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All about trigeminal neuralgia

Published in: Health & Medicine


  2. 2. Demotivating , of the most painful neuropathic painsIASP definition: Sudden, recurrent, severe pain in thedistribution of one or more branches of the fifth cranial nerveno universal treatment is capable of reverting completelyimpairment of daily functionality, reduced quality of life anddepressionoverwhelming fear that pain can suddenly return again
  3. 3. Peculiar neuropathic painnot accompanied by sensory deficitCan be cured by a small nerve or root lesionCause ? Now… sound hypothesis of neurovascular conflict(NVC) [ Are we still hearing sounds of conflict? ]tic douloureux = since painful brief muscle spasms
  4. 4. EPIDEMIOLOGY3-5/ one lac; 52- 69 years most commonMore recent estimates suggest the prevalence isapproximately 1.5 cases per 10,000 population, with anincidence of approximately 15,000 cases per yearMultiple sclerosis is found to be a risk factor; ?HTN I‟m also having..[youngest 12m] 3.4/lac 5.9/lac
  5. 5. Anatomy - whereabouts• Emerge as a larger sensory and smaller motor root• Fibres in sensory root are axons of cells in trigeminal ganglion which occupies Meckels cave• Neurons of the unipolar cells of the ganglion divides into central and peripheral processes• Peripheral ophthalmic,maxillary and sensory part of mandibular• Central fibres of the sensory root
  6. 6. Whereabouts……
  7. 7. origin of the…..pain....nerve .
  8. 8. Course and relevance in TN The sensory fibers arise from the gasserian ganglion (lying near the petrous part of the temporal bone in the dura matter), pass backward, enter the pons, and divide into upper and lower roots. The upper roots end in the principal or superior sensory nucleus and locus caeruleus. The lower roots descend through the pons and medulla and terminate in the spinal tract nucleus, which consists of subnucleus caudalis, subnucleus inter-polates, and subnucleus oralis. The subnucleus caudalis serves as the principal brainstem relay site for orofacial pain, and the superior sensory nucleus and subnucleus oralis are sites relaying orofacial
  9. 9. No monopoly; already a lot of members to control• 1 motor and 3 sensory nuclei• Motor upper pons• Mesencephalic midbrain ; for proprioception• Main sensory nucleus upper pons ; for touch• Spinal nucleus in lower pons, medulla and upper cervical spinal cord; for pain and temperature
  10. 10. Complex routes…. .
  11. 11. The Spinal TrigeminalNucleus .
  12. 12. Principal brainstem relaysites…. Subnucleus caudalis  orofacial pain Superior sensory nucleus , subnucleus oralis  Tactile informationThe similarity…. Neurons in dorsal horn   Thalamus Neurons in subnucleus caudalis    ThalamusMotor root…. Motor roots from the superior and lower nucleus then joins the sensory root as it emerges from the pons
  13. 13. Eagerly waiting for chaos..Nociceptive neurons in subnucleus caudalis respond tonoxious stimulation of the  Orofacial tissues Tooth pulp TMJ Dura Jaw Tongue Neck musclesMechanoreceptive neurons in the superior sensory nucleus Light tactile stimuli to Skin Mucosa teeth
  14. 14. Ophthalmic nerve
  15. 15. Maxillary nerve
  16. 16. Mandibular nerve
  17. 17. ETIOLOGY AND PATHOPHYSIOLOGY“Pain is temporary. Quitting lasts forever”…Lance ArmstrongHis quotes also are loosing integrity...???
  18. 18. Central vs PeripheralCentral theories emphasize the role of deafferentation(secondary to compression of the trigeminal roots organglion) in the genesis of neural hyperactivity.Peripheral theories note that changes in peripheral axonsand myelin may lead to altered nerve sensitivity to chemicaland mechanical stimuli.Starts as a peripheral lesion; response of central synapsesto this sets stage for the war; SO BOTH MECHANISMSPLAY
  19. 19. Painful and annoying conflict…In 85%, no structural lesion is seenClassic [idiopathic] form: “Neurovascular conflict” i.e.vascular compression of nerve most commonly @ its entryinto pons [REZ]Significant NVC= an artery (not a vein), crossing (notparallel to) the nerve and provoking displacement/groovingof it (Casselman,2000)
  20. 20. Amplifying….compression results in focal trigeminal nerve demyelinationleads to ephaptic transmission [action potentials jump fromone fiber to another]A lack of inhibitory inputs from large myelinated nerve fibersplays a role.a reentry mechanism causes an amplification of sensoryinputs
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  22. 22. Two types....One feature..Trigeminal neuralgia is divided into classic [idiopathic] andsymptomatic typesThe classic form includes the cases that are due to a normalartery present in contact with the nerve, such as the SCA oreven a primitive trigeminal arterySymptomatic forms can have multiple origins: Aneurysms,tumors, chronic meningeal inflammation.An abnormalvascular course of the superior cerebellar artery is oftencited as the causeUncommonly, an area of demyelination from multiplesclerosis may be the precipitant
  23. 23. ETIOLOGY• compression of nerve root [most common-vascular; rarely tumor/vein/avm] usually when pain @ v2 / v3, compression is by SCA ; pain @ v1  by AICA• Inflammatory causes: multiple sclerosis [in1-5% of patients with MS;more likely if patient with TN is 20-40ys] ; Damage to myelin sheath [Myelin gone….signals blend….nerves may sense light touch as pain!!!!!] ), sarcoidosis, and Lyme disease neuropathy• traumatic accidents• unsuccessful dental work
  24. 24. ETIOLOGYTumor-related causes : (most commonly in the cerebello-pontine angle) include acoustic neurinoma, chordoma at thelevel of the clivus, pontine glioma orglioblastoma,epidermoid, metastases, and lymphoma andparaneoplastic etiologies.Vascular causes include a pontine infarct and arteriovenousmalformation or aneurysm in the vicinity.infections , varicella virusfoci of abscessesbone resorption with irritation of the trigeminal nerve in themaxilla or mandible
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  27. 27. Don‟t get deceived by imitations DIFFERENTIAL DIAGNOSIS variety of tumours and other lesions involving, or impinging on, the trigeminal nerve, ganglion or sensory root  tumours of the C-P angle, MCF, cranium or extracranial tissues (often metastatic), and from the envelopes of the Gasserian ganglion.OTHERSatypical facial pain syndromescluster headachepostherpetic neuralgiageniculate neuralgia (Ramsay Hunt)sphenopalatine ganglion neuralgiaglossopharyngeal neuralgiadental disease, orbital diseasetemporomandibular dysfunctiontemporal arteritis
  28. 28. I doubt….you are having….Headache Classification Subcommitee of the InternationalHeadache Society. Cephalalgia 2004
  29. 29. Difficult to bearAlmost always u/lComes like electric shockBrief; but will recur„Paralysing‟Light pressure on trigger points will trigger the attackUnpredictable symptom free intervalsAtypical pain patterns are thereMy patients‟ biggest ambitions: Eating…. Shaving…. Make up face….
  30. 30. Please don‟t touch on these areas ..Ok..?.
  31. 31. DIAGNOSIS
  32. 32. Keep a low threshold for MRI inyounger patients atypical clinical featuressensory lossdull burning pain between paroxysmspatients who do not respond to initial medical therapy
  33. 33. ImagingC.T.M.R.I. : CONVENTIONAL: can rule out tumour / multiple sclerosis 3-D VOLUME ACQUISITION, with contrast injection and thin cuts (ie, 0.8 mm) without gaps can see Trigeminal nerve and associated blood vessels The trigeminal nerve is easily observed in the axial plane when the MRI series is centered at die midpoint of the 4th ventricle. To ensure adequate evaluation, the nerve should be observed on 3 adjacent cuts. when an offending vessel is present, it will be detected 80% of the time OTHERS: TOF, CISTERNOGRAPHYAlso look for tumours, multiple sclerosis, abnormalities of
  34. 34. ImagingMeckel‟s cave, the cavernous sinus, the skull baseforamina, the pterygopalatine fossa and the peripheraltrigeminal nerve coursealways look for a normal gray and white matter andbrainstem, a normal cisternal segment, a fluid fi lledMeckel‟s cave, a homogeneously enhancing cavernoussinus, a fat-filled superior orbital fissure and pterygopalatinefossa, normal foramen rotondum and ovale, and asymmetrical appearance of the masticator muscles with
  35. 35. DIFFERENTIATION• paroxysms of pain last longer• pain tends to be constant• Involvement of forehead alone +/- autonomic symptoms• neurologic deficit is often detected (cutaneous hypoesthesia, loss of corneal reflex, masticatory muscle weakness).
  36. 36. . Treatment
  37. 37. PHARMACOLOGICALenormous belief in CarbamazepinePhenytoin is the second treatment of choice 3 weeks over,adequate serum levels obtained…..but no relief DISCONTINUE because higher doses may lead to toxicity. The short-term efficacy rate is 60%; decreases to 30% after 2 yearsLamotrigene useful in failure/intolerance withCarbamazepineGabapentin : benign adverse effect profile, can be used asadjuvant alsoTopiramate: proved to be effective where combinationtherapy fails
  38. 38. Treatment Your Text here Take @ meals Use long acting preparationsfewer drug interactions and side effects;but cross reactivity with carbamazepine +
  39. 39. TreatmentYour Text here
  40. 40. SURGICAL Rx-FACTSaimed at either destroying parts of nerve fibers ordecompressing the trigeminal nerve to relieve painalthough surgical treatment may initially be successful,trigeminal neuralgia may recur retry medical therapy[because drugs that were previously ineffective maybecome effective later]patients with classic trigeminal neuralgia, evidence ofvascular compression, shorter duration of disease, and noprevious surgery respond better to all treatment options.In such patients, MVD can be considered the “goldstandard” surgical procedure, and it offers the best longterm cure rates.
  41. 41. SURGICAL Rx-FACTSAll procedures have high initial response rate, except forstereotactic radiosurgery, which usually takes maximumeffect at one to two monthsAblative Rxs are used to a greater extent in patients withhigh operative risk
  42. 42. Microvascular decompression (MVD) of the posterior fossajunction of the Vth nerve with the pons is exploredblood vessels and tumors removed from direct contact withthe nerve. The SCA, PICA, VA, and AICA (& smallbranches) are separated from the nerve by a piece ofDacron fabricEfficacy is reported to be 85% initially, and 80% at 5 years.carries a relatively low risk of painrecurrence, dysthesia, corneal analgesia, and trigeminalmotor weakness
  43. 43. .
  44. 44. MVD-RisksRisks higher in patients who have an ecstatic(atherosclerotic) and a tortuous vertebrobasilar arterial treethe risk for perioperative mortality [around 0.4%], seriousmorbidity (eg, stroke, hemorrhage, venous occlussion,M.I.,HCP), permanent hearing loss, and facial palsy ishigher after MVD than after percutaneous procedures.But ablative procedures are less effective in the long termand more likely to produce facial numbness and other minorcomplications than MVD
  45. 45. MVD-Follow up• OPERATIVE FINDINGS (97%)• arterial channels 374 (80,3%) Russel R. Lonser and Ronald I. Apfelbaum “Operative Neurosurgical Techniques”• venous channels 65 (13,9%) Vol 2, pp 1531-1538 (2006)• tumor 12 (2,6%)• negative 15 (3,2%)• total 466• COMPRESSIVE ARTERY• SCA – 80%• SCA+AICA – 9%• AICA – 8%• Basilar – 2%• Others--1%
  46. 46. MVD-Follow up• INITIAL RESULTS• complete relief – 91% Russel R. Lonser and Ronald I. Apfelbaum “Operative Neurosurgical Techniques”• pain reduced – 6% Vol 2, pp 1531-1538 (2006)• pain not relieved – 2%• death – 1%• COMPLICATIONS• cranial nerve dysfunction – 12,6%• dizziness, ataxia – 3%• infarction – 1,8%• seizures – 1%• death – 1%
  47. 47. MVD-Follow up• LONG-TERM RESULTS• no recurrence - 62% Russel R. Lonser and Ronald I. Apfelbaum “Operative Neurosurgical Techniques”• mild pain (no medication) - 5% Vol 2, pp 1531-1538 (2006)• pain controlled with medication -14%• severe pain not controlled “ - 18%• died - 1%
  48. 48. PREOPERATIVE SIMULATIONfusion imaging technique of three-dimensional (3-D) MRcisternography and co-registered 3-D MRAThe presence of offending vessels and compressive site ofneurovascular conflict was assessed from the variousviewpoints within the cisternsurgeons-eye view, birds-eye view
  49. 49. PREOPERATIVE SIMULATIONPresurgical Virtual Endoscopy: is a novel technique thatprovides excellent visualization of the three-dimensionalrelations between neurovascular structures and allowssimulation of MVD
  50. 50. Percutaneous radiofrequency thermocoagulation of the gasserian ganglionA high-frequency current used to destroy precisely the A-delta and C-fiber nociceptorsbased on the theory that lower temperatures selectivelydestroys the nociceptive unmyelinated C-fibers & the poorlymyelinated A-delta fibers while sparing the heavilymyelinated A-alpha & A-beta fibers which convey the touch,proprioceptive & motor impulses.
  51. 51. Percutaneous radiofrequency thermocoagulation of the gasserian ganglionUnder fluoroscopic guidance, an insulated needle is passedthrough the foramen ovale next to the gasserian ganglionThe initial efficacy ̴ 90%, with 80% patients remaining free ofpain at 1 year and 50% remaining pain free at 5 years.appropriate for elderly and for those with poor medicalconditionsRisks : numbness, paresthesia, and anesthesiadolorosa,corneal anesthesia [may develop after lesioning ofthe ophthalmic division]
  52. 52. Percutaneous radiofrequency thermocoagulation of the gasserian ganglionUnder fluoroscopic guidance, an insulated needle is passedthrough the foramen ovale next to the gasserian ganglionForamen ovale accessed under flouroscopyEnsure CSF flow…Needle advanced to petrous clivus junctionTest stimulus which will elicit the patients original neuralgicpainThermocoagulation
  53. 53. .
  54. 54. Percutaneous radiofrequency thermocoagulation of the gasserian ganglionA
  55. 55. Percutaneous microcompression of the gasserian ganglioninvolves passing a fine balloon catheter through the foramenovale.Inflation of the balloon produces an ischemic or mechanicaldestruction of cells in the ganglion.38associated with the highest risk for postoperative motortrigeminal weakness.the best choice for patients who have ophthalmic nerve painand who are not candidates for MVD
  56. 56. Gamma knife irradiation [NIHCE,U.K. APPROVED]radiation is aimed at the proximal nerve and root entry zonein the ponsgamma knife projects 201 very fine beams of gamma rays(generated by RA Cobalt) through the skull and brain.The dose of radiation along any one beam is too small toeffect any change by itselfbut when all 201 beams intersect, a very high dose ofradiation can be administered with little or no radiation tosurrounding tissue.41has been shown to affect abnormal ephaptic transmissionbut not normal axonal conduction
  57. 57. Glycerol injectionInjected behind the ganglion, which destroys small and largemyelinated and unmyelinated fibers.Under fluoroscopic guidance, glycerol is injected into thecistern of Meckles cave.OTHERS METHODS : Laser irradiation of the skin overlyingperipheral nerves with a heliium-neon laser
  58. 58. Weighing once more….Your Text here
  59. 59. Proparacaine eye dropsIs a local anesthetic agent that anesthetizes the eye andpossibly the nerves around it.It is shown that it can give short-term relief in someinstancesusually effective if the pain is in the distribution of theophthalmic division of the trigeminal nerve.almost certainly ineffective for classic trigeminal neuralgia.relatively harmless, but can damage the eye if usedextensivelySo it cannot be considered a long-term treatment.
  60. 60. Final words….patients with trigeminal neuralgia deserve an accurate anddispassionate explanation of the merits and drawbacks of allmethods of treatment from the outset.
  61. 61. References• Trigeminal neuralgia Pathophysiology and treatment A. JOFFROY, M. LEVIVIER and N. MASSAGER• Manish K Singh, MD; Chief Editor: Robert A Egan, MD[2012] Medscape• Pain Management: Trigeminal Neuralgia;Meraj N. Siddiqui, Hospital Physician;Turner White;2003• BMJ Luke Bennetto, Nikunj K Patel and Geraint Fuller ;2008• John tew, Mayfield Clinic Update,2012• review on the causes of trigeminal neuralgia symptomatic to other diseases florin popovici1, ROMANIAN JOURNAL OF NEUROLOGY – VOLUME X, NO. 2, 2011