Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Brain Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed1999

Border zone neovascularization in cerebral ischemic infarct.

Immunocytochemical and quantitative studies on vascular reaction (angiogenesis) in cortical border zone of infarct were undertaken. Intensity and temporal profile of angiogenesis was assessed in 60 patients aged between 48 and 69 (younger group), and between 70 and 92 (older group), with cerebral infarct in the area of middle cerebral artery vascularization, who died during the first six weeks following the stroke. We have found that angiogenesis was a multistage process in which four stages were distinguished: phase of primary activation of endothelial cells, two consecutive phases of active angiogenesis and final phase of only sporadic proliferation of vessels. The distinction of phases in a multiphase angiogenic cascade helped us to evaluate the correlation with survival time and the age of patients. The most pronounced intensification of angiogenesis and increased density of CD 31 positive capillaries in penumbra were observed in the second phase, especially in younger patients. The duration of the penumbral neovascularization decreased in the older age patient. Our results indicate that sprouting angiogenesis is a quantitatively significant source of vessels in the cerebral infarct border zone. However, non-therapeutically stimulated angiogenesis developed only 3-4 days after the stroke, that is beyond the period of reversible changes in ischemic penumbra recognized as a "therapeutical window" in the human brain. The angiogenic therapy opens a new way towards the revascularization of ischemic brain infarct.

Aged↗
PubMed1998

Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats.

We have recently shown that long-term, but not acute, treatment with lithium robustly protects cultured CNS neurons against excitotoxicity mediated by NMDA receptors. Since NMDA receptor over-excitation has been strongly implicated in the ischemic brain injury, we examined the effects of chronic lithium treatment on neurological deficit and brain infarct induced by occlusion of the left middle cerebral artery in rats. Subcutaneous injection of LiCl for 16 days significantly improved neurological deficits, including abnormal posture and hemiplegia, measured 24 h after artery occlusion. Importantly, the size of ischemic infarct was reduced by 56% after lithium pretreatment. These results raise the possibility that lithium may be useful for reducing focal ischemia-induced brain damage and neurological abnormalities.

Animals↗
PubMed2003

Increased expression of neuronal apolipoprotein E in human brain with cerebral infarction.

BACKGROUND AND PURPOSE: Cellular origin of apolipoprotein E (ApoE) in the human brain and its roles in physiological and pathological conditions remain to be clarified. METHODS: Immunolocalization of ApoE was investigated in a series of autopsied human brains with or without infarction. ApoE expression was also estimated on immunoblot on protein extracts from autopsied brains and a cultured neuroblastoma cell line of human origin (GOTO) subjected to an oxidative stress induced by exposure to hydrogen peroxide (0.2 mmol/L). RESULTS: In addition to astrocytes and microglia, neurons and degenerated axons in and around the ischemic foci contained ApoE-like immunoreactivity, which was more intense in recent ischemic foci. Immunoblot demonstrated an increase in expression of ApoE in brain extracts from ischemic lesion, and this increase was also pronounced in the cultured neuroblastoma cell line after the stress. CONCLUSIONS: Accumulation of ApoE in neurons in and around ischemic foci of the human brain is related to an increase in ApoE synthesis in neurons, as seen in cultured neuronal cells after oxidative stress. Intrinsic regenerative activity of neuron in reaction to external insults may be related to this increase in ApoE of neuronal origin.

Aged↗
PubMed1994

TGF-beta 1 post-treatment in a rabbit model of cerebral ischaemia.

Transforming growth factor-beta 1 (TGF-beta 1), suggested in some studies to suppress astrocyte and neutrophil function, has also reduced ischaemic brain injury when administered immediately prior to clot embolization in models of thromboembolic stroke. The effect of TGF-beta 1 as a post-treatment paradigm was investigated in a rabbit model of thromboembolic stroke. Following clot embolization, regional cerebral blood flow fell to < 10 cc 100 g-1 min-1 in all animals. TGF-beta 1 (10 micrograms) or vehicle (n = 5 each group) was infused via the contralateral carotid artery. TGF-beta 1 administration resulted in a rapid and selective reduction in the peripheral neutrophil count as compared to a significant (p < 0.05) increase in control values (2336 +/- 817 vs 4320 +/- 928 neutrophils mm3, mean +/- SEM). Neutrophil aggregation was increased within 30 min of TGF-beta 1 infusion when compared to control (2.07 +/- 0.70 vs 1.09 +/- 0.17 ohms, p < 0.05); neutrophil chemiluminescence, an index of the oxygen respiratory burst was not significantly affected by TGF-beta 1 administration. No difference in platelet counts or aggregation was noted. There was no significant difference between the two groups regarding brain infarct size (47.5 +/- 10.9 vs 56.5 +/- 10.4, n = 4, TGF-beta vs control, mean +/- SEM), intracranial pressure, or brain excitatory amino acid levels (aspartate and glutamate) within ischaemic regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed2006

Activation of cerebral peroxisome proliferator-activated receptors gamma promotes neuroprotection by attenuation of neuronal cyclooxygenase-2 overexpression after focal cerebral ischemia in rats.

Up-regulation of cyclooxygenase (COX)-2 exacerbates neuronal injury after cerebral ischemia and contributes to neuronal cell death. The present study clarifies the function of cerebral peroxisome-proliferator-activated receptor(s) gamma (PPARgamma) in the expression of COX-2 in neurons of the rat brain after middle cerebral artery occlusion (MCAO) with reperfusion by immunohistochemistry, Western blot, and immunofluorescence staining. In peri-infarct cortical areas the PPARgamma was located in both microglia and neurons, whereas COX-2 was almost exclusively expressed in neurons. PPARgamma immunolabeling reached the peak 12 h after MCAO, whereas the number of COX-2 immunostained cells gradually rose and reached its peak at 48 h. Intracerebroventricular infusion of pioglitazone, an agonist of the PPARgamma, over a 5-day period before and 2 days after MCAO, reduced the infarct size, the expression of tumor necrosis factor alpha (TNF-alpha), COX-2, and the number of cells positively stained for COX-1 and COX-2 in the peri-infarct cortical regions. COX-2 induction was also attenuated in the ipsilateral but not in the contralateral hippocampus. In primary cortical neurons expressing the PPARgamma, pioglitazone suppressed COX-2 expression in response to oxidative stress. This protective effect was reversed after cotreatment with GW 9662, a selective antagonist of the PPARgamma, clearly demonstrating a PPARgamma-dependent mechanism. Our data provide evidence that activation of neuronal PPARgamma considerably contributes to neuroprotection by prevention of COX-2 up-regulation in vitro and in peri-infarct brain areas.

Animals↗
PubMed1983

Triglycerides as a risk factor in extracranial atherosclerotic cerebrovascular disease.

A retrospective study was carried out on a group of 138 patients undergoing carotid endarterectomy for extracranial vascular disease. Risk factors of cerebrovascular disease and routine laboratory evaluations were assessed. Of the laboratory evaluations of blood lipids, only mean triglycerides were found to be significantly different from laboratory normals. Stroke as a clinical event has been suggested not to be correlated with blood lipids in a number of large studies, but the present investigation supports the notion that extracranial vascular disease may be associated with blood lipid concentrations. Previous studies of stroke and lipids have not separated out the anatomical site responsible for the cerebral infarction, and thus probably have underestimated the effect of lipids as a risk factor in cervical extracranial atherosclerosis and brain infarction.

Aged↗
PubMed1998

Carotid plaque characterization using digital image processing and its potential in future studies of carotid endarterectomy and angioplasty.

PURPOSE: To corroborate the validity of a computerized methodology for evaluating carotid lesions at risk for stroke based on plaque echogenicity. METHODS: The records of 96 carotid endarterectomy patients (59 men; median age 69.5 years, range 52 to 83) with stenoses > 50% were studied retrospectively. Forty-one patients (43%) had been symptomatic preoperatively. All patients had undergone computed tomography (CT) to detect infarction in the carotid territory and a duplex scan to measure carotid stenosis. Plaque echogenicity was analyzed by computer, expressing the echodensity in terms of the gray scale median (GSM). The incidence of CT-documented cerebral infarction was analyzed in relation to symptomatology, percent stenosis, and echodensity. RESULTS: Symptoms correlated well with CT evidence of brain infarction: 32% of symptomatic patients had a positive CT scan versus 16% for asymptomatic plaques (p = 0.076). The mean GSM value was 56 +/- 14 for plaques associated with negative CT scans and 38 +/- 13 for plaques from patients with positive scans (p < 0.0001). However, there was no difference in the GSM value between plaques with > or < 70% stenosis. Furthermore, the incidence of CT infarction was 40% in the cerebral territory of carotid plaques with a GSM value < 50 and only 9% in those with a GSM > 50 (p < 0.001). CONCLUSIONS: Computerized analysis of plaque echogenicity appears to provide clinically useful data that correlates with the incidence of cerebral infarction and symptoms. This method of analyzing plaque echolucency could be used as a screening tool for carotid stent studies to identify high-risk lesions better suited to conventional surgical treatment.

Aged↗
PubMedDate not supplied

[Neurologic manifestations of infective endocarditis: a diagnostic and prognostic challenge].

INTRODUCTION: Infective endocarditis (IE) is an ongoing challenge in terms of excess morbidity and mortality. Neurologic complications occur in 20-40% of patients, and the brain is the main location of IE extracardiac complications. AIM: To analyse clinical characteristics of the neurologic complications found in patients with IE, focused on the diagnostic and prognostic aspects. PATIENTS AND METHODS: We studied retrospectively the cases of patients with IE admitted to the Hospital de Valme and Hospital de la Merced between 1998 and 2003. Laterly, patients with and without neurologic manifestations were compared. Sixty episodes of IE were evaluated. RESULTS: Neurological complications occurred in 12 patients (20%). The most frequent neurologic manifestation was unilateral hemi paresis, which occurred in seven cases (58.3%), three cases with acute confusional state (25%) and two patients developed meningitis (16.6%). Brain infarction was the most common lesion found in neuroimaging, in 6 patients (50%), followed by 2 cases (16.6%) of brain hemorrhage, and without significant findings in the cases left. Cases with neurologic complications had significantly higher mortality (p < 0.001) and higher frequency of negative blood culture (p < 0.001). CONCLUSIONS: Neurologic complications of IE are frequent during the evolution of the disease, and they still constitute a significant problem in clinical practice because they often are not accurately diagnosed and significantly increase patients' mortality.

Adolescent↗
PubMed1993

Contributions of ions and albumin to the formation and resolution of ischemic brain edema.

Changes in brain water, sodium, potassium, and albumin contents and blood-brain barrier (BBB) permeability were determined at various times between 1 hour and 6 weeks following occlusion of the middle cerebral artery (MCA) in rats. In the center of the infarct, brain edema increased to a maximum level by 12 hours, remained elevated for 7 days, and then returned to normal. The change in water content was accompanied by a parallel increase in sodium and decrease in potassium contents; however, the increase in sodium always exceeded the decrease in potassium, resulting in a net gain in brain cations during edema formation which returned to normal with edema resolution. The BBB permeability to 3H-alpha-aminoisobutyric acid was increased by 24 hours after MCA occlusion and returned to normal by 1 week after the edema had resolved. The time course for changes in brain albumin content was different than that for brain edema formation. Large increases in brain albumin content were not apparent until 6 hours after the onset of ischemia, rose to a peak at 3 days after occlusion of the MCA, and returned to normal several weeks after the edema had resolved. Albumin appeared to spread from the central infarct zone to surrounding, less ischemic areas. The relative contributions of the osmotic force produced by the increase in brain cations and the oncotic force produced by the increase in brain albumin to the observed change in water content were calculated. At all time points, the increase in brain cations accounted for nearly all of the observed brain edema, while the increase in albumin played essentially no role in edema development.

Albumins↗
PubMed2000

A glycine site antagonist ZD9379 reduces number of spreading depressions and infarct size in rats with permanent middle cerebral artery occlusion.

Spreading depressions (SDs) occur in experimental focal ischemia and contribute to lesion evolution. N-methyl-D-aspartate (NMDA) antagonists inhibit SDs and reduce infarct size. The glycine site on the NMDA receptor complex offers a therapeutic target for acute focal ischemia, potentially devoid of many side effects associated with competitive and non-competitive NMDA antagonists. We evaluated the effect of the glycine antagonist, ZD9379, on SDs and brain infarction. Male Sprague-Dawley rats (n = 18) weighing 290 to 340 g undergoing permanent middle cerebral artery occlusion (MCAO) were randomly and blindly assigned to receive drug or placebo: Group 1 (pre-MCAO treatment group, n = 5) a 5 mg/kg bolus of ZD9379 over 5 minutes followed by 5 mg/kg/hour drug infusion for 4 hours beginning 30 minutes before MCAO; Group 2 (post-MCAO treatment group, n = 7) a 5 mg/kg bolus of ZD9379 30 minutes after MCAO followed by 5 mg/kg/hour drug infusion for 4 hours; and Group 3 (control group, n = 6) vehicle for 5 hours beginning 30 minutes before MCAO. SDs were monitored electrophysiologically for 4.5 hours following MCAO by continuous recording of cortical direct current (DC) potentials and electrocorticogram (ECoG). Infarct volume was measured 24 hours after MCAO by 2,3,5 triphenyltetrazolium chloride (TTC) staining. Corrected infarct volume was 90 +/- 72 mm3 (mean +/- standard deviation) in Group 1, 105 +/- 46 mm3 in Group 2, and 226 +/- 41 mm3 in Group 3 (P < .001). The corresponding numbers of SDs in the 3 groups were 8.2 +/- 5.8, 8.1 +/- 2.5, and 16.0 +/- 5.1, respectively (P < .01). When all animals (n = 18) were analyzed, infarct volumes and the number of SDs were significantly correlated (r = .68, P = .002). This study demonstrated that ZD9379 initiated before or after MCAO significantly reduced the number of SDs and infarct volume in a permanent focal ischemia model, implying that ZD9379 is neuroprotective and its neuroprotective effect may be related to inhibiting ischemia-related SDs.

Animals↗
PubMed1988

Silent stroke in the NINCDS Stroke Data Bank.

Previous brain infarctions seen on CT are common in the absence of history of stroke. Eleven percent of patients (135/1,203) without stroke history had ischemic lesions on their first CT, unrelated to the presenting stroke. Stroke Data Bank files were reviewed to determine whether the occurrence, location, and CT characteristics of those lesions are associated with their undetected status. Two distinct patterns were seen: (1) Small lesions of 1 cm or less were left hemisphere predominant and involved the deep structures of the brain; the majority of these were clinically silent. (2) Lesions greater than 1 cm occurred more frequently in the right hemisphere and were mostly superficial; these infarcts produced signs unrecognized by the patient or family. Risk factors for silent stroke were similar to those for stroke in general. Frequencies of in-hospital complications and 30-day fatality rates from the presenting stroke were not influenced by the existence of a prior silent stroke.

Adult↗
PubMed1994

Prevention of periinfarct direct current shifts with glutamate antagonist NBQX following occlusion of the middle cerebral artery in the rat.

The effect of the glutamate (AMPA subtype) receptor antagonist NBQX on periinfarct direct current (DC) shifts and cortical ATP depletion volume was examined in rats subjected to 3 h of occlusion of the middle cerebral artery (MCA). MCA occlusion produced an immediate DC shift in the periphery of the ischemic territory. Vehicle-treated (untreated) animals developed one to five additional DC shifts (median, 2) during the 3-h occlusion time. NBQX treatment (2 x 30 mg/kg i.v. immediately after MCA occlusion and 1 h later) significantly reduced the number of DC deflections (median, 0; range, 0-2; p < 0.05) without changing blood flow in the border zone of the infarct (untreated, 50.6 +/- 10.6%; NBQX-treated: 51.9 +/- 7.7% of control; mean +/- SD). NBQX treatment significantly decreased the cortical volume of ATP depletion (untreated, 75.3 +/- 11.4 mm3; NBQX-treated, 47.9 +/- 10.1 mm3; p < 0.05). Moreover, a significant linear relationship between the number of periinfarct DC shifts and the volume of cortical ATP depletion was obtained (y = 38.3 + 9.4x; r = 0.866; p < 0.001). The reduction of brain infarct volume by NBQX treatment is explained by the suppression of DC shifts and the decrease of metabolic workload in hemodynamically compromised cortex.

Animals↗
PubMed1990

Clinical study of 227 patients with lacunar infarcts.

We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p less than 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p less than 0.005) or the internal capsule (p less than 0.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (21.1%), and severe disability was recorded in one case (0.4%). Lacunar infarcts are a clearly defined entity with characteristic clinical features and an excellent short-term prognosis. Magnetic resonance imaging is the current method of choice for demonstrating these small brain lesions.

Age Factors↗
PubMed1993

MK-801, a glutamate antagonist, lowers flow threshold for inhibition of protein synthesis after middle cerebral artery occlusion of rat.

The effect of the glutamate antagonist MK-801 on the ischemic threshold of energy metabolism and protein synthesis (CPS) was studied in rats submitted to 3 h occlusion of the left middle cerebral artery (MCA). Local blood flow and CPS were measured by double tracer autoradiography, and local ATP content by bioluminescence imaging. In untreated animals breakdown of energy metabolism occurred at flow values below 15 +/- 1 and CPS inhibition below 51 +/- 15 ml/100 g/min (means +/- S.D.). MK-801 treatment (3 mg/kg immediately after MCA occlusion) did not change the ischemic flow threshold of energy failure (16 +/- 3 ml/100 g/min) but lead to a highly significant decline of the perfusion threshold for the inhibition of CPS to 19 +/- 4 ml/100 g/min (P < 0.01). Our data demonstrate that MK-801 dramatically reduces the threshold for the suppression of protein synthesis which could explain previously reported therapeutical effects on the reduction of brain infarct size.

Adenosine Triphosphate↗
PubMed2003

Tamoxifen, a selective estrogen receptor modulator, reduces ischemic damage caused by middle cerebral artery occlusion in the ovariectomized female rat.

Previous work has demonstrated that physiological concentrations of 17beta-estradiol can protect the female rat brain against middle cerebral artery occlusion (MCAO)-induced ischemic damage. The present study examined whether therapeutic doses of the clinically relevant selective estrogen receptor modulator (SERM), tamoxifen, can similarly protect the female rat brain against ischemic stroke damage. Adult female rats were bilaterally ovariectomized and implanted subcutaneously with either a placebo or tamoxifen time-release pellet (0.1, 0.8 or 2.4 mg/kg/day). One week later, the animals underwent permanent MCAO to assess the protective ability of the different tamoxifen doses on brain infarct size. As expected, MCAO produced a large infarct ( approximately 53%) of the affected cerebral hemisphere in placebo (control) animals. The 0.1 mg/kg/day dose of tamoxifen did not exhibit any significant protective effects, however; the 0.8 and 2.4 mg/kg/day doses of tamoxifen, which are in the therapeutic range, dramatically reduced infarct of the affected cerebral hemisphere ( approximately 70% reduction) as compared to the controls. The reduction of infarct size was primarily due to protection of two major structures, the cerebral cortex and striatum. Laser Doppler analysis further revealed that tamoxifen had no significant effect on cerebral blood flow either before or after MCAO, suggesting that tamoxifen protection is independent of cerebral blood flow changes. Further studies showed that tamoxifen pellets implanted at the time of MCAO did not reduce infarct size, suggesting that pretreatment with tamoxifen is necessary to observe a protective effect. These studies suggest that clinically important SERMs may have an additional unrecognized beneficial effect of protection of the female brain.

Animals↗
PubMedDate not supplied

[Computerized electroencephalography in acute cerebral ischaemia (author's transl)].

Physiopathological, clinical and therapeutical problems of acute cerebral ischaemia and brain infarction are briefly discussed. In the opinion of the Authors, a first valuable approach to the diagnosis and treatment of these conditions is afforded by the computerized electroencephalography (Berg Fourier Analysis). This investigations proved to be a safe, easy and reliable tool for testing and monitoring the effectiveness of individually selected drugs in early phases of cerebral ischaemia.

Acute Disease↗
PubMed1999

Voxel-based mapping of irreversible ischaemic damage with PET in acute stroke.

Objective mapping of irreversible tissue damage in the acute stage of ischaemic stroke would be useful for prognosis and in assessing the efficacy of therapeutic manoeuvres in impeding extension of infarction. From our database of 30 patients studied with 15O-PET within 5-18 h after onset of first-ever middle cerebral artery territory stroke, we extracted a subgroup of 19 survivors (age 74.6 +/- 8.5 years) in whom late CT coregistered with PET was available to determine final infarct topography. By means of a voxel-based analysis of the PET data, we determined putative thresholds for irreversible tissue damage as the lower limit of the 95% confidence interval calculated from all voxels within the ultimately non-infarcted brain parenchyma ipsilateral to the insult. The following values were found: 8.43 ml/100 ml/min, 0.87 ml/100 ml/min, 1.64 ml/100 ml, 0.27 and 2.21/min, for cerebral blood flow (CBF), oxygen consumption (CMRO2), blood volume (CBV), oxygen extraction fraction and the ratio CBF : CBV, respectively. Voxels below these thresholds occurred significantly more frequently in the final infarct region than in the non-infarcted parenchyma for CBF and CMRO2 (P = 0.016 and P = 0.0045, respectively, Wilcoxon test), but not for the other PET variables. Furthermore, with both CBF and CMRO2, the percentage of irreversible tissue damage voxels in the affected hemisphere relative to the opposite hemisphere was significantly positively correlated to both the volume of final infarct and the neurological outcome at 2 months (all P < 0.005, Spearman ranked test). These findings validate our voxel-based CBF and CMRO2 thresholds for probabilistic mapping of irreversible tissue damage within the 5-18 h interval after stroke onset; however, whether they would be applicable to earlier intervals remains to be determined. Transfer of our procedure for determination of irreversible tissue damage thresholds to other imaging modalities such as single proton emission computed tomography and diffusion-weighted MRI should be straightforward.

Aged↗