Full-Length Original Research
Altered thalamocortical functional connectivity in idiopathic generalized epilepsy
Version of Record online: 20 MAR 2014
Wiley Periodicals, Inc. © 2014 International League Against Epilepsy
Volume 55, Issue 4, pages 592–600, April 2014
How to Cite
Epilepsia, 55(4):592–600, 2014
- Issue online: 22 APR 2014
- Version of Record online: 20 MAR 2014
- Manuscript Accepted: 27 JAN 2014
- Korean Government. Grant Numbers: 20100004827, 20110005418
- Korea University Grant
- Idiopathic generalized epilepsy;
- Resting-state functional connectivity;
- Thalamocortical network;
- Frontal cognitive dysfunction
Aberrant thalamocortical network has been hypothesized to play a crucial role in the fundamental pathogenesis underlying idiopathic generalized epilepsy (IGE). We aimed to investigate alterations of thalamocortical functional network in patients with IGE using thalamic seed-based functional connectivity (FC) analysis, and their relationships with frontal cognitive functions and clinical characteristics.
Forty-nine IGE patients (31 with juvenile myoclonic epilepsy, 17 with IGE with generalized tonic–clonic seizures only, one with juvenile absence epilepsy) and 42 control subjects were prospectively recruited. Voxel-based morphometry (VBM) was first performed to detect thalamic region of gray matter (GM) reduction in patients compared to controls. Between-group comparison of thalamocortical FC was then carried out using resting-state functional magnetic resonance imaging (MRI) analysis seeding at thalamic region of volume difference. In addition, thalamocortical FC was correlated with frontal cognitive performance and clinical variables.
Neuropsychological assessment revealed that patients with IGE had poorer performance than controls on most of the frontal cognitive functions. VBM detected a reduction in GM in the anteromedial thalamus in patients relative to controls. FC analysis seeding at the anteromedial thalamus revealed a reduction of thalamocortical FC in the bilateral medial prefrontal cortex and precuneus/posterior cingulate cortex in patients with IGE compared to controls. Thalamocortical FC strength of bilateral medial prefrontal cortex correlated negatively with disease duration, but did not correlate with seizure frequency or frontal cognitive functions in patients with IGE.
Our results indicate that IGE is associated with decreased thalamocortical FC between anteromedial thalamus and medial prefrontal cortex and precuneus/posterior cingulate cortex. Our finding of greater reduction of medial prefrontal FC in relation to increasing disease duration suggests that thalamoprefrontal network abnormality, the proposed pathophysiologic mechanism underlying IGE, may be the consequence of the long-standing burden of the disease.