Using the Aperiodic Exponent from Resting-state Magnetoencephalography (MEG) to Assess Excitation/Inhibition (E/I) in Temporal Lobe Epilepsy Patients
Gurwinder Johal1, Giovanni Pellegrino1, Victoria Ros-Castelló2, Christophe Grova3, Eliane Kobayashi4
1Schulich School of Medicine & Dentistry, Western University, 2Epilepsy Unit, Hospital de la Santa Creu i Sant Pau, 3Physics, Concordia University, 4Peter O'Donnell Jr. Brain Institute, University of Texas Southwestern Medical Center
Objective:
To assess excitation/inhibition (E/I) alterations in temporal lobe epilepsy (TLE) patients using resting-state magnetoencephalography (MEG) and explore the relationship between E/I and cortical thickness.
Background:
TLE, the most common form of focal epilepsy, involves recurrent seizures originating in the temporal lobe and is characterized by E/I imbalance and cortical thinning. Given the challenges of measuring E/I balance in vivo, a non-invasive measure of E/I would be valuable in patients with epilepsy and other excitability disorders. The aperiodic exponent of M/EEG signals, representing the brain’s background noise, is one such measure recently studied. A larger exponent suggests lower E/I, while a smaller exponent suggests higher E/I. The potential applications of this measure remain unknown in epilepsy and TLE, specifically.
Design/Methods:
MEG recordings and 3T MRI images were obtained from 32 TLE patients (17=left, 15=right) and 87 healthy controls at Montreal Neurological Institute-Hospital. Using Brainstorm and CAT12, head modelling and cortical thickness assessment was completed. MEG recordings were coregistered with MRI images to reconstruct six minutes of wakefulness resting state cortical activity. By applying FOOOF to the power-spectrum density of the MEG signals, we extracted the exponent of the aperiodic components. The aperiodic exponent and cortical thickness were modeled vertex-wise, and resulting maps were thresholded after cluster-based permutation statistics.
Results:
Compared to controls, the aperiodic exponent was broadly and significantly lower in TLE patients, indicating higher E/I, with largest differences in posterior head regions. Additionally, a thicker cortex was significantly associated with a larger exponent, or lower E/I, in widespread regions in healthy controls and to a greater extent in left TLE than right TLE.
Conclusions:
This research demonstrates modulations in the aperiodic exponent in TLE patients that correlate with cortical thickness, supporting its potential as a non-invasive measure of E/I alterations in epilepsy. Future studies should further evaluate its translation into clinical practice.
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