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Epilepsia. 2010 Aug;51(8):1436-45. doi: 10.1111/j.1528-1167.2009.02413.x. Epub 2009 Dec 1.

Involvement of the thalamocortical network in TLE with and without mesiotemporal sclerosis.

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  • 1Center for Imaging of Neurodegenerative Diseases, San Francisco, California, USA. susanne.mueller@ucsf.edu

Abstract

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:

T₁ and high-resolution T₂ 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 T₂ 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.

Wiley Periodicals, Inc. © 2009 International League Against Epilepsy.

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