Cortical and Subcortical Structural Abnormalities in Juvenile Myoclonic Epilepsy: Tract-based Spatial Statistics (TBSS) and Constrained Laplacian-based Anatomic Segmentation with Proximity (CLASP) Algorithm
Abstract number :
2.205
Submission category :
5. Neuro Imaging
Year :
2015
Submission ID :
2327402
Source :
www.aesnet.org
Presentation date :
12/6/2015 12:00:00 AM
Published date :
Nov 13, 2015, 12:43 PM
Authors :
S. Lim, S. Kim, W. Kim, J. Kim, Y. Shon
Rationale: Some previous neuroimaging studies reported the evidence that the pathophysiology of juvenile myoclonic epilepsy (JME) is associated with structural abnormalities of thalamo-frontal circuit. But recent studies suggest that structural abnormalities exist extend beyond frontal area. In this study, we studied to investigate the anatomical and pathophysiological nature of JME using multimodal neuroimaging method.Methods: High-resolution T1 and diffusion tensor images (DTI) were acquired on a 1.5T MRI in 18 patients of JME and 22 normal controls. The group comprasions of white matter (WM) water diffusivity and cortical thickness were analyzed by tract-based spatial statistics (TBSS) and Constrained Laplacian-based Anatomic Segmentation with Proximity (CLASP) algorithm, respectively. Volume of bilateral thalamus and hippocampus was also obtained by manual volumetry.Results: In patients with JME, compare to normal control, structural abnormalities were detected by multimodal neuroimaging analysis. TBSS revealed that patients with JME had WM alterations in both anterior superior corona radiate, genu and body of corpus callosum, multiple frontal WM, left temporal WM and posterior part of corpus callosum. CLASP demonstrated that patients with JME had lesions of cortical thickness reduction in both medial frontal, parietal, dorsolateral parietal, left medial temporal, right superior temporal and both inferior temporal area. Comparing to control subjects, we could observe the definitely significant volume reduction in both thalami and hippocampus by using manual volumetry in JME patients.Conclusions: Our results of WM diffusivity changes of frontal lobe, anterior part of corpus callosum, cortical thickness reduction of frontal lobe and thalamic volume loss could support the hypothesis of thalamofrontal dysfunction in JME. Moreover, derangement of WM diffusivity in temporal lobe, posterior part of corpus callosum and reduced cortical thickness reduction of temporal lobe and hippocampus volume loss were observed. These finding of our study suggest that structural abnormalities in JME extend beyond frontal lobe, especially temporal lobe. Our result may suggest that the JME pathophysiology is associated to not only frontal connection but also temporal or extra-frontal connectivity.
Neuroimaging