bluuebunny/crossref_metadata_2025_split huggingface dataset:
Does cerebral infarction after a previous warning occur in the same vascular territory?
Authors: Cillessen J P , Kappelle L J , van Swieten J C , Algra A , van Gijn J 
Published: June 2011

The aim of this study was to compare the territory of cerebral infarcts on follow-up with that of the preceding transient ischemic attack or nondisabling stroke.
The Dutch TIA Trial was a randomized, double-blind, controlled trial, in which the secondary preventive effects of two doses of aspirin were compared in patients with a transient ischemic attack or nondisabling stroke. On the basis of clinical symptoms and computed tomography, qualifying events were classified as pertaining to the left carotid, right carotid, or vertebrobasilar circulation.
In 2,993 patients the territory of the qualifying event was that of the left carotid in 1,281 (43%), the right carotid in 1,090 (36%), and the vertebrobasilar in 444 (15%); the territory was uncertain in 178 (6%). On follow-up (mean, 2.6 years), 184 of the 2,371 patients with a baseline event in the carotid circulation suffered a recurrent ischemic stroke (7.8%), as did 28 of the 444 patients in the vertebrobasilar group (6.3%); 117 of these 212 infarcts (55%; 95% confidence interval, 49-62) occurred in the same territory (108 in the ipsilateral carotid and nine in the vertebrobasilar territory) as the event at baseline, compared with 39% to be expected by chance alone (95% confidence interval, 32-45). In the carotid groups patients were significantly more likely to have a subsequent ischemic event in the same territory as at entry than patients in the vertebrobasilar group (relative risk, 1.8; 95% confidence interval, 1.1-3.2). The average interval between the qualifying event and the subsequent stroke was significantly shorter (mean, 167 days; 95% confidence interval, 77-257) if the vascular territory was the same.
These results suggest that single artery disease accounts for at most one half of the strokes on follow-up, relatively more often in the carotid territory, and that recurrent strokes from the same arterial lesion occur sooner than strokes associated with other lesions.
Lupus anticoagulant and the fibrinolytic system in young patients with stroke.
Authors: Ferro D , Quintarelli C , Rasura M , Antonini G , Violi F 
Published: June 2011

Our purpose was to assess the presence of lupus anticoagulant and fibrinolytic system abnormalities in young patients with stroke.
We studied 33 consecutive ischemic patients aged < 50 years. Lupus anticoagulant was screened by four different coagulation tests, and the fibrinolytic system was studied by analyzing tissue plasminogen activator antigen and plasminogen activator inhibitor activity.
Six patients (18%), two of whom were affected by systemic lupus erythematosus, had lupus anticoagulant. Plasminogen activator inhibitor activity was significantly higher in those positive for lupus anticoagulant than in those negative for lupus anticoagulant and control subjects (p < 0.001).
In young patients with stroke, lupus anticoagulant is associated with an imbalance of the fibrinolytic system as a result of higher levels of plasminogen activator inhibitor.
Sustained decrease in brain regional blood flow after microsphere embolism in rats.
Authors: Miyake K , Takeo S , Kaijihara H 
Published: June 2011

An experimental model that induces sustained ischemia and infarction may provide useful information relevant to prevention of the development of ischemic brain disease. The purpose of the present study was to elucidate the pathophysiological consequences of cerebral blood flow under sustained cerebral ischemia or oligemia and infarction in rats after microsphere embolism.
We injected 900 microspheres (48 microns in diameter) into the right internal carotid artery of 146 rats and determined the time course of changes in blood flow of the cerebral cortex, striatum, and hippocampus of both hemispheres by the hydrogen clearance method for a period of 28 days after the operation. Infarct area was determined by triphenyltetrazolium chloride staining and hematoxylin and eosin staining methods.
Cortical and striatal blood flow of the right hemisphere of microsphere-injected rats was significantly decreased after the embolism, and this was sustained throughout the experiment. Hippocampal blood flow of the microsphere-injected hemisphere was also decreased on days 1 and 3 but tended to return toward control levels thereafter. In the left hemisphere, reduction in regional blood flow was detected in the cortex and hippocampus on day 1 and the striatum on day 3. A triphenyltetrazolium chloride-unstained area had developed by day 3 after the embolism. The extent of the area was similar to that on days 7 and 28. Microscopic examination revealed degenerative areas scattered mainly in the parietotemporal cortex, corpus callosum, hippocampus, thalamus, and lenticular nucleus of the embolized hemisphere, demonstrating the induction of widespread necrosis after embolism.
Microsphere embolism resulted in a sustained decrease in regional blood flow and production of cerebral infarction in the brain regions of the microsphere-injected hemisphere.
Dynamic computed tomographic imaging of regional cerebral blood flow and blood volume. A clinical pilot study.
Authors: Steiger H J , Aaslid R , Stooss R 
Published: June 2011

The advent of faster computed tomography scanners has evoked considerable interest in using this technology as a more practical method of regional cerebral hemodynamic evaluation than the currently available positron emission and single-photon emission computed tomography. The theoretical concepts have been worked out and validated in the laboratory by several groups. The aim of the present study was the development of a clinically useful system.
Software was developed for dynamic computed tomography-based calculation and color-coded representation of regional cerebral blood flow and blood volume. Normal values, reproducibility, and sensitivity to acetazolamide challenge were established in 13 volunteers. The method was applied to an additional three patients with internal carotid artery occlusion and known decreased vascular reserve capacity as diagnosed by transcranial Doppler ultrasonography.
Normal regional cerebral blood flow was determined as 50 +/- 13 ml/100 ml per minute and normal fractional cerebral blood volume as 58 +/- 12 ml/1,000 ml (mean +/- SD). In five volunteers, two examinations were performed within 15 minutes for determination of reproducibility. Intermeasurement variability of hemispheric blood flow and blood volume was determined as +/- 23% and +/- 16%, respectively. Intravenous administration of 1 g acetazolamide resulted on the average in a 75% increase of blood flow and a 65% increase of fractional blood volume. In the patients with decreased cerebrovascular reserve capacity, baseline fractional blood volume in the ischemic hemispheres was significantly increased. Baseline regional cerebral blood flow in the ischemic territories was overestimated. Reactivity to acetazolamide of both regional blood flow and fractional blood volume was clearly reduced in the ischemic hemispheres.
The present results demonstrate that the method is a simple and effective means of determining regional cerebral blood volume. Spatial resolution is superior to that of the radioactive tracer methods. Hemodynamic evaluation of ischemic conditions can be performed on the basis of increased resting cerebral blood volume and a diminished increase after acetazolamide. Accuracy of cerebral blood flow measurements, on the other hand, is affected by abnormal cerebral blood volume, and corresponding adjustments need to be made in pathological conditions.
Expression of thrombomodulin in patients with spontaneous occlusion of the circle of Willis.
Authors: Ikeda E , Maruyama I , Hosoda Y 
Published: June 2011

We examined the expression of thrombomodulin, a recently isolated anticoagulant protein, in endothelial cells from patients with spontaneous occlusion of the circle of Willis (cerebrovascular moyamoya disease) to determine whether lack of the expression of thrombomodulin might lead to the thrombogenicity in patients with this disease.
The intracranial internal carotid arteries, the external carotid arteries, and the vertebral or basilar arteries from 12 autopsied patients who had this disease and eight control autopsied patients were examined immunohistochemically by using the antiserum against human thrombomodulin.
All of the endothelial cells from the patients with this disease and from the control patients were positive for thrombomodulin. Immunoelectron microscopy also disclosed normal localization of thrombomodulin on the luminal plasma membrane. Immunohistochemically, we could find no significant differences in the expression of thrombomodulin among the arteries examined in this study.
We conclude that as far as we investigated immunohistochemically, the thrombogenicity in this disease is almost unlikely to depend on the abnormal expression of thrombomodulin.
Contrast-enhanced transcranial color-coded real-time sonography. Results of a phase-two study.
Authors: Bogdahn U , Becker G , Schlief R , Reddig J , Hassel W 
Published: June 2011

Transcranial color-coded real-time sonography has been developed as a promising new bedside procedure to monitor central nervous system parenchymal and vascular pathology; the present study was designed to investigate the potential role of galactose microparticles (SH U 508 A) as a new ultrasound contrast-enhancing agent for transcranial sonography.
Ten patients (four women and six men, 24-63 years of age) with a broad spectrum of central nervous system pathology were investigated by transcranial color-coded real-time sonography in a phase-two clinical study. After conventional ultrasound examination, all patients received a maximum of six injections of 10 ml with 200, 300, or 400 mg/mL SH U 508 A. The intracranial vessels were scanned by color flow imaging in the axial and coronal planes through a transtemporal acoustic bone window; in addition, the vertebrobasilar system was followed through the foramen magnum.
SH U 508 A was well tolerated without side effects. In axial and coronal scans, the application of SH U 508 A resulted in detection of peripheral branches of the anterior, middle, and posterior cerebral arteries, as well as the posterior communicating and superior cerebellar arteries. In addition, the deep cerebral veins (i.e., inferior sagittal sinus, internal cerebral veins, great cerebral vein of Galen, straight sinus, and the confluence sinuum) were revealed. The transforaminal approach led to detection of the main infratentorial branches (anterior inferior, posterior inferior, and superior cerebellar arteries). One patient could not be insonated without contrast, but after SH U 508 A the trunks of the large intracranial arteries were detected. No obvious changes in the ultrasound pattern of the central nervous system parenchyma were observed.
These preliminary data indicate that the use of a transpulmonary ultrasound contrast agent (SH U 508 A) may substantially broaden the spectrum and potential diagnostic utility of transcranial ultrasound by allowing detection of supratentorial peripheral central nervous system arteries, deep cerebral veins, and (through the foramen magnum) the entire vertebrobasilar system, including the cerebellar arteries.
Cardiovascular changes during focal cerebral ischemia in rats.
Authors: Perez-Trepichio A D , Williams J L , Block C H , Jones S C 
Published: June 2011

Recent studies have suggested that cerebral infarction influences autonomic activity and may contribute to sudden death. The goal of this study was to examine effects of focal cerebral infarction on mean arterial pressure and heart rate.
Halothane-anesthetized rats were assigned to two groups: stroke (n = 10), in which the middle cerebral artery or an adjacent vessel was embolized with a silicone cylinder, and sham (n = 8), in which rats were sham embolized (saline). Arterial pressure and heart rate were measured for 90 minutes and again 24 hours after vascular occlusion. A change in electroencephalographic amplitude of -45% after embolization was used to determine if a significant degree of infarction was present.
Vascular occlusion produced a significant increase in mean arterial pressure at 10, 60, and 90 minutes (p < 0.05). Changes in heart rate were significantly greater (p < 0.05) than in sham-treated rats at 10 and 30 minutes after embolization. In contrast, mean arterial pressure and heart rate measured 24 hours after embolization were similar in both groups. Anatomic analysis of the infarcted areas demonstrated that either insular cortex or amygdala was affected in all embolized rats.
This study indicates that cerebral infarction produces a transient elevation of mean arterial pressure and heart rate. However, within 24 hours both parameters returned to preinfarcted levels. Our findings are consistent with clinical reports that indicate that mean arterial pressure and heart rate of stroke patients are similar to those of other groups when they are admitted to the hospital, although other cardiovascular parameters are greatly altered.
Protective efficacy of a hypothermic pharmacological agent in gerbil forebrain ischemia.
Authors: Hall E D , Andrus P K , Pazara K E 
Published: June 2011

The novel muscarinic cholinergic partial agonist U-80816E was tested in the gerbil brief bilateral carotid occlusion ischemia model based on the rationale that the compound's hypothermic properties might afford effective protection of the selectively vulnerable hippocampal CA1 region.
Male gerbils were subjected to either 10 or 15 minutes of bilateral carotid occlusion, followed by histopathological assessment of the CA1 neuronal survival 7 days later.
In saline-treated animals, 10 minutes of bilateral carotid occlusion resulted in a 30.5% loss of CA1 neurons, whereas a 15-minute insult resulted in a 49.6% loss. Administration of U-80816E (6 mg/kg i.p. 30 minutes before bilateral carotid occlusion and again 2 hours after reperfusion) resulted in a significant protective effect of the CA1 neuronal population with either duration of ischemia; neuronal loss was reduced to 12.6% in the milder model (p < 0.05 versus saline-treated) and 24.9% in the more severe model (p < 0.04 versus saline). However, the 6 mg/kg i.p. dose of U-80816E was found to produce a 1.0 degree C decrease in brain temperature (measured with a tympanic temperature probe) at 10 minutes of ischemia compared with that of saline-treated gerbils. At 10 minutes of reperfusion, after the 10-minute episode of ischemia, the brain temperature of the U-80816E-treated gerbils was 2.2 degrees C lower than that of saline-treated animals. When the U-80816E-treated gerbils were subjected to either 10 or 15 minutes of ischemia but placed in a heated chamber that prevented the hypothermic effects, no cerebroprotection was observed.
These results show that the anti-ischemic efficacy of U-80816E is mediated through its hypothermic properties, thus suggesting the feasibility of pharmacologically induced hypothermia as a cerebroprotective approach.
The antioxidant LY231617 reduces global ischemic neuronal injury in rats.
Authors: Clemens J A , Saunders R D , Ho P P , Phebus L A , Panetta J A 
Published: June 2011

In the rat four-vessel occlusion model with 30 minutes of ischemia most agents have failed to be of benefit when given after ischemia. Because postischemia administration is more clinically relevant, we evaluated the antioxidant LY231617 (2,6-bis(1,1-dimethylethyl)-4-[[(1-ethyl)amino]methyl]phenol hydrochloride]) when administered after 30 minutes of four-vessel occlusion.
Male Wistar rats were subjected to 30 minutes of four-vessel occlusion. LY231617 was either given orally 30 minutes before ischemia or intravenously beginning at 30 minutes after the onset of ischemia. Hippocampal CA1 layer and striatal damage were rated on a scale of 0-3 (0, no damage; 3, > 90% cell loss). We also evaluated the ability of LY231617 to prevent iron-dependent lipid peroxidation and to prevent hydrogen peroxide-induced neuronal death of hippocampal neurons in primary culture by exposing cultures to a 50-microM concentration of hydrogen peroxide for 15 minutes in the presence of LY231617.
Oral administration of LY231617 reduced both striatal and hippocampal CA1 damage by > 75% (p < 0.0001). In two separate experiments in which LY231617 was given intravenously beginning 30 minutes after occlusion, hippocampal and striatal damage were reduced by approximately 50% (p < 0.03) in the first experiment and by approximately 41% (p < 0.02) in the second experiment. Addition of 5 microM of LY231617 to primary hippocampal neuronal cultures antagonized the lethal effect of hydrogen peroxide (p < 0.05). Iron-dependent lipid peroxidation was also inhibited in a dose-related fashion.
The significant reduction of ischemia-induced or hydrogen peroxide-induced neuronal damage and inhibition of lipid peroxidation by LY231617 observed in this study suggest that reactive oxygen intermediates play an important role in the events leading to neuronal death after global ischemia/reperfusion.
Geographic variation in the incidence of nonfatal stroke in Finland. Are the observed differences real? FINMONICA Stroke Register Study Group.
Authors: Sarti C 
Published: June 2011

We sought to find an explanation for the geographical variation in the incidence of nonfatal stroke detected in the FINMONICA stroke register during the period 1983-1985.
Two separate investigations were made. In the first, a sample of approximately 100 nonfatal events drawn from each of the three monitoring areas (North Karelia, Kuopio, and Turku/Loimaa) participating in FINMONICA was recoded by an independent coder. In the second, 29 nonfatal events from Kuopio and 29 from North Karelia were recorded by the neurologist of the other area. Kappa coefficients (kappa) were calculated to measure the proportion of agreement beyond chance among the different coders.
A good level of agreement with the independent coder was found for each of the three areas; it was best for the cases from Turku/Loimaa (kappa = 0.896), followed by Kuopio (kappa = 0.792) and North Karelia (kappa = 0.616). In the second part of the investigation, agreement was higher for the stroke cases originating from Kuopio (kappa = 0.861) than for those from North Karelia (kappa = 0.563). In the latter there was discrepancy in the classification of the cases originally classified as no stroke.
The results from the first part of the investigation suggest that the lower incidence of nonfatal stroke in Turku/Loimaa was real, confirming findings in previous studies. Differences in data entry, rather than in the interpretation of signs and symptoms of stroke, were the main cause of disagreement in the second part of the investigation, where the disagreement primarily concerned the cases classified as no stroke in North Karelia. The results also indicate that the different proportions of patients submitted to computerized brain tomography conceivably account for a good part of the difference in the incidence rates of nonfatal stroke between Kuopio and North Karelia.
Noninvasive detection of vertebral artery dissection.
Authors: Hoffmann M , Sacco R L , Chan S , Mohr J P 
Published: June 2011

We sought to identify the use of duplex and transcranial Doppler sonography in the noninvasive diagnosis of vertebral dissection.
Ten patients with a diagnosis of symptomatic vertebral artery dissection confirmed by cerebral angiography were retrospectively analyzed.
Computed tomographic scanning and magnetic resonance imaging together delineated lateral medullary or cerebellar infarcts in 7 patients. Angiography documented a total of 21 vertebral artery lesions (16 stenoses and 5 occlusions), with 7 of 10 patients having multiple sites of vertebral artery dissection. Vertebral Doppler was abnormal in 8 of the 10 patients. A high resistance signal in the relevant vertebral artery was found in 6 patients, no flow in a well-imaged vertebral artery in 1, and bilateral retrograde vertebral artery flow in 1 patient. Transcranial Doppler was abnormal in only 2 patients, with reduced pulsatility index in 1 and high resistance vertebral signal in another. A hyperintense intramural signal of the affected vertebral artery by magnetic resonance imaging was documented in 1 patient in whom Doppler sonography was nondiagnostic.
Vertebral artery dissection can be detected and monitored by noninvasive vertebral Doppler and magnetic resonance imaging in the setting of a clinically suggestive presentation.
Thromboxane antagonism in experimental canine carotid artery thrombosis.
Authors: Rote W E , Mu D X , Lucchesi B R 
Published: June 2011

The two objectives of this study were to assess the potential of BAY U 3405 to prevent arterial thrombosis in response to vessel wall injury and to determine the ability of BAY U 3405 to prevent thrombotic reocclusion after thrombolysis with anisoylated plasminogen streptokinase activator complex.
Dogs were instrumented with a carotid flow probe, stimulating electrode, and a stenosis. Current (150 microA) was applied to the intimal surface of the right carotid artery, and time to occlusive thrombus formation was noted. BAY U 3405 was administered, and the procedure for thrombus formation was repeated for the left carotid artery.
BAY U 3405 administration prevented occlusive arterial thrombosis formation. Ex vivo platelet aggregation was inhibited, bleeding time increased, and thrombus weight reduced after BAY U 3405 treatment. In a second group, thrombi were formed initially in both carotid arteries, BAY U 3405 was administered as before, and anisoylated plasminogen streptokinase activator complex was infused in the right carotid artery proximal to the occlusive thrombus. BAY U 3405 did not alter the incidence of rethrombosis compared with the lytic agent alone.
BAY U 3405 prevented primary arterial thrombosis, corresponding to inhibition of platelet aggregation, and increased bleeding times. BAY U 3405, however, did not prevent rethrombosis after successful thrombolysis with anisoylated plasminogen streptokinase activator complex, despite the fact that platelet reactivity was inhibited. The data are consistent with the concept that the residual thrombus represents a more effective thrombogenic stimulus as compared with arterial wall injury alone and that the mechanisms associated with primary versus secondary thrombus formation may require separate therapeutic approaches.
Oxyhemoglobin-induced cytotoxicity and arachidonic acid release in cultured bovine endothelial cells.
Authors: Takenaka K , Kassell N F , Foley P L , Lee K S 
Published: June 2011

An impairment of endothelial function is associated with vasospasm after subarachnoid hemorrhage. Oxyhemoglobin is considered to be a critical trigger in the pathogenesis of vasospasm. The present studies examined the direct effects of oxyhemoglobin on cultured endothelial cells from bovine carotid artery.
Confluent endothelial cells were treated with oxyhemoglobin, and the following were studied: 1) cell morphology, 2) cell density, and 3) the release of radiolabel from [3H]arachidonic acid-treated cells.
Endothelial cells exposed to oxyhemoglobin exhibited detachment vacuoles, and cell density was significantly decreased in time- and dose-dependent manners. Superoxide dismutase, a free radical scavenger, provided partial protection against the cytotoxic effects of oxyhemoglobin. The release of radiolabel from [3H]arachidonic acid-treated cells was increased by oxyhemoglobin in time- and dose-dependent manners. Treatment with an inhibitor of phospholipase A2 or a calcium chelator inhibited the effects of oxyhemoglobin on arachidonic acid release and cellular viability.
Oxyhemoglobin exerts a direct cytotoxic effect on cultured endothelial cells, and this effect is associated with increased release from [3H]arachidonic acid-labeled cells. Phospholipase A2 and free radicals appear to participate in the pathogenesis of endothelial cell damage. Oxyhemoglobin-induced compromise of endothelial cells may contribute to cerebrovascular pathology.