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Updated: Jan 29, 2026

Psychophysiological Assessment of the Effectiveness of Emotion Regulation Strategies in Childhood
Published on: February 11, 2017
Emotional neglect in childhood modulates aperiodic offset in the left pars orbitalis in adulthood
Sota Inoue1,2, Naofumi Otsuru2,3, Hitomi Ikarashi2,3
1Graduate School, Niigata University of Health and Welfare, Niigata, Japan.
Introduction:
Early life stress (ELS) has been identified as a major risk factor for the development of various disorders in adulthood. This study aimed to investigate the impact of ELS on adult brain function by focusing on the aperiodic component (exponent and offset) of neural activity-a novel neurophysiological marker thought to reflect the excitation and inhibition (E/I) balance.
Methods:
We recruited 65 healthy adults as participants in this study. Resting-state magnetoencephalography (MEG) data were recorded for 5 min with eyes closed. ELS was assessed using the Childhood Trauma Questionnaire-Japanese version, National Institute of Mental Health (CTQ-JNIMH), and current psychological status was evaluated with the Beck Depression Inventory (BDI) and the State-Trait Anxiety Inventory (STAI). Aperiodic components were extracted from the MEG power spectra using the FOOOF algorithm, and their relationships with CTQ-JNIMH scores were analyzed.
Results:
According to the CTQ-JNIMH, 40% of the participants reported experiencing emotional neglect and 27.7% reported physical neglect, while reports of abuse were relatively rare. A significant negative correlation was observed between emotional neglect severity and the aperiodic offset in the left pars orbitalis, which remained significant after false discovery rate correction. In contrast, the aperiodic offset in the left pars orbitalis did not correlate with the current psychological measures (BDI and STAI).
Discussion:
These findings suggest that emotional neglect in early life may induce long-lasting alterations in brain function, potentially shifting the E/I balance, as reflected by the aperiodic offset, toward increased excitability in the left pars orbitalis.
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