Trigeminal Neuralgia
RUDOLPH M. KRAFFT, MD, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio
Trigeminal neuralgia is an uncommon disorder characterized by recurrent attacks of lancinat-
ing pain in the trigeminal nerve distribution. Typically, brief attacks are triggered by talking,
chewing, teeth brushing, shaving, a light touch, or even a cool breeze. The pain is nearly always
unilateral, and it may occur repeatedly throughout the day. The diagnosis is typically deter-
mined clinically, although imaging studies or referral for specialized testing may be necessary
to rule out other diseases. Accurate and prompt diagnosis is important because the pain of tri-
geminal neuralgia can be severe. Carbamazepine is the drug of choice for the initial treatment
of trigeminal neuralgia; however, baclofen, gabapentin, and other drugs may provide relief
in refractory cases. Neurosurgical treatments may help patients in whom medical therapy is
unsuccessful or poorly tolerated. (Am Fam Physician.
2008;77(9):1291-1296. Copyright 2008
American Academy of Family Physicians.)

Trigeminal neuralgia was first 1and2percent,makingitthemostcommon associated disease.2 Patients with hyperten- sion have a slightly higher incidence of tri- of the distinctive facial spasms that often population.2 There is no racial predilection.2 Trigeminal neuralgia is generally sporadic, Headache Society has published criteria for although there have been reports of the dis- the diagnosis of classical and symptomatic trigeminal neuralgia (Table 1).1 In classi- same family. Spontaneous remission is pos- cal trigeminal neuralgia, no cause of the sible, but most patients have episodic attacks symptoms can be identified other than vas- cular compression. Symptomatic trigeminalneuralgia has the same clinical criteria, but Pathophysiology
another underlying cause is responsible for It has been proposed that the symptoms of elination of the nerve leading to ephaptic geminal nerve (Figure 1), with the maxillary transmission of impulses. Surgical speci- branch involved the most often and the oph- mens have demonstrated this demyelination thalmic branch the least.2,3 The right side of and close apposition of demyelinated axons the face is affected more commonly than the in the trigeminal root of patients with tri- left (ratio of 1.5:1), which may be because of axons are prone to ectopic impulses, which The annual incidence of trigeminal neural- may transfer from light touch to pain fibers gia has been reported as 4.3 per 100,000 pop- in close proximity (ephaptic conduction).5 ulation, with a slight female predominance (age-adjusted ratio of 1.74:1).2 Primary care physicians might expect to encounter this compression of the nerve root by aberrant condition two to four times over the course or tortuous vessels. Pathologic and radio- of a 35-year career. The peak incidence is at logic studies have demonstrated proximity 60 to 70 years of age, and classical trigeminal of the nerve root to such vessels, usually neuralgia is unusual before age 40 years.2,3 the superior cerebellar artery.5 Relief of symptoms by surgical techniques that sepa- patients with multiple sclerosis is between rate the offending vessels from the nerve Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright 2008 American Academy of Family Physicians. For the private, noncommercial use of one individual user of the Web site. All other rights reserved. Contact copyrights@aafp.org for copyright questions and/or permission requests.
Trigeminal Neuralgia
Physicians should obtain magnetic resonance imaging in all patients with suspected trigeminal neuralgia. Carbamazepine (Tegretol) should be the initial treatment for patients with classical trigeminal neuralgia because it has been found to be successful in most cases and no other medication has been shown to be superior in large studies.
Surgical options should be considered for patients who have persistent pain after trials with several medications or who have a relapse after initial success with medical treatment.
A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 1205 or http://www.aafp.org/afpsort.xml. further strengthens this hypothesis. Demyelination has nerve and the generation of ectopic impulses that are also been demonstrated in cases of trigeminal neuralgia spread ephaptically to precipitate the typical attack.
associated with multiple sclerosis or tumors affectingthe nerve root.
Multiple other causes of trigeminal neuralgia have The diagnosis of trigeminal neuralgia should be consid- been described, including amyloid infiltration, arterio- ered in all patients with unilateral facial pain. Accurate venous malformations, bony compression, and small and prompt diagnosis is important because the pain of infarcts in the pons and medulla. In most of these situ- trigeminal neuralgia can be severe. Other diagnoses must ations, demyelination may also be an underlying cause.
also be considered, particularly in patients with atypical Most investigators now accept the theory that classical features of the disease or “red flags” in the history or phys- trigeminal neuralgia results from vascular compression ical examination (Table 2). In addition, it is important to of the nerve root. This leads to demyelination of the distinguish classical from symptomatic trigeminal neu-ralgia for the purpose of treatment. Symptomatic trigemi-nal neuralgia is always secondary to another disorder, and Table 1. IHS Diagnostic Criteria
treatment should focus on the underlying condition.
for Trigeminal Neuralgia
Because trigeminal neuralgia is a clinical diagnosis, the A. Paroxysmal attacks of pain lasting from a fraction of a second patient’s history is critical in the evaluation. Patients with to two minutes, affecting one or more divisions of the trigeminal neuralgia present with a primary description trigeminal nerve, and fulfilling criteria B and C B. Pain has at least one of the following characteristics: of recurrent episodes of unilateral facial pain. Attacks 1. Intense, sharp, superficial, or stabbing last only seconds and may recur infrequently or as often 2. Precipitated from trigger zones or by trigger factors as hundreds of times each day; they rarely occur during C. Attacks are stereotyped in the individual patient sleep. The pain is generally severe, and is described as a D. There is no clinically evident neurologic deficit stabbing, sharp, shock-like, or superficial pain in the dis- tribution of one or more of the trigeminal nerve divisions.
Patients generally are asymptomatic between episodes, A. Paroxysmal attacks of pain lasting from a fraction of a second although some patients with long-standing trigeminal to two minutes, with or without persistence of aching between neuralgia have a persistent dull ache in the same area.
paroxysms, affecting one or more divisions of the trigeminal Talking, smiling, chewing, teeth brushing, and shaving have all been implicated as triggers for the pain. Even a B. Pain has at least one of the following characteristics: breeze touching the face may cause a paroxysm of pain 1. Intense, sharp, superficial, or stabbing in some patients. In trigger zones—small areas near the 2. Precipitated from trigger zones or by trigger factors nose or mouth in patients with trigeminal neuralgia— C. Attacks are stereotyped in the individual patient minimal stimulation initiates a painful attack. Patients D. A causative lesion, other than vascular compression, has been with trigeminal neuralgia can pinpoint these areas and demonstrated by special investigations and/or posterior fossa exploration will assiduously avoid any stimulation of them. Not allpatients with trigeminal neuralgia have trigger zones, but IHS = International Headache Society. trigger zones are nearly pathognomonic for this disorder.
The patient’s history is also important for ruling out other causes of facial pain. Because of the association 1292 American Family Physician
Volume 77, Number 9 V May 1, 2008 Trigeminal Neuralgia
attacks; a change in the location, severity, orquality of the pain should alert the physician to the possibility of an alternative diagnosis.
The physical examination in patients withtrigeminal neuralgia is generally normal.
Therefore, physical examination in patients with facial pain is most useful for identifying abnormalities that point to other diagno-ses. The physician should perform a careful examination of the head and neck, with an emphasis on the neurologic examination.
dibular joint (TMJ) should be examined for problems that might cause facial pain.
The finding of typical trigger zones verifies Figure 1. Trigeminal nerve.
the diagnosis of trigeminal neuralgia. Patientswith classical trigeminal neuralgia have a between trigeminal neuralgia and multiple sclerosis, normal neurologic examination. Sensory abnormalities patients should be asked about other neurologic symp- in the trigeminal area, loss of corneal reflex, or evidence toms, particularly those common in multiple sclerosis of any weakness in the facial muscles should prompt the (e.g., ataxia, dizziness, focal weakness, unilateral vision physician to consider symptomatic trigeminal neuralgia changes). An evaluation for other diagnoses is indicated or another cause of the patient’s symptoms.
in younger patients, because classical trigeminal neural-gia is unusual in persons younger than 40 years.3 ANCILLARY TESTING
Trigeminal neuralgia pain is nearly always unilateral.
Laboratory studies generally are not helpful in patients In rare cases of bilateral trigeminal neuralgia, individ- with typical symptoms of trigeminal neuralgia. Occasion- ual attacks are usually unilateral, with distinct episodes ally, TMJ or dental radiographs may be useful when TMJ involving each side of the face at separate times. Symp- syndrome or dental pain is in the differential diagnosis.
toms are always confined to the trigeminal nerve distri- Magnetic resonance imaging (MRI) of the brain is use- bution, with most cases involving the second or third ful to look for multiple sclerosis, tumors, or other causes division, or both. The asymptomatic period between of symptomatic trigeminal neuralgia, and it should be attacks is important to distinguish classical trigeminal performed in the initial evaluation of all patients pre- neuralgia from other causes of facial pain, as well as senting with trigeminal neuralgia symptoms. One study from symptomatic trigeminal neuralgia. Patients with found that specific clinical variables may be helpful indetermining the likely utility of MRI, which may be use-ful in prioritizing MRI studies when there is limited MRIcapacity.6 Some studies have indicated that MRI may pre- Table 2. Atypical Features Suggesting
dict surgery outcomes based on findings of neurovascular Symptomatic Trigeminal Neuralgia or
contact or the volume of the affected trigeminal nerve.7-9 an Alternative Diagnosis
One recent study demonstrated that trigeminal reflex testing could distinguish classical from symptomatic trigeminal neuralgia with a sensitivity of 96 percent and a specificity of 93 percent.10 Trigeminal reflex test- ing involves electrical stimulation of the divisions of the trigeminal nerve and measurement of the response with standard electromyography apparatus. This testing is not readily available to most physicians, and its indica-tions and clinical utility are still unclear.
May 1, 2008 V Volume 77, Number 9 American Family Physician 1293
Trigeminal Neuralgia
Table 3. Differential Diagnosis of Trigeminal Neuralgia
Features that differentiate from trigeminal treatment of trigeminal neuralgia is pro- Longer-lasting pain; orbital or supraorbital; may cause patient to wake from sleep; autonomic symptoms Treatment
Localized; related to biting or hot or cold foods; visible abnormalities on oral examination The initial treatment of choice for trigemi- Persistent pain; temporal; often bilateral; jaw nal neuralgia is medical therapy, and most patients have at least temporary relief with Pain in tongue, mouth, or throat; brought on by the use of selected agents. Patients who have no response to or who relapse with medical May have other neurologic symptoms or signs therapy should be considered for surgical Longer-lasting pain; associated with photophobia treatment.12-14 Surgery may also be consid- ered for patients who are intolerant of medi- MEDICAL TREATMENT
Pain in forehead or eye; autonomic symptoms; Carbamazepine (Tegretol) has been studied extensively in trigeminal neuralgia, with one Continuous pain; tingling; history of zoster; often meta-analysis finding good evidence for its effectiveness.15 A Cochrane review confirmed Persistent pain; associated nasal symptoms that carbamazepine is effective for the treat- ment of trigeminal neuralgia.16 The number Persistent pain; localized tenderness; jaw needed to treat has been calculated at 2.5 for trigeminal neuralgia. The number needed to harm for minor adverse events is 3.7, which SUNCT = shorter lasting, unilateral neuralgiform, conjunctival injection, and tearing. was calculated using data for all conditions.16 bamazepine is useful as a diagnostic trialfor classical trigeminal neuralgia. Lack of DIFFERENTIAL DIAGNOSIS
response would suggest symptomatic trigeminal neu- Some disorders that might be included in the differential ralgia or another diagnosis, both of which are less likely diagnosis of trigeminal neuralgia are listed in Table 3.11 A to respond to the drug. Dosages used have ranged from careful examination may disclose local findings indica- 100 to 2,400 mg per day, with most patients responding tive of otitis, sinusitis, dental disorders, or TMJ dysfunc- to 200 to 800 mg per day in two or three divided doses.
tion. A history of persistent pain or pain that occurs Carbamazepine should be the initial treatment for episodically in attacks lasting longer than two minutes patients with classical trigeminal neuralgia. Other medi- eliminates classical trigeminal neuralgia and should lead cations may be tried if carbamazepine is unsuccessful or to a search for other diagnoses. The pain of glossopha- provides only partial relief. These may be substituted or ryngeal neuralgia, which may be triggered by talking or added to carbamazepine as necessary. Baclofen (Liore- swallowing, is located in the tongue and pharynx.
sal) in dosages of 10 to 80 mg daily has been shown to be Symptomatic trigeminal neuralgia is usually caused by useful.17 Additional medications with reported success in multiple sclerosis or by tumors arising near the trigeminal smaller studies or case reports include phenytoin (Dilan- nerve root. A history of previous neurologic symptoms tin), lamotrigine (Lamictal), gabapentin (Neurontin), and typical findings on MRI assist with the diagnosis of topiramate (Topamax), clonazepam (Klonopin), pimo- multiple sclerosis. Tumors involving the trigeminal nerve zide (Orap), and valproic acid (Depakene).13,18-23 Most usually cause additional symptoms or examination find- patients will respond, at least temporarily, to single or combination therapy with these agents.
A variety of other medications and modalities have The initial choice of treat-
been tried for treatment of trigeminal neuralgia. There ment for trigeminal neural-
are small studies reporting success with botulinum toxin gia is medical therapy.
type A (Botox) in some patients,24 and one case report of relief being experienced after an accidentally high 1294 American Family Physician
Volume 77, Number 9 V May 1, 2008 Trigeminal Neuralgia
discharge from a transcutaneous electrical nerve stim- was insufficient evidence from randomized controlled ulation unit.25 Topical capsaicin (Zostrix) was helpful trials to show significant benefit from non-antiepileptic for trigeminal neuralgia pain in one open-label trial,26 drugs in patients with trigeminal neuralgia.32 and intramuscular sumatriptan (Imitrex) was benefi-cial in one small, single-dose study.27 One recent study SURGICAL TREATMENT
found that intranasal lidocaine (Xylocaine) significantly Surgical procedures may be percutaneous or open. The decreased second-division trigeminal neuralgia pain choice of procedure should be made after patient preference for more than four hours.28 Acupuncture, high-dose and the experience of the surgeon have been considered dextromethorphan (Delsym), and topical ophthalmic and the potential risks and benefits of each procedure have anesthetic have been tried unsuccessfully in small tri- been evaluated. Most procedures provide effective short- als.29-31 A recent Cochrane review concluded that there term relief, but studies suggest that recurrence is likely within several years for many patients.33-40 Diagnosis and Treatment of Trigeminal Neuralgia
injection, balloon compression, radiofre-quency rhizotomy, and gamma knife stereo- Patient with unilateral, episodic facial pain tactic radiosurgery. These techniques offerthe advantage of being relatively noninvasive, only a short hospital stay, and lacking life-threatening adverse effects. However, theymay provide less long-lasting relief than the more invasive techniques and have a higher incidence of sensory loss, which may cause abnormal examination, or age < 40 years the patient significant discomfort and can beextremely difficult to treat.
nal rhizotomy and microvascular decom-pression. These procedures involve posterior fossa exploration with its attendant risks, although the reported incidence of thesecomplications with microvascular decom- pression is less than 2 percent. Microvasculardecompression appears to provide the longestlasting relief, with persistent relief at 10 years in more than 70 percent of patients.36,41,42 It has low risks of symptom recurrence andsensory loss, and is therefore a good choicefor young, healthy patients, who have lower risks of adverse outcomes with the invasivesurgery involved. The author thanks Brian Selius, DO, and Azfar Ahmed, MD, for their assistance in the preparation and review of The Author
RUDOLPH M. KRAFFT, MD, is an associate professor of family medicine at Northeastern Ohio Universities Col-lege of Medicine in Rootstown and director of the Fam- Figure 2. Algorithm for the diagnosis and treatment of trigeminal ily Medicine Residency at St. Elizabeth Health Center in
neuralgia. (MRI = magnetic resonance imaging.) Youngstown, Ohio. He received his medical degree from Jefferson Medical College of Thomas Jefferson University, May 1, 2008 V Volume 77, Number 9 American Family Physician 1295
Trigeminal Neuralgia
Philadelphia, Pa., and completed a residency in family medicine at St. Vin- trigine (lamictal) in refractory trigeminal neuralgia: results from a dou- ble-blind placebo controlled crossover trial. Pain. 1997;73(2):223-230.
20. Cheshire WP. Defining the role for gabapentin in the treatment of tri- Address correspondence to Rudolph M. Krafft, MD, FAAFP, 1053 Bel- geminal neuralgia: a retrospective study. J Pain. 2002;3(2):137-142.
mont Ave., Youngstown, OH 44504 (e-mail: rudolph_krafft@hmis. 21. Gilron I, Booher SL, Rowan JS, Max MB. Topiramate in trigeminal neu- org). Reprints are not available from the author. ralgia: a randomized, placebo-controlled multiple crossover pilot study. Author disclosure: Nothing to disclose.
Clin Neuropharmacol. 2001;24(2):109-112.
22. Lechin F, van der Dijs B, Lechin ME, et al. Pimozide therapy for trigeminal neuralgia. Arch Neurol. 1989;46(9):960-963.
23. Peiris JB, Perera GLS, Devendra SV, Lionel ND. Sodium valproate in tri- 1. Headache Classification Subcommittee of the International Headache geminal neuralgia. Med J Aust. 1980;2(5):278.
Society. The international classification of headache disorders: 2nd ed. 24. Piovesan EJ, Teive HG, Kowacs PA, Della Coletta MV, Werneck LC, Sil- Cephalalgia. 2004;24(Suppl 1):9-160.
berstein SD. An open study of botulinum-A toxin treatment of trigemi- 2. Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence and clinical fea- nal neuralgia. Neurology. 2005;65(8):1306-1308.
tures of trigeminal neuralgia, Rochester, Minnesota, 1945-1984. Ann 25. Thorsen SW, Lumsden SG. Trigeminal neuralgia: sudden and long-term remission with transcutaneous electrical nerve stimulation. J Manipula- 3. Cruccu G, Biasiotta A, Galeotti F, et al. Diagnosis of trigeminal neu- tive Physiol Ther. 1997;20(6):415-419.
ralgia: a new appraisal based on clinical and neurophysiological find- 26. Epstein JB, Marcoe JH. Topical application of capsaicin for treatment of ings. In: Cruccu G, Hallett M, eds. Brainstem Function and Dysfunction. oral neuropathic pain and trigeminal neuralgia. Oral Surg Oral Med Oral Amsterdam, the Netherlands: Elsevier; 2006:171-186.
4. Neto HS, Camilli JA, Marques MJ. Trigeminal neuralgia is caused by 27. Kanai A, Saito M, Hoka S. Subcutaneous sumatriptan for refractory tri- maxillary and mandibular nerve entrapment: greater incidence of right- geminal neuralgia. Headache. 2006;46(4):577-582.
sided facial symptoms is due to the foramen rotundum and foramen 28. Kanai A, Suzuki A, Kobayashi M, Hoka S. Intranasal lidocaine 8% spray ovale being narrower on the right side of the cranium. Med Hypotheses.
for second-division trigeminal neuralgia. Br J Anaesth. 2006;97(4):559- 5. Love S, Coakham HB. Trigeminal neuralgia: pathology and pathogen- 29. Millán-Guerrero RO, Isáis-Millán S. Acupuncture in trigeminal neuralgia esis [published correction appears in Brain. 2002;125(pt 3):687]. Brain.
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30. Gilron I, Booher SL, Rowan JS, Smoller MS, Max MB. A randomized, 6. Majoie CB, Hulsmans FJ, Castelijns JA, et al. Symptoms and signs related controlled trial of high-dose dextromethorphan in facial neuralgias. to the trigeminal nerve: diagnostic yield of MR imaging. Radiology.
Neurology. 2000;55(7):964-971.
31. Kondziolka D, Lemley T, Kestle JR, Lunsford LD, Fromm GH, Janetta 7. Erbay SH, Bhadelia RA, Riesenburger R, et al. Association between neu- PJ. The effect of single-application topical ophthalmic anesthesia in rovascular contact on MRI and response to gamma knife radiosurgery in patients with trigeminal neuralgia. A randomized double-blind pla- trigeminal neuralgia. Neuroradiology. 2006;48(1):26-30.
cebo-controlled trial. J Neurosurg. 1994;80(6):993-997.
8. Kress B, Schindler M, Rasche D, et al. MRI volumetry for the preoperative 32. He L, Wu B, Zhou M. Non-antiepileptic drugs for trigeminal neuralgia. diagnosis of trigeminal neuralgia. Eur Radiol. 2005;15(7):1344-1348.
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9. Kuncz A, Vörös E, Barzó P, et al. Comparison of clinical symptoms and 33. Zakrzewska JM. Trigeminal neuralgia and facial pain. Semin Pain Med.
magnetic resonance angiographic (MRA) results in patients with tri- geminal neuralgia and persistent idiopathic facial pain. Medium-term 34. Kannan V, Deopujari CE, Misra BK, Shetty PG, Shroff MM, Pendse AM. outcome after microvascular decompression of cases with positive MRA Gamma-knife radiosurgery for trigeminal neuralgia. Australas Radiol.
findings. Cephalalgia. 2006;26(3):266-276.
10. Cruccu G, Biasotta A, Galeotti F, Ianetti GD, Truini A, Gronseth G. Diag- 35. Oturai AB, Jensen K, Eriksen J, Madsen F. Neurosurgery for trigemi- nostic accuracy of trigeminal reflex testing in trigeminal neuralgia. Neu- nal neuralgia: comparison of alcohol block, neurectomy, and radiofre- quency coagulation. Clin J Pain. 1996;12(4):311-315.
11. Zakrzewska JM. Diagnosis and differential diagnosis of trigeminal neu- 36. Barker FG, Janetta PJ, Bissonette DJ, Larkins MV, Jho HD. The long- ralgia. Clin J Pain. 2002;18(1):14-21.
term outcome of microvascular decompression for trigeminal neuralgia. 12. Delzell JE, Grelle AR. Trigeminal neuralgia. New treatment options for a N Engl J Med. 1996;334(17):1077-1083.
well-known cause of facial pain. Arch Fam Med. 1999;8(3):264-268.
37. Kondziolka D, Lunsford LD, Flickenger JC, et al. Stereotactic radio- 13. Scrivani SJ, Mathews ES, Maciewicz RJ. Trigeminal neuralgia. Oral Surg surgery for trigeminal neuralgia: a multiinstitutional study using the Oral Med Oral Pathol Oral Radiol Endod. 2005;100(5):527-538.
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14. Haanpää M, Truini A. Neuropathic facial pain. Suppl Clin Neurophysiol.
38. Mendoza N, Illingworth RD. Trigeminal neuralgia treated by micro- vascular decompression: a long-term follow-up study. Br J Neurosurg.
15. McQuay H, Carroll D, Jadad AR, Wiffen P, Moore A. Anticonvulsant drugs for management of pain: a systematic review. BMJ. 1995;311(7012): 39. Hai J, Li ST, Pan QG. Treatment of atypical trigeminal neuralgia with microvascular decompression. Neurol India. 2006;54(1):53-56.
16. Wiffen PJ, McQuay HJ, Moore RA. Carbamazepine for acute and chronic 40. Taha JM, Tew JM. Comparison of surgical treatments for trigeminal pain. Cochrane Database Syst Rev. 2005;(3):CD005451.
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17. Fromm GH, Terrence CF, Chattha AS. Baclofen in the treatment of tri- geminal neuralgia: double-blind study and long-term follow-up. Ann 41. Tronnier VM, Rasche D, Hamer J, Kienle A, Kunze S. Treatment of idio- pathic trigeminal neuralgia: comparison of long-term outcome after 18. McCleane GJ. Intravenous infusion of phenytoin relieves neuropathic radiofrequency rhizotomy and microvascular decompression. Neurosur- pain: a randomized, double-blinded, placebo-controlled, crossover study. Anesth Analg. 1999;89(4):985-988.
42. Lichtor T, Mullan JF. A 10-year follow-up review of percutaneous micro- 19. Zakrzewska JM, Chaudhry Z, Nurmikko TJ, Patton DW, Mullens EL. Lamo- compression of the trigeminal ganglion. J Neurosurg. 1990;72(1):49-54.
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