AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

The clinical description of severe facial pain, which is now known as trigeminal neuralgia (TN), can be traced back more than 300 years. Aretaeus of Cappadocia, known for one of the earliest descriptions of migraine, is credited with the first indication of TN. He described a headache in which "spasms and distortions of the countenance took place." John Fothergill was the first to give a full and accurate description of TN in a paper titled "On a Painful Affliction of the Face," which he presented to the medical society of London in 1773. Nicholaus Andre coined the term tic douloureux in 1756.

Idiopathic TN is the most common type of facial pain neuralgia. The pain typically occurs in the distribution of one of the branches of the trigeminal nerve, usually on one side. Rarely, it can affect both sides, although simultaneous bilateral trigeminal neuralgia is uncommon. It involves both the mandibular and maxillary divisions of the trigeminal nerve in 35% of affected patients. Isolated involvement of the ophthalmic division is much less common (2.8% of TN cases).

TN reportedly is one of the most excruciating pain syndromes. It has been known to drive patients with TN to the brink of suicide. The name tic douloureux was first used to describe TN and remains synonymous with the classic form of TN. The tic refers mainly to the visible effects of the brief and paroxysmal pain that, in classic TN, lasts only a few seconds. The pain is so severe that it often causes the patient to wince or make an aversive head movement, as if trying to escape the pain, thus producing an obvious movement, or tic.

An interactive Web site now allows patients to self-diagnose facial pain based on a brief series of questions. An artificial intelligence method (neural network modeling) provides immediate feedback to the patient regarding the diagnosis and patient education resources.¹

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), Tic Douloureux, and Pain Medications.

Problem

A lack of clear definitions for facial pain has hampered the understanding of trigeminal neuralgia. The condition has no clear natural history, and no long-term follow-up study of the progression of the disorder has ever been published. In an attempt to rationalize the language of facial pain, recently, a new classification scheme that divides facial pain into several distinct categories was introduced:²

• Trigeminal neuralgia type 1 (TN1): This is the classic form of trigeminal neuralgia in which episodic lancinating pain predominates.
• Trigeminal neuralgia type 2 (TN2): This is the atypical form of trigeminal neuralgia in which more constant pains (aching, throbbing, burning) predominate.
• Trigeminal neuropathic pain (TNP): This is pain that results from incidental or accidental injury to the trigeminal nerve or the brain pathways of the trigeminal system.
• Trigeminal deafferentation pain (TDP): This is pain that results from intentional injury to the system in an attempt to treat trigeminal neuralgia. Numbness of the face is a constant part of this syndrome, which has also been referred to as anesthesia dolorosa or one of its variants.
• Symptomatic trigeminal neuralgia (STN): This is trigeminal neuralgia associated with multiple sclerosis (MS).
• Postherpetic neuralgia (PHN): This is chronic facial pain that results from an outbreak of herpes zoster (shingles), usually in the ophthalmic division (V1) of the trigeminal nerve on the face and usually in elderly patients.
• Geniculate neuralgia (GeN): This is typified by episodic lancinating pain felt deep in the ear.
• Glossopharyngeal neuralgia (GPN): This is typified by pain in the tonsillar area or throat, usually triggered by talking or swallowing.

Frequency

The disease begins after age 40 in 90% of patients and is slightly more common in women. The incidence is said to be approximately 4-5 per 100,000 persons, although this is likely an underestimate. TN is observed with increased frequency in one disease category, ie, multiple sclerosis (MS). TN occurs in up 4% of these patients, in whom it is often bilateral. About 2% of patients with TN have MS.

Etiology

The etiology of most cases of TN is chronic vascular compression and injury to the trigeminal nerve at its entrance into the brainstem (pons). In one study, 64% of the compressing vessels were identified as an artery, most commonly the superior cerebellar (81%). Venous compression was identified in 36% of cases.³

Pathophysiology

Vascular compression of the trigeminal nerve appears to cause demyelination and remyelination of the nerve with persisting abnormalities of myelination (dysmyelination).

The most common theoretical explanation for TN proposes that high-frequency ectopic impulses are either generated from or augmented by areas of dysmyelination.⁴ These abnormal discharges may ignite a chain reaction of neuronal depolarization in the trigeminal ganglion.⁵ The subsequent cascade of neuronal activity is progated centrally into the trigeminal nucleus and is then perceived by the patient as an overwhelming burst of pain.

Although most cases of TN are caused by vascular compression, other structural disease is present in secondary TN, which can produce either typical or atypical pain. For example, a mass may displace and damage the nerve, resulting in pain. Alternatively, inflammation secondary to multiple processes may be due to the underlying lesion. (See Differentials).

In MS, lesions in the pons at the root entry zone (REZ) of the trigeminal fibers have been demonstrated. This is one form of "symptomatic" trigeminal neuralgia related to visible pathology. 

Clinical

TN presents with multiple episodes of severe and spontaneous pain that usually lasts seconds to minutes. The pain is often described as shooting, lancinating, shocklike, or stabbing. The episodes frequently are triggered by painless sensory stimulation to perioral trigger zones, eg, a patch of facial skin, mucosa, or teeth innervated by the ipsilateral trigeminal nerve. Triggers include touch, certain head movements, talking, chewing, swallowing, shaving, brushing teeth, or even a cold draft. The most commonly affected dermatomal zones are innervated by the second and third branches of the trigeminal nerve.

The episodes may be repetitive, recurring, and remitting randomly. Pain-free intervals, which might last for years early in the course of TN, typically grow shorter as the disease progresses. During episodes of pain, some patients have difficulty talking, eating, and maintaining facial hygiene out of fear of triggering the pain.

Physical: Standard bedside neurological examination findings are normal in TN. Patients may refuse examinations of the face, fearing the triggering of pain. Male patients may present with an area of the face, the trigger zone, that is unshaven and unkempt. The finding of numbness in the trigeminal distribution of TN suggests secondary TN and more extensive damage to the trigeminal nerve.

Differentials: Most of the following conditions are not easily confused with TN:

• Trigeminal neuropathy: Sensory loss is usually prominent; pain is slight.
• Herpetic and postherpetic neuralgia (PHN): This condition usually affects the first branch of the trigeminal nerve. The diagnosis of PHN usually requires the outbreak of shingles (herpes zoster) in the forehead or eye. Acute herpetic neuralgia is the norm in shingles, but pain that persists after the lesions have healed is PHN. The risk of PHN development is directly related to patient age.
• Neoplasms: These may present as a compressing mass or neoplastic cell infiltration of the trigeminal nerve. Pain is usually more constant than in TN1, and facial numbness is more common.
• Granulomatous inflammation (eg, tuberculosis, sarcoidosis, Behçet syndrome, collagen vascular diseases): These and other vasculitides may affect the trigeminal nerve and simulate TN.
• Other conditions that may mimic TN include odontogenic pain, geniculate neuralgia, glossopharyngeal neuralgia, temporomandibular disorders, cluster headache, hemicrania, and SUNCT (short-lasting, unilateral neuralgia from headache attacks with conjunctival injection and tearing) syndrome.

INDICATIONS

Section 3 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Surgical treatment is indicated for patients whose trigeminal neuralgia (TN) is intractable despite medical therapy, in those who are intolerant to the adverse effects of the medications, and in those in whom previous procedures failed.

Microvascular decompression (MVD) is usually indicated for patients younger than 70 years who are at lower risk for complications during general anesthesia, although healthy older patients can tolerate it well. Percutaneous approaches (eg, radiofrequency ablation, glycerol injection, balloon compression, radiosurgery) are more frequently offered to elderly patients, those in poor medical condition, those with MS, and those in whom previous MVD has failed.

RELEVANT ANATOMY

Section 4 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

The trigeminal nerve is the largest of all the cranial nerves. It exits laterally at the mid-pons level and has 2 divisions—a smaller motor root (portion minor) and a larger sensory root (portion major). The motor root supplies the temporalis, pterygoid, tensor tympani, tensor palati, mylohyoid, and anterior belly of the digastric. The motor root also contains sensory nerve fibers that particularly mediate pain sensation.

The gasserian ganglion is located in the trigeminal fossa (Meckel cave) of the petrous bone in the middle cranial fossa. It contains the first-order general somatic sensory fibers that carry pain, temperature, and touch. The peripheral processes of neurons in the ganglion form the 3 divisions of the trigeminal nerve, ie, ophthalmic, maxillary, and mandibular. The ophthalmic division exits the cranium via the superior orbital fissure; the maxillary and mandibular divisions exit via the foramen rotundum and foramen ovale, respectively.

The proprioceptive afferent fibers travel with the efferent and afferent roots. They are peripheral processes of unipolar neurons located centrally in the mesencephalic nucleus of the trigeminal nerve.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Lab Studies

• The diagnosis of facial pain is almost entirely based on the patient's history. In most cases of facial pain, no specific laboratory tests are needed. A blood count and liver function tests are required if therapy with carbamazepine is contemplated. Oxycarbazine can cause hyponatremia, so the serum sodium should be tested after institution of therapy.
• Although rarely indicated, appropriate blood work for rheumatic diseases, such as scleroderma (trigeminal neuropathy is reported in up to 5% of patients with this collagen vascular disease) and systemic lupus erythematosus, should be undertaken in patients with atypical features of facial pain and a systemic presentation of collagen vascular disease. Appropriate blood work includes a sedimentation rate, antinuclear antibody titer, double-stranded DNA, anti-Sm antibody, lupus erythematosus cell preparation, and complete blood count to look for hematological abnormalities (eg, hemolytic anemia, leukopenia, thrombocytopenia). Particularly in the case of scleroderma, creatinine kinase and aldolase levels may be elevated with muscle involvement. Antibody titers to SCL-86 and SCL-70 may also be present.
• When surgical procedures are contemplated, appropriate and routine preoperative laboratory tests are in order.

Imaging Studies

• In cases of typical (TN1) and atypical TN (TN2), a brain MRI with contrast is required. An MRI is sensitive for the exclusion of intracranial lesions that can rarely cause trigeminal neuralgia.
• Obtain contrast-enhanced brain MRIs prior to surgery to evaluate for vascular malformations or other lesions. Devote particular attention to the posterior fossa. High-resolution imaging of the nerve at the brainstem entry zone may reveal vascular compression of the nerve.³
• Imaging procedures have improved to the degree that reliably imaging neurovascular compression of the trigeminal nerve using high-resolution MRI sequences is possible.⁶

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Medical therapy

The most effective medication for the treatment of trigeminal neuralgia (TN) is carbamazepine. It acts by inhibiting the neuronal sodium channel activity, thereby reducing the excitability of neurons. The effective dose ranges from 600-1200 mg/d, with serum concentrations between 40-100 mcg/mL. However, many adverse 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.

Obtain a blood count during the first few weeks of therapy and yearly thereafter. Agranulocytosis and aplastic anemia are extremely rare adverse effects, but suppression of the WBC count in the range of 200-3000 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.

Oxycarbazine 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.

Gabapentin, lamotrigine topiramate, and several other newer anticonvulsants are being used to treat trigeminal neuralgia. Further outcome studies on their use in the treatment of trigeminal neuralgia are needed.

Surgical therapy

In some studies, more than 50% of patients with TN eventually had some kind of surgical procedure. Experience would indicate that medical management eventually fails in most patients with TN, and those patients undergo surgery.

Microvascular decompression (MVD) is the classic and most effective surgical procedure. It involves a posterior fossa craniotomy and dissection of vascular elements that compress the trigeminal nerve in the subarachnoid space. Teflon felt is used to pad the nerve away from the offending artery or vein.

The effectiveness of MVD is based on the hypothesis that compression from vessels in the vicinity of the trigeminal nerve leads to abnormal nerve activity.

Percutaneous approaches

• Radiofrequency (RF) rhizotomy (thermocoagulation): This is an outpatient procedure performed by placing a needle into the gasserian ganglion, through which an electrical current passes, heating the probe and producing a thermal lesion in the ganglion. The reported rate of pain recurrence is the lowest compared with other percutaneous procedures, with the average patient experiencing 3 years of excellent pain relief.⁷ Complications of RF rhizotomy depend on the amount of numbness created by the lesion. Dysesthesia has been reported in up to 5-25% of patients, corneal numbness in up to 15%, and masseter weakness in about 4%. These complications are markedly reduced if the numbness produced by the procedure is limited. Some of these complications may be reversible. To avoid ophthalmic complications, some experts do not recommend this approach when the ophthalmic division is involved.⁸
• Glycerol rhizotomy: The rate of pain recurrence with percutaneous rhizotomy is between that of radiofrequency ablation and percutaneous compression. The rate of significant facial numbness (5%) is low. About half of the patients have pain recurrence at 2 years.⁹
• Percutaneous balloon microcompression: Recent studies indicate that this procedure carries about the same complications and average pain-free outcome as glycerol rhizotomy (2 y).^{10, 11}
• Gamma knife radiosurgery (GKRS): This is the least invasive procedure. Administered as a single dose of 70-90 Gy delivered to the trigeminal root, this procedure is an option when medical and surgical techniques fail. Contemporary studies indicate that the average pain-free outcome of GKRS is about the same as for RF rhizotomy, or around 3 years.^{12, 13}
• Other procedures
• • Peripheral neurectomy, although safe and effective, is rarely used but may be of value in patients who have TN and a limited life span.¹⁴
  • Trigeminal tractotomy (cutting of the descending trigeminal tract in the medulla), retrogasserian glycerol instillation in trigeminal cistern, peripheral alcohol blocks, and partial trigeminal rhizotomy via a posterior fossa craniotomy are other rarely used options.

COMPLICATIONS

Section 7 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Morbidity associated with trigeminal nerve decompression stems from hemorrhage, infection, and possible damage to the brainstem around the area of decompression.

In centers where MVD is frequently performed, complications include facial dysesthesia (0.3%), facial numbness (0.15%), cerebellar injuries and hearing loss (<1%), and CSF leakage (<2%).

With thermocoagulation, dysesthesia can occur in 5-25% of patients, although this complication is uncommon when the degree of facial numbness is controlled. Corneal numbness can occur in up to 15% of patients, and masseter weakness can occur in about 4%. Many of these complications are reversible over time.

OUTCOME AND PROGNOSIS

Section 8 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Accurate data on surgical outcome are still difficult to obtain. Most surgical series do no meet modern criteria for evidence-based medicine. Recently, an evidence-based approach has been applied to both the diagnosis of trigeminal neuralgia, and its surgical management. These results will be published in the journal Neurology in 2008. 

The challenges of the field are exemplified by a paper published by Zakrzewska and Lopez.¹⁵ They assessed the quality of 222 reports of surgical management of trigeminal neuralgia and found only 3 randomized controlled trials (RCTs) on peripheral techniques. The vast majority of the evidence was of case series reports (class 3 evidence), and a very high proportion was of poor quality.

The difficulties center around the following important issues:

• Lack of clear diagnostic criteria and baseline assessments
• Poor methodology - Low numbers, short follow-up period, high percentage lost to follow-up, mixture of cases (eg, previous surgery, including repeated treatments)
• Lack of Kaplan-Meier assessment of pain relief, poorly defined outcome measures (eg, partial success), incomplete reporting of all complications, and no quality-of-life evaluations
• Lack of independent evaluation

Certain principles seem to transcend even the relatively poor outcomes studies performed thus far on procedures for trigeminal neuralgia. The chance of success is seemingly less likely the longer the duration of symptoms. Of all the procedures, MVD carries the lowest rate of facial dysesthesia at 0.3%. Facial numbness caused by MVD is not common (0.15%) compared with that caused by the percutaneous procedures; in addition, MVD is the procedure of choice in younger patients who desire no sensory deficit. MVD is also the most likely treatment to provide sustained postoperative pain relief.

One study found that 70% of patients had excellent results (defined as a cure or significant pain relief) 10 years after the procedure, with a recurrence rate of less than 1%.¹⁶ Possible reasons for failure include new vascular compression from scarred implants or other sources, but these are rarely identified during posterior fossa re-exploration for failed MVD. After an initial 10% risk of recurrence of TN within one year after MVD, the risk of pain recurrence is about 3.5% every succeeding year.¹⁷ The reasons for this recurrence are not clear.

In a 1999 study, cerebellar injuries and hearing loss occurred in less than 1% of the patients, and CSF leakage occurred in 1.85%.¹⁸ As expected, these complication rates were inversely proportional to the total number of procedures performed.

FUTURE AND CONTROVERSIES

Section 9 of 10  

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

Once developed, trigeminal neuralgia (TN) is likely to have an exacerbating and remitting course. Over time, the pain-free intervals appear to diminish, and the pain becomes progressively more medically intractable. Temporary spontaneous remission may occur at any time, but permanent remission never occurs.

Without treatment, typical TN (TN1) may transform over time to become atypical TN (TN2), with a change in the character of the pain to more constant and background pain and the development of sensory impairment. Therefore, some authorities recommend early intervention to give the opportunity of pain relief without sensory deficits.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Indications
• Relevant Anatomy
• Workup
• Treatment
• Complications
• Outcome and Prognosis
• Future and Controversies
• References

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3. Anderson VC, Berryhill PC, Sandquist MA, Ciaverella DP, Nesbit GM, Burchiel KJ. High-resolution three-dimensional magnetic resonance angiography and three-dimensional spoiled gradient-recalled imaging in the evaluation of neurovascular compression in patients with trigeminal neuralgia: a double-blind pilot study. Neurosurgery. Apr 2006;58(4):666-73; discussion 666-73. [Medline].
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8. Taha JM, Tew JM Jr. Comparison of surgical treatments for trigeminal neuralgia: reevaluation of radiofrequency rhizotomy. Neurosurgery. May 1996;38(5):865-71. [Medline].
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10. Abdennebi B, Mahfouf L, Nedjahi T. Long-term results of percutaneous compression of the gasserian ganglion in trigeminal neuralgia (series of 200 patients). Stereotact Funct Neurosurg. 1997;68(1-4 Pt 1):190-5. [Medline].
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12. Sheehan J, Pan HC, Stroila M, Steiner L. Gamma knife surgery for trigeminal neuralgia: outcomes and prognostic factors. J Neurosurg. Mar 2005;102(3):434-41. [Medline].
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16. Barker FG 2nd, Jannetta PJ, Bissonette DJ, Larkins MV, Jho HD. The long-term outcome of microvascular decompression for trigeminal neuralgia. N Engl J Med. Apr 25 1996;334(17):1077-83. [Medline].
17. Burchiel KJ, Clarke H, Haglund M, Loeser JD. Long-term efficacy of microvascular decompression in trigeminal neuralgia. J Neurosurg. Jul 1988;69(1):35-8. [Medline].
18. McLaughlin MR, Jannetta PJ, Clyde BL, Subach BR, Comey CH, Resnick DK. Microvascular decompression of cranial nerves: lessons learned after 4400 operations. J Neurosurg. Jan 1999;90(1):1-8. [Medline].
19. Anderson VC, Berryhill PC, Sandquist MA, Ciaverella DP, Nesbit GM, Burchiel KJ. High-resolution three-dimensional magnetic resonance angiography and three-dimensional spoiled gradient-recalled imaging in the evaluation of neurovascular compression in patients with trigeminal neuralgia: a double-blind pilot study. Neurosurgery. Apr 2006;58(4):666-73; discussion 666-73. [Medline].
20. Broggi G, Ferroli P, Franzini A, Servello D, Dones I. Microvascular decompression for trigeminal neuralgia: comments on a series of 250 cases, including 10 patients with multiple sclerosis. J Neurol Neurosurg Psychiatry. Jan 2000;68(1):59-64. [Medline].
21. Burchiel KJ, Slavin KV. On the natural history of trigeminal neuralgia. Neurosurgery. Jan 2000;46(1):152-4; discussion 154-5. [Medline].
22. Carrazana EJ, Schachter SC. Alternative uses of lamotrigine and gabapentin in the treatment of trigeminal neuralgia [letter; comment]. Neurology. Apr 1998;50(4):1192. [Medline].
23. Gass A, Kitchen N, MacManus DG, Moseley IF, Hennerici MG, Miller DH. Trigeminal neuralgia in patients with multiple sclerosis: lesion localization with magnetic resonance imaging. Neurology. Oct 1997;49(4):1142-4. [Medline].
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Article Last Updated: Jun 5, 2008