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Trigeminal neuralgia induced by brainstem infarction treated with pontine descending tractotomy: illustrative case

Rachyl M. Shanker, Miri Kim, Chloe Verducci, Elhaum G. Rezaii, Kerry Steed, Atul K. Mallik, and Douglas E. Anderson

Trigeminal neuralgia (TN) most commonly presents as neuropathic pain secondary to neurovascular compression (NVC) at the nerve root entry zone (NREZ) 1 , 2 or as a result of a space-occupying lesion impacting the trigeminal nerve. 3 However, there exists a subset of patients in whom trigeminal pain is induced by brainstem ischemia, interrupting the NREZ, spinal trigeminal nucleus, or descending spinal trigeminal tract (SpTV). While cases of TN induced by a brainstem infarct have been reported, there are no clear treatment recommendations for this

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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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Intraoperative application of indocyanine green and temporary venous occlusion test to assess collateral flow during microvascular decompression for venous-related trigeminal neuralgia: illustrative case

Kentaro Fujimoto, Yosuke Akamatsu, Yasumasa Nishikawa, and Kuniaki Ogasawara

Trigeminal neuralgia (TN) is caused by various types of compression from offending vessels, including arteries, veins, and nonvascular structures 1–4 such as venous angiomas or thickened arachnoids. 5 , 6 Of these, the involvement of the superior petrosal vein (SPV) and its branches in the etiology of TN has been reported in up to 15% of the cases, suggesting that vein-related TN is relatively common. 3 , 7–10 Although transposition of the offending vein is desirable during microvascular decompression (MVD) for vein-related TN, sacrificing the offending

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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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Computational hemodynamic analysis of the offending vertebral artery at the site of neurovascular contact in a case of hemifacial spasm associated with subclavian steal syndrome: illustrative case

Keita Tominaga, Hidenori Endo, Shin-ichiro Sugiyama, Shin-ichiro Osawa, Kuniyasu Niizuma, and Teiji Tominaga

Neurovascular compression syndromes such as hemifacial spasm (HFS) and trigeminal neuralgia (TN) are generally caused by neurovascular contact between the vascular structure and the cranial nerves. In HFS, neurovascular compression occurs along the root exit zone (REZ) of the facial nerve, most commonly by either the anterior inferior cerebellar artery or the posterior inferior cerebellar artery (PICA) and rarely by vertebral artery (VA). Microvascular decompression (MVD) is an effective microsurgical treatment option for HFS through releasing the contact of

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Hemifacial spasm caused by multiple vascular attachments due to remote compression effects of a dermoid cyst in the cerebellar hemisphere: illustrative case

Kento Hirayama, Takafumi Tanei, Takenori Kato, Toshinori Hasegawa, Eiji Ito, Yusuke Nishimura, and Ryuta Saito

posterior fossa are extremely rare, and they are located close to occipital bone at the asterion, intradural space, and cerebellar hemisphere. 3–8 These cases are summarized in Table 1 . Clinical symptoms of patients with these lesions included headache, ataxia, hearing loss, gait disturbance, dizziness, vertigo, and trigeminal neuralgia. The mechanisms of onset of these symptoms were mainly direct compression or increased intracranial pressure. Even though there is normal cerebellar tissue between the lesion and the cranial nerve, remote effects due to indirect

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Complete resolution of chronic cluster headache following central lateral thalamotomy using incisionless MRI-guided focused ultrasound with 6 years of follow-up: illustrative case

Anouk E. Magara, Marc N. Gallay, David Moser, and Daniel Jeanmonod

; 1 : 3 . 10.1186/2050-5736-1-3 31 Gallay MN , Moser D , Jeanmonod D . MR-guided focused ultrasound central lateral thalamotomy for trigeminal neuralgia . Front Neurol . 2020 ; 11 : 271 . 10.3389/fneur.2020.00271 32 Headache Classification Committee of the International Headache Society (IHS) . The International Classification of Headache Disorders . 3rd edition . Cephalalgia . 2018 ; 38 ( 1 ): 1 – 211 . 33 Jeanmonod D , Magnin M , Morel A . A thalamic concept of neurogenic pain . In: Proceedings of the 7th World

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Microvascular decompression for developmental venous anomaly causing hemifacial spasm: illustrative case

Margaret Tugend and Raymond F Sekula Jr.

DVA or a decrease in outflow from the DVA. Symptoms from flow-related causes include headache, neurological deficit, seizures, and coma secondary to hemorrhage or infarction. Mechanical causes include obstructive hydrocephalus and nerve compression, causing trigeminal neuralgia and HFS. Cases with symptoms attributed to DVA, such as headache, but with no identifiable patho-mechanism, are classified as idiopathic. 5 Here, we present an example of mechanical compression of the facial nerve by a pontine DVA ostensibly causing HFS. Although the patient ultimately had a

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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