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Updated: May 13, 2026

A Multimodal Imaging- and Stimulation-based Method of Evaluating Connectivity-related Brain Excitability in Patients with Epilepsy
Published on: November 13, 2016
Volumetric and shape analysis of thalamus in idiopathic generalized epilepsy
Ji Hyun Kim1, Jung Bin Kim, Woo-Keun Seo
1Department of Neurology, Korea University Guro Hospital, Korea University College of Medicine, Guro-dong Ro 148, Guro-gu, Seoul 152-703, Republic of Korea. jhkim.merrf@gmail.com
Abstract:
Previous studies using voxel-based morphometry (VBM) provided emerging evidence of structural changes of the thalamus in idiopathic generalized epilepsy (IGE). However, the location of atrophy within the thalamus in IGE has been somewhat inconsistent across the studies. We, therefore, examined the location of thalamic atrophy and its relationship with clinical factors in IGE, using multiple analytic methods. Fifty IGE patients and 50 controls were scanned on a 3T MRI. Structural evaluation consisted of automated thalamic volumetry, VBM, and thalamic shape analysis. Group comparison between patients and controls was made to assess thalamic atrophy. Within-group correlations between thalamic atrophy and clinical variables were further performed in patients. Both thalamic volumes were reduced in IGE patients, and were negatively correlated with disease duration. The VBM showed a significant regional grey matter volume reduction in bilateral anterior-medial thalami in patients compared to controls. Voxel values extracted from the anterior-medial thalamic cluster were negatively correlated with disease duration. Vertex-based shape analysis revealed regional atrophy on the anterior-medial and posterior-dorsal aspects of thalamus bilaterally in patients compared to controls. Correlation analysis showed that anterior-medial and posterior-dorsal aspects of bilateral thalami were negatively correlated with disease duration. Combining multiple analyses, we demonstrated regional atrophy of anterior-medial and posterior-dorsal thalamus in patients with IGE. Given the anatomical connection of these thalamic regions with the frontal lobe, our finding of greater thalamic atrophy in relation to increasing disease duration further supports the pathophysiological concept of thalamo-frontal network abnormality underlying IGE, and may implicate frontal cognitive dysfunctions and disease progression.
