Titlebook: Cerebral Vasospasm: Neurovascular Events After Subarachnoid Hemorrhage; Mario Zuccarello,Joseph F. Clark,Opeolu M. Adeoye Book 2013 Spring

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Protein Biomarkers in Patients with Subarachnoid Hemorrhage, Vasospasm, and Delayed Ischemic Neurological deficits (DINDs). We explored the blood proteome in patients with aSAH using transcranial Doppler (TCD) velocity as a guide to patients who are at risk for symptomatic vasospasm and DIND. Blood was drawn on all days that patients were observed in the neurocritical care unit (NCCU) after aSAH.

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Randomised Trial of Clazosentan, an Endothelin Receptor Antagonist, in Patients with Aneurysmal Sub = 768) or placebo (. = 389) administered for up to 14 days in patients with aneurysmal subarachnoid hemorrhage (SAH) repaired by surgical clipping. The primary endpoint was a composite of all-cause mortality, new cerebral infarction or delayed ischemic neurological deficit due to vasospasm, and res

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Angiographic Vasospasm Versus Cerebral Infarction as Outcome Measures After Aneurysmal Subarachnoidemorrhage (SAH) remains challenging. While there is general consensus that vasospasm is associated with delayed cerebral ischemia (DCI), cerebral infarction, poor functional outcome, and mortality after SAH, causal relationships are subject to discussion. Therefore, it was the aim of our study to in

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Prolonged Intravenous Infusion of Sodium Nitrite Delivers Nitric Oxide (NO) in Humans,fety and toxicity of intravenous nitrite administration in healthy volunteers infused with increasing doses of sodium nitrite for 48 h. Twelve volunteers (5 men, 7 women; mean age was 38.8 years, range 27–56 years) participated in the study. The starting sodium nitrite dose was 4.2 mg/kg/h, and it w

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Proposed Mechanism of Cerebral Vasospasm: Our Hypothesis and Current Topics,ascular contractility can be attributed to either endothelial dysfunction or increased contractility of vascular smooth muscle. Endothelial damage and dysfunction cause impairment of endothelium-dependent vasodilation of the cerebral artery after SAH. In addition to endothelial damage and dysfunctio

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Monitoring of Cerebral Hemodynamics and Oxygenation to Detect Delayed Ischemic Neurological Deficitc neurologic deficits (DINDs) to prevent cerebral infarction and thus poor outcome or even death. The complex changes of cerebral metabolism, hemodynamics, and oxygenation after SAH are underestimated if they are considered exclusively based on angiographic cerebral vasospasm (CVS). The discrepancie

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Usefulness of Three-Dimensional Computed Tomography to Quantify the Subarachnoid Hemorrhage Volume:on between the SAH volume and the occurrence of symptomatic vasospasm (SVS). We studied 64 patients with SAH onset (day 0) and on days 1, 4, 7, and 14. We compared the hematoma volume by 3D-CT with 2D-CT on day 0 and examined the correlation between the hematoma volume and the occurrence of SVS. The