bluuebunny/crossref_metadata_2025 huggingface dataset:
Leukoencephalopathy in patients with ischemic stroke.
Authors: Bogousslavsky J , Regli F , Uske A
Published: June 2011

Thirty-one (16 women, 15 men; mean age 68 years) of 1,000 consecutive patients with an ischemic stroke investigated systematically with computed tomography (CT), Doppler, electrocardiography (ECG), and biological tests had a diffuse hypodensity of the cerebral hemispheric white matter on CT, a sign indicative of leukoencephalopathy. In 25 of the 31 patients, the acute infarct was deep. Leukoencephalopathy was more frequent in patients with a deep infarct (8%) than in patients in whom the cortex was involved (0.8%) (p less than 0.01). A history of progressive intellectual impairment (23%) and the finding of a mild or moderate impairment, or severe dementia (84%) were more frequent in study patients (p less than 0.05) than in 31 sex- and age-matched controls with an acute infarct of same size and topography but without leukoencephalopathy. A history of hypertension (81%) and high blood pressure on admission (166 +/- 19/96 +/- 12 mm Hg) were the most common risk factors and were more frequent in study patients (p less than 0.05) than in controls. On the other hand, study patients had a greater than or equal to 50% stenosis or occlusion of the carotid artery (13%) less often than controls (35%) (p less than 0.05). Diabetes (23%), elevated blood cholesterol (13%), hematocrit greater than 45% (23%), smoking (32%), and myocardial ischemia by history or ECG (45%) did not differ. These findings suggest that hypertension may be more strongly associated with leukoencephalopathy than with deep infarcts. In acute stroke patients, leukoencephalopathy on CT should not be considered a fortuitous finding.
Ultrastructural studies of pial vascular endothelium following damage resulting in loss of endothelium-dependent relaxation.
Authors: Rosenblum W I , Povlishock J T , Wei E P , Kontos H A , Nelson G H
Published: June 2011

The changes in pial arterioles of 7 cats were examined by electron microscopy after injury that eliminates endothelium-dependent relaxation to acetylcholine or bradykinin. The injury was produced by exposing the vessels to mercury light in situ in the presence of intravascular sodium fluorescein dye. Previous studies showed that, at the time of initial injury and loss of endothelium-dependent responses, the endothelial cells displayed minimal ultrastructural evidence of injury. Because these changes might indicate the beginning of a sequence of irreversible alterations representing or leading to cell death, the present study was carried out 31/2-4 hours later, when ultrastructural evidence of progressive cell degeneration should readily be recognized. No such changes were observed. Instead, most vessels showed only the minimal alterations observed initially (endothelial vacuolation, blebs, and lucencies). Four of 19 vessels were completely normal. The findings fail to support the hypothesis that irreversible cell damage or death caused by the light + dye injury has caused the associated loss of endothelium-dependent relaxation. Rather, the findings support the concept that much lesser degrees of trauma are sufficient to impair the dilating responses of cerebral microvessels. This greatly expands the potential spectrum of pathologic states that might result in loss of endothelium-dependent relaxation.
Hypoglycemic hemiplegia: two cases and a clinical review.
Authors: Foster J W , Hart R G
Published: June 2011

Hypoglycemic hemiplegia mimics cerebrovascular disease. Two patients are reported who experienced multiple attacks of transient hemiplegia associated with hypoglycemia and who were initially diagnosed as having transient ischemic attacks. In both, angiography was normal and the attacks resolved with reduction of insulin dose. Recognition of hypoglycemia as the cause of transient hemiplegia is important, often obviating the need for cerebrovascular evaluation.
Michaelis-Gutmann bodies in a healing brain infarct.
Authors: Gal R , Gukovsky-Oren S , Sandbank U , Baharav E , Kessler E
Published: June 2011

A case of Michaelis-Gutmann bodies in a healing brain infarct is described. Morphologically this was consistent with cerebral malacoplakia. There are only 6 previously reported cases of cerebral malacoplakia, and only 1 of them was a consequence of postpartum stroke. The histologic and ultrastructural features of the malacoplakia lesion are reported and compared with the previously reported cases.
Mycotic aneurysm, subarachnoid hemorrhage, and indications for cerebral angiography in infective endocarditis.
Authors: Salgado A V , Furlan A J , Keys T F
Published: June 2011

We compared the clinical course of 68 patients with infective endocarditis and mycotic aneurysm and 147 patients with infective endocarditis but no mycotic aneurysm. Among the patients with mycotic aneurysm, 57% had subarachnoid hemorrhage without warning. Forty-three percent had a neurologic prodrome 2 days to 18 months (median 17 days) prior to discovery of the mycotic aneurysm. A focal deficit consistent with embolism was the most common prodrome (23%). However, there was no significant difference in the frequency of neurologic symptoms between patients with and without mycotic aneurysm. During an average follow-up of 40 months, there were no instances of subarachnoid hemorrhage/mycotic aneurysm among 121 patients discharged after a full course of antibiotic therapy. Therefore, the risk of rupture of an unsuspected mycotic aneurysm following a full course of antibiotics is low. When a prodrome does precede a mycotic aneurysm, it most often is a focal deficit consistent with embolism. We favor angiography in all patients with infective endocarditis who experience a focal deficit with good recovery. The timing and other indications for angiography in infective endocarditis are discussed.
Relation between spinal cord and epidural blood flow.
Authors: Shimoji K , Sato Y , Endoh H , Taga K , Fujiwara N , Fukuda S
Published: June 2011

To test applicability of monitoring regional spinal cord blood flow by measuring regional epidural blood flow, both were simultaneously measured by the hydrogen clearance method in response to changes in PaCO2 and mean arterial blood pressure in rats anesthetized with pentobarbital. An excellent correlation was found between regional spinal and epidural blood flow over a physiological range of PaCO2 (27.8-66.7 torr) and blood pressure (30-130 torr), while a poor correlation was demonstrated between regional spinal or epidural blood flow and regional muscle blood flow in response to these same physiological parameters. Moreover, the rates of change in regional spinal and epidural blood flows were almost the same in response to both PaCO2 and blood pressure. These results suggest that both regional spinal and epidural blood flow are regulated by a similar mechanism and suggest that regional spinal cord blood flow can be monitored by regional epidural blood flow.
Selective proprioceptive loss from a thalamic lacunar stroke.
Authors: Sacco R L , Bello J A , Traub R , Brust J C
Published: June 2011

In an elderly woman a small thalamic infarct, documented by computed tomography and nuclear magnetic resonance imaging, caused proprioceptive loss contralaterally without impairment of other sensory modalities. This patient, the first so reported, demonstrates the anatomic separation of spinothalamic and dorsal column/medial lemniscus sensory modalities in the human thalamus.
Pure motor hemiplegia secondary to a saccular basilar artery aneurysm.
Authors: Fisher M , Smith T W , Jacobs R
Published: June 2011

Pure motor hemiplegia is the most commonly encountered lacunar syndrome and is classically associated with small infarctions in the contralateral internal capsule or basis pontis. Pure motor hemiplegia has also been observed secondary to a wide variety of other vascular and nonvascular focal central nervous system processes. We describe a patient with pure motor hemiplegia associated with a saccular basilar artery aneurysm causing a lacunar infarction of the cerebral peduncle.
Aging modifies the asymmetry in brain microvascular regulation.
Authors: Magnoni M S , Govoni S , Kobayashi H , Battaini F , Trabucchi M
Published: June 2011

Cerebral ischemia induced by unilateral carotid occlusion in rats decreases in an asymmetric manner the number of beta-adrenergic receptors in microvessels prepared from cerebral cortexes ipsilateral and contralateral to the side of the ligature. In particular, the reduction is more pronounced in the left hemisphere in case of both right and left carotid ligature. The greater receptor decrease in the left side of the brain was shown to depend on the integrity of interhemispheric connections. We show that the changes in capillary beta-adrenergic receptors in response to unilateral carotid occlusion are qualitatively modified during aging. In particular, the asymmetry in the response pattern observed in young rats is lost. The mechanisms underlying this phenomenon may be based on an age-related impairment in the transfer of neuronal information between the two sides of the brain.
Biomechanics of brain edema in acute cerebral ischemia in cats.
Authors: Hatashita S , Hoff J T
Published: June 2011

We studied whether the biomechanical properties of brain play an important role in the development of early ischemic brain edema in cats with middle cerebral artery occlusion. Brain tissue pressure, tissue compliance, and tissue resistance were measured from the gray matter in the core and the periphery of the middle cerebral artery territory for 6 hours after occlusion. Regional cerebral blood flow and water content were also measured from the same areas. Ventricular fluid pressure was recorded. Tissue pressure rose gradually in the core, where flow was 6 ml/100 g/min, over 4 hours and then stabilized. The pressure gradient measured between edematous tissue and ventricular fluid was 5.3 mm Hg. Tissue resistance increased 1 hour after occlusion when water content increased to 10 mg/g. Later, when water content increased by 40 mg/g, tissue resistance decreased and tissue compliance increased significantly. In the periphery, where flow was 17.6 ml/100 g/min, tissue pressure rose slightly while tissue compliance and tissue resistance did not change within 6 hours. Our data indicate that as ischemic injury progresses, edema fluid accumulates in highly compliant brain parenchyma, then migrates through highly conductive tissue into the cerebrospinal fluid spaces, driven by the hydrostatic pressure gradient between the edematous tissue and the cerebrospinal fluid.
Danish very-low-dose aspirin after carotid endarterectomy trial.
Authors: Boysen G , Sørensen P S , Juhler M , Andersen A R , Boas J , Olsen J S , Joensen P
Published: June 2011

The effect of very-low-dose aspirin as an antithrombotic agent was evaluated blindly in 301 patients who had recently undergone carotid endarterectomy. After randomization, 150 patients received aspirin and 151 received placebo. The two groups were comparable with regard to age, sex, blood pressure, previous cerebrovascular events, and smoking habits. The effect of the study medication on platelet aggregation was measured twice in each patient during the first 2 months and at each follow-up visit; the dose was individually adjusted. In 76% of the patients receiving aspirin, 50 mg/day gave satisfactory platelet inhibition, 13% needed 60 mg/day, 8% needed 70 mg/day, and 3% needed 100 mg/day. Platelet aggregation was found to be inhibited in only 1.2% of the measurements in the patients receiving placebo. Observation during treatment averaged 21 months; total intention-to-treat follow-up averaged 25 months. For the combined outcome events of transient ischemic attack, stroke, acute myocardial infarction, and vascular death, aspirin reduced risk by 11% (95% confidence limits: -38% to 48%, p greater than 0.1). Thus, there was no significant effect of very-low-dose aspirin in our trial.
Carotid endarterectomy. Clinical results in a community-based teaching hospital.
Authors: Friedmann P , Garb J L , Berman J , Sullivan C , Celoria G , Rhee S W
Published: June 2011

Since 1971, 688 consecutive carotid endarterectomies were performed in 612 patients in a community-based teaching hospital by 16 surgeons; 82% of the procedures were performed in patients who had suffered a transient ischemic attack, amaurosis fugax, or a previous stroke. Seven patients (1%) died, five of perioperative stroke and two of myocardial infarction. Thirty-one patients suffered a perioperative stroke (4.5% of the 688 endarterectomies); 20 patients (2.9% of 688) were left with moderate to severe neurologic deficits. The combined mortality/major neurologic deficit morbidity rate (number of patients divided by number of endarterectomies) is 3.2%. Both operative mortality and morbidity have progressively declined in successive 5-year periods, with no deaths and a 2.7% stroke rate in 148 endarterectomies performed after 1984. Our results indicate that carotid endarterectomy as practiced in a community-based teaching hospital can be performed without excessive risk.
Effect of the aminosteroid U74006F after cardiopulmonary arrest in dogs.
Authors: Natale J E , Schott R J , Hall E D , Braughler J M , D'Alecy L G
Published: June 2011

The oxygen free radical-induced lipid peroxidative reactions that occur during resuscitation from normothermic cardiac arrest may contribute to the degree of neurologic dysfunction sustained. A blinded, randomized experimental trial was performed to determine whether U74006F, a potent inhibitor of lipid peroxidation, reduces morbidity and 24-hour mortality after 10 minutes of normothermic cardiopulmonary arrest; ventricular fibrillation was induced by electrical stimulation in 24 open-chest, halothane-anesthetized dogs, and circulation was reestablished by direct cardiac compressions, administration of a standardized drug regime, and internal countershocks. When spontaneous circulation was restored, a bolus injection of 1.5 mg/kg U74006F (n = 12) or 25 mM citrate vehicle (n = 12) was infused intravenously in 15 minutes and an infusion was continued at 0.125 mg/kg/hr for the next 12 hours. In the drug-treated group, plasma U74006F concentration averaged 0.13 microgram/ml between 3 and 12 hours after cardiac arrest. By 24 hours after arrest, 10 of 12 (83%) vehicle-treated dogs had died but only four of 12 (33%) U74006F-treated dogs had died (p = 0.017). U74006F-treated dogs survived significantly longer (mean +/- SEM 22 +/- 1 hr) than vehicle-treated dogs (18 +/- 1 hr), with significantly better neurologic function 1, 2, and 24 hours after arrest. Plasma fatty acid hydroperoxide concentrations 12 hours after arrest were 88 +/- 81 pmol/ml in U74006F-treated and 241 +/- 49 pmol/ml in vehicle-treated dogs (p less than 0.05). Vitamin E concentrations were significantly higher in the plasma of U74006F-treated dogs 2, 3, and 6 hours after arrest compared with vehicle-treated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
Endothelium dependence of dilation of pial arterioles in mouse brain by calcium ionophore.
Authors: Rosenblum W I , Nelson G H
Published: June 2011

Previous studies have shown that local selective in situ injury of pial arteriolar endothelium eliminates the dilations produced by acetylcholine or bradykinin. One means of producing such injury employs a helium-neon laser in the presence of intravascular Evans blue. Since the endothelium-dependent dilations produced by acetylcholine or bradykinin may be initiated by interaction with endothelial surface receptors, it is possible that the light simply inactivates or destroys these receptors. We used calcium ionophore A-23187, another dilating agent known from in vitro studies of large arteries to be endothelium-dependent, which moves calcium into endothelial cells rather than interacting with surface receptors. Our data in 10 mice show that before injury, 10(-5)M A-23187 dilated arterioles to 109 +/- 2% of control diameter. After selective endothelial injury by helium-neon laser, dilation was essentially abolished (101 +/- 1% of baseline diameter; p less than 0.01, Wilcoxon test). Undamaged sites along the arteriole still dilated to A-23187. Our data indicate that the laser must do more than inactivate surface receptors and are the first in vivo microvascular (vessels of less than 100 micron diameter) data showing endothelium dependence of the response to A-23187.
Endothelium-dependent and -independent responses to vasodilators of isolated dog cerebral arteries.
Authors: Onoue H , Nakamura N , Toda N
Published: June 2011

We compared responses to calcium ionophore A23187, vasopressin, and substance P in helical strips of dog middle cerebral, basilar, and posterior communicating arteries to obtain a better understanding of humoral control of cerebrovascular tone in different brain regions and its potential impact on mechanisms of cerebral vasospasm. A23187 relaxed these different arterial strips partially precontracted with prostaglandin F2 alpha to a similar extent. Vasopressin produced concentration-dependent relaxation in basilar and posterior communicating arterial strips, whereas middle cerebral arterial strips either contracted or relaxed slightly. Relaxations induced by A23187 and vasopressin were either abolished or converted to contractions by removal of the endothelium. In contrast, the relaxation of cerebral arterial strips to substance P was markedly attenuated but not abolished by endothelium denudation; the remaining relaxation was suppressed by indomethacin. In some cerebral arterial strips with intact endothelium, substance P caused a transient contraction that was reversed to a relaxation by indomethacin or ONO-3708, a prostaglandin antagonist. In arterial strips denuded of endothelium from the same dogs, substance P always produced relaxations. Relaxations of cerebral arterial strips to A23187 and vasopressin appear to be mediated by endothelium-derived relaxing factor. The function of vasopressin receptors in endothelial cells differs markedly in basilar and posterior communicating arteries versus middle cerebral arteries. Substance P-induced relaxations appear to be primarily associated with endothelium-derived relaxing factor and with prostaglandin I2, whereas contractions appear to be mediated by endothelium-derived prostaglandins.
Blood components contribute to rise in gerbil brain levels of leukotriene-like immunoreactivity after ischemia and reperfusion.
Authors: Saito K , Levine L , Moskowitz M A
Published: June 2011

The mean +/- SEM concentrations of immunoreactive leukotriene C4 and D4 (iLTD4) and prostaglandin D2 (iPGD2) increased from 3.0 +/- 1.2 and 0.71 +/- 0.33 to 16.3 +/- 4.7 and 3.0 +/- 1.14 ng/g forebrain, respectively (p less than 0.05, iLTD4; p less than 0.01, iPGD2), in the forebrains of 12 gerbils after 15 minutes of bilateral common carotid artery occlusion and 15 minutes of reperfusion. Removal of blood from ischemic brain of 11 gerbils by intracardiac perfusion with ice-cold saline for 10 minutes decreased iLTD4 concentrations significantly to 7.0 +/- 0.9 (p less than 0.05) but did not change iPGD2 concentrations. Severe granulocytopenia (4.98 +/- 1.79 to 0.05 +/- 0.03 x 10(3)/mm3, p less than 0.01) in seven gerbils following intraperitoneal injection of 50 mg/kg busulfan was associated with decreased iLTD4 accumulation in the brain to 3.46 +/- 1.36 ng/g forebrain (p less than 0.01). Taken together, our results suggest that blood components (most likely leukocytes) are a source of leukotriene-like immunoreactivity in the ischemic and reperfused brain.
Comparison of [125I]HIPDm and [125I]iodoantipyrine in quantifying regional cerebral blood flow in rats.
Authors: Albright R E , Friedman A H , Fram E K , Harbury O L , Molter B A , Skatoff J H , Harris C C , Coleman R E , Drayer B P
Published: June 2011

We determined regional cerebral blood flow (rCBF) using [125I]HIPDm [N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propanediamin e] and [125I]iodoantipyrine autoradiography under control and pathologic conditions (hypercapnia [acidosis], hypocapnia [alkalosis], and disrupted blood-brain barrier) conditions in 35 rats. In control rats, HIPDm rCBF (indicator fractionation method, n = 5) was lower than the corresponding IAP rCBF (diffusible indicator method, n = 4), most notably in the infratentorial regions and subcortical nuclei. In hypercapnia, rCBF increased by 100% and 37% in the HIPDm (n = 5) and IAP (n = 5) groups, respectively. In hypocapnia, IAP rCBF (n = 4) decreased 34% but HIPDm rCBF (n = 4) did not change. Following disruption of the blood-brain barrier by intracarotid infusion of mannitol in eight rats, both radiotracers (HIPDm n = 4, IAP n = 4) showed decreased rCBF to regions of disruption as defined by trypan blue extravasation. Our work indicates that modeling HIPDm uptake to quantify rCBF using the indicator fractionation method will underestimate blood flow and that HIPDm kinetics are influenced by compartmental pH dynamics that will limit the accuracy of this method in quantifying rCBF in pathologic conditions.
Insulin administration protects neurologic function in cerebral ischemia in rats.
Authors: LeMay D R , Gehua L , Zelenock G B , D'Alecy L G
Published: June 2011

Hyperglycemia exacerbates neurologic damage in clinical and experimental central nervous system ischemia. The purpose of our study was to determine if insulin administration before significantly alters neurologic deficit and survival after ischemia using a newly developed rat cerebral ischemia model. One hour before the onset of ischemia, 40 200-300-g Sprague-Dawley rats received intraperitoneal injections of either 1 ml normal saline or 0.4, 0.5, or 0.6 units regular insulin in 1 ml normal saline. Rats were then intubated and ventilated with 1-1.5% halothane. The aortic arch was exposed, and snares were placed on the innominate, left carotid, and left subclavian arteries. A 20-minute occlusion was begun, and anesthesia was discontinued. Baseline plasma glucose concentration was similar (p = 0.48, Student's t test) in both groups, but it subsequently was significantly lower in the 0.4 unit insulin-treated group up to 4 hours after occlusion (p less than or equal to 0.0035, Student's t test). Neurologic deficit was scored on a 50-point scale (0 = normal, 50 = severe deficit) 1, 4, 18, and 24 hours after occlusion. In the 0.4 unit insulin-treated group the neurologic deficit score was significantly lower than in the saline-treated group 1, 4, 18, and 24 hours after occlusion (p less than or equal to 0.005, Student's t test). Survival was significantly higher (p = 0.001) in the 0.4 unit insulin-treated (1.7 unit/kg dose) group than in the saline-treated group. No rats died when preocclusion plasma glucose concentration was between 65 and 175 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)
Timing of autopsy-confirmed hemorrhagic infarction with reference to cardioembolic stroke.
Authors: Lodder J , Krijne-Kubat B , van der Lugt P J
Published: June 2011

We studied the temporal profile of hemorrhagic transformation in 34 cases with autopsy-confirmed hemorrhagic infarction who died within 15 days following a supratentorial brain infarct, provided they had undergone computed tomography. It appeared that within 4 days, at least 76% (95% confidence interval 39-100%) of 21 cardioembolic strokes had become hemorrhagic. We conclude that if anticoagulation is considered in cardioembolic stroke, such treatment should not be started sooner than at least 4 days after the onset of stroke, provided that computed tomography at that time shows no hemorrhagic infarction.
Comparison of intraluminal and extraluminal inhibitory effects of hemoglobin on endothelium-dependent relaxation of rabbit basilar artery.
Authors: Hongo K , Ogawa H , Kassell N F , Nakagomi T , Sasaki T , Tsukahara T , Lehman R M
Published: June 2011

To determine whether extraluminal or intraluminal hemoglobin inhibits endothelium-dependent relaxation, we measured the vascular responsiveness of rabbit basilar artery in an in vitro perfusion system and we performed immunohistochemical staining for hemoglobin. In the in vitro study, we applied agents from either the intraluminal or the extraluminal side of excised basilar arteries. KCl-induced contraction was the same with either application. Acetylcholine-induced maximal relaxations were 57.6 +/- 8.5% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 3.3 +/- 0.3% for intraluminal, and 34.9 +/- 8.6% for extraluminal applications. Adenosine triphosphate-induced maximal relaxations were 64.2 +/- 4.1% of the contraction induced by 10(-5) M 5-hydroxytryptamine for control, 26.9 +/- 3.8% for intraluminal, and 42.2 +/- 6.0% for extraluminal applications. Hemoglobin's inhibition of acetylcholine- and adenosine triphosphate-induced relaxation was significantly greater with intraluminal than with extraluminal application (p less than 0.05). The immunohistochemical study revealed hemoglobin in the outer layer of the smooth muscle and in the adventitia when 10(-5) M hemoglobin was applied extraluminally for 5 minutes, whereas hemoglobin was observed on the surface of the endothelial cells after intraluminal application. Our findings suggest that hemoglobin inhibits acetylcholine- or adenosine triphosphate-induced relaxation by binding to endothelium-derived relaxing factor (EDRF) and by inhibiting production of EDRF. Hemoglobin's inhibitory effect on endothelium-dependent relaxation may be important in the pathogenesis of vasospasm after subarachnoid hemorrhage.
Alcoholic intracerebral hemorrhage.
Authors: Weisberg L A
Published: June 2011

Six alcoholic patients developed extensive cerebral hemispheric hemorrhages with both intraventricular and subarachnoid blood. All patients had evidence of liver damage, low platelet counts, and abnormal prothrombin and partial thromboplastin times. Four patients presented with seizures; in two of the four, these seizures were initially diagnosed as alcohol withdrawal seizures. Four patients were comatose with lateralizing neurologic deficit; two patients were comatose without lateralizing neurologic deficit, suggesting a metabolic encephalopathy. In one patient there was delayed neurologic deterioration. In all six patients, computed tomography showed large diffuse cerebral hemispheric hemorrhages, prominent intraventricular blood, and breakthrough into the subarachnoid spaces, which was confirmed by necropsy findings. There was marked mass effect but minimal surrounding edema. All six patients died. In three, autopsy showed no evidence of aneurysm, vascular malformation, neoplasm, or amyloid angiopathy and no arteriolar hypertensive changes.
Multiple strokes due to atrial myxoma with a negative echocardiogram.
Authors: Thompson J , Kapoor W , Wechsler L R
Published: June 2011

We report a patient with three cerebrovascular events involving the posterior circulation, one of which occurred in conjunction with central retinal artery occlusion. The patient had constitutional findings but had a normal cardiac examination, negative echocardiogram, and negative blood cultures. Angiography on two separate occasions revealed left vertebral artery occlusion. Repeat echocardiography 10 months later, at the time of the third stroke, revealed a left atrial mass consistent with myxoma. In patients with repetitive unexplained embolic events in different vascular distributions and constitutional findings suggestive of atrial myxoma, repeat noninvasive studies are indicated even if the initial workup is negative.
Aneurysmal subarachnoid hemorrhage in Izumo City and Shimane Prefecture of Japan. Incidence.
Authors: Inagawa T , Ishikawa S , Aoki H , Takahashi M , Yoshimoto H
Published: June 2011

During the 5-year period from 1980 to 1984, the incidence of subarachnoid hemorrhage due only to rupture of aneurysms was investigated in Izumo City, a small city with a population of 79,026. Additionally, to ascertain the relation of incidence to the size of the geographic area and/or population, a similar analysis was made on a larger area of Shimane Prefecture, including Izumo City, with a total population of 789,712. During this 5-year period, a total of 83 patients with aneurysmal subarachnoid hemorrhage were hospitalized in Izumo City, 548 patients in Shimane Prefecture. Ruptured aneurysms were confirmed in 77 cases (93%) in Izumo City and 466 cases (85%) in Shimane Prefecture. The crude annual incidences of aneurysmal subarachnoid hemorrhage for Izumo City and Shimane Prefecture were 21.0 and 13.9 per 100,000 population for all ages, and the age-adjusted annual incidences (adjusted to the 1980 population of Japan) were 18.3 and 11.0 per 100,000 for all ages, respectively. For both Izumo City and Shimane Prefecture, the age-specific annual incidences peaked at the ages of 50-69 years, and the highest incidence was 92.3 per 100,000 men from Izumo City in the eighth decade of life. The annual incidence of subarachnoid hemorrhage for Izumo City is the highest reported to date. If a wider area, such as Shimane Prefecture, were studied many patients in poor condition, particularly elderly patients, would be missed. To determine accurately the incidence of aneurysmal subarachnoid hemorrhage, it thus might be better to conduct the study in a small city such as Izumo City.
Effects of CDP-choline on neurologic deficits and cerebral glucose metabolism in a rat model of cerebral ischemia.
Authors: Kakihana M , Fukuda N , Suno M , Nagaoka A
Published: June 2011

The effects of cytidine 5'-diphosphocholine (CDP-choline) on neurologic deficits and cerebral glucose metabolism were studied in a rat model of transient cerebral ischemia. Cerebral ischemia was induced by occluding both common carotid arteries for 20 or 30 minutes 24 hours after the vertebral arteries were permanently occluded by electrocautery. CDP-choline was administered intraperitoneally twice daily for 4 days after reestablishing carotid blood flow. CDP-choline at two dosages (50 and 250 mg/kg) shortened the time required for recovery of spontaneous motor activity in a dose-related manner; recovery time was measured early after reperfusion. Neurologic signs were observed for 10 days. High-dose CDP-choline improved neurologic signs in the rats within 20-30 minutes of ischemia. When cerebral glucose metabolism was assessed on Day 4, increases in the levels of glucose and pyruvate were accompanied by decreases in the synthesis of labeled acetylcholine from uniformly labeled [14C]glucose measured in the cerebral cortex of rats with 30 minutes of ischemia. High-dose CDP-choline also attenuated changes in these variables. CDP-[1,2-14C]choline injected intravenously 10 minutes after reperfusion was used for membrane lipid biosynthesis. These results indicate that CDP-choline has beneficial effects on brain dysfunction induced by cerebral ischemia, which may be due in part to the restorative effects of CDP-choline on disturbed cerebral glucose metabolism, probably by stimulating phospholipid biosynthesis.
Regulation of cerebral blood flow after asphyxia in neonatal lambs.
Authors: Rosenberg A A
Published: June 2011

In a postasphyxia neonatal lamb model, the responses of the cerebral circulation to hypoxic hypoxia and changes in systemic arterial blood pressure were examined. Ventilated newborn lambs (n = 14) were subjected to a gradual asphyxial insult, resuscitated, and returned to control ventilator settings. During the time 2-5 hours after asphyxia, the responses of cerebral blood flow (CBF), cerebral oxygen delivery (OD), cerebral oxygen consumption (CMRO2), and cerebral fractional oxygen extraction (E) to changes in either arterial oxygen content (CaO2) or mean arterial blood pressure (MAP) were assessed. These data were compared with measurements from nonasphyxiated lambs (n = 7). With hypoxia (n = 7), cerebral blood flow increased (CBF = 646/CaO2 + 44) compared with nonasphyxiated lambs (CBF = 1121/CaO2 + 11). In asphyxiated lambs, cerebral oxygen delivery decreased (OD = 0.41 CaO2 + 6.87), but cerebral oxygen consumption remained stable due to a proportional increase in cerebral fractional oxygen extraction (E = -0.014 CaO2 + 0.65). In nonasphyxiated lambs, cerebral oxygen delivery, consumption, and fractional extraction were unchanged with hypoxia. In response to alterations in blood pressure, both cerebral blood flow (CBF = 0.84 MAP + 6.62) and oxygen delivery (OD = 0.13 MAP + 0.77) were pressure-passive. With hypotension, cerebral fractional oxygen extraction increased (E = -0.003 MAP + 0.69) but not enough to prevent a decrease in cerebral oxygen consumption (CMRO2 = 0.042 MAP + 1.79). In nonasphyxiated lambs, cerebral blood flow, oxygen delivery, consumption, and fractional extraction did not vary with blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
Regional creatine kinase, adenylate kinase, and lactate dehydrogenase in normal canine brain.
Authors: Chandler W L , Fine J S , Emery M , Weaver D , Reichenbach D , Clayson K J
Published: June 2011

Following acute stroke, creatine kinase and other enzymes are released into the cerebrospinal fluid and blood from injured brain tissue. To determine whether regional differences in brain enzyme activity might exist and therefore affect the amount of enzyme released, we quantified the levels of creatine kinase, adenylate kinase, and lactate dehydrogenase in 12 regions of normal canine brain (n = 4). Adenylate kinase activity varied the least among regions (49 +/- 7 units/g), followed by lactate dehydrogenase activity (122 +/- 28 units/g). The pattern for both adenylate kinase and lactate dehydrogenase was higher activity in predominantly gray matter areas, lower activity in white matter, and intermediate activity in mixed regions. The distribution of creatine kinase brain isoenzyme and mitochondrial creatine kinase in canine brain was less predictable, showing wider variations among regions (isoenzyme, 462 +/- 116 units/g; mitochondrial, 42 +/- 20 units/g). Even cerebral gray matter demonstrated substantial regional variations in creatine kinase brain isoenzyme, ranging from 606 units/g in the parietal cortex to 329 units/g in the temporal cortex. We conclude that the content of creatine kinase brain isoenzyme varies more than twofold among areas of brain. This regional variation may be important in the interpretation of creatine kinase brain isoenzyme measurements in cerebrospinal fluid and serum used to assess neurologic injury following stroke.
Benign disappearance of ventricular thrombus after embolic stroke. A case report.
Authors: DeWitt L D , Pessin M S , Pandian N G , Paulker S G , Sonnenberg F A , Caplan L R
Published: June 2011

The source for a patient's middle cerebral artery territory embolic stroke was found by echocardiography to be a left ventricular cardiac thrombus. The apical mass was large, pedunculated, and moved with systole into the ventricular cavity. The absence of ventricular dyskinesia was thought to favor a tumor, and surgery was considered before repeat echocardiography showed disappearance of the mass, making thrombus the likely diagnosis. No further embolic events occurred during or since the disappearance of the thrombus while on anticoagulation therapy. Serial echocardiography for change in or disappearance of a ventricular mass may be critical in distinguishing thrombus from tumor.
Cerebral ischemia and mitral valve prolapse: case-control study of associated factors.
Authors: Kelley R E , Pina I , Lee S C
Published: June 2011

We evaluated 36 patients with cerebral ischemia and mitral valve prolapse and compared them with 36 age-matched controls with cerebral ischemia who had similar attributes but who did not have mitral valve prolapse. Stepwise logistic regression analysis revealed an inverse relation between cerebral ischemia in the presence of mitral valve prolapse and hypertension, diabetes mellitus, occlusive cerebrovascular disease, and completed stroke at p less than 0.01. We also found, by correlation analysis, a negative correlation between both hypertension and diabetes mellitus versus mitral valve prolapse at p less than 0.05. Overall, 10 study patients compared with two control patients had no risk factors for cerebrovascular disease detected (chi 2 = 4.9, p less than 0.05). These data indicate that the association of mitral valve prolapse and cerebral ischemia is of special importance in patients who do not have other detected risk factors for cerebrovascular disease.
Efficacy and mechanism of action of a calcium channel blocker after global cerebral ischemia in rats.
Authors: Grotta J C , Pettigrew L C , Rosenbaum D , Reid C , Rhoades H , McCandless D
Published: June 2011

Dihydropyridine calcium channel blockers such as nicardipine are under evaluation for treating acute cerebral ischemia because they may increase cerebral blood flow by causing vasodilation and because they may be cytoprotective in part by limiting production of arachidonic acid metabolites. We demonstrated in a previous study that nicardipine improves postischemic neuronal function, as measured by somatosensory evoked potentials, without reducing the extent of light-microscopic CA-1 hippocampal histologic damage. To characterize further the effect of nicardipine on global ischemic injury, we administered the drug beginning 24 hours before 30 minutes of four-vessel ischemia in Wistar rats. We then measured hippocampal ATP, phosphocreatine, and glucose contents immediately and 2 hours after ischemia, and measured learning ability (working and reference errors) on an eight-arm radial maze beginning 30 days after ischemia. To gain insight into the possible mechanism of action, we measured production of arachidonic acid metabolites (eicosanoids: TXB2 and 6-keto-PGF1 alpha) and hemispheric and hippocampal cerebral blood flow by the [14C]butanol indicator fractionation technique immediately and 2 hours after ischemia. Nicardipine was associated with fewer working errors (p less than 0.02) but no difference in reference errors. The drug had no effect on energy metabolites, cerebral blood flow, or eicosanoids immediately after ischemia, but ATP, phosphocreatine, and cerebral blood flow all returned to normal levels significantly more rapidly during reperfusion in treated rats. Nicardipine improves behavioral, electrophysiologic, and mitochondrial function after ischemia without preventing cellular damage and improves postischemic reperfusion. The drug's positive effect appears to occur during reperfusion.
The postorbital approach to the middle cerebral artery in cats.
Authors: Berkelbach van der Sprenkel J W , Tulleken C A
Published: June 2011

The study of the relation between behavior, cerebral blood flow, and metabolism in animal models of cerebral ischemia has gained interest in the last 10 years. The most suitable models are those with the fewest side effects. One-sided blindness caused by decompression of the eye and coagulation of the optic nerve has been an inevitable side effect of transorbital occlusion of the middle cerebral artery. The postorbital technique is a new surgical approach to the middle cerebral artery that leaves the intraorbital structures intact. After resection of the postorbital processes and gentle retraction of the eye, the optic foramen is approached with the help of an operating microscope. This approach is possible because cats have no lateral bony orbital wall. A subperiostal approach to the optic foramen is made, after which the optic foramen is enlarged. Opening of the dura gives access to the middle cerebral artery in the same way as the transorbital approach. In this way, occlusion of the middle cerebral artery is possible with minimal impairment of vision.
Hyperglycemia enlarges infarct size in cerebrovascular occlusion in cats.
Authors: de Courten-Myers G , Myers R E , Schoolfield L
Published: June 2011

We investigated the influence of serum glucose concentration on infarct size following middle cerebral artery occlusion in cats. These animals were deprived of food for 48 hours and infused with 1) saline for 1 hour before and 8 hours after occlusion (n = 8), 2) 10% glucose solution for 1 hour before and 6 hours after occlusion and saline for 2 additional hours (n = 8), or 3) 10% glucose for 1 hour before and saline for 8 hours after occlusion (n = 5). Nineteen cats killed after 2 weeks' survival were subjected to morphometric infarct size determinations. Eight normoglycemic and 11 hyperglycemic cats exhibited infarcts affecting 10.2 +/- 3.4% and 29.5 +/- 6.5% (mean +/- SEM) of their middle cerebral artery territories, respectively (p less than 0.02). Cats of the two hyperglycemic groups showed similarly sized infarcts. However, two of eight (25%) of cats with preocclusion and postocclusion hyperglycemia died 8 and 24 hours after occlusion with infarction of the entire middle cerebral artery territory, marked hemispheral edema, and brainstem compression. Our results demonstrate that serum glucose concentration at the time of large cerebral vessel occlusion influences stroke outcome.
Blood rheology in patients with transient ischemic attacks.
Authors: Ernst E , Matrai A , Marshall M
Published: June 2011

A complete ischemic stroke is associated with a significant hemorheologic disturbance leading to a rise of the viscous component of the peripheral resistance. This abnormality represents a consequence of the acute event. Nonetheless, it could be causally related to ischemia. In an attempt to clarify this question, 26 patients suffering from transient ischemic attacks were compared with controls in terms of blood and plasma viscosity, hematocrit, blood cell filterability, and erythrocyte aggregation. In patients there was a significant impairment of blood fluidity comprising plasma viscosity, blood cell filterability, and erythrocyte aggregation, suggesting that the flow properties of blood are jeopardized even before an acute stroke. Most likely this is due to the underlying arteriosclerotic process. Our results open the way to speculating that hemorheologic mechanisms might predispose to the development of a stroke by decreasing cerebral blood flow. If this hypothesis were true, it would have important therapeutic implications.
Thromboxane B2 levels in serum during continuous administration of nimodipine to patients with aneurysmal subarachnoid hemorrhage.
Authors: Vinge E , Brandt L , Ljunggren B , Andersson K E
Published: June 2011

Twenty-four patients with subarachnoid hemorrhage due to rupture of a supratentorial aneurysm underwent surgery within 72 hours after subarachnoid hemorrhage. Immediately after clipping of the aneurysm the patients were treated with intravenous nimodipine for at least 7 days and then received the drug orally for another week. Nine patients had a documented or probable intake of aspirin or other nonsteroid anti-inflammatory drug during the days preceding admission. In all patients there was a gradual increase in serum thromboxane B2 concentration from low to normal levels during the treatment period, the increase being most pronounced in patients with prior nonsteroid anti-inflammatory drug intake. Thromboxane B2 concentrations were similar to those of four control patients not receiving nimodipine. In three patients who developed delayed ischemic dysfunction despite "therapeutic" nimodipine plasma concentrations, the thromboxane B2 levels were low or normal. Our present results do not support the idea that nimodipine exerts an effect on platelet function in patients with aneurysmal subarachnoid hemorrhage.
Correlation of cardiac arrhythmias with brainstem compression in patients with intracerebral hemorrhage.
Authors: Stober T , Sen S , Anstätt T , Bette L
Published: June 2011

Neurogenically caused cardiac arrhythmias and their correlation to lesions within the central nervous system were examined prospectively in 54 patients with spontaneous intracerebral hemorrhage. All patients were examined neurologically daily for 3 weeks, with special attention given to signs of brainstem compression resulting from transtentorial herniation. Electrocardiograms were continuously recorded over an average of 5 days. A significant correlation was established between the clinical manifestations of brainstem compression and sinus arrhythmias, multifocal premature ventricular contractions, couplets, and ventricular tachycardias. An explanation for this correlation may be found in the localization of the autonomous cardiovascular centers in the hypothalamus and brainstem. Transtentorial herniation frequently leads to a bilateral lesion of these structures. However, the cardiac arrhythmias are only a partial phenomenon within a complex cardiovascular reaction.
Ischemic stroke after cardiac pacemaker implantation in sick sinus syndrome.
Authors: Fisher M , Kase C S , Stelle B , Mills R M
Published: June 2011

The risk of embolic stroke during sick sinus syndrome before cardiac pacemaker insertion is substantial, but stroke after pacemaker insertion has not been well studied. We observed 10 sick sinus syndrome patients who developed an ischemic stroke 4 days to 112 months after pacemaker insertion. Nine patients represented 6% of the 156 ischemic stroke patients observed during a 30-month period. Eight had a ventricular-demand pacemaker, one had a dual-chamber pacemaker, and one had an atrial-inhibited pacemaker. Six patients were in atrial fibrillation at stroke onset, but none had atrial fibrillation when the pacemaker was inserted. Six patients were taking aspirin, and one was anticoagulated when stroke occurred. Stroke in sick sinus syndrome after pacemaker insertion is not rare, and pacing does not appear to be protective. Sick sinus syndrome patients who convert to atrial fibrillation or who have a ventricular-demand pacemaker might represent high-risk groups for stroke.
Pentoxifylline in acute nonhemorrhagic stroke. A randomized, placebo-controlled double-blind trial.
Authors: Hsu C Y , Norris J W , Hogan E L , Bladin P , Dinsdale H B , Yatsu F M , Earnest M P , Scheinberg P , Caplan L R , Karp H R
Published: June 2011

The efficacy and safety of pentoxifylline were assessed in 297 adult patients with ischemic stroke in a multicenter, double-blind, randomized and placebo-controlled trial. Treatment was started within 12 hours after the stroke onset. Study medication was administered intravenously continuously (16 mg/kg/day, maximum 1,200 mg/day) for 3 days and per os (400 mg t.i.d.) for the remainder of 28 days. Demographic data were comparable, and functional impairment and mortality (pentoxifylline 12%, placebo 10%) were not different between the two groups. Neurologic deficit scores improved from baseline admission scores during the 4-week study in both groups but did not differ between groups at admission or throughout the study except during the first few days when the consciousness level (Days 1 and 2), motor function (Days 1 and 2), cranial nerve function (Days 1-4), and total neurologic deficit scores (Days 1 and 2) were better in the pentoxifylline group than in the placebo group, especially in a subset of patients with severe deficits at admission. Laboratory values and side effects were also comparable between groups. Our study indicates that pentoxifylline can be given safely in patients with acute ischemic stroke. Although pharmacologic effects were present during the first few days, the clinical benefits were small and not sustained.