A thinner cortex has higher potential for binding GABA receptor A which is associated with larger amplitudes of intrinsic brain activity(i BA). However, the relationship between cortical thickness and i BA is unknown in intact and epileptic brains. To this end, we investigated the relationship between cortical thickness measured by highresolution MRI and surface-based i BA derived from resting-state functional MRI in normal controls(n = 82) andpatients with generalized tonic–clonic seizures(GTCS)only(n = 82). We demonstrated that the spatial distribution of cortical thickness negatively correlated with surface-based i BA amplitude at both whole-brain and within independent brain functional networks. In GTCS patients,spatial coupling between thickness and i BA amplitude decreased in the default mode, dorsal attention, and somatomotor networks. In addition, the vertex-wise acrosssubject thickness–i BA amplitude correspondence altered in the frontal and temporal lobes as well as in the precuneus in GTCS patients. The relationship between these two modalities can serve as a brain-based marker for detecting epileptogenic changes. A, thinner cortex has higher potential for binding GABA receptor A which is associated with larger amplitudes of intrinsic brain activity (i BA). However, the relationship between cortical thickness and i BA is unknown in intact and epileptic brains. To this end, we the relationship between cortical thickness by high resolution MRI and surface-based i BA derived from resting-state functional MRI in normal controls (n = 82) andpatients with generalized tonic-clonic seizures (GTCS) only (n = 82) the spatial distribution of cortical thickness negatively correlated with surface-based i BA amplitude at both whole-brain and within independent brain functional networks. In GTCS patients, spatial coupling between thickness and i BA amplitude decreased in the default mode, dorsal attention, and somatomotor networks. In addition, the vertex-wise acrosssubject thickness-i BA amplitude correspondence altered in the frontal and temporal lobes as well as in th The relationship between these two modalities can serve as a brain-based marker for detecting epileptogenic changes.