Metabolic characteristics of mesial temporal lobe epilepsy with hippocampal sclerosis based on quantitative analysis of 18F-FDG PET

Abstract

Background Mesial temporal lobe epilepsy with hippocampal sclerosis (mTLE?HS) is the most common type of focal epilepsy involving complex networks. 18F?fluoro?2?deoxy?D?glucose (18F?FDG) PET provides unique brain metabolic information for epilepsy. This study aims to explore the spatial metabolic characteristics of mTLE?HS based on a quantitative analysis of 18F?FDG PET.  Methods A total of 23 patients with mTLE?HS and 26 sex? and age?matched healthy controls were enrolled in this study. All of them were performed head MRI and 18F?FDG PET scanning. PET images were registered to standard template and further divided into 90 regions of interest (ROIs) based on anatomical automatic labeling (AAL). Normalized standard uptake value (SUV) in whole brain, bilateral cerebral hemispheres and each ROI were calculated.  Results The normalized SUV of whole brain in mTLE?HS patients was significantly lower than healthy controls (1.13 ± 0.06 vs. 1.20 ± 0.10; t = ? 3.245, P = 0.002). The normalized SUV of left hemisphere was significantly lower than right hemisphere (1.10 ± 0.06 vs. 1.15 ± 0.06; t = ? 2.710, P = 0.010) in mTLE?HS patients. Compared with controls, the normalized SUV in 15 ROIs of mTLE?HS patients were identified with hypometabolism significantly, which were located in left temporal lobe (hippocampus, parahippocampal gyrus, amygdala, superior temporal pole, middle emporal pole, inferior temporal gyrus and fusiform gyrus, transverse temporal gyrus) and left extratemporal cortex (inferior frontal operculum, Rolandic operculum, insular lobe, median cingulate gyrus, caudate nucleus, putamen and thalamus).  Conclusions This study revealed the spatial metabolic characteristics of mTLE?HS based on a quantitative analysis of 18F?FDG PET from the metabolic perspective, deepened the understanding on pathophysiological mechanisms of

mTLE?HS, and provided a framework for further analyzing the functional change and seizure progression of mTLE?HS.

DOI: 10.3969/j.issn.1672-6731.2018.05.007