Auditory stimulation during sleep suppresses spike activity in benign epilepsy with centrotemporal spikes

Benign epilepsy with centrotemporal spikes (BECTS) is a common form of childhood epilepsy linked to diverse cognitive abnormalities. The electroencephalogram of patients shows focal interictal epileptic spikes, particularly during non-rapid eye movement (NonREM) sleep. Spike formation involves thalamocortical networks, which also contribute to the generation of sleep slow oscillations (SOs) and spindles. Motivated by evidence that SO-spindle activity can be controlled through closed-loop auditory stimulation, here, we show in seven patients that auditory stimulation also reduces spike rates in BECTS. Stimulation during NonREM sleep decreases spike rates, with most robust reductions when tones are presented 1.5 to 3.5 s after spikes. Stimulation further reduces the amplitude of spikes closely following tones. Sleep spindles are negatively correlated with spike rates, suggesting that tone-evoked spindle activity mediates the spike suppression. We hypothesize spindle-related refractoriness in thalamocortical circuits as a potential mechanism. Our results open an avenue for the non-pharmacological treatment of BECTS. [Display omitted] Spikes in BECTS epilepsy and sleep spindles may share thalamocortical generationAuditory stimulation during sleep evokes sleep spindles and suppresses spikesStimulation may reduce spiking by inducing thalamocortical refractoriness Interictal spikes hallmarking benign epilepsy with centrotemporal spikes (BECTS) have been hypothesized to emerge from thalamocortical networks. These networks likewise generate spindle activity during sleep. Klinzing et al. demonstrate that auditory stimulation during sleep suppresses interictal spikes in BECTS, possibly by inducing refractoriness in shared thalamocortical networks.