The ischemic penumbra: how does tissue injury evolve?

Abstract

An ischemic penumbra has the potential for functional recovery provided that local blood flow can be reestablished, but irreversible damage will develop without sufficient reperfusion, depending on the interaction of severity and duration of ischemia. With acute flows below the threshold required for maintenance of basic housekeeping, injury in the core is established within a few minutes. During the subacute phase, the irreversible damage expands into the penumbra: multiple electrical and biological signals are triggered by periinfarct, spreading depression-like depolarizations leading to hypoxia and stepwise increase in lactate. Usually within 6 to 8 hours, all the penumbra are converted into irreversible infarcts. In a delayed phase, secondary phenomena may cause additional tissue damage: disruption of the tight junctions results in vasogenic edema, leading to increase of water content and damage expansion. Neutrophils and cytokinins cause secondary inflammation, inducing further damage in periinfarct regions and connecting fiber tracts. Multimodal imaging might be able to differentiate among the tissue compartments affected by acute, subacute, or delayed ischemic damage, and thereby might provide the basis for phase-specific treatment strategies.