FLAIR vascular hyperintensities may reflect physiological hemodynamic adaptation in acute ischemic stroke patientsNew insights into how brain blood flow affects stroke recovery

With advances in reperfusion therapies for acute large vessel occlusion (LVO), stroke imaging evaluation has progressively shifted from time-based treatment selection toward comprehensive assessment of tissue status and hemodynamic adaptation. However, current imaging approaches primarily characterize vascular patency, perfusion status, and tissue injury, while remaining limited in their ability to directly capture the dynamic regulatory processes of cerebral circulation after arterial occlusion. In patients with LVO, ischemic tissue outcome is determined not only by the occlusion site and time to reperfusion but also by collateral circulation capacity, cerebral hemodynamic status, and tissue tolerance to ischemia. Therefore, imaging biomarkers capable of reflecting cerebral circulatory adaptation under ischemic conditions are of substantial research interest. FLAIR vascular hyperintensities (FVHs) are MRI findings characterized by linear or serpentine hyperintense signals along the cortical surface, within cortical sulci, or along the Sylvian fissure on fluid-attenuated inversion recovery (FLAIR) sequences. They are generally associated with reduced distal blood flow velocity, prolonged blood transit time, and hemodynamic alterations mediated by leptomeningeal collateral pathways. In recent years, numerous studies have investigated the role of FVHs in the diagnosis of acute ischemic stroke, evaluation of reperfusion therapy, and prediction of clinical outcomes. However, the clinical significance of FVHs remains incompletely understood. Some studies have suggested that FVHs are associated with favorable collateral status and smaller infarct volumes, whereas others have demonstrated that FVHs may also occur in patients with more pronounced hemodynamic impairment. These discrepancies suggest that FVHs may not simply represent favorable collateral circulation or ischemic severity, but may instead reflect the dynamic hemodynamic response of the cerebral circulation to reduced perfusion following arterial occlusion. From the perspective of precision stroke imaging, this review systematically summarizes the mechanisms underlying FVH formation, their biological significance, and clinical implications. Particular emphasis is placed on the relationships between FVHs and collateral circulation, FVHs-DWI mismatch, ischemic tissue status, and potential benefit from reperfusion therapy. Furthermore, current challenges related to FVH standardization and clinical translation are discussed, with particular emphasis on their potential role as a candidate dynamic hemodynamic imaging phenotype reflecting physiological hemodynamic adaptation.