Neurovascular contact in trigeminal neuralgia

While selectively sectioning the pain fibers in trigeminal neuralgia (which usually lie posteriorly) of the trigeminal nerve via an occipital craniectomy Walter Edward Dandy, as quoted in Wilkins, noted that vascular compression of the trigeminal nerve at the pons was a frequent finding 1).

However some patients may present with clinically classical trigeminal neuralgiabut no vascular conflict on MRI or even at surgery. Several factors have been cited as alternative or supplementary factors that may cause neuralgia.

The vessel that most often causes TN is the superior cerebellar artery (SCA), other known offending vessels include the anterior inferior cerebellar artery(AICA) and the vertebrobasilar artery and vein.

Veins as the source of trigeminal neuralgias (TN) lead to controversies. Only a few studies have specifically dealt with venous implication in neurovascular conflicts (NVC).

A study shows the frequent implication of veins not only at TREZ but also at mid-cisternal portion and porus of Meckel cave 2).

Trigeminal neuralgia in pediatric patients is very rare. A case of typical trigeminal neuralgia in a child, demonstrating the pathogenesis of the neurovascular conflict due to subarachnoidal adhesions after meningoencephalitis was reported 3).


It is widely accepted that a neurovascular contact in the cisternal segment of the trigeminal nerve is the primary cause of classical trigeminal neuralgia 4). However, previous studies have cast doubt on this hypothesis because a neurovascular contact was reported to be prevalent on both the symptomatic and the asymptomatic side and therefore suggested that the severity of the neurovascular contact should be taken into account 5)6) 7). The previous studies were limited by small sample size, lack of blinding, MRI was done with low magnetic field strength or study populations were highly selected consisting only of patients from neurosurgical departments.

Grading the neurovascular contact in classical trigeminal neuralgia is scientifically and probably also clinically important. Findings demonstrate that neurovascular contact is highly prevalent on both the symptomatic and asymptomatic sides. Maarbjerg et al., demonstrated that severe neurovascular contact is involved in the aetiology of classical trigeminal neuralgia and that it is caused by arteries located in the root entry zone. Findings also indicate that in some patients with classical trigeminal neuralgia a neurovascular contact is not involved in the aetiology of the disease or may only be a contributing factor in combination with other unknown factors. The degree of neurovascular contact could thus be important when selecting patients for surgery 8).


Jani et al., from the University of Pittsburgh Medical Centerprospectively recruited 27 patients without facial pain who were undergoing microvascular decompression for hemifacial spasm and had undergone high-resolution preoperative MRINeurovascular contact/compression (NVC/C) by artery or vein was assessed both intraoperatively and by MRI, and was stratified into 3 types: simple contact, compression (indentation of the surface of the nerve), and deformity (deviation or distortion of the nerve).

Intraoperative evidence of NVC/C was detected in 23 patients. MRI evidence of NVC/C was detected in 18 patients, all of whom had intraoperative evidence of NVC/C. Thus, there were 5, or 28% more patients in whom NVC/C was detected intraoperatively than with MRI (Kappa = 0.52); contact was observed in 4 of these patients and compression in 1 patient. In patients where NVC/C was observed by both methods, there was agreement regarding the severity of contact/compression in 83% (15/18) of patients (Kappa = 0.47). No patients exhibited deformity of the nerve by imaging or intraoperatively.

There was moderate agreement between imaging and operative findings with respect to both the presence and severity of NVC/C 9).

References

1)

Wilkins RH: Historical perspectives, in Rovit RL, Murali R, Jannetta PJ (eds): Trigeminal Neuralgia. Baltimore: Williams & Wilkins, 1990, pp 1–25
2)

Dumot C, Sindou M. Trigeminal neuralgia due to neurovascular conflicts from venous origin: an anatomical-surgical study (consecutive series of 124 operated cases). Acta Neurochir (Wien). 2015 Jan 22. [Epub ahead of print] PubMed PMID: 25604274.
3)

Solth A, Veelken N, Gottschalk J, Goebell E, Pothmann R, Kremer P. Successful vascular decompression in an 11-year-old patient with trigeminal neuralgia. Childs Nerv Syst. 2008 Jun;24(6):763-6. doi: 10.1007/s00381-008-0581-0. Epub 2008 Feb 22. PubMed PMID: 18293001.
4)

Devor M, Amir R, Rappaport ZH. Pathophysiology of trigeminal neuralgia: the ignition hypothesis. Clin J Pain. 2002 Jan-Feb;18(1):4-13. Review. PubMed PMID: 11803297.
5)

Masur H, Papke K, Bongartz G, Vollbrecht K. The significance of three-dimensional MR-defined neurovascular compression for the pathogenesis of trigeminal neuralgia. J Neurol. 1995 Jan;242(2):93-8. PubMed PMID: 7707097.
6)

Anderson VC, Berryhill PC, Sandquist MA, Ciaverella DP, Nesbit GM, Burchiel KJ. High-resolution three-dimensional magnetic resonance angiography and three-dimensional spoiled gradient-recalled imaging in the evaluation of neurovascular compression in patients with trigeminal neuralgia: a double-blind pilot study, Neurosurgery , 2006, vol. 58 pg. 666-73
7)

Miller JP, Acar F, Hamilton BE, Burchiel KJ. Radiographic evaluation of trigeminal neurovascular compression in patients with and without trigeminal neuralgia, J Neurosurg , 2009a, vol. 110 pg. 627-632
8)

Maarbjerg S, Wolfram F, Gozalov A, Olesen J, Bendtsen L. Significance of neurovascular contact in classical trigeminal neuralgia. Brain. 2015 Feb;138(Pt 2):311-9. doi: 10.1093/brain/awu349. Epub 2014 Dec 24. PubMed PMID: 25541189.
9)

Jani RH, Hughes MA, Gold MS, Branstetter BF, Ligus ZE, Sekula RF Jr. Trigeminal Nerve Compression Without Trigeminal Neuralgia: Intraoperative vs Imaging Evidence. Neurosurgery. 2019 Jan 1;84(1):60-65. doi: 10.1093/neuros/nyx636. PubMed PMID: 29425330.

Medically refractory trigeminal neuralgia treatment

see Trends in surgical treatment for trigeminal neuralgia

see Cost effectiveness in surgical treatment for trigeminal neuralgia.

Microvascular decompression

see Microvascular decompression for trigeminal neuralgia

Percutaneous procedures

see Percutaneous trigeminal rhizotomy.

Gamma Knife radiosurgery

see Gamma Knife radiosurgery for trigeminal neuralgia.


Microvascular decompression should be performed more prudently in elderly patients (>80 years old), and the indications for PR should be relatively relaxed. MVD + PR could improve the curative effect in patients with trigeminal neuralgia >80 years. Gamma knife treatment of trigeminal neuralgia had high safety, less complications, and positive curative effect, especially suitable for patients >80 years 1).


MVD results in superior rates of short- and long-term pain relief, facial numbness and dysesthesia control, and less recurrence amongst those in whom pain freedom was achieved, at the cost of greater postoperative complications when compared to SRS. Although no significant difference was found in terms of the need for retreatment surgery, there was a trend towards less procedures favoring MVD. First treatment by either technique represents the overall trends reported 2).

References

1) Yu R, Wang C, Qu C, Jiang J, Meng Q, Wang J, Wei S. Study on the Therapeutic Effects of Trigeminal Neuralgia With Microvascular Decompression and Stereotactic Gamma Knife Surgery in the Elderly. J Craniofac Surg. 2018 Nov 30. doi: 10.1097/SCS.0000000000004999. [Epub ahead of print] PubMed PMID: 30507874. 2) Lu VM, Duvall JB, Phan K, Jonker BP. First treatment and retreatment of medically refractive trigeminal neuralgia by stereotactic radiosurgery versus microvascular decompression: a systematic review and Meta-analysis. Br J Neurosurg. 2018 May 10:1-10. doi: 10.1080/02688697.2018.1472213. [Epub ahead of print] PubMed PMID: 29745268.

Update: Microvascular decompression for glossopharyngeal neuralgia

Microvascular decompression for glossopharyngeal neuralgia

For glossopharyngeal neuralgia treatment, should pharmacologic management be ineffective, surgical intervention is indicated. The first-choice treatment is typically microvascular decompression (MVD), as it has the highest initial and long-term success rates.
In 1932, Walter Edward Dandy 1) thought that the operative approach of GPN was the same with trigeminal neuralgia or Meniere’s disease.
Laha and Jannetta 2) proposed that GPN could be treated by surgically relieving the pressure that offending vascular structures imposed on the glossopharyngeal nerves.
Resnick et al. 3) reporteded excellent postoperative surgical results for 79%.
Patel et al. reported in 217 a immediate success rate of 90% 4).
There are three types of neurovascular compression (NVC): type I – NVC at the root entry zone (REZ) of the IX CN within the retro-olivary sulcus; type II – the vertebral artery causes NVC at the IX CN REZ by the shoulder of the artery, and the type III – a “sandwich-like” compression where the vertebral artery and the PICA perform a combination of NVC 5).

Technique

Once the anesthetic induction and intubation have been performed, the patient should be positioned in lateral decubitus fashion, fixing the head with a Mayfield head clamp, followed by the placement of an axillary roll. The neck should be narrowed with slight flexion and rotated approximately 10 degrees to the affected side. The vertex is tilted 15 degrees toward the floor. The shoulder is pulled out of the way and finally the patient is accommodated in such a way that the table can be rotated laterally or adjusted for a Trendelenburg position or reverse Trendelenburg position. For the incision, the mastoid eminence is initially demarcated, then a line is drawn from the external auditory canal to the inion to mark the transverse sinus. Then, a 3-4 cm arcuate or linear incision is performed, with the concave side toward the ear. Half of the incision should be above the mastoid notch or even more posteriorly in large, muscular or dolichocephalic patients. Subsequently, a retractor is placed and the bone is opened with a perforator, making sure to use bone wax in case of bleeding and filling the mastoid cells.
Ordónez-Rubiano et al. propose to target the opening of the bone depending on the CN affected. Three different approaches could be performed. The superior for the V CN (mini extreme-lateral or microasterional), the middle for VII and VIII CNs (usual for the cerebellopontine angle), and the inferior for the IX to XII CNs (mini far-lateral).
Once the dura is exposed, it is incised and stretched. The form in which the dura is opened includes the L or reverse L shape, 3-5 mm parallel to the sigmoid sinus and to the floor of the posterior fossa, after which they are secured with sutures for a wider exposure. A retractor is placed under the cerebellum and raised from its inferolateral margin, after which the microscope is introduced, and the retractor is advanced anteriorly until the spinal part of the XI CN is observed, the arachnoid is dissected, which allows to elevate the cerebellum and expose the remaining CNs within the jugular foramen. Once the rootlets of the IX CN are identified, they are separated from the rootlets of the X and XI CNs. The involved vessel is identified and dissected before the decompression and finally, the Teflon is placed between the two structures 6).
If there is no NVC, the glossopharyngeal nerve and the upper bundle of the X CN can be sectioned 7).

Case series

2018

Between 2006 and 2016, 228 idiopathic GPN patients underwent MVD in our department. Those cases were retrospectively reviewed with emphasis on intraoperative findings and long-term postoperative outcomes. The average period of follow-up was 54.3 ± 6.2 months.
Intraoperatively, the culprit was identified as the posterior inferior cerebellar artery (PICA) in 165 cases (72.3%), the vertebral artery (VA) in 14 (6.1%), vein in 10 (4.4%), and a combination of multiple arteries or venous offending vessels in 39 (17.2%). The immediately postoperative outcome was excellent in 204 cases (89.5%), good in 12 (5.3%), fair in 6 (2.6%) and poor in 6 (2.6%). More than 5-year follow-up was obtained in 107 cases (46.9%), which presented as excellent in 93 (86.9%), good in 6 (5.6%), fair in 3 (2.8%) and poor in 5 (4.7%). Thirty-seven (16.2%) of the patients experienced some postoperative neurological deficits immediately, such as dysphagia, hoarseness and facial paralysis, which has been improved at the last follow-up in most cases, except 2.
This investigation demonstrated that MVD is a safe and effective remedy for treatment of GPN 8).

2017

30 patients with intractable primary typical GPN who underwent MVD without rhizotomy and were followed for more than 2 years were included in the analysis. Each MVD was performed using one of four different surgical techniques: interposition of Teflon pieces, transposition of offending vessels using Teflon pieces, transposition of offending vessels using a fibrin-glue-coated Teflon sling, and removal of offending veins.
The posterior inferior cerebellar artery was responsible for neurovascular compression in 27 of 30 (90%) patients, either by itself or in combination with other vessels. The location of compression on the glossopharyngeal nerve varied; the root entry zone (REZ) only (63.3%) was most common, followed by both the REZ and distal portion (26.7%) and the distal portion alone (10.0%). In terms of detailed surgical techniques during MVD, the offending vessels were transposed in 24 (80%) patients, either using additional insulation, offered by Teflon pieces (15 patients), or using a fibrin glue-coated Teflon sling (9 patients). Simple insertion of Teflon pieces and removal of a small vein were also performed in five and one patient, respectively. During the 2 years following MVD, 29 of 30 (96.7%) patients were asymptomatic or experienced only occasional pain that did not require medication. Temporary hemodynamic instability occurred in two patients during MVD, and seven patients experienced transient postoperative complications. Neither persistent morbidity nor mortality was reported.
This study demonstrates that MVD without rhizotomy is a safe and effective treatment option for GPN 9).


From January 2004 to June 2006, 35 consecutive patients were diagnosed with GPN. All of them underwent MVD. Demographic data, clinical presentation, operative findings, clinical results, operative complications were reviewed.
A total of 33 patients (94.3%) experienced complete pain relief immediately after MVD. Long-term follow-up was available for 30 of these 35 patients, and 28 of these 30 patients continued to be pain-free. There was no long-term operative morbidity in all cases. One patient had a cerebrospinal fluid leak and 1 case presented with delayed facial palsy.
Classic GPN is usually caused by pulsatile neurovascular compression of the glossopharyngeal and vagus rootlets. MVD is a safe, effective, and durable operation for GPN 10).

2015

A retrospective review of the case notes of patients who had undergone surgery for GPN in the authors’ department between 2008 and 2013 was performed to investigate baseline characteristics and immediate outcomes during the hospitalization. For the long-term results, a telephone survey was performed, and information on pain recurrence and permanent complications was collected. Pain relief meant no pain or medication, any pain persisting after surgery was considered to be treatment failure, and any pain returning during the follow-up period was considered to be pain recurrence. For comparative study, the patients were divided into 2 cohorts, that is, patients treated with GPNR alone and those treated with GPNR+VNR.
One hundred three procedures, consisting of GPNR alone in 38 cases and GPNR+VNR in 65 cases, were performed in 103 consecutive patients with GPN. Seventy-nine of the 103 patients could be contacted for the follow-up study, with a mean follow-up duration of 2.73 years (range 1 month-5.75 years). While there were similar results (GPNR vs GPNR+VNR) in immediate pain relief rates (94.7% vs 93.8%), immediate complication rates (7.9% vs 4.6%), and long-term pain relief rates (92.3% vs 94.3%) between the 2 cohorts, a great difference was seen in long-term complications (3.8% vs 35.8%). The long-term complication rate for the combined GPNR+VNR cohort was 9.4 times higher than that in the GPNR cohort. There was no operative or perioperative mortality. Immediate complications occurred in 6 cases, consisting of poor wound healing in 3 cases, and CSF leakage, hoarseness, and dystaxia in 1 case each. Permanent complications occurred in 20 patients (25.3%) and included cough while drinking in 10 patients, pharyngeal discomfort in 8 patients, and hoarseness and dysphagia in 1 case each.
In general, this study indicates that GPNR alone or in combination with VNR is a safe, simple, and effective treatment option for GPN. It may be especially valuable for patients who are not suitable for the microvascular decompression (MVD) procedure and for surgeons who have little experience with MVD. Of note, this study renews the significance of GPNR alone, which, the authors believe, is at least valuable for a subgroup of GPN patients, with significantly fewer long-term complications than those for rhizotomy for both glossopharyngeal nerve and rootlets of the vagus nerve 11).

2002

Patel et al. present the experience with more than 200 patients and conducted a retrospective review of the database and identified patients who presented for treatment of presumed GPN. When possible, patients were contacted by telephone for collection of follow-up information regarding symptom relief, complications, functional outcomes, and patient satisfaction. Univariate and multivariate analyses were performed to identify predictors of good outcomes after MVD. Subgroup analyses were performed with quartiles of approximately 50 patients each, for assessment of the effects of improvements in techniques and anesthesia during this 20-year period.
They observed GPN to be more common among female (66.8%) than male (33.2%) patients, with an overall mean patient age of 50.2 years (standard deviation, 14.4 yr). The most common presenting symptoms were throat and ear pain and throat pain alone, and the mean duration of symptoms was 5.7 years (standard deviation, 5.8 yr; range, 1-32 yr). Symptoms appeared almost equally on the left side (54.8%) and the right side (45.2%). The overall immediate success rate exceeded 90%, and long-term patient outcomes and satisfaction were best for the typical GPN group (with pain restricted to the throat and palate). Complication rates decreased across quartiles for all categories evaluated.
MVD is a safe, effective form of therapy for GPN. It may be most beneficial for patients with typical GPN, especially when symptoms are restricted to deep throat pain only 12).

1995

Since 1971, 40 patients have undergone microvascular decompression of the glossopharyngeal and vagus nerves for treatment of typical glossopharyngeal neuralgia. This procedure provided excellent immediate results (complete or > 95% relief of pain) in 79%, with an additional 10% having a substantial (> 50%) reduction in pain. Long-term follow-up (mean, 48 mo; range, 6-170 mo) reveals excellent results (complete or > 95% reduction in pain without any medication) in 76% of the patients and substantial improvement in an additional 16%. There were two deaths at surgery (5%) both occurring early in the series as the result of hemodynamic lability causing intracranial hemorrhage. Three patients (8%) suffered permanent 9th nerve palsy 13).

1986

20 patients who had undergone microvascular decompression for the treatment of “idiopathic” trigeminal neuralgia (9 cases), hemifacial spasm (7 cases), glossopharyngeal neuralgia (3 cases) and paroxysmal vertigo and tinnitus (1 case) were followed up for 25 months on average. Permanent relief of symptoms was observed in 19 (95%), with sparing of cranial nerve function. Analysis of the clinical data shows that the patients described in the present series did not differ from those considered to suffer from “idiopathic” cranial nerve dysfunction syndromes. The importance of vascular cross compression as etiological factor in such conditions is stressed and the pathophysiology discussed. The term “cryptogenic” applied to trigeminal neuralgia or hemifacial spasm thus needs revising. Lastly, the indications of microvascular decompression in the treatment of “cryptogenic” cranial nerve dysfunction syndromes are defined 14).

1977

Microsurgical observations werw made of the cranial nerve root entry or exit zones 117 patients operated upon for the treatment of hyperactive-hypoactive dysfunction syndromes (trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction, and glossopharyngeal neuralgia). Cross-compression or distortion of the appropriate nerve root at its entry or exit zone was noted in all patients. This compression or distortion was usually caused by normal or arteriosclerotic, elongated arterial loops, it was usually relieved by decompressive microsurgical techniques. A small percentage of patients were found to have compression of the nerve root at the entry-exit zone by a tumor, a vein, or some other structural abnormality; they were relieved by tumor excision or other measures as described. Relief was gradual postoperatively if the treated nerve was not stroked or manipulated at operation but it was immediate if the nerve was manipulated. Preoperative evidence of decreased nerve function improved postoperatively 15).

Case reports

A case of coexistent glossopharyngeal neuralgia and hemifacial spasm was treated by transposition of the vertebral artery. A 60-year-old man was referred to our hospital due to pain in the left posterior part of the tongue that was difficult to control with oral medication at a local hospital. The diagnosis was left glossopharyngeal neuralgia based on the symptoms, imaging findings, and lidocaine test results. Moreover, the patient had left hemifacial spasm. Microvascular decompression was performed, which confirmed that the vertebral artery was compressing the lower cranial nerve and the posterior inferior cerebellar artery was compressing the root exit zone of the facial nerve. The vertebral artery and posterior inferior cerebellar artery were transposed using TachoSil. After the surgery, both glossopharyngeal neuralgia and hemifacial spasm disappeared, and the patient was discharged 16).

1985

A case of combined trigeminal and glossopharyngeal neuralgia is described. The superior cerebellar artery and normal choroid plexus compressed and indented the root entry zones of the trigeminal and glossopharyngeal nerves, respectively. Complete relief was obtained after microvascular decompression and resection of the choroid plexus 17).


A case of glossopharyngeal neuralgia associated with episodic cardiac arrest and syncope is presented. Posterior fossa exploration showed that the left glossopharyngeal and vagus nerves were compressed by the posterior inferior cerebellar artery. Microvascular decompression resulted in complete relief of glossopharyngeal neuralgia, cardiac syncope, and seizure. The mechanism of glossopharyngeal neuralgia associated with cardiac syncope is discussed 18).


Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848 19).
1)

Dandy WE (1932) The treatment of trigeminal neuralgia by the cerebellar route. Ann Surg 96:787–795
2)

Laha RK, Jannetta PJ (1977) Glossopharyngeal neuralgia. J Neurosurg 47:316–320
3) , 13)

Resnick DK, Jannetta PJ, Bissonnette D, Jho HD, Lanzino G. Microvascular decompression for glossopharyngeal neuralgia. Neurosurgery. 1995 Jan;36(1):64-8; discussion 68-9. PubMed PMID: 7708170.
4) , 12)

Patel A, Kassam A, Horowitz M, Chang YF. Microvascular decompression in the management of glossopharyngeal neuralgia: analysis of 217 cases. Neurosurgery. 2002 Apr;50(4):705-10; discussion 710-1. PubMed PMID: 11904019.
5)

Tanrikulu L, Hastreiter P, Dörfler A, Buchfelder M, Naraghi R. Classification of neurovascular compression in glossopharyngeal neuralgia: Three-dimensional visualization of the glossopharyngeal nerve. Surg Neurol Int. 2015 Dec 24;6:189. doi: 10.4103/2152-7806.172534. eCollection 2015. PubMed PMID: 26759734; PubMed Central PMCID: PMC4697202.
6)

Ordónez-Rubiano EG, García-Chingaté CC, Rodríguez-Vargas S, Cifuentes-Lobelo HA, Perilla-Cepeda TA. Microvascular Decompression for a Patient with a Glossopharyngeal Neuralgia: A Technical Note. Cureus. 2017 Jul 20;9(7):e1494. doi: 10.7759/cureus.1494. PubMed PMID: 28948114; PubMed Central PMCID: PMC5606712.
7)

Rey-Dios R, Cohen-Gadol AA. Current neurosurgical management of glossopharyngeal neuralgia and technical nuances for microvascular decompression surgery. Neurosurg Focus. 2013 Mar;34(3):E8. doi: 10.3171/2012.12.FOCUS12391. Review. PubMed PMID: 23451790.
8)

Xia L, Li YS, Liu MX, Zhong J, Dou NN, Li B, Li ST. Microvascular decompression for glossopharyngeal neuralgia: a retrospective analysis of 228 cases. Acta Neurochir (Wien). 2018 Jan;160(1):117-123. doi: 10.1007/s00701-017-3347-1. Epub 2017 Nov 4. PubMed PMID: 29103137.
9)

Kim MK, Park JS, Ahn YH. Microvascular Decompression for Glossopharyngeal Neuralgia: Clinical Analyses of 30 Cases. J Korean Neurosurg Soc. 2017 Nov;60(6):738-748. doi: 10.3340/jkns.2017.0506.010. Epub 2017 Oct 25. PubMed PMID: 29142635; PubMed Central PMCID: PMC5678068.
10)

Zhao H, Zhang X, Zhu J, Tang YD, Li ST. Microvascular Decompression for Glossopharyngeal Neuralgia: Long-Term Follow-Up. World Neurosurg. 2017 Jun;102:151-156. doi: 10.1016/j.wneu.2017.02.106. Epub 2017 Mar 2. PubMed PMID: 28263933.
11)

Ma Y, Li YF, Wang QC, Wang B, Huang HT. Neurosurgical treatment of glossopharyngeal neuralgia: analysis of 103 cases. J Neurosurg. 2015 Sep 4:1-5. [Epub ahead of print] PubMed PMID: 26339847.
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Michelucci R, Tassinari CA, Samoggia G, Tognetti F, Calbucci F. Intracranial microvascular decompression for “cryptogenic” hemifacial spasm, trigeminal and glossopharyngeal neuralgia, paroxysmal vertigo and tinnitus: II. Clinical study and long-term follow up. Ital J Neurol Sci. 1986 Jun;7(3):367-74. PubMed PMID: 3733417.
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Jannetta PJ. Observations on the etiology of trigeminal neuralgia, hemifacial spasm, acoustic nerve dysfunction and glossopharyngeal neuralgia. Definitive microsurgical treatment and results in 117 patients. Neurochirurgia (Stuttg). 1977 Sep;20(5):145-54. PubMed PMID: 198692.
16)

Fujii T, Otani N, Otsuka Y, Matsumoto T, Tanoue S, Ueno H, Tomura S, Tomiyama A, Toyooka T, Wada K, Mori K. [A Case of Coexistent Glossopharyngeal Neuralgia and Hemifacial Spasm Successfully Treated with Transposition of the Vertebral Artery]. No Shinkei Geka. 2017 Jun;45(6):503-508. doi: 10.11477/mf.1436203540. Review. Japanese. PubMed PMID: 28634310.
17)

Yoshioka J, Ueta K, Ohmoto T, Fujiwara T, Tabuchi K. Combined trigeminal and glossopharyngeal neuralgia. Surg Neurol. 1985 Oct;24(4):416-20. PubMed PMID: 4035551.
18)

Tsuboi M, Suzuki K, Nagao S, Nishimoto A. Glossopharyngeal neuralgia with cardiac syncope. A case successfully treated by microvascular decompression. Surg Neurol. 1985 Sep;24(3):279-83. PubMed PMID: 4023909.
19)

Murasawa A, Yamada K, Hayakawa T, Aragaki Y, Yoshimine T. Glossopharyngeal neuralgia treated by microvascular decompression–case report. Neurol Med Chir (Tokyo). 1985 Jul;25(7):551-3. PubMed PMID: 2415848.

Update: Geniculate neuralgia treatment

Geniculate neuralgia treatment

The treatment for geniculate neuralgia has not been established, although it seems reasonable that the therapeutic approaches used in other more common craniofacial neuralgias, such as trigeminal neuralgia, should be effective.
Conservative medical treatment is always the first-line therapy.
Mild cases may respond to carbamazepine sometimes in combination with phenytoin.
May responde to valproic acid.
Topical antibiotics for secondary infections of herpetic lesions.
Local anesthetic to external auditory canal.

Surgery

Surgical treatment should be offered if medical treatment fails. The two commonest surgical options are transection of the nervus intermedius, and microvascular decompression of the nerve at the nerve root entry zone of the brainstem. However, extracranial intratemporal division of the cutaneous branches of the facial nerve may offer a safer and similarly effective treatment.
The response to medical treatment for this condition varies between individuals. The long-term outcomes of surgery remain unknown because of limited data 1).
Rupa et al., postulate that geniculate ganglionectomy may be ineffective as the sole treatment for certain cases of geniculate neuralgia, and that nervus intermedius section may also be required to achieve a more complete deafferentation 2).
Excision of the nervus intermedius and/or of the geniculate ganglion by the middle cranial fossa approach without the production of facial paralysis, sometimes in combination with selective section of the Vth cranial nerve, has been successful in relieving the pain of geniculate neuralgia.

Microvascular decompression

Microvascular decompression may be effective as a treatment. Along its cisternal course, the nerve may be difficult to distinguish from the facial nerve. Based on case reports and small series, long-term pain control can be seen after nerve sectioning or microvascular decompression, but no prospective studies exist. Such studies are now necessary to shed light on the efficacy of surgical treatment of nervus intermedius neuralgia 3).

Complications

High-frequency hearing loss occurred after MVD for TGN, GPN, or GN, and the greatest incidence occurred on the ipsilateral side. This hearing loss may be a result of drill-induced noise and/or transient loss of cerebrospinal fluid during the course of the procedure. Changes in intraoperative BAEP waveforms were not useful in predicting HFHL after MVD. Repeated postoperative audiological examinations may be useful in assessing the prognosis of HFHL 4).

Case series

2002

Surgically excision of the nervus intermedius and geniculate ganglion via the middle cranial fossa approach, Review the long-term outcomes in 64 patients who were treated in this manner. Findings indicate that excision of the nervus intermedius and geniculate ganglion can be routinely performed without causing facial paralysis and that it is an effective definitive treatment for intractable geniculate neuralgia 5).

1991

A total of 31 surgical procedures were performed. Seventeen patients had sequential rhizotomies and one patient had microvascular decompression alone. Based on the clinical diagnosis, the nerves sectioned were singly or in combination: the nervus intermedius (14 patients), geniculate ganglion (10 patients), ninth nerve (14 patients), 10th nerve (11 patients), tympanic nerve (four patients), and chorda tympani nerve (one patient). Microvascular decompression of the involved nerves was undertaken in nine patients, in whom vascular loops were discovered. Adhesions (six patients), thickened arachnoid (three patients), and benign osteoma (one patient) were other intraoperative abnormalities noted. The overall success of these procedures in providing pain relief was 72.2%, and the mean follow-up period was 3.3 years (range 1 month to 14.5 years). There was no surgical mortality. Expected side effects were: decreased lacrimation, salivation, and taste related to nervus intermedius nerve section, and transient hoarseness and diminished gag related to ninth and 10th nerve section. Four patients developed sequelae consisting of sensorineural hearing loss, vertigo, and transient facial nerve paresis. One patient had a cerebrospinal fluid leak and another developed aseptic meningitis as postoperative complications. Except when primary glossopharyngeal neuralgia is the working diagnosis, a combined posterior cranial fossa-middle cranial fossa approach is recommended for adequate exploration and/or section of the fifth, ninth, and 10th cranial nerves as well as the geniculate ganglion and nervus intermedius 6).

1976

Excision of the nervus intermedius and/or of the geniculate ganglion by the middle cranial fossa approach without the production of facial paralysis, in any of 15 cases with geniculate neuralgia is reported. Use of these new techniques, sometimes in combination with selective section of the Vth cranial nerve, has been successful in relieving the pain of geniculate neuralgia 7).

Case reports

A 39-year-old man presented with a history of left “deep” ear pain within his ear canal. He noted occasional pain on the left side of his face around the ear. He had been treated with neuropathic pain medications without relief. His wife described suicidal ideations discussed by her husband because of the intense pain.
The patient’s neurologic examination was normal, and otolaryngologic consultation revealed no underlying structural disorder. Anatomic imaging revealed a tortuous vertebral artery-posterior inferior cerebellar artery complex with the posterior inferior cerebellar artery loop impinging on the root entry zone of the nervus intermedius-vestibulocochlear nerve complex and just inferior to the root entry zone of the facial nerve and a small anterior inferior cerebellar artery loop interposed between the cranial nerve VII-VIII complex and the hypoglossal and glossopharyngeal nerves. A left-sided retromastoid craniotomy was performed, and the nervus intermedius was transected. An arterial loop in contact with the lower cranial nerves at the level of the brainstem was mobilized with a polytetrafluoroethylene implant.
The patient indicated complete relief of his preoperative pain after surgery. He has remained pain-free with intact hearing and balance 8).
1)

Tang IP, Freeman SR, Kontorinis G, Tang MY, Rutherford SA, King AT, Lloyd SK. Geniculate neuralgia: a systematic review. J Laryngol Otol. 2014 May;128(5):394-9. doi: 10.1017/S0022215114000802. Review. PubMed PMID: 24819337.
2)

Rupa V, Weider DJ, Glasner S, Saunders RL. Geniculate ganglion: anatomic study with surgical implications. Am J Otol. 1992 Sep;13(5):470-3. PubMed PMID: 1443083.
3)

Tubbs RS, Steck DT, Mortazavi MM, Cohen-Gadol AA. The nervus intermedius: a review of its anatomy, function, pathology, and role in neurosurgery. World Neurosurg. 2013 May-Jun;79(5-6):763-7. doi: 10.1016/j.wneu.2012.03.023. Epub 2012 Apr 3. Review. PubMed PMID: 22484073.
4)

Thirumala P, Meigh K, Dasyam N, Shankar P, Sarma KR, Sarma DR, Habeych M, Crammond D, Balzer J. The incidence of high-frequency hearing loss after microvascular decompression for trigeminal neuralgia, glossopharyngeal neuralgia, or geniculate neuralgia. J Neurosurg. 2015 Dec;123(6):1500-6. doi: 10.3171/2014.10.JNS141101. Epub 2015 May 1. PubMed PMID: 25932612.
5)

Pulec JL. Geniculate neuralgia: long-term results of surgical treatment. Ear Nose Throat J. 2002 Jan;81(1):30-3. Review. PubMed PMID: 11816385.
6)

Rupa V, Saunders RL, Weider DJ. Geniculate neuralgia: the surgical management of primary otalgia. J Neurosurg. 1991 Oct;75(4):505-11. PubMed PMID: 1885967.
7)

Pulec JL. Geniculate neuralgia: diagnosis and surgical management. Laryngoscope. 1976 Jul;86(7):955-64. PubMed PMID: 933690.
8)

Tubbs RS, Mosier KM, Cohen-Gadol AA. Geniculate neuralgia: clinical, radiologic, and intraoperative correlates. World Neurosurg. 2013 Dec;80(6):e353-7. doi: 10.1016/j.wneu.2012.11.053. Epub 2012 Nov 23. PubMed PMID: 23178920.

Update: Microvascular decompression for trigeminal neuralgia

Microvascular decompression (MVD) via lateral suboccipital approach is the standard surgical intervention for trigeminal neuralgia (TN).

Outcome

It has proven to be the most successful and durable surgical approach for trigeminal neuralgia (TN).
However, not all patients with TN manifest unequivocal neurovascular compression (NVC). Furthermore, over time patients with an initially successful MVD manifest a relentless rate of TN recurrence.
It does not achieve 100 % cure rate. Re-exploration of the posterior fossa may carry increased risk over first-time MVD and is not always successful, so other treatments are needed.

Case series

2017

Clinical characteristics, intraoperative findings, and postoperative curative effects were analyzed in 72 patients with trigeminal neuralgia who were treated by microvascular decompression. The patients were divided into arterial and venous compression groups based on intraoperative findings. Surgical curative effects included immediate relief, delayed relief, obvious reduction, and invalid result. Among the 40 patients in the arterial compression group, 32 had immediate pain relief of pain (80.0%), 5 cases had delayed relief (12.5%), and 3 cases had an obvious reduction (7.5%). In the venous compression group, 12 patients had immediate relief of pain (37.5%), 13 cases had delayed relief (40.6%), and 7 cases had an obvious reduction (21.9%). During 2-year follow-up period, 6 patients in the arterial compression group experienced recurrence of trigeminal neuralgia, but there were no recurrences in the venous compression group. Simple artery compression was followed by early relief of trigeminal neuralgia more often than simple venous compression. However, the trigeminal neuralgia recurrence rate was higher in the artery compression group than in the venous compression group 1).

2016

Indocyanine green videoangiography was performed in 17 TN patients undergoing microvascular decompression.
von Eckardstein et al., focused on whether ICG angiography is helpful in determining the site of conflict, particularly when not directly visible via the microscope, and whether fluorescence is strong enough to shine through the nerve obliterating the direct view of the compressing vessel.
In four patients, the site of conflict was immediately apparent after opening the cerebellopontine cistern, and ICG angiography did not provide the neurosurgeon with additional information. In another two patients, imaging quality and fluorescence were too poor. Of the remaining 11 patients with a hidden site of nerve-vessel conflict, ICG angiography was found to be helpful in anticipating the site of compression and the course of the artery in 7 patients, particularly in regard to the so-called shining-through effect through fiber bundles of the thinned nerve. Of all the patients, 88% reported at least improvement or cessation of their symptoms, including all of the patients with a shine-through effect.
ICG angiography could be a helpful adjunct in decompressing the trigeminal nerve and can guide the surgeon to the nerve-vessel conflict. Intensity of the fluorescence is powerful enough to shine through thinned and splayed trigeminal nerve fiber bundles 2).


A retrospective review of patient records from 1998 to 2015 identified a total of 942 patients with TN and 500 patients who underwent MVD. After excluding several cases, 306 patients underwent MVD as their first surgical intervention and 175 patients underwent subsequent MVD. Demographics and clinicopathological data and outcomes were obtained for analysis.
In patients who underwent subsequent MVD, surgical intervention was performed at an older age (55.22 vs 49.98 years old, p < 0.0001) and the duration of symptoms was greater (7.22 vs 4.45 years, p < 0.0001) than for patients in whom MVD was their first surgical intervention. Patients who underwent initial MVD had improved pain relief and no improvement in pain rates compared with those who had subsequent MVD (95.8% and 4.2% vs 90.3% and 9.7%, respectively, p = 0.0041). Patients who underwent initial MVD had significantly lower rates of facial numbness in the pre- and postoperative periods compared with patients who underwent subsequent MVD (p < 0.0001). The number of complications in both groups was similar (p = 0.4572).
The results demonstrate that patients who underwent other procedures prior to MVD had less pain relief and a higher incidence of facial numbness despite rates of complications similar to patients who underwent MVD as their first surgical intervention 3).

2015

A retrospective analysis of clinical data was performed in 99 patients who underwent MVD from May 2012 to June 2015. The outcome data from 27 MVD operations for 27 patients aged 70-80 years (mean 74.6 years) were compared with 72 MVD operations with 72 patients aged 25-69 years (mean 55.7 years). Preoperative comorbidities were recorded and postoperative worsening comorbidities and non-neurological complications were evaluated at discharge. Efficacy of the surgery and neurological complications were evaluated in July 2015.
No decrease in activity of daily living was found in any patient. Complete pain relief without medication was achieved in 77.8% and partial pain relief in 14.8% in the elderly group, and 83.3% and 9.7%, respectively, in the non-elderly group (p=0.750). Permanent neurological complication was not observed in the elderly group, whereas Vth nerve and VIIIth nerve complications were observed in the non-elderly group. Rates of preoperative multiple comorbidities and of cardiovascular comorbidity were significantly higher in the elderly group (p<0.01). Worsening comorbidity and new pathology at discharge were mainly hypertension in both groups, but glaucoma attack and asthma attack were observed in the elderly group. All pathologies were successfully managed.
MVD for elderly patients with TN can be achieved safely with careful perioperative management. Information of comorbidity should be shared with all staff involved in the treatment, who should work as a team to avoid worsening comorbidity. The possibility of unpredictable events in the elderly patients should always be considered 4).


Since 2004, there were a total of 51 patients with TIC and 12 with HS with available MRI scans. All patients underwent preoperative MRI to rule out non-surgical etiologies for facial pain and facial spasm, and confirm vascular compression. Follow-up after surgery was 13±22 months for the patients with TIC and 33±27 months for the patients with HS.
There were 45 responders to MVD in the TIC cohort (88%), with a Visual analog scale (VAS) of 1±3. All patients with HS responded to MVD between 25 and 100%, with a mean of 75±22%. Wound complications occurred in 10% of patients with MVD for TIC, and 1 patient reported hearing loss after MVD for HS, documented by audiogram. The congruence rate between the preoperative MRI and operative findings of vascular compression was 84% in TIC and 75% in HS.
MVD is an effective and safe modality of treatment for TIC and HS. In addition to ruling out structural lesions, MRI can offer additional information by highlighting vascular loops associated with compressions. On conventional scans as obtained here, the resolution of MRI was congruent with operative findings in 84% in TIC and 75% in HS. This review emphasizes that the decision to undertake MVD in TIC or HS should be based on clinical diagnosis and not visualization of a compressing vessel by MRI. Conversely, the presence of a compressing vessel by MRI demands perseverance by the surgeon until the nerve is decompressed 5).


The trigeminal nerve was sectioned into 5 zones. Zone 1, 2, 3, 4 was located at the rostral, caudal, ventral, and dorsal part of the nerve root entry zone (REZ) respectively, and zone 5 was located at the distal of the nerve root. This study contained 86 patients with trigeminal neuralgia underwent microvascular decompression. Every zone was exposed through preoperative imaging. During the operation, offending vessels were explored from zone 1 to zone 5, and different decompression techniques were used for different types of vessels.
Through zone exploration, the sensitivity of preoperative imaging was 96.5% and specificity was 100%. Location of the neurovascular conflict was in the zone 1 in 53.5% of the patients, zone 2 in 32.6%, zone 3 in 45.3%, zone 4 in 29.1%, and zone 5 in 34.9%. In total, 2 zones were both involved in 59.3%, and 3 zones were involved in 18.6%. All offending arteries were moved away and interposed with Teflon sponge. Offending veins of 11 patients were too small to interpose, and coagulated and cut was adopted. The other offending veins were interposed with wet gelatin and Teflon sponge, respectively 6).

2014

Lee et al. performed a retrospective review of cases of TN Type 1 (TN1) or Type 2 (TN2) involving patients 18 years or older who underwent evaluation (and surgery when indicated) at Oregon Health & Science University between July 2006 and February 2013. Surgical and imaging findings were correlated.
The review identified a total of 257 patients with TN (219 with TN1 and 38 with TN2) who underwent high-resolution MRI and MR angiography with 3D reconstruction of combined images using OsiriX. Imaging data revealed that the occurrence of TN1 and TN2 without NVC was 28.8% and 18.4%, respectively. A subgroup of 184 patients underwent surgical exploration. Imaging findings were highly correlated with surgical findings, with a sensitivity of 96% for TN1 and TN2 and a specificity of 90% for TN1 and 66% for TN2. Conclusions Magnetic resonance imaging detects NVC with a high degree of sensitivity. However, despite a diagnosis of TN1 or TN2, a significant number of patients have no NVC. Trigeminal neuralgia clearly occurs and recurs in the absence of NVC 7).

2002

A study comprises 42 cases of trigeminal neuralgia that underwent operation with endoscopic-assisted microvascular decompression between October 1992 and October 1998. This study was performed in the Ear, Nose, and Throat Department, Nord Hospital, in Marseille, France. The decompression was performed by means of a minimally invasive retrosigmoid approach without a cerebellar retractor. The cerebellopontine angle was then explored by a 30-degree endoscope that gives a panoramic view of this space, with clear visualization of the trigeminal nerve from the pons to Meckel’s cave, allowing for the identification of the precise location of the site of the conflict. Microvascular decompression was performed under the microscope by separating the offending vessel from the trigeminal nerve; separation was maintained by the insertion of a piece of Teflon.
The site of conflict was detected at the root entry zone of the nerve in 35 patients (83.3%) and at Meckel’s cave in 7 patients (16.7%). In 32 cases (76.2%), the type of contact between the vessel and the nerve was of the simple type (1 vessel coming in contact with the nerve in a single point); in 6 cases (14.3%), it was a multiple type (2 vessels touching the nerve in the same point); and in 4 cases (9.5%), it was a nutcracker type (2 vessels compressing the nerve between them). After at least 1-year follow-up and a single operation (cases that required a second operation for revision were considered failures), a successful result was obtained in 31 cases (73.8%), and an improvement was obtained in 4 cases (9.5%). The operation was a failure or early recurrence occurred in 7 cases (16.7%). Postoperative complications were rare. A cerebrospinal fluid leak occurred in only 1 case (2.4%) and was subsequently treated with lumbar puncture and a compressive bandage.
The minimally invasive retrosigmoid endoscopic-assisted microvascular decompression is an acceptable treatment of primary trigeminal neuralgia. Endoscopy provides a unique way to explore the cerebellopontine angle and to identify the exact location of the neurovascular conflict 8).

1) Shi L, Gu X, Sun G, Guo J, Lin X, Zhang S, Qian C. After microvascular decompression to treat trigeminal neuralgia, both immediate pain relief and recurrence rates are higher in patients with arterial compression than with venous compression. Oncotarget. 2017 Jan 20. doi: 10.18632/oncotarget.14765. [Epub ahead of print] PubMed PMID: 28122347.
2) von Eckardstein KL, Mielke D, Akhavan-Sigari R, Rohde V. Enlightening the Cerebellopontine Angle: Intraoperative Indocyanine Green Angiography in Microvascular Decompression for Trigeminal Neuralgia. J Neurol Surg A Cent Eur Neurosurg. 2016 Sep 23. PubMed PMID: 27704490.
3) Theodros D, Rory Goodwin C, Bender MT, Zhou X, Garzon-Muvdi T, De la Garza-Ramos R, Abu-Bonsrah N, Mathios D, Blitz AM, Olivi A, Carson B, Bettegowda C, Lim M. Efficacy of primary microvascular decompression versus subsequent microvascular decompression for trigeminal neuralgia. J Neurosurg. 2016 Jul 15:1-7. [Epub ahead of print] PubMed PMID: 27419826.
4) Amagasaki K, Watanabe S, Naemura K, Shono N, Nakaguchi H. Safety of microvascular decompression for elderly patients with trigeminal neuralgia. Clin Neurol Neurosurg. 2015 Dec 31;141:77-81. doi: 10.1016/j.clineuro.2015.12.019. [Epub ahead of print] PubMed PMID: 26765772.
5) Hitchon PW, Zanaty M, Moritani T, Uc E, Pieper CL, He W, Noeller J. Microvascular decompression and MRI findings in trigeminal neuralgia and hemifacial spasm. A single center experience. Clin Neurol Neurosurg. 2015 Oct 22;139:216-220. doi: 10.1016/j.clineuro.2015.10.012. [Epub ahead of print] PubMed PMID: 26519891.
6) Feng BH, Zheng XS, Liu M, Wang XQ, Wang XH, Ying TT, Li ST. Microvascular Decompression for Trigeminal Neuralgia: Zone Exploration and Decompression Techniques. J Craniofac Surg. 2015 Oct 21. [Epub ahead of print] PubMed PMID: 26501973.
7) Lee A, McCartney S, Burbidge C, Raslan AM, Burchiel KJ. Trigeminal neuralgia occurs and recurs in the absence of neurovascular compression. J Neurosurg. 2014 May;120(5):1048-54. doi: 10.3171/2014.1.JNS131410. Epub 2014 Feb 7. PubMed PMID: 24506241.
8) El-Garem HF, Badr-El-Dine M, Talaat AM, Magnan J. Endoscopy as a tool in minimally invasive trigeminal neuralgia surgery. Otol Neurotol. 2002 Mar;23(2):132-5. PubMed PMID: 11875338.

Update: Geniculate neuralgia

J.Sales-Llopis
Neurosurgery Department, University General Hospital of Alicante, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO), Alicante, Spain
Geniculate neuralgia is a pain syndrome associated with the nervus intermedius.

Epidemiology

Fewer than 150 reported cases were published in English between 1932 and 2012 1).

Etiology

The etiology of the condition remains unknown 2).

Symptoms

The pain may also be of gradual onset and of a dull, persistent nature, with occasional sharp, stabbing pain like an electric shock, deep in the ear 3).
Some people have reported additional symptoms during pain attacks:
Salivation
Bitter taste
Tinnitus
Vertigo

Diagnosis

The clinical presentation varies. Non-neuralgic causes of otalgia should always be excluded by a thorough clinical examination, audiological assessment and radiological investigations before making a diagnosis of geniculate neuralgia 4).

Differential diagnosis

Due to the close anatomical proximity, temporomandibular joint (TMJ) pathologies should be included in the differential diagnosis.
Easily confused with trigeminal neuralgia and glossopharyngeal neuralgia. However, nerves intermedius has its characteristic clinical syndroms to be diagnosed.
see Ramsay Hunt syndrome.

Treatment

The treatment has not been established, although it seems reasonable that the therapeutic approaches used in other more common craniofacial neuralgias, such as trigeminal neuralgia, should be effective.
Conservative medical treatment is always the first-line therapy.
Surgical treatment should be offered if medical treatment fails. The two commonest surgical options are transection of the nervus intermedius, and microvascular decompression of the nerve at the nerve root entry zone of the brainstem. However, extracranial intratemporal division of the cutaneous branches of the facial nerve may offer a safer and similarly effective treatment.
The response to medical treatment for this condition varies between individuals. The long-term outcomes of surgery remain unknown because of limited data 5).

Geniculate ganglion section

Rupa et al., postulate that geniculate ganglionectomy may be ineffective as the sole treatment for certain cases of geniculate neuralgia, and that nervus intermedius section may also be required to achieve a more complete deafferentation 6).

Case series

2015

Thirumala et al., analyzed preoperative and postoperative audiogram data and brainstem auditory evoked potentials (BAEPs) from 8 patients with GN who underwent MVD. Differences in pure tone audiometry > 10 dB at frequencies of 0.25, 0.5, 1, 2, 4, and 8 kHz were calculated preoperatively and postoperatively for both the ipsilateral and the contralateral sides. Intraoperative monitoring records were analyzed and compared with the incidence of HFHL, which was defined as a change in pure tone audiometry > 10 dB at frequencies of 4 and 8 kHz.
High-frequency hearing loss occurred after MVD for TGN, GPN, or GN, and the greatest incidence occurred on the ipsilateral side. This hearing loss may be a result of drill-induced noise and/or transient loss of cerebrospinal fluid during the course of the procedure. Changes in intraoperative BAEP waveforms were not useful in predicting HFHL after MVD. Repeated postoperative audiological examinations may be useful in assessing the prognosis of HFHL 7).

2002

Excision of the nervus intermedius and/or of the geniculate ganglion by the middle cranial fossa approach without the production of facial paralysis, in any of 15 cases with geniculate neuralgia is reported. Use of these technique, sometimes in combination with selective section of the Vth cranial nerve, has been successful in relieving the pain of geniculate neuralgia 8).
In 2002 Pulec, review the long-term outcomes in 64 patients who were treated in this manner. Findings indicate that excision of the nervus intermedius and geniculate ganglion can be routinely performed without causing facial paralysis and that it is an effective definitive treatment for intractable geniculate neuralgia 9).

1997

After failing conservative treatment and after undergoing neurologic, otologic, and dental evaluations, 14 patients underwent 20 intracranial procedures consisting of retromastoid craniectomies with microvascular decompression of cranial nerves V, IX, and X with section of the nervus intermedius in most cases.
At operation, vascular compression of the nerves and nervus intermedius was found, which implicated vascular compression as an etiology of this disorder. Initially, 10 of 14 patients had an excellent outcome (71.5%), 3 experienced partial relief (21.5%), and there was 1 failure (7%). Ten patients were available for long-term (> 12 months) follow-up. Of these 10, 3 retained the excellent result (30%), 6 experienced partial relief (60%), and there was 1 failure (10%). Complications included one transient facial paresis, one facial numbness, one paresis of cranial nerves IX and X, one chemical meningitis, two cerebrospinal fluid leaks, and one superficial wound infection. Of those that fell from the excellent to partial category, this usually involved a return of atypical facial pain, but otalgia remained resolved.
Overall, good results (with excellent or partial relief) were found long term for 90% of patients in this series. The authors recommend microvascular decompression of cranial nerves V, IX, and X with nervus intermedius section for the treatment of geniculate neuralgia 10).

Case reports

2014

A case illustration was presented that demonstrates the novel brainstem functional imaging findings for geniculate neuralgia. A 39-year-old man presented with a history of left “deep” ear pain within his ear canal. He noted occasional pain on the left side of his face around the ear. He had been treated with neuropathic pain medications without relief. His wife described suicidal ideations discussed by her husband because of the intense pain.
The patient’s neurologic examination was normal, and otolaryngologic consultation revealed no underlying structural disorder. Anatomic imaging revealed a tortuous vertebral artery-posterior inferior cerebellar artery complex with the posterior inferior cerebellar artery loop impinging on the root entry zone of the nervus intermedius-vestibulocochlear nerve complex and just inferior to the root entry zone of the facial nerve and a small anterior inferior cerebellar artery loop interposed between the cranial nerve VII-VIII complex and the hypoglossal and glossopharyngeal nerves. A left-sided retromastoid craniotomy was performed, and the nervus intermedius was transected. An arterial loop in contact with the lower cranial nerves at the level of the brainstem was mobilized with a polytetrafluoroethylene implant.
The patient indicated complete relief of his preoperative pain after surgery. He has remained pain-free with intact hearing and balance 11).

2007

Figueiredo et al., present a case report of a female patient who was successfully managed with pharmacological treatment 12).

1984

A patient had combined otalgia and intractable unilateral facial spasm, relieved by microsurgical vascular decompression of the seventh and eighth cranial nerve complex in the cerebellopontine angle without section of the intermediate nerve. A dolicho-ectatic anterior inferior cerebellar artery compressed the seventh and eighth cranial nerves complex, suggesting that vascular compression of the intermediate nerve or of the sensory portion of the facial nerve may cause geniculate neuralgia. “Tic convulsif” seems to be a combination of geniculate neuralgia and hemifacial spasm. This combination could be due to vascular compression of the sensory and motor components of the facial nerve at their junction with the brainstem 13).

1) , 2) , 4) , 5) Tang IP, Freeman SR, Kontorinis G, Tang MY, Rutherford SA, King AT, Lloyd SK. Geniculate neuralgia: a systematic review. J Laryngol Otol. 2014 May;128(5):394-9. doi: 10.1017/S0022215114000802. Review. PubMed PMID: 24819337.
3) , 8) Pulec JL. Geniculate neuralgia: diagnosis and surgical management. Laryngoscope. 1976 Jul;86(7):955-64. PubMed PMID: 933690.
6) Rupa V, Weider DJ, Glasner S, Saunders RL. Geniculate ganglion: anatomic study with surgical implications. Am J Otol. 1992 Sep;13(5):470-3. PubMed PMID: 1443083.
7) Thirumala P, Meigh K, Dasyam N, Shankar P, Sarma KR, Sarma DR, Habeych M, Crammond D, Balzer J. The incidence of high-frequency hearing loss after microvascular decompression for trigeminal neuralgia, glossopharyngeal neuralgia, or geniculate neuralgia. J Neurosurg. 2015 Dec;123(6):1500-6. doi: 10.3171/2014.10.JNS141101. PubMed PMID: 25932612.
9) Pulec JL. Geniculate neuralgia: long-term results of surgical treatment. Ear Nose Throat J. 2002 Jan;81(1):30-3. Review. PubMed PMID: 11816385.
10) Lovely TJ, Jannetta PJ. Surgical management of geniculate neuralgia. Am J Otol. 1997 Jul;18(4):512-7. PubMed PMID: 9233495.
11) Tubbs RS, Mosier KM, Cohen-Gadol AA. Geniculate neuralgia: clinical, radiologic, and intraoperative correlates. World Neurosurg. 2013 Dec;80(6):e353-7. doi: 10.1016/j.wneu.2012.11.053. PubMed PMID: 23178920.
12) Figueiredo R, Vazquez-Delgado E, Okeson JP, Gay-Escoda C. Nervus intermedius neuralgia: a case report. Cranio. 2007 Jul;25(3):213-7. Review. PubMed PMID: 17696039.
13) Yeh HS, Tew JM Jr. Tic convulsif, the combination of geniculate neuralgia and hemifacial spasm relieved by vascular decompression. Neurology. 1984 May;34(5):682-3. PubMed PMID: 6538661.

New Book: Trigeminal Neuralgia, An Issue of Neurosurgery Clinics of North America

Trigeminal Neuralgia, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)
By John Y.K. Lee MD, Michael Lim MD

Trigeminal Neuralgia, An Issue of Neurosurgery Clinics of North America, 1e (The Clinics: Surgery)

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This issue of Neurosurgery Clinics offers a broad review of current topics surrounding trigeminal neuralgia including:
Overview and History, Diagnosis/Etiology, Scales of measuring TN pain and response, Medical Therapy, Role of Imaging, Rhizotomy, SRS, Microscopic MVD, Neuromodulation, and many more articles that focus on trigeminal neuralgia.


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  • Published on: 2016-07-14
  • Original language: English
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Editorial Reviews

Trigeminal neuralgia caused by a trigeminocerebellar artery

The trigeminocerebellar artery (TCA) is a unique branch of the basilar artery supplying both the trigeminal nerve root and the cerebellar hemisphere.
The close relationship of the TCA to the trigeminal nerve root may have clinical implications including for the etiology of trigeminal neuralgia, thus the neurosurgeon must be aware of the vasculature of the trigeminal nerve root area and the anatomical variations 1).
The trigeminocerebellar artery supplied two roots (6.89%) of the trigeminal nerves 2).
The trigeminocerebellar artery was found on the left side in one of 22 brainstems, with the vasculature injected with India ink or methylmethacrylate. The trigeminocerebellar artery, which measured 910 microns in diameter, arose from the basilar artery. The artery was divided into the pontine, trigeminal, cerebellopontine, and cerebellar segments. The artery supplied the anterolateral and lateral part of the pons, the trigeminal nerve root, the middle cerebellar peduncle, and most of the petrosal surface of the cerebellar hemisphere.
Occlusion of this artery would cause a syndrome similar to the lateral midpontine syndrome. The trigeminocerebellar artery could be misinterpreted on angiograms as the anterior inferior cerebellar artery with a high origin from the basilar artery 3).


A 31-year-old woman presented with typical right trigeminal neuralgia caused by a trigeminocerebellar artery, manifesting as pain uncontrollable with medical treatment. Preoperative neuroimaging studies demonstrated that the offending artery had almost encircled the right trigeminal nerve. This finding was confirmed intraoperatively, and decompression was completed. The neuralgia resolved after the surgery; the patient had slight transient hypesthesia, which fully resolved within the 1st month after surgery. The neuroimaging and intraoperative findings showed that the offending artery directly branched from the upper part of the basilar artery and, after encircling and supplying tiny branches to the nerve root, maintained its diameter and coursed toward the rostral direction of the cerebellum, which indicated that the artery supplied both the trigeminal nerve and the cerebellum. The offending artery was identified as the trigeminocerebellar artery. This case of trigeminal neuralgia caused by a trigeminocerebellar artery indicates that this variant is important for a better understanding of the vasculature of the trigeminal nerve root 4).
1) Tuccar E, Sen T, Esmer AF. Anatomy and clinical significance of the trigeminocerebellar artery. J Clin Neurosci. 2009 May;16(5):679-82. doi: 10.1016/j.jocn.2008.06.025. Epub 2009 Mar 9. PubMed PMID: 19269826.
2) Marinković SV, Gibo H. The blood supply of the trigeminal nerve root, with special reference to the trigeminocerebellar artery. Neurosurgery. 1995 Aug;37(2):309-17. PubMed PMID: 7477784.
3) Marinković S, Gibo H, Nikodijević I. Trigeminocerebellar artery–anatomy and possible clinical significance. Neurol Med Chir (Tokyo). 1996 Apr;36(4):215-9. PubMed PMID: 8741249.
4) Amagasaki K, Abe S, Watanabe S, Naemura K, Nakaguchi H. Trigeminal neuralgia caused by a trigeminocerebellar artery. J Neurosurg. 2014 Oct;121(4):940-3. doi: 10.3171/2014.6.JNS132292. Epub 2014 Jul 11. PubMed PMID: 25014438.

Actualización de Esclerosteosis y neuralgia del trigémino

La esclerosteosis es una enfermedad ósea poco frecuente, caracterizada por una hiperostosis craniotubular progresiva. El diagnóstico de esclerosteosis se basa en las características clínicas y radiológicas, así como antecedentes familiares de herencia autosómica recesiva. El crecimiento excesivo del cráneo puede dar lugar a la elevación letal de la presión intracraneal , la distorsión de la cara , y el atrapamiento de los nervios craneales , lo que da como resultado una parálisis facial o neuralgia del trigémino secundaria y recurrente.
El tratamiento de la neuralgia del trigémino secundaria a la hiperostosis y resistente a los medicamentos presenta un dilema . El estrechamiento del foramen oval y la dificultad en la identificación del agujero hace que la técnica percutánea sea un desafío.
La descompresión microvascular no debe ser considerada ya que la causa primaria de la neuralgia del trigémino es el atrapamiento del nervio por el estrechamiento del forámen y no el conflicto neurovascular relacionado con neuralgia del trigémino esencial . La radiocirugía estereotáctica, puede ser una buena opción de tratamiento , pero hay una falta de datos publicados que apoyen el uso de este método.
El artículo es gratuito en http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858807/

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