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Commentary In any form of epilepsy associated with distinct anatomical lesions within the brain, questions arise as to whether the lesional tissue alone is epileptogenic, whether perilesional cortex is also epileptogenic, or whether even more remote cortical regions that appear structurally normal may serve as independent epileptic foci. In disorders associated with multiple distinct lesions, these questions become progressively more complex yet are potentially critical to answer when patients with such lesions who have medically refractory epilepsy are considering the possibility of resective surgery as a treatment option. The paper by Mohamed et al. from Melbourne, Australia, provides us with detailed and well-reported data that suggest important answers to these questions for patients with tuberous sclerosis complex, which is one of the archetypal examples of multilesional epilepsy in pediatrics (1) but for which we have only limited direct evidence regarding epileptogenicity (2, 3). The authors report on a total of 23 intracranial EEG monitoring studies performed in 17 children with TSC-associated refractory epilepsy, most of whom had epileptic spasms and all of whom had at least two distinct seizure foci by scalp EEG monitoring. Individually tailored intracranial electrode paradigms included subdural grids and strips overlying cortical tubers and perituberal cortex and, in some patients, depth electrodes implanted into tubers themselves. The authors present details on the ictal and interictal epileptiform activity seen in this cohort (which included a total of 60 electroclinically distinct seizures), as well as the specific relationship of this activity to the anatomical lesions themselves. The highlights of their findings are:

Tuber or Not Tuber: The Question of Epileptogenic Lesions in Tuberous Sclerosis Complex (TSC)