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DOI: 10.1055/s-0045-1809909
Microvascular Decompression for Trigeminal Neuralgia Secondary to Vertebrobasilar Dolichoectasia: a Case Report and Review of the Literature
Funding None
Abstract
Vertebrobasilar dolichoectasia (VBD) is a vasculopathy characterized by elongation and dilation of the affected artery. We present a case of trigeminal neuralgia (TN) secondary to VBD, successfully treated with microvascular decompression (MVD) using an autologous muscle graft (AMG). Additionally, we conducted a review of the literature and meta-analysis of 14 studies involving 303 patients to evaluate the efficacy of this surgical approach. A 63-year-old man experienced recurrent, lancinating pain in the V1, V2, and V3 branches of the right trigeminal nerve. Due to the intractable symptoms, he underwent MVD with an AMG after thorough neurological evaluation. At the 1-year follow-up, he was pain-free without the need for further medication. TN secondary to VBD is a rare and challenging condition, often refractory to medical treatment. MVD with an AMG offers significant symptom relief. Further research, including prospective studies or randomized controlled trials comparing AMG with other graft materials, is necessary to confirm its efficacy.
Keywords
microvascular decompression - autologous muscle grafts - trigeminal neuralgia - vertebrobasilar dolichoectasia - systematic review - meta-analysisIntroduction
Vertebrobasilar dolichoectasia (VBD) is a condition characterized by the elongation, dilation, and tortuosity of the vertebrobasilar arteries, which may compress adjacent neural structures.[1] This uncommon vascular anomaly is often associated with vascular risk factors such as atherosclerosis and hypertension.[2] The dilation of these arteries can lead to mechanical compression, typically at the root entry zone (REZ), most notably the trigeminal nerve, leading to trigeminal neuralgia (TN). In cases where medical treatment fails, surgical interventions such as microvascular decompression (MVD) or Gamma Knife radiosurgery (GKRS) are considered to alleviate the pain by relieving the pressure on the nerve.[3]
The choice of interposition material in MVD is critical for optimizing outcomes and minimizing complications. Autologous muscle grafts (AMGs) offer a biocompatible, low-risk alternative, yet their application in MVD for TN remains underexplored. This study presents the first detailed report on AMG in MVD for TN secondary to VBD, emphasizing its safety and efficacy through a case report, a systematic review, and a single-arm meta-analysis.
Case Presentation
A 63-year-old male presented to our neurology clinic with a 7-year history of paroxysmal shooting pain in the right V1, V2, and V3 branches of the trigeminal nerve, occurring more than 10 times a day, and triggered by chewing, drinking, and brushing his teeth. He had no significant medical history or comorbidities.
Diagnosed with TN, he was initially treated with carbamazepine, which was progressively increased to 1,200 mg/day. However, the medication was ineffective, and caused side effects, including postural imbalance and drowsiness. Additional antiepileptic drugs—lamotrigine 400 mg/day, phenytoin 300 mg/day, and clonazepam 4 mg/day—were tried at maximum tolerated doses but failed to control symptoms, indicating a refractory condition, prompting referral to our neurosurgery department.
Given findings consistent with TN, the patient underwent a magnetic resonance imaging scan using the Fast Imaging Employing Steady-state Acquisition (FIESTA) sequence to assess for neurovascular compression ([Fig. 1]), revealing a dolichoectatic basilar artery (BA), with compression of the right trigeminal nerve. TN was classified as Grade V according to the Barrow Neurological Institute scale.[4]


Surgery
The patient was considered for a surgical procedure to alleviate the neurovascular compression. A right retrosigmoid approach to access the cerebellopontine angle was performed, and the dura mater was opened and suspended, followed by the emptying of the cisterna magna (see [Fig. 2] for surgical images).


Using an operating microscope, a retractor was used to expose the cerebellar hemisphere to expose the cerebellopontine angle, revealing cranial nerves VII, VIII, and lower cranial nerves. The right trigeminal nerve was compressed by an enlarged vertebral artery (VA) loop at the REZ, classified as Grade III, according to Sindou's classification.[5] Muscle fragments harvested from the suboccipital region during surgery were used to buffer the vessel's pulsatility against the nerve. Arachnoid adhesions were sectioned, and the VA was displaced using a cerebral retractor, allowing placement of an AMG, fixed with biological glue (see [Fig. 2]). Hemostasis was confirmed, and the surgical site was irrigated with sterile saline. The dura mater was closed with an epicranial flap and biological glue, followed by a layered anatomical closure without drainage, and a compressive dressing was applied.
Postoperative Course
Pharmacological therapy was progressively tapered and discontinued within 60 days. Notably, the paroxysmal pain disappeared immediately after surgery. No postoperative complications were observed. At 1-year follow-up, the patient remained pain-free, required no pharmacological treatment, and reported significant improvements in quality of life and daily functioning.
Literature Review
Materials and Methods
Following the standard PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines, we performed a systematic review and meta-analysis of the available literature reporting cases of TN secondary to VBD (see [Fig. 3] for PRISMA flow diagram). PubMed, Scopus, Embase, and Virtual Health Library were searched from inception until June 2024. The search strategy was carried out as follows: (((vertebrobasilar dolichoectasia) OR (dolichoectasia) OR (vertebrobasilar))) AND (trigeminal neuralgia). We excluded case reports, articles with unavailable full texts, articles not published in English, abstracts not followed by a peer-reviewed publication, and cases not treated with MVD (see [Supplementary Methods 1] [available in the online version] for full search strategy).


Three authors independently extracted data (F.C.P.C., P.R.M.N., L.A.L.V.) following predefined search criteria and quality assessment methods. After applying the exclusion criteria, three reviewers (F.C.P.C., P.R.M.N., and L.A.L.V.) analyzed the remaining articles for quality assessment. Disagreements were resolved through consensus among all authors until agreement was achieved. The data extracted included article characteristics (publication year, authors, follow-up), population characteristics (age, sex, affected side, pain distribution, disease duration, hypertension prevalence), and outcomes (pain-free status, pain recurrence, facial numbness, facial palsy, hearing loss, diplopia). Pain-free status was defined as complete or partial pain relief.
Statistical Analysis
Statistical analyses were performed using R software (version 4.3.1) and extension package “meta” for all statistical analyses. Proportions were pooled using a random-effects model with 95% confidence intervals (CIs). Heterogeneity was assessed with the chi-square test.
Review Results
From 609 relevant publications identified, 389 duplicates were removed, leaving 220 articles. Subsequently, 191 studies were removed after reading the title and abstract. Then, 29 articles were selected for full-text reading. In sequence, 15 articles were excluded after full-text reading. Ultimately, 14 articles were included, all retrospective reviews ([Fig. 3]).
Our series included 303 patients, 182 men (60.1%) and 121 women (39.9%), with a mean age of 61.77 years ([Table 1] for summary of included studies). Among them, 132 patients (43.6%) had hypertension. The pain was localized on the left side in 185 cases (61.1%) and on the right in 118 cases (38.9%). In 108 cases (35.6%), only one branch of the trigeminal nerve was affected. In 31 cases (10.2%), both the V1 (ophthalmic) and V2 (maxillary) branches were affected. In 123 cases (40.6%), the V2 (maxillary) and V3 (mandibular) branches were affected. In 30 cases (9.9%), all three branches—V1 (ophthalmic), V2 (maxillary), and V3 (mandibular)—were affected simultaneously. Lastly, there was only 1 case (0.3%) where the V1 (ophthalmic) and V3 (mandibular) branches were affected, without involvement of V2.
Author (first author), year (country) |
Sample |
Sex (M/F) |
Age |
Side (L/R) |
Pain distribution |
Disease duration |
Outcome[6] |
---|---|---|---|---|---|---|---|
Linskey,1994 (United States)[6] |
31 |
21/1 0 |
62 ± 6.7 |
20/11 |
V1–2: 4; V2 3; V1–2–3: 5; V2–3: 15; V3: 4 |
6.8 ± 5.7 y |
28 (90.4%) pain-free; 3 (9.6%) partial relief |
Zhong, 2011 (China)[7] |
9 |
5/4 |
60 |
6/3 |
NA |
5.44 y |
7 (77.8%) pain-free, 2 (22.2) partial relief |
El-Ghandour, 2010 (Egypt)[8] |
10 |
6/4 |
54 |
6/4 |
V1–V2: 1; V2: 1; V3: 1; V2–V3: 5; V1–V2–V3: 2 |
4.5 y |
8 (80%) pain-free; 2 (20%) partial relief |
Yang, 2012 (China)[9] |
10 |
5/5 |
64 |
5/5 |
V1–V2: 2; V2: 3; V3:1; V2–V3: 4 |
6.45 y |
8 (80%) pain free; 2 (20%) partial relief[10] |
Ma, 2013 (China)[10] |
11 |
8/3 |
62.5 |
8/3 |
V2: 3; V2–V3: 8 |
3.87 y |
11 pain-free (100%) |
Juretschke, 2016 (Spain)[11] |
7 |
6/1 |
67 |
6/1 |
V1–V2: 3; V2: 1; V3: 1; V2–V3: 1; V1–V2–V3: 1 |
8 y |
7 pain-free (100%)[12] |
Vanaclocha, 2016 (United Kingdom)[12] |
7 |
5/2 |
64.88 |
6/1 |
V2: 1; V3: 2; V2 + V3: 4 |
NA |
7 pain-free (100%) |
Sun, 2017 (China)[13] |
15 |
8/7 |
60.8 |
6/9 |
V1V1: 1, V2: 7, V3: 1; V1 + V2: 1; V2 + V3: 3; V1 + V2 + V3: 1; V1 + V3: 1 |
2.9 y |
15 pain-free (100%) |
Honey, 2018 (Canada)[2] |
13 |
10/3 |
67.3 |
8/5 |
V1: 1; V2: 3; V3: 3; V1–V2: 2; V2–V3: 3; V1–V2–V3: 1 |
NA |
11 (84.6%) pain-free; 2(15.4%) no relief |
Chai, 2020 (China)[3] |
39 |
24/1 5 |
60.9 |
11/5 |
V2: 4; V3: 1; V2–V3: 8; V1–V2–V3: 3 |
3.7 ± 2.3 y |
10 (62.5%) pain-free; 2 (12.5%) partial relief; 4 (25%) no relief |
61.9 |
14/9 |
V1–V2: 2; V2: 6; V3: 3; V2–V3: 10; V1–V2–V3: 2 |
3.4 ± 2.6 y |
21 (91.3%) pain-free; 1 (4.3%) partial relief; 1 (4.3%) no relief |
|||
Shulev, 2020 (Russia)[14] |
14 |
4/10 |
66 ± 9 |
10/4 |
V1–V2: 2; V2–V3: 6; V3: 3; V1–V2–V3: 2; 1 missing |
Mean: 4.9 y |
14 pain-free (100%) |
Zhao, 2021 (China)[15] |
46 |
28/1 8 |
61.1 |
30/16 |
Single branch (V1 or V2 or V3): 16; V1 + V2: 3; V2 + V3: 20; V1 + V2 + V3: 7 |
3.8 ± 2.3 y |
36 (78.2%) pain-free; 4 (8.7%) partial relief; 6 no relief (13%) |
Yu, 2022 (China)[16] |
30 |
21/9 |
63.03 |
22/8 |
V2: 6; V3: 1; V1 + V2: 5; V2 + 3: 15; V1 + V2 + V3: 3 |
4.67 ± 2.46 y |
27 pain-free (90%); 3 (10%) partial relief |
Zheng, 2023 (China)[17] |
61 |
31/3 0 |
59.8 ± 1 .73 |
27/34 |
V1: 6; V2: 11; V3: 14; V1–V2: 6; V2–V3: 21; V1–V2–V3: 3 |
46.8 ± 1.14 mo |
51 (83.6%) pain-free; 6 (9.8%) partial relief; 4 no relief (6.6%) |
Total |
303 |
182/ 121 |
61.77 |
185/118 |
Single branch: 108; V1–V2: 31; V2–V3: 123; V1–V2–V3: 30; V1–V3: 1 |
4.9 y |
Pain-free: 261 (86.1%); partial relief: 25 (8.3%); no relief: 17 (5.6%) |
Vascular compression involved the BA alone in 50 cases (16.5%), while compression by the VA alone was reported in 101 cases (33.3%). Compression by both arteries was observed in 16 cases (5.3%). Simultaneous compression by the vertebral, basilar, and anterior inferior cerebellar arteries (VA + BA + AICA) was identified in 24 cases (7.9%), while the combination of VA and AICA was seen in 21 cases (6.9%). Other vascular compression patterns accounted for 91 cases (30.0%).
Of 301 patients treated with MVD, 4 (1.3%) underwent MVD combined with selective partial posterior rhizotomy of the trigeminal nerve and 2 (0.7%) had nerve section. Post-surgically, 261 patients (86.7%) achieved complete pain relief, 25 (8.3%) partial relief, and 17 (5.6%) had no relief. Facial numbness was the most common complication, occurring in 35 cases (11.6%), suggesting nerve damage or irritation may have occurred during or after the procedure. Facial palsy was reported in 12 cases (4.0%), possibly linked to trauma to adjacent cranial nerves. Hearing loss was observed in 17 cases (5.6%), indicating some damage to the cochlear nerve during the surgical process. Diplopia, reported in 12 cases (4.0%), potentially involved cranial nerve VI. The 17 cases (5.6%) of other complications include various less frequent but significant issues, such as cerebrospinal fluid leaks or infections.
Teflon was the most common interposition material, used in 270 cases[2] [3] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] (90%), followed by biological glue slings in 23 cases[3] (7.7%), Ivalon in 3 cases (1.0%), muscle in 2 cases (0.7%),[6] silicone in 1 case (0.3%), and human fibrin glue in 1 case (0.3%).
Pooled Analysis of all Included Studies
The pooled pain-free rate post-MVD was 89.64% (95% CI: 84.19–94.23%; I2 = 32.7%; [Fig. 4A]). Conversely, the rate of pain recurrence during follow-up was 4.83% (95% CI: 1.84–8.73%; I2 = 0%; [Fig. 4B]). Our analyses of safety outcomes revealed that the rate of facial palsy was 2.16% (95% CI: 0.23–5.26%; I2 = 0%; [Supplementary Methods 2] [available in the online version]), the rate of facial numbness was 6.59% (95% CI: 1.93–13.00%; I2 =38.5%; [Supplementary Methods 3] [available in the online version]), hearing loss occurred in 3.38% of cases (95% CI: 1.02–6.59%; I2 = 0.3%; [Supplementary Methods 4] [available in the online version]), and diplopia in 4.23% (95% CI: 0.27–10.89%; I2 = 55.0%; [Supplementary Methods 5] [available in the online version]).


Discussion
Epidemiology
Intracranial dolichoectasia is observed in approximately 2.8 to 7.7% of patients with vascular compression, being an uncommon cause of TN.[18] Although most cases occur in older adults, instances have also been documented in younger individuals. The condition is more prevalent in patients with hypertension and atherosclerosis.[3] [16] [17] Our systematic review of 14 studies, including 303 patients, highlights that VBD is more prevalent in older adults, often associated with hypertension.
Etiologies
Dolichoectasia involves increased arterial diameter and length, primarily affecting the basilar and VAs. However, it can also involve other arteries. Microscopically, it results from degeneration of the internal elastic lamina in the media of the affected blood vessels. Its etiology is multifactorial, including genetic predispositions, congenital arterial defects, and hemodynamic factors such as chronic hypertension.[17]
Diagnosis
The diagnosis of VBD is typically made through imaging studies such as magnetic resonance angiography or 3D time-of-flight techniques. These imaging methods help visualize the enlargement, elongation, and tortuosity of the vertebro BAs. VBD is confirmed when the basilar or VA's diameter exceeds 4.5 mm, there is a deviation of more than 10 mm from the normal course, or when the BA is longer than 29.5 mm, or the VA exceeds 23.5 mm.[17] While vascular compression can be asymptomatic, it may cause transient ischemic attacks, strokes, intracranial bleeding, brainstem compression, hemifacial spasm, or TN.[1] [7]
Treatment
TN caused by VBD typically begins with medication, with carbamazepine as the first-line drug. However, many patients fail to respond or experience side effects such as drowsiness and imbalance. For these patients, MVD is the most effective surgical option, offering immediate pain relief by repositioning the compressing blood vessels. In our review, 94.3% of patients had full or partial relief, with complications such as facial numbness and hearing loss occurring in fewer than 12%. Less invasive alternatives, such as GKRS, carry a higher risk of recurrence.[19] MVD remains the preferred treatment for severe and refractory TN cases, offering long-term relief.
Use of Autologous Muscle Graft
The use of AMG in MVD for TN presents several significant advantages.[20] As a biocompatible and natural material, AMG reduces the risk of complications associated with synthetic materials, such as granuloma formation or chemical inflammation.[21] Since the muscle graft is harvested from the patient's own body, the likelihood of rejection is minimized. Additionally, its soft texture allows it to better absorb neurovascular pulsations, protecting the trigeminal nerve without exerting additional pressure. This technique also offers a practical and cost-effective solution, as the muscle is readily available, making AMG a safe and effective alternative for patients undergoing MVD.
Although synthetic materials such as Teflon are commonly used, they have been associated with adverse events such as foreign body granulomas and persistent inflammation, especially when in contact with the REZ.[22] Recent data reinforce the strategic value of using AMGs in MVD. In a recent multicenter analysis involving over 1,000 patients, AMG showed excellent clinical performance, with over 86% achieving immediate pain relief and recurrence rates remaining below 14% at long-term follow-up.[23] Unlike synthetic materials, muscle grafts carry a significantly lower risk of foreign-body reaction, particularly important in cases of VBD, where extensive arterial contact further increases the potential for implant-related inflammation.
An alternative approach is the biomedical glue sling, which fixes the artery to the dura mater with adhesive, avoiding direct contact with the nerve. Although effective, it involves greater vascular manipulation and may lead to complications such as fixation failure, symptom recurrence, or indirect nerve compression.[24] This technique may be particularly useful when a decompression interface is not feasible due to anatomical constraints.
Prognosis
The prognosis for treating VBD with MVD is generally positive. In most cases, patients achieve complete or significant pain relief. Ninety percent of patients experienced immediate improvement in pain and 75% achieved a satisfactory result within 15 years.[16] In our single-arm meta-analysis, 89.64% of patients achieved complete or partial pain relief after surgery. Furthermore, the effectiveness of MVD for treatment can reach 98%.[14] The main factors that influence the few cases of poor prognosis are the degrees of vertical elongation and lateral displacement of the artery.[12] Complications include new or worsening hypoalgesia or hypoesthesia, facial numbness, diplopia, facial palsy, or hearing loss.[4] Our meta-analysis of postoperative morbidities showed that facial numbness was the most common complication, occurring in 6.59% of cases. In contrast, the combined incidence of the other three complications remained below 10%. That said, recurrence of pain may be present, occurring in approximately 4.83% of cases according to our meta-analysis, although 86% of patients are medication-free for pain control within the first 10 years after surgery.[15]
Limitations
This study has limitations. The 14 included studies vary in design, patient populations, and clinical approaches, potentially affecting result consistency. Their retrospective nature increases risks of selection and reporting biases. As for the present case report, its intrinsic limitations—such as the lack of generalizability and potential observer bias—must also be acknowledged. These factors limit the strength of the conclusions and reinforce the need for well-designed prospective studies on VBD.
Conclusion
TN secondary to VBD is a rare and challenging condition, often refractory to medical treatment. Our case report demonstrates MVD with AMG achieving complete symptom relief without complications, consistent with the literature. This systematic review and meta-analysis of 14 articles, including 303 patients, reinforces the effectiveness of MVD, with 89.64% of cases showing complete or partial pain relief. AMG is a safe, biocompatible alternative, reducing risks associated with synthetic materials. MVD remains a first-line surgical option for refractory cases, emphasizing the need for personalized treatment based on vascular compression patterns and clinical conditions.
To further strengthen the current understanding and therapeutic approach to VBD-related neuralgias, future research should prioritize prospective studies and randomized controlled trials comparing the effectiveness of different surgical techniques and materials, including the use of AMG, in MVD. Such studies may contribute to establishing standardized treatment protocols and improving long-term outcomes for patients with this rare but impactful condition.
Conflict of Interest
None declared.
Authors' Contributions
F.C.P.C. formulated the research question and developed the search strategy, screened the articles and extracted the data, synthesized the results, and drafted the manuscript. J.F.C.-N. performed the quality assessment and provided critical insights and supervision. F.J.A.N. performed the statistical analysis and drafted the manuscript. P.R.M.-N. screened the articles, extracted the data, and drafted the manuscript. L.A.L.V. screened the articles, extracted the data, and drafted the manuscript. G.C.-F. revised the manuscript and provided expert input. P.R.L.L. revised the manuscript and provided expert input.
Patients' Consent
Informed consent was obtained from the patient included in this study.
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References
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- 2 Honey CM, Kaufmann AM. Trigeminal neuralgia due to vertebrobasilar artery compression. World Neurosurg 2018; 118: e155-e160
- 3 Chai S, Xu H, Wang Q. et al. Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar dolichoectasia: interposition technique versus transposition technique. Acta Neurochir (Wien) 2020; 162 (11) 2811-2821
- 4 Rogers CL, Shetter AG, Fiedler JA, Smith KA, Han PP, Speiser BL. Gamma knife radiosurgery for trigeminal neuralgia: the initial experience of The Barrow Neurological Institute. Int J Radiat Oncol Biol Phys 2000; 47 (04) 1013-1019
- 5 Sindou M, Leston J. Microvascular decompression for trigeminal neuralgia. In: Samii M, Ammirati M. eds Practical Handbook of Neurosurgery: From Leading Neurosurgeons. Vienna, Austria: Springer; 2009: 455-464
- 6 Linskey ME, Jho HD, Jannetta PJ. Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. J Neurosurg 1994; 81 (01) 1-9
- 7 Zhong J, Zhu J, Li ST, Guan HX. Microvascular decompressions in patients with coexistent hemifacial spasm and trigeminal neuralgia. Neurosurgery 2011; 68 (04) 916-920 , discussion 920
- 8 El-Ghandour NMF. Microvascular decompression in the treatment of trigeminal neuralgia caused by vertebrobasilar ectasia. Neurosurgery 2010; 67 (02) 330-337
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- 10 Ma X, Sun X, Yao J. et al. Clinical analysis of trigeminal neuralgia caused by vertebrobasilar dolichoectasia. Neurosurg Rev 2013; 36 (04) 573-577 , discussion 577–578
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- 14 Shulev YA, Gordienko KS, Trashin AV, Pechiborshch DA. Mikrovaskulyarnaya dekompressiya pri nevralgii troinichnogo nerva vsledstvie vertebrobazilyarnoi dolikhoektazii. Vopr Neirokhir 2020; 84 (05) 50-63
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- 16 Yu F, Yin J, Lu PG, Zhao ZY, Zhang YQ, Men XZ. Microvascular decompression by interposition method for treatment of trigeminal neuralgia due to vertebrobasilar dolichoectasia: a retrospective single-center study. Neurosurg Rev 2022; 45 (04) 2709-2715
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Publication History
Article published online:
25 June 2025
© 2025. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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References
- 1 Wolters FJ, Rinkel GJE, Vergouwen MDI. Clinical course and treatment of vertebrobasilar dolichoectasia: a systematic review of the literature. Neurol Res 2013; 35 (02) 131-137
- 2 Honey CM, Kaufmann AM. Trigeminal neuralgia due to vertebrobasilar artery compression. World Neurosurg 2018; 118: e155-e160
- 3 Chai S, Xu H, Wang Q. et al. Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar dolichoectasia: interposition technique versus transposition technique. Acta Neurochir (Wien) 2020; 162 (11) 2811-2821
- 4 Rogers CL, Shetter AG, Fiedler JA, Smith KA, Han PP, Speiser BL. Gamma knife radiosurgery for trigeminal neuralgia: the initial experience of The Barrow Neurological Institute. Int J Radiat Oncol Biol Phys 2000; 47 (04) 1013-1019
- 5 Sindou M, Leston J. Microvascular decompression for trigeminal neuralgia. In: Samii M, Ammirati M. eds Practical Handbook of Neurosurgery: From Leading Neurosurgeons. Vienna, Austria: Springer; 2009: 455-464
- 6 Linskey ME, Jho HD, Jannetta PJ. Microvascular decompression for trigeminal neuralgia caused by vertebrobasilar compression. J Neurosurg 1994; 81 (01) 1-9
- 7 Zhong J, Zhu J, Li ST, Guan HX. Microvascular decompressions in patients with coexistent hemifacial spasm and trigeminal neuralgia. Neurosurgery 2011; 68 (04) 916-920 , discussion 920
- 8 El-Ghandour NMF. Microvascular decompression in the treatment of trigeminal neuralgia caused by vertebrobasilar ectasia. Neurosurgery 2010; 67 (02) 330-337
- 9 Yang XS, Li ST, Zhong J. et al. Microvascular decompression on patients with trigeminal neuralgia caused by ectatic vertebrobasilar artery complex: technique notes. Acta Neurochir (Wien) 2012; 154 (05) 793-797 , discussion 797
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