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Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution.

Nature clinical practice. Neurology

pathology, metabolism, etiology, Vasospasm, Intracranial, complications, Subarachnoid Hemorrhage, Humans, Brain Ischemia, Animals

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      Abstract

      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.

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      Most cited references 9

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      Case-fatality rates and functional outcome after subarachnoid hemorrhage: a systematic review.

      During the last three decades, new management strategies have been developed for patients with aneurysmal subarachnoid hemorrhage. To assess whether the case-fatality rate has improved after the introduction of new management strategies, we studied outcome in all population-based studies from 1960 onward. To identify population-based studies that reported on case-fatality rate in subarachnoid hemorrhage, we performed a MEDLINE search and checked all reference lists of the studies found. Two authors (J.W.H. and G.J.E.R.) independently assessed all studies for eligibility, using predefined criteria for case finding and diagnosis, and extracted data on case-fatality rates. We used weighted linear regression analysis to quantify change in case-fatality rate over time. We found 21 studies, describing 25 study periods between 1960 and 1992. Case-fatality rates varied between 32% and 67%, with the exception of one recent study. The case-fatality rate decreased by 0.5% per year (95% confidence interval, -0.1 to 1.2); the decline was steeper after adjustment for age and sex (0.9% per year; 95% confidence interval, -0.7 to 2.6; data from 12 studies). The case-fatality rate after subarachnoid hemorrhage has decreased during the last three decades. A plausible explanation for this decrease is the improved management of patients with subarachnoid hemorrhage.
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        The burden, trends, and demographics of mortality from subarachnoid hemorrhage.

        The objective of this study was to describe the recent epidemiology of mortality from subarachnoid hemorrhage in the United States. Subarachnoid hemorrhage is distinct from other forms of stroke in its risk factors, demographics, and treatment. However, it is often clustered with other stroke subtypes, obscuring its unique epidemiology. We analyzed subarachnoid hemorrhage mortality data from the National Center for Health Statistics of the United States for the years 1979 to 1994 and compared it with other stroke subtypes. Age-adjusted mortality rates of subarachnoid hemorrhage were 62% greater in females than in males and 57% greater in blacks than in whites. The median age of death from subarachnoid hemorrhage was 59 years compared with 73 years for intracerebral hemorrhage and 81 years for ischemic stroke. Mortality rates of subarachnoid hemorrhage have decreased by approximately 1% per year since 1979, and the mean age of death has steadily increased from 57 years in 1979 to 60 years in 1994. Subarachnoid hemorrhage accounted for 4.4% of stroke mortality but 27.3% of all stroke-related years of potential life lost before age 65, a measure of premature mortality. The proportion of years of potential life lost due to subarachnoid hemorrhage was comparable with ischemic stroke (38.5%) and intracranial hemorrhage (34.2%). Subarachnoid hemorrhage is an uncommon cause of stroke mortality but occurs at a young age, producing a relatively large burden of premature mortality, comparable with ischemic stroke.
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          Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

          Cerebral microcirculatory changes during cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) are still controversial and uncertain. The aim of this study was to investigate the changes of cerebral microcirculation during cerebral vasospasm and to clarify the roles of microcirculatory disturbances in cerebral ischemia by measuring cerebral circulation time (CCT) and regional cerebral blood flow (rCBF). In 24 cases with aneurysmal SAH, rCBF studies by single-photon emission CT and digital subtraction angiography (DSA) were performed on the same day between 5 and 7 days after SAH and/or within 4 hours after the onset of delayed ischemic neurological deficits. CCT was obtained by analyzing the time-density curve of the contrast media on DSA images and was divided into proximal CCT, which was the circulation time through the extraparenchymal large arteries, and peripheral CCT, which was the circulation time through the intraparenchymal small vessels. They were analyzed in association with rCBF and angiographic vasospasm. Severe angiographic vasospasm statistically decreased rCBF, and correlation between the degree of angiographic vasospasm and rCBF was seen (r=0.429, P=0.0006). Peripheral CCT showed strong inverse correlation with rCBF (r=-0.767, P<0.0001). Even in none/mild or moderate angiographic vasospasm, prolonged peripheral CCT was clearly associated with decreased rCBF. In addition to the marked luminal narrowing of large arteries detected as severe angiographic vasospasm, microcirculatory changes detected as prolonged peripheral CCT affected cerebral ischemia during cerebral vasospasm. These results suggested that impaired autoregulatory vasodilation or decreased luminal caliber in intraparenchymal vessels may take part in cerebral ischemia during cerebral vasospasm.
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            Journal
            10.1038/ncpneuro0490
            17479073

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