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 1,495 records · Page 83Linked to original sources
PubMed1994

Brain microvessels: factors altering their patency after the occlusion of a middle cerebral artery (Wistar rat).

The progression from ischemic injury to pannecrosis that occurs in the rat brain several hours after occluding a large artery may be partly attributable to a worsening of the circulation through the microvessels. The objective of this study was to quantitate selected structural changes involving astrocytes and endothelial cells within an area of focal brain ischemia created by the occlusion of a middle cerebral artery. The magnitude of these structural changes was correlated with alterations in the patency to a circulating macromolecule through the microvessels (< or = 15 mu in diameter) located within the territory of the occluded artery. One hundred eighty-five adult male Wistar rats had the right middle cerebral artery occluded after threading a nylon monofilament through the external carotid artery. Experiments were terminated by either cardiovascular perfusion or decapitation and immersion fixation at intervals ranging between 30 minutes and 7 days after the arterial occlusion. Randomly selected animals from each experimental subgroup were injected intravenously with horseradish peroxidase (molecular weight 44 kd) approximately 20 minutes before death. The progressive decline in the area fraction comprised by the vessels filled with horseradish peroxidase was preceded at 30 to 60 minutes by an increase in the surface area occupied (on a cross-section of a microvessel) by endothelial cells (both nucleus and cytoplasm). This was followed by an increase of 23.7% in the mean diameter of astrocytes nuclei and a decrease of approximately 35% in lumenal surface of the microvessels. These observations suggest that the occlusion of a large cerebral artery causes prompt swelling of endothelial cells and astrocytes; both of these early biological responses may interfere with erythrocyte circulation and oxygen delivery, which (after the arterial occlusion) are entirely dependent on the circulation provided by the collateral arterial connections. Through its interference with microvascular patency and oxygen delivery, cell swelling may influence the rate at which neurons become necrotic. In this model of brain infarct the number of necrotic neurons peaks approximately 72 hours after middle cerebral artery occlusion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Brain Embolism Monitoring with Transcranial Doppler Ultrasound.

Embolism is considered to be the main mechanism leading to brain infarction today; with the introduction of sophisticated neuroimaging tools, its impact is increasingly appreciated. Transcranial Doppler ultrasound allows noninvasive monitoring of in vivo embolism. Acute stroke, internal carotid artery stenosis, several cardiac conditions, internal carotid endarterectomy, and coronary artery bypass graft surgery have been extensively monitored. These investigations and other clinical and neuroimaging studies have expanded the understanding of brain embolism; they suggest it may be appropriate to think of it as a process that occurs in the context of other hemodynamic factors. Differences have been identified among several conditions regarding the temporal profile of embolism and the characteristics of embolic particles. This article presents a brief review of brain embolism monitoring with transcranial Doppler ultrasound.

Journal Article↗
PubMedDate not supplied

Muscle histopathology in spastic cerebral palsy.

We studied the histopathology of spastic muscles in patients with spastic cerebral palsy using specimens obtained from the gastrocnemius muscles during orthopedic operations. Though there was no disease-specific abnormality, we found changes in fiber type distribution, i.e., type-1 fiber predominance and type-2B fiber deficiency. These changes were not found in the patient with brain infarction at age 1 year 5 months. Variation in fiber size, especially in type-1 fibers, was also detected in older patients and at the more severely affected sides. We speculated that the influence on the spinal motor unit from upper motor cortex might be applicable to the muscle histological findings and the time of the onset of the brain damage might be important.

Adenosine Triphosphatases↗
PubMedDate not supplied

Non-rheumatic atrial fibrillation as a risk factor for stroke.

The association between non-rheumatic atrial fibrillation (AF) and stroke has been studied in 402 patients consecutively admitted to a stroke unit. Brain infarction patients with sinus rhythm (n = 196) and non-rheumatic AF (n = 92) were further compared. Some findings supported an embolic origin of the stroke: half of the deceased AF patients (n = 24) at autopsy either had left atrial thrombosis or arterial embolism compared to none of the ten with sinus rhythm. Patients with AF also had a higher mortality and more severe brain lesions, findings compatible with a sudden occlusion of blood flow. However, these differences might also be explained by an atherothrombotic occlusion with impaired autoregulation in the ischaemic region in conjunction with heart failure, which was more common in the AF patients. Other findings supporting an atherothrombotic mechanism were: the prevalence of AF was higher (19-29%) in all kinds of stroke, including haemorrhage, than in age-matched controls (3-9%). Also patients with previous AF and no present embolic source resembled the whole AF group and differed from patients with sinus rhythm. Thus embolism is a plausible cause of stroke in many AF patients, whereas an atherothrombotic origin is more likely in others. Characteristics identifying the mechanism in an individual case were not found.

Aged↗
PubMed1988

Clinical and neuropathological findings in systemic lupus erythematosus: the role of vasculitis, heart emboli, and thrombotic thrombocytopenic purpura.

We reviewed the medical records and autopsy reports of 50 patients with systemic lupus erythematosus to determine the clinical and neuropathological features of this disease. Neuropsychiatric disturbances were found in the majority (74%) of the patients, occurring as psychiatric illness only (5 patients), neurological disorders only (15 patients), and both together (17 patients). Central nervous system (CNS) lesions were present in half the patients; embolic brain infarcts (10 patients) and CNS infections (8 patients) were the most common. Cardiac sources of emboli were Libman-Sacks endocarditis (5 patients), chronic valvulitis (2 patients), and left side of heart mural thrombus (2 patients). There was no evidence of active CNS vasculitis. Clinical features of thrombotic thrombocytopenic purpura (TTP) developed during the terminal illness in 14 patients, 7 of whom also had pathological evidence of TTP. Correlation between neuropsychiatric disorders and brain lesions could be made in approximately half the patients. This study indicates that cardiac emboli from Libman-Sacks endocarditis and TTP are common pathogenetic factors of CNS disease in systemic lupus erythematosus, whereas CNS vasculitis is rare.

Adolescent↗
PubMed2006

Early carotid endarterectomy after ischemic stroke: the results of a prospective multicenter Italian study.

OBJECTIVES: To evaluate safety of early carotid endarterectomy (CEA) in patients with acute brain ischemia presenting to the emergency department stroke units (EDSU). METHODS: The neurologists, neuroradiologists and vascular surgeons on duty in emergency departments enrolled 96 patients who underwent very early CEA according to a predefined protocol within two years. The protocol included evaluation of neurological status by National Institute of Health Stroke Scale (NIHSS), neuroimaging assessment, ultrasound of the carotid arteries and Transcranial Doppler. Patients with NIHSS>22 or whose neuroimaging showed brain infarct >2/3 of the middle cerebral artery territory were excluded. All eligible patients underwent CEA as soon as possible. Primary end points of the study were mortality, neurological morbidity by NIHSS and postoperative hemorrhagic conversion on neuroimaging. Statistical analysis was performed by univariate analysis. RESULTS: The mean time elapsing between the onset of stroke and endarterectomy was 1.5 days (+/-2 days). The overall 30-day morbidity mortality rate was 7.3% (7/96). No neurological mortality occurred. On hospital discharge, three patients (3%) experienced worsening of the neurological deficit (NIHSS score 1 to 2, 1 to 3 and 9 to 10 respectively). Postoperative CT demonstrated there were no new cerebral infarcts nor hemorrhagic transformation. At hospital discharge 9/96 patients (9%) had no improvement in NHISS scores, 37 were asymptomatic and 45 showed a median decrease of 4.5 NIHSS points (range 1-18). By univariate analysis none of the considered variables influenced the clinical outcome. CONCLUSION: Our protocol selected patients who can safely undergo very early (<1.5 days) surgery after acute brain ischemia. Large randomized multicenter prospective trials are warranted to compare very early CEA versus best medical therapy.

Aged↗
PubMed1988

Dystonia in homocystinuria.

Three patients with homocystinuria due to cystathionine beta-synthase deficiency who developed progressive generalised dystonia are described. Although cerebrovascular thrombosis is usually thought to be responsible for neurological dysfunction in homocystinuric patients, neuropathological studies in one case and clinical and radiological evidence in the other two suggested that dystonia was not caused by brain infarction. Movement disorder associated with homocystinuria may result from the neurochemical changes in the basal ganglia related to the inherited defect in sulphur amino acid metabolism.

Adolescent↗
PubMed2004

Inhibition of MEK/ERK 1/2 pathway reduces pro-inflammatory cytokine interleukin-1 expression in focal cerebral ischemia.

It has been proposed that mitogen-activated protein kinase (MAPK) pathways may play a role in the regulation of pro-inflammatory cytokines, such as interlukine-1, during cerebral ischemia. Our previous study showed that extracellular-signal-regulated kinases 1 and 2 (ERK 1/2) were activated during focal cerebral ischemia in mice [J. Cereb. Blood Flow Metab. 20 (2000) 1320]. However, the effect of ERK 1/2 activation in focal cerebral ischemia is still unclear. In this study we reported that in vivo phospho-ERK 1/2 expression increased following 30 min of middle cerebral artery occlusion (MCAO) in the mouse brain in both the ischemic core and perifocal regions. Western blot analysis and immunohistochemistry demonstrated that pro-treatment with 1,4-diamino-2,3-dicyano-1,4-bis butadiene (U0126) [J. Biol. Chem. 273 (1998) 18623] could significantly inhibit mouse brain phospho-MEK 1/2 and phospho-ERK 1/2 expression after 1-2 h of MCAO (p<0.05). Compared to the control group of mice, brain infarct volume was significantly decreased after 24 h of MCAO in the U0126-treated mice (27+/-6 vs. 46+/-9 mm(2), p<0.05). Inhibition of the MEK/ERK 1/2 pathway also prevented downstream kinase Elk-1 phosphorylation, and further reduced cytokine IL-1beta mRNA, but not TNFalpha, IL-1alpha, or chemokine MIP-1alpha mRNA expression. Our data demonstrates that in vivo the close linking of MEK 1/2, ERK 1/2, Elk-1, and IL-1 mRNA expression in the cerebral ischemia animals suggests that ERK 1/2 pathway activation is important in pro-inflammatory cytokine IL-1beta signaling, which induces an inflammatory response and exacerbates ischemic brain injury. Inhibiting the ERK 1/2 pathway may therefore provide a novel approach for the reduction of ischemia-induced IL-1beta overexpression.

Animals↗
PubMed2004

Prophylactic creatine administration mediates neuroprotection in cerebral ischemia in mice.

Creatine mediates remarkable neuroprotection in experimental models of amyotrophic lateral sclerosis, Huntington's disease, Parkinson's disease, and traumatic brain injury. Because caspase-mediated pathways are shared functional mechanistic components in these diseases, as well as in ischemia, we evaluated the effect of creatine supplementation on an experimental stroke model. Oral creatine administration resulted in a remarkable reduction in ischemic brain infarction and neuroprotection after cerebral ischemia in mice. Postischemic caspase-3 activation and cytochrome c release were significantly reduced in creatine-treated mice. Creatine administration buffered ischemia-mediated cerebral ATP depletion. These data provide the first direct correlation between the preservation of bioenergetic cellular status and the inhibition of activation of caspase cell-death pathways in vivo. An alternative explanation to our findings is that creatine is neuroprotective through other mechanisms that are independent of mitochondrial cell-death pathways, and therefore postischemic ATP preservation is the result of tissue sparing. Given its safety record, creatine might be considered as a novel therapeutic agent for inhibition of ischemic brain injury in humans. Prophylactic creatine supplementation, similar to what is recommended for an agent such as aspirin, may be considered for patients in high stroke-risk categories.

Adenosine Triphosphate↗
PubMed2005

Inhibition of the cerebral ischemic injury by ethyl pyruvate with a wide therapeutic window.

BACKGROUND AND PURPOSE: Ethyl pyruvate (EP) is a pyruvate derivative that has been reported recently to prevent lethality in mice with established lethal sepsis and systemic inflammation. In this study, we examined the neuroprotective effect of EP in a rat cerebral ischemia model of middle cerebral artery occlusion (MCAO). METHODS: Male Sprague-Dawley rats were subjected to 1 hour of MCAO, and EP was administered at various time points before or after MCAO. The changes in the brain infarction, neurological deficits, microglia activation, and proinflammatory cytokine expression were evaluated. BV2 microglial cells were also used to access the anti-inflammatory effect of EP. RESULTS: The administration of EP intraperitoneally at 30 minutes before or at 4 or 12 hours after MCAO reduced the infarct volume to 10.3+/-3.4% (n=6; P<0.05), 21.5+/-2.7% (n=6; P<0.05), and 44.3+/-4.0% (n=6; P<0.05), respectively, of that of the control group. The significant reduction in infarct volume was accompanied by the suppression of the clinical manifestations associated with cerebral ischemia, including motor impairment and neurological deficits, microglial activation, and proinflammatory cytokine expression. The neuroprotective effect of EP was yet evident when it was administered as late as 24 hours after MCAO/reperfusion (76.5+/-4.70%; n=6; P<0.05). EP suppressed lipopolysaccharide induced activation of BV2 cells, as was evidenced by a reduction in NO release and the accompanying induction of proinflammatory cytokines. CONCLUSIONS: These results suggest that EP affords the strong protection of the delayed cerebral ischemic injury with a wide therapeutic window.

Animals↗
PubMed1980

Familial oculoleptomeningeal amyloidosis.

Members of a German family living in Ohio (United States) have been found to have dominantly inherited amyloidosis causing dementia, seizures, strokes, coma and visual deterioration. Pathological examination of affected individuals has shown severe, diffuse amyloidosis of the leptomeninges and subarachnoid vessels associated with patchy fibrosis and obliteration of the subarachnoid space. Amyloid deposits were prominent on the ependymal surfaces and severe and diffuse neuronal loss and generalized subpial gliosis were found in the cerebrum and cerebellum. On occasion superficial brain infarcts were seen. Amyloid was also found in the vitreous, the retinal internal limiting membrane and the retinal vessels, particularly those in the nerve fibre layer. There was only minimal amyloid elsewhere.

Adult↗
PubMed2006

Involvement of cell adhesion molecules in polydatin protection of brain tissues from ischemia-reperfusion injury.

Previous studies have demonstrated that polydatin, a crystal component extracted from the root stem of the perennial herbage Polygonum Cuspidatum Sieb.et Zucc, exerts a neuroprotective effect on cerebral injury induced by ischemia/reperfusion. To investigate the possible mechanism of this action, we determined the effects of polydatin on the expression of cell adhesion molecules (CAMs) after ischemia-induced cerebral injury. Rats were treated with polydatin (i.v.) immediately after the operation of middle cerebral artery occlusion (MCAO) for 1 h. It was found that polydatin improved neurological deficits and reduced the volume of brain infarction. In addition, polydatin decreased the levels of CAMs relative to the control (MCAO alone); these included intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, L-selectin and Integrins. These results suggest that polydatin exerts protective effects likely via inhibition of the expression of various CAMs; polydatin may be a potential agent for treatment of brain injury associated with stroke.

Analysis of Variance↗
PubMedDate not supplied

Cardioprotective effects of sodium gamma-hydroxybutyrate (GHB) on brain induced myocardial injury.

Gamma-hydroxybutyrate (GHB) was evaluated as a protective agent in a gerbil model of non-lethal myocardial injury that follows brain ischaemia. The accumulation of fat droplets in myocardial fibers following brain infarction was measured by electron microscopic morphometry and expressed as a percentage of the area of the sarcoplasm. GHB treatment significantly reduced the area occupied by lipid droplets compared with that found in saline treated controls measured both 10 hours (p less than .005) and 24 hours (p less than 0.05) after unilateral carotid ligation. GHB did not affect the ischaemic swelling of the brain.

Animals↗
PubMed1979

The protective effects of dietary fish oil on focal cerebral infarction.

The protective effect of the (n-3) fatty acids in menhaden fish oil on acute cerebral ischemia was investigated in cats. Cerebral ischemia was produced by ligation of the left middle cerebral artery of cats fed either a basal diet of feline cat chow or the basal diet supplemented with 8% of the calories as menhaden oil for 18-24 days. Fatty acids esters of 20:5 (n-3) were increased and the 18:2 (n-6) decreased in the heart and liver of cats fed supplemental fish oil, but the brain lipid showed no effect of the diet. We found that the neurological deficit and the volume of brain infarction in the group treated with fish oil was less than that of the control group. The present findings suggest that moderate dietary supplements of fish oil may be beneficial in the prophylactic treatment of ischemic cerebral vascular disease.

Animals↗
PubMed2005

High titers of CA-125 may be associated with recurrent ischemic strokes in patients with cancer.

In addition to etiologies common in the general population, strokes in cancer patients may be caused by hypercoagulable states, hyperviscosity, cardiogenic embolism, and neoplastic vessel infiltration. Intravascular mucins were reported in patients with recurrent thromboembolism. The authors report four patients with metastatic cancer, brain infarcts, and other thromboembolic disease with markedly elevated levels of the tumor marker CA-125 and explore possible associations between this mucinous protein and strokes.

Aged↗