International journal of cerebrovascular disease and stroke最新文献

{"title":"Selective Vulnerability to Transcellular Pathway of Blood-Brain Barrier in Chronic Stage of the Kainate Model of Temporal Lobe Epilepsy in Rats","authors":"C. U. Yılmaz, N. Orhan, N. Arican, B. Ahishali, C. Gürses, M. Küçük, I. Elmas, E. Taşkıran, M. Kaya","doi":"10.29011/2688-8734.100008","DOIUrl":"https://doi.org/10.29011/2688-8734.100008","url":null,"abstract":"Background: The blood-brain barrier (BBB) integrity is severely affected in many epilepsy syndromes including temporal lobe epilepsy (TLE). Aim: In the present study, we investigated the effects of acute and chronic seizures induced by kainic acid (KA) on the transport pathways of BBB in rats. Methods: Electroencephalography (EEG) was recorded to evaluate seizure activity. Immunohistochemistry for claudin-5, a tight junction protein, caveolin-1, and the glial fibrillary acidic protein (GFAP), a marker of astrocyte activation, was performed. Electron microscopy was used to ultrastructurally assess the presence and route of extravasation of horseradish peroxidase (HRP), a permeability marker, in barrier type of brain capillary endothelial cells. Results: The immunoreactivity of claudin-5 and caveolin-1 in hippocampus increased by both acute and chronic seizures (p<0.01), while an increase in GFAP immunoreactivity was found in the hippocampus by only acute seizures (p<0.01). The endothelial cells of brain capillaries in hippocampus and amygdala regions of animals in acute and chronic sham groups showed occasional HRP reaction products. Acute and chronic seizures led to the observation of significantly greater extent of accumulation of HRP reaction products in both brain regions of rats compared to acute and chronic sham groups (p<0.01), while tight junctions were intact in all experimental groups. Conclusion: This study provides immunohistochemical and ultrastructural evidence of BBB disruption through a selective vulnerability of the transcellular transport via an increase in caveolar vesicles in the endothelial cells brain capillaries rather than activation of paracellular pathway in the KA-induced rat model of TLE. Citation: Yilmaz CU, Orhan N, Arican N, Ahishali B, Gürses C, et al. (2018) Selective Vulnerability to Transcellular Pathway of Blood-Brain Barrier in Chronic Stage of the Kainate Model of Temporal Lobe Epilepsy in Rats. Int J Cerebrovasc Dis Stroke : IJCDS-108. DOI: 10.29011/ IJCDS-106. 100008 2 Volume 2018; Issue 01","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81728859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Coexistence of Familial Mediterranean Fever and Stroke","authors":"M. Batum, A. Kısabay, M. Akgul, D. Selçuki","doi":"10.29011/2688-8734.100007","DOIUrl":"https://doi.org/10.29011/2688-8734.100007","url":null,"abstract":"Familial Mediterranean Fever (FMF) is a hereditary disease that is characterized by fever, peritonitis, arthritis, skin lesions in the form of erysipelas and has recurrent episodes of fever and features of autosomal recessive autoimmunity. In FMF, which is an inflammatory disease, while procoagulant factors increase both during episodes and inter-episode periods, the anticoagulant and fibrinolytic activity decrease. As a result, predisposition to thrombosis occurs. A 46-year-old female patient, while she was being followed-up because of acute FMF episode in the Rheumatology department, she was admitted to the stroke unit due to the right shift of the mouth, speech disorder, the left side weakness and numbness. In the brain and diffusion Magnetic Resonance (MR) imaging of the patient, it was seen that there was the diffusion restriction in the field irrigated by right middle cerebral artery, and the intra-infarct hematoma on right side at the level of basal ganglia in follow-up. It was thought to be appropriate to present the case, which applied with ischemic stroke symptom and had development of intra-infarct hematoma in follow-up, due to the coexistence of two clinical forms. There were no similar cases that had coexistence of two different clinical symptoms, in the literature.","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"80 1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77304941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of Cilostazol + Nimodipine on Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage","authors":"K. Lara, S. Villaraza, J. Navarro","doi":"10.29011/2688-8734.100002","DOIUrl":"https://doi.org/10.29011/2688-8734.100002","url":null,"abstract":"Introduction: Cerebral Vasospasm (VSP) accounts for 39% of morbidity following aneurysmal Subarachnoid Hemorrhage (SAH), occurring between days 4 and 14, with mean time of onset of 7.7 days after the ictus. Nimodipine has shown to prevent cerebral VSP after SAH. Objective: This clinical trial aimed to determine the efficacy of oral nimodipine and cilostazol combination in preventing vasospasm following aneurysmal SAH. Methodology: This is a prospective, randomized, open-label, blinded end point study to establish whether the combination of nimodipine and cilostazol will reduce the incidence of VSP arising from spontaneous aneurysmal SAH. The primary endpoint is the onset of cerebral VSP as manifested by increasing trend of Lindergaard Index (LI) during Transcranial Doppler (TCD) monitoring. A total of 144 patients were recruited from May 2014 to December 2015 and randomized to 2 groups. Group A (control) received nimodipine 60mg every 4 hours for 21 days. Group B (treatment) received nimodipine 60mg every 4 hours for 21 days, and cilostazol 100mg every 12 for 14 days. Transcranial Doppler (TCD) monitoring was done daily for measurement of LI. Conclusion: The combination of oral nimodipine 60 mg every 4 hours for 21 days and cilostazol 100 mg every 12 hours for 14 days is well tolerated and reduced the incidence of vasospasm following aneurysmal SAH compared to nimodipine alone. Introduction Aneurysmal Subarachnoid Hemorrhage (SAH) accounts for only 2%-5% of all strokes but carries a high mortality of 22%-25% of deaths secondary to cerebrovascular diseases [1]. For patients who survive, a high morbidity has been recorded secondary to its complications such as rebleeding, hydrocephalus, seizures and cerebral vasospasm. Cerebral Vasospasm (VSP) accounts for 39% of morbidity following aneurysmal SAH [2], occurring between days 4 and 14, with mean time of onset of 7.7 days after the ictus [3]. Following a well-utilized scoring system, the Fisher grading determines the degree of subarachnoid blood and the risk of VSP [4]. Detection of the onset of VSP with high confidence after aneurysmal SAH is important. The Digital Subtraction Angiography (DSA) and the Transcranial Doppler (TCD) are the two most commonly employed procedures. DSA is the gold standard imaging modality [5,6], with nearly 100% sensitivity and specificity for detection of VSP. However, its use has been limited by its relative invasiveness, high cost, along with the tedious time-consuming performance of serial studies. On the other hand, TCD is a noninvasive, and safe tool that is also widely used for detection of VSP. It is highly specific (89%98%) and sensitive (84%-93%) [7] and may be used daily with minimal cost and risk to patients. Aside from absolute increase in mean flow velocity, determining the LI, is an important information to support the presence of VSP [1,3]. Numerous studies have been published regarding the medical management on the prevention of VSP after aneurysmal SAH. ","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74642089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing the Utility of Sex-Specific Organotypic Hippocampal Sliced Cultures for In Vitro Ischaemia Studies","authors":"Asha Akram, Raeed Altaee, B. Grubb, C. Gibson","doi":"10.29011/2688-8734.100004","DOIUrl":"https://doi.org/10.29011/2688-8734.100004","url":null,"abstract":"In vitro models of ischaemia are commonly used in neuroscience research yet can be difficult to establish in a reproducible manner due to lack of experimental details commonly reported in publications. This study describes a series of optimization steps in order to produce a reliable model of organotypic hippocampal sliced cultures used for in vitro ischaemia studies. In addition, we describe the process by which sex-specific cultures were produced. Optimization data is provided regarding the age of animals used, time course of culture maintenance in vitro and optimal time of Oxygen and Glucose Deprivation (OGD) in order to produce a sufficient level of cell death. In addition, we demonstrate the effect of the age and sex of the pups on the amount of cell death produced. This study provides detailed optimization steps required to produce a reliable and reproducible sex-specific organotypic hippocampal sliced culture model which would then be suitable for exposure to OGD in order to model in vitro ischaemia and assess potential neuroprotective compounds.","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"255 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73301619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What Fibrinolytic Therapy Can Learn from Endogenous Fibrinolysis; Both Activators Rather Than Only One are Required","authors":"V. Gurewich","doi":"10.29011/2688-8734.100005","DOIUrl":"https://doi.org/10.29011/2688-8734.100005","url":null,"abstract":"Fibrinolytic therapy with Tissue Plasminogen Activator (tPA) alone has been the standard for three decades, but due to its inefficacy and bleeding risk, tPA has been replaced by Primary Percutaneous Coronary Intervention (PPCI) as the treatment of choice for Acute Myocardial Infarction (AMI). By contrast to tPA mono-therapy, natural fibrinolysis uses a sequential combination of both biological activators, tPA and uPA, the native form of which is a proenzyme, prouPA. Both in vitro and in vivo, tPA and prouPA have complementary modes of action in fibrinolysis and are synergistic when combined. In a published clinical trial, the PATENT study, 101 patients with AMI were treated with a 5 mg tPA bolus (5% of the standard dose) followed by a modest infusion of prouPA. This sequential combination virtually doubled the coronary TIMI-3 infarct artery patency rate and reduced the mortality six-fold compared to the best results with tPA alone. Introduction Fibrinolysis is the body’s natural defense that prevents physiological fibrin, needed for the repair of wear and tear vascular injuries, from building up and interfering with blood flow. Evidence that this system is ongoing comes from the invariable presence of the fibrinolytic degradation product D-dimer in plasma (110-250 ng/ml). This normal concentration goes up as much as twenty-fold in the presence of thromboembolism, representing endogenous fibrinolysis. The idea that tPA alone was responsible for this efficient system represents a fundamental misunderstanding of this biological system, which remains to be addressed [1]. Ever since the FDA approved tPA for the treatment of AMI in 1987, it has been the activator choice and it has been used alone. As a result, the current understanding of the clinical benefit of fibrinolysis is based almost exclusively on tPA monotherapy. At the same time, it was well established that there are two plasminogen activators, the second one being Urokinase Plasminogen Activator (uPA), the native form of which is a proenzyme (prouPA) [2]. Both are required for clot lysis in vitro, and their fibrinolytic properties are complementary and synergistic in combination. Therefore, the clinical benefits of the full potential of fibrinolytic therapy remains to be established. Discussion With few exceptions, the fibrinolytic clinical experience has been that of tPA or one of its two longer half-life mutant forms. This experience has been sufficiently disappointing that fibrinolysis has become discredited, and it has been replaced by Primary Percutaneous Coronary Intervention (PPCI) as the treatment of choice for AMI. For ischemic stroke, the tPA bleeding risk is higher and has obliged a one third tPA dose reduction which further diminished its efficacy. Even with this reduction, a 6-7% risk of intracranial hemorrhage remains [3]. Due to this risk, reperfusion therapy must be delayed until a careful history and diagnostic studies have eliminated a bleeding risk. Because of these risks","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87072223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Predictors of Mortality Following PEG Insertion in Stroke Patients","authors":"","doi":"10.29011/2688-8734.000028","DOIUrl":"https://doi.org/10.29011/2688-8734.000028","url":null,"abstract":"","PeriodicalId":92795,"journal":{"name":"International journal of cerebrovascular disease and stroke","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73663501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}