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 1,477 records · Page 82Linked to original sources

Idiopathic cerebral arterial infarction with paucity of symptoms in the full-term neonate.

Two full-term neonates, one with convulsions and intermittent generalized hypotonia and one with poor sucking, temperature instability, and lethargy, are reported. CT scan findings suggested cerebral arterial infarction. Arteriography revealed occlusion of the middle cerebral artery, unilaterally in the first and bilaterally in the second patient. The evolution of the infarct could be followed on serial CT scans. No predisposing factors during pregnancy or delivery were found, and serious neurologic deficits developed in both children. These cases demonstrate that, even in full-term neonates with discrete or moderate neurologic symptoms and born after normal pregnancy and delivery, the possibility of vasoocclusive brain infarction should be considered. The diagnosis is suggested by imaging techniques, of which CT scanning seems to have the greatest value at present. This technique also permits the follow-up of the lesions. The prognosis for neurologic development appears to be variable: minor neurologic deficits as well as unexplained spastic hemiplegia in older children may be the consequence of inapparent cerebral arterial infarction in the neonatal period.

Adult↗

Postvaricella angiopathy: report of a case with pathologic correlation.

Varicella is a common childhood illness, and central nervous system complications occur frequently. Delayed angiopathy has been described, although there are few reports of clinicopathologic correlation. A previously well 4-year-old male is presented. He suffered varicella 2 months before presentation with extensive right middle cerebral artery (MCA) territory infarction. Cerebral angiography demonstrated an isolated 89% stenosis of the right proximal MCA. He developed cerebral edema refractory to medical treatment and progressed to transtentorial herniation. Right frontal temporoparietal craniotomies were performed with evacuation of infarcted brain tissue. Pathologic studies revealed small vessel vasculitis with lymphocytic infiltration of the vessel wall. Areas of demyelination were present within the white matter. Polymerase chain reaction for varicella was negative on brain tissue. Postvaricella angiopathy, although an uncommon complication, may affect both small and large blood vessels, with catastrophic results.

Cerebral Cortex↗

Early and late results of carotid endarterectomy: retrospective study of 70 operations.

CONTEXT: Indications and results of carotid endarterectomy have been defined from clinical multicentric trials like the European Carotid Surgery Trialists, North-American Symptomatic Carotid Endarterectomy Trial and Asymptomatic Carotid Atherosclerosis Study. The patients included in these trials were highly selected, as were the surgeons performing the operations. Clinical practice is different but the same results should be achieved. OBJECTIVE: To study indications, technique, early and late results, and whether carotid endarterectomy has been performed in accordance with standards defined by multicentric trials. DESIGN: Retrospective case report study. SETTING: A tertiary care private hospital. PARTICIPANTS: 57 patients, on whom 70 carotid endarterectomies were performed over a 10-year period. The median age was 66.4 +/- 7.8 years; 43 (75.4%) were male, 41 (71.9%) hypertensive, 36 (63.1%) current smokers and 24 (21.0%) had diabetes. Bilateral carotid stenosis was present in 31 (54.3%) patients, peripheral arterial occlusions in 32 (56.1%) and ischemic cardiopathy in 25 (43.1%). All patients had had angiography and 41 (71.9%) had also had a duplex-scan of neck arteries. Cerebral imaging via computerized tomography scan or magnetic resonance imaging was obtained for 36 patients. Patients were followed up over a period of one to 122 months. MAIN MEASUREMENTS: early and late post-operative death, early and late post-operative stroke, and recurrence of atheroma plaque and symptoms relative to carotid stenosis. RESULTS: There was one post-operative death (1.4%) caused by myocardial infarction and two early strokes (2.8%): a total complication rate of 4.2%. After 3 and 5 years, 95.4% and 81.3% of patients respectively were stroke-free and 72.8% and 67.3% were alive. There were four recurrences and two of them related to stroke. Forty-nine (70%) stenoses operated on were symptomatic. Brain infarction was detected in 59.2% of patients who underwent computerized tomography scan or magnetic resonance imaging. CONCLUSIONS: Carotid endarterectomy was done in accordance with international standards. The most frequent cause of late death was myocardial infarction, and recurrences were related to stroke. Patients should be followed up closely.

Aged↗

Neurofilament expression in the rat brain after cerebral infarction: effect of age.

In this study the role of neurofilaments (NFs) in brain plasticity after cerebral infarction in young and middle aged rats was evaluated. Focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery in 3- and 20-month-old male Sprague-Dawley rats. After 1 week, brains were removed and in situ hybridization and immunostaining was performed for NF-68 kDa, 160 kDa and 200 kDa in different phosphorylation states. After focal cerebral ischemia the levels of gene and protein expression of neurofilament proteins were increased in the border zone of the infarcted area compared with the unaffected contralateral site. Furthermore, the level of gene expression was significant lower in aged as in young animals. Focal cerebral ischemia resulted in a clearly increased number of immunostained axons in the penumbral region in both young and aged rats. On the other hand the immunostained apical dendrites became thicker and vacuolization appeared. Our results suggest that that neurofilament proteins are involved in response of brain to focal ischemia.

Aging↗

[Tumor embolism with fatal cerebral infarct in pneumonectomy. Case report and review of the literature].

Carcinomas of the bronchi often infiltrate veins, particularly in advanced stages. Tumor propagation in pulmonary veins with intra-atrial extension has been reported. Systemic arterial tumor embolism is a potentially fatal hazard that is caused by surgery or it can be the initial manifestation of a bronchogenic carcinoma. The importance of early pulmonary venous ligation in lung cancer surgery, first stressed by Aylwin in 1951, is evident, particularly when intravenous tumor progression has been diagnosed preoperatively by echocardiography or CT scan. We report a case of lethal hemispheric brain infarction following tumor embolism during lobectomy for bronchus carcinoma. A review of the literature on this subject is presented; there were 38 cases of arterial tumor embolism because of primary lung neoplasms.

Aged↗

Chronic daily administration of ethyl docosahexaenoate protects against gerbil brain ischemic damage through reduction of arachidonic acid liberation and accumulation.

Recently, we reported that dietary ethyl docosahexaenoate (Et-DHA) intake decreases the level of membrane arachidonic acid (AA), which reduces the generation of AA metabolites in ischemic gerbil brain. As an extended study, we further investigated the influence of the chronic administration of Et-DHA on free AA levels after ischemia. In addition, Na,K-ATPase activity, cation content, cerebral edema and brain damage were also evaluated. Weanling male gerbils were orally pretreated with either Et-DHA (200 mg/kg) or vehicle, once a day for 10 weeks, and subjected to transient forebrain ischemia by bilateral common carotid occlusion for 30 min. Time-course analyses revealed that pretreatment with Et-DHA, compared with pretreatment with the vehicle, significantly decreased the brain's free AA levels during ischemia (5, 15 and 30 min) and after reperfusion (5, 10, 15 and 30 min), and attenuated the decline of Na,K-ATPase activity at examined time points. Pretreatment with Et-DHA significantly prevented an increase in Na(+) concentration and a decrease in K(+) concentration after 24 h of reperfusion, which resulted in lower cerebral water content. Reduced brain infarct volume and low animal mortality were also observed in Et-DHA-treated animals. These data suggest that the reduction of ischemia-induced AA liberation and accumulation by Et-DHA pretreatment may be attributable to (a) protection against the decline of Na,K-ATPase activity, (b) postischemic cerebral edema and brain damage and (c) animal mortality.

Animals↗

Intrathecal release of pro- and anti-inflammatory cytokines during stroke.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of ischaemic brain damage. We have recently demonstrated that stroke patients display an intrathecal production of proinflammatory cytokines, such as IL-1beta and IL-6 already within the first 24 h after the beginning of symptoms (Tarkowski et al., 1995). The aim of the present study was to investigate patterns of local inflammatory responses as a consequence of acute stroke. Thirty stroke patients were studied prospectively on days 0-3, 7-9, 21-26 and after day 90 with clinical evaluations, radiological assessments and analysis of cerebrospinal fluid (CSF) cytokine levels. In addition, 15 healthy control CSF samples were used. Significantly increased CSF levels of IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-10 were observed early during the stroke with a peak on day 2 for the proinflammatory cytokines IL-8 and GM-CSF, and on day 3 for the immunoregulatory cytokine IL-10. Patients with a brain infarct predominantly located in the white matter showed significantly higher levels of IL-8 in CSF than patients with an infarct mainly located in the grey matter. Also, high levels of intrathecal tumour necrosis factor-alpha (TNF-alpha) were associated with the presence of white matter disease. Our study demonstrates an intrathecal production of proinflammatory and immunoregulatory cytokines in patients with stroke, supporting the notion of localized immune response to the acute brain lesion. A better understanding of the inflammatory response in stroke may lead to new treatment strategies.

Adult↗

[Stroke unit: requirements for diagnostic imaging and interventions].

Stroke Units are specialised centers of expertise with the aim to optimize acute therapy of stroke. More specifically, the aims are (a) to reduce the area of brain infarction, (b) to prevent or appropriately react to complications, (c) to ensure an optimal strategy of secondary stroke prevention after having clarified etiopathogenesis, and (d) to establish a basis for subsequent rehabilitation. Stroke Units should collaborate for the evaluation and development of new diagnostic and therapeutic means. Patients' medical history, their clinical presentation and brain imaging create the basis for therapeutical decisions. The value of interventional therapy is presently evaluated for acute stroke therapy (e.g. intra-arterial thrombolysis) and secondary stroke prevention (Stent-protected angioplasty of carotid stenosis).

Austria↗

C-11-labeled glucose and its utilization in positron-emission tomography.

Carbon-11-labeled glucose was prepared photosynthetically using the green alga Scenedesmus obtusiusculus Chod. The carbohydrates were extracted from the cells with dilute HCI and the glucose was isolated and purified using high-performance liquid chromatography. The manipulations in the hot cell are described. Analysis of the material (gas liquid chromatography and HPLC) showed that the glucose obtained was radiochemically pure. The total incorporation of the 11CO2 added to the algae was 60-80%. The radiochemical yield of pure carrier-added glucose was approximately 25%, at 40 min after E.O.B. including the HPLC purification and sterile filtration. The C-11 glucose uptake in rat brain was compared with that of commercial D[U-14C]glucose, and preliminary PET studies with D-[11C]glucose in a patient with a brain infarct are presented.

Animals↗

Possible pitfalls with clinical imaging of indium-111 leukocytes: concise communication.

Indium-111 leukocyte imaging is a reliable procedure for detecting abscesses. Problems such as cell clumping can occur before injection, thus altering the normal distribution. Furthermore, accumulation of the labeled leukocytes in the colon, brain infarcts, and accessory spleens has been observed. Thus, these physiologic and pathologic conditions other than abscesses must be borne in mind to avoid false-positive diagnoses of abscess.

Abscess↗

[The correlation of the clinical and the computed tomographic changes in patients with atherosclerotic circulatory encephalopathy].

Correlation has been carried out between hemodynamic, structural and clinical changes in stenotic lesions of major brain arteries in 175 patients with atherosclerotic dyscirculatory encephalopathy. The paper analyses the results of ultrasonic and radioopaque diagnosis of vascular lesions of the head and neck, those of clinical, neurological observations and data from computerized tomography scans of the brain. Topographic connections have been established between hemodynamic, structural and neurological manifestations of the disease. It was not infrequently that moderately severe hydrocephaly as one of the manifestations of atrophy of the brain in these patients outstripped brain infarction. Vascular aspect is considered of paresthesias in the extremities by monotype in lesions of major arteries of one of the extremities.

Adult↗

Transcranial Doppler in acute ischemic stroke of the middle cerebral artery territories.

UNLABELLED: We have investigated the reliability of transcranial doppler compared with cerebral angiography in acute ischemic stroke in the middle cerebral artery territories. We studied 48 patients, 28 men and 21 women, mean age 68.1 (range 54-75), observed within 5 h of the onset of ischemic stroke in the middle cerebral artery territory. Ultrasound evaluation (duplex scanner and transcranial doppler) and cerebral angiography were carried out in close sequence immediately after CT scan. CT was repeated by Day 7 to estimate the infarct size: 27/48 patients had intracranial arterial obstructions. An acoustic temporal "window" was not found in 6.25%. Transcranial doppler showed a sensitivity of 80.0% and a specificity of 90.0% compared with cerebral Angiography for patients with patent acoustic temporal "windows". Accuracy was 79.2%, when patients with no "windows" were included. With respect to intracranial internal carotid artery and middle cerebral artery mainstem, transcranial doppler showed a sensitivity of 95.0%, and a specificity of 92.0%. Including patients with no windows, accuracy was 87.5%. CONCLUSIONS: Our data suggest that Transcranial Doppler can be reliably used to demonstrate intracranial internal carotid artery or middle cerebral artery mainstem obstructions in the acute phase of a brain infarction.

Acute Disease↗

Silent cortical strokes associated with atrial fibrillation.

To clarify whether silent cortical strokes (SCS) could be a predictor of symptomatic stroke in patients with atrial fibrillation (AF), 72 patients with AF (50 with chronic AF, 22 with paroxysmal AF) were studied. Patients with mitral stenosis, history of myocardial infarction, or dilated cardiomyopathy were excluded from this study. Using cranial magnetic resonance imaging (MRI), the patients were divided into those with SCS (23 patients, Group 1) and those without SCS (49 patients, Group 2). The incidence of symptomatic stroke was then compared between the two groups. Three patients (13%) in Group 1 developed symptomatic brain infarction; this is statistically significant (p < 0.05), compared with the patients in Group 2, none of whom experienced symptomatic stroke. We suggest that SCS is a predictor of symptomatic cerebral infarct in patients with AF. Therefore, it is thought to be important to diagnose SCS using cranial MRI or computed tomography and to keep patients with SCS under close surveillance.

Aged↗

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for lipid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results, showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage.

Animals↗

Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy.

Over the past 10 years, 10 cats with primary central nervous system infection by larvae of Cuterebra flies have been documented at Cornell University. Clinical abnormalities noted in all cats were progressive and most commonly consisted of depression (6/10), blindness (6/10), and behavior changes (2/10). Affected cats presented most commonly in July (2/10) and August (7/10); one cat was presented in September. The diverse histopathologic changes are unique to this aberrant migration and consist of a combination of five characteristic features: 1) parasitic track lesion (7/10), 2) superficial laminar cerebrocortical necrosis (10/10), 3) cerebral infarction (8/10), 4) subependymal rarefaction and astrogliosis with or without ependymal cell loss (7/10), and 5) subpial astrogliosis (7/10). Changes 2-5 occurred throughout the parenchyma unassociated with the track lesion or the parasite in the affected tissue. The larvae have been recovered most commonly in the region of the olfactory bulbs and peduncles, optic nerves, and cribriform plate, suggesting entry from the nasal cavity. Many of the changes noted are suggestive of a toxic factor elaborated by the parasite and borne within the cerebrospinal fluid, as well as vascular compromise as a component in those cats with brain infarction. Because of the prevalence of infarction associated with this syndrome and the lack of reported cases of such lesions in regions of the world devoid of the fly, we propose that aberrant cuterebral larval migration in the brain is the cause of feline ischemic encephalopathy.

Animals↗

The novel and systemically active metabotropic glutamate 1 (mGlu1) receptor antagonist 3-MATIDA reduces post-ischemic neuronal death.

We examined the pharmacological properties of 3-methyl-aminothiophene dicarboxylic acid (3-MATIDA) by measuring second messenger responses in baby hamster kidney cells stably transfected with mGlu1a, mGlu2, mGlu4a or mGlu5a receptors and ionotropic glutamate receptor agonist-induced depolarizations in mouse cortical wedges. 3-MATIDA was a potent (IC(50)=6.3 microM, 95% confidence limits 3-15) and relatively selective mGlu1 receptor antagonist. When tested on mGlu2, mGlu4 or mGlu5 receptors its IC(50) was >300 microM. When tested in cortical wedges, however, 3-MATIDA was also able to antagonize AMPA or NMDA responses with an IC(50) of 250 microM. When present in the incubation medium of cultured murine cortical cells, 3-MATIDA (1-100 microM) significantly reduced the death of neurons induced by 60 min of oxygen and glucose deprivation (OGD), even when added up to 60 min after OGD. A similar neuroprotective activity was observed when 3-MATIDA was present at 10-100 microM in the medium of rat organotypic hippocampal slice cultures exposed to 30 min OGD. Systemic administration of 3-MATIDA (3-10 mg/kg, immediately and 1 h after the onset of ischemia) reduced the volume of brain infarcts following permanent middle cerebral artery occlusion in rats. Our results show that 3-MATIDA is a potent and possibly selective mGlu 1 receptor antagonist that may be considered as a novel prototype neuroprotective agent.

Animals↗

Bilateral extensive cerebral infarction and mesenteric ischemia associated with segmental arterial mediolysis in two young women.

Segmental arterial mediolysis (SAM) is a rare non-atherosclerotic non-inflammatory vascular disease that affects mainly muscular arteries of the splanchnic and cerebral territories. Reported herein are two cases of SAM in young women with fatal outcome. One of the patients had an atypical form of the disease, which primarily affected small intestinal submucosal and subserosal arteries, and resulted in acute mesenteric ischemia. The other had bilateral brain infarction with SAM of internal carotid arteries (ICA). Pathological examination of both cases did not reveal the cause of blood flow disturbance: large mesenteric branches of the former and ICA of the latter were free of either dissection or thrombosis; in addition, small intestinal arteries of the first patient did not show signs of vasculitis. These findings suggest that unusual pathways of arterial occlusion and dissection may occur in the context of SAM.

Adult↗

Cell proliferation after ischemic infarction in gerbil brain.

In order to study cell proliferation after ischemic infarction, a model of bilateral common carotid artery occlusion in the gerbil was developed. A comparison of survival rates after 15, 30, 45 and 60 min of occlusion revealed that 45 min was the maximum duration of ischemia after which most (72%) of the gerbils were alive at 1 week. The administration of pentobarbital (single dose, 30 mg/kg) postoperatively to badly seizing animals increased survival to 100%. Large, well-demarcated infarcts were present in posterior thalamus or midbrain in 62% of gerbils subjected to 45 min bilateral occlusion. In 60% of these animals the infarcts were unilateral; in 40% they were bilateral. To quantitate cell proliferation in the infarcts from 12 h to 25 days after ischemia, gerbils were injected with [3H]thymidine 4 h prior to sacrifice, and autoradiographs were prepared from sectioned brains. Proliferation took place from 2 to 7 days after occlusion, with a maximum of 24% labeled cells at 6 days.

Animals↗