Disseminated coccidioidomycosis complicated by vasculitis: a cause of fatal subarachnoid hemorrhage in two cases.
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We describe two cases of disseminated coccidioidomycosis that were complicated by fatal subarachnoid hemorrhage. In the first case, a left middle cerebral artery aneurysm and long-segment vasculitis occurred. In the second case, MR imaging revealed an enlarging coccidioidal granuloma at the tip of the basilar artery, and the artery subsequently ruptured. Fatal intracranial hemorrhage is a rare complication of disseminated coccidioidomycosis. (+info)
Initial loss of consciousness and risk of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
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BACKGROUND AND PURPOSE: Delayed cerebral ischemia (DCI) is a major cause of death and disability in patients with aneurysmal subarachnoid hemorrhage. We studied the prognostic value for DCI of 2 factors: the duration of unconsciousness after the hemorrhage and the presence of risk factors for atherosclerosis. METHODS: In 125 consecutive patients admitted within 4 days after hemorrhage, we assessed the presence and duration of unconsciousness after the hemorrhage, the neurological condition on admission, the amount of subarachnoid blood, the size of the ventricles, and a history of smoking, hypertension, stroke, or myocardial infarction. The relationship between these variables and the development of DCI was analyzed by means of the Cox proportional hazards model. RESULTS: The univariate hazard ratio (HR) for the development of DCI in patients who had lost consciousness for >1 hour was 6.0 (95% CI 3.0 to 12.0) compared with patients who had no loss or a <1-hour loss of consciousness. The presence of any risk factor for atherosclerosis yielded an HR of 1.4 (95% CI 0.6 to 3.5). The HR for unconsciousness remained essentially the same after adjustment for other risk factors for DCI. The HR for a poor World Federation of Neurological Surgeons score (grade IV or V) on admission was 2.9 (95% CI 1.5 to 5. 5); that for a large amount of subarachnoid blood on CT was 3.4 (95% CI 1.6 to 7.3). CONCLUSIONS: The duration of unconsciousness after subarachnoid hemorrhage is a strong predictor for the occurrence of DCI. This observation may contribute to a better understanding of the pathogenesis of DCI and increased attention for patients at risk. (+info)
Clinical course, surgical management, and long-term outcome of moyamoya patients with rebleeding after an episode of intracerebral hemorrhage: An extensive follow-Up study.
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BACKGROUND AND PURPOSE: Revascularization surgery for moyamoya patients is believed to prevent cerebral ischemic attacks by improving cerebral blood flow. However, measures preventing the occurrence of hemorrhagic moyamoya in patients have not yet been established in the literature due to the low rate of hemorrhage onset as well as the originally limited numbers of patients with moyamoya disease, poor understanding of the clinical course of rebleeding, correct surgical management, and long-term outcome. We present here the results of an overall survey of patients with hemorrhagic moyamoya disease in a district of Miyagi Prefecture in Japan and examine their clinical course, efficacy of revascularization surgery, and long-term outcome. METHODS: This study included 28 moyamoya patients with episodes of intracranial hemorrhage between 1976 and 1988. The mean follow-up period was 14.2 years. There were 4 males and 24 females, aged 7 to 69 years (mean 39.2 years). Cerebral angiography and CT scans were performed for all patients. Surgical treatment was performed in 19 patients (67. 9%), and 10 patients (35.7%) underwent revascularization surgery. We observed the clinical course of all 28 patients. We also studied the relationship between the efficacy of surgical treatment and long-term outcome. RESULTS: Five of the 28 patients (17.9%) died of the initial intracranial hemorrhage, and 2 patients died of other causes. Rebleeding occurred in 6 of the remaining 21 patients (28. 6%). The interval to rebleeding ranged from 2 to 20 years (mean 7.3 years). Of these 6 patients, 4 died of rebleeding. Rebleeding was observed in 1 of 8 patients who underwent bypass surgery and in 5 of 13 patients who did not, which suggested that rebleeding was less likely to occur in patients who had undergone bypass surgery. However, there was no significant difference in rebleeding ratio or mortality between patients with and those without revascularization surgery (P>0.05). CONCLUSIONS: In this study, we compiled the results of meticulous follow-up conducted over the past 10 years for patients with hemorrhagic moyamoya disease. Because hemorrhagic moyamoya disease is known for its high rate of mortality at the time of rebleeding and often causes rebleeding long after the initial episode (as much as 20 years later), implementation of long-term preventive measures for rebleeding is necessary. This suggests that a long-term prospective study of a large number of patients with hemorrhagic moyamoya disease is required to determine whether bypass surgery prevents rebleeding of hemorrhagic moyamoya disease. (+info)
Acquired pial arteriovenous fistula following cerebral vein thrombosis.
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BACKGROUND: We report a unique case of an acquired pial arteriovenous fistula occurring after an asymptomatic thrombosis of a superficial cerebral vein. CASE DESCRIPTION: A cerebral angiogram performed in a 51-year-old man with subarachnoid hemorrhage revealed a 10-mm ruptured anterior communicating artery aneurysm and a thrombosed left superficial middle cerebral vein. Coil embolization of the anterior communicating aneurysm was performed. Follow-up angiography 18 months later revealed a new, asymptomatic, pial arteriovenous fistula between the previously thrombosed left superficial middle cerebral vein and a small sylvian branch of the left middle cerebral artery. CONCLUSIONS: This case provides evidence that pial arteriovenous fistulas may develop as acquired lesions and furthermore may rarely follow cerebral vein thrombosis. Several cases of dural arteriovenous fistulas, as well as a single case of a mixed pial-dural arteriovenous fistula, occurring after dural sinus thrombosis have been reported previously. However, to our knowledge, this is the first report of an acquired pial arteriovenous fistula following a cerebral vein thrombosis. (+info)
Very late-onset symptomatic cerebral vasospasm caused by a large residual aneurysmal subarachnoid hematoma--case report.
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A 70-year-old female developed delayed ischemic neurological deficits at 35 days after subarachnoid hemorrhage (Hunt and Kosnik grade III, Fisher group 4) caused by a ruptured aneurysm of the left middle cerebral artery. Angiography indicated late-onset cerebral vasospasm probably due to the mass effect of a large hematoma remaining in the sylvian fissure and an intracerebral hematoma after surgery. Patients with a large subarachnoid hematoma after subarachnoid hemorrhage should receive therapy to prevent cerebral vasospasm until the mass effect of the hematoma has diminished. (+info)
Impaired cerebral vasodilator responses to NO and PDE V inhibition after subarachnoid hemorrhage.
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Subarachnoid hemorrhage (SAH) is associated with impaired nitric oxide (NO)-mediated cerebral vasodilatation. We tested the hypothesis that SAH causes alterations in the production of, hydrolysis of, or responsiveness to cGMP in the rat basilar artery in vivo. Rats were injected with saline or autologous blood into the cisterna magna. Two days later, effects of vasoactive drugs on basilar artery diameter were examined using a cranial window preparation. Vasodilator responses to ACh, sodium nitroprusside (SNP), and low concentrations (+info)
Identification of genes differentially expressed in canine vasospastic cerebral arteries after subarachnoid hemorrhage.
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To understand the molecular processes of continuous vasospasm of cerebral arteries after subarachnoid hemorrhage, mRNA differential display and screening of cDNA expression array were performed to identify genes that are differentially expressed in vasospastic arteries of canine two-hemorrhage models. The expression levels of 18 genes were found to be upregulated, and those of two genes to be downregulated. Of these, 12 represent known genes or homologues of genes characterized previously, and the other eight genes are not related to any sequences in the databases. The known genes include five upregulated inflammation-related genes encoding monocyte chemotactic protein-1, cystatin B, inter-alpha-trypsin inhibitor family heavy chain-related protein, serum amyloid A protein, and glycoprotein 130, suggesting that inflammatory reaction may be involved in the development of cerebral vasospasm. The upregulation of three known genes encoding stress-related proteins of vascular endothelial growth factor, BiP protein, and growth-arrest and DNA-damage-inducible protein may be involved in possible cell survival in the damaged arteries. A full-length cDNA for the unknown clone DVS 27, whose expression was most highly upregulated, was isolated from the cerebral artery cDNA library by hybridization. Characterization of these genes should help to clarify the molecular mechanism of continuous cerebral vasospasm after subarachnoid hemorrhage. (+info)
Different risk factors for different stroke subtypes: association of blood pressure, cholesterol, and antioxidants.
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BACKGROUND AND PURPOSE: Blood pressure is an important risk factor for stroke, but the roles of serum total and HDL cholesterol, alpha-tocopherol, and beta-carotene are poorly established. We studied these factors in relation to stroke subtypes. METHODS: Male smokers (n=28 519) aged 50 to 69 years without a history of stroke participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, a controlled trial to test the effect of alpha-tocopherol and beta-carotene supplementation on cancer. From 1985 to 1993, a total of 1057 men suffered from primary stroke: 85 had subarachnoid hemorrhage; 112, intracerebral hemorrhage; 807, cerebral infarction; and 53, unspecified stroke. RESULTS: Systolic blood pressure > or = 160 mm Hg increased the risk of all stroke subtypes 2.5 to 4-fold. Serum total cholesterol was inversely associated with the risk of intracerebral hemorrhage, whereas the risk of cerebral infarction was raised at concentrations > or = 7.0 mmol/L. The risks of subarachnoid hemorrhage and cerebral infarction were lowered with serum HDL cholesterol levels > or = 0.85 mmol/L. Pretrial high serum alpha-tocopherol decreased the risk of intracerebral hemorrhage by half and cerebral infarction by one third, whereas high serum beta-carotene doubled the risk of subarachnoid hemorrhage and decreased that of cerebral infarction by one fifth. CONCLUSIONS: The risk factor profiles of stroke subtypes differ, reflecting different etiopathology. Because reducing atherosclerotic diseases, including ischemic stroke, by lowering high serum cholesterol is one of the main targets in public health care, further studies are needed to distinguish subjects with risk of hemorrhagic stroke. The performance of antioxidants needs confirmation from clinical trials. (+info)