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Updated: Aug 5, 2026
EEG Mu Rhythm in Typical and Atypical Development
Published on: April 9, 2014
Atypical Development of Resting-State Periodic and Aperiodic Electroencephalography Activity in 22q11.2 Deletion
Caren Latrèche1, Valentina Mancini2, Vincent Rochas3
1Developmental Imaging and Psychopathology Laboratory, University of Geneva School of Medicine, Geneva, Switzerland.
Background:
22q11.2 deletion syndrome (22q11DS) carries increased psychosis risk, making it a valuable model for identifying neurobiological markers. Electrophysiological alterations similar to idiopathic psychosis have been reported, particularly in gamma-band oscillations. However, the aperiodic 1/f component, a putative marker of excitatory-inhibitory balance, is rarely separated from periodic activity, and the developmental trajectories of both remain largely unexplored in 22q11DS.
Methods:
This longitudinal study included 117 individuals with 22q11DS and 96 healthy control participants (HCs) ages 6 to 35 years, and a total of 451 eyes-closed resting-state electroencephalography (EEG) recordings. Spectral relative power (RP) was computed across 6 frequency bands over whole scalp, frontal, and occipital electrodes. Aperiodic exponent and offset were extracted across the whole scalp. Mixed-model regression analyses examined developmental trajectories in individuals with 22q11DS and HCs.
Results:
Deletion carriers showed atypical trajectories across frequency bands. From adolescence, frontal delta RP declined more steeply, whereas beta and low-gamma RP showed more pronounced and widespread increases compared with HCs. Moreover, a consistently higher aperiodic offset was found in 22q11DS. While periodic and aperiodic components did not distinguish participants with and without psychotic symptoms, lower low-gamma RP was associated with higher symptom severity.
Conclusions:
Atypical maturation of neural oscillations emerged from adolescence in 22q11DS, particularly in delta, beta, and low-gamma frequencies. A higher aperiodic offset may reflect elevated broadband neural activity, while the preserved exponent suggests that group differences are primarily driven by periodic changes. Elevated low-gamma RP may represent a neurodevelopmental marker of psychosis vulnerability, whereas its inverse association with symptom severity points to stage-dependent gamma alterations consistent with idiopathic psychosis.
