Abstracts

Temporal Dynamics of Amygdala-Hippocampal Beta Synchrony Reveal Trait-Level Depression in Temporal Lobe Epilepsy

Abstract number : 1.277
Submission category : 3. Neurophysiology / 3G. Computational Analysis & Modeling of EEG
Year : 2025
Submission ID : 117
Source : www.aesnet.org
Presentation date : 12/6/2025 12:00:00 AM
Published date :

Authors :
Presenting Author: Sebastian Hanna, MD – UC Irvine Medical Center

Victoria Ho, MD, PhD – UCLA
Melanie Lucas, PhD – UC Irvine Medical Center
Sumeet Vadera, MD – UC Irvine Medical Center
Kurt Qing, MD, PhD – UC Irvine Medical Center
Doris Deng, MD – UC Irvine Medical Center
David King-Stephens, MD – University of California Irvine
Mona Sazgar, MD – UC Irvine Medical Center
Lilit Mnatsakanyan, MD – UC Irvine Medical Center
Beth Lopour, PhD – UC Irvine
Jack Lin, MD – UC Davis Medical Center
Brian Jung, MD – UC Irvine Medical Center

Rationale:

Beta-frequency synchrony between the amygdala and hippocampus has been associated with instantaneous negative mood. However, it remains unclear whether the temporal structure of this synchrony reflects longer-lasting traits such as depression. Persistent, scale-free fluctuations—where moment-to-moment changes tend to continue in the same direction—may indicate a failure to regulate network dynamics. In this study, we investigated whether the temporal structure of fluctuations in beta synchrony between the amygdala and hippocampus could reflect depression severity.



Methods:

We analyzed awake-state intracranial EEG recordings from 14 patients with temporal lobe epilepsy (TLE). Beta-band (13-30 Hz) functional connectivity (FC) between the amygdala and hippocampus was estimated using the imaginary part of the phase locking value across 5-second sliding windows, generating dynamic FC time series. Temporal structure was quantified using detrended fluctuation analysis, which produces a scaling exponent (α), where α ≈ 0.5 reflects uncorrelated (white noise) dynamics, while α > 0.5 indicates persistent dynamics—i.e., if FC increases at one time point, it is likely to continue increasing over time (and vice versa for decreases).



Results:

Both depressed (n=6; Beck Depression Inventory [BDI] ≥ 19) and non-depressed (n=8; BDI < 19) patients exhibited α values significantly higher than phase-randomized surrogate controls (P< 0.00001), indicating temporally structured, non-random FC dynamics in both groups. Depressed patients showed significantly higher α [stronger directional persistence] than non-depressed patients (noisier/more random FC;

Neurophysiology