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 1,153 records · Page 64Linked to original sources
PubMed1980

[Morphologic verification in computer tomography of the brain].

A comparison of computer-aided tomograms of the brain with the results of morphological examinations of the latter in 51 autopsy cases was carried out. The causes of the death were brain infarctions, hemorrhages, and tumours. It was found that roentgenological diagnosis of cerebral infarctions entailed no difficulties, if the examinations were performed within 24 hours after the disease onset and the focus size was over 1 to 2 cm. There were some difficulties in diagnosing small foci in the brain stem and in the cortex of brain hemispheres as well as infarctions with hemorrhages irrespectively of their size and location. The diagnoses of cerebral hemorrhages were rather precise in the early stages of hemorrhagic strokes, but extremely difficult later, in a definite stage of the hemorrhagic focus organization when computer-aided tomography revealed densities characteristic for unaffected brain. A high diagnostic efficiency of the computer-aided tomography was noted in brain tumours. Certain difficulties sometimes arose in determining the character of the tumour in cases of multiple of small-size foci. The morphological verification of the results of the computer-aided brain tomography is of a decisive importance for developing roentgenomorphological criteria for diagnosing CNS pathologies with the aid of this method, and contributes to further improvement of the latter.

Brain↗
PubMed2005

[Antithrombotic drugs in the prevention of ischemic stroke].

Stroke prevention cannot be dissociated from cardiovascular prevention in general. It is based on the correction of vascular risk factors, particularly hypertension and tobacco smoking, and on antithrombotic drugs which tackle the thrombo-embolic process which is the immediate cause of the ischemic event. Ischemic strokes exhibit considerable etiopathogenic diversity, the underlying cause modifying thrombus composition. In atherothrombotic brain infarction, platelets play a major role and antiplatelet drugs have a benefit/risk ratio better than that of oral anticoagulants, with a 25% reduction in the combined risk of ischemic stroke, myocardial infarction and vascular death. Antiplatelet drugs are also used in small artery diseases of the brain although the role of thrombosis is unknown and no specific trial has been devoted to this variety of cerebrovascular disease. In emboligenic cardiac diseases, atrial fibrillation in particular, stasis of the dilated left atrium favors coagulation phenomena, hence the much better efficacy of oral anticoagulants (presently vitamin K antagonists) both in primary and secondary prevention with a 70% risk reduction in cerebral infarction, compared with only 20% for aspirin. The expected benefit of antithrombotic drugs must be weighed against their inherent hemorrhagic risk, which is greatest for oral anticoagulants, slightly less for association of antiplatelet drugs and even less for each antiplatelet drug given alone. The use of antithrombotic drugs allows a targeted prevention of cerebral infarction. It is based on a triple case by case evaluation: that of the cause and of the risk it carries, that of the benefit expected from antithrombotic drugs, and that of their inherent hemorrhagic risk.

Brain Ischemia↗
PubMed1995

Delayed tissue-plasminogen activator therapy in a rabbit model of thromboembolic stroke.

This study investigated the efficacy and safety of delayed therapy with tissue-plasminogen activator (t-PA) in a rabbit model of thromboembolic stroke. The t-PA therapy was started 3, 4, or 5 hours after autologous clot embolization. New Zealand rabbits were randomized to receive a 2-hour intravenous infusion of either t-PA (6.3 mg/kg) or a saline solution (0.9% saline) after an autologous clot had embolized the anterior cerebral circulation. Regional cerebral blood flow (rCBF), intracranial pressure (ICP), and infarct size were measured to determine the effects of the delayed administration of the t-PA after intracranial embolization. Additionally, the following physiological parameters were monitored throughout the protocol: mean arterial pressure, hematocrit, arterial blood gases, glucose, and core and brain temperatures. All animals were studied for 4 hours after the administration of the t-PA or control solution; thus, the duration of each experiment was 7, 8, or 9 hours after autologous clot embolization. In control animals, brain infarct size and final ICP values were directly related to the length of time studied after clot embolization; among control animals, the largest infarct size and greatest rise in ICP were seen 9 hours after embolization.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

[Attenuation of reperfusion injury in the mouse transfected interleukin-1 receptor antagonist].

OBJECTIVE: To investigate the therapeutic effects of overexpression of interleukin-1 receptor antagonist (IL-1ra), administered by gene transfer, on the transient cerebral ischemic injury in an experimental mice suture model. METHODS: Adenovirus vector encoding human IL-1ra gene (Ad.RSVIL-1ra) or LacZ gene (Ad.RSVLacZ) or normal saline was administered by injection into the right lateral ventricle in adult CD-1 mice. Five days after the virus injection, the mice received 1 h transient middle cerebral artery occlusion with 23 h reperfusion. Surface cerebral blood flow was measured using laser Doppler flowmetry. Brain infarct volume was evaluated on the sections with hematoxylin-eosin staining. Blood-brain barrier (BBB) permeability was determined using immunostaining of extravasated endogenous albumin. The number of intracellular adhesion molecular-1-positive vessels was determined by immunohistochemistry. RESULTS: The infarct volume in the Ad. RSVIL-1ra transfected mice was markedly reduced compared with the Ad. RSVLacZ transfected or saline mice (36.0 +/- 5.3 mm(3) vs 60.0 +/- 6.2 mm(3), 69.5 +/- 6.3 mm(3), P < 0.05). BBB disruption area was also smaller in the Ad. RSVIL-1ra transfected mice than in the Ad. RSVLacZ transfected and saline mice (P < 0.05). The expression of intracellular adhesion molecular-1 (ICAM-1) positive vessels in the ischemic cortex and basal ganglia was greatly attenuated in the Ad. RSVIL-1ra transfected mice (cortex: 135 +/- 23, vs 311 +/- 40 and 357 +/- 51 pound sterling basal ganglia: 90 +/- 21, vs 207 +/- 43 and 259 +/- 43, P < 0.05. CONCLUSION: IL-1ra has neuroprotective property during ischemia/reperfusion injury. Overexpression of IL-1ra via gene transfer can attenuate the expression of ICAM-1 in the ischemic area.

Adenoviridae↗
PubMed2006

Reduction of apoptosis in the amygdala by an A2A adenosine receptor agonist following myocardial infarction.

It has been observed that a cytokine synthesis inhibitor, pentoxifylline, prevents the apoptotic processes taking place in the amygdala following myocardial infarction. However, it is unknown if the cardioprotective effect of A(2A) adenosine receptor agonist, CGS21680, which reduces cytokine synthesis, would lead to such amygdala apoptosis regression. Thus, this study was designed to investigate whether cardioprotective A(2A) adenosine receptor activation reduces apoptosis in the amygdala following myocardial infarction. Anesthetized rats were subjected to left anterior descending coronary artery occlusion for 40 min, followed by 72 h of reperfusion. The A(2A) agonist CGS21680 (0.2 mug/kg/min i.v.) was administered continuously for 120 min, starting (1) five minutes prior to instituting reperfusion (Early) or (2) five minutes after the beginning of reperfusion (Late). After reperfusion, myocardial infarct size was determined and the amygdala was dissected from the brain. Infarct size was reduced significantly in the Early compared to the Control group (34.6 +/- 1.8% and 52.3 +/- 2.8% respectively; p < 0.05), with no difference compared to the Late group (40.1 +/- 6.1%). Apoptosis regression was documented in the amygdala of the Early group by an enhanced phosphatidylinositol 3-kinase-Akt pathway activation and Bcl-2 expression concurrently to a caspase-3 activation limitation and reduction in TUNEL-positive cells staining. On the other hand, amygdala TUNEL-positive cell numbers were not reduced in the Late group. Moreover, TNFalpha was significantly reduced in the amygdala of the Early group compared to the Control and Late groups. These results indicate that A(2A) adenosine receptor stimulation is associated with apoptosis regression in the amygdala following myocardial infarction.

Adenosine↗
PubMed1993

Stroke rates in patients with lacunar and large vessel cerebral infarctions.

A stroke registry was developed to determine the value of various clinical data in distinguishing lacunar from large vessel infarctions. Adequate localization was achieved in 98% of 246 patients with brain infarcts. These and 30 transient ischemic attack patients were followed for a median of 1082 days (range 2-1657). Follow-up data on TIA patients were invalidated by evidence of serious underreporting of TIAs in our general population. Among 212 male patients with cerebral infarcts not due to cardiogenic embolism, syphilis, migraine, vasculitis, or other unusual etiologies, 1-, 12-, and 36-month recurrence rates were 23%, 31% and 39% among patients with large vessel anterior circulation infarcts; 15%, 20% and 28% among patients with large vessel posterior circulation infarcts; and 8%, 16% and 21% among patients with lacunar anterior circulation infarcts, respectively. Six patients with posterior circulation lacunes did not experience recurrence. Comparative case fatality data were also compiled. Large vessel infarcts tended to be followed by further large vessel infarcts, usually in the same vascular distribution, whereas lacunar infarcts were not predictive of the type or location of subsequent events.

Cerebral Arteries↗
PubMed2004

Detection of the founder effect in Finnish CADASIL families.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited cerebrovascular disease characterized by brain infarcts, cognitive decline and dementia. The disease is caused by at least 91 missense mutations, four deletions and one splice site mutation in the NOTCH3 gene, which maps to 19p13.1. In 18 out of the 21 Finnish CADASIL families so far identified, the causative mutation is an arginine to cysteine substitution in position 133 (R133C). Most of the families carrying this mutation originate from the western coast of Finland, thus suggesting a founder effect. No previous reports of a founder effect in CADASIL have been published. We haplotyped 60 patients from these 18 families for 10 microsatellite markers in order to determine whether the families descend from a common ancestor. We found a similar haplotype linked to the mutation in all 18 pedigrees, which indicates a single common ancestor for all the Finnish R133C families. The age analysis of the founder mutation places the introduction of the mutation in the late 1600s or early 1700s.

Amino Acid Substitution↗
PubMedDate not supplied

Hypoxia preconditioning in the brain.

Exposure to moderate hypoxia alone does not cause neuronal death as long as blood pressure and cerebral blood flow are maintained in mammals. In neonatal and adult mammals including rats and mice, carotid occlusion in combination with hypoxia produces neuronal death and brain infarction. However, preexposure to 8% oxygen for 3 h protects the brain and likely other organs of neonatal and adult rats against combined hypoxia-ischemia 24 h later. In this paper, the possible mechanisms of this so-called hypoxia-induced tolerance to ischemia is discussed. One mechanism likely involves hypoxia-inducible factor-1alpha (HIF-1alpha). HIF-1alpha is a transcription factor that - during hypoxia - binds with a second protein (HIF-1beta) in the nucleus to promoter elements in hypoxia-responsive target genes. This causes upregulation of HIF target genes including VEGF, erythropoietin, iNOS, glucose transporter-1, glycolytic enzymes, and many other genes to protect the brain against ischemia 24 h later. In addition, non-HIF pathways including MTF-1, Egr-1 and others act directly or indirectly on other target genes to also promote hypoxia-induced preconditioning. Hypoxia preconditioning can be mimicked by iron chelators like desferrioxamine and transition metals like cobalt chloride that inhibit prolyl hydroxylases, increase HIF-1alpha levels in the brain, and produce protection of the brain against combined hypoxia-ischemia 24 h later. This hypoxia preconditioning has potential clinical usefulness in protecting high-risk newborns or to provide protection prior to surgery.

Animals↗
PubMed2001

The levels of TNF-alpha in cerebrospinal fluid and serum do not correlate with the counts of the white blood cells in acute phase of ischaemic stroke.

Stroke-induced inflammatory reaction, which leads to invasion of leukocytes into the evolving brain infarct, seems to play a key role in the deterioration of brain ischaemic impairment. We have studied CSF and serum levels of tumour necrosis factor-alpha (TNF-alpha), the potent proinflammatory cytokine, and peripheral white blood cells (WBC) counts in patients within the first 24 hours of ischaemic stroke. TNF-alpha levels in CSF and serum as well as WBC counts were increased. There was no correlation between TNF-alpha levels either in CSF and serum or in WBC counts. The results of our study suggest that increased CSF TNF-alpha levels may represent acute intracerebral inflammation in stroke, whereas elevated levels of TNF-alpha in serum may reflect the peripheral proinflammatory state as well as stroke-induced systemic inflammatory reaction. Increased CSF and serum TNF-alpha levels do not correlate with the elevation of WBC counts, suggesting that TNF-alpha overexpression observed in early phase of stroke is not dependent on increased total number of peripheral leukocytes.

Acute Disease↗
PubMed2003

Results of vascular reconstructions for a associated lesion of the brachiocephalic arteries and paroxysmal disorders of cardiac rhythm.

Annually, about 400,000 new patients with strokes are recorded in Russia. Of these, 80% of patients may develop ischemic brain infarctions. In approximately 30-40% of cases, ischemic lesion of the brain eventuates in lethal outcome; the same number of patients remain heavily disabled and only 15-20% of patients return to the previous level of work fitness. In 30-50% of cases, the development of ischemic stroke and other forms of cerebrovascular insufficiency is caused by stenotic and occlusive lesion of aortic arch branches, being more frequently of atherosclerotic origin. Patients with brachiocephalic artery (BCA) lesion face an important problem of the origin and progression of different forms of cardiac rhythm disorders. In the presence of hemodynamically significant stenotic and occlusive lesion of brain vessels, even transient changes in cardiac rhythm may induce an additional deterioration of cerebral flow. In turn, the origin of arrhythmias in the immediate postoperative period in patients after reconstructions on the BCA is a serious complication which may lead to sudden death. The aim of the present study was to examine the long-term results of the surgical treatment in patients with associated BCA lesion and paroxysmal disorders of cardiac rhythm (PDCR). The treatment results were analyzed in 89 patients aged 35 to 70 years. There were 66 (74.2%) men and 23 (25.8%) women. All the patients had undergone different BCA reconstructions. In the long-term period, this resulted in the lowering of the death rate. Besides, in the long-term period, vascular reconstructions carried out in patients with associated BCA lesion and PDCR not only improved the neurologic status but also favoured the positive course of changes in arrhythmias in 36.4% of patients.

Adult↗
PubMed1988

The effect of postischemic blood glucose levels on ischemic brain damage in the rat.

The effect of insulin-induced hypoglycemia following 10.5 minutes of forebrain ischemia was studied in the rat. All groups received preischemic glucose loading (2 gm/kg) to promote brain infarction. Following completion of ischemia, rats received either 2 to 3 IU/kg (low-dose group) or 8 to 20 IU/kg (high-dose group) insulin. During the survival period, blood glucose concentrations were maintained in the ranges of 1.2 to 2.9 mM and 2.9 to 4.9 mM, respectively, for the low-dose and high-dose insulin groups. Control rats were given 2 gm/kg glucose immediately following ischemia. During the recovery period, until perfusion at 7 days, they were given glucose, 2 gm/kg, twice daily by intraperitoneal injection, and their drinking water was supplemented with 25% glucose. Mortality (p less than 0.05) and postischemic seizure incidence (p less than 0.01) were significantly reduced in the low-dose insulin group compared to the control group. Mortality was increased in the high-dose insulin group compared to the control group and was associated with an increased incidence of postischemic seizures. Neuropathological examination revealed no cortical infarction in the low-dose or high-dose insulin-treated rats compared to a 60% incidence of cortical infarction in the control group. In addition, the high-dose insulin-treated group showed a significant reduction in striatal and hippocampal CA1 selective neuronal necrosis compared to control rats with comparable survivals (p less than 0.05). The findings suggest that postischemic blood glucose concentrations play an important role in modulating both ischemic infarction and selective neuronal necrosis.

Animals↗
PubMed1996

Medial medullary infarction: analyses of eleven patients.

Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.

Adult↗
PubMed1980

[Morphologo-histochemical characteristics of ischemic cerebral infarcts in the acute stage of the stroke in patients with atherosclerosis].

Morphological and histochemical investigations of the activity of succinate, malate, lactate, isocitrate, and glucoso-6-phosphate dehydrogenases, and NAD-diaphorase in the central, marginal, borderline and perifocal zones of ischemic brain infarctions were carried out. Deep changes in the activity of the enzymes listed, and peculiarities of this activity in various brain structures and tissues were revealed. A connection between the activity of the enzymes, the duration of the infarction, and the structural and biochemical peculiarities of the affected brain part is demonstrated. A suggestion is made on the pathogenesis of the ischemic infarctions and on the possibility of using histochemical data for the purposes of the pathoanatomic diagnosis.

Aged↗
PubMed1991

Pathogenetic basis of vascular dementia.

Vascular dementia (VAD) was studied with reference to pathogenetic aspects, especially the importance of brain infarcts. A VAD diagnosis was chosen when the patients showed dementia in combination with transitory ischemic attacks (TIA), stroke episodes, or other pronounced vascular diseases judged to be causally related to the dementia. Computed tomography (CT) white matter lesions were shown to occur frequently (85%); a pronounced decrease in myelin lipids was common in subcortical white matter; a fronto-subcortical symptom complex was the prevailing clinical pattern; and an overall increased albumin ratio without relation to TIA/stroke was noted, indicating blood-brain barrier (BBB) dysfunction. When infarcts were present, they appeared to be endpoint manifestations of the vascular pathology rather than the cause of the disease. Today, thromboembolism with multiple cerebral infarcts is considered more or less the only pathogenetic substrate of VAD, with multi-infarct dementia (MID) as its clinical counterpart. Our findings suggest that subcortical white matter changes are another important VAD substrate.

Aged↗
PubMed1995

[Inversion recovery RARE: clinical use of a T2-weighted CSF-suppressed rapid sequence].

Inversion-Recovery RARE is a strongly T2-weighted fast sequence in which the CSF appears dark. This sequence was used in more than 100 patients. Retrospective analysis of 80 patients with cerebrovascular and inflammatory disease was carried out. The IR-RARE sequence proved to be particularly suitable for identifying small lesions in the neighbourhood of the subarachnoid space. We illustrate the typical contrast provided by this sequence, and describe its characteristics, exemplifying the advantages it offers for the diagnosis of multiple sclerosis, cerebral microangiopathy and brain infarction.

Adolescent↗
PubMed2004

Cerebral neutrophil recruitment, histology, and outcome in acute ischemic stroke: an imaging-based study.

BACKGROUND AND PURPOSE: Evidence now exists for a pathogenic role for neutrophils in acute cerebral ischemia. We have studied the patterns and temporal profile of cerebral neutrophil recruitment to areas of acute ischemic stroke (IS) and have attempted to correlate this with neurological status and outcome. METHODS: Patients with cortical middle cerebral artery (MCA) IS were recruited within 24 hours of clinical onset. Neutrophil recruitment was studied using indium-111 (111In) troponolate-labeled neutrophils, planar imaging, and single-photon emission computed tomography (SPECT). Volume of brain infarction was calculated from concurrent computed tomography (CT). Hematoxylin and eosin sections were obtained postmortem (n=2). Outcome was measured using Barthel, Rankin, and National Institute of Health Stroke (NIHSS) scales. RESULTS: Fifteen patients were studied. Significant 111In-neutrophil recruitment to ipsilateral hemisphere, as measured by asymmetry index (AI), was demonstrated within 24 hours of onset in 9 patients; this response was heterogenous between patients and on repeated measurement attenuated over time. Histologically, recruitment was confirmed within intravascular, intramural, and intraparenchymal compartments. Interindividual heterogeneity in neutrophil response did not correlate with infarct volume or outcome. In an exploratory analysis, neutrophil accumulation appeared to correlate significantly with infarct expansion (Spearman rho=0.66; P=0.03, n=12). CONCLUSIONS: Neutrophils recruit to areas of ischemic brain within 24 hours of symptom onset. This recruitment attenuates over time and is confirmed histologically. While neutrophil accumulation may be associated with either the magnitude or the rate of infarct growth, these results require confirmation in future studies.

Brain Ischemia↗
PubMed1996

Fructose-1,6-bisphosphate after hypoxic ischemic injury is protective to the neonatal rat brain.

Fructose-1,6-bisphosphate (FBP) has been shown to attenuate central nervous system injury in adult animals. We evaluated whether FBP given after an ischemic-hypoxic insult is protective to the developing brain in a neonatal rat model of hypoxia-ischemia. Postnatal day 7 rat pups were subjected to focal ischemia followed by global hypoxia and then administered either FBP or saline intraperitoneally. A dose of 500 mg/kg or greater of FBP significantly reduced the amount of injury such that 55% of FBP- vs. 17% of saline-treated rats had no injury; 6% of FBP- and 47% of saline-treated rats had severe damage (P = 0.004). There was less infarcted brain in FBP-treated rats (12 +/- 11% vs. 37 +/- 32%; P = 0.005); and fewer FBP-treated rats had > 30% ipsilateral cortical injury (12% of FBP- vs. 50% of saline-treated rats; P = 0.002). FBP lowered serum calcium levels during the first 24 h after the insult without significant changes in ionized calcium or osmolarity. These results indicate that FBP treatment administered systemically after hypoxia-ischemia reduces CNS injury in neonatal rats.

Animals↗
PubMed2001

The role of cerebral microdialysis in predicting the outcome after experimental hypothermic circulatory arrest.

OBJECTIVE: To evaluate whether and which of the cerebral microdialysis parameters are predictive of postoperative outcome after an experimental 75-min period of hypothermic circulatory arrest (HCA) in a chronic porcine model. DESIGN: Seventy-four juvenile female pigs underwent a 75-min period of HCA at 20 degrees C. A microdialysis catheter was placed into the cortex gray matter and brain extracellular concentrations of glucose, lactate, glycerol and glutamate were measured throughout the experiment by enzymatic methods using a microdialysis analyzer. Surviving animals were sacrificed on the 7th postoperative day and histopathological examination of the brain was performed. RESULTS: Brain glucose concentrations were higher in animals that survived (p = 0.017), especially from the 90-min until the 7-h interval after the start of rewarming. The blood venous concentrations of glucose were also higher among survivors, and correlated significantly with the brain glucose levels at 2-h and 4-h intervals after the start of rewarming. Higher concentrations of brain lactate, glycerol and glutamate were observed throughout the study among animals that died postoperatively. Brain glutamate and glycerol concentrations were significantly, negatively correlated with brain glucose concentrations. The lactate/glucose ratio was significantly lower among survivors during the postoperative period (p=0.014). Furthermore, brain glucose concentrations were higher and brain glycerol concentrations lower among the animals that did not develop brain infarction, but such differences did not reach statistical significance. CONCLUSION: Cerebral microdialysis is a useful tool for cerebral monitoring during experimental HCA. Low brain glucose concentrations and high brain lactate/glucose ratios after HCA are strong predictors of postoperative death. Brain glucose concentrations are negatively correlated with brain glycerol and glutamate concentrations.

Animals↗