Compromised Arousal Circuitry in Temporal Lobe Epilepsy: Potential Neural Substrates of Respiratory Vulnerability
Abstract number :
1.143
Submission category :
2. Translational Research / 2A. Human Studies
Year :
2025
Submission ID :
1158
Source :
www.aesnet.org
Presentation date :
12/6/2025 12:00:00 AM
Published date :
Authors :
Presenting Author: Anas Reda, MS – Vanderbilt University Medical Center
Derek Doss, PhD – Vanderbilt University
Ghassan Makhoul, BS – Vanderbilt University Medical Center
Bruno Hidalgo, BS – Vanderbilt University Medical Center
Graham Johnson, MD, PhD – Mayo Clinic
Lucas Sainburg, BS – Vanderbilt University
Addison Cavender, BS – Vanderbilt University Medical Center
Sameer Sundrani, – Vanderbilt University Medical Center
Emily Liao, BE – University of Minnesota
Alexandra Roche, BA – Vanderbilt University Medical Center
Hakmook Kang, PhD – Vanderbilt University Medical Center
Benoit Dawant, PhD – Vanderbilt University Medical Center
Catie Chang, PhD – Vanderbilt University
Sarah Bick, MD – Vanderbilt University Medical Center
Victoria Morgan, PhD – Vanderbilt University Medical Center
Dario Englot, MD PhD – Vanderbilt University Medical Center
Rationale: Temporal lobe epilepsy (TLE) is characterized by recurrent ictal discharges that progressively remodel critical arousal and respiratory circuitry [1], putting patients at risk for adverse respiratory events, autonomic instability, and sudden unexpected death in epilepsy (SUDEP). Recent evidence has implicated the bed nucleus of the stria terminalis (BNST) as a critical chemosensory hub that serves as a relay between brainstem respiratory nuclei and cortical arousal networks [2]; however, it remains unclear how directional information flow within these circuits becomes compromised in TLE. We hypothesize that the BNST loses causal influence on important arousal and respiratory circuitry, indicating a loss in its ability to regulate hypercapnic arousal.
Methods: Using simultaneous multislice imaging (SMS) with a multiband (MB) acceleration factor of 3 (TR=1.3s), we measured both non-directed functional connectivity (FC) and effective connectivity using Granger causality (GC) in 37 TLE patients compared to 33 controls. Using the CONN functional connectivity toolbox atlas and Harvard Ascending Arousal Network (AAN) Atlas, along with BNST masks defined from recent high-resolution structural imaging protocols, we compared functional connectivity and effective connectivity of the ipsilateral and contralateral BNST to the whole brain, major cortical networks, and key brainstem respiratory nuclei.
Results: TLE patients demonstrated bilateral reductions in BNST FC and causal influence on the whole brain (p< 0.01, Figures 1A, 1B).
Translational Research