Stroke; a journal of cerebral circulation
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An increased risk of hemorrhagic transformation is a major factor limiting the use of tissue plasminogen activator for stroke. Increased hemorrhagic transformation is also found in animals undergoing transient focal cerebral ischemia with hyperglycemia; this study examined whether hyperbaric oxygen (HBO) could reduce such hemorrhagic transformation in a rat model. ⋯ Early intraischemic HBO treatment reduces the blood-brain barrier disruption, hemorrhagic transformation, and mortality after focal cerebral ischemia suggesting that HBO could be used to reduce hemorrhagic conversion in patients with stroke.
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Subarachnoid hemorrhage (SAH) can be devastating, yet its initial presentation may be limited to common symptoms and subtle signs, potentially leading to misdiagnosis. Little is known about population rates of misdiagnosis of SAH, or hospital factors that may contribute to it. We estimated the population-based rate of missed SAH among emergency department (ED) patients and examined its relationship with hospital characteristics. ⋯ About 1 in 20 SAH patients are missed during an ED visit. Lower acuity patients are at higher risk of misdiagnosis, suggesting the need for heightened suspicion among patients with minimal clinical findings. The risk is also greater in nonteaching hospitals, but this is not explained by the annual volume of SAHs seen in the ED or access to CT.
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Acute basilar artery occlusion portends high risk of stroke and death. Thrombolysis or endovascular therapy has been limited to patients who present within hours of symptom onset. Without recanalization, acute basilar artery occlusion almost always results in death or severe disability. ⋯ Endovascular therapy can be feasible and safe for symptomatic basilar artery occlusion at chronic stage.
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Hemodynamic compromise due to occlusive cerebrovascular disease is associated with an increased stroke risk. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been suggested to stimulate collateral blood vessel growth in various models of hemodynamic compromise. The purpose of this study was to investigate the effects of GM-CSF on cerebral hemodynamics and vessel growth in a rat model of chronically impaired cerebral blood flow (CBF). ⋯ Long-term GM-CSF treatment in a BCO model in rats leads to restoration of impaired cerebral hemodynamics and accompanies structural changes in the resistance-vessel network.
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Clinical Trial
Autonomic ganglionic blockade does not prevent reduction in cerebral blood flow velocity during orthostasis in humans.
The underlying mechanisms for reductions in cerebral blood flow (CBF) during orthostasis are not completely understood. This study tested the hypothesis that sympathetic activation causes cerebral vasoconstriction leading to reductions in CBF during lower body negative pressure (LBNP). ⋯ These data, contrary to our hypothesis, demonstrate that sympathetic vasoconstriction is not the primary mechanism underlying reductions in CBF during moderate LBNP. We speculate that diminished pulse arterial pressure or pulsatile blood flow may reduce cerebral vessel wall shear stress and contribute to reductions in CBF during orthostasis through flow mediated regulatory mechanisms.