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Mauricio Campos-Benitez and Anthony M. Kaufmann

M icrovascular decompression has become a well-established treatment for HFS, providing an excellent potential for achieving disease cure. 2 , 11 Direct surgical treatment of the facial nerve for HFS was first developed by Gardner. 4–6 He described a series of patients successfully treated with “gentle” mechanical trauma delivered by rubbing the cisternal portion of the facial nerve. He noted contact between the CP of the facial nerve and the AICA and postulated that pulsatile neurovascular compression might be the cause of HFS. It was Jannetta, however

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Arterial hypertension and neurovascular compression at the ventrolateral medulla

A comparative microanatomical and pathological study

Ramin Naraghi, Michael R. Gaab, Gerhard F. Walter and Berthold Kleineberg

A fter reports of Dandy 18, 19 and Gardner and Sava, 26, 27 Jannetta 36 – 38 developed the concept of neurovascular compression as the etiology of hyperactive cranial nerve dysfunction syndromes. Pathological contacts between vessels and the root entry zones of cranial nerves close to the brain stem are regarded as causes of hyperactive cranial nerve dysfunction syndromes such as trigeminal neuralgia, hemifacial spasm, or glossopharyngeal neuralgia. 18, 36, 38, 45 Although this concept is still the subject of controversy, these entities are currently

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Andrew L. Ko, Albert Lee, Ahmed M. Raslan, Alp Ozpinar, Shirley McCartney and Kim J. Burchiel

I n 1934, Dandy proposed neurovascular compression (NVC) as an etiology for trigeminal neuralgia (TN). In his series, he reported that the superior cerebellar artery caused NVC in 30.7% of patients. 6 He noted veins, tumors, and vascular and cranial malformations as other “gross findings” causing compression of the trigeminal nerve; nevertheless, in 40% of cases, he observed no evidence of a gross lesion. 6 He did document, however, that his posterior fossa approach did not allow for visualization of the entire root entry zone (REZ). After years of

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Carlo A. Pagni, Michele Naddeo and Giuliano Faccani

sternocleidomastoideus muscle. The pioneer work of Dandy 6 and Gardner, 8 relating to compression at the root entry zone of the trigeminal nerve by vascular loops as a cause of trigeminal neuralgia, 13 formed the basis for current concepts of neurovascular compression in other cranial nerve disorders. 14–18 To our knowledge, spinal accessory nerve dysfunction due to neurovascular compression as a cause of spasmodic torticollis has not been previously reported. Case Report This 68-year-old woman had for 5 years suffered from painful spasmodic tilting of the neck to the left

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Demonstration of neurovascular compression in trigeminal neuralgia with magnetic resonance imaging

Comparison with surgical findings in 52 consecutive operative cases

James F. M. Meaney, Paul R. Eldridge, Lawrence T. Dunn, Thomas E. Nixon, Graham H. Whitehouse and John B. Miles

D espite a large body of supportive evidence, the concept of neurovascular compression (NVC) in the etiology of trigeminal neuralgia (TGN) is not yet universally accepted. 1 Some of the reluctance to accept this theory stems from lack of a standardized definition of the “root entry zone,” 18 conflicting evidence regarding the incidence of vascular compression both in patients undergoing exploratory surgery for TGN 2, 5, 7, 9, 11, 18, 21, 22, 30 and in controls examined at postmortem, 17–19, 26, 31 and the possibility that the neurovascular relationships

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Dirk De Ridder and Tomas Menovsky

used to obtain high contrast high-resolution images of small anatomical structures in cerebrospinal fluid, such as small cranial nerves and arteries. 8 , 18 In this patient, the clinical evolution followed a similar pattern often seen in hemifacial spasm due to neurovascular compression. 6 , 7 At first, paroxysmal attacks of intermittent irregular tonic or clonic contractions of the muscles innervated by the facial nerve are present, and in time these attacks diminish and a progressive paresis of the facial nerve occurs. 6 , 7 The clinical symptoms of our patient

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Hieronymus D. Boogaarts, Tomas Menovsky, Joost de Vries, André L. M. Verbeek, Jacques W. Lenders and J. André Grotenhuis

-analysis. Methods Sample of Studies Studies were identified through literature searches of MEDLINE by using the website at the National Library of Medicine. The searches were based on the following medical subject heading categories: “hypertension,” “neurogenic,” “primary,” “essential,” “neurovascular,” “compression,” “medulla oblongata,” “RVLM,” “cranial nerves,” “magnetic resonance imaging,” “vagal nerve,” and “glossopharyngeal nerve.” These terms were also used for the search in Embase. The search was conducted in November 2009. Search strategies and results are given in

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Jonathan P. Miller, Feridun Acar, Bronwyn E. Hamilton and Kim J. Burchiel

Shirley McCartney, Ph.D., for editorial assistance and to Valerie Anderson, Ph.D., for electronic institutional review board assistance. References 1 Akimoto H , Nagaoka T , Nariai T , Takada Y , Ohno K , Yoshino N : Preoperative evaluation of neurovascular compression in patients with trigeminal neuralgia by use of three-dimensional reconstruction from two types of high-resolution magnetic resonance imaging . Neurosurgery 51 : 956 – 962 , 2002 2 Anderson VC , Berryhill PC , Sandquist MA , Ciaverella DP , Nesbit GM , Burchiel

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Marion A. Hughes, Ronak H. Jani, Saeed Fakhran, Yue-Fang Chang, Barton F. Branstetter IV, Parthasarathy D. Thirumala and Raymond F. Sekula Jr.

C lassical trigeminal neuralgia (cTN) is a neuropathic pain disorder marked by evoked and spontaneous attacks in the distribution of the trigeminal nerve, and the disorder is further associated with periods of complete remission and subsequent recurrence in most patients. The pain of cTN is considered to be among the most debilitating types of pain. Neurovascular compression (NVC) of the trigeminal nerve has been accepted as the cause of cTN in the majority of patients by the International Headache Society (IHS). 6 A recent prospective study of patients meeting

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Ricardo Segal, Peter J. Jannetta, Sidney K. Wolfson Jr., Manuel Dujovny and Eugene E. Cook

situations in which there is compression of nervous elements in the region of the brain stem or other areas by aberrant or ectatic branches of normal arteries. Description of Device and Methods The neurovascular compression simulator (NCS) consists of four parts: an intra-aortic balloon, a smaller balloon for placement in the cephalic subarachnoid space, connecting tubing, and an injection port ( Fig. 1 ). The aortic balloon is an enclosed cylindrical bag, 5 mm in diameter and 8 cm long. The blood-contacting surface is composed of a complex band of polyurethane