Endovascular treatment is a highly effective therapy for acute ischemic stroke due to large vessel occlusion and has recently revolutionized stroke care. Oftentimes, ischemic core extent on baseline imaging is used to determine endovascular treatment-eligibility. There are, however, 3 fundamental issues with the core concept: First, computed tomography and magnetic resonance imaging, which are mostly used in the acute stroke setting, are not able to precisely determine whether and to what extent brain tissue is infarcted (core) or still viable, due to variability in tissue vulnerability, the phenomenon of selective neuronal loss and lack of a reliable gold standard. Second, treatment decision-making in acute stroke is multifactorial, and as such, the relative importance of single variables, including imaging factors, is reduced. Third, there are often discrepancies between core volume and clinical outcome. This review will address the uncertainty in terminology and proposes a direction towards more clarity. This theoretical exercise needs empirical data that clarify the definitions further and prove its value.

This trial showed an obviously higher rate of large and giant aneurysm obliteration with the Tubridge FD over Enterprise stent-assisted coiling. However, this higher obliteration rate came at the cost of a nonsignificantly higher rate of complications. Investigational site comparisons suggested that a learning curve for flow-diverter implantation should be recognized and factored into trial designs.

PurposeTo compare the safety and efficiency of stent assisted coiling (SAC) with non-SAC for the management of ruptured intracranial aneurysms.MethodsA meta-analysis that compared SAC with coiling alone and balloon assisted coiling was conducted by database searching. The primary outcomes of this study were immediate occlusion and progressive thrombosis rate, overall perioperative complication rate, and angiographic recurrence. Secondary outcomes included mortality at discharge, hemorrhagic and ischemic complications, and favorable clinical outcome at discharge and at follow-up.ResultsEight retrospective cohort studies with 1408 ruptured intracranial aneurysms (SAC=499; non-SAC=909) were included. The SAC group tended to show a lower immediate complete occlusion rate than the non-SAC group (54.3% vs 64.2%; RR 0.90; 95% CI 0.83 to 0.99; I2=17.4%) and achieved a significantly higher progressive complete rate at follow-up (73.4% vs 61.0%; RR 1.30; 95% CI 1.16 to 1.46; I2=40.5%) and a lower recurrence rate (4.8% vs 16.6%; RR 0.28; 95% CI 0.16 to 0.50; I2=0.0%). With respect to safety concerns, overall perioperative complications in the SAC group were significantly higher (20.2% vs 13.1%; RR 1.70; 95% CI 1.36 to 2.11; I2=0.0%). However, no significant difference was found for mortality rate at discharge (6.3% vs 6.2%; RR 1.29; 95% CI 0.86 to 1.94; I2=0.0%), or favorable clinical outcome rate at discharge (73.4% vs 74.2%; RR 0.95; 95% CI 0.88 to 1.02; I2=12.1%) and at follow-up (85.6% vs 87.9%; RR 0.98; 95% CI 0.93 to 1.02; I2=0.0%; P=0.338).ConclusionsSAC has a lower recurrence rate than non-SAC. Nevertheless, further validation by well designed prospective studies is warranted for determining whether stents improve angiographic outcome without an increased complication rate or unfavorable clinical outcome.

Moyamoya disease (MMD) is a cerebrovascular disease characterized by progressive stenosis of the intracranial internal carotid arteries and their proximal branches. However, the etiology of this rare disease remains unknown. Serum microRNA (miRNA) profiles have been screened to identify novel biomarkers of prognostic values. Here, we identified serum miRNAs that might play an important role in the pathogenesis of MMD. A genome-wide miRNA array analysis of two pooled serum samples from patients with MMD and controls revealed 94 differentially expressed serum miRNAs, including 50 upregulated and 44 downregulated miRNAs. In an independent MMD cohort, real-time PCR confirmed that miR-106b, miR-130a and miR-126 were significantly upregulated while miR-125a-3p was significantly downregulated in serum. GO analysis showed that the differentially expressed serum miRNAs were enriched in metabolic processes, transcription and signal transduction. Pathway analysis showed that the most enriched pathway was mTOR signaling pathway with 16 potential, functional targets. Finally, we found that 16 and 13 aberrant serum miRNAs coordinately inhibited RNF213 and BRCC3 protein expression at the posttranscriptional level, respectively, resulting in defective angiogenesis and MMD pathogenesis. To our knowledge, this is the first study to identify a serum miRNA signature in MMD. Modulation of the mechanism underlying the role of serum miRNAs in MMD is a potential therapeutic strategy and warrants further investigations.