Bidirectional Causal Relationship Between Sleep Duration, Insomnia, and Cerebral Infarction: A Two-Sample Mendelian Randomization Study

2026-08-05T08:20:49+08:00

Objective: Observational studies suggest that abnormal sleep duration and insomnia are associated with stroke, but residual confounding factors, reverse causal bias, and the nonlinear characteristics of exposure-response relationships limit precise causal inference. This study employed a two-sample Mendelian randomization (MR) approach to systematically investigate the bidirectional causal relationship between sleep duration, insomnia, and cerebral infarction, clarifying their genetic causal effects. Methods: Genome-wide association study (GWAS) summary statistics were retrieved from the IEU OpenGWAS platform for sleep duration (ieu-a-1088; 128,266 participants of European descent), insomnia (ukb-b-3957; 462,341 participants of European descent), and cerebral infarction (ukb-d-I63; 361,194 participants of European descent). The inverse variance weighted (IVW) method was used as the core analytical approach, combined with the maximum likelihood method, MR-Egger regression, weighted median method, and weighted mode method for sensitivity analysis. Cochran’s Q test quantified heterogeneity across genetic instruments, while the MR-Egger intercept test was applied to detect directional horizontal pleiotropy. Results: After data harmonization, 26, 38, 24, and 128 genetic variants were included in the analyses of sleep duration → cerebral infarction, insomnia → cerebral infarction, cerebral infarction → sleep duration, and cerebral infarction → insomnia, respectively. IVW analysis revealed no significant causal effect of genetically predicted sleep duration on cerebral infarction [OR=1.002, 95% confidence interval (CI): 0.998-1.006, P=0.252], nor did genetic susceptibility to insomnia significantly affect the risk of cerebral infarction (OR=0.994, 95% CI: 0.988-1.001, P=0.100). In reverse analyses, genetic susceptibility to cerebral infarction showed no significant causal relationship with sleep duration (β=0.394, 95% CI: -1.620-2.408, P=0.701) or the insomnia phenotype (β=0.057 SD, 95% CI: -0.245-0.360, P=0.711). The results of various supplementary analyses were consistent with the core IVW results, demonstrating stable conclusions. Neither the Cochran’s Q test nor the MR-Egger intercept test detected significant heterogeneity or directional horizontal pleiotropy. Conclusion: This bidirectional MR study indicates that there is currently no reliable genetic evidence supporting a bidirectional causal relationship between sleep duration, insomnia, and cerebral infarction. Their clinical correlation may be largely mediated by non-genetic confounding factors.

The Impact of Cerebral Small Vessel Disease on Hemorrhagic Transformation After Mechanical Thrombectomy in Acute Large Vessel Occlusion Ischemic Stroke

2026-08-05T08:20:50+08:00

With the intensification of population aging and the rapid development of neuroimaging, cerebral small vessel disease (CSVD) has garnered increasing attention. Endovascular thrombectomy (EVT) can significantly improve functional outcomes in patients with intracranial large vessel occlusion and has become the standard treatment for acute large vessel occlusion ischemic stroke. Numerous studies suggest that pre-existing CSVD before acute ischemic stroke may increase the risk of hemorrhagic transformation (HT) after EVT, yet results remain controversial. This article primarily discusses the impact of different subtypes of CSVD and the total burden on magnetic resonance imaging on HT after EVT in patients with acute large vessel occlusion ischemic stroke, aiming to provide a clinical reference.

Clinical Neuroscience Research

Bidirectional Causal Relationship Between Sleep Duration, Insomnia, and Cerebral Infarction: A Two-Sample Mendelian Randomization Study

The Impact of Cerebral Small Vessel Disease on Hemorrhagic Transformation After Mechanical Thrombectomy in Acute Large Vessel Occlusion Ischemic Stroke