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PubMed2004

Carotid haemodynamic parameters as risk factors for cerebral infarction in Type 2 diabetic patients.

AIMS: The purpose of this study was to investigate the usefulness of carotid haemodynamic parameters, i.e. the resistive index (RI) and the pulsatility index (PI), in estimating the risk of cerebral infarction in Type 2 diabetic patients. METHODS: Three hundred and eighty-two Type 2 diabetic patients (223 men and 159 women; mean age 61 years, range 40-88; 40 had a history of cerebral infarction) and 110 control subjects were analysed in a cross-sectional study. All subjects underwent ultrasonography of the common carotid artery, with determination of intima-media thickness (IMT), RI, and PI. A SMART (Second Manifestations of ARTerial Disease) atherosclerosis risk score was determined for all diabetic patients. RESULTS: The mean values for IMT, RI, and PI were increased in diabetic patients compared with control subjects, and they were significantly elevated in patients with previous cerebral infarction compared with patients without cerebral infarction. (IMT 0.88 +/- 0.22 vs. 0.77 +/- 0.19, P < 0.005; RI 0.77 +/- 0.07 vs. 0.75 +/- 0.06, P < 0.05; PI 1.88 +/- 0.36 vs. 1.71 +/- 0.36, P < 0.01) Significant but weak correlations were found between SMART risk scores and IMT, RI and PI (IMT r = 0.390, P < 0.0001; RI r = 0.346, P < 0.0001; PI r = 0.393, P < 0.0001). The multiple logistic model showed that both the IMT [odds ratio (OR) 6.50, 95% confidence interval (CI) 3.42, 12.34] and the PI (OR 4.16, 95% CI 2.36, 7.34) were independent risk factors for cerebral infarction. The subjects who had an IMT of > 1.0 and a PI > 2.00 had a greater risk of developing a cerebral infarction than did the subjects who had an IMT of < 1.0 and a PI < 2.00 (OR 6.21, 95% CI 2.26, 17.05). CONCLUSIONS: The results of this cross-sectional study showed that the measurement of haemodynamic parameters was useful, together with IMT, in estimating the risk of previous cerebral infarction in Type 2 diabetic patients. The predictive value of these parameters in identifying the risk of future cerebral infarction must await the results of future prospective studies.

Adult↗
PubMed2005

Microglia, apoptosis and interleukin-1beta expression in the effect of sophora japonica l. on cerebral infarct induced by ischemia-reperfusion in rats.

Sophora Japonica L. (SJ) is a traditional Chinese herb used to cool blood, stop bleeding and to treat hemorrhoids with bleeding. Although several recent studies found that both SJ and Ginkgo biloba have the same components of quercetin and rutin, only Ginkgo biloba has been widely used to treat cerebrovascular disorders and dementia in humans. This study investigated the effect of SJ on cerebral infarct in rats. A total of 66 Sprague-Dawley (SD) rats were studied. Focal cerebral infarct was established by occluding the bilateral common carotid arteries and the right middle cerebral artery for 90 minutes. After 24 hours of reperfusion, the neurological status was evaluated. The rats were then killed, and brain tissue was stained with 2,3,5-triphenyl-tetrazolium chloride. The grading scale of neurological deficit and the ratio of cerebral infarction area were used as an index to evaluate the effect of SJ on cerebral infarct. In addition, the number of ED1 and interleukin-1beta immunostaining positive cells, and apoptotic cells were measured in the cerebral infarction zone. The results indicated that pre-treatment with 100 or 200 mg/kg SJ and post-treatment with 200 mg/kg SJ significantly reduced the grade of neurological deficit and the ratio of cerebral infarction area. In addition, pre-treatment with 200 mg/kg SJ also significantly reduced ED1 and interleukin-1beta immunostaining positive cells, and apoptotic cells in ischemia-reperfusion cerebral infarct rats. This study demonstrated that SJ could reduce the cerebral infarction area and neurological deficit induced by ischemia-reperfusion in rats, suggesting its potential as a treatment for cerebral infarct in humans. This effect of SJ involves its suppressive action of microglia, interleukin-1beta and apoptosis.

Animals↗
PubMed1993

Risk factors for carotid atherosclerosis and silent cerebral infarction in patients with coronary heart disease.

In this study, the authors examined relations between coronary and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction. They ascertained the risk factors for carotid atherosclerosis and silent cerebral infarction complicating coronary heart disease (CHD) in 77 Japanese subjects. As coronary atherosclerosis progressed, the carotid ultrasonographic score and the brain computed tomographic score increased. Multivariate analyses showed that the significant and independent risk factors for carotid atherosclerosis in patients with CHD were age (p < 0.01) and apolipoprotein (apo) B (p < 0.05) and the factors for silent cerebral infarction were age (p < 0.05) and hypertension (p < 0.05). Their study confirms a positive relation between coronary atherosclerosis and carotid atherosclerosis and between coronary atherosclerosis and silent cerebral infarction in patients with CHD. Their data suggest that carotid atherosclerosis should be looked for in patients with CHD who are old and have a high value of apo B, and silent cerebral infarction should be looked for in those who are old and have hypertension, to prevent complicating symptomatic cerebral vascular disease (CVD). If severe carotid atherosclerosis or silent cerebral infarction are detected, antithrombotic medication should be given.

Age Factors↗
PubMed1981

[Vascular surgery in ischemic cerebral infarction (author's transl)].

Ischemic cerebral infarction requires surgical treatment, if based on stenosis or occlusion of an internal carotid or middle cerebral artery. The selection of the patients and the indications for carotid thrombendarterectomy or extracranial-intracranial arterial bypass are discussed. Preoperative testing of patients under hyperbaric oxygenation may be important for the success of an operation. Report on the experience with 128 surgically treated cases.

Adult↗
PubMed1986

Characterization of plasma lipoproteins in survivors of cerebral infarction.

To characterize the plasma lipoproteins in survivors of cerebral infarction, plasma lipoproteins were ultracentrifugally fractionated into VLDL, LDL, HDL2 and HDL3, and the concentrations of cholesterol, phospholipid, apolipoprotein and triglyceride in each lipoprotein class were determined. Subjects examined were 15 male healthy controls and 15 male survivors of cerebral infarction situated in the distribution of cerebral cortical artery. The concentrations of VLDL-cholesterol and VLDL-triglyceride and the percent content of VLDL-cholesterol were higher in survivors than in controls. The concentration of LDL-triglyceride was higher and the percent content of LDL-cholesterol was lower in survivors than in controls. While the plasma concentration of triglyceride was higher in survivors than in controls, those of HDL, HDL2 and HDL3 were lower in survivors. The concentrations of cholesterol, phospholipid and apolipoprotein in either HDL2 or HDL3 were also reduced in survivors as compared with controls. In either HDL2 or HDL3, the percent content of triglyceride was higher and that of phospholipid was lower in survivors than in controls. These results were in good agreement with those reported for survivors of myocardial infarction, suggesting that the underlying derangement in lipoprotein metabolism is common to myocardial and cerebral infarction.

Adult↗
PubMed1982

Cerebral infarction caused by vasospasm.

Fifteen patients with cerebral infarction, the majority of them being under the age of 40 years, were reviewed. Patients in whom an underlying structural disease, such as atheroma or thromboembolism, was suspected on clinical grounds were excluded. On the basis of either a personal or family history of migraine, or a concomitant vascular headache, or a migratory pattern of evolution of the neurological deficit, a migrainous disorder was considered possible in 14 patients. It is postulated that cerebral vasospasm is a cause of cerebral infarction, especially in younger people.

Adolescent↗
PubMed2004

[Traumatic cerebral infarction: a histopathological study of 17 cases].

OBJECTIVE: To assess the morphologic changes in traumatic cerebral infarction and to discuss its mechanism. METHODS: Specimens from seventeen cases of cerebral infarction were selected from 81 patients with severe brain injury, and subject to routine gross and histological examinations. RESULTS: (1) The cerebral infarction in all cases was hemorrhagic in nature with a wedged or irregular shape upon gross inspection. The lesions were found in occipital gyrus (8 cases), occipital lobes (3 cases), basal nuclei (3 cases), cingulate gyrus (2 cases), and lateral occipitotemporal gyrus (1 case). Histologically, the lesions were located at the junction between the cortex and medulla, showing congestion, edema, hemorrhage, necrotic nerve tissue and blood vessels. In severe cases, the lesion extended into the entire cortex and subarachnoid spaces. (2) Swelling of the brain and cerebral hernia were found in all cases, 8 of which demonstrated that the posterior cerebral artery was compressed and stenotic within the space between the crus cerebri and uncus. CONCLUSION: Brain tissue necrosis in traumatic cerebral infarction is the result of brain swelling and cerebral hernia formation, following congestion, bleeding and ischemia due to vasculature compression.

Adolescent↗
PubMed2005

Effects of the cyclooxygenase-2 inhibitor nimesulide on cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion in the rat.

BACKGROUND: Previous studies suggest that the cyclooxygenase-2 (COX-2) inhibitor nimesulide has a remarkable protective effect against different types of brain injury including ischemia. Since there are no reports on the effects of nimesulide on permanent ischemic stroke and because most cases of human stroke are caused by permanent occlusion of cerebral arteries, the present study was conducted to assess the neuroprotective efficacy of nimesulide on the cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion (pMCAO) in the rat. METHODS: Ischemia was induced by permanent occlusion of the middle cerebral artery in rats, via surgical insertion of a nylon filament into the internal carotid artery. Infarct volumes (cortical, subcortical and total) and functional recovery, assessed by neurological score evaluation and rotarod performance test, were performed 24 h after pMCAO. In initial experiments, different doses of nimesulide (3, 6 and 12 mg/kg; i.p) or vehicle were administered 30 min before pMCAO and again at 6, 12 and 18 h after stroke. In later experiments we investigated the therapeutic time window of protection of nimesulide by delaying its first administration 0.5-4 h after the ischemic insult. RESULTS: Repeated treatments with nimesulide dose-dependently reduced cortical, subcortical and total infarct volumes as well as the neurological deficits and motor impairment resulting from permanent ischemic stroke, but only the administration of the highest dose (12 mg/kg) was able to significantly (P < 0.01) diminish infarct volume. The lower doses failed to significantly reduce infarction but showed a beneficial effect on neurological function. Nimesulide (12 mg/kg) not only reduced infarct volume but also enhanced functional recovery when the first treatment was given up to 2 h after stroke. CONCLUSIONS: These data show that nimesulide protects against permanent focal cerebral ischemia, even with a 2 h post-treatment delay. These findings have important implications for the therapeutic potential of using COX-2 inhibitors in the treatment of stroke.

Journal Article↗
PubMed1998

[Apolipoprotein(a) and cortical cerebral infarction].

OBJECTIVE: To elucidate the correlation of apolipoprotein(a)[apo(a)] with cerebral infarction at the level of molecule and protein. METHODS: The serum Lp(a) level, by means of ELISA, the polymorphism of apo(a) protein, by SDS-PAGE/Western blotting combined with silver staining assays, and the sequence polymorphism in 5' control region, the first exon and intron of apo(a) gene, by PCR-SSCP/AFLP assays, were detected in 85 healthy controls and 42 cases of cortical cerebral infarction. RESULTS: The serum Lp(a) level was remarkadly higher in the patients (153 +/- 3 mg/L) than that in the controls(56 +/- 4 mg/L) (t = 4.15, P < 0.001), even in the subjects with the same apo(a) phenotype. The allele frequency of low molecular weight phenotype containing B, S1 and S2 isoforms was also significantly higher in the patients than that in the controls (0.5238 vs. 0.2941). There were 2 sites of sequence variance in the 5' control region of apo(a) gene in the studied population, which were of significant difference between the patients and controls, and were related to the variation of serum Lp(a) level. CONCLUSION: On the basis of proving further the risk of high serum Lp(a) level for AS event, we found that the low molecular weight phenotype of apo(a) is closely associated with cerebral infarction. The variation of serum Lp(a) level is also related to the sequence of apo(a) gene, indicating that both the size and sequence of apo(a) are associated with the susceptibility to cerebral infarction due to its impact on serum Lp(a) level.

Aged↗
PubMed1990

[Cerebral infarct in a young adult, as the presenting form of myeloencephalopathic syndrome with lactic acidosis and cerebral ischemia].

We report a 26-year-old male who developed aphasia due to an ischemic cerebral infarction caused by MELAS (myoencephalophatic syndrome with lactic acidosis and cerebral ischemia). The most common causes of cerebral infarction in young patients were ruled out by laboratory investigations. The diagnosis of MELAS was suspected on the basis of past history of epilepsy, migraine and progressive sensory deafness, and increased resting blood lactic acid. Cerebral computed tomography showed bilateral caudate-putamen-pallidal calcification and nuclear magnetic resonance scan disclosed a left ischemic parietal-temporal-occipital infarction. The diagnosis was confirmed by muscular biopsy, which was characteristic of mitochondrial myopathy showing "red disarrayed" fibers in the histologic modified trichromic Gomori stain. Our patient showed that MELAS should be considered in young adults with cerebral infarction. The diagnosis should initially be suspected on a clinical basis, and confirmed by the presence of "red disarrayed" fibers with modified trichromic Gomori stain histologic muscle study.

Acidosis, Lactic↗
PubMed1987

A comparative study of electroencephalography and computed axial tomography in recent cerebral infarction.

In order to re-assess the present role of electroencephalography in the investigation of cerebral infarct, we prospectively studied 50 adults with recent supratentorial cerebral infarction over a ten-month period. All 50 patients had EEG's and CT scans within the first two weeks of the apoplectic event. The time span between the two procedures was one week or less in all patients. We monitored the following EEG parameters: characteristics of alpha rhythm (depressed, unchanged, or enhanced); prevalence, type, rhythmicity, and topography of focal slowing; and presence or absence of FIRDA. We grouped the patients on the basis of CT findings as follows: depth of the infarct (cortical-subcortical, deep white matter, or lacunar); size of the infarct (large, medium, or small); and presence or absence of mass effect. Statistical analysis revealed no differences with regard to the EEG parameters between the groups. However, when patients were categorized according to topography of the infarct, the group with parietal infarct showed a significantly higher incidence of depressed alpha rhythm compared with the groups with frontal or occipital infarct. Of the 50 patients, four patients whose history and clinical presentation suggested infarct had normal CT scans despite the presence of EEG abnormality. On the contrary, in two patients, the EEG was normal, whereas the CT confirmed the infarct. Our data suggested that physiological factors may play a major role in the pathogenesis of EEG abnormalities in cerebral infarct, thus accounting for the discrepancies between the EEG parameters and CT findings observed in our population. It was also suggested that EEG's be included routinely in the investigation of cerebral infarct.

Adult↗
PubMedDate not supplied

Neonatal cerebral infarction: USS or CT for imaging?

Neonatal cerebral infarction or neonatal stroke is the second most common cause of neonatal seizures in term new born babies. It remains one of the least recognised entities in the neonatal text books and the awareness of its existence among general practitioners and practising paediatricians is very low. Cranial Ultrasound Scan (USS) is the standard imaging used by neonatologists and many neonatal intensive care units have their own scanners. However, USS may give a false sense of security especially in the term neonates and we report a case of neonatal cerebral infarction here and the need for computerised tomography (CT) for imaging.

Cerebral Infarction↗
PubMed1993

High serum lipoprotein(a) levels are an independent risk factor for cerebral infarction.

BACKGROUND AND PURPOSE: This study was conducted to evaluate the role of high serum lipoprotein(a) levels in a group of patients with a relatively early onset of cerebral infarction as a whole and in a subgroup with the perforating artery occlusion subtype of cerebral infarction. METHODS: Fifty-four patients with cerebral infarction, the onset of which was before age 65 years (37 men, 17 women; mean age, 61.9 +/- 7.7 years) were examined in this study. When patients with atrial fibrillation were excluded to omit cardiac embolic strokes from analysis, the group consisted of 45 patients. The patients were classified into two subtype groups, the perforating artery occlusion group and the cortical artery occlusion group, by using magnetic resonance imaging. Lipoprotein(a) levels were measured by an enzyme-linked immunosorbent assay. Four biochemical variables (serum levels of lipoprotein(a), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides) and other potential risk factors such as hypertension, diabetes mellitus, smoking habits, alcohol intake, and family history were analyzed by stepwise logistic regression to determine the independent and significant risk factors for cerebral infarction without atrial fibrillation. RESULTS: The incidence of subjects with serum lipoprotein(a) levels > or = 42.6 mg/dL, which is the 95th percentile level of the control subjects, was significantly increased in the total cerebral infarction group (P < .025) and the perforating artery occlusion group (P < .025) compared with the control group. In addition, by using stepwise logistic regression analysis in the total and perforating artery occlusion patient groups we identified three independent and significant risk factors: hypertension, a low high-density lipoprotein cholesterol level, and a high serum lipoprotein(a) level. In the cortical artery occlusion group, the sample size was not large enough for the statistical analysis. Diabetes mellitus is the only known factor that correlates with serum lipoprotein(a) levels, but there were no significant correlations between serum lipoprotein(a) levels and history of diabetes mellitus or fasting blood sugar. CONCLUSIONS: These findings indicate that high serum lipoprotein(a) levels are an independent risk factor in the development of cerebral infarction when subjects with atrial fibrillation were excluded from the total group and the perforating artery occlusion subtype group.

Adult↗
PubMed1988

Unilateral hyperhidrosis after cerebral infarction.

Unilateral hyperhidrosis occurred contralateral to acute cerebral infarctions in six patients. Two patients had localized infarctions of opercular cortex, while the other four had large strokes involving both superficial cortical and deep subcortical structures. The unilateral hyperhidrosis typically involved the face and arm and was transient, lasting 1 to 3 days. No other autonomic dysfunction occurred. One patient died, and the others had significant residual neurologic disability, thus indicating poor prognosis when this sign is present. Disruption of a pathway of cortical origin, inhibitory to contralateral sweating, is a proposed mechanism for the hyperhidrosis seen contralateral to acute cerebral infarction in these patients.

Adult↗
PubMed1989

[Cerebral infarction in 141 cases treated by traditional Chinese medicine and Western medicine].

Acute cerebral infarction of 141 cases with treatment combining TCM and WM was reported. The significant effective rate and the effective rate were 65% and 84% in the LT group (low molecular dextran + TCM) respectively; in the LN group (low molecular dextran + Nicotinic acid) were 29% and 41% respectively; in the T group (Salvia miltiorrhiza + Astragalus + Puraria) were 40% and 81.8% respectively. Among them the therapeutic effect in the LT group was the best. The LT group was also superior to the other two groups in serious cases. Cerebral edema developed following cerebrovascular dilator in a week after cerebral infarction; in the early stage, the therapeutic effect could be improved by giving mannitol first and then cerebrovascular dilator. Heart failure could be easily induced by low molecular dextran in the cerebral infarction following rheumatic heart disease. The therapeutic effect was poor in those cases with recurrent cerebral infarction.

Adult↗
PubMed1995

A pilot study of streptokinase for acute cerebral infarction.

We evaluated intravenous streptokinase in the treatment of cerebral infarction. Following neurological assessment and cerebral computed tomography (CT), patients aged 40-80 years with symptoms of anterior circulation acute ischaemic stroke were given 1.5 M units streptokinase or saline placebo in a double-blind randomized study. Twenty patients (10 streptokinase, 10 placebo), 11 males, 9 females, aged 57-79 years, were treated out of 512 consecutive admissions to the acute stroke unit over a 2-year period. Initial CT was normal in 11 (6 placebo, 5 streptokinase) and showed early signs of cerebral infarction in nine (4 placebo, 5 streptokinase). Median times from symptom onset to treatment were 5.2 h (placebo) and 5.8 h (streptokinase). Streptokinase treatment was associated with symptomatic hypotension in one patient. Repeat CT at 72 h demonstrated intracerebral haematoma in two patients and haemorrhagic infarction in one patient in the streptokinase group; the two cases of haematoma formation were associated with neurological deterioration and death. One patient in the placebo group had evidence of haemorrhagic infarction at 72 h. There were three deaths in each treatment group, all within the first 14 days. Patients with acute stroke can be evaluated with CT and treated with streptokinase within 6 h, but the opportunity for treatment is currently limited to few patients. Streptokinase treatment is not without risk, but potential clinical benefit justifies ongoing multicentre randomized trials.

Acute Disease↗
PubMed2002

[Acute cerebral infarction--diagnosis of subgroups].

BACKGROUND: Subclassification of cerebral infarcts is crucial in order to optimise and differentiate therapy. If we are to apply specific treatment modalities early while neurological deficits are still reversible, we need a fast diagnosis that reliably predicts etiology. MATERIAL AND METHODS: The early clinical classification into Oxford subgroups is presented with an assessment of their predictive value in relation to aetiology (TOAST classification). RESULTS: The various Oxford subgroups correlate well to the topography of the infarction demonstrated by neuroradiology, to the vascular aetiology as demonstrated by ultrasound techniques, and to the "aetiologic" subgroup as determined by a full diagnostic work-up. However, the correlation is not sufficient to guide potentially specific treatments of subgroups if the treatment in question has serious side effects (e.g. thrombolysis). However, if the clinical diagnosis is supplemented with diffusion-weighted MRI and perhaps MR angiography, the predictive value of the diagnosis is extremely high. INTERPRETATION: Very early clinical diagnosis of cerebral infarction must be supplemented with diffusion-weighted MRI to make the diagnostic precision sufficiently high to guide the application of specific treatments with potentially serious side effects.

Acute Disease↗