Disrupted Signal Flow in Episodic Memory Associated with Temporal and Frontal Lobe Epilepsy
Abstract number :
1.378
Submission category :
5. Neuro Imaging / 5B. Functional Imaging
Year :
2024
Submission ID :
806
Source :
www.aesnet.org
Presentation date :
12/7/2024 12:00:00 AM
Published date :
Authors :
Presenting Author: Donna Gift Cabalo, RN, MSc – Montreal Neurological Institute, McGill University, Montreal, QC, Canada
Jordan DeKraker, PhD – McGill University
Ke Xie, MSc – McGill University
Jessica Royer, PsyD – McGill University
Shahin tavakol, PhD – McGill University
Raul Rodriguez-Cruces, PhD – McGill University
Hans Auer, BSc – Multimodal Imaging and Connectome Analysis Laboratory, McConnell Brain Imaging Centre, Montreal Neurological Institute and Hospital, McGill University, Montreal, QC, Canada
Alexander Ngo, BS – McGill University
Ella Sahlas, BS – McGill University
Judy Chen, BS – McGill University
Thaera Arafat, MD – Montreal Neurological Institute and Hospital, McGill University
Andrea Bernasconi, MD – McGill University
Neda Bernasconi, MD,PHD – McGill University
Raluca Pana, MD – McGill University
Elizabeth Jefferies, PhD – University of York, North Yorkshire, United Kingdom
Jonathan Smallwood, PhD – Queens University, Kingston, Ontario, Canada
Lorenzo Caciagli, MD, PhD – Department of Bioengineering, University of Pennsylvania, Philadelphia, USA
Boris Bernhardt, PhD – McGill University
Rationale: Temporal lobe epilepsy (TLE) and frontal lobe epilepsy (FLE), the two most common pharmaco-resistant epilepsies[1], are linked to significant, yet differential impairments in episodic memory[2]. TLE patients exhibit marked episodic memory difficulties[3], and while FLE patients are less frequently investigated, reports to date suggest mild episodic impairment[4]. In this study, we examine the directionality of signal flow between two models of epilepsies with variations of structural alterations to assess how local disruptions due to lesions integrate with broader cognitive architectures and impact global brain function in health and epilepsies.
Methods: We studied 20 mesial TLE (left/right=12/8, age=32土7 years; F/M: 13/7), 15 FLE (left/right=8/7, age=30土8 years; F/M: 9/6 patients as well as 78 healthy controls (age=32土9 years, F/M: 38/40). Participants underwent fMRI while performing an episodic retrieval task (Fig.1A). To infer signal flow, we concatenated the pre-processed neocortical[5] and hippocampal[6] data and computed the subject-specific effective connectivity[7] (EC). The model specified the design matrix as the driving inputs or the experimental manipulations influencing neuronal activity (Fig. 1B). The EC matrix was then divided into sources (out) and targets (in) nodes. Out/in-degree scores were computed by summing the connectivity weights (Fig.1C, D). Group differences were evaluated using surface-based multivariate analysis, controlling for age and sex, and correcting for multiple comparisons. We also examined the association between memory impairments and disruption in signal flow.
Results: Behaviourally, patients exhibited markedly reduced episodic memory accuracy relative to healthy controls (Fig. 2A). In TLE, there was an atypical signal flow compared to controls in the ipsilateral neocortex, encompassing lateral temporal, fronto-parietal regions, as well as lateral regions of the hippocampus (Fig. 2B). In FLE, while no significant differences were observed at the neocortical level, disrupted signal flow was recorded in the ipsilateral anterior hippocampus. Furthermore, in TLE, neocortical and hippocampal in-degree scores were correlated with episodic performance, while out-degree scores did not. No significant associations were observed for out/in-degree scores in FLE (Fig. 2C).
Conclusions: Our data-driven analysis of task fMRI data reveals disrupted signal flow of episodic memory systems in both TLE and FLE patients. Atypical signal flow was particularly evident in the ipsilateral hemisphere of both groups, with cognitive associations observed only in TLE. These findings provide novel insights into reorganization of episodic memory state, which may underpin impairments in some patients but potentially serve as compensatory adaptations.
[1]Elger, (2002). Brain Pathology, 12(2):193; [2] Helmstaedter, C (2002). Prog in Brain Research, 135:439-5; [3]Barret-Jones (2022). Applied Neuropsych, 29(6):1352-61;[4]Rocchetta A & Milner, (1993), Neuropsychologia, 31(6) 503-524 [5]Cruces et al. (2022). NeuroImage, 263,119612. [6] Dekraker (2022), 11. [7] Frässle, S. (2017). NeuroImage, 155, 406–421
Funding: Savoy Foundation and Fonds de recherche du Québec- Sante
Neuro Imaging