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PubMed1996

Gender influences the magnitude of the inflammatory response within embolic cerebral infarcts in young rats.

BACKGROUND AND PURPOSE: The inflammatory response within cerebral infarcts may have an influence on tissue damage. Since old animals with an impaired immune response have decreased inflammation after experimental cerebral infarction, we postulated that female animals with an increased immune response will have an increased inflammatory response after cerebral infarction. METHODS: Embolic cerebral infarcts were produced by photochemical irradiation of the right carotid artery in 12 female Fischer rats. The inflammatory response within 4-day-old infarcts was quantitated by histology with the use of computer-assisted image analysis and compared with that in 12 male rats from a previous series. RESULTS: Severe infarcts had the most pronounced inflammatory response. Female rats had an increased inflammatory response in infarcts of all severity, which was statistically significant in severe cerebral infarcts even after adjustment for infarct size. Severe infarcts in males were significantly larger than those in females. CONCLUSIONS: Gender influences the outcome of embolic cerebral infarcts after photochemical damage to the carotid artery, both in terms of the magnitude of the inflammatory response and infarct size. There are numerous gender-related differences in neurochemicals, cytokine production, and drug metabolism that may influence tissue damage after stroke and responsiveness to therapeutic intervention. The preponderance of male animals in stroke research may produce results not applicable to female stroke patients. The use of female animals will be required to provide adequate models for the study of stroke in women.

Animals↗
PubMed1995

The use of computed tomography in the prediction of delayed cerebral infarction following acute aneurysm surgery for subarachnoid haemorrhage.

In order to predict the occurrence of cerebral infarction after aneurysmal surgery in patients with subarachnoid haemorrhage, we measured the amount of subarachnoid blood on initial and on postoperative computed tomograms. We used a reliable grading method to estimate the amount of blood on computed tomograms in 24 patients with infarction due to vasospasm and 45 patients without cerebral infarction, all of whom underwent aneurysmal surgery within 48 hours after the ictus. The total amount of subarachnoid blood on admission and on the day after operation was more in the cerebral infarction group than in the non-infarction group. The clearance rate of subarachnoid blood by surgery was lower in patients with cerebral infarction than in patients without infarction and the predominant site of subarachnoid blood corresponded with the site of the infarct. Of 24 patients with cerebral infarction, 22 (92%) belonged to the group whose initial total blood score was more than 10 on admission and whose clearance rate by surgery was less than 50%. Therefore, we propose this range to be an indication for the occurrence of cerebral infarction in postoperative patients due to cerebral vasospasm. The presence of intracerebral haematoma and the amount of ventricular blood and their clearance by surgery were also estimated for the prediction of delayed cerebral infarction after aneurysmal surgery. However, they had no relation to the occurrence of cerebral infarction due to vasospasm.

Adult↗
PubMedDate not supplied

Posttraumatic cerebral infarction diagnosed by CT: prevalence, origin, and outcome.

Posttraumatic cerebral infarction is a recognized complication of craniocerebral trauma, but its frequency, cause, and influence on mortality are not well defined. To ascertain this information, all cranial CT studies demonstrating posttraumatic cerebral infarction and performed during a 40-month period at our trauma center were reviewed. Posttraumatic cerebral infarction was diagnosed by CT within 24 hr of admission (10 patients) and up to 14 days after admission (mean, 3 days) in 25 (1.9%) of 1332 patients who required cranial CT for trauma during the period. Infarcts, in well-defined arterial distributions, were diagnosed either uni- or bilaterally in the posterior cerebral (17), proximal and/or distal anterior cerebral (11), middle cerebral (11), lenticulostriate/thalamoperforating (nine), anterior choroidal (three), and/or vertebrobasilar (two) territories in 23 patients. Two other patients displayed atypical infarction patterns with sharply marginated cortical and subcortical low densities crossing typical vascular territories. CT findings suggested direct vascular compression due to mass effects from edema, contusion, and intra- or extraaxial hematoma as the cause of infarction in 24 patients; there was postmortem verification in five. In one patient, a skull-base fracture crossing the precavernous carotid canal led to occlusion of the internal carotid artery and ipsilateral cerebral infarction. Mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction, 68% in this series, did not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow Coma Score results. Thus, aggressive management should be considered even in the presence of posttraumatic cerebral infarction.

Adult↗
PubMed1990

Posttraumatic cerebral infarction diagnosed by CT: prevalence, origin, and outcome.

Posttraumatic cerebral infarction is a recognized complication of craniocerebral trauma, but its frequency, cause, and influence on mortality are not well defined. To ascertain this information, all cranial CT studies demonstrating posttraumatic cerebral infarction and performed during a 40-month period at our trauma center were reviewed. Posttraumatic cerebral infarction was diagnosed by CT within 24 hr of admission (10 patients) and up to 14 days after admission (mean, 3 days) in 25 (1.9%) of 1332 patients who required cranial CT for trauma during the period. Infarcts, in well-defined arterial distributions, were diagnosed either uni- or bilaterally in the posterior cerebral (17), proximal and/or distal anterior cerebral (11), middle cerebral (11), lenticulostriate/thalamoperforating (nine), anterior choroidal (three), and/or vertebrobasilar (two) territories in 23 patients. Two other patients displayed atypical infarction patterns with sharply marginated cortical and subcortical low densities crossing typical vascular territories. CT findings suggested direct vascular compression due to mass effects from edema, contusion, and intra- or extraaxial hematoma as the cause of infarction in 24 patients; there was postmortem verification in five. In one patient, a skull-base fracture crossing the precavernous carotid canal led to occlusion of the internal carotid artery and ipsilateral cerebral infarction. Mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction, 68% in this series, did not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow Coma Score results. Thus, aggressive management should be considered even in the presence of posttraumatic cerebral infarction.

Adult↗
PubMed2005

Relation of serum total cholesterol and other factors to risk of cerebral infarction in Japanese men with hypercholesterolemia.

BACKGROUND: Risk factors for cerebral infarction have not been well clarified, except for hypertension (HT), and few studies have examined the risk factors in the elderly. METHODS AND RESULTS: Clinical and behavioral risk factors for cerebral infarction were examined in 4,349 Japanese men aged 45-74 years with a serum total cholesterol (TC) concentration of 220 mg/dl or greater who participated in the Kyushu Lipid Intervention Study. A total of 81 men developed definite cerebral infarction in a 5-year follow-up period. The Cox proportional hazards model was used with serum TC at baseline and during the follow-up, serum high-density lipoprotein-cholesterol (HDL-C), HT, diabetes mellitus (DM), and other factors as covariates. Serum TC during the follow-up, not at baseline, was positively associated with cerebral infarction, showing a stronger association in the elderly (>or=65 years old) than in the middle-aged (<65 years old). Statin use was related to a moderate decrease in the risk of cerebral infarction when follow-up TC was not considered, but the decrease was almost nullified after adjustment for follow-up TC. A low concentration of serum HDL-C, diabetes mellitus, hypertension, and angina pectoris were each related to an increased risk. No clear association was observed for body mass index, smoking or alcohol use. CONCLUSIONS: Lowering cholesterol is important in the prevention of cerebral infarction in men with moderate hypercholesterolemia. A low concentration of HDL-C, DM, and HT are independent predictors of cerebral infarction.

Aged↗
PubMedDate not supplied

Epidemiologic studies of stroke in Shibata, a Japanese provincial city: preliminary report on risk factors for cerebral infarction.

A 6.5-year prospective study of cerebral infarction among residents 40 years and older was conducted at the Akadani-Ijimino district in Shibata City, Niigata Prefecture, Japan. The response rate for the initial examination was 85% of 1,182 males and 93% of 1,469 females. Nine hundred and sixty males and 1,339 females who were initially free of stroke were followed up from July 1977 through December 1983. Statistically significant risk factors for cerebral infarction appeared to be age, elevated blood pressure, high R, ST-T changes and atrial fibrillation on ECG, and albuminuria. The ECG abnormalities and albuminuria were due to the high blood pressure persisted over a long period of time. The strength of association of blood pressure with cerebral infarction got weak in comparison with other factors, and funduscopic changes which had been regarded as a risk factor for stroke in 1965-1974 did not reach statistical significance because of the spread of the community-based hypertension control. Even in 1977-1983 when Japanese dietary habits were westernized, neither hyperlipidemia nor obesity appeared to be related to the development of cerebral infarction.

Adult↗
PubMed1994

Accumulation of L-[2-(F-18)]fluorophenylalanine in peri-infarct area in a patient with acute cerebral infarction.

We studied the brain uptake of amino acid in a patient with acute cerebral infarction with L-[2-(F-18)]fluorophenylalanine and positron emission tomography. The increased accumulation of the ligand was specifically found in the peri-infarct area where oxygen metabolism was still maintained but decreased later in the 72-day follow-up period. The kinetic analysis revealed that increased accumulation was not due to increased transport from the blood to the brain but delayed washout from the brain to the blood. Although the mechanism is still unknown, abnormally high accumulation of L-[F-18]fluorophenylalanine may predict delayed neuronal changes after ischemic insults of the brain.

Aged↗
PubMedDate not supplied

Neurological deficit and cerebral infarction after temporary middle cerebral artery occlusion in unanesthetized cats.

Forty-four unanesthetized cats underwent temporary middle cerebral artery (MCA) occlusion with an implanted, externally controlled balloon cuff occluder. The occlusion was reversed to allow reperfusion of the MCA after 2 min to 24 hr of ischemia. Fourteen cats had temporary occlusions lasting 2 min to 3 hr; their neurological deficits improved or resolved after reperfusion, and brain sections showed only scattered microscopic areas of necrosis. After a 4-hr occlusion, five of nine cats (55%) recovered completely within 24 hr; two had persistent deficit when sacrificed, 10 days later, and each had a circumscribed infarct. All 18 cats undergoing 5-, 6-, 8-, and 24-hr occlusions sustained permanent neurological deficits. Three 3-hr occlusions at 2-day intervals in three cats resulted in permanent deficits and infarcts that were 25% larger than those after single 8-hr occlusions. Ten cats underwent permanent MCA occlusion; three deteriorated neurologically and died, and the survivors showed no improvement. Infarcts after 5-, 6-, and 8-hr occlusions followed by reperfusion were 66% smaller (p less than 0.05) than those after permanent occlusion; reperfusion after 24 hr of occlusion did not reduce infarct size. Hemorrhagic infarction occurred after two permanent occlusions, but after only one 5-hr temporary occlusion. The results obtained with this method of temporary regional ischemia indicate that restoration of flow after 1-8 hr, but not after 24 hr, of MCA occlusion resulted in less severe neurological deficit and smaller infarcts than did permanent occlusion. The infarct size correlated with the duration of MCA occlusion (p less than 0.05) rather than with the degree of deficit during occlusion.

Animals↗
PubMed2004

Early external decompressive craniectomy with duroplasty improves functional recovery in patients with massive hemispheric embolic infarction: timing and indication of decompressive surgery for malignant cerebral infarction.

BACKGROUND: Extensive cerebral hemispheric infarction associated with massive brain swelling is known as malignant infarction because of the rapid clinical deterioration and mortality as high as 80% unless appropriate treatment is performed. Decompressive craniectomy is an effective treatment, but patient selection, timing, functional recovery, and complications remain unclear. METHODS: Seventy-one patients with massive embolic hemispheric infarctions (infarct volume >200 cm(3)) associated with brain swelling were retrospectively divided into 3 groups according to the therapeutic modalities: 21 patients were treated conservatively (conservative group); 50 patients were treated by external decompressive craniectomy with duroplasty in 2 groups; 29 patients treated after the appearance of clinical and radiologic findings of brain herniation (late surgery group); and 21 patients treated before the onset of brain herniation (early surgery group). RESULTS: The mortality at 1 and 6 months in the conservative group were 61.9% and 71.4%, respectively. The mortality at 1 and 6 months in the late surgery group were significantly improved to 17.2% and 27.6%, respectively, (p < 0.01) and in the early surgery group were further improved to 4.8% and 19.1%, respectively. The functional recovery of the patients was estimated by the Glasgow Outcome Scale (GOS) and Barthel Index (BI) at 6 months after the ictus. The GOS scores of the early surgery group were significantly better than that of the late surgery group (p < 0.05). The mean BI score of the survivors in the late surgery group (26.9 +/- 30.4) was not significantly different from that of the conservative group (28.3 +/- 42.2), but was significantly improved in the early surgery group (52.9 +/- 34.2) compared with the late surgery group (p < 0.05). CONCLUSIONS: Early decompressive craniectomy with duroplasty before the onset of brain herniation should be performed to achieve satisfactory functional recovery if the infarct volume of the hemispheric cerebral infarction is more than 200 cm(3) and computed tomography on the second day after the ictus shows mass effect.

Adult↗
PubMed1995

[An analysis on the activity status of fibrinolytic system in Chinese patients with acute cerebral infarction].

The fibrinolytic activity status of the patients with cerebral infarction can affect their clinical prognosis. In this case-controlled study, the plasma fibrinolytic system activities in 30 cases of cortical artery territory cerebral infarction (CACI) and 32 cases of perforating artery territory cerebral infarction (PACI) with a disease duration less than 3 days were assayed with a comprehensive panel including the plasma tPA activity, PAI activity, tPA releasing capacity from vascular endothelium and PAI/tPA ratio values. 30 subjects without cardiovascular and cerebrovascular disorders were served as control. The results showed that the plasma fibrinolytic system activities of the patients with aforementioned two subtypes of cerebral infarction were significantly lower than those of the controls, the results provide a theoretical basis for carrying out thrombolytic therapy in patients with ischemic stroke and suggest that recurrent cerebral infarction might be related to the high activity of plasma PAI.

Adult↗
PubMed2003

Effect of salvia miltiorrhiza bunge on cerebral infarct in ischemia-reperfusion injured rats.

According to the theory of traditional Chinese medicine, cerebral infarction results from blood stasis, and the method of quickening the blood and dispelling stasis is used to treat cerebral infarct. salvia miltorrhiza bunge (SM) is a Chinese herb, which is considered to have an action of quickening the blood and dispelling stasis, and is frequently used to treat related disorders of blood stasis such as cerebrovascular accident and ischemic heart disease. The aim of the present study was to investigate the effect of SM on cerebral infarct in ischemia-reperfusion injured rats. A total of 30 Sprague-Dawley (SD) rats were studied. A model of focal cerebral infarct was developed by occluding both common carotid arteries and the right middle cerebral artery for 90 minutes. After 24 hours reperfusion, the rats were killed and the brain tissue was stained with 2, 3, 5-triphenyl-tetrazolium chloride (TTC). The areas of cerebral infarct were calculated, and lumino-chemiluminesence (CL) counts and lucigenin-CL counts of peripheral blood taken at this time were measured. The changes in the area of cerebral infarct were used as an index to evaluate the effect of SM on cerebral infarct. The results indicated that pretreatment with intraperitoneal injection of 30 mg/kg and 15 mg/kg SM reduced the area of cerebral infarct and also reduced the luminol-CL counts of peripheral blood in ischemia-reperfusion injured rats. This study has demonstrated that SM can reduce the area of cerebral infarct in ischemia-reperfusion injured rats, suggesting it may be useful in the treatment of cerebral infarct in humans. The therapeutic effect of SM may be partly due to its free radical scavenging activities.

Acridines↗
PubMed2001

Cerebroprotective action of a Na+/Ca2+ channel blocker NS-7. II. Effect on the cerebral infarction, behavioral and cognitive impairments at the chronic stage of permanent middle cerebral artery occlusion in rats.

We have previously shown that NS-7 [4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy)pyrimidine hydrochloride] reduces the size of cerebral infarction measured by 2,3,5-triphenyltetrazolium chloride staining at 48 h after permanent middle cerebral artery occlusion (MCAO) in rats. To determine whether NS-7 improves the pathological and behavioral changes at the chronic stage of MCAO, the effect of this compound on the cerebral infarction as well as the neurological and cognitive impairments was investigated 7 days after MCAO. Single or five daily injections of NS-7 (0.125-0.5 mg/kg, i.v.) significantly reduced the infarct volume and improved the neuronal dysfunction including the hind leg paralysis, walking disability and motor incoordination, and the deficit of passive avoidance task, although the neuroprotective efficacy was not different among these dosing regimens. On the other hand, the effects of single versus repeated injections of NS-7 at 0.1 or 0.2 mg/kg on the neurological symptoms were compared at 4 weeks after MCAO. At a lower dose, repeated but not single injection of NS-7 significantly improved the neurological symptoms, although the single injection was effective at a higher dose. From these findings, it is suggested that NS-7 reverses the behavioral and cognitive dysfunction observed at the chronic stage of cerebral ischemia by suppressing the cerebral infarction.

Animals↗
PubMed1990

[Relation of the changes in hemorheologic indices and the site and size of cerebral infarction].

According to the CT findings, 83 cases of cerebral infarction were divided into two groups. One group consisted of cases with occlusion of the cerebral arterial main trunks and the other of those with occlusion of the penetrating arteries. The HCT and the whole blood viscosity were higher in the former group, whereas the rate of platelet aggregation was higher in the latter group. These results suggested that the physiopathology involved in the formation of the large cerebral infarction in the cerebral cortex and subcortex was different from that of the small infarction in the deep cerebral structures. Besides, it was found that the blood viscosity has positive relationship with the size of the cerebral infarction in the former group. It was presumed that the HCT and the blood viscosity should be reduced immediately for treating the larger cerebral infarction, but to lower the rate of platelet aggregation for treating the small infarction in the deep cerebral structures would be of benefit.

Adult↗
PubMed1984

Atrial fibrillation as a cause of myocardial and cerebral infarctions.

Pathogenetic role of atrial fibrillation (AF) on myocardial and cerebral infarctions was studied in 2340 consecutive autopsies of the aged. AF was found in 405 cases or 17.3%, and the incidence of AF increased with age. Myocardial infarction and scar were found in 56.8% in AF, but in 36.4% in non-AF (p less than 0.001). Small myocardial infarction was 2.9 times (12.6% vs. 4.3%), and the scar was 1.5 times (27.2% vs. 18.7%) as prevalent in AF as in non-AF. Intracardiac mural thrombus was found in 14.8% in AF and in 4.8% in non-AF, 8 to 10 times as prevalent in small myocardial infarction (29.4% vs. 3.7%) and scar (17.4% vs. 1.7%) in AF as in non-AF. Coronary stenotic index revealed no difference between AF and non-AF. Large cerebral infarction was observed in 21.9% in AF and 7.3% in non-AF, and this difference was prominent in cases with myocardial infarction or myocardial scar indicating the common pathogenetic role of AF. In cases with large cerebral infarction severe cerebral atherosclerosis was less frequent in AF than in non-AF. Medium sized cortical infarction was also prevalent in AF. The prevalences of myocardial and cerebral infarctions were not different in AF complicated with valvular heart disease from those without it, but increased in the permanent AF in comparison to the transient AF. AF induced small myocardial infarction and large or medium sized cerebral infarctions by embolism from mural thrombus. The mechanism for the difference in size is discussed.

Aged↗
PubMed1998

[Prevention of cerebral infarct caused by atherosclerosis].

Atherosclerosis of the cerebral arteries is the main cause of cerebral infarction but the frequency with which this cause is implicated is very variable from one trial to another depending on the criteria used. Primary prevention of this type of infarction is mostly based on the correction of arterial risk factors and on carotid artery surgery in selected cases. Aspirin does not appear to the effective in this indication. The respective indications of heparin and aspirin in the acute phase of cerebral infarction remain controversial despite the recent publications of large scale therapeutic trials. The benefits of these treatments is, at best, globally modest. Thrombolytics could, on the other hand, revolutionize the treatment of acute cerebral infarction if the encouraging results of a recent trial using rt-PA in the first 3 hours, are confirmed by other trials. After the acute phase, antiplatelet agents (aspirin, ticlopidine, clopidogrel or aspirin associated with dipyridamole) and surgery in patients with symptomatic carotid artery stenosis greater than 50% or 70-80% (according to the method of measurement) have been shown to be effective. Several large scale trials are under way to assess the benefits and risks: a) of antihypertensive therapy in patients with previous cerebrovascular accidents, b) of treatment with statins of patients at high risk of infarction due to atherosclerosis, c) of oral anticoagulants at low dosage (versus antiplatelet agents) in secondary prevention, d) of thrombolytics in the acute phase of cerebral infarction, e) of carotid angioplasty (versus surgery) in patients with symptomatic severe stenosis.

Arteriosclerosis↗
PubMedDate not supplied

Double-blind controlled trial of prostacyclin in cerebral infarction.

Thirty-two patients with acute cerebral infarction received either prostacyclin or placebo intermittently for 65 hours. Pulse and blood pressure were not altered by prostacyclin. After infusion there was no change in infarct volume or cerebral blood flow in either group. After normalisation for starting values, age and site of cerebral infarction there was a greater than 10% improvement in speech in the prostacyclin group, but minimal changes in neurological score or disability status. Age is related to neurological score at 14 days after stroke by decreasing improvement by 6.8% for each additional 10 years. This study has not been able to demonstrate that prostacyclin is effective in the treatment of ischaemic stroke, but due to the sample size the chance of proving this statistically (the power) was small. Similarly any conclusion that prostacyclin is not effective may be wrong because of the Type II error probability being high.

Aged↗
PubMed2002

Effects of selective beta2 and beta3-adrenoceptor agonists on detrusor hyperreflexia in conscious cerebral infarcted rats.

PURPOSE: We evaluated the effects of beta-adrenoceptor agonists on detrusor hyperreflexia in cerebral infarcted rats. MATERIALS AND METHODS: To produce cerebral infarction in Sprague-Dawley rats the left middle cerebral artery was occluded by introducing a monofilament nylon thread into the artery. In sham operated rats the same artery was exposed but not occluded. After these operations cystometric and cardiovascular experiments were performed with no anesthesia or restraint. RESULTS: After the operation bladder capacity was significantly decreased and voiding pressure was significantly increased in cerebral infarcted but not in sham operated animals. The difference in cerebral infarcted and sham operated rats was significant for each parameter (p <0.01). Post-void residual urine volume was not affected in either group. In the cerebral infarction group intravenous administration of CL316243 ([R,R]-5-2-[[2-(3-chlorophenyl-2-hydroxyethyl]-amino]propyl] -1,3-benzodioxole-2,2-dicarboxylate) (Kissei Central Laboratories, Hotaka, Japan) a selective beta3-adrenoceptor agonist, significantly increased bladder capacity at 10 and 100 microgram./kg. without affecting voiding pressure or post-void residual urine volume. Procaterol, a selective beta2-adrenoceptor agonist, significantly increased bladder capacity and post-void residual urine volume at 10 microgram/kg. intravenously without affecting voiding pressure. In separate experiments procaterol (1 to 100 microgram./kg. intravenously) decreased mean blood pressure and increased heart rate in a dose dependent manner. In contrast, the effects of CL316243 (0.1 to 100 microgram./kg. intravenously) on mean blood pressure and heart rate were minimal. CONCLUSIONS: These results indicate that in cerebral infarcted rats detrusor hyperreflexia can be suppressed by the selective beta3-adrenoceptor agonist CL316243 without increasing post-void residual volume and without significant cardiovascular side effects. If the current results hold true in humans, selective beta3-adrenoceptor agonists may prove useful for treating detrusor hyperreflexia associated with cerebral infarction.

Adrenergic beta-2 Receptor Agonists↗
PubMed2004

Hemicraniectomy for massive cerebral infarction.

The most important acute phase complication of massive cerebral infarction is cerebral herniation secondary to brain edema. In the past decade, there has been heightened interest in surgical treatment of this problem with the use of the techniques of hemicraniectomy and dural augmentation. In this article, we review the theoretical and clinical data supporting the use of hemicraniectomy in malignant cerebral infarction and the range of outcomes expected in patients who undergo this procedure.

Brain Diseases↗