The Experts below are selected from a list of 20928 Experts worldwide ranked by ideXlab platform
John H. Zhang - One of the best experts on this subject based on the ideXlab platform.
-
recombinant osteopontin in cerebral vasospasm after Subarachnoid Hemorrhage
Annals of Neurology, 2010Co-Authors: Hidenori Suzuki, Yu Hasegawa, Wanqiu Chen, Kenji Kanamaru, John H. ZhangAbstract:Objective Osteopontin (OPN), a pleiotropic extracellular matrix glycoprotein, has been reported to be protective against ischemic lesions, but effects of OPN on vascular functions have not been investigated. The aim of this study was to assess whether recombinant OPN (r-OPN) could prevent cerebral vasospasm after Subarachnoid Hemorrhage (SAH) in rats.
-
cerebral vasospasm after Subarachnoid Hemorrhage the emerging revolution
Nature Reviews Neurology, 2007Co-Authors: R. Loch Macdonald, Ryszard M Pluta, John H. ZhangAbstract:Cerebral vasospasm is the classic cause of delayed neurological deterioration after Subarachnoid Hemorrhage (SAH). Surprisingly, however, patient outcome after SAH was not improved in recent trials of the endothelin antagonist clazosentan, which prevents vasospasm. In light of this result, Macdonald et al. highlight the need for reconsideration of the pathophysiology of SAH. Cerebral vasospasm is the classic cause of delayed neurological deterioration after aneurysmal Subarachnoid Hemorrhage, leading to cerebral ischemia and infarction, and thus to poor outcome and occasionally death. Advances in diagnosis and treatment—principally the use of nimodipine, intensive care management, hemodynamic manipulations and endovascular neuroradiology procedures—have improved the prospects for these patients, but outcomes remain disappointing. Recent clinical trials have demonstrated marked prevention of vasospasm with the endothelin receptor antagonist clazosentan, yet patient outcome was not improved. This Review considers possible explanations for this result and proposes alternative causes of neurological deterioration and poor outcome after Subarachnoid Hemorrhage, including delayed effects of global cerebral ischemia, thromboembolism, microcirculatory dysfunction and cortical spreading depression.
-
Cerebral vasospasm after Subarachnoid Hemorrhage: the emerging revolution.
Nature Clinical Practice Neurology, 2007Co-Authors: R. Loch Macdonald, Ryszard M Pluta, John H. ZhangAbstract:Cerebral vasospasm is the classic cause of delayed neurological deterioration after aneurysmal Subarachnoid Hemorrhage, leading to cerebral ischemia and infarction, and thus to poor outcome and occasionally death. Advances in diagnosis and treatment-principally the use of nimodipine, intensive care management, hemodynamic manipulations and endovascular neuroradiology procedures-have improved the prospects for these patients, but outcomes remain disappointing. Recent clinical trials have demonstrated marked prevention of vasospasm with the endothelin receptor antagonist clazosentan, yet patient outcome was not improved. This Review considers possible explanations for this result and proposes alternative causes of neurological deterioration and poor outcome after Subarachnoid Hemorrhage, including delayed effects of global cerebral ischemia, thromboembolism, microcirculatory dysfunction and cortical spreading depression.
-
mechanisms of early brain injury after Subarachnoid Hemorrhage
Journal of Cerebral Blood Flow and Metabolism, 2006Co-Authors: Julian W Cahill, John H Calvert, John H. ZhangAbstract:Apoptosis is the term given to programmed cell death, which has been widely connected to a number of intracranial pathologies including stroke, Alzheimer's disease, and more recently Subarachnoid Hemorrhage (SAH). Subarachnoid Hemorrhage is a disease, without any form of effective treatment, that affects mainly the young and middle aged and as a result is responsible for severe disability in otherwise healthy and productive individuals. Despite intense research efforts in the field, we currently possess a very limited understanding of the underlying mechanisms that result in injury after SAH. However, a number of studies have recently indicated that apoptosis may be a major player in the pathogenesis of secondary brain injury after SAH. As a result, the apoptotic cascades present a number of potential therapeutic opportunities that may ameliorate secondary brain injury after SAH. Experimental data suggest that these cascades occur very early after the initial insult and may be related directly to physiologic sequela commonly associated with SAH. It is imperative, therefore, to obtain a thorough understanding of the early events that occur after SAH, which will enable future therapies to be developed.
-
molecular mechanisms of early brain injury after Subarachnoid Hemorrhage
Neurological Research, 2006Co-Authors: Robert P Ostrowski, Austin R T Colohan, John H. ZhangAbstract:Abstract Objectives: Increasing body of experimental and clinical data indicates that early brain injury after initial bleeding largely contributes to unfavorable outcome after Subarachnoid Hemorrhage (SAH). This review presents molecular mechanisms underlying brain injury at its early stages after SAH. Methods: PubMed was searched using term 'Subarachnoid Hemorrhage' and key words referring to molecular and cellular pathomechanisms of SAH-induced early brain injury. Results: The authors reviewed intracranial phenomena and molecular agents that contribute to the early development of pathological sequelae of SAH in cerebral and vascular tissues, including cerebral ischemia and its interactions with injurious blood components, blood–brain barrier disruption, brain edema and apoptosis. Discussion: It is believed that detailed knowledge of molecular signaling pathways after SAH will serve to improve therapeutic interventions. The most promising approach is the protection of neurovascular unit including anti-a...
Stephan A Mayer - One of the best experts on this subject based on the ideXlab platform.
-
angiographic vasospasm is strongly correlated with cerebral infarction after Subarachnoid Hemorrhage
Stroke, 2011Co-Authors: Webster R Crowley, Stephan A Mayer, Ricky Medel, Aaron S Dumont, Don Ilodigwe, Neal F Kassell, Daniel Ruefenacht, Peter Schmiedek, S Weidauer, Alberto PasqualinAbstract:Background and Purpose—The long-standing concept that delayed cerebral infarction after aneurysmal Subarachnoid Hemorrhage results exclusively from large artery vasospasm recently has been challenged. We used data from the CONSCIOUS-1 trial to determine the relationship between angiographic vasospasm and cerebral infarction after Subarachnoid Hemorrhage. Methods—We performed a post hoc exploratory analysis of the CONSCIOUS-1 data. All patients underwent catheter angiography before treatment and 9±2 days after Subarachnoid Hemorrhage. CT was performed before and after aneurysm treatment, and 6 weeks after Subarachnoid Hemorrhage. Angiograms and CT scans were assessed by centralized blinded review. Angiographic vasospasm was classified as none/mild (0%–33% decrease in arterial diameter), moderate (34%–66%), or severe (≥67%). Infarctions were categorized as secondary to angiographic vasospasm, other, or unknown causes. Logistic regression was conducted to determine factors associated with infarction. Results...
-
cardiac troponin elevation cardiovascular morbidity and outcome after Subarachnoid Hemorrhage
Circulation, 2005Co-Authors: Andrew M Naidech, Kurt T Kreiter, Brian-fred Fitzsimmons, Christopher Commichau, Nazli Janjua, Sander E Connolly, Noeleen Ostapkovich, Augusto Parra, Stephan A MayerAbstract:Background— Cardiac troponin I (cTI) release occurs frequently after Subarachnoid Hemorrhage (SAH) and has been associated with a neurogenic form of myocardial injury. The prognostic significance a...
-
dobutamine versus milrinone after Subarachnoid Hemorrhage
Neurosurgery, 2005Co-Authors: Andrew M Naidech, Yunling Du, Kurt T Kreiter, Augusta Parra, Brian-fred Fitzsimmons, Sean D Lavine, Stephan A Mayer, Sander E Connolly, Christopher CommichauAbstract:OBJECTIVE: Neurogenic stunned myocardium is a well-recognized complication of Subarachnoid Hemorrhage. Dobutamine and milrinone are both used for neurogenic stunned myocardium, but there are few data comparing them after Subarachnoid Hemorrhage. METHODS: We compared the physiological dose response of dobutamine and milrinone in patients with Subarachnoid Hemorrhage requiring a pulmonary artery catheter. We located 11 patients who received either inotrope. Physiological data were fitted to a mixed model accounting for drug, dose, and between-patient variation. RESULTS: There were 11 patients who had 152 pulmonary artery catheter measurements. Two received both inotropes (but not within 4 h of each other), 2 only milrinone, and 7 only dobutamine. The groups had similar clinical and physiological characteristics. After adjustment for vasopressin, milrinone was significantly more potent in increasing cardiac output (P <0.0001) and stroke volume (P=0.03), while decreasing vascular resistance (P <0.0001) and systolic blood pressure (P=0.008), than dobutamine. CONCLUSION: These data suggest that milrinone and dobutamine should be used in different clinical situations. Milrinone may be more effective in patients with severely depressed systolic function but who have at least normal vascular resistance and blood pressure and in whom raising cardiac output is the primary goal. Dobutamine may be superior when vascular resistance or blood pressure is low.
-
cerebral vasospasm after Subarachnoid Hemorrhage
Current Opinion in Critical Care, 2003Co-Authors: Nazli Janjua, Stephan A MayerAbstract:Purpose of reviewTo summarize new pathophysiologic insights and recent advances in the diagnosis and treatment of cerebral vasospasm after aneurysmal Subarachnoid Hemorrhage.Recent findingsImportant, newly recognized mediators of cerebral arterial spasm after Subarachnoid Hemorrhage include superoxi
Owen Samuels - One of the best experts on this subject based on the ideXlab platform.
-
hyperchloremia is associated with acute kidney injury in patients with Subarachnoid Hemorrhage
Critical Care Medicine, 2017Co-Authors: Ofer Sadan, Kai Singbartl, Prem Kandiah, Kathleen S Martin, Owen SamuelsAbstract:Objective To assess the prevalence of acute kidney injury in patients with Subarachnoid Hemorrhage patients. Design Retrospective analysis of all Subarachnoid Hemorrhage admissions. Settings Neurocritical care unit. Patients All patients with a diagnosis of Subarachnoid Hemorrhage between 2009 and 2014. Interventions None. Measurements and main results Of 1,267 patients included in this cohort, 16.7% developed acute kidney injury, as defined by Kidney Disease Improving Global Outcome criteria (changes in creatinine only). Compared to patients without acute kidney injury, patients with acute kidney injury had a higher prevalence of diabetes mellitus (21.2% vs 9.8%; p Conclusions Critically ill patients with Subarachnoid Hemorrhage show a strong association between hyperchloremia and acute kidney injury as well as acute kidney injury and mortality.
Jan Regelsberger - One of the best experts on this subject based on the ideXlab platform.
-
terson syndrome in Subarachnoid Hemorrhage intracerebral Hemorrhage and traumatic brain injury
Neurosurgical Review, 2015Co-Authors: Patrick Czorlich, Christos Skevas, Volker Knospe, Eik Vettorazzi, G Richard, Lars Wagenfeld, Manfred Westphal, Jan RegelsbergerAbstract:This prospective trial was designed to evaluate the incidence of Terson syndrome in patients suffering from Subarachnoid Hemorrhage, intracerebral Hemorrhage, or traumatic brain injury and whether consequences necessarily derive from the intraocular Hemorrhage itself. Two ophthalmologic examinations were performed to identify patients with Terson syndrome. Data on initial Glasgow Coma Scale, Hunt and Hess and Fisher grades, aneurysm site and diameter, and volume of Hemorrhage in intracerebral Hemorrhage patients were correlated to the location and course of Terson syndrome. Follow-up was performed after 3 months, including clinical and ophthalmologic investigations. The data showed that 16 of 83 Subarachnoid Hemorrhage patients (19.3 %), 2 of 22 intracerebral Hemorrhage patients (9.1 %), and 1 of 32 traumatic brain injury patients (3.1 %) suffered from Terson syndrome. Low Glasgow Coma Scale (p = 0.002), high Hunt and Hess grade (p < 0.001), and high Fisher grade (p = 0.002) were found to be associated with a higher incidence of Terson syndrome. The neurological outcome in Subarachnoid Hemorrhage patients suffering from Terson syndrome was worse compared with that of Subarachnoid Hemorrhage patients without Terson syndrome (p = 0.005), and vitrectomy was performed in seven eyes of six patients due to poor visual acuity. Terson syndrome is underestimated in patients with Subarachnoid Hemorrhage and a rare pathology in intracerebral Hemorrhage as well as in traumatic brain injury patients. Spontaneous regression of the intraocular Hemorrhage may be seen, but in half of the patients, vitrectomy is necessary to prevent permanent visual deterioration.
Joshua M Levine - One of the best experts on this subject based on the ideXlab platform.
-
brain lactate metabolism in humans with Subarachnoid Hemorrhage
Stroke, 2012Co-Authors: Mauro Oddo, Joshua M Levine, Suzanne Frangos, Eileen Maloneywilensky, Roy Thomas Daniel, Marc Levivier, Emmanuel Carrera, Pierre J. Magistretti, Peter D LerouxAbstract:Background and Purpose— Lactate is central for the regulation of brain metabolism and is an alternative substrate to glucose after injury. Brain lactate metabolism in patients with Subarachnoid Hemorrhage has not been fully elucidated. Methods— Thirty-one Subarachnoid Hemorrhage patients monitored with cerebral microdialysis (CMD) and brain oxygen (PbtO2) were studied. Samples with elevated CMD lactate (>4 mmol/L) were matched to PbtO2 and CMD pyruvate and categorized as hypoxic (PbtO2 119 μmol/L) versus nonhyperglycolytic. Results— Median per patient samples with elevated CMD lactate was 54% (interquartile range, 11%–80%). Lactate elevations were more often attributable to cerebral hyperglycolysis (78%; interquartile range, 5%–98%) than brain hypoxia (11%; interquartile range, 4%–75%). Mortality was associated with increased percentage of samples with elevated lactate and brain hypoxia (28% [interquartile range 9%–95%] in nonsurvivors versus 9% [interquartile range 3%–17%] in survivors; P =0.02) and lower percentage of elevated lactate and cerebral hyperglycolysis (13% [interquartile range, 1%–87%] versus 88% [interquartile range, 27%–99%]; P =0.07). Cerebral hyperglycolytic lactate production predicted good 6-month outcome (odds ratio for modified Rankin Scale score, 0–3 1.49; CI, 1.08–2.05; P =0.016), whereas increased lactate with brain hypoxia was associated with a reduced likelihood of good outcome (OR, 0.78; CI, 0.59–1.03; P =0.08). Conclusions— Brain lactate is frequently elevated in Subarachnoid Hemorrhage patients, predominantly because of hyperglycolysis rather than hypoxia. A pattern of increased cerebral hyperglycolytic lactate was associated with good long-term recovery. Our data suggest that lactate may be used as an aerobic substrate by the injured human brain.
-
reversible cerebral vasoconstriction syndrome associated with Subarachnoid Hemorrhage
Neurocritical Care, 2007Co-Authors: Brian L Edlow, Scott E Kasner, Robert W Hurst, John B Weigele, Joshua M LevineAbstract:Introduction Reversible cerebral vasoconstriction syndrome (RCVS) is a rare vasculopathy of unknown etiology. Ischemic stroke and intracerebral Hemorrhage are well-documented sequelae, but Subarachnoid Hemorrhage is an uncommon complication of RCVS.
