Abstract
This study aimed to show a novel visualization method to investigate neurovascular compression of the trigeminal nerve (TN) using a volume-rendering fusion imaging technique of 3D fast imaging employing steady-state acquisition (3D FIESTA) and coregistered 3D time of flight MR angiography (3D TOF MRA) sequences, which we called “neurovascular study of the trigeminal nerve”.
We prospectively studied 30 patients with unilateral trigeminal neuralgia (TN) and 50 subjects without symptoms of TN (control group), on a 3 Tesla scanner. All patients were assessed using 3D FIESTA and 3D TOF MRA sequences centered on the pons, as well as a standard brain protocol including axial T1, T2, FLAIR and GRE sequences to exclude other pathologies that could cause TN. Post-contrast T1-weighted sequences were also performed.
All cases showing arterial imprinting on the trigeminal nerve (n = 11) were identified on the ipsilateral side of the pain. No significant relationship was found between the presence of an artery in contact with the trigeminal nerve and TN. Eight cases were found showing arterial contact on the ipsilateral side of the pain and five cases of arterial contact on the contralateral side.
The fusion imaging technique of 3D FIESTA and 3D TOF MRA sequences, combining the high anatomical detail provided by the 3D FIESTA sequence with the 3D TOF MRA sequence and its capacity to depict arterial structures, results in a tool that enables quick and efficient visualization and assessment of the relationship between the trigeminal nerve and the neighboring vascular structures.
Keywords: trigeminal neuralgia, magnetic resonance imaging, brain, trigeminal nerve diseases, facial pain
Introduction
Trigeminal neuralgia (TN) is a syndrome characterized by intense facial pain like electrical discharges, paroxysmal, usually unilateral, comprising one or more innervations territories of the trigeminal nerve branches. Pain may last few seconds, but several consecutive episodes may occur, producing a feeling of discomfort and desperation for the patient. TN affects elderly adults, with an incidence rate of four to five every 400,000 inhabitants. It is uncommon in patients younger than 30 years of age. Only 1% of TN cases involves patients under 20 years of age.1–3
The most common cause of TN is focal compression of the trigeminal nerve root, close to its point of entry into the pons (root entry zone, REZ), produced by a neighboring arterial or venous vessel. This cause was identified by Jannetta (Jannetta, 1967),4 however, in 1934 Walter Dandy suggested a causal relationship between an impinging superior cerebellar artery and TN.5 Several authors believe that neurovascular compression (NVC) accounts for 80–90% of the cases of TN (Haines et al., 1980; Jannetta, 1980; Richards et al., 1983; Fukushima, 1990; Meaney et al., 1995, Bowser, 1997; Hamlyn, 1997; McLaughlin et al., 1999). Rarely, trigeminal neuralgia results from vascular compression of the nerve root by a saccular aneurysm or an arteriovenous malformation (AVM). A wide range of other compressive lesions can also cause TN, including: vestibular schwannomas, meningiomas and epidermoid cysts. Compression of the trigeminal nerve root may be mediated by the tumor itself, by an interposed blood vessel, or by distortion of the contents of the posterior fossa, with displacement of the nerve root against a blood vessel or the skull base. Rarely, TN results from bony compression of the nerve, for example, due to an osteoma or deformity resulting from osteogenesis imperfecta.4,5
The mechanism through which TN is believed to originate is that compression by arteries and veins lying on the trigeminal nerve roots may cause nerve demyelination, causing aberrant impulse generation, which manifests as severe pain. It is believed that compression of the nerve fibers causes hyperexcitability. A study of 12 surgical biopsies from patients with TN presumably caused by vascular compression reported demyelination and dysmyelination.5
The purpose of our study was to describe a novel visualization method for the study of trigeminal nerve NVC using a volume-rendering fusion imaging technique of 3D fast imaging employing steady-state acquisition (3D FIESTA) and coregistered 3D time of flight MR angiography (3D TOF MRA) sequences performed on a 3 Tesla scanner, which we called “neurovascular study of the trigeminal nerve”. We will also make a brief bibliographical review of articles on NVC in patients with TN.
Materials and Methods
For the present study, we prospectively studied 80 patients, 30 with unilateral TN and 50 without symptoms of TN (control group), on a 3 Tesla MR imaging unit (Signa HDx3T GE Healthcare, Milwaukee, WS, USA) with a 12-channel head coil during a 12-month period. Written informed consent was obtained from all patients.
Patients and study protocol
Patients with TN
A total of 30 patients with characteristic symptoms of unilateral TN were evaluated, 19 females and 11 males, age range 28–73 years (mean age, 53 years) (Table 1). Seventeen patients reported right neuralgia and 13 left neuralgia. The study was requested by the treating neurologist or neurosurgeon.
Table 1.
Patients with characteristic symptoms of trigeminal neuralgia (n = 30).
| Patient N° | Age | Sex | Neuralgia | Ipsilateral to the pain | Contralateral to the pain |
|---|---|---|---|---|---|
| 1 | 44 | F | Right | Normal | SCA contacts |
| 2 | 44 | M | Right | SCA contacts- Vein contacts | SCA contacts |
| 3 | 70 | F | Right | Vein contacts | Vein contacts |
| 4 | 53 | F | Right | Normal | Vein contacts |
| 5 | 36 | M | Right | Normal | SCA contacts |
| 6 | 28 | F | Right | Vein contacts | Normal |
| 7 | 71 | F | Right | SCA contacts | SCA contacts |
| 8 | 64 | F | Right | AICA contacts – Vein contacts | Normal |
| 9 | 50 | M | Right | Vein contacts | Normal |
| 10 | 71 | F | Right | SCA imprints | Normal |
| 11 | 34 | M | Right | SCA imprints | Normal |
| 12 | 73 | F | Right | Vein contacts | Normal |
| 13 | 66 | M | Right | SCA contacts | Normal |
| 14 | 56 | M | Right | SCA imprints | Vein imprints |
| 15 | 47 | F | Left | SCA imprints | Normal |
| 16 | 48 | F | Left | SCA imprints | Normal |
| 17 | 44 | M | Left | AICA contacts | Normal |
| 18 | 50 | M | Left | SCA contacts | Vein contacts |
| 19 | 45 | F | Left | Normal | Vein contacts |
| 20 | 67 | F | Left | SCA imprints | SCA contacts |
| 21 | 41 | F | Left | Vein contacts | Vein contacts |
| 22 | 56 | F | Left | SCA contacts – Vein contacts | Normal |
| 23 | 68 | F | Left | SCA and AICA imprint | Normal |
| 24 | 53 | F | Left | SCA imprints | Normal |
| 25 | 43 | F | Right | Normal | Normal |
| 26 | 65 | M | Left | VA and PICA imprint | Normal |
| 27 | 63 | M | Left | Vein contacts | Normal |
| 28 | 35 | F | Right | SCA contacts | Normal |
| 29 | 63 | F | Left | VA imprints | Vein contacts |
| 30 | 52 | M | Right | SCA imprints | Normal |
Control group
A total of 50 patients without symptoms of TN were selected for the control group, whose neurologist had ordered an MRI scan of the inner ear due to unilateral hearing loss. Of the total patients in the control group (n = 50), 32 were female and 18 male, age range 25–78 years.
Imaging protocol
All patients were assessed using 3D FIESTA and 3D TOF MRA sequences centered on the pons, as well as a standard brain protocol including axial T1, T2, FLAIR and GRE sequences to exclude other pathologies that could cause TN. Post-contrast T1-weighted sequences were also performed on conventional transverse, sagittal and coronal sections.
The parameters used in the 3D FIESTA sequence were: TR, 5.5 ms; TE, 2.1 ms; flip angle; 60°; matrix, 360 x 360; FOV, 18 mm; section thickness, 0.6 mm; acquisition time, 4 minutes 10 seconds; transverse sections; 76 slices. The imaging parameters used in the 3D TOF MRA sequence were: TR, 38 ms; TE, 2.3 ms; flip angle, 20°; matrix, 320 x 224; FOV 22 (80%); section thickness, 0.8 mm; acquisition time; 4 minutes 22 seconds; transverse sections; 74 slices. 3D FIESTA sequence is a high-resolution volumetric sequence, which increases the contrast between CSF and tissues, allowing a fine anatomical analysis of the vasculo-nervous structures of the cerebellopontine cistern. The CSF appears hyperintense, the blood vessels hypointense and the cranial nerves isointense relative to the brain stem. With this sequence alone, a trained neuroradiologist can detect NVC. Furthermore, following the path of the blood vessel involved, it can be determined whether it is an artery or a vein. This sequence is usually applied in the protocol of inner ear studies, since it enables a thorough assessment of the morphology of the inner ear and the vestibulocochlear and facial nerves.
The 3D TOF MRA sequence demonstrates fast flowing blood, allowing excellent depiction of the arterial anatomy, since arteries appear hyperintense contrasting with venous structures and the trigeminal nerves which appear as isointense structures relative to the brain stem. CSF appears iso-hypointense. The problem arising with this sequence is that, in many cases, there is no clear contrast difference between the trigeminal nerves and CSF, making its visualization difficult. This technique allows us to make a 3D reconstruction of the posterior arterial circuit, to evaluate its anatomical variants and its relationship with the cranial nerves.
Image analysis
Images were transferred to a Workstation with GE Readyview software for post-processing and analysis.
Fusion of the 3D FIESTA and 3D TOF MRA volumetric sequences was performed, using the volume rendering module, obtaining a single 3D image, where the vascular anatomy and the trigeminal nerve are visible in different colors. We can see the arteries color-rendered in red, and the veins in black. Thus, we can objectively distinguish and identify the type of blood vessels (arteries or veins) from the trigeminal nerve, which appears isointense relative to the brain stem (Figure 1). Therefore, this high-resolution fused technique facilitates the visualization and interpretation of the NVC, through the differentiation and depiction of the trigeminal nerve, arterial and venous structures as well as their relationship from various viewpoints. This fusion technique enables not only to assess neurovascular compression of the trigeminal nerve, but also of other cranial nerves, such as the facial nerve and its relationship with the anterior inferior cerebellar artery (AICA) in case there is a loop in the AICA, and the oculomotor nerve with the posterior cerebral arteries or their branches.
Figure 1.
Normal trigeminal nerves. Fusion imaging technique of 3D FIESTA and 3D TOF MRA sequences, coronal view. Both trigeminal nerves (green arrows) are observed, located in the cerebellopontine cistern. The nerves maintain their normal morphology and trajectory. No NVC with neighboring blood vessels is identified.
Data analysis
All the studies (TN and control groups) were analyzed by two neuroradiologists (ten and 12 years of experience), who were blinded to the clinical findings, reaching a consensus on the results obtained.
NVC of the trigeminal nerve was evaluated in TN patients on the side of the pain, as well as on the contralateral side. In the control group it was also evaluated whether there was NVC in both trigeminal nerves. When evaluating NVC of the trigeminal nerve, the presence of NVC was considered if there was contact between a blood vessel and the trigeminal nerve. In a second step, it was determined whether the blood vessel involved was an artery or a vein, and in the case of arteries, we determined which artery was responsible for the compression.
In addition, we distinguished whether there was contact or imprinting of the neighboring blood vessel on the nerve. It was considered contact when the blood vessel did not alter the morphology of the trigeminal nerve, or its trajectory (Figure 2). It was considered imprinting when the blood vessel produced deformation of the trigeminal nerve in its circumference (Figure 3).
Figure 2.
SCA contacts with the trigeminal nerve. Fusion technique of 3D FIESTA and 3D TOF MRA sequences, coronal view. The left SCA is contacting with the internal surface of the left trigeminal nerve (blue arrow), without deforming it or causing a trajectory change.
Figure 3.
SCA imprints on the trigeminal nerve. Fusion technique of 3D FIESTA and 3D TOF MRA sequences, coronal view, a duplication of the left SCA is identified (anatomical variant). The upper branch, of dominant caliber, imprints on the superior and internal surface of the left trigeminal nerve (blue arrow), deforming it.
Therefore, the relation between the trigeminal nerve and its neighboring blood vessels was divided into three types: normal (without contact), with contact and with imprinting.
Statistical analysis
In order to investigate if there was a correlation between the presence of TN and a blood vessel contacting or imprinting on the trigeminal nerve, the X2 (Chi-square) statistical method was used.
The type of blood vessel (artery or vein) was evaluated separately, as well as the type of relationship between the blood vessel and nerve (if the blood vessel contacts with or imprints on the nerve). Differences were considered statistically significant if p value was under .01.
Results
In the group of patients with TN, the findings on the symptomatic side versus the contralateral asymptomatic side were compared. Results are shown in Table 2, which highlights the higher number of normal results on the contralateral side of the pain (18/30) compared to the side of the pain (5/30).
Table 2.
Results obtained from the evaluation of neurovascular compression in patients with trigeminal neuralgia and in the control group. Three types of findings are distinguished: NORMAL, when there is no contact between the neighboring blood vessel and the trigeminal nerve; CONTACT, when there is contact between the neighboring blood vessel and the trigeminal nerve without deformation or trajectory alteration; IMPRINTING, when the neighboring blood vessel causes deformation of the trigeminal nerve, with a possibility of trajectory alteration.
| Trigeminal nerve |
Control group |
||
|---|---|---|---|
| Side of pain | Contralateral | 50 patients | |
| Total trigeminal nerves | 30 | 30 | 100 |
| Normal (without contact) | 5 | 18 | 64 |
| Vein contacts | 6 | 6 | 19 |
| Vein imprints | – | 1 | – |
| Artery contacts | 5 | 5 | 11 |
| Artery imprints | 9 | – | 1 |
| Artery and vein contact | 3 | – | 5 |
| Two arteries imprint | 2 | – | – |
All cases showing arterial imprinting on the trigeminal nerve (n = 11) were identified on the ipsilateral side of the pain (Figure 3), and in two patients, two arteries were found imprinting on the trigeminal nerve ipsilateral to the side of the pain. Statistical analysis reported a significant association between TN and the presence of an artery imprinting on the trigeminal nerve, compared to the contralateral side of the pain (X2 = 21, p < .001).
Regarding the offending arterial vessel involved, the superior cerebellar artery (SCA) was identified in eight cases, the vertebral artery (VA) in one case, both the VA and the posterior inferior cerebellar artery (PICA) in one case, and both the SCA and the AICA in one case (Table 1).
In five cases there was conflict with more than one blood vessel and the trigeminal nerve, all located on the ipsilateral side of the pain; in three patients there was contact with both an artery and a vein, and in two patients there was imprinting of two arteries, as mentioned above (Figure 4). No contact of more than one blood vessel with the trigeminal nerve was observed on the contralateral side of the pain.
Figure 4.
VA and PICA imprinting on the trigeminal nerve. Fusion technique of the 3D FIESTA and 3D TOF MRA sequences, coronal view. The left VA is observed, of redundant caliber and flexuous course which, together with the PICA, imprint on the left trigeminal nerve, displacing it cranially and deforming it, giving it a ribbon-like shape (blue arrow).
No significant relationship was found between the presence of an artery contacting with the trigeminal nerve and TN (X2 = 2.65, p = .104) (Figure 2). Eight cases were found showing arterial contact on the ipsilateral side of the pain (three of which also showed contact with a vein), and five cases of arterial contact on the contralateral side.
No significant association was found either between the presence of a vein contacting with or imprinting on the nerve and TN (X2 = .583, p = .445) (Figure 5). In nine cases, veins making contact with the trigeminal nerve were identified on the ipsilateral side (three of which showed associated arterial contact), and seven cases on the contralateral side of the pain (six contacting and one imprinting).
Figure 5.
Vein contacting with the trigeminal nerve. Fusion technique of 3D FIESTA and 3D TOF MRA sequences, coronal view. A vein that contacts with the inferior edge of the left trigeminal nerve is identified (blue arrow), without deforming it or changing its trajectory.
Results obtained at control group assessment of a total of 100 trigeminal nerves (Table 2) were the following: 64 were normal without evidence of neurovascular contact (64%), 19 showed contact with a venous structure (19%), 11 showed contact with an artery with no deformation of the trigeminal nerve in its circumference or trajectory alteration (11%), five showed contact with an artery and a vein (5%), and only one case showed arterial imprinting with deformation of the circumference of the trigeminal nerve (1%). Results obtained at the contralateral side of the pain in patients with TN were the following: 60% showed no vascular conflict (18/30), 20% showed contact of the trigeminal nerve with a vein (6/30), and 16% had contact with a vein (6/30). On the ipsilateral side of the pain, 20% showed contact with only one vein (6/30), 16% showed contact with only one artery (5/30), and 10% showed contact with an artery and a vein (3/30).
Among the arteries involved in the control group, the SCA was the most frequent (n = 14), followed by the AICA (n = 3). In the case of arterial imprinting on the trigeminal nerve, the blood vessel involved was the AICA, which, in this case, showed a loop in its trajectory.
Discussion
Several studies have used 3D TOF sequences and sequences similar to 3D FIESTA to detect neurovascular compression (NVC). Our aim is to show a novel technique of visualization of NVC through the fusion of both sequences.
Satoh et al. published a study in which they evaluated 66 patients with TN on a 1.5 T scanner, applying T2-weighted 3D Fast spin echo and 3D TOF sequences, developing a fusion technique with inner view window, finding NVC in the trigeminal nerve ipsilateral to the pain in 85% of cases. They also found NVC in the trigeminal nerve contralateral to the pain in 35% of cases. They classified NVC into simple, moderate and severe, finding severe NVC only on the ipsilateral side of the pain.6
Garcia et al. evaluated 47 patients with NVC, TN, hemifacial spasm and glossopharyngeal neuralgia, comparing 1.5 and 3 Tesla scanners, and using 3D TOF and 3D CISS sequences (3D constructive interference in steady-state, similar to 3D FIESTA). They found that overall image quality (better anatomic resolution and fewer signal artifacts) was significantly higher at 3 T than at 1.5 T for both sequences. NVC could not be identified in six patients with TN at 1.5 T, but defined findings were obtained with the 3 Tesla scanners.7
Yoshino et al. examined 54 patients with TN comparing 3D TOF and 3D CISS sequences with a 1.5-Tsystem, and obtained similar results regarding the detection of arterial NVC with both sequences. 3D TOF sequence was not able to diagnose venous compressions, which were clearly identified with 3D CISS sequence.8
We believe that a well-trained neuroradiologist can detect arterial and venous NVC with the 3D FIESTA sequence alone (or similar sequences) if the blood vessel trajectory is followed correctly. 3D TOF MRA sequence would confirm arterial NVC. The fusion imaging technique that we used for the present study, which has been very well accepted by the requesting neurosurgeons and neurologists, allowed us to better visualize and easily detect NVC.
This fusion technique enabled us to accurately evaluate the topographic anatomy of the cerebellopontine cistern, and to visualize it on any plane, since they are volumetric sequences. We consider that the coronal plane is the best view to assess NVC correctly, because we can see the front (a perpendicular section) of both trigeminal nerves.
Lacerda et al. evaluated 40 patients with TN who underwent a preoperative 3 T MRI, applying 3D TOF, 3D T2-weighted driven equilibrium (DRIVE) (a sequence similar to 3D FIESTA) and 3D T1-weighted gadolinium-enhanced sequences, and compared the results obtained with the surgical findings. On surgical exploration, NVC was found in 38 of the 40 patients. On MRI, NVC was found in 37 patients, without false positives. It was concluded that MRI sensitivity was 97.4% and specificity was 100% compared with the surgical findings. Regarding the blood vessel involved, there was agreement between MRI and surgery in 33 of the 37 positive cases. The blood vessel with moderate agreement was the superior petrosal vein. There were no discrepancies on the arterial NVC diagnosed with MRI. It was also observed that arterial compressions on the trigeminal nerve were visualized more proximally to the brain stem than venous compressions.9 The same group of authors performed a similar study with 100 patients with TN, obtaining 96.7% sensitivity and 100% specificity for the diagnosis of NVC with MRI.10
Sindou et al. reported a study of 579 patients with TN, who were treated by microvascular decompression, finding that only 3.3% of patients (n = 19) did not present NVC. Ninety-seven percent of cases (n = 560) showed NVC. In 37.8% of patients (n = 212), they found more than one blood vessel involved with the trigeminal nerve. An interesting finding was that in 42% of patients with NVC, the trigeminal nerve affected showed a significant degree of atrophy.11
Lutz et al. studied 20 patients with TN using diffusion tensor imaging on a 3 T scanner, and measured the mean fractional anisotropy (FA) in the trigeminal nerves, finding lower values of FA on the TN side compared to the contralateral side. They correlated such finding with the demyelination that the nerve suffers, axonal loss and abnormal remyelinization.12 These phenomena usually occur in the nerve root entry zone, since this is a susceptible transition area between the central and peripheral myelin.4
Trigeminal nerves without NVC
In our study, 64% of the trigeminal nerves in the control group did not show either contact with or imprinting of the neighboring blood vessels (normal result). In the group of patients with TN, 60% of cases (18/30) showed neither contact nor imprinting on the contralateral side of the pain, and 16.7% of cases (5/30) did not show either contact or imprinting on the ipsilateral side of the pain.
The percentage of trigeminal nerves without NVC was similar between the control group (64%) and the contralateral side of the pain in the group with TN (60%).
Arterial compression
Our study found no significant association between an artery contacting with the trigeminal nerve (without deforming or displacing it) and TN (X2 = 2.65, p = .104), but we did find a significant association between TN and an artery imprinting on the trigeminal nerve, compared with the contralateral side of the pain (X2 = 21, p < .001).
In the group of patients with TN, the most common artery identified on the symptomatic side (contacting or imprinting) was the SCA (n = 15), followed by the AICA (n = 10), the VA (n = 2) and the PICA (n = 1).
Sindou et al. found that in 88% of patients operated with NVC (n = 493) the arterial vessel involved was the SCA alone or in association with another blood vessel, in 25.1% of cases (n = 155) the artery responsible was the AICA alone or in association with another blood vessel, and in 3.5% of cases (n = 20) it was the basilar artery.11
In several publications on TN, the blood vessel most frequently associated with NVC is SCA, with a percentage of 57–88%, followed by AICA: 5–39%, PICA: 1–13%, basilar artery; 1–3% and VA: 2%.5,8,10,11,13
Venous compression
Our study found no significant association between a vein contacting with the nerve and TN (X2 = .583, p = .445). We identified the same number of cases (n = 6) with venous contact (20%) both on the ipsilateral and contralateral sides of the pain. The percentage is similar to that found in the control group, where 19% of the trigeminal nerves evaluated showed venous contact.
It is less easy to explain the origin of pain as a consequence of venous compression than arterial compression, since veins lack the pulsatile pressure that could explain the mechanism of artery compression. However, Apfelbaum stated that veins which drain to the cerebral venous sinuses can pulsate due to the lack of valves between them and the heart.5
Conclusion
The fusion imaging technique of 3D FIESTA and 3D TOF MRA sequences, “neurovascular study of the trigeminal nerve”, combining the high anatomical detail provided by the 3D FIESTA sequence with the 3D TOF MRA sequence and its capacity to depict arterial structures, results in a tool that enables the quick and efficient visualization and assessment of the relationship between the trigeminal nerve and the neighboring vascular structures. We suggest that the “neurovascular study of the trigeminal nerve” may be a useful, safe and non-invasive method for the diagnosis of neurovascular compression of the trigeminal nerve and for surgical planning in patients with trigeminal neuralgia.
Funding
This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Conflict of interest
The authors declare no conflict of interest.
References
- 1.Bahat D, Ray D, Raslan A, et al. Trigeminal neuralgia in young adults. J Neurosurg 2011; 114: 1306–1311. [DOI] [PubMed] [Google Scholar]
- 2.Cruccu G, Gronseth G, Alksne J, et al. AAN-EFNS guidelines on trigeminal neuralgia management. Eur J Neurol 2008; 15: 1013–1028. doi: 10.1111/j.1468–1331.2008.02185.x. [DOI] [PubMed] [Google Scholar]
- 3.Gronseth G, Cruccu G, Alksne J, et al. Practice parameter: The diagnostic evaluation and treatment of trigeminal neuralgia (an evidence-based review): Report of the Quality Standards Subcommittee of American Academy of Neurology and the European Federation of Neurological Societies. Neurology 2008; 71: 1183–1190. doi: 10.1212/01.wnl.0000326598.83183.04. [DOI] [PubMed] [Google Scholar]
- 4.Love S, Coakham H. Trigeminal neuralgia pathology and pathogenesis. Brain 2001; 124: 2347–2360. doi: 10.1093/brain/124.12.2347. [DOI] [PubMed] [Google Scholar]
- 5.Thomas K, Vilensky J. The anatomy of vascular compression in trigeminal neuralgia. Clin Anat 2014. [DOI] [PubMed] [Google Scholar]
- 6.Satoh T, Omi M, Nabeshima M, Onoda K, Date I. Severity analysis of neurovascular contact in patients with trigeminal neuralgia: assessment with the inner view of the 3D MR cisternogram and angiogram fusion imaging. Am J Neuroradiol 2009; 30: 603–607. doi: 10.3174/ajnr.A1409. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Garcia M, Naraghi R, Zumbrunn T, et al. High-resolution 3D-constructive interference in steady-state MR imaging and 3D time-of-flight MR angiography in neurovascular compression: a comparison between 3T and 1.5T. Am J Neuroradiol 2012; 33: 1251–1256. doi: 10.3174/ajnr.A2974. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Yoshino N, Akimoto H, Yamada I, et al. Trigeminal neuralgia: evaluation of neuralgic manifestation and site of neurovascular compression with 3D CISS MR imaging and MR angiography. Radiology 2003; 228(2): 539–545. doi: 10.1148/radiol.2282020439. [DOI] [PubMed] [Google Scholar]
- 9.Lacerda P, Hermier M, Souza M, et al. Visualization of vascular compression of the trigeminal nerve with high-resolution 3T MRI: a prospective study comparing preoperative imaging analysis to surgical findings in 40 consecutive patients who underwent microvascular decompression for trigeminal neuralgia. Neurosurgery 2011; 69(1): 15–26. doi: 10.1227/NEU.0b013e318212bafa. [DOI] [PubMed] [Google Scholar]
- 10.Lacerda P, Hermier M, Froment J, et al. Preoperative demonstration of the neurovascular compression characteristics with special emphasis on the degree of compression, using high-resolution magnetic resonance imaging: a prospective study, with comparison to surgical findings, in 100 consecutive patients who underwent microvascular decompression for trigeminal neuralgia. Acta Neurochir (Wien) 2010; 152: 817–825. doi: 10.1007/s00701-009-0588-7. [DOI] [PubMed] [Google Scholar]
- 11.Sindou M, Howeidy T, Acevedo G. Anatomical observations during microvascular decompression for idiopathic trigeminal neuralgia (with correlations between topography of pain and site of the neurovascular conflict). Prospective study in a series of 579 patients. Acta Neurochir (Wien) 2002; 144: 1–13. doi: 10.1007/s007010200081. [DOI] [PubMed] [Google Scholar]
- 12.Lutz J, Linn J, Mehrkens J, et al. Trigeminal neuralgia due to neurovascular compression: high-spatial-resolution diffusion-tensor imaging reveals microstructural neural changes. Radiology 2011; 258(2): 524–530. doi: 10.1148/radiol.10100477. [DOI] [PubMed] [Google Scholar]
- 13.Anqi X, Ding L, Jiahe X, Zhenlin L, Chunchao X, Chao Y. MR Cisternography in the posterior fossa: the evaluation of trigeminal neurovascular compression. Turk Neurosurg 2013; 23(2): 218–225. [DOI] [PubMed] [Google Scholar]





