Transient and chronic seizure‐induced inflammation in human focal epilepsy. (6th July 2016)

• Record Type: Journal Article
• Authors: Butler, Tracy; Li, Yi; Tsui, Wai; Friedman, Daniel; Maoz, Anat; Wang, Xiuyuan; Harvey, Patrick; Tanzi, Emily; Morim, Simon; Kang, Yeona; Mosconi, Lisa; Talos, Delia; Kuzniecky, Ruben; Vallhabjosula, Shankar; Thesen, Thomas; Glodzik, Lidia; Ichise, Masanori; Silbersweig, David; Stern, Emily; de Leon, Mony J.; French, Jacqueline
• Is Part Of: Epilepsia. Volume 57:issue 9(2016)
• Page Start: e191
• Page End: e194
• Publication Date: 2016-07-06
• Subjects: Positron emission tomography -- Microglia -- Translocator protein -- Supplementary motor area -- Frontal lobe epilepsy -- Focal cortical dysplasia; Epilepsy -- Periodicals; 616.853
• DOI: 10.1111/epi.13457
• Languages: English
• ISSNs: 0013-9580

Abstract

Summary: In animal models, inflammation is both a cause and consequence of seizures. Less is known about the role of inflammation in human epilepsy. We performed positron emission tomography (PET) using a radiotracer sensitive to brain inflammation in a patient with frontal epilepsy ~36 h after a seizure as well as during a seizure‐free period. When statistically compared to a group of 12 matched controls, both of the patient's scans identified a frontal (supplementary motor area) region of increased inflammation corresponding to his clinically defined seizure focus, but the postseizure scan showed significantly greater inflammation intensity and spatial extent. These results provide new information about transient and chronic neuroinflammation in human epilepsy and may be relevant to understanding the process of epileptogenesis and guiding therapy.