Evidence of Thalamocortical Network Activation During Epileptic Spasms: A Thalamic SEEG Case Series
Abstract number :
1.257
Submission category :
3. Neurophysiology / 3C. Other Clinical EEG
Year :
2024
Submission ID :
1293
Source :
www.aesnet.org
Presentation date :
12/7/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Atsuro Daida, MD,PhD – UCLA Mattel Children's Hospital
Saarang Panchavati, BS – UCLA
Shingo Oana, MD, PhD – University of California, Los Angeles
Sotaro Kanai, MD, PhD – Tottori University, Faculty of Medicine
Yipeng Zhang, Dr. – UCLA
Yuanyi Ding, MS – University of California, Los Angeles
Rajsekar Rajaraman, MD, MS – UCLA Mattel Children's Hospital
Shaun Hussain, MD, MS – UCLA Mattel Children's Hospital, David Geffen School of Medicine
Raman Sankar, MD, PhD – University of California, Los Angeles
Aria Fallah, MD, MS – UCLA Mattel Children's Hospital
William Speier, PhD – University of California, Los Angeles,
Vwani Roychowdhury, PhD – UCLA
Hiroki Nariai, MD, PhD, MS – UCLA Mattel Children's Hospital
Rationale: High-voltage slow waves are a distinctive ictal EEG feature during epileptic spasms. Ictal low-voltage fast activity is associated with these slow waves, and such fast waves are speculated to be of cortical origin. However, the origin of the ictal slow waves remains a subject of debate between subcortical and cortical sources.
Methods: We analyzed four patients (3 females, age: 2.7 — 16.9 years) with epileptic spasms who underwent intracranial EEG monitoring with thalamic sampling, including the anterior, centromedian, and/or pulvinar nuclei. These patients underwent thalamic sampling to guide potential neurostimulation therapy. We selected a 4-second window for each epileptic spasm, centering on the first slow-wave peak. For the quantitative analysis, we separated the slow waves (0.5 —10 Hz) and fast waves (10 — 80 Hz). We conducted time-frequency analyses and measured both undirected and directed connectivity metrics (coherence and spectral Granger causality) involving the thalamus and the seizure onset zone (SOZ) to investigate ictal changes in slow and fast waves. Finally, we performed phase-amplitude coupling, which was measured as a modulation index, to examine the interaction between ictal slow and fast waves.
Results: A total of 84 epileptic spasms were analyzed across the subjects, with a median of 23 spasms per patient (range: 6 — 32). Two subjects had generalized epileptic spasms, while the other two had focal epileptic spasms. One of the focal epileptic spasms was clinically subtle, presenting solely as eye movement. Ictal EEG changes were visually confirmed in nine thalamic sites across subjects and were used for further analysis. Time-frequency plots for each thalamic nucleus showed an increase in slow band components, even in the case of subtle epileptic spasms (Fig 1: left, generalized spasms; right, subtle spasms; red dashed line indicates a significant increase at the individual level). Group analysis showed a significant increase in power in both the slow wave (p< 0.01) and the fast wave components (p< 0.05) compared to the interictal baseline (at least 10 minutes away from the ictal segment) in both SOZ and thalamic channels. Coherence analysis showed a significant increase in both slow and fast wave components during epileptic spasms (both p < 0.01; Fig. 2A). Directed connectivity of slow waves was equally increased from the thalamus to SOZ (outflow) and vice versa (inflow) (all p < 0.05; Fig. 2 B). Although fast wave activity also showed a bidirectional increase, the inflow to the thalamus was more pronounced than the outflow (all p < 0.05; Fig. 2C). Moreover, modulation index in the thalamus significantly increased during generalized epileptic spasms (p < 0.05), but not in focal spasms.
Neurophysiology