Ischemic brain injury first causes direct cell damage through energy failure, resulting in necrosis and delayed apoptosis of brain cells. Despite promising results using experimental anti-inflammatory therapies after focal brain ischemia in animal studies, no such therapy has been proven effective in human stroke studies to date. Hematogenous granulocytes are the first cells entering the ischemic brain parenchyma within hours of stroke onset. Therapeutic interventions after stroke are still scarce, and only recombinant tissue plasminogen activator has been shown to be effective in human stroke patients, when given in the first 6 h after stroke onset. Since invasive histological or immunohistochemical techniques to detect and monitor the postischemic response after focal brain ischemia are feasible in human stroke studies, attempts have been made to study cellular macrophage activity after brain ischemia with molecular imaging techniques, like positron emission tomography or magnetic resonance imaging.