bluuebunny/crossref_metadata_2025 huggingface dataset:
Prediction of symptomatic vasospasm after subarachnoid hemorrhage by rapidly increasing transcranial Doppler velocity and cerebral blood flow changes.
Authors: Grosset D G , Straiton J , du Trevou M , Bullock R
Published: June 2011

Increased transcranial Doppler velocities and regional cerebral perfusion defects have been well demonstrated in patients with subarachnoid hemorrhage, but the clinical significance of these changes has not been clearly defined, particularly in the presymptomatic stage of cerebral vasospasm. We have tested the hypothesis that a rapid, massive rise in Doppler velocity denotes progressive vasospasm by relating Doppler velocity increases to regional cerebral blood flow changes and to the subsequent clinical course.

Serial transcranial Doppler sonography was performed in 121 patients; 20 of these patients were selected for blood flow mapping on the basis of rapid increases (greater than 50 cm/sec/24 hr) in blood flow velocity. Cerebral blood flow was mapped by single-photon emission computed tomography using technetium-99m hexamethylpropyleneamine oxime.

Ten of 15 patients studied before the onset of any deficit subsequently developed a focal neurological abnormality. In 14 of these 15 patients, and in a further five in which single-photon emission computed tomography was performed after the onset of a delayed neurological deficit, perfusion patterns were abnormal and correlated with sites of increased Doppler velocities. Four patients had zones of cerebral hypoperfusion but did not develop neurological deficit.

Transcranial Doppler measurements can assist in identifying patients at risk of delayed ischemic deficit. Selection of patients for regional cerebral blood flow mapping studies and for prophylactic anti-ischemic therapy may be considered on this basis.
Ischemic brain damage is not ameliorated by 1,3-butanediol in hyperglycemic rats.
Authors: Lundgren J , Smith M L , Mans A M , Siesjö B K
Published: June 2011

Treatment with the ketone body precursor 1,3-butanediol has been suggested to ameliorate hypoxic/ischemic brain damage. Butanediol could provide an alternative energy substrate for the brain, thereby decreasing the amount of glycolytically produced lactate. Hyperglycemia aggravates brain damage after brain ischemia and causes fatal postischemic seizures, probably by increasing the production of lactate and decreasing the pH. We studied whether butanediol treatment altered the adverse consequences following ischemia complicated by hyperglycemia.

Hyperglycemic adult male rats were given 25 or 50 mmol.kg-1 body wt butanediol intravenously 30 minutes before 10 minutes of transient forebrain ischemia. Morphological evaluation was performed following perfusion-fixation after 15 hours of recovery. Blood concentrations of beta-hydroxybutyrate, acetoacetate, glucose, and lactate and brain tissue concentrations of energy metabolites were measured before and after ischemia.

Blood levels of ketone bodies increased in the butanediol-treated rats. Ischemia decreased the blood levels of acetoacetate but increased the levels of beta-hydroxybutyrate by a similar amount, resulting in unchanged high levels of total ketone bodies in the animals that received butanediol. Brain tissue levels of glucose, energy metabolites, and lactate showed no difference between butanediol- and saline-treated rats. Furthermore, compared with saline-treated animals butanediol-treated rats showed no decrease in brain damage and no attenuation in the development of postischemic seizures.

The ketone body precursor 1,3-butanediol offers no protective effect in transient forebrain ischemia complicated by hyperglycemia.
Polyethylene glycol superoxide dismutase and catalase attenuate increased blood-brain barrier permeability after ischemia in piglets.
Authors: Armstead W M , Mirro R , Thelin O P , Shibata M , Zuckerman S L , Shanklin D R , Busija D W , Leffler C W
Published: June 2011

Transport of urea across the blood-brain barrier is increased during postischemic cerebral reperfusion in the piglet. Ischemia/reperfusion also has been observed to increase apparent superoxide anion generation on the surface of the brain. The present study was designed to address the hypothesis that the increased transfer of urea into the brain after ischemia/reperfusion could be due to superoxide anion-induced alterations in blood-brain barrier permeability.

Blood-to-brain transfer of carbon-14-labeled urea was measured in four groups (n = 7 each) of newborn pigs: 1) control (no ischemia, no pretreatment), 2) pretreatment with polyethylene glycol superoxide dismutase (1,000 IU/kg) and polyethylene glycol catalase (10,000 IU/kg i.v.) but no ischemia, 3) no pretreatment and 20 minutes of ischemia followed by 2 hours of reperfusion, and 4) pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase in addition to ischemia/reperfusion. The following brain regions were investigated: cerebrum, caudate, midbrain, pons, medulla, and cerebellum.

Polyethylene glycol superoxide dismutase inhibited generation of superoxide anion by the brain during reperfusion after ischemia. Regional transfer of [14C]urea from blood to brain increased at 2 hours' reperfusion. This ischemia-induced increase in blood-to-brain transfer of [14C]urea was attenuated by pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase: e.g., cerebrum Kin was 28 +/- 2 in the control group, 26 +/- 3 in the pretreated/no ischemia group, 67 +/- 5 in the untreated/ischemia group, and 40 +/- 2 ml.g-1.s-1.10(6) in the pretreated/ischemia group. After ischemia/reperfusion, cerebral blood flow was unchanged by pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase.

These data suggest that production of a partially reduced species of oxygen contributes to the increased urea transfer across the blood-brain barrier after ischemia in the newborn pig.
Stroke and Parkinson's disease.
Authors: Levine R L , Jones J C , Bee N
Published: June 2011

We sought to determine whether the recently reported decreased incidence of stroke and atherosclerotic disease in a university hospital-based Parkinson's disease patient population would be demonstrated in our patient population.

We performed a retrospective case-control review of the last 119 Parkinson's disease patients discharged from the Middleton Veterans Affairs Hospital Neurology Service to study the incidence of ischemic stroke, myocardial ischemia, tobacco use, and other stroke risk factors. Controls were age and sex matched and were randomly taken from 238 non-Parkinson's disease discharges in which stroke or myocardial infarction was not the reason for hospitalization.

The cumulative incidences of ischemic stroke, hypertension, and diabetes mellitus were not significantly different between groups. Myocardial infarction, coronary artery disease, tobacco use, atrial fibrillation, cancer, and ethanol abuse were significantly more prevalent in the controls, whereas dementia and congestive heart failure were the only variables studied that were more prevalent in the Parkinson's disease patients.

Our study failed to demonstrate that Parkinson's disease patients from a Veteran population were protected from ischemic stroke.
Influence of tissue plasminogen activator and heparin on cerebral ischemia in a rabbit model.
Authors: Carter L P , Guthkelch A N , Orozco J , Temeltas O
Published: June 2011

The aims of this study were to verify that tissue-type plasminogen activator given either 1 or 2 hours after experimental embolic stroke in rabbits diminishes the volume of resulting ischemic brain and to ascertain the effect of the simultaneous administration of heparin.

We embolized the middle cerebral artery of rabbits by injecting performed autologous arterial ("white") thrombus into one internal carotid artery. Treatment with 2 mg/kg tissue-type plasminogen activator, alone or in combination with heparin, was commenced either 1 or 2 hours after embolization. The animals were killed 5 hours after treatment commenced, and their brains were examined for evidence of ischemia and hemorrhage.

Administration of tissue-type plasminogen activator significantly diminished the size of the resulting brain ischemia. Administration of heparin, with or instead of tissue-type plasminogen activator, did not result in a significant decrease in the volume of cerebral ischemia, but it also did not lead to hemorrhagic transformation of the stroke.

In the rabbit model, administration of tissue-type plasminogen activator within 2 hours diminished the volume of brain rendered acutely ischemic by embolic stroke. Since the simultaneous administration of heparin during this same period did not result in any instances of hemorrhagic transformation, tissue-type plasminogen activator may have some place for use in such circumstances to mitigate a tendency to further embolic or thrombotic events.
Effects of hypothermia on evoked potentials, magnetic resonance imaging, and blood flow in focal ischemia in rabbits.
Authors: Lo E H , Steinberg G K
Published: June 2011

Mild hypothermia has been shown to ameliorate neuronal damage due to cerebral ischemia. In our study, the influence of mild-to-moderate hypothermia was examined in a rabbit model of focal cerebral ischemia.

After 4 hours of permanent ischemia induced by occlusion of the anterior and middle cerebral and internal carotid arteries, somatosensory evoked potentials and regional cerebral blood flow were measured. Ex vivo magnetic resonance imaging scans were also obtained to determine the degree of ischemic brain injury. Three temperature (temporalis muscle) groups were studied: 37 degrees C, 33 degrees C, and 30 degrees C (n = 5 per group). An additional two animals were used to confirm that temporalis muscle temperatures were well correlated with brain temperature. Rectal temperatures were kept constant (37.5 degrees C) in all groups.

After 4 hours of focal ischemia, evoked potentials in the normothermic animals remained depressed (2.2 +/- 2.1% [mean +/- SEM] preocclusion values). Recovery of potentials was significantly enhanced in both hypothermic groups (p less than 0.05): 18.2 +/- 6.5% (33 degrees C) and 43.6 +/- 12.2% (30 degrees C). Quantitative magnetic resonance measurements showed that T1 and T2 relaxation times were increased in the core ischemic regions within the cortex (20.4 +/- 4.0% and 25.3 +/- 5.9%, respectively). These elevations in T1 and T2 were reduced by hypothermia. However, blood flow was not improved by lowered temperature; in fact, flow in the 30 degrees C group was significantly decreased compared with the other groups (p less than 0.01). There was no statistically significant correlation between specific cerebral blood flow values and T1 or T2 elevations.

These results demonstrate that hypothermia can improve evoked potentials and magnetic resonance parameters in permanent focal ischemia. However, moderate hypothermia (30 degrees C) appears to also significantly decrease blood flow in the ischemic brain.
Tirilazad reduces cortical infarction after transient but not permanent focal cerebral ischemia in rats.
Authors: Xue D , Slivka A , Buchan A M
Published: June 2011

We examined the cytoprotective effect of the lipid peroxidation inhibitor tirilazad mesylate (U74006F) in rodent models of neocortical infarction induced by transient and permanent focal cerebral ischemia.

Wistar rats (experiment 1) and spontaneously hypertensive rats (experiment 2) were subjected to 2 hours of transient middle cerebral artery occlusion followed by 22 hours of reperfusion and pretreated with 10 mg/kg i.p. tirilazad, vehicle, or saline. Repeat doses were given at 4 and 10 hours after reperfusion. Spontaneously hypertensive rats were also subjected to permanent middle cerebral artery occlusion and either pretreated with tirilazad, vehicle, or saline intraperitoneally (experiment 3) or treated with either tirilazad or vehicle intravenously after ischemia (experiment 4). Cortical infarct volumes were measured 24 hours after the onset of either transient or permanent ischemia, and changes in core regional cerebral blood flow were monitored with laser Doppler flowmetry.

Tirilazad reduced infarct volume after transient ischemia by 40% in Wistar rats (p = 0.08) (experiment 1) and 23% in spontaneously hypertensive rats (p less than 0.05) (experiment 2) but did not reduce infarction after permanent ischemia whether it was given intraperitoneally (experiment 3) or intravenously (experiment 4). Ischemic core blood flows were not affected during ischemia, nor were they affected during reperfusion after transient ischemia.

Tirilazad reduces cortical infarction in transient but not permanent ischemia, an effect not related to improvement in regional cerebral blood flow. Tirilazad might prove to be useful as an adjuvant therapy after successful thrombolysis in acute stroke patients.
Early recurrent ischemic stroke. A case-control study.
Authors: Goldstein L B , Perry A
Published: June 2011

Data concerning potentially treatable risk factors for early recurrent stroke are limited. Therefore, we carried out a retrospective case-control study to identify factors predisposing to early reinfarction.

We identified all patients admitted to Duke University Hospital or the Durham Veterans Administration Medical Center during 1 year having two documented ischemic strokes within 90 days (n = 12 of 273). Twelve randomly selected patients matched for age, sex, and race but having only a single stroke served as controls. There were no significant differences between the groups with respect to a variety of factors including the presence of hypertension, diabetes, a history of transient ischemic attack, a history of stroke, cerebral site of the index stroke, and subtype of the index stroke. A potential cardioembolic source was more frequently identified in the patients with early recurrent stroke (seven of the 12 case-control pairs were discordant for a potential cardioembolic source; McNemar's chi 2 test, p less than or equal to 0.02).

Of the variables examined, the presence of a potential cardioembolic source was the single statistically significant factor associated with reinfarction within the first 90 days after ischemic stroke. The limitations and possible therapeutic implications of these results are discussed.
Progression of carotid atherosclerosis in Japanese patients with coronary artery disease.
Authors: Tanaka H , Nishino M , Ishida M , Fukunaga R , Sueyoshi K
Published: June 2011

Along with the recent changes in lifestyle in Japan, the incidence of coronary artery disease has increased while the incidence of stroke appears to be decreasing. We investigated the relation between the progression of carotid atherosclerosis and the severity of coronary artery disease in the Japanese population.

The 2-year change in extracranial carotid atherosclerosis in 50 Japanese patients who underwent coronary angiography was evaluated using carotid echotomography. To quantify the extent of carotid atherosclerosis, the maximal thickness measurements of all plaques were summed for an individual plaque score, except for new plaques found on reexamination. Carotid disease progression was evaluated by the sum of plaque score change and the thickness of the new plaque found on reexamination.

The plaque score changed by -3.2 to 10.1 mm (mean +/- SD, 1.06 +/- 2.42 mm). The extent of coronary atherosclerosis (p less than 0.02) and serum total cholesterol level (p less than 0.01) were different between the progressing (n = 17) and the nonprogressing (n = 30) groups of carotid atherosclerosis when the progressing group included the patients with a delta plaque score of greater than or equal to 1.0 mm. Neither age, serum triglyceride level, serum high-density lipoprotein cholesterol level, pack-years of smoking, percentage of smokers, percentage of hypertensive patients, nor percentage of diabetic patients was different between the two groups. Carotid disease progression was significantly higher in patients with three-vessel coronary disease than in patients without significant coronary artery disease (p less than 0.005). There was a significant positive linear correlation between carotid disease progression and Gensini's coronary artery disease score (R = 0.411, p less than 0.005).

Our data showed that severe coronary artery disease and a high serum total cholesterol level were strong predictors for carotid disease progression in Japanese patients with high rates of coronary artery disease.
Aortogenic embolic stroke: a transesophageal echocardiographic approach.
Authors: Toyoda K , Yasaka M , Nagata S , Yamaguchi T
Published: June 2011

We studied the frequency and grade of atherosclerotic changes in the thoracic aorta and their significance as embologenic lesions in patients with stroke.

Using transesophageal echocardiography, we evaluated complicated lesions in the thoracic aortas of 62 patients who met our clinical criteria for embolic stroke. A complicated lesion was defined as a raised lesion with an irregular surface or acoustic shadow based on a comparative study of echocardiographic and histopathologic findings. The results were compared with plain radiographic findings and in some cases with computed tomographic or aortographic findings.

Twenty-six patients (42%) showed complicated aortic arch lesions on echocardiogram. Transesophageal echocardiography brought us more abundant information than other techniques. Aortic knob calcification by plain radiography correlated well with the presence of echocardiographically complicated lesions, suggesting its utility for rough screening of atherosclerotic changes. Fifty-two patients had other potential embolic sources in the heart or cervical arteries. Among the remaining 10 patients without extra-aortic embolic sources, three showed complicated lesions and were diagnosed as having aortogenic embolic stroke.

Aortic atherosclerosis should be recognized as an embolic source of stroke and the advantage of transesophageal echocardiography recognized in its evaluation.
Transcranial Doppler correlation with cerebral angiography in sickle cell disease.
Authors: Adams R J , Nichols F T , Figueroa R , McKie V , Lott T
Published: June 2011

Cerebral infarction in sickle cell disease is associated with arterial narrowing or occlusions of intracranial arteries. Primary stroke prevention would be feasible if a noninvasive screening test could be developed to detect intracranial disease in patients before symptoms develop.

To determine the sensitivity and specificity of transcranial Doppler in detecting significant (greater than or equal to 50% lumen diameter reduction) intracranial arterial lesions, we compared transcranial Doppler and cerebral angiography in a primarily young, symptomatic group of 33 patients (18 males and 15 females) with sickle cell disease.

From a total of 34 examinations, transcranial Doppler detected significant abnormalities in 26 of 29 (sensitivity 90%, specificity 100%). Five were normal by both techniques. The transorbital examination detected abnormalities in two patients whose studies were otherwise unremarkable.

Transcranial Doppler is sensitive and specific for the detection of arterial vasculopathy of sickle cell disease. Screening should include a transorbital examination of the distal internal carotid artery as well as examination using the transtemporal approach.
Platelet-activating factor acetylhydrolase in plasma lipoproteins from patients with ischemic stroke.
Authors: Satoh K , Yoshida H , Imaizumi T , Takamatsu S , Mizuno S
Published: June 2011

Platelet-activating factor is a potent bioactive phospholipid and may play an important role in occlusive vascular diseases. To assess the inactivation of this autacoid in plasma, we measured platelet-activating factor acetylhydrolase activity in plasma low density and high density lipoproteins from patients with ischemic stroke.

Low density and high density lipoproteins were separated by ultracentrifugation from plasma of 33 patients with cerebral thrombosis and 31 age-matched healthy control subjects, and platelet-activating factor acetylhydrolase activity in each fraction was assayed.

The average values of platelet-activating factor acetylhydrolase activity in low density lipoprotein from patients and control subjects were 41 +/- 18 and 29 +/- 17 nmol/ml per minute, respectively, and the difference was statistically significant (p less than 0.01 U test). There was no difference in activity in high density lipoprotein between the two groups (16 +/- 11 versus 14 +/- 9 nmol/ml per minute, respectively).

The increased plasma platelet-activating factor acetylhydrolase activity in stroke patients is primarily attributable to the increased binding to low density lipoprotein, and this increase may be an adaptation to the augmented generation of platelet-activating factor in ischemic stroke.
Stroke risk from alcohol consumption using different control groups.
Authors: Ben-Shlomo Y , Markowe H , Shipley M , Marmot M G
Published: June 2011

Our aim in this study was to investigate the relation between chronic alcohol consumption and stroke.

A case-control study was carried out using two hospital-based control groups and the results of a community-based survey of alcohol consumption. Hospital-based control subjects were chosen either from "general" medical admissions or a subset of "select" admissions that excluded possible alcohol-related admissions. Cases were selected from hospital inpatients.

The relative risk for stroke associated with alcohol consumption greater than 300 grams per week for general control subjects was 0.73 (95% confidence interval [CI], 0.54-3.49) compared with 1.30 (95% CI, 0.42-4.05) for select control subjects. The odds ratio was further increased to 1.93 (95% CI, 0.87-4.28) using data from the community-based survey. None of these estimates were statistically significant.

These results illustrate how the risk associated with alcohol consumption varies depending on the choice of control groups and may explain the contradictory results from previous case-control studies. Because of different biases associated with control selection, we believe that the results of this study are consistent with those of other studies that demonstrate a modest increased risk for stroke associated with alcohol consumption.
Combined magnetic resonance imaging and proton magnetic resonance spectroscopy of patients with acute stroke.
Authors: Felber S R , Aichner F T , Sauter R , Gerstenbrand F
Published: June 2011

The prospect for a therapeutic window for treatment of ischemic stroke encourages the noninvasive investigation of metabolic changes in acute ischemia. Recently, localized proton spectroscopy became available at 1.5-T magnetic resonance systems. In this study we evaluated the usefulness of combined magnetic resonance imaging and spectroscopy on the diagnosis of acute and chronic infarctions.

Combined magnetic resonance imaging and spectroscopy investigations were carried out with a 1.5-T system in 16 volunteers, eight patients with chronic infarction (greater than 8 months), and 10 patients with acute ischemic stroke (less than 8 hours). We used a stimulated echo sequence to acquire localized spectra from image-guided volumes of interest (16-27 ml).

There were no significant interindividual differences of choline, creatine, phosphocreatine, and N-acetyl aspartate resonances in the spectra from volunteers. In chronic infarctions, N-acetyl aspartate was decreased in relation to choline. Acute ischemic infarctions were characterized by decreased N-acetyl aspartate resonances and elevation of lactate.

The study demonstrates the feasibility of proton spectroscopy in stroke patients. Metabolic alterations in ischemic tissue can be monitored and can distinguish acute from chronic lesions.
Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage.
Authors: Hatake K , Wakabayashi I , Kakishita E , Hishida S
Published: June 2011

The goal of this study was to determine the alterations in vascular reactivity of human basilar artery after subarachnoid hemorrhage.

Human basilar arteries were obtained from subjects who died within 1 day after subarachnoid hemorrhage and control subjects who died from causes other than brain involvement. Basilar artery strips were suspended for isometric tension recording in Krebs-Ringer solution. Morphometric study was also carried out on paraffin-embedded sections stained with van Gieson's elastica stain of preselected sites from the basilar arteries. The intimal and medial area and the intimal index ([intimal area/area circumscribed by internal elastic lamina] x 100) were evaluated.

Contractile responses to KCl, norepinephrine, and 5-hydroxytryptamine did not differ between subarachnoid hemorrhage and control groups. The endothelium-dependent relaxation responses to thrombin, bradykinin, and calcium ionophore A23187 were less for the subarachnoid hemorrhage group than for the control group. However, the endothelium-independent response to sodium nitroprusside of the subarachnoid hemorrhage group did not differ from that of the control group. Morphometric measurements were comparable between the two groups.

These results suggest that the decreased relaxation responses to thrombin and bradykinin occur at the level of endothelial cells and not smooth muscle cells and that decreased relaxation may be involved in delayed vasospasm after subarachnoid hemorrhage. Although the decreased relaxation was observed within 1 day after subarachnoid hemorrhage, a period in which delayed spasm does not occur, this time difference may be dependent on the severity of bleeding after rupture of an aneurysm.
Reduction of infarct volume and mortality by thrombolysis in a rat embolic stroke model.
Authors: Overgaard K , Sereghy T , Boysen G , Pedersen H , Diemer N H
Published: June 2011

Thrombolytic therapy with recombinant tissue plasminogen activator was tested in a rat embolic stroke model.

The rat carotid territory was embolized with arterial-like microthrombi formed under pressure. Hemispheric cerebral blood flow before and after embolization was measured by the intraarterial Xenon-133 injection method. Fifteen minutes after embolization, 24 rats were treated with 3 mg/kg or 10 mg/kg tissue plasminogen activator, and 27 were treated with saline. Carotid angiography displayed the rate of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed and evaluated neuropathologically and infarct volume was measured.

Cerebral blood flow was reduced 70-86% after embolization. The comparison of pretreatment and posttreatment angiography showed significant (p = 0.0005) reperfusion in the treated rats. Thrombolytic therapy significantly reduced the infarct volume from 55.1% to 24.4% of embolized hemisphere volume (p = 0.007) and increased the survival rate from 0.48 to 0.96 (p = 0.0004). Fifty-three percent of the embolized rats recanalized completely after thrombolytic treatment and developed almost no infarction (median volume 2.8%), and all survived. No hemorrhagic complications were observed.

Early thrombolytic therapy induced recanalization and reduced mortality and infarct volume after embolic stroke in this model.
Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group.
Authors: Herderscheê D , Hijdra A , Algra A , Koudstaal P J , Kappelle L J , van Gijn J
Published: June 2011

We studied silent stroke (i.e., infarcts on computed tomographic scan not related to later symptoms) in patients after transient ischemic attack or minor ischemic stroke.

Ours is a cross-sectional study of 2,329 patients who were randomized in a secondary prevention trial after transient ischemic attack or minor ischemic stroke and had no residual deficit after the qualifying event.

Silent stroke was observed in 13% of the 2,329 patients. Lacunes formed 79%, cortical lesions 14%, and border zone lesions 7% of all silent strokes. Silent lacunes were most often located in the basal ganglia and symptomatic lacunes most often in the corona radiata. Age, hypertension, and current cigarette smoking were related to the presence of silent stroke. Silent stroke was equally common in different types of transient ischemic attack, including transient monocular blindness. Residual symptoms of any kind were more common in patients with silent stroke than in those without.

Because only the sites of silent stroke infarcts differed slightly from those of symptomatic infarcts and the frequency of vascular risk factors was similar to that of symptomatic infarcts, silent stroke may have the same bearing on future risk as known prior stroke.
Restriction fragment length polymorphism of the apoprotein A-I-C-III gene cluster in control and stroke-prone white and black subjects: racial differences.
Authors: Kasturi R , Yatsu F M , Alam R , Rogers S
Published: June 2011

The presence of known restriction fragment length polymorphisms in the apoprotein A-I-C-III gene cluster, which encodes their respective apoproteins, was investigated using the restriction enzymes Sac I and Pst I to determine the potential role of genetic variations for stroke risk in an American population.

Ninety-eight subjects (70 white, 28 black subjects), both normal controls with no carotid stenosis and those with carotid stenosis believed at risk for stroke, defined as showing stenosis focally or diffusely at that site, composed the study population.

Sac I polymorphic S2 allele frequency was higher in stroke-risk groups, whereas Pst I polymorphic P2 allele frequency was similar in control and stroke-risk groups. Significantly higher levels of serum cholesterol, triglycerides, and low density lipoprotein (p less than 0.05) and significantly lower levels of high density lipoprotein (p less than 0.05) were observed in stroke-risk groups with diffuse stenosis. Results of our study with the two racial groups show the following: the frequency of Sac I polymorphism was significantly higher in American black compared with American white subjects (chi 2 = 3.92, p less than 0.05). Among serum lipids, triglycerides were significantly higher in white compared with black subjects (p less than 0.05). In white subjects, carotid artery stenosis was associated with significantly elevated total cholesterol and low density lipoprotein (p less than 0.01) but not with Sac I polymorphism. In black subjects the converse was observed, namely, the Sac I polymorphic S2 allele seemed to be associated with carotid bifurcation stenosis but did not reach statistical significance because of the small number of subjects. In addition, Sac I polymorphism did not correlate with any lipid profile. Pst I polymorphism was not associated with any lipid profile or carotid artery stenosis abnormalities.

Our results indicate that carotid artery stenosis identifies white subjects with increased plasma total cholesterol and low density lipoprotein, an atherogenic profile, but not with Sac I polymorphism. These findings suggest that carotid bifurcation stenosis in white subjects is associated with an atherogenic lipid profile but not with apoprotein A-I-C-III restriction fragment length polymorphisms. In black subjects, Sac I polymorphism seems to identify those individuals with significant carotid stenosis, a necessary precursor to atherothrombotic brain infarction, but not those with elevated total cholesterol, elevated low density lipoprotein, and/or reduced high density lipoprotein. These results suggest that Sac I polymorphism may identify black subjects at increased risk for atherothrombotic brain infarctions.
Magnetoencephalography of focal cerebral ischemia in rats.
Authors: Chen Q , Chopp M , Chen H , Tepley N
Published: June 2011

The purpose of this study was to use magnetoencephalography to record magnetic field changes in the brain during middle cerebral artery occlusion.

A direct-current electrocorticogram (two channels) and a direct-current magnetoencephalogram (seven channels) were simultaneously recorded from five rats subjected to middle cerebral artery occlusion for 1-2 hours.

Direct-current electrocorticographic and direct-current magnetoencephalographic signal deflections were observed after the onset of middle cerebral artery occlusion and occurred repeatedly throughout the ischemic period, with a mean +/- SD time interval of 12 +/- 5 minutes. A one-to-one correspondence of the electrocorticographic and magnetoencephalographic signal deflections was demonstrated.

Direct-current magnetoencephalography can provide a new noninvasive technique for studying depolarization and/or spreading depression in focal cerebral ischemia.
Level of function predicts first stroke in the elderly.
Authors: Colantonio A , Kasl S V , Ostfeld A M
Published: June 2011

Our aim in this study was to assess physical function as a predictor of stroke incidence in a probability sample of noninstitutionalized elderly subjects with no previous history of stroke.

The data were obtained from a prospective longitudinal study of 2,812 individuals aged 65 years of age and older living in New Haven, Connecticut. Incidence of stroke was monitored from the baseline interview in 1982 until December 1988 (n = 167). Physical function was measured by the Katz scale of activities of daily living and a three-item scale measuring gross mobility function (Rosow scale). Both measures of impairment of function were independently associated with stroke incidence controlling for age, sex, diabetes, hypertension, and angina (p less than 0.001).

Our findings suggest that in elderly persons, physical disability is a newly identified risk factor for stroke.
The preponderance of posterior circulatory events is independent of the route of cardiac catheterization.
Authors: Keilson G R , Schwartz W J , Recht L D
Published: June 2011

Central nervous system complications of cardiac catheterization are most often attributed to embolic events that occur at the time of catheter manipulation. Nevertheless, the reason that over 50% of these events are localized to the posterior circulation remains unexplained. One potential explanation offered for this preponderance is the use of the brachial artery approach. In this report, we examined the relation between the route of catheterization and central nervous system complications.

We retrospectively analyzed all central nervous system complications that occurred after cardiac catheterization through a femoral route at our institution over a 3 1/2-year period. Thirteen patients were identified as having central nervous system complications. Using defined criteria, posterior circulatory events still accounted for at least 54% of central nervous system complications.

The preponderance of posterior circulatory events is apparently independent of the route of catheterization. Furthermore, given the array of neurological symptoms and their often complete resolution, we feel it is unlikely that embolism is the sole pathophysiological mechanism involved in these events.
Moderate hyperglycemia worsens acute blood-brain barrier injury after forebrain ischemia in rats.
Authors: Dietrich W D , Alonso O , Busto R
Published: June 2011

Clinical and experimental data indicate that hyperglycemia can aggravate the consequences of stroke and cerebral ischemia. The purpose of this study was to examine the effects of moderate hyperglycemia on the response of the blood-brain barrier to normothermic (37 degrees C) and hypothermic (30 degrees C) global forebrain ischemia.

Sixteen rats underwent 20 minutes of four-vessel occlusion followed by 30 minutes of postischemic recirculation. We used the protein tracer horseradish peroxidase as an indicator of increased vascular permeability, and rats were perfusion-fixed for microscopic analysis. To produce moderate hyperglycemia, we gave an intraperitoneal injection of 50% dextrose 15 minutes before the ischemic insult.

After normothermic brain ischemia, normoglycemic rats (plasma glucose level, 115 +/- 3 mg/dl) demonstrated extravasated horseradish peroxidase mainly restricted to the cerebral cortex. In contrast, more severe and widespread protein extravasation was documented throughout the neuraxis of hyperglycemic (plasma glucose level, 342 +/- 27) rats. Sites of protein leakage included the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum. Foci of protein extravasation were associated with pial and large penetrating vessels. Intraischemic hypothermia significantly attenuated the blood-brain barrier consequences of hyperglycemic brain ischemia.

Under normothermic ischemic conditions, hyperglycemia significantly worsens the degree of acute blood-brain barrier breakdown compared with normoglycemia. Postischemic blood-brain barrier disruption may play an important role in the pathogenesis of increased brain damage associated with systemic hyperglycemia.
Magnetic resonance angiography of cervicocranial dissection.
Authors: Nguyen Bui L , Brant-Zawadzki M , Verghese P , Gillan G
Published: June 2011

A retrospective study of five patients with the clinical or magnetic resonance-based diagnosis of carotid dissection was done. Clinical data, imaging studies, treatment, and outcome were reviewed. The potential applicability of three-dimensional time-of-flight magnetic resonance angiography in these settings was evaluated.

This modality reliably showed vascular abnormalities and focal, segmental, or aneurysmal dilatation when correlated with conventional angiograms in three patients. Turbulence and magnetic susceptibility at the acute turn of the carotid in the petrous canal led to a false-positive diagnosis on magnetic resonance angiography in one patient (in whom subtle fibromuscular hyperplasia was found with conventional angiography but missed with magnetic resonance angiography).

When combined with appropriate clinical signs, magnetic resonance imaging and magnetic resonance angiography can reliably establish the diagnosis of carotid dissection. Pitfalls of magnetic resonance angiography are discussed.
Different linkage of depression to hypercortisolism early versus late after stroke. A 3-year longitudinal study.
Authors: Aström M , Olsson T , Asplund K
Published: June 2011

Using the dexamethasone suppression test, we studied the suppressibility of the cortisol axis and its clinical determinants at various time points after stroke. A major aim was to examine the dexamethasone test as a diagnostic tool for the diagnosis of major depression in stroke patients.

The dexamethasone suppression test, major depression, functional ability, and disorientation were assessed in a cohort of 70 patients with acute stroke and after 3 months (n = 63) and 3 years (n = 43).

Early after stroke, 24% of the patients were nonsuppressors, with about the same proportion at 3 months (22%) and 3 years (21%). None of the controls (17 healthy elderly volunteers) were nonsuppressors. High cortisol levels early after stroke were significantly associated with functional impairment (r = 0.35; p = 0.003) and disorientation (r = 0.27; p = 0.03). Three years after stroke, high postdexamethasone cortisol levels were significantly associated with major depression (r = 0.57; p < 0.001). The sensitivity of the dexamethasone test was 70% and the specificity 97%. In a longitudinal analysis of the long-term survivors (n = 42), postdexamethasone cortisol values at 3 months predicted major depression at 3 years.

Hypercortisolism is associated with major depression late (3 years) but not early (0-3 months) after stroke. Patients with hypercortisolism 3 months after stroke are at risk of major depression later in the course and warrant careful follow-up from a psychiatric viewpoint.
Impact of social support on outcome in first stroke.
Authors: Glass T A , Matchar D B , Belyea M , Feussner J R
Published: June 2011

The purpose of this study is to examine the impact of social support on outcome after first stroke in a prospective cohort study. Although modest evidence exists for the importance of several psychosocial factors, studies have failed to use widely recognized measures of outcome and social support, have failed to control for time since onset, and have not used longitudinal techniques.

Forty-six surviving patients were followed for 6 months after stroke. Recovery was measured using repeated measures of functional status as indicated by the Barthel Index of activities of daily living. Perceived social support was measured at 1, 3, and 6 months after onset. Repeated-measures multivariate analysis of variance was used to analyze changes in functional status.

Significant differences were found across levels of social support in trajectories of functional status (p = 0.002). A significant three-way interaction between stroke severity, social support, and outcome was also found (p = 0.012). Patients with more severe stroke and the largest amount of social support attained an average Barthel Index that was 68 points (65%) higher than the group reporting the least support.

High levels of social support were associated with faster and more extensive recovery of functional status after stroke. Social support may be an important prognostic factor in recovery from stroke. Socially isolated patients may be at particular risk for poor outcome.
Hypoperfusion and vasoreactivity in the thalamus and cerebellum after stroke.
Authors: Sakashita Y , Matsuda H , Kakuda K , Takamori M
Published: June 2011

Cerebellar hypoperfusion in the contralateral hemisphere after stroke is well studied and termed crossed cerebellar diaschisis. However, studies of hypoperfusion in the ipsilateral thalamus have been few. The purpose of this study was to investigate the prevalence of hypoperfusion and vasoreactivity to acetazolamide in the thalamus and cerebellum after stroke.

We studied cerebral blood perfusion in the thalamus and cerebellum of 14 patients with unilateral cerebral infarction using [123I]isopropyliodoamphetamine single-photon emission computed tomography (123I-IMP SPECT). We also administered acetazolamide-stressed 123I-IMP SPECT to determine vasodilator capacity in these two areas. Regions of interest were drawn over the bilateral thalami and bilateral cerebellar cortices, and asymmetry indexes were obtained.

We found ipsilateral thalamic hypoperfusion in 12 (85.7%) and contralateral cerebellar hypoperfusion in 11 (78.6%) of 14 patients. Hypoperfusion was improved (p < 0.01 by the Wilcoxon signed rank test) in 11 (91.7%) of the 12 patients with ipsilateral thalamic hypoperfusion and in seven (63.6%) of the 11 patients with contralateral cerebellar hypoperfusion.

Hypoperfusion in the ipsilateral thalamus and contralateral cerebellum is common, and vasoreactivity to acetazolamide is preserved in both the thalamus and the cerebellum with hypoperfusion.
Platelet aggregation in patients with atrial fibrillation taking aspirin or warfarin.
Authors: Helgason C M , Hoff J A , Kondos G T , Brace L D
Published: June 2011

Although warfarin and perhaps aspirin may be effective in preventing thromboembolism in patients with nonvalvular atrial fibrillation, some patients develop cerebral infarction despite these therapies. The purpose of this study was to determine inhibition of platelet aggregation in patients on aspirin and platelet reactivity in those on warfarin in the Stroke Prevention in Atrial Fibrillation study.

Twenty-four patients in the Stroke Prevention in Atrial Fibrillation study at the University of Illinois at Chicago, 17 on enteric-coated aspirin 325 mg/d and 7 on warfarin to produce an International Normalized Ratio of 2.0 to 4.5, had platelet aggregation studies performed during a 10-month period and interpreted by an investigator blinded to therapy. Epinephrine, adenosine diphosphate, collagen, and arachidonic acid were used as aggregating agents. Compliance was determined by pill count for those patients on aspirin.

Seven patients taking aspirin had partial and 10 had complete inhibition of platelet aggregation. Three of seven patients on warfarin had hyperaggregable platelets. Compliance was 80% or greater for those patients taking aspirin. One patient on warfarin had partial inhibition of platelet aggregation.

Some patients in the Stroke Prevention in Atrial Fibrillation trial on aspirin 325 mg/d did not achieve complete inhibition of platelet aggregation. Others had hyperaggregable platelets. These findings suggest platelet-dependent mechanisms for aspirin and warfarin failure to prevent stroke in these patients.
Risk factors of stroke incidence and mortality. A 12-year follow-up of the Oslo Study.
Authors: Håheim L L , Holme I , Hjermann I , Leren P
Published: June 2011

The objective of this study was to determine the risk factors of stroke incidence and mortality.

Our data are based on a prospective cohort study of men aged 40 to 49 years after 12 years of follow-up.

In age-adjusted Cox proportional-hazards regression analysis of 14,403 healthy men, diastolic blood pressure was a stronger predictor for stroke incidence and mortality than systolic blood pressure. Smoking was a stronger predictor of mortality than of incidence. However, there was no dose-response relation among smokers by increased cigarette consumption. Total serum cholesterol was a significant (P < .05) risk factor for stroke mortality and of borderline significance (P = .08) for stroke incidence. Increased physical activity at leisure was associated with reduced stroke incidence but not mortality. The myocardial infarction risk score comprising systolic blood pressure, total serum cholesterol, and daily cigarette smoking was a strong predictor of mortality and incidence. Body mass index, triglycerides, blood glucose, and physical activity at work were not found to be risk factors for stroke.

Reduction of blood pressure, cessation of smoking, lowered cholesterol, and increased physical activity at leisure are individual measures to reduce the risk of stroke.
Altered cerebral hemodynamics and metabolism in Takayasu's arteritis with neurological deficits.
Authors: Takano K , Sadoshima S , Ibayashi S , Ichiya Y , Fujishima M
Published: June 2011

Takayasu's arteritis is a nonspecific arteritis involving major cerebral arteries. The aim of our study is to examine cerebral hemodynamics and metabolism in Takayasu's arteritis with neurologic symptoms.

We measured cerebral blood flow and metabolism using positron emission tomography in seven patients (14 to 59 years of age) with Takayasu's arteritis who developed transient ischemic attacks (2 patients), ischemic stroke (4) or putaminal hemorrhage with multiple brain infarction (1).

All patients had severe stenosis or occlusion of one or more major cerebral arteries. There were no significant differences in the values of cerebral blood flow, oxygen extraction fraction, and cerebral blood volume in the infarcted and noninfarcted hemisphere. By contrast, the value of cerebral metabolic rate for oxygen in the infarcted hemisphere was markedly reduced (1.87 mL/100 mL per minute, P < .01) compared with controls. Mean transit time in the infarcted hemisphere was significantly greater than in the noninfarcted one, both in patients and controls (P < .01 and P < .05, respectively).

Collateral blood flow to the hemisphere without brain damage may be relatively well developed in Takayasu's arteritis, although hemodynamic reserve as well as oxygen metabolism were impaired in the infarcted hemisphere with ischemic lesions.