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Hubert Lee, Jeffrey J. Perry, Shane W. English, Fahad Alkherayf, Joanne Joseph, Steven Nobile, Linghong Linda Zhou, Howard Lesiuk, Richard Moulton, Charles Agbi, John Sinclair, and Dar Dowlatshahi

discharge home, 38.1% (no DCI: 52.5%). TABLE 1. Demographic, clinical, and radiological characteristics of 463 patients presenting with aSAH Characteristic Pts w/ Delayed Cerebral Ischemia (n = 97) Pts w/o Delayed Cerebral Ischemia (n = 366) p Value Demographics  Age, yrs   Mean 54.62 ± 11.56 56.35 ± 13.58 0.25   <40 7 (7.2) 39 (10.7)   40–49 26 (26.8) 80 (21.9)   50–59 34 (35.1) 107 (29.2) 0.15   60–69 20 (20.6) 67 (18.3)   ≥70 10 (10.3) 73 (20.0)  No. of females 73 (75.3) 252 (68.9) 0.22 Comorbidities  Hypertension 42 (43.3) 171 (46.7) 0.55  Hypercholesterolemia 11 (11

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Menno R. Germans, Blessing N. R. Jaja, Airton Leonardo de Oliviera Manoel, Ashley H. Cohen, and R. Loch Macdonald

A pproximately 30% of patients with ruptured intracranial aneurysms causing subarachnoid hemorrhage (SAH) develop delayed cerebral ischemia (DCI) or delayed cerebral infarction. 6 , 21 , 24 These complications of SAH are recognized as the most important reasons for poor outcome; hence, considerable effort is devoted to monitoring and preventing their occurrence or mitigating their effect during hospital admission. 6 , 21 , 24 There is a growing realization that DCI and delayed cerebral infarction have a complex pathophysiology involving the interaction of

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Robert A. Solomon, Stephen T. Onesti, and Louise Klebanoff

of delayed cerebral ischemia: 1) Does the timing of aneurysm surgery during the first 7 days after subarachnoid hemorrhage (SAH) play a role in the development of delayed cerebral ischemia secondary to vasospasm? 2) Should aneurysm surgery be avoided within a certain time following SAH because of an unacceptably high risk of permanent ischemic complications in the postoperative period? and 3) Should the clinical condition of the patient influence the surgeon's decision regarding timing of aneurysm surgery? The following is a prospective analysis of the incidence

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Michael Veldeman, Daniel Lepore, Anke Höllig, Hans Clusmann, Christian Stoppe, Gerrit Alexander Schubert, and Walid Albanna

D espite general advancement in intensive care treatment, the outcome after aneurysmal subarachnoid hemorrhage (aSAH) remains poor. 1 , 2 Following early mortality, delayed cerebral ischemia (DCI) is an important contributing factor to additional morbidity and mortality. 3 DCI affects approximately 20%–30% of survivors of aSAH and typically occurs between days 4 and 14 after the initial hemorrhage. The concept of angiographic vasospasm as the sole culprit of delayed cerebral infarctions has been largely abandoned, and clinical as well as experimental research

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Paul M. Foreman, Michelle Chua, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Beverly C. Walters, R. Shane Tubbs, Mohammadali M. Shoja, and Christoph J. Griessenauer

A neurysmal subarachnoid hemorrhage (aSAH) is a unique form of hemorrhagic stroke associated with high morbidity and mortality. Delayed cerebral ischemia (DCI) is a recognized complication of aSAH that contributes to poor outcome, 28 , 31 and it occurs in approximately 30% of patients. 30 Early efforts to identify patients at risk for DCI focused on the diagnosis of large-vessel cerebral vasospasm. However, contemporary evidence suggests that DCI negatively affects outcome independent of angiographic vasospasm, suggesting that other factors are involved

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Johannes Platz, Erdem Güresir, Marlies Wagner, Volker Seifert, and Juergen Konczalla

T he development of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) is the most important complication after SAH and has a severe impact on outcome for the patients. It accounts for up to 30% of new neurological deficits after the initial hemorrhage. 20 , 34 Yet, to date, the occurrence of DCI still cannot be predicted reliably for the individual patient. Furthermore, the importance of angiographic cerebral vasospasm (CVS) for the occurrence of DCI has recently been critically discussed. 20 , 29 , 42 One of the standard

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Bartosz T. Grobelny, Andrew F. Ducruet, Peter A. DeRosa, Ivan S. Kotchetkov, Brad E. Zacharia, Zachary L. Hickman, Luis Fernandez, Reshma Narula, Jan Claassen, Kiwon Lee, Neeraj Badjatia, Stephan A. Mayer, and E. Sander Connolly Jr.

D elayed cerebral ischemia is associated with death and functional disability following aSAH. 13 Delayed cerebral ischemia has typically been thought to result from cerebral blood flow reductions caused by spasm of the cerebral macrovasculature. 4 Thus, investigations have focused on establishing a role for several key vasoactive molecules in the pathogenesis of cerebral vasospasm such as NO and endothelin. 18 , 22 Despite the evidence implicating macrovascular spasm in the pathogenesis of DCI, emerging work supports a more complex pathophysiology. 16

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Fawaz Al-Mufti, David Roh, Shouri Lahiri, Emma Meyers, Jens Witsch, Hans-Peter Frey, Neha Dangayach, Cristina Falo, Stephan A. Mayer, Sachin Agarwal, Soojin Park, Philip M. Meyers, E. Sander Connolly, Jan Claassen, and J. Michael Schmidt

aneurysmal rupture. 2 , 28 Two retrospective analyses of data obtained from the Tirilazad Mesylate in SAH clinical trial studies conducted between 1990 and 1997 have investigated the importance of UEAV. 2 , 28 These studies found that UEAV was associated with poor functional outcome, but the characterization of UEAV was limited by the trial design and data available. In the current study we sought to assess the clinical significance of UEAV by determining its frequency, association to delayed cerebral ischemia (DCI), and impact on functional outcome. Methods Study

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Hussain Jafri, Michael N. Diringer, Michelle Allen, Allyson R. Zazulia, Gregory J. Zipfel, and Rajat Dhar

I t has been known for many decades that cerebral blood flow (CBF) is reduced in patients suffering from aneurysmal subarachnoid hemorrhage (SAH). 12 While such impairments may initially relate to early brain injury and the concomitant impairment in cerebral metabolism, 2 delayed reductions in CBF may lead to neurological deficits and cerebral infarction. 10 This process, termed delayed cerebral ischemia (DCI), is a serious complication that contributes to poor outcomes in survivors of SAH. 20 The optimal means of assessing course and severity of DCI remains

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Christoph J. Griessenauer, Robert M. Starke, Paul M. Foreman, Philipp Hendrix, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Beverly C. Walters, Jean-Francois Pittet, and Mali Mathru

A neurysmal subarachnoid hemorrhage (aSAH) is the common end point of environmental, biomechanical, cellular, molecular, and genetic processes that underlie the formation and rupture of cerebral aneurysms. Genetic polymorphisms have been associated with aSAH and its sequelae, clinical vasospasm, and delayed cerebral ischemia (DCI). 19 Endothelin-1 (END1), a potent vasoconstrictor, and its receptors may be components in this complex multifactorial process and have been investigated as therapeutic targets in aSAH. The purpose of the present study was to