Focal cerebral ischemia elicits strong inflammatory responses involving activation of resident microglia and recruitment of monocytes/macrophages. These cells express peripheral benzodiazepine receptors (PBRs) and can be visualized by positron emission tomography (PET) using [ 11 C]PK11195 that selectively binds to PBRs. Earlier research suggests that transient ischemia in rats induces increased [11 C]PK11195 binding within the infarct core. In this study, we investigated the expression of PBRs during permanent ischemia in rats. Permanent cerebral ischemia was induced by injection of macrospheres into the middle cerebral artery. Multimodal imaging 7 days after ischemia comprised (1) 18 F]FDG metabolic rate constant with accumulated activated microglia and macrophages. These results suggest that after permanent focal ischemia, neuroinflammation occurring in the normoperfused peri-infarct zone goes along with increased energy demand, therefore extending the tissue at risk to areas adjacent to the infarct.

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Over the past years, severe difficulties in translating experimental stroke research from bench-to-bedside have become apparent, and call for fresh ideas on why bench results get "lost in translation". In an attempt to close this gap, we suggest to perform experimental stroke studies in an intraindividual, longitudinal and translational way using multi-modal in vivo imaging protocols. Besides allowing us to stratify experimental animals in vivo, non-invasive imaging can also generate specific read-outs that allow monitoring the efficiency of individual treatments. Such an experimental design may specifically overcome the disadvantageous effects of increased variability in embolic stroke models. The quite novel "macrosphere model" of embolic stroke comprises a number of advantages, both regarding its particular usefulness for longitudinal imaging as well as its interesting pathophysiological aspects linking it to human stroke.