Galovic et al have answered the call with a longitudinal study of a cohort with epilepsy compared to 3 cohorts without epilepsy. The authors studied 190 patients with focal epilepsy and 141 age and gender-matched healthy controls. All patients and controls had at least 2 high-resolution T1-weighted magnetic resonance imaging (MRI) scans performed on the same scanner at least 6 months apart. Cortical thickness was estimated using the projection-based thickness method in the fully automated and validated Computational Anatomy Toolbox (CAT12). Annualized cortical thinning was determined by subtracting vertexwise thickness values of aligned baseline and follow-up MRI scan pairs and dividing by the interscan interval. This step obviated the need of finding patients and controls with the exact interscan interval. To analyze whether the spatial patterns of progressive cortical thinning reflected areas of connectivity to the epileptic focus, the authors performed a set of connectivity analyses with probabilistic tractography based on 10 high-quality diffusion data sets from BCBtoolkit. This analysis was accomplished for the TLE subgroup because the seed location (ie, hippocampus) is a well-established and well-defined location of the epileptogenic zone in most cases of TLE. A similar analysis could not be made for extra-TLE because of the high variability of epileptogenic foci location(s). People with epilepsy had a higher mean yearly rate of global cortical thinning compared with healthy volunteers (P = .01), with greater thinning associated with increasing age. A total of 76.8% of people with epilepsy in their cohort showed progressive cortical thinning that was distinct from that seen with normal aging. Cortical thinning was not associated with seizure frequency, number of antiepileptic drugs taken, or history of secondarily generalized seizures. In the TLE subgroup, accelerated cortical thinning was seen in functionally connected areas.