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CASE REPORT
Year : 2018  |  Volume : 45  |  Issue : 2  |  Page : 102-105

Trigeminal neuralgia - microvascular decompression by teflon patch


1 Department of Neurosurgery, KLE'S JN Medical College, Belgaum, Karnataka, India
2 Department of Otorhinolaryngology, KLE'S JN Medical College, Belgaum, Karnataka, India

Date of Web Publication10-Dec-2018

Correspondence Address:
Ravi Ichalakaranji
Department of Neurosurgery, KLE'S JN Medical College, Belgaum, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jss.JSS_47_18

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  Abstract 


According to the international headache society (IHS), trigeminal neuralgia (TN) is a disorder characterized by recurrent unilateral brief, shock-like pain abrupt in onset and termination, limited to the distribution of one or more divisions of the trigeminal nerve. Peak incidence is between the ages of 50 and 60 years, more common in women. Patients with TN are best managed by coordinated multidisciplinary approach (medical and surgical management). Early surgery helps the patient to have a better quality of life rather than waiting with the medical therapy alone. Here we present a case of an old aged male patient with h/o right side facial pain in V1 and V2 distribution, diagnosed with trigeminal neuralgia, and was on prolonged drug therapy for the same with no signs of improvement. We subjected the patient for Microvascular decompression after confirming the vascular loop compressing the ipsilateral trigeminal nerve. Patient showed improvement with symptom free interval subsequently.

Keywords: Microvascular decompression, Teflon patch, trigeminal neuralgia


How to cite this article:
Shenoy R, Ichalakaranji R, Mahantashetti P, Soni S. Trigeminal neuralgia - microvascular decompression by teflon patch. J Sci Soc 2018;45:102-5

How to cite this URL:
Shenoy R, Ichalakaranji R, Mahantashetti P, Soni S. Trigeminal neuralgia - microvascular decompression by teflon patch. J Sci Soc [serial online] 2018 [cited 2019 Jul 17];45:102-5. Available from: http://www.jscisociety.com/text.asp?2018/45/2/102/247158




  Introduction Top


According to the international headache society (IHS), trigeminal neuralgia (TN) is a disorder characterized by recurrent unilateral brief, shock-like pain abrupt in onset and termination, limited to the distribution of one or more divisions of the trigeminal nerve. In the United States, the annual incidence of TN is 5.9/100,000 women and 3.4/100,000 men.[1]

Peak incidence is between the ages of 50 and 60 years, more common in women. Patients with TN are best managed by coordinated multidisciplinary approach (medical and surgical management).

Early surgery helps the patient to have a better quality of life rather than waiting with the medical therapy alone.


  Case Report Top


A 73-year-old male patient presented to us with h/o right side facial pain in V1 and V2 distribution, shock-like sensation triggered by chewing of food, and allodynia over the right face for 2 years which was gradual and progressive type. The patient consulted the physician and was prescribed carbamazepine initially and later added with pregabalin and nortriptyline for nonsubsidence of pain. The patient is on these drugs for 2 years but still having persistent pain and for the same patient was referred to us.

On examination

The patient conscious oriented, wincing with pain over the right face.

Sensory examination - hypersensitivity over the distribution of the right V1 and V2 corneal reflex decreased on the right side. Other lower cranial nerves were within normal limit.

Magnetic resonance imaging (MRI) brain with constructive interference steady state (CISS) three-dimensional (3D) images was taken which showed vascular compression over trigeminal nerve [Figure 1].
Figure 1: CISS three-dimensional images showing vascular compression over trigeminal nerve

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Neurosurgical intervention, that is, microvascular decompression (MVD) was planned for this patient since the symptoms were refractory to medical therapy and had worsening symptoms.

Standard right side suboccipital retromastoid approach was done after placing the patient in the left lateral position with head held with Mayfield pin and burr hole placed at the asterion and craniectomy done. Dura mater was opened, and cerebellum retracted gently exposing brainstem and cranial nerves V, VII, and VIII. Superior cerebellar artery in the posterosuperior and superior petrosal vein in the anterior were noted by compressing the trigeminal nerve. Gentle arachnoid dissection was done with skeletonizing the nerve and the vessels. Tiny piece of Teflon patch was placed in between the vessel and the nerve. Hemostasis was achieved followed by closure done [Figure 2] and [Figure 3].
Figure 2: Intraoperative image showing superior cerebellar artery and superior petrosal vein compressing over trigeminal nerve

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Figure 3: Intraoperative images showing Teflon patch and trigeminal nerve

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Postoperatively, the patient recovered well subsequently with significant reduction of pain and with no deficits.

The patient was on regular follow-up for 6 months with symptom-free interval.


  Discussion Top


According to the headache classification committee of the IHS, TN is a disorder characterized by recurrent unilateral brief, electric, shock-like pains, abrupt in onset and termination, and limited to the distribution of one or more divisions of the trigeminal nerve, often triggered by innocuous trigeminal tactile stimuli.[2]

It may develop without apparent cause (classic or typical TN) or may be a result of another diagnosed disorder (secondary or symptomatic TN).[3],[4],[5] Other diagnosed disorders that can lead to secondary TN include intrinsic brainstem pathology with trigeminal nerve, nuclei, or tract involvement (e.g., multiple sclerosis [MS] or lacunar infarction), or extrinsic cerebellopontine angle pathology (e.g., neoplasms, benign or malignant or nonneoplastic cysts such as epidermoid, dermoid, or arachnoid cysts, or vascular lesions such as aneurysms or arteriovenous malformations).

In the majority of patients with classic TN, the pain is generated because of the compression of the trigeminal nerve at the root entry zone (point in the proximal nerve root central oligodendrocyte myelin persists and has not yet given way to peripheral Schwann cell myelin). The plaques of demyelination that occurs lead to hyperexcitability of exposed and potentially injured afferents, which results in after discharges large enough to cause a nonnociceptive signal being perceived as pain.[6] At present, the most widely accepted theory to explain TN is the one proposed by Devor et al., the ignition theory.[7] It is likely that both the central nervous system and nerve root changes occur over time, which would account for why not all patients get permanent relief after relief of vascular compression of the nerve root.

There may also be genetic and/or myelin biologic predispositions, given that rare reports of genetic and familial associations do exist.[8]

The major risk factor for TN is MS.[9] Despite this risk factor, <5% of patients with unilateral TN will be found to have MS. Conversely, <2% of patients with MS will eventually develop TN, and in approximately 85% of patients, the diagnosis of MS will already have been made based on the basis of other symptoms, imaging, or laboratory findings before TN develops.[10] TN is a characteristic pain in the distribution of one or more branches of the fifth cranial nerve. In the majority of cases, the pain begins in the second or third divisions of the trigeminal nerve (V2 and V3, respectively). With time, it can spread to other divisions including the first division (V1). However, TN involves V1 in isolation in only 5% of cases.[9]

The diagnosis is made on the history alone, based on characteristic features of the pain.[2] It occurs in sudden paroxysms, with each pain lasting a few seconds to several minutes. The pain is usually described as sharp, stabbing, electric, or shock like. It characteristically resolves as suddenly as it started. Between paroxysms, the person is asymptomatic. Typically, the pain can be triggered by light touch on any area innervated by the trigeminal nerve, including such things as wind, chewing, talking, washing the face, applying or removing makeup, shaving, or cleaning the teeth.

Diagnosis

TN is a purely clinical diagnosis; there is no confirmatory laboratory or imaging study for this disease. However, there are electrophysiologic and imaging studies that may be useful as an adjunct to clinical acumen. Trigeminal-evoked potentials and electrophysiologic studies are not widely used but are complementary diagnostic tools.[11],[12] MRI and magnetic resonance angiography processed as 3D images have been used to verify vascular compression and other causes for secondary TN.[13]

Treatment

Carbamazepine is considered the most proven, the first-line treatment for TN. Oxcarbazepine has also been shown to be effective for treating patients with TN.[6]

Although gabapentin has been shown to be effective in treating some neuropathic pain conditions, particularly MS, evidence for its use in TN is weak.[14]

Baclofen is also used for patients with TN, despite very weak evidence in the literature supporting its use.[6] Consensus suggests that it may be useful in people with MS who develop TN.

Lamotrigine is also used for patients with TN, despite very weak evidence in the literature supporting its use. Consensus suggests that it may be useful in people who cannot tolerate or are allergic to carbamazepine, or as an add-on agent augmenting either carbamazepine or oxcarbazepine as their effectiveness wains.[6]

Patients with TN are best managed by a coordinated multidisciplinary approach. This approach includes early referral to a surgeon experienced and skilled in TN surgery for initial consultation and counseling.

Surgery is generally offered to patients who fail medical treatment, has only partial relief of pain after 1 year; MVD remains the surgical option of choice for TN, with percutaneous procedures generally reserved for patients who experience recurrent pain after MVD or is a high surgical risk owing to medical comorbidity. Percutaneous procedures are usually offered to patients with MS.[10] MVD was first performed by W. James Gardner in 1959, who described mobilizing a vessel from the trigeminal nerve and placing a piece of absorbable gelatin sponge (Gelfoam) between them without any intentional damage to the nerve itself. Various materials such as muscle patch, fascia, and, nowadays, Teflon patch are more commonly used. Multiple investigators have found MVD to be an effective treatment for TN. In one study of 1204 patients, 75% had complete relief and 9% had partial relief after 1 year. After 10 years, 64% had complete relief and 4% had partial relief. The annual rate of recurrence was <2% by 5 years and <1% by 10 years.[7] Although initial results are similar, MVD offers a much higher likelihood than destructive procedures for a long-term cure. In one study comparing 378 MVD recipients with 316 radiofrequency (RF) rhizotomy recipients over 20 years, patients undergoing RF rhizotomy had a 75% chance of pain recurrence in the first 5 years. By contrast, 63% of patients undergoing MVD were pain free at 20 years.[15]

Neuroendoscopic microvascular decompression

It was first described in 2001 by Eby et al. The endoscope offers a very good panoramic visualization and illumination. Multiple groups have demonstrated that endoscope-assisted approaches (where the bulk of the procedure is done with the operating microscope but an endoscope is used to inspect the nerve before or after decompression) lead to increasing identification of vascular contact and compression, which were not appreciated with microscopy alone. One of the putative advantages of the endoscope as compared with the microscope is that hidden compression may be more easily identified. Indeed, Teo et al. reported that in their series of endoscope-assisted MVDs, they identified vascular compression in all patients with the aid of the endoscope. They report that in 8% of the cases no vessel was identified with the microscope but was identified with the endoscope.

Radiofrequency rhizotomy

RF rhizotomy was popularized by Sweet and Wepsic, as reported in 1974. The concept behind the technique is to use RF stimulation (alternating electrical field with an oscillating frequency of 500,000 Hz) to cause a thermal lesion in the retrogasserian root or ganglion.

In 98%–99% of the patients, pain relief is obtained immediately after surgery. A recurrence rate of 20% at 9 years has been described with this procedure. Because hypoesthesia is the endpoint of the procedure, numbness is present in 100% of patients after surgery.[16]

Glycerol rhizotomy

The procedure for injecting anhydrous glycerol (99.5%), a mild neurolytic, can be performed both in an operating room with fluoroscopic facilities and in a radiology suite setting with anesthetic support.

Most patients experience relief immediately or within 1–2 days after surgery, although it can take up to 2 weeks to achieve pain relief in some cases.

Balloon compression

Percutaneous balloon microcompression of the trigeminal ganglion using a balloon catheter was introduced by Mullanand Lichtor. Microcompression of the trigeminal ganglion takes place during the procedure; it has also been documented in anatomic study on cadavers that, when the balloon is fully inflated, there is stretching of the dura, relieving what is called the dural compression of the trigeminal ganglion and its root.

Radiosurgery

Stereotactic radiosurgery was first used by Leksell for the treatment of TN in 1971. The mechanism of action of radiosurgery is presumed to be axonal degeneration as a result of radiation. Arteriolar thickening that occurs after radiation insult to the vessel in contact with the nerve has been postulated to have a possible therapeutic effect.


  Conclusion Top


TN is associated with and is likely to be caused by pulsatile mechanical compression of the trigeminal nerve by a blood vessel near the dorsal root entry zone. MVD is found to be a safe and an effective procedure to relieve typical TN in patients of all ages. Careful patient selection is the most important determinant of outcome, and morbidity is rare when the procedure is performed by an experienced surgeon.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Zakrzewska JM, Hamlyn PJ. Facial pain. In: Crombie IK, Croft PR, Linton SJ, editors. Epidemiology of Pain. Seattle: IAS Press; 1999. p. 171-202.  Back to cited text no. 1
    
2.
Headache Classification Committee of the International Headache Society (IHS). The international classification of headache disorders, 3rd edition (beta version). Cephalalgia 2013;33:629-808.  Back to cited text no. 2
    
3.
Zakrzewska JM, Linskey M. Trigeminal neuralgia. In: Zakrzewska JM, edtior. Orofacial Pain. London: Oxford University Press; 2009. p. 119-34.  Back to cited text no. 3
    
4.
Linskey ME, Jannetta PJ. Differential diagnosis of trigeminal neuralgia: Look-a-like diseases and atypical trigeminal neuralgia. In: Jannetta PJ, editor. Trigeminal Neuralgia. London: Oxford University Press; 2010. p. 74-86.  Back to cited text no. 4
    
5.
Zakrzewska JM, Linskey ME. Trigeminal neuralgia. Clinical Evidence handbook. Available from: https://www.aafp.org/afp/2016/0715/p133.html. [Last accessed on 2018 Dec 01].  Back to cited text no. 5
    
6.
Zakrzewska JM, Linskey ME. Trigeminal neuralgia. BMJ 2015;350:h1238.  Back to cited text no. 6
    
7.
Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: The ignition hypothesis. Clin J Pain 2002;18:4-13.  Back to cited text no. 7
    
8.
Duff JM, Spinner RJ, Lindor NM, Dodick DW, Atkinson JL. Familial trigeminal neuralgia and contralateral hemifacial spasm. Neurology 1999;53:216-8.  Back to cited text no. 8
    
9.
Katusic S, Beard CM, Bergstralh E, Kurland LT. Incidence and clinical features of trigeminal neuralgia, Rochester, Minnesota, 1945-1984. Ann Neurol 1990;27:89-95.  Back to cited text no. 9
    
10.
Brisman R. Trigeminal neuralgia and multiple sclerosis. Arch Neurol 1987;44:379-81.  Back to cited text no. 10
    
11.
Lunsford LD, Bennett MH. Percutaneous retrogasserian glycerol rhizotomy for tic douloureux: Part 1. Technique and results in 112 patients. Neurosurgery 1984;14:424-30.  Back to cited text no. 11
    
12.
Szapiro J Jr., Sindou M, Szapiro J. Prognostic factors in microvascular decompression for trigeminal neuralgia. Neurosurgery 1985;17:920-9.  Back to cited text no. 12
    
13.
Fukuda H, Ishikawa M, Okumura R. Demonstration of neurovascular compression in trigeminal neuralgia and hemifacial spasm with magnetic resonance imaging: Comparison with surgical findings in 60 consecutive cases. Surg Neurol 2003;59:93-9.  Back to cited text no. 13
    
14.
De Santi L, Annunziata P. Symptomatic cranial neuralgias in multiple sclerosis: Clinical features and treatment. Clin Neurol Neurosurg 2012;114:101-7.  Back to cited text no. 14
    
15.
Tronnier VM, Rasche D, Hamer J, Kienle AL, Kunze S. Treatment of idiopathic trigeminal neuralgia: Comparison of long-term outcome after radiofrequency rhizotomy and microvascular decompression. Neurosurgery 2001;48:1261-7.  Back to cited text no. 15
    
16.
Taha JM, Tew JM Jr. Comparison of surgical treatments for trigeminal neuralgia: Reevaluation of radiofrequency rhizotomy. Neurosurgery 1996;38:865-71.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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