Abstracts

Rationale: We aimed to study the role of inflammation in focal epilepsy using a PET marker for the translocation protein 18 kDa, a protein complex associated with activated microglia and reactive astrocytes. In a previous study we found increased binding in limbic structures in patients with temporal lobe epilepsy, particularly associated with hippocampal sclerosis.Methods: We studied ten adult patients (6 women) not reported previously. They were evaluated with ictal video-EEG, T1, FLARE, and T2-weighted MRI, screened with a leucocyte binding assay to exclude non-binders, and scanned on an Advance Tomograph (GE Healthcare) after injection of ~740 MBq of [11C]PBR28 (n=2), [11C]DPA (n=1) or both ligands (n=7). Scans were co-registered to 3D-t1-weighted MRI and normalized to a standard template. The images were analyzed by an investigator blinded to clinical, electrographic, T2 and FLARE MRI sequences. In addition to visual inspection, regions of interest were drawn on the co-registered images and asymmetry indices calculated for comparison between regions of increased uptake and contralateral cortex. Results: Five of 10 subjects had increased binding with [11C]PBR, [11C]DPA, or both ligands, including 2 of 2 with MRI + HS, and 2 of 3 with MRI + focal cortical dysplasia. One MRI negative patient, found to have focal cortical dysplasia (FCD) type 2A with CD 68 + astrocytes on surgical pathology, had positive [11C]DPA; [11C]PBR was not performed. Conclusions: Our results confirm and extend our previous findings in focal epilepsy. In addition to hippocampal sclerosis, we have now detected increased TSPO binding in focal cortical dysplasia. These results provide further evidence for a possible role of inflammatory mechanisms in two pathological substrates of uncontrolled focal epilepsy.