Search

Objective: Epilepsy surgery is an effective treatment for drug‐resistant patients. However, how different surgical approaches affect long‐term brain structure remains poorly characterized. Here, we present a semiautomated method for quantifying structural changes after epilepsy surgery and compare the remote structural effects of two approaches, anterior temporal lobectomy (ATL), and selective amygdalohippocampectomy (SAH). Methods: We studied 36 temporal lobe epilepsy patients who underwent resective surgery (ATL = 22, SAH = 14). All patients received same‐scanner MR imaging preoperatively and postoperatively (mean 2 years). To analyze postoperative structural changes, we segmented the resection zone and modified the Advanced Normalization Tools (ANTs) longitudinal cortical pipeline to account for resections. We compared global and regional annualized cortical thinning between surgical treatments. Results: Across procedures, there was significant cortical thinning in the ipsilateral insula, fusiform, pericalcarine, and several temporal lobe regions outside the resection zone as well as the contralateral hippocampus. Additionally, increased postoperative cortical thickness was seen in the supramarginal gyrus. Patients treated with ATL exhibited greater annualized cortical thinning compared with SAH cases (ATL: −0.08 ± 0.11 mm per year, SAH: −0.01 ± 0.02 mm per year, t = 2.99, P = 0.006). There were focal postoperative differences between the two treatment groups in the ipsilateral insula (P = 0.039, corrected). Annualized cortical thinning rates correlated with preoperative cortical thickness (r = 0.60, P < 0.001) and had weaker associations with age at surgery (r = −0.33, P = 0.051) and disease duration (r = −0.42, P = 0.058). Significance: Our evidence suggests that selective procedures are associated with less cortical thinning and that earlier surgical intervention may reduce long‐term impacts on brain structure. [ABSTRACT FROM AUTHOR]

Introduction: Drug‐resistant epilepsy patients show worse outcomes after resection when standard neuroimaging is nonlesional, which occurs in one‐third of patients. In prior work, we employed 2‐D glutamate imaging, Glutamate Chemical Exchange Saturation Transfer (GluCEST), to lateralize seizure onset in nonlesional temporal lobe epilepsy (TLE) based on increased ipsilateral GluCEST signal in the total hippocampus and hippocampal head. We present a significant advancement to single‐slice GluCEST imaging, allowing for three‐dimensional analysis of brain glutamate networks. Methods: The study population consisted of four MRI‐negative, nonlesional TLE patients (two male, two female) with electrographically identified left temporal onset seizures. Imaging was conducted on a Siemens 7T MRI scanner using the CEST method for glutamate, while the advanced normalization tools (ANTs) pipeline and the Automated Segmentation of the Hippocampal Subfields (ASHS) method were employed for image analysis. Results: Volumetric GluCEST imaging was validated in four nonlesional TLE patients showing increased glutamate lateralized to the hippocampus of seizure onset (p =.048, with a difference among ipsilateral to contralateral GluCEST signal percentage ranging from −0.05 to 1.37), as well as increased GluCEST signal in the ipsilateral subiculum (p =.034, with a difference among ipsilateral to contralateral GluCEST signal ranging from 0.13 to 1.57). Conclusions: The ability of 3‐D, volumetric GluCEST to localize seizure onset down to the hippocampal subfield in nonlesional TLE is an improvement upon our previous 2‐D, single‐slice GluCEST method. Eventually, we hope to expand volumetric GluCEST to whole‐brain glutamate imaging, thus enabling noninvasive analysis of glutamate networks in epilepsy and potentially leading to improved clinical outcomes. [ABSTRACT FROM AUTHOR]