bluuebunny/crossref_metadata_2025 huggingface dataset:
Time course of early brain edema following reversible forebrain ischemia in rats.
Authors: Mellergård P , Bengtsson F , Smith M L , Riesenfeld V , Siesjö B K
Published: June 2011

Cerebral ischemia is known to be accompanied by brain edema. This increase in brain tissue water content probably influences the final outcome of an ischemic insult negatively. Despite extensive investigations on different aspects of brain edema, information on edema development during the early recirculation period following ischemia is sparse. We assessed changes in brain water content, as reflected by changes in tissue density, during the early recirculation period following severe forebrain ischemia. Fasted rats were subjected to 5, 15, or 30 minutes of ischemia and 5 to 180 minutes of recirculation. The specific gravity of specimens from the caudoputamen, frontoparietal cortex, hippocampus, and mesencephalon were measured with a Percoll linear density gradient. Five minutes of ischemia followed by recirculation did not produce any significant regional brain edema. However, following 15 minutes of ischemia, transient edema developed in the caudoputamen, frontoparietal cortex, and hippocampus. This edema was maximal after 30 minutes of reperfusion and was normalized after 180 minutes of reperfusion. Similar edema was seen following 30 minutes of ischemia. In the mesencephalon (where blood flow is approximately 50% of control during the ischemic insult) no brain edema was noted following 5, 15, or 30 minutes of ischemia. We discuss to what extent this transient regional brain edema may influence the selective neuronal vulnerability and cell damage observed in rats subjected to reversible forebrain ischemia and how these findings may correlate with neurochemical alterations observed during the early recirculation period.
Intracranial thrombolysis via a catheter embedded in the clot.
Authors: Jungreis C A , Wechsler L R , Horton J A
Published: June 2011

We treated a patient with acute stroke by clot lysis with urokinase. The drug was administered via an arterial catheter that had been positioned in the middle cerebral artery with the catheter tip embedded in the thrombus. The use of a microcatheter that is not flow-directed was essential to performing this procedure. Thrombolysis was successful, but an underlying high-grade vascular stenosis caused rethrombosis. Nevertheless, the techniques used in treating this patient are relatively uncomplicated. They make intracranial arterial thrombolytic drug infusions practical and are an important subject for further clinical evaluation.
Rodent models of cerebral ischemia.
Authors: Ginsberg M D , Busto R
Published: June 2011

The use of physiologically regulated, reproducible animal models is crucial to the study of ischemic brain injury--both the mechanisms governing its occurrence and potential therapeutic strategies. Several laboratory rodent species (notably rats and gerbils), which are readily available at relatively low cost, are highly suitable for the investigation of cerebral ischemia and have been widely employed for this purpose. We critically examine and summarize several rodent models of transient global ischemia, resulting in selective neuronal injury within vulnerable brain regions, and focal ischemia, typically giving rise to localized brain infarction. We explore the utility of individual models and emphasize the necessity for meticulous experimental control of those variables that modulate the severity of ischemic brain injury.
Preoperative training modifies radial maze performance in rats with ischemic hippocampal injury.
Authors: Volpe B T , Davis H P , Colombo P J
Published: June 2011

Rats exposed to 30 minutes of four-vessel occlusion reliably develop severe bilateral CA1 hippocampal injury; under certain conditions of radial maze training, such rats perform the reference memory component as well as controls yet perform the working memory component worse than controls. Reference memory is thought to depend on invariable and working memory on variable spatial information. We assessed the effect of training before ischemia. In Experiment 1, rats trained for 36 trials on 12-arm radial mazes before ischemia demonstrated a persistent impairment on the working memory task but eventually performed the reference memory task comparable to controls. Ischemic rats made more working memory errors as the number of choices increased. This pattern of working memory errors was similar to that in controls except, as expected, ischemic rats made many more errors. In Experiment 2, training for 80 trials before ischemia in rats decreased the severity of both the working and the reference memory impairment. Ischemia did not affect motor behavior in either experiment. These results characterize the working memory deficit in ischemic rats and demonstrate the importance of experimental factors, particularly in the design of treatment strategies to reduce functional impairments caused by ischemia.
Estimation of error limits for cerebral blood flow values obtained from xenon-133 clearance curves.
Authors: Ryding E
Published: June 2011

I provide the theoretical basis for an error calculus for measurements of cerebral blood flow using a freely diffusible tracer substance such as xenon-133. The use of the error calculus is exemplified by a study of the effect on the error margins in measurements of gray matter blood flow from flow level, relative weight of the gray matter compartment, and use of the earliest parts of the clearance curves. The clinical value of the error calculus is illustrated by its ability to separate different sources of measurement error. As a consequence, it is possible to optimize the method for blood flow calculation from the clearance curves, depending on the type of cerebral blood flow measurement. I show that if a true picture of the regional gray matter blood flow distribution is sought, the earliest part of the clearance curves should be used. This does, however, increase the error in the estimate of the average cerebral blood flow value.
Lupus anticoagulants, anticardiolipin antibodies, and cerebral ischemia.
Authors: Kushner M , Simonian N
Published: June 2011

We studied 23 patients suffering cerebral ischemia who also had laboratory evidence of either a lupus anticoagulant (LA) or an abnormal anticardiolipin antibody (ACA). Four patients had lupus or a lupus-like illness, three had drug-induced lupus, and 16 had no overt evidence of collagen-vascular disease. Cerebral ischemic events were multiple in 71% of the patients; two patients presented with multi-infarct dementia. Recognized cerebrovascular disease risk factors were present in 57% of the patients. The partial thromboplastin time was prolonged in only 35% of the patients. An LA was identified in 15 of 21 patients tested, and an elevated ACA titer was identified in 10 of 12 patients tested. Simultaneous assays for LA and ACA were discordant in eight of 10 patients tested. LA- and ACA-associated brain ischemia is often recurrent, but other risk factors for cerebrovascular disease are often present. The laboratory findings in such patients may display considerable heterogeneity.
Atherosclerosis potentiates constrictor responses of cerebral and ocular blood vessels to thromboxane in monkeys.
Authors: Faraci F M , Williams J K , Breese K R , Armstrong M L , Heistad D D
Published: June 2011

The goal of our study was to examine the effects of infusion of serotonin and the thromboxane A2 analogue U46619 into one carotid artery to stimulate their release from platelets during aggregation. We measured blood flow to the brain and eye using microspheres and cerebral microvascular pressure in the pial arteries of normal and atherosclerotic cynomolgus monkeys. Unilateral intracarotid infusion of 10-30 micrograms/min serotonin did not affect cerebral blood flow in normal or atherosclerotic monkeys; serotonin did not alter blood flow to the eye in normal monkeys but decreased flow to the retina and choroid in atherosclerotic monkeys by 39 +/- 11% and 44 +/- 10% (mean +/- SEM), respectively. Infusion of 30 ng/min U46619 did not alter cerebral blood flow but increased the pressure gradient from the aorta to the pial artery, which is an index of large-artery resistance, in atherosclerotic monkeys. U46619 had no effect on blood flow to the eye in normal monkeys but decreased blood flow to the retina and choroid by 71 +/- 14% and 53 +/- 13%, respectively, in atherosclerotic monkeys. Thus, atherosclerosis potentiates the constrictor responses of large cerebral arteries to thromboxane and the responses of blood vessels of the eye to thromboxane and serotonin.
Beta-endorphin in experimental canine spinal ischemia.
Authors: De Riu P L , Petruzzi V , Palmieri G , Gentili C , Melis F , Caria M A , Azzena G B , Casu A R , Marras G , Madeddu G
Published: June 2011

Plasma and cerebrospinal fluid beta-endorphin concentrations were radioimmunologically assayed in dogs subjected to spinal cord ischemia induced by infrarenal aortic ligature and in control sham-operated dogs. Plasma beta-endorphin levels rose significantly following surgery in control dogs but were unaffected by spinal ischemia. On the other hand, a significant increase in cerebrospinal fluid beta-endorphin concentration occurred after spinal ischemia, while surgical stress had no significant effect. Thus, the origins of plasma and cerebrospinal fluid beta-endorphin may be different, with the former secreted from the hypophysis and the latter from nervous tissue. Observed changes in cerebrospinal fluid beta-endorphin concentration could be related to the ischemic lesion of nervous tissue while the changes in plasma levels may reflect general stressing factors such as the surgery in our experiments.
Role for gamma-aminobutyric acid in selective vulnerability in gerbils.
Authors: Sternau L L , Lust W D , Ricci A J , Ratcheson R
Published: June 2011

We tested the efficacy of various putative neuroprotective agents in the gerbil model of delayed neuronal death. The selective loss of anterior CA1 neurons of the hippocampus 4 days after 5 minutes of bilateral ischemia was complete in greater than 90% of the gerbils examined. We tested 11 agents for their ability to protect against neuronal loss. Only those agents that were associated with the GABAergic system exhibited protection and only when administered before the ischemic insult. The possibility that delayed neuronal death is the result of a primary defect in inhibitory neurotransmission is considered.
Infarction of the medulla and cervical cord after fitness exercises.
Authors: Pryse-Phillips W
Published: June 2011

The clinical association of a left lateral medullary syndrome with left corticospinal and posterior column deficits is reported in the case of a young woman with a left vertebral artery dissection. The signs are explicable on the basis of occlusion of branches of the vertebral artery to both the upper cervical cord and the medulla. The dissection may have been due to sustained rotation of the neck during fitness classes. In view of the undocumented benefits and the potential unwanted effects of this exercise, it is doubtful whether it should be recommended.
Prospective analysis of carotid endarterectomy and silent cerebral infarction in 97 patients.
Authors: Sise M J , Sedwitz M M , Rowley W R , Shackford S R
Published: June 2011

To determine the incidence of perioperative silent cerebral infarction, 97 patients who underwent carotid endarterectomy were prospectively studied with preoperative and postoperative computed tomograms. Thirty-one of 96 patients (32%) had findings of cerebral infarction on preoperative computed tomograms. Silent cerebral infarction was found preoperatively in 17 patients (18%) (lacunar infarction in 10, cortical infarction in five, both cortical and lacunar infarctions in one, and cerebellar infarction in one). Transient ischemic attacks occurred in 10 of the 17 patients with silent cerebral infarction; however, symptoms were appropriate to the site in only five of these 10 patients. Fourteen of the 17 patients with silent cerebral infarction had a hemodynamically significant carotid stenosis, and seven patients had an ulcerated plaque on preoperative angiogram. The incidence of these lesions was similar to that found in the group of 66 patients without cerebral infarction. Endarterectomy specimens revealed a higher but not significantly different incidence of ulcerated plaque in the silent cerebral infarction group. There were no perioperative deaths. Following surgery, one patient (1%) with a preoperative silent cerebral infarction suffered a transient ischemic attack, and two patients (2%) with normal preoperative computed tomograms developed permanent neurologic deficits with new cortical infarctions on postoperative computed tomograms. No new silent cerebral infarctions were found on postoperative computed tomograms in any of the 97 patients. Our data suggest that silent cerebral infarction is a common preoperative finding with an as-yet unclear etiology and that carotid endarterectomy does not appear to be a cause.
Streptokinase treatment versus calcium overload blockade in experimental thromboembolic stroke.
Authors: De Ley G , Weyne J , Demeester G , Stryckmans K , Goethals P , Leusen I
Published: June 2011

Thromboembolic brain ischemia was produced in dogs using an autologous blood clot model. The effect of postembolic treatment with flunarizine and streptokinase on hemispheric cerebral metabolic rate for oxygen (CMRO2), oxygen extraction ratio (OER), and cerebral blood flow (CBF) was studied by positron emission tomography (oxygen-15 technique) 24 hours after the insult. We studied five groups of experimental dogs and compared them with a control group of nonembolized dogs. Group I received no treatment, Group II was treated locally with 500,000 IU streptokinase starting 30 minutes after the insult, Group III received streptokinase locally 30 minutes after the insult and 0.1 mg/kg i.v. flunarizine immediately after the insult and 2 hours later, Group IV received flunarizine as Group III, and Group V was orally pretreated with 0.5 mg/kg/day flunarizine during 2 weeks preceding embolization. Compared with the contralateral hemisphere, in the embolized hemisphere a significant reduction of CMRO2 (-25% to -40%) and CBF in normocapnia (-35%) and hypercapnia (-50%) was observed in Groups I, II, and V. In Groups III and IV, CMRO2, OER, and CBF of the embolized hemisphere were within the normal range during normocapnia and hypercapnia; the extent of the ischemic lesions was markedly less than in the other groups of experimental dogs. We conclude that flunarizine treatment after experimental thromboembolic stroke had a favorable influence on brain tissue. Chronic preventive flunarizine treatment failed to have a beneficial effect.
Tolerance of the cerebral venous system to retrograde perfusion pressure in focal cerebral ischemia in rats.
Authors: Ueda T , Yamamoto Y L , Takara E , Diksic M
Published: June 2011

Using quantitative double-tracer autoradiography, we examined the tolerance of the rat cerebral venous system in focal cerebral ischemia to retrograde perfusion pressure into the inferior cerebral vein. At perfusion pressures of less than 150 mm Hg, there was no significant change in local cerebral blood flow (LCBF) and blood-brain barrier (BBB) permeability. At pressures of greater than 170 mm Hg, significant changes occurred in BBB permeability in the superficial cortical layers and there was a mild reduction of LCBF. In the group of rats subjected to 200 mm Hg perfusion pressure, the change in BBB permeability extended to the entire cortical zone and significant reduction of LCBF occurred. Our results indicate for the first time that during conditions of focal cerebral ischemia, the rat cerebral venous system can tolerate up to 150 mm Hg of retrograde perfusion pressure into the cerebral venous system without any change in BBB permeability or in LCBF. However, progressive change in BBB permeability and reduction in LCBF occur once the perfusion pressure exceeds 170 mm Hg. This finding may permit more efficient delivery of cytoprotective agents into ischemic tissue.
Occipital infarction with hemianopsia from carotid occlusive disease.
Authors: Pessin M S , Kwan E S , Scott R M , Hedges T R
Published: June 2011

Extracranial internal carotid artery occlusive disease usually produces stroke in the middle cerebral artery territory or the border zone between the middle and anterior cerebral arteries. It is unusual for occipital infarction in the posterior cerebral artery territory to be caused by internal carotid artery disease despite the fact that the posterior cerebral artery may arise directly from the internal carotid artery as an anatomic variation. We describe a patient with a fetal posterior cerebral artery originating from the internal carotid artery, and the initial manifestation of his extracranial internal carotid artery occlusive disease was hemianopsia from occipital infarction.
Patch angioplasty in carotid endarterectomy. Advantages, concerns, and controversies.
Authors: Awad I A , Little J R
Published: June 2011

There is much controversy in the literature regarding the precise role of patch angioplasty in carotid endarterectomy. Our report summarizes the theoretical and experimental considerations, including the hemodynamic effects and biologic behavior of the graft, associated with this technique. We present a detailed review of the literature regarding the clinical efficacy of patch angioplasty in carotid endarterectomy, including the early results, the late results, and the incidence and nature of carotid restenosis. We address concerns about the use of patch angioplasty, including the duration of cross-clamping, potential problems with the graft and suture-line disruption, and graft atherogenesis. We conclude that most recent literature indicates that patch angioplasty decreases acute complications (notably carotid occlusion) after carotid endarterectomy and prevents or delays carotid restenosis. As pressure increases to achieve a minimal rate of perioperative morbidity, many surgeons are expected to adopt patch angioplasty in more of their cases. However, in the absence of conclusive results from a prospective randomized study, opinion will continue to be divided regarding the routine versus the selective use of patch grafting in carotid endarterectomy. We present criteria for randomized trials of this technique.
The potential role for ultrafast cardiac computed tomography in patients with stroke.
Authors: Helgason C M , Chomka E , Louie E , Rich S , Zajac E , Roig E , Wilbur A , Brundage B H
Published: June 2011

We studied 40 patients with stroke of potential cardioembolic origin by cardiac ultrafast computed tomography and two-dimensional echocardiography. Cardiac ultrafast computed tomography was more sensitive (positive in eight of 14 instances) than two-dimensional echocardiography (positive in two of 14 instances) for the detection of intracardiac thrombus, which was found in 13 patients. Mitral anular calcification was diagnosed more often by two-dimensional echocardiography (four of five instances) than by cardiac ultrafast computed tomography (one of five instances); this implies a high incidence of false-positives for the former. Cardiac ultrafast computed tomography showed that one half of the patients (21 of 40) had coronary artery calcification, indicating a high incidence of coronary atheroma in this patient population. Future studies comparing brain and cardiac pathology with the findings of cardiac ultrafast computed tomography and patient prognosis are needed to define the significance and utility of this technique in patients with stroke.
Morning increase in onset of ischemic stroke.
Authors: Marler J R , Price T R , Clark G L , Muller J E , Robertson T , Mohr J P , Hier D B , Wolf P A , Caplan L R , Foulkes M A
Published: June 2011

The time of onset of ischemic stroke was determined for 1,167 of 1,273 patients during the collection of data by four academic hospital centers between June 30, 1983, and June 30, 1986. More strokes occurred in awake patients from 10:00 AM to noon than during any other 2-hour interval. The incidence of stroke onset declined steadily during the remainder of the day and early evening. The onset of stroke is least likely to occur in the late evening, before midnight.
Allopurinol and dimethylthiourea reduce brain infarction following middle cerebral artery occlusion in rats.
Authors: Martz D , Rayos G , Schielke G P , Betz A L
Published: June 2011

Free radicals have been shown to play an important role in ischemia-reperfusion injury in several organ systems; however, the role of free radicals in central nervous system ischemia has been less well studied. Many potential free radical-generating systems exist. The primary products of these reactions, superoxide and hydrogen peroxide, may combine to produce hydroxyl radicals. Of the many potential sources of free radical generation, the enzyme xanthine oxidase has been shown to be important in ischemia in noncerebral tissue. We investigated the effect of the hydroxyl radical scavenger dimethylthiourea and the xanthine oxidase inhibitor allopurinol on infarct volume in a model of continuous partial ischemia. Male Sprague-Dawley rats were treated with dimethylthiourea or allopurinol before middle cerebral artery occlusion. Infarct volume was measured by triphenyltetrazolium chloride staining of brains removed 3 or 24 hours after occlusion. Stroke volume was reduced by 30% after dimethylthiourea treatment and by 32-35% after allopurinol treatment. At 24 hours after stroke, cortical tissue was more effectively protected than caudate tissue with both agents. Pretreatment with dimethylthiourea and allopurinol also significantly reduced cerebral edema formation and improved blood-brain barrier function as measured by fluorescein uptake. Our results imply that hydroxyl radicals are important in tissue injury secondary to partial cerebral ischemia and that xanthine oxidase may be the primary source of these radicals.
Biosynthesis of leukotrienes in canine cerebral vasospasm.
Authors: Yokota M , Tani E , Maeda Y
Published: June 2011

We produced cerebral vasospasm in 29 dogs by the "two-hemorrhage" method of intracisternal injections, 2 days apart, of autogenous arterial blood. Leukotriene (LT) C4, LTD4, and LTE4 were purified from incubated basilar artery, medulla oblongata, hypothalamus, median eminence, and blood clot from around the basilar artery using reverse-phase high-performance liquid chromatography, and the amount of each LT was quantified separately by bioassay with guinea pig ileum. The biosynthetic capacity for total LTs was approximately three times higher in the hypothalamus and median eminence than in the basilar artery and medulla oblongata in the eight normal dogs. In the dogs with subarachnoid hemorrhage, the biosynthetic capacity was increased significantly both before and 2 hours after the second injection of blood on Day 2 and was normal on Day 7 in the basilar artery and medulla oblongata, whereas the biosynthetic capacity was decreased significantly 2 hours after the first and second injections of blood and was increased significantly on Day 7 in the hypothalamus and median eminence. In blood clot the biosynthetic capacity was increased continuously after the first injection of blood. Thus, the biosynthetic capacity for total LTs showed a time- and tissue-specific change after subarachnoid hemorrhage.
Acute effects of isovolemic hemodilution with crystalloids in a canine model of focal cerebral ischemia.
Authors: Hyodo A , Heros R C , Tu Y K , Ogilvy C , Graichen R , Lagree K , Korosue K
Published: June 2011

We used 44 splenectomized dogs to study the effects of isovolemic hemodilution with a crystalloid solution. The dogs were randomly divided into a hemodilution and a control group. In each group, 17 dogs were subjected to 6 hours of internal carotid and middle cerebral artery occlusion, and five dogs received sham operations. Isovolemic hemodilution by phlebotomy and Ringer's lactate infusion was performed 30 minutes after arterial occlusion and resulted in an average hematocrit of 32-33%. Hemodilution significantly reduced viscosity, fibrinogen and total protein concentrations, and plasma oncotic pressure. Systemic arterial blood pressure and pulmonary wedge pressure decreased slightly with hemodilution, but central venous pressure and pulmonary arterial pressure did not change significantly. There was a similar decrease in cardiac index in both hemodiluted and control dogs, which may have been due to the effects of barbiturate anesthesia. Intracranial pressure increased significantly with time in all dogs subjected to arterial occlusion, but this increase was significantly more severe in the hemodiluted dogs. Specific gravity, measured just after the dogs were killed, 6 hours after hemodilution, was significantly lower in the white matter and basal ganglia of the left (ischemic) hemisphere in hemodiluted dogs than in controls. Regional cerebral blood flow decreased significantly in the left hemisphere after arterial occlusion. This decrease was almost completely reversed by hemodilution except in the basal ganglia, where the increase in edema caused by hemodilution was the greatest.
Postischemic cerebral microvascular responses to norepinephrine and hypotension in newborn pigs.
Authors: Leffler C W , Busija D W , Beasley D G , Armstead W M , Mirro R
Published: June 2011

We examined the effects of 20 minutes' cerebral ischemia on cerebral microcirculatory responses to topical norepinephrine and systemic hypotension in three groups (sham-operated control, 2-3 hours postischemia, and 24 hours postischemia) of anesthetized newborn pigs equipped with closed cranial windows. Cerebral ischemia may eliminate the prostanoid vasodilator system from the cerebral circulation. Norepinephrine (10(-4) M) decreased pial arteriolar diameters similarly in all three groups (27%, 28%, and 21%, respectively), but only the sham-operated group exhibited pial arteriolar dilation in response to hypotension (28% at 33 mm Hg). Two-three and 24 hours after cerebral ischemia, hypotension decreased pial arteriolar diameters (21% and 17%, respectively). In sham-operated piglets, norepinephrine and hypotension increased cortical periarachnoid cerebrospinal fluid prostanoid concentrations. However, neither norepinephrine nor hypotension altered cerebral prostanoid production 2-3 or 24 hours after cerebral ischemia. Therefore, we conclude that after cerebral ischemia, autoregulatory pial arteriolar dilation in response to hypotension is absent, while vasoconstriction in response to norepinephrine is intact.
Bilateral loss of vision in bright light.
Authors: Wiebers D O , Swanson J W , Cascino T L , Whisnant J P
Published: June 2011

We describe four patients with episodic bilateral vision impairment related exclusively to light exposure. Each had angiographically documented bilateral high-grade stenosis or occlusion of the internal carotid arteries. This phenomenon appears to be related to bilateral simultaneous retinal ischemia delaying regeneration of visual pigments in the pigment epithelial layer. It must be distinguished from bilateral occipital lobe ischemia caused by vertebrobasilar system disease.
Incidence rates of stroke in the eighties: the end of the decline in stroke?
Authors: Broderick J P , Phillips S J , Whisnant J P , O'Fallon W M , Bergstralh E J
Published: June 2011

Studies of the population of Rochester, Minnesota, have provided the only data on temporal trends for the incidence of stroke in North America. Among the residents of Rochester, the average annual incidence rate of stroke declined by 46%, from 213 to 115 per 100,000 population, between 1950-1954 and 1975-1979. The decline occurred in all age and sex groups, but it occurred earlier in women than in men. The rates stabilized in the 1970s, and did so earlier in women. For 1980-1984, the incidence rate of stroke was 17% higher than that for 1975-1979. The onset of the decline in incidence rates coincided with the introduction of effective antihypertensive therapy, but stabilized and increased rates were associated with continuing improvement in the control of hypertension. The increase in the incidence rates of stroke coincided with the introduction of computed tomography, which appeared to increase the detection of less severe strokes.
Hemorrhagic transformation in cerebral embolism.
Authors: Okada Y , Yamaguchi T , Minematsu K , Miyashita T , Sawada T , Sadoshima S , Fujishima M , Omae T
Published: June 2011

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients greater than or equal to 70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or less than 50 years (seven of 27, 25.9%) (greater than or equal to 70 vs. less than 50, p less than 0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p less than 0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytic and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical correlates of Doppler/ultrasound errors in the detection of internal carotid artery occlusion.
Authors: Bridgers S L
Published: June 2011

One recognized limitation of carotid Doppler/ultrasound is its accuracy in differentiating occlusion from near-total occlusion of the internal carotid artery, which is a crucial issue in management decisions. Clinical histories were reviewed in 58 patients with apparent occlusion of an internal carotid artery diagnosed by Doppler/ultrasound who also underwent angiography. False-positive results were detected in eight patients, for an overall accuracy of 86%. Among a group of 25 patients with acute cerebral or ocular events ipsilateral to an apparently occluded artery, false-positive results occurred in seven (accuracy of 72%). Among a group of 33 patients with asymptomatic or remotely symptomatic apparent occlusions, only one false-positive occurred, for an accuracy of 97%. This difference in accuracy between groups was significant. Thus, a Doppler/ultrasound diagnosis of occlusion was most inexact in those patients for whom the detection of continued patency was most likely to influence management.
Nuclear magnetic resonance study of regional metabolism after forebrain ischemia in rats.
Authors: Peeling J , Wong D , Sutherland G R
Published: June 2011

Proton nuclear magnetic resonance (NMR) spectroscopy of perchloric acid tissue extracts has been used to follow serial postischemic changes in the levels of metabolites in the hippocampus, cerebellum, frontal lobes, and parietal/occipital lobes in a rat model of short-duration (10 minutes) forebrain ischemia. Shortly (10 minutes, 1 hour) after the ischemic insult, the levels of the amino acids alanine and gamma-aminobutyric acid are elevated and that of glutamate is depressed in all regions except the cerebellum. The levels of these species return to control values by 24 hours postischemia. No changes are observed in the levels of aspartate or N-acetylaspartate. Greatly elevated levels of acetate 10 minutes postischemia, particularly in the hippocampus, may be due in part to metabolic degradation of fatty acids released due to membrane breakdown. Elevated levels of lactate persist for up to 7 days postischemia, suggesting that normal mitochondrial functioning is not fully restored following the ischemic insult.
Influence of monosialoganglioside inner ester on neurologic recovery after global cerebral ischemia in monkeys.
Authors: Cahn R , Borzeix M G , Aldinio C , Toffano G , Cahn J
Published: June 2011

We assessed the consequences of transitory global cerebral ischemia and the influence of monosialoganglioside inner ester (AGF 2) treatment on neurologic outcome, cerebral blood flow, and cerebral metabolic rate in monkeys over 48 hours. Global cerebral ischemia was produced by a cervical tourniquet and a lowering of blood pressure to 6.65 kPa; recirculation followed after 30 minutes. AGF 2 (30 mg/kg) was administered intravenously immediately after initiation of recirculation and intramuscularly twice a day for 48 hours. Our results show that treatment with AGF 2 significantly accelerated the rate of neurologic recovery. Improvement was evident 5 hours after ischemia; full neurologic recovery was observed in half of the monkeys 48 hours after ischemia. This recovery was associated with a less severe reduction in cerebral blood flow without a concomitant increase in the cerebral metabolic rate.
Prolonged exposure to oxyhemoglobin modifies the response of isolated dog middle cerebral arteries to vasoactive substances.
Authors: Onoue H , Nakamura N , Toda N
Published: June 2011

We exposed helical strips of dog middle cerebral arteries to oxyhemoglobin for 5 hours, rinsed them with bathing medium, and stored them overnight; we compared the responses of strips thus treated with the responses of strips without oxyhemoglobin treatment. Relaxation induced by nicotine was abolished by hexamethonium and was markedly inhibited after exposure to oxyhemoglobin. A low concentration of KCl (5 mM) elicited relaxation that was abolished by ouabain and significantly reduced by oxyhemoglobin. Endothelium-dependent relaxation caused by calcium ionophore A23187 was attenuated, and that caused by substance P was reversed to contraction after exposure to oxyhemoglobin. Contraction elicited by substance P also depended on endothelium and was abolished by indomethacin. Relaxation induced by TRK-100, a stable analogue of prostaglandin I2, was moderately attenuated by oxyhemoglobin. On the other hand, concentration-dependent relaxation induced by papaverine and contractile responses to KCl, serotonin, and prostaglandin F2 alpha were not affected by oxyhemoglobin. Our results indicate that vasodilations mediated by vasodilator nerves, the electrogenic sodium pump, endothelium-derived relaxing factor, and prostaglandin I2 were impaired in dog cerebral arteries exposed to oxyhemoglobin. After exposure to oxyhemoglobin, vascular endothelium appears to participate in cerebroarterial contraction via a release of vasoconstrictor prostaglandins. These actions of oxyhemoglobin may be involved in the genesis of cerebral vasospasm after subarachnoid hemorrhage.
Spontaneous calcific cerebral embolus from a calcific aortic stenosis in a middle cerebral artery infarct.
Authors: Rancurel G , Marelle L , Vincent D , Catala M , Arzimanoglou A , Vacheron A
Published: June 2011

Calcific emboli from a calcific aortic stenosis is an uncommon event, usually following local trauma, as from cardiac surgery or left heart catheterization or as a sequel to bacterial endocarditis. We report what we believe to be the first case of a spontaneous calcareous emboli demonstrated by cranial computed tomography. In this patient, systemic hypertension and mild aortic insufficiency may have caused increasing mechanical forces acting on the aortic cusps and may have precipitated embolism.
Has there been a decline in subarachnoid hemorrhage mortality?
Authors: Ingall T J , Whisnant J P , Wiebers D O , O'Fallon W M
Published: June 2011

We studied subarachnoid hemorrhage in the population of Rochester, Minnesota, for the 40-year period from 1945 through 1984. The average annual incidence rate of subarachnoid hemorrhage in Rochester has remained constant at approximately 11 per 100,000 population. Age-specific incidence rates increased with age. However, the average annual mortality rate for subarachnoid hemorrhage in Rochester has shown a decreasing trend, from 6.8 per 100,000 population in 1955-1964 to 4.3 in 1975-1984. It is likely that this is due to a decrease in case-fatality rates from 57% in 1945-1974 to 42% in 1975-1984 (p = 0.10). This decreasing trend was also evident in annual mortality rates from subarachnoid hemorrhage for US white men and women. The reason for the improved case-fatality rate is unclear, but it may be related to changes in management. The interval from onset of subarachnoid hemorrhage to surgery decreased from a median of 12 days in 1975-1979 to 2 days in 1980-1984, and of those who survived to receive medical attention, more patients received some form of medical treatment in 1980-1984. Whether either or both of these changes have led to the decrease in the case-fatality rate is uncertain.
Protection from cerebral ischemia by brain cooling without reduced lactate accumulation in dogs.
Authors: Natale J A , D'Alecy L G
Published: June 2011

Hypothermia protects tissue function in ischemia. This study determined if selective brain cooling inhibits cerebral cortical lactate accumulation and thus accounts for imporved neurologic outcome after complete cerebral ischemia in dogs. The brain was selectively cooled (hippocampal temperature 33 degrees C) by nasal lavage with water at 5 degrees C. Control dogs received nasal lavage with water at 39 degrees C. Mean +/- SEM rectal temperature in both groups was 39 +/- 1 degree C prior to ischemia. Selective brain cooling before and during 10 minutes of cardiac arrest was associated with significantly improved neurologic function and 100% survival, whereas normothermic cardiac arrest produced marked neurologic dysfunction and 100% mortality. Cerebral cortical lactate accumulation was measured in a complementary series of dogs exposed to the same two treatments but with the addition of six cerebral cortical brain biopsies taken before, during, and immediately after cardiac arrest. Brain and rectal temperatures of dogs in the brain biopsy protocol were similar to those of dogs in the recovery protocol. There was no difference detected in cerebral lactate accumulation during ischemia between brain-cooled and control dogs. Thus, reduction in cortical brain lactate during ischemia cannot account for the postischemic functional protection afforded by preischemic selective brain cooling.
The value of magnetic resonance imaging in the detection of type II hemorrhagic lacunes.
Authors: Challa V R , Moody D M
Published: June 2011

Lacunar infarcts (lacunes) are small necrotic/cystic lesions of the brain associated with hypertension. Many are clinically silent, but some are associated with localizing symptoms and signs. Lacunes recently were classified into three types, namely, those resulting from small infarcts (type I), those arising as small hemorrhages (type II), and those due to dilatation of perivascular spaces (type III). The type II lacunes are thought to be much less common than those of type I. Type II lacunes have not previously been reported during life. We report a case of subacute type II lacune in the pontine tegmentum that was detected by magnetic resonance imaging and later verified by histopathologic examination. The patient was hypertensive and had numerous other type I lacunes. This case shows that the magnetic resonance imaging features of hemorrhagic lacunes are identical to those of small hemorrhages or small hemorrhagic infarcts and that magnetic resonance imaging is a useful tool in the detection of lacunes and their correlation with clinical neurologic symptoms and signs.
Prevalence of silent stroke in patients presenting with initial stroke: the Framingham Study.
Authors: Kase C S , Wolf P A , Chodosh E H , Zacker H B , Kelly-Hayes M , Kannel W B , D'Agostino R B , Scampini L
Published: June 2011

It is common to find computed tomography scan evidence of prior stroke without a history of such an event. The frequency, risk factors for, and relevance of silent strokes are unknown. The Framingham cohort of 5,184 men and women aged 30-62 years and free of stroke at entry to the study have been followed with periodic examinations since 1950. We studied the silent strokes found on computed tomography scan of all initial strokes that occurred between January 1, 1979, and July 31, 1987. During these 8 1/2 years, 164 initial strokes occurred; 124 had computed tomography scans performed. There were 13 (10%) with silent stroke, 71 had abnormalities related to their presenting acute stroke, and 40 had normal computed tomography scans. There were 15 silent lesions; eight were lacunar infarcts in the basal ganglia-internal capsule area, seven were small cortical infarcts. Glucose intolerance was the sole risk factor that occurred significantly more frequently (11 of 13) in the group with silent lesions (p less than 0.04) than in the group with computed tomography evidence of acute stroke. Silent stroke is not rare; it was present in at least 10% of acute initial stroke patients arising in a general population. The relation of these silent lesions to the development of "vascular" dementia and poststroke disability deserves further study.
Measurements of acute cerebral infarction: a clinical examination scale.
Authors: Brott T , Adams H P , Olinger C P , Marler J R , Barsan W G , Biller J , Spilker J , Holleran R , Eberle R , Hertzberg V
Published: June 2011

We designed a 15-item neurologic examination stroke scale for use in acute stroke therapy trials. In a study of 24 stroke patients, interrater reliability for the scale was found to be high (mean kappa = 0.69), and test-retest reliability was also high (mean kappa = 0.66-0.77). Test-retest reliability did not differ significantly among a neurologist, a neurology house officer, a neurology nurse, or an emergency department nurse. The stroke scale validity was assessed by comparing the scale scores obtained prospectively on 65 acute stroke patients to the patients' infarction size as measured by computed tomography scan at 1 week and to the patients' clinical outcome as determined at 3 months. These correlations (scale-lesion size r = 0.68, scale-outcome r = 0.79) suggested acceptable examination and scale validity. Of the 15 test items, the most interrater reliable item (pupillary response) had low validity. Less reliable items such as upper or lower extremity motor function were more valid. We discuss methods for improving the reliability and validity of brief examination scales to be used in stroke therapy trials.
Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke.
Authors: Ogata J , Yutani C , Imakita M , Ishibashi-Ueda H , Saku Y , Minematsu K , Sawada T , Yamaguchi T
Published: June 2011

We examined the brains of 14 patients (four men and 10 women, mean age 68.9 years) who died from brain herniation after cardioembolic stroke with persistent occlusion of the internal carotid-middle cerebral arterial axis. Our examination showed hemorrhagic infarct in seven patients and pale infarct in the other seven, contradicting the commonly proposed pathophysiologic mechanism for the development of hemorrhagic infarct that the opening of previously occluded vessels makes an infarct hemorrhagic. Analysis of blood pressure after stroke revealed one or more surges of arterial hypertension or rapid rise of blood pressure in patients with hemorrhagic infarct without a reopening of the occluded artery. Such arterial hypertension was not always present in patients with pale infarct. Hemorrhage into an infarct with persisting occlusion of the proximal artery is assumed to occur when the involved blood vessels are exposed to the force of arterial blood pressure from the leptomeningeal collaterals. This occurs when arterial blood pressure rises after stroke in the presence of efficient leptomeningeal collaterals and before occlusion of these collaterals by a swollen cerebral hemisphere containing a large infarct.
Hemodilution increases cerebral blood flow in acute ischemic stroke.
Authors: Vorstrup S , Andersen A , Juhler M , Brun B , Boysen G
Published: June 2011

We measured cerebral blood flow in 10 consecutive, but selected, patients with acute ischemic stroke (less than 48 hours after onset) before and after hemodilution. Cerebral blood flow was measured by xenon-133 inhalation and emission tomography, and only patients with focal hypoperfusion in clinically relevant areas were included. Hemodilution was done according to the hematocrit level: for a hematocrit greater than or equal to 42%, 500 ml whole blood was drawn and replaced by the same volume of dextran 40; for a hematocrit between 37% and 42%, only 250 ml whole blood was drawn and replaced by 500 cc of dextran 40. Mean hematocrit was reduced by 16%, from 46 +/- 5% (SD) to 39 +/- 5% (SD) (p less than 0.001). Cerebral blood flow increased in both hemispheres by an average of 20.9% (p less than 0.001). Regional cerebral blood flow increased in the ischemic areas in all cases, on an average of 21.4 +/- 12.0% (SD) (p less than 0.001). In three patients, a significant redistribution of flow in favor of the hypoperfused areas was observed, and in six patients, the fractional cerebral blood flow increase in the hypoperfused areas was of the same magnitude as in the remainder of the brain. In the last patient, cerebral blood flow increased relatively less in the ischemic areas. Our findings show that cerebral blood flow increases in the ischemic areas after hemodilution therapy in stroke patients. The marked regional cerebral blood flow increase seen in some patients could imply an improved oxygen delivery to the ischemic tissue.
Vertebrobasilar insufficiency revealed by xenon-133 inhalation SPECT.
Authors: Delecluse F , Voordecker P , Raftopoulos C
Published: June 2011

A study of cerebral and cerebellar blood flow reactivity to acetazolamide by xenon-133-inhalation single photon emission computed tomography (133Xe SPECT) was carried out in a patient with bouts of transient basilar ischemia, whose neurological examination, computed tomographic scan, and auditory evoked potentials were normal. Though the patient was symptom-free at the time of the study, 133Xe SPECT demonstrated vertebrobasilar insufficiency by showing an impaired vasodilatory response in both the occipital lobes and the right cerebellar hemisphere. Three weeks later, the patient suffered an extensive stroke in these same areas. We therefore suggest that this method could be of great value in the assessment of vertebrobasilar insufficiency.
Cerebral infarction and ventricular septal defect.
Authors: Shuiab A
Published: June 2011

With the availability of contrast echocardiography, patent foramen ovale is frequently detected in patients with stroke, especially in those with no clear etiology and/or the young patient with stroke. Before this report, an association of stroke with ventricular septal defect had not been reported. In this communication, we describe a 38-year-old patient who developed an occipital lobe infarction and who, on investigation, was found to have a ventricular septal defect. Other investigations, which included four-vessel cerebral angiography, collagen disease workup, and coagulation profile, were all normal. We believe this case further extends the spectrum of cerebral ischemic events that may occur with intracardiac shunts.