Hemorrhage detected using MR imaging in the setting of acute stroke: an in vivo model.
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BACKGROUND AND PURPOSE: The treatment algorithm for acute cerebrovascular accidents has traditionally sorted these accidents as either hemorrhagic or nonhemorrhagic, and MR imaging, with its ability to allow expeditious assessment of vascular substrates and regional blood volume, is well suited for this purpose. Our purpose was to delineate the accuracy of MR imaging in acute, hemorrhagic forms of stroke during the time frame considered beneficial for intervention in an animal model. METHODS: Eighteen dogs with small, iatrogenic parenchymal, subarachnoid hemorrhage (SAH), or both were serially scanned over the initial 6-hour postictal period. Confirmatory pathologic specimens and 3-hour postictal CT scans were obtained in all animals. The MR and CT studies were then interpreted in a blinded fashion by two neuroradiologists for the presence of hemorrhage. The results were subjected to receiver operating characteristic analysis. RESULTS: MR imaging depicted acute parenchymal hemorrhage and SAH with a high degree of accuracy at 1.5 T. This finding was independent of each of the time points studied during the 6-hour window. For SAH, the MR accuracy for reader 1 was 0.86 (95% CI, 0.76-0.97); for reader 2, accuracy was 0.85 (95% CI, 0.71-0.99). The CT accuracy for the two readers was 0.42 (95% CI, 0.26-0.58) and 0.66 95% CI, 0.43-0.89), respectively. Fluid-attenuated inversion-recovery images improved the conspicuity of SAH on MR images and, along with spin-density-weighted spin-echo sequences, helped to establish the hemorrhagic nature. For parenchymal hemorrhage, the MR accuracy for reader 1 was 0.90 (95% CI, 0.81-0.99); for reader 2, accuracy was 0.93 (95% CI, 0.84-1.00). With CT, the accuracy of reader 1 was 0.91 (95% CI, 0.85-0.97) whereas for reader 2 accuracy was 0.76 (95% CI, 0.69-.83). Parenchymal hemorrhage detection and diagnosis was best with T2*-weighted gradient-echo images. CONCLUSION: MR imaging with appropriately selected sequences appears able to provide information regarding the presence (or absence) of hemorrhage in an acute stroke model requisite to the initiation of treatment. (+info)
Treatment of intradural paraclinoidal aneurysms.
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Intradural paraclinoidal aneurysm still presents conceptual confusion and technical surgical problems. The clinical features of 68 consecutive patients with paraclinoidal aneurysms were analyzed. The pterional approach was used in all patients. Subarachnoid hemorrhage (SAH) occurred in 37 patients from the paraclinoidal aneurysm and in 10 patients from another associated aneurysm. Thirty-four of the 37 ruptured paraclinoidal aneurysms were clipped, two blister-like aneurysms required trapping, and one blister-like aneurysm was coated. Thirteen of the 31 unruptured paraclinoidal aneurysms, consisting of 10 with ruptured associated aneurysm, four symptomatic, and 17 incidental, were clipped and 18 were coated. Favorable outcomes were obtained in 38 of 47 patients with SAH and 17 of 21 patients without SAH. Nine unfavorable outcomes in SAH patients were caused by primary brain damage (5), vasospasm (2), cerebral infarction after trapping (1), and pneumonia (1). All four unfavorable outcomes in non-SAH patients were due to surgical procedures for giant aneurysms or associated basilar artery aneurysm. Removal of the anterior clinoid process was performed to secure the proximal neck in 15 patients with large or giant aneurysms. Multiple clips with or without fenestrated clips were required in all giant aneurysms, and exposure of the cervical internal carotid artery (ICA) in 17 giant or large aneurysms. Fenestrated clips were also useful for one small aneurysm projecting posteriorly. A favorable outcome was achieved in 17 of 19 patients undergoing coating. Coating without clipping might be better for some blister-like ICA aneurysms, even if ruptured. Paraclinoidal aneurysms can be clipped with favorable results using these techniques except for giant aneurysms and associated basilar artery aneurysm. (+info)
Sudden death in a rat subarachnoid hemorrhage model.
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The pathogenesis of sudden death during subarachnoid hemorrhage (SAH) still remains to be elucidated. A new rat common carotid artery-prechiasmal extracorporeal shunt model was designed to study the effect of different severities of SAH on intracranial pressure (ICP), regional cerebral blood flow (rCBF), and mortality. Different severities of SAH were induced by controlling the bleeding period (from 30 to 90 sec) and number of bleedings (one or three times). SAH caused a dramatic increase in ICP and immediate depression of rCBF, which recovered slowly to a certain extent. ICP increased sharply within the first 30 seconds and reached a plateau concomitant with nearly zero rCBF, which suggested the occurrence of cerebral circulation arrest. Bleeding of more than 60 seconds and increased ICP over 80 mmHg were directly correlated with the mortality. Respiratory arrest was the first sign of death, immediately followed by cardiac depression resulting in sudden death. This model combines arterial bleeding with systemic blood pressure and controlled bleeding time to simulate the acute period of SAH. (+info)
Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage. Clinical and TCD correlations.
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BACKGROUND AND PURPOSE: Hyponatremia has been shown in association with cerebral vasospasm (CVS) following aneurysmal subarachnoid hemorrhage (SAH). In the past few years there has been increasing evidence that brain natriuretic peptide (BNP) is responsible for natriuresis after SAH. The purpose of the present study was to investigate the relationship between BNP plasma concentrations and CVS after aneurysmal SAH. METHODS: BNP plasma concentrations were assessed at 4 different time periods (1 to 3 days, 4 to 6 days, 7 to 9 days, and 10 to 12 days) in 19 patients with spontaneous SAH. BNP plasma levels were investigated with respect to neurological condition, SAH severity on CT, and flow velocities measured by means of transcranial Doppler. RESULTS: Thirteen patients had Doppler evidence of CVS; 7 of these had nonsymptomatic CVS. In 6 patients, CVS was severe and symptomatic, with delayed ischemic lesion on CT in 5 of these. CVS was severe and symptomatic in 6 patients, and delayed ischemic lesions were revealed on CT in 5 of these. BNP levels were found to be significantly elevated in SAH patients compared with control subjects (P=0.024). However, in patients without CVS or with nonsymptomatic CVS, BNP concentrations decreased throughout the 4 time periods, whereas a 6-fold increase was observed in patients with severe symptomatic CVS between the first and the third periods (P=0.0096). A similar trend in BNP plasma levels was found in patients with severe SAH compared with those with nonvisible or moderate SAH (P=0.015). CONCLUSIONS: In conclusion, our results show that BNP plasma levels are elevated shortly after SAH, although they increase markedly during the first week in patients with symptomatic CVS. The present findings suggest that secretion of BNP secretion after spontaneous SAH may exacerbate blood flow reduction due to arterial vasospasm. (+info)
Distal calcarine fusiform aneurysm: a case report and review of literature.
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A 50 year old female who was operated for atrial septal defect 8 years back, presented with clinical features suggestive of subarachnoid haemorrhage (grade I, Hunt and Hess). CT scan of brain revealed haemorrhage in all the supratentorial basal cisterns, sylvian cistern and small haematoma in the left occipital lobe. Conventional CT and MR angiography revealed aneurysm in relation to distal part of the calcarine branch of the left posterior cerebral artery (PCA). Left occipital craniotomy in prone position followed by deep dissection in the occipital lobe showed fusiform aneurysm of the distal part of the calcarine branch. PCA aneurysms constitute only 0.2 to 1% of all intracranial aneurysms and among them distal PCA aneurysms are most rare, constituting only 1.3%. They too are mostly seen at the bifurcation of the PCA. The present case however, is unique in the sense that it has developed as a fusiform aneurysm in the distal part of the calcarine branch. To the best of our knowledge this is rare among the rarest. (+info)
Risk of subarachnoid haemorrhage in first degree relatives of patients with subarachnoid haemorrhage: follow up study based on national registries in Denmark.
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OBJECTIVE: To estimate the risk of occurrence of subarachnoid haemorrhage in first degree relatives (parents, siblings, children) of patients with subarachnoid haemorrhage. DESIGN: Population based cohort study using data from the Danish National Discharge Registry and the Central Person Registry. SUBJECTS: Incident cases of subarachnoid haemorrhage admitted to hospital from 1977 to 1995 (9367 patients) and their first degree relatives (14 781). MAIN OUTCOME MEASURES: The incidence rate of subarachnoid haemorrhage was determined for the relatives and compared with that of the entire population, standardised for age, sex, and calendar period. This process was repeated for patients discharged from neurosurgery units, as diagnoses from these wards had high validity (93%). RESULTS: 18 patients had a total of 19 first degree relatives with subarachnoid haemorrhage during the study period, corresponding to a standardised incidence ratio of 2.9 (95% confidence interval 1.9 to 4.6). Patients discharged from neurosurgery wards had a higher standardised incidence ratio (4.5, 2.7 to 7.3). CONCLUSIONS: First degree relatives of patients with subarachnoid haemorrhage have a threefold to fivefold increased risk of subarachnoid haemorrhage compared with the general population. (+info)
Controlled trial of alpha-tocopherol and beta-carotene supplements on stroke incidence and mortality in male smokers.
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Observational data suggest that diets rich in fruits and vegetables and with high serum levels of antioxidants are associated with decreased incidence and mortality of stroke. We studied the effects of alpha-tocopherol and beta-carotene supplementation. The incidence and mortality of stroke were examined in 28 519 male cigarette smokers aged 50 to 69 years without history of stroke who participated in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC Study). The daily supplementation was 50 mg alpha-tocopherol, 20 mg beta-carotene, both, or placebo. The median follow-up was 6.0 years. A total of 1057 men suffered from incident stroke: 85 men had subarachnoid hemorrhage; 112, intracerebral hemorrhage; 807, cerebral infarction; and 53, unspecified stroke. Deaths due to stroke within 3 months numbered 38, 50, 65, and 7, respectively (total 160). alpha-Tocopherol supplementation increased the risk of subarachnoid hemorrhage 50% (95% CI -3% to 132%, P=0.07) but decreased that of cerebral infarction 14% (95% CI -25% to -1%, P=0.03), whereas beta-carotene supplementation increased the risk of intracerebral hemorrhage 62% (95% CI 10% to 136%, P=0.01). alpha-Tocopherol supplementation also increased the risk of fatal subarachnoid hemorrhage 181% (95% CI 37% to 479%, P=0.01). The overall net effects of either supplementation on the incidence and mortality from total stroke were nonsignificant. alpha-Tocopherol supplementation increases the risk of fatal hemorrhagic strokes but prevents cerebral infarction. The effects may be due to the antiplatelet actions of alpha-tocopherol. beta-Carotene supplementation increases the risk of intracerebral hemorrhage, but no obvious mechanism is available. (+info)
Postpartum dissecting aneurysm of the superior cerebellar artery--case report.
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A 37-year-old female with toxemia of pregnancy suffered sudden headache and loss of consciousness on the day following a cesarean delivery. Computed tomography revealed subarachnoid hemorrhage (SAH). Vertebral angiography revealed a fusiform dilatation near the origin of the right superior cerebellar artery (SCA) with distal luminal narrowing. She underwent surgery within 24 hours of the ictus. A SAH clot was carefully removed from the prepontine cistern, and subadventitial discoloration was seen in the wall of the right SCA just distal to the aneurysmal protuberance (rupture site). The dissecting aneurysm was treated with body clipping by directly clipping the rupture site and with additional wrapping of the proximal SCA, including the aneurysmal protuberance and discolored site. The postoperative clinical course was uneventful. Postoperative angiography revealed complete obliteration of the aneurysm and patency of the SCA. Therapeutic intervention should be considered for patients with ruptured dissecting aneurysm who present with recurrent SAH. (+info)