bluuebunny/crossref_metadata_2025_split huggingface dataset:
Optimality principles and flow orderliness at the branching points of cerebral arteries.
Authors: Rossitti S , Löfgren J 
Published: June 2011

The cerebral arteries present an optimum blood flow/vessel radius relation. However, branch angles may vary widely in the cerebral arteries because the parametric optimization of branch angles is irrelevant in terms of energy cost. The position of the flow divider in extracranial arteries has been suggested to be optimum in flow orderliness. No data exist on the flow divider of cerebral arteries. Thus, we hypothesized that in the cerebral arteries the apex of the bifurcations, which is known to be the site of maximum hemodynamic stress in a vascular network, may normally lie in a non-optimum position relative to the dividing flow streamline in the parent vessel, leading to disturbed laminar flow and increased vessel wall shear stress at the apical region despite the optimum blood flow/vessel radius relation. The objective of this study was to test our hypothesis.
We measured the branch angles and diameters of parent and branch segments of the anterior cerebral artery system from lateral projections to minimize the measurement error on angiographs chosen at random from normal sets. The position of the apex of the bifurcations in relation to the ostium of the parent artery (gamma) and the ratio of the branch diameters (d2/d1) were compared. Optimum curves for these parameters were calculated by a mathematical model. In addition, the separation of flow streamlines according to gamma was calculated for each bifurcation and related to the division of flow required by each branch according to the optimum blood flow/vessel radius relation.
The data points on gamma and d2/d1 and the separation of flow according to gamma and the division of flow required by the branches were found to scatter around the optimum curves. However, a trend toward the theoretical optimum is discernible. The data points are suggested to be a random sample from a normal distribution around the optimum (.40 < P < .50).
The bifurcations of the cerebral arteries appear to be optimized to avoid increased hemodynamic stresses both globally and locally in the same manner as extracranial arteries.
Fulminant brain necrosis from atrial myxoma showers.
Authors: Browne W T , Wijdicks E F , Parisi J E , Viggiano R W 
Published: June 2011

Atrial myxoma is uncommon and may be associated with brief isolated ischemic events. We describe a patient with atrial myxoma and an incompletely evaluated ischemic stroke followed 1 year later with almost complete brain necrosis.
A 63-year-old woman presented with a rapidly progressive illness resulting in coma within 24 hours from multiple myxomatous emboli. Cranial computed tomographic scan demonstrated multiple hypodensities in both cerebellar and cerebral hemispheres. Postmortem examination revealed virtually complete brain necrosis, multiple peripheral artery embolizations, embolization in the coronary arteries with acute myocardial infarction, and tumor emboli in the spleen and kidneys.
Although uncommon, atrial myxoma may present as a fatal multiple organ embolization that includes both anterior and posterior circulation territories of the brain.
Posterior ischemia during an attack of transient global amnesia.
Authors: Lin K N , Liu R S , Yeh T P , Wang S J , Liu H C 
Published: June 2011

The popular concept that cerebral ischemia causes transient global amnesia has been difficult to prove by cerebral blood flow studies during attacks because the transient global amnesia attacks are so short.
We performed single-photon emission computed tomography (SPECT) of the brain and neuropsychological assessment in a 37-year-old woman during a 10-hour attack and twice thereafter. A neuropsychological evaluation 3 hours after the onset of transient global amnesia revealed severe impairment of recent memory and verbal fluency, both of which returned to normal 2 and 28 days later, respectively. A 99mTc-labeled hexamethylpropyleneamine oxime SPECT of the brain performed 6 hours after the onset showed multiple perfusion defects in both occipital lobes, the medial left temporal lobe, and the left thalamus. A second brain SPECT performed 3 days later showed perfusion defects in only the occipital regions. A third brain SPECT performed 28 days later was normal. The patient's brain computed tomographic scan, electroencephalogram, duplex ultrasound of the carotid artery, and echocardiogram were normal.
The perfusion defects revealed by the brain SPECT during the transient global amnesia attack indicated ischemia in the territory of the posterior cerebral arteries, which partially resolved in 3 days and completely resolved by 28 days.
Increased immunoglobulin binding to cerebral endothelium in patients with antiphospholipid antibodies.
Authors: Hess D C , Sheppard J C , Adams R J 
Published: June 2011

There is a strong link between antiphospholipid antibodies and stroke. The mechanism of action of antiphospholipid antibodies is unknown. Most theories of pathogenesis center around platelet or endothelial cell dysfunction. Our aim was to determine if there were immunoglobulins in the sera of patients with antiphospholipid antibodies that bind human brain microvascular endothelial cells.
We studied sera from three groups of subjects: patients with antiphospholipid antibodies and stroke (group 1), healthy control subjects (group 2), and patients with stroke but without antiphospholipid antibodies (group 3). We isolated human brain microvascular endothelial cells from temporal lobectomy specimens and used a cellular enzyme-linked immunosorbent assay (ELISA) to measure immunoglobulin binding to endothelial cells derived from human brain and from human umbilical vein. We used a chromium release assay to measure cytotoxicity.
Patients with antiphospholipid antibodies and stroke had significantly higher immunoglobulin binding to human brain microvascular endothelial cells than subjects in the other groups ([ELISA index+standard deviation], 63 +/- 37 [group 1] versus 7 +/- 7 [group 2] versus 7 +/- 7 [group 3], P < .001). There was, however, poor correlation between binding to brain endothelial cells and binding to cardiolipin. The binding to brain microvascular cells was not specific to brain endothelium, as similar results were found in an ELISA using human umbilical vein cells. There was no evidence of complement-mediated brain endothelial cell cytotoxicity.
Patients with stroke and antiphospholipid antibodies frequently have human brain microvascular endothelial-reactive antibodies in their serum. These antibodies are distinct from those to cardiolipin. We found no evidence that these antibodies are cytotoxic.
Stroke mortality and case-fatality rates in three geographic areas of Finland from 1983 to 1986.
Authors: Sarti C , Tuomilehto J , Sivenius J , Kaarsalo E , Narva E V , Salmi K , Salomaa V , Torppa J 
Published: June 2011

Our aim was to describe the mortality and early case-fatality rates of stroke in three geographic areas of Finland during 1983 to 1986 by means of a community-based stroke register and to estimate the accuracy of registration of stroke deaths in the official statistics compared with the FINMONICA stroke register.
Annual and average mortality and case-fatality rates of stroke were derived from data collected in the FINMONICA stroke register during 1983 to 1986. Age-specific and age-standardized rates were calculated for the three areas, and the results were compared with the official mortality statistics and with the case-fatality figures published previously in the literature for Finland and elsewhere.
Mortality from stroke in the three FINMONICA areas was between 73 and 90 per 100,000 per year among men aged 25 to 74 years and between 42 and 55 per 100,000 per year among women in the same age group. Average case-fatality was similar in the three areas and globally high: 20% to 27% in men and 24% to 28% in women. Approximately half of the fatal strokes occurred within less than 2 days from the onset of the attack, and a further 25% within the first week. Hemorrhagic strokes accounted for 54% to 81% of all fatal strokes occurring in less than 2 days among men, while among women the corresponding proportions varied in the three areas between 35% and 74%. Of cerebral infarctions, approximately 28% to 37% among men and 19% to 20% among women were fatal within less than 2 days. Although the number of fatal strokes was similar in both the FINMONICA register and official mortality statistics, only 82% to 85% of the stroke cases were common in both registers; a further 13% to 14% of the cases classified as stroke deaths in the FINMONICA register could also be found in the official mortality statistics, but the underlying cause of death was something other than stroke.
The reliability of the Finnish official mortality statistics with regard to stroke deaths is reasonably good in aggregate numbers, but at the individual level considerable discrepancies seem to occur. Mortality from stroke in Finland has not declined further after 1979 and remains high internationally. Early case-fatality of stroke also seems higher in Finland than in most other countries. We believe that both the high incidence of stroke and the severity of the attacks are contributing to mortality and case-fatality rates of stroke in Finland.
Bilirubin levels in subarachnoid clot and effects on canine arterial smooth muscle cells.
Authors: Trost G R , Nagatani K , Goknur A B , Haworth R A , Odell G B , Duff T A 
Published: June 2011

Previous studies have suggested that bilirubin is a potential contributor to cerebral vasospasm. The purpose of this investigation was to determine whether bilirubin accrues in subarachnoid clot, whether its vasoconstrictive effect could involve a direct action on arterial smooth muscle cells, and, if so, whether bilirubin affects their Ca2+ uptake.
Subarachnoid clots were analyzed for bilirubin using high-performance liquid chromatography. The length and 45Ca2+ uptake of vascular smooth muscle cells enzymatically dissociated from canine carotid arteries were measured before and after exposure to bilirubin solution. Additional experiments were conducted on cultured smooth muscle cells from canine basilar artery and on ATP-depleted cardiac myocytes.
Mean +/- SE bilirubin concentration in experimental clot was 263 +/- 35.7 mumol/L. Vascular smooth muscle cells exposed to bilirubin showed progressive shortening (P < .01) and an increased uptake of 45Ca2+ (P < .001). Contraction was prevented by Ca(2+)-free media but not by verapamil. Experiments with heart myocytes showed that bilirubin caused an increased uptake of 45Ca2+ but not of [14C]sucrose.
The results indicate that bilirubin accrues in subarachnoid clot, that it exerts a direct constrictive effect on arterial smooth muscle cells, and that this effect is associated with an increased uptake of Ca2+. Studies on heart myocytes suggest that the Ca2+ uptake induced by bilirubin could be due to a selective increase in membrane permeability to Ca2+.
Morphometry of structural preservation of tunica media in aged and hypertensive human intracerebral arteries.
Authors: Masawa N , Yoshida Y , Yamada T , Joshita T , Sato S , Mihara B 
Published: June 2011

Medial smooth muscle cell necrosis has been reported as a lesion that may precede angionecrosis, which is a major cause of not only hypertensive brain hemorrhage but also lacunar infarct. We morphometrically studied a loss of smooth muscle cells in the media of cerebral arteries in relation to clinical risk factors.
The lateral striate, ie, perforating arteries and the medullary arteries in the subcortical white matter of the temporal lobe (100 to 400 microns in diameter) were histologically investigated in 121 autopsied brains. Medial area was measured quantitatively, and the number of nuclei of smooth muscle cells in the area was calculated in 1210 cross-sectional arteries of histological sections. The influence on the structural (ie, smooth muscle cell) preservation of the tunica media (ratio of number of smooth muscle cell nuclei to medial area [N-MA ratio]) of age, blood pressure, serum lipids, and presence of absence of extracerebral severe atherosclerosis was investigated.
The N-MA ratio decreased slightly with age in both arteries. A reverse correlation between N-MA ratio and age was seen in groups both with and without hypertension. The mean N-MA ratio in the hypertensive group was significantly lower than that of the nonhypertensive group (P < .001) in all decades of life. The mean N-MA ratio of the perforating arteries was slightly lower than that of the medullary arteries in both groups. Severe atherosclerosis of the internal carotid arteries, even with hypertension, mitigated a decrease of the N-MA ratio, which was as slight as that in the nonhypertensive group. Serum cholesterol in this group was higher than in both the conventional hypertensive group (P < .005) and the nonhypertensive group (P < .001).
Although both hypertension and age were significant risk factors for medial smooth muscle cell necrosis, hypertension was relatively more significant. Medial smooth muscle cells of the perforating arteries in the basal ganglia were more vulnerable than those of the medullary arteries. Cerebral small arteries in subjects with severe atherosclerosis of the carotid and major cerebral arteries (hypertension in eight of nine subjects) may have been protected from extensive loss of medial smooth muscles presumably because of both high serum cholesterol and decreased wall tensile stress associated with reduced blood perfusion due to severe atherosclerotic stenosis.
Cerebral blood flow in frontal lesions of aneurysms of the anterior communicating artery.
Authors: Rousseaux M , Huglo D , Steinling M 
Published: June 2011

The aim of this study was to investigate local and remote regional cerebral blood flow in patients with prefrontal lesions resulting from rupture (and operation) of aneurysms of the anterior communicating artery.
The localization and severity of the lesions were evaluated by magnetic resonance imaging on T2 sequences. Blood flow measurements were performed in 21 patients at least 3 weeks after surgery using single-photon emission computed tomography. Flow values were calculated in 10 regions of interest in each cerebral hemisphere and compared with those of 21 control subjects matched for age.
A drop in regional cerebral blood flow, predominating on the right side, was observed in the frontal areas. Flow values were not reduced in the thalamus and striatum but were significantly elevated in the posterior cortical areas and cerebellum. This latter phenomenon was significantly correlated with the severity of frontal lesions on magnetic resonance imaging.
Blood flow drop in frontal areas was correlated with the cerebral lesions, which predominated in the anterior prefrontal lobe, on the side of the surgical flap; most of these prefrontal lesions were likely due to the surgical procedure and not to classic arterial spasm. Elevated perfusion in the temporo-parieto-occipital cortex and cerebellum might be due to the release of a physiological inhibition exerted by the prefrontal cortex.
Effect of moderate hypothermia on lipid peroxidation in canine brain tissue after cardiac arrest and resuscitation.
Authors: Lei B , Tan X , Cai H , Xu Q , Guo Q 
Published: June 2011

We sought to examine the effect of moderate hypothermia (30 degrees C to 32 degrees C) initiated after resuscitation on the scavenging systems of free radicals and lipid peroxidation in canine brain tissue after cardiac arrest and resuscitation.
Twenty-one dogs were divided into four groups: group A, nonischemic controls (shams) (n = 4); group B, 15-minute cardiac arrest without reperfusion (n = 4); group C, 15-minute cardiac arrest and standard resuscitation (n = 6); and group D, 15-minute cardiac arrest and hypothermic resuscitation (n = 7). During the period of 10 to 120 minutes after resuscitation, brain temperature and core temperature in group D remained at 30 degrees C to 32 degrees C and were 4 degrees C to 5 degrees C lower than in group C. For each dog, a sample of right parietal cerebral cortex was obtained from group A, group B, or from group C and group D at 2 hours after resuscitation. The sample was assayed for tissue malondialdehyde (MDA), the content of reduced glutathione (GSH), and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX).
In group B, a 15-minute cardiac arrest induced an increase in MDA, a significant reduction of GSH, and no change in SOD and GSH-PX activities compared with group A. In group C, there were further increases in MDA and reductions in GSH content and GSH-PX activity compared with group A; SOD activity remained substantially unchanged. The content of MDA was higher in group D than in group A but less elevated in group D than in group C. The GSH content and SOD and GSH-PX activities were significantly higher in group D than in group C.
Moderate hypothermia initiated after resuscitation can significantly inhibit the accumulation of lipid peroxidation products and the consumption of free radical scavengers in the brain tissue.
Influence of pH on calcium influx during hypoxia in rat cortical brain slices.
Authors: O'Donnell B R , Bickler P E 
Published: June 2011

Acidity of brain intracellular and extracellular fluids appears to increase brain injury from stroke, but low extracellular pH decreases the activity of N-methyl-D-aspartate receptor ion channels and decreases calcium influx into isolated neurons. To further investigate the role of acid-base balance in hypoxic brain injury, we studied the influences of intracellular and extracellular pH on calcium influx in cortical brain slices during hypoxia.
Intracellular calcium ([Ca2+]i) and pH (pHi) were measured fluorometrically with the dyes fura-2 and biscarboxyethyl carboxyfluorescein, respectively, during two types of hypoxia: (1) slice perfusate equilibrated with N2/CO2 at pH 6.6 or 6.2 ("gaseous hypoxia") or (2) perfusate equilibrated with 95% O2/5% CO2 plus 100 mumol/L NaCN at pH 7.3, 6.6, or 6.2 ("chemical hypoxia").
Changes in perfusate pH under aerobic conditions did not change [Ca2+]i. However, influx of calcium caused by gaseous or chemical hypoxia increased significantly with decreasing perfusate pH. During chemical hypoxia, the elevation in [Ca2+]i at perfusate pH 6.2 was twice that at perfusate pH 7.3. Change in [Ca2+]i was correlated with perfusate pH but not pHi.
These results, which differ from previous studies showing acid inhibition of calcium influx in isolated neurons, suggest that low extracellular pH may exacerbate cellular injury during severe hypoxia or ischemia in the intact brain.
Basilar artery occlusion in a young patient with Wegener's granulomatosis.
Authors: Savitz J M , Young M A , Ratan R R 
Published: June 2011

Stroke is an uncommon sequela of Wegener's granulomatosis, resulting primarily from vasculitic infiltration of small to medium-sized vessels. We describe a young patient with Wegener's granulomatosis and basilar artery occlusion.
A 26-year-old man with histopathologically confirmed Wegener's granulomatosis suffered a brain stem stroke 24 hours after open lung biopsy. Angiography revealed midbasilar artery occlusion.
Patients with Wegener's granulomatosis may experience premature large cerebral vessel occlusion. Putative etiologies in our patient include vasculitis, postoperative hypercoagulability, and/or intraoperative neck positioning leading to embolization.
Initial experience with intravascular ultrasound imaging during carotid endarterectomy.
Authors: Karnik R , Ammerer H P , Winkler W B , Valentin A , Slany J 
Published: June 2011

To assess the feasibility of intravascular ultrasound imaging during carotid endarterectomy.
Intravascular ultrasound imaging was performed during carotid endarterectomy in eight patients using an over-the-wire catheter system with a 30-MHz ultrasound probe. In vitro studies were carried out before the intraoperative application, paying special attention to visualization of the wall layers of normal carotid arteries, structures of more or less diseased vessels, and surgically placed materials such as patch, suture material, and fibrin glue. Although intravascular ultrasound failed to distinguish between intima and media in areas of normal intima, fibrotic and calcified plaques were detected clearly. Dacron patch as well as sutures were identified as highly reflective structures.
In seven of the eight patients studied, intravascular ultrasound yielded cross-sectional images of good quality allowing identification of the vessel layers and the structures at the endarterectomy site. In all patients the three layers of the vessel wall were clearly differentiated and the transition zone between the site of endarterectomy and the genuine vessel appeared smooth without intimal flaps or residual arteriosclerotic plaques. In one patient severe eccentric thickening of the media was detected in the distal internal carotid artery. Neither damage of the vessel layers by the shunt nor thrombus formation in the operating area and the internal carotid artery were detected.
Intravascular ultrasound lends itself as a potentially valuable method of quality control during carotid endarterectomy. The method seems to enable an accurate evaluation of the endarterectomy site and the search for residual plaques.
Denial of eye closure in acute stroke.
Authors: Ellis S J , Small M 
Published: June 2011

Many patients suffering from stroke exhibit denial of illness. As part of this symptom complex we observed denial of eye closure. We therefore aimed to document the frequency and phenomenology of denial of eye closure in acute stroke.
Denial of eye closure was sought in 43 cases of denial of illness from a series of 400 acute strokes. Subjects underwent a neurological examination, and audiotaped interviews were performed during which they were asked to finger count through their closed eyes and their denial was challenged.
Five of 43 patients with denial of hemiplegia after acute stroke were also found to have denial of eye closure (12%). Denial of eye closure was associated with drowsiness and in all but one patient with disorientation. In the three cases with imaging or autopsy data available, lesions were moderate to large, in the right hemisphere, and involved the frontal lobe. Three subjects confabulated as to what they saw through their closed eyes. One subject mislocalized the hospital closer to her home.
Denial of eye closure occurs in a minority of patients with denial of illness after acute stroke. This phenomenon sheds light on denial as a whole and cannot easily be accounted for by unilateral explanations, such as inattention to one half of the body or loss of sensory input. There are aspects of denial, such as denial of eye closure, mislocalization, and the delusional intensity of beliefs, that can only be understood in cognitive terms.