Beta oscillations in the sensorimotor cortex correlate with disease and remission in benign epilepsy with centrotemporal spikes

Abstract

Introduction Benign epilepsy with centrotemporal spikes (BECTS) is a common form of childhood epilepsy with the majority of those afflicted remitting during their early teenage years. Seizures arise from the lower half of the sensorimotor cortex of the brain (e.g. seizure onset zone) and the abnormal epileptiform discharges observed increase during NREM sleep. To date no clinical factors reliably predict disease course, making determination of ongoing seizure risk a significant challenge. Prior work in BECTS have shown abnormalities in beta band (14.9–30 Hz) oscillations during movement and rest. Oscillations in this frequency band are modulated by state of consciousness and thought to reflect intrinsic inhibitory mechanisms. Methods We used high density EEG and source localization techniques to examine beta band activity in the seizure onset zone (sensorimotor cortex) in a prospective cohort of children with BECTS and healthy controls during sleep. We hypothesized that beta power in the sensorimotor cortex would be different between patients and healthy controls, and that beta abnormalities would improve with resolution of disease in this self‐limited epilepsy syndrome. We further explored the specificity of our findings and correlation with clinical features. Statistical testing was performed using logistic and standard linear regression models. Results We found that beta band power in the seizure onset zone is different between healthy controls and BECTS patients. We also found that a longer duration of time spent seizure‐free (corresponding to disease remission) correlates with lower beta power in the seizure onset zone. Exploratory spatial analysis suggests this effect is not restricted to the sensorimotor cortex. Exploratory frequency analysis suggests that this phenomenon is also observed in alpha and gamma range activity. We found no relationship between beta power and the presence or rate of epileptiform discharges in the sensorimotor cortex or a test of sensorimotor performance. Conclusion These results provide evidence that cortical beta power in the seizure onset zone may provide a dynamic physiological biomarker of disease in BECTS.

A prediction model integrating synchronization biomarkers and clinical features to identify responders to vagus nerve stimulation among pediatric patients with drug‐resistant epilepsy

“… 15 , 17 Usami et al 37 found that beta oscillations may enhance the responsiveness of cortex to input from distant cortical sites besides gating local cortical processing, indicating the importance of beta oscillations in functional connectivity. Song et al 38 reported longer duration of time spent seizure‐free correlated with lower beta power in the seizure onset zone of patients with benign epilepsy with centrotemporal spikes, suggesting beta oscillations might relate with epileptogenicity. When comparing the difference in the PLI at the beta bandwidth in different efficacies (R100 and R80 subgroups) and different age ranges (3–9 years and 9–16 years subgroups), the significance still had good consistency.…”

“…15,17 Usami et al37 found that beta oscillations may enhance the responsiveness of cortex to input from distant cortical sites besides gating local cortical processing, indicating the importance of beta oscillations in functional connectivity.Song et al38 reported longer duration of time spent seizure-free correlated with lower beta power in the seizure onset zone of patients…”

Source EEG reveals that Rolandic epilepsy is a regional epileptic encephalopathy

“…The union of this label and the pre- and post-central gyri labels was used to define the inferior Rolandic cortex label. The overlap between this sphere and the pre- and post-central gyrus labels was the inferior Rolandic cortex ROI ( Song et al, 2019 ) ( Fig. 1 C).…”

Transient, developmental functional and structural connectivity abnormalities in the thalamocortical motor network in Rolandic epilepsy

“…The inferior Rolandic cortex was targeted here to approximate the seizure onset zone in RE, based on the stereotyped seizure semiology and spike localization observed in this disease ( Boor et al, 2007 , Pataraia et al, 2008 ). The inferior Rolandic cortex was defined using a sphere from the most inferior vertex in Rolandic cortex with a radius equal to half of the distance between the most superior and inferior vertices in Rolandic cortex ( Ostrowski et al, 2019 , Song et al, 2019 , Spencer et al, 2022 ). All ROIs were inspected visually for accuracy.…”