Trigeminal neuralgia/TN/ NEURALGIA
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The International Association for the Study of Pain (IASP)1 defines trigeminal neuralgia (TN) as a sudden, usually unilateral, severe brief stabbing recurrent pain in one or more branches of the fifth cranial nerve synonyms Idiopathic trigeminal neuralgia / Tic Doulourex. Trifacial Neuralgia. Fothergell’s disease. In 1677 John Locke, a American physician and philosopher, accurately identified the major clinical features of TN In 1756 the French physician Nicolaus Andre coined the term “Tic douloureux” to the condition. The English physician John Fothergill in 1773 published detailed description of TN, since then, it has been referred to as ‘Fothergill’s disease’. Peripheral injections Long acting LA Alcohol Glycerol Peripheral neurectomy/ nerve avulsion Cryotherapy Gasserian ganglion procedures Percutaneous stereotactic radiofrequency thermal lesioning of the trigeminal ganglion and/or root (rfl) percutaneous glycerol gangliolysis of the trigeminal ganglion percutaneous balloon microcompression of the trigeminal ganglion Intracranial procedures MVD Partial sensory rhizotomy Gamma knife radiation to the trigeminal root entry zone GKR
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Trigeminal neuralgia/TN/ NEURALGIA
- 1. GOOD MORNING
- 3. Outline: 1. Introduction 2. History 3. Aetiology 4. Clinical feature 5. Diagnosis 6. Management 7. Summary 8. References
- 4. Introduction • The International Association for the Study of Pain (IASP)1 defines trigeminal neuralgia (TN) as a sudden, usually unilateral, severe brief stabbing recurrent pain in one or more branches of the fifth cranial nerve • synonyms Idiopathic trigeminal neuralgia / Tic Doulourex. Trifacial Neuralgia. Fothergell’s disease.
- 5. History • In 1677 John Locke, a American physician and philosopher, accurately identified the major clinical features of TN • In 1756 the French physician Nicolaus Andre coined the term “Tic douloureux” to the condition. • The English physician John Fothergill in 1773 published detailed description of TN, since then, it has been referred to as ‘Fothergill’s disease’.
- 6. Etiology and Pathogenesis • Condition known for centuries, but pathogenesis has remained ENIGMA • Vascular factors • transient ischemia, • autoimmune hypersensitivity • Mechanical factors: pressure from aneurysms of ICA →erode intra cranial fossa → pulsatile irritation of trigeminal ganglion → demyelenation → pain
- 7. Etiology • Anomaly of superior cerebellar artery: lies in contact with sensory root of trigeminal ganglion → anomaly → demyelenation • Dental etiology: Westrum and Black ,1976 differentiation from loss of teeth & degeneration of nerve → proceeds proximally to involve nucleus • Infections: various granulomatous & nongranulomatous infections invoving 5th nr
- 8. Etiology • Ratner’s jaw bone cavities (1979): Cavities in the alveolar and jaw bones are the causative factor. • Multiple sclerosis: Olfson (1966), sclerotic plaque located at root entry zone of TNr • Petrous ridge compression: Lee (1937),compression of nerve at dural foramen • Post traumatic neuralgia: traumatic neuromas following injury
- 9. ‘Ignition Hypothesis’ proposed by Devor et al • In this model, a trigeminal injury induces physiologic changes that result in a population of hyper excitable and functionally linked primary sensory neurons. • The discharge of any individual neuron in this group can quickly spread to activate the entire population. • Such a sudden synchronous discharge could underlie the sudden jolt of pain characteristic of a TN pain attack.
- 10. Etiology • Intracranial tumours: epidermoid tumors, meningiomas of cerebellopontine angle & meckel’s cave, arteriovenous malformations, aneurysms, vascular compressions & trigeminal neuromas may impinge on the nerve • Intracranial vascular abnormality: • Viral etiology: post herpetic neuralgia is seen in elderly patients. Viral lesions of the ganglion can be etiologic factor
- 11. General characteristics • Incidence: 4:1,00,000 • Occurs at middle age or later (5th or 6th decade) • Female predisposition (58%) • Predilection for RT side • V3 > V2 > V1
- 12. Clinical features Sudden, unilateral, intermittent paroxysmal, sharp, shooting, stabbing, lancinating, recurring pain, elicited by slight touching superficial “trigger points”. Pain radiates from that point, across the distribution of one more branches Pain usually confined to 1 branch
- 13. Clinical features • Rarely crosses the mid line • Pain is of short duration, lasts for few seconds • "tic douloureux" because of a characteristic muscle spasm that accompanies the pain.
- 14. Clinical features • Male patients avoid shaving, poor oral hygiene • Occasionally a cold breeze blowing on the face can be enough to initiate an attack. • Paroxysms occur in cycles, each cycle lasting for weeks or months • No attacks during sleep • Patients lead poor quality of life due to pain
- 15. Clinical features • The condition can lead to • Irritability • Severe anticipatory anxiety and Depression • Life-threatening malnutrition. • Suicidal depression is not uncommon
- 16. Trigger zones
- 17. Diagnosis White and Sweet - ‘‘Sweet criteria’’ • 1. The pain is paroxysmal. • 2. The pain may be provoked by light touch to the face (trigger zones). • 3. The pain is confined to the trigeminal distribution. • 4. The pain is unilateral. • 5. The clinical sensory examination is normal.
- 18. • International Classification of Headache Disorders II (ICHD-II) subdivides TN into • 1. Classic TN and 2. Symptomatic TN.
- 19. Classical trigeminal neuralgia: A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting one or more divisions of the trigeminal nerve and fulfilling criteria B and C: B. Pain has at least one of the following characteristics: 1. intense, sharp, superficial or stabbing 2. Precipitated from trigger areas or by trigger factors C. Attacks are stereotyped in the individual patient. D. There is no clinically evident neurological deficit. E. Not attributed to another disorder.
- 20. Symptomatic trigeminal neuralgia: A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, with or without persistence of aching between paroxysms, affecting one or more divisions of the trigeminal nerve and fulfilling criteria B and C B. Pain has at least one of the following characteristics: 1. Intense, sharp, superficial or stabbing 2. Precipitated from trigger areas or by trigger factors C. Attacks are stereotyped in the individual patient D. A causative lesion, other than vascular compression, has been demonstrated by special investigations and/or posterior fossa exploration.
- 21. Steps in Diagnosis • History • Diagnostic nerve block Material Required • 3–1 cc syringes • 3–25 gauge needles • Sterile normal saline • Two percent lignocaine without adr • Several alcohol wipes
- 22. Inject 0.5 cc of normal saline •psychogenic pain inject 0.5 ml of 2 percent lignocaine without adrenaline at surface site •Direct therapy at small nociceptor fibers. persists–inject little deeper •Musculoskeletal origin of pain. more proximal portionof nerve •direct therapy at site, when relief occurred. selective inferior alveolar, lingual, buccal, infraor bital, posterior superior alveolar blocks
- 23. Steps in Diagnosis • History • Diagnostic nerve block • Carbamazepine • MRI Material Required • 3–1 cc syringes • 3–25 gauge needles • Sterile normal saline • Two percent lignocaine without adr • Several alcohol wipes
- 27. Medicinal • Phenytoin was first introduced in 1942, and in 1962 carbamazepine became the most commonly used drug. • Baclophen may add to the effectiveness of these drugs. • Recently - Neurontin has been widely used because of reduced side effects, although is more expensive.
- 28. Blom (1962), showed a response to anticonvulsants
- 29. Carbamazepine (Tegretol) • Dose- initial- 100mg bid Maintainance- 1200 -2400mg • Drug dosage should be taken at night, so that adequate serum concentration can be present in early morning, when pain most occurs. • Side effects: Visual blurring, dizziness, somnolence, skin rashes and ataxia and in rare cases hepatic dysfunction, leukopenia, thrombocytopenia— aplastic anemia (It is known to suppress the bone marrow. Patients should be monitored to avoid agranulocytosis). Whenever the side effects appear, a reduction of 200 mg of drug will often eliminate them. Once the pain remission has been achieved, the drug dose should be kept at maintenance level or withdrawn and restarted if symptoms appear.
- 30. Oxcarbazepine • Dose- initial-300mg Maintainance-1200 mg/day. • Side effects: Hypona tremia, double vision.
- 31. Clonazepam • Dose- initial- 0.5mg maintainance- 4 mg max 20mg • Side effects: Drowsiness, fatigue, lethargy.
- 32. Phenytoin • Dose—100 mg three times a day. • Side effects: nystagmus, ataxia, dysarthria, ophthalmoplegia (paralysis of eye movements) as well as drowsiness and mental confusion. • Gingival hyperplasia (enlargement of the gums in the mouth) and hypertrichosis (excessive hair growth).
- 33. Valproic acid • Dose—600 mg/day. • Side effects: irritability, tremors, confusion, hepatoxicity, weight gain.
- 34. Baclofen (Lioresal) • Dose- initial-5mg tds Maintainence- 80 mg max • One tenth of sufferers cannot tolerate baclophen. • Should not be discontinued abruptly after prolonged use because hallucinations or seizures may occur. • Side effects: drowsiness, dizziness, nausea and leg weakness.
- 35. Gabapentin • An anti-epileptic drug that is structurally related to the neurotransmitter GABA. • This drug is almost as effective as carbamazepine but involves fewer side effects. • The starting dose is usually 300mg three times a day and this is increased to a maximal dose.
- 36. Multiple drug therapy • AED therapy routinely begins with a single agent, given in gradually increasing doses until pain attacks are either suppressed or satisfactorily reduced. • When a patient only partially responds to single drug therapy at dosages that evoke side effects, adding a second AED may enhance the therapeutic response. • Because AEDs have differing mechanisms of action as well as differing side effect patterns, combining agents is a reasonable approach.
- 37. Treatment of Acute Exacerbations • Peripheral local anesthetic block • Intravenous lidocaine. • Intravenous AED Role of Analgesic medication Ineffective in TN
- 38. Surgical managements • Peripheral injections • Long acting LA • Alcohol • Glycerol • Peripheral neurectomy/ nerve avulsion • Cryotherapy
- 39. Surgical managements • Gasserian ganglion procedures • Percutaneous stereotactic radiofrequency thermal lesioning of the trigeminal ganglion and/or root (rfl) • percutaneous glycerol gangliolysis of the trigeminal ganglion • percutaneous balloon microcompression of the trigeminal ganglion • Intracranial procedures • MVD • Partial sensory rhizotomy • Gamma knife radiation to the trigeminal root entry zone GKR
- 40. Other procedure • TENS • Deep brain stimulation • Biofeedback • Hypnosis/ Autosuggestion • Psychiatric counselling
- 41. PERIPHERAL INJECTIONS • Produces anesthesia in the trigger zones • Care should be taken to avoid IV injections • Very effective in relieving pain
- 42. Long acting anesthetic agents • Emergency pain relieving technique • Injected proximally to nerve site • Pain free period will be very short
- 43. Alcohol injections • 95% alchohol injectionproduces anesthesia of the region • May cause local tissue toxicity inflammation and fibrosis. • It may also cause alcohol neuritis. • Pain relief for 6-12 months may be seen.
- 44. Peripheral neurectomy • Carried out under GA • Most effective pain peripheral nerve destructive technique. • Pain may return after amputed nerve stump regenerates . • Done in patients where craniotomy contraindicated due to age , systemic diseases.
- 45. Infra orbital neurectomy • 1) conventional • 2)brauns trans antral
- 46. Intra oral approach • U – shaped caldwell luc incision is made • Infra-orbital foramen located. • The nerve is located and avulsed from the skin surface. • The foramen may be plugged with poly ethylene plug.
- 47. Brauns trans-antral approach • An intra oral incision is made from the maxillary tubarosity to the midline of vestibule. • Mucoperiosteal flap is reflected to anterior and lateral maxillary wall. • A 3 cm window is created, the lining of the posterior superior portion of the antrum is carefully exised..
- 48. • Complications (i) inadvertent section of the vessels in the pterygopalatine fossa • (ii) inadvertent sectioning of the branches of the sphenopalatine ganglion entering the posterior aspect of the ganglion.
- 49. THANK YOU
- 56. Inferior alveolar neurectomy • 1) extra oral approach • 2) intra oral approach ( Ginwllas incision )
- 57. Extra-oral approach • Risdons incision,where after reflection of masseter , a bony window is created in Outer cortex and nerve is reflected with nerve hook and is avulsed from its superior attatchment. • mental nerve is avulsed anteriorly through the same approach
- 58. Intra-oral apprroach • Dr GINWALLAS incision.: incision is made along anterior border of ascending ramus, extending lingualy and buccaly in a fork like an inverted “Y”. • The incision is deepend on the medial aspect of ascending ramus . • Temporal and medial pterygoid muscles are split and INFERIOR ALVEOLAR NERVE IS LOCATED.
- 59. Lingual neurectomy • A vertical incision is made at the inner border of the ascending ramus, extending from the coronoid process down the level of the floor of the mouth. • nerve lies even more superficially and it can be easily found between the anterior pillar of the fauces at the root of the tongue. • After dissection, the nerve is grasped with a hemostat and is then either avulsed or cauterized and cut.
- 60. Cryotherapy temperature colder than -60° centigrade. Produce wallerian degeneration. Nitrous oxide cryo probe is used .
- 61. THERMOCOAGULATION • PERIPHERAL RADIOFREQUENCY NEUROLYSIS • GREGG AND SMALL in 1986 • 65° centigrade for 1-2 min. • 20% recurrence rate is there. • Used in elderly patients
- 62. Gasserian ganglion procedures • Glycerol injection • Controlled radio frequency thermocoagulation • Balloon compression
- 63. • 1900, first open surgeries done on gasserian ganglion for trigeminal neuralgia. • 1910, harris , hartel introduced approaches to ganglion via foramen ovale. • 1931, kirschner introduced percutaneous electrocoagulation of gasserian ganglion.
- 64. Radio frequency thermocoagulation • Percutaneous radiofrequency thermal lesioning of the trigeminal nerve was repopularized by Sweet and Wepsic in 1974 • It preserves motor function of trigeminal nerve. • Lower recurrence rate • well tolerated by elderly and medically compromised patients.
- 65. • Principle- This technique is based on the findings that the compound action potentials of nociceptive fibers (A-d and C fibers) in nerves are blocked at lower temperatures than those of larger A-a and A-b fibers carrying tactile sensations.
- 67. • A ALTERNATING CURRENT OF HIGH FREQUENCY CAUSES IONISATION OF BIOLOGICAL TISSUES . WHICH FURTHER LEADS TO COAGULATION OF TISSUES.
- 68. Percutaneous glycerol chemoneurolysis • Percutaneous chemoneurolysis with glycerol was introduced in 1981 by Hakanson. • Glycerol, a mild neurolytic, provides excellent pain relief while largely sparing trigeminal nerve function in most patients. • pure anhydrous (99.5%) glycerol is instilled into the trigeminal cistern.
- 69. Balloon compression • Percutaneous balloon compression of the gasserian ganglion with a balloon catheter was introduced by Mullan and Lichtor in 1983 • a technique to traumatize the trigeminal ganglion and preganglionic rootlets mechanically using a percutaneously inserted balloon-tipped catheter. • It is then inflated using a radiopaque contrast agent to a predetermined pressure to compress the neural structures. • 1.3 – 1.5 atm pressure.
- 70. OPEN PROCEDURS • MICROVASCULAR DECOMPRESSION OF THE SENSORY ROOT • Popularized by jannetta in 1967 • Open craniotomy approach is used to gain access to the trigeminal root entry zone and adjacent brain stem. • Most commonly performed intra cranial procedure done to decompress superior ceribellar artery has mortality rate of 2%
- 71. TRIGEMINAL ROOT SECTION • Extradural sensory root section(fraziers approach1901) • Intra dural root section – discribed by wilkins in1966 • less chances of damage to sup petrosal n. and facial n. • Can cause damage to 5,7,8 cranial nerves.
- 72. • Trigeminal tract totomy or medullary tract totomy – done at the cervico medullary junction • Very useful in patients with glossopharyngeal and pharyngeal pain distribution • Causes loss of pain and temperature sensation in ipsilateral face and pharynx.
- 73. Gamma knife radiation to the trigeminal root entry zone GKR • Relatively recent procedure, that employs computerized stereotactic methods to concentrate gamma radiation on the trigeminal root entry zone. • It has gained wide acceptance, however long term results of GKR in TN remain to be established. Advocated in old, frail patients.
- 74. Summary • An early and accurate diagnosis of TN is important. • Patients with TN are usually initially treated pharmacologically. • The best treatment for the patient depends on the age of the patient, medical comorbidities, and the risks the patient is willing to assume.
- 75. Summary • Surgical approaches • MVD • PSR
- 76. Summary • Three percutaneous ablative procedures • GKS • Partial sectioning of the trigeminal nerve
- 77. Summary • Peripheral procedures • stereotactic radiosurgery
- 78. References 1. Toda K. Operative treatment of trigeminal neuralgia: review of current techniques. Oral Pathol Oral Radiol Endod 2008;106:788-805. 2. Scrivani SJ, Mathews SE, Maciewicz RJ. Trigeminal neuralgia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:527-38. 3. Liu JK, Apfelbaum RI. Treatment of trigeminal neuralgia. Neurosurg Clin N Am 2004;15: 319–334 4. Textbook of oral and maxillofacial surgery by Neelima malik.
- 79. THANK YOU
Hinweis der Redaktion
- It is a truly agonizing condition, in which patient may clutch the hand over the face and experience severe, lancinating pain associated with spasmodic contractions of the facial muscles during attacks—a feature that led to the use of the term (its archaic name) ‘Tic Douloureux’ (painful jerking)
- Trigeminal neuralgia is not a specific disease , but a symptom ellicited by pathology of 5th cranial nerve. Lloyd, etal JOMSI 1992 ; 58;621-628
- The cause of this disease process is unknown it is usually idiopathic. However , the fact that benign tumors and vascular anomalies that compress the TN root can produce symptoms clinically indistinguishable from classical tn strongly implies that injury to the nerve root is an imp initiating factor in this ds
- based on the morphologic and physiologic changes following partial nerve injury,
- The condition may begin at any age, although it tends to occur more frequently with advancing age and it afflicts women somewhat more often than men.
- During attack, patient grimaces with pain, clutches his hands over the affected side, stops all activities, rubs his face, which may redden or the eyes may water.
- Patients may experience many attacks daily and, although they are pain-free between attacks, they live in fear of impending pain. Despite their repeated occurrence, the painful spasms occur infrequently at night, and periods of spontaneous remission are common.
- Trigger zones: A TN ‘‘trigger zone’’ is an area of facial skin or oral mucosa where low-intensity mechanical stimulation (such as light touch, an air puff, or even hair-bending) can elicit a typical pain attack. TN trigger zones are typically only a few millimeters in size and are nearly exclusively found in the perioral region.
- An accurate history is paramount for proper diagnosis, because physical findings are minimal or absent; few syndromes are as consistent and no other condition has this Diagnosis is made from well taken history White and Sweet made a significant contribution by articulating precise diagnostic criteria for TN.
- Classic TN is the most common idiopathic form of the disorder (although it also includes cases associated with vascular compression). Symptomatic TN has the same key features of TN but results from another disease process (such as multiple sclerosis or a cerebellopontine angle tumor).
- A detailed intraoral examination of the dentition, oral cavity, oropharynx, salivary glands, and associated oral structures should be performed to rule out any odontogenic or nonodontogenic source for the pain • Always begin injections at surface site of pain and then move proximally. For example, if the pain is perceived in the lower lip, then inject lower lip, then mental nerve and then inferior alveolar nerve.
- • Inject 0.5 cc of normal saline at test site. Wait for 5 minutes. If pain is relieved, then psychogenic pain is likely. • If the pain persists, then inject 0.5 ml of 2 percent lignocaine without adrenaline at surface site and wait for 5 minutes. If pain is relieved, then direct therapy at small nociceptor fibers. • If the pain persists–inject little deeper and wait for 5 minutes. If pain is relieved, then consider musculoskeletal origin of pain. • If pain is not relieved, inject at more proximal portion of nerve—If pain is relieved, direct therapy at site, when relief occurred. • Thus, selective inferior alveolar, lingual, buccal, infraor bital, posterior superior alveolar blocks can be given to know the involvement of the branch of the trigeminal nerve.
- Carbamazepine is highly specific in only relieving pain of TN and not any other type of facial pain. It has, therefore, suggested that its response can be used as a diagnostic indicator. Carbamazepine MRI
- Mathews and Scrivani40 have proposed a simple algorithm for the differential diagnosis and management of TN
- Today trigeminal neuralgia is usually treated with drugs called anti-convulsants, Modification of the Paroxysmal Pain at Cortical Level which include Bourguignon (1942), used anticonvulsant phenytoin to effectively control attacks of pain in TN. Blom (1962), showed a response to anticonvulsants Anti-convulsants are thought to reduce TN attacks by decreasing the hyperactivity of the trigeminal nerve nucleus in the brain stem
- Today trigeminal neuralgia is usually treated with drugs called anti-convulsants, Modification of the Paroxysmal Pain at Cortical Level which include Bourguignon (1942), used anticonvulsant phenytoin to effectively control attacks of pain in TN. Blom (1962), showed a response to anticonvulsants
- Anti-convulsants are thought to reduce TN attacks by decreasing the hyperactivity of the trigeminal nerve nucleus in the brain stem. Treatment - initiated with one drug such as Tegretol or Neurontin. The dose is increased as needed and tolerated. If any single drug proves ineffective, alternative drugs may be tried alone or in combination with other drugs. Medical therapy is initially effective for most patients with TN. Surgical treatments are then considered.
- Currently, carbamazepine is the initial drug of choice for the management of trigeminal neuralgia [26–28] because it controls the pain in approximately 90% of patients 100 mg twice daily with meals, increasing by 100 mg every other day until pain control is achieved or toxicity develops. The gradual increase in dosage allows many patients to tolerate large doses of this medication. Response to medication and clinical side effects are the most useful dosing indicators; blood levels do not correlate well with clinical response. Twenty percent to 40% of patients treated with carbamazepine experience drug-related side effects, The most common idiosyncratic side effects are hematologic, including neutropenia, thrombocytopenia, and, rarely, aplastic anemia A baseline complete blood cell count and liver and renal function tests should be obtained before initiating carbamazepine therapy. These studies should be repeated at 2-week intervals initially and then periodically thereafter. Carbamazepine should be discontinued if the peripheral white blood cell count drops below 3000 cells/lL or if side effects become intolerable.
- Oxcarbazepine, a derivative of carbamazepine, is a newer drug that is reported to have similar clinical effectiveness but fewer side effects than carbamazepine [29,30]. Because there are fewer side effects, higher doses of oxcarbazepine are often tolerated. Patients with trigeminal neuralgia refractory to carbamazepine have demonstrated a good response when they were switched to oxcarbazepine.
- Clonazepam, a benzodiazepine derivative, has been used in the treatment of trigeminal neuralgia since 1975 [19]. clinical efficacy in 60% to 70% of patients with trigeminal neuralgia [17,18]. A typical maintenance dose of clonazepam for trigeminal neuralgia is 6 to 8 mg/d. S sedation, which is the major dose-related side effect, limits its usefulness
- Phenytoin may also be administered intravenously to treat severe exacerbations of TN. Less effective than carbamazepine, may be useful in many patients because it has lower toxicity [31]. Patients who have obtained effective pain relief while on carbamazepine but can no longer tolerate it seem to be the best candidates for phenytoin. Can be used in conjunction with carbamazepine. Plasma levels are useful for dosage regulation and to avoid toxicity. Because only 25% to 60% of patients achieve satisfactory control [31 A morbilliform rash can commonly occur.
- Baclofen, a gamma-aminobutyric acid (GABA) agonist, has some efficacy in the treatment of trigeminal neuralgia [24,25,32]. There seems to be a synergism between baclofen and either carbamazepine or phenytoin; therefore, combination therapy in specific cases is a reasonable option [33]. The initial dose is 10 mg three times daily. The dose should be increased incrementally until pain relief is achieved or toxicity is encountered. Baclofen is typically well tolerated and does not have the potentially life-threatening side effects of carbamazepine or phenytoin.
- Gabapentin (Neurontin) has apparently been widely promoted for the treatment of trigeminal neuralgia, its effectiveness in classical trigeminal neuralgia is low, probably less than 10%. It is more useful for deinnervation and dysesthetic pain syndromes.
- Peripheral local anesthetic block. Many clinicians find that a standard local block that anesthetizes the facial region containing the trigger often results in an immediate reduction in TN attacks. The local anesthetic block frequently allows the patient to talk and provides a practical way for the clinician to get a full history before making decisions regarding definitive treatment. Local anesthetic blocks have also been reported to potentially eliminate the bouts of pain for prolonged periods of time, outlasting the duration of the particular anesthetic agent utilized Intravenous lidocaine. A standard loading dose of 100 mg infused at 20 mg/min has few contraindications, and rapidly provides a therapeutic blood level associated with symptomatic relief. This effect is relatively transient, however, because the drug redistributes in tissue. Although often highly effective, intravenous infusions of lidocaine carry additional risks. These treatments should be administered only where monitoring and emergency care are available. Intravenous AED. initial treatment with a parenteral ‘‘loading’’ dose of an AED. Intravenous drug therapy also should be administered only where monitoring and emergency care are available. Analgesic medication. Patients with unrelieved TN pain attacks are frequently given opioid and nonopioid analgesics as part of the therapeutic regimen. These medications are largely ineffective in TN, given the nature and quality of pain attacks. The present authors believe standard analgesics should be avoided in this patient group.
- It has got the potential to have sound treatment for intractable V2 neuralgia, because of the direct access and visualization it provides. Careful dissection is now performed to expose the descending palatine branches of V2, which are then traced superiorly to the sphenopalatine ganglion In order to provide anatomical verification, the infraorbital nerve is identified in the roof of the maxillary sinus and is carefully followed posteriorly to the trunk of V2 near the sphenopalatine ganglion. Dissection is then completed by isolating and identifying the trunk of V2 superiorly and posteriorly to the sphenopalatine ganglion. The trunk of the maxillary nerve (V2) is then sectioned posterior to the sphenopalatine ganglion near the foramen rotundum and close to the inferior orbital fissure
- or the vidian nerve
- Fig. 1. Coronal Tl-weighted MRI shows round trigeminal nerve (arrows) at the root entry zone with signal similar to the surrounding brain tissue. There is no significant lesion or vascular contact or compression in this patient. (P, pons; T, temporal lobe; I, interpenduncular cistern; and Th, third ventricle.)
- Fig. 2. Patient is 60-year-old women with MS for more than 10 years and new onset of trigeminal neuralgia. T2- weighted MRI shows hyperintense lesions (arrows), consistent with MS plaques, scattered throughout the white matter. (L, lateral ventricle.)
- Fig. 3. Patient is 74-year-old women with left trigeminal neuralgia in the distribution of V2. Tl-weighted coronal (A) and axial (B) images with contrast show the left pons and the preganglionic segment are compressed by a meningioma (arrows) arising from the surface of the left tentorium cerebelli. Removal of the tumor relieved pain. (L, lateral ventricle; Th, third ventricle; P, pons; SS, sphenoid sinus; I, internal carotid artery; T, temporal lobe; A, aqueduct.)
- Fig. 4. Patient is 37-year-old woman with trigeminal neuralgia involving V2 and V3. T 1-weighted coronal (A) and axial (B) images show an extraaxial lobulated mass (M) (epidermoid tumor) in the left cerebellar pontine cistern compressing the trigeminal nerve and pons (arrow). Removal of the tumor relieved pain. (Th, third ventricle; P, pons; SS, sphenoid sinus; T, temporal lobe.)
- Fig. 5. Coronal T 1-weighted without gadolinium (A), with gadolinium (B), and axial T 1-weighted with gadolinium ((2) images show vessel contact (arrows) the left trigeminal nerve. The vessel enhancement with contrast (gadolinium) help to identify the vascular contact. (P, pons, T, temporal lobe.)
- Fig. 6. Dolichoectatic basilar artery (arrow heads) causing compression and displacement of the right preganglionic segment the trigeminal nerve (arrow). (L, lateral ventricle; Th, third ventricle; P, pons; T, temporal lobe.)
- Two heavy black linen threads are then looped around the nerve using nerve hook and then divided between the 2 threads. This is done as high as possible and the upper end is cauterized, while dividing and lower end is held with the hemostat. Another linear incision is made in the buccal vestibule overlying the mental foramen. A mucoperiosteal flap is reflected to expose the mental nerve. It is then tied with heavy black linen just little away from the foramen. The nerve is then caught with the hemostat distal to the knot and is divided between the two. The distal part held between the hemostat and is wound around it and the peripheral branches entering the mucosa are avulsed out. There is puckering of the skin surface seen during this procedure. Now after the mental nerve is freed, then at the mandibular foramen, the distal part of the nerve which is held with the hemostat is pulled until the entire nerve length of the canal is avulsed out. If any obstruction is encountered, a window may be made in the buccal cortex posterior to the mental foramen, along the level of the inferior alveolar canal and the nerve is lifted out of the canal through the window. The wound is closed with interrupted sutures.
- the dissection is continued downwards until the lingual nerve comes into view at the border of the medial pterygoid muscle. In the region of the floor of the mouth, the The wound is closed with interrupted sutures.
- Direct applications of cryotherapy probe at temperatures colder than –60ºC are known to produce Wallerian degeneration without destroying the nerve sheath itself. For this procedure the nerve is exposed as described in peripheral neurectomy procedure and is frozen with a cryoprobe (Nitrous oxide probe) for a period of 1 to 2 minutes followed by 3 minutes thaw, to be repeated three times. The pain remission follows the procedure. But regeneration of axons is expected. But the procedure is relatively simple.
- A radiofrequency electrode that has the capacity to definitely destroy the pain fibers is used in this procedure. RF neurolysis has been shown to induce pain remission in 80 percent of cases with a 20 percent/year recurrence rate. Topical anesthesia with mild sedation is used. The patient is grounded in an electronic circuit and the 22 gauge lesion probe is positioned adjacent to nerve to be lesioned. Paresthesias are elicited to ensure proximity to the nerve and tissue temperature is measured with the probe tip through the probe thermocouple. Lesioning is then carried out at 65 to 75ºC for 1 to 2 minutes. Repositioning may be required to ensure adequate RF wave effect on the nerve fibers. Advantages: Low morbidity in high risk/elderly patients. Disadvantages: Needs specific electronic armamen tarium and reasonable patient cooperation.
- Modificn of electro 22 guage probe is used .30-90 sec duration 65-75 degree current is passed
- Operative room with radiology suite Short acting sedative Along with neuroleptic fentanyl with domperodone The patient is placed in the supine position. Using the Hartel technique [52], a standard 100- mm length 18- to 20-gauge needle or cannula with a stylet is inserted in the cheek approximately 2.5 cm lateral to the oral commissure and through the foramen ovale under fluoroscopic guidance Medial side of foramen
- Guide lines on the patient’s face help to orient the needle close to the foramen ovale. The entry site is 2.5 to 3 mm lateral to the corner of the mouth. Two guide lines through this point are drawn, one to a point one third of the way from the external auditory canal to the lateral canthus of the eye and another toward the medial side of the iris of the eye. A needle kept perpendicular to both of these lines will arrive at the skull base in close proximity to the foramen ovale. Final placement through the medial end of the foramen is performed using a fluoroscope Fluoroscopic view of a right-sided percutaneous approach to the foramen ovale. The patient’s neck is hyperextended, and the head is rotated to the contralateral side about 15( to 20 Stylet removed Radioectrode inserted along with thermocouple Current
- Stylet removed 25 watts 40-45 volts current 120-140mA is used .
- It is not known whether the glycerol works by direct chemical action or by hyperosmotic damage to the nerve Needle puncture. Canula is left insitu Pt is transfer to hospital bed and glycerol is injected Pt is instructed to be in sitting position for 2 hr Most pt relieved pain if pain persist more than 7 days procedur is repeated
- 14 gause needle is used Placed ext end of fpramen ovale Priciple- technique is based on the observation that mechanical trauma could relieve the pain of trigeminal neuralgia, often for a significant period. effective for first-division trigeminal neuralgia because of its low risk of corneal anesthesia and because unmyelinated fibers that control the corneal reflex are not injured by compression. It is less likely to cause corneal anesthesia because it does not selectively impair A-d and C fibers, as does the radiofrequency thermocoagulation technique.
- This operation is based on the observation made by Dandy that the cause of trigeminal neuralgia is compression of the trigeminal nerve at its root entry zone adjacent to the brain stem The usual cause aberrantly located and elongated arterial loop; . This approach allows dissection at the root entry zone of the trigeminal nerve and displacement of the offending vascular structure, usually by the insertion of a small synthetic sponge prosthesis interposed between the nerve and artery.
- , because therapeutic interventions can reduce or eliminate pain attacks in the large majority of TN patients. no strict rules are set and each patient should be evaluated individually.
- Surgical approaches are performed when medication cannot control pain, patients cannot tolerate the adverse effects of the medication, or in medically complex patients with polypharmacy for other conditions. MVD is generally performed when the patient is healthy and relatively young. PSR is performed in addition to or in place of MVD, in whom posterior fossa exploration fails to reveal significant compression of the trigeminal sensory root or in whom MVD is technically infeasible.
- Three percutaneous ablative procedures (radiofrequency thermocoagulation, glycerol gangliolysis, and balloon microcompression) and GKS are also performed in cases where MVD cannot be performed. Gsk is inf to mvd and……, but superior in terms of infrequency of technical failure and incidence of complications. Partial sectioning of the trigeminal nerve may be considered in patients who have negative explorations during a microvascular decompression or when other less invasive procedures have failed to provide adequate relief.
- Peripheral procedures (cryotherapy, peripheral neurectomy, glycerol injection, and peripheral alcohol block) are usually performed in patients not suitable for or not wishing to have other procedures. Although their pain free period is relatively short and recurrence rates are relatively high, they have a low morbidity; however. The role of stereotactic radiosurgery in the treatment of trigeminal neuralgia will be better defined in the future.