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- W2093984243 abstract "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." @default.
- W2093984243 created "2016-06-24" @default.
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- W2093984243 date "2007-05-01" @default.
- W2093984243 modified "2023-10-11" @default.
- W2093984243 title "Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution" @default.
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- W2093984243 doi "https://doi.org/10.1038/ncpneuro0490" @default.
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