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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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Dallas L. Sheinberg, David J. McCarthy, Omar Elwardany, Jean-Paul Bryant, Evan Luther, Stephanie H. Chen, John W. Thompson, and Robert M. Starke

nucleotide polymorphism on aneurysm size . J Neurosurg 102 : 68 – 71 , 2005 2 Akimoto S , Mitsumata M , Sasaguri T , Yoshida Y : Laminar shear stress inhibits vascular endothelial cell proliferation by inducing cyclin-dependent kinase inhibitor p21(Sdi1/Cip1/Waf1) . Circ Res 86 : 185 – 190 , 2000 3 Aoki T , Kataoka H , Morimoto M , Nozaki K , Hashimoto N : Macrophage-derived matrix metalloproteinase-2 and -9 promote the progression of cerebral aneurysms in rats . Stroke 38 : 162 – 169 , 2007 4 Aoki T , Nishimura M , Kataoka H

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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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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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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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Fredric B. Meyer, Thoralf M. Sundt Jr., Nicolee C. Fode, Michael K. Morgan, Glen S. Forbes, and James F. Mellinger

(20%). This may again reflect the referral nature of our practice, as an equal number of reports do not verify this fact. Despite these apparent discrepancies, it appears reasonable to conclude that pediatric aneurysms are distinct from their counterparts in adults on the basis of sex predominance, location, and size. Perhaps this information can facilitate an understanding concerning the genesis of cerebral aneurysms.4 Discussion on the evolution of cerebral aneurysms has always focused on the question of the congenital versus the acquired nature of these lesions

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Toru Satoh, Yuji Yamamoto, Syoji Asari, Masaru Sakurai, and Kenji Suzuki

C ases of cerebral aneurysms associated with moyamoya disease have been reported occasionally. We report another such case, which is unique in that sequential angiographic studies revealed the reduction and disappearance of internal carotid artery (ICA) aneurysms and the development and enlargement of basilar artery (BA) aneurysms in conjunction with the advancement of moyamoya disease. Case Report This 44-year-old woman, who had been suffering from hypertension for a long time, visited our service on September 11, 1978, complaining of progressive left

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Collagen deficiency and ruptured cerebral aneurysms

A clinical and biochemical study

Glenn Neil-Dwyer, John R. Bartlett, Alan C. Nicholls, Paolo Narcisi, and F. Michael Pope

I n the United Kingdom, 4000 deaths yearly are directly caused by bleeding into the subarachnoid space, 14 mainly from ruptured cerebral aneurysms. There are blister-like arterial outpouchings which affect between 1% and 2% of the population, and are most commonly situated on the anterior half of the circle of Willis. 4 The abnormalities originate at arterial bifurcations where the internal elastic lamina becomes interrupted and the medial layer thins. As the elastic interruptions or gaps occur in normal individuals as well as in patients with aneurysms, 10

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Richard Leblanc, Andrés M. Lozano, Michel van der Rest, and Ronald David Guttmann

T he etiology of cerebral aneurysms has long been the subject of debate. Two general theories have been proposed to explain their occurrence. The degeneration theory holds that cerebral aneurysms result from an acquired degeneration of cerebral arteries under the influence of atherosclerosis and hypertension. The congenital theory proposes that cerebral aneurysms result from an inborn structural deficiency of the cerebral vessel harboring them. Other factors invoked in the formation of cerebral aneurysms include incomplete involution of fetal arteries at

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Grant Sinson, Matthew F. Philips, and Eugene S. Flamm

difficult to approach surgically. An important adjunct in the treatment of difficult aneurysms is the use of intravascular and intraluminal surgical maneuvers to facilitate the definitive surgical clipping of these lesions. Our experience with a variety of intraoperative techniques is reviewed. Clinical Material and Methods All cases of cerebral aneurysms treated surgically by the senior author (E.S.F.) between 1973 and 1993 were evaluated. Those cases in which intraoperative endovascular techniques were used before or during clip placement are the subject of this