Abstract

Niklas Brake, Flavie Duc, Alexander Rokos, Francis Arseneau, Shiva Shahiri, Anmar Khadra, Gilles Plourde For nearly a century, EEG has been parsed through the familiar lexicon of oscillations: alpha, beta, delta, and their kin. Yet the non-rhythmic, or aperiodic, background of the EEG —often characterized by broadband, 1/f-like, spectral features—is also sensitive to cognitive states and pathology. Compared to EEG oscillations, however, the physiological basis of these aperiodic signals remains largely unknown. Using biophysical models, we found two broad classes of mechanisms capable of driving differences in broadband EEG features. First, we found that cortical circuits can synchronize with aperiodic fluctuations that are capable of producing detectable, low-frequency, broadband scalp potentials. Second, we found that the kinetics of GABA receptors strongly shape EEG spectra across all frequencies. This model prediction was validated by administrating human subjects with propofol, an anesthetic and GABA -A agonist that slows inhibitory decay. Building on this, we developed a spectral analysis method that infers GABA receptor kinetics from EEG and corrects their broadband filtering effects. Applied to propofol data, the method revealed a robust increase in delta rhythms at loss of consciousness, previously obscured by inhibition-driven filtering. Together, these findings extend EEG theory beyond oscillations, linking macroscopic spectral features to receptor-level mechanisms. They offer a framework for mechanistic biomarkers of unconsciousness and for interpretable EEG -based monitoring in clinical care.