bluuebunny/crossref_metadata_2025_split huggingface dataset:
Postpartum cerebral angiopathy. Is there a role for sympathomimetic drugs?
Authors: Raroque H G , Tesfa G , Purdy P 
Published: June 2011

Postpartum cerebral angiopathy is associated with the use of of ergot alkaloids. The exact mechanism is unclear but may be related to their sympathomimetic properties, as evidenced in patients already on other ergot derivatives who deteriorated only after taking additional sympathomimetic drugs. We postulate that sympathomimetic agents, independent of ergot alkaloids, may produce the same complication.
A postpartum patient, initially presenting with headaches, subsequently manifested rapid neurological deterioration after ingesting isometheptene, a sympathomimetic drug. She was not on any ergot derivative but presented similar clinical and radiological manifestations. She experienced increased headache severity, visual disturbance, and seizures associated with multiple segmental cerebral vasoconstriction on angiography and increased T2-weighted signal in the occipital areas on magnetic resonance imaging.
This case is additional evidence that sympathomimetic actions of some drugs, such as ergot derivatives and isometheptene, may lead to postpartum cerebral angiopathy. Documentation of medication used by postpartum women suffering similar complications is needed to verify these findings.
The use of expected value as an aid to decisions regarding anticoagulation in patients with atrial fibrillation.
Authors: Nadeau S E 
Published: June 2011

The method described provides a rational means for determining whether to institute chronic anticoagulation to prevent stroke in patients with chronic atrial fibrillation under a variety of clinical circumstances.
The concept of expected value is used in conjunction with data from clinical studies to define the net value of anticoagulation to the patient. A full year of anticoagulation is warranted in patients with recent stroke or transient ischemic attack thought to be due to cardiogenic embolism who feel that stroke is a very serious event with nearly as much disvalue as death. If stroke has a lesser degree of negative value to the patient, or it is uncertain whether the stroke was in a large-vessel distribution, or it is uncertain whether a large-vessel distribution stroke was due to cardiogenic embolism, 6 months or less of anticoagulation may be warranted. Indefinite anticoagulation is justifiable in most patients with chronic atrial fibrillation without a history of stroke or transient ischemic attack but may be contraindicated in certain patients at extremely low risk for embolism and in patients who place a low value on stroke relative to death and who have a modest increase in risk for fatal hemorrhage.
The method described provides a means readily usable by clinicians to make anticoagulation decisions in patients with chronic atrial fibrillation that will address risk-benefit tradeoffs with somewhat greater precision than current approaches.
Distribution of atherosclerosis and risk factors in atherothrombotic occlusion.
Authors: Yasaka M , Yamaguchi T , Shichiri M 
Published: June 2011

The present study was performed to determine the relation between distribution of atherosclerosis and risk factors in Japanese patients with atherothrombotic occlusion.
We studied 154 patients with atherothrombotic occlusion of the extracranial internal carotid artery (n = 75, ICA group), the horizontal portion of the middle cerebral artery (n = 47, MCA group), and the basilar artery (n = 32, BA group), all of which were confirmed by cerebral angiography. We investigated the distribution of atherosclerosis of the three sites and compared the risk factors for atherosclerosis between the three groups. We used 113 subjects without stroke as the control group.
A strong correlation was present between atherosclerosis of the extracranial internal carotid artery and that of the basilar artery. However, only a weak correlation existed between atherosclerosis of the middle cerebral artery and that of the other vessels. Although the prevalence of smoking and hypertension was higher and high density lipoprotein cholesterol levels were lower in the three groups than in the control subjects, no significant differences were found in age, sex, prevalence of smoking and hypertension, serum levels of triglycerides, and high density lipoprotein cholesterol among the three groups. The prevalence of coronary heart disease and diabetes mellitus and the serum levels of hemoglobin A1c, total cholesterol, and low density lipoprotein cholesterol were higher in the ICA and BA groups than in the MCA group. The prevalence of electrocardiographic evidence of left ventricular hypertrophy was higher in the MCA group than in the other groups.
In addition to smoking, hypertension, and low concentration of high density lipoprotein cholesterol, diabetes mellitus and hypercholesterolemia seem to be associated with atherosclerosis of the extracranial internal carotid artery and the basilar artery, and advanced hypertension may play a role in the development of middle cerebral artery occlusion.
Neuropathologic changes in the gerbil brain after chronic hypoperfusion.
Authors: Kudo T , Takeda M , Tanimukai S , Nishimura T 
Published: June 2011

An animal model has been developed to elucidate the pathological changes in brain cytoskeletal proteins during chronic hypoperfusion.
Newly designed coiled clips were placed around both carotid arteries of Mongolian gerbils (n = 10) to cause stenosis without occlusion. Those gerbils showing impaired learning ability by the passive avoidance paradigm were killed for neuropathologic study after 12 weeks.
The brains showed ventricular dilatation, cortical atrophy, and rarefaction of the white matter. Immunoreactivity to anti-microtubule-associated protein 2 antibody in the cerebral cortex and the hippocampus was diminished, indicating dendritic changes of neurons. In the thalamic axonal regions, staining with anti-neurofilament 200K protein antibody was increased, suggesting increased amounts of neurofilament proteins or increased phosphorylation of the protein. Increased immunoreactivity to anti-glial fibrillary acidic protein antibody was observed in a wedge-shaped configuration, corresponding to the border zone of perfusion by small vessels.
These findings suggest that changes in the cytoskeletal proteins in dendrites, axons, and glial cells may cause neuronal death under conditions of chronic cerebral hypoperfusion.
Cerebral blood flow in mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes.
Authors: Ooiwa Y , Uematsu Y , Terada T , Nakai K , Itakura T , Komai N , Moriwaki H 
Published: June 2011

The precise mechanism of neurological symptoms with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) is still controversial. We investigated the correlation between strokelike episodes and cerebral blood flow in two patients with MELAS and discuss the pathogenesis of strokelike episodes with MELAS.
Cerebral dynamic computed tomography and cerebral angiography were used to measure cerebral circulation in the first case, that of a 20-year-old woman with MELAS. The second subject was a 13-year-old female who was studied with xenon-enhanced computed tomography. The cerebral blood flow studies were performed 3-72 hours after the onset of strokelike episodes. Serial cerebral angiography, dynamic computed tomography, and xenon-enhanced computed tomography showed vasodilation localized in the affected cerebral cortexes during strokelike episodes, without any reduction in regional cerebral blood flow.
Our study suggests that the strokelike episodes associated with MELAS are different in origin from ischemic stroke.
Aspirin response and failure in cerebral infarction.
Authors: Helgason C M , Tortorice K L , Winkler S R , Penney D W , Schuler J J , McClelland T J , Brace L D 
Published: June 2011

The purpose of this study was to assess the biological effect of aspirin as measured by the inhibition of platelet aggregation in patients taking aspirin for stroke prevention and in patients with acute stroke.
We administered increasing doses of aspirin (325, 650, 975, and 1,300 mg daily) to 113 patients for stroke prevention and measured the inhibition of platelet aggregation in these patients and in 33 patients with acute stroke taking aspirin before stroke onset.
Eighty-five patients on < or = 325 and six on > or = 650 mg aspirin had complete inhibition of platelet aggregation. Increase of the dose by 325 mg in nine of the 22 patients with partial inhibition of platelet aggregation produced complete inhibition in five patients at 650 mg and in one at 975 mg. At 1,300 mg, three patients still had only partial inhibition of platelet aggregation (aspirin resistance). Of the 33 inpatients with acute stroke, 24 had platelet aggregation studies done before further administration of aspirin. Of these, 19 had complete inhibition of platelet aggregation and three had partial inhibition, with production of complete inhibition of platelet aggregation at dose escalation; one patient was aspirin-resistant and the other noncompliant.
How the inhibition of platelet aggregation relates to stroke prevention remains unclear. The ability of aspirin and the dose required to inhibit platelet aggregation may depend upon the individual.
Vascular dimensions of the cerebral arteries follow the principle of minimum work.
Authors: Rossitti S , Löfgren J 
Published: June 2011

The principle of minimum work is a parametric optimization model for the growth and adaptation of arterial trees. It establishes a balance between energy dissipation due to frictional resistance of laminar flow (shear stress) and the minimum volume of the vascular system, implying that the radius of the vessel is adjusted to the cube root of the volumetric flow. The purpose of this study is to verify whether the internal carotid artery system obeys the principle of minimum work.
Measurements of the radius of parent and branch segments of the internal carotid, anterior, and middle cerebral arteries were performed on analog angiographs chosen at random from a set classified as normal. The branch angles were measured from lateral projections in bifurcations of the anterior cerebral artery. The relation of the calibers of parent and branch vessels was analyzed.
The area ratio of the bifurcations (N = 174) was 1.2 +/- 0.4 (mean +/- SD). The equation (r0)n = (r1)n + (r2)n was solved for n, resulting in n = 2.9 +/- 0.7 (mean +/- SD, N = 157). Optimum proportions between the radii of parent (r0) and branch (r1 and r2) vessels in the internal carotid artery system were verified in normal carotid angiographs up to four branch generations, according to the theoretical equation r0(3) = r1(3) + r2(3) (r = 0.989, N = 174). No clear correlation was found between the measured branch angles, the relative branch cross-sectional area, and the theoretical optimum angles.
This study demonstrates that the process of branching of the internal carotid artery system obeys the principle of minimum work, as the diameter exponent approximates 3. The principle of minimum work establishes strict functional relations between volumetric flow, flow velocity, and vessel radius. This model was extended to parametric optimization of branch angles, which has proved irrelevant in terms of functional optimization. Our results corroborate this finding. Shear stress-induced endothelial mediation seems to be the regulating mechanism for the maintenance of this optimum vessel design. The magnitude of wall shear stress is the same at every point in a vascular network obeying the principle of minimum work, because the flow rate influences the shear stress proportionally to the third power of the vessel radius. This observation has implications for understanding the remodeling of the cerebral vascular network in the presence of arteriovenous malformations and for the pathogenesis of saccular aneurysms.
Data analysis in behavioral cerebral blood flow activation studies using xenon-133 clearance.
Authors: Lagrèze H L , Hartmann A 
Published: June 2011

Three mainstream strategies exist to detect the responses of regional cerebral blood flow to functional activation. We tested the significance of changes in raw regional cerebral blood flow data, regional cerebral blood flow data normalized by division by global cerebral blood flow (dependent model of the regional-to-global cerebral blood flow relation), and regional cerebral blood flow data treating global cerebral blood flow as a covariate (independent model). Both latter models attempt to enhance regional sensitivity by removing global effects. We examined the sensitivity and pitfalls of these three strategies in behavioral activation studies.
These three strategies of data analysis were applied to changes in regional cerebral blood flow induced by a visuospatial problem-solving task in 38 healthy subjects as measured by the intravenous xenon-133 method with 32 stationary detectors.
Mental activation increased blood flow in all regions of interest. Raw data were most sensitive and reliable to detect responses to mental stimulation. Both the independent and dependent models to remove global effects were less sensitive and falsely indicated deactivation in regions that were clearly stimulated.
In behavioral activation paradigms, safe data analysis should be restricted to using raw regional cerebral blood flow increases without normalization or separation of global from regional effects. Studies using complex stimulation tasks should be scrutinized for global cerebral blood flow effects confounding regional responses.
Measurement of cerebrovascular changes in cats after transient ischemia using dynamic magnetic resonance imaging.
Authors: Hamberg L M , Macfarlane R , Tasdemiroglu E , Boccalini P , Hunter G J , Belliveau J W , Moskowitz M A , Rosen B R 
Published: June 2011

Hemodynamic changes associated with acute ischemia cannot be measured with conventional nuclear magnetic resonance imaging. In this study, we used dynamic susceptibility-contrast magnetic resonance imaging to measure the changes in vascular transit time and relative cerebral blood volume in a feline occlusion-reperfusion model.
Dynamic susceptibility-contrast measurements were obtained before and during 10 minutes of global cerebral ischemia and for up to 3 hours after the onset of reperfusion. A cerebral blood flow index was calculated from the vascular transit time and relative cerebral blood volume measurements. Functional maps were constructed to demonstrate the regional hemodynamic differences resulting from the induced ischemia.
During the early phase after reperfusion, both the relative cerebral blood volume and blood flow index rose sharply, followed by a fall to near-basal levels at 45 minutes (1 x control and 1.3 x control, respectively). Thereafter, the volume rose slowly, whereas the flow index continued to drop. At 3 hours, cerebral blood volume had reached 1.6 times its control value, whereas the flow index had returned to its base value.
The hemodynamic behavior we observed in our model reflects the independent responses of the cerebral blood volume and flow index to ischemic insult. Measurements acquired by our method were consistent with the temporal behavior reported in previous radionuclide studies. Susceptibility-contrast nuclear magnetic resonance tomographic imaging proved to be valuable in detecting and quantifying both immediate and subsequent changes in the hemodynamic state of the ischemic and hyperemic feline brain.
Effects of repeated cerebral ischemia on extracellular amino acid concentrations measured with intracerebral microdialysis in the gerbil hippocampus.
Authors: Nakata N , Kato H , Kogure K 
Published: June 2011

To clarify the role of elevated extracellular amino acid concentrations during ischemia on the cumulative neuronal damage after repeated cerebral ischemic insults, using a microdialysis technique we measured concentrations of the amino acids glutamate, glutamine, glycine, taurine, and gamma-aminobutyric acid in the gerbil hippocampus over three 2-minute forebrain ischemic insults induced at 1-hour intervals.
Under light anesthesia, the bilateral common carotid arteries were occluded with aneurysm clips at 1-hour intervals. Samples were collected by microdialysis at 10-minute intervals, and the amino acid concentrations were determined using a high-performance liquid chromatography system.
During and immediately after the first ischemic insult, concentrations of glutamate, glycine, and taurine, but not glutamine, increased significantly. Glutamate and taurine concentrations rose again during the second and third ischemic insults, but the increases were smaller than those during the first insult. By contrast, glutamine concentrations increased slightly but significantly during the second and third ischemic insults. The extracellular concentration of gamma-aminobutyric acid before the ischemic insults was below the level of detectability but increased markedly during each ischemic insult, with similar declines in the amounts released during later insults. Concentrations of all amino acids returned to baseline after 10 minutes of reperfusion and remained at baseline until the subsequent ischemic insult was induced.
It is well established that glutamate released during ischemia plays a crucial role in ischemia-induced neuronal death. However, the present results indicate that cumulative neuronal damage following sublethal ischemic insults is not caused by an exaggerated release of excitatory amino acids during subsequent ischemic insults but strongly suggest that increased intracellular reactions leading to cell death play a major role.
Myocardial infarction, thrombolytic therapy, and stroke. A community-based study. The MITI Project Group.
Authors: Longstreth W T , Litwin P E , Weaver W D 
Published: June 2011

Thrombolytic therapy used in patients with acute myocardial infarction may increase the risk of stroke. Scant information is available from community-based studies.
Among 5,635 consecutive patients admitted with acute myocardial infarction to hospitals in Seattle and surrounding suburban King County, Washington, 116 (2.1%) experienced strokes during hospitalization. Of these strokes, 82 (71%) were ischemic and 34 (29%) were hemorrhagic, defined by a patient's having had a computed tomographic scan of the head that showed blood. Thrombolytic therapy was given to 1,413 of these patients (25%) and was associated with increased risk of hemorrhagic stroke but reduced risk of ischemic stroke. The relative risk of stroke with thrombolytic therapy was estimate using multiple logistic regression to adjust for potential confounding factors. The adjusted relative risk for hemorrhagic stroke was 3.6 (95% confidence interval [CI], 1.7-8.0); for ischemic stroke, 0.4 (95% CI, 0.2-0.9); and for overall stroke, 1.0 (95% CI, 0.6-1.7). The adjusted risk for death from any cause following stroke was 3.0 (95% CI, 1.4-6.4).
Although thrombolytic therapy had little effect on the overall occurrence of stroke, thrombolytic therapy increased the risk of stroke death because more patients with hemorrhagic than ischemic strokes died during their hospitalization. The rates of hemorrhagic stroke with thrombolytic therapy reported in the present study are higher than those reported in clinical trials in which treatment is given to select patients under strict protocols.
An unusual cause of cerebral venous thrombosis in a four-year-old child.
Authors: Rich C , Gill J C , Wernick S , Konkol R J 
Published: June 2011

Inherited protein S deficiency has been associated with an increased risk of thromboembolic disease. It is possible that such a coagulopathy could predispose children to the development of strokes by permitting clot formation in response to stimuli that ordinarily would be insufficient to cause thrombus formation.
We evaluated a previously well 4-year-old boy who developed cerebral venous thrombosis after suffering minor head trauma. Crossed-immunoelectrophoresis of his plasma showed a marked decrease of the free, active form of protein S. Family studies revealed that the patient's father and other paternal relatives had a similar abnormality of protein S.
We suggest that the cerebral venous thrombosis in this child was initially precipitated by minor head trauma and pathological thrombus formation was then potentiated by inherited protein S deficiency. This case extends the clinical spectrum for protein S deficiency and emphasizes the importance of evaluating family members to establish a specific diagnosis and therapeutic intervention.
Prevalence of apolipoprotein E phenotypes in ischemic cerebrovascular disease. A case-control study.
Authors: Couderc R , Mahieux F , Bailleul S , Fenelon G , Mary R , Fermanian J 
Published: June 2011

Apolipoprotein E polymorphism may influence the early development of coronary artery disease. We investigated the putative role of apolipoprotein E phenotypes in cerebral infarction.
The apolipoprotein E phenotypes of 69 patients (mean +/- SD age, 72 +/- 11 years) who had suffered completed stroke or a transient ischemic attack and 68 sex- and age-matched control subjects free of cerebrovascular disease were determined by isoelectric focusing. The relative frequency of the apolipoprotein E phenotypes in the general population was estimated in 498 healthy blood donors (mean age, 37 years).
The prevalences of hypertension, diabetes mellitus, obesity, and intermittent claudication were significantly higher in patients than in control subjects. Serum lipid and apolipoprotein B concentrations and the composition of very low density lipoproteins were not significantly different between patients and control subjects. Apolipoprotein A-I and E levels were significantly lower in patients. Cholesterol levels were higher in male patients than in male control subjects (5.10 +/- 1.46 versus 4.41 +/- 0.80 mmol/L; p = 0.036), and the ratio of apolipoprotein A-I to B was lower (0.77 +/- 0.29 versus 1.03 +/- 0.37; p < 0.001). The E3/E3 phenotype was more frequent in control subjects (85%) than in patients (72.5%; p < 0.05) and healthy blood donors (64%; p < 0.02). The E3/E2 phenotype was more frequent in patients (10.1%) than in control subjects (1.4%; p < 0.05). A stepwise logistic regression showed that the presence of stroke was significantly related to high blood pressure (p < 0.0001), low apo E levels (p < 0.008), obesity (p < 0.041), the apo E phenotype (p < 0.05), and diabetes mellitus (p < 0.05).
The E3/E3 phenotype may protect against early vascular morbidity, and the epsilon 2 gene may be a risk factor for cerebrovascular morbidity, possibly related to diabetes, hypertension, and/or obesity.