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 1,135 records · Page 63Linked to original sources
PubMed1999

Soluble intercelluar adhesion molecule-1, E-selectin, vascular cell adhesion molecule-1 and von Willebrand factor in stroke.

We investigated the role of endothelial cell and leukocyte adhesion in the pathophysiology of acute stroke. The immunocytochemical expression of adhesion molecules in brain tissue from six patients who died following acute ischaemic stroke showed weak endothelial expression of intercellular adhesion molecule-1 (ICAM-1), but intense expression of vascular cell adhesion molecule-1 (VCAM-1) by astrocytes and endothelial cells from the infarcted, but not the non-infarcted areas. We also measured soluble adhesion molecules E-selectin, ICAM-1, VCAM-1 and von Willebrand factor (all by enzyme-linked immunosorbent assay) in 21 patients after an acute ischaemic stroke (ictus < 12 h), and again 3 months later. Blood levels in the stroke patients were compared with 82 healthy controls and 22 subjects with carotid atherosclerosis. Compared with healthy controls, both patient groups had raised levels of von Willebrand factor (P < 0.02) but the level of soluble VCAM-1 was raised only in patients with acute stroke (P < 0.02). Levels of von Willebrand factor and soluble VCAM-1 in the stroke patients were still high at 3 months follow-up. We suggest that there might be changes in adhesion molecule expression and release in the acute and chronic stages of ischaemic stroke, where blood levels are related to immunocytochemical findings on infarcted brain. These changes may perhaps be part of the complex pathophysiological responses to infarction and repair of brain tissue following stroke.

Aged↗
PubMed1996

Experimental acute cerebral ischemia with reperfusion. Evaluation with gadolinium-texaphyrin.

RATIONALE AND OBJECTIVES: The authors explore the potential usefulness of the new contrast medium gadolinium (Gd)-texaphyrin (PCI-0101) in magnetic resonance imaging of experimental acute cerebral ischemia with reperfusion. METHODS: Four New Zealand white rabbits underwent 2 hours of transorbital occlusion of the left internal carotid, anterior, and middle cerebral arteries, followed by 2 hours of reperfusion with normal saline. Immediately thereafter, the rabbits were injected with 25 mumol/kg of 2 mmol/L Gd-texaphyrin and killed by barbiturate overdose. Postmortem T1- and T2-weighted coronal scans were performed at 1.5 Tesla and correlated with histopathologic findings. RESULTS: Postcontrast T1-weighted images showed high signal within extensive cortical and basal ganglia infarcts. Areas of high signal on T1-weighted images were less extensive than on T2-weighted images, and corresponded to only a portion of the region of neuronal damage seen histologically. Signal intensity of infarcted brain on postcontrast T1-weighted images was significantly greater than normal brain in the contralateral hemisphere (P < 0.0014). CONCLUSIONS: Experimental reperfused infarcts only 2 hours old demonstrate contrast enhancement with Gd-texaphyrin.

Acute Disease↗
PubMed2003

Vascular territories and watersheds: a zonal frequency analysis of the gyral and sulcal extent of cerebral infarcts. Part I: the anatomic template.

Our purpose was to establish a template of upper cerebral anatomy suitable for analysis of infarct distribution and for comparison among infarct types. We made a standard diagram of the key gyri and sulci of the supraventricular and occipital regions, partitioned the gray matter and white matter into specific zones useful for analyzing infarcts by CT and MRI, and numbered each zone uniquely in to establish a template suitable for tabulating the precise regions affected by each infarct and for analyzing differences among infarcts. The template provides a method for extracting a standardized set of data from CT or MRI performed at any angle, reconfiguring those data into a standard image, and characterizing the specific portions of infarcted brain in terms of unique numbers suitable for tabulation, collation and comparison. Standardization of the format provides for later computer analysis of increasing numbers of diverse infarcts. This method may be extended to any other type of pathology, although successful analysis of different lesions may require partitioning the gray and white matter zones in different ways.

Brain↗
PubMed2005

Inhibition of iNOS activity by 1400W decreases glutamate release and ameliorates stroke outcome after experimental ischemia.

BACKGROUND AND PURPOSE: It has been shown that the reversed operation of glutamate transporters when ATP levels fall accounts for most glutamate release induced by severe cerebral ischemia. Nitric oxide (NO) is formed after ischemia and causes ATP depletion. Our purpose is to test if NO release from inducible NO synthase (iNOS) after stroke may cause a delayed glutamate release due to ATP depletion that might underlie progression of the ischemic infarct. We have studied the effect of the highly selective inhibitor of iNOS activity 1400W on brain ATP levels, extracellular glutamate, and stroke outcome after transient focal cerebral ischemia in rats. METHODS: To induce focal ischemia, the middle cerebral artery (MCA) was occluded by using the intraluminal thread technique (tMCAO). 1400W was administered, after tMCAO, by using an Alzet osmotic pump to yield a drug delivery rate of 2.5 mg/kg/h. Results. Postischemic treatment with 1400W induced a reduction in the neurofunctional impairment and in the total volume of brain infarct. Western blot analysis showed ischemia-induced expression of iNOS. Treatment with 1400W partially prevented delayed ATP reduction and produced inhibition of the subsequent delayed increase in glutamate levels caused by the ischemic insult. CONCLUSIONS: Our data indicate that 1400W improves stroke outcome, an effect concomitant to the inhibition of both ischemia-induced decrease in brain ATP levels and increase in glutamate release. These results provide evidence indicating that the expression of iNOS induced by ischemia may contribute to the progression of the ischemic infarct and have important therapeutic implications for the management of stroke.

Adenosine Triphosphate↗
PubMed1998

Demographic study of first-ever stroke and acute myocardial infarction in Okinawa, Japan.

We performed a cross-sectional survey of stroke and acute myocardial infarction (AMI) in Okinawa, Japan with a census population of about 1.2 million. A total of 3,644 cases of first-ever stroke and 898 cases of initial acute myocardial infarction (AMI) were detected. The age-adjusted annual incidence rate for stroke was 105 per 100,000 standard population of Japan, and that of AMI was 26. The case-fatality rate of stroke within 28 days of onset was 12.8%, and that of AMI was 22.2%. Of the stroke cases, 51.4% were diagnosed as brain infarction, 38.7% as brain hemorrhage, and 9.3% as subarachnoid hemorrhage. The diagnosis of stroke subtypes were confirmed by computed tomography or magnetic resonance imaging in 98.4% of all stroke cases. In Okinawa, the incidence rate of AMI was still considerably lower than that in the Western population, and the rate of stroke was similar to that in the Western population.

Adult↗
PubMed2004

Delayed shrinkage of the brain after ischemic stroke: preliminary observations with voxel-guided morphometry.

BACKGROUND AND PURPOSE: The most important effect of cerebral ischemia is brain infarction. In this magnetic resonance imaging (MRI) study, the authors aimed at assessing postischemic brain atrophy. METHODS: Ten patients suffering from their first acute cerebral ischemia in the territory of the middle cerebral artery were studied retrospectively. Three-dimensional MRI volume scans were recorded in the acute and chronic stage after infarction and analyzed voxel by voxel intraindividually with the newly developed voxel-guided morphometry. RESULTS: Shrinkage of brain tissue was detected in all patients, not only in the perilesional cortical structures but also in contralateral homolog cortex areas and subcortically in the striatum and thalamus. This secondary shrinkage was not related to the size of the infarcts or to the clinical outcome of patients. CONCLUSIONS: Our study suggests that delayed brain atrophy after acute ischemic stroke involved areas anatomically connected with the ischemic brain lesion but nevertheless was accompanied by a simultaneous improvement of the neurological deficit.

Atrophy↗
PubMed2007

Aphasia: an early uncommon complication of ovarian stimulation without ovarian hyperstimulation syndrome.

Thromboembolic disease associated with assisted reproductive techniques is extremely rare. A 21-year-old woman with primary infertility underwent an ovulation induction cycle with luteal long protocol. Twenty-four hours following oocyte retrieval, the patient complained of difficulty in speaking. On neurological examination, mild disorientation, motor aphasia, and right-sided hypoesthesia were noted. Brain computed tomography scanning without contrast revealed left parietal lob infarct. Brain magnetic resonance imaging (MRI), MRI angiography (MRA) and perfusion MRI demonstrated an occlusion of the posterior division of the left middle cerebral artery (MCA). Physical, ultrasound examinations and laboratory test evaluation failed to reveal ovarian hyperstimulation syndrome. Except for ovarian stimulation, no additional risk factors for stroke were shown. Following anticoagulation and speech therapy, the patient recovered completely within eight months. One year after the left MCA thrombosis, she conceived spontaneously and had an uncomplicated vaginal delivery of a live male infant weighing 2900 g at 38 weeks gestation. This case supports that ovulation induction and assisted reproductive techniques may be a newly recognized cause of cerebral infarction in otherwise healthy women.

Adult↗
PubMed2006

Targeting coagulation factor XII provides protection from pathological thrombosis in cerebral ischemia without interfering with hemostasis.

Formation of fibrin is critical for limiting blood loss at a site of blood vessel injury (hemostasis), but may also contribute to vascular thrombosis. Hereditary deficiency of factor XII (FXII), the protease that triggers the intrinsic pathway of coagulation in vitro, is not associated with spontaneous or excessive injury-related bleeding, indicating FXII is not required for hemostasis. We demonstrate that deficiency or inhibition of FXII protects mice from ischemic brain injury. After transient middle cerebral artery occlusion, the volume of infarcted brain in FXII-deficient and FXII inhibitor-treated mice was substantially less than in wild-type controls, without an increase in infarct-associated hemorrhage. Targeting FXII reduced fibrin formation in ischemic vessels, and reconstitution of FXII-deficient mice with human FXII restored fibrin deposition. Mice deficient in the FXII substrate factor XI were similarly protected from vessel-occluding fibrin formation, suggesting that FXII contributes to pathologic clotting through the intrinsic pathway. These data demonstrate that some processes involved in pathologic thrombus formation are distinct from those required for normal hemostasis. As FXII appears to be instrumental in pathologic fibrin formation but dispensable for hemostasis, FXII inhibition may offer a selective and safe strategy for preventing stroke and other thromboembolic diseases.

Animals↗
PubMed2003

Rye, lignans and human health.

Rye bran contains a high content not only of dietary fibre, but also of plant lignans and other bioactive compounds in the so-called dietary fibre complex. Blood concentrations of lignans such as enterolactone have been used as biomarkers of intake of lignan-rich plant food. At present,evidence from studies in human subjects does not warrant the conclusion that rye, whole grains orphyto-oestrogens protect against cancer. Some studies, however, have pointed in that direction,especially in relation to cancers of the upper digestive tract. A number of prospective epidemiological studies have clearly shown a protective effect of wholegrain cereals against myocardial infarctions. A corresponding protective effect against diabetes and ischaemic stroke(brain infarct) has also been demonstrated. It seems reasonable to assume that these protective effects are associated with one or more factors in the dietary fibre complex.

Cardiovascular Diseases↗
PubMedDate not supplied

Brain atrophy evaluated by computed tomography in independent and institutionalized hip fracture patients.

PURPOSE: To examine if there is an association between brain computed tomography (CT) findings and place of residence in a series of hip fracture patients. METHOD: The CT scans taken immediately after hip fracture of 215 patients (mean age 81.6 years) living in their own homes or otherwise independently (home-dwelling group) and 95 patients (mean age 82.5 years) permanently institutionalized (institutionalized group) were analysed. RESULTS: The institutionalized patients had significantly more cortical cerebral (frontal, p = 0.004; temporal, p = 0.007; parietal, p < 0.001) and central cerebral (third ventricle width, p < 0.001; frontal horn width, p < 0.001; midbody width, p < 0.001) atrophy than the home-dwelling ones. This was also true of atrophy in the white-matter (WM) area (p < 0.001). The institutionalized patients also had more atrophy of the cerebellar hemisphere (atrophy of the cerebellopontine angle cistern, p = 0.002, greater fourth ventricle width, p = 0.020). No significant difference was seen in the incidence of brain infarcts. CONCLUSIONS: Hip fracture patients living in institutions have more brain atrophy than those living independently. The brain atrophy may be one factor in the multiple mechanism underlying their institutional admission.

Aged↗
PubMed2001

[Memory disturbance caused by medial temporal lesion].

The memory disturbance caused by medial temporal lesion is reported concerning 6 cases of cerebral hemorrhage, infarction, brain tumor, and contusion. The memory disturbance was significant compared with the patient's intact orientation and normal intelligence. In the category of memory, recent memory was more markedly disturbed than the immediate or remote memory. From the viewpoint of the lesion, the memory disturbance was more severe when, in addition to the hippocampus, the entorhinal gyrus or amygdala was damaged. The visual memory disturbance was mild and no difference was observed in the verbal or visual memory according to whether the lesion was right or left. The memory disturbance was usually transient and marked improvement was observed in some cases.

Adult↗
PubMed2002

Prereperfusion saline infusion into ischemic territory reduces inflammatory injury after transient middle cerebral artery occlusion in rats.

BACKGROUND AND PURPOSE: In ischemic stroke, the ischemic crisis activates a cascade of events that are potentiated by reperfusion, eventually leading to cell death. The chief aim in this study was to investigate whether our new experimental model for stroke therapy, flushing the ischemic territory with saline before reperfusion, could minimize this damage by (1) reducing the inflammatory reaction and (2) improving regional microcirculation. METHODS: Stroke in Sprague-Dawley rats (n=39) was induced by a 2-hour middle cerebral artery occlusion with the use of a novel intraluminal hollow filament. Before 48-hour reperfusion, 20 of the ischemic rats received 7 mL isotonic saline at 23 degrees C or 37 degrees C infused into the ischemic area through the filament. Regional cerebral blood flow in cortex supplied by the right middle cerebral artery was measured by laser-Doppler flowmetry during ischemia and reperfusion. Leukocyte infiltration, microvascular plugging, and infarct volume were compared with the use of hematoxylin and eosin staining. Expression of intercellular adhesion molecule 1 (ICAM-1) was determined by immunocytochemistry. Neurological deficits were evaluated. RESULTS: After the prereperfusion infusion of saline, significantly (P<0.001) improved cerebral blood flow (105+/-12% of baseline) was obtained up to 48 hours after reperfusion, compared with 45+/-7% at 24 hours and 25+/-3% at 48 hours after reperfusion without local saline infusion. Significant (P<0.001) reductions in leukocyte infiltration (61%), vascular plugging (45%), infarct volume (approximately 65%), and neurological deficits were also produced. ICAM-1 expression in the infarct region was significantly (P<0.05) minimized by 37%. CONCLUSIONS: The reduced brain infarct and neurological deficits may be attributed to adequate reperfusion and ameliorated inflammation induced by local prereperfusion infusion.

Animals↗
PubMed1993

Increased plasma levels of brain natriuretic peptide in patients with acute myocardial infarction.

BACKGROUND: Brain natriuretic peptide is a novel natriuretic peptide that is secreted predominantly from the ventricles, and its plasma levels have been shown to be markedly increased in patients with chronic congestive heart failure. This study was designed to examine the plasma levels of brain natriuretic peptide as well as atrial natriuretic peptide in patients with acute myocardial infarction. METHODS AND RESULTS: We examined the plasma levels of brain natriuretic peptide as well as atrial natriuretic peptide in 50 consecutive patients (36 men and 14 women; mean age, 66 years) with acute myocardial infarction over the time course of 4 weeks. The plasma level of brain natriuretic peptide was significantly increased on admission in patients with acute myocardial infarction compared with controls (92 +/- 28 versus 5.2 +/- 0.5 pg/mL, P < .01) and reached the peak level of 319 +/- 58 pg/mL at 16.4 +/- 0.7 hours after admission. Thereafter, the level decreased and then again increased, forming the second peak of 277 +/- 66 pg/mL on day 5. The level then decreased gradually but was still much higher in the fourth week than that of controls (149 +/- 47 versus 5.2 +/- 0.5 pg/mL, P < .001). On the other hand, the plasma atrial natriuretic peptide level already had been increased at the time of admission compared with controls (116 +/- 14 versus 39.5 +/- 2.6 pg/mL, P < .01) and decreased thereafter, again increasing and making a small peak on day 2 to 3. The time course of the plasma brain natriuretic peptide level could be divided into two patterns: a monophasic pattern with one peak at about 16 hours after admission and a biphasic pattern with two peaks at about 16 hours and 5 days after admission. There were significantly more patients with anterior infarction, congestive heart failure, higher level of maximal creatine kinase-MB isoenzyme, and lower left ventricular ejection fraction in the biphasic group than in the monophasic group. CONCLUSIONS: We conclude that the plasma level of brain natriuretic peptide is increased markedly in patients with acute myocardial infarction and may reflect the degree of left ventricular dysfunction in these patients.

Aged↗
PubMed1993

Postoperative brainstem and cerebellar infarcts.

OBJECTIVE: To study the clinical features and causes of postoperative brainstem and cerebellar infarcts. METHODS: Two groups were studied. The 10 group 1 patients had cardiac (eight) or aortic (two) surgery. The 12 group 2 patients had noncardiac-nonvascular surgery, including orthopedic (five), gynecologic (four), and general (three). Patients were studied by stroke services at university hospitals in Boston (13), Charlottesville (three), Baltimore (three), and Mainz (three) during 2 consecutive years. RESULTS: Onset of strokes was immediately postoperative (six), during the first 48 postoperative hours (nine), and delayed 3 days or more (seven). Clinical syndromes were altered level of consciousness or cognition (15), vestibulocerebellar (four), and hemiparesis with focal brainstem signs (three). Infarction involved the brainstem (13), cerebellum (13), and posterior cerebral artery hemispheric territory (10). Causes: In group 1, five infarcts were due to cardiogenic embolism and three to embolism from the aorta. One patient had a postoperative pontine lacunar infarct and one developed an infarct in the territory of a known stenotic basilar artery. In group 2, one patient had vertebral artery injury from instrumentation, one had medical complications with severe hemorrhage and hypotension, and 10 most likely had position-related vertebral artery thromboses. CONCLUSIONS: Patients with postoperative brainstem and cerebellar infarcts present with altered consciousness or vestibulocerebellar syndromes. The major cause of brain infarcts after cardiac surgery is embolism from the heart and aorta. The causes of infarction after general surgery are less clear, but neck positioning during or after surgery may play an important role by promoting thrombi in compressed arteries that later embolize intracranially when neck motion becomes free.

Adolescent↗
PubMed1992

Depletion of brain glutathione by buthionine sulfoximine enhances cerebral ischemic injury in rats.

Oxygen free radicals have been implicated in the pathogenesis of brain injury induced by ischemia/reperfusion. We studied the role of endogenous reduced glutathione (GSH) in brain infarction associated with focal cerebral ischemia caused by permanent ligation of the right middle cerebral artery (MCA) and the right common carotid artery (CCA) plus temporary occlusion of the left CCA. GSH levels in the ischemic side of cortex decreased with time after ischemia and preceded cortical infarction estimated by the staining of mitochondrial respiratory enzymes with 2,3,5-triphenyltetrazolium chloride. GSH levels in the contralateral cortex were unchanged through the experimental periods. The extent of decrease of GSH levels and the severity of infarction in the ischemic cortex at 24 h after ischemia depended on the duration of occlusion of the left CCA. Depletion of brain GSH with buthionine sulfoximine, a selective inhibitor for gamma-glutamylcysteine synthetase, exacerbated cortical infarction and edema after ischemia. These results suggest that the endogenous brain GSH is an important determinant in the defense mechanisms against lesion formation after ischemia and support the possible role of oxygen radicals in the pathogenesis of ischemic brain injury.

Animals↗
PubMed1975

[Reliability of positive findings in serial cerebral scintigraphy. Evaluation of a prospective series of 1700 cases].

The cerebral sequential scintigraphy enables a process to be described according to its hemodynamics (Stage I), its degree of vascularization (Stage II), and the extent of the localized disturbance of the blood-brain barrier function (Stage III). For a given lesion, typical scintigraphic behaviour patterns can be described. This report presents the results of a prospective series with 1722 patients examined using this method. The accuracy of the different scintigraphic diagnoses, according to tumor type, was: cerebrovascular accident with brain infarction - 92% (= CVA), metastasis - 90%, bone or meningital process - 89%, malignant glioma - 91%, meningioma - 74%, highly differentiated glioma - 67%, chronic subdural hematoma - 54%, A-V angioma - 54%, brain abscess - 45%. The differential diagnosis between brain tumor and CVA with infarction was possible in approximately 97% of the patients, the differential diagnosis of intracranial space-occupying lesion versus CVA with infarction in approximately 95%. There were 14 false positive results recorded (0.8% of the 1722 patients).

Brain Abscess↗
PubMed2000

Failure to demonstrate peri-infarct depolarizations by repetitive MR diffusion imaging in acute human stroke.

BACKGROUND AND PURPOSE: Peri-infarct depolarizations (PIDs) have been demonstrated with diffusion-weighted MRI (DWI) in experimental stroke and are regarded as an important mechanism of ischemic injury. We tested the hypothesis that PIDs are of relevance for the early enlargement of human brain infarcts. METHODS: Ten stroke patients were investigated by repetitive imaging of the apparent diffusion coefficient (ADC) in the acute phase (7 patients) or subacute phase (3 patients) of developing cortical infarction. In each patient, 20 ADC maps were obtained from serially measured echo-planar DWI (interval of 45 seconds). Data analysis focused on the potential spatial and temporal ADC changes, including structured qualitative analysis, calculation of subtraction images, serial analysis of regions of interest positioned in the infarct core and border, and calculation of hemispheric lesion areas, depending on various ADC thresholds ranging between 0 and 800 microm(2)/s. RESULTS: Data analysis was unable to disclose any time-dependent changes in ADC that would resemble PID. In ischemic regions, the ADC reduction significantly progressed from the infarct border (555+/-96 microm(2)/s) to the infarct core (431+/-104 microm(2)/s, P:<0.01). CONCLUSIONS: By using an MRI protocol with high temporal resolution and elaborated postprocessing, we were unable to demonstrate a pattern of diffusion changes that would be indicative of PID in human stroke. Experimental infarction and human stroke may differ in the detectability of PID.

Acute Disease↗
PubMed2000

Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance.

A low dose (0.5 mg/kg) of lipopolysaccharide (LPS), administered 72 hours before 60-minute middle cerebral artery occlusion, induced a delayed neuroprotection proven by the significant decrease (-35%) of brain infarct volume in comparison with control, whereas infarct volumes remained unchanged in rats treated 12, 24, or 168 hours before ischemia. This delayed neuroprotective effect of LPS was induced only with low doses (0.25 to 1 mg/kg), whereas this effect disappeared with a higher dose (2 mg/kg). The delayed neuroprotection of LPS was induced in the cortical part of the infarcted zone, not in the subcortical part. The beneficial effect of LPS on consequences of middle cerebral artery occlusion was suppressed by dexamethasone (3 mg/kg) and indomethacin (3 mg/ kg) administered 1 hour before LPS, whereas both drugs had no direct effect on infarct volume by themselves, suggesting that activation of inflammatory pathway is involved in the development of LPS-induced brain ischemic tolerance. Preadministration of cycloheximide, an inhibitor of protein synthesis, also blocked LPS-induced brain ischemic tolerance suggesting that a protein synthesis is also necessary as a mediating mechanism. Superoxide dismutase (SOD) could be one of the synthesized proteins because lipopolysaccharide increased SOD brain activity 72 hours, but not 12 hours, after its administration, which paralleled the development of brain ischemic tolerance. In contrast, catalase brain activity remained unchanged after LPS administration. The LPS-induced delayed increase in SOD brain content was suppressed by a previous administration of indomethacin. These data suggest that the delayed neuroprotective effect of low doses of LPS is mediated by an increased synthesis of brain SOD that could be triggered by activation of inflammatory pathway.

Adaptation, Physiological↗