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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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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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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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A child with unilateral abducens nerve palsy and neurovascular compression in Chiari malformation type 1 resolved with posterior fossa decompression: illustrative case

Olivia A Kozel, Belinda Shao, Cody A Doberstein, Natalie Amaral-Nieves, Matthew N Anderson, Gita V Harappanahally, Michael A Langue, and Konstantina A Svokos

instances of contact between the abducens nerve and the AICA. 28 Symptomatic neurovascular compression of the abducens nerve is rare. A few reported cases have implicated compression from the AICA or a dolichoectatic VA. 29 , 30 Given the difficult skull base approach to the prepontine cistern 31 and the rarity of the condition, microvascular decompression of the abducens nerve is seldom undertaken, in contrast to more commonly decompressed pathologies such as hemifacial spasm and trigeminal neuralgia. 32 – 35 One review noted that only 6 of 22 cases of abducens nerve