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Fred G. Barker II, Peter J. Jannetta, David J. Bissonette, Philip T. Shields, Mark V. Larkins and Hae Dong Jho

H emifacial spasm is an uncommon disorder characterized by involuntary paroxysmal movement of one side of the face. Since the 1960s 13, 14 there has been increasing consensus that this disorder may be relieved by repositioning of arteries in contact with the facial nerve in its course through the subarachnoid cisterns of the posterior fossa. 23, 26, 41 This report describes our experience with microvascular decompression for hemifacial spasm in 703 patients (705 sides) over a 20-year period. Clinical Material and Methods Patient Population All

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Microvascular decompression for trigeminal neuralgia

Results with special reference to the late recurrence rate

Robert Breeze and Ronald J. Ignelzi

procedures, and nine had been treated with percutaneous thermal coagulation of the Gasserian ganglion. Four had received some other form of treatment. Table 1 summarizes the therapies utilized prior to microvascular decompression surgery. TABLE 1 Therapy tried before microvascular decompression in 51 patients in this series Therapy Cases No. Percent medical treatment   carbamazepine 42 82   phenytoin 26 51   carbamazepine or phenytoin 48 94   narcotics 3 6   non

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Tomomi Okamura, Yasushi Kurokawa, Norio Ikeda, Seisho Abiko, Makoto Ideguchi, Kousaku Watanabe and Toshishige Kido

S oon after reports of the effectiveness of microvascular decompression for treating disabling positional vertigo, 4, 11 studies began to appear in which NVC syndrome of the eighth cranial nerve was described. 16, 18 Since then the correlation between vestibular symptoms and neuropathological findings 3 has become more clear. Just what symptoms are caused by direct or indirect compression of the cochlear nerve, however, is a matter of controversy. This makes it difficult to evaluate the results of various surgical techniques used to treat NVC of the eighth

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Microvascular decompression for hemifacial spasm

Patterns of vascular compression in unsuccessfully operated patients

Shinji Nagahiro, Akira Takada, Yasuhiko Matsukado and Yukitaka Ushio

M icrovascular decompression via retromastoid craniectomy is the preferred method for treating hemifacial spasm. 1, 2, 4–8, 10, 11 However, treatment failure, failure to relieve the spasm, and recurrence of the spasm have been reported. 1, 2, 3–8, 10, 11 Little work has been carried out to determine the factors causing unsuccessful microvascular decompression. We examined the causative factors in patients who had undergone unsuccessful microvascular decompression in a retrospective study of the relationship between the follow-up results and the pattern of

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Nancy McLaughlin and Michel W. Bojanowski

postoperative analyses (lower) revealing normalization of the visual field defects. Discussion Compression of the optic nerve or the chiasm by intracranial vessels, most often the ICA, has been reported in the literature. Indeed, enlargement or dolichoectasia of the ICA has been associated with a variety of visual field defects, depending on the site of compression on the visual apparatus. 4 , 5 Microvascular decompression has been performed in few cases, with improvement of visual field defects in some cases. 1 , 3 Compression of the visual apparatus by an

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Brenton Nash, Matthew L. Carlson and Jamie J. Van Gompel

I n 1959, W. James Gardner performed the first microvascular decompression (MVD) without concomitant neurolysis for trigeminal neuralgia (TN) to good effect. 21 Microvascular decompression for TN and other neurovascular compression (NVC) syndromes was subsequently refined and popularized by Peter Jannetta. 12 The success of the procedure lent credence to Walter Dandy's observations made decades prior that NVC of cranial nerves (CNs) may lead to hyperactive disorders. 6 With these etiological assumptions supported by the success of MVD for TN

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Kazuya Nagata, Tomio Sasaki and Norihiko Basugi

S ince the report of Jannetta, 2 microvascular decompression has been widely used for the treatment of hemifacial spasm and trigeminal neuralgia. In some cases, symptoms may recur after the operation, or residual vasospasm may be observed for 2 to 4 weeks postoperatively. 1 In such cases, dislocation of the prosthesis may be the cause of the problem; however, this cannot be ascertained without reoperation. A radiopaque synthetic sponge has been developed to overcome this disadvantage. Description and Use of the Device The x-ray-detectable absorbent

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Madjid Samii, Steffen K. Rosahl, Gustavo A. Carvalho and Thomas Krzizok

phenomenon restricted to the superior oblique motor unit. Electromyographic evidence has pointed to a lesion in the lower motor neuron. 22, 28, 56 Superior oblique myokymia has been classified as a specific type of nystagmus 53 and was previously referred to as one of the brainstem eye signs. 9 In a variety of cases it also involves functional weakness of the superior oblique muscle. 25, 31, 45, 46 We report the case of a patient who was referred to our department as a candidate for microvascular decompression (MVD) of the trochlear nerve root exit zone. Case

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Tracy M. Flanders, Rachel Blue, Sanford Roberts, Brendan J. McShane, Bryan Wilent, Vijay Tambi, Dmitriy Petrov and John Y. K. Lee

most frequently implicated vessels in HFS. 31 In 1962, Gardner first described the treatment of HFS with elimination of the neurovascular conflict between compressive arterial vessels and the facial nerve. 8 Jannetta et al. revolutionized the treatment of HFS with microvascular decompression (MVD) via the suboccipital approach to the cerebellopontine angle (CPA). MVD has now become the standard and accepted surgical technique for HFS treatment with long-term success rates (within 10 years) of 83%–97%. 5 , 14 In recent years, endoscopy has entered the neurosurgical

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Debebe Theodros, C. Rory Goodwin, Matthew T. Bender, Xin Zhou, Tomas Garzon-Muvdi, Rafael De la Garza-Ramos, Nancy Abu-Bonsrah, Dimitrios Mathios, Ari M. Blitz, Alessandro Olivi, Benjamin Carson, Chetan Bettegowda and Michael Lim

(GR), radiofrequency-thermocoagulation GR (RFTC-GR), and more invasive procedures such as microvascular decompression (MVD). MVD aims to reverse the presumed etiology of TN via placement of a Teflon pledget between the compressed nerve and, most commonly, an overlying vascular structure. It is considered the gold standard surgical treatment for patients with medically intractable TN and demonstrable compression. 15 , 26 , 31 Although MVD has been shown to exhibit the most durable outcomes, some patients elect to undergo less invasive procedures or are poor surgical