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: Trigeminal schwannoma radiosurgery

Stereotactic radiosurgery (SRS) is an effective and minimally invasive management option for patients with residual or newly diagnosed trigeminal schwannomas. The use resulted in good tumor control and functional improvement 1).
Predictors of a better treatment response included female sex, smaller tumor volume, root or ganglion tumor type, and the application of SRS as the primary treatment 2).
Cranial neuropathies are bothersome complications of radiosurgery, and tumor expansion in a cavernous sinus after radiosurgery appears to be the proximate cause of the complication. Loss of central enhancement could be used as a warning sign of cranial neuropathies, and for this vigilant patient monitoring is required 3).
Larger studies with open-ended follow-up review will be necessary to determine the long-term results and complications of GKS in the treatment of trigeminal schwannomas 4).
It is a promising alternative to conventional microsurgery in cases of neurinomas of the trigeminal nerve including neurotrophic keratopathy, to keep or restore vision 5).

Case series

2013

The records of 52 patients who underwent stereotactic radiosurgery (SRS) for trigeminal schwannoma were reviewed using a retrospective study. The median patient age was 47.1 years (range, 18-77); 20 patients (38.5%) had undergone prior tumor resection and 32 (61.5%) underwent radiosurgery on the basis of imaging diagnosis only. The most frequent presenting symptoms were facial numbness (29 patients), jaw weakness (11 patients), facial pain (10 patients) and diplopia (4 patients). Fifty-two cases with solid tumors were mainly solid in 44 cases (84.6%), mostly cystic in 2 cases (3.8%), and cystic and solid mixed in 6 cases (11.5%). Two cases of mostly cystic tumor first underwent stereotactic cystic fluid aspiration and intracavitary irradiation, and then had MRI localization scan again for gamma knife treatment. The mean tumor volume was 7.2 ml (range, 0.5-38.2). The mean prescription radiation dose was 13.9 Gy (range, 11-17), and the mean prescription isodose configuration was 47.9%.
At a mean follow-up of 61 months (range, 12-156), neurological symptoms or signs improved in 35 patients (67.3%), 14 patients (26.9%) had a stable lesion, and worsening of the disease occurred in 2 patients (3.8%). On imaging, the schwannomas almost disappeared in 8 (15.4%), shrank in 32 (61.5%), remained stable in 5 (9.6%), and increased in size in 7 patients (13.5%). Tumor growth control was achieved in 45 (86.5%) of the 52 patients.
SRS is an effective and minimally invasive management option for patients with residual or newly diagnosed trigeminal schwannomas. The use of SRS to treat trigeminal schwannomas resulted in good tumor control and functional improvement 6).

2009

The records of 33 consecutive patients with trigeminal schwannoma treated via Gamma Knife surgery were retrospectively reviewed. The median patient age was 49.5 years (range 15.1-82.5 years). Eleven patients had undergone prior tumor resection. Two patients had neurofibromatosis Type 2. Lesions were classified as root type (6 tumors), ganglion type (17 tumors), and dumbbell type (10 tumors) based on their location. The median radiosurgery target volume was 4.2 cm3 (range 0.5-18.0 cm3), and the median dose to the tumor margin was 15.0 Gy (range 12-20 Gy).
At an average of 6 years (range 7.2-147.9 months), the rate of progression-free survival (PFS) at 1, 5, and 10 years after SRS was 97.0, 82.0, and 82.0%, respectively. Factors associated with improved PFS included female sex, smaller tumor volume, and a root or ganglion tumor type. Neurological symptoms or signs improved in 11 (33.3%) of 33 patients and were unchanged in 19 (57.6%). Three patients (9.1%) had symptomatic disease progression. Patients who had not undergone a prior tumor resection were significantly more likely to show improvement in neurological symptoms or signs.
Stereotactic radiosurgery is an effective and minimally invasive management option in patients with residual or newly diagnosed trigeminal schwannomas. Predictors of a better treatment response included female sex, smaller tumor volume, root or ganglion tumor type, and the application of SRS as the primary treatment 7).

2007

Phi et al. reviewed the clinical records and radiological data in 22 consecutive patients who received GKS for a trigeminal schwannoma. The median tumor volume was 4.1 ml (0.2-12.0 ml), and the mean tumor margin dose was 13.3 +/- 1.3 Gy at an isodose line of 49.9 +/- 0.6% (mean +/- standard deviation). The median clinical follow-up period was 46 months (range 24-89 months), and the median length of imaging follow-up was 37 months (range 24-79 months).
Tumor growth control was achieved in 21 (95%) of the 22 patients. Facial pain responded best to radiosurgery, with two thirds of patients showing improvement. However, only one third of patients with facial hypesthesia improved. Six patients (27%) experienced new or worsening cranial neuropathies after GKS. Ten patients (46%) showed tumor expansion after radiosurgery, and nine of these also showed central enhancement loss. Loss of central enhancement, tumor expansion, and a tumor in a cavernous sinus were found to be significantly related to the emergence of cranial neuropathies.
The use of GKS to treat trigeminal schwannoma resulted in a high rate of tumor control and functional improvement. Cranial neuropathies are bothersome complications of radiosurgery, and tumor expansion in a cavernous sinus after radiosurgery appears to be the proximate cause of the complication. Loss of central enhancement could be used as a warning sign of cranial neuropathies, and for this vigilant patient monitoring is required 8).


Twenty-six patients with trigeminal schwannomas underwent GKS at the University of Virginia Lars Leksell Gamma Knife Center between 1989 and 2005. Five of these patients had neurofibromatosis and one patient was lost to follow up. The median tumor volume was 3.96 cm(3), and the mean follow-up period was 48.5 months. The median prescription radiation dose was 15 Gy, and the median prescription isodose configuration was 50%. There was clinical improvement in 18 patients (72%), a stable lesion in four patients (16%), and worsening of the disease in three patients (12%). On imaging, the schwannomas shrank in 12 patients (48%), remained stable in 10 patients (40%), and increased in size in three patients (12%). These results were comparable for primary and adjuvant GKSs. No tumor growth following GKS was observed in the patients with neurofibromatosis.
Gamma Knife surgery affords a favorable risk-to-benefit profile for patients harboring trigeminal schwannomas. Larger studies with open-ended follow-up review will be necessary to determine the long-term results and complications of GKS in the treatment of trigeminal schwannomas 9).

2001

A patient developed severe corneal neovascularization within four weeks and the contact lens had to be removed. Three months later an MRI scan was performed, which showed an intracranial tumor originating from the first branch of the trigeminal nerve. Neurinoma of the trigeminal nerve was suspected, and this presumed diagnosis was confirmed by fine needle biopsy. The patient underwent radiosurgery seven weeks later. The epithelium closed, the cornea recovered and stayed stable until the last examination 18 months after radiosurgery.
Radiosurgery is a promising alternative to conventional microsurgery in cases of neurinomas of the trigeminal nerve including neurotrophic keratopathy, to keep or restore vision 10).

References

1) , 6)

Sun J, Zhang J, Yu X, Qi S, Du Y, Ni W, Hu Y, Tian Z. Stereotactic radiosurgery for trigeminal schwannoma: a clinical retrospective study in 52 cases. Stereotact Funct Neurosurg. 2013;91(4):236-42. doi: 10.1159/000345258. Epub 2013 Mar 26. PubMed PMID: 23548989.
2) , 7)

Kano H, Niranjan A, Kondziolka D, Flickinger JC, Dade Lunsford L. Stereotactic radiosurgery for trigeminal schwannoma: tumor control and functional preservation Clinical article. J Neurosurg. 2009 Mar;110(3):553-8. PubMed PMID: 19301456.
3) , 8)

Phi JH, Paek SH, Chung HT, Jeong SS, Park CK, Jung HW, Kim DG. Gamma Knife surgery and trigeminal schwannoma: is it possible to preserve cranial nerve function? J Neurosurg. 2007 Oct;107(4):727-32. PubMed PMID: 17937215.
4) , 9)

Sheehan J, Yen CP, Arkha Y, Schlesinger D, Steiner L. Gamma knife surgery for trigeminal schwannoma. J Neurosurg. 2007 May;106(5):839-45. PubMed PMID: 17542528.
5) , 10)

Ardjomand N, Can B, Schaffler G, Eustacchio S, Scarpatetti M, Pendl G. [Therapy of neurotrophic keratopathy in trigeminal schwannoma with radiosurgery]. Wien Klin Wochenschr. 2001 Aug 16;113(15-16):605-9. German. PubMed PMID: 11571839.

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.

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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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.

Update: Trigeminal nerve deficit after vestibular schwannoma treatment

Microsurgery

In 333 patients after microsurgery (Koos grading scale 1: 12, grade 2: 34, grade 3: 62, and grade 4: 225) permanent trigeminal nervedysfunction was found in 1% 1).
In large/compressive, trigeminal nerve deficit has to be sought to avoid corneal complications in particular. Trigeminal hypoesthesia occurs preoperatively in about half of the cases. It remains relatively stable after tumor removal, but there appears to be an increased rate of absentcorneal reflex and neurotrophic keratitis postoperatively. Karkas et al. were able to correlate pre/postoperative trigeminal hypoesthesia with pre/postoperative MRI findings 2).
Radiosurgery
In 386 patients treated with single-fraction radiosurgery, tumor volume was the only predictor of trigeminal neuropathy 3).
New facial numbness occurred in one patient (2.2%) with normal fifth cranial nerve function prior to stereotactic radiotherapy in 50 patients 4)
Patients receiving > 13 Gy were significantly more likely to develop trigeminal nerve neuropathy than those receiving < 13 Gy (p < 0.001) 5).
1) Betka J, Zvěřina E, Balogová Z, Profant O, Skřivan J, Kraus J, Lisý J, Syka J, Chovanec M. Complications of microsurgery of vestibular schwannoma. Biomed Res Int. 2014;2014:315952. doi: 10.1155/2014/315952. Epub 2014 May 28. PubMed PMID: 24987677; PubMed Central PMCID: PMC4058457.
2) Karkas A, Lamblin E, Meyer M, Gay E, Ternier J, Schmerber S. Trigeminal nerve deficit in large and compressive acoustic neuromas and its correlation with MRI findings. Otolaryngol Head Neck Surg. 2014 Oct;151(4):675-80. doi: 10.1177/0194599814545440. Epub 2014 Aug 1. PubMed PMID: 25085321.
3) Wowra B, Muacevic A, Fürweger C, Schichor C, Tonn JC. Therapeutic profile of single-fraction radiosurgery of vestibular schwannoma: unrelated malignancy predicts tumor control. Neuro Oncol. 2012 Jul;14(7):902-9. doi: 10.1093/neuonc/nos085. Epub 2012 May 3. PubMed PMID: 22561798; PubMed Central PMCID: PMC3379795.
4) Selch MT, Pedroso A, Lee SP, Solberg TD, Agazaryan N, Cabatan-Awang C, DeSalles AA. Stereotactic radiotherapy for the treatment of acoustic neuromas. J Neurosurg. 2004 Nov;101 Suppl 3:362-72. PubMed PMID: 15537191.
5) Sughrue ME, Yang I, Han SJ, Aranda D, Kane AJ, Amoils M, Smith ZA, Parsa AT. Non-audiofacial morbidity after Gamma Knife surgery for vestibular schwannoma. J Neurosurg. 2013 Dec;119 Suppl:E4. Review. PubMed PMID: 25077327.
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