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PubMedDate not supplied

[Subfractions of high-density cholesterol lipoproteins in patients with ischemic cerebrovascular disorders].

Aiming to detect the most sensitive markers of increased risk of ischemic cerebrovascular diseases HDL, HDL2 and HDL3 cholesterol levels were examined using the ultracentrifugation method in 36 patients with acute brain infarction and 34 healthy subjects of the control group. The results of the study have shown significant reduction of the total HDL cholesterol levels in both subfractions, and especially of HDL3 in patients with brain infarction. This finding was discussed in the light of recent studies of lipid disorders in patients with ischemic cerebrovascular diseases. It has been concluded that further studies of these diseases should be directed toward apolipoproteins.

Acute Disease↗
PubMed2005

Post-ischemic delivery of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin protects against focal cerebral ischemia in mice via inhibition of extracellular-regulated kinase-1/-2.

After recent clinical trials, statins have gained increasing significance in secondary stroke prevention. From experimental studies, it is well established that statins have beneficial action when delivered prophylactically prior to a stroke. Conversely, much less is known about the effects of statins on injury development when delivered after ischemia. We here examined the effects of a post-ischemic delivery of rosuvastatin (0.5, 5 or 20 mg/kg, administered i.p. immediately after reperfusion onset), a potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on brain injury and cell signaling after focal cerebral ischemia, induced by 90 min of intraluminal middle cerebral artery occlusion in mice. In animals receiving normal saline, 0.5 or 5 mg/kg rosuvastatin, middle cerebral artery occlusions resulted in reproducible brain infarcts at 24 h after reperfusion onset, which did not differ in size. However, rosuvastatin, administered at higher doses (20 mg/kg), reduced infarct volume at 24 and 48 h after ischemia (by 34+/-16% and 18+/-3%, respectively, P<0.05). Western blots revealed that rosuvastatin decreased phosphorylated extracellular-regulated kinase-1/-2 and reduced activated caspase-3 levels in ischemic brain areas, while endothelial NO synthase expression, p38 and Jun kinase phosphorylation were not influenced by the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Rosuvastatin also significantly diminished expression levels of inducible NO synthase in the ischemic brain. Our results indicate that rosuvastatin may have utility not only as stroke prophylaxis but also as acute therapy inhibiting executive cell death pathways.

Animals↗
PubMed2003

Trends in stroke incidence and 10-year survival in Söderhamn, Sweden, 1975-2001.

BACKGROUND AND PURPOSE: Stroke mortality rates have declined in many countries. Stroke incidence rates have also declined, but not to the same extent and not always in parallel with stroke mortality. The aim of the present study was to investigate trends in stroke incidence and long-term survival in a Swedish population. METHODS: A population-based survey of the incidence of first-ever stroke was performed prospectively in the periods 1975 to 1977, 1983 to 1986, and 1987 to 1990. Case fatality ratios and survival rates were followed to 2001. RESULTS: Crude incidence rates increased between 1975 to 1977 and 1983 to 1986, but age- and sex-adjusted incidence rates were stable during the whole period of 1975 to 1990. The incidence of intracerebral hemorrhage decreased by approximately two thirds, whereas the incidence of mild brain infarction almost doubled. The case fatality ratio at 28 days did not change, but the 10-year survival ratio increased from 13% to 35%. Mean survival time increased significantly among patients with intracerebral hemorrhage and brain infarction but not among patients with subarachnoidal hemorrhage or stroke of undetermined origin. CONCLUSIONS: Stroke incidence and short-term case fatality did not change between 1975 and 1990 in the Söderhamn population. Long-term survival after stroke, on the other hand, has continued to improve to 2001. The implication of these changes is that the burden of stroke is likely to increase unless strokes are becoming less severe.

Adolescent↗
PubMed2003

Overexpression of monocyte chemoattractant protein 1 in the brain exacerbates ischemic brain injury and is associated with recruitment of inflammatory cells.

Brain cells produce cytokines and chemokines during the inflammatory process after stroke both in animal models and in patients. Monocyte chemoattractant protein 1 (MCP-1), one of the proinflammatory chemokines, can attract monocytes to the tissue where MCP-1 is overexpressed. However, the role of MCP-1 elevation in stroke has not been explored in detail. The authors hypothesized that elevated MCP-1 levels would lead to increased influx of monocytes and increased brain infarction size in stroke induced by middle cerebral artery occlusion with partial reperfusion. There were no differences in blood pressure, blood flow, or vascular architecture between wild-type mice and transgenic MBP-JE mice. Twenty-four to 48 hours after middle cerebral artery occlusion, brain infarction volumes after ischemia were significantly larger in MBP-JE mice than in wild-type controls and were accompanied by increased local transmigration and perivascular accumulation of macrophages and neutrophils. These results indicate that MCP-1 can contribute to inflammatory injury in stroke.

Animals↗
PubMed2004

Evidence for a protective role played by the Na+/Ca2+ exchanger in cerebral ischemia induced by middle cerebral artery occlusion in male rats.

In the present paper, the role played by Na+/Ca2+ exchanger (NCX) in focal cerebral ischemia was investigated. To this aim, permanent middle cerebral artery occlusion (pMCAO) was performed in male rats. The effects on the infarct volume of some inhibitors, such as tyrosine-6 glycosylated form of the exchanger inhibitory peptide (GLU-XIP), benzamil derivative (CB-DMB) and diarylaminopropylamine derivative (bepridil), and of the NCX activator, FeCl3, were examined. FeCl3, CB-DMB, bepridil and GLU-XIP, a modified peptide synthesized in our laboratory in order to facilitate its entrance into the cells through the glucose transporter, were intracerebroventricularly (i.c.v.) infused. FeCl3 (10 microg/kg) was able to reduce the extension of brain infarct volume. This effect was counteracted by the concomitant icv administration of CB-DMB (120 microg/kg). All NCX inhibitors, GLU-XIP, CB-DMB and bepridil, caused a worsening of the brain infarct lesion. These results suggest that a stimulation of NCX activity may help neurons and glial cells that are not irreversibly damaged in the penumbral zone to survive, whereas its pharmacological blockade can compromise their survival.

Animals↗
PubMedDate not supplied

Studies of the endothelial origin of cells in systemic angioendotheliomatosis and other vascular lesions of the brain and meninges using ulex europaeus lectin stains.

Ulex europaeus agglutinin I (UEA-I) is a plant lectin which binds specifically to alpha-L-fucose moieties on the surface glycoproteins of human endothelial cells. The binding is completely inhibited by preincubation of the lectin with fucose. UEA-I can be conjugated directly to fluorescein or peroxidase and can be used to stain endothelium of paraffin embedded tissues. UEA-I staining was evaluated on normal and infarcted brain, systemic angioendotheliomatosis, metastatic epidural angiosarcoma, hemangioendothelioma, hemangioblastoma, angioblastic meningioma of both the hemangioblastic and hemangiopericytic types, and vascular meningioma. The endothelium, but not neuropil of normal and infarcted brain was positive for UEA-I. The tumor cells of hemangioendothelioma and angiosarcoma also stained. However, no staining was seen in malignant intravascular cells of angioendotheliomatosis, the stromal cells of hemangioblastoma, or pericytes of angioblastic meningioma. It is concluded that the malignant cells in angioendotheliomatosis, the stromal cells of hemangioblastoma and the pericytes of angioblastic meningioma do not produce surface glycoproteins characteristic of endothelial cells.

Brain Neoplasms↗
PubMed1987

Clinical profiles of cerebrovascular disorders in a population-based patient sample.

Clinical features of different types of stroke were investigated in a sample of 409 patients representative of all cases admitted for acute stroke, except subarachnoidal hemorrhages, within a well defined population. A specific cerebrovascular diagnosis was obtained by detailed clinical investigation, including CT scan. In people greater than 50 years old, men/women risk for stroke was estimated to be 1.40:1. The risk was higher in men up to the age of 80; above this age similar risk for the two genders was observed. Eleven per cent had intracerebral hemorrhage, 13% TIA, 51% non-embolic and 25% embolic brain infarction. In all diagnostic categories there were similar proportions of patients who had a history of hypertension and previous stroke, neither did hemoglobin and hematocrit levels differ between the different stroke disorders. TIA preceded intracerebral hemorrhage in 11% and brain infarction in 15-20%. As opposed to patients with ischemic lesions, subjects with intracerebral hemorrhage had higher systolic blood pressure levels and more severe symptoms on admission to hospital. Ischemic stroke was associated with male predominance, different ischemic manifestations of heart diseases and diabetes.

Age Factors↗
PubMed1980

[Erythrocyte deformability in patients with acute cerebral circulatory disorders].

The capacity of erythrocytes to deformation was examined in patients with acute disturbances of the cerebral circulation. It was shown that in patients with transient cerebral circulation disturbances and brain infarctions this capacity of erythrocytes was sharply lowered. It was accompanied by a greater capacity of erythrocytes to aggregation and by a lability of weakly linked proteins of the erythrocytic membranes. It was also shown that in patients with brain infarction the lipid fraction of the erythrocytic membranes was more viscous.

Acute Disease↗
PubMed2001

[Treatment for recurrent paradoxical brain embolism through the patent foramen ovale].

We report here two patients with recurrent paradoxical brain embolism through the patent foramen ovale(PFO). The TIAs, which occurred frequently under antiplatelet therapy, resolved soon after commencing the anticoagulation therapy. Case 1, a 57-year-old woman, was diagnosed as having lacunar brain infarction and was treated with ticlopidine hydrochloride. Eleven months later, she suffered from frequent TIAs. Anticoagulation therapy was started after the presence of PFO was documented on transesophageal echocardiography(TEE). Thereafter, her TIA disappeared. Case 2 was a 67-year-old man with a history of lacunar brain infarction. Although he was treated with aspirin for 9 months, he showed transient monoplegia in his right leg. His TEE study also revealed the presence of PFO. After the anticoagulation therapy reached the proper level(PT-NR = 2), he never experienced the recurrence of TIA. If the antiplatelet therapy failed to prevent the recurrence of TIA, it is recommended to find out the presence of PFO which is a potential source of paradoxical brain embolism. In such a case, anticoagulation therapy should be instituted.

Aged↗
PubMed1992

[Prognosis in brain stem infarction].

UNLABELLED: A retrospective study of patients who suffered cerebrovascular accidents (CVA particularly brainstem damage) was conducted to look for risk factors which, present on admission, indicated the chance of survival. The evolution of 100 patients, hospitalized in the Neurology Department, University Hospital Lausanne, after having had their first CVA was studied. The risk factors chosen were age, sex, hypertension, smoker, late onset diabetes, hypercholesterolemia as well as the conscious state, the location of the lesion and whether it was bi- or unilateral. Analysis of the data was performed by means of a stepwise multiple logistic regression program. The results demonstrated that diabetes or bilateral lesions, regardless of their position in the brainstem, or the combination of these two factors, indicated an unfavorable outcome, associated with a short term mortality rate greater than 30%. In their absence and despite the presence of the other risk factors, it was less than 2%. At one month the mortality rate was shown to be very high. At two month it was non insignificant and thereafter it became similar to that of the Swiss population. Brainstem lesions extending to the vital centres or respiratory complications related to the state of dependence were the most common causes of short term deaths. At long term the aetiology of death was the same as for the population as a whole. CONCLUSION: The results obtained show the importance of the prevention and treatment of patients at risk of CVA, particularly diabetes. To avoid the fatal complications, that arise from severe handicap in bedridden patients, the management must be rapid and efficient (physiotherapy and drugs).

Adult↗
PubMed2006

Improved regional cerebral blood flow is important for the protection seen in a mouse model of late phase ischemic preconditioning.

INTRODUCTION: Ischemic preconditioning (IPC) induces protection to cerebral ischemia. However, it was previously unclear whether this protection resulted from altered susceptibility to ischemia. The current study examines the effects of late phase ischemic preconditioning in a mouse model of middle cerebral artery occlusion (MCAO). Specific examination of the regional cerebral blood flow (rCBF) was conducted. EXPERIMENTAL PROCEDURE: Intra-abdominal radiofrequency probes were implanted in animals and core temperature was regulated. Mice were subjected to MCAO: (1) brief 15 min duration (preconditioning ischemia) and (2) 45 min MCAO (injurious ischemia). Naive (i.e. not preconditioned) animals were compared with preconditioned animals (preconditioning ischemia plus injurious ischemia at 72 h reperfusion). rCBF was measured using laser Doppler flowmetry (LDF) and magnetic resonance cerebral perfusion (MRP) arterial spin labeling. Percentage of brain infarcted was compared between groups. RESULTS: rCBF was significantly improved in the preconditioned cohorts of mice. Naive animals showed flow reductions to 16+/-3.59% (MCAO_45; injurious, unpreconditioned) and 17.1+/-8.6% (MCAO_15; preconditioning ischemia alone) of baseline, while preconditioned animals had flows 33.9+/-13.2% (IPC_45; preconditioned animals with injurious ischemia at 72 h reperfusion) of baseline (p=0.001). Percentage of brain infarcted was 17.2+/-6.2% in naive animals, while it was 5.1+/-4.6% in the preconditioned animals (p=0.003). MRP of the perfusion to the ischemic hemisphere, in a striatal coronal slice of the brain was 26.7+/-5.8% of the contralateral hemisphere in naive animals while preconditioned mice had flows of 38.7+/-6.8% of contralateral (p=0.04). CONCLUSIONS: Improved rCBF is an important factor in the protection of IPC, during injurious MCAO in the mouse. Stringent monitoring of rCBF is required in future studies of IPC.

Animals↗
PubMed1997

Aortic plaque morphology and vascular events: a follow-up study in patients with ischemic stroke. FAPS Investigators. French Study of Aortic Plaques in Stroke.

BACKGROUND: Atherosclerotic disease of the aortic arch has been found to be associated with the risk of ischemic stroke. We have shown that atherosclerotic plaques > or = 4 mm in thickness in the ascending aorta and proximal arch detected by transesophageal echocardiography are a risk factor for ischemic stroke. The purpose of this study was to evaluate the impact, if any, of plaque morphology (ulceration, hypoechoic plaques or calcification) on the risk of subsequent vascular events. METHODS AND RESULTS: We followed for a period of 2 to 4 years, a cohort of 334 patients 60 years or older who were consecutively admitted with brain infarction and who had transesophageal echocardiography. The risk of vascular events in patients with plaques in the aortic arch according to the presence of surface ulceration, calcifications, and sessile or mobile thrombus was estimated during a total of 788 person-years of follow-up. Hypoechoic plaques, calcifications, and ulceration were more frequently found in patients with plaques > or = 4 mm as compared with those with plaques < 4 mm. The presence of ulceration did not increase the relative risk of vascular events in patients with plaque > or = 4 mm (the relative risk was 4.3 [P<.001] in those with ulceration and 5.7 [P<.001]) in those without ulceration. The lack of calcification did increase the risk of vascular events in patients with plaque > or = 4 mm. The highest relative risk of events was found among the patients with noncalcified plaques (relative risk, 10.3; 95% confidence interval, 4.2 to 25.2; P<.001). The risk of events was systematically higher in patients without calcifications than in patients with calcifications regardless of what other morphological features were considered. CONCLUSIONS: In patients with brain infarction, the risk associated with aortic plaque thickness (> or = 4 mm) is markedly increased by the absence of plaque calcifications. These findings are important for the design of therapeutic trials in such patients.

Aged↗
PubMed1991

[Dissections of the internal carotid artery--new diagnostic and pathogenetic aspects].

Initial and follow-up investigations were done systematically in 15 cases of internal carotid artery (ICA) dissections by means of angiography, computerized tomography, Magnetic Resonance Imaging, extracranial and transcranial Doppler sonography, as well as B-mode imaging. Cerebral hemodynamic reserve was evaluated by means of both SPECT and CO2-dependent vasomotor reactivity. The findings are focussed on two major issues: Do modern diagnostic tools permit to make the diagnosis of ICA dissection without angiographical proof? What is the pathogenesis of brain infarctions due to ICA dissections? Our findings demonstrate that the diagnosis of carotid artery dissection can reliably be done noninvasively by means of ultrasound techniques and MRI. These methods also allow for frequent follow-up investigations without any inconvenience for the patient. Embolic brain infarctions caused by carotid artery dissections are equally frequent as low flow induced lesions. Acute and follow-up findings suggest that surgical intervention is contraindicated in the acute phase, but may be considered for chronic pseudoaneurysms. Initial anticoagulation with high dose heparin is safe and seems to be efficacious. In certain cases, subsequent cumarine therapy may be indicated for a maximum of six months. Measures improving hemodynamics, e. g. induced hypertension, are reasonable, as long as the vasomotor reserve is exhausted.

Carotid Artery Diseases↗
PubMed2004

Tau protein in the cerebrospinal fluid is a marker of brain injury after aortic surgery.

BACKGROUND: Tau is a protein localized primarily in neurons, especially in the axonal compartment. Cerebrospinal fluid tau levels are elevated in acute stroke and head traumas. The purpose of this study is to elucidate the alterations of cerebrospinal fluid tau levels in patients with or without neurologic complication after aortic surgery. METHODS: Twenty-eight patients undergoing descending thoracic (n = 8) or thoracoabdominal (n = 20) aortic surgery were enrolled. Cerebrospinal fluid tau levels were measured before operation and at seven time points up to the 72nd postoperative hour, and were compared with cerebrospinal fluid S100B levels. RESULTS: Two patients developed brain infarction, including the one with paraplegia. In these patients, 20-fold to 100-fold tau elevation was observed, but S100B elevation was less evident in the patient without paraplegia. Three other patients developed spinal cord injury. Additional three patients suffered from temporary neurologic dysfunction of the brain. Tau levels in the latter three patients showed tenfold elevation and were higher than those in the three patients with spinal cord injury or those in the patients without neurologic complication up to 24 postoperative hours. The S100B levels were also higher in the three patients with temporary neurologic dysfunction of the brain than in the patients without neurologic complication at the conclusion of surgery. From 6 to 24 postoperative hours, they were higher in the three patients with spinal cord injury than in the patients without neurologic complication. CONCLUSIONS: These preliminary results suggest that cerebrospinal fluid tau levels reflect brain injury. Because tau levels may separate the patients with temporary neurologic dysfunction, they may serve as a useful marker of brain injury.

Adult↗
PubMedDate not supplied

[Should asymptomatic carotid stenosis be operated on?].

Should asymptomatic carotid stenosis be operated on? The aim of the present editorial is to stress that there is no simple answer to this question. The only undisputed point is that mild non hemodynamic stenosis carry such a low risk of ipsilateral brain infarct that surgery is unjustified. For tight asymptomatic stenosis ( > or = 75% at angiography according to the European method of measurement, > or = 60% according to the American method), the indication of surgery should be discussed on a case by case basis. Four main factors should be taken into account: the spontaneous risk of ipsilateral brain infarct (2% per year for stenosis > or = 75%) the risk of surgery (which should be less than 3%); the patient's life expectancy, and his own will as regards a surgical operation. It is thus possible to evaluate for each patient, the pertinence of preventive surgery and the benefit/risk ratio of the operation in order to optimize the surgical decision.

Brain Ischemia↗
PubMed1978

Cerebrospinal fluid beta 2-microglobulin in neurological disorders.

Beta-2-microglobulin was measured in specimens of cerebrospinal fluid (CSF) collected from 167 patients classified in 14 diagnostic categories at an outpatient Department of Neurology. In the control group of 29 subjects without any obvious disease of the nervous system, the concentration of beta-2-microglobulin was 1.15 +/- 0.37 mg/1 (M +/- s.d.). The concentration was almost significantly elevated in the groups with fresh brain infarct, central nervous system infection, and polyneuropathy. The serum concentrations of beta-2-microglobulin did not differ significantly among these diagnostic categories. The mean ratio between CSF and serum beta-2-microglobulin was 0.79 +/- 0.32 in the control group and more than 1.0 in the patients with brain infarcts, CNS infections and spinal paresis, but the differences were not statistically significant.

Adolescent↗
PubMed1994

c-fos protein expression and ischemic changes in neurons vulnerable to ischemia/hypoxia, correlated with basic fibroblast growth factor immunoreactivity.

Injuries to the brain induce rapid expression of c-fos and c-jun proto-oncogenes in neurons. The protein products (Fos and Jun) of these cellular immediate early genes are thought to regulate target genes that participate in fundamental biological responses. In recent studies of rat brain infarct we demonstrated that gliosis and angiogenesis, two of the fundamental biological responses, are related to neuronal expression of basic fibroblast growth factor (bFGF). In the present study, we explore the linkage between c-fos and bFGF genes by comparing the temporal and spatial domains of Fos and bFGF immunoreactivities (IR) in brain infarct and in transient global ischemia. We demonstrate colocalization of Fos-IR and ischemic changes in neurons at infarct periphery and in regions of "selective vulnerability" beginning 3 hours post-infarction and lasting up to 1-2 weeks. These are: cortical neurons in layers II-III and V, interneurons in hippocampal formation, cerebellar Purkinje cells, and many subcortical nuclei and brainstem nuclei. bFGF-IR appears 12-24 hours later than Fos-IR in the same region but in non-ischemic neurons and the expression persists beyond 2 weeks. Persistent and not transient c-fos expression appears to be associated with ischemic neuronal death, although some of these neurons may survive beyond 2 weeks postinfarction.

Animals↗
PubMedDate not supplied

Changes in frequency of cerebrovascular diseases in Oslo, Norway, 1958-1977. An autopsy study.

The frequency of lethal stroke was examined over a 20-year period in a large collection of autopsy material and was compared with the official mortality statistics for the same period. The frequency of lethal stroke in the autopsy material was calculated as a percentage of the total number of autopsied patients in the corresponding age groups. The frequency of strokes found in mortality statistics was calculated as a percentage of all deaths in the corresponding age groups. In the autopsy material the over-all stroke frequency fell by 14 percent. For patients between 40 and 69 years the decline was 25 percent while for patients over 70 years only a minor drop was observed. The most marked decline was 25 percent while for patients over 70 years only a minor drop was observed. The most marked decline was found for intracerebral hemorrhage which decreased by 70 percent in patients between 40 and 69 and by 33 percent for those over 70. For brain infarction the decline was 32 percent in the youngest age group while patients over 70 showed no decrease at all. MOrtality statistics showed a steady decline in the frequency of stroke death and the overall figures in the 2 sources were similar. Figures fo the stroke sub-groups (brain infarction and intracranial hemorrhage) were markedly different from those found in the autopsy records. Frequency of hemorrhage was several times greater than that of infarction in mortality statistics while the reverse was true in the autopsy records. The sources of error are discusses for both materials. It is concluded that the over-all figures for stroke deaths are largely reliable for both autopsy records and mortality statistics. In the mortality statistics the separate figures for hemorrhages and infarction were not correct and long term changes in frequency of these conditions would be interpreted with caution. The figures from the autopsy material are considered to be more reliable and it is concluded that the decline in hemorrhage and infarction described is real.

Adult↗