■尽管先前的研究报道了缺血性卒中(IS)和癫痫之间的双向关系,因果关系的存在及其方向性仍然是一个有争议的话题。
■与IS相关的单核苷酸多态性(SNP)从全基因组关联研究(GWAS)数据库中提取。包含所有癫痫病例的汇总遗传数据,以及全身性和局灶性癫痫亚型,是从国际抗癫痫联盟的GWAS研究中获得的。在这项研究中,主要分析方法使用方差逆加权(IVW)方法作为主要分析技术。为了增强研究结果对潜在多效性的稳健性,进行了额外的敏感性分析.
■在正向分析中,IVW方法显示IS与所有癫痫(比值比(OR)=1.127,95%置信区间(CI)=1.038~1.224,P=0.004)和全身性癫痫(IVW:OR=1.340,95%CI=1.162~1.546,P=5.70×10~5)的风险增加相关.IS与局灶性癫痫之间无显著因果关系(P>0.05)。此外,全身性癫痫,局灶性癫痫,所有癫痫均未显示与IS有因果关系.
■这项孟德尔随机化(MR)分析表明,IS会增加患癫痫的风险,尤其是全身性癫痫.相反,在癫痫发作和卒中发作之间没有明确的因果关系.因此,癫痫对IS发病机制的影响可能机制仍需进一步研究。
UNASSIGNED: Although previous studies have reported a bidirectional relationship between ischemic stroke (IS) and epilepsy, the existence of a causal nexus and its directionality remains a topic of controversy.
UNASSIGNED: The single nucleotide polymorphisms (SNPs) associated with IS were extracted from the Genome-Wide Association Study (GWAS) database. Pooled genetic data encompassing all epilepsy cases, as well as generalized and focal epilepsy subtypes, were acquired from the International League Against Epilepsy\'s GWAS study. In this study, the primary analysis approach utilized the inverse variance weighting (IVW) method as the main analytical technique. To enhance the robustness of the findings against potential pleiotropy, additional sensitivity analyses were conducted.
UNASSIGNED: In the forward analysis, the IVW method demonstrated that IS was associated with an increased risk of all epilepsy (odds ratio (OR) = 1.127, 95 % confidence interval (CI) = 1.038-1.224, P = 0.004) and generalized epilepsy (IVW: OR = 1.340, 95 % CI = 1.162-1.546, P = 5.70 × 10-5). There was no substantial causal relationship observed between IS and focal epilepsy (P > 0.05). Furthermore, generalized epilepsy, focal epilepsy, and all epilepsy did not show a causal relationship with IS.
UNASSIGNED: This Mendelian randomization (MR) analysis demonstrates that IS increases the risk of developing epilepsy, especially generalized epilepsy. Conversely, no clear causal association was found between epilepsy and the onset of stroke. Therefore, the possible mechanisms of the effect of epilepsy on the pathogenesis of IS still need to be further investigated.