bluuebunny/crossref_metadata_2025_split huggingface dataset:
Computed tomography in prognostic stroke evaluation.
Authors: Rasmussen D , Køhler O , Worm-Petersen S , Blegvad N , Jacobsen H L , Bergmann I , Egeblad M , Friis M , Nielsen N T 
Published: June 2011

Computed tomography is now routinely used in many hospitals to investigate cerebrovascular disease. The purpose of our prospective study was to determine whether cranial computed tomography in connection with neurological assessment was useful in prognostic evaluation of survival after acute stroke.
Two-hundred forty-five consecutive stroke patients were included in the project during a 1-year period. Each had a detailed neurological assessment 24-72 hours after stroke onset and underwent cranial computed tomography without intravenous contrast injection within the first week after admission. The lesions were divided according to neuroanatomic regions. In the statistical analyses we used a multiple logistic regression model with survival/death as the binary variable.
Computed tomography showed 76% of the patients had infarcts, 11% had hemorrhages, and 13% had no acute lesion. Forty-three patients had more than one acute lesion, and 57 had one or more old infarctions. The temporal, parietal, and frontal regions and the basal ganglia were most often affected.
We conclude that age, level of consciousness, and involvement of the temporal lobe on computed tomography were factors of prognostic significance regarding survival in the acute phase.
Release of superoxide dismutase into cerebrospinal fluid as a marker of brain lesion in acute cerebral infarction.
Authors: Strand T , Marklund S L 
Published: June 2011

Evaluation of biochemical patterns in cerebrospinal fluid may add diagnostic and prognostic information. We tested to determine whether the concentration of superoxide dismutase in cerebrospinal fluid is a marker of brain tissue damage in acute ischemic stroke.
We investigated 36 acute ischemic stroke patients for cerebrospinal fluid activity of the enzyme superoxide dismutase on two occasions shortly after symptom onset (average, day 1 and day 4).
In 75% of the patients, the first of two lumbar punctures revealed the maximal superoxide dismutase value. The amount in the cerebrospinal fluid was significantly correlated with the size of infarction on computed tomographic scan (p less than 0.001 by analysis of variance) and to functional impairment and stroke-related mortality during initial hospital stay (p less than 0.002). The correlation of initial superoxide dismutase concentration with the need for long-term institutional care and mortality at 3 months after the stroke was also significant (p less than 0.03).
We conclude that superoxide dismutase in cerebrospinal fluid is a marker of an acute brain lesion and has some value as a prognostic predictor. This small enzyme leaks rapidly from ischemically injured cells.
A rat model of severe neonatal hypoxic-ischemic brain injury.
Authors: Schwartz P H , Massarweh W F , Vinters H V , Wasterlain C G 
Published: June 2011

Perinatal hypoxic-ischemic brain injury is a common problem with severe neurological sequelae. In this report we describe in detail a simple model of hypoxia-ischemia in the neonatal rat that gives rise to severe neocortical infarction and to selective hippocampal neuronal necrosis.
Seven-day-old Simonsen Wistar rat pups underwent bilateral carotid artery ligation under methoxyflurane anesthesia and, after a 4 to 6-hour recovery, were exposed to 60 minutes of hypoxia (6.5% O2); they were perfusion-fixed 3 days later for histological study. Brain temperature was monitored throughout this treatment.
We found that 64 +/- 3% of neocortex above the rhinal sulcus was infarcted; this infarction was evenly distributed through the cerebral hemispheres. In the hippocampus, neuronal necrosis was selective for the internal (hilar) layers of granule cells of the dentate gyrus, with relative sparing of CA1 pyramidal cells. In addition, brain temperature was tightly controlled throughout the experimental manipulations.
The present model is easy and sensitive and provides an infarct of sufficient severity and homogeneity to make it well suited for pharmacological and biochemical studies directed toward therapeutic amelioration and mechanisms of hypoxic-ischemic brain damage, respectively. In addition, the pattern of damage in the hippocampus is quite different from that seen in the adult brain, which should be helpful in studying the ontogeny of selective vulnerability.
Effects of carbon dioxide inhalation on cerebral blood flow and oxygen tissue level in spontaneously hypertensive rabbits.
Authors: Hegedüs K , Fekete I , Molnár L 
Published: June 2011

Because previous studies have yielded conflicting results, this study was designed to investigate the efficiency of cerebrovascular reactivity to carbon dioxide in hypertension associated with moderate diffuse cerebral ischemic lesions.
The effects of carbon dioxide inhalation on mean arterial blood pressure, heart and respiration rates, cerebral cortical blood flow, polarographically detected oxygen currents (oxygen availability), and cerebral electrical activity were compared in 14 spontaneously hypertensive and 16 normotensive rabbits anesthetized with urethane and alpha-chloralose. Blood flow was measured with the hydrogen clearance and thermal clearance methods.
In the resting state the frequency of electrical activity shifted to slower components, the levels of oxygen availability and cerebral blood flow were lower (p less than 0.01), and the ratio of the two latter parameters was greater (p less than 0.01) in hypertensive rabbits than in normotensive animals. Carbon dioxide inhalation induced more marked increases in cerebral blood flow, respiration rate, and oxygen availability in hypertensive (p less than 0.01) than in normotensive (p less than 0.05) rabbits. The ratio of oxygen availability to cerebral blood flow decreased (p less than 0.01) in the former and did not change significantly in the latter group. The carbon dioxide-induced rise in blood flow was also slower and more protracted in hypertensive rabbits (p less than 0.01). Histological investigation revealed groups of neurons with ischemic changes in the cortex of the hypertensive rabbits.
We suggest that in hypertensive rabbits the mild multiple ischemic lesions are the basis of functional disturbances, including reduced resting cerebral blood flow, greater oxygen tissue level, slower response to carbon dioxide, and greater vasodilatory capacity.
Evaluation of long-term outcome and safety after hemodilution therapy in acute ischemic stroke.
Authors: Strand T 
Published: June 2011

In a previous single-center, randomized controlled trial including 102 patients treated in a stroke unit, we showed that rapid, modest hemodilution improved short-term clinical outcome in ischemic stroke patients. I now evaluate the long-term outcome and potential risks of this combined venesection/dextran 40 therapy in the same 52 treated and 50 control patients.
Mortality, need for institutional care, and recurrent strokes were registered during 1 year following inclusion in the trial, and a final evaluation of functional outcome was performed at 12 months after the stroke. Cerebrospinal fluid was analyzed for protein content and hemorrhagic admixture at two occasions during the acute phase.
Thirty-six hemodiluted and 30 control patients survived the first year following the stroke (difference not significant). One year after the stroke, persistent neurological deficits were less frequent among the hemodiluted patients and a larger proportion of hemodiluted survivors was independent in walking (92% versus 73%, p less than 0.05). Two hemodiluted patients (6%) and nine control patients (30%) were totally dependent in the activities of daily living (p less than 0.05). Three hemodiluted patients (8%) and eight control patients (27%) remained hospitalized 1 year after the stroke (p less than 0.05). With the possible exception of patients with a medical history of congestive heart failure, subset analyses revealed a tendency toward improved outcome for hemodiluted patients in all clinically important subgroups compared with the controls. When analyzing cerebrospinal fluid, signs of blood-brain barrier breakdown and hemorrhagic admixture to the cerebrospinal fluid during the acute phase were less frequent in the hemodiluted subjects.
These results suggest that, when applied in a stroke unit, the combination of venesection and dextran 40 administration is a clinically safe, therapeutic regimen in the treatment of acute cerebral infarction that improves long-term clinical outcome.
Stroke with negative brain magnetic resonance imaging.
Authors: Alberts M J , Faulstich M E , Gray L 
Published: June 2011

Magnetic resonance imaging (MRI) of the brain is replacing computed tomography in the diagnostic evaluation of acute ischemic strokes. Past studies have suggested that MRI may not visualize all acute strokes, but few clinical details were included. To better understand the clinical characteristics of strokes not detected by MRI, we collected and reviewed case histories of several patients with acute stroke who had negative MRI scans.
Patients with a clinical diagnosis of stroke and negative brain MRI scans were ascertained from hospital records dating from 1989 to mid-1991. Patients with transient ischemic attacks, postictal paralysis, functional examinations, central nervous system infections, other nonstroke diagnoses, or equivocal findings were excluded. The MRI scans were performed with a GE Signa 1.5-T magnet in an axial plane (spin-echo repetition time/echo time: 500 msec/20 msec; 2,500 msec, 30 msec/80 msec). One patient received contrast material.
We identified seven patients with clinically diagnosed ischemic stroke and negative brain MRI scan. Six of seven patients were scanned within 7 days of symptom onset and two patients within 24 hours. One patient was scanned 3 months after symptom onset. The strokes not detected by MRI were clinically localized to the cortex (n = 3), brain stem (n = 3), and subcortical/lacunar area (n = 1). One patient underwent two MRI scans, one with gadolinium.
These cases, while selected, illustrate some potential limitations of MRI for diagnosing stroke.
Prediction of symptomatic vasospasm after subarachnoid hemorrhage by rapidly increasing transcranial Doppler velocity and cerebral blood flow changes.
Authors: Grosset D G , Straiton J , du Trevou M , Bullock R 
Published: June 2011

Increased transcranial Doppler velocities and regional cerebral perfusion defects have been well demonstrated in patients with subarachnoid hemorrhage, but the clinical significance of these changes has not been clearly defined, particularly in the presymptomatic stage of cerebral vasospasm. We have tested the hypothesis that a rapid, massive rise in Doppler velocity denotes progressive vasospasm by relating Doppler velocity increases to regional cerebral blood flow changes and to the subsequent clinical course.
Serial transcranial Doppler sonography was performed in 121 patients; 20 of these patients were selected for blood flow mapping on the basis of rapid increases (greater than 50 cm/sec/24 hr) in blood flow velocity. Cerebral blood flow was mapped by single-photon emission computed tomography using technetium-99m hexamethylpropyleneamine oxime.
Ten of 15 patients studied before the onset of any deficit subsequently developed a focal neurological abnormality. In 14 of these 15 patients, and in a further five in which single-photon emission computed tomography was performed after the onset of a delayed neurological deficit, perfusion patterns were abnormal and correlated with sites of increased Doppler velocities. Four patients had zones of cerebral hypoperfusion but did not develop neurological deficit.
Transcranial Doppler measurements can assist in identifying patients at risk of delayed ischemic deficit. Selection of patients for regional cerebral blood flow mapping studies and for prophylactic anti-ischemic therapy may be considered on this basis.
Ischemic brain damage is not ameliorated by 1,3-butanediol in hyperglycemic rats.
Authors: Lundgren J , Smith M L , Mans A M , Siesjö B K 
Published: June 2011

Treatment with the ketone body precursor 1,3-butanediol has been suggested to ameliorate hypoxic/ischemic brain damage. Butanediol could provide an alternative energy substrate for the brain, thereby decreasing the amount of glycolytically produced lactate. Hyperglycemia aggravates brain damage after brain ischemia and causes fatal postischemic seizures, probably by increasing the production of lactate and decreasing the pH. We studied whether butanediol treatment altered the adverse consequences following ischemia complicated by hyperglycemia.
Hyperglycemic adult male rats were given 25 or 50 mmol.kg-1 body wt butanediol intravenously 30 minutes before 10 minutes of transient forebrain ischemia. Morphological evaluation was performed following perfusion-fixation after 15 hours of recovery. Blood concentrations of beta-hydroxybutyrate, acetoacetate, glucose, and lactate and brain tissue concentrations of energy metabolites were measured before and after ischemia.
Blood levels of ketone bodies increased in the butanediol-treated rats. Ischemia decreased the blood levels of acetoacetate but increased the levels of beta-hydroxybutyrate by a similar amount, resulting in unchanged high levels of total ketone bodies in the animals that received butanediol. Brain tissue levels of glucose, energy metabolites, and lactate showed no difference between butanediol- and saline-treated rats. Furthermore, compared with saline-treated animals butanediol-treated rats showed no decrease in brain damage and no attenuation in the development of postischemic seizures.
The ketone body precursor 1,3-butanediol offers no protective effect in transient forebrain ischemia complicated by hyperglycemia.
Polyethylene glycol superoxide dismutase and catalase attenuate increased blood-brain barrier permeability after ischemia in piglets.
Authors: Armstead W M , Mirro R , Thelin O P , Shibata M , Zuckerman S L , Shanklin D R , Busija D W , Leffler C W 
Published: June 2011

Transport of urea across the blood-brain barrier is increased during postischemic cerebral reperfusion in the piglet. Ischemia/reperfusion also has been observed to increase apparent superoxide anion generation on the surface of the brain. The present study was designed to address the hypothesis that the increased transfer of urea into the brain after ischemia/reperfusion could be due to superoxide anion-induced alterations in blood-brain barrier permeability.
Blood-to-brain transfer of carbon-14-labeled urea was measured in four groups (n = 7 each) of newborn pigs: 1) control (no ischemia, no pretreatment), 2) pretreatment with polyethylene glycol superoxide dismutase (1,000 IU/kg) and polyethylene glycol catalase (10,000 IU/kg i.v.) but no ischemia, 3) no pretreatment and 20 minutes of ischemia followed by 2 hours of reperfusion, and 4) pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase in addition to ischemia/reperfusion. The following brain regions were investigated: cerebrum, caudate, midbrain, pons, medulla, and cerebellum.
Polyethylene glycol superoxide dismutase inhibited generation of superoxide anion by the brain during reperfusion after ischemia. Regional transfer of [14C]urea from blood to brain increased at 2 hours' reperfusion. This ischemia-induced increase in blood-to-brain transfer of [14C]urea was attenuated by pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase: e.g., cerebrum Kin was 28 +/- 2 in the control group, 26 +/- 3 in the pretreated/no ischemia group, 67 +/- 5 in the untreated/ischemia group, and 40 +/- 2 ml.g-1.s-1.10(6) in the pretreated/ischemia group. After ischemia/reperfusion, cerebral blood flow was unchanged by pretreatment with polyethylene glycol superoxide dismutase and polyethylene glycol catalase.
These data suggest that production of a partially reduced species of oxygen contributes to the increased urea transfer across the blood-brain barrier after ischemia in the newborn pig.
Stroke and Parkinson's disease.
Authors: Levine R L , Jones J C , Bee N 
Published: June 2011

We sought to determine whether the recently reported decreased incidence of stroke and atherosclerotic disease in a university hospital-based Parkinson's disease patient population would be demonstrated in our patient population.
We performed a retrospective case-control review of the last 119 Parkinson's disease patients discharged from the Middleton Veterans Affairs Hospital Neurology Service to study the incidence of ischemic stroke, myocardial ischemia, tobacco use, and other stroke risk factors. Controls were age and sex matched and were randomly taken from 238 non-Parkinson's disease discharges in which stroke or myocardial infarction was not the reason for hospitalization.
The cumulative incidences of ischemic stroke, hypertension, and diabetes mellitus were not significantly different between groups. Myocardial infarction, coronary artery disease, tobacco use, atrial fibrillation, cancer, and ethanol abuse were significantly more prevalent in the controls, whereas dementia and congestive heart failure were the only variables studied that were more prevalent in the Parkinson's disease patients.
Our study failed to demonstrate that Parkinson's disease patients from a Veteran population were protected from ischemic stroke.
Influence of tissue plasminogen activator and heparin on cerebral ischemia in a rabbit model.
Authors: Carter L P , Guthkelch A N , Orozco J , Temeltas O 
Published: June 2011

The aims of this study were to verify that tissue-type plasminogen activator given either 1 or 2 hours after experimental embolic stroke in rabbits diminishes the volume of resulting ischemic brain and to ascertain the effect of the simultaneous administration of heparin.
We embolized the middle cerebral artery of rabbits by injecting performed autologous arterial ("white") thrombus into one internal carotid artery. Treatment with 2 mg/kg tissue-type plasminogen activator, alone or in combination with heparin, was commenced either 1 or 2 hours after embolization. The animals were killed 5 hours after treatment commenced, and their brains were examined for evidence of ischemia and hemorrhage.
Administration of tissue-type plasminogen activator significantly diminished the size of the resulting brain ischemia. Administration of heparin, with or instead of tissue-type plasminogen activator, did not result in a significant decrease in the volume of cerebral ischemia, but it also did not lead to hemorrhagic transformation of the stroke.
In the rabbit model, administration of tissue-type plasminogen activator within 2 hours diminished the volume of brain rendered acutely ischemic by embolic stroke. Since the simultaneous administration of heparin during this same period did not result in any instances of hemorrhagic transformation, tissue-type plasminogen activator may have some place for use in such circumstances to mitigate a tendency to further embolic or thrombotic events.
Effects of hypothermia on evoked potentials, magnetic resonance imaging, and blood flow in focal ischemia in rabbits.
Authors: Lo E H , Steinberg G K 
Published: June 2011

Mild hypothermia has been shown to ameliorate neuronal damage due to cerebral ischemia. In our study, the influence of mild-to-moderate hypothermia was examined in a rabbit model of focal cerebral ischemia.
After 4 hours of permanent ischemia induced by occlusion of the anterior and middle cerebral and internal carotid arteries, somatosensory evoked potentials and regional cerebral blood flow were measured. Ex vivo magnetic resonance imaging scans were also obtained to determine the degree of ischemic brain injury. Three temperature (temporalis muscle) groups were studied: 37 degrees C, 33 degrees C, and 30 degrees C (n = 5 per group). An additional two animals were used to confirm that temporalis muscle temperatures were well correlated with brain temperature. Rectal temperatures were kept constant (37.5 degrees C) in all groups.
After 4 hours of focal ischemia, evoked potentials in the normothermic animals remained depressed (2.2 +/- 2.1% [mean +/- SEM] preocclusion values). Recovery of potentials was significantly enhanced in both hypothermic groups (p less than 0.05): 18.2 +/- 6.5% (33 degrees C) and 43.6 +/- 12.2% (30 degrees C). Quantitative magnetic resonance measurements showed that T1 and T2 relaxation times were increased in the core ischemic regions within the cortex (20.4 +/- 4.0% and 25.3 +/- 5.9%, respectively). These elevations in T1 and T2 were reduced by hypothermia. However, blood flow was not improved by lowered temperature; in fact, flow in the 30 degrees C group was significantly decreased compared with the other groups (p less than 0.01). There was no statistically significant correlation between specific cerebral blood flow values and T1 or T2 elevations.
These results demonstrate that hypothermia can improve evoked potentials and magnetic resonance parameters in permanent focal ischemia. However, moderate hypothermia (30 degrees C) appears to also significantly decrease blood flow in the ischemic brain.
Tirilazad reduces cortical infarction after transient but not permanent focal cerebral ischemia in rats.
Authors: Xue D , Slivka A , Buchan A M 
Published: June 2011

We examined the cytoprotective effect of the lipid peroxidation inhibitor tirilazad mesylate (U74006F) in rodent models of neocortical infarction induced by transient and permanent focal cerebral ischemia.
Wistar rats (experiment 1) and spontaneously hypertensive rats (experiment 2) were subjected to 2 hours of transient middle cerebral artery occlusion followed by 22 hours of reperfusion and pretreated with 10 mg/kg i.p. tirilazad, vehicle, or saline. Repeat doses were given at 4 and 10 hours after reperfusion. Spontaneously hypertensive rats were also subjected to permanent middle cerebral artery occlusion and either pretreated with tirilazad, vehicle, or saline intraperitoneally (experiment 3) or treated with either tirilazad or vehicle intravenously after ischemia (experiment 4). Cortical infarct volumes were measured 24 hours after the onset of either transient or permanent ischemia, and changes in core regional cerebral blood flow were monitored with laser Doppler flowmetry.
Tirilazad reduced infarct volume after transient ischemia by 40% in Wistar rats (p = 0.08) (experiment 1) and 23% in spontaneously hypertensive rats (p less than 0.05) (experiment 2) but did not reduce infarction after permanent ischemia whether it was given intraperitoneally (experiment 3) or intravenously (experiment 4). Ischemic core blood flows were not affected during ischemia, nor were they affected during reperfusion after transient ischemia.
Tirilazad reduces cortical infarction in transient but not permanent ischemia, an effect not related to improvement in regional cerebral blood flow. Tirilazad might prove to be useful as an adjuvant therapy after successful thrombolysis in acute stroke patients.