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PubMed2005

Risk of carotid endarterectomy in patients with cerebral infarction.

Stroke is a clinical diagnosis, but there is uncertainty as to the relative risks of surgery in patients with a visible infarction on brain CT. It is not clear whether visible infarction is associated with higher operative risk and poor outcome or is simply an indicator of a more "severe" stroke. Some studies have indicated that CT evidence of stroke carries an increased risk, other studies have found that patients with a low density and without significant shift on CT, with a stable neurological deficit and a normal level of consciousness can safely undergo carotid endarterectomy. Our aim was to answer a the specific question whether visible brain infarction on CT increases the operative risk of carotid endarterectomy, with special attention to the neurological complications. This analysis involved 105 patients with a visible brain infarct on CT scan who underwent carotid endarterectomy in Vilnius University Emergency Hospital. Carotid endarterectomy was performed in 86 men and in 19 women with mean carotid stenosis 87%, ranging from 42% to 99% by angiography. Clinical symptoms of stroke were present in 95 patients (86 carotid and 9 vertebrobasilar). Carotid endarterectomy underwent 76 patients with symptomatic carotid stenosis, 16 patients with symptoms of contralateral carotid artery, 9 patients with vertebrobasilar symptoms and 4 patients with nonspecific symptoms. Among symptomatic patients there were 46 patients with unilateral carotid stenosis and 30 patients with bilateral stenosis. Angiography of asymptomatic patients (n=29) revealed unilateral carotid lesions in 9 cases, bilateral stenosis in 8 patients and concomitant bilateral carotid and vertebral stenosis in 12 patients. The postoperative mortality rate was 2.9%, a new stroke occurred in 1.9%. The total rate of complications--4.8%. Patients with visible brain infarction on CT scan can safely undergo carotid endarterectomy with a standard operative risk, but risks modelling will be required if we are to target surgery most effectively at individuals.

Adult↗
PubMed2000

Volumetric measurements of right cerebral hemisphere infarction: use of a semiautomatic MRI segmentation technique.

The applications of a new segmentation software, Anatomatic, in the evaluation of volumetric measurements of brain infarctions and the new Medimag 3D software in the evaluation of 3D image representation of infarctions are described. These programs are applied to magnetic resonance imaging. The aim of this study is to evaluate the use of these software packages in making accurate volumetric measurements in 40 patients with right cerebral infarctions, in determining the correlations between the quantitated lesions and neurological/neuropsychological dysfunctions and in creating realistic 3D views of the infarctions. Using Anatomatic, reproducible infarction volumes were achieved with ease and within a reasonably fast time. Medimag helped achieve realistic 3D representations of the infarctions. When compared, the semiautomatic segmentation proved to be much faster and yielded higher infarction volumes than the manual segmentation technique. Significantly positive correlations between the infarction volumes and neurological dysfunctions and neuropsychological deficit (neglect) helped to explain the effect of volumes on the clinical status of the patients.

Adult↗
PubMed1992

[Adverse prognostic influence of diabetes mellitus and hyperglycemia on the clinical course of cerebral infarction].

We accessed the potential impact of diabetes mellitus and hyperglycemia on early prognosis in a study of 109 cases of CT proved brain infarction. Main end-points of this study were 30-days case-fatality rates and the probability of early discharge or prolonged hospitalization. Proportions of patients exhibiting diverse evolutions were compared by Fisher's test and, when the number of observations permitted, by chi-square test. Diabetes mellitus was diagnosed by history in 15.6% (17 patients). In 86 cases analysed within 72 hours of admission, hyperglycemia (glucose level higher than 110 mg/dL) was detected in 67.4% (including all 14 diabetic patients (35.3% vs 21.7%; p = 0.18), but these patients probably were discharged early less frequently (23.5% vs 51.1%; p = 0.06). Compared to the normoglycemic patients, hyperglycemic patients also fared worse, when considering altogether the early discharge and case fatality rates and the need for prolonged hospitalization (p = 0.06). They also exhibited a nonsignificant increase in early case fatality rate (31% vs 15.4%; p = 0.21) and a markedly reduced chance of obtaining early hospital discharge (37.9% vs 65.4%; p = 0.03). Case fatality rates were maximal in diabetic hyperglycemic patients (42.9%) and seemed intermediate in non-diabetic hyperglycemic patients (27.3%). Considering the three end-points evaluated, the apparent differences between non-diabetic hyper and normoglycemic patients did not reach statistical significance (p = 0.19). These results suggest that both diabetes mellitus and hyperglycemia "per se" have deleterious effects on the clinical evolution of patients with cerebral infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

AMPA receptor antagonist, YM90K, reduces infarct volume in thrombotic distal middle cerebral artery occlusion in spontaneously hypertensive rats.

We examined the effects of a potent and selective antagonist of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) subtype of glutamate receptor, YM90K, on brain infarction using a newly developed stroke model of thrombotic distal middle cerebral artery occlusion. Male spontaneously hypertensive rats (5-7 months old) were subjected to photochemically-induced distal middle cerebral artery occlusion as previously described [Stroke 26 (1996) 333-336]. Intravenous infusion of YM90K (n = 8) (5 mg/kg per h for 1 h) or the same amount of vehicle (n = 8) (alkaline saline) was started 5 min after distal middle cerebral artery occlusion. Penumbral cerebral blood flow was determined with laser-Doppler flowmetry. Three days after the ischemic insult, brains were stained with 2,3,5-triphenyltetrazolium chloride and infarct volumes were determined. One hour infusion of YM90K significantly reduced infarct volume by 34% (93 +/- 23 mm3 in control group vs. 61 +/- 25 mm3 in YM90K-treated group, P = 0.017). There were no significant differences in the degrees of cerebral blood flow reduction after distal middle cerebral artery occlusion between the YM90K treated and control groups. YM90K reduces infarct volume in experimental ischemia produced by photothrombotic distal middle cerebral artery occlusion in rats. The present results demonstrated beneficial effects of AMPA receptor blockade on acute ischemic stroke.

Animals↗
PubMed1997

Stat1 in developing and adult rat brain. Induction after transient focal ischemia.

Stat1 has a dual function as signal transducer and activator of transcription, and is activated in response to growth factors and cytokines. We examined Stat1 in the rat brain during development and following transient focal ischemia, using Western immunoblotting. Two bands of 91 and 84 kDa, corresponding to Stat1 alpha and Stat1 beta forms, were found with an intensity that increased from postnatal day 0 to adulthood in cerebellum and cerebral cortex. Ischemia caused a strong induction of Stat1 in the ipsilateral cortex after 4, 7 and 15 days, but not at 6 or 24 h. These results show that Stat1 is normally expressed in the postnatal and adult rat brain and is induced under brain infarction.

Animals↗
PubMed1982

Watershed infarcts in the brain caused by microemboli.

Multiple vascular occlusions are frequently found in the leptomeningeal arteries over watershed infarcts in the brain. These occlusions have largely been interpreted as thrombi secondary to slowing of the blood flow. This report suggests that most of the occlusions are microemboli, which may lodge preferentially in these areas, and that they are the cause of the infarcts rather than secondary events. These suggestions are based upon the analysis of three groups of patients. The first group consists of four cases, two of which had atheromatous masses and the other two, tumor emboli in the overlying leptomeningeal arteries. These cases prove beyond doubt that microemboli can lodge preferentially in the watershed areas and cause infarcts in the brain. The second group consists of the cases of watershed infarcts that were precipitated by hypotensive episodes. Only one of these showed occlusion of the overlying arteries, although all of them obviously had slowing of the blood flow during the acute phase. These cases thus discredit the concept that stagnation thrombosis is a frequent event. Finally, three cases with watershed infarcts and vascular occlusions interpreted as platelet microemboli are presented to demonstrate different pathogenetic mechanisms effective in the process of embolization.

Adenocarcinoma↗
PubMed1990

Methionine sulfoximine reduces cortical infarct size in rats after middle cerebral artery occlusion.

The methionine analogue methionine sulfoximine was administered to 10 rats 24 hours before occlusion of the proximal left middle cerebral artery. Three days later the rats were decapitated and the brain infarct volumes were compared with those in 10 control rats that received saline before middle cerebral artery occlusion. The mean volume of the infarct in the cerebral cortex was reduced by 33% in the group treated with methionine sulfoximine (p less than 0.01). This protective effect may be mediated by a presynaptic mechanism; methionine sulfoximine profoundly inhibits brain glutamine synthetase, thereby interrupting the astrocyte-neuron glutamate shuttle and impairing neuronal glutamate release. Methionine sulfoximine also increases brain glycogen stores, and this increased energy reserve may benefit penumbral tissue during the peri-infarct period. Further study of the mechanisms by which methionine sulfoximine decreases infarct volume could lead to new therapeutic approaches for stroke.

Animals↗
PubMed1997

Cerebroprotective effects of a novel pyrazoline derivative, MS-153, on focal ischemia in rats.

MS-153 ((R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline) is a novel pyrazoline compound that has potent cerebroprotective effects in the rat focal cerebral ischemia model. Middle cerebral artery (MCA) occlusion in rats allows detailed assessment of both functional and morphological sequelae of brain infarct. Using this model, we evaluated the cerebroprotective effects of MS-153. Treatment with MS-153 (12.5 mg/kg, i.v. bolus followed by 6.25 mg/kg/hr or 25.0 mg/kg, i.v. bolus followed by 12.5 mg/kg/hr infusion for 7 days) significantly reduced infarct volumes and improved neurological deficits in MCA occluded rats 7 days after occlusion. Delayed treatment significantly reduced infarct volume 24 hr after MCA occlusion when MS-153 (25.0 mg/kg, i.v. bolus followed by 12.5 mg/kg/hr infusion for 21 hr) administration was started 3 hr after occlusion. Brain edema was also significantly improved when MS-153 (25.0 mg/kg, i.v. bolus followed by 12.5 mg/kg/hr infusion for 18 hr) administration was started 6 hr after occlusion.

Analysis of Variance↗
PubMed2004

Protective effect of vitamin E against focal brain ischemia and neuronal death through induction of target genes of hypoxia-inducible factor-1.

Vitamin E has been shown to have protective effects against cerebral ischemia, possibly due to its anti-oxidant effects. However, its non-anti-oxidant, intracellular molecular mechanism remains elusive. For in vivo experiments in rats, orally administered vitamin E significantly reduced not only the brain infarct volume but also space navigation disability after permanent middle cerebral artery (MCA) occlusion. The level of anti-oxidant after MCA occlusion was significantly increased specifically in the ipsilateral brain tissues of vitamin E-treated rats. For in vitro experiments, posttreatment with vitamin E protected primary cultured neurons from nitric oxide-induced insult. Vitamin E induced the expression of the alpha subunit of hypoxia-inducible factor-1 (HIF-1) and its target genes, including vascular endothelial growth factor (VEGF) and heme oxygenase-1. The hypoxia response element on the VEGF promoter was responsible for this vitamin E-induced transcriptional activation of VEGF gene. Taken together, these results suggest that cerebral infarction increased the permeability of vitamin E across the blood-brain barrier, and this increased vitamin E in brain tissue elicited neuroprotective effects not only through scavenging oxidants, as are previously well reported, but also by transactivating HIF-1-dependent genes, which results in protection of brains from ischemic insults.

Animals↗
PubMed1988

Protective effect of fasting upon cerebral hypoxic-ischemic injury.

This study was designed to determine the effect of fasting upon cerebral hypoxic-ischemic injury. In the first part of the study the effect of fasting was determined for survival, brain tissue water and kation contents, and blood-brain barrier integrity. In the second part of the study the administration of the substrates beta-hydroxybutyrate (BHB) and glucose has been evaluated regarding their influence upon the effect of fasting. The study used the Levine-Klein model of unilateral carotid occlusion and hypoxia because it mimics clinical situations of ischemia with hypoxia. The data show that fasting did protect rats from developing brain infarction following hypoxia-ischemia. Hypoglycemia seems to be involved in the mitigation of ischemic blood-brain barrier disruption. The plasma glucose level seems to be not the only factor involved in the genesis of the tissue kation changes. Starvation-induced ketosis probably does not play a role in the protection mechanism.

Acetoacetates↗
PubMed2005

Oral clopidogrel load in aspirin-resistant capsular warning syndrome.

INTRODUCTION: Capsular warning syndrome (CWS) carries a significant risk of permanent stroke. There are no proven therapies for preventing completed stroke in this unstable situation. METHODS: Clinical observation in two patients with aspirin-resistant CWS treated with a loading dose of oral clopidogrel. RESULTS: Both patients had excellent neurological outcome, although one sustained an asymptomatic brain infarction. CONCLUSION: High-dose oral clopidogrel plus aspirin merits formal evaluation in high-risk transient brain ischemia such as CWS, preferably in a randomized trial compared to aspirin alone.

Administration, Oral↗
PubMed1999

Location of the primary motor cortex in schizencephaly.

BACKGROUND AND PURPOSE: Functional reorganization of the brain can result from congenital brain disorders as well as from brain infarction. The purpose of our study was to use functional MR imaging to determine whether reorganization of brain function occurs in patients with schizencephaly. METHODS: Four patients with schizencephaly (three right-handed, one ambidextrous) presented with seizures. Associated lesions included agenesis of the corpus callosum (n = 1) and absence of the septum pellucidum (n = 1). Functional MR imaging was performed in each patient using a single-section fast low-angle shot (FLASH) blood oxygen level-dependent (BOLD) technique at 1.5 T in a standard head coil. The motor cortex was initially identified on an axial T1-weighted anatomic image. Thirty consecutive images were obtained during a motor task consisting of repetitive finger-to-thumb opposition. The percentage of change in increased signal intensity was calculated for the primary motor area. An ipsilateral activation index was used to compare the affected with the unaffected hemisphere. RESULTS: The percentage of change in increased signal intensity in the area of activation ranged from 4.8% +/- 0.9 to 9.2% +/- 1.2 (mean, 5.6% +/- 1.5). The ipsilateral activation index in the affected hemisphere was 0.00 to 0.38, whereas that in the unaffected hemisphere was 15.4 to infinity. The difference in the ipsilateral activation index between each hemisphere was considered significant. CONCLUSION: Our results showed increased activation in the unaffected hemisphere in patients with schizencephaly, which may reflect functional reorganization of the motor area in patients with this congenital disorder.

Adolescent↗
PubMed1992

[Revising the principles and improving the methods of differential therapy of ischemic stroke].

In accordance with the clinical and coagulographic data on 172 patients with ischemic brain stroke (IBS), the authors developed a method of the use of some medicamentous agents (heparin, platelet inhibitors, fresh-frozen blood plasma, plasminogen activators, proteolytic enzymes), adapted to concrete characteristics of the coagulation status at different stages of brain infarction formation and permitting the rate of lethal outcomes to be reduced. In disseminated intravascular coagulation seen in patients with the gravest patterns of IBS, heparin may be indicated.

Blood Coagulation↗
PubMed1983

The effects of chronic alcoholism on development of ischemic cerebral infarcts following unilateral carotid artery ligation in gerbils.

To test if chronic alcoholism potentiates mortality and accentuates cerebral infarcts associated with ischemia, 32 male and 33 female Mongolian gerbils were chronically fed ethanol in their diet for 6 weeks. Cerebral ischemia was then induced by ligation and sectioning of the right common carotid artery. Postoperatively, there was a mean difference in survival in the control versus the alcoholic gerbils. Whereas 76% of controls survived the operation, only 55% of alcoholic gerbils survived. Also, the alcoholic gerbils died earlier, usually in the initial 3 postoperation days. The incidence of cerebral infarcts was identical (52%) in both control and alcohol-treated gerbils. There was, however, a difference in the extent (size) of the infarcts and tolerance to them. The alcoholic gerbils tended to develop either large infarcts which were usually lethal, or smaller infarcts but with decreased tolerance. The cerebral infarcts in the controls tended to be smaller with better survival. These findings suggest that chronic alcohol consumption contributes significantly to the risk of mortality associated with ischemic brain infarction reported in human alcoholics, and indicate that the alcoholic gerbil is a good experimental model to study the pathophysiology of this phenomenon.

Alcoholism↗
PubMed1984

A microcomputer assisted method for obtaining composite pictures of focal brain damage.

A method used to produce composite drawings of superimposed areas of brain infarction is described. The method uses a microcomputer interfaced to a digitising pad and linear plotter. Areas of brain damage are drawn on standardised maps, digitised, manipulated in computer memory, and summated using computer graphics facilities. The composites show the position of brain damage in groups of patients as a contour map of the extent of lesion overlap. The method can be used to study neurological and neuropsychological deficits using CT-scan, or other imaging techniques. Deep and superficial lesions may be displayed equally well.

Cerebral Infarction↗
PubMed1994

Oedema-related tissue damage after temporary and permanent occlusion of the middle cerebral artery.

Eleven adults spontaneously-hypertensive male rats (SHR) were studied 22 h or 7 days after a 2 h unilateral occlusion of the right middle cerebral artery (MCA). Another 11 SHR were studied after 24 h or 7 days of permanent MCA ligation. The brain infarcts were significantly larger (P < 0.05) after permanent occlusion than after a 2 h occlusion. More extensive and widespread vasogenic oedema, emanating from the infarcts, was visualized immunohistochemically in the temporarily-ligated animals and the relative number of astrocytes in their contralateral hemispheres was greater, thereby indicating that the vasogenic oedema influences the degree of gliosis. An immunopositivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where cytolytic nerve cell damage, severely shrunken and karyorrhectic nerve cells as well as gliosis were found one week after permanent and temporary MCA ligation. The histological changes in the thalamus indicated a difference in timing between lateral and medial parts of the lesion as well as between temporarily- and permanently-ligated SHR. These findings together with the close spatial correlation with albumin immunoreactivity indicate that the spread of extravasated plasma constituents or degradation products with the oedema bulk flow from the infarct influences the timing, character and extent of thalamic lesions after cerebral infarction.

Animals↗
PubMed2005

CD40/CD40 ligand signaling in mouse cerebral microvasculature after focal ischemia/reperfusion.

BACKGROUND: CD40/CD40 ligand (CD40L) signaling contributes to proinflammatory and prothrombogenic responses in the vasculature. CD40/CD40L expression is elevated in patients after a transient ischemic attack or stroke. The purpose of this study was to investigate the role of CD40/CD40L signaling in cerebral microvascular dysfunction and tissue injury response to middle cerebral artery occlusion (MCAO) and reperfusion. METHODS AND RESULTS: Intravital fluorescence microscopy was used to visualize the cerebral microcirculation of wild-type (WT), CD40-deficient, and CD40L-deficient mice subjected to 1-hour MCAO and 4-hour reperfusion. The adhesion of platelets and of leukocytes and vascular permeability were measured in postcapillary venules after 4-hour and 1-hour reperfusions, respectively. Cerebral infarct volume was analyzed 24 hours after reperfusion. Platelet and leukocyte adhesion was elevated and blood/brain barrier function was compromised by MCAO in WT mice. Blood cell recruitment and increased permeability were blunted in both CD40-deficient and CD40L-deficient mice. Infarct volume was also reduced in CD40- and CD40L-deficient mice compared with WT mice. CONCLUSIONS: Our findings indicate that CD40/CD40L signaling contributes to inflammatory and prothrombogenic responses and brain infarction induced by MCAO and reperfusion. The CD40/CD40L dyad may play a significant pathogenic role in the acute phase of ischemic stroke.

Animals↗