[18F]DPA-714 PET in presurgical evaluation of drug-resistant epilepsy: from clinical to pathology

Fluorine 18 ([18F])–labeled DPA-714 binds to the translocator protein (TSPO), which can be used for monitoring activated glial cells during inflammatory process, and be potentially helpful for localizing the epileptogenic zone. In this study, we aimed to analyze the application of [18F] DPA-714 PET in preoperative evaluation of epilepsy, and to validate the results through surgical outcome and pathological results. Patients who underwent epilepsy surgery with both preoperative [18F]DPA-714 PET and 18F-fluorodeoxyglucose ([18F]FDG) PET were retrospectively reviewed. We visually compared [18F]DPA-714 PET, [18F]FDG PET findings and clinical data. The asymmetry index (AI) were also analyzed for both PET modalities. Pathological correlations with TSPO-positive findings ([18F]DPA-714 PET positive regions) were assessed using CD68 antibodies to identify microglial cells. Eight patients were included in this study. All patients were seizure-free after one-year follow-up. Three patients underwent resection of regions that showed increased uptake on [18F]DPA-714 PET. These three patients had temporal lobe resection or temporal and opercular epileptogenic lesion resection, and their [18F]DPA-714 PET results showed hypermetabolism in ipsilateral mesial temporal lobe. We compared the microglial cells density in the gray matter and white matter separately, and found that microglial cells density was higher in the mesial temporal regions ([18F]DPA-714 PET positive regions) than in the anterior lateral temporal regions ([18F]DPA-714 PET negative regions) in both gray matter (p = 0.003) and white matter (p < 0.001). [18F]DPA-714 PET was more restricted than [18F]FDG PET in patients with temporal lobe epilepsy by visual analysis, whereas [18F]FDG PET showed greater asymmetry in frontal lobe epilepsy. The [18F]DPA-714 PET positive regions correlated with increased microglial density, and it showed a different sensitivity in the recognition of the epileptogenic lesions in temporal and frontal lobe epilepsy.