bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal leukocyte antibody does not decrease the injury of transient focal cerebral ischemia in cats.
Authors: Takeshima R , Kirsch J R , Koehler R C , Gomoll A W , Traystman R J 
Published: June 2011

We tested the hypothesis that inhibition of leukocyte function by administration of monoclonal antibody 60.3 (MoAb 60.3) improves electrophysiological recovery and decreases injury volume following transient focal cerebral ischemia in cats.
Halothane-anesthetized cats underwent 90 minutes of left middle cerebral artery and bilateral common carotid artery occlusion followed by 180 minutes of reperfusion. Cats were assigned to receive either 2 mg/kg MoAb 60.3 (n = 8) directed at the CDw18 leukocyte antigen complex or an equal volume of diluent (sterile saline; n = 10) at 45 minutes of ischemia in a blinded fashion.
Blood flow to the left temporoparietal cortex decreased to less than 5 ml/min/100 g with ischemia, but was minimally affected on the right side. Postischemic hyperemia occurred in the left caudate nucleus, whereas blood flow in other brain regions returned to control. No region demonstrated delayed hypoperfusion, and there were no differences between groups. Somatosensory evoked potential recorded over the left cortex was ablated during ischemia and recovered to less than 10% of baseline amplitude at 180 minutes of reperfusion in both groups. Left hemispheric injury volume, as assessed by 2,3,5-triphenyltetrazolium chloride staining, was not affected by drug treatment (mean +/- SE values: MoAb 60.3, 37 +/- 5%; placebo, 38 +/- 7% of hemisphere).
Inhibition of leukocyte function with MoAb 60.3 does not afford protection from severe focal ischemia and reperfusion in cats.
Neurological and behavioral outcomes of focal cerebral ischemia in rats.
Authors: Wahl F , Allix M , Plotkine M , Boulu R G 
Published: June 2011

The aim of this study was to investigate the neurobehavioral consequences of focal ischemia in rats.
We induced permanent occlusion of the left middle cerebral artery in 14 Sprague-Dawley rats, and used 13 sham-operated rats as controls. During surgery, brain temperature and body temperature were kept at normothermia. Neurobehavioral studies (neurological examination, passive avoidance task, Y maze test, and modified open-field test) were carried out 4 days after ischemia before killing the rats to evaluate histological damage.
Ischemia induced large infarcts in the cortex (138.6 +/- 8.5 mm3) and caudate-putamen (48.8 +/- 2.6 mm3) and, compared with sham-operated rats, produced a dramatic neurological deficit (p less than 0.001) characterized by sensorimotor dysfunctions and hemiplegia. Memory retention was significantly (p less than 0.05) impaired in the passive avoidance task, but neither vigilance and exploratory behavior measured in the modified open-field test nor working memory evaluated in the Y maze test were disturbed. Infarct size was not correlated with the neurological or behavioral deficits.
This lack of correlation indicates the necessity of carrying out parallel histological, neurological, and behavioral studies in any assays of new drugs using this model of focal ischemia.
Bilateral middle cerebral artery occlusions in neurocysticercosis.
Authors: terPenning B , Litchman C D , Heier L 
Published: June 2011

Bilateral hemispheric strokes in a young adult are very rare. We describe a case of neurocysticercosis in a young male with bilateral middle cerebral artery occlusions.
Axial tomographic imaging revealed lesions compatible with cysticerci adjacent to each middle cerebral artery initial segment, and occlusion of both arteries at that level was demonstrated by angiography. Extensive medical workup disclosed no other risk factors for stroke.
Neurocysticercosis should be considered in the differential diagnosis of stroke in a young patient.
Provokable bilateral vertebral artery compression diagnosed with transcranial Doppler.
Authors: Brautaset N J 
Published: June 2011

Head and neck movements may cause vascular compression that produces a syndrome of vertebrobasilar insufficiency. Vertebrobasilar circulation was examined noninvasively in two patients who were able to provoke these symptoms repeatedly on demand.
Blood flow velocities in the basilar artery (case 1) and both posterior cerebral arteries (both cases) were measured continuously by transcranial Doppler sonography while the patients voluntarily performed the offending maneuvers and reproduced their symptoms. The provocative maneuvers evoked an immediate and precipitous drop in blood flow velocity, producing symptoms within seconds. Upon relief, the blood flow velocities showed a transient overshoot before returning to baseline values.
These observations indicate that the symptoms of vertebrobasilar insufficiency were due to real reductions in blood flow and demonstrate the usefulness of transcranial Doppler sonography to diagnose bilateral extracranial vertebral artery compression.
Prevalence and significance of hyperdense middle cerebral artery in acute stroke.
Authors: Leys D , Pruvo J P , Godefroy O , Rondepierre P , Leclerc X 
Published: June 2011

Early noncontrast computed tomographic scans may visualize a hyperdense middle cerebral artery before the infarct becomes visible. This sign disappears within a few days, corresponds to the clot itself, and might be associated with a poor prognosis. The aim of the study was to determine its prevalence, diagnostic value, relationship to demographic data, ability to separate embolic from nonembolic causes, short-term prognostic value, evolution over time, and relationship to arterial occlusion on angiography.
We performed this study using computed tomographic scans performed within 12 hours after onset in 272 consecutive unselected patients with a first acute cerebrovascular event.
Seventy-three subjects had the hyperdense middle cerebral artery sign, leading to a prevalence of 26.8% in the whole group and 41.2% in patients with a middle cerebral artery infarct. Specificity was 100%, but sensitivity was only 30%. This sign was not dependent on cerebrovascular risk factors, but was more likely to occur in cortical and in large, deep, middle cerebral artery infarcts (p less than 0.01). It provided only a 3.5% gain in predicting death, and one fifth of patients with the sign recovered within 2 weeks; this sign was not an independent variable of poor outcome on multiple linear regression. It spontaneously disappeared within a few days and was always related to an occlusion of the middle cerebral artery in patients who underwent early angiography.
The hyperdense middle cerebral artery sign is useful in the diagnosis of middle cerebral artery occlusion but does not always predict a poor prognosis.
Degeneration of the ipsilateral substantia nigra following cerebral infarction in the striatum.
Authors: Nakane M , Teraoka A , Asato R , Tamura A 
Published: June 2011

In rats, degeneration of the ipsilateral substantia nigra occurs a few weeks after occlusion of the middle cerebral artery. The aim of this study was to clarify whether similar change is observed in stroke patients.
Eighteen patients with striatal infarction and six patients with cortical infarction in the territory of the middle cerebral artery were examined by means of sequential magnetic resonance imaging.
In all patients with striatal infarction, T2-weighted images revealed a high-signal-intensity spot in the ipsilateral substantia nigra. Changes in the ipsilateral substantial nigra appeared at day 14 after stroke on average and then became less intense and smaller a few months after the stroke. By contrast, we observed no nigral changes in any patient with cortical infarction.
The degenerative change in the ipsilateral substantia nigra initially found in the rat model similarly occurred in patients with striatal infarction. This remote change in the substantia nigra may represent magnetic resonance imaging detection of neuropathologic changes in this region through the striatonigral pathway.
Proton magnetic resonance spectroscopy of cerebral lactate and other metabolites in stroke patients.
Authors: Graham G D , Blamire A M , Howseman A M , Rothman D L , Fayad P B , Brass L M , Petroff O A , Shulman R G , Prichard J W 
Published: June 2011

Proton magnetic resonance spectroscopy can measure in vivo brain lactate and other metabolites noninvasively. We measured the biochemical changes accompanying stroke in 16 human subjects with cortical or deep cerebral infarcts within the first 3 weeks after symptom onset, and performed follow-up studies on six.
One-dimensional proton spectroscopic imaging encompassing the infarct region was performed with a 2.1-T whole-body magnet using the stimulated echo pulse sequence and an echo time of 270 msec.
All but one of the cortical stroke patients had increased lactate within or near the infarct. Persistently elevated cerebral lactate was documented in five of six cases studied serially as long as 251 days after infarction. N-acetylaspartate levels were decreased in most cortical strokes. Elevated lactate, accompanied by minimal reduction in N-acetylaspartate, was recorded in two of four patients in the first week following a small subcortical infarct.
Long-term elevation of lactate commonly occurs after stroke. This lactate may arise from ongoing ischemia or infiltrating leukocytes, or it may be a residual of the lactate formed during the initial insult. The ability to observe stroke-elevated lactate pools at any time after lesion onset provides an approach to distinguishing among these possibilities in the future.
Predictive value of repeated systolic blood pressure measurements for stroke risk. The Zutphen Study.
Authors: Keli S , Bloemberg B , Kromhout D 
Published: June 2011

The strength of the association between blood pressure and stroke incidence is dependent on the number of blood pressure measurements. Different summary variables of repeated blood pressure measurements taken during 10 years were evaluated in relation to the long-term risk of stroke in the Zutphen Study.
During the period 1960-1970 repeated blood pressure measures were taken yearly in 603 men aged 50-69 years in 1970 in the town of Zutphen, The Netherlands. The individual average systolic blood pressure between 1960 and 1970, the predicted systolic blood pressure for 1970 (based on regression of blood pressure readings on time), and the single observed systolic blood pressure in 1970 were used as systolic blood pressure estimates. Their strength in predicting the 15-year stroke incidence was assessed using Cox proportional hazards models. Adjustment was made for the confounding effects of age, cigarette smoking, and serum total cholesterol.
The average systolic blood pressure between 1960 and 1970 was the strongest predictor of 15-year stroke incidence. The strength of the association was underestimated by 55% when a casual systolic blood pressure measurement was used instead of 11 yearly measurements.
It can be concluded that a casual blood pressure measurement leads to a substantial underestimation of the long-term stroke risk of an individual.
Blood flow and metabolism during and after repeated partial brain ischemia in neonatal piglets.
Authors: Laptook A R , Corbett R J , Ruley J , Olivares E 
Published: June 2011

Our investigation sought to determine whether neonatal brain ischemic vascular and metabolic effects were altered by repeated episodes of ischemia.
We studied twelve piglets using in vivo magnetic resonance spectroscopy to obtain multiple, simultaneous measurements of cerebral blood flow and phosphorylated metabolites from the same tissue volume. The relationship between cerebral blood flow and energy metabolism was examined over a range of reduced cerebral blood flow (90-10% of control). Three episodes of partial ischemia were studied, each lasting 10 minutes and separated by 45 minutes.
During each interval of ischemia, plots of the percent reduction in cerebral blood flow versus the percent change in phosphorylated metabolites (phosphocreatine, inorganic phosphorus) or unit change in intracellular pH did not differ in slope and intercept. The relationship between beta-ATP and cerebral blood flow during repeated ischemia revealed similar slopes, but a lower intercept during the third interval of ischemia (p = 0.029). After ischemia, cerebral blood flow was reduced as a function of the severity of the preceding ischemia. After each interval of ischemia, phosphocreatine and intracellular pH were unchanged from preischemic values. Inorganic phosphorus remained elevated after ischemia (117 +/- 16 and 118 +/- 11% of control, p less than 0.005, following the first and second intervals of ischemia), and beta-ATP was restored to progressively lower values (92 +/- 10 and 83 +/- 11% of control, p less than 0.025). Calculated free ADP decreased after ischemia and correlated with the postischemic level of beta-ATP (r = 0.63, p = 0.001).
These results demonstrate that the relationship between cerebral blood flow and metabolism was reasonably preserved during repeated partial ischemia. However, following ischemia, alterations occurred in both cerebral blood flow and metabolism. These alterations may reflect a relative inhibition of ATP production by metabolic regulators such as ADP on either glycolysis or oxidative phosphorylation or both.
Neuroprotective effects of SKF 10,047 in cultured rat cerebellar neurons and in gerbil global brain ischemia.
Authors: Lysko P G , Gagnon R C , Yue T L , Gu J L , Feuerstein G 
Published: June 2011

Excitatory amino acids and their receptors are involved in mediating ischemic neuronal damage. The sigma-agonists are believed to interact with the N-methyl-D-aspartate receptor. Therefore, we studied the neuroprotective, hypothermic, and motor deficit effects of the sigma-agonist SKF 10,047 and the N-methyl-D-aspartate antagonist MK-801.
Neuroprotective effects were compared using an in vitro ischemia model of cultured rat cerebellar granule cells and the gerbil model of global brain ischemia induced by 5 minutes of bilateral carotid artery occlusion followed by 7 days of reperfusion.
In vitro, (+)MK-801 protected against 100 microM glutamate with a 50% protective concentration of 30 nM, followed by (-)MK-801 (150 nM), cyclazocine (0.5 microM), (+)SKF 10,047 (3.3 microM), pentazocine (5 microM), and (-)SKF 10,047 (10 microM). In vivo, (+)SKF 10,047 pretreatment (60 mg/kg) or multiple postischemic treatments provided neuroprotection comparable with MK-801 pretreatment (10 mg/kg). When ischemic animals were administered the multiple dosing regimen of (+)SKF 10,047, no hypothermic effect was noted in the temporalis muscle over 4 hours' postischemia. Motor deficits monitored by a swing grid test showed that 50% recovery from (+)SKF 10,047 was 5.5 times faster than recovery from MK-801.
These results are the first to report a hypothermia-free, in vivo neuroprotective effect of (+)SKF 10,047, a prototypical drug of the sigma-agonist class.
Significance of low perfusion with increased oxygen extraction fraction in a case of internal carotid artery stenosis.
Authors: Yamauchi H , Fukuyama H , Fujimoto N , Nabatame H , Kimura J 
Published: June 2011

Decreased cerebral blood flow with an increased oxygen extraction fraction, the so-called misery perfusion syndrome, suggests a vulnerability to reduction in cerebral perfusion pressure and a tendency to develop cerebral infarction. It is uncertain, however, whether the infarct would occur in the brain region specifically exhibiting this condition.
We report the case of a patient with right intracranial internal carotid artery stenosis who presented with mild left hemiparesis resulting from a right frontal watershed infarct. Positron emission tomography 2 months after the stroke showed decreased cerebral blood flow with an increased oxygen extraction fraction in noninfarcted areas of the affected hemisphere. Maximal changes were detected in the watershed area between the middle cerebral artery and the posterior cerebral artery. Three months later, while on antiplatelet therapy, he suffered a new infarct in the right temporo-occipital watershed area that had shown the highest oxygen extraction fraction value on the first positron emission tomographic study. One month after the recurrence of stroke, a second study showed that low perfusion with increased oxygen extraction fraction persisted in the affected hemisphere to a lesser degree than in the first study.
This observation suggests that the area of low perfusion exhibiting the highest oxygen extraction fraction has the highest risk for infarction. Increased oxygen extraction fraction may be an important factor in the development of hemodynamic infarction.
Early clinical differentiation of cerebral infarction from severe atherosclerotic stenosis and cardioembolism.
Authors: Timsit S G , Sacco R L , Mohr J P , Foulkes M A , Tatemichi T K , Wolf P A , Price T R , Hier D B 
Published: June 2011

Hyperacute cerebral infarction trials require early differentiation of infarction subtype. Our aim was to determine clinical factors predictive of infarction subtype from data collected in the early hours of admission.
Using the 1,273 patients enrolled in the Stroke Data Bank, stroke risk factors and demographic, clinical, and radiological features were compared between the 246 cardioembolic and 113 large-vessel atherosclerotic cerebral infarcts.
Stroke Data Bank definitions ensured more transient ischemic attacks in atherosclerotic infarcts and more cardiac disease in cardioembolic infarcts, but the diagnosis was distinguished further using a logistic regression model. Fractional arm weakness (shoulder different from hand) (odds ratio 3.1, 95% confidence interval [CI] 1.6-5.8), hypertension (odds ratio 2.8, CI 1.4-5.3), diabetes (odds ratio 2.5, CI 1.2-5.1) and male gender (odds ratio = 2.2, CI 1.2-4.1) occurred more frequently in patients with atherosclerotic than cardioembolic infarcts. Reduced consciousness (odds ratio = 3.2, CI 1.4-7.3) was more frequent in cardioembolism. For a male patient with hypertension, diabetes, and fractional arm weakness, the estimated odds of an atherosclerotic infarction were 47-fold that of a cardioembolic infarction. Patients with atherosclerotic infarcts were more likely to have a fractional arm weakness regardless of infarct size, whereas, for those with cardioembolic infarctions, fractional weakness was more frequent in infarcts less than 20 cc in volume.
Clinical features that are observed at stroke onset can help distinguish cerebral infarction subtypes and may allow for early stratification in therapeutic trials.
Correlations between cerebral arterial velocities, blood flow, and delayed ischemia after subarachnoid hemorrhage.
Authors: Davis S M , Andrews J T , Lichtenstein M , Rossiter S C , Kaye A H , Hopper J 
Published: June 2011

Elevated middle cerebral erythrocyte velocities and tissue hypoperfusion have been correlated with delayed ischemia after subarachnoid hemorrhage, but few studies have compared serial arterial velocities with cerebral blood flow and neurological deficits.
Serial measurements of middle cerebral velocities, using transcranial Doppler ultrasonography, were performed in 34 patients after subarachnoid hemorrhage and correlated with cerebral blood flow, measured in 20 of the 34 using single-photon emission computed tomography with technetium-99m hexamethylpropylene amine oxime and neurological evidence of delayed ischemia.
In 16 patients without delayed ischemia, eight had evidence of vasospasm (greater than 120 cm/sec), but only one of seven had hypoperfusion, suggesting that vasospasm might be more common than hypoperfusion in this group (p = 0.1). In 10 patients with delayed ischemia and a lateralizing deficit, both asymmetrical middle cerebral vasospasm (eight of nine with vasospasm) and hypoperfusion (six of six studied) were concordant with the clinically ischemic hemisphere (p less than 0.05). Vasospasm occurred with nonlateralized delayed ischemia in seven of eight patients and with hypoperfusion in five of six, affecting the anterior cerebral territory in three.
Concordant vasospasm and hypoperfusion were most often present in patients with delayed ischemia and lateralizing neurological deficits. Discordant results reflect inherent limitations and the different levels of the circulation monitored by the two techniques.
Penumbral tissues salvaged by reperfusion following middle cerebral artery occlusion in rats.
Authors: Memezawa H , Smith M L , Siesjö B K 
Published: June 2011

The rat is now extensively used for studies on focal cerebral ischemia, and several novel pharmacological principles have been worked out in rat models of middle cerebral artery occlusion. The objective of the present study was to assess how ischemic tissue can be salvaged by reperfusion in a model of transient focal ischemia that gives infarction of both the caudoputamen and the neocortex.
The middle cerebral artery of anesthetized rats was occluded for 15, 30, 60, 90, 120, or 180 minutes by an intraluminal filament, and recirculation was instituted for 7 days to allow assessment of the density and localization of ischemic brain damage using histopathologic techniques. Local cerebral blood flow was measured in separate animals to verify that removal of the filament was followed by adequate recirculation.
Following 15 minutes of middle cerebral artery occlusion seven of eight rats showed selective neuronal necrosis in the caudoputamen, while the neocortex was normal. After 30 minutes of occlusion, seven of eight animals had infarcts localized to the lateral caudoputamen, and four of eight had selective neuronal necrosis in the neocortex. Prolongation of the ischemia to 60 minutes induced cortical infarction in all eight rats. The infarct size increased progressively with increasing occlusion time, up to 120-180 minutes, when the infarcts were as extensive as those observed following 24 hours of permanent middle cerebral artery occlusion.
The results demonstrate a time window for salvage of penumbral tissues by reperfusion that is shorter than that suggested on the basis of previous data in other species. The results probably reflect a lower collateral blood flow in the rat than in other species. This should be taken into account when the effect of pharmacological agents is studied in rats.