Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cerebral 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 163 records · Page 9Linked to original sources
PubMed2003

Effect of TTC-909 on cerebral infarction following permanent occlusion of the middle cerebral artery in stroke prone spontaneously hypertensive rats.

We investigated the effect of TTC-909, a drug preparation of the stable prostaglandin I(2) analogue clinprost (isocarbacyclin methylester; methyl 5-[(1S,5S,6R,7R)-7-hydroxy-6-[(E)-(S)-3-hydroxy-1-octenyl] bicyclo[3.3.0]oct-2-en-3-yl] pentanoate) incorporated into lipid microspheres, on cerebral infarction 7 days after permanent occlusion of the middle cerebral artery (MCA) in stroke prone spontaneously hypertensive rats (SHRSP). Under the anesthesia, the MCA was permanently occluded above the rhinal fissure. In schedule 1, vehicle or TTC-909 was injected i.v. once daily over 7 days starting immediately after MCA occlusion. In schedule 2, vehicle or TTC-909 was infused for 3 h starting immediately after MCA occlusion. In schedule 3, vehicle or TTC-909 was infused for 3 h starting immediately after MCA occlusion followed by bolus injection once daily over 6 days. Seven days later, the infarct volume was estimated following hematoxylin and eosin staining. Cerebral infarction produced by permanent occlusion of MCA was limited to the cerebral cortex. While this volume was reduced significantly in case of schedule 3, the infarct volume was not reduced significantly in schedules 1 and 2. Ozagrel, a thromboxane A(2) synthetase inhibitor, had no effect on the infarct volume in schedule 3. These results suggest that cerebral infarction can be developed progressively not only during the first few hours but also after a permanent occlusion of MCA in SHRSP. TTC-909 inhibited cerebral infarction, maybe by improving cerebral blood flow and by protecting against neuronal damage.

Animals↗
PubMed2005

The management of large hemispheric cerebral infarcts.

Large hemispheric cerebral infarcts have significant morbidity and mortality. Our understanding of this pathophysiological process involved with secondary neurological deterioration in large hemispheric infarctions has increased in the past few decades. New experimental strategies designed to improve outcome are reviewed.

Critical Care↗
PubMed2004

Evaluation and management of transient ischemic attack and minor cerebral infarction.

After immediate intervention for cerebral infarction or transient ischemic attack (TIA), the primary goal is secondary prevention of future cerebral ischemia and prevention of complications related to the initial ischemic event. The goals of the diagnostic evaluation are to (1) determine potential contributing mechanisms (cardioembolic, large-vessel disease of the extracranial and intracranial vessels, small-vessel disease, coagulation defects, and cryptogenic), (2) identify contributing risk factors (hypertension, hyperlipidemia, tobacco use, diabetes), and (3) complete the evaluation in a cost-effective and safe manner. We provide a sequential approach to the diagnostic evaluation of cerebral infarction or TIA to optimize diagnostic yield of testing, minimize cost and potential harm to the patient, and provide information that will change management. This systematic approach focuses on 6 important questions: (1) Are the symptoms consistent with a cerebral infarction or TIA (versus nonischemic pathology)? (2) Where does the ischemic event localize? (3) What etiologies and mechanisms of cerebral infarction and TIA are possible? (4) What is the prevalence of each potential etiology? (5) What treatments are available for this etiology? (6) What tests and studies are useful to evaluate this etiology?

Adult↗
PubMed1983

[Dynamic pathophysiology of cerebral infarction and revascularization. III. Changes of regional cerebral blood flow].

Thirty-eight patients with occlusive cerebrovascular disease were followed with regional cerebral blood flow (rCBF) measurement, angiography and computerized tomography (CT) to know the time course of rCBF in cerebral infarction. The rCBF study was carried out by the 133Xe intracarotid injection method with 16 scintillation detectors. They were allocated to two groups according to the findings on angiograms; 15 patients having any change of occlusive lesion (the group of no-recanalization ) and 23 patients showing reopening of occluded vessels (the group of recanalization). A mass sign and an extent of cerebral infarction were observed on CT. In the group of no-recanalization, a mean value of rCBF (mean rCBF) in acute stage was well correlated to the severity of ischemic stroke. In minor completed strokes the average mean rCBF was 35.8 +/- 3.7 ml/100g/min, which is significantly higher than that in major strokes and progressing strokes of 24.8 +/- 3.9 ml/100 g/min (p less than 0.001). Sequential change of mean rCBF was not prominent in the group of no-recanalization. However, rCBF change was conspicuous in the group of recanalization. In acute stage of recanalization, rCBF were markedly affected by the presence of mass sign (cerebral edema) on CT. When CT showed midline shift of structure, mean rCBF was markedly reduced, and when without midline shift, focal hyperemic areas were sometimes observed in the revascularized area. Thus, the inhomogeneity of rCBF was characteristic in cases with recanalization. The focal hyperemia usually disappeared within one week in cases of minor stroke and lasted until 2 or 3 weeks in cases of major stroke. In chronic stage, mean rCBF decreased, and there was no significant difference of averaged rCBF between two groups. Those findings suggests that the main factor influenced on the sequential change of rCBF is reopening of occluded vessels. Regional CBF may depends both on the degree of cerebral edema and the extent of vasoparesis after revascularization. In chronic stage CBF value is not always dependent to the presence of occlusive lesion but might be reflected in the total brain function.

Aged↗
PubMed1989

Impairment and recovery of ipsilateral sensory-motor function following unilateral cerebral infarction.

After unilateral cerebral hemisphere stroke, resulting in contralateral arm symptoms but largely sparing higher cerebral function, ipsilateral arm function is generally considered to be unaffected. In this study, 8 subjects with acute unilateral cerebral infarction (confirmed by CT scan) and primarily motor deficits underwent 11 computerized and 6 clinical assessments between 11 days and 12 months poststroke, and were compared with 12 normal subjects. Computerized tests comprised 3 pursuit tracking tasks (preview-random, step and a combination of these), designed to measure different aspects of integrated sensory-motor (S-M) function, and 12 tasks aimed at breaking tracking into various sensory, perceptual and motor components (joint movement sense, visual resolution, object perception, static and dynamic visuospatial perception, range of movement, grip and arm strength, reaction time, speed, static and dynamic steadiness). The asymptomatic arm was impaired on all but one of the computerized tests throughout the 12-month period, although to a lesser degree than the symptomatic arm. Grip strength was marginally impaired initially. Incomplete neurological recovery was seen in the asymptomatic arm for all functions except strength, speed and steadiness, possibly indicating their resistance to improvement. Clinical assessment detected no asymptomatic arm impairment and only a mild transient deficit of higher mental function. Our data suggest that (1) all cerebral hemisphere areas involved in S-M functions can exert some degree of bilateral motor control; (2) ipsilateral influence is never greater than contralateral influence, and is usually considerably less; and (3) the proportion of ipsilateral to contralateral control is closely related to the degree of continuous sensory feedback required by the particular task. The mechanism and degree of ipsilateral dysfunction can be explained by a 3-tier cerebral model of S-M integration comprising a lower level of functions with high contralateral specificity (somatosensory and motor), a middle level of non-limb-specific partially lateralized functions (ideomotor praxis and visuospatial perception) and an upper level of global mental activities (intellect, alertness, etc.).

Adult↗
PubMed2002

Pretreatment with melatonin reduces volume of cerebral infarction in a rat middle cerebral artery occlusion stroke model.

Melatonin is a potent scavenger of free radicals and an indirect antioxidant. Recent studies have shown that melatonin possesses beneficial effects in experimental models of brain trauma and global cerebral ischemia. The effects of pretreatment with melatonin on volume of cerebral infarction were investigated in the present study. Adult male Sprague-Dawley rats were anesthetized with sodium pentobarbital to undergo right-sided endovascular middle cerebral artery occlusion (MCAO) for 3 hr. A single dose of melatonin (1.5, 5, 15, or 50 mg/kg in 1 mL normal saline) or its vehicle was given via an intraperitoneal injection at 0.5 hr before MCAO. Relative infarction volumes on day 3 after MCAO were significantly reduced in the groups treated with melatonin at 5 (mean +/- S.E.M., 15.7 +/- 2.5%) or 15 (21.4 +/- 3.1 %) mg/kg but not at 1.5 (30.6 +/- 3.5%) or 50 (26.7 +/- 2.8%) mg/ kg when compared with the vehicle group (33.9 +/- 3.5%). There was no significant difference in the arterial blood pressure (BP), heart rate (HR) and relative cerebral blood flow among the experimental groups. These results indicate that pretreatment with melatonin at a dose between 5 and 15 mg/kg protects against focal cerebral ischemia.

Animals↗
PubMed1987

The predictive value of cerebral anaerobic metabolism with cerebral infarction after head injury.

Cerebral ischemia is a common mechanism of secondary brain injury following severe head injury. The cerebral metabolic rate of oxygen (CMRO2) and of lactate (CMRL), as well as cerebral blood flow (CBF) were measured daily for 5 days after head injury in 44 comatose head-injured patients to determine if metabolic changes could identify the patients who would develop cerebral infarction. Of 41 patients whose CBF remained at levels regarded as adequate to prevent infarction (CBF greater than or equal to 0.2 ml/gm/min), the six who showed a cerebral infarction on computerized tomography (CT) scans exhibited characteristic cerebral metabolic patterns: a CMRO2 of less than 0.6 mumol/gm/min on one or more of the days monitored, and markedly elevated cerebral lactate production (CMRL less than -0.06 mumol/gm/min) on Days 1 and/or 2 after injury. Patients who had no areas of infarction on serial CT scans typically had a CMRO2 and CMRL can be obtained at the bedside and can indicate the presence of an evolving ischemic infarct after head injury.

Adult↗
PubMed2003

[An epidemiologic study for relation between the snore and cerebral infarction].

OBJECTIVE: To explore the relation between cerebral infarction and simple, apneic snore. METHOD: A case control comparative study with the exception of influencing factors such as ages, sex, obesity and so on in 60 patients with cerebral infarction and 60 control subjects. RESULT: The probability of cerebral infarction is a little high in all snorer compared with the no snorer. The Odds ratio is 1.709 (95% confidence limits 0.798-3.705). The probability persist high in apneic snore compared with other kind of snore. The Odds ratio is 3.571 (95% CL 1.295-9.849, P < 0.05). The Odds ratio of cerebral infarction is highest in apneic snore compared with normal subjects (Odd ratio = 4.107, 95% CL 1.407-11.99, P < 0.01). CONCLUSION: Cerebral infarction is not obviously related with common snore. It is related significantly with the apneic snore. It indicated that snore is a possible cause of cerebral infarction. The possibility suffering from cerebral infarction is more in people especially in apneic snorer than no snorer.

Aged↗
PubMed2002

Acute cerebral infarction caused by congenital hypoplasty of cerebral artery in a severe burn case.

An 81-year-old man who had been healthy died 1 week after suffering severe burns. The autopsy revealed a fresh unilateral cerebral infarction with hemorrhagic transformation within the territory of the anterior cerebral artery (ACA) and hypoplasty of the A1 portion of the ACA. Since no other cause which could have resulted in this infarction was detected and since the victim had been healthy before the fire broke out, we concluded that this infarction occurred because of congenital hypoplasty of the left ACA and hypovolemic shock suffered after the burn injuries. Since cerebral infarction itself can lead to burn injuries or other accidents due to acute motor disturbance or syncope, detailed macroscopic and histological examinations of the brain of severe burn victims is important for evaluating the correlation between the infarction and a fire or other accidents.

Journal Article↗
PubMed2001

High- and moderately high-methionine uptake demonstrated by PET in a patient with a subacute cerebral infarction.

In patients with cerebral tumors, high accumulations of L-methyl-11C-methionine (11C-Met) have been reported in some cases of cerebral ischemic disease, but no high accumulations of 11C-Met in areas where only transient arterial occlusions are most likely to occur have been reported. Herein we present a case of a high accumulation of 11C-Met in an area of frontal interhemispheric cerebral infarction and a moderately high accumulation with an unclear margin in a distant frontal convexity area. A craniotomy revealed a subacute stage of cerebral infarction in the interhemispheric lesion, and an ischemic change in the distant convexity area. Sixteen months after onset, CT scans demonstrated an infarction area in the interhemispheric lesion only, and no atrophic changes were observed in the distant convexity area indicating that no serious tissue damage had occurred.

Adult↗
PubMed2004

Contralateral cerebral infarction following vacuum extraction.

Cerebral infarction is a rare complication following a vacuum-assisted delivery occurring on the side of the vacuum application and often accompanied by a cephalhematoma. We report a case of cerebral infarction that was contralateral to the side of the vacuum application in a term baby. The baby presented with seizures in the immediate neonatal period. There was no fracture of the skull to account for a contusion injury. We discuss the mechanisms of intracranial vascular injuries during the process of natural and assisted birth.

Adult↗
PubMed1997

[Segmental arteriographic anomalies in migranous cerebral infarct].

A migranous cerebral infarct (ICM) has the appearance of an ischaemic cerebral lesion which occurs during a migraine crisis and is shown by neuroimaging techniques to be in the corresponding vascular area. Four young patients are described. They fulfilled the clinical and neuroimaging criteria for compatibility with ICM and the protocol for the aetiological study of stroke was normal. Angiography ruled out other causes of ischaemia (dissection, fibromuscular dysplasia, etc.) and showed segmental images of 'vasculitis appearance' similar to these described in Call's syndrome, in 'benign intracranial angiopathy' and in other intracranial vasculopathies or criteria of 'reversible segmental cerebral vasoconstriction'. The pathogenic significance, as with migraine, is still unknown.

Adolescent↗
PubMed1985

Snoring and cerebral infarction.

The association of snoring with cerebral infarction was tested in a case-control study of 50 male patients with cerebral infarction and 100 male patients with other disorders. Cerebral infarction was significantly associated with habitual (almost always or always) snoring; the risk ratio of cerebral infarction between those who did and did not snore habitually was 10.3 (95% confidence limits 3.5-30.1). The corresponding risk ratio was 2.8 (95% CL 1.3-5.8) for snoring often, almost always, or always compared with snoring occasionally or never, but the association was still significant. The association was also found when age and body mass index were taken into account.

Adult↗
PubMed1997

Confirmation of CT criteria to distinguish pathophysiologic subtypes of cerebral infarction.

PURPOSE: To determine whether cerebral infarctions classified as embolic or hemodynamic by their appearance on CT scans reflect distinct pathophysiologic entities. METHODS: Cerebral infarctions were retrospectively classified into two groups according to their morphologic appearance on CT scans: territorial infarctions and watershed, or terminal supply area, infarctions. Specific CO2 reactivity for both groups of patients was determined with the xenon-133 method and 32 stationary detectors. Twenty-one patients with unilateral, supratentorial, ischemic cerebral infarctions were selected. CT findings were highly suggestive of a territorial infarction in 14 patients (mean age, 56 years) and of a watershed infarction in seven patients (mean age, 52 years). RESULTS: The initial slope index of the territorial and watershed infarction groups during CO2 inhalation was 55.1 +/- 2.4 sec-1 and 52.0 +/- 1.9 sec-1, respectively, in the infarcted hemispheres and 58.3 +/- 2.3 sec-1 and 55.1 +/- 1.5 sec-1, respectively, in the noninfarcted hemispheres. CO2 reactivity of the unaffected detectors was 1.75 +/- 0.3 sec-1 mm Hg-1 and 1.51 +/- 0.2 sec-1 mm Hg-1 for the territorial and watershed infarction groups, respectively. CO2 reactivity of the affected detectors was 1.75 +/- 0.3 sec-1 mm Hg-1 and 1.27 +/- 0.2 sec-1 mm Hg-1 for the two groups, respectively. The CO2 reactivity difference between affected detectors of the hemodynamic group and age-matched healthy control subjects was significant. CONCLUSIONS: The difference in CO2 reactivity between the two groups supports the concept that CT criteria can identify two pathophysiologic entities. In addition, we conclude that during the chronic stage, lower CO2 reactivity of the watershed infarction indicates that the global hemodynamic situation in these infarcts is more severely compromised than in territorial infarctions.

Aged↗