Authors :
Presenting Author: Caren Armstrong, MD PhD – Children's Hospital of Philadelphia
Rudy Whitney, student – University of Pennsylvania; Samuel Tomlinson, MD – University of Pennsylvania; Benjamin Kennedy, MD – neurosurgery – CHOP; Sudha Kilaru Kessler, MD – CHOP; Erin Conrad, MD MA – University of Pennsylvania; Eric Marsh, MD PhD – neurology – CHOP
Rationale:
Low frequency electrical stimulation of cerebral cortex produces waveforms known as cortico-cortical evoked potentials (CCEPs) which can be used to probe functional connectivity during intracranial EEG monitoring.
1,2 Increasingly CCEPs are being investigated as a method to evaluate seizure onset networks. CCEP data from pediatric patients is relatively sparse, but recent evidence from subdural grid recordings and a large group of patients < 16 years of age provide evidence of age-related changes in CCEP responses.
3,4,5 Methods:
The CHOP institutional review board approved this study. Informed consent was obtained from parents or guardians, and assent was obtained from subjects when applicable. We studied 37 patients who participated in research based CCEP recording while undergoing stereoelectroencephalographic (sEEG) monitoring for epilepsy, aged 1.8-23 years (median age 14 years) at Children’s Hospital of Philadelphia from 2019 to 2023. CCEP stimulation consisted of sequential 30s trains of 1Hz biphasic stimulation in a bipolar configuration with pulse width 300-500us, amplitude 2-7mA (charge density 12-42µC/cm2). Adjacent pairs of electrode contacts across the implant were stimulated. An automated pipeline was used to synchronize sweeps, remove artifact-corrupted data, and generate an averaged waveform for each response channel.6 The amplitude (expressed as Z score compared with pre-stimulation baseline) and the latency of the averaged N1 and N2 responses were calculated. Reconstructions from pre and post implant images were generated using GARDEL software7 and electrode locations were mapped to a standardized atlas using Freesurfer.8
Results:
Average amplitude of the N1 and N2 responses increased with patient age (r
2 for N1 24% p=0.004; N2 30% p=0.001). This effect was most pronounced with stimulation in frontal and insular regions (r
2 for N1: frontal 31% p=0.001, insular 27% p=0.003; N2: frontal 43% p< 0.001, insular 31% p< 0.001). Average latency of the responses decreased with age (r
2 for N1: 12% p=0.05; N2: 32% p< 0.001), most evident for the N2 response when stimulating outside the seizure onset zone (r
2 for N2: 5% p=0.22 for stimulation of seizure onset zone contacts, 36% p< 0.001 with stimulation outside the seizure onset zone).