Hypothesizing the interplay of thrombus formation, wall enhancement, and perifocal edema as predictive factors for rupture in brain AVMs

•Imaging features in ruptured AVMs indicate an underlying inflammatory process.•Blood recirculation and stasis in venous pouches may initiate local thrombosis.•Local thrombosis may cause hypoxemia and trigger inflammatory changes.•Inflammatory changes might ultimately increase rupture risk. The presence of shear stress within intracranial AVMs (arteriovenous malformations) due to high flow, perinidal angiogenesis, intranidal aneurysms, and biological factors are presumed risk factors for rupture. However, emerging imaging and histological evidence suggests that risk factors for AVM rupture may extend beyond the classical understanding. The presence of perifocal edema at the time of rupture, luminal thrombosis, and vessel wall enhancement on vessel wall MRI elucidate the possibility of an underlying inflammatory process within AVMs, which may predispose them to instability and eventual rupture. We hypothesize that for some AVM ruptures, the occurrence of thrombosis within vascular outpouchings of the AVM initiates a cascade of events, including local hypoxia, inflammation, breakdown of the blood–brain barrier and wall matrix degradation, which is evident from the presence of perifocal edema and vessel wall enhancement observed on imaging. These changes might ultimately raise the risk of AVM rupture and subsequent hemorrhage. Understanding this inflammatory component offers promising insights into AVM pathogenesis and may facilitate the development of preventive strategies to mitigate rupture risk.