bluuebunny/crossref_metadata_2025_split huggingface dataset:
Progressive intracranial occlusive disease associated with deficiency of protein S. Report of two cases.
Authors: Barinagarrementeria F , Cantú Brito C , Izaguirre R , de la Peña A 
Published: June 2011

Deficiency of the free fraction of protein S has been associated with arterial or venous stroke. The pathogenesis of vascular occlusion in patients with protein S deficiency is not known. We present two cases of cerebral infarction and deficiency of protein S in which the subjects had progressive intracranial occlusions.
A 16-year-old girl was admitted because of left brain stem infarction and protein S deficiency. Cerebral angiography disclosed stenosis of the right intracranial vertebral artery and occlusion of the left posterior cerebral artery. A second angiogram performed 18 months later disclosed occlusion of the right vertebral intracranial artery. In the second case, a 17-year-old girl was admitted because of left hemispheric cerebral infarction and protein S deficiency. Cerebral angiography showed stenosis of the left anterior cerebral artery, left supraclinoid internal artery, and left middle cerebral artery. A second cerebral angiogram performed 5 months later disclosed occlusion of the left anterior cerebral artery and poor hemispheric perfusion through the left middle cerebral artery.
Based on our cases, we postulate that some patients with prothrombotic states may develop progressive intracranial arterial occlusions, possibly secondary to a permanent thrombogenic stimulus. We suggest routinely searching for prothrombotic states in young patients with intracranial occlusion, especially if the occlusion is progressive and other causes are not obvious.
One-year reduction and longitudinal analysis of carotid intima-media thickness associated with colestipol/niacin therapy.
Authors: Mack W J , Selzer R H , Hodis H N , Erickson J K , Liu C R , Liu C H , Crawford D W , Blankenhorn D H 
Published: June 2011

The Cholesterol Lowering Atherosclerosis Study has reported significant reduction of coronary artery disease and of carotid arterial intima-media thickness (IMT) at 2 and 4 years with colestipol/niacin therapy. We now report on treatment effects on carotid IMT at 6 months and 1 year.
One hundred eighty-eight nonsmoking men, aged 40 to 59 years, with prior coronary artery bypass graft surgery were randomized to colestipol/niacin plus diet therapy or placebo plus diet therapy. Computerized image processing of carotid ultrasound films was used to measure IMT in the right common carotid artery. Treatment group comparisons were made at 6 months and 1 year (46 and 33 subjects, respectively, with baseline and 6-month or 1-year ultrasound measures). The time course of the treatment effect on carotid IMT was estimated using the complete sample of 78 subjects with baseline and on-trial data.
No significant treatment group differences on carotid IMT were found at 6 months. At 1 year, the treated group showed significant reduction of carotid IMT (P = .01 between groups). The placebo group showed continuing progression of IMT during the 4-year study period (estimated progression rate, 0.018 mm/y). The treated group showed reduction of IMT during the first 3 years and a plateau during the remainder of the study.
Reduction of carotid IMT was found with aggressive lipid-lowering therapy. Ultrasound measures of IMT offer a noninvasive and precise measure of early carotid atherosclerosis that will decrease sample size requirements, potentially decrease dropout rates, and widen the study population of antiatherosclerotic clinical trials.
Predicting length of stay, functional outcome, and aftercare in the rehabilitation of stroke patients. The dominant role of higher-order cognition.
Authors: Galski T , Bruno R L , Zorowitz R , Walker J 
Published: June 2011

Research in recent years has revealed factors that are important predictors of physical and functional rehabilitation: demographic variables, visual and perceptual impairments, and psychological and cognitive factors. However, there is a remaining uncertainty about prediction of outcome and a need to clinically apply research findings. This study was designed to identify the relative importance of medical, functional, demographic, and cognitive factors in predicting length of stay in rehabilitation, functional outcome, and recommendations for postdischarge continuation of services.
The influence of these factors was determined by comparing diagnostic, medical, demographic, functional, and neuropsychological information that was retrospectively obtained by reviewing the records of 86 patients admitted for comprehensive rehabilitation due to stroke (n = 36) or orthopedic injury (n = 50). Multiple linear regression with statistical adjustment to control for overprediction of variance was used to predict outcomes.
The study revealed the primary importance of higher-order cognitive impairments (comprehension, judgment, short-term verbal memory, and abstract thinking) in extending length of stay and increasing referrals for outpatient therapies and home services after discharge for the cerebrovascular accident patients in comparison with orthopedic cohorts.
The need is discussed for early, comprehensive assessment of deficits in cognition that affect a stroke survivor's ability to participate in a rehabilitation program and remediation that facilitates functional improvement by building on residuals of impaired abilities or teaching compensatory behaviors.
Relation of laboratory and clinical variables to the grade of carotid atherosclerosis.
Authors: Szirmai I G , Kamondi A , Magyar H , Juhász C 
Published: June 2011

To clarify diagnostic entities in ischemic stroke we analyzed the relation between the severity of carotid atherosclerosis, coagulation parameters, lipoproteins, neurological status, and risk factors in 232 patients.
Duplex ultrasonography, computed tomography scan, and laboratory investigations were performed between the third and tenth days after stroke. Based on carotid ultrasound scores, we categorized the patients into four groups (A, B, C, and D) according to severity of atherosclerosis. Corresponding laboratory variables and clinical data were statistically analyzed.
Ultrasound scores were significantly (P < .05) higher in the male (n = 126) versus female (n = 106) patients. The hematocrit was significantly higher and thrombin time was significantly shorter in the male group compared with the female group. Severe atherosclerosis (group C) and occlusion (group D) of the internal carotid artery was associated with smoking (C = 56%; D = 78%), hypertension (C = 43%; D = 35%), claudication (C = 13%; D = 5%), and antecedent myocardial infarction (C = 9%; D = 13%). There was no statistical correlation between ultrasound scores and the patients' neurological condition. Cholesterol and plasma fibrinogen levels were significantly higher and high-density lipoprotein cholesterol was significantly lower in groups with severe atherosclerosis compared with patients with slight intimal damage. The presence of multiple plaques or thrombosis of the internal carotid artery was concordant with the prevalence of single cerebral infarcts.
Severity of carotid atherosclerosis corresponded well with the following factors: age, smoking, and low concentration of high-density lipoprotein cholesterol. Elevation of plasma fibrinogen combined with a loss of high-density lipoprotein cholesterol is strongly associated with severe atherosclerosis and results in brain infarction.
A model for management of patients with stroke during the acute phase. Outcome and economic implications.
Authors: Odderson I R , McKenna B S 
Published: June 2011

The purpose of the study was to develop a clinical pathway for patients with nonhemorrhagic stroke during the acute hospital phase to improve the quality of care and reduce costs.
The pathway included standard admission orders and a swallow screen on day 1 of hospitalization. Physical therapy, occupational therapy, speech therapy, and social worker assessments were done on day 2. A physiatry consult was performed on day 3 if indicated, and by day 4 a discharge target date and disposition were addressed.
Outcomes for 121 patients during the first year of pathway implementation are reported. The average length of stay on the acute service decreased from 10.9 days to 7.3 days (P < .05), reducing the charges per patient by 14.6%. Complications in the form of urinary tract infections and aspiration pneumonia rates decreased by 63.2% (P < .05) and 38.7%, respectively.
We conclude that the implementation of a clinical pathway for patients with acute, nonhemorrhagic stroke resulted in a significant reduction in length of stay, charges, and complications while improving the quality of care.
Relationship of transcranial Doppler flow velocities and arteriovenous malformation feeding artery pressures.
Authors: Fleischer L H , Young W L , Pile-Spellman J , terPenning B , Kader A , Stein B M , Mohr J P 
Published: June 2011

Feeding mean arterial pressure immediately proximal to the nidus of arteriovenous malformations may influence the frequency of spontaneous intracerebral hemorrhage. This study assessed the usefulness of transcranial Doppler ultrasound velocities as a noninvasive estimate of feeding mean arterial pressure.
We studied 41 patients undergoing 73 staged treatments of arteriovenous malformations with endovascular embolization, surgery, or both. Before treatment during the awake state, transcranial Doppler mean and peak velocities were recorded in proximal Willisian vessels. During superselective angiography with the patient under conscious sedation or during surgery with the patient under general anesthesia, feeding mean arterial pressure was measured through a 1.5F transfemoral intracranial microcatheter or a 26-g needle by direct puncture. Measurement of insonated artery diameter was possible in 41 embolizations, and a flow velocity index (mL/min) and Reynolds' number were estimated.
Mean +/- SEM feeding mean arterial pressure was 38 +/- 2 mm Hg at a systemic mean arterial pressure of 77 +/- 2 mm Hg; mean velocity was 102 +/- 4 cm/s. There was an inverse correlation between feeding mean arterial pressure and parent artery mean velocity (y = -0.74x + 130, r = .35, P = .0025). The best correlation was for the first treatment in each patient (n = 27) using the highest peak velocity obtainable in a Willisian vessel ipsilateral to the arteriovenous malformation (y = -1.61x + 221, r = .62, P = .0005). Flow velocity index (775 +/- 106 mL/min) did not correlate with feeding mean arterial pressure, but there was a weak correlation with Reynolds' number (y = -12x + 1616, r = .27, P = .1283). Mean Reynolds' number was 1257 +/- 119.
Transcranial Doppler mean velocity is correlated with feeding mean arterial pressure but only weakly predictive. Considerations influencing the relation of distal feeding mean arterial pressure to proximal mean velocity might include the influence of other fistulae in the circuit between major inflow and outflow channels as well as turbulent flow at vascular branch points between point of insonation and the nidus, as suggested by Reynolds' number values of more than 400.
Clinical features, pathogenesis, and computed tomographic characteristics of internal watershed infarction.
Authors: Bladin C F , Chambers B R 
Published: June 2011

Infarction in the internal border-zone region has been described radiologically and pathologically. The aim of this study was to define the clinical and pathophysiological correlates of internal watershed infarction.
Eighteen consecutive stroke patients with evidence of internal watershed infarction on computed tomography (CT) were studied.
Two CT patterns were identified: 6 patients had confluent internal watershed infarction (CIWI), and 12 patients had partial internal watershed infarction (PIWI). Syncopal symptoms and/or documented hypotension were prominent in both groups. Patients with CIWI usually presented with stepwise onset of contralateral hemiplegia and recovered poorly; patients with PIWI usually had discrete episodes of brachiofacial sensorimotor deficit and good recovery. Both groups had evidence of cortical involvement as part of their clinical deficit. Severe carotid occlusive disease was seen in 10 patients, and 12 patients had evidence of transiently impaired cardiac output. Carotid disease (P < .001), cardiac disease (P < .01), and diabetes mellitus (P < .01) were more prevalent in patients with internal watershed infarction compared with our stroke population as a whole.
Distinguishing internal watershed infarction from lacunar and other subcortical infarctions is important because the different pathological mechanisms demand different therapeutic strategies.
A quantitative investigation of the variability of the major cerebral arterial territories.
Authors: van der Zwan A , Hillen B , Tulleken C A , Dujovny M 
Published: June 2011

We have previously reported that the topographic variability of the territories of the anterior, middle, and posterior cerebral arteries is much larger than is generally considered in the literature. In the current study, we quantitatively investigated the variability of the territorial distribution of the major cerebral arteries and analyzed its relation to the variability of the circle of Willis.
In 23 human brains, the volumes of the major cerebral territories were calculated and the diameters of the contributing arteries were measured and standardized for size.
The variability of the standardized territorial volumes proved to be considerably large and strongly correlated with the variability of the diameters of the arteries emanating from the circle of Willis. Furthermore, the relative vascular densities in the gray and white matter were determined. Taking these densities into account, an estimation of the relative peripheral resistance of the contributing arteries was made.
We hypothesize that the morphological variability of the cerebral vascular system is related to the peripheral resistance of the major cerebral arteries and, consequently, to flow patterns, both of which are hemodynamic factors. We suggest that hemodynamic factors predominantly determine the form and size of the cerebral vascular system.
The ultrastructure of photochemically induced thrombi with embolization in a rat model.
Authors: Futrell N , Riddle J M 
Published: June 2011

Photochemical techniques, currently used in stroke and cancer research, produce endothelial damage and thrombosis. To further characterize these thrombi and to determine whether they embolize, we studied the ultrastructure of photochemically damaged carotid arteries and small vessels distal to the irradiated carotid.
The right carotid artery of 9 Wistar rats was irradiated with a laser (632 nm, 200 mW/cm2, 15 minutes) after the injection of the photosensitizing dye Photofrin II, 12.5 mg/kg. There were 6 additional control rats: laser only, 2 rats; dye only, 2; carrier only (5% dextrose), 1; and normal, 1. The carotid artery and cerebral arterioles were studied using scanning and transmission electron microscopy.
Endothelial damage was present in all irradiated carotid arteries, and consisted of exposure of the subendothelium and the formation of a nonocclusive thrombus. Although most cerebral arterioles were normal, 32 of these vessels contained peripheral blood elements, with platelet or red blood cell aggregates present in 15. The endothelium adjacent to the aggregates was intact. A few scattered endothelial cells had been lost in the carotid artery of control animals (compatible with normal cell turnover), with a few platelets adhering to the exposed subendothelium.
Aggregates of blood cells and platelets in cerebral vessels in the absence of endothelial denudation verifies embolism as the mechanism for cerebral vascular occlusion in this experimental model. The possibility of embolization distal to the site of photochemical irradiation has implications for potential applications of photochemistry for cancer treatment and the ablation of vascular malformations and/or aneurysms.
The kinetics of lymphocyte subsets and macrophages in subarachnoid space after subarachnoid hemorrhage in rats.
Authors: Kubota T , Handa Y , Tsuchida A , Kaneko M , Kobayashi H , Kubota T 
Published: June 2011

Although it has been suggested that humoral immunity plays a role in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage, there has been no quantitative assay for cellular immunity. We studied the kinetics of immune cells in the subarachnoid space after subarachnoid hemorrhage in the rat.
One hundred fourteen Sprague-Dawley rats were used in this study. The animals were divided into two groups and injected with either autologous blood (0.3 mL) or saline into the major cistern. They were killed at the specified time: 10 minutes or 1, 2, 3, 5, or 7 days after subarachnoid hemorrhage. For immunohistochemical analysis, the rats' whole brains were frozen, and cryostat sections were prepared. For flow cytometric analysis of immune cell presence, their whole brains underwent enzymatic digestion.
Histopathologic study revealed pathological change of the arterial wall, and immunohistochemical study revealed the existence of macrophages and T cells in the subarachnoid space in animals with a survival time of 2 to 5 days after subarachnoid hemorrhage. A flow cytometric study revealed the peak of appearance of T cells and macrophages 2 days after subarachnoid hemorrhage. The helper-suppressor T cell ratio also reached a peak 2 days after subarachnoid hemorrhage.
A serial response of immunoreactive cells, which resembles that of the chronic allergic reaction observed in autoimmune diseases or delayed-type hypersensitivity, exists in the subarachnoid space after subarachnoid hemorrhage. The present results suggest that the initial response in cellular immunity, which is followed by humoral immunity and eicosanoid reactions, plays a role in eliciting the development of cerebral vasospasm.
The effect of nitric oxide synthase inhibition on infarct volume after reversible focal cerebral ischemia in conscious rats.
Authors: Kuluz J W , Prado R J , Dietrich W D , Schleien C L , Watson B D 
Published: June 2011

Previous in vitro and in vivo studies of the effects of nitric oxide synthase inhibition in the central nervous system have yielded conflicting results concerning the role of nitric oxide in the events that lead to ischemic injury. In this study, we tested the hypothesis that preischemic inhibition of nitric oxide synthase increases infarct volume after reversible focal cerebral ischemia in rats.
NG-nitro-L-arginine methyl ester hydrochloride 15 mg/kg IV or an equivalent volume of saline was administered to adult Wistar rats 15 minutes before middle cerebral artery occlusion by the intraluminal suture method. After 2 hours of ischemia, the suture was withdrawn, and rats were allowed to survive for 3 days. Areas of infarction in 10 hematoxylin-eosin-stained sections were measured and used to determine infarct volume.
Administration of NG-nitro-L-arginine methyl ester hydrochloride increased hemispheric infarct volume by 137% over control (60.9 +/- 30.5 to 144.3 +/- 19.6 mm3, P < .05; mean +/- SEM). Cortical and subcortical infarct volumes were increased by 176% (33.8 +/- 21.9 to 93.3 +/- 15.2 mm3, P < .05) and 103% (25.1 +/- 9.4 to 51.0 +/- 5.5 mm3, P < .03), respectively.
Nitric oxide synthase inhibition increases infarct volume and decreases the variability of the response to middle cerebral artery occlusion in Wistar rats, a strain that is normally resistant to focal cerebral ischemic injury owing to extensive collateralization. The mechanism of the deleterious effect of nitric oxide synthase inhibition likely involves a more severe degree of blood flow reduction during and after middle cerebral artery occlusion, primarily by preventing the vasodilatory response of collateral vessels to proximal middle cerebral artery occlusion. Maintenance of nitric oxide synthase activity during and after focal cerebral ischemia appears to minimize ischemic injury.
In vivo mapping of brain benzodiazepine receptor changes by positron emission tomography after focal ischemia in the anesthetized baboon.
Authors: Sette G , Baron J C , Young A R , Miyazawa H , Tillet I , Barré L , Travère J M , Derlon J M , MacKenzie E T 
Published: June 2011

Recent reports have shown an increase in specific binding (in vitro) of [3H]PK 11195 to peripheral-type benzodiazepine receptors in both experimental animals and humans, reflecting a glial/macrophagic reaction within and around focal ischemic insults. We have evaluated by positron emission tomography the time course of changes in brain uptake in vivo of 11C-labeled PK 11195 and flumazenil (an antagonist of central benzodiazepine receptors) as indirect and direct markers of neuronal loss, respectively, after focal cerebral ischemia.
Ten anesthetized baboons were submitted to sequential positron emission tomography studies between day 1 and day 91 after unilateral middle cerebral artery occlusion. The studies consisted of successive assessments, in the same positron emission tomography session, of [11C]PK 11195, [11C]flumazenil, cerebral blood flow, and oxygen consumption; late computed tomographic scans were obtained to map the approximate contours of infarction and to define a concentric peri-infarct area.
We found a significant time-dependent increase in [11C]PK 11195 uptake in the peri-infarcted area, maximum at 20 to 40 days after occlusion. In contrast, there was a time- and perfusion-independent significant decrease in [11C]flumazenil uptake in the infarcted area, stable from day 2 onward, and already present in one baboon at day 1. Challenge studies with saturating doses of cold ligands confirmed that these changes represented alterations in specific binding. [11C]Flumazenil uptake was not affected in hypometabolic (but apparently noninfarcted, ie, deafferented) cortical areas.
The delayed and apparently transient increases in [11C]PK 11195 specific uptake in vivo presumably represent glial/macrophage reaction; the marked depression in [11C]flumazenil specific binding, which appears selective for synaptic damage, is both precocious and sustained and thus may be better suited for the early assessment of ischemic damage in humans.
The Stroke Prevention Patient Outcomes Research Team. Goals and methods.
Authors: Matchar D B , Duncan P W , Samsa G P , Whisnant J P , DeFriese G H , Ballard D J , Paul J E , Witter D M , Mitchell J P 
Published: June 2011

The aim of the present study, based at Duke University and involving 14 other institutions, is to identify the most appropriate and cost-effective clinical strategies for prevention of ischemic (thrombotic or embolic) stroke in high-risk individuals and to design and test an intervention to disseminate this information to providers and the public.
The study uses (1) secondary data from literature review, Medicare claims, and population-based data from three epidemiological studies and (2) primary data generated in national physician and patient surveys and in demonstration trials. Phases I through III involve data collection and analysis using a decision/cost-effectiveness model and consensus development methods. Phase IV includes intervention in physicians' practice patterns. Data is collected by literature survey and abstraction, review of medical records, claims analysis, and patient and physician surveys.
A structured decision model and a well-defined clinical focus provide a successful organization for a PORT on stroke prevention.