bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dipyridamole increases oxygen-glucose deprivation-induced injury in cortical cell culture.
Authors: Lobner D , Choi D W 
Published: June 2011

Adenosine transport inhibitors attenuate ischemic central neuronal damage in vivo, but the locus of this protective action is presently unknown. To help address the question of whether adenosine transport inhibitors have a protective effect directly on brain parenchyma, we tested the effect of the adenosine transport inhibitor dipyridamole on neuronal loss induced by oxygen-glucose deprivation in vitro.
Murine cortical cultures were exposed to combined oxygen and glucose deprivation, N-methyl-D-aspartate, or kainate. The extracellular concentrations of glutamate and adenosine were measured by high-performance liquid chromatography; neuronal cell death was assessed by morphological examination and measurement of lactate dehydrogenase release.
Cultures exposed to oxygen-glucose deprivation for 30 to 75 minutes exhibited an insult-dependent increase in extracellular adenosine, followed shortly by an increase in extracellular glutamate and 24 hours later by neuronal death. Addition of the A1 receptor antagonist 8-cyclopentyltheophylline during oxygen-glucose deprivation enhanced both glutamate release and neuronal damage. Addition of 10 mumol/L dipyridamole decreased extracellular adenosine and also enhanced extracellular glutamate and neuronal death. In contrast, dipyridamole increased the levels of extracellular adenosine stimulated by N-methyl-D-aspartate or kainate.
These results are consistent with the idea that endogenous adenosine has a neuroprotective effect directly on cortical cells exposed to oxygen-glucose deprivation. However, inhibition of adenosine transport with dipyridamole was surprisingly not an effective strategy for enhancing this protective effect. The beneficial effects of adenosine transport inhibitors observed in vivo may be mediated indirectly--for example, by effects on the vasculature.
Urgent therapy for acute stroke. Effects of a stroke trial on untreated patients.
Authors: Barsan W G , Brott T G , Broderick J P , Haley E C , Levy D E , Marler J R 
Published: June 2011

As part of the recruitment efforts for the National Institutes of Health Tissue Plasminogen Activator Pilot Study, public education and awareness campaigns were conducted to encourage early hospital arrival. We evaluated the change in arrival times during the course of the study for all stroke patients, including those who were not entered into study.
Data were gathered on all patients presenting within 24 hours of stroke onset to all of the study hospitals. Coincident with the start of the study, educational and promotional programs, which stressed signs and symptoms of stroke and the need to call 911, were presented to physicians, paramedical personnel, and the public. The study was divided into four quartiles to analyze differences in time to hospital arrival and use of 911.
Of 2099 patients screened, time data were available on 1116. During the course of the study, the mean time from symptom onset to hospital arrival declined significantly (3.2 hours versus 1.5 hours). Patients arrived for treatment sooner at community hospitals than at university/teaching hospitals. The use of 911 increased from 39% in the first quartile of the study to 60% in the fourth quartile. This was a consistent finding in all study sites. Increased use of 911 was seen almost exclusively in patients with nonhemorrhagic stroke.
Times from stroke onset to hospital arrival decreased significantly during the course of the National Institutes of Health Tissue Plasminogen Activator Pilot Study. Significantly increased use of 911 was the likely major explanation for the shortened arrival times. The decrease in arrival times may be a consequence of the public and professional education programs conducted at all study sites.
Diagnosis of moyamoya disease with magnetic resonance angiography.
Authors: Houkin K , Aoki T , Takahashi A , Abe H 
Published: June 2011

Present criteria for the diagnosis of moyamoya disease emphasize the use of conventional cerebral angiography as an indispensable requirement. However, magnetic resonance angiography (MRA) is fast becoming a reliable diagnostic modality for occlusive cerebrovascular diseases. The purpose of this study is to assess the accuracy of MRA compared with conventional angiography.
Thirty-nine patients (23 children and 16 adults) with moyamoya disease confirmed by conventional angiography (78 side views) were examined with MRA (three-dimensional time-of-flight technique with a 256 x 256 or 256 x 512 matrix). T1- and T2-weighted MR images were also taken.
The stenotic or occlusive change at the carotid fork was clearly revealed by MRA, which correlated well with conventional angiography (83% good correlation, 17% overestimation). Apparent moyamoya vessels were clearly shown as a signal void on the MR image and fine unusual vessels on MRA, particularly in children with moyamoya disease (82%). However, small moyamoya vessels were poorly shown on both MR images and MRA, particularly in adults (63%).
MRA can be an alternative to conventional angiography in typical moyamoya disease cases (the bilateral type of moyamoya disease in children). However, in the early or the end stages of moyamoya disease, diagnosis by means of MRA should be carefully evaluated.
Prognostic value of transcranial magnetic stimulation in acute stroke.
Authors: Araç N , Sağduyu A , Binai S , Ertekin C 
Published: June 2011

The aim of this study is to evaluate the role of motor-evoked potentials (MEPs) in predicting functional recovery of hemiparesis and hemiplegia in acute stroke patients.
Twenty-seven acute stroke patients were evaluated clinically and electrophysiologically within the first week and 3 to 6 months after the event. Clinical assessment included a quantitative evaluation of motor ability and activities of daily living. MEPs were recorded from the abductor pollicis brevis and tibialis anterior muscles bilaterally. Correlations between clinical parameters and MEPs were assessed.
In the acute period, no MEP could be detected in 17 of 27 patients. In these 17 patients, the clinical scores were worse than in the patients whose MEPs could be elicited. However, in the follow-up period (3 to 6 months), no significant differences in motor function were observed between the two groups.
In the acute phase of stroke, neurophysiological parameters were correlated with the clinical findings, but MEPs had no value in predicting the outcome of hemiparesis and hemiplegia.
Nitric oxide regulates cerebral arteriolar tone in rats.
Authors: Kimura M , Dietrich H H , Dacey R G 
Published: June 2011

Although cerebral penetrating arterioles are main regulators of the brain microcirculation, little is known about the effect of endothelium-derived relaxation factor on these vessels. This study examined the effects of nitric oxide synthase inhibitors on the spontaneous tone of isolated rat cerebral arterioles.
Intraparenchymal penetrating arterioles (53 to 102 microns in passive diameter) isolated from Sprague-Dawley rats were cannulated with glass pipettes and subjected to 60 mm Hg of intraluminal pressure. The diameter response to intraluminal and extraluminal treatments was observed with an inverted microscope.
Extraluminal application of Nw-nitro-L-arginine (10(-5) mol/L) contracted the arterioles to 63.9 +/- 2.8% (P < .05) of the control diameter. This contracting effect was stereospecific and easily reversed by L-arginine dose dependently (10(-3), 10(-2) mol/L) but not by D-arginine. Intraluminally applied Nw-nitro-L-arginine also induced a similar degree of contraction. Another nitric oxide synthase inhibitor, NG-monomethyl L-arginine (10(-5), 10(-4) mol/L), applied extraluminally induced a dose-dependent contraction to 77.5 +/- 6.6% and 68.6 +/- 5.4% of the control (P < .05), which was also reversed by L-arginine. L-Arginine alone did not significantly affect vessel diameter, however. Treatment with indomethacin, a cyclooxygenase inhibitor, dilated the vessel to 115.2 +/- 7% (P < .05) but did not change the constricting effect of Nw-nitro-L-arginine.
Nw-Nitro-L-arginine and NG-monomethyl L-arginine produce substantial contraction in isolated brain arterioles, suggesting that nitric oxide of brain arterioles is continuously produced within the vessel wall. The dilatory effect of indomethacin appears to be independent of the vasoconstriction induced by nitric oxide synthase inhibitor. In these vessels, the effect of nitric oxide synthase inhibitors is not mediated by an indomethacin-sensitive mechanism. A balance probably exists between factors tending to constrict these arterioles and the elaboration of nitric oxide from endothelial cells, which tends to dilate them. The production of nitric oxide from isolated vessels indicates that parenchymal and vessel wall sources of nitric oxide are probably important in brain microcirculatory regulation.
Stability of thrombosis induced by electrocoagulation of rat middle cerebral artery.
Authors: el-Sabban F , Reid K H , Zhang Y P , Edmonds H L 
Published: June 2011

Although it is often assumed in experimental stroke studies that cautery-induced occlusion is permanent, surgeons commonly expect cauterized vessels to recanalize spontaneously. We used the rat middle cerebral artery to determine if electrocoagulation would produce a permanent occlusion in this preparation.
A standard bipolar coagulator, calibrated to determine actual power output, was adjusted to induce platelet aggregation in the middle cerebral artery of anesthetized Sprague-Dawley rats without inducing bleeding through the arterial wall. A reliable temporary thrombosis was induced by a Malis Bipolar Coagulator set to deliver 10 bursts of 1.5 seconds each at a rate of 24 min-1 and a power setting of 3 W. This thrombus was responsive to the antithrombotic agent flunarizine. An apparently permanent occlusion was produced by 30 bursts at 3 W followed by 20 bursts at 5 W. To our surprise, seven of seven such occlusions recanalized spontaneously within 4 hours.
The electrocoagulation process commonly used in experimental stroke studies may produce only a temporary occlusion of the rat middle cerebral artery.
Sjögren's syndrome presenting as ischemic stroke.
Authors: Bragoni M , Di Piero V , Priori R , Valesini G , Lenzi G L 
Published: June 2011

We describe a young woman who presented with minor stroke as a first clinical symptom of Sjögren's syndrome (SS) in the absence of well-known risk factors for cerebrovascular disease.
The medical history included recurrent miscarriages and sun rashes, which directed the diagnosis toward immunologic disorders such as systemic lupus erythematosus and antiphospholipid antibody syndrome, which are often associated with stroke. Only complete laboratory testing, including SSB antibody studies, and ophthalmologic and salivary gland evaluation revealed the correct diagnosis.
Sjögren's syndrome should be considered among the causes of stroke, especially in a young female patient.
Use of Medicare claims data to estimate national trends in stroke incidence, 1985-1991.
Authors: May D S , Kittner S J 
Published: June 2011

Although stroke mortality has been declining in the United States for decades, recent trends in stroke incidence based on national data have not been described. We used Medicare hospitalization data to estimate national trends in the incidence of stroke among Americans aged 70 years or older, and we provide evidence of the validity of the estimate.
We defined stroke as a principal diagnosis with International Classification of Diseases, 9th Revision, Clinical Modification codes 430 to 434 or 436 to 437. We excluded many recurrent cases from the analysis by eliminating persons hospitalized for stroke during the 5 years preceding the index stroke. We calculated annual adjusted incidence rates and examined trends graphically. We investigated the effect of different exclusion periods, trends in in-hospital mortality of stroke patients, and trends in out-of-hospital stroke mortality. We examined trends in relation to sex, race, and age.
The estimated age- and sex-adjusted stroke incidence declined 9.5% from 1985 to 1989, then increased 3.3% to 1991. The pattern did not vary with the length of the exclusion period or when all listed diagnosis rather than principal diagnoses were used to identify stroke cases. Incidence trends resembled the overall trend for both men and women, for 5-year age groups, and for whites; the trend did not change for blacks.
Stroke incidence declined steadily from 1985 to 1989 and then increased slightly to 1991. Several postulated potential sources of bias were investigated and found to be unlikely to account for the incidence decline, although some may have contributed to the subsequent incidence increase.
Body mass index and thromboembolic stroke in nonsmoking men in older middle age. The Honolulu Heart Program.
Authors: Abbott R D , Behrens G R , Sharp D S , Rodriguez B L , Burchfiel C M , Ross G W , Yano K , Curb J D 
Published: June 2011

While evidence suggests that obesity has an independent relation to coronary artery disease, similar findings for stroke have not been established. The purpose of this study was to examine the relation between body mass index and the risk of thromboembolic stroke independently of other risk factors.
Since 1965, the Honolulu Heart Program has followed a cohort of men in a prospective study of cardiovascular disease. This article examines the relationship between the baseline measurement of body mass index and the risk of thromboembolic stroke in 1163 nonsmoking men in older middle age (55 to 68 years). Men who had an elevated risk of stroke due to hypertension, diabetes, and other risk factors were excluded from the analysis.
After 22 years of follow-up, the rate of stroke increased significantly with increasing levels of body mass (P < .01). In the bottom tertile of the body mass index, the rate of thromboembolic stroke was 28.7 per 1000 (11/383). In the middle tertile, the rate was increased by 40% to 40.7 per 1000 (16/393), and in the top tertile, the rate of thromboembolic stroke was 55.4 per 1000 (21/387), a twofold excess compared with the bottom tertile. After adjustment for age and the residual effects of confounding risk factors, including systolic blood pressure and serum glucose, the estimated relative risk of stroke for the average body mass index in the top tertile (26.6 kg/m2) compared with that in the bottom tertile (20.3 kg/m2) was 2.1 (95% confidence interval, 1.1 to 4.1). These findings were not affected by coronary events that occurred in the course of follow-up, nor did they appear to be influenced by deaths from other causes.
We conclude that elevated body mass is associated with an increased risk of thromboembolic stroke in nonsmoking men in older middle age who are free of commonly observed conditions related to cardiovascular disease.
Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality.
Authors: Boon A , Lodder J , Heuts-van Raak L , Kessels F 
Published: June 2011

We wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT.
We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis.
Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P = .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P = .005) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P = .011; and OR, 1.58; 95% CI, 1.13 to 2.21; P = .007; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI, 1.10 to 2.79; P = .018; and OR, 1.57; 95% CI, 1.09 to 2.24; P = .014; respectively). A cardioembolic source or atrial fibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction > 50%) was not significantly associated with any type of silent lesion. Initial severe handicap (Rankin Scale score > 3), 30-day case fatality rate, and 1-year mortality were not affected by the presence of silent infarcts.
The strong association of silent small deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), whereas cardiogenic embolism and large-vessel thromboembolism are the most likely causes in both silent and first symptomatic territorial infarcts. Single or multiple silent infarcts do not predict a cardioembolic stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influence the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality. The significance of silent infarcts for predicting possible future cognitive decline and risk of recurrent stroke deserves further study.
Detection of reverse flow by duplex ultrasonography in orthostatic hypotension.
Authors: Yonehara T , Ando Y , Kimura K , Uchino M , Ando M 
Published: June 2011

The aim of this study is to elucidate the effect of orthostatic hypotension on changes in cerebral blood flow.
Blood flow velocities of both the common carotid artery and vertebral artery were measured using duplex ultrasonography in 12 patients: 6 with familial amyloidotic polyneuropathy, 3 with Shy-Drager syndrome, 2 with pandysautonomia, and 1 with senile orthostatic hypotension. Simultaneously, peripheral blood flow was also evaluated by laser-Doppler flowmetry.
The patients showing dizziness or syncope when tilted to a 70 degrees upright position exhibited characteristic reverse flow at the end-diastolic phase on the Doppler flow image of both the common carotid and vertebral arteries, which was effectively treated by infusion of 2.5 micrograms/min norepinephrine for 10 minutes. This end-diastolic reverse flow was not seen in any patients who did not have dizziness or syncope. After subjects were tilted from a supine to a 70 degrees upright position, decrease in the peripheral blood flow of the patients with orthostatic hypotension remained unchanged for at least 5 minutes, whereas that of control subjects was recovered within 2 minutes. However, no significant difference between the patients with and without clinical symptoms was observed.
These results suggest that detection of this specific echographic pattern may be quantitatively useful in examination of clinical symptoms accompanying orthostatic hypotension and that duplex ultrasonography may be a helpful tool to evaluate the effect of drugs used for controlling these clinical signs.
Increased proportion of docosahexanoic acid and high lipid peroxidation capacity in erythrocytes of stroke patients.
Authors: Imre S G , Fekete I , Farkas T 
Published: June 2011

Intracellular accumulation of lipid peroxides that derive from the autoxidation of membrane polyunsaturated fatty acids reduces the deformability of erythrocytes contributing to the hemorheological disturbances observed in acute cerebral ischemia. The present study deals with the biochemical background of increased lipid peroxidation capacity in the erythrocytes of stroke patients.
A complete clinical and laboratory assessment was made of 24 men and 18 women (aged 50 to 78 years; 64.5 +/- 13.9 years, mean +/- SD) who had an ischemic hemispheric lesion of the brain. Lipid peroxide content, lipid peroxidation capacity, superoxide dismutase activity, and fatty acid composition of erythrocytes were compared in stroke patients and 22 healthy subjects matched for age. The lipid peroxide content of the erythrocytes was estimated before and after the autoxidative test; the results were expressed as nanomoles of malondialdehyde per gram of hemoglobin. The increase of the lipid peroxide content in the erythrocytes during the autoxidative test measures the lipid peroxidation capacity.
In comparison with healthy subjects (1.45 +/- 0.30 nmol MDA/g Hb per 24 hours), the lipid peroxidation capacity was found to be significantly higher (4.18 +/- 0.41 nmol MDA/g Hb per 24 hours) (P < .01) in the erythrocytes of stroke patients. The stroke patients could be divided into two groups on the basis of lipid peroxidation capacity of their erythrocytes. Twenty patients had erythrocytes with high lipid peroxidation (< 4 nmol MDA/g Hb per 24 hours), and 22 patients had very high lipid peroxidation capacity (> 4 nmol MDA/g Hb per 24 hours). There was no significant difference in superoxide dismutase activity in the erythrocytes of patients compared with healthy subjects. Before the autoxidative test was conducted, the fatty acid composition in the erythrocytes of stroke patients with very high lipid peroxidation capacity was measured and found to be generally normal; only the proportion of docosahexanoic acid (22:6 n-3) was markedly (P < .01) increased.
The results suggest that the erythrocytes of ischemic stroke patients with very high lipid peroxidation capacity displaying an abnormal fatty acid composition are much more vulnerable to lipid peroxidation. The increased proportion of docosahexanoic acid and the high lipid peroxidation capacity of erythrocytes play a pathogenetic role and explain the hemorheological disturbances observed in the microcirculation of stroke patients.