Abstract 3456: Incidence of Vasospasm and Outcomes in Angiography-negative Perimesencephalic Subarachnoid Hemorrhage with and without Ventricular Extension
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Background: Angiography negative perimesencephalic subarachnoid hemorrhage (SAH) is considered a relatively benign entity compared to aneurysmal SAH. However, some patients with angiography negative perimesencephalic subarachnoid hemorrhage with extension of hemorrhage beyond the perimesencephalic area are at increased risk for vasospasm. Here we present a series of 21 patients with angiography negative perimesencephalic pattern of SAH both with and without ventricular extension and describe their incidence of vasospasm and clinical outcomes. Methods: Retrospective chart review was performed among patients who underwent invasive angiography from 8/2007-6/2010. Inclusion criteria were presenting clinical symptoms typical of SAH, computed tomography (CT) evidence of perimesencephalic SAH with or without ventricular extension, no recent trauma or stroke, and cerebral angiography negative for aneurysm or arteriovenous malformation. 21 patients, 8 men and 13 women, with a mean age of 55.1 years met these criteria. The presenting CTs were examined and a modified Fisher Grade assigned. The patients’ clinical course was reviewed for incidence and treatment of vasospasm. The patients’ discharge summaries were evaluated and each patient given a modified Rankin Scale score. Results: The modified Fisher Scale score derived from the presenting CT was 1 for 29% (n=6), 2 for 5% (n=1), 3 for 19% (n=4), and 4 for 47% (n=10) of the patients. Amongst the 52% (n=11) of patients with intraventricular hemorrhage as defined by a modified Fisher Scale score of 2 or 4, 24% (n=5) developed angiographical evidence of vasospasm. 10% (n=2) of the patients required intra-arterial verapamil. 90% (n=9) of patients without intraventricular extension had good outcomes at discharge as defined by modified Rankin Scale score less than or equal to 2, while only 36% (n=4) of patients with angiography negative SAH with intraventricular extension had good outcomes. Conclusions: Although angiography negative perimesencephalic SAH is considered to have less associated morbidity and mortality than aneurysmal perimesencephalic SAH, patients with extension of hemorrhage into the ventricles are at increased risk for vasospasm and poor functional outcomes.Keywords:
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Cerebral Vasospasm
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BACKGROUND: Cerebral vasospasm is delayed-onset cerebral arterial narrowing in response to blood clots left in the subarachnoid space after spontaneous aneurysmal subarachnoid hemorrhage (SAH). Ideally, studies on the pathogenesis and treatment of cerebral vasospasm in humans should be conducted using human cerebral arteries. Because in vivo experiments using human vessels are not possible, and postmortem pathological examination of human arteries in vasospasm provides only a limited amount of information, a number of animal models of vasospasm have been developed. METHODS: The literature was searched to find all references to in vivo animal models of SAH and vasospasm. An online search of the medical database MEDLINE was initially performed using the key words "cerebral," "vasospasm," "subarachnoid," "hemorrhage," "animal," and "model." References were checked to determine the first description of each in vivo animal model. RESULTS: Fifty-seven models of SAH and vasospasm were identified. These models used one of three techniques to simulate SAH: 1) an artery was punctured allowing blood to escape and collect around the artery and its neighbors; 2) an artery was surgically exposed, and autologous blood obtained from another site was placed around the artery; or 3) blood from another site was injected into the subarachnoid space and was allowed to collect around arteries. Each technique has advantages and disadvantages. The majority of animal models of SAH and vasospasm use intracranial arteries; however, extracranial arteries have also been used recently in vasospasm experiments. These studies seem easier and less costly to perform, but concerns exist regarding the physiological dissimilarity between systemic and cerebral arteries. CONCLUSION: The model of SAH and vasospasm used most frequently is the canine "two-hemorrhage" model, in which two injections of blood into the dog's basal cistern performed 48 hours apart result in greater arterial vasoconstriction than that effected by a single injection of blood. On the basis of its ability to accurately predict what occurs in human SAH, the best model of vasospasm seems to be the primate model in which a blood clot is surgically placed around the large cerebral vessels at the base of the monkey's brain.
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Object. It is not known whether the factors responsible for vasospasm after subarachnoid hemorrhage (SAH) cause the cerebral arteries to be narrowed independent of the subarachnoid blood clot or whether the continued presence of clot is required for the entire time of vasospasm. The authors undertook the present study to investigate this issue. Methods. To distinguish between these possibilities, bilateral SAH was induced in monkeys. The diameters of the monkeys' cerebral arteries were measured on angiograms obtained on Days 0 (the day of SAH), 1, 3, 5, 7, and 9. The subarachnoid blood clot was removed surgically on Day 1, 3, or 5 or, in control animals, was not removed until the animals were killed on Day 7 or 9. The concentrations of hemoglobins and adenosine triphosphate (ATP), substances believed to cause vasospasm, were measured in the removed clots and the contractile activity of the clots was measured in monkey basilar arteries in vitro. If the clot was removed 1 or 3 days after placement, vasospasm was significantly diminished 4 days after clot removal. Clot removal on Day 5 had no marked effect on vasospasm. There was a significant decrease over time in hemoglobin and ATP concentrations and in the contractile activity of the clots, although substantial hemoglobin and contractile activity was still present on Day 7. Conclusions. The authors infer from these results that vasospasm requires the presence of subarachnoid blood for at least 3 days, whereas by Day 5 vasospasm is less dependent on subarachnoid blood clot. Because the clot still contains substantial amounts of hemoglobin and contractile activity after 5 days, there may be an adaptive response in the cerebral arteries that allows them to relax in the presence of the stimulus that earlier caused contraction.
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✓ This study investigates the relationship between vasospasm and repeated subarachnoid hemorrhages in 18 monkeys. Sixteen received weekly 4 cc injections of autogenous blood into the subfrontal subarachnoid space. The weekly mortality rate for 4 weeks was 6%, 33%, 20%, and 37% respectively. The over-all mortality was 75%. The degree of vasospasm did not correlate with the morbidity and mortality. Vasospasm was limited to the intradural cerebral vessels and was diffuse. It never lasted longer than a few hours, late vasospasm did not occur, and the degree of vasospasm did not alter with repeated occasions of “subarachnoid hemorrhage.” Immediate electrocardiogram abnormalities were related to the height of the cerebrospinal fluid pressure rise following the subarachnoid hemorrhage (injected blood). Pathological examination of the vessels shown to be in spasm was normal. The study suggests that the increased mortality associated with repeated subarachnoid hemorrhage is due to cumulative structural damage rather than a heightened vasospastic response to repeated hemorrhages.
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Cerebral Vasospasm
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Cerebral vasospasm is the most common and most dangerous complication of subarachnoid hemorrhage (SAH). If it can not be diagnosed and treated early, it will result in delayed cerebral ischemia and delayed ischemic neurological deficits, and seriously affect the outcomes of patients. SAH can cause oxidative stress and inflammation, causing vasospasm, and leading to brain tissue damage. Numerous studies have shown that the concentrations and activities of numerous metabolites will change in these pathological physiological processes. Identification of the changes of location, time and trend of these markers has important clinical significance for investigating the mechanism of cerebral vasospasm after SAH and seeking better therapeutic targets. This article reviews the molecular markers of cerebral vasospasm after SAH.
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Subarachnoid Hemorrhage; Vasospasm, Intracranial; Biological Markers
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