Abstracts

Rationale: Benign epilepsy with centrotemporal spikes (BECTS) is the most common childhood focal epilepsy syndrome, characterized by a transient period of sleep-activated seizures and interictal spikes arising from the sensorimotor cortex. The pathophysiology of this developmental epilepsy is unknown. We recently identified that children with BECTS have an abnormal developmental trajectory of thalamocortical white matter connectivity to the sensorimotor cortex. Median nerve somatosensory evoked potentials (SEPs) and magnetic fields (SEFs) are summated neural responses measured in the primary somatosensory cortex to peripheral nerve sensory stimulation. The early neural activity measured in the somatosensory cortex reflects the transmission along peripheral nerves, dorsal medial lemniscus, and thalamocortical white matter. We hypothesized that median nerve SSEP conduction time would be abnormal in children with BECTS compared to controls, reflecting aberrant structural connectivity of the thalamocortical sensorimotor circuit. Methods: We recorded MEG median nerve SEFs in 7 children in the active phase of BECTS (<12 months seizure free), 7 children entering resolution (>12 months seizure free), and 7 healthy control children. MEG was recorded with 306-sensor system at 2350 Hz sampling rate (Neuromag, 204 planar gradiometers and 102 magnetometers) inside a magnetically shielded room. The sources of MEG signals were estimated on each subject’s cortical surface (reconstructed using FreeSurfer) using the MNE software. The forward solution was computed using a three-compartment boundary-element model with the inner and outer skull surfaces and the scalp surface segmented from the T1 MultiEcho MPRAGE images. The noise covariance matrix was estimated for each MEG recording. Anatomically constrained dynamic statistical parametric mapping was used to estimate the cortical generators. The N20m SEF responses and P100m Visually Evoked Field (VEF) responses were averaged and visualized in each subject. We compared the N20 latency between groups. We then evaluated VEF latency as a control. Results: We found significantly delayed SEF conduction in resolving BECTS compared to active BECTS (p=0.003, age adjusted p=0.057) and controls (p=0.001, age adjusted p=0.019). There was no difference in VEF conduction time between groups (p>0.18). Conclusions: These results demonstrate a focal conduction delay in the early median nerve somatosensory evoked responses in children with resolving BECTS. These data are consistent with our previous findings demonstrating that children with BECTS have decreasing thalamocortical structural connectivity to the sensorimotor cortex across the same age-period that healthy children show increasing connectivity. These data suggest that the structural integrity of this thalamocortical sensorimotor circuit is abnormal in BECTS, and that a decrease in thalamocortical connectivity may be a feature of disease resolution. Funding: NIH NINDS K23-NS092923