scholarly journals Seizures and epilepsy in patients with ischaemic stroke

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Johann Philipp Zöllner ◽  
Friedhelm C. Schmitt ◽  
Felix Rosenow ◽  
Konstantin Kohlhase ◽  
Alexander Seiler ◽  
...  

Abstract Background With the increased efficacy of stroke treatments, diagnosis and specific treatment needs of patients with post-stroke seizures (PSS) and post-stroke epilepsy have become increasingly important. PSS can complicate the diagnosis of a stroke and the treatment of stroke patients, and can worsen post-stroke morbidity. This narrative review considers current treatment guidelines, the specifics of antiseizure treatment in stroke patients as well as the state-of-the-art in clinical and imaging research of post-stroke epilepsy. Treatment of PSS needs to consider indications for antiseizure medication treatment as well as individual clinical and social factors. Furthermore, potential interactions between stroke and antiseizure treatments must be carefully considered. The relationship between acute recanalizing stroke therapy (intravenous thrombolysis and mechanical thrombectomy) and the emergence of PSS is currently the subject of an intensive discussion. In the subacute and chronic post-stroke phases, important specific interactions between necessary antiseizure and stroke treatments (anticoagulation, cardiac medication) need to be considered. Among all forms of prevention, primary prevention is currently the most intensively researched. This includes specifically the repurposing of drugs that were not originally developed for antiseizure properties, such as statins. PSS are presently the subject of extensive basic clinical research. Of specific interest are the role of post-stroke excitotoxicity and blood–brain barrier disruption for the emergence of PSS in the acute symptomatic as well as late (> 1 week after the stroke) periods. Current magnetic resonance imaging research focussing on glutamate excitotoxicity as well as diffusion-based estimation of blood–brain barrier integrity aim to elucidate the pathophysiology of seizures after stroke and the principles of epileptogenesis in structural epilepsy in general. These approaches may also reveal new imaging-based biomarkers for prediction of PSS and post-stroke epilepsy. Conclusion PSS require the performance of individual risk assessments, accounting for the potential effectiveness and side effects of antiseizure therapy. The use of intravenous thrombolysis and mechanical thrombectomy is not associated with an increased risk of PSS. Advances in stroke imaging may reveal biomarkers for PSS.

2018 ◽  
Vol 28 (3) ◽  
pp. 283-288 ◽  
Author(s):  
Zhong‐Song Shi ◽  
Gary R. Duckwiler ◽  
Reza Jahan ◽  
Satoshi Tateshima ◽  
Viktor Szeder ◽  
...  

2021 ◽  
Author(s):  
Wen Jiang ◽  
Jie Li ◽  
Yuefang Cai ◽  
Wenchen Liu ◽  
Mei Chen ◽  
...  

Abstract Ischemic stroke (IS) is a major neurological disease with high fatality and residual disability burdens. Increasing amount of long noncoding RNAs (lncRNAs) have been revealed to play an important role in ischemic stroke. However, the roles and significances of most lncRNAs in ischemic stroke are still unknown.This study was performed to identify differentially expressed lncRNAs using a lncRNA microarray in whole blood samples of patients suffered from acute cerebral ischemia. Bioinformatics analyses including GO, KEGG pathway enrichment analysis, and proximity to putative stroke risk location analysis were performed. A novel lncRNA ENST00000530525 significantly decreased after ischemic stroke. Furthermore, we evaluated lncRNA ENST00000530525 expression in cultured hCMEC/D3 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions using fluorescent in situ hybridization (FISH) and quantitative real-time polymerase chain reaction (RT-qPCR) analysis. To investigate the function of lncRNA ENST00000530525, the plasmid of overexpression(OE) and negative control(NC) were transfected into hCMEC/D3, then cell viability was detected by cell counting kit-8 (CCK-8) Assay after OGD/R,lncRNA ENST00000530525 and ANO1 expression were investigated using RT-qPCR and Immunofluorescence. For blood-brain barrier(BBB) permeability,FITC-dextran transendothelial permeability assay and Tight junction(Tj) protein was detected.There were 3352 differentially expressed lncRNAs in blood samples of acute ischemic stroke patients. The validation results were consistent with gene chip data.GO and KEGG results showed these lncRNAs were mainly related to oxygen and glucose metabolism, leukocyte transendothelial migration,mitophagy and cellular senescence.Among these, lncRNA ENST00000530525 was the highly down-regulated lncRNA and mapped within the ischemic stroke associated gene anoctamin-1 (ANO1). We furtherly found lncRNA ENST00000530525 was down-regulated in hCMEC/D3 cells under 4h OGD and 20h reoxygenation(OGD4/R20) conditions. Up-regulating lncRNA ENST00000530525 decreased the cell viability while increased ANO1 expression and contributed to BBB injury of hCMEC/D3 cells after OGD4/R20.The lncRNA ENST00000530525 might plays deleterious roles in post-stroke pathogenesis. The results show light on some differentially expressed lncRNAs in human certainly participate through characteristic roles in post-stroke pathogenesis, thus, the roles and significances of some novel lncRNAs in ischemic stroke thereby warranting further study.


2020 ◽  
Vol 11 ◽  
Author(s):  
Parisa Heidari ◽  
Sarah Blayney ◽  
Jarrhett Butler ◽  
Emi Hitomi ◽  
Marie Luby ◽  
...  

Background: Penumbral brain tissue identified with multimodal imaging can be salvaged with reperfusion in an extended time window. The risk of severe hemorrhagic complications after reperfusion therapy increases with worsening disruption of the blood-brain barrier (BBB). The relationship between penumbral tissue and BBB disruption has not been previously studied.Methods: Stroke patients presenting in an extended time window without a large vessel occlusion who underwent diffusion-perfusion MRI within 24 h of last-seen-normal were included. The volume of penumbral tissue was calculated using mismatch on MRI. Mean permeability derangement (MPD) of the BBB was measured within the ischemic lesion. A target profile (TP) for treatment was defined based on the EXTEND trial.Results: 222 patients were included with a median age of 73 and 55% women. The median NIHSS was 6, the mean core volume was 14 ml, the mean ischemic volume was 47 mL and the mean mismatch volume was 33 mL. Higher MPD was significantly associated with less mismatch volume (p = 0.001). A target profile was associated with lower MPD (OR 0.97; CI 0.96:0.99; p < 0.001). Of the 105 patients who had a TP, 31 (30%) had a MPD > 20% suggesting an increased risk of hemorrhage. Thus, 33% (74/222) of patients had a favorable profile for benefit and safety.Conclusions: Patients presenting in an extended time window with a favorable penumbral profile for treatment have less severe BBB disruption. Up to a third of patients who currently go untreated could be considered for enrollment in a clinical trial of thrombolysis in an extended time window.


Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Shameena Bake ◽  
Farida Sohrabji

Background and Purpose: Although insulin-like growth factor (IGF)-1 treatment has been shown to reduce stroke-induced infarct volume, the mechanisms underlying its neuroprotective actions are not fully understood. The present study tested the hypothesis that IGF-1 may regulate the neuroinflammatory cascade initiated by ischemic stroke, specifically, by promoting the integrity of the blood brain barrier. Methods: Middle-aged (10-12 month old) female rats were implanted with a cannula directed toward the lateral ventricle. One week later, animals were anesthetized using isoflurane and the middle-cerebral artery was occluded using an intraluminal suture maintained in place for 90 mins. IGF-1 or vehicle was delivered icv, via a mini-pump, following reperfusion. All animals were terminated at 4h or 24h post MCAo. Blood brain barrier permeability was determined using Evan’s blue extravasation and infarct volumes were determined from TTC-stained brain sections. Inflammatory cytokines were analyzed from brain lysates by ELISA. Results: IGF-1 treatment to middle-aged females resulted in a 39% reduction in infarct volume when measured 24h post MCAo, confirming the neuroprotective action of this peptide hormone. In order to assess the effects of IGF-1 on early stroke induced effects, we next determined blood brain permeability 4h post stroke as well as the expression of cytokines in the ischemic hemisphere. IGF-1 treatment resulted in a significant reduction of blood brain barrier permeability at 4h post-stroke compared to vehicle treated animals. Moreover, multiplex cytokine analysis showed that IGF-1 significantly reduced inflammatory markers such as IL-6, IFN-gamma, TNF-alpha, eotaxin, GM-CSF. Brain infarct volume at 4h was similar in both IGF-1 and vehicle groups, indicating that the effects of IGF-1 on inflammatory markers precede its effects on infarct volume. IGF-1 also suppressed IL-6, MIP-2, GRO-KC, MCP-1, EGF and MIP-1-alpha expression at 24h post stroke, indicating a persistent anti-inflammatory effect for this growth factor. Conclusions: The above findings support the hypothesis that IGF-1 has unique anti-inflammatory action in the aging female brain, and suggest that brain endothelial cells may be a primary target of IGF-1.


Sign in / Sign up

Export Citation Format

Share Document