Titlebook: Neurovascular Events After Subarachnoid Hemorrhage; Towards Experimental Javier Fandino,Serge Marbacher,Emanuela Keller Book 2015 Springer

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,Vasospasm: My First 25 Years—What Worked? What Didn’t? What Next?,cologic angioplasty) if the patient develops DCI. Well-designed clinical trials of tirilazad, clasozentan, antiplatelet drugs, and magnesium have been conducted using more than a 1,000 patients each. Some of these drugs have almost purely vascular effects; other drugs are theoretically neuroprotecti

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Molecular Basis for Intracranial Aneurysm FormationA, have revealed some of the molecular mechanisms linking hemodynamic stress and long-lasting inflammation in IA walls. Currently, we propose that IA is a chronic inflammatory disease regulated by a positive feedback loop consisting of the cyclooxygenase (COX)-2 – prostaglandin (PG) E. – prostagland

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Mouse Genetic Background Is Associated with Variation in Secondary Complications After Subarachnoid ow much brain injury and vasospasm occur after SAH. Future investigations may provide insight into the causes of these differences between strains and into which genetic contributors may be responsible for vasospasm and brain injury after SAH.

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The Value of Perfusion Computed Tomography (PCT) Imaging After Aneurysmal Subarachnoid Hemorrhage: An relevant publications were identified, nine of which focused on early PCT and seven on subsequent PCT diagnostics after aSAH. Early PCT provided relevant details on the extent of EBI and identified patients at risk for developing DCI, whereas subsequent PCT imaging facilitated the monitoring and d

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Neurovascular Events After Subarachnoid Hemorrhage: Focusing on Subcellular Organellesk of review articles addressing the direction of organelle dysfunction after SAH. In this review, we discuss the roles of organelle dysfunction in the pathogenesis of SAH and present the opportunity to develop novel therapeutic strategies of SAH via modulating the functions of organelles.

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