Despite upstream recanalization in acute ischemic stroke, it is now increasingly recognized that blood flow may fail to reach downstream tissue microvascular beds in a phenomenon termed “no-reflow”. This pathology is associated with poor clinical outcomes and presents as one explanation for futile recanalization in human stroke patients. Experimental data from animal stroke models have shown that this incomplete microcirculation reperfusion may be due to multiple mechanisms such as microthrombi, vasoconstriction, pericyte dysfunction, and capillary cellular clogging.

To date, clinical data on the no-reflow remain sparse. There is ongoing debate regarding the prevalence, natural history, significance, and optimal mode of detection in acute ischemic stroke. Better understanding of this phenomenon will clarify the importance of this pathology and facilitate potential development of novel therapeutics for prevent or treatment.

This Research Topic aims to comprehensively highlight the current advancement and controversies of no-reflow in the brain across experimental and clinical studies. We welcome submissions of Original Research, Review articles, and Mini-reviews focusing on, but not limited to, the following sub-topics:

- Identification of no-reflow/incomplete microcirculation reperfusion in preclinical animal models of ischemic stroke and in clinical ischemic stroke population

- Pathogenesis of no-reflow/incomplete microcirculation reperfusion, including cellular mechanism and molecular pathways

- Potential treatment of no-reflow/incomplete microcirculation reperfusion

- Predictors of no-reflow/incomplete microcirculation reperfusion in clinical studies

- Insights from population-based investigations on incidence, risk factors, and symptoms of no-reflow/incomplete microcirculation reperfusion

- Natural history and evolution of cerebral hypoperfusion upstream recanalization.

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Futile recanalization after successful thrombectomy for acute ischemic stroke, including incomplete microvascular reperfusion