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Results for “Brain Infarction”

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PubMed1984

Visualization of brain infarction with nuclear magnetic resonance imaging.

Nine patients with cerebral or cerebellar hemispheric infarction and two patients with brain stem lesions were studied with NMR imaging in order to examine the lesion with different weightings on the various NMR parameters. The time interval between examination and the acute onset of the stroke varied from one day to six months. The lesions were clearly detected by the T1 weighted inversion recovery sequence but the tissue contrast was better using the spin echo sequence with a long repetition rate and a long echo delay (SE2000/100). In two patients the brain stem lesions were invisible with CT, but were easily depicted with NMR. In one of them the further progress of the lesion was also confirmed and visualized with the follow-up NMR study.

Adult↗
PubMed1996

Kainate-induced brain lesion: similar local and remote histopathological and molecular changes as in ischemic brain infarct.

Cerebral ischemia/hypoxia induces histopathological changes characterized by nuclear and cytoplasmic condensation and sustained c-fos expression. The ischemic changes are thought to be initiated by excessive glutamate released by the ischemic neurons. However, no comparative study has been made between the pathological and molecular changes caused by local injection of excitotoxin and by ischemia. In the present study, we investigated the histopathological changes in rat brains induced by an intracerebral microinjection of kainic acid, a potent analogue of glutamate using two newly available markers for ischemic neurons: Fos immunohistochemistry and EA 50 stain. The rats were sacrificed at intervals from 1 hour (h) to 28 days. We demonstrated that the neurons at the site of injection developed changes typical of ischemia 1 h post-lesion: nuclear and cytoplasmic condensation, strong Fos immunoreactivity and positive EA 50 stain. By 1 day, the neurons underwent necrosis and an infarct-like picture was produced. The neuronal degeneration rapidly spread to the bilateral neocortex, CA3 and CA4 regions of hippocampus, piriform gyrus, amygdala and cerebellar Purkinje cells. After 3 days, there was neovascularization and macrophage production in the lesion center and astrocytic proliferation at the lesion periphery. The CA1 of hippocampus showed delayed neuronal necrosis typical of ischemia. Thus, intracerebral microinjection of KA induces similar histopathological and molecular changes as those occurring in brain infarct and is a simple and reliable model for studying changes related to focal brain infarct.

Animals↗
PubMed2004

Silent brain infarcts in patients with manifest vascular disease.

BACKGROUND AND PURPOSE: Silent infarcts are frequently found on MRIs of brains of healthy elderly persons (aged >60 years). The purpose of this study was to investigate the prevalence and determinants of silent infarcts in a population of patients with clinically manifest vascular disease. METHODS: To detect silent infarcts, MR images were made in 308 participants of the Second Manifestations of ARTerial disease (SMART) study (mean age, 58 years) without prior stroke or transient ischemic attack. These are patients referred to the University Medical Center Utrecht because of atherosclerotic vascular disease. Risk factors were assessed by questionnaire and by physical, ultrasonographic, and laboratory examinations. RESULTS: Silent infarcts were found in 51 patients (17%). Most infarcts (62%) were located in white matter, 20% in basal ganglia, 14% in brain stem and cerebellum, and 4% in cortical area. Categorical determinants for presence of silent infarct(s) that remained (borderline) significant after adjustment for age were hypertension (odds ratio [OR]=2.2; 95% CI, 1.2 to 4.2), abdominal aortic aneurysm (OR=2.4; 95% CI, 0.9 to 6.4), severe renal failure (OR=7.3; 95% CI, 2.1 to 25.2), and hyperhomocysteinemia (OR=2.6; 95% CI, 1.1 to 5.9). CONCLUSIONS: Patients with manifest vascular disease are at risk for silent infarcts at a younger age. In particular, patients with the aforementioned risk factors should be considered for treatment or (secondary) prevention.

Adult↗
PubMed2000

Hyperkinetic movement disorders caused by corpus striatum infarcts: brain MRI/CT findings in three cases.

Three patients with hemichorea/hemiballismus/hemidystonia caused by discrete contralateral infarction of the corpus striatum are presented. The infarcts were all small on CT or MRI brain scan and were lacunar in type. Small discrete infarction of basal ganglionic structures allows such adventitious movements to be manifested. Involvement of contiguous areas, seen with larger infarcts, can suppress such movements. The infrequency of such hyperkinetic movement disorders, and the subtle infarct appearance on brain scan, can lead to a delay in the diagnosis.

Adult↗
PubMed1996

VEGF and flt. Expression time kinetics in rat brain infarct.

BACKGROUND AND PURPOSE: Vascular endothelial growth/vascular permeability factor (VEGF) is a candidate for an angiogenic and hyperpermeability inducing factor in an infarct because it is a secretable mitogen specific for endothelial cells and is upregulated by hypoxia. Our study attempts to clarify the chronological expression of VEGF and its receptor (flt) system in experimental cerebral infarction. METHODS: With the use of a reproducible middle cerebral artery occlusion model in rats, VEGF expression was identified by Western blotting with anti-VEGF antibody. The chronological expression of the VEGF/flt system was analyzed semiquantitatively by immunohistochemical means in infarcts with different time courses from 3 hours to 3 weeks. RESULTS: VEGF and flt were expressed exclusively in the ischemic brain. The bands obtained on the immunoblot at 38 and 45 kD are related to those of VEGF121 and VEGF165 isoforms. Macrophages, neurons, and glial cells chronologically expressed VEGF immunoreactivity in a different fashion. Both VEGF (bound) and flt were detected in endothelial cells along with the development of angiogenesis. CONCLUSIONS: In the ischemic brain the macrophages, neurons, and glial cells appear to contain VEGF. The VEGF receptor flt was induced in endothelial cells along with the progression of angiogenesis in infarct. The VEGF/flt system is thus considered to be involved in the healing process of brain infarct.

Animals↗
PubMed1999

Single lacunar brain infarction with transient signs versus those with long-lasting signs.

BACKGROUND: In order to find out the difference between single brain lacunar infarctions with transient signs and those with long-lasting signs, cerebral blood flow studies and blood tests were performed. METHODS: Ten cases of single lacunar infarction with transient signs and 10 of single lacunar infarction with long-lasting signs were studied. Subcortical cystic infarctions with a diameter of less than 1.5 cm were defined as lacunar infarction. Episodes lasting less than 24 hours were classified as transient signs and those lasting 24 hours or more as long-lasting signs. MEASUREMENTS: cerebral blood flows were measured using the stable xenon computed tomography method. The regional cerebral blood flows were measured before and 20 minutes after the intravenous injection of 17 mg/kg acetazolamide. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were determined at the Special Reference Laboratories. RESULTS: Blood flows in the cerebral cortex and cerebral white matter contralateral to the lacunar infarction were lower in the group with long-lasting signs than in that with transient signs. Cerebrovascular acetazolamide reactivity in the cerebral cortex and white matter contralateral to the lacunar infarction were lower in the group with long-lasting signs than in that with transient signs. Plasma fibrinopeptide A, platelet factor 4 and beta-thromboglobulin concentrations were higher in the long-lasting signs group than in that with transient signs. CONCLUSIONS: There may be some differences in pathogenesis between single lacunar infarction with transient signs and those with long-lasting signs.

Acetazolamide↗
PubMed1992

In vivo relaxation of N-acetyl-aspartate, creatine plus phosphocreatine, and choline containing compounds during the course of brain infarction: a proton MRS study.

Localized water suppressed proton spectroscopy has opened up a new field of pathophysiological studies of severe brain ischemia. The signals obtained with the pulse sequences used so far are both T1 and T2 weighted. In order to evaluate the extent to which changes in metabolite signals during the course of infarction can be explained by changes in T1 and T2 relaxation times, eight patients with acute stroke were studied. STEAM sequences with varying echo delay times and repetition times were used to measure T1 and T2 of N-acetyl-aspartate (NAA), creatine plus phosphocreatine (Cr+PCr) and choline containing compounds (CHO) in a 27-ml voxel located in the affected area of the brain. Ten healthy volunteers served as controls. We found no difference in T1 or T2 of the metabolites between the patients and the normal controls. The T2 of CHO was longer than that of NAA and Cr+PCr. Our results indicate that spectra obtained in brain infarcts and normal tissue with the same acquisition parameters are directly comparable with respect to relative signal intensities as well as signals scaled with internal and external standards.

Adult↗
PubMed1986

Morphometric evaluation of brain infarcts in rats and gerbils.

The Levine rat preparation, the gerbil stroke model, and appropriate control animals were used to determine if the 2,3,5-triphenyltetrazolium chloride (TTC) would selectively identify noninfarcted versus infarcted cerebral tissue. The TTC is frequently used to quantify infarcted myocardial tissue and has been shown to have great specificity, reproducibility, and efficacy. The TTC produces a red product upon reaction with the respiratory enzymes (dehydrogenases) present in non-infarcted tissues. Irreversibly damaged tissues, lacking dehydrogenases, do not form red reaction products. Six gerbil brains and seven rat brains were incubated with the TTC, and the unreacted areas were macroscopically identified. The brains were fixed and sectioned for routine hematoxylin and eosin staining to determine the specificity of the TTC. The TTC was found to react selectively only with non-infarcted cerebral tissue. The gross brain sections were evaluated by macroscopic morphometric analysis, and the unreacted area was always ipsilateral to ligation and correlated with histologic identification of infarct. The brains from neurologically intact animals demonstrated neither macroscopic nor histological evidence of infarction. This technique allows macroscopic quantification of infarct size by planimetry. The average area of infarct for the neurologically impaired rats was 34.7% and it was 31.4% for the impaired gerbils. The percentage of surface area of each infarcted slice was found to correlate with the severity of the neurologic deficit. We conclude that TTC staining is effective for macroscopically delineating cerebral infarcts in rats and gerbils, thus permitting quantification of infarct size.

Animals↗
PubMed1999

Prevalence and associations of MRI-demonstrated brain infarcts in elderly subjects with a history of transient ischemic attack. The Cardiovascular Health Study.

BACKGROUND AND PURPOSE: MRI is more sensitive than CT, but the significance of brain abnormalities seen on MR images obtained in older subjects with transient ischemic attack (TIA) is not clear. We studied the prevalence and risk factors associated with MRI-demonstrated infarcts in elderly subjects with a history of TIA. METHODS: Participants of the Cardiovascular Health Study, aged 65 years or more and without prior stroke, were studied with brain MRI (n=3456). The prevalence of brain infarcts (>/=3 mm) on MRI was determined in subjects with and without TIA. The cardiovascular risk factors and clinical and subclinical cardiovascular disease associated with MRI infarcts were studied in subjects with TIA. RESULTS: Subjects with TIA (n=100) had a higher prevalence of MRI infarcts than subjects without TIA (46% versus 28%; P<0.001). The unadjusted odds ratio for having MRI infarcts in subjects with TIA was 2.20 (95% CI, 1.47 to 3.30) and remained significantly elevated after adjustments for risk factors and cerebrovascular disease (odds ratio, 1.86; 95% CI, 1.23 to 2.83). In subjects with TIA, diastolic blood pressure (P=0.01) and internal carotid artery intima-media thickness (P=0.01) were the only factors predictive of the presence of MRI infarcts by stepwise logistic regression analysis. CONCLUSIONS: MRI infarcts are imaging manifestations of clinically important cerebrovascular disease in subjects with a history of TIA, given their increased prevalence and positive association with increased diastolic blood pressure and internal carotid artery intima-media thickness.

Aged↗