Articles: subarachnoid-hemorrhage.
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The outcome of subarachnoid hemorrhage in patients with familial occurrence of subarachnoid hemorrhage (familial SAH) is an important but neglected factor in balancing the risks of screening for asymptomatic aneurysms and repairing these in unaffected members of such families. ⋯ Patients with familial SAH have a greater risk of poor outcome than patients with sporadic SAH. This adds to the factors in favor of screening unaffected first-degree relatives of patients with familial SAH.
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Journal of neurosurgery · Jun 1995
Aspirin and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
This follow-up study was designed to evaluate whether the use of aspirin either before or after aneurysm rupture affects the occurrence of delayed cerebral ischemia. Aspirin inhibits platelet function and thromboxane production and has been shown to reduce the risk of various cardiovascular and cerebrovascular ischemic diseases. Following admission, the patients in this study was interviewed regarding their use of aspirin and other medicines prior to and after hemorrhage, and their urine was screened qualitatively for salicylates. ⋯ This reduced risk of ischemic complications with aspirin use was restricted to those patients who used aspirin before hemorrhage, when the risk of ischemia was 0.21 (95% CI, 0.03 to 1.63) and the risk of infarct was 0.18 (95% CI, 0.04 to 0.84) compared with those who had not used aspirin. The reduced risk of cerebral infarction remained significant after adjustment for several potential confounding factors (adjusted risk 0.19; 95% CI, 0.04 to 0.89). These observations suggest that platelet function at the time of subarachnoid hemorrhage may be associated with delayed cerebral ischemia after aneurysm rupture.
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Comment Letter Case Reports
Isolated basilar traumatic subarachnoid hemorrhage: an observer's 25 year re-evaluation of the pathogenetic possibilities.
This paper was inspired by Leadbeatter's recent review [1] on the subject, and consists primarily of a recapitulation of this author's observations in the 25 years since publication of his paper [2] describing three cases of traumatic basilar subarachnoid hemorrhage resulting from direct trauma to the upper lateral neck. Those observations include personal experience and case reports personally communicated or published. Leadbeatter's analysis makes the following three salient points to which the author considers a response to be appropriate: 1. ⋯ Accordingly, empirical factors have to be considered for a diagnosis in most cases. Four diagnostic criteria have been established for a firm conclusion of death due to traumatic basilar subarachnoid hemorrhage. 3. While over half of traumatic basilar subarachnoid hemorrhages involve a completely different site of trauma, and many indirect mechanisms of injury may come into play, the author still considers that in the commonly observed syndrome as described by him in 1971, direct trauma to the vertebral artery is the primary causative factor.
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The clinical characteristics of vertebrobasilar dissecting aneurysms occurring with subarachnoid hemorrhage (SAH) were reviewed in 42 patients, with particular focus on the time, incidence, and outcome in association with subsequent rupture. Twenty-nine patients underwent 31 surgical procedures, and the remaining 13 patients were managed without surgery. Surgical details included 19 proximal vertebral artery obliterations (including 1 case of endovascular surgery using balloon occlusion), 9 trappings, 1 wrapping, 1 bleb clipping, and 1 bleb clipping combined with wrapping. ⋯ The mortality (46.7%) of the patients with subsequent rupture was significantly higher (P < 0.05) than that (8.3%) of the patients without subsequent rupture. Seventeen (56.7%) of the 30 subsequent ruptures occurred within 24 hours after the first SAH, and 24 (80%) occurred within the first week. Six (66.7%) of the 9 patients operated on within 24 hours after the first SAH and 11 (68.8%) of the 16 patients operated on within a week suffered preoperative subsequent ruptures.(ABSTRACT TRUNCATED AT 250 WORDS)
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Journal of neurosurgery · May 1995
Randomized Controlled Trial Clinical TrialPhase II trial of tirilazad in aneurysmal subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study.
Tirilazad mesylate, a 21-aminosteroid free-radical scavenger, has been shown to ameliorate cerebral vasospasm and reduce infarct size in animal models of subarachnoid hemorrhage (SAH) and focal cerebral ischemia. In preparation for performing large-scale clinical trials in humans with aneurysmal SAH, the safety of varying doses of tirilazad was tested in a randomized, double-blind, vehicle-controlled, sequential dose-escalation study at 12 Canadian neurosurgical centers. Two hundred forty-five patients with an aneurysmal SAH documented by angiography were enrolled in the study sequentially within 72 hours of hemorrhage. ⋯ No serious side effects of tirilazad treatment were identified at any of the three doses, despite close monitoring of hepatic and cardiac toxicity. A trend toward improvement in overall 3-month patient outcome was seen in the 2 mg/kg per day tirilazad-treated group compared to the outcomes in the vehicle-treated groups. We conclude that tirilazad mesylate is safe in SAH patients at doses up to 6 mg/kg per day for up to 10 days and is a promising drug for the treatment of patients with aneurysmal SAH.