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PubMed1996

[The role of preparation LB in forming a thrombotic infarct of the cerebral cortex].

Non-invasion model for photochemically induced brain infarction was used to study the effect of a the new anti-ischemic drug LB ("Plaferon") in albino rats. Intensity of a local blood flow was measured so as oxygen tension in brain cortex. Square and volume of the disturbed nervous tissue region, capillary length and density of distribution of different caliber vessels were detected by means of light microscopy in serial sections of brain cortex. Preliminary introduction of LB was found to prevent formation of thrombotic infarction (the volume of cortical zone damaged is 85% lower as compared to the control). Anti-ischemic effect of LB implicates in vasodilatory action on cerebral vessels and also breaking pathogenic chain of ischemia development.

Animals↗
PubMed2006

[A clinicoanatomical study of thalamic cheiro-oral syndrome].

We report 6 patients with Cheiro-oral syndrome (COS), with special reference to clinical features and responsible lesions. The time intervals from the onset of symptoms to arrival in our department were less than 24 hours in 3 patients, 2 days in 2, and 5 days in 1. All patients had subjective sensory disturbance involving the unilateral hand and ipsilateral perioral regions, and 4 patients presented with objective sensory disturbance. The body parts of tingling sensation tended to be larger than those of superficial sensory disturbance. Three patients developed motor disturbance including hemiparesis with or without ataxia, clumsiness of fine finger movements, and dysarthria. Magnetic resonance imaging revealed fresh infarctions around the thalamus, including lacunar infarctions in 5 patients and branch atheromatous disease in 1 patient. The lesion sites responsible for COS were ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei in the thalamus in 4 patients, thalamic pulvinar nucleus and medial geniculate body in 1, thalamic ventroposterior region-internal capsule-corona radiata in 1. Three patients had asymptomatic brain infarctions. Risk factors were hyperlipidemia, hypertension, diabetes mellitus, smoking, arteriosclerosis of the carotid artery, and polycythemia. In the convalescent stage, 5 patients suffered from residual sensory-motor disturbance, whereas 1 patient recovered from COS. COS has been attributed mainly to small infarctions in the thalamic ventroposterior nuclei. However, it is suggested that damage to ascending sensory fibers projecting to the thalamic VPL and VPM nuclei can cause COS. Because initial symptoms of COS are apt to be overlooked, early diagnosis and treatment are necessary to avoid residual sensory-motor disturbance.

Aged↗
PubMed2004

Regulation of GABA transporter mRNA and protein after photothrombotic infarct in rat brain.

Animal models of focal ischemic infarcts reveal an impaired GABAergic (gamma-aminobutyric acid) neurotransmission. GABA, the main inhibitory neurotransmitter, is primarily taken up by specific sodium-dependent transporters. As these transporters play a crucial role in maintaining levels of GABA concentration, they may be functionally involved in ischemic processes. We investigated whether the mRNA and protein expression of GAT-1, the dominant neuronal GABA transporter, is altered after cortical infarct induced by photothrombosis in Wistar rats. In situ hybridization was performed to analyze GAT-1 mRNA-positive cells in cortical brain regions and the hippocampus. The lesion dramatically raised the number of GABA transporter mRNA-expressing cells in all investigated cortical regions. Double-labeling studies with a general neuronal marker and a marker for astrocytes revealed that cells expressing GAT-1 mRNA after photothrombosis are neurons. The mRNA expression pattern of all hippocampal subfields remained unchanged. In contrast, cortical GAT-1 protein density was only slightly affected and surprisingly in the opposite way. In the primary and secondary somatosensory cortex, density values were significantly reduced. Immunoreactivity was not altered in all investigated hippocampal areas. We found a marked discordance between the increased number of cells expressing GAT-1 mRNA in the cortex and the reduced tissue GAT-1 protein content. Focal brain ischemia obviously triggers mechanisms that interfere with GAT-1 transcriptional regulation and protein synthesis or turnover.

Animals↗
PubMed2003

Ethanol attenuates ischemic and hypoxic injury in rat brain and cultured neurons.

Reactive oxygen species play a critical role in ischemic injury and oxidative stress induces apoptosis and triggers inflammation in neural cells. The effect of ethanol on ischemic brain injury was examined. Ethanol attenuated ischemia/reperfusion-induced brain infarction and elevation of inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha) expression, metalloproteinase-9, and neutrophil-associated myeloperoxidase activities. In cultured neurons, ethanol suppressed combined oxygen and glucose deprivation (COGD)/reoxygenation-induced oxidative stress and neuronal apoptosis. Furthermore, ethanol suppressed COGD/reoxygenation-induced activation of NF-kappaB, a free-radical-sensitive regulator, leading to the attenuation of TNF-alpha expression in glial cultures. We propose that scavenging of free radicals and attenuation of free-radical-induced alterations might account for ethanol's beneficial action against ischemic brain injury.

Animals↗
PubMed2006

Cerebrovascular disease in the elderly: lipoprotein metabolism and cognitive decline.

Data concerning the treatment of lipoprotein disturbances in patients with cerebrovascular disease (CVD) are less robust than those for coronary heart disease (CHD), raising clinical questions as to which is the appropriate therapeutic approach to stroke patients. Although observational cohort studies have failed to demonstrate an association between lipoprotein disorders and stroke incidence, recently completed trials of subjects at risk for CHD have shown that statins reduce not only the risk of myocardial infarction and death, but also that of brain infarction and transient ischemic attacks. At present, it seems reasonable to conclude that stroke patients with undesirable lipid profiles who have a history of CHD should receive specific treatment for the lipid disorder. Recommendations are more problematic for stroke patients with lipid disorder but no history of CHD. Furthermore, many of the risk factors for CVD and vascular dementia (VaD), including serum total cholesterol (TC), lipoprotein(a), diabetes, atrial fibrillation, hypertension, apolipoprotein E levels, and atherosclerosis, have also been shown to increase the risk of Alzheimer's disease (AD). In a recent study, we estimated the prevalence, incidence and rate of progression of Mild Cognitive Impairment (MCI) to dementia, and correlated vascular risk factors with incident MCI and its progression to dementia. We evaluated 2963 individuals from the population-based sample of 5632 subjects 65-84 years old of the Italian Longitudinal Study on Aging, with a 3.5-year follow-up. We found a progression rate to dementia (all causes) of 3.8/100 person-years. Furthermore, age was a risk factor for incident MCI, while education was protective, and serum TC evidenced a non-significant borderline trend for a protective effect. There was a non-significant trend for stroke as a risk factor of progression of MCI to dementia. In conclusion, in our population, among MCI patients who progressed to dementia, 60% progressed to AD and 33% to VaD. Vascular risk factors and CVD may influence the development of MCI and the rate of progression to dementia.

Aged↗
PubMed2002

Treatment of lipid disorders after stroke.

The efficacy of lipid disorder therapy for the primary and secondary prevention of coronary heart disease is established. There are, however, no completed studies specifically directed at reducing the risk of stroke with lipid therapy. Although observational cohort studies have failed to demonstrate an association between lipid disorders and stroke incidence, recently completed trials of subjects at risk for coronary heart disease have shown that statins and fibric acid derivatives reduce not only the risk of myocardial infarction and death, but also that of brain infarction and transient ischemic attacks. Lipid drugs are well tolerated and treatment complications are relatively low. It seems prudent to conclude that the stroke patient with an undesirable lipid profile who has a history of coronary heart disease should receive specific treatment for the lipid disorder. Recommendations are more problematic for stroke patients with lipid disorders but no history of coronary heart disease; most should receive therapy for primary prevention of heart disease. Lipid treatment trials focused on stroke risk reduction are urgently needed.

Humans↗
PubMed1999

CT findings in head scans at Moi Teaching and Referral hospital.

BACKGROUND: The first CT scanner in western Kenya was launched on 20th February, 1998. OBJECTIVE: To determine the pattern of CT findings in head scans. DESIGN: Prospective study over a one year period. SETTING: Moi Teaching and Referral Hospital, Eldoret, Kenya. SUBJECTS: Four hundred and ninety five consecutive patients who underwent CT head scans. RESULTS: Intracranial haemorrhage was the leading disorder with 17.8%, followed by brain infarcts at 10.5%, hydrocephalus at 6.3% and brain tumours at 5.9%. CONCLUSION: Intracranial disorders secondary to trauma, stroke and their sequelae are major causes of head disease in western Kenya.

Brain Diseases↗
PubMed1990

[P300 and dementia: diagnostic relevance. I].

Visual evoked potentials, including the P300 response, and reaction time were recorded from 20 patients with multi-infarct dementia, 20 nondemented patients with brain-infarct diseases, and 20 age-matched control subjects. Additionally the patients were assessed using the WAIS-index. Prolonged P300 latency and reaction time occurred in both of the patient-groups, correlated significantly with the WAIS-index. However, effects regarding to P300 latency and reaction time were not strong enough to allow individual classifications.

Adult↗
PubMed1992

Cranial computed tomographic observations in multi-infarct dementia. A controlled study.

BACKGROUND AND PURPOSE: We compared cranial computed tomography findings among 58 multi-infarct dementia index cases and 74 multi-infarct control subjects without cognitive impairment to identify potential determinants of multi-infarct dementia. METHODS: The cranial computed tomography records of acute ischemic stroke patients with a history of multiple cerebral infarcts were compared to determine the number, location, and size of cerebral infarcts; the pattern of infarction; brain volume loss; and the degree of white matter lucency, sulcal enlargement, and ventricular enlargement. Multi-infarct patients were divided into two groups: 1) index cases were defined as those with multi-infarct dementia as defined by the Diagnostic and Statistical Manual of Mental Disorders, edition 3 (DSM-III) criteria; and 2) control subjects were defined as those multi-infarct patients without dementia or multi-infarct dementia according to DSM-III criteria. RESULTS: Overall, multi-infarct index cases had more cerebral infarcts, more cortical and subcortical left hemisphere infarcts, higher mean ventricular volume to brain volume ratio, more extensive enlargement of the body of the lateral ventricles and cortical sulci, and a higher prevalence of white matter lucencies. Among multi-infarct cases and control subjects the most frequent site of infarction was the subcortical region, and the most frequent pattern of infarction was lacunar. Stepwise logistic regression analysis examined cranial computed tomography as well as other factors and showed that level of education, stroke severity, left cortical infarction, and diffuse enlargement of the left lateral ventricle were the best overall predictors of multi-infarct dementia. CONCLUSIONS: Level of education, stroke severity, and left hemisphere infarction may be predictors of multi-infarct dementia.

Brain↗
PubMed2000

Contribution of tumor necrosis factor alpha to the pathogenesis of stroke.

Tumor necrosis factor alpha (TNF-alpha) is a protein of a cellular origin belonging to a group of proinflammatory cytokines. A rapid overproduction of TNF-alpha in a cerebral post-ischemic inflammatory response leads to the stimulation of adhesive molecules expression with subsequent accumulation of leukocytes in the ischemic focus, which is preceded by their adhesion and migration. The TNF-alpha proinflammatory activity results mainly in extending the area of the brain infarct, which brings about negative clinical implications. Being the final morphological effect of ischemic stroke, TNF-alpha appears also to contribute to neuronal necrosis by its involvement in the process of apoptosis as well as in the death of neurons. The present study describes and discusses mainly the contribution of TNF-alpha to the formation of ischemic focus in the brain.

Animals↗
PubMed2003

Evaluating non-invasive medical imaging for diagnosis of carotid artery stenosis with ischemic cerebrovascular disease.

OBJECTIVES: To assess the value of non-invasive medical imaging for diagnosis of carotid artery stenosis and to study the relationship between carotid stenosis and brain infarction. METHODS: Thirty-one patients with a total of 62 carotid arteries were studied using Doppler ultrasound (DUS) and magnetic resonance angiography (MRA). Eleven of the 31 patients were studied using CT angiography (CTA). CT and MRI of the brain were also done in all patients. The imaging results in 5 patients were compared with those of digital subtraction angiography (DSA). Eight patients with severe stenosis received carotid endarterectomy. The comparisons between the imaging results and pathological data were conducted in 2 patients. RESULTS: Of the 62 carotid arteries, mild stenosis was seen in 11, moderate in 14, severe in 21, obstructed in 4 and normal in 12. In 25 patients with severe stenosis or occlusion of carotid arteries, there were a total of 35 focal or multifocal infarcts on the ipsilateral cerebral hemisphere, and 15 infarcts on the contrary side. Compared with the results of the operations, DUS correctly diagnosed 6 stenoses, while MRA identified 7 correctly and CTA 8. Agreement on location of stenosis as performed by endarterectomy, DUS, MRA and CTA occurred in all patients. Histologically, areas of calcification and fibrousness were related to high densities on CTA, strong echoes on DUS, and low signal intensities on MRA. Relatively large amounts of necrotic material and foam cells filled with lipolytic materials on the intimal surface of arteries were observed during pathologically, corresponding to low and iso-densities on CTA, low echoes on DUS, and inhomogeneous signal intensities on MRA. CONCLUSIONS: A strong link exists between carotid stenosis and brain infarction. The combined use of DUS, MRA and CTA can improve diagnostic accuracy for the assessment of carotid artery stenosis, as well as assist in ascertaining the nature of the plaque.

Adult↗
PubMed2004

Post-ischemic hypothermia-induced tissue protection and diminished apoptosis after neonatal cerebral hypoxia-ischemia.

Hypothermia is possibly the single most effective method of neuroprotection developed to date. However, the mechanisms are not completely understood. The aim of this study was to investigate the effects of post-ischemic hypothermia on brain injury and apoptotic neuronal cell death as well as related biochemical changes after neonatal hypoxia-ischemia (HI). Seven-day-old rats were subjected to left common carotid artery ligation and hypoxia (7.8%) for 1 h. Systemic hypothermia was induced immediately after hypoxia-ischemia, and body temperature was maintained at 30 degrees C for 10 h. The normothermic group was kept at 36 degrees C. Brain infarct volumes and neuronal loss in the CA1 area of the hippocampus were significantly reduced at 72 h post-HI in the hypothermia group. Cytochrome c release and activation of caspase-3 and -2 at 24 h post-HI were significantly diminished by hypothermia. The numbers of cytochrome c- and TUNEL-positive cells in the cortex and dentate gyrus of the hippocampus were significantly reduced in the hypothermia group compared with the normothermia group at 72 h post-HI. These results indicate that hypothermia may, at least partially, act through inhibition of the intrinsic pathway of caspase activation in the neonatal brain, thereby preventing apoptotic cell death.

Animals↗
PubMed1996

Detectability of cerebral hemisphere ischaemic infarcts by CT within 6 h of stroke.

To determine how early and how reliably ischaemic brain infarcts can be detected on CT within 6 h of the onset of cerebral hemisphere strokes, 44 such studies were interpreted by an experienced neuroradiologist blinded to clinical signs, but aware that the cohort was a stroke population. He was asked to detect and localise an area of parenchymal low density and/or focal brain swelling. A follow-up study showing the definite infarct served as a reference in each case. In 38 patients areas of slightly low density were seen, and in 36 follow-up CT confirmed infarcts in the locations indicated. In 2 patients the reading was false positive. In 6 patients no low density focus could be detected. In these 8 patients examined by CT within 180 min of the stroke, no low density could be identified, even in retrospect with the knowledge of the findings on follow-up. Thus, 42 readings (95%) were true positive or true negative; 2 were false positive; and none was a false negative. CT within 6 h of the onset of symptoms has a mean sensitivity of 82% (36/44) for ischaemic cerebral hemisphere infarcts. By contrast, its sensitivity to ischaemic parenchymal low density is low during the initial 2 h. The early development of hemispheric infarcts can be detected reliably if the radiologist is familiar with the signs.

Adult↗
PubMed2003

Preconditioning with isoflurane produces dose-dependent neuroprotection via activation of adenosine triphosphate-regulated potassium channels after focal cerebral ischemia in rats.

UNLABELLED: In this study, we determined whether repeated brief isoflurane (Iso) anesthesia induces ischemic tolerance to focal cerebral ischemia in a dose-response manner and whether the effect is dependent on adenosine triphosphate-regulated potassium channels. In Experiment 1, 40 rats were randomly assigned to 4 groups: control animals received 100% oxygen 1 h/d for 5 days, whereas the isoflurane (Iso)1, Iso2, and Iso3 groups received 0.75%, 1.5%, or 2.25% Iso in oxygen 1 h/d for 5 days. In Experiment 2, 36 rats were randomly assigned to 4 groups: controls received 100% oxygen 1 h/d for 5 days; animals in the Iso and I+G (Iso+glibenclamide) groups received 2% Iso in oxygen 1 h/d for 5 days, and the I+G group received glibenclamide (GLB) (5 mg/kg intraperitoneally) before each Iso pretreatment. Animals in the GLB group received GLB (5 mg/kg intraperitoneally) once a day for 5 days. Twenty-four hours after the last pretreatment, the right middle cerebral artery was occluded for 120 min. Neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 h. The NDS and infarct volumes of Iso2 and Iso3 were less than those of the controls (P < 0.05). The infarct volume in Iso3 was smaller than in Iso2 (P < 0.05). The NDS and infarct volume in the Iso group were less than in the control and I+G groups (P < 0.05). There was no statistical difference among the control, I+G, and GLB groups. The study demonstrated that repeated Iso anesthesia induces ischemic tolerance in rats in a dose-response manner. GLB, an adenosine triphosphate-regulated potassium channel blocker, abolished the tolerance induced by Iso. IMPLICATIONS: Brief isoflurane anesthesia induces ischemic tolerance in the brain. The effect was found to be dose dependent in a rat focal cerebral ischemia model. Ischemic tolerance induced by isoflurane preconditioning is dependent on activation of adenosine triphosphate-regulated potassium channels.

ATP-Binding Cassette Transporters↗
PubMed2002

Neuroprotective effect of cilostazol against focal cerebral ischemia via antiapoptotic action in rats.

This study examined the protective effects of cilostazol on cerebral infarcts produced by subjecting rats to 2-h occlusion of the left middle cerebral artery followed by 24-h reperfusion. The ischemic cerebral infarct consistently involved the cortex and striatum. The infarct size was significantly reduced, when rats received 10 mg/kg cilostazol intravenously 5 min or 1 h after the completion of 2-h ischemia. Cyclic AMP level was significantly elevated in the cortex of 4- and 12-h reperfusion (P < 0.01) following treatment with cilostazol (10 mg/kg, 5 min after 2-h ischemia) accompanied by decreased tumor necrosis factor-alpha level. Samples from the regions corresponding to the penumbra showed markedly reduced Bcl-2 protein level and, in contrast, high levels of Bax protein and cytochrome c release. Cilostazol decreased Bax protein and cytochrome c release and increased the levels of Bcl-2 protein. Cilostazol (10(-7)-10(-5) M) potently and concentration dependently scavenged hydroxyl and peroxyl radicals. In conclusion, cilostazol treatment decreases ischemic brain infarction in association with inhibition of apoptotic and oxidative cell death.

Animals↗
PubMed2001

Characterization of polymorphic structure of cathepsin G gene: role in cardiovascular and cerebrovascular diseases.

Cathepsin G (CTSG), a serine protease released from activated neutrophils, may cause platelet activation, leading to intravascular thrombosis, thus contributing to cardiovascular and cerebrovascular disease. Applying the candidate gene approach, we screened the 5'-flanking region and the entire coding region of the CTSG gene for genetic variation by using polymerase chain reaction/single-strand conformation polymorphism analysis from 96 patients at high risk for myocardial infarction (MI). We identified 4 polymorphisms in the 5'-flanking region (G-618C, G-315A, C-179T, and C-160T) and 1 polymorphism in the coding region (Asn125Ser) of the gene and genotyped the participants in the Etude Cas-Temoins sur l'Infarctus du Myocarde (ECTIM Study), a case-control study for MI, and in the Etude du Profil Génétique de l'Infarctus Cérébral (GENIC Study), a case-control study for brain infarction (BI), for all identified genetic variants. The potential in vitro functionality of the 4 variants in the 5'-flanking region was investigated with transient transfection analyses in U937 cells with different allelic promoter constructs by using a luciferase assay. Our in vitro analyses did not reveal any differences for the investigated allelic constructs with respect to promoter activity, and none of the polymorphisms in the 5'-flanking region was associated with the available phenotypes in either study. Allele and genotype distributions of all identified polymorphisms did not globally differ between cases and controls in the ECTIM Study. However, in patients from the ECTIM Study, the Ser125 allele was significantly associated with elevated plasma fibrinogen levels (P=0.006), but this effect was not seen in controls (case-control heterogeneity, P=0.04). There was a significant interaction between CTSG Asn125Ser and the beta-fibrinogen gene polymorphism G-455A on plasma fibrinogen levels (P=0.04). In the GENIC Study, the odds ratio for BI associated with CTSG Ser125 carrying was 1.82 (95% CI 1.16 to 2.84, P=0.008) in patients without a history of cardiovascular or cerebrovascular diseases. Our results indicate that the CTSG Ser125 allele is associated with plasma fibrinogen levels in MI patients from the ECTIM Study and with BI in the GENIC Study. Further studies should be carried out to define the underlying mechanisms.

Adult↗
PubMed1989

[Clinical study of watershed infarct dementia].

This clinical study of watershed infarct was carried out in two hospitals for elderly patients. The purpose of this study was an investigation of the clinical specificity of this type of infarct as compared with other types of infarcts. The most important point was to determine which patients with this type of infarct usually become demented. The items of investigation were brain CT findings, measurements of the width of the ventricles and the extent of sylvian fissures from CT images, blood pressure, past history of hypertension, diabetes mellitus, alcohol use and smoking, blood analysis of total cholesterol, HDL-cholesterol, hematocrit, hemoglobin A1 and uric acid and the incidence of patients in whom dementia had improved from the previous state. From CT findings, we classified all patients with brain infarcts into 4 groups; 173 patients with central infarcts, 56 patients with watershed infarcts, 20 patients with subcortical lesions of the Binswanger type and 11 patients with occlusion of main brain arteries. Among all investigated patients, there were 56 non-demented and 162 demented (74.3%) patients. Among the patients with watershed infarcts, there were 10 non-demented and 45 (81.8%) demented patients. In the group of demented patients with watershed infarcts, females were four times as many as males. Demented patients with watershed infarcts in the right hemisphere were twice as frequent as those with infarcts in the left hemisphere, while the number of non-demented patients with this type of infarct in right hemisphere was the same as that in the left hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗