bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stroke incidence and mortality in rural and urban Shanghai from 1984 through 1991. Findings from a community-based registry.
Authors: Hong Y , Bots M L , Pan X , Hofman A , Grobbee D E , Chen H 
Published: June 2011

Mortality from stroke has declined in many countries. This decline may result from a fall in incidence of stroke or a decrease in case fatality from stroke. The present study was conducted to investigate the temporal trends of incidence rate, mortality rate, and case fatality of stroke in an urban and rural Chinese population.
A community-based registry study was established in 1983 in defined rural and urban areas of Shanghai with a population aged 35 to 74 years of approximately 86,000 subjects, adhering to the methods and definitions of the World Health Organization MONICA protocol. All stroke events occurring in the population aged 35 to 74 years in these areas were registered by a special three-level case-registration system.
From 1984 through 1991, 1391 stroke cases were identified. No significant change in the incidence rate of stroke was observed from 1984 through 1991 in men and women living in rural and urban areas. Age-standardized mortality rates (per 100,000 person years) of stroke declined significantly during this period, except for rural women. The annual changes and 95% confidence intervals of age-standardized mortality rates were: for rural men -4.6% (-5.4, -3.9), for rural women -0.6% (-1.6, 0.5), for urban men -2.5% (-3.5, -1.6), and for urban women -4.7% (-5.2, -4.2). A significant decrease in case fatality from stroke from 1984 through 1991 was found among men living in rural areas (from 62.4% to 46.0%) and among women living in urban areas (from 48.4% to 33.3%). Overall case fatality, however, showed a nonsignificant decline over time.
We observed a decline in stroke mortality rate in a rural and urban Chinese population. No significant changes in stroke incidence were found in this study, whereas case fatality appeared to have decreased, in particular among men living in rural areas and women living in urban areas.
Coagulation activity and emboli counts in patients with prosthetic cardiac valves.
Authors: Georgiadis D , Mallinson A , Grosset D G , Lees K R 
Published: June 2011

The underlying embolic material detected by transcranial Doppler ultrasound in patients with prosthetic heart valves remains unknown. We undertook this study to evaluate the relation between the number of Doppler emboli signals and the activity of the coagulation system.
Patients with various types of prosthetic valves (n = 120) and patients in atrial fibrillation (n = 20) were monitored for 30 minutes using transcranial Doppler with a 2-MHz probe. The plasma concentrations of cross-linked D-dimer, antithrombin-III, and thrombin-antithrombin III complex were measured.
No correlation between the levels of any of the hematologic parameters and the number of emboli was demonstrated in the studied groups. The D-dimer levels were significantly higher in patients with mechanical prosthetic valves with an international normalized ratio under 2.0 compared with those with an international normalized ratio between 2 and 3.5 or above 3.5, and in patients with Medtronic-Hall versus Björk-Shiley or Carpentier-Edwards valve prostheses.
The lack of correlation between the activity of the coagulation system and the number of Doppler emboli in patients with prosthetic valves suggests that the underlying embolic material in these patients is not thrombotic. Our results also suggest that an increase of the anticoagulation intensity to an international normalized ratio above 3.5 does not result in a further decrease of the activity of the unstimulated coagulation system in patients with mechanical prosthetic valves.
Chimeric 7E3 prevents carotid artery thrombosis in cynomolgus monkeys.
Authors: Rote W E , Nedelman M A , Mu D X , Manley P J , Weisman H , Cunningham M R , Lucchesi B R 
Published: June 2011

We compared the current antithrombotic strategy of antiplatelet therapy with aspirin, and anticoagulant therapy with heparin, with a specific genetically engineered chimeric antibody (c7E3 Fab) directed against the human glycoprotein IIb/IIIa receptor in an animal model of arterial thrombosis.
Anesthetized cynomolgus monkeys (Macaca fascicularis) were instrumented for monitoring of arterial blood pressure, heart rate, and carotid artery flow velocity. Animals were treated with saline (n = 6), aspirin (25 mg PO daily for 3 days; n = 6), heparin (100 U/kg i.v. plus infusion adjusted to maintain activated partial thromboplastin time at 2 to 3 times baseline; n = 6), aspirin plus heparin (as administered separately, n = 6), or c7E3 Fab (0.10 mg/kg i.v., n = 7; 0.15 mg/kg i.v., n = 6; 0.20 mg/kg i.v., n = 6; 0.25 mg/kg i.v., n = 6). Thrombus formation via anodal electrolytic stimulation (100 microA) to the intimal surface of the right carotid artery was initiated 15 minutes after drug administration and continued for 180 minutes. Electrolytic injury to the left carotid artery began 210 minutes after drug administration and continued for 180 minutes. Whole blood cell counts, glycoprotein IIb/IIIa receptor blockade, ex vivo platelet aggregation, template bleeding time, and activated partial thromboplastin time were assessed at various time points throughout the experimental protocol.
Hemodynamic and hematologic parameters were comparable among groups at baseline. Treatment with c7E3 Fab inhibited ex vivo platelet aggregation, increased bleeding time, decreased thrombus weight, and increased time to occlusion in a dose-dependent manner in both vessels. Treatment with aspirin, heparin, or the combination of aspirin plus heparin was ineffective for the prevention of carotid artery thrombosis in this model.
Inhibition of the platelet glycoprotein IIb/IIIa receptor with c7E3 Fab was found to be safe and effective for the prevention of primary thrombus formation, whereas treatment with either aspirin or heparin or the combination of the two agents failed to protect against occlusive thrombus formation in cynomolgus monkeys.
Stroke: the way things really are.
Authors: Scheinberg P 
Published: June 2011

To comply with governmental requirements regarding the validity of therapeutic modalities and for medico-legal purposes, it is important to distinguish between what has been scientifically proven and what is anecdotal in the prevention and management of stroke.
This review summarizes the evidence for many of the modalities used to prevent stroke in high-risk patients, including antiplatelet drugs, anticoagulants, and endarterectomy, and the limitations of each. Controversial therapeutic modalities for which no scientific proof exists, such as anticoagulation of progressing stroke, are also discussed. The term "standard of care" should apply to modalities proven to be effective by scientifically controlled studies, not because they are used by many physicians. Treatment of acute stroke is still disappointing despite the development of many promising pharmacological strategies in experimental animals. An important part of the reason may be that the window of therapeutic opportunity is much shorter than the usual entry time of patients in most clinical trials. This logistic problem merits serious attention.
Numerous controlled, randomized, multiple-center clinical trials have demonstrated that the efficacy or lack thereof of various therapies directed at preventing or treating stroke can be determined and that anecdotal data may be misleading and harmful. At the least we should be aware of what we know and what we do not.
The impact of microemboli during cardiopulmonary bypass on neuropsychological functioning.
Authors: Pugsley W , Klinger L , Paschalis C , Treasure T , Harrison M , Newman S 
Published: June 2011

Microemboli have been implicated in the etiology of neuropsychological deficits after cardiopulmonary bypass. This study examined the incidence of high-intensity transcranial signals (microemboli) and their relation to changes in neuropsychological performance after surgery.
Transcranial Doppler ultrasonography was used to measure middle cerebral artery blood flow velocity and detect microemboli. The number of high-intensity transcranial signals was determined and related to a neurological examination and absolute changes in neuropsychological performance as well as the number of patients considered to exhibit a neuropsychological deficit. Data were available on 100 consenting patients undergoing routine cardiopulmonary bypass. Fifty of the patients were randomly assigned to a procedure that included a 40-microns arterial line filter, and 50 had the procedure without any arterial line filter.
Significantly more patients were found to have neuropsychological deficits in the group without the arterial line filter at both 8 days (P < .05) and 8 weeks (P < .03) after surgery. In addition, more "soft" neurological signs were found in the nonfiltered group 24 hours after surgery (P < .05). More high-intensity transcranial signals were found in the nonfiltered group, and the number of high-intensity transcranial signals was found to be related to the likelihood of a patient having a neuropsychological deficit at 8 weeks.
These data suggest that neuropsychological deficits after routine cardiopulmonary bypass are related to the number of microemboli delivered during surgery. Furthermore, the numbers of microemboli may be reduced by including a 40-microns filter on the arterial line.
Cerebral blood flow in subcortical global aphasia. Perisylvian cortical hypoperfusion as a crucial role.
Authors: Okuda B , Tanaka H , Tachibana H , Kawabata K , Sugita M 
Published: June 2011

Global aphasia after subcortical stroke is very rare, and its pathophysiology remains unsolved. To clarify the mechanism underlying subcortical global aphasia, we investigated lesion sites and cerebral blood flow in patients with subcortical global aphasia and nonaphasic patients with subcortical stroke.
We examined four patients with global aphasia and four nonaphasic patients. Language testing was performed more than 4 weeks after the onset. Measurement of cerebral blood flow was done between 35 and 75 days after stroke by using single-photon emission computed tomography (SPECT) with N-isopropyl-p[123I]iodoamphetamine as a tracer and three-dimensional surface display generated from SPECT.
All aphasic patients had subcortical lesions in the putamen, posterior internal capsule, temporal isthmus, and periventricular white matter in the left hemisphere. No cortical lesions were found on either magnetic resonance imaging or computed tomographic scanning. The nonaphasic patients had smaller periventricular white matter lesions and no temporal isthmus lesions. All aphasic patients showed cortical hypoperfusion mainly in the perisylvian areas, including Broca's and Wernicke's areas. In contrast, cortical cerebral blood flow of the nonaphasic patients was decreased in smaller areas and spared the perisylvian language areas.
These results suggest that cortical hypoperfusion in the perisylvian language areas, presumably due to undercutting of the white matter, is crucial for the development of subcortical global aphasia.
Pure sensory stroke caused by a pontine infarct. Clinical, radiological, and physiological features in four patients.
Authors: Shintani S , Tsuruoka S , Shiigai T 
Published: June 2011

We conducted this retrospective study to evaluate the clinical, neuroradiological, and neurophysiological findings in patients with pure sensory stroke due to pontine lacuna.
Four patients with pontine lacuna, three men and one woman (mean age, 64.5 years; range, 55 to 75 years), were evaluated. Magnetic resonance images were obtained with a 0.5-T superconducting magnet using the SE technique. Short-latency somatosensory evoked potentials were evaluated by unilateral stimulation of the median nerve at the wrist. These tests were done at a mean of 22.5 months (range, 9 to 34 months) after symptom onset. Deep sensory disturbances were present in one half of the patient's body with no other neurological deficits found. The sensory deficit was characterized by a prolonged period of refractory dysesthesia and a discrepancy between the superficial and deep sensory disturbances. Lesions were localized in the medial lemniscus of the middle and lower pons, with a sparing of the spinothalamic tracts. The central conduction times of short-latency somatosensory evoked potentials were prolonged (patients 1, 2, and 4), and the amplitudes were significantly reduced (patients 1 and 2) when stimulating the paresthetic-sided median nerve (contralateral side of the lesion) compared with stimulating the other side.
In all cases, the clinical and radiological findings indicated a dysfunction of the medial lemniscal tract in the pons. The observed somatosensory evoked potentials were probably related to the persistent refractory dysesthesias present in these patients.
Bilateral occipital infarctions associated with carotid stenosis in a patient with persistent trigeminal artery. The Collaborators of the North American Carotid Endarterectomy Trial (NASCET).
Authors: Gasecki A P , Fox A J , Lebrun L H , Daneault N 
Published: June 2011

Embolization via a persistent trigeminal artery, one of the embryonic vascular connections that may persist between the carotid and basilar arteries, is an unusual occurrence.
We describe a 76-year-old man with bilateral occipital infarctions presumably related to an ulcerated left carotid stenosis. Clinically, a left inferior homonymous quadrantanopia was present.
Anomalous connections between the carotid and the usual posterior circulation territory should be considered in evaluating patients with vertebrobasilar stroke. When they are identified, patients with symptoms attributable to the pontine vertebrobasilar territory supplied by the anomaly may be considered for carotid endarterectomy in the presence of concomitant severe carotid stenosis detected angiographically. Proper identification and treatment of such cases would be expected to prevent recurrence of disabling strokes in the vertebrobasilar circulation. These anomalies will likely be overlooked by ultrasound techniques and depend on good intracranial arteriographic images.
Shear-induced platelet aggregation in cerebral ischemia.
Authors: Uchiyama S , Yamazaki M , Maruyama S , Handa M , Ikeda Y , Fukuyama M , Itagaki I 
Published: June 2011

Recent evidence has suggested that shear-induced platelet aggregation is an important mechanism of thrombosis at arterial bifurcations or stenoses. We measured shear-induced platelet aggregation with a new apparatus in patients with cerebral ischemia and also studied correlations with other hemostatic parameters as well as the effect of antiplatelet agents.
The subjects were 75 patients with cerebral ischemia and 26 control subjects. Platelet aggregation was induced in citrated platelet-rich plasma by a high shear stress (108 dynes/cm2) that was applied by means of a cone-plate streaming chamber based on turbidimetry. We studied the correlation of test results with hemostatic parameters and also the effects of antiplatelet agents.
Compared with the control subjects, an increase of shear-induced platelet aggregation was observed in 21 patients with atherothrombotic stroke and 12 with transient ischemic attacks, but not in 11 with cardioembolic stroke or 31 with lacunar stroke. There was no significant correlation of shear-induced platelet aggregation with platelet count, agonist-induced platelet aggregation, fibrinogen level, or beta-thromboglobulin level. The extent of shear-induced aggregation was not correlated with von Willebrand factor antigen levels but was significantly correlated with the amounts of larger von Willebrand factor multimers. Oral aspirin (81 mg/d) did not inhibit shear-induced platelet aggregation, whereas oral ticlopidine (200 mg/d) significantly inhibited it.
These results indicate that shear-induced platelet aggregation is increased in patients with atherothrombotic stroke and transient ischemic attacks, is correlated with the increase of larger von Willebrand factor multimers, and is corrected by ticlopidine but not by low-dose aspirin.
Factors affecting changes in blood pressure after acute stroke.
Authors: Harper G , Castleden C M , Potter J F 
Published: June 2011

We sought to establish the pattern of blood pressure (BP) change after hospitalization for acute hemispheric stroke.
In 292 patients from the Leicester teaching hospitals with acute hemispheric stroke within the previous 24 hours (139 men; median age, 75 years [range, 42 to 98 years]), we prospectively studied BP changes between admission, 24 hours, 1 week, and 4 to 6 weeks. Changes were assessed in relation to the main stroke risk factors, stroke type and severity, and antihypertensive drug treatment. All subjects were followed up for 1 week, with 117 subjects followed up for 4 to 6 weeks. Changes were assessed by repeated-measures ANOVA, and Student's t tests were used to compare group pairs.
Systolic and diastolic BP fell by 12 mm Hg (95% confidence interval [CI], 8 to 15 mm Hg) and 7 mm Hg (95% CI, 5 to 9 mm Hg), respectively, in the first 24 hours and 22 mm Hg (95% CI, 18 to 25 mm Hg) and 12 mm Hg (95% CI, 10 to 14 mm Hg), respectively, during the first week (all changes significant at P < .01) but no further thereafter. In those patients receiving no antihypertensive medication before or after stroke, the pattern of change was similar to that of the whole group. Previously diagnosed hypertensive subjects (n = 106) had higher initial BP values than did normotensive subjects, although by 1 week the levels were not significantly different. Patients with cerebral hemorrhage confirmed by computed tomography (n = 20) had higher systolic BP, but not diastolic BP, throughout the first week than those with cerebral infarction (n = 89). The severity of stroke, age, and previous stroke history did not appear to alter the BP pattern. Stroke patients who were moderate to heavy alcohol consumers had lower convalescent systolic BP levels than lighter drinkers or abstainers.
We have demonstrated a marked fall in systolic and diastolic BP levels during the first 7 days after acute hemispheric stroke, with little change thereafter. Higher initial systolic BP values were found in patients with cerebral hemorrhage compared with those with cerebral infarct. Moderate to heavy alcohol consumption before stroke was associated with a greater systolic BP decline in the first week after the event compared with stroke patients who were light drinkers or abstainers.
Evaluation of cerebral vasoreactivity by three-dimensional time-of-flight magnetic resonance angiography.
Authors: Mandai K , Sueyoshi K , Fukunaga R , Nukada M , Tsukaguchi I , Matsumoto M , Kamada T 
Published: June 2011

Cerebral vasoreactivity is an important indicator of the reserve capacity of the cerebral circulation. To make a quantitative analysis of cerebral vasoreactivity in individual major arterial territories, we evaluated the response to acetazolamide using three-dimensional time-of-flight magnetic resonance angiography.
We examined 10 healthy volunteers and 6 patients with unilateral stenosis of the middle cerebral artery by a 1.5-T superconducting magnetic resonance imaging system. After a baseline vascular image was obtained, each subject received 17 mg/kg IV of acetazolamide; a second scan was performed 20 minutes later. Using a generally available personal computer and image analysis software, we measured the areas of the individual major arteries on collapsed axial vascular images and then calculated the vasoreactivity.
The average vasoreactivity of individual major cerebral arterial territories in the healthy volunteers was as follows: anterior cerebral artery complex, 33%; right middle cerebral artery, 71%; left middle cerebral artery, 74%; right posterior cerebral artery, 68%; and left posterior cerebral artery, 68%. In the patient group, the vasoreactivity of the stenotic middle cerebral arteries was significantly smaller than that of the nonstenotic arteries (P < .05). In addition, the nonstenotic middle cerebral arteries showed significantly less vasoreactivity than the right arteries of the healthy volunteers (P < .01).
Three-dimensional time-of-flight magnetic resonance angiography can be used to quantitatively evaluate acetazolamide-induced vasoreactivity in individual major cerebral arterial territories.
Reduced mortality and brain damage after locomotor activity in gerbil forebrain ischemia.
Authors: Stummer W , Weber K , Tranmer B , Baethmann A , Kempski O 
Published: June 2011

Preischemic spontaneous locomotor activity was distinguished in this laboratory as a factor influencing outcome after 15 and 20 minutes of forebrain ischemia in gerbils. Histological investigations were carried out to analyze potential relations between postischemic survival and a reduction of cerebral damage by spontaneous locomotor activity.
Male Mongolian gerbils were divided into two groups, one with access to running wheels ("runners") and one kept in conventional cages ("nonrunners") for 2 weeks preceding forebrain ischemia of 15 or 20 minutes. A total of 99 gerbils were divided in subgroups and were allowed to recover for 2 weeks for assessment of survival. Other subgroups (n = 7 to 9) were killed at day 4 for quantitative histology of selectively vulnerable areas such as hippocampus, cortex, striatum, and thalamus.
Two weeks after 15-minute ischemia, 44% of non-runners had survived compared with 90% of runners (P < .01). With 20-minute ischemia all runners survived compared with 21% of nonrunners. Quantitative histology (15-minute ischemia) revealed selective nerve cell injury in various cerebral regions in both groups. In runners, however, with the exception of the CA1 sector, damage was attenuated in cortex, striatum, and hippocampus. Furthermore, the extent of thalamic infarction was reduced (P < .05).
Locomotor activity before global cerebral ischemia is highly efficient in protecting the brain as demonstrated by enhanced survival and a reduction of tissue damage in Mongolian gerbils. The mechanisms underlying this protection are currently unclear. However, further understanding of this intriguing phenomenon should enhance the understanding of ischemia pathophysiology and lead to the development of new treatment strategies.