bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lacunar infarction as an embolic complication of cardiac and arch angiography.
Authors: Cacciatore A , Russo L S 
Published: June 2011

Lacunar infarcts are small, deep cerebral infarcts resulting from occlusion of small, penetrating cerebral arteries. They are most commonly associated with hypertension. Cardiac sources of embolization are sometimes present in patients with lacunes, but direct proof of a causal relationship is lacking. This report attempts to support the contention that emboli can cause lacunar syndromes and lacunar infarction.
We report two cases of pure motor hemiplegia, each of which developed while the patient was undergoing cardiac or aortic arch angiography. Neither patient had a history of previous transient ischemic attack or stroke. Initial computed tomography of the brain was normal in each. Repeat computed tomography in one confirmed a small, low-density lesion in the posterior limb of the internal capsule on the side appropriate to the patient's symptoms and remained normal in the second patient.
These two cases offer evidence that the classic lacunar stroke syndrome of pure motor hemiplegia can occur on an embolic basis.
A comparison of transcranial Doppler and cerebral blood flow studies to assess cerebral vasoreactivity.
Authors: Dahl A , Lindegaard K F , Russell D , Nyberg-Hansen R , Rootwelt K , Sorteberg W , Nornes H 
Published: June 2011

The aim of this study was to determine the ability of transcranial Doppler ultrasonography when used to assess cerebral vasoreactivity. The results of this method were compared with regional cerebral blood flow measurements.
Forty-three patients with symptoms suggesting cerebrovascular disease took part. Transcranial Doppler findings in the middle cerebral arteries were compared with regional cerebral blood flow in the corresponding perfusion territories before and after acetazolamide administration.
There was a significant positive correlation between the absolute increase in cerebral blood flow in milliliters per 100 g per minute and the percent increase in velocity (r = 0.63). The right-left, side-to-side difference of the acetazolamide response obtained by the two methods also showed a positive correlation (r = 0.80). Control limits obtained from healthy subjects were used for both the blood flow increase (absolute values and asymmetry in absolute values) and the velocity increase (percent increase and asymmetry in percent increase). The two methods then agreed in their evaluation of vasoreactivity in 74 (86%) of the 86 middle cerebral artery perfusion territories; 20 (23%) were assessed by both methods as having a reduced vasodilatory reserve. Eleven hemispheres with a slightly reduced regional cerebral blood flow response to acetazolamide were not detected by transcranial Doppler, whereas all territories with a marked reduction were identified by Doppler. Only one hemisphere with a normal cerebral blood flow increase after acetazolamide administration was assessed by Doppler as having reduced vasoreactivity.
Transcranial Doppler and the acetazolamide test may be used in clinical situations to assess cerebral vasoreactivity.
Stroke incidence in Copenhagen, 1976-1988.
Authors: Lindenstrøm E , Boysen G , Nyboe J , Appleyard M 
Published: June 2011

Temporal trends in stroke incidence in Denmark have not been previously reported. The Copenhagen City Heart Study is a prospective study based on a randomly selected sample of an urban population of, initially, 19,698 participants followed since 1976. Over a period of 12 years, we studied three important aspects of stroke incidence in 848 identified cases: temporal trends, dependence on age and sex, and comparison of responders and nonresponders.
The participants were invited to two health examinations at 5-year intervals. The participants who attended at least one of the two examinations are termed responders and those who attended none nonresponders. The cases of first-ever stroke were collected from responders, the National Patient Register, and the National Register of Deaths and were verified by study of hospital records and death certificates.
For responders aged 35-64 years and greater than or equal to 65 years, there were no significant changes in the weighted rates in four consecutive 3-year periods. There was a tendency toward decreasing rates among younger women, but not in older women or men. The age- and sex-adjusted rates per 1,000 (based on the Danish population in 1982) in responders in the entire 12-year follow-up period were 1.61 in women, 2.67 in men, and 2.14 in both sexes combined. Stroke incidence rates increased exponentially with age in both sexes, with rates in men generally twice those in women, even in the greater than or equal to 75 years of age group. Age-adjusted rates were higher in nonresponders than in responders. For women, this ratio was 1.7; for men, 1.1.
The stroke incidence in Copenhagen is relatively high and has shown no decreasing tendency over the period 1976-1988.
Effect of 33% xenon inhalation on whole-brain blood flow and metabolism in awake and fentanyl-anesthetized monkeys.
Authors: Yao L P , Bandres J , Nemoto E M , Boston J R , Darby J M , Yonas H 
Published: June 2011

Despite the documented diagnostic value of local cerebral blood flow maps by xenon-enhanced computed tomography, reports of cerebral blood flow activation by inhaled 33% Xe raised concerns about the method's safety and accuracy. We evaluated the effect of 33% Xe inhalation on cerebral blood flow and cerebral metabolic rates for oxygen and glucose in four awake and six fentanyl-anesthetized rhesus monkeys.
Platinum microelectrodes and catheters in the torcular Herophili were used to measure cerebral blood flow by hydrogen clearance, and oxygen and glucose concentrations. Cerebral variables were measured after 5 and 35 minutes of exposure to room air followed randomly by 67% O2 in 33% N2 or Xe. Five- and 35-minute measurements were combined because the duration of exposure had no effect.
In awake monkeys, 33% Xe compared with 33% N2 reduced (p less than 0.05) cerebral blood flow from 75 +/- 12 to 66 +/- 9 (mean +/- SD) ml.100 g-1.min-1 and oxygen consumption from 6.1 +/- 0.7 to 5.1 +/- 0.6 ml.100 g-1.min-1. In fentanyl-anesthetized monkeys, cerebral variables during 33% N2 versus 33% Xe were cerebral blood flow, 84 +/- 26 versus 79 +/- 23 ml.100 g-1.min-1; oxygen consumption, 5.0 +/- 0.7 versus 4.9 +/- 0.5 ml.100 g-1.min-1; and glucose consumption, 8.4 +/- 1.9 versus 7.9 +/- 2.0 mg.100 g-1.min-1.
In awake monkeys, 33% Xe reduced rather than activated cerebral blood flow and oxygen consumption by 12% and 16%, respectively; it had no effect in fentanyl-anesthetized monkeys.
Effect of calcium antagonists on postischemic protein biosynthesis in gerbil brain.
Authors: Xie Y , Seo K , Ishimaru K , Hossmann K A 
Published: June 2011

Prolonged inhibition of protein synthesis precedes delayed neuronal death in the CA1 sector of the hippocampus after transient cerebral ischemia. Organic calcium antagonists have been recommended for alleviation of ischemic neuronal damage. The present study was undertaken to investigate whether these drugs improve the recovery of protein biosynthesis after interruption of cerebral blood flow.
Cerebral protein synthesis was measured biochemically and autoradiographically in gerbils submitted to 5 minutes of bilateral occlusion of the common carotid arteries followed by 2 hours or 2 days of recirculation. Flunarizine (25 mg/kg) or nimodipine (1.5 mg/kg) were applied intraperitoneally shortly after ischemia.
Treatment with either calcium antagonist did not markedly influence postischemic recovery of protein synthesis in the resistant regions of the brain and did not prevent the persisting inhibition in the vulnerable stratum pyramidale of the CA1 sector of the hippocampus.
The postischemic application of the organic calcium antagonists nimodipine and flunarizine does not promote postischemic recovery of protein synthesis. The beneficial effects of these drugs must, therefore, be based on other mechanisms.
Infarct reduction by the platelet activating factor antagonist apafant in rats.
Authors: Bielenberg G W , Wagener G , Beck T 
Published: June 2011

Recent findings suggest a key role for platelet activating factor in neuroinjury. For this reason we evaluated the effects of the platelet activating factor antagonist apafant (4-(2-chlorophenyl)-9-methyl-2[3(4-morpholinyl)-3-propanol-1- yl[6H-thieno[3.2-f[[1.2.4]triazolo]4,3-1]]1.4]diazepine on farct volume and local cerebral blood flow following irreversible occlusion of the left middle cerebral artery in rats to assess the direct and vascular components of apafant's action.
We measured infarct volume 48 hours after middle cerebral artery occlusion. The effect of multiple doses of apafant (30 mg/kg p.o.) was tested in both pretreatment (n = 8) and posttreatment (n = 8) groups. In the pretreatment group apafant was given 30 minutes before and 2, 6, and 18 hours after occlusion. Rats of the posttreatment group received apafant 1, 6, and 18 hours after middle cerebral artery occlusion. We also examined the effect of a single dose of apafant given 30 minutes prior to occlusion (n = 9) on local cerebral blood flow determined 2 hours after middle cerebral artery occlusion.
Both regimens of apafant effectively decreased infarct volume. The reduction in cortical infarct volume was 59% (p less than 0.01; H test, U test) when the rats were treated before and after vessel occlusion whereas the decrease was 47% (p less than 0.05; H test, U test) when treatment began 1 hour after occlusion. Apafant did not change local cerebral blood flow after occlusion compared with controls.
We suggest that the cytoprotection afforded by apafant occurs mainly via a direct effect on brain tissue and has no major vascular component.
Hematogenous factors and prediction of delayed ischemic deficit after subarachnoid hemorrhage.
Authors: Ameriso S F , Wong V L , Ishii H , Quismorio F P , Giannotta S L , Meiselman H J , Fisher M 
Published: June 2011

Delayed ischemic deficits contribute to the high morbidity and mortality rates associated with subarachnoid hemorrhage. We evaluated the potential usefulness of measuring coagulation and hemorheological variables and cardiolipin antibodies for prediction of delayed ischemic deficit after subarachnoid hemorrhage.
Consecutive patients with subarachnoid hemorrhage were studied. Coagulation and hemorheological variables and cardiolipin antibodies were measured on admission, within 7 days of subarachnoid hemorrhage. A subset of patients was studied on admission and at two subsequent occasions.
Sixty-nine patients were studied. Sixty-one of these were without clinical manifestations of vasospasm at admission, and 16 developed delayed ischemic deficit during their hospitalization. None of the laboratory variables measured were significantly different between patients with or without later development of delayed ischemic deficit. Elevation of the fibrin fragment D-dimer was found in the group of eight patients admitted with ischemic symptoms and in 49% (34 of 69) of all patients, but this was not associated with delayed ischemic deficit. Sixteen patients were studied on three occasions; this group showed a significant decrease in hematocrit, an increased white blood cell count, and no change in fibrinogen concentration. Fibrin D-dimer levels rose significantly after surgery (from 5.01 +/- 0.69 to 5.53 +/- 0.58 ln-ng/ml, p less than 0.025) and after onset of delayed ischemic deficit (from 4.71 +/- 0.64 to 5.84 +/- 0.34 ln-ng/ml, p less than 0.01).
Hemostatic measurements, hemorheological variables, and cardiolipin immunoreactivity did not predict delayed ischemic deficit in this population.
Effect of diabetes mellitus on responses of the basilar artery in rats to products released by platelets.
Authors: Mayhan W G 
Published: June 2011

Aggregation and adherence of platelets to vascular endothelium are increased during diabetes mellitus, and thus responses of cerebral arteries to products released by platelets may have important implications for the pathogenesis of stroke during diabetes. The goal of this study was to determine whether responses of the basilar artery to products released by platelets are altered during diabetes.
A craniotomy was performed over the ventral medulla to expose the basilar artery. Diameter of the basilar artery was measured using intravital microscopy in nondiabetic and diabetic (50-60 mg/kg i.p. streptozotocin) rats in response to adenosine 5'-diphosphate, serotonin, and the thromboxane analogue U-46619.
Topical application of 10 and 100 microM adenosine 5'-diphosphate produced only minimal changes in diameter of the basilar artery that were similar in nondiabetic and diabetic rats (p greater than 0.05). At 0.01, 0.1, and 1.0 microM serotonin produced dose-related constriction of the basilar artery that was similar in nondiabetic and diabetic rats (p greater than 0.05). At 0.1 and 1.0 microM U-46619 also produced similar dose-related constriction of the basilar artery in nondiabetic and diabetic rats (p greater than 0.05).
These findings suggest that responses of the basilar artery to products released by platelets are not altered by diabetes mellitus. Thus, it does not appear that alterations in reactivity of the basilar artery to products released by platelets contribute to the pathogenesis of stroke during diabetes.
Glucose-associated alterations in ischemic brain metabolism of neonatal piglets.
Authors: Laptook A R , Corbett R J , Arencibia-Mireles O , Ruley J 
Published: June 2011

During global brain ischemia or hypoxia-ischemia in adults, hyperglycemia is deleterious to the brain. In contrast, similar adverse effects have not been found in neonatal animals. This investigation examined neonatal piglets to determine if there were specific alterations of ischemic brain metabolism associated with different systemic glucose concentrations and to potentially clarify the effects of hyperglycemia during ischemia in neonates.
Two groups of animals (n = 12 in each group) were studied during partial ischemia to compare the effects of hyperglycemia (plasma glucose concentration, 258 +/- 97 mg% [mean +/- SD]) with modest hypoglycemia (plasma glucose concentration, 62 +/- 23 mg%). A broad spectrum of cerebral blood flow reduction was achieved by combining inflation of a cervical pressure cuff with varying degrees of hemorrhagic hypotension. High-energy phosphorylated metabolites, intracellular pH, and cerebral blood flow were simultaneously measured using a magnetic resonance spectroscopic technique. Brain metabolic variables (beta-ATP, inorganic phosphorus, phosphocreatine, intracellular pH) were plotted as a function of blood flow reduction during partial ischemia for each group.
During ischemia values of cerebral blood flow were comparably distributed between groups and ranged from 15% to 110% of those of control. At a given reduction of cerebral blood flow, hyperglycemic piglets maintained a higher concentration of beta-ATP (p = 0.011) and had a smaller increase in inorganic phosphorus (p less than 0.001). At cerebral blood flow less than 50% of control, the intracellular pH of piglets with modest hypoglycemia during partial ischemia was never reduced to less than 6.46, whereas intracellular pH fell as low as 5.97 for hyperglycemic animals.
ATP preservation may account for the differing effects of glucose during ischemia in neonates compared with adults, provided that the accentuated brain acidosis is not deleterious to neonatal brain tissue.
Bilateral medial medullary infarction with oculomotor disorders.
Authors: Toyoda K , Hasegawa Y , Yonehara T , Oita J , Yamaguchi T 
Published: June 2011

We describe the first case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging. We discuss the relation between this lesion and the oculomotor signs that were observed clinically.
A 71-year-old man initially presented with pure motor hemiparesis, which progressed to complete quadriplegia. He also developed nearly complete vertical and horizontal ophthalmoplegia. Magnetic resonance imaging revealed upper medial medullary infarctions bilaterally that extended to the pontomedullary junction.
We propose that the vertical oculomotor disorders resulted from involvement of the oculomotor system in the caudal brain stem, especially the caudal paramedian pontine reticular formations on both sides.
Incidence and prognosis of stroke in the Valle d'Aosta, Italy. First-year results of a community-based study.
Authors: D'Alessandro G , Di Giovanni M , Roveyaz L , Iannizzi L , Compagnoni M P , Blanc S , Bottacchi E 
Published: June 2011

We sought to determine the incidence rate, risk factors, and prognosis of stroke in Valle d'Aosta, Italy, to provide information for planning regional health-care facilities.
We undertook a prospective study of all new cases of stroke in the geographically defined population of 114,325 residents of Valle d'Aosta in northern Italy.
In the first year of the study (January 1-December 31, 1989), 254 cases of first stroke were registered. The crude annual incidence rate was 2.23/1,000, 1.98/1,000 for men and 2.46/1,000 for women. After adjustment to the 1988 Italian population, the incidence rate for first stroke was 2.15/1,000 per year, 2.48/1,000 per year for men and 1.99/1,000 per year for women. The pathological diagnosis was cerebral infarction in 67%, intracranial hemorrhage in 15%, and unknown in 18%. The overall 30-day case-fatality rate was 31%. In survivors, Barthel Index Score recorded at 30 days from stroke onset showed that 100 patients (62%) were dependent in activities of daily living.
Our results do not differ significantly from those reported in Umbria, the only similar study performed in Italy, and support non-Italian data as to risk factors in stroke.
Antioxidants attenuate microvascular changes in the early phase of experimental pneumococcal meningitis in rats.
Authors: Pfister H W , Koedel U , Lorenzl S , Tomasz A 
Published: June 2011

We tested in a rat meningitis model 1) whether pneumococcal cell wall components are capable of producing changes in regional cerebral blood flow, brain water content, and intracranial pressure similar to those we have already observed after intracisternal inoculation of live pneumococci and 2) whether antioxidants would modulate these alterations in the early phase of meningitis.
Regional cerebral blood flow as measured by laser Doppler flowmetry and intracranial pressure were monitored continuously for 4 hours after intracisternal challenge. Brain edema formation was assessed by brain water content determinations. We investigated the following groups: rats challenged intracisternally with the whole intact pneumococcal cell wall (n = 7) or the pneumococcal cell wall hydrolyzed by the M1-muramidase (n = 7); rats injected intracisternally with phosphate-buffered saline (n = 6); rats pretreated intravenously with superoxide dismutase conjugated with polyethylene glycol (10,000 units/kg) and injected intracisternally with cell wall components (n = 5) or phosphate-buffered saline (n = 6); rats injected intracisternally with phosphate-buffered saline and pretreated intravenously with polyethylene glycol (10% solution, 1.2 ml/kg, n = 5) or continuously treated with intravenous free superoxide dismutase (22,000 units/kg per hour, n = 6); and rats continuously treated intravenously with deferoxamine mesylate (10 mg/kg per hour) and injected intracisternally with cell wall components (n = 6) or phosphate-buffered saline (n = 7).
Both pneumococcal cell wall preparations produced a significant increase in regional cerebral blood flow, intracranial pressure, and brain water content. Conjugated superoxide dismutase as well as deferoxamine prevented the increase in intracranial pressure and brain water content. In addition, the increase in regional cerebral blood flow as observed in untreated, cell wall-challenged rats (baseline, 100%; 183.1 +/- 12.3% after 4 hours, mean +/- SEM) was significantly attenuated by administration of both conjugated superoxide dismutase (136.6 +/- 14.1%) and deferoxamine (149.8 +/- 8.2%) (p < 0.05). Polyethylene glycol-conjugated superoxide dismutase alone produced an increase in regional cerebral blood flow (125.6 +/- 8.7% after 4 hours). We found that polyethylene glycol per se accounts for this action.
These data show that pneumococcal cell wall components containing teichoic acid produce changes in regional cerebral blood flow, intracranial pressure, and brain water content and that oxygen radicals contribute to these pathophysiological alterations in the early phase of experimental pneumococcal meningitis.
Cerebral infarction in a heterozygote with variant antithrombin III.
Authors: Arima T , Motomura M , Nishiura Y , Tsujihata M , Okajima K , Abe H , Nagataki S 
Published: June 2011

We report a heterozygous case of familial qualitative deficiency of antithrombin III associated with cerebral infarction.
A 33-year-old man had a history of recurrent transient ischemic attacks from the age of 28. Cerebral computed tomography at age 29 disclosed a low-density area in the left frontal lobe, and an internal carotid angiogram showed branch occlusion of the right anterior cerebral artery and stenosis of the left middle cerebral artery. Occlusion of the right middle cerebral artery developed thereafter. The plasma antithrombin III antigen concentration and progressive antithrombin activity were normal, but plasma heparin cofactor activity was low in the patient and his father. Nucleotide sequence analysis of the proband's deoxyribonucleic acid showed no mutation in exons II and VI of antithrombin III.
We conclude that abnormal antithrombin III with defective heparin binding, even though heterozygous, may cause ischemic stroke in young adults. We named this antithrombin III variant "Antithrombin III Nagasaki."
Transcranial Doppler sonography monitoring of local intra-arterial thrombolysis in acute occlusion of the middle cerebral artery.
Authors: Karnik R , Stelzer P , Slany J 
Published: June 2011

The aim of this study is to report on the use of transcranial Doppler ultrasonography as a noninvasive diagnostic monitoring tool during local intra-arterial thrombolysis in a patient with acute embolic occlusion of the middle cerebral artery.
We describe a 41-year-old woman with mitral valve stenosis suffering from embolism of the middle cerebral artery. Local thrombolysis was performed with tissue plasminogen activator at a dosage of 0.05 mg/kg/hr. Progress of the thrombolysis was monitored by transcranial Doppler. The steps of recanalization could be ascertained by transcranial ultrasound showing a hemodynamically relevant residual stenosis after the first 120 minutes and complete patency of the M1 segment of the middle cerebral artery 180 minutes later. One branch of the middle cerebral artery still showed a filling defect.
Our report demonstrates the potential usefulness of transcranial Doppler monitoring during thrombolysis of a proximal occlusion of the middle cerebral artery for guiding the treatment by assessing the reperfusion of the obstructed artery.