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Background Mechanical thrombectomy is established for large‐vessel occlusions in acute ischemic stroke, but the potential role in distal vessel occlusions of medium arteries is less well established. Such medium or distal arterial segments have not been assessed with respect to thrombectomy devices used during endovascular therapy. We conducted an analysis of arterial size, segmental anatomy, and stent‐retriever device performance with respect to vessel size during thrombectomy. Methods The STRATIS registry angiography core laboratory adjudicated the exact location of the occlusion, proximal, and distal device deployment, relationship to arterial bifurcations, and anatomic nomenclature. Arterial diameters were measured at all these sites. Statistical analyses examined the relationship between vessel and stent size, and arterial recanalization using expanded Thrombolysis in Cerebral Infarction reperfusion score. Results Overall, 665 patients with stroke were included following thrombectomy using various Solitaire device sizes, including Solitaire 4×40, Solitaire 6×30, Solitaire 4×20, Solitaire 6×20, and Solitaire 4×15. Arterial diameter at the occlusion site was a median of 2.17 mm (interquartile range [IQR], 1.88–2.60 mm) in the distal M1, 1.67 mm (IQR, 1.47–2.06 mm) in the proximal M2 middle cerebral artery, 1.50 mm (IQR, 1.15–1.61 mm) in the distal M2 middle cerebral artery, 1.24 mm (IQR, 1.11–1.24 mm) in the M3 middle cerebral artery, and 1.88 mm (IQR, 1.49–1.94 mm) in the P1 posterior cerebral artery. Expanded Thrombolysis in Cerebral Infarction 2b to 3 reperfusion was achieved in all M3 or P1 segment occlusions. The rate of first‐pass recanalization was significantly higher in patients with medium (0.75–2 mm) versus large (>2 mm) vessel occlusion (69.5% versus 57.1%; P = 0.003). Conclusion Considerable overlap was noted between arterial sizes at occlusion sites carrying different segmental arterial nomenclature or vessel names. Substantial reperfusion may be achieved with currently available mechanical thrombectomy devices in medium arteries.

Insult-provoked transformation of neuronal networks into epileptic ones involves multiple mechanisms. Intervention studies have identified both dysregulated inflammatory pathways and NRSF-mediated repression of crucial neuronal genes as contributors to epileptogenesis. However, it remains unclear how epilepsy-provoking insults (e.g., prolonged seizures) induce both inflammation and NRSF and whether common mechanisms exist. We examined miR-124 as a candidate dual regulator of NRSF and inflammatory pathways. Status epilepticus (SE) led to reduced miR-124 expression via SIRT1—and, in turn, miR-124 repression—via C/EBPα upregulated NRSF. We tested whether augmenting miR-124 after SE would abort epileptogenesis by preventing inflammation and NRSF upregulation. SE-sustaining animals developed epilepsy, but supplementing miR-124 did not modify epileptogenesis. Examining this result further, we found that synthetic miR-124 not only effectively blocked NRSF upregulation and rescued NRSF target genes, but also augmented microglia activation and inflammatory cytokines. Thus, miR-124 attenuates epileptogenesis via NRSF while promoting epilepsy via inflammation.