bluuebunny/crossref_metadata_2025_split huggingface dataset:
Experimental evidence of ischemic thresholds and functional recovery.
Authors: Heiss W D 
Published: June 2011

Impaired blood flow below certain critical levels and an insufficient supply of energy-rich substrates cause failure of neuronal function, triggering biochemical disturbances that eventually lead to ischemic cell damage.
This article reviews experimental studies that attempted to define those ischemic thresholds using functional and histological markers and, more recently, chemical markers of ischemic damage.
The duration of ischemia causing irreversible cell damage still is ill defined. Reestablishment of sufficient perfusion must be induced very early after an ischemic attack to ameliorate the potentially harmful biochemical sequelae of transient ischemia.
Ticlopidine versus aspirin for the prevention of recurrent stroke. Analysis of patients with minor stroke from the Ticlopidine Aspirin Stroke Study.
Authors: Harbison J W 
Published: June 2011

Ticlopidine has not been formally compared with aspirin in patients with a completed stroke. We therefore performed an analysis on a subgroup of patients from the Ticlopidine Aspirin Stroke Study (TASS) with a recent minor completed stroke as the qualifying ischemic event.
This was a multicenter, double-blind, randomized trial of patients with a recent history of cerebral ischemia. Eligible patients had a qualifying minor stroke within 3 months of study entry. All patients received either 650 mg aspirin twice daily or 250 mg ticlopidine twice daily for up to 5.8 years. The primary study end point was the first occurrence of nonfatal stroke or death from any cause. A secondary end point was the first occurrence of a fatal or nonfatal stroke.
Minor stroke was the qualifying ischemic event in 927 patients (463 received ticlopidine and 464 received aspirin). The cumulative event rate at 1 year for nonfatal stroke or death was 6.3% for patients receiving ticlopidine and 10.8% for patients receiving aspirin, a 42% risk reduction in favor of ticlopidine. For fatal or nonfatal stroke, the cumulative event rate at 1 year was 4.8% for patients receiving ticlopidine and 7.5% for those receiving aspirin, a risk reduction of 36% for ticlopidine relative to aspirin. The overall risk reductions were 22.1% for nonfatal stroke or death and 19.9% for fatal or nonfatal stroke. Adverse reactions were reported in 58% of the ticlopidine patients and 51% of the aspirin patients.
The results in this subgroup are consistent with the overall TASS results and show that ticlopidine is somewhat more effective than aspirin for reducing the risk of stroke in patients with a completed minor stroke.
Cerebral blood flow velocity after hyperventilation-induced vasoconstriction in hypertensive patients.
Authors: Malatino L S , Bellofiore S , Costa M P , Lo Manto G , Finocchiaro F , Di Maria G U 
Published: June 2011

The aim of our study was to evaluate by transcranial Doppler ultrasonography the dynamics of blood flow velocity changes in the middle cerebral artery during and after hypocapnia-induced vasoconstriction in untreated essential hypertensive patients.
Sixteen hypertensive patients (10 men and six women, 29-62 years of age) and 10 healthy control subjects (six men and four women, 30-62 years of age) were studied. Patients with mild-to-moderate essential hypertension (mean +/- SE blood pressure, 171/106 +/- 3/2 mm Hg) belonged to stage I or II of the World Health Organization classification. Mean blood flow velocity in the middle cerebral artery, arterial blood pressure, and end-tidal CO2 partial pressure were recorded at baseline, during 2-minute hyperventilation, and every 30 seconds up to 5 minutes after hyperventilation.
End-tidal CO2 partial pressure values overlapped in the two groups throughout the study. Baseline values of mean blood flow velocity in hypertensive patients were similar to those in normotensive subjects (mean +/- SE values, 64.7 +/- 3.9 cm/sec versus 58.6 +/- 3.7 cm/sec). A similar fall in mean blood flow velocity was observed in hypertensive patients and normotensive subjects (43.2 +/- 2.8% versus 46.7 +/- 3.6%). Mean blood flow velocity reverted to baseline more quickly in hypertensive patients: 1.5 minutes after hyperventilation, mean blood flow velocity was 60.7 +/- 3.1% and 84.9 +/- 1.8% of control in normotensive subjects and hypertensive patients, respectively. No changes in arterial blood pressure were observed in either group throughout the study.
This study demonstrates that the recovery of blood flow velocity in the middle cerebral artery after hyperventilation is faster in hypertensive patients than in normal subjects, thus providing further evidence that chronic hypertension is associated with changes in the dynamics of cerebral blood vessel reactivity.
Distribution and correlates of sonographically detected carotid artery disease in the Cardiovascular Health Study. The CHS Collaborative Research Group.
Authors: O'Leary D H , Polak J F , Kronmal R A , Kittner S J , Bond M G , Wolfson S K , Bommer W , Price T R , Gardin J M , Savage P J 
Published: June 2011

This article describes the prevalence of extracranial carotid atherosclerosis assessed by ultrasonography, its association with risk factors, and its relation to symptomatic coronary disease and stroke in men and women aged > or = 65 years.
Maximum percent stenosis, maximum common carotid artery wall thickness, and maximum internal carotid artery wall thickness were assessed using duplex ultrasound in 5,201 men and women aged > or = 65 years in the Cardiovascular Health Study, a study of the risk factors and natural history of cardiovascular disease in the elderly. Existing coronary disease and stroke were assessed by physical examination and participant history.
Detectable carotid stenosis was present in 75% of men and 62% of women, although the prevalence of > or = 50% stenosis was low, 7% in men and 5% in women. Maximum stenosis and maximum wall thickness measurements increased with age and were uniformly greater at all ages in men than in women (p < 0.00001). Established risk factors for atherosclerosis (hypertension, smoking, diabetes) and indications of vascular disease (left ventricular hypertrophy, major electrocardiographic abnormality, bruits, and history of heart disease or stroke) related to all three carotid artery measures in the elderly. Of the three ultrasound measures, the best correlate for a history of coronary disease was maximum internal carotid artery wall thickness. For stroke the best correlate was common carotid artery wall thickness. Multiple logistic regression models of prevalent coronary heart disease and stroke that included the ultrasound findings indicated, after adjustment for age and sex, that maximum internal wall thickness and maximum common carotid wall thickness were significant correlates of both. Maximum stenosis did not add significantly to the correlation.
In the elderly the incidence of carotid atherosclerosis was high, although the frequency of severe disease was low. The prevalence and severity of carotid atherosclerosis continued to increase with age even in the late decades of life, and more disease was found in men than in women at all ages. Known risk factors for atherosclerosis continued to relate to carotid abnormalities in the later decades of life, both in symptomatic and asymptomatic subjects.
Spontaneous cerebral hypothermia diminishes focal infarction in rat brain.
Authors: Moyer D J , Welsh F A , Zager E L 
Published: June 2011

Brain temperature during ischemia is known to strongly influence the extent of cellular injury. The objectives of the present study were to determine the effect of severe focal ischemia on brain temperature and to assess the influence of those changes on focal infarction.
Severe focal ischemia was produced in rats using permanent occlusion of the distal middle cerebral artery combined with transient (60-minute) bilateral carotid artery occlusion. The temperature of the ischemic focus was measured with a small subdural probe. Three groups of rats were studied. In the first group, brain temperature was permitted to decline spontaneously to 32 degrees C after occlusion. In the second, brain temperature was maintained at 37.5 degrees C during occlusion. In the third group, the brain temperature was maintained at 37.5 degrees C for 40 minutes postocclusion before cooling. After recovery for 24 hours, the volume of infarction was measured in histological sections.
In the absence of cranial heating, the brain temperature fell to 33 degrees C by 10 minutes postocclusion, and infarct volume was 19 +/- 9 mm3 (mean +/- SEM; n = 6). Maintaining brain temperature at 37.5 degrees C increased the volume of infarction to 82 +/- 16 mm3 (n = 7; p < 0.001). Delayed cooling did not prevent the increase in infarct volume (75 +/- 16 mm3; n = 6).
These results demonstrate that in the present model of transient focal ischemia, spontaneous cooling of the brain during ischemia diminishes the extent of focal infarction, relative to that observed when cerebral hypothermia is prevented or delayed for 40 minutes.
Thrombolysis in acute ischemic stroke: does it work?
Authors: Wardlaw J M , Warlow C P 
Published: June 2011

This article is presented to provoke further discussion regarding the use of thrombolytic drugs to treat acute ischemic stroke.
Overview analysis of the six randomized trials of thrombolysis in acute ischemic stroke available in the world literature shows a 20% increase in the odds of death and a 30% reduction in the odds of death or deterioration (both with wide confidence intervals, neither result significant) after thrombolytic treatment for acute ischemic stroke. Exclusion of the two trials conducted without the benefit of computed tomographic scanning shows a 37% reduction in the odds of death (95% confidence interval, 74% reduction to 40% excess) and a significant reduction of 56% in the odds of death or deterioration after thrombolytic treatment (95% confidence interval, 20-76% reduction; 2p = 0.007). Analysis of all published studies (randomized and nonrandomized) shows that there does not appear to be an excess risk of hemorrhagic transformation of the cerebral infarct or of severe edema formation.
We believe the present evidence is sufficiently encouraging to warrant proper testing of thrombolysis in sufficiently large and well-designed randomized clinical trials to influence clinical practice.
Custom-tailored hemodilution with albumin and crystalloids in acute ischemic stroke.
Authors: Goslinga H , Eijzenbach V , Heuvelmans J H , van der Laan de Vries E , Melis V M , Schmid-Schönbein H , Bezemer P D 
Published: June 2011

Hemodilution in the acute phase of ischemic stroke is still controversial. Multicenter studies have failed to demonstrate any benefit. The present study focuses attention on analysis of circulation in stroke and on individual restabilization of circulation.
The Amsterdam Stroke Study is a prospective, single-center, randomized clinical trial (n = 300). Normovolemic hemodilution is accomplished in a customized procedure by administration of 20% albumin plus crystalloids under hemodynamic and rheological monitoring in the acute phase of stroke. All patients receive general intensive care treatment and monitoring with a pulmonary artery catheter. This custom-tailored fluid therapy is guided on the basis of a target pulmonary capillary wedge pressure (12 +/- 3 mm Hg) and hematocrit (0.32 +/- 0.02). The control group receives only customized rehydration by infusion of crystalloids.
We obtained significant (p less than 0.05) reduction in mortality at 3 months (from 27% to 16%) and an increase in independence at home (from 35% to 48%) after viscosity reduction by means of hemodilution with albumin in the subgroup with a hematocrit less than 0.45 (n = 201) (specific viscosity effect). We also obtained a significant (p less than 0.005) reduction in mortality at 3 months (from 27% to 8%) and an increase in independence (from 35% to 59%) after only rehydration with crystalloids in the subgroup with overt dehydration (hematocrit greater than or equal to 0.45; n = 51) as compared with the normal-hematocrit group without signs of dehydration (hematocrit less than 0.45; n = 103) (specific rehydration effect).
This study may provide an explanation for the failures in former hemodilution trials and may re-establish proper hemodilution and rehydration as a valuable therapy in the acute phase of stroke, thus reducing mortality and improving independence after 3 months.
Measurement variability in duplex scan assessment of carotid atherosclerosis.
Authors: Sutton-Tyrrell K , Wolfson S K , Thompson T , Kelsey S F 
Published: June 2011

The reproducibility of duplex scan measures of carotid atherosclerosis was evaluated as part of a study assessing the prevalence of carotid disease in elderly adults.
Doppler measures of blood flow velocity were used to evaluate disease severity, and extent of carotid plaque was scored from the B-mode image. A reader assigned a grade from 0 to 3 to each of seven segments in the carotid system, based on the number and size of lesions present. Reproducibility data were obtained from 30 study participants who underwent a repeat scan by a second sonographer. Each scan was then scored by two readers.
Doppler measures of blood flow velocity were found to be highly reproducible, with intraclass correlation coefficients of 0.81 for the common carotid artery, 0.84 for the internal carotid artery, and 0.77 for the internal carotid artery velocity to common carotid artery velocity ratio. Reproducibility of plaque grade was evaluated using segment as the unit of analysis, and both sonographer and reader variation were analyzed. When readers differed perfect agreement was achieved in 84% of the segments (K = 0.67), and when sonographers differed perfect agreement was obtained in 78% of the segments (K = 0.56). When both sonographer and reader differed, perfect agreement was obtained in 77% of the segments (K = 0.53). The plaque index, created by summing plaque grades from selected segments, was highly reproducible, with an intraclass correlation coefficient of 0.86.
The duplex scan protocol described here provides reliable measures of both extent and severity of carotid disease that are appropriate for use in cross-sectional studies.
A study of twins and stroke.
Authors: Brass L M , Isaacsohn J L , Merikangas K R , Robinette C D 
Published: June 2011

Although there are strong genetic contributions to coronary artery disease, only a few studies have considered heritable influences on stroke.
We investigated the role of genetic factors in stroke using the Twin Registry maintained by the National Academy of Sciences-National Research Council. The registry includes 15,948 male twin pairs born between 1917 and 1927. In 1985, 9,475 twins responded to a mailed questionnaire, which covered vascular risk factors, cardiac events, and stroke.
Analysis of twin pairs in which both responded to the questionnaire, and a question on stroke, indicated proband concordance rates of 17.7% for monozygotic pairs and 3.6% for dizygotic pairs (relative risk = 4.3; chi 2 = 4.94, df = 1; p less than 0.05).
This nearly fivefold increase in the prevalence of stroke among the monozygotic compared with the dizygotic twin pairs suggests that genetic factors are involved in the etiology of stroke. The twin study paradigm holds considerable promise for identifying both genetic and environmental influences on stroke.
Failure of GM1 ganglioside to influence outcome in experimental focal ischemia.
Authors: Mayer S A , Pulsinelli W A 
Published: June 2011

Reports of improved short-term (less than 72 hours) outcome in experimental models of mechanical and ischemic central nervous system injury suggest that exogenous ganglioside administration may confer a protective effect on neural tissue. We studied the effect of the monosialoganglioside GM1 on cerebral infarction and edema in spontaneously hypertensive rats subjected to permanent focal cerebral ischemia.
GM1 or normal saline was injected intramuscularly once a day for 3 days before and 30 and 120 minutes after occlusion of the right middle and common carotid arteries. Following a 24-hour survival period, the volume of infarction was measured by computer-assisted image analysis, and the extent of edema was assessed by measurements of tissue water content and hemispheric volume.
Infarct volume was similar among the GM1-treated (n = 10) and saline-treated (n = 10) rats (212 +/- 10 versus 220 +/- 13 microliters, respectively). In a second series of experiments, the brain water content and edema volume of the ischemic right hemisphere in GM1-treated rats (n = 10) did not differ from saline-treated controls (n = 10).
GM1 ganglioside does not effectively reduce cerebral infarction caused by permanent focal ischemia.
Infarction after aneurysm rupture does not depend on distribution or clearance rate of blood.
Authors: Brouwers P J , Wijdicks E F , Van Gijn J 
Published: June 2011

We sought to determine the contribution of the amount, distribution, and clearance rate of extravasated blood in relation to occurrence of infarction and outcome in patients with aneurysmal subarachnoid hemorrhage.
We prospectively studied 59 consecutive patients with aneurysmal subarachnoid hemorrhage admitted within 72 hours by means of serial computed tomographic scanning, close clinical observation, and assessment of outcome after 3 months.
Infarction occurred in 17 of the 59 patients. The arterial territories involved hardly reflected the distribution of subarachnoid blood in the basal cisterns on computed tomography, and even the side of the infarcts corresponded only weakly with the side on which most extravasated blood was seen. Infarction occurred twice as often in patients with large amounts of subarachnoid blood; this difference was not significant on its own but is in agreement with previous studies. A low clearance rate of cisternal blood was not related to the occurrence of infarction; a relation between clearance rate and poor outcome was largely explained by the amount of subarachnoid blood on the initial computed tomogram and by a low Glasgow Coma Scale score on admission.
The fact that infarction is related to the total amount but not to the distribution or clearance rate of extravasated blood argues against a direct role of extravasated blood and in favor of systemic factors, dependent on the severity of the initial hemorrhage.
Silent stroke and carotid stenosis.
Authors: Norris J W , Zhu C Z 
Published: June 2011

Silent cerebral infarction is often found on computed tomographic scan in patients with asymptomatic carotid stenosis, but its relation to the arterial stenosis is uncertain.
We compared computed tomographic scans and carotid Doppler in 115 patients with asymptomatic carotid stenosis, 203 with carotid transient ischemic attacks and carotid stenosis, and 63 with transient ischemic attacks but without carotid stenosis. There was no group with normal carotid arteries for comparison.
Lesions seen on CT scan were most common in the transient ischemic attack with carotid stenosis group (47%) compared with the other groups (30%, 19%) (p less than 0.001). Cerebral infarcts ipsilateral to the carotid stenosis were found in 10% of patients with mild (35-50%) stenosis, 17% in moderate (50-75%) stenosis, and 30% with severe (greater than 75%) carotid stenosis (p less than 0.001). In patients with asymptomatic carotid stenosis, 68% of infarcts were ipsilateral to the stenosis; in those with transient ischemic attacks and carotid stenosis, 86% of infarcts were ipsilateral to the stenosis.
The more severe the carotid stenosis, the higher the incidence of cerebral infarction ipsilateral to the stenosis. This finding applied to central infarcts as well as to peripheral infarcts in both symptomatic and asymptomatic patients. Silent cerebral infarction may be an indication for carotid endarterectomy in asymptomatic patients.
Somatosensory evoked potentials sensitivity relative to electroencephalography for cerebral ischemia during carotid endarterectomy.
Authors: Kearse L A , Brown E N , McPeck K 
Published: June 2011

The relation between electroencephalographic pattern changes and cerebral ischemia during carotid endarterectomy under general anesthesia is well established. Pattern changes seen on somatosensory evoked potentials under the same conditions are reported to be more sensitive indicators of cerebral ischemia. We estimated the sensitivity and specificity of somatosensory evoked potentials relative to electroencephalography for detecting cerebral ischemia during carotid endarterectomy under general anesthesia.
We simultaneously monitored electroencephalographs and somatosensory evoked potentials in 53 carotid endarterectomies performed on 51 patients under general anesthesia, and we determined the extent to which somatosensory evoked potentials detected cerebral ischemia defined by electroencephalographic pattern changes at the time of carotid cross-clamp.
Twenty-three of the 53 cases studied had electroencephalographic evidence of ischemia following carotid cross-clamp. Ten of these 23 cases had an increased somatosensory evoked potential latency of 0.1 msec or greater (sensitivity 0.43). One of these 23 patients had a decrease in somatosensory evoked potential amplitude of 50% or greater (sensitivity 0.04). Of the 30 subjects who had no electroencephalographic evidence of ischemia, 13 had either no change or a decrease in somatosensory evoked potential latency (specificity 0.45). None of these 30 cases had a significant decrease in somatosensory evoked potential amplitude (specificity 1.0). If somatosensory evoked potential latencies were a sensitive method for detecting cerebral ischemia (true sensitivity of 0.95 or higher), the probability of only 10 subjects having somatosensory evoked potential latency increases would be less than 0.001. Therefore, our observed sensitivity cannot be attributed to chance.
We conclude that measuring somatosensory evoked potentials is not a sensitive method for detecting cerebral ischemia during carotid endarterectomy.
Design and baseline results of the monosialoganglioside early stroke trial. The EST Study Group.
Authors: Rocca W A , Dorsey F C , Grigoletto F , Gent M , Roberts R S , Walker M D , Easton J D , Bruno R , Carolei A , Sancesario G 
Published: June 2011

The Early Stroke Trial is a randomized, placebo-controlled, double-masked, multicenter study to assess the safety and efficacy of monosialoganglioside in patients who have suffered an ischemic stroke of the cerebral hemispheres.
Only patients who could be evaluated and treated within 5 hours after the onset of stroke were considered; within each center, subjects were stratified by age, sex, and clinical severity. Patients were randomly allocated to receive a specified sequence of intravenous and intramuscular doses of either monosialoganglioside or identical-appearing placebo for 21 days. Patients were followed up for 4 months after randomization. Neurological status was measured primarily by using the Canadian Neurological Scale. After assessing the effect of treatment on survival, the principal measure of efficacy will be the change in neurological status between baseline and the 4-month follow-up among survivors.
Sixteen clinical centers, 15 in Europe and one in North America, entered a total of 792 eligible patients during a 36-month recruitment period (from May 1987 to April 1990). In our series there were more men than women, and the relative frequency of patients increased with advancing age. The most frequently associated cardiovascular conditions were hypertension, atrial fibrillation, and peripheral vascular disease. Approximately 46% of the patients were admitted to a hospital within 1 hour and 81%, within 2 hours after the onset of stroke. About 22% first received the study treatment within 3 hours and 57%, within 4 hours.
This study demonstrates the feasibility of large-scale trials with the onset of treatment within 5 hours after an ischemic stroke.