Medical Student Texas Tech University Health Sciences Center Laredo, Texas
Rationale: Seizure onset and evolution result from a complex interaction between seizure focus, initiating circuit, pathway of spread, and modulatory center.1 There may be sites within the seizure circuitry that can initiate seizures independently.1,2 Seizure recurrence after months or years of seizure freedom post successful neocortical lesion resection is a rare but known complication. The etiology of this process is currently unknown. In animal models for epilepsy, repeated electrical stimulation of limbic structures has been shown to produce focal seizures through kindling.3The applicability to mesial temporal onset seizures in humans is controversial.3 Seizure recurrence after focal neocortical resection-induced seizure freedom in an approximating region is often attributed to incomplete removal of the epileptogenic zone. We hypothesize that after neocortical resection, non-adjacent mesial temporal lobe structures may be activated, leading to mesial temporal sclerosis and subsequent recurrence of seizures. Methods: A retrospective chart review was performed for all patients who underwent neocortical resection for drug-resistant focal epilepsy between May 2008 and May 2020 at Dell Children’s Medical Center and who subsequently became seizure-free for at least six months following the intervention. Individuals with new temporal lobe seizures and MTS were identified. Results: Two hundred four patients who met criteria were identified. Out of the 204 patients, five patients (2.45%) developed recurrent seizures from the ipsilateral or contralateral temporal lobe after a period of presumed seizure freedom lasting between six months and five years. Seizure semiology was different compared to prior seizures in 4/5 (80%) children. Repeat imaging showed new MTS in all five individuals. Atypical symptoms were reported by two without initial scalp EEG correlates. One individual underwent repeat intracranial depth electrode placement showing subclinical seizures with spread to the mesial temporal lobe that were not detectable by scalp EEG. Conclusions: This study revealed that 2.45% of our cohort with prior neocortical resections to treat drug-resistant epileptic seizures and temporary seizure freedom developed mesial temporal sclerosis. Timed EEG’s pre- and post-weaning of meds, or with subtle non-descript behaviors may or may not optimize early identification of ongoing events. Future research would be needed to demonstrate whether ongoing AED management could be preventative. Funding: Please list any funding that was received in support of this abstract.: There was no funding that was received in support of this abstract.