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Decompressive hemicraniectomy without clot evacuation in dominant-sided intracerebral hemorrhage with ICP crisis

Simon G. Heuts, Samuel S. Bruce, Brad E. Zacharia, Zachary L. Hickman, Christopher P. Kellner, Eric S. Sussman, Michael M. McDowell, Rachel A. Bruce, and E. Sander Connolly Jr.

, 2011 10.1161/STROKEAHA.110.608166 4 Auer LM , Deinsberger W , Niederkorn K , Gell G , Kleinert R , Schneider G , : Endoscopic surgery versus medical treatment for spontaneous intracerebral hematoma: a randomized study . J Neurosurg 70 : 530 – 535 , 1989 10.3171/jns.1989.70.4.0530 5 Bor-Seng-Shu E , Figueiredo EG , Amorim RLO , Teixeira MJ , Valbuza JS , de Oliveira MM , : Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain

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Extracranial-intracranial bypass for ischemic cerebrovascular disease: what have we learned from the Carotid Occlusion Surgery Study?

Matthew R. Reynolds, Colin P. Derdeyn, Robert L. Grubb Jr., William J. Powers, and Gregory J. Zipfel

criteria were used to select those high-risk patients who were most likely to benefit from revascularization. 41 , 51 This latter criticism was particularly germane given that ICA occlusion does not always predict cerebral hemodynamic impairment in individual patients. 34 This key issue formed the basis for the St. Louis Carotid Occlusion Study (STLCOS) 19 and, subsequently, COSS. 32 Stages of Cerebral Hemodynamic Impairment Complete ICA occlusion may precipitate a reduction in cerebral perfusion pressure (CPP) in the distal cerebral circulation, depending on

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A review of selective hypothermia in the management of traumatic brain injury

Eisha Christian, Gabriel Zada, Gene Sung, and Steven L. Giannotta

(< 50%) with the cooling method as compared with the control group. Epidural cerebral cooling appears to offer a potent neuroprotective benefit, but to date this method has only been attempted in animal studies. Discussion Although a large multicenter RCT by Clifton et al. 8 did not demonstrate an overall benefit of hypothermia in severe TBI, subsequent clinical trial data have suggested that systemic methods of inducing hypothermia provide effective control of ICP and cerebral perfusion pressure, as well as improvements in neurological outcome. 15 Several

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Pathophysiology and genetic factors in moyamoya disease

Achal S. Achrol, Raphael Guzman, Marco Lee, and Gary K. Steinberg

bilateral revascularization surgery for a diagnosis of moyamoya disease. The exact mechanism for this rare de novo brain AVM formation is unknown. The authors proposed decreased cerebral perfusion pressure and hypoxia in the setting of moyamoya disease as one possible mechanism, acting through elaboration of angiogenic cascades. However, this seems less likely given that revascularization was deemed effective on pancerebral angiography. It may be more likely that de novo brain AVM formation occurred in the setting of an increased angiogenic environment 82 induced by the

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Symptomatic intracranial arterial disease: incidence, natural history, diagnosis, and management

Ananth K. Vellimana, Andria L. Ford, Jin-Moo Lee, Colin P. Derdeyn, and Gregory J. Zipfel

“failed.” One of the main reasons for failure of the International Cooperative Extracranial-Intracranial Bypass Trial was thought to be the absence of cerebral hemodynamic assessment to help identify patients with reduced cerebral perfusion pressure in whom STA-MCA bypass may be more beneficial. 16 , 63 , 88 Subsequently, several quantitative methods have been developed to examine cerebral hemodynamic impairment in patients with ischemic cerebrovascular disease (for a review, see Grubb et al. 30 ). Two prospective observational studies in which PET was used for

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Patterns in neurosurgical adverse events: open cerebrovascular neurosurgery

Judith M. Wong, John E. Ziewacz, Allen L. Ho, Jaykar R. Panchmatia, Albert H. Kim, Angela M. Bader, B. Gregory Thompson, Rose Du, and Atul A. Gawande

in the management of intracranial aneurysms . Neurosurgery 34 : 22 – 29 , 1994 93 Sandalcioglu IE , Schoch B , Regel JP , Wanke I , Gasser T , Forsting M , : Does intraoperative aneurysm rupture influence outcome? Analysis of 169 patients . Clin Neurol Neurosurg 106 : 88 – 92 , 2004 10.1016/j.clineuro.2003.10.011 94 Schmidt JM , Ko SB , Helbok R , Kurtz P , Stuart RM , Presciutti M , : Cerebral perfusion pressure thresholds for brain tissue hypoxia and metabolic crisis after poor-grade subarachnoid hemorrhage

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An overview of the basic science of concussion and subconcussion: where we are and where we are going

Matthew L. Dashnaw, Anthony L. Petraglia, and Julian E. Bailes

-mediated disturbances, and metabolic disturbances may further contribute to, or prolong, BBB breakdown. Breakdown of the BBB has several untoward consequences. First and foremost, fluid exudation from BBB breakdown results in brain edema. This edema may result in increased intracranial pressure, and lower cerebral perfusion pressure can ensue with sufficient fluid accumulation. Excitotoxicity from neuronal membrane damage may be further exacerbated by the loss of ionic flux control from BBB breakdown, resulting in extravasation of excitatory amino acids. Similarly, as other ions

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Cerebral venous sinus thrombosis: review of the demographics, pathophysiology, current diagnosis, and treatment

Aristotelis Filippidis, Eftychia Kapsalaki, Gianna Patramani, and Kostas N. Fountas

perfusion pressure, and finally increases the blood volume. Collateral pathways of blood flow are recruited, while the function of the venous system in high pressures leads to the blood-brain barrier disruption and the development of vasogenic edema. Cerebral perfusion pressure and cerebral blood flow drops, lead to the failure of the most important indirect regulator of intracellular water content, the Na + /K + ATPase dependent pump. This cascade of events results in the development of cytotoxic edema. 38 The described theoretical pathophysiological model implies the

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Superficial temporal artery to middle cerebral artery bypass: past, present, and future

Marcelo D. Vilela and David W. Newell

with different states of hemodynamic insufficiency, and whether any of these subpopulations could benefit from a revascularization procedure. 38 , 47 , 62 , 97 The occurrence of ischemic symptoms and stroke in occlusive cerebrovascular disease can usually be attributed to either thromboembolic phenomena or a decrease in cerebral perfusion pressure. 9 , 62 , 99 Only recently the overall risk of subsequent stroke in patients with CAO has been clarified. A major prospective study by Powers et al. 97 revealed a stroke risk of 0% at 2 years and 4.4% at 3 years in the

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Cell therapies for traumatic brain injury

Matthew T. Harting, James E. Baumgartner, Laura L. Worth, Linda Ewing-Cobbs, Adrian P. Gee, Mary-Clare Day, and Charles S. Cox Jr.

highly variable nature of the disease, but has been estimated in the tens of billions of dollars annually. 44 Current acute treatment of TBI is limited to controlling intracranial pressure and optimizing cerebral perfusion pressure to prevent further cerebral edema, inflammation, and cell death, while chronic treatment centers on motor, cognitive, and behavioral rehabilitation. 2 Advances in early recognition, acute care, the overall trauma system, and rehabilitation strategies have led to improved survival and, consequently, survivors with significant motor