Abstract
AbstractElectroconvulsive therapy (ECT) is one of the most efficacious interventions for treatment-resistant depression. Despite its efficacy, ECT’s neural mechanism of action remains unknown. Although ECT has been associated with “slowing” in the electroencephalogram (EEG), how this change relates to clinical improvement is unresolved. Until now, increases in slow-frequency power have been assumed to indicate increases in slow oscillations, without considering the contribution of aperiodic activity, a process with a different physiological mechanism. Here we show that aperiodic activity, indexed by the aperiodic exponent, increases with ECT treatment. This increase better explains EEG “slowing” when compared to power in oscillatory peaks in the delta (1-3 Hz) range, and is correlated to clinical improvement. In accordance with computational models of excitation-inhibition balance, these increases in aperiodic exponent are linked to increasing levels of inhibitory activity, indicating that ECT might ameliorate depressive symptoms by restoring healthy levels of inhibition in frontal cortices.
Publisher
Cold Spring Harbor Laboratory
Cited by
5 articles.
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