Abstracts

Functional Segregation of Epileptogenicity within the Human Amygdala

Abstract number : 1.554
Submission category : 3. Neurophysiology / 3C. Other Clinical EEG
Year : 2025
Submission ID : 1308
Source : www.aesnet.org
Presentation date : 12/6/2025 12:00:00 AM
Published date :

Authors :
Presenting Author: Odile Feys, MD, PhD – Hôpital de la Timone

Julia Makhalova, MD, PhD – Hôpital de la Timone
Samuel Medina Villalon, Eng – Hôpital de la Timone
Maria Fratello, Eng – Aix-Marseille Université
Hugo Dary, PhD – Aix-Marseille Université
Stanislas Lagarde, MD, PhD – Hôpital de la Timone
Francesca Pizzo, MD, PhD – Hôpital de la Timone
Agnès Trébuchon, MD, PhD – Hôpital de la Timone
Maxime Guye, MD, PhD – Aix-Marseille Université
Jean-Philippe Ranjeva, PhD – Aix-Marseille Université
Romain Carron, MD, PhD – Hôpital de la Timone
Didier Scavarda, MD, PhD – Hôpital de la Timone
Christian Bénar, PhD – Aix-Marseille Université
Bernard Giusiano, MD, PhD – Hôpital de la Timone
Fabrice Bartolomei, MD, PhD – Hôpital de la Timone

Rationale:

Temporal lobe epilepsy (TLE) is the most frequent type of epilepsy in adults, yet the amygdala remains less investigated than the hippocampus. Recent advances in neuroimaging and neurophysiological analyses could help better understand the implication of different amygdala nuclei in the genesis of temporal lobe seizures.



Methods:

We retrospectively included 51 patients suffering from TLE who underwent stereoelectroencephalography (SEEG) over the last five years. A virtual epileptic patient atlas with integrated amygdala atlas was used to automatically localize SEEG contacts within the brain regions including nine amygdala nuclei (Mourre et al, 2025; adapted from Tyszka and Pauli, 2016). The epileptogenicity index (EI; Bartolomei et al, 2008) and connectivity epileptogenicity index (Balatsakaya et al, 2020) were computed on the ictal SEEG recordings. We used a linear mixed model to differentiate the effect of amygdala nuclei, TLE subtypes, and lateralization of the epileptogenic zone on the epileptogenicity and Wilcoxon rank sum test to study the links between ictal semiology (present vs. absent) and epileptogenicity of different amygdala nuclei. In patients with mesial TLE (mTLE), correlations between epileptogenicity of the amygdala nuclei, the rhinal cortex and the hippocampus were investigated. Seizure-onset patterns were described using visual and time-frequency analyses (Lagarde et al, 2019).



Results:

We found higher EI values within the basolateral (BL) nucleus compared to other nuclei of the basolateral complex (lateral (LA), accessory basal (BM) and paralaminar (PL) nuclei) across all TLE subtypes and a trend for a higher epileptogenicity in LA and BL in patients with mTLE. For the semiology aspect, BL was more epileptogenic in patients with sensory phenomena and LA in patients with autonomic phenomena while PL was less epileptogenic in patients with cognitive phenomena. In patients with mTLE, PL epileptogenicity correlated with hippocampal epileptogenicity. Seizure onset patterns included low-voltage fast activity (LVFA), rhythmic theta activity, preictal spiking followed by LVFA and bursts of polyspikes followed by LVFA.



Conclusions:

Our findings allow to disentangle the role of different nuclei in amygdala epileptogenicity in temporal lobe seizures. The observed epileptogenicity variance across amygdala nuclei can be explained by underlying neuronal and cytoarchitectural substrates. The higher BL epileptogenicity in all TLE subtypes could be due to its ability to generate intrinsic gamma bursts (Feng et al, 2018). LA, BM, and BL involve rather homogenous masses of cells with a cortical-like character (Równiak et al, 2003), supporting the tendency for higher LA and BM epileptogenicity in mTLE. Surprisingly, affective phenomena were not related to amygdala epileptogenicity, that could be due to the relationship between ictal semiology and the propagation network more than the EZ (McGonigal et al, 2021). Some speculative hypotheses on the pathophysiology of the observed semiological associations with epileptogenicity of BL and LA could be proposed.



Funding: No funding

Neurophysiology