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Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis
Author(s) -
Mueller Susanne G.,
Laxer Kenneth D.,
Barakos Jerome,
Cheong Ian,
Finlay Daniel,
Garcia Paul,
CardenasNicolson Valerie,
Weiner Michael W.
Publication year - 2010
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2009.02413.x
Subject(s) - thalamus , temporal lobe , epilepsy , neuroscience , hippocampal sclerosis , anatomy , lobe , psychology , medicine
Summary Purpose: The thalamus plays an important role in seizure propagation in temporal lobe epilepsy (TLE). This study investigated how structural abnormalities in the focus, ipsilateral thalamus and extrafocal cortical structures relate to each other in TLE with mesiotemporal sclerosis (TLE‐MTS) and without hippocampal sclerosis (TLE‐no). Methods: T 1 and high‐resolution T 2 images were acquired on a 4T magnet in 29 controls, 15 TLE‐MTS cases, and 14 TLE‐no. Thalamus volumes were obtained by warping a labeled atlas onto each subject’s brain. Deformation‐based morphometry was used to identify regions of thalamic volume loss and FreeSurfer for cortical thickness measurements. CA1 volumes were obtained from high‐resolution T 2 images. Multiple regression analysis and correlation analyses for voxel‐ and vertex‐based analyses were performed in SPM2 and FreeSurfer. Results: TLE‐MTS had bilateral volume loss in the anterior thalamus, which was correlated with CA1 volume and cortical thinning in the mesiotemporal lobe. TLE‐no had less severe volume loss in the dorsal lateral nucleus, which was correlated with thinning in the mesiotemporal region but not with extratemporal thinning. Discussion: The findings suggest that seizure propagation from the presumed epileptogenic focus or regions close to it into the thalamus occurs in TLE‐MTS and TLE‐no and results in circumscribed neuronal loss in the thalamus. However, seizure spread beyond the thalamus seems not to be responsible for the extensive extratemporal cortical abnormalities in TLE.