| Literature DB >> 27381590 |
Tracy Butler1,2,3, Yi Li1, Wai Tsui1, Daniel Friedman2, Anat Maoz4, Xiuyuan Wang1,2, Patrick Harvey1, Emily Tanzi1, Simon Morim4, Yeona Kang4, Lisa Mosconi1, Delia Talos2, Ruben Kuzniecky2, Shankar Vallhabjosula4, Thomas Thesen2, Lidia Glodzik1, Masanori Ichise5, David Silbersweig3, Emily Stern3, Mony J de Leon1, Jacqueline French2.
Abstract
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. Wiley Periodicals, Inc.Entities:
Keywords: Focal cortical dysplasia; Frontal lobe epilepsy; Microglia; Positron emission tomography; Supplementary motor area; Translocator protein
Mesh:
Year: 2016 PMID: 27381590 PMCID: PMC5266563 DOI: 10.1111/epi.13457
Source DB: PubMed Journal: Epilepsia ISSN: 0013-9580 Impact factor: 5.864