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Trigeminal neuralgia secondary to vascular compression and neurocysticercosis: illustrative case

Mao Vásquez, Luis J. Saavedra, Hector H. García, Evelyn Vela, Jorge E. Medina, Miguel Lozano, Carlos Hoyos, and William W. Lines-Aguilar

Trigeminal neuralgia (TN) is the most common type of facial pain, negatively affecting quality of life and work capacity in 34% of patients. 1 TN has a prevalence of 4–13 cases per 100,000 inhabitants 1–3 and generally affects patients older than 50 years, with a female-to-male ratio of 1.5 to 1. In primary (classic) TN, compression by vascular loops is found at the entrance of the trigeminal nerve to the brainstem. 4 , 5 In secondary TN, 6 , 7 extrinsic compression of the trigeminal nerve triggers the pain. The most common causes of extrinsic TN are

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Radiofrequency thermocoagulation for the treatment of trigeminal neuralgia associated with a focal pontine lesion: illustrative case

Vadym Biloshytsky, Anna Skorokhoda, Inna Buvailo, and Maryna Biloshytska

Trigeminal neuralgia (TN) is a debilitating neurological condition with brief attacks of facial pain restricted to the trigeminal distribution and with an electric shock-like shooting, stabbing, or sharp quality. TN-associated pain is one of the most severe pains known, often referred to as “suicidal,” and is triggered by innocuous stimulation of the face and intraoral mucosa such as touching the face, talking, chewing, drinking, washing the face, shaving, etc. 1 , 2 TN etiology can be classified as classic, secondary, or idiopathic. The classic type

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Simultaneous microvascular decompression for trigeminal neuralgia and hemifacial spasm involving a dolichoectatic vertebral artery in an elderly patient: illustrative case

Neelan J. Marianayagam, Hanya M. Qureshi, Sagar Vasandani, Shaurey Vetsa, Muhammad Jalal, Kun Wu, and Jennifer Moliterno

Trigeminal neuralgia (TN) and hemifacial spasm (HFS) refractory to medical management can commonly be the result of direct contact by an aberrant vessel compressing the root entry zone (REZ) of the trigeminal and facial nerves, respectively. Microvascular decompression (MVD) has been shown to provide lasting relief. 1 In TN, the offending vessel is usually the superior cerebellar artery, whereas in HFS, it is usually the anterior inferior cerebellar artery. There are instances, however, in which an enlarged or dolichoectatic vertebral artery (DVA) can be the

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Bipolar, high-voltage, long-duration pulsed radiofrequency ablation of the Gasserian ganglion for the treatment of trigeminal neuralgia in a patient with a cardiac implantable electronic device: illustrative case

Albert A Sufianov, Nargiza A Garifullina, Andrey G Shapkin, Egor S Markin, Matias Baldoncini, Luis A. B Borba, Manuel J Encarnacion Ramirez, and Rinat A Sufianov

Patients with drug-resistant forms of trigeminal neuralgia (TN) are usually subjected to interventional neurosurgical procedures. 1 Despite the gold-standard treatment of microvascular decompression (MVD), a great deal of attention is given to percutaneous procedures. 2–5 Nowadays, an alternative percutaneous treatment for TN gaining scientific support is high-voltage, long-duration pulsed radiofrequency therapy (PRFT) of the Gasserian ganglion (GG) because of its neuromodulation effect with minimal risk of thermal neuronal damage. 6 PRFT is a novel and

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Trigeminal neuralgia caused by a persistent primitive trigeminal artery: preoperative three-dimensional multifusion imaging and computational fluid dynamics analysis. Illustrative case

Toru Satoh, Takao Yasuhara, Michiari Umakoshi, and Isao Date

Trigeminal neuralgia (TN) is mainly caused by compression of the trigeminal nerve by blood vessels at the site of neurovascular contact (NVC). 1 However, the detailed mechanism of its onset is unknown. The superior cerebellar artery (SCA), anterior inferior cerebellar artery, and basilar artery and veins are responsible for this condition. TN caused by the persistent primitive trigeminal artery (PTA) and its variants is extremely rare, accounting for 0.2%–0.6% of TN cases. 2 , 3 Herein, we describe a case of TN in which the PTA trunk was fused with the SCA

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Pterygoid venous plexus anastomosis in trigeminal percutaneous glycerol rhizotomy: illustrative case

Kevin Cordeiro, Jason Kim, Niall Buckley, Mark Kraemer, Conrad Pun, and Daniel Resnick

Percutaneous glycerol rhizotomy (PGR) is a safe and effective treatment for medication-refractory trigeminal neuralgia, 1 , 2 although it may lead to trigeminal distribution sensory loss. 3 , 4 Computed tomography (CT)-guided PGR has been shown to improve procedural efficiency, reduce operator radiation exposure, and allow definitive needle placement within the foramen ovale. 5 In addition to the foramen ovale, CT guidance allows the visualization of key skull base anatomy, such as the infratemporal fossa. 5 The infratemporal fossa houses the pterygoid

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Middle meningeal artery pseudoaneurysm and pterygoid plexus fistula following percutaneous radiofrequency rhizotomy: illustrative case

Rahim Ismail, Derrek Schartz, Timothy Hoang, and Alexander Kessler

The percutaneous approach to the trigeminal nerve via the foramen ovale originated in the early 20th century from Taptas and Hartel in 1911 and 1913, 1 respectively, with electrocoagulation developed by Rethi in 1913. 2 Over the subsequent century, much advancement in the percutaneous techniques has occurred including chemodenervation, radiofrequency ablation, cryoablation, nerve blocks, Botox injections, nerve stimulation, and balloon decompression. 2 Percutaneous treatment for trigeminal neuralgia is generally considered a well-tolerated procedure, with

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Utilization of three-dimensional fusion images with high-resolution computed tomography angiography for preoperative evaluation of microvascular decompression: patient series

Takamitsu Iwata, Koichi Hosomi, Naoki Tani, Hui Ming Khoo, Satoru Oshino, and Haruhiko Kishima

Neurovascular compression syndromes, such as trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia, are abnormal conditions that can substantially affect the quality of life of patients. 1–3 Microvascular decompression (MVD) is an effective surgical treatment for drug-resistant cases. 1–4 The overall success rate of MVD varies from 73% to 90%, and the most common complications include hearing loss, facial weakness or numbness, and cerebrospinal fluid leakage. 3 , 5 However, the success of MVD depends on accurate preoperative imaging and