Abstract

See related article, pages 1638–1643. In the past decade there has been considerable scientific discussion about the metabolic state of the tissue surrounding a brain hemorrhage. The scientific discussion has focused mostly on the question of whether brain ischemia is present in this “penumbral tissue,” which has great clinical relevance because the presence of ischemia would drive clinical treatment considerations such as blood pressure management and surgery.1 Ischemia has classically been considered to be the deprivation of oxygen to tissue caused by arterial occlusion, with a resulting increase in oxygen extraction fraction (OEF) followed by local tissue acidosis and eventually cell death. This model of ischemia has been used to define tissue at risk and is a core principal used for ischemic stroke. The exact PET thresholds that define ischemia2 have been proposed and are presently being used in research settings. In an important study, Zazulia et al3 reported that the tissue immediately surrounding a brain hemorrhage did not exhibit classical ischemia as defined by PET OEF, and that small reductions in cerebral blood flow did not elicit much change in cerebral blood flow.4 This implies that ischemia is not present in the perihematomal tissue. PET OEF imaging in traumatic hemorrhage similarly shows no increase in OEF …

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