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Kimon Bekelis, Joanna S. Kerley-Hamilton, Amy Teegarden, Craig R. Tomlinson, Rachael Kuintzle, Nathan Simmons, Robert J. Singer, David W. Roberts, Manolis Kellis and David A. Hendrix

C erebral aneurysm rupture is a devastating event with extremely high morbidity and mortality. 32 The molecular mechanisms behind cerebral aneurysm formation and rupture remain poorly understood. Some investigators have attempted to identify the genetic basis of their development. These studies have focused mainly on linkage analyses, 14 , 18 in cases of familial aneurysms, or association analyses 40 of single nucleotide polymorphisms. Most recently, limited gene expression studies 25 , 27 , 30 , 33–35 have identified genes (mainly related to

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Kimon Bekelis, Dan Gottlieb, Nicos Labropoulos, Yin Su, Stavropoula Tjoumakaris, Pascal Jabbour and Todd A. MacKenzie

, with a growing number of hybrid neurosurgeons performing both clipping and coiling. 1 Endovascular coiling is also performed by radiologists and other proceduralists who solely focus on this approach for the treatment of cerebral aneurysms. It is often questioned whether hybrid neurosurgeons can perform endovascular surgery as successfully and safely as providers focusing only on coiling. However, limited literature exists that has attempted to answer this question. De Vries and Boogaarts published a single-center series 6 on the outcomes of coiling of ruptured

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Kimon Bekelis, Daniel J. Gottlieb, Yin Su, A. James O'Malley, Nicos Labropoulos, Philip Goodney, Michael T. Lawton and Todd A. MacKenzie

paradigm shift in the treatment of cerebral aneurysms with an increased focus on coiling as the preferred intervention for patients with subarachnoid hemorrhage. 3 , 30 This trend has been paralleled by similar practices for unruptured cerebral aneurysms, 3 despite the lack of randomized studies in this population. However, lessons learned in trials on ruptured cerebral aneurysms may not necessarily apply to patients presenting with intact cerebral aneurysms. 3 The lack of cerebral edema in patients with the latter has been used as an argument supporting the

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Nobuo Hashimoto, Choegon Kim, Haruhiko Kikuchi, Masayuki Kojima, Yoo Kang and Fumitada Hazama

A lthough intracranial arterial aneurysms are of considerable importance in cerebrovascular pathology and neurosurgery, many problems concerning their etiology, pathogenesis, and treatment are still unsolved. The difficulties in studying the problems are partly caused by the extreme rarity of the disease in animals and the lack of an appropriate animal model of the disease. 16 As described previously, this laboratory has developed an experimental model for inducing cerebral aneurysms in rats by ligation of one or both of the common carotid arteries and the

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Tomohiro Aoki, Masaki Nishimura, Ryota Ishibashi, Hiroharu Kataoka, Yasushi Takagi and Nobuo Hashimoto

C erebral aneurysms can cause a devastating SAH, with quite high mortality and morbidity rates. 24 Despite its high prevalence and the severity of subsequent SAH, 57 we have no option for medical treatment of unruptured cerebral aneurysms because detailed mechanisms of cerebral aneurysm formation and rupture remain to be elucidated. Our recent studies have revealed that chronic inflammatory response in arterial walls to hemodynamic stress is an active participant in cerebral aneurysm formation. 33 , 47 , 48 The transcriptional factor NF-κB is a key

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Marcus A. Stoodley, Jason D. Warren and Peter E. Oatey

S ubarachnoid hemorrhage is the most common presentation of cerebral aneurysms, but unruptured cerebral aneurysms may present with cranial nerve palsy, visual failure, embolic phenomena, or they may be incidental. Giant aneurysms may cause neurological deficits due to mass effect, but this is uncommon with small lesions. Thalamic syndrome as a presentation of an unruptured aneurysm is a rare occurrence 3, 10 and has been attributed to ischemia from the compression of perforating vessels. We present a case of thalamic syndrome as the presenting feature of an

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Gerard Bruno, Roxanne Todor, Isabel Lewis and Douglas Chyatte

biology of cerebral aneurysm formation and rupture remains an enigma. Early investigators hypothesized that aneurysm formation occurs when cerebral blood vessels passively respond to exaggerated hemodynamic forces. 50 Experimental and clinical data, however, both suggest that hemodynamic forces alone are not sufficient to produce cerebral aneurysms, 21 pointing toward an active, rather than a passive role of cerebral arteries in aneurysm formation. Remodeling of the arterial extracellular matrix has been linked to the occurrence of other types of vascular diseases

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Nobutake Sadamasa, Kazuhiko Nozaki, Yasushi Takagi, Takuya Moriwaki, Yoshifumi Kawanabe, Masatsune Ishikawa and Nobuo Hashimoto

C EREBRAL aneurysm is regarded as a major cause of subarachnoid hemorrhage, but the mechanisms of aneurysm initiation, progression, and rupture remain unclear. Studies on human cerebral aneurysms (specimens obtained during operations or autopsies) have been performed to elucidate these mechanisms, but such studies are inevitably limited by the fact that the development of the aneurysms cannot be followed over time. We have overcome this limitation by producing experimental intracranial aneurysms in rats, 6 mice, 12 and monkeys. 7 The induced aneurysms

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Hao Li, Haiyan Yue, Yajing Hao, Haowen Li, Shuo Wang, Lanbing Yu, Dong Zhang, Yong Cao and Jizong Zhao

T he prevalence of cerebral aneurysms (CAs) in the world's population ranges from 1% to 6%. 24 The rupture of a CA can cause aneurysmal subarachnoid hemorrhage (SAH), which results in a high fatality rate of 65% and disables 50% of the patients who survive it. 19 Current therapeutics for treating CAs include mainly microsurgical clipping and endovascular treatment. However, both of these treatments are invasive and confer a nonnegligible risk of procedural morbidity. 4 Great efforts have been made to investigate the molecular mechanisms of CA formation and

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Michael Pullar, Peter C. Blumbergs, Gael E. Phillips and Paul G. Carney

review revealed eight cases of neoplastic cerebral aneurysm from gestational choriocarcinoma. 11, 13, 15, 19, 20, 23, 24 Only two reports presented both radiological evidence of aneurysm formation and histopathological documentation of trophoblastic invasion and destruction of the vessel wall. 13, 24 Our case demonstrates focal destruction of the media and internal elastic lamina, with aneurysm formation. Neoplastic aneurysms are also reported in cardiac myxoma (18 cases), 6, 17 bronchogenic carcinoma (two cases), 6, 9 and undifferentiated carcinoma (three cases