Publication

Different structural correlates for verbal memory impairment in temporal lobe epilepsy with and without mesial temporal lobe sclerosis

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Last modified
  • 05/21/2025
Type of Material
Authors
    Susanne G. Mueller, University of California, San FranciscoKenneth D. Laxer, California Pacific Medical CenterCathy Scanlon, University of California, San FranciscoPaul Garcia, University of California, San FranciscoWilliam J. McMullen, California Pacific Medical CenterDavid W Loring, Emory UniversityKim J Meador, Emory UniversityMichael W. Weiner, University of California, San Francisco
Language
  • English
Date
  • 2012-02-01
Publisher
  • Wiley: 12 months
Publication Version
Copyright Statement
  • © 2011 Wiley Periodicals, Inc.
Final Published Version (URL)
Title of Journal or Parent Work
ISSN
  • 1065-9471
Volume
  • 33
Issue
  • 2
Start Page
  • 489
End Page
  • 499
Grant/Funding Information
  • National Institutes of Health; Contract grant number: RO1-NS31966.
Supplemental Material (URL)
Abstract
  • Objectives: Memory impairment is one of the most prominent cognitive deficits in temporal lobe epilepsy (TLE). The overall goal of this study was to explore the contribution of cortical and hippocampal (subfield) damage to impairment of auditory immediate recall (AIMrecall), auditory delayed recall (ADMrecall), and auditory delayed recognition (ADMrecog) of the Wechsler Memory Scale III (WMS-III) in TLE with (TLE-MTS) and without hippocampal sclerosis (TLE-no). It was hypothesized that volume loss in different subfields determines memory impairment in TLE-MTS and temporal neocortical thinning in TLE-no. Methods: T1 whole brain and T2-weighted hippocampal magnetic resonance imaging and WMS-III were acquired in 22 controls, 18 TLE-MTS, and 25 TLE-no. Hippocampal subfields were determined on the T2 image. Free surfer was used to obtain cortical thickness averages of temporal, frontal, and parietal cortical regions of interest (ROI). MANOVA and stepwise regression analysis were used to identify hippocampal subfields and cortical ROI significantly contributing to AIMrecall, ADMrecall, and ADMrecog. Results: In TLE-MTS, AIMrecall was associated with cornu ammonis 3 (CA3) and dentate (CA3&DG) and pars opercularis, ADMrecall with CA1 and pars triangularis, and ADMrecog with CA1. In TLE-no, AIMrecall was associated with CA3&DG and fusiform gyrus (FUSI), and ADMrecall and ADMrecog were associated with FUSI. Conclusion: The study provided the evidence for different structural correlates of the verbal memory impairment in TLE-MTS and TLE-no. In TLE-MTS, the memory impairment was mainly associated by subfield-specific hippocampal and inferior frontal cortical damage. In TLE-no, the impairment was associated by mesial-temporal cortical and to a lesser degree hippocampal damage.
Author Notes
  • Susanne G. Mueller, Department of Veterans Affairs (DVA) Medical Center, Center for Imaging of Neurodegenerative Diseases, Clement Street 4150, San Francisco, CA 94121, USA. susanne.mueller@ucsf.edu.
Keywords
Research Categories
  • Biology, Neuroscience
  • Health Sciences, Radiology

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