What Is Trigeminal Neuralgia? Comprehensive treatment analysis

Trigeminal neuralgia (TN) (also known as tic douloureux) is a disorder of the fifth cranial (trigeminal) nerve that causes episodes of intense, stabbing, electric shock-like pain in the areas of the face where the branches of the nerve are distributed  (eg, lips, eyes, nose, scalp, forehead, upper jaw, lower jaw). TN is often accompanied by a brief facial spasm or tic. It is a relatively rare neurological disorder that produces intense pain in one side (or in a few cases both sides at different times) of the face. The condition has been known to drive patients to the brink of suicide, and the disorder has sometimes been called "the suicide disease."[1[,[2]  It is widely considered the most debilitating form of pain known in medical practice.[3]   

The trigeminal nerve

The trigeminal nerve is the nerve responsible for sensation in the face and motor functions such as biting and chewing. It supplies three major branches to the face, the ophthalmic nerve (V1), the maxillary nerve (V2) and the mandibular nerve (V3).[5] 

• The ophthalmic nerve (V1) carries sensory information from the scalp and forehead, the upper eyelid, the conjunctiva and cornea of the eye, the nose, the nasal mucosa, the frontal sinuses and parts of the meninges (lining of the spinal cord).
• The maxillary nerve (V2) carries sensory information from the lower eyelid and cheek, the nose and upper lip, the upper teeth and gums, the nasal mucosa, the palate and roof of the pharynx, the maxillary, ethmoid and sphenoid sinuses and parts of the meninges.
• The mandibular nerve (V3) carries sensory information from the lower lip, the lower teeth and gums, the chin and jaw (except the angle of the jaw, which is supplied by C2-C3), parts of the external ear and parts of the meninges. The mandibular nerve is the only division of the trigeminal nerve that also carries a motor component. The mandibular nerve controls the movements of eight muscles all of which are involved in the process of mastication including the temporalis, the masseter, the medial and lateral pterygoids, the digastric muscle, the tensor tympani, the tensor veli palatini, and the pair of mylohyoid muscles.[6]

Some practitioners recognise two forms of Trigeminal neuralgia: "Type I" or "Classic" TN and "Type II" or "Atypical" TN.

Classic TN is said to present as volleys of intense, brief, sharp, electric-shock  jabbing pain, each jab lasting up to 90 seconds and volleys tapering off after one to two hours. 

Atypical TN pain is described as less-intense, constant 24-7 burning, boring, aching pain.8  Both forms of pain may occur in the same person, sometimes at the same time. The intensity of pain can be physically and mentally incapacitating. The number of attacks may vary from less than 1 per day to 12 or more per hour and up to hundreds per day.

What Causes Trigeminal Neuralgia?

Although the exact pathophysiology remains controversial, many investigators agree that vascular compression, typically venous or arterial loops at the trigeminal nerve entry into the brainstem, is critical to the pathogenesis of the idiopathic variety. This compression results in focal trigeminal nerve demyelination (loss of the myelin sheath that normally surrounds certain nerves). Rarely, symptoms of TN may be caused by nerve compression from a tumour, or a tangle of arteries and veins called an arteriovenous malformation. Injury to the trigeminal nerve (perhaps the result of sinus surgery, oral surgery, stroke, or facial trauma) may also produce neuropathic facial pain.

TN occurs most often in people over age 50, but it can occur at any age, and is more common in women than in men. There is some evidence that the disorder runs in families, perhaps because of an inherited pattern of blood vessel formation.[9]

What Triggers the Onset of an Attack?

Triggers of pain attacks include the following:

• Chewing, talking, or smiling
• Drinking cold or hot fluids
• Touching, shaving, brushing teeth, blowing the nose
• Encountering cold air from an open automobile window

A valuable clue to the diagnosis is the triggering of the pain with certain activities. Patients carefully avoid rubbing the face or shaving a trigger area, in contrast to other facial pain syndromes, in which they massage the face or apply heat or ice. Also, many patients try to hold their face still while talking to avoid precipitating an attack. According to one researcher, trigger zones, or areas of increased sensitivity, are present in one half of patients and often lie near the nose or mouth.[10] 

In contrast to migrainous pain, persons with this condition rarely suffer attacks during sleep, which is another key point in the history. People with TN avoid social contact and daily activities such as eating and talking because they fear an attack. Many have been known to lose their jobs because of the debilitating nature of the pain. Marriages have dissolved due to the difficulty of providing care and support to persons with TN.

Pain from TN is frequently very isolating and depressing for the individual. Depression and sleep disturbance may render individuals more vulnerable to pain and suffering. Thus, there are individual, family, and societal costs of TN.[11]

Primary Features of an Attack

Patients can localise their pain precisely. The pain is not confined exclusively to one of the three divisions of the trigeminal nerve but more commonly runs along the line dividing either the mandibular and maxillary nerve dermatomal distribution or along the line dividing the mandibular and ophthalmic dermatomal distribution. The pain quality is characteristically severe, paroxysmal, and lancinating. It begins with a sensation of electrical shocks in an affected area, then quickly crescendos in less than 20 seconds to an excruciating discomfort felt deep in the face, often contorting the patient's expression. The pain then begins to fade within seconds, only to give way to a burning ache lasting seconds to minutes. During attacks, patients may grimace, wince, or make an aversive head movement, thus producing an obvious movement, or tic; hence the term "tic douloureux."[12]

Diagnosing Trigeminal Neuralgia

No laboratory, electrophysiologic, or radiologic testing is routinely indicated for the diagnosis of TN, as patients present with a characteristic history and normal neurologic examination. Nevertheless, other disorders that cause facial pain should be ruled out before TN is diagnosed. Some disorders that cause facial pain include post-herpetic neuralgia (nerve pain following an outbreak of shingles), cluster headaches, and temporomandibular joint dysfunction which causes pain and dysfunction in the jaw joint and muscles that control jaw movement.

A diagnosis of Type I or "Classic" TN may be supported by an individual’s positive response to a short course of carbamazepine. Diagnosis of Type II or 'atypical' TN is more complex and difficult, but tends to be supported by a positive response to low doses of tricyclic antidepressant medications. Strict criteria for the diagnosis of TN have been defined by the International Headache Society as follows:[13]

• A - Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting 1 or more divisions of the trigeminal nerve and fulfilling criteria B and C
• B - Pain has at least 1 of the following characteristics: (1) intense, sharp, superficial or stabbing; or (2) precipitated from trigger areas or by trigger factors
• C - Attacks stereotyped in the individual patient
• D - No clinically evident neurologic deficit
• E - Not attributed to another disorder

Treatment for Trigeminal Neuralgia 

Antiepileptic medicines—used to block nerve firing—are generally effective in treating Type I TN but often less effective in Type II TN. These antiepileptic drugs include carbamazepine, oxcarbazepine, lamotrigene, topiramate, gabapentin, pregabalin, and phenytoin. Baclofen and tizanidine, classified as muscle relaxants, are also of benefit in the treatment of TN. Other interventions include neurosurgery and complementary approaches.

Medications

The earliest study on the use of anticonvulsants in TN dates back to 1942 when a complete cure of essential facial neuralgia was reported in three patients treated with the use of phenytoin.[14] Carbamazepine (CBZ) was initially reported as effective in relieving TN in 1962.[15]  Since then, multiple studies have confirmed its efficacy.[16-18]  So predictable and powerful is the relief that if the patient does not respond at least partially to carbamazepine, the diagnosis of TN should be reexamined.

Carbamazepine and oxcarbazepine: Carbamazepine (Tegretol) and oxcarbazepine (Trileptal) are now considered first-line therapy in TN. Although the evidence for the efficacy of CBZ is stronger,[19-22] oxcarbazepine (OXC) has a better safety profile[.23] The mechanism of analgesia is unknown. The effective dose in newly diagnosed TN may be less than that required to treat epilepsy. Pain in some patients may resolve on as little as 100mg two to three times a day. For the remaining patients the daily dose should be increased by 100mg every other day until adequate pain relief is established or until intolerable side effects prevent further upward titration. Typical maintenance doses range from 300 to 800mg/day divided into two to three daily doses. Efficacy is approximately 80% initially. Over time, higher doses may be needed to maintain efficacy, which declines to approximately 50% of patients due to autoinduction of CBZ.[21]   Autoinduction is defined as the ability of a drug to induce enzymes that enhance its own metabolism, resulting in tolerance and reduction in efficacy. Many adverse central nervous system effects (eg, dizziness, sedation, gait disturbance, double vision) 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.

Lamotrigine: Lamotrigine (Lamictal) is considered second-line therapy for TN. Lamotrigine was shown to be superior to placebo in a randomised, controlled trial investigating 14 patients with TN refractory to CBZ.[24]  The initial dose of 25mg/day is slowly increased to a target dose of 200–400mg/day divided between two doses. Potential side effects include dizziness, nausea, blurred vision and ataxia. Approximately 7–10% of patients will report a skin rash during the first 4–8 weeks of therapy[25] that most often resolves with continued therapy. With severe rash, desquamation or associated symptoms of fever or lymphadenopathy indicative of Stevens–Johnson syndrome requires prompt discontinuation. The slower the titration, the less likely it is that these side effects will occur.

Baclofen: Along with lamotrigine, baclofen (Lioresal) (40-80mg/day) is considered second-line treatment of TN. Baclofen has been shown in double-blind studies to be effective in 70% of patients at doses of 10–60mg per day.[26] Follow-up of 60 patients over 1–5 years showed that efficacy was maintained in only 30% of patients.26  Potential side effects include lassitude, drowsiness, dizziness and gastrointestinal discomfort. To date, baclofen has the strongest scientific evidence for efficacy in the treatment of TN next to CBZ.

Gabapentin: Gabapentin (Neurontin) has shown adequate efficacy alone and in combination with local injections of ropivacaine used to block trigger points in TN patients. In a small study of 36 patients,[27] this combination appeared to be safe and effective in the treatment of TN.27 Gabapentin has demonstrated effectiveness in TN, especially in patients with multiple sclerosis (MS).[28, 29]  Gabapentin is initiated recommended at 300mg daily and may be gradually increased by 300mg each 2–3 days as tolerated. Gabapentin has no interaction with other drugs and relatively minor side effects that may include dizziness, somnolence, headache, diarrhoea, confusion, nausea, and ankle swelling.

Pregabalin: Pregabalin (Lyrica) was tested in an open-label study including 53 patients with 1-year follow-up. Pregabalin (150–600mg/day) proved to be effective in reducing TN pain by over 50% in 74% of patients with minor efficacy reduction over the 1-year observational period.[30]

Topiramate: Topiramate (Topamax) (100–400mg/day) was effective in 75% of patients in a very small sample of only eight patients.[31]

Levetiracetam: A pilot study investigated the efficacy and tolerability of levetiracetam (Keppra) in 10 patients with TN over a period of 10 weeks in an open-label prospective design. Patients were treated with up to 4000mg daily and 40% reported an improvement of 50–90%.[32]

Tizanidine: Tizanidine (Zanaflex) has proven efficacy in a double-blind crossover study in 8 out of 10 patients with TN. However, all patients that were followed-up after 1–3 months experienced recurrence of pain.[33]

Botulinum neurotoxin type A (Bo-Tox): Reports of isolated TN patients treated with botulinum neurotoxin type A (BoNT-A) and a small, uncontrolled clinical trial (n=13) showed significant relief from symptoms after treatment with BoNT-A. Mean BoNT-A dose was 3.22 units/cm2 administered directly into the affected facial regions subcutaneously. At 60 days follow-up, the pain began to slowly return in most patients.[34]

Phenytoin: Phenytoin (Dilantin), although not approved by the US Food and Drug Administration (FDA) for idiopathic TN and believed to be less effective than carbamazepine, is probably effective for some patients with this disorder. According to one small study,  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.[35]

Tricyclic antidepressants (TCAs): Tricyclic antidepressants such as amitriptyline or nortriptyline can be used to treat neuropathic pain.  However, only a minority of patients may respond. Anticholinergic side effects may limit tolerance of these medications.

Opioids. Common analgesics and opioids (narcotic analgesics) are not usually helpful in treating the sharp, recurring pain caused by Type I TN, although some individuals with Type II TN do respond to opioids.

Neurosurgery

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. It is estimated that 25-50% of patients eventually stop responding to drug therapy and require some form of alternative treatment.[36]  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 one 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.[12] Among patients who develop trigeminal neuralgia when younger than 60 years, surgery is the definitive treatment.

Three operative strategies are applied to TN: percutaneous procedures, gamma knife surgery, and microvascular decompression.[12] Ninety percent of patients are pain-free immediately or soon after any of the operations,[37] although the relief is much more long-lasting with microvascular decompression.

Percutaneous surgeries are preferable for older patients with medically unresponsive TN. Younger patients and those expected to do well under general anaesthesia should first consider microvascular decompression—presently, this is the most cost-effective surgery although it is also more invasive.

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

Balloon compression: A tube called a cannula is inserted through the cheek and guided to where one branch of the trigeminal nerve passes through the base of the skull. A soft catheter with a balloon tip is threaded through the cannula and the balloon is inflated to squeeze part of the nerve against the hard edge of the brain covering and the skull.  Pain-free intervals after percutaneous balloon compression last 1.5 to 2 years.[40]

Glycerol injection: A thin needle is passed through the cheek, next to the mouth, and guided through the opening in the base of the skull where the third division of the trigeminal nerve (mandibular) exits. The needle is moved into the pocket of spinal fluid that surrounds the trigeminal nerve center (called the ganglion). The glycerol injection bathes the ganglion and damages the insulation of trigeminal nerve fibers. This form of rhizotomy is likely to result in recurrence of pain within a year to two years.[40] However, the procedure can be repeated multiple times.

Radiofrequency thermal lesioning: This procedure is also known as "RF Ablation" or "RF Lesion."  A hollow needle is passed through the cheek through the same opening at the base of the skull where the balloon compression and glycerol injections are performed. The individual is briefly awakened and a small electrical current is passed through the needle, causing tingling in the area of the nerve where the needle tips rests. When the needle is positioned so that the tingling occurs in the area of TN pain, the person is then sedated and the nerve area is gradually heated with an electrode, injuring the nerve fibers. Approximately half of the people have symptoms that reoccur three to four years following RF lesioning.[40]

Gamma knife surgery: Gamma knife surgery 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 uses computer imaging to direct highly focused beams of radiation at the site where the trigeminal nerve exits the brain stem. This causes the slow formation of a lesion on the nerve that disrupts the transmission of sensory signals to the brain. People usually leave the hospital the same day or the next day following treatment but will not typically experience relief from pain for several weeks (or sometimes several months) following the procedure. 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. For individuals who were treated successfully, almost half have recurrence of pain within three years.

Microvascular decompression: This procedure is commonly performed in younger, healthier patients, especially those with pain isolated to the ophthalmic division or in all three divisions of the trigeminal nerve and in those with secondary trigeminal neuralgia (TN). It is now the most common surgery performed for TN and general anaesthesia is required. Microvascular decompression is the most invasive of all surgeries for TN, but also offers the lowest probability that pain will return. Initial efficacy is greater than 80%. About half of individuals undergoing microvascular decompression for TN will experience recurrent pain within 12 to 15 years.[38], [39]  This inpatient procedure, which is performed under general anesthesia, requires that a small opening be made through the mastoid bone behind the ear. While viewing the trigeminal nerve through a microscope or endoscope, the surgeon moves away the vessel (usually an artery) that is compressing the nerve and places a soft cushion between the nerve and the vessel. 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.[40]

Surgery for Type II TN. Surgical treatment for Type II TN is usually more problematic than for Type I TN, particularly where vascular compression is not detected in brain imaging prior to a proposed procedure. Many neurosurgeons advise against the use of microvascular decompression or rhizotomy in individuals for whom Type II TN symptoms predominate over Type I TN.

Alternative Complementary Approaches to TN?

Some individuals manage TN using complementary techniques, usually in addition to drug treatment. These therapies include low-impact exercise, yoga, creative visualisation, aroma therapy, or meditation. Other options include acupuncture, upper cervical chiropractic, biofeedback, vitamin therapy, and nutritional therapy. Supportive counseling and/or psychiatric care may be of benefit for depressive symptoms.

References

1. Lawhern RA. Demographics of Neurological Face Pain at a Social Networking Website. http://www.livingwithtn.org/page/who-gets-tn Updated 16 Mar 2012. Accessed 6 Mar 2015. 
2. Trigeminal neuralgia. Wikipedia. http://en.wikipedia.org/wiki/Trigeminal_neuralgia Updated 2012. Accessed 6 Feb 2015.
3. Dela Cruz Y. Salamat doc -- the Suicide Disease. ABS-CBN News. http://www.abs-cbnnews.com/current-affairs-programs/10/30/11/salamat-dok-trigeminal-neuralgia-suicide-disease   Published 30 Oct 2011. Accessed 8 Mar 2015.
4. Trigeminal neuralgia. Medicine.org http://medicine.org/trigeminal-neuralgia-the-suicide-disease-may-be-the-most-painful-condition-known-to-medical-science/ Published 2012. Accessed 8 Mar 2015.
5. The trigeminal nerve. Fotosearch. http://www.fotosearch.com/CSP898/k8983264/#   Accessed 6 Mar 2015.
6. Tewfik TL. Trigeminal nerve anatomy. Medscape. http://emedicine.medscape.com/article/1873373-overview#aw2aab6b3  Updated 19 June 2013. Accessed 6 Feb 2015.
7. Trigeminal neuralgia. Wikipedia. http://en.wikipedia.org/wiki/Trigeminal_nerve Updated 13 Feb 2015. Accessed 6 Feb 2015.
8. Eller JL, Raslan AM, Burchiel KJ.  Trigeminal Neuralgia -- Definition and Classification", Neurosurgical Focus. 2005;18(5).
9. Trigeminal neuralgia. American Academy of Neurology. http://patients.aan.com/disorders/index.cfm?event=view&disorder_id=1094  Published 2015. Accessed 6 Mar 2015.
10. Sands GH. Pain in the face. Headaches in Adults, Annual Course, American Academy of Neurology Annual Meeting. 1994;3:146:130-2.
11. What is trigeminal neuralgia? The Facial Pain Association. http://fpa-support.org/trigeminal-neuralgia/  (n.d.) Accessed 6 Mar 2015.
12. Singh MK.  Trigeminal Neuralgia. Medscape.  http://emedicine.medscape.com/article/1145144-overview  Updated 1 May 2014. Accessed 6 Mar 2015.
13. The International Classification of Headache Disorders: 2nd edition. Cephalalgia. 2004;24 Suppl 1:9-160.
14. Bergouignan, M., Successful cures of essential facial neuralgias by sodium diphenylhydantoinate, Rev. Laryng. (Bordeaux), 63: 34-41, 1942.
15. Blom S. Trigeminal neuralgia: its treatment with a new anticonvulsant drug (G-32883). Lancet. Apr 21 1962;1:839-40.
16. Talor JC. Trigeminal neuralgia treated with G32883. Journal of Neurology. Neurosurgery and Psychiatry. 1963; 26, 443.
17. Spillane JD. The treatment of trigeminal neuralgia. Practitioner. 1964; 192, 71.
18. Graham JG. & Zilkha KJ. Treatment of trigeminal neuralgia with carbamazepine; a follow-up study. BMJ. 1966; 1, 210.
19. Nicol CF. A four year double-blind study of tegretol in facial pain. Headache. 1969; 9: 54–57.
20. Killian JM., Fromm GH. Carbamazepine in the treatment of neuralgia. Use of side effects. Arch Neurol. 1968; 19: 129–136.
21. Campbell FG, Graham JG, Zilkha KJ. Clinical trial of carbazepine (tegretol) in trigeminal neuralgia. J Neurol Neurosurg Psychiatry. Jun 1966;29(3):265-7.
22. Rockliff BW, Davis EH. Controlled sequential trials of carbamazepine in trigeminal neuralgia. Arch Neurol. Aug 1966;15(2):129-36.
23. Beydoun A. Safety and efficacy of oxcarbazepine: results of randomized, double-blind trials. Pharmacotherapy 2000; (8 Pt 2): 152S–158S.
24. Zakrzewska JM, Chaudhry Z, Nurmikko TJ, Patton DW, Mullens EL. Lamotrigine (Lamictal) in refractory trigeminal neuralgia: results from a double-blind placebo controlled crossover trial. Pain. 1997; 73: 223–230.
25. Wiffen PJ, Rees J. Lamotrigine for acute and chronic pain. Cochrane Database Syst Rev 2. 2007; CD006044–CD006044.
26. Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of trigeminal neuralgia: double-blind study and long-term follow-up. Ann Neurol 1984;15: 240–244.
27. Lemos L., Flores S., Oliveira P., Almeida A. Gabapentin supplemented with ropivacain block of trigger points improves pain control and quality of life in trigeminal neuralgia patients when compared with gabapentin alone. Clin J Pain 2008; 24: 64–75.
28. Khan OA. Gabapentin relieves trigeminal neuralgia in multiple sclerosis patients. Neurology. Aug 1998;51(2):611-4.
29. Solaro C, Lunardi GL, Capello E, et al. An open-label trial of gabapentin treatment of paroxysmal symptoms in multiple sclerosis patients. Neurology. Aug 1998;51(2):609-11.
30. Obermann M, Yoon MS, Sensen K, Maschke M, Diener HC, Katsarava Z. Efficacy of pregabalin in the treatment of trigeminal neuralgia. Cephalalgia. 2008; 28: 174–181.
31. Domingues RB, Kuster GW, Aquino CC. Treatment of trigeminal neuralgia with low doses of topiramate. Arq Neuropsiquiatr 2007;65: 792–794.
32. Jorns T.P., Johnston A., Zakrzewska J.M. (2009) Pilot study to evaluate the efficacy and tolerability of levetiracetam (Keppra) in treatment of patients with trigeminal neuralgia. Eur J Neurol 16: 740–744.
33. Fromm GH, Aumentado D, Terrence CF. A clinical and experimental investigation of the effects of tizanidine in trigeminal neuralgia. Pain 1993; 53: 265–271.
34. Piovesan EJ., Teive HG., Kowacs PA, et al. An open study of botulinum-A toxin treatment of trigeminal neuralgia. Neurology 2005; 65: 1306–1308.
35. Braham J. Pain in the face. Br Med J. Aug 3 1968;3(5613):316.
36. Dalessio DJ. Trigeminal neuralgia. A practical approach to treatment. Drugs. Sep 1982;24(3):248-55.
37. Burcheil KJ. Trigeminal neuralgia. In: Conn's Current Therapy. 1999:948-50.
38. Pollock BE, Ecker RD. A prospective cost-effectiveness study of trigeminal neuralgia surgery. Clin J Pain. Jul-Aug 2005;21(4):317-22.
39. Olson S, Atkinson L, Weidmann M. Microvascular decompression for trigeminal neuralgia: recurrences and complications. J Clin Neurosci. Sep 2005;12(7):787-9.
40. Sweet WH. Percutaneous methods for the treatment of trigeminal neuralgia and other faciocephalic pain; comparison with microvascular decompression. Semin Neurol. Dec 1988;8(4):272-9.