuralgia (TN), especially in patients with multiple sclerosis (MS). In an early study, Sist et al reported 2 patients with trigeminal neuralgia whose condition had a response to gabapentin,[32] 1 of whom was previously unresponsive to carbamazepine.

In another study, Khan reported complete relief of secondary trigeminal neuralgia in 6 of 7 patients with multiple sclerosis who received gabapentin doses of 900-2400 mg/d.[33] The patients previously had not responded to a variety of drugs. Once on gabapentin, 2 subjects were able to discontinue all other pain medications, and the remaining 5 could stop all but one other pain medication.[33] All patients maintained the response at 1 year of therapy with minimal adverse effects. In a similar, uncontrolled, small study of patients with multiple sclerosis, Solaro et al reported that 5 of 6 individuals found complete and sustained relief with gabapentin.[34]

To date, the efficacy of gabapentin and lamotrigine versus placebo or their efficacy in patients whose pain is refractory to carbamazepine has not been established. In paclitaxel-induced neuropathic pain, lamotrigine appears to be a promising drug. The difference in responses shown by different antiepileptic drugs depends on the etiology of the underlying mechanisms in neuropathic pain.[35] As stated by Carrazana and Schachter, of these 2 agents, gabapentin has advantages, which include faster titration, no known drug interactions, and no known idiosyncratic skin reaction.[36]


Lamotrigine Therapy

Lamotrigine (Lamictal) has been proven more effective than placebo in trigeminal neuralgia (TN). This agent provided impressive and sustained relief in A small, open-label, prospective study,[37] in which all 5 patients with symptomatic trigeminal neuralgia associated with multiple sclerosis (MS) and 11 of 15 patients with idiopathic disease gained complete relief. This was maintained during a follow-up period of 3-8 months. Drug levels closely predicted pain relief, although the dosage required for adequate relief varied widely from 100 to 400 mg/d.[37]

The dosage should be increased slowly for better tolerance (eg, 25-mg daily dose each week; up to 250 mg twice a day).[38]


Phenytoin Therapy

Phenytoin, although not approved by the US Food and Drug Administration (FDA) for idiopathic trigeminal neuralgia (TN) and believed to be less effective than carbamazepine, is probably effective for some patients with this disorder.[39]

Phenytoin has the same mechanism of action as carbamazepine and poses a similar risk panel, except for the risk of aplastic anemia. Of those patients who fail to attain relief with carbamazepine alone, an additional 8-20% of patients may have an adequate response if phenytoin is added to the treatment regimen.

According to a small study by Braham, phenytoin produced complete relief of pain in 30-40% of 43 patients and partial relief in an additional 30-40% at 300-600 mg/d.[40] Blom stated that doses of 300 mg/d were less effective, although doses of 400-600 mg caused more adverse effects.[27]

No correlation has been found between blood levels of phenytoin and therapeutic effect. Loeser recommended that the dose can be increased until relief is obtained or undesirable adverse effects appear (eg, dizziness, ataxia, diplopia, nystagmus, nausea).[39]

Raskin reported relief of intolerable pain with 250 mg of intravenous phenytoin over 5 minutes, allowing relief for hours to 3 days, sufficient for an adequate history and reexamination.[41]


Non-antiepileptic Drug Therapy

In 2006, He et al reported that the evidence from randomized controlled trials was insufficient to show significant benefit from non-antiepileptic drugs in trigeminal neuralgia (TN).[42]

Baclofen therapy

Baclofen may be effective in patients with trigeminal neuralgia.[43, 44] Tizanidine was investigated in a few trials but did not show significant benefit. Commonly, baclofen is added to anticonvulsants when breakthrough symptoms occur.

In an early small, uncontrolled study, Fromm et al demonstrated baclofen to be useful.[15] Of the 14 patients with idiopathic trigeminal neuralgia resistant to carbamazepine, 10 found relief with 60-80 mg/d of baclofen.[15] The starting dosage is 10 mg/d, which can be increased, if needed, to 60-80 mg/d administered 3-4 times per day (it has a short half-life of 3-4 h).[15] According to Parekh et al and Raskin, the dose of carbamazepine then may be reduced to 500 mg/d to maintain a putative synergistic effect.[41, 45]

In another study, Fromm and Terrence suggested that L-baclofen represents a significant improvement over racemic baclofen in the treatment of trigeminal neuralgia.[46]

Other agents

The National Institutes of Health (NIH) is also investigating the use of dextromethorphan in doses much higher than those used in over-the-counter cough preparations. A randomized, double-blind, cross-over trial compared 6 weeks of oral dextromethorphan with active placebo (low-dose lorazepam) in 19 patients, stratified into 3 groups: 11 with facial pain and possible trigeminal neuropathy, 5 with anesthesia dolorosa, and 3 with idiopathic trigeminal neuralgia.[47] Dosage was titrated in each patient to the highest level reached without disrupting normal activities.

Dextromethorphan shows little or no analgesic efficacy in pain due to possible trigeminal neuropathy and anesthesia dolorosa. Additional trials are necessary to conclusively evaluate the efficacy of NMDA-receptor antagonists in trigeminal neuralgia.

Botulinum toxin was shown to be successful for at least 90 days in a single case report in a patient with trigeminal neuralgia in whom carbamazepine and rhizolysis had previously failed.[48]

Trials of newer N- methyl-D-aspartate receptor blockers have not been done. A nonsteroidal anti-inflammatory agent (NSAID), misoprostol, has shown modest efficacy in a small prospective open study in patients with multiple sclerosis (MS).[49]


Surgical Considerations

Over time, the drugs used for the treatment of trigeminal neuralgia (TN) often lose effectiveness as patients experience breakthrough pain. For patients in whom medical therapy has failed, surgery is a viable and effective option. According to Dalessio, 25-50% of patients eventually stop responding to drug therapy and require some form of alternative treatment.[28] The clinician then may consider referral to a surgeon for one of the procedures discussed below. Among patients who develop trigeminal neuralgia when younger than 60 years, surgery is the definitive treatment.

Many operations have been offered to patients in recent decades. Local ablation of the peripheral nerve and wide sectioning of the sensory roots largely have been abandoned. In the past, alcohol or phenol injection was given to the affected nerve, with the goal to destroy selective pain fibers. Although it was an easy procedure, the success rate is low, in part because of a low selectivity of effect on the fiber type with this substance; recurrence rates are around 50% at 1 year. Rhizotomy or tractotomy was recommended if pharmacologic treatment was unsuccessful.

In a review of surgical options by Tatli et al, which mostly included microvascular decompression and radiofrequency thermorhizotomy, each surgical technique for treatment of trigeminal neuralgia had merits and limitations.[50] The investigators also found that microvascular decompression provides the highest rate of long-term patient satisfaction with the lowest rate of pain recurrence.[50]

Neurosurgery is generally more helpful in those patients with paroxysmal rather than constant pain and in patients whose pain follows the anatomic distribution of one or more trigeminal distributions rather than being spread diffusely. The various operations often fail after 1 or several years of initial relief. This requires a repeat procedure, often with improved but still incomplete results. Thus, many patients eventually restart pain medication after surgery.

Surgery appears to be less effective for trigeminal neuralgia secondary to multiple sclerosis (MS).

For more information, see the following:

  • International RadioSurgery Association Stereotactic radiosurgery for patients with intractable typical trigeminal neuralgia who have failed medical management. Harrisburg, Pa: IRSA; 2009. Harrisburg, Pa: IRSA; 2009. (Radiosurgery practice guideline report; no. 1-03). Available at: Accessed April 8, 2011. [51]
  • Gronseth G, Cruccu G, Alksne J, et al. Practice parameter: the diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the European Federation of Neurological Societies. Neurology. 2008 Oct 7;71(15):1183-90. Available at: Accessed April 8, 2011. [23]

Current techniques

The success rate varies according to the experience of the surgeon or the anesthesiologist, and, therefore, surgical correction should be performed only by experienced surgeons. Surgical therapy can be divided into procedures on the nerve or gasserian ganglion (external or percutaneous, usually performed by pain management specialists) and on the nerve root (open skull surgery called microvascular decompression and performed by neurosurgeons, and gamma-knife radiation performed by radiation therapists).

Three operative strategies now prevail: percutaneous procedures, gamma knife surgery (GSK), and microvascular decompression (MVD). Ninety percent of patients are pain-free immediately or soon after any of the operations,[2] although the relief is much more long-lasting with microvascular decompression. Percutaneous surgeries make sense for older patients with medically unresponsive trigeminal neuralgia. Younger patients and those expected to do well under general anesthesia should first consider microvascular decompression—presently, this is the most cost-effective surgery although it is also more invasive.

Pain-free intervals after percutaneous procedures (percutaneous retrogasserian glycerol rhizotomy [PRGR] and percutaneous balloon microcompression [PBM]) last 1.5-2 years, 3-4 years after another (percutaneous radiofrequency trigeminal gangliolysis [PRTG]), and 15 years commonly after microvascular decompression.[52] Those in whom the first percutaneous procedure fails may undergo a repeat procedure, which usually provides relief.

More recently, however, posterior fossa exploration has frequently revealed some structural cause for neuralgia (despite normal findings on computed tomography [CT] scans, magnetic resonance images [MRI], or arteriograms), such as an anomalous artery or vein impinging on the trigeminal nerve root. In such cases, simple decompression and separation of the anomalous vessel from the nerve root produces lasting relief of symptoms.

In elderly patients with limited life expectancy, radiofrequency rhizotomy is sometimes preferred, as it is easy to perform, has few complications, and provides symptomatic relief for a period.


The cost per quality adjusted pain-free year was $6,342 for glycerol rhizotomy, $8,174 for microvascular decompression, and $8,269 for stereotactic radiosurgery, according to Pollock and Ecker.[53] In 2005, approximately 8000 patients with trigeminal neuralgia underwent surgery in the United States, at an estimated cost exceeding $100 million.


The timing for surgery is debatable, and no randomized study has addressed this question. However, the earlier a surgical technique is applied, it seems the better the outcome. At least 2 medication trials should be performed and carefully evaluated before more invasive techniques are instituted.[50]


Surgery exposes the patient to operative risks and the risk of permanent, residual facial numbness and dysesthesias. The primary complications of surgery include permanent anesthesia over the face or the troubling dysesthetic syndrome of anesthesia dolorosa—often disabling, is occasionally worse than the original trigeminal neuralgia, and is often untreatable. For this reason, procedures with the best long-term success and the least risk of a residual facial dysesthetic syndrome are the most promising.

Many patients require pain medication even after surgery.


Microvascular Decompression

Jannetta pioneered microvascular decompression (MVD). This procedure is commonly performed in younger, healthier patients, especially those with pain isolated to the ophthalmic division or in all 3 divisions of the trigeminal nerve and in those with secondary trigeminal neuralgia (TN). It is now the most common surgery performed for trigeminal neuralgia and general anesthesia is required.

Microvascular decompression 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 greater than 80%. Recurrence rates are among the lowest (20% at 1 year, 25% at 5 years) compared with other invasive treatments.[54, 53] 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. A 2015 systematic review and meta-analysis found that MVD had a significantly higher rate of initial pain-free outcomes (BNI grade 1) and a significantly lower pain-free recurrence rate when compared with GKS.[55]

See a surgical image below.

Microvascular decompression (Jannetta procedure) u 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

Patients spend 4-10 days in the hospital and another week convalescing at home. Thus, recovery is more prolonged than with percutaneous procedures. In addition, mortality for this more invasive procedure approaches 0.5%. Serious morbidity includes dizziness, temporary facial palsy, cerebrospinal fluid leaks, meningitis, cerebellar stroke, and hearing loss, which may occur in 1-5% of cases.

Also see Trigeminal Neuralgia Surgery.


Percutaneous Procedures

Percutaneous procedures usually can be performed on an outpatient basis under local or brief general anesthesia at acceptable or minimal risk of morbidity. For these reasons, they commonly are performed in debilitated persons or those older than 65 years.

Zakrzweska and Thomas described 3 types of procedures: percutaneous radiofrequency trigeminal gangliolysis (PRTG), percutaneous retrogasserian glycerol rhizotomy (PRGR), and percutaneous balloon microcompression (PBM).[56] Patients are left with minor, local, residual facial numbness after PRTG; may occasionally lose sensation after PRGR; and rarely do so after PBM. In each procedure, the surgeon introduces a trocar or needle lateral to the corner of the mouth and, under fluoroscopic guidance, into the ipsilateral foramen ovale. The ganglion is lysed at this location.

Percutaneous procedures and surgery yield the best results when applied early in the course of trigeminal neuralgia. Even if medical treatment comes first, trials, when they are adequately completed and the agent is deemed ineffective, should be followed promptly by the next trial in order not to delay and decrease the efficacy of more invasive treatments.

Percutaneous radiofrequency rhizotomy and percutaneous microcompression with balloon inflation are relatively inexpensive and accessible techniques, and they are less invasive than surgery, with a lower (long-term) efficacy-to-recurrence ratio. A comparison of the two techniques found them both effective with a median duration of pain relief of 21 months after PRGR and 20 months after PBC.[57] The result is highly dependent on the surgeon's skill. General anesthesia is required.

Also see Trigeminal Neuralgia Surgery.


In PRTG, a radiofrequency heating tip sears the ganglion until the area of facial pain becomes numb. This procedure has gained wide acceptance according to several investigators, because the patient is awake during the procedure, recovers quickly, and goes home the day of the procedure or the next day. However, according to Tan et al, the recurrence rate approaches 25% with PRTG, and occasionally patients suffer complications of jaw weakness and corneal anesthesia.[58]

In PRGR, a spinal needle likewise penetrates the face, this time to the trigeminal cistern, at which point a cisternogram is obtained with water-soluble contrast material. After removing this material, the surgeon instills anhydrous glycerol, asking the patient to remain seated for an additional 2 hours to fully ablate the nerve.

PRGR may be the favored procedure, as it has a higher efficacy rate and a lower recurrence rate than the alcohol injection and includes only a minimal risk of disturbed facial sensitivity postoperatively. In addition, it is easy to perform, and anesthesia is not needed. However, Cappiabianca et al and Taha and Tew, who favor the radiofrequency rhizotomy, argue that PRGR has the highest rate of pain recurrence.[59, 60]

With PBM, the operator inserts a balloon catheter through the foramen ovale into the region of the ganglion and inflates it for 1-10 minutes. As related by Meglio and Cioni, some surgeons report excellent results with PBM, comparable to those with PRTG.[61]


Gamma Knife Surgery

In 1953, Leksell irradiated the trigeminal nerve in 2 patients with good initial success but did not publish this data until 1971.[62] Progress really began when, in the 1990s, surgeons learned to target the nerve precisely with stereotactic magnetic resonance imaging (MRI), determine the proper radiation dose to quickly relieve pain without incurring facial sensory loss, and ascertain the length of nerve to be radiated.[63]

Gamma knife surgery (GKS) has become more widely available since 2000. This surgery is less technically demanding, less operator-dependent, and less invasive than the percutaneous procedures. It is among the newer techniques for treating trigeminal neuralgia and has fewer complications. Gamma knife surgery appears to be about as effective (80% of patients) as the percutaneous procedures but takes weeks to months to bring relief, which may be too long for some patients, and costs slightly more.

This procedure consists of multiple rays (>200) of high-energy photons concentrated with high accuracy on the target (ie, trigeminal nerve root),[64, 65] destroying specific components of the nerve. Of those treated, 60% of patients are immediately free of pain, and more than 75% of patients have greater than 50% relief after 1.5 years. Recurrence rates are around 25 % between 1 and 3 years. The device contains a stable source of radiation (60-Co) that frees this technique from requiring an external source of radioactivity (eg, cyclotron). See the image below.

Magnetic resonance image (MRI) with high resolutio 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.

The pain recurrence rate is low for patients who initially attain complete relief. Gamma knife surgery is generally effective, even in patients in whom previous surgery or medication trials failed.

In one study, most patients already had no relief with either microvascular decompression or glycerol rhizotomy, whereas following gamma knife surgery, at a median follow-up point of 18 months, 60% of patients were pain free, 17% were moderately improved, and 23% were minimally or not improved.[64] The investigators concluded that this technique is minimally invasive, is associated with a low risk (10%) of facial paresthesias or sensory loss, and offers a high rate (86%) of significant, initial pain relief.[64]

New facial numbness or paresthesias develop slowly over the first 12-15 months after gamma knife surgery, reaching bothersome levels in 9-20% of patients.

Also see Trigeminal Neuralgia Surgery.



Neurosurgical consultation is needed when medical treatment does not effectively control episodes of breakthrough facial pain. Pain management specialists may also be consulted for intractable pain.


Long-Term Monitoring

Longitudinal follow-up care is important because of the chronicity of trigeminal neuralgia, and because many treatments fail to maintain their efficacy (eg, pharmacologic, procedural).

In patients treated with carbamazepine or phenytoin, obtain a blood count during the first few weeks of therapy (ie, monthly for at least 3 mo for carbamazepine, once after 2 wk for phenytoin), every time the dose is adjusted or adverse effects appear, and yearly thereafter. Agranulocytosis and aplastic anemia are extremely rare adverse effects, but suppression of the white blood cell (WBC) count in the range of 2000-3000 103/µL is not uncommon. This mild suppression of the WBC count does not warrant discontinuation of carbamazepine therapy. Hepatic function should also be monitored. Up to 70% of patients receive complete or acceptable partial relief, at least temporarily.

Oxcarbazepine is a newer agent that may have fewer side effects, but it can cause hyponatremia, which should be monitored with serial serum sodium measurements in the first few weeks of therapy.

Patients who experience breakthrough pain may need an increase in the dosage of their medication, if tolerated, or the addition of a second anticonvulsant medication or baclofen. No published data from randomized, prospective, controlled studies are available to guide clinicians regarding multidrug therapy, leaving providers to empiric trials of one agent or another.

Neurologists caring for younger patients (< 60 y at onset) should consider early neurosurgical consultation, even after a negative magnetic resonance image (MRI) of the brain. Surgical procedures occasionally can afford complete relief, delaying the need for anticonvulsant medications for many years, if not permanently.

Monitoring patients after procedures or open skull surgery helps screen for complications such as corneal abrasions and anesthesia dolorosa.

Contributor Information and Disclosures

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 Headache Society, American Association of Physicians of Indian Origin, American Medical Association, American Society of Regional Anesthesia and Pain Medicine

Disclosure: Nothing to disclose.


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 is a member of the following medical societies: American Academy of Neurology

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, OHSU Stroke Center

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

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Siddharth Gautam, MBBS Resident Physician, Jersey Neuroscience Institute

Disclosure: Nothing to disclose.

Chief Editor

Robert A Egan, MD Director of Neuro-Ophthalmology and Stroke Service, 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, Oregon Medical Association

Disclosure: Received honoraria from Biogen Idec for speaking and teaching; Received honoraria from Teva for speaking and teaching.


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
Condition Male:Female Ratio Age of onset, y Localization Accompanying Symptoms Attack Duration Cycles Provocation
Trigeminal neuralgia 1:2 >50 Unilateral None Seconds Month intervals Trigger zones
Cluster headache 31:1 30-40 Always unilateral Horner syndrome, conjunctival injection, epiphora 15-180 minutes Clusters with weeks to months intervals Nocturnal attacks
Migraine 1:1 10-20 Variable Photophobia, phonophobia, gastrointestinal symptoms 4-72 hours Days to weeks intervals Variable
Table 2. Distinguishing Features Between Trigeminal Neuralgia and Atypical Facial Pain
Feature Trigeminal Neuralgia Atypical Facial Pain
Prevalence Rare Common
Main location Trigeminal area Face, neck, ear
Pain duration Seconds to 2 minutes Hours to days
Character Electric jerks, stabbing Throbbing, dull
Pain intensity Severe Mild to moderate
Provoking factors Light touch, washing, shaving, eating, talking Stress, cold
Associated symptoms None Sensory abnormalities
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