Ischemic Stroke Patients (ischemic + stroke_patient)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Ischemic Stroke Patients

  • acute ischemic stroke patient


  • Selected Abstracts


    CADISP-genetics: an International project searching for genetic risk factors of cervical artery dissections

    INTERNATIONAL JOURNAL OF STROKE, Issue 3 2009
    S. Debette
    Background Cervical artery dissection (CAD) is a frequent cause of ischemic stroke, and occasionally death, in young adults. Several lines of evidence suggest a genetic predisposition to CAD. However, previous genetic studies have been inconclusive mainly due to insufficient numbers of patients. Our hypothesis is that CAD is a multifactorial disease caused by yet largely unidentified genetic variants and environmental factors, which may interact. Our aim is to identify genetic variants associated with an increased risk of CAD and possibly gene,environment interactions. Methods We organized a multinational European network, Cervical Artery Dissection and Ischemic Stroke Patients (CADISP), which aims at increasing our knowledge of the pathophysiological mechanisms of this disease in a large group of patients. Within this network, we are aiming to perform a de novo genetic association analysis using both a genome-wide and a candidate gene approach. For this purpose, DNA from approximately 1100 patients with CAD, and 2000 healthy controls is being collected. In addition, detailed clinical, laboratory, diagnostic, therapeutic, and outcome data are being collected from all participants applying predefined criteria and definitions in a standardized way. We are expecting to reach the above numbers of subjects by early 2009. Conclusions We present the strategy of a collaborative project searching for the genetic risk factors of CAD. The CADISP network will provide detailed and novel data on environmental risk factors and genetic susceptibility to CAD. [source]


    Thrombolysis in patients with acute ischemic stroke due to arterial extracranial dissection

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2009
    M. D. I. Vergouwen
    Background and purpose:, No data of randomized controlled trials investigating the effect of thrombolysis in patients with ischemic stroke caused by an extracranial dissection are available. Previous case series suggested that thrombolysis in this group of patients is safe and improves outcome, however publication bias may play a role. The purpose of the present study was to describe outcome of consecutive patients with ischemic stroke caused by an extracranial dissection treated with recombinant tissue plasminogen activator (rtPA), derived from a well-defined ischemic stroke cohort. Methods:, All consecutive patients with a transient ischemic attack (TIA) or ischemic stroke admitted to the Academic Medical Center Amsterdam between January 1, 2007 and September 1, 2007 were prospectively registered. Cause of TIA/stroke, treatment, and 6-months outcome were recorded. Results:, During the study period 252 patients were evaluated with TIA or ischemic stroke. Eight patients (3%) had an extracranial dissection. Of the six rtPA treated patients, five had good clinical outcome and one patient died. The two patients who were not treated with rtPA, because of minor stroke, had good clinical outcome 6 months after index event. Discussion:, Treatment with rtPA seems to be safe and feasible in ischemic stroke patients with an extracranial dissection. [source]


    ADP-induced platelet aggregation in acute ischemic stroke patients on aspirin therapy

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 12 2008
    J.-K. Cha
    Background and purpose:, Aspirin is an important therapeutic regimen to prevent the recurrent ischemic events or death after acute ischemic stroke. In this study, we evaluated the relationship between the extent of adenosine diphosphate (ADP) -induced platelet aggregation and outcome in acute ischemic stroke patients on aspirin therapy. Methods:, We selected 107 acute ischemic stroke patients who had been prescribed aspirin and evaluated platelet function test by using optic platelet aggregometer test after 5 days of taking it and investigated the prognosis 90 days after ischemic events. Kaplan,Meyer curve was used for survival analysis. Results:, After stratification of the subjected patients by tertiles of ADP-induced platelet aggregation, the events rates were 7.4%, 9.3% and 30.8% (P = 0.023). In multiple logistic regression analysis, old age over 70 years (OR, 13.7; 95% CI, 2.14,88.07; P = 0.001) and the increased ADP-induced platelet aggregation had independent significance to the risk of primary end-points after acute ischemic stroke (OR, 1.1; 95% CI 1.01 to 1.20; P = 0.026). Conclusions:, This study showed that the increased ADP-induced platelet aggregation under using aspirin is associated with poor outcome after acute ischemic stroke. [source]


    The influence of anaemia on stroke prognosis and its relation to N-terminal pro-brain natriuretic peptide

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007
    M. Nybo
    Anaemia is a negative prognostic factor for patients with heart failure and impaired renal function, but its role in stroke patients is unknown. Furthermore, anaemia has been shown to influence the level of N-terminal pro-brain natriuretic peptide (NT-proBNP), but this is only investigated in patients with heart failure, not in stroke patients. Two-hundred-and-fifty consecutive, well-defined ischemic stroke patients were investigated. Mortality was recorded at 6 months follow-up. Anaemia was diagnosed in 37 patients (15%) in whom stroke severity was worse than in the non-anaemic group, whilst the prevalence of renal affection, smoking and heart failure was lower. At 6 months follow-up, 23 patients were dead, and anaemia had an odds ratio of 4.7 when adjusted for age, Scandinavian Stroke Scale and a combined variable of heart and/or renal failure and/or elevation of troponin T using logistic regression. The median NT-proBNP level in the anaemic group was significantly higher than in the non-anaemic group, and in a multivariate linear regression model, anaemia remained an independent predictor of NT-proBNP. Conclusively, anaemia was found to be a negative prognostic factor for ischemic stroke patients. Furthermore, anaemia influenced the NT-proBNP level in ischemic stroke patients, an important aspect when interpreting NT-proBNP in these patients. [source]


    Assessment of corticodiaphragmatic pathway and pulmonary function in acute ischemic stroke patients

    EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2000
    E. M. Khedr
    This study investigates the effect of stroke on the corticodiaphragmatic pathway and attempts to clarify the relationship between neurophysiological data and degree of motor disability, site of infarction in computerized tomography (CT) scan, diaphragmatic excursion, blood gases and pulmonary function in stroke patients. Using magnetic stimulation of the scalp sites and cervical roots, an assessment of corticodiaphragmatic pathway was made. The study included 34 sequentially selected patients from a total of 250 patients with acute ischemic stroke. Twenty-five (age- and sex-matched) volunteers served as controls. Sixteen patients had cortical infarction, 13 had subcortical infarction and five had both cortical and subcortical infarction. The mean according to the Scandinavian Stroke Scale was 32.2. Decreased diaphragmatic excursion was observed in 41% of the patients. Twenty-four patients (70.5%) had abnormal magnetic evoked potentials (MEPs) in the affected hemisphere. In five patients MEPs could not be elicited from the affected hemisphere; the remaining 19 patients had abnormal values of both cortical latency and central conduction time (CCT). Cortical latency, CCT, amplitude of compound muscle action potentials (CMAPs) and excitability threshold of the affected hemisphere were significantly altered compared with both the unaffected hemisphere and the control group. Those patients with hemiplegia had a greater degree of hypoxia, hypocapnia and decreased serum bicarbonate level compared with the control group. Also, hemiplegic patients had different degree of respiratory dysfunction. A statistically significant association was found between neurophysiological data and disability score, diaphragmatic excursion, site of infarction in CT scan and degree of respiratory dysfunction. Central diaphragmatic impairment may occur in acute stroke and could contribute to the occurence of hypoxia in those patients. [source]


    Role of hyperlipidemia in atherosclerotic plaque formation in the internal carotid artery

    JOURNAL OF CLINICAL ULTRASOUND, Issue 6 2006
    Levente Kerenyi MD
    Abstract Purpose. The role of hyperlipidemia in atherosclerotic changes of the carotid artery is controversial. The aims of this retrospective study were to assess (1) the relationship between total serum cholesterol and triglyceride and the grade of internal carotid artery stenosis and (2) whether total serum cholesterol and triglyceride levels are independent risk factors for internal carotid artery atherosclerosis. Methods. The files of 1,934 acute ischemic stroke patients were investigated retrospectively. The atherosclerotic involvement of the internal carotid artery was assessed via duplex sonography as percent of stenosis and was graded as follows: group 1, no plaque; group 2, <30% stenosis; group 3, 30,99% stenosis; and group 4, occlusion. Results. The mean age of the patients was 66.9 ± 12.8 years. Patients without any plaque had significantly lower cholesterol levels compared with those with any degree of internal carotid artery stenosis. Univariate analysis revealed that age (p < 0.001), sex (p < 0.001), hypertension (p < 0.05), cholesterol (p < 0.01), triglycerides(p < 0.05), and smoking (p < 0.001) were significant contributors to atherosclerosis. In the ordinal logistic regression model, age (p < 0.001), sex (p < 0.001), smoking(p < 0.001), and cholesterol (p < 0.05) remained independent predictors of internal carotid artery atherosclerosis. Conclusions. Total serum cholesterol level seems to be an independent risk factor of atherosclerosis in the carotid artery. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound 34:283,288, 2006 [source]


    Improved dynamic susceptibility contrast (DSC)-MR perfusion estimates by motion correction

    JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2007
    Robert K. Kosior BSc
    Abstract Purpose To investigate the effect of patient motion on quantitative cerebral blood flow (CBF) maps in ischemic stroke patients and to evaluate the efficacy of a motion-correction scheme. Materials and Methods Perfusion data from 25 ischemic stroke patients were selected for analysis. Two motion profiles were applied to a digital anthropomorphic brain phantom to estimate accuracy. CBF images were generated for motion-corrupted and motion-corrected data. To correct for motion, rigid-body registration was performed. The realignment parameters and mean CBF in regions of interest were recorded. Results All patient data with motion exhibited visibly reduced intervolume misalignment after motion correction. Improved flow delineation between different tissues and a more clearly defined ischemic lesion (IL) were achieved in the motion-corrected CBF. A significant difference occurred in the IL (P < 0.05) for patients with severe motion with an average difference between corrupted and corrected data of 4.8 mL/minute/100 g. The phantom data supported the patient results with better CBF accuracy after motion correction and high registration accuracy (<1 mm translational and <1° rotational error). Conclusion Motion degrades flow differentiation between adjacent tissues in CBF maps and can cause ischemic severity to be underestimated. A registration motion correction scheme improves dynamic susceptibility contrast (DSC)-MR perfusion estimates. J. Magn. Reson. Imaging 2007;26:1167,1172. © 2007 Wiley-Liss, Inc. [source]


    Combination of T2*W and FLAIR Abnormalities for the Prediction of Parenchymal Hematoma Following Thrombolytic Therapy in 100 Stroke Patients

    JOURNAL OF NEUROIMAGING, Issue 4 2009
    Jens Fiehler MD
    ABSTRACT INTRODUCTION The objective of our study was to determine whether the combination of hypointense spots ("cerebral microbleeds," CMBs) with a leukoaraiosis is associated with the risk of parenchymal hematoma (PH) after thrombolytic therapy. PATIENTS AND METHODS We analyzed magnetic resonance imaging (MRI) scans acquired within 6 hours after symptom onset from 100 ischemic stroke patients. Multiparametric MRI including a T2*-weighted (T2*w) MRI and fluid attenuated inversion recovery (FLAIR) was performed before thrombolysis in all patients. Initial T2*w imaging was rated by two independent observers for the presence of CMBs smaller than 5 mm. White matter changes were evaluated using an adapted scale of Fazekas and Schmidt. PH was defined in follow-up imaging. FINDINGS A PH was observed in seven per 100 patients. CMBs were detected by observer 1 in 22 and observer 2 in 20 patients. We found a very low sensitivity (0.14) for prediction of PH by the presence of CMBs. We found a concordant increase in the rate of PH when the periventricular hyperintensity in FLAIR was larger than a thin lining. Sensitivity was good-to-perfect (0.86 and 1.00, observers 1 and 2) and specificity was substantial (0.65 and 0.66). Using the combination of a periventricular matter lesion (PVML)>1 and the presence of CMBs did not improve the prediction of PH. DISCUSSION A marked periventricular hyperintensity in FLAIR imaging seems to be associated with a substantially increased risk of PH. A combination of CMBs with leukoaraiosis scores did not appear to be beneficial for prognosis. [source]


    Topographic Patterns of Small Subcortical Infarcts Associated with MCA Stenosis: A Diffusion-Weighted MRI Study

    JOURNAL OF NEUROIMAGING, Issue 3 2006
    Xin Wang MD
    ABSTRACT Background and Purpose. Small subcortical infarcts (SSI, maximum lesion diameter ,2.0 cm) are usually considered as infarcts caused by small vessel disease. However, SSI can also be associated with large artery occlusive disease such as middle cerebral artery (MCA) stenosis. We performed a prospective study to investigate the relationship between MCA stenosis and SSI distribution and further to investigate the mechanism of SSI caused by MCA stenosis. Methods. Magnetic resonance angiography (MRA) and diffusion-weighed MRI (DWI) of consecutive acute ischemic stroke patients with recent SSI were studied. The distribution of acute infarcts on DWI was categorized as cortical infarct (CI), border zone infarct (BI), or perforating artery infarct (PAI). Results. Totally, 93 cases were recruited, among which 12 had single SSI with MCA stenosis (group 1) and 26 patients had multiple SSI with MCA stenosis (group 2), while 55 patients without MCA stenosis had single SSI (group 3). For patients with single SSI and MCA stenosis, 6 had BI and 6 had PAI; for patients with multiple SSI and MCA stenosis, 25 had BI, 4 had PAI and 9 had CI (compared with group1: P= .001); for patients with single SSI but without MCA stenosis, 20 had BI and 35 had PAI (compared with group1: P= .58). Conclusion. Multiple acute infarcts along the border zone are the commonest pattern in small infarcts with MCA stenosis, especially among those with multiple acute infarcts. Our data suggest that hemodynamic compromise and artery-to-artery embolism may be both important factors for infarcts in patients with MCA stenosis. [source]


    Intravenous administration of melatonin reduces the intracerebral cellular inflammatory response following transient focal cerebral ischemia in rats

    JOURNAL OF PINEAL RESEARCH, Issue 3 2007
    Ming-Yang Lee
    Abstract:, We have previously shown that exogenous melatonin improves the preservation of the blood,brain barrier (BBB) and neurovascular unit following cerebral ischemia,reperfusion. Recent evidence indicates that postischemic microglial activation exaggerates the damage to the BBB. Herein, we explored whether melatonin mitigates the cellular inflammatory response after transient focal cerebral ischemia for 90 min in rats. Melatonin (5 mg/kg) or vehicle was given intravenously at reperfusion onset. Immunohistochemistry and flow cytometric analysis were used to evaluate the cellular inflammatory response at 48 hr after reperfusion. Relative to controls, melatonin-treated animals did not have significantly changed systemic cellular inflammatory responses in the bloodstream (P > 0.05). Melatonin, however, significantly decreased the cellular inflammatory response by 41% (P < 0.001) in the ischemic hemisphere. Specifically, melatonin effectively decreased the extent of neutrophil emigration (Ly6G-positive/CD45-positive) and macrophage/activated microglial infiltration (CD11b-positive/CD45-positive) by 51% (P < 0.01) and 66% (P < 0.01), respectively, but did not significantly alter the population composition of T lymphocyte (CD3-positive/CD45-positive; P > 0.05). This melatonin-mediated decrease in the cellular inflammatory response was accompanied by both reduced brain infarction and improved neurobehavioral outcome by 43% (P < 0.001) and 50% (P < 0.001), respectively. Thus, intravenous administration of melatonin upon reperfusion effectively decreased the emigration of circulatory neutrophils and macrophages/monocytes into the injured brain and inhibited focal microglial activation following cerebral ischemia,reperfusion. The finding demonstrates melatonin's inhibitory ability against the cellular inflammatory response after cerebral ischemia,reperfusion, and further supports its pleuripotent neuroprotective actions suited either as a monotherapy or an add-on to the thrombolytic therapy for ischemic stroke patients. [source]


    Carboxypeptidase U (TAFIa) activity is induced in vivo in ischemic stroke patients receiving thrombolytic therapy

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 1 2008
    J. L. WILLEMSE
    No abstract is available for this article. [source]


    Stromelysin-1 (MMP-3) is critical for intracranial bleeding after t-PA treatment of stroke in mice

    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2007
    Y. SUZUKI
    Summary.,Background:,Tissue-type plasminogen activator (t-PA) is approved for treatment of ischemic stroke patients, but it may increase the risk of intracranial bleeding (ICB). Matrix metalloproteinases (MMPs), which can be activated through the plasminogen/plasmin system, may contribute to ICB after ischemic stroke. Objectives:,To explore the contribution of plasminogen, MMP-3 and MMP-9 to ICB associated with t-PA treatment after ischemic stroke. Methods:,Using a thrombotic middle cerebral artery occlusion (MCA-O) model, ICB was studied in mice with genetic deficiencies of plasminogen (Plg,/,), stromelysin-1 (MMP-3,/,), or gelatinase B (MMP-9,/,) and their corresponding wild-type (WT) littermates. The induction of MMP-3 and MMP-9 was also studied in C57BL/6 WT mice. Results:,ICB induced by t-PA (10 mg kg,1) was significantly less than WT in Plg,/, (P < 0.05) and MMP-3,/, (P < 0.05) but not in MMP-9,/, mice. Furthermore, administration of the broad-spectrum MMP inhibitor GM6001 after t-PA treatment reduced ICB significantly (P < 0.05) in MMP-3+/+ mice, but had no effect on MMP-3,/, mice. MMP-3 expression was significantly enhanced at the ischemic hemisphere; with placebo treatment, it was expressed only in neurons, whereas it was up-regulated in endothelial cells with t-PA treatment. Although MMP-9 expression was also significantly enhanced at the ischemic brain, the amount and the distribution were comparable in mice with and without t-PA treatment. Conclusions:,Our data with gene-deficient mice thus suggest that plasminogen and MMP-3 are relatively more important than MMP-9 for the increased ICB induced by t-PA treatment of ischemic stroke. [source]


    Coagulopathy and embolic signal in cancer patients with ischemic stroke

    ANNALS OF NEUROLOGY, Issue 2 2010
    Jin Myoung Seok MD
    Objective It has been reported that embolic signal (ES) detected by transcranial Doppler (TCD) has clinical significance, especially in patients with recent stroke attributable to arterial or cardiac embolism. Therefore, we conducted this study to determine whether the prevalence of ES is high in ischemic stroke patients with cancer and related to hypercoagulopathy. Methods We prospectively studied cancer patients with acute ischemic stroke within the middle cerebral artery (MCA) distribution on diffusion-weighted imaging. Conventional stroke mechanisms (CSMs) were determined using cardiologic and vascular studies. Additionally, the coagulation status was assessed based on the serum D-dimer levels, and TCD monitoring was performed on both MCAs for 30 minutes to detect ES. Clinical features including vascular risk factors, characteristics of ischemic stroke, and cancer and laboratory findings associated with the presence of ES were evaluated. Results A total of 74 patients were finally included in this study. ES was more commonly observed in patients without CSMs (22 of 38 patients, 57.9%) than in those with CSMs (12 of 36 patients, 33.3%) (p = 0.034). Moreover, ES was more commonly detected in patients with high D-dimer levels (p < 0.001), and D-dimer levels were significantly correlated with the number of ESs in patients without CSMs (r = 0.732, p < 0.001), but were poorly correlated in patients with CSMs (r = 0.152, p = 0.375). Higher levels of D-dimer (odds ratio [OR], 1.082 per 1,g/ml increase; 95% confidence interval [CI], 1.014,1.154) and adenocarcinoma (OR, 3.829; 95% CI, 1.23,13.052) were independently associated with the presence of ES. The use of anticoagulants dramatically decreased the D-dimer levels. Interpretation A high prevalence of ES was observed in cancer patients with ischemic stroke, especially in those without CSMs. Elevated D-dimer levels were independently associated with ES, and decreased dramatically with the use of anticoagulants. ANN NEUROL 2010;68:213,219 [source]


    Characterizing the diffusion/perfusion mismatch in experimental focal cerebral ischemia

    ANNALS OF NEUROLOGY, Issue 2 2004
    Xiangjun Meng MD
    Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) can rapidly detect lesions in acute ischemic stroke patients. The PWI volume is typically substantially larger than the DWI volume shortly after onset, that is, a diffusion/ perfusion mismatch. The aims of this study were to follow the evolution of the diffusion/ perfusion mismatch in permanent and 60- minute temporary focal experimental ischemia models in Sprague-Dawley rats using the intraluminal middle cerebral artery occlusion (MCAO) method. DWI and arterial spin-labeled PWI were performed at 30, 60, 90, 120, and 180 minutes after occlusion and lesion volumes (mm3) calculated At 24 hours after MCAO, and infarct volume was determined using triphenyltetrazolium chloride staining. In the permanent MCAO group, the lesion volume on the ADC maps was significantly smaller than that on the cerebral blood flow maps through the first 60 minutes after MCAO; but not after 90 minutes of occlusion. With 60 minutes of transient ischemia, the diffusion/perfusion mismatch was similar, but after reperfusion, the lesion volumes on ADC and cerebral blood flow maps became much smaller. There was a significant difference in 24- hour infarct volumes between the permanent and temporary occlusion groups. [source]


    Early magnetic resonance imaging findings in patients receiving tissue plasminogen activator predict outcome: Insights into the pathophysiology of acute stroke in the thrombolysis era,

    ANNALS OF NEUROLOGY, Issue 1 2004
    Julio A. Chalela MD
    We measured ischemic brain changes with diffusion and perfusion MRI in 42 ischemic stroke patients before and 2 hours (range approximately 1.5 to 4.5 hours) after standard intravenous tissue plasminogen activator (tPA) therapy. The median time from stroke onset to tPA was 131 minutes. Clinical and MRI variables (change in perfusion and/or diffusion weighted lesion volume) were compared between those with excellent outcome defined as 3-month modified Rankin score (mRS) of 0 to 1 and those with incomplete recovery (mRS >1). In multivariate logististic regression analysis, the most powerful independent predictor for excellent outcome was improved brain perfusion: hypoperfusion volume on mean transit time (MTT) map decrease >30% from baseline to 2-hour post tPA scan (p=0.009; odds ratio [95% confidence interval], 20.7 [2.1-203.9]). Except for age < 70 years, no other baseline clinical or imaging variable was an independent predictor of outcome. We propose MTT lesion volume decrease more than 30% 2 hours after tPA as an early marker of long-term clinical benefit of thrombolytic therapy. [source]


    Magnetic resonance cerebral metabolic rate of oxygen utilization in hyperacute stroke patients

    ANNALS OF NEUROLOGY, Issue 2 2003
    Jin-Moo Lee MD
    The purpose of this study was to explore the feasibility of obtaining magnetic resonance,measured cerebral metabolic rate of oxygen utilization (MR-CMRO2) in acute ischemic stroke patients. Seven stroke patients were serially imaged: 4.5 ± 0.9 hours (tp1), 3 to 5 days (tp2), and 1 to 3 months (tp3) after symptom onset. Diffusion-weighted, perfusion-weighted, and multiecho gradient-echo/spin-echo images were acquired; cerebral blood flow and oxygen extraction fraction maps were obtained from which CMRO2 was calculated as the product of cerebral blood flow and oxygen extraction fraction. The final infarct lesions obtained from tp3 T2-weighted images and the "penumbra" obtained from the tp1 perfusion-weighted image,defined lesion were coregistered onto tp1 CMRO2 maps. CMRO2 values in the region of brain that eventually infarcted were reduced to 0.40 ± 0.24 of the respective region on the contralateral hemisphere. The "salvaged penumbra" defined by the area of mismatch between the final infarct and the tp1 perfusion-weighted lesion demonstrated an average CMRO2 value of 0.55 ± 0.11 of the contralateral hemisphere. Although our results are preliminary and require further evaluation, the ability to obtain in vivo measurements of MR-CMRO2 noninvasively potentially can provide information for determining brain tissue viability in acute ischemic stroke patients. [source]


    Strongly increased levels of fibrinogen elastase degradation products in patients with ischemic stroke

    BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2008
    Lonneke M. L. De Lau
    Summary Ischemic stroke is associated with leucocyte activation. Activated leucocytes release elastase, an enzyme that can degrade fibrinogen. Fibrinogen elastase degradation products (FgEDP) may serve as a specific marker of elastase proteolytic activity. In a case-control study of 111 ischemic stroke patients and 119 controls, significantly higher FgEDP levels were observed in cases than in controls, both in the acute phase and in the convalescent phase. Results were only slightly affected by adjustment for cardiovascular risk factors, C-reactive protein and fibrinogen. Our findings suggest that FgEDP might be involved in the pathogenesis of stroke. [source]


    A randomized controlled trial of rivastigmine in patients with cognitive impairment no dementia because of cerebrovascular disease

    ACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010
    K. Narasimhalu
    Narasimhalu K, Effendy S, Sim CH, Lee JM, Chen I, Hia SB, Xue HL, Corrales MP, Chang HM, Wong MC, Chen CP, Tan EK. A randomized controlled trial of rivastigmine in patients with cognitive impairment no dementia because of cerebrovascular disease. Acta Neurol Scand: 2010: 121: 217,224. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, The safety and efficacy of early acetylcholinesterase inhibitors therapy in patients with cognitive impairment no dementia (CIND) after a cerebrovascular accident have not been examined. In this study, we investigated the safety and efficacy of rivastigmine in cognition, particularly executive function in patients with CIND because of cerebrovascular disease. Methods,,, This study was a 24-week, double-blind, randomized, placebo-controlled trial of ischemic stroke patients seen at a tertiary hospital who had cognitive impairment no dementia because of cerebrovascular disease. The intervention was either rivastigmine or placebo up to 9 mg/day. The primary outcome of interest was mean change from baseline in the Ten-Point Clock Drawing and Color Trails 1 and 2. Results,,, Fifty patients were randomized into rivastigmine (n = 25) and placebo (n = 25) arms. Patients in the rivastigmine group showed statistically significant improvement (1.70 vs 0.13, P = 0.02) on the animal subtask of the verbal fluency measure compared with placebo. There was also a trend (non-significant) towards improvement in Color Trails II. Conclusions,,, In this pilot study, we demonstrated that rivastigmine was well tolerated in patients with CIND because of cerebrovascular disease and may potentially improve executive functioning. [source]


    Why ischemic stroke patients do not receive thrombolytic treatment: results from a general hospital

    ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009
    J. S. P. Van Den Berg
    Objectives,,, To determine the proportion of patients with an ischemic stroke that received intravenous (IV) thrombolytic treatment, and reasons why patients are not treated. Methods,,, A prospective registry of all patients with an ischemic stroke admitted to our emergency department (ED). Results,,, A total of 286 patients with an ischemic stroke were admitted. Eighty-one patients were admitted within 3 h of onset of neurological deficit, of which 28 received IV thrombolysis. In 25 patients no thrombolytic treatment was given because of the presence of the National Institute of Neurological Disorders and Stroke (NINDS) exclusion criteria, and one patient refused treatment. No thrombolytic treatment was given to 27 patients because of mild neurological deficit or rapid clinical improvement, and after 3 months all these patients were independently living at home without nursing help. Despite a public campaign to gain awareness concerning stroke, the majority of the patients arrived too late at the ED for thrombolytic treatment. Conclusions,,, A large proportion of the patients with an ischemic stroke are admitted too late to receive IV thrombolysis. More needs to be done to increase both public and medical awareness of stroke as a treatable emergency. [source]


    Serum creatinine is an inadequate screening test for renal failure in ischemic stroke patients

    ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2009
    G. Piñol-Ripoll
    Objective,,, Serum creatinine (SCr) level is the most commonly used screening test for renal function, but its concentration is affected by factors other than glomerular filtration rate (GFR). We hypothesized that SCr would underestimate the degree of renal failure in ischemic stroke patients. Material and methods,,, We conducted a prospective study of 273 patients admitted to our institution for ischemic stroke within a year. GFR was calculated using the Cockcroft,Gault formula (CG). Patients were grouped according to the SCr with stages of renal failure according to CG values. Results,,, Of the 273 patients studied, 231 had normal SCr. Of this group 46.8% (108), 24.7% (57) and 4 (1.7%) had mild, moderate and severe renal failure according to GFR estimation. Among patients with normal SCr, abnormal CG values were identified in 86.2% (150) , 65 years old, 33.3% (19) <65 years old, 69% (89) in men and 78.4% (80) in women. An SCr greater than 1.7 mg/dl had only a sensitivity of 14.7%. Conclusions,,, This study documents the substantial prevalence of significantly abnormal renal function among patients with normal-range SCr. Routine estimation of GFR be preferred to SCr as a screening method for the early detection of renal impairment in stroke patients. [source]


    Long-term mortality among young ischemic stroke patients in western Norway

    ACTA NEUROLOGICA SCANDINAVICA, Issue 3 2007
    U. Waje-Andreassen
    Objectives,,, To obtain data on long-term mortality among young ischemic stroke patients compared with controls in this population-based study. Material and methods ,, We used Kaplan,Meier survival analysis to compare 232 patients aged 15,49 years with first-ever cerebral infarction in 1988,1997 and 453 controls followed from inclusion to death or 1 August 2005 for 2515 and 5558 person-years respectively. In a subanalysis of 192 patients, we compared risk factor variables using the Kaplan,Meier method and log-rank testing. We applied a Cox proportional hazards model to adjust for multiple risk factors. Results ,, Forty-five patients and nine controls died during follow-up (P < 0.0005). Independent risk factors for mortality were active tumor disease (P < 0.0005), high consumption of alcohol (P < 0.0005), coronary atherosclerosis (P < 0.001), living alone (P < 0.02), seizures (P < 0.04) and smoking (P = 0.08). Conclusions ,, Long-term mortality was significantly increased among young stroke patients, mainly due to such lifestyle factors as high consumption of alcohol and tobacco. [source]