ABS 011: Electrophysiological Markers of PTSD: Linking EEG Signal Entropy to Symptom Severity

Sophia Bililies¹, Yumna Magzoub¹, Nicola Sharp¹, Eva Franks¹, Sanne van Rooij², Jessica Maples-Keller², Barbara O. Rothbaum², Kerry Ressler¹, Mohammad Sendi¹

¹ McLean Hospital, Harvard Medical School Teaching Hospital, Belmont, MA, USA ² Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA

The Van Wickle Journal (2026) Volume 2, ABS011

Introduction: Traumatic events are widespread in the United States, with more than half of individuals experiencing at least one over the course of their lives. Post-traumatic stress disorder (PTSD), a serious and often debilitating response to trauma, affects approximately 5-10% of the general population, with prevalence rising to nearly 46% in groups exposed to severe or repeated trauma. Entropic EEG measures have been increasingly used as a proxy for neural flexibility, with lower entropy reflecting more predictable, or less adaptable, brain dynamics. While PTSD has been hypothesized to disrupt neural flexibility, empirical evidence directly linking PTSD symptom severity to EEG-derived entropy measures is limited. Here, we have examined whether PTSD symptom severity does in fact correspond to reduced neural entropy, or predictability, across canonical scalp electrodes. Ultimately, this study aims to identify electrophysiological biomarkers of PTSD by examining how EEG-derived entropy measures relate to symptom severity, providing insight into the neural signatures associated with clinical burden.

Methods: We analyzed resting-state EEG data from an N=331 sample and recorded from a 19-channel EEG system. Each participant completed the PLC-5, which provided us with a continuous measure of PTSD symptom severity. For each participant, entropy was measured from each EEG channel, and a linear mixed-effects (LME) model was used to estimate the association between PCL-5 scores and neural entropy. We controlled for age, sex, and other covariates that are known to influence EEG signals.

Results: Across all 19 channels, higher PTSD symptom severity was consistently associated with lower EEG entropy measures (r=~-0.17 to -0.11, all FDR p<0.05). This uniform, negative direction across channels is indicative of a global pattern of reduced neural flexibility, or predictability, as PTSD symptom severity increases. This suggests that individuals with more severe PTSD exhibit more predictable, less flexible brain dynamics.

Discussion: EEG entropy measures show a robust, sound relationship with PTSD severity, with lower entropy suggesting a larger symptom burden. These findings support an interpretation that PTSD is, in part, characterized by diminished neural flexibility. This also highlights entropy as a potentially sensitive biomarker of symptom severity. Further work may be needed to clarity whether neural entropy measures reflect a more fundamental neurophysiological mechanism of trauma-related dysregulation.