If validated, the finding that progressive cortical atrophy in patients with epilepsy was not associated with disease severity or duration is significant on a couple of levels. First, if seizure frequency, seizure severity, or the number of antiseizure drugs trialed has no effect on cortical thinning, this suggests that effective pharmacologic interventions to stop or minimize seizures are not likely to influence the loss of gray matter. Thus, a major part of what clinicians feel is successful treatment of patients with epilepsy (ie, achieving seizure freedom) appears to have no bearing on a process that is decreasing overall brain health. Would a surgical “cure” of epilepsy be more effective in stopping neuronal degeneration? The preliminary data are not reassuring. One recent study suggests there is ongoing contralateral hippocampal atrophy after successful anterior temporal lobe surgery.9 Second, these findings appear to overturn the traditional thinking that epilepsy is a progressive disease because of the damaging effects of continued seizures.1,10 If the absence of ongoing seizure activity does not stop the progressive cortical atrophy seen in patients with epilepsy, we will be forced to consider that the neuronal damage is secondary to other etiologies such as low-level inflammation or an autoimmune process, to name just two of many speculative possibilities. This would certainly produce a paradigm shift in a field which has long regarded seizure activity as the main driver of adverse cognitive sequelae in patients with nonsyndromic focal epilepsy.