bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebrovascular responsiveness to hypercapnia in Alzheimer's dementia and vascular dementia of the Binswanger type.
Authors: Kuwabara Y , Ichiya Y , Otsuka M , Masuda K , Ichimiya A , Fujishima M 
Published: June 2011

Alzheimer's dementia is thought to be a primary degenerative dementia, whereas vascular dementia of the Binswanger type is an entity of vascular dementia. We evaluated the cerebrovascular responsiveness to hypercapnia to clarify the differences in the cerebral hemodynamics between two groups of patients. The subjects were eight younger control subjects, five age-matched control subjects, five Alzheimer's patients, and five patients with vascular dementia of the Binswanger type.
In the resting state, the regional cerebral blood flow was low in both Alzheimer's dementia and vascular dementia of the Binswanger type. The responsiveness to hypercapnia was preserved in Alzheimer's dementia, whereas it was impaired in vascular dementia of the Binswanger type in the cerebral cortices and in the deep white matter.
These results suggest that small vascular lesions exist in vascular dementia of the Binswanger type but not in Alzheimer's dementia, even though regional cerebral blood flow was thought to decrease by hypometabolism in both types of dementia.
Cheiro-oral syndrome due to lesions in the corona radiata.
Authors: Omae T , Tsuchiya T , Yamaguchi T 
Published: June 2011

We describe three patients with cheiro-oral syndrome caused by a small lesion in the corona radiata confirmed by high-resolution magnetic resonance imaging.
Case 1: A 56-year-old hypertensive man who developed hypesthesia and paresthesia in the left perioral area and hand was found to have a small hematoma just lateral to the right internal capsule. Case 2: A 67-year-old man noticed hypesthesia around the left mouth angle and thumb and index finger. Magnetic resonance imaging revealed a lesion in the right corona radiata. Case 3: A 45-year-old hypertensive man developed numbness in his perioral region and left hand that later spread to his shoulder. Magnetic resonance imaging revealed a recent small infarct in the lower lateral aspect of the right corona radiata.
A small lesion in the corona radiata can cause cheiro-oral syndrome, whose pathogenetic mechanism in such patients may be explained by the somatotopical location or by the differing vulnerability of the neuropils in the corona radiata.
Urgent therapy for stroke. Part II. Pilot study of tissue plasminogen activator administered 91-180 minutes from onset.
Authors: Haley E C , Levy D E , Brott T G , Sheppard G L , Wong M C , Kongable G L , Torner J C , Marler J R 
Published: June 2011

Renewed interest in thrombolytic therapy as potential treatment for patients with acute ischemic stroke prompted a dose-escalation safety study of tissue plasminogen activator in patients with very early (less than or equal to 90 minutes; see Part I) neurological symptoms. To test whether this stringent entry window might be safely lengthened, a second study was organized to test tissue plasminogen activator in patients with symptoms of 91-180 minutes' duration before treatment.
An open-label, dose-escalation design was chosen. Eligible patients had pretreatment head computerized tomographic scanning and treatment begun 91-180 minutes from stroke onset. End points examined included the incidence of symptomatic and asymptomatic intracranial hemorrhage, other bleeding, and clinical outcome at 2 hours, 24 hours, and 3 months after treatment.
Twenty patients were treated at three hospitals in 13 months. Three doses were tested: 0.6 mg/kg (n = 8), 0.85 mg/kg (n = 6), and 0.95 mg/kg (n = 6). Two patients, one each at the two highest doses, sustained fatal intracerebral hemorrhages. Three patients (15%) improved by greater than or equal to 4 points on the National Institutes of Health Stroke Scale by 24 hours.
These observations suggest that tissue plasminogen activator treatment of acute ischemic stroke 91-180 minutes from onset in doses of greater than or equal to 0.85 mg/kg is attended by a risk of intracerebral hemorrhage approximating 17% (range 3-44%, 95% confidence interval). The rate of early neurological improvement observed in this study was small but does not exclude an improvement over the natural history. Future study with placebo control subjects and stratification by time to treatment is indicated.
Changing pattern of brain hemorrhage during 12 years of computed axial tomography.
Authors: Schuetz H , Dommer T , Boedeker R H , Damian M , Krack P , Dorndorf W 
Published: June 2011

We examined whether the pattern of cerebral hemorrhage changed after the introduction of computed tomography.
Using a prospective data base we analyzed the case-fatality ratio, early mortality, and the incidences of hypertension and anticoagulant medication in 488 consecutive cases with supratentorial hemorrhage between 1978 and 1989. Blood pressure at admission of all patients for the years 1978-1979 and 1988-1989 and the Mathew and activities of daily living scores for the years 1978-1979, 1982-1983, and 1988-1989 were assessed retrospectively.
The case-fatality ratio decreased from 49% in the period 1978-1981 to 31% in 1986-1989 (p = 0.006); early mortality (day 1-4) decreased from 28% to 12% (p = 0.0017). The incidence of hypertension decreased from 78% in the period 1978-1981 to 64% in 1986-1989 (p = 0.01). Systolic and diastolic blood pressure at admission sank (p = 0.09). The decrease of the case-fatality ratio correlated best with a less severe initial disturbance of consciousness (p less than 0.01) and with a higher Mathew score (p = 0.038). The activities of daily living score remained unchanged.
The case-fatality ratio and early mortality decreased after the introduction of computed tomography. This was basically due to a decreased incidence of comatose and stuporous patients with severe neurological deficit paralleled by a decrease of mean systolic and diastolic blood pressure values at admission.
Antithrombotic effects of a platelet fibrinogen receptor antagonist in a canine model of carotid artery thrombosis.
Authors: Willette R N , Sauermelch C F , Rycyna R , Sarkar S , Feuerstein G Z , Nichols A J , Ohlstein E H 
Published: June 2011

Platelet-fibrin thrombi in the lumen of atherostenotic carotid arteries may underlie transient ischemic attacks and cerebral infarction. For this reason, we investigated the antiplatelet and antithrombotic effects of a novel and potent platelet fibrinogen receptor (glycoprotein IIb/IIIa) antagonist (SK&F 106760).
The effects of 0.1-3.0 mg/kg i.v. SK&F 106760 on platelet aggregation were examined ex vivo in canine platelet-rich plasma (n = 20). In addition, the antithrombotic effects of SK&F 106760 were compared with those of aspirin in an acute canine model of extracranial carotid artery thrombosis with high-grade stenosis. Sham-operated (n = 4), vehicle-treated (n = 6), SK&F 106760-treated (n = 8), aspirin-treated (n = 9), and SK&F 106760+aspirin-treated (n = 5) dogs were examined.
The intravenous administration of SK&F 106760 caused a dose-related inhibition of ex vivo platelet aggregation. In the carotid artery thrombosis model, an occlusive thrombus formed at stenotic sites in the region of the carotid bifurcation. The thrombogenic process caused a progressive reduction in carotid blood flow and reduced the cortical microvascular perfusion and electroencephalographic power. Based on nuclear magnetic resonance spectroscopy, the occlusive events depleted the stores of high-energy phosphates (adenosine triphosphate and phosphocreatine) and increased the lactate concentration in the forelimb somatosensory area of the parietal cortex. In this model, the administration of 1 mg/kg i.v. SK&F 106760 prevented thrombosis of the stenotic carotid artery. Consequently, neurophysiological, cerebral hemodynamic, and metabolic parameters were all improved significantly in the SK&F 106760-treated group. No dog receiving SK&F 106760 reoccluded during the 1-hour posttreatment observation period. In contrast, thrombosis of the carotid artery was associated with neurophysiological deterioration in six of the nine dogs treated with 5 mg/kg i.v. aspirin. Both spontaneous and evoked (increased carotid stenosis) aspirin-resistant thrombosis were abolished by SK&F 106760 treatment.
These results suggest that antagonism of fibrinogen binding to platelet glycoprotein IIb/IIIa (the final common pathway for aggregation) may represent a new and more effective antithrombotic approach to the treatment of cerebral transient ischemic attacks and infarction associated with extracranial carotid artery disease.
Emphasized selective vulnerability after repeated nonlethal cerebral ischemic insults in rats.
Authors: Inoue T , Kato H , Araki T , Kogure K 
Published: June 2011

We examined the density and distribution of brain damage after repeated periods of nonlethal ischemic insult in rats in comparison with damage after single lethal periods of ischemic insult.
Transient cerebral ischemia was induced by four-vessel occlusion for 3, 10, 20, and 30 minutes, and 3-minute periods of ischemia were repeated two, three, or five times at 1-hour intervals, followed by 7 days of survival.
Three minutes of ischemia produced no brain damage, but 10-30 minutes of ischemia produced neuronal damage, depending on the length of ischemia, to the selectively vulnerable forebrain regions such as hippocampal CA1 and CA4 subfields, neocortex, striatum, and ventral thalamus, as well as to the brain stem structures (medial geniculate body, substantia nigra, and inferior colliculus) and cerebellar Purkinje cells. Two 3-minute periods of ischemic insult produced neuronal damage to the hippocampal CA1 subfield. Three and five 3-minute insults produced neuronal damage extensively to the selectively vulnerable forebrain areas. An intense cumulative effect of damage was observed in the ventral thalamus, whereas the substantia nigra and the inferior colliculus were resistant to repeated ischemic insults.
Our data indicate that the density and distribution of neuronal damage after repeated ischemic insults are altered as compared with after single ischemia.
Postprandial triglyceridemia and carotid atherosclerosis in middle-aged subjects.
Authors: Ryu J E , Howard G , Craven T E , Bond M G , Hagaman A P , Crouse J R 
Published: June 2011

It has been suggested that a postprandial accumulation of triglyceride-rich lipoproteins promotes the development of atherosclerosis. This study was designed to test the hypothesis that postprandial lipemia is independently associated with intima-media thickening of the extracranial carotid arteries.
Forty-seven middle-aged, moderately hypercholesterolemic individuals were recruited for a 1-day study of the lipemic response to a standard high-fat test meal. The formula was fed at a dose of 65 g fat/m2 body surface area, after a 14-hour fast, and blood was obtained for triglyceride analysis hourly for 8 hours. A baseline lipid profile was obtained. Each subject underwent a carotid ultrasound examination. The extent of alimentary lipemia (peak triglyceride response) was correlated with the carotid artery wall thickness as measured by B-mode ultrasound.
Univariate analyses indicated an inverse correlation between peak triglyceride response and high density lipoprotein cholesterol concentration and a direct correlation with male sex, baseline triglyceride concentration, background fat intake, and waist-to-hip ratio. Of these, the only variable that showed a univariate correlation with B-mode score was peak triglyceride response. Age and cigarette smoking were also correlated with B-mode score in univariate analyses. The correlation coefficient (r = 0.52) between peak triglyceride response to a fat-rich meal and B-mode score was significant (p less than 0.002) and remained so in multivariate analysis. Forward-selection stepwise regression resulted in the inclusion of only peak triglyceride response (p = 0.001) and smoking history (p = 0.005) as important predictors of carotid wall thickness in a linear model.
The association between lipemic response and carotid wall thickness suggests that prolonged exposure of arterial wall cells to triglyceride-rich chylomicron remnants enhances the atherogenic process.
Lifestyle factors and risk of cerebral infarction.
Authors: Ellekjaer E F , Wyller T B , Sverre J M , Holmen J 
Published: June 2011

We evaluated the impact of lifestyle factors on the risk of ischemic stroke.
We used a nested case-control design. The cases comprised 163 persons (median age 69 years) admitted to a stroke unit and diagnosed with acute cerebral infarction. All cases had earlier participated in the North Trøndelag Health Survey. The controls comprised 567 participants from the North Trøndelag Health Survey, matched by sex and year of birth.
Raised systolic (p less than 0.001) and diastolic (p = 0.02) blood pressure, antihypertensive treatment (p less than 0.001), previous myocardial infarction (p less than 0.001), prior stroke (p = 0.002), diabetes (p less than 0.001), and former daily smoking (p = 0.02) were identified as significant risk factors by univariate conditional logistic regression. No difference in risk was detected at different levels of alcohol consumption, salt intake, physical activity, or body mass index. Current smokers had virtually the same risk as nonsmokers. No association was found between stroke and the number of cigarettes smoked per day or the number of years of smoking. Multivariate conditional logistic regression identified diabetes (p = 0.002), raised systolic blood pressure (p less than 0.001), and former daily smoking (p = 0.01) as significant and independent risk factors. Previous myocardial infarction (p = 0.07), previous stroke (p = 0.1), and current daily smoking (p = 0.1) were of marginal significance.
The established medical risk factors for stroke are confirmed. With the possible exception of smoking, we have not identified any lifestyle factor with a significant impact on the risk of ischemic stroke.
Brain and tissue distribution of polyethylene glycol-conjugated superoxide dismutase in rats.
Authors: Yoshida K , Burton G F , McKinney J S , Young H , Ellis E F 
Published: June 2011

The purpose of this study was to determine the distribution of polyethylene glycol-conjugated superoxide dismutase in the brain, cerebrospinal fluid, and various organs.
Distribution of iodine-125-labeled polyethylene glycol-conjugated superoxide dismutase was determined in three groups of male Sprague-Dawley rats: a normotensive sham control group (n = 9) and groups given 125I-labeled polyethylene glycol-conjugated superoxide dismutase either 30 minutes before (n = 10) or 30 minutes after (n = 7) norepinephrine-induced hypertensive injury.
In the first 30 minutes after intravenous administration, polyethylene glycol-conjugated superoxide dismutase plasma activity declined to 70% of the initial value and then decreased negligibly between 30 and 90 minutes. Levels of 125I-labeled polyethylene glycol-conjugated superoxide dismutase in normotensive animals were low in the brain and cerebrospinal fluid and highest in kidney. Brain levels of polyethylene glycol-conjugated superoxide dismutase were elevated only in those rats that received it before hypertensive injury; however, cerebrospinal fluid levels were elevated in animals receiving the drug either before or after hypertensive injury.
Our results suggest that the blood-brain barrier becomes more permeable to polyethylene glycol-conjugated superoxide dismutase only during the hypertensive period but that the blood-cerebrospinal fluid barrier sustains more permanent injury. We suggest that the therapeutic effectiveness of polyethylene glycol-conjugated superoxide dismutase in hypertensive brain injury is due to its action in the vascular wall or to its extracellular activity in the cerebrospinal fluid.
Serotonin release into plasma during common carotid artery thrombosis in rats.
Authors: Wester P , Dietrich W D , Prado R , Watson B D , Globus M Y 
Published: June 2011

We have tested the hypothesis that platelet-derived serotonin is released into the bloodstream during cerebrovascular thrombosis.
Nonocclusive common carotid artery thrombosis was produced photochemically in 22 anesthetized adult male Wistar rats using the photosensitizing dye rose bengal and irradiation with an argon-pumped dye laser. Plasma serotonin levels were recorded before, during, and after photothrombosis by intra-arterial in vivo microdialysis with the probe placed distal to the site of thrombosis.
During and immediately after the common carotid artery thrombosis, serotonin levels increased significantly to a peak value of 781 nmol/l (p less than 0.001 by analysis of variance), representing a 15-fold increase compared with baseline levels. The increased serotonin levels gradually decreased but remained significantly elevated for 90 minutes. Ultrastructural analysis of the carotid thrombi identified a dense mass of aggregated platelets at various stages of degranulation.
These results are the first to demonstrate directly that serotonin accumulation occurs in plasma during and after the acute phase of common carotid artery thrombosis. Increased plasma serotonin levels may play a major role in the cerebral blood flow and blood-brain barrier abnormalities previously documented in this model of large-vessel thrombotic stroke.
Temporal relation of calcium-calmodulin binding and neuronal damage after global ischemia in rats.
Authors: DeGraba T J , Ostrow P T , Strong R A , Earls R M , Zong Z J , Grotta J C 
Published: June 2011

This study explores the temporal relation of the severity of ischemia and calcium-calmodulin binding in vulnerable and resistant brain regions in a commonly used model of global ischemia.
Immunohistochemical assay of free calmodulin unbound to calcium and light microscopic histological damage were measured in rats after 5, 10, or 20 minutes of global ischemia.
After 24 hours of reperfusion, decreased calmodulin staining, representing increased calcium influx and calcium-calmodulin binding, correlated with increasing durations of ischemia across all brain regions. Based on a 4-point scale (4, extensive stain; 0, no staining), calmodulin staining after 5 minutes versus 10 minutes of ischemia was 3.2 versus 1.9, respectively (p less than 0.05) and after 10 minutes versus 20 minutes of ischemia was 1.9 versus 1.0, respectively (p less than 0.01). The CA1 region displayed the greatest sensitivity to ischemia. Similar but less dramatic results were seen after 2 hours of reperfusion. After 72 hours of reperfusion, histological damage closely correlated with calcium-calmodulin binding after variable durations of ischemia. A threshold of 10 minutes of ischemia was required to cause calcium-calmodulin binding and irreversible neuronal damage. Surviving neuronal populations showed recovery of calmodulin staining 7 days after ischemia, representing a return of free calmodulin and normal calcium homeostasis.
These correlations between calcium-calmodulin binding, histological damage, and duration of ischemia support the causal role of calcium influx in global ischemic injury and suggest the need for very rapid intervention after ischemia if calcium-mediated damage is to be prevented.
Increased plasma endothelin-1 in acute ischemic stroke.
Authors: Ziv I , Fleminger G , Djaldetti R , Achiron A , Melamed E , Sokolovsky M 
Published: June 2011

Endothelins are a recently discovered group of most powerful vasoconstrictor peptides. Endothelin-1 is produced by endothelial cells, and endothelin-3 is derived from neuronal tissue. Theoretically, endothelin-mediated vasoconstriction may enhance ischemic neuronal damage. This study aimed to measure plasma levels of both endothelins in patients with acute nonhemorrhagic cerebral infarction.
Plasma levels of endothelin-1 and endothelin-3 were measured by radioimmunoassay in 16 consecutive patients within the first 72 hours after the onset of nonhemorrhagic cerebral infarct, as diagnosed clinically and by computed tomography. There was a marked (fourfold) elevation in plasma endothelin-1 levels in the patients (median, 11.7 pg/ml; 25th and 75th centiles, 5.4 and 13.2 pg/ml) compared with those in a control group of 13 age-matched subjects (median, 2.56 pg/ml; 25th and 75th centiles, 2.4 and 3.0 pg/ml; p less than 0.0001). The first 24 hours after stroke onset were associated with higher endothelin-1 levels, and there was a trend to elevated levels with more severe neurological deficits. In all patients and controls endothelin-3 levels were below 0.5 pg/ml.
Ischemic stroke is associated with acute and marked increases in plasma levels of endothelin-1. This may reflect enhanced production by damaged endothelial cells within the infarcted tissue. Local leakage of endothelin-1 may induce severe and prolonged constriction of collateral vessels and may therefore have a deleterious role in the pathogenesis and final outcome of cerebral infarction.
Spontaneous vertebral artery dissection initially mimicking myocardial infarction.
Authors: Linden D , Steinke W , Schwartz A , Hennerici M 
Published: June 2011

Vertebral and carotid artery dissections may present with very different signs and symptoms, making early recognition difficult. However, diagnosis should be established as soon as possible to prevent unnecessary diagnostic investigations and to institute adequate treatment.
A 46-year-old man presented with severe intermittent pain of his left upper arm and general discomfort. During extensive cardiological evaluation for suspected myocardial infarction, a severe brain stem syndrome occurred. Ultrasound Doppler studies detected vertebral artery dissection, which was confirmed by angiography.
The unusual initial presentation of vertebral artery dissection delayed an early diagnosis and adequate treatment. Because noninvasive methods are available today, their applications are recommended in similarly uncharacteristic circumstances.
Coronary artery disease and cardiac events with asymptomatic and symptomatic cerebrovascular disease.
Authors: Love B B , Grover-McKay M , Biller J , Rezai K , McKay C R 
Published: June 2011

The purpose of this study was to evaluate the prevalence of coronary artery disease and coronary events during follow-up in patients with asymptomatic carotid stenosis, transient ischemic attacks, or small strokes.
We prospectively studied 60 consecutive patients with thallium-201 scintigraphy followed by coronary arteriography according to an established protocol.
The 201Tl testing was abnormal in seven of 15 patients (47%) with asymptomatic carotid stenosis and in 19 of 44 patients (43%) with transient ischemic attacks or small strokes (p greater than 0.05). In 33 patients with no history of coronary artery disease, 11 (33%) had reversible 201Tl defects. In 26 patients with a history of coronary artery disease, 15 (58%) had reversible and/or fixed defects (p = 0.054 compared with patients with no history). A history of peripheral vascular disease was the only risk factor significantly associated with an abnormal 201Tl test (p = 0.032). Coronary artery stenosis of greater than 50% was identified in one or more vessels in 14 of 15 patients undergoing coronary arteriography. Over a mean follow-up period of 311 days, four patients (7%) developed new onset of angina. There were four coronary events among 14 patients (29%) with both a reversible area on the 201Tl and abnormal coronary arteriography. In comparison, there were only four coronary events among 46 patients (9%) without reversible defects on the 201Tl studies (p = 0.055).
Our study demonstrates that one third of patients with no history of coronary artery disease had an abnormal 201Tl test and that nearly one half of patients with either symptomatic or asymptomatic cerebrovascular disease had abnormal 201Tl tests. Patients with a reversible 201Tl defect and significant stenosis by coronary arteriography were at higher risk for subsequent cardiac events. These findings demonstrate the utility of screening patients with asymptomatic and symptomatic cerebrovascular disease for cardiac disease.