bluuebunny/crossref_metadata_2025_split huggingface dataset:
Magnetic resonance imaging findings associated with cardiac arrest.
Authors: Roine R O , Raininko R , Erkinjuntti T , Ylikoski A , Kaste M 
Published: June 2011

The frequency and prognostic significance of neuroradiological findings after cardiac arrest are unknown. Using healthy volunteers as control subjects, we studied the magnetic resonance imaging (MRI) findings associated with cardiac arrest, adjusted for confounding factors.
The presence of cerebral infarcts, leukoaraiosis, atrophy, and edema on ultra-low-field MRI was assessed in 88 community volunteers and 52 cardiac arrest survivors enrolled in a placebo-controlled, randomized, double-blind trial of nimodipine in out-of-hospital ventricular fibrillation.
Cardiac arrest was an independent risk factor for the presence of infarcts in a logistic regression model adjusted for age, sex, and history of myocardial infarction, stroke, coronary heart disease, cardiac failure, and hypertension (odds ratio, 3.6; 95% confidence interval, 1.3 to 9.9; P = .01). Leukoaraiosis was associated with increasing age but not with cardiac arrest. Adjusted for age, the delay of advanced life support had an inverse correlation with the degree of atrophy in placebo-treated patients (r = -.62, P < .0001) but not in patients treated with nimodipine (r = -.10, P = .43). Lack of age-related atrophy, possibly implicating the presence of brain edema, predicted poor outcome after cardiac arrest (odds ratio, 4.6; 95% confidence interval, 1.4 to 15.8; P = .01).
Cardiac arrest was associated with deep cerebral infarcts but not with leukoaraiosis. MRI findings did not predict the functional outcome at 1 year. Nimodipine treatment had no significant effect on the MRI findings, but delayed resuscitation was associated with probable brain edema only in placebo-treated patients.
Comparison of diagnostic techniques for the detection of a patent foramen ovale in stroke patients.
Authors: Di Tullio M , Sacco R L , Venketasubramanian N , Sherman D , Mohr J P , Homma S 
Published: June 2011

The prevalence of a patent foramen ovale has been shown to be increased in patients with ischemic stroke. Transesophageal echocardiography, transthoracic echocardiography, and transcranial Doppler examination with contrast injection can all be used to search for a patent foramen ovale. We compared the accuracy of these techniques for identifying a patent foramen ovale in 49 patients with acute ischemic stroke or transient ischemic attack.
Transcranial Doppler examination of the right middle cerebral artery was performed during simultaneous transthoracic echocardiography with aerated saline injection, and again during transesophageal echocardiography; the latter was adopted as the "gold standard" for assessing the sensitivity of the other two tests.
Contrast transesophageal echocardiography detected a patent foramen ovale in 19 of 49 patients (39%), during normal respiration in 15 of them and during Valsalva maneuver in 4. Transcranial Doppler correctly identified 13 patients with a patent foramen ovale and all 30 patients without it. Therefore, the sensitivity of transcranial Doppler was 68% (13/19), and its specificity 100% (30/30). The 6 patients misclassified by transcranial Doppler (false negatives) had a very small right-to-left shunt detected by transesophageal echocardiography. Contrast transthoracic echocardiography was found to be the least sensitive test, detecting a patent foramen ovale in only 9 of 19 patients (47%). The specificity of transthoracic echocardiography was 100% (30/30 patients). The low sensitivity of transthoracic echocardiography was principally due to the suboptimal image quality obtained in false-negative patients. Both transcranial Doppler and transthoracic echocardiography were more sensitive in patients with cryptogenic stroke than in patients with stroke of determined origin. This may indicate the presence of larger, more easily detectable shunts in patients with cryptogenic stroke.
Transesophageal echocardiography is more sensitive than transcranial Doppler examination in detecting a patent foramen ovale, but only in cases of minimal right-to-left shunts, the clinical relevance of which remains to be established. The sensitivity of transthoracic echocardiography is heavily hampered by the frequency of inadequate heart visualization.
Endothelium-dependent effects of substance P and calcitonin gene-related peptide on mouse pial arterioles.
Authors: Rosenblum W I , Shimizu T , Nelson G H 
Published: June 2011

The effects of substance P (SP) and calcitonin gene-related peptide (CGRP) were tested on pial arterioles of mice. This was done because (1) perivascular peptidergic nerves may play an important role in modulation of cerebrovascular responses; (2) there are conflicting data concerning the mechanism of action of CGRP; (3) there are few or no studies directly testing the endothelium dependence of dilation by these peptides in the cerebral circulation; and (4) we wished to extend previous observations of mice by comparing peptidergic responses in the mouse with those published for other species.
The pial arterioles were monitored in vivo using video microscopy and image-shearing techniques for measuring diameter. Focal endothelial injury was produced with a laser-Evans blue technique. Responses to SP and CGRP were tested before and after endothelial injury. They were also tested before and during treatment with agents that interfere with responses mediated by endothelium-derived relaxing factor (EDRFACh). They were also tested before and during treatment with indomethacin.
Both CGRP and SP produced dilation that was blocked by endothelial injury and by agents interfering with responses mediated by EDRFACh. Indomethacin had no effect.
SP and CGRP produce endothelium-dependent dilations. These dilations are probably mediated by EDRFACh. With respect to SP, these results are similar to those reported for other vessels and species. With respect to CGRP, the finding of endothelium dependence has not been previously reported for cerebral vessels. However, very few species have been tested. Reports of other vascular beds in other species sometimes parallel and sometimes contradict our findings with CGRP.
Glucose affects the severity of hypoxic-ischemic brain injury in newborn pigs.
Authors: LeBlanc M H , Huang M , Vig V , Patel D , Smith E E 
Published: June 2011

The administration of glucose has been shown to worsen brain injury in adult animals but has no effect on the severity of injury in newborn rats. We wished to see whether the results in newborn rats could be extended to another newborn animal.
In 44 0- to 3-day-old piglets, hypoxic-ischemic central nervous system damage was induced by ligation of both carotid arteries and reduction of their blood pressure to two-thirds normal for one-half hour. In the last 15 minutes of this half hour, oxygen concentration was reduced to 6%. The piglets were randomized to receive either 2 mL/kg 50% dextrose in water followed by 2 mL/kg per hour for 2.5 hours beginning before ischemia or enough insulin to reduce their resting blood sugar to approximately 2 mmol/L.
Neurological exam scores in the glucose-treated piglets at 1 day after injury were significantly worse than those in the insulin-treated group. Pathological examination scores were poorer in the glucose-treated group (13.6 +/- 1.9 [mean +/- SEM]) than in the insulin-treated group (24.7 +/- 1.4, P < .01).
Increasing serum glucose during hypoxic-ischemic injury to the newborn piglet's brain worsens brain injury.
Delayed therapy of experimental ischemia with competitive N-methyl-D-aspartate antagonists in rabbits.
Authors: Madden K P , Clark W M , Zivin J A 
Published: June 2011

N-methyl-D-aspartate antagonists are effective in limiting ischemic damage to the brain and spinal cord if treatment is begun at time of ischemic injury. More clinically relevant delayed therapy has not been adequately investigated. We report the temporal profile of efficacy for two competitive N-methyl-D-aspartate antagonists in therapy of central nervous system ischemia.
CGS-19755 (30 mg/kg) or LY233053 (100 mg/kg) was administered 5, 30, or 60 minutes after reversible spinal cord ischemia in rabbits, induced by temporary occlusion of the infrarenal aorta. Duration of occlusion for individual animals was varied to provide a range of ischemia for each experimental group. The P50 represents the duration (in minutes) associated with a 50% probability of resultant permanent paraplegia. Neuroprotection is demonstrated if a drug prolongs the P50.
CGS-19755 significantly prolonged the P50 (t test, P = .003) when given 5 minutes after ischemia, but not if delayed by 30 or 60 minutes (P50: control, 24.1; 5 minutes, 31.4; 30 minutes, 30.1; 60 minutes, 26.6). LY233053 was efficacious at 5 (P = .0008) and 30 (P = .002) minutes, but not at 60 minutes (P50: control, 26.8; 5 minutes, 39.4; 30 minutes, 36.0; 60 minutes, 25.6).
These competitive N-methyl-D-aspartate antagonists are effective in limiting ischemic damage, but protection is lost if therapy is not initiated within 60 minutes of injury.
Ticlopidine improves the enhanced erythrocyte aggregability in patients with cerebral infarction.
Authors: Tanahashi N , Fukuuchi Y , Tomita M , Matsuoka S , Takeda H 
Published: June 2011

We examined the effect of ticlopidine hydrochloride on the enhanced erythrocyte aggregability in 14 patients with cerebral infarction during the chronic phase (over 1 month after onset).
Ticlopidine (100 mg BID) was administered for 8 weeks. We measured the rate of erythrocyte aggregation (aggregability), using the whole-blood erythrocyte aggregometer that we developed, before and at 4 and 8 weeks after the initiation of ticlopidine administration. Concomitant measurements were made of such blood factors as the hematocrit, albumin-globulin ratio, and fibrinogen concentration. The erythrocyte aggregation rates before and at 4 and 8 weeks after were 0.147 +/- 0.017/s, 0.138 +/- 0.019/s, and 0.133 +/- 0.017/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly lower (P < .05 by Bonferroni's modified t test) than those before ticlopidine administration. At 4 and 8 weeks after the initiation of ticlopidine treatment, the hematocrit value and concentration of fibrinogen were also significantly (P < .05) reduced.
Our results suggest that ticlopidine can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.
Association between low bone density and stroke in elderly women. The study of osteoporotic fractures.
Authors: Browner W S , Pressman A R , Nevitt M C , Cauley J A , Cummings S R 
Published: June 2011

To determine whether women with low bone mineral density are at increased risk of stroke, the present study was conducted.
We studied 4024 ambulatory women aged 65 years or older participating in the prospective Study of Osteoporotic Fractures. Bone mineral density was measured at baseline using single photon absorptiometry; strokes were ascertained using a computerized Medicare data base and death certificates.
During a mean of 1.98 years of follow-up, 83 women suffered first strokes (five fatal). Osteopenia was associated with an increased stroke risk: Each SD decrease in bone mineral density at the calcaneus (0.09 g/cm2) was associated with a 1.31-fold increase in stroke (95% confidence interval, 1.03-1.65), adjusted for age, follow-up time, and several potential confounders, including diabetes, systolic blood pressure, use of alcohol, cigarettes or postmenopausal estrogens, cognitive ability, grip strength, and functional ability. The observed relation between bone density and stroke was strongest for intracerebral hemorrhages and occlusions.
Most likely, low bone density does not cause stroke; some other process probably results in both osteopenia and cerebrovascular disease.
Transient ischemic attacks in younger and older patients. A comparative study of 798 patients in South Africa.
Authors: Giovannoni G , Fritz V U 
Published: June 2011

The literature concerning transient ischemic attacks in young adults compared with strokes in young adults is scanty. This study evaluates the profile of transient ischemic attacks in young patients (aged 45 years or younger) compared with older patients (aged older than 45 years).
Between 1981 and 1991, 75 young patients (aged 45 years or younger) and 723 older patients (aged older than 45 years) were diagnosed as having a transient ischemic attack and included in the study. History of presenting transient ischemic attack, risk factors, clinical features, investigations, and etiology were compared on the basis of the above age groups.
In younger patients the presenting transient ischemic attack occurred less frequently in the vertebrobasilar territory (9% versus 21%, P = .03). Risk factor analysis revealed significant differences between the groups, with hypertension, previous smoking history, ischemic heart disease, and peripheral vascular disease being more common in the older group. Migraine and valvular heart disease were more common in the younger group. Approximately 60% of the patients in each group had multiple etiologies. The most common etiology was atheromatous cerebrovascular disease in both groups (74% versus 37% [P < .0001] in the older and younger groups, respectively). Other significant etiologic differences included fibromuscular dysplasia, mitral valve prolapse, and use of oral contraceptives occurring more frequently in the younger group, and ischemic heart disease occurring more frequently in the older group.
This study reveals the clinical and etiologic differences between younger and older patients with transient ischemic attack. The importance of multiple etiologies in both groups of patients has diagnostic and management implications.
Treatment of acute cortical infarct with intravenous glycerol. A double-blind, placebo-controlled randomized trial.
Authors: Yu Y L , Kumana C R , Lauder I J , Cheung Y K , Chan F L , Kou M , Fong K Y , Cheung R T , Chang C M 
Published: June 2011

This clinical trial investigates the effectiveness of intravenous glycerol therapy in patients with acute cortical infarction in whom intracerebral hemorrhage was rigorously excluded.
Within 48 hours of symptoms from their first ischemic stroke, 113 hospital inpatients were randomized into the trial, provided that hemorrhage was excluded by computed tomography and informed consent was obtained. Patients were stratified into alert, semicoma, and coma groups using the Glasgow Coma Scale. Treatment was allocated according to a double-blind, randomized protocol; 56 patients received 500 mL of 10% glycerol in saline over 4 hours on 6 consecutive days, and 57 patients received corresponding placebo treatment with saline. Using a variety of objective scoring systems, patient follow-up was up to 6 months.
Corresponding measures of outcome in the glycerol and placebo groups were similar. At 6 months, respective mortality rates were 17 of 56 and 16 of 57, and mean +/- SD improvements in scores were 9.98 +/- 14.40 vs 10.51 +/- 12.68 (long-term), 1.12 +/- 7.20 vs 1.57 +/- 6.30 (prognostic), -1.94 +/- 5.53 vs -2.06 +/- 5.34 (Glasgow Coma Scale), and 21.72 +/- 23.40 vs 11.94 +/- 18.10 (Barthel Index rating in survivors). Hemolysis (generally subclinical) was the only adverse effect.
There was no clinically or statistically significant difference in outcome between the groups; a trend toward greater functional recovery among survivors was evident after treatment with glycerol.
Color Doppler imaging of orbital arteries for detection of carotid occlusive disease.
Authors: Hu H H , Sheng W Y , Yen M Y , Lai S T , Teng M M 
Published: June 2011

Distal to a hemodynamically significant stenosis, the Doppler effect becomes dampened. Thus, measuring the flow profile in the ophthalmic artery and the central retinal artery with color Doppler imaging may provide hemodynamic information about the carotid circulation.
To validate the flow profile measurement with color Doppler imaging in the ophthalmic and central retinal arteries and to determine the sensitivity and specificity of this examination in the detection of hemodynamically significant carotid stenosis, we compared color Doppler imaging examinations with ocular pneumoplethysmography and ophthalmodynamometry examinations in 66 patients with atherothrombotic ischemic cerebrovascular disease. The degree of carotid stenosis in these patients was determined by a duplex scan with color Doppler imaging, and 57 patients underwent angiography to verify the stenosis.
The flow velocities (systolic peak velocity and end-diastolic velocity) and pulsatility indices (A/B ratio and resistance index) in the ophthalmic and central retinal arteries decreased as the degree of carotid stenosis increased. There is a statistically significant difference in the mean of systolic peak velocity and the mean of end-diastolic velocity of the ophthalmic and central retinal arteries among groups with various degrees of carotid stenosis (P < .02). Using the flow velocities of the ophthalmic and central retinal arteries to diagnose carotid stenosis (> or = 75% stenosis and occlusion), 8 cm/s for systolic peak velocity in the central retinal artery and 29 cm/s for systolic peak velocity plus flow direction reversal in the ophthalmic artery gave the maximum accuracy (sensitivities, 84% and 85.7% and specificities, 89.6% and 81.7%, respectively). The systolic peak velocity in the central retinal artery varied directly with the systolic pressure of the ophthalmic and central retinal arteries.
The flow velocity and pulsatility in orbital arteries examined by color Doppler imaging provide further hemodynamic information; this test can be used to complement current sonographic examination of carotid disease.
Threshold of calcium disturbances after focal cerebral ischemia in rats. Implications of the window of therapeutic opportunity.
Authors: DeGraba T J , Ostrow P T , Grotta J C 
Published: June 2011

One explanation for inconclusive results with calcium channel blockers in human acute stroke trials may be incomplete information about the time course of calcium-mediated ischemic neuronal injury. This study explores the temporal relation between duration of focal ischemia and the functional activity of increased intracellular calcium as measured by calcium-calmodulin binding.
Calcium-calmodulin binding, determined by immunohistochemical assay of free calmodulin, was measured in 60 male spontaneously hypertensive rats after 2 minutes and after 1, 2, 4, and 24 hours of permanent tandem common carotid and middle cerebral artery occlusion, and after 1 and 2 hours of reversible middle cerebral artery occlusion followed by 1 and 22 hours of reperfusion, respectively. Light microscopic histological damage was measured after 1 hour of occlusion with 23 hours of reperfusion and after 24 hours of occlusion.
Significant loss of calmodulin staining in the core of the infarction was noted by 1 hour and became maximal after 4 hours of ischemia. No reversal of calmodulin staining loss was noted after reperfusion following 1 and 2 hours of ischemia. Cortical necrosis seen by light microscopy correlated well with the area of maximal calcium-calmodulin binding. The border zone area, represented by a mild loss of calmodulin staining surrounding the central core of maximal binding, gradually decreased in size and became incorporated into the central core after 4 hours of ischemia; it may represent an area of reversible ischemia.
Calcium-calmodulin binding correlates with duration of focal ischemia, and histological neuronal necrosis corresponds to the cortical areas displaying a significant loss of calmodulin staining. Inasmuch as loss of calmodulin staining represents a marker for calcium-mediated activity after ischemia, it suggests a window of opportunity within 4 hours after acute stroke for therapeutic intervention with calcium antagonists.
Effect of S-emopamil, nimodipine, and mild hypothermia on hippocampal glutamate concentrations after repeated cerebral ischemia in rabbits.
Authors: Matsumoto M , Scheller M S , Zornow M H , Strnat M A 
Published: June 2011

We sought to determine the effects of two different calcium channel antagonists, S-emopamil and nimodipine, on hippocampal glutamate and glycine release and to compare their effects to those of mild hypothermia.
New Zealand White rabbits were subjected to two 7.5-minute episodes of global cerebral ischemia at a 1-hour interval produced by neck tourniquet inflation (20 psi) combined with hypotension during halothane anesthesia. Hippocampal extracellular concentrations of glutamate and glycine were monitored using in vivo microdialysis. Animals were randomized to receive either S-emopamil (1 mg.kg-1 bolus, 0.1 mg.kg-1.min-1 infusion), nimodipine (10 micrograms.kg-1 bolus, 1 microgram.kg-1.min-1 infusion), hypothermia (32 degrees C), or saline (control) before ischemia. Drug infusion and hypothermia were continued throughout the study periods.
In all four groups, both ischemic episodes resulted in significant elevations of hippocampal extracellular concentrations of glutamate and glycine (baseline vs peak, P < .01 in all groups). However, glutamate levels were significantly lower in the S-emopamil (P = .0001) and hypothermia (P = .0003) groups when compared with the control group after the onset of the first ischemic episode through 1 hour after the second ischemic episode. There was no significant difference between the four groups in the concentrations of glycine. There was no significant difference between the peak concentrations of glutamate or glycine after each ischemic period.
These results suggest that preischemic administration of S-emopamil, but not nimodipine, attenuates the increase in hippocampal extracellular concentrations of glutamate in the peri-ischemic period in this model, and that this effect is also observed when mild hypothermia is instituted before ischemia. Decreased concentrations of glutamate after ischemic episodes may be a possible mechanism for the observed neuroprotective properties of S-emopamil and mild hypothermia (32 degrees C).
Postischemic (1 hour) hypothermia significantly reduces ischemic cell damage in rats subjected to 2 hours of middle cerebral artery occlusion.
Authors: Zhang R L , Chopp M , Chen H , Garcia J H , Zhang Z G 
Published: June 2011

We investigated the effect of hypothermia induced 1 hour after transient (2-hour) middle cerebral artery occlusion on the extent of ischemic cell damage in the rat.
Middle cerebral artery occlusion was induced extracranially by insertion of a nylon filament into the right internal carotid artery. Two groups of rats were investigated: (1) rats (n = 10) subjected to normothermic (37 degrees C) ischemia and normothermic reperfusion; and (2) rats (n = 10) subjected to normothermic ischemia and 1 hour of normothermic reperfusion followed by 3 hours of hypothermia (30 degrees C). All rats were killed 1 week after the experiment, and brain sections were stained with hematoxylin and eosin for evaluation of ischemic cell damage.
Infarct volume in normothermic rats involved 20.9 +/- 4.6% of the hemisphere, whereas hypothermic rats exhibited a significantly smaller (P < .001) infarct volume of 11.1 +/- 2.7%. The numbers of surviving (or structurally intact) neurons within large sections of the cortex and striatum were significantly greater for hypothermic compared with normothermic rats (P < .01).
Our data suggest that postischemic induction of hypothermia significantly reduces ischemic cell damage after 2 hours of middle cerebral artery occlusion in the rat, and that an interval of time of at least 1 hour after ischemia exists in which hypothermic intervention is effective in either salvaging or postponing irreversible neuronal injury.