bluuebunny/crossref_metadata_2025_split huggingface dataset:
Decrease in cerebral blood flow with blood pressure reductions in patients with chronic stroke.
Authors: Mori S , Sadoshima S , Fujii K , Ibayashi S , Iino K , Fujishima M 
Published: June 2011

Possible effects of changes in blood pressure on the cerebral circulation were studied in patients with chronic stroke and age-matched nonstroke control subjects at 28 +/- 10 months (mean +/- SD) (range, 18 to 54 months) and 27 +/- 6 months (range, 19 to 44 months), respectively, after the first measurement.
Cerebral blood flow was measured by the 133Xe inhalation method in 55 patients (mean +/- SD age, 62 +/- 11 years; 39 with brain infarction and 16 with hemorrhage) and 10 control subjects (mean +/- SD age, 61 +/- 9 years). Correlations between changes in cerebral blood flow and blood pressure were evaluated.
Among brain infarctions, average cerebral blood flow did not change from the first study; however, changes in cerebral blood flow in each individual were closely related to changes in systolic and mean arterial blood pressures (P < .01 and P < .05, respectively). Of these, in 10 patients with cerebral blood flow decreased more than 15% from the initial levels, systolic and mean arterial blood pressures decreased by 25 +/- 32 mm Hg and 16 +/- 14 mm Hg (P < .05 and P < .005, respectively). In contrast, in 29 patients with unchanged or increased cerebral blood flow, changes in systolic (0 +/- 19 or -2 +/- 12 mm Hg, respectively) and mean arterial blood pressures (3 +/- 22 or -1 +/- 11 mm Hg, respectively) were not significant, and their systolic blood pressure levels were maintained above 110 mm Hg.
Blood pressure importantly correlates with cerebral circulatory changes among patients with chronic brain infarction. Early detection of cerebral hemodynamic changes should be useful for determining the most favorable levels of blood pressure and for selecting appropriate therapy.
Angiotensin II administration improves cerebral blood flow in cardiopulmonary arrest in swine.
Authors: Little C M , Brown C G 
Published: June 2011

Cerebral blood flow during cardiopulmonary resuscitation is inadequate to meet cerebral metabolic demand. Adrenergic agonists improve cerebral blood flow, but clinical trials of increased doses in adults have not shown improved outcome from cardiac arrest. This may be due to adverse beta-agonist-mediated effects. The purpose of this study was to determine the effect of angiotensin II, a potent nonadrenergic vasopressor, on cerebral blood flow in cardiac arrest.
Eleven immature swine were anesthetized and instrumented for regional blood flow measurements with radiolabeled microspheres. A sagittal sinus catheter was placed for blood gas determination. A blood flow measurement was performed in normal sinus rhythm and ventricular fibrillation induced. After 10 minutes of ventricular fibrillation, cardiopulmonary resuscitation was begun and a blood flow measurement performed. Angiotensin II at a dose of 50 micrograms/kg was administered intravenously at 13 minutes of ventricular fibrillation. A blood flow measurement was performed and defibrillation attempted. A fourth blood flow measurement was obtained if return of spontaneous circulation occurred.
Total cerebral blood flow was 46.4 mL/min per 100 g in normal sinus rhythm. This fell to 6.9 mL/min per 100 g with cardiopulmonary resuscitation alone and rose to 30.8 mL/min per 100 g after the administration of angiotensin II. The improvement following angiotensin II was statistically different (P = .002). Cerebral blood flow further rose in the animals that had return of spontaneous circulation to 73.9 mL/min per 100 g.
Angiotensin II in a dose of 50 micrograms/kg significantly improves cerebral blood flow in this model of cardiac arrest.
Combination therapy protects ischemic brain in rats. A glutamate antagonist plus a gamma-aminobutyric acid agonist.
Authors: Lyden P D , Lonzo L 
Published: June 2011

The excitotoxic effects of glutamate can be blocked almost completely with gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, in cell culture, tissue slices, and in some animal models. After stroke in rats, we showed previously that an agonist of GABA, muscimol, was as neuroprotective as MK-801, an antagonist of glutamate. To obtain further neuroprotection and to avoid the side effects associated with high doses of MK-801, we wanted to assess the efficacy of the two agents in combination.
Treatment was administered 5 minutes after embolic cerebral ischemia in Sprague-Dawley rats. The subjects were rated using a neurological evaluation 48 hours later. Visual-spatial learning was measured 8 to 10 weeks after stroke, after which we measured the volume of each cerebral hemisphere and several large cerebral compartments. Treatment groups included saline (n = 27), MK-801 1.0 mg/kg (n = 23), muscimol 1.0 mg/kg (n = 17), and both agents together using a dose of 0.5 mg/kg each (n = 25).
A probit analysis of the neurological ratings revealed a protective effect of muscimol used alone (MK-801 potency ratio, 2.0; P = NS; muscimol potency ratio, 4.0; P < .05) and a protective effect of the combination (potency ratio, 5.0; P < .05). Focal ischemia caused a moderate to severe delay in the acquisition of visual-spatial information, which was completely eliminated by the combination treatment but only partially ameliorated with MK-801 or muscimol alone. Ischemia reduced the cerebral hemisphere volume from 0.42 mm3 to 0.34 mm3 (P < .0001), the volume density of cortex from 22% to 17% of total cerebral volume (P < .01), and that of hippocampus from 4.3% to 3.0% (P < .05). Only the combination was neuroprotective, as measured by the ratio of the lesioned to the contralateral hemisphere volume (P = .013). The combination treatment and MK-801 protected the hemisphere volume, the cortex, and the hippocampus and reduced the size of visible infarction.
Combination therapy, using a glutamate antagonist and a GABA-A agonist, appeared to protect the brain and ameliorate a defect in learning behavior after stroke. The combination may have been more effective than either agent used alone, although further study of higher doses is needed.
Silent infarction in acute stroke patients. Prevalence, localization, risk factors, and clinical significance: the Copenhagen Stroke Study.
Authors: Jørgensen H S , Nakayama H , Raaschou H O , Gam J , Olsen T S 
Published: June 2011

Our objective was to study age-specific prevalence, computed tomographic (CT) characteristics, risk factors, and the prognostic influence on stroke outcome of silent infarction in acute stroke patients.
The study was prospective and community-based and included 801 acute stroke patients, of whom 587 had first-ever stroke. A CT scan was performed in 500 (85%) of the 587 patients with first-ever stroke. CT was reviewed blindly, and infarcts were classified according to patient history as silent or symptomatic. Patients were evaluated initially with the Mini-Mental State Examination (MMSE) and weekly with both the Scandinavian Stroke Scale (SSS) and the Barthel Index (BI) from the onset of stroke to completion of rehabilitation. CT characteristics, risk factors, and stroke outcome were compared in stroke patients with and without silent infarction.
The prevalence of silent infarction in patients with first-ever stroke and recurrent strokes was similar, at 29% (group aged 0 to 54 years, 16%; 55 to 64 years, 22%; 65 to 74 years, 30%; 75 years or older, 33%). Silent infarcts were small and subcortical. Independent risk factors were increasing age (odds ratio [OR], 1.95 per 25 years; confidence interval [CI], 1.19 to 3.15), hypertension (OR, 1.75; CI, 1.13 to 2.70), claudication (OR, 1.74; CI, 1.01 to 3.00), and male sex (OR, 1.72; CI, 1.12 to 2.64); other stroke risk factors such as atrial fibrillation and former transient ischemic attack were not independent risk factors. Patients with and without silent infarction did not differ in frequency of prestroke home care (P = .2). MMSE (P = .56), initial BI (P = .62) and SSS score (P = .08), BI (P = .85) and SSS score (P = .75) after completion of rehabilitation, or in the speed of recovery (P = .85). Length of hospital stay, mortality rate, and discharge rate to nursing home also did not differ between the two groups.
This community-based study shows that silent infarction in stroke patients is more related to certain stroke risk factors than others and that silent infarction does not seem to influence the prognosis of stroke.
Dementia after stroke is a predictor of long-term survival.
Authors: Tatemichi T K , Paik M , Bagiella E , Desmond D W , Pirro M , Hanzawa L K 
Published: June 2011

The aim of this study was to determine whether dementia after stroke adversely influences long-term survival.
Subjects were 251 patients > or = 60 years of age with ischemic stroke who were given neurological, neuropsychological, and functional examinations 3 months after hospitalization and were followed up prospectively. Using criteria modified from the Diagnostic and Statistical Manual of Mental Disorders-III-R, dementia was found in 66 (26.3%) patients at the 3-month baseline examination. Life-table methods were used to estimate mortality rates in the groups with and without dementia after 1 to 5 years of follow-up, Kaplan-Meier curves to estimate the cumulative proportion surviving with and without dementia, and Cox proportional-hazards analysis to compute the relative risk of mortality associated with dementia at baseline, after adjusting for other potential predictors of stroke mortality.
The mortality rate was 19.8 deaths per 100 person-years with dementia compared with 6.9 deaths per 100 person-years without dementia. The cumulative proportion surviving after a median follow-up of 58.6 months was 38.9 +/- 0.08% for those with dementia and 74.5 +/- 0.04% for those without dementia. The relative risk associated with dementia was 3.11 (95% confidence interval, 1.79 to 5.41) after adjusting for the effects of demographic factors, cardiac disease, severity of stroke (Barthel Index), stroke type (lacunar versus nonlacunar), and recurrent stroke (examined as a time-dependent variable). When the Mini-Mental State Examination score at baseline was examined instead of the diagnosis of dementia, the results of the model were similar.
Our study is the first to demonstrate that dementia or cognitive impairment adversely influences long-term survival after stroke, even after adjusting for other commonly accepted predictors of stroke mortality. Impairment in intellectual function after stroke, independent of physical disability, has a significant impact on prognosis. Both cognitive and physical functions should be assessed in clinical studies of stroke outcome.
Code stroke. An attempt to shorten inhospital therapeutic delays.
Authors: Gomez C R , Malkoff M D , Sauer C M , Tulyapronchote R , Burch C M , Banet G A 
Published: June 2011

Significant delays often occur during the treatment of patients with acute stroke. Some of those delays occur in the hospital. We attempted to shorten inhospital treatment intervals by creating a rapid-response system, similar to that available for cardiac arrest, that would allow the stroke team to be available within a few minutes to care for stroke victims.
We connected all beepers (pocket pagers) of stroke team members to a common access number and instructed the emergency staff to activate that number immediately upon arrival of a stroke victim. We monitored the response time and treatment interval for patients who were treated after this system was activated (Code Stroke patients) during the first 3 months of its availability and compared the results to those of patients seen for similar reasons during the study period but without the use of Code Stroke (control patients).
A total of 12 Code Stroke patients were available for analysis, representing 12% of all patients (n = 98) seen in the emergency department for ischemic stroke during the study period. The remaining 86 patients constituted the control group. The mean time to evaluation of a Code Stroke patient by a stroke team member was 4.8 minutes (range, 2 to 7 minutes), and the mean time to treatment institution was 30 minutes (range, 10 to 120 minutes). There were significant differences between the consultation intervals in the two groups (P < .05). There was only a trend of a difference between treatment institution intervals (P = .06).
It is possible to shorten inhospital treatment delays by instituting rapid-response systems within individual institutions.
Pure dysarthria, isolated facial paresis, or dysarthria-facial paresis syndrome.
Authors: Kim J S 
Published: June 2011

Pure dysarthria, isolated supranuclear facial paresis, and their combination without somatic motor dysfunction are rarely encountered clinical syndromes and have not yet been clearly characterized.
Thirteen patients (9 men, 4 women; aged 33 to 72 [mean, 56] years) with unilateral strokes who developed dysarthria with or without facial paresis but without somatic motor dysfunction were reviewed in addition to case reports from previous literature.
Computed tomographic scan and/or magnetic resonance imaging showed infarcts on the corona radiata in 4 patients, basal ganglia abutting the internal capsule in 3, basal ganglia-corona radiata in 1, pontine base in 3, and cortical-subcortical bulbar motor area in 2. The dysarthria and facial paresis were usually mild and transient, and either one was likely to be unnoticed.
It is suggested that pure dysarthria or isolated facial paresis syndrome be considered as an extreme continuum of dysarthria-facial paresis syndrome, which is likely to be a variant of dysarthria-clumsy hand syndrome.
Preoperative noninvasive coronary risk stratification in candidates for carotid endarterectomy.
Authors: Urbinati S , Di Pasquale G , Andreoli A , Lusa A M , Carini G , Grazi P , Labanti G , Passarelli P , Corbelli C , Pinelli G 
Published: June 2011

Patients with symptomatic carotid stenosis who are candidates for carotid endarterectomy are at high short- and long-term risk of coronary events. To stratify patients at different risk of coronary events we investigated the usefulness of a noninvasive preoperative cardiological workup.
We studied 172 consecutive patients admitted to the Neurosurgical Department for symptomatic high-grade (70% to 99%) carotid stenosis (age, 42 to 74 years; mean, 57.8 years). Patients without history of coronary artery disease (CAD) and able to exercise were submitted to exercise electrocardiographic testing (EET) and, if abnormal, to exercise thallium myocardial imaging (TMI). Patients were classified into four groups: group 1, patients without CAD: no history of CAD, normal EET, or normal TMI in the presence of indeterminant EET (n = 93, 54%); group 2, patients with silent CAD: no history of CAD and concordant abnormal EET and TMI (n = 28, 16%); group 3, patients unable to exercise: no history of CAD and inability to perform adequate EET because of previous stroke or claudication (n = 29, 17%); and group 4, patients with known CAD: history of angina or myocardial infarction (MI) (n = 22; 13%).
The four groups were comparable in regard to age, sex, and computed tomographic scan of the brain. The prevalence of stroke was higher in patients unable to exercise; hypercholesterolemia was more frequent in patients with known CAD. During the perioperative period (< or = 30 days after carotid endarterectomy), coronary events occurred in 3 patients (2%): fatal MI in 2 patients in group 4 and 1 patient in group 3. One hundred percent of patients were followed up for 6.2 years. Coronary events occurred in 23 of the 168 patients discharged from the hospital (13.7%); these were fatal in 11 (6.5%): 3 patients of group 1 (3%; sudden death in 2, fatal MI in 1), 8 patients of group 2 (29%; fatal MI in 5, unstable angina in 3), 8 patients of group 3 (28%; fatal MI in 4, nonfatal MI in 4), and 4 patients of group 4 (18%; fatal MI in 2, sudden death in 1, unstable angina in 1). Kaplan-Meier estimated curves of survival free from fatal and nonfatal coronary events were 97%, 51%, 49%, and 59%, respectively (P < .001, group 1 versus groups 2 and 3; P < .01, group 1 versus group 4).
Among patients undergoing carotid endarterectomy, coronary events occurred twice as often as cerebral recurrences. A preoperative noninvasive cardiac investigation, including EET, can adequately identify groups of patients with diverse short- and long-term prognoses. In addition to patients with known CAD, those with silent CAD or who are unable to exercise represent, without the need of further investigation, groups at high risk of coronary events in long-term follow-up.
Evaluation of delayed treatment of focal cerebral ischemia with three selective kappa-opioid agonists in cats.
Authors: Baskin D S , Widmayer M A , Browning J L , Heizer M L , Schmidt W K 
Published: June 2011

The purpose of this study was to determine the therapeutic efficacy of three kappa-opioid agonists used for delayed treatment of experimental focal cerebral ischemia.
Forty halothane-anesthetized cats underwent permanent occlusion of the right intracranial internal carotid, middle cerebral, and anterior cerebral arteries via a transorbital, microsurgical approach. Six hours after occlusion, animals received a blinded bolus injection, and a subcutaneous osmotic pump was implanted to provide continuous release for 7 days. The injection and pump contained either saline or one of three kappa-agonists: dynorphin (1-13), U-50,488, or DuP E3800. Survival, neurological function, tissue damage, and brain weight were assessed.
As a group, kappa-agonist-treated animals had higher survival (P < .02), less tissue damage (P < .02), and lower brain weight (P < .05) than saline controls. U-50,488 more effectively improved survival (P < .03) than dynorphin (P < .07) or E3800 (P < .07). Each of the three kappa compounds improved tissue damage (dynorphin, P < .02; U-50,488, P < .05; E3800, P < .05). Greater improvement in neurological function was seen after treatment with dynorphin (P < .05) than with U-50,488 (P < .6) or E3800 (P < .7). The only significant reduction in brain weight was seen after dynorphin treatment (P < .01).
Compounds that act at the kappa subclass of opiate receptors are effective in increasing survival, improving neurological function, and decreasing tissue damage and edema in a cat model of focal cerebral ischemia. The current study provides support for the benefits of treatment of acute cerebrovascular ischemia with kappa-opioid agonists. The agents may prove to be of superior clinical utility because of efficacy even when administered 6 hours after the onset of stroke.
Calcitonin gene-related peptide reduces brain injury in a rat model of focal cerebral ischemia.
Authors: Holland J P , Sydserff S G , Taylor W A , Bell B A 
Published: June 2011

Calcitonin gene-related peptide is an endogenous vasodilating neuropeptide with a dense concentration in the trigeminocerebrovascular system. It is hypothesized that depletion of this peptide contributes to delayed cerebral ischemia after subarachnoid hemorrhage and that an exogenous supply of calcitonin gene-related peptide will augment ischemic cerebral blood flow and reduce neuronal injury.
In this study we have investigated the effect of an intravenous infusion of calcitonin gene-related peptide (100 ng/kg per minute), started 1 hour before and continued throughout 4 hours of focal cerebral ischemia, on cerebral blood flow and the volume of brain injury in a rat model of middle cerebral artery occlusion.
Calcitonin gene-related peptide produces a significant improvement in ischemic cerebral blood flow (32 +/- 2 compared with 13 +/- 2 mL/100 g per minute in the controls; t = 6.92, P < .0001) with a concomitant reduction in the volume of ischemic brain injury (102 +/- 22 compared with 234 +/- 19 mm3; t = 4.47, P < .001).
These findings lend support for the potential use of this peptide in the prophylactic treatment of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
Dihydropyridine ligand binding decreases earlier in adolescent than in infant swine after global cerebral ischemia.
Authors: Hoehner P J , Kirsch J R , Helfaer M A , Ganunis T F , Murphy M T , Traystman R J 
Published: June 2011

Voltage-dependent calcium channels (VDCCs) are thought to play a major role in the alteration of calcium homeostasis during ischemia. Tissue functional state as well as responsiveness to therapy with calcium channel blockers may be a function of regional changes in the density of VDCCs. This study determined whether VDCCs are altered by global ischemia in infant and adolescent swine.
We employed the radioligand 3HPN200-110 to quantify the binding characteristics of VDCCs in cerebral cortex, caudate, and hippocampus by equilibrium binding analysis. Adolescent and infant pigs underwent 3, 5, 10, and 20 minutes of global cerebral ischemia without reperfusion by ligation of the brachiocephalic and left subclavian arteries combined with hypotension to a mean arterial blood pressure of 50 mm Hg. Brain cortex, hippocampus, and caudate samples were taken during ischemia and frozen immediately in liquid nitrogen, and crude synaptosomal membranes were isolated by differential centrifugation/filtration. 3HPN200-110 equilibrium binding assays were performed in the presence or absence of 1.0 mumol/L unlabeled nitrendipine to determine total and nonspecific binding.
Infant cortex maximal binding (Bmax) increased to 176% of control after 5 minutes of global cerebral ischemia and remained significantly elevated (172% of control) after 10 minutes before falling to near control levels by 20 minutes. Adolescent cortex Bmax increased to 157% of control levels after 5 minutes but did not remain elevated, falling to 131% of control by 10 minutes and near control by 20 minutes. Infant caudate and hippocampus binding were significantly elevated after 10 (124% and 149% of control, respectively) and 20 (115% and 120% of control, respectively) minutes of ischemia. Adolescent caudate and hippocampus binding was either not significantly different from control levels (hippocampus at 10 minutes) or less than control after 10 and 20 minutes of global cerebral ischemia. The decrease in binding following the initial upregulation, which appeared earlier in the adolescent than the infant pigs, may indicate decreased tolerance to ischemia in the adolescent.
The binding of 3HPN200-110 in brain is altered during 20 minutes of global cerebral ischemia, and these changes are region- and age-dependent.