Preoperative demonstration of neurovascular relationship in trigeminal neuralgia by using 3D FIESTA sequence

Zhou, Quan; Liu, Zhiling; Qu, Chun-cheng; Ni, Shilei; Xue, Feng; Zeng, Qingshi

doi:10.1016/j.mri.2011.12.022

Cited by 38 publications

(18 citation statements)

References 23 publications

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“…Few animal models have been developed to study compression of the trigeminal nerve root [20]. Advances in imaging techniques have allowed for detailed examination of neurovascular structures and studies in patients with trigeminal neuralgia have demonstrated contact between vessels and the trigeminal nerve [21–24]. The majority of the evidence for vascular compression of the trigeminal nerve as the cause of trigeminal neuralgia is from studies examining outcomes after microsurgical decompression [12–15, 17].…”

Section: Discussionmentioning

confidence: 99%

Arterial compression of nerve is the primary cause of trigeminal neuralgia

Chen

Wang

et al. 2013

Neurol Sci

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Whether arterial or venous compression or arachnoid adhesions are primarily responsible for compression of the trigeminal nerve in patients with trigeminal neuralgia is unclear. The aim of this study was to determine the causes of trigeminal nerve compression in patients with trigeminal neuralgia. The surgical findings in patients with trigeminal neuralgia who were treated by micro vascular decompression were compared to those in patients with hemifacial spasm without any signs or symptoms of trigeminal neuralgia who were treated with microvascular decompression. The study included 99 patients with trigeminal neuralgia (median age, 57 years) and 101 patients with hemifacial spasm (median age, 47 years). There were significant differences between the groups in the relationship of artery to nerve (p < 0.001) and the presence of arachnoid adhesions (p < 0.001) but no significant difference in relationship of vein to nerve. After adjustment for age, gender, and other factors, patients with vein compression of nerve or with artery compression of nerve were more likely to have trigeminal neuralgia (OR = 5.21 and 42.54, p = 0.026 and p < 0.001, respectively). Patients with arachnoid adhesions were less likely to have trigeminal neuralgia (OR = 0.15, p = 0.038). Arterial compression of the trigeminal nerve is the primary cause of trigeminal neuralgia and therefore, decompression of veins need not be a priority when performing microvascular dissection in patients with trigeminal neuralgia.

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Section: Discussionmentioning

confidence: 99%

Arterial compression of nerve is the primary cause of trigeminal neuralgia

Chen

Wang

et al. 2013

Neurol Sci

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“…Advances in MRI have been playing an important role in the diagnostic setting, especially in the presurgical evaluation of TN patient in order to identify secondary causes of TN and/or the neurovascular conflict. Studies have been published17,18 on the usefulness of three-dimensional fast imaging employing steady-state acquisition and magnetic resonance angiography (MRA) in surgical planning and prediction of surgical findings during micro-vascular decompression (MVD). A correlation more than 95% between this method and surgical findings has been demonstrated 17,18…”

Section: Advances In Diagnosismentioning

confidence: 99%

Advances in diagnosis and treatment of trigeminal neuralgia

Montano¹,

Conforti²,

Bonaventura³

et al. 2015

TCRM

142

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Various drugs and surgical procedures have been utilized for the treatment of trigeminal neuralgia (TN). Despite numerous available approaches, the results are not completely satisfying. The need for more contemporaneous drugs to control the pain attacks is a common experience. Moreover, a number of patients become drug resistant, needing a surgical procedure to treat the neuralgia. Nonetheless, pain recurrence after one or more surgical operations is also frequently seen. These facts reflect the lack of the precise understanding of the TN pathogenesis. Classically, it has been related to a neurovascular compression at the trigeminal nerve root entry-zone in the prepontine cistern. However, it has been evidenced that in the pain onset and recurrence, various neurophysiological mechanisms other than the neurovascular conflict are involved. Recently, the introduction of new magnetic resonance techniques, such as voxel-based morphometry, diffusion tensor imaging, three-dimensional time-of-flight magnetic resonance angiography, and fluid attenuated inversion recovery sequences, has provided new insight about the TN pathogenesis. Some of these new sequences have also been used to better preoperatively evidence the neurovascular conflict in the surgical planning of microvascular decompression. Moreover, the endoscopy (during microvascular decompression) and the intraoperative computed tomography with integrated neuronavigation (during percutaneous procedures) have been recently introduced in the challenging cases. In the last few years, efforts have been made in order to better define the optimal target when performing the gamma knife radiosurgery. Moreover, some authors have also evidenced that neurostimulation might represent an opportunity in TN refractory to other surgical treatments. The aim of this work was to review the recent literature about the pathogenesis, diagnosis, and medical and surgical treatments, and discuss the significant advances in all these fields.

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“…3 Zou and colleagues 17 found a similar somatotopic distribution when they correlated preoperative fast imaging employing steady state acquisition (FIESTA) MRI imaging with the distribution of symptoms in TGN patients. Thus, lateral and inferior neurovascular compression corresponded to symptoms predominantly in the V.3 distribution.…”

Section: Imaging Of Neurovascular Contactmentioning

confidence: 83%

“…For example, in a series with 37 patients with TGN, Zhou and colleagues 17 found that preoperative imaging correctly identified the site of neurovascular compression in 35 of 36 patients with proved intraoperative neurovascular conflict. Importantly, visualization of neurovascular conflict may be difficult intraoperatively, particularly in the setting of distal compression near the porus trigeminus, when a prominent bony ridge along the posterior wall of the petrous temporal bone obscures visualization of CN V, or when the offending vessel is small and located medial and parallel to the nerve.…”

Section: Imaging Of Neurovascular Contactmentioning

confidence: 99%