bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of a new calcium antagonist, TA3090 (clentiazem), on experimental transient focal cerebral ischemia in cats.
Authors: Sakaki T , Tsujimoto S , Sasaoka Y , Tsunoda S , Shintomi K 
Published: June 2011

TA3090 (Clentiazem) has been shown to have cerebrovascular protective properties in three experimental studies. An in vivo investigation was undertaken to determine its effects on pial arteries and cerebral blood flow and its therapeutic value in transient focal cerebral ischemia.
This experiment was divided into two protocols. In the first, 200 or 400 micrograms/kg per hour TA3090 was administered continuously for 3 hours in cats without ischemic insult (n = 6 for each group). The effects on pial arteries and cerebral blood flow were estimated. In the second protocol, 400 micrograms/kg per hour TA3090 (treated group, n = 14) or physiological saline (control group, n = 10) was administered 5 minutes before 1 hour of middle cerebral artery occlusion in cats. The effects on the pial arteries and cerebral blood flow were observed continuously, followed by autoradiography for a quantitative measurement of cerebral blood flow 5 hours after middle cerebral artery recirculation. The volumes of the cerebral edema and infarct were estimated by planimetry from cerebral preparations made for histological examination.
Pial arteries dilated by up to approximately 10% in the 400-micrograms group and 3% in the 200-micrograms group 30 minutes after administration of TA3090. Increases in cerebral blood flow of about 10% in the 400-micrograms group and 2% in the 200-micrograms group were demonstrated with laser Doppler flowmetry. In the second protocol, dilatation of pial arteries was significantly smaller during and after the ischemic insult in the treated group compared with the control group (p < 0.01). Cerebral blood flow decreased less significantly during ischemia (p < 0.01 at the end of ischemia) and increased less significantly after ischemia (p < 0.01 at the end) in the treated group compared with the control group. Autoradiography showed a more remarkable increase in cerebral blood flow due to luxury perfusion in the cerebral cortex, which was mainly perfused by the middle cerebral artery on the affected side in the control group (p < 0.01). Cerebral blood flow in the cerebral cortex, thalamus, and caudate nucleus on the contralateral side of the treated group increased by about 20% more than that of the control group (p < 0.05). Cerebral edema and infarction were much smaller in the treated group than in the control group (p < 0.01).
1) TA3090 dilates pial arteries and increases cerebral blood flow in normal brain regions in a dose-response fashion; 2) in ischemic regions compared with those in untreated animals, TA3090 results in a lesser reduction of cerebral blood flow during ischemia and in a lesser degree of hyperemia during reperfusion; 3) TA3090 is associated with less pial artery dilatation during ischemia, presumably due to improved collateral flow; and 4) the improved hemodynamic state with TA3090 is associated with significant reduction of cerebral edema and infarct size.
Pilot randomized trial of tissue plasminogen activator in acute ischemic stroke. The TPA Bridging Study Group.
Authors: Haley E C , Brott T G , Sheppard G L , Barsan W , Broderick J , Marler J R , Kongable G L , Spilker J , Massey S , Hansen C A 
Published: June 2011

Early thrombolytic therapy with recombinant tissue-type plasminogen activator is a theoretically attractive approach to the treatment of acute focal cerebral ischemia. In preparation for a larger multicenter trial, three centers piloted a protocol for a randomized, double-blind, placebo-controlled trial of intravenous recombinant tissue-type plasminogen activator begun within 3 hours of the onset of symptoms of acute stroke to test its feasibility and to explore trends.
Eligible patients had pretreatment computed tomographic scanning, gave informed consent, and began treatment with either 0.85 mg/kg recombinant tissue-type plasminogen activator or placebo as soon as possible, but no later than 180 minutes after stroke onset. Patients were stratified by whether treatment was begun within 90 minutes or 91 to 180 minutes from onset. The primary end point was the proportion of patients in each group who improved by 4 or more points on the National Institutes of Health Stroke Scale at 24 hours, as determined by a separate blinded evaluator.
Twenty-seven patients were randomized: 20 (10 recombinant tissue-type plasminogen activator, 10 placebo) within 90 minutes, and 7 (4 recombinant tissue-type plasminogen activator, 3 placebo) from 91 to 180 minutes. Median baseline Stroke Scale scores were 16 (minimum = 5, maximum = 26) for the recombinant tissue-type plasminogen activator-treated group and 11 (minimum = 3, maximum = 21) for the control subjects in the group treated within 90 minutes. Six patients treated with recombinant tissue-type plasminogen activator within 90 minutes improved by 4 or more points at 24 hours compared with 1 patient in the placebo group (P < .05, Fisher's Exact Test). Two patients in each group in the 91- to 180-minute arm improved. One fatal intracerebral hemorrhage occurred in the placebo group.
A randomized, double-blind, placebo-controlled trial of recombinant tissue-type plasminogen activator very early in acute stroke is feasible. Preliminary observations suggest that recombinant tissue-type plasminogen activator treatment within 90 minutes may be associated with early neurological improvement. Larger studies are needed so that the potentially serious short-term risks of this treatment can be assessed in relation to meaningful long-term benefit.
Unilateral amnesic stroke. Six new cases and a review of the literature.
Authors: Ott B R , Saver J L 
Published: June 2011

Although persistent amnesia due to bilateral limbic system infarction is well described, reports of amnesic syndromes due to unilateral stroke have appeared infrequently and unsystematically. We report six new cases and review previously published reports to expand and consolidate knowledge regarding amnesic stroke.
Six patients developed acute amnesia associated with unilateral stroke. Brain computed tomography or magnetic resonance imaging revealed lesions in limbic structures, which accounted for the memory deficit. Based on these as well as similar cases in the literature, we delineate three distinct syndromes of unilateral amnesic stroke involving the territories of the posterior cerebral, anterior choroidal, and thalamic penetrating arteries. Eighty-five percent of reported cases have involved the left hemisphere.
Persistent as well as transient amnesia may be the sole or primary manifestation of unilateral hemispheric stroke. The vascular mechanisms of amnesic stroke are diverse. Patients presenting with acute amnesia possibly related to cerebral ischemia should be classified by documented or presumed lesion site as well as the involved vascular territory. Left amygdalohippocampal or diencephalic dysfunction may produce a particular vulnerability to global amnesia.
Regional differences in the vasodilator response to vasopressin in canine cerebral arteries in vivo.
Authors: Suzuki Y , Satoh S , Oyama H , Takayasu M , Shibuya M 
Published: June 2011

The aim of this study was to investigate the regional differences in the in vivo vasodilator responses to vasopressin, which is thought to stimulate the release of nitric oxide from the endothelium, in canine cerebral arteries by angiography.
Angiograms were performed through a catheter inserted directly into the right vertebral artery and were taken periodically after the infusion of vasopressin. The diameters of various segments of the major arteries were measured using a computerized image analysis system.
The bolus administration of vasopressin (10 pmol to 1 nmol) into the vertebral artery produced a long-lasting, dose-dependent vasodilation in the major cerebral arteries centering around the circle of Willis. One nanomole of vasopressin appeared to be the optimal dose for producing maximal vasodilation. The internal diameters of the basilar, posterior communicating, and internal carotid arteries experienced the most dilation (approximately 150% that of control) 2 minutes after the infusion of 1 nmol of vasopressin, followed by those of the middle cerebral, the intracranial portion of the vertebral, and the anterior spinal arteries (approximately 130% that of control). The extracranial portion of the vertebral artery (109.8 +/- 4.8% that of control, n = 4) was less sensitive to 1 nmol of vasopressin. Pretreatment with an intracisternal injection of 10 mumol of NG-monomethyl L-arginine suppressed the vasodilator effect of vasopressin and substance P, whereas it did not affect the response to vasoactive intestinal peptide.
These results suggest that the arteries composing the circle of Willis at the base of the brain are more sensitive to nitric oxide release induced by vasopressin compared with other intracranial and extracranial arteries.
Major depression in stroke patients. A 3-year longitudinal study.
Authors: Aström M , Adolfsson R , Asplund K 
Published: June 2011

This prospective study was designed to examine the contributions of neurobiological, functional, and psychosocial factors to major depression after stroke. In addition, the prevalence and longitudinal course of major depression were studied.
Major depression, functional ability, and social network were assessed repeatedly for a period of 3 years in a population-based cohort of 80 patients with acute stroke (mean age, 73 years). Cerebral atrophy and brain lesion parameters were determined from computed tomographic scans performed acutely and after 3 years.
The prevalence of major depression was 25% at the acute stage and approximately the same at 3 months (31%). It decreased to 16% at 12 months, was 19% at 2 years, and increased to 29% at 3 years. The most important predictors of immediate major depression were left anterior brain lesion, dysphasia, and living alone. Dependence in activities of daily living was the most important predictor at 3 months. From 12 months on, the patient's having few social contacts outside the immediate family contributed most to depression, and at 3 years cerebral atrophy also contributed. At 1 year, 60% of the patients with early depression (0 to 3 months) had recovered; those not recovered at this follow-up had a high risk of development of chronic depression.
The study has provided evidence of a differentiation of factors likely to be implicated in the development of depression after stroke based or the period of time since the stroke event.
Do anger and aggression affect carotid atherosclerosis?
Authors: Matsumoto Y , Uyama O , Shimizu S , Michishita H , Mori R , Owada T , Sugita M 
Published: June 2011

Although a number of metabolic and psychosocial factors have been identified as coronary risk factors, no studies have evaluated the relation between personality and cerebrovascular disease. The purpose of the present study was to elucidate the relation between the characteristics of anger or aggression and the severity of carotid atherosclerosis on the basis of the findings of B-mode ultrasonography.
The Cornell Medical Index was used to measure anger in 34 patients with signs of atherosclerosis or at least one of four recognized risk factors for atherosclerosis (hypertension, hypercholesterolemia, diabetes mellitus, and cigarette smoking). The Rosenzweig Picture Frustration Study and Yatabe-Guilford Personality Test were used to evaluate aggression. High-resolution B-mode ultrasonography was performed, and the severity of carotid atherosclerosis was determined by plaque score. The occurrence of risk factors for carotid atherosclerosis was compared among the patients.
The correlation of plaque score with one item that endorses anger was r = .65 (P < .01) and with "extrapersistive" in aggression was r = .50 (P < .01). Multivariate analysis identified significant correlations between plaque score and age, hypercholesterolemia, and anger.
Our results suggest that anger and, perhaps, aggression may be risk factors for cerebrovascular disease.
Regional cerebral blood flow in chronic hypertension. A correlative study.
Authors: Nobili F , Rodriguez G , Marenco S , De Carli F , Gambaro M , Castello C , Pontremoli R , Rosadini G 
Published: June 2011

Cerebral hypoperfusion has occasionally been reported during essential hypertension. We explored regional cerebral blood flow in a large series of neurologically asymptomatic hypertensive patients to determine relations among cerebral blood flow, concomitant main vascular risk factors, and the most common signs of end-organ damage.
Regional cerebral blood flow was measured by the 133Xe inhalation method in 101 hypertensive patients without clinically apparent central nervous system involvement, including 39 mild to moderate untreated and 62 mild to severe treated patients.
Compared with age- and sex-matched normal control subjects, cerebral blood flow was significantly reduced in untreated hypertensive patients (P < .01) and to a lesser extent in treated patients (P = .047). Both regional and global cerebral blood flow reductions were observed in approximately one third of patients in both groups. Analysis of variance failed to show significant correlations between cerebral blood flow and total cholesterol concentration, mean arterial blood pressure, duration of disease, or the presence of retinopathy or left ventricular hypertrophy. In the treated group, the quality of control of hypertension significantly influenced both global cerebral blood flow (P = .007) and cerebrovascular resistance (P < .0001).
Focal or diffuse cerebral hypoperfusion is present even in neurologically asymptomatic hypertensive patients, especially when untreated; good control of blood pressure may preserve cerebral perfusion and reduce cerebrovascular resistance. Regional cerebral blood flow examination represents a relatively simple and low-cost technique to explore the perfusional condition of the brain, one of the main target organs of hypertensive disease.
Cerebral blood flow velocity and systemic vascular resistance after acute reduction of low-density lipoprotein in familial hypercholesterolemia.
Authors: Rubba P , Faccenda F , Di Somma S , Gnasso A , Scarpato N , Iannuzzi A , Nappi G , Postiglione A , De Divitiis O , Mancini M 
Published: June 2011

Low-density lipoprotein apheresis is currently used for the treatment of familial hypercholesterolemia, an inherited disorder of metabolism associated with premature development of cardiovascular disease. We wanted to evaluate cerebral blood flow velocity, cardiac output, and systemic vascular resistance in patients with familial hypercholesterolemia before and after low-density lipoprotein apheresis.
Ten patients (age range, 14 to 46 years; 4 males, 6 females) with familial hypercholesterolemia (8 homozygotes, 2 heterozygotes) and 10 healthy control subjects of comparable age and sex distribution participated in the study. Low-density lipoprotein apheresis by dextran sulfate was performed in 8 patients (7 homozygotes, 1 heterozygote). Six patients (4 homozygotes, 2 heterozygotes) underwent a procedure of extracorporeal erythrocyte filtration with the same extracorporeal volume as for low-density lipoprotein apheresis, but with the exclusion of the passage of plasma through the dextran sulfate column. Cerebral blood flow velocity (transcranial Doppler), cardiac output, and systemic vascular resistance (electric bioimpedance cardiography) were determined by noninvasive techniques before and 1 day and 7 days after low-density lipoprotein apheresis or extracorporeal erythrocyte filtration. Plasma and blood viscosities were measured at the same time.
Before apheresis, mean and diastolic cerebral flow velocities were abnormally low in hypercholesterolemic patients (P < .01 and P < .02 vs healthy control subjects, respectively). After apheresis, low-density lipoprotein cholesterol was lowered by 40% to 60% from baseline, and cerebral blood flow velocities (mean, systolic, and diastolic velocities) were increased (P < .01). Cardiac output, systemic vascular resistance, and viscosity values were not significantly modified. Extracorporeal erythrocyte filtration (without passage of plasma through the dextran sulfate column) did not modify serum lipids, hemodynamic parameters, or viscosity values.
Low-density lipoprotein apheresis produces potentially useful hemodynamic effects. They are not adequately explained by changes in blood viscosity alone and might reflect a restoration of endothelium-mediated vasodilation, which is inhibited by high concentrations of low-density lipoprotein.
Brain stem infarction and diaschisis. A SPECT cerebral perfusion study.
Authors: Fazekas F , Payer F , Valetitsch H , Schmidt R , Flooh E 
Published: June 2011

We studied six patients suffering from pure, unilateral brain stem infarction to explore the association of remote cerebral and cerebellar blood flow changes with damage at different sites of this region of the brain.
We used single-photon emission computed tomography and [123I]iodoamphetamine to measure regional differences in tracer uptake. Qualitative image analysis and calculated asymmetry indexes were correlated to the location of the infarcted area on magnetic resonance imaging and to the patients' clinical findings.
Significant perfusion asymmetries were noted in the two patients with infarction in the upper pons but not in those with lesions below this level. They comprised a contralateral cerebellar and ipsilateral supratentorial hypoactivity that was most marked in the frontoparietal cortex. There was no clear relation between the patterns of cerebral or cerebellar tracer uptake and specific neurological findings.
Remote perfusion changes after pure brain stem infarction may be seen both infratentorially and supratentorially and depend on the lesion site rather than on the neurological deficit. In this context, our study confirmed damage to the corticopontocerebellar pathways as the key event in the genesis of a crossed cerebellar diaschisis. The exact mechanisms causing ipsilateral cerebral hemispheric diaschisis await further clarification.
Regional cerebral blood flow measured with N-isopropyl-p-[123I]iodoamphetamine and its redistribution in ischemic cerebrovascular disease.
Authors: Odano I , Tsuchiya T , Nishihara M , Sakai K , Abe H , Tanaka R 
Published: June 2011

The relation between the redistribution phenomenon and regional cerebral blood flow and its clinical significance were investigated in stroke patients.
Single-photon emission computed tomography studies using N-isopropyl-p-[123I]iodoamphetamine were performed on 16 patients (26 to 77 years old) with chronic infarction and 10 age-matched normal control subjects. Regional cerebral blood flow was quantitatively measured by a microsphere model, and the redistribution on delayed images was analyzed in ischemic lesions.
Supratentorial mean cerebral blood flow and the ratio of gray matter to white matter in normal subjects were 52.7 +/- 5.0 mL/100 g per minute and 2.34, respectively. Low-activity areas of ischemic lesions on early images were classified into two abnormal zones, an infarct area and a peri-infarct area. These regions were characterized by regional blood flow averaging 9 to 20 mL/100 g per minute and 22 to 41 mL/100 g per minute, respectively. Redistribution, which was minimally present in the infarct area, was markedly enhanced in the peri-infarct area. After bypass surgery, we observed a significant increase of blood flow (+22%) in the peri-infarct area.
The data indicate that the redistribution phenomenon depends on the maintenance of a minimal blood flow that would sustain cellular function and that this phenomenon is useful to evaluate bypass surgery in patients with chronic infarction.
Value of single-photon emission-computed tomography in acute stroke therapeutic trials.
Authors: Hanson S K , Grotta J C , Rhoades H , Tran H D , Lamki L M , Barron B J , Taylor W J 
Published: June 2011

New therapeutic interventions for acute ischemic stroke are aimed at improving cerebral blood flow in the first 3 to 6 hours after symptom onset. Single-photon emission-computed tomography (SPECT) performed in the setting of clinical therapeutic trials may give us a better understanding of the physiological response to new forms of treatment and could impact acute management decisions.
We prospectively studied 15 patients with hemispheric ischemic stroke with SPECT within 6 hours of symptom onset and again at 24 hours. The ischemic defect was assessed in a semiquantitative manner that used computer-generated regions of interest (SPECT graded scale). This measure was correlated with clinical presentation (National Institutes of Health [NIH] Stroke Scale), initial clinical course (change in NIH Stroke Scale), long-term outcome (Barthel Index at 3 months), and complications of cerebral hemorrhage and edema.
The severity of the SPECT graded scale on the admission scan correlated with the severity of neurological deficit (admission NIH Stroke Scale) (P < .05) and was positively associated with poor long-term outcome as measured with the Barthel Index (P < .001) and the complications of cerebral hemorrhage and massive cerebral edema (P < .005). In fact, there was a threshold value for the SPECT graded scale above which all patients suffered poor long-term outcome and the complications of cerebral hemorrhage and edema.
The measurement of an ischemic defect using SPECT is a valid assessment of hemispheric stroke severity in the hyperacute setting and may be useful for selecting or stratifying patients in clinical therapeutic trials.
Pathogenesis of subcortical hyperintense lesions on magnetic resonance imaging of the brain. Observations in patients undergoing controlled therapeutic internal carotid artery occlusion.
Authors: Awad I A , Masaryk T , Magdinec M 
Published: June 2011

Factors associated with the pathogenesis of subcortical hyperintense lesions on magnetic resonance imaging of the brain are not known. We describe four cases of de novo genesis of subcortical hyperintense lesions in patients undergoing controlled therapeutic internal carotid artery occlusion, and we speculate on associated pathophysiological mechanisms.
Twelve consecutive patients underwent controlled therapeutic internal carotid artery occlusion for symptomatic giant cerebral aneurysm using the detachable balloon technique under full anticoagulation. Preocclusion (within 2 weeks) and postocclusion (within 6 weeks) magnetic resonance imaging of the brain was performed in eight cases and evaluated for preexisting and new appearance of subcortical hyperintense lesions.
There were four instances of de novo genesis of subcortical hyperintense lesions after carotid occlusion. New subcortical hyperintense lesions were ipsilateral to carotid occlusion in every instance and in two cases were associated with ipsilateral hemispheric ischemic symptoms despite anticoagulant therapy. In one instance, there were transient hemispheric symptoms without the appearance of new subcortical hyperintense lesions. Age, vascular risk factors, and preexisting subcortical hyperintense lesions did not appear to predispose patients to de novo genesis of new hyperintensities.
This is the first documentation of de novo genesis of subcortical hyperintense lesions in a controlled setting of hemodynamic ischemic insult. Symptomatic and asymptomatic lesions can be detected in this setting. Anticoagulation does not appear to provide protection from this phenomenon. Careful prospective studies are required to further evaluate risk factors and possible clinical consequences associated with the genesis of new subcortical hyperintense lesions.