AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

First detailed in the 18th century, trigeminal neuralgia is a severe, lightninglike pain in the trigeminal nerve territory that can be triggered by various stimuli (eg, touch).

Diagnostic criteria for idiopathic trigeminal neuralgia by the International Headache Society are as follows:

• Paroxysmal attacks of facial or frontal pain occur, lasting a few seconds to less than 2 minutes.
• Pain has at least 4 of the following characteristics:
  • Distribution along 1 or more divisions of the trigeminal nerve
  • Sudden, intense, sharp, superficial, stabbing, or burning in quality
  • Severe pain intensity
  • Precipitation from trigger areas or by certain daily activities (eg, eating, talking, washing the face, cleaning the teeth)
  • No symptoms between paroxysms
• No neurologic deficit is present.
• Attacks are stereotyped in the individual patient.
• Other causes of facial pain are excluded by history, physical examination, and special investigations (when necessary). In symptomatic cases, a persistence of aching can occur between paroxysms, as well as signs of sensory impairment in the trigeminal division. Then, a cause is demonstrated by appropriate investigation.

Pathophysiology

Trigeminal neuralgia is the prototype of neuropathic pain, meaning that the pain mechanisms themselves are altered. Evidence of both small and large fiber damage is present, as suggested by the potential for vibration to trigger an attack. Demyelination of the nerve, primary or secondary, leads to uncontrolled firing of small unmyelinated trigeminal nerve fibers. This occurs, in part, because of the lack of inhibitory inputs from large myelinated nerve fibers. However, features also suggest a partly central mechanism (eg, delay between stimulation and pain, refractory period). The central abnormalities are still poorly understood. See Image 1.

Frequency

United States

Prevalence in the United States is approximately 1.5 cases per 10,000 population. Incidence in the United States is about 15,000 cases per year. Although a questionable family clustering exists, trigeminal neuralgia most likely is multifactorial.

International

No geographic tendency exists.

Mortality/Morbidity

Mortality is virtually nonexistent; however, the severity of the pain may lead to suicide. This disease has no significant morbidity, except for the burden of long-term pain and possible reactive depression.

Race

No racial differences regarding this disease have been reported.

Sex

Females are affected twice as often as males.

Age

Most cases develop in patients older than 50 years, but occasional reports of pediatric cases indicate a large range of age at onset.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Although it may be interrupted by remissions of a few months, trigeminal neuralgia is a long-term condition, consisting of episodic headache. This disease has the typical characteristics of neuropathic pain.

• The pain is lightninglike and hardly lasts for longer than a second. Because multiple bouts frequently follow each other, the patient often misleadingly describes a continuous pain. A refractory period that can be as short as a couple of seconds occurs. The intense pain is followed by a bothersome sensation in the area. If prominent, the painful sensation is indicative of a potential underlying lesion (eg, tumor) in the posterior fossa.
• In most cases, pain is located in V3 or V2; it is located rarely in both and exceptionally in V1. Pain is unilateral and does not shift sides. Although very rare, bilateral cases have been described.
• Different stimuli can trigger pain, often consistent in each patient. These stimuli include the following:
• • Touching or applying heat or cold to the cheek or gum
  • Chewing, yawning, or talking
  • Wind blowing in the face
  • Gustatory stimuli and vibration (In experimental studies, these stimuli have been described, demonstrating the role of large myelinated fibers in the pathophysiology.)

Physical

Except for a trigger zone, usually in the face, general and neurologic examinations should be normal. Although they may be observed transitorily in idiopathic trigeminal neuralgia, hypesthesia or dysesthesia in the face should be considered part of the secondary forms.

Causes

Trigeminal neuralgia is divided into 2 categories, idiopathic and secondary. Secondary forms can have multiple origins, as outlined below. (This list is not exclusive.)

• Tumor
• • Acoustic neurinoma
  • Chordoma at the level of the clivus
  • Pontine glioma or glioblastoma
  • Epidermoid
  • Metastases
  • Lymphoma
• Vascular
• Pontine infarct
• Arteriovenous malformation in the vicinity
• Persistence of a primitive trigeminal artery
• Pulsatile compression by the adjacent superior cerebellar artery (more rarely, anteroinferior artery)
• Inflammatory
• Multiple sclerosis (MS)
• Sarcoidosis
• Lyme disease neuropathy
• Paraneoplastic (possibly)

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

The differential diagnosis will be most critical with related trigeminal autonomic cephalgias, such as cluster headache and chronic paroxysmal hemicrania.

Cluster headache: Pain is not restricted to a branch of the trigeminal nerve but is periocular, lasts longer (15-120 min), is not triggerable, is accompanied by prominent autonomic symptoms, and usually has fewer episodes a day.

Raeder syndrome: Ophthalmoparesis is present.

Atypical facial pain: In addition to pain that is of vague localization and long duration (usually chronic and daily), psychiatric disturbances are associated.

SUNCT: Pain is of longer duration (2-3 min), and prominent autonomic symptoms (eg, lacrimation, rhinorrhea) are associated.

Tolosa-Hunt syndrome: Pain is of longer duration but not triggerable.

Dental abscess, sinusitis, and sinusal adenocarcinoma are possible differential diagnoses.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• No routine laboratory studies are performed in the initial workup. Laboratory work is not frequently helpful but should be directed by the clinical context.
• An inflammatory disease might be supported by an elevated erythrocyte sedimentation rate (ESR). Lyme titers can be demonstrated by serology.
• Cerebrospinal fluid (CSF) may confirm metastatic carcinomatosis.

Imaging Studies

• Imaging studies are indicated because distinguishing between idiopathic and secondary forms of trigeminal neuralgia is not always clear.
• CT scan provides a poor resolution in the posterior fossa.
• MRI is the imaging modality of choice. It can reveal MS plaques and pontine gliomas.
• Magnetic resonance angiography (MRA) can be useful in locating a vascular compression; however, the sensitivity remains low.
• Newer techniques, with enlarged and/or tridimensional views of the pontine area, can demonstrate a neurovascular conflict (eg, posteroinferior cerebellar artery compresses the trigeminal root). See Image 2.
• Conventional angiogram is only useful if a vascular malformation is suspected, but it fails to directly demonstrate the relationship with the nerve.

Other Tests

• Clinical neurophysiology testing with a blink reflex study may be helpful to demonstrate a lesion of the trigeminus in which a bilateral delay occurs in response to the stimulation on the pathologic side. The blink reflex can clearly help distinguish between the symptomatic form and the idiopathic form of the syndrome.

Histologic Findings

Although not a diagnostic test, histologic findings reveal focal demyelination as the ultimate lesion in both secondary and idiopathic cases. In secondary cases, the underlying lesion can be assessed by histology in some instances (eg, tumor).

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Section 7 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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.

Drug Category: Anticonvulsants

Reduce firing of nerve potentials in the trigeminal nerve.

Drug Name	Phenytoin (Dilantin)
Description	Not as efficient as carbamazepine; use is based on same potential mechanisms.
Adult Dose	300 mg PO qhs (range 100-400 mg/d qd/bid)
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	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)

Drug Name	Lamotrigine (Lamictal)
Description	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 Dose	25 mg PO qd initially, increase q2wk by 25 mg bid; increase until efficacy or adverse effects, up to 250 mg PO bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	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)

Drug Name	Gabapentin (Neurontin)
Description	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 Dose	1200-3600 mg/d PO tid/qid 300 mg PO qd initially, then titrate 300 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Caution in impaired renal or hepatic function

Drug Category: GABA-agonists

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

Drug Category: 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.

Drug Category: Toxin

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

FOLLOW-UP

Section 8 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Except for surgical procedures, trigeminal neuralgia is not an affliction to treat on an inpatient basis.

Further Outpatient Care

• Longitudinal follow-up care is important because of the chronicity of the disease and because many treatments fail to maintain their efficacy (eg, pharmacologic, procedural).
• Monitor treatment for adverse effects. Monitoring of blood levels is advised in the case of carbamazepine or phenytoin (ie, monthly for at least 3 mo for carbamazepine, once after 2 wk for phenytoin) and every time the dose is adjusted or adverse effects appear.
• In the case of carbamazepine, a CBC should be performed every month for 3 months to rule out bone marrow suppression.
• Monitoring patients after procedures or open skull surgery will help screen for complications, such as corneal abrasions and anesthesia dolorosa.
• Transcranial magnetic stimulation appears promising, but results are still scarce.

Deterrence/Prevention

• Percutaneous procedures and surgery yield the best results when applied early in the course of the disease. Even if medical treatment comes first, trials, when they are adequately completed and ineffective, should be followed promptly by the next trial in order not to delay and decrease the efficacy of more invasive treatments.
• No specific preventative therapy exists. Patients may suffer from a premonitory atypical pain for months; therefore, appropriate recognition of this pretrigeminal neuralgia syndrome may lead to earlier and more efficient treatment.

Complications

• A partial destruction of the nerve due to procedures and, sometimes, surgery can result in anesthesia dolorosa, a condition where pain is still present but sensation is decreased. Whether pain is or is not present, the decreased pain perception can lead to lesions that remain unnoticed to the patient.
• Corneal ulceration can result because of trophic disturbances from nerve deafferentation. Therefore, assessing the integrity of facial sensation immediately before and after a procedure, as well as in the long term, is paramount.
• After any invasive treatments, reactivation of a herpes simplex infection is not uncommon.

Prognosis

• Idiopathic trigeminal neuralgia is a chronic affliction and needs constant follow-up care; however, its disease course does not progressively worsen.

Patient Education

• Patients should be aware of potential adverse effects. They should report any altered sensation in the face, especially after a procedure.
• Patients should be educated about the importance of being compliant with their medication regimen. They should be informed about the potential for anesthesia dolorosa.
• Patients should be informed that carbamazepine is not prescribed (at this time) for a seizure disorder.
• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center. Also, see eMedicine's patient education articles Trigeminal Neuralgia (Facial Nerve Pain) and Tic Douloureux.

MISCELLANEOUS

Section 9 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Neoplastic infiltration of the nerve should not be overlooked. (A case of lymphoma revealed by trigeminal neuralgia has been seen.)
• Failure to diagnose a brainstem tumor and bone marrow aplasia as an idiosyncratic adverse effect of carbamazepine are common pitfalls to avoid. Standard care must be applied to invasive procedures, which are most subject to potential claims.

Special Concerns

• Anesthesia dolorosa should be a main special concern.

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Microscopic demonstration of demyelination in primary trigeminal neuralgia. A tortuous axon is surrounded by abnormally discontinuous myelin. Electron microscope, 3, 300 X.
	View Full Size Image
Media type:  Image

Media file 2:  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.
	View Full Size Image
Media type:  MRI

Media file 3:  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.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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Article Last Updated: Mar 17, 2006