Vagal Nerve Stimulation Modulates EEG Functional Connectivity and Cortical Responsiveness in People with Drug-resistant Epilepsy
Abstract number :
2.072
Submission category :
3. Neurophysiology / 3G. Computational Analysis & Modeling of EEG
Year :
2022
Submission ID :
2204907
Source :
www.aesnet.org
Presentation date :
12/4/2022 12:00:00 PM
Published date :
Nov 22, 2022, 05:27 AM
Authors :
MARILISA BOSCARINO, MD – Campus Bio-Medico University of Rome; Lorenzo Ricci, MD – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome; Jacopo Lanzone, MD – IRCCS Salvatore Maugeri Foundation, Institute of Milan; Tommaso Tufo, MD – Neurosurgery – Policlinico A. Gemelli Foundation, Institute of Hospitalization and Care of a Scientific Character, Catholic University; Flavia Narducci, MD – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome; Carlo Vico, MD – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome; Biagio Sancetta, MD – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome; Mario Tombini, MD, PhD – University Campus Bio Medico in Rome; Vincenzo Di Lazzaro, Professor – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome; Eleonora Tamilia, PhD – Fetal-Neonatal Neuroimaging and Developmental Science Center, Division of Newborn Medicine, Department of Pediatrics – Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts; Giovanni Assenza, MD – Unit of Neurology, Neurophysiology, Neurobiology – Campus Bio-Medico University of Rome
Rationale: Vagal nerve stimulation (VNS) is a viable choice in non-surgical cases of drug-resistant epilepsy (DRE). However, its specific mechanisms of action remain still unclear. In addition to a good response in terms of seizure reduction, improved global quality of life has also been reported in people with epilepsy (PwE) after VNS implantation. We performed a longitudinal study with quantitative EEG analysis and with somatosensory evoked potentials (SEPs) in ten people with DRE before and after VNS therapy, aiming to explore its neuromodulatory effects and identify potential neurophysiological biomarkers of response.
Methods: Ten patients eligible for VNS therapy (4 male, mean age 43,3±13,7 years, with a history of epilepsy of 36,6±11,9 years) were enrolled. All participants underwent a 35-minutes recording with a high density 64-channels EEG before VNS therapy (T0) and after three (T1), six (T2), and 12 (T3) months in both modalities (ON and OFF). SEPs were recorded from the right hand before (T0) and after three months (T1) of VNS therapy, both in VNS ON and OFF mode (T1-ON and T1-OFF, respectively; Figure 1). We assessed changes in intermittent alpha frequency (IAF), power spectrum density (PSD), and network connectivity with graph theory metrics (Figure 1).
Results: Only one patient could be defined seizure responder; however, 50% of them had a reduction in seizure severity on the McHugh scale and 60% was considered improved on the GCI-I scale after VNS therapy. PSD analysis revealed a decrease in delta and an increase in alpha power after VNS therapy with significant differences between T0 and T1 in the OFF modality (p=0.04; Fig. 2A). SEP analysis evidenced an increased amplitude of the N20 potential from T0 to T1 both in ON and OFF mode (p=0.038 and p=0.004, respectively). Moreover, the amplitude of the P24/N24 potential significantly increased when comparing T1-OFF with T1-ON (p=0.048; Figure 2A). EEG connectivity analysis showed a global modification in connectivity values (closeness) across different times (T0, T1, T2, and T3) and frequency bands (delta, theta, alpha, beta, gamma; p < 0.05). In detail, we found a general reduction in low frequencies (i.e., delta and theta) connectivity values after VNS coupled with an increase in faster frequencies (i.e., beta and gamma; p < 0.05; Figure 2B). Functional connectivity in the alpha frequency band revealed an initial increase in connectivity values (T1 and T2) followed by a decrease (T3, p < 0.01, Figure 2B)._x000D_
Neurophysiology