Journal ofNeurology, Neurosurgery, and Psychiatry 1995;59:253-259

Association between trigeminal neuralgia andmultiple sclerosis: role of magnetic resonance

imaging

J F M Meaney, JW G Watt, P R Eldridge, G H Whitehouse, J C D Wells, J B Miles

AbstractSeven consecutive patients with multiplesclerosis and trigeminal neuralgia wereinvestigated with MRI to determine theoccurrence of a lesion which wouldaccount for the patients' pain. Twopatients had bilateral symptoms. In thepatients with unilateral trigeminal neu-ralgia vascular compression of the nerveby an artery at the root entry zone on thesymptomatic side was confirmed in threepatients and an epidermoid tumour dis-torting the nerve on the symptomatic sidewas identified in one patient. A demyeli-nating plaque was identified in only onepatient, affecting the trigeminal nerve atthe root entry zone at the pons. In thosewith bilateral symptoms neurovascularcompression was identified on both sidesin one patient and on one side only in theremanng patient. Microvasculardecompression cured the pain in twopatients with neurovascular compres-sion. The variable aetiology of trigeminalneuralgia is stressed even in patients withcoexistent neurological conditions suchas multiple sclerosis, which can causetrigeminal neuralgia independent ofother causes.

(7 Neurol Neurosurg Psychiatry 1995;59:253-259)

Keywords: trigeminal neuralgia; magnetic resonanceimaging; multiple sclerosis

UniversityDepartment ofRadiodiagnosis, 2ndfloor JohnstonBuilding, Universityof Liverpool, L69 3BX,UKJ F M MeaneyG H WhitehousePain ResearchInstitute, Rice Lane,Liverpool, L9 IAEJW G WattJ C D WellsWalton Centre forNeurology andNeurosurgery, RiceLane, Liverpool,L9 1AE, UKP R EldridgeJ B MilesCorrespondence to:Mr J B Miles.Received 8 June 1994and in final revised form16 March 1995

Accepted 20 April 1995

The aetiology of trigeminal neuralgia is multi-factorial, but it is becoming increasinglyrecognised that most so called "idiopathic"cases are due to vascular compression of thenerve by a looping blood vessel where thenerve enters the pons.l4 About 1-2% arecaused by demyelinating plaques of multiplesclerosis affecting the trigeminal pathway andthe results of many postmortem examinationssupport this notion.5-8 About 10% of cases aredue to cerebellopontine masses compressingor invading the nerve.9We emphasise that trigeminal neuralgia in

patients with multiple sclerosis must not beattributed solely to demyelination, withoutexclusion of other causes such as vascularcompression or tumours.

Patients and methodsSeven consecutive patients with both multiplesclerosis and trigeminal neuralgia were inves-

tigated by MRI. Two patients had bilateraltrigeminal neuralgia. All images wereobtained on a Siemens Magnetom 1-5 TeslaMR scanner. All patients had a sagittal TIweighted localiser (TR/TE 500/15 ms).Conventional T2 weighted and proton densityweighted images (TR/TE 2,000/80/20 ms) orfast spin echo T2 weighted images (TRITE3800/93 ms) were obtained in four patients.Magnetic resonance tomoangiograms(MRTAs) of the intracranial vasculature wereobtained by a three dimensional fast inflowwith steady state precession sequence, whichis routinely employed for depiction of theintracranial vasculature at our institution.Images were acquired axially over the pons.Scanning parameters were TR 29-36 ms, TE7 ms, flip angle 150, 64 partitions, 55 mmslab, 22 cm field of view. This techniqueyielded 64 slices each of 0 9 mm thick.Operator defined reconstructions centredaround the trigeminal nerves were performedto determine the presence or absence of vas-cular compression. So as not to confuse thistechnique with MR angiography, which pro-vides information about the vessels only, theterm magnetic resonance tomoangiographyhas been used.'0

Case reportsPATIENT 1A 40 year old woman presented with a oneyear history of second division trigeminal neu-ralgia on the right side. She had had a series ofattacks 19 years earlier, which had respondedto carbamazepine. Five years previously anepisode of optic neuritis led to a diagnosis ofmultiple sclerosis. A conventional MRIshowed several areas of increased signal con-sistent with multiple sclerosis.

Carbamazepine (600 mg daily) initiallycontrolled the pain but one year after theonset of symptoms she was taking 1400 mgcarbamazepine and 0 5 mg clonazepam daily.A glycerol trigeminal ganglion block gave onlylimited relief, and so a trial of dorsal columnstimulation was performed. High cervicalstimulation gave complete pain relief for threehours after stimulation was stopped.Permanent dorsal column stimulation wasplanned.An MRTA clearly showed compression of

the right trigeminal nerve at the root entryzone by the superior cerebellar artery (fig IA,B) This finding prompted microvasculardecompression of her right trigeminal nerve(rather than implantation of a permanent dor-

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Figure 1 (patient 1): (A) Coronal MRTA ofpons. Both trigeminal nerves are indicat(large curved arrows). Note compression of the right trigeminal nerve by a caudallylooping superior cerebellar artery (small curved arrows). No evidence of compression on tleft side. (B) Sagittal MRTA along the right trigeminal nerve (solid arrows) showingcompression of the nerve superiorly at the root entry zone by the superior cerebellar artery(open arrow)

sal column stimulator), which completelycured her neuralgia.

PATIENT 2

A 54 year old woman presented with a seven

year history of left second division trigeminalneuralgia. She had multiple sclerosis mani-

fested as optic atrophy and ataxic spasticquadriparesis for 12 years. Carbamazepinewas effective in relieving trigeminal neuralgiabut exacerbated her multiple sclerosissymptoms to such a degree that she becameconfined to a wheelchair on high doses. Shetook 800 mg carbamazepine daily increasingto 1600 mg during exacerbations. A posteriorfossa trigeminal nerve rhizotomy had previ-ously been planned but was cancelled due tothe severity of her multiple sclerosis. Aradiofrequency lesion of the second divisiongave three months of complete relief, andpartial relief for a further six months. She iscurrently well controlled on 800 mg ofcarbamazepine daily.An MRTA showed no evidence of vascular

contact with the nerve. Conventional T2Wand proton density MRI showed multipleareas of increased signal intensity consistentwith multiple sclerosis, and a large discreteplaque affecting the pons at the level of thetrigeminal nerve on the symptomatic side(fig 2).

PATIENT 3After 25 years of multiple sclerosis, a 54 yearold man had no movement below the neckand a bulbar palsy. He had left third divisiontrigeminal neuralgia for six years and was tak-ing 800 mg of carbamazepine daily, whichgave only limited pain relief.An MRTA disclosed a single artery com-

pressing and displacing his left trigeminalnerve at the root entry zone. Unfortunately hiscondition was so severe that surgery was notoffered. Radiofrequency nerve destructionwas not performed because of his inability tocommunicate, which would have made itimpossible for the operator to assess the nee-dle position during sensory testing.Reasonable pain relief was achieved by injec-tion of absolute alcohol into the trigeminalganglion.

PATIENT 4A 60 year old woman had multiple sclerosisfor 20 years and was wheelchair bound due tolower limb weakness. Two years previouslyshe had developed severe shooting pains inthe second division of her left trigeminalnerve. Initially attacks lasted 20 minutes butat presentation they were almost constant.Carbamazepine relieved her pain but caused aflorid skin rash. Phenytoin was ineffective andcaused hallucinations. Sodium valproate gaveonly limited relief and at a high dose exacer-bated her ataxia and induced tremor.An MRTA showed no evidence of vascular

compression but the nerve was medially devi-ated by a well circumscribed mass (fig 3A),and T2W MRI (fig 3B) showed a mass lesionextending along the left petrous ridge, distort-ing the left trigeminal nerve. Changes consist-ing of extensive demyelination with severalsmall demyelinating areas in the midbrain andpons were also noted. She is currently await-ing surgery for her tumour.

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* 4~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.XtFigure 2 (patient 2): T2 weighted magnified image at the level of the pons. Bothtrigeminal nerves are visible as low signal intensity structures (black arrows) suspendedwithin the high signal CSF. Note high signal intensity plaque (white arrow) extendingposteriorly from the left tigeminal nerve root enty zone.

PATIENT 5A 64 year old man had bilateral leg and leftarm weakness after 36 years of multiple scle-rosis. Fourteen years ago he developed leftsecond division trigeminal neuralgia whichwas effectively treated by a radiofrequencynerve lesion. Three years later he developedneuralgia in his left first division, which alsoresponded to a radiofrequency lesion that lefthim with left sided facial anaesthesia.

Eight years ago he developed right seconddivision trigeminal neuralgia. To limit theextent of nerve destruction, the infraorbitalnerve was exposed and frozen with a cryo-probe. This gave only six months of relief.Over the next six years he underwent fourradiofrequency lesions of the right trigeminalnerve. Although the first lesion gave two yearsof relief, subsequent lesions had a shorterduration of action until the final lesion had noeffect. He was now anaesthetic in all threedivisions of the left trigeminal nerve, anaes-thetic in the second division, and hypoaes-thetic in the first division of the righttrigeminal nerve. Carbamazepine (600 mgdaily) gave only limited relief but worsenedhis multiple sclerosis symptoms such that hecould no longer feed himself and his speechbecame incomprehensible.An MRTA showed vascular compression

and distortion of the right trigeminal nervebetween the superior cerebellar artery aboveand a further small artery below (fig 4A, B).Vascular compression on the left side by a

single vessel was also noted.The pain of his trigeminal neuralgia was

now intolerable, carbamazepine was not toler-ated, and radiofrequency lesions were ineffec-tive. Despite the severity of his multiple

sclerosis the patient and his family consideredthat the risks of surgery were justified. Aftersuccessful microvascular decompression ofthe right trigeminal nerve he was completelyfree of pain. Unfortunately, he subsequentlydeveloped a chest infection from which hedied five days later.At postmortem, multiple, sclerotic, translu-

cent plaques were seen throughout the whitematter of the cerebral hemispheres, the cere-bellum, pons, medulla, and spinal cord. Serialsections through the pons showed typicaldemyelinating plaques in the root entry zonesof both trigeminal nerves, most pronouncedon the right side. On the left there was alsoconsiderable axonal loss with secondarydemyelination along the whole length of thetrigeminal nerve tract, assumed to be due toradiofrequency thermocoagulation of pregan-glionic nerves 10 years earlier.

PATIENT 6A 44 year old woman had multiple sclerosisfor 25 years, manifested as optic neuritis onseveral occasions and persistent spastic para-paresis of the lower limbs. Three years ago,she had been referred by her dentist who hadbeen unable to cure a right sided mandibularpain with tooth extractions. She gave a clearhistory of third division trigeminal neuralgiaand gained good pain relief with carba-mazepine (1600 mg daily). This dose madeher dizzy and sedated, however.Radiofrequency lesioning gave complete relieffrom pain and numbness in the third division.She was then able to discontinue carba-mazepine. Two years later she developedsymptoms of trigeminal neuralgia in themandibular division of her left trigeminalnerve. A combination of carbamazepine(2400 mg daily) with amitriptyline,desipramine, and clonazepam was only par-tially effective.An MRTA showed vascular compression of

the right trigeminal nerve by an ectatic artery,but no evidence of compression on the leftside. The patient was reluctant to undergosurgery. A diagnostic trigeminal ganglionblock with 1 5 ml of 1% lignocaine resulted in48 hours of total pain relief. As she remainedanaesthetic in the third division on the right itwas considered that radiofrequency ablationof the left trigeminal nerve carried too great arisk of bilateral sensory and motor dysfunc-tion. Her pain was therefore treated by inject-ing 0 5 ml of glycerol into the right Meckel'scave which resulted in complete anaesthesiaof her face on the symptomatic side. She hasbeen able to stop all medication except carba-mazepine at a daily dose of 200 mg.Microvascular decompression will be carriedout if her symptoms recur.

PATIENT 7After 14 years of multiple sclerosis, mani-fested as spastic paraparesis affecting bothlower limbs and the left upper limb, bladderdisturbance, and diplopia, this 40 year oldwoman developed left sided first and seconddivision trigeminal neuralgia six years ago. A

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Figure 3 (patient 4): (A) AxialMRTA showing medial deviation of the left trigeminalnerve (straight arrow) by a well circumscribed low signal intensity rounded lesion (curvedarrows). Note also low signal intensity area within the pons (open arrow) consistent with a

demyelinating plaque. (B) Axial T2W image showingflattening of the left side of the pons(straight white arrows) by a tumour (T) which has a signal intensity slightly higher thanCSF. The appearances are consistent with an epidermoid tumour. Note also areas ofincreased signal intensity (curved arrows) consistent with multiple sclerosis plaques

diagnostic trigeminal block afforded completepain relief, which lasted for three years. Theprocedure was successfully employed on twofurther occasions to treat recurrence. AnMRTA on the last occasion showed compres-sion of the left trigeminal nerve at the pons

between the superior cerebellar artery aboveand a small vessel below. At present the painis fairly well controlled with a combination ofketoprofen and paracetamol. Surgery is notplanned unless oral medication and anaes-thetic blocks cease to be effective.

DiscussionConventional opinion is that trigeminal neu-ralgia in patients with multiple sclerosis is dueto a demyelinating plaque affecting thetrigeminal nociceptive pathway.5-8 11 In thissmall series of nine instances of trigeminalneuralgia (seven patients; two bilateral) asso-ciated with multiple sclerosis, a potentiallytreatable cause was discovered in seveninstances. In only one case of unilateraltrigeminal neuralgia was demyelination shownto affect the trigeminal nerve root entry zoneon the symptomatic side. In four otherpatients with unilateral trigeminal neuralgia,vascular compression of the nerve was presentin three instances, and an epidermoid tumourin one. In two patients with bilateral trigemi-nal neuralgia, vascular compression was iden-tified on both sides in one patient and on oneside only in the other patient. In the patientwith bilateral compression radiofrequencycoagulation of the trigeminal root had previ-ously effected a cure on one side.

Postmortem examination of the brain hasrarely been performed in patients with trigem-inal neuralgia and multiple sclerosis. In mostcases reported demyelination affected thepons at the root entry zone.6 8 Although neu-rovascular compression of the nerve accountsfor most cases of "idiopathic" trigeminal neu-ralgia,4 the neurovascular relations of thetrigeminal nerve have not previously beenstudied in patients with multiple sclerosis andthe possibility that vascular compression maybe responsible in some instances has beensummarily dismissed by most authors. Forinstance Brisman states that microvasculardecompression is contraindicated in patientswith multiple sclerosis and trigeminal neural-gia8 and even Jannetta and colleagues,2 12 whopopularised microvascular decompression,have agreed with this statement. None theless, Lazar and Kirkpatrick reported thedemonstration of a plaque affecting thetrigeminal nerve at the root entry zone in apatient with multiple sclerosis, in whom a ves-sel was seen to compress the nerve at opera-tion.'3 This vessel was dismissed asunimportant, the fact that demyelination wasdemonstrated histologically being regarded asevidence to refute the relevance of the vessel.We question this assertion, as we are unawareof any firm criteria distinguishing unimpor-tant from important compression as disclosedat operation, and secondly, demyelination is anon-specific response to injury and has beenreported in trigeminal nerves at the root entryzone in patients with trigeminal neuralgia whodid not have multiple sclerosis. 14

Furthermore, postmortem examination of thepons disclosed demyelinating plaques bilater-ally affecting the root entry zone in patient 5

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Figure 4 (patient 5): (A) CoronalMRTA showing the right trigeminal nerve (straightarrow), barely visible because ofpronounced compression, sandwiched between the superiorcerebeUlar artery above (open arrow), and another vessel below (curved arrow),presumably a branch of the anterior inferior cerebellar artery. (B) Maximum intensityprojection angiogram showing caudal looping of the superior cerebellar artery (open curvedarrow) and a further small vessel inferiorly (solid white arrow). The site at which thenerve was compressed between these two vessels is indicated (black arrow)

who experienced immediate pain relief afterdecompression of the right trigeminal nerve,which was sandwiched between two vessels.The concept of vascular compression of the

nerve as a cause of trigeminal neuralgia was

first proposed by Dandy,' and the techniqueof microvascular decompression, in which thevessel is displaced from the nerve at the rootentry zone by interposition of a small non-resorbable sponge between the two structures,was popularised by Jannetta.2 The notion ofneurovascular compression is a widely, butnot universally accepted, cause of trigeminalneuralgia.'- Until recently, demonstration ofvascular compression of the nerve was notpossible by imaging means. Work at our insti-tute and others has shown that MRTA canconfirm or exclude vascular compression ofthe nerve root and potentially predict whichpatients will benefit from microvasculardecompression.4 101516 In a prospective seriesof patients with trigeminal neuralgia and ageand sex matched controls, vascular compres-sion of the nerve was identified in 85% ofsymptomatic cases compared with 8% of con-trols.4 In the present series, vascular compres-sion of the nerve was seen in 66% of patients inwhom trigeminal neuralgia was assumed to bedue to multiple sclerosis. Whereas response tomicrovascular decompression remains theultimate test of the importance of vascularcompression, the high incidence of vascularcompression in the present study strongly sug-gests a causal relation rather than a chanceassociation of vascular compression inpatients with trigeminal neuralgia associatedwith multiple sclerosis. The relevance of neu-rovascular compression in one patient with anundistorted nerve, as well as the importanceof vascular compression of the nerve on theside which had been cured by a radiofre-quency lesion of the trigeminal root in thepatient with bilateral trigeminal neuralgiawhose pain on the second side responded onlyto microvascular decompression, remainunproved.The pathophysiological processes underly-

ing trigeminal neuralgia remain anenigma.'7-20 It is known that compression, dis-tortion, or stretching of the trigeminal nerveby a slow growing tumour, aberrant vessels, orvascular malformations, can cause typicaltrigeminal neuralgia. Intrinsic brain lesionssuch as syringobulbia, brain stem infarcts and,most commonly multiple sclerosis, may alsocause trigeminal neuralgia. The most plaus-ible hypothesis regarding pathophysiology,which explains the fact that both extrinsic andintrinsic brain lesions may produce typicaltrigeminal neuralgia as well as the paroxysmalnature of the pain, is that trigeminal neuralgiahad a peripheral cause and a central patho-genesis. Fromm et al have postulated thatchronic irritation of the peripheral nerve leadsboth to ectopic action potentials within thenerve and failure of segmental inhibition inthe trigeminal nucleus.'7 This theory explainsthe origin of pain in the case of tumours andaberrant vessels compressing the nerve, whenectopic action potentials generated in thenerve would presumably be responsible, andalso the cause of pain in patients with intrinsicbrain lesions such as multiple sclerosis when aplaque would lead to increased activity withinthe trigeminal nucleus. Regardless of which of

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Table 1 Summary of clinical history, MRI, and treatment outcome of seven consecutive patients with trigeminalneuralgia and multiple sclerosis

DurationPatient of multiple Side andNo sclerosis Age division(s) Pathology Treatment Outcome1 5 40 Right 1-3 Vessel MVD Pain free2 12 54 Left 2 Plaque CBZ Partial control3 25 54 Left 3 Vessel Alcohol Pain free4 20 60 Left 2-3 Epidermoid Acupuncture, Partial control

tumour awaitingsurgery5 36 71 Bilateral, Two vessels MVD right side Pain free

Left 1 Right side, RFL left side DiedRight 2 single vessel left side

6 25 44 Bilateral, Vessel Alcohol Pain freeRight V3,Left V3

7 20 40 Left, Two vessels Nerve block Pain free1 and 2

MVD = microvascular decompression; CBZ = carbamezepine; RFL = radiofrequency lesion.

these mechanisms operates, episodic activa-tion of the trigeminal neurons may result inparoxysms of pain whenever these bursts ofactivity exceed the threshold for activation ofpain neurons in the trigeminothalamic tract.To satisfactorily explain the unexpectedlyhigh incidence of vascular compression of thenerve in patients with trigeminal neuralgiaand multiple sclerosis, we wish to extend thistheory further. Given the occurrence oftrigeminal neuralgia in about 1-2% ofpatients with multiple sclerosis, and thattrigeminal neuralgia is encountered in only0-01% of the general population in whom an8% incidence of vascular contact with thenerve is expected, we postulate that vascularcompression is more likely to cause trigeminalneuralgia in patients with multiple sclerosisthan it is in the population without this condi-tion, because of underlying hyperexcitabilityin the trigeminal nucleus. This same argu-ment may explain the higher incidence ofbilateral occurrence of trigeminal neuralgia inpatients with multiple sclerosis, and perhapsalso the earlier onset. It also satisfactorilyexplains the cause of symptoms in a patientwe have recently encountered with bilateraltrigeminal neuralgia associated with Charcot-Marie-Tooth syndrome, in whom bilateralmicrovascular decompression cured thetrigeminal neuralgia on both sides after failureof all other treatments. In such cases an

Table 2 Outcomes offour procedures for the treatment of trigeminal neuralgiaProcedure Outcome Duration of action Sensorylmotor loss

Glycerol injection 85% effective Short Slight sensory lossAbout 6 months Corneal anaesthesia possible

Masseter weakness rare

Alcohol injection 85% effective Variable, may be Sensory losslong Other cranial nerve loss

Comeal anaesthesia

Radiofrequency 90% effective Long Frequent sensory losslesion 25% relapse rate Corneal anaesthesia if V,

Masseter weaknessoccasionally

Microvascular 90% effective Long 3% morbidity (damage todecompression other cranial nerves)

1% mortality

intrinsic neurological abnormality is assumedto form the basis for the provocation oftrigeminal neuralgia by neurovascular com-

pression.Jannetta2 has suggested that the pain of

trigeminal neuralgia in patients with multiplesclerosis is milder than that seen in theidiopathic group. All the patients in thepresent study had severe symptoms unrespon-sive to drug treatment and had been referredto a pain institute with a special interest intrigeminal neuralgia; therefore we cannotconclude that our cohort is representative ofthe overall population of patients with mul-tiple sclerosis and trigeminal neuralgia, andwe eagerly await validation of our results byothers.The fact that most patients with trigeminal

neuralgia respond to drug treatment andpercutaneous procedures on the ganglion,presumably even those with vascular com-pression, highlights the fact that cure of paincan be effected by interruption of the painpathway at one of many sites.2124 As eventu-ally there is a poor response to both drugtreatment and percutaneous ablative proce-dures in patients with trigeminal neuralgiaand multiple sclerosis, as is the case to a lesserextent in trigeminal neuralgia in general, it isimportant to identify vascular compression toeffect appropriate treatment.The discovery of trigeminal nerve compres-

sion by an epidermoid tumour was almostcertainly a chance finding. In a patient with acondition such as multiple sclerosis whichmay cause neurological deficit, a search for acoexistent potentially curable cause of thesame clinical manifestation is unlikely to becarried out.2' 24 The same is true of idiopathictrigeminal neuralgia. In a large recent studythe 10% of cases secondary to tumours werediscovered only after an average delay of 6-3years.9 All patients with trigeminal neuralgiahave been equally disadvantaged in the pastby the inability to demonstrate vascularcompression of the nerve without recourse toexploratory surgery. In addition, patients withmultiple sclerosis are further disadvantaged bya disease process which might have explainedtheir symptoms irrespective of a coexistent

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Association between trigeminal neuralgia and multiple sclerosis: role of magnetic resonance imaging

cause such as tumour or vascular compres-sion.

Despite advances in both MRI and labora-tory technology, the diagnosis of multiplesclerosis remains a clinical one, and most clin-icians should remain extremely reluctant toforward a diagnosis of multiple sclerosis with-out firm clinical evidence. "1 25 Poser et al havedeveloped criteria to aid the clinician in com-ing to the correct diagnosis.26 The presence ofabnormalities referable to multiple lesionswithin the CNS, separated both in time andspace, with evidence of remissions, stronglyfavours a diagnosis of multiple sclerosis. In a

patient with one CNS abnormality and coex-

istent trigeminal neuralgia, it seems reason-

able to attribute both to the same underlyingpathological process. Although we suspectthat trigeminal neuralgia is simply more likelyto develop in patients with multiple sclerosisand vascular compression of the nerve, thisremains unproved; we emphasise that trigemi-nal neuralgia can only be used as corrobora-tive evidence to support a diagnosis ofmultiple sclerosis if secondary causes such as

vascular compressions and tumours have firstbeen excluded.

ConclusionAdvances in MRI may allow demonstration ofthe cause of symptoms in most patients withtrigeminal neuralgia. Failure to investigatefully the cause of pain in each individualcase of trigeminal neuralgia associated withmultiple sclerosis may deprive an alreadydisabled patient of a potential surgical cure.

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