Enhancing Epilepsy Zone Localization: Integrating SD Analysis with Conventional EEG
Abstract number :
1.245
Submission category :
3. Neurophysiology / 3A. Video EEG Epilepsy-Monitoring
Year :
2024
Submission ID :
932
Source :
www.aesnet.org
Presentation date :
12/7/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Zoya JR.Bastany, PhD – UBC
Ali Gorji, PhD, MD, Prof. – University of Münster
Guy Dumont, PhD, Prof – UBC
Rationale: 40% of epileptic patients endure medically refractory epilepsy, wherein surgical excision of the seizure zone (EZ) is a primary therapeutic approach. However, two-thirds of patients encounter impediments as conventional detection methods often struggle to precisely locate the EZ. Cortical spreading depression (SD), a pathological DC-EEG, is associated with seizures in patients with medically intractable epilepsy (Clinical Neurophysiology 2020;131; 2861-2874). SD signifies localized ionic shifts in cells, spreading slowly across the brain and causing temporary loss of electrical activity and neuron morphology changes. While conventional EEG (AC-EEG, 0.1< frequency< 90Hz) is vital for identifying epileptiform potentials during long-term video EEG monitoring, it lacks sensitivity in detecting DC-potentials like SD. Considering the crucial importance of accurate EZ localization in pre-surgical assessment, this study aims to examine both DC-EEG (including SD) and conventional EEG to enhance EZ localization.
Methods: We conducted a study involving 20 patients with drug-resistant epilepsy, employing our novel DC/AC EEG device during long-term video EEG monitoring. The study followed the ethical guidelines of the World Medical Association for human experiments and received approval from the UBC C & W Research Ethics Board (CW15-0318/ H15-02837 and H22-01534). Our analysis included the examination of AC-EEG, comprising ictal EEG, alongside the assessment of SD through simultaneous DC-EEG (frequency < 0.015 Hz) and AC-EEG recordings. Subsequently, MRI scans were employed to pinpoint lesion sites and generate 3D head models, signal processing methods, and tailored brain mapping analyses to examine the epileptogenic zone.
Results: Our research revealed a prevailing occurrence of SD proximate to the EZ. Moreover, a significant alignment was observed between the lesion site identified by MRI and the SD (19/20; %95). Notably, while AC-EEG suggested the localization of the EZ at a singular site, both MRI imaging and SD zone analysis indicated the involvement of two distinct locations within the epileptogenic zone (Figure1). Furthermore, whereas MRI findings indicated a solitary epileptic lesion, our recordings captured SD waves emanating from two separate lesions, with AC-EEG analysis further corroborating the presence of these dual lesion sites (Figure2).
Conclusions: The findings underscore the limitations inherent in exclusively relying on AC-EEG and MRI for the localization of the epilepsy zone. They highlight the enhanced precision achieved by incorporating DC-EEG and SD analysis in EZ localization during long term video EEG monitoring.
Funding: UBC funding
Neurophysiology