bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stroke subtypes among Hispanics living in Guayaquil, Ecuador. Results from the Luis Vernaza Hospital Stroke Registry.
Authors: Del Brutto O H , Mosquera A , Sánchez X , Santos J , Noboa C A 
Published: June 2011

Racial differences in stroke subtypes have been documented. Asians have a higher rate of cerebral hemorrhage than whites; however, there is little information about stroke subtypes among Hispanics. The purpose of this study was to determine the patterns of stroke subtypes in a population of Hispanics.
Five hundred consecutive patients with a first stroke were included. Patients were collected from hospital wards, the emergency department, and the outpatient clinic to ensure inclusion of patients with a wide range of stroke severity. Computed tomography was available in all cases. Patients with pure subarachnoid hemorrhage were excluded.
There were 313 (62.6%) patients with an infarct and 187 (37.4%) with a hemorrhage. Hypertensive arteriolopathy was the most common cause of both infarcts and hemorrhages. The carotid territory was involved in 70.6% of the 313 patients with infarcts, the vertebrobasilar territory in 17.9%, multiple territories in 6.7%, and a watershed area in 4.8%. Hemorrhages were most often lobar (36.4%), followed by putaminal (30.5%), brain stem (9.1%), cerebellar (8%), thalamic (8%), ventricular (5.3%), and caudate (2.7%).
This hospital-based stroke registry suggests that stroke in Hispanics has a pattern different from that in whites but similar to that in Asians. Cerebral hemorrhages occur three times more frequently in Hispanics than in whites.
Hemodilution improves cerebral hemodynamics in internal carotid artery occlusion.
Authors: Yamauchi H , Fukuyama H , Ogawa M , Ouchi Y , Kimura J 
Published: June 2011

Hemodilution may be a useful form of therapy for patients with carotid occlusive disease and hemodynamic ischemia. Accordingly, we evaluated the effects of hemodilution on cerebral hemodynamics and oxygen metabolism in patients with carotid artery occlusion.
Using positron emission tomography, we analyzed regional cerebral blood flow, oxygen extraction fraction, oxygen metabolic rate, and blood volume before and after isovolemic hemodilution in five patients with unilateral internal carotid artery occlusion and minor stroke. Hemodilution was accomplished by phlebotomy of 400 mL and infusion of 400 mL of hydroxyethyl starch.
Before hemodilution, the patients had a significant decrease in blood flow and oxygen transport along with significantly elevated oxygen extraction fraction in the cerebral hemisphere with carotid artery occlusion compared with six control subjects. After hemodilution, the hematocrit and arterial oxygen content decreased from 41.2% and 18.6 mL/dL to 36.3% and 16.5 mL/dL, respectively. Both cerebral blood flow and oxygen transport were increased and oxygen extraction fraction was decreased without any change in oxygen consumption. The degree of increase in blood flow and oxygen transport was positively correlated with the ratio of oxygen extraction fraction to blood volume before hemodilution.
These findings indicate that hemodilution improves oxygen transport as well as blood flow in patients with internal carotid occlusion and decreased perfusion and that this improvement may be more prominent in patients with a severely compromised hemodynamic state. Thus, hemodilution may be useful in patients with hemodynamic ischemia.
Hematologic abnormalities occur in both cortical and lacunar infarction.
Authors: Kilpatrick T J , Matkovic Z , Davis S M , McGrath C M , Dauer R J 
Published: June 2011

Primary hematologic abnormalities are a rare but established cause of ischemic stroke. In addition, activation of hemostatic parameters is often present during the acute phase of stroke. However, it is uncertain whether these abnormalities occur in both cortical and lacunar infarction; this study aimed to further assess this issue.
Hematologic parameters (prothrombin, activated partial thromboplastin, thrombin clotting, and euglobulin lysis times; and fibrinogen, fibrinopeptide A, antithrombin III, protein C, protein S, and plasminogen levels) were measured in 19 patients within 48 hours of the onset of acute cerebral infarction. These patients included 10 with cortical infarcts and 9 with lacunar infarcts, as determined by standard clinical and radiological criteria.
Five patients with lacunar infarction and 7 patients with cortical infarction demonstrated raised fibrinopeptide A levels, indicating enhanced thrombin activity. Fibrinolysis, assessed by the euglobulin lysis time, was impaired in 6 of 9 patients with lacunar infarction and in 2 of 10 patients with cortical infarction. Lupus anticoagulants were detected in 3 patients with lacunar infarction and in 1 patient with cortical infarction. Three patients in each group displayed decreased antithrombin III function, and 1 patient with a lacunar infarction had a low protein C level.
Primary hematologic disorders and secondary hemostatic derangements may occur in patients with either cortical or lacunar infarction.
Evidence supporting a role for programmed cell death in focal cerebral ischemia in rats.
Authors: Linnik M D , Zobrist R H , Hatfield M D 
Published: June 2011

Cells die by one of two mechanisms, necrosis or programmed cell death. Necrosis has been implicated in stroke and occurs when the cytoplasmic membrane is compromised. Programmed cell death requires protein synthesis and often involves endonucleolytic cleavage of the cellular DNA. We assessed the potential contribution of programmed cell death to ischemia-induced neuronal death.
Cycloheximide (protein synthesis inhibitor; 1 mg/kg per 24 hours) or vehicle (1 mL/kg per 24 hours) was continuously infused into the right cerebral ventricle of spontaneously hypertensive rats. Neocortical focal ischemia was produced by tandem occlusion of the right common carotid artery and the ipsilateral middle cerebral artery. After 24 hours the brain was stained with 2% 2,3,5-triphenyltetrazolium and the ischemic zone quantitated. Protein synthesis was determined by [3H]methionine incorporation into acid-precipitated protein. DNA integrity was determined in isolated DNA by gel electrophoresis and in whole cells by flow cytometry.
Continuous cycloheximide infusion caused approximately 70% reduction in cortical protein synthesis. Cycloheximide also reduced the size of the infarction produced by focal cerebral ischemia when compared with controls (ischemic brain volume, 147.5 +/- 25.9 and 188.7 +/- 16.8 mm3 for cycloheximide and saline, respectively; P < .01), suggesting that protein synthesis may contribute to cell death. Purified DNA from the ischemic zone showed evidence of endonucleolytic degradation when fractionated by gel electrophoresis. Flow cytometric analysis demonstrated increased propidium iodide fluorescence in intact cells isolated from ischemic cortex, indicating an increased accessibility of degraded DNA to the intercalating dye.
New protein synthesis appears to contribute to ischemic cell death in which endonucleolytic DNA degradation is apparent. These observations implicate programmed cell death in ischemic injury and may open unique therapeutic approaches for the preservation of neurons in stroke.
Cerebral endothelial nitric oxide synthase expression after focal cerebral ischemia in rats.
Authors: Zhang Z G , Chopp M , Zaloga C , Pollock J S , Förstermann U 
Published: June 2011

The purpose of this study was to measure the temporal profile of expression of the endothelial nitric oxide synthase (NOS) in cerebral microvessels after middle cerebral artery occlusion in the rat.
Middle cerebral artery occlusion was performed on 24 male Wistar rats by extracranial insertion of a 4-0 nylon monofilament into the internal artery. Three additional rats were used as controls. Animals were killed at 1, 2, 4, 6, 24, 48, 72, and 168 hours after middle cerebral artery occlusion (n = 3 per time point). Rat brains were perfused with buffer, frozen, sectioned, and stained with a monoclonal antibody against endothelial NOS. Adjacent sections were stained with hematoxylin and eosin for evaluation of neuronal damage.
The endothelial NOS in the cerebral vessels was upregulated at 1 hour after induction of ischemia throughout the ischemic region. The induction of the endothelial NOS progressively increased up to 24 hours of ischemia. In the periphery of the area of necrosis in the cortex, a delayed (24-hour) upregulation of the endothelial NOS remained constant throughout the duration of ischemia.
The rapid and intense differential expression of the endothelial NOS in the core and peripheral areas of the lesion indicates a role for endothelial NOS in ischemic cell damage and suggests that the increased expression of NOS may mediate changes in the cerebral blood flow.
Diffusion and perfusion magnetic resonance imaging studies to evaluate a noncompetitive N-methyl-D-aspartate antagonist and reperfusion in experimental stroke in rats.
Authors: Minematsu K , Fisher M , Li L , Sotak C H 
Published: June 2011

Diffusion magnetic resonance imaging (MRI) can quantitatively detect focal ischemic injury within minutes of onset, and perfusion MRI can evaluate the brain's microcirculation. N-Methyl-D-aspartate (NMDA) antagonists and reperfusion can reduce lesion size in stroke models. We used diffusion and perfusion MRI to evaluate the in vivo effects of a noncompetitive NMDA antagonist, CNS 1102, in a temporary ischemia model.
Sixteen Sprague-Dawley rats underwent suture occlusion of the middle cerebral artery. Fifteen minutes after occlusion, animals were randomly assigned to treatment with CNS 1102 (n = 10) or placebo (n = 6), receiving a bolus of 1.13 mg/kg at that time and an infusion of 0.785 mg.kg-1.h-1 for the next 165 minutes. The placebo group received a saline bolus and infusion. Diffusion MRI studies by a spin-echo technique were initiated 30 minutes after occlusion and repeated every 30 minutes for the next 3 hours. Perfusion MRI studies were obtained using echo-planar imaging after injection of superparamagnetic iron oxide particles, immediately before and 15 minutes after withdrawal of the occluder at 3 hours after middle cerebral artery occlusion. At 24 hours, the animals were clinically evaluated (scale of 0 to 5) and electively killed, and the brain was stained with triphenyltetrazolium chloride to evaluate infarct size.
Diffusion imaging demonstrated markedly reduced ischemic lesion area in the CNS 1102 group during occlusion--10.5 +/- 7.3% (mean +/- SEM) of the ischemic hemisphere (optic chiasm slice) at 30 minutes after occlusion versus 50.0 +/- 2.7% of the hemisphere in controls (P < .02). With reperfusion after 3 hours of temporary ischemia, diffusion imaging documented an additional 29% reduction of the ischemic lesion area in the CNS 1102-treated group (P < .01) compared with the prereperfusion ischemic lesion area, with no change in the placebo group. During occlusion, perfusion imaging demonstrated a relative signal intensity decline of 31.5 +/- 7.7% in controls and 83.4 +/- 7.6% in the CNS 1102 group (P < .005), indicating better perfusion in the latter group. After removal of the occluder, perfusion improved in both groups and was not significantly different. Post mortem infarct volume was 53.8 +/- 20.0 mm3 in the CNS 1102 group and 216.8 +/- 16.1 mm3 in the controls (P < .0001). Clinical outcome at 24 hours was 1.1 +/- 0.4 in the CNS 1102 group and 4.0 +/- 0.5 (scale of 0 to 5) in the controls (P < .005).
This study demonstrates that CNS 1102 reduces early postischemic injury as documented by diffusion MRI and improves perfusion as documented by perfusion MRI and that reperfusion confers additional reduction of ischemic lesion size.
Reversed alterations of hippocampal parvalbumin and protein kinase C-gamma immunoreactivity after stroke in spontaneously hypertensive stroke-prone rats.
Authors: De Jong G I , Van der Zee E A , Bohus B , Luiten P G 
Published: June 2011

Aging spontaneously hypertensive stroke-prone rats (SHR-SP) were previously shown to develop neocortical strokes. Because the hippocampal CA1 is selectively vulnerable to abnormal brain perfusion, the neuropathological effects of spontaneous strokes were investigated on specific neurochemical alterations in two major cell types of the hippocampal CA1 in SHR-SP.
The immunoreactivity for the gamma-isoform of protein kinase C (in pyramidal cells) and parvalbumin (in interneurons) was determined in the hippocampal CA1 by applying monoclonal antibodies. Because chronic treatment with the calcium antagonist nimodipine prevents the development of strokes in SHR-SP, we compared SHR-SP (stroke) with age-matched nimodipine-treated rats (nonstroke).
After stroke in control animals, we observed a strikingly enhanced immunoreactivity for protein kinase C-gamma in CA1 pyramidal cells compared with nimodipine-treated rats, which can be interpreted as the result of an increased activation of these cells. The pathological increase of protein kinase C-gamma immunoreactivity was accompanied by a reduced parvalbuminergic innervation of these pyramidal cells in symptomatic SHR-SP.
Because parvalbumin is present in a subset of GABAergic inhibitory interneurons, these data suggest that increased activity of CA1 pyramidal cells after spontaneous stroke may partially be related to a decreased inhibitory input on these cells.
Cerebral infarction due to painless thoracic aortic and common carotid artery dissections.
Authors: Veyssier-Belot C , Cohen A , Rougemont D , Levy C , Amarenco P , Bousser M G 
Published: June 2011

Aortic arch dissection is usually lethal unless emergency surgery is performed. The dissection rarely may have a benign outcome or may occur without pain and be revealed by cerebral infarction. It is then likely to be seen primarily by a neurologist. In such cases, the value of new noninvasive diagnostic testing has not been reported.
A 51-year-old man had a sudden left-sided hemiplegia due to hemorrhagic capsular and caudate infarcts on the right side. Cervical ultrasound examination with color flow imaging showed a bilateral common carotid artery dissection extending up to the bifurcation. Transesophageal echocardiography showed an aortic arch dissection, involving the innominate and left common carotid artery origins, which was confirmed by magnetic resonance imaging and aortography. The patient spontaneously fully recovered and is still alive 24 months after the stroke onset.
This case emphasizes the usefulness of new noninvasive techniques such as transesophageal echocardiography and color-coded Doppler echocardiography in the diagnosis and follow-up of painless dissection of aortic and common carotid arteries. This cause of stroke may be underestimated.
Persistent primitive proatlantal intersegmental artery (proatlantal artery I) results in 'top of the basilar' syndrome.
Authors: Bahşi Y Z , Uysal H , Peker S , Yurdakul M 
Published: June 2011

Persistent primitive proatlantal intersegmental artery (proatlantal artery I) is an anastomotic channel between the carotid and vertebrobasilar arterial systems. Persistence of this embryonic anastomosis is very rare. The "top of the basilar" syndrome is usually due to occlusion of thalamoperforating arteries by emboli that rise from the vertebrobasilar arterial system. In this case, however, the emboli stemmed from atherosclerotic plaques in the carotid system.
A 55-year-old woman was hospitalized with top of the basilar syndrome. A brain scan showed hypodense lesions extending from the mesencephalon to both thalami. Digital subtraction angiography of the cerebral circulation was performed, which revealed a proatlantal artery I on the left side. In addition, atheromatous plaques were seen along the internal and common carotid arteries on the same side.
The occurrence of proatlantal artery I is extremely rare. Top of the basilar syndrome is also rarely encountered. To our knowledge, this is the first report of a patient with both conditions.
Discrete cortical infarction with prominent impairment of thumb flexion.
Authors: Terao Y , Hayashi H , Kanda T , Tanabe H 
Published: June 2011

Intracortical efferent zones in the primary motor cortex for thumb movements, namely thumb flexion, extension, adduction, and abduction, have been described in Macaca mulatta monkeys but not in humans. Even recent cortical mapping based on intraoperative monitoring does not provide information about intracortical efferent zones as it is not ethically possible to search the human motor cortex extensively by punctate electrodes.
A 78-year-old man with discrete cortical embolism over the left central sulcus is described. Only a mild weakness of his right thumb was observed. Thumb flexion was affected to a greater degree than thumb extension, adduction, and abduction. The lesion ran along the bottom of the central sulcus and affected part of the precentral and postcentral gyri on both sides of it. Animal studies in Macaca mulatta monkeys have shown that the intracortical efferent zones for thumb movement, especially for thumb flexion, are located in the part of the motor cortex just adjoining the central sulcus that folds down from the "bank" to the depth of the central sulcus. It was possible to explain the prominent weakness of thumb flexion if we applied the results of the animal studies.
Our case suggests that the same arrangement of intracortical efferent zones found in monkeys may also exist in human beings.
Altered gene expression in cerebral ischemia.
Authors: Kogure K , Kato H 
Published: June 2011

Using the techniques of molecular biology, recent experimental studies have shown that cerebral ischemia induces a variety of changes in gene expression in the brain.
During the early postischemic stages, protein synthesis in the brain is generally suppressed, but specific genes are expressed and their corresponding proteins may be synthesized, such as immediate-early gene products (c-fos, c-jun, and zinc finger gene), heat-shock proteins, and amyloid precursor protein. The ability of neurons to induce such stress responses, which depends on both the severity of ischemia and the intrinsic nature of the neuronal populations, may be directly associated with neuronal death and survival after ischemia. Nerve growth factor and fibroblast growth factor are also induced after ischemia and may be related to repair processes, in which a role of glial cells is suggested. Postischemic events that may be associated with the altered gene expression include (1) induction of tolerance to ischemia after pretreatment with sublethal ischemia, (2) slow, progressive neuronal changes and the development of neuronal plasticity after ischemia, and (3) delayed neuronal changes in remote areas outside the cerebral ischemic focus.
Because a variety of harmful stresses, including ischemia, elicit the same stress response and because this response is induced when total protein synthesis in the brain is nearly completely suppressed, this response may be vital to cell survival and repair. A successful induction of this response may induce resistance and survival of neurons after ischemia. However, failure or abortion of the response and persistent stresses may lead to neuronal death and possibly long-term changes and degeneration.
Differentiation of multi-infarct and Alzheimer dementia by intracranial hemodynamic parameters.
Authors: Ries F , Horn R , Hillekamp J , Honisch C , König M , Solymosi L 
Published: June 2011

The differentiation between the Alzheimer and multi-infarct types of dementia may still be equivocal considering clinical criteria, neuropsychological tests, and imaging techniques. Cerebral microangiopathic alterations underlying multi-infarct dementia should allow the characterization of dementia subgroups.
Patients with a diagnosis of multi-infarct dementia (n = 17; mean age, 69.1 +/- 8.5 years) or Alzheimer dementia (n = 24, mean age, 65.8 +/- 9.0 years) according to standard testing criteria, clinical findings, and neuroimaging techniques (computed tomography and magnetic resonance imaging) were investigated prospectively by transcranial Doppler sonography and compared with a normal reference group (n = 64; mean age, 61.0 +/- 11.1 years). Transcranial Doppler sonography allows an indirect evaluation of peripheral flow resistance in the microcirculatory bed by quantifying pulsatility characteristics, as reflected in the effective pulsatility range (time-averaged mean blood flow velocity minus the peak-systolic to end-diastolic amplitude, in centimeters per second).
A total of 204 vessels were investigated in 105 subjects. Mean and diastolic blood flow velocities as well as the effective pulsatility range were significantly lower in the multi-infarct dementia group compared with the Alzheimer and the normal reference groups (p < 0.001). By using receiver operating characteristic analysis, a cutoff point for effective pulsatility range values of -5 cm/sec gives a side-dependent sensitivity of 90.48-95.24% and a specificity of 64.71-70.59% in diagnosing Alzheimer-type dementia; the corresponding sensitivity and specificity for a value of -2 cm/sec are 82.35-88.24% and 80.95-90.48%, respectively.
Pulsatility changes as reflected by the effective pulsatility range are a noninvasive additional criterion in the differential diagnosis of dementia.
Predictors of carotid stenosis in older adults with and without isolated systolic hypertension.
Authors: Sutton-Tyrrell K , Alcorn H G , Wolfson S K , Kelsey S F , Kuller L H 
Published: June 2011

This study was designed to determine the prevalence of carotid stenosis and atherosclerosis in older adults with and without isolated systolic hypertension and to determine risk factors for carotid artery disease in these two groups.
Duplex scans were performed on 187 participants of the Systolic Hypertension in the Elderly Program and on 187 normotensive control subjects. Doppler measures of blood flow velocity were used to determine the prevalence of internal carotid artery stenosis.
Carotid stenosis was found in 25% of hypertensive participants but in only 7% of normotensive participants (p < 0.001). Among hypertensive participants, carotid stenosis was correlated with lower diastolic blood pressure (p = 0.022). In multivariate analysis, systolic blood pressure of > or = 160 mm Hg was the strongest predictor of carotid stenosis. Other variables independently related to stenosis were diastolic blood pressure of < 75 mm Hg (p = 0.001), alcohol use (p = 0.005), heart rate of > or = 80 beats per minute (p = 0.013), smoking (p = 0.034), high concentration of apoprotein B (p = 0.001), and low concentration of high density lipoprotein cholesterol (borderline significant, p = 0.069). Among hypertensive participants, the strongest predictor of carotid stenosis was low diastolic blood pressure. This relation persisted even after taking into account differences in pulse pressure.
Isolated systolic hypertension is strongly correlated with carotid stenosis, and among those with isolated systolic hypertension low diastolic blood pressure is a marker for carotid stenosis.