# The different subtypes of temporal lobe seizures networks

F. Bartolomei, J. Makhalova, J. Benoit, S. Lagarde

► To cite this version:

F. Bartolomei, J. Makhalova, J. Benoit, S. Lagarde. The different subtypes of temporal lobe seizures networks. Revue Neurologique, 2025, 181 (5), pp.368 - 381. 10.1016/j.neurol.2025.03.004. hal-05490578

HAL Id: hal-05490578

https://amu.hal.science/hal-05490578v1

Submitted on 3 Feb 2026

HAL is a multi-disciplinary open access
archive for the deposit and dissemination of sci-
entific research documents, whether they are pub-
lished or not. The documents may come from
teaching and research institutions in France or
abroad, or from public or private research centers.

L'archive ouverte pluridisciplinaire HAL, est
destinée au dépôt et à la diffusion de documents
scientifiques de niveau recherche, publiés ou non,
émanant des établissements d'enseignement et de
recherche français ou étrangers, des laboratoires
publics ou privés.

<figure><img src="image_1.png" /></figure>

Distributed under a Creative Commons CC BY 4.0 - Attribution - International License
<figure><img src="image_2.png" /></figure>

ELSEVIER

Available online at

ScienceDirect

www.sciencedirect.com

Elsevier Masson France

EM|consulte

www.em-consulte.com

<figure><img src="image_3.png" /></figure>

Advances in epilepsy

# The different subtypes of temporal lobe seizures networks

<figure><img src="image_4.png" /></figure>

F. Bartolomei<sup>a,b,*</sup>, J. Makhalova<sup>a,b,c</sup>, J. Benoit<sup>a,d,e</sup>, S. Lagarde<sup>a,b</sup>

## INFO ARTICLE

Article history:

Received 15 January 2025

Received in revised form

1st March 2025

Accepted 4 March 2025

Available online 29 March 2025

Keywords:

Temporal lobe epilepsy (TLE)

Epileptogenic zone (EZ)

Stereoelectroencephalography
(SEEG)

Epileptogenic networks

Mesial temporal lobe epilepsy
(MTLE)

Lateral temporal seizures

Temporal-PLUS EPILepsy

## ABSTRACT

Temporal lobe epilepsies (TLEs) are among the forms of epilepsy most frequently encountered in surgical evaluations, characterized by a wide range of anatomical, functional, and electroclinical subtypes. Traditional classifications, such as mesial and lateral TLE, have been broadened by advances in stereoelectroencephalography (SEEG), revealing more complex forms such as mesio-lateral and temporal-plus seizures. These findings support the concept of epileptogenic networks, emphasizing interconnected regions rather than isolated focal areas in the genesis of seizures. Quantitative tools, such as the epileptogenicity index (EI), are improving the accuracy of SEEG interpretation, which is closely correlated with surgical results. Temporal-plus epilepsies, in particular, require full SEEG exploration due to their broader involvement in the network, necessitating tailored surgical approaches. A better understanding of TLEs subtypes and epileptogenic networks is an essential basis for advancing minimally invasive surgical techniques, including laser interstitial thermal therapy (LITT) and neuromodulation. These methods rely on the precise localization of epileptogenic networks. This network-based framework represents an important step towards optimizing surgical outcomes and advancing personalized epilepsy care.

© 2025 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

## 1. Introduction

Temporal lobe epilepsies (TLEs) are among the most commonly encountered forms of epilepsy in surgical evaluation, accounting for approximately 60% of cases referred to epilepsy surgery centers [1]. These epilepsies are characterized

by an epileptogenic zone (EZ, the brain region producing seizures) in the temporal lobe. TLEs have numerous etiologies, particularly in the context of presurgical evaluation, including lesions such as hippocampal sclerosis, low-grade epilepsy-associated tumors, and developmental malformations [2-4]. Some cases remain of unknown etiology, without specific

<footnote><sup>a</sup> Aix-Marseille université, Inserm, INS, Institut de Neurosciences des Systèmes, 13005 Marseille, France</footnote>

<footnote><sup>b</sup> AP-HM, Timone Hospital, Epileptology and Cerebral Rhythmology, 13005 Marseille, France</footnote>

<footnote><sup>c</sup> Aix Marseille University, CNRS, CRMBM, Marseille, France</footnote>

<footnote><sup>d</sup> UF EEG-Épileptologie, Service de neurologie, University Hospitals of Nice, Nice, France</footnote>

<footnote><sup>e</sup> Université Côte d'Azur, CHU Nice, UR2CA-URRIS, Nice, France</footnote>

<footnote>* Corresponding author. Service d'épileptologie et de rythmologie cérébrale, hôpital Timone, 264, rue Saint-Pierre, 13005 Marseille, France.</footnote>

<footnote>E-mail address: fabrice.bartolomei@ap-hm.fr (F. Bartolomei).</footnote>

<footnote>https://doi.org/10.1016/j.neurol.2025.03.004</footnote>

<footnote>0035-3787/© 2025 The Authors. Published by Elsevier Masson SAS. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).</footnote>
histological findings. Beyond this etiological classification, examining the anatomical organization of temporal lobe seizures is likely more insightful, particularly through recording seizures and their origin using stereoelectroencephalography (SEEG). Indeed, there is no strict correlation between the epileptogenic zone and the location of a visible lesion [5-8]. This discordance underscores the importance of accurately defining the epileptogenic zone as a prerequisite for effective, tailored epilepsy surgery. SEEG recordings have expanded our understanding of temporal lobe seizures, uncovering a variety of seizure types beyond the traditional mesial and lateral classifications [3]. Historically, the medial form, known as mesial temporal lobe epilepsy (MTLE), is the most recognized due to its association with hippocampal sclerosis [2]. However, TLE is a heterogeneous condition encompassing different anatomical, functional, and electroclinical subtypes. This was illustrated early in the history of SEEG, with the first classification of temporal seizures by J. Bancaud in 1965, highlighting distinct anatomical and functional areas involved in seizure genesis [9]. More recent SEEG-based analyses have led to the description of various forms, such as mesio-lateral seizures [10], temporo-polar seizures [11], temporo-basal seizures [12], and the different forms of “temporal-plus” seizures [13]. In general, SEEG recordings of the epileptogenic zone in temporal epilepsies have served as a prototype for developing a network-based view of the epileptogenic process instead of the classic notion of a zone or even a focus [10,14-16].

In this article, we will recall the concept of epileptogenic networks before exploring the various forms of temporal lobe seizure networks based on SEEG investigations, with particular emphasis on the works provided by our group for more than twenty years.

## 2. The model of “epileptogenic networks”

In the 1960s, the introduction of SEEG facilitated electro-anatomical-clinical correlations during seizure recordings and enabled a better understanding of the genesis and organization of human focal seizures [9]. The advent of digitized EEG systems and advances in imaging further enhanced the exploration of the epileptic brain [17]. In particular, progress in SEEG signal quantification and ictal imaging has increasingly aligned with understanding of normal brain function, specifically within the framework of distributed brain networks characterized by their functional and structural connectivity [10,18,19].

Based on SEEG observations and signal quantification methods, we proposed a theoretical framework called “epileptogenic networks,” which describes three primary network types producing abnormal electrophysiological activity: the epileptogenic zone network (EZN), the propagation network (PN), and the non-involved networks (NIN) [20,21] (Fig. 1A). An ultimate goal of SEEG interpretation is precisely delineating the brain regions associated with these network types. Brain networks can be modeled as nodes, representing distinct brain regions, interconnected by functional or structural links. SEEG-based quantification of epileptogenic networks involves evaluating functional connectivity during

ictal events [18,22-24]. In temporal lobe seizures, the EZN is characterized by distinct coupling patterns: initial heightened synchrony preceding rapid ictal discharges, followed by transient desynchronization (or decorrelation) during the fast discharge phase, and a subsequent re-increase in coupling [25,26]. This dynamic interplay of functional coupling is a hallmark feature of the EZN. In contrast, propagation networks exhibit more intricate dynamics, often characterized by hypersynchronization phenomena [27,28].

Clinical ictal quantification increasingly relies on methods that focus on spectral changes in specific regions, particularly the generation of high-frequency activity at seizure onset [29]. For example, the epileptogenicity index (EI) [30] is based on two parameters: the delay of structural involvement and the relative amount of fast activity in the initial discharge. EI values are normalized at the seizure level ranging from 0 (no epileptogenicity) to 1 (maximum epileptogenicity) for each channel/region. EZN regions typically have EI values above 0.4 [31]. Ictal biomarkers have demonstrated better correlations with surgical outcomes than interictal measures [31].

The EZN comprises brain regions with the highest epileptogenicity, responsible for seizure initiation [30]. These regions exhibit altered excitability [32] and connectivity [21]. Three features characterize SEEG-recorded seizure onset patterns in the EZN [33]:

* transient changes from interictal to preictal periods (e.g., increase in spikes, slow waves, or polyspike bursts);

* emergence of rhythmic discharges, often manifesting as fast activity in the beta/gamma range and loss of theta/alpha background activity;

* the spatial extent of discharges, potentially involving multiple regions. The first two features are collectively termed “seizure onset patterns” (SOPs). In 20% of SEEG cases, SOPs do not include fast discharges [34,35].

From a large series of SEEG recordings, we found that the EZN is focal, confined to a single region in approximately 40% of cases, while in 60%, it involves a network comprising at least two epileptogenic regions [34]. For instance, most temporal lobe seizures are organized as EZ networks [16]. The number of regions in the EZ varies, ranging from one to nine depending on the subtype of temporal epilepsy [16]. Moreover, temporal lobe cases with negative magnetic resonance imaging (MRI) findings tend to have a more extensive EZN [16,30].

The EZN may include a visible lesion, particularly in the case of intrinsically epileptogenic lesions. However, in this network concept, it is crucial to note that the lesion may be only one node within the EZN, and in some cases, only a part of the lesion belongs to the EZN [8]. The propagation network (PN) comprises regions with lower epileptogenicity, less-altered biological properties, and an inability to generate seizures under typical conditions [32,36]. The PN is typically activated with some delay, may include slower-frequency discharges, and often does not exhibit clear changes during the preictal state. These networks involve both cortical and subcortical structures, especially within propagation systems [37]. Thalamic regions, such as the anterior nucleus or pulvinar, are highly involved in temporal lobe seizures, contributing to the spread and hypersynchronization of
<figure><img src="image_5.png" /></figure>

Fig. 1 – A. Schematic representation of the Epileptogenic networks model. The epileptogenic zone network is responsible for seizure generation (EZN). The propagating network (PZN) is characterized by cerebral structures that are less epileptogenic and involved in seizure diffusion. Non-involved networks (NI) have little or no altered activity during seizures. During the interictal period, these networks have modified connectivity, represented schematically here. The lines between small circles represent the functional connectivity (FC) strength within the structures of a sub-network. B. Anatomofunctional subtypes of temporal lobe epilepsies (TLEs) with implications for surgical strategies. EZN: epileptogenic zone networks. Blue (Mesial and mesial lateral) forms are accessible to standardized anterior lobectomy (ATL). Pink (Lateral TLE) and orange (the different forms of temporal plus) generally require a tailored cortectomy and prior SEEG.

discharges [38,39]. Recently, computational macroscopic models have validated the empirical description of epilepto- genic networks [40]. The virtual epileptic patient (VEP) is a large-scale computational model that can reproduce SEEG- recorded seizures and generate synthetic data mimicking epileptogenic network dynamics, including seizure genesis in hyperexcitable, interconnected regions [41,42]. This model is particularly powerful for studying temporal lobe seizures.

### 3. Anatomo-functional subtypes of temporal lobe seizures networks

It is traditionally recognized that TLEs can involve two principal types of epileptogenic zones, defining the mesial temporal subtype (where the epileptogenic zone is localized in

the mesial part of the temporal lobe) and the lateral subtype (where the epileptogenic zone is localized in the neocortex) [43,44]. However, this dichotomy appears too simplistic in light of findings from SEEG studies, which have shown the existence of additional forms of temporal lobe seizures [9,13,14,45,46].

Notably, some TLEs have been demonstrated to involve more complex EZNs, encompassing both mesial (M) and lateral (L) cortices, referred to as mesio-lateral subtypes [10,14]. Additionally, temporal EZNs involving the cortices bordering the Sylvian fissure ("perisylvian cortex") and/or including the insula have long been described in the SEEG literature [45,46]. Other temporal lobe seizures may involve the frontal cortex (temporo-frontal seizures) or the occipital region (temporo-occipital seizures). Collectively, these complex epileptogenic networks, including both temporal
and extratemporal cortices, have been designated by the acronym “temporal-plus” [47]. The extension of the epileptogenic zone (EZ) beyond the boundaries of surgical resection is a major cause of epilepsy surgery failure, particularly in cases where standardized anterior temporal lobectomy (ATL) interventions have been performed [47].

In practical terms, it is helpful to propose a framework for classifying the various forms of epileptogenic networks in temporal epilepsies based on surgical strategy. This is illustrated in Fig. 1B. The EZN of these different forms of TLEs can be broadly categorized into temporal networks and temporal-plus networks. Concerning temporal networks, the surgical strategy is typically based on standard ATL for the mesial temporal and mesio-lateral networks. In contrast, lateral temporal networks often require a tailored corticectomy guided by SEEG recordings to address the extent of the EZN accurately. For temporal-plus networks, the epileptogenic zone extends beyond the boundaries of the temporal lobe, requiring SEEG exploration in all suspected cases [48]. These include temporo-insular/perisylvian networks, temporo-frontal networks, and temporo-occipital networks.

Some forms of temporal lobe seizures have less clearly defined boundaries. This is particularly true for seizures originating in the temporo-basal region, which will be briefly discussed [12]. Furthermore, some TLEs, especially MTLEs, can be bilateral. This issue will not be addressed in this article. Noteworthy, temporal lobe epilepsies in infants and young children may present with spasms, especially in association with temporo-basal EZNs [49].

### 3.1. Mesial temporal lobe subtype of EZN

Mesial temporal seizures (MT) have long been recognized and are well-characterized through intracranial recordings [50]: these seizures arise within a network of limbic temporal structures, including the hippocampus, the amygdala, the limbic mesial portion of the temporal pole, and the entorhinal cortex [10], which are highly interconnected and share a common phylogenetic origin [51].

Mesial temporal seizures represent the prototype of an epileptogenic zone network being generated often simultaneously within a network of mesio-temporal structures rather than a single structure (Figs. 2A, 3, 4). Thus, incomplete surgical resection of this network carries the risk of failure. For example, the resection of the anterior parahippocampal gyrus is a significant prognostic factor when a selective amygdalo-hippocampectomy is performed surgically or by laser interstitial therapy [52–54]. Modes of onset that are more limited to certain structures, notably the amygdala or hippocampus, can also be observed [55].

Two main ictal seizure onset patterns have been described in MTLE [50]. The first type (“hypersynchronous”) is characterized by the emergence of large rhythmic spikes followed (preictal spiking) by rapid discharge (RD). A second type (“non synchronous”) is characterized by the emergence of RD without prior interictal activity changes. The average duration of the RD is about eight seconds before it slows down, with frequency typically ranging from 12 to 35 Hz [25].

Preferential interactions (functional connectivity) are observed between these structures at the onset of mesial

temporal seizures [10,14,56–58] (Fig. 3). Using directed connectivity methods, it is possible to demonstrate that the entorhinal cortex drives certain seizures, while others are primarily driven by the amygdalo-hippocampal complex [59]. The role of sub-hippocampal structures (entorhinal cortex) was found to be more frequent in seizures with a non-synchronous pattern [59].

Studies from our team have precisely quantified ictal activity using the EI [16,30]. The profile of mesial temporal seizures is distinct from other subtypes. Fig. 4 illustrates that the peak epileptogenicity is distributed within mesial temporal structures while epileptogenicity in neocortical and extratemporal cortices is low. The quantification of mesial temporal seizures using EI demonstrates a gradient of epileptogenicity, with maximal values in the hippocampus and entorhinal cortex, followed by the amygdala, the limnic/medial temporal pole, and the parahippocampal cortex [30] (Fig. 5A).

Mesial temporal seizures are predominantly caused by hippocampal sclerosis but can also occur in cryptogenic forms or, less commonly, in lesion-related forms, which tend to cause other seizure types [16,60] (Fig. 5B).

### 3.2. Mesio-lateral temporal subtype of EZN

This subtype involves epileptogenicity affecting both the medial part of the temporal lobe and neocortical structures [16], often anterior neocortical structures, particularly the temporal pole [11] (Figs. 2B, 4A). A continuum exists with temporal-perisylvian forms, and the epileptogenicity profile shows high epileptogenicity values in both mesial and lateral cortices (Fig. 4A).

These forms are more frequently encountered in lesional epilepsies (Fig. 5B), particularly involving the anterior and medial temporal regions [16,60,61]. They may be amenable to standardized ATL when they remain well-confined in these areas. Fig. 6 [62] shows an example of a mesial-lateral seizure with a slow seizure onset pattern in a patient cured by an ATL. In contrast, tailored resections are required when the more posterior lateral neocortex is involved. These resections may depend on the relationship between the EZ and eloquent cortices responsible for language.

### 3.3. Lateral temporal lobe subtype of EZN

This subtype is relatively rare and defined by an EZN limited to neocortical lateral temporal structures (superior, middle, and inferior temporal gyri) [43]. The epileptogenicity profile of these EZN is shown in Fig. 4A [16]. This profile mirrors the MTLE profile with maximal epileptogenic values in the temporal neocortex. These EZN tend to be more focal (less epileptogenic regions, Fig. 4). It has been suggested that this subtype is often confined to the superior temporal gyrus, possibly due to limited direct connectivity with mesial temporal structures [14]. An illustrative case is shown in Fig. 7.

### 3.4. Temporal-Plus (T+) subtypes of EZN

This term defines epilepsies where epileptogenicity extends beyond the temporal lobe [47,63]. The suspicion of T+ TLE is a formal indication for SEEG exploration, with electrodes
<figure><img src="image_6.png" /><figcaption>Fig. 2 – Examples of SEEG recordings in Mesial (A) and Mesial lateral (B) temporal lobe seizures. Selected traces from different structures during a seizure (adapted from [16]). Mesial seizure is characterized by a fast discharge affecting only the mesial brain structures (EC, A, HIA); while the Mesial-lateral is characterized by a fast discharge affecting mesial (iTP; A, HIA, HIP, EC) and the lateral neocortex (eTP; aMTG). Abbreviation: iTP: internal part of the temporal pole; A: amygdala; HIA: anterior hippocampus; HIP: posterior hippocampus; EC: entorhinal cortex; aMTG: anterior middle temporal gyrus; pMTG: posterior part middle temporal gyrus; STG: superior temporal gyrus; INS: insular cortex</figcaption></figure>

exploring the temporal lobe and adjacent insular, frontal, and, in some cases, posterior regions. They require subsequent adjustment of surgical strategy.

In temporal-plus epilepsies, the number of epileptogenic regions is generally larger, and the quantified values of epileptogenicity in extra-temporal cortices are more significant (Fig. 4B, Fig. 5C) [64,65]. The surgical prognosis tends to correlate with the involvement of extra-temporal cortices, particularly perisylvian regions [65], which can, in some cases, pose a limitation to the surgical outcome [66]. This has been recently confirmed in a study showing that insular involvement in TLE, identified through SEEG, may influence surgical outcomes. Early temporal-insular spreading time (< 400 ms) was a key predictor of poorer surgical outcome following ATL [67].

The relative frequency of these forms is not well-established. In a study on the surgical prognosis of TLEs

involving a cohort of 168 patients, 18 (10%) were classified as temporal-plus. Among these, the majority presented with temporo-insulo-opercular forms (11/18). Other forms included temporo-frontal epileptogenic zones (2/18) and temporo-occipito-parietal EZ (5/18) [66].

Forms of temporo-insular or temporo-frontal epilepsy have been well-documented in cases of epilepsy with an enlarged amygdala [68]. Temporo-insulo-opercular seizure often the antero-ventral part of the insula (agranular cortex) and anterior frontal operculum: Temporo-frontal seizures are distinct due to their epileptogenic network, which tends to preferentially involve the temporal pole and paralimbic regions, particularly the ventromedial prefrontal cortex [69,70]. In these seizures, involvement of the anterior insular cortex may also be observed (Fig. 8). This phylogenetically related triangle [70] should be systematically explored in this
<figure><img src="image_7.png" /><figcaption>Fig. 3 – Example of a mesial temporal seizure (red arrow indicates the seizure start). As indicated by the EI, the most epileptogenic regions are A1-A2 (amygdala) and TB1-TB2 (entorhinal cortex). (c) Time-frequency representation of the seizure; increase of high-frequency activity at seizure onset is visible on channel A1-A2. (d) Examples of connectivity (non linear correlation, h2) graphs corresponding to different time windows during the seizure. The delay between channels permits to estimate a direction for each link. Maximum interactions are visible between the mesial regions before the fast discharge (period 202-204s) and after the discharge extending to other regions (period 2016-220s). EI; Epileptogenicity Index; SEEG; stereotaxic electroencephalography. Adapted from [26].</figcaption></figure>

type of epilepsy. The clinical manifestations resemble prefrontal seizures, often presenting with complex motor, emotional, and hyperkinetic semiology [69].

3.5. *The Temporo-basal EZN*

Basal temporal seizures are more challenging to classify and
have not been extensively studied in the literature [12]. They

are defined as TLE with maximal epileptogenicity within the
temporo-basal regions, either anterior (including the rhinal
cortex, anterior collateral sulcus, anterior fusiform gyrus, and
anterior occipito-temporal sulcus) or posterior (including the
posterior fusiform gyrus, collateral sulcus, and posterior
occipito-temporal sulcus), or a combination of these areas.
These seizures have been often grouped with anterior
temporal epilepsies (mesial or mesio-lateral subtypes) and
<figure><img src="image_8.png" /></figure>

Fig. 4 – A. Individual profiles of epileptogenicity in a cohort of patients explored with SEEG adapted from [16]. Epileptogenicity is quantified in regions of the temporal lobe and in the extratemporal cortices thanks to the Epileptogenicity Index method. Values range from 0 (no epileptogenicity) to 1 (maximum epileptogenicity), based on the propensity of each region to generate fast activities. EI values are plotted for each patient and for each studied structure. Abbreviations: M: Mesial, L: Lateral, ML: Mesio-Lateral, TPS: temporal perisylvian/temporal plus, iTP: internal part of the temporal pole, eTP: external part of the temporal pole, A: amygdala, HIA: anterior hippocampus, HIP: posterior hippocampus, EC: entorhinal cortex, aMTG: anterior middle temporal gyrus, pMTG: posterior part middle temporal gyrus, STG: superior temporal gyrus, OP: opercular cortex, OFC: orbitofrontal cortex, INS: insular cortex. B/Histograms showing the number of patients disclosing high EI values (NEI = 0.3) in each subgroup. Only four patients disclose only one epileptogenic structure (1 in M group and 3 in L group). Adapted from [16].
<figure><img src="image_9.png" /><figcaption>Fig. 5 – A. Values of the Epileptogenicity Index (EI) computed from mesial and lateral temporal lobe structures in 17 patients (P1-P17) with MTLE. Adapted from Bartolomei F et al. [30]. EI values are averaged over the 17 patients. Mean EI values are significantly higher in mesial (EI averaged from the mesial structures) than lateral structures (EI averaged from the lateral structures). B. Etiology according to the Subtype (M: mesial, L: lateral, ML: mesial-lateral, TPS: temporal plus/perisylvian). HS: hippocampal sclerosis, Le: lesion other than HS, N: normal MRI. The ML type is frequently associated with epileptogenic lesions in the temporal lobe. Adapted from [16]. C. Maximal EI values obtained in extra-temporal cortices in 34 patients with SEEG explored TLEs. EI values are indicated by ascending order and according to the corresponding subtypes. We can notice that TPS patients have the highest values. Adapted from [16].</figcaption></figure>

with temporal-plus epilepsies, particularly temporo-occipital forms, in cases of posterior involvement. They are often associated with MRI lesion.

### 3.6. Thalamic Involvement in TLE networks

The role of thalamic involvement in TLE has been increasingly recognized as a crucial factor influencing seizure dynamics, therapeutic interventions, and surgical prognosis. The thalamus, particularly its anterior nucleus (ANT) and pulvinar nucleus (PuM), plays a key role in epileptic network dynamics. SEEG studies have shown that thalamocortical synchronization increases significantly during seizures, reinforcing the concept that the thalamus serves as a hub for epileptic activity spread [27]. More recent studies demonstrated through multisite thalamic recordings that

thalamic involvement in seizure propagation is not uniform, with the pulvinar often engaged earlier than ANT in many cases [38,71]. The degree of thalamo-cortical synchrony may influence the clinical manifestation of seizures, including the presence of loss of consciousness [27,72]. The medial pulvinar, in particular, has been implicated in seizure termination, suggesting a potential regulatory role in seizure cessation [38,39]. The degree of thalamic involvement in seizure activity has been correlated with surgical outcomes in TLE patients. Studies have found that higher thalamic epileptogenicity is associated with a poorer post-surgical prognosis, likely due to the extension of epileptic networks beyond the temporal lobe [37]. The recognition of the thalamus as a key component of the epileptogenic network has led to the exploration of deep brain stimulation (DBS) as a potential therapeutic approach [73]. Stimulation of the ANT
A

<figure><img src="image_10.png" /></figure>

B

<figure><img src="image_11.png" /></figure>

C

<figure><img src="image_12.png" /></figure>

Fig. 6 – An example of temporal mesial-lateral seizure. Twenty-three-year-old man with drug-resistant epilepsy. A. SEEG traces show rhythmic discharge affecting simultaneously the mesial temporal regions and the lateral neocortex. B. Connectivity Epileptogenicity Index estimation projected into the MRI Mesh with electrodes. This connectivity measure estimates the directed connectivity plus the epileptogenicity index [80]. C. Anterior standard lobectomy removing both mesial and anterior lateral cortex. The patient is seizure free since this surgery.

has been FDA-approved for drug-resistant epilepsy, showing a significant reduction in seizure frequency over time [74]. The pulvinar has also emerged as a promising target due to its role in functional connectivity with mesial temporal structures and associative cortices [75]. Preliminary results from open studies using pulvinar DBS have shown encouraging results [76,77], but the indications for this stimulation have yet to be clearly defined, particularly in temporal

epilepsies that have failed surgery or are considered inoperable.

4. Clinical differential semiology

A significant portion of temporal seizure semiology is due to the extension of ictal discharges to numerous cortical and
<figure><img src="image_13.png" /><figcaption>Fig. 7 – Example of Lateral temporal EZN. A. SEEG recording showing fast discharge emerging in the neocortical contacts of the temporal lobe electrodes. B. Projection of the epileptogenicity values within the post-operative MRI Mesh showing the limit of the cortectomy (dashed lines) and the electrodes.</figcaption></figure>

subcortical structures [72]. Therefore, absolute electroclinical
correlations between different subtypes of temporal seizures
are challenging to establish.

No recent study has comprehensively assessed the
temporal seizure semiology according to the different EZN
networks. Our team investigated the main differences
between the clinical signs of mesial, lateral, and mesial-
lateral temporal seizures [60]. MTLEs were characterized by
viscerosensory sensations, particularly epigastric sensa-
tions, and emotional experiences like fear. Dreamy states
or déjà vu were frequently reported. Oroalimentary auto-
matisms and upper-limb automatisms typically occur later
in the seizure. Loss of contact is delayed, with initial
preservation of awareness and interaction. Seizure duration
is generally long, over 60 s, with a long post-ictal recovery

time [78]. Secondary generalizations are rare in this subtype.
Mesial-lateral TLE shares similarities with mesial seizures,
such as epigastric sensations, and may include fear and
dreamy states. Early onset of oroalimentary automatisms,
verbal automatisms, or vocalizations is a hallmark. Loss of
contact occurs earlier compared to purely mesial seizures.
Seizure duration is similar to mesial seizures, mostly
exceeding 60 s. Lateral TLEs were characterized by promi-
nent auditory illusions or hallucinations, often accompanied
by other sensory signs (e.g., visual, vestibular). Initial loss of
contact is common while oroalimentary and upper-limb
automatisms are rare. Seizures tend to be shorter compared
to mesial and mesial-lateral subtypes. Secondary generali-
zations are more frequent in this subtype compared to the
others.
A

<figure><img src="image_14.png" /></figure>

B

<figure><img src="image_15.png" /></figure>

C

<figure><img src="image_16.png" /></figure>

D

<figure><img src="image_17.png" /></figure>

Fig. 8 – An illustrative case of Temporal plus epilepsy presenting as temporo-frontal seizures. Seizure semiology was characterized by a subjective feeling of anxiety, ascending thoracic sensation, followed by a loss of consciousness, right-hand gestural automatisms, pelvic thrusts, and pedaling automatisms, eventually followed by bilateral tonic posture and vocalizations. Brain MRI revealed large right frontal periventricular nodular heterotopia (PNH), A. SEEG recording of a habitual seizure out of sleep that starts with spike-DC-shift followed by LVFA simultaneously affecting the right temporal pole, amygdala, anterior hippocampus, as well as the right orbitofrontal cortex. The left amygdala is simultaneously involved by the tonic fast discharge, which spares the left hippocampus and orbitofrontal cortex. The prefrontal heterotopic cortex and the ipsilateral anterior insula are involved simultaneously, however expressing a less rapid fast discharge. The temporal lateral region, anterior cingulate, and lateral prefrontal and premotor regions belong to the propagation network. B. A quantitative SEEG-signal analysis by the Connectivity Epileptogenicity Index [80] demonstrates a temporo-prefrontal EZN, with the highest epileptogenicity values within the right temporal pole (TP3-4), amygdala (A1-2), and hippocampus (B3-4), followed by the right insula-gyri longi (T1-2) and the right orbitofrontal cortex (OR1-2). The right frontal heterotopic cortex (OF1-2) discloses moderate cEI values. C. Patient's three-dimensional (3D) brain mesh with SEEG electrodes. The maximal cEI values across seizures are represented as spheres on the respective electrode contacts according to a color map. D. Maximal cEI values represented on the patient's axial and coronal brain MRI views showing the heterotopic cortex. Abbreviations: ACC: anterior cingulate cortex; Amy: amygdala; DLPFC: dorsolateral prefrontal cortex; EZN: epileptogenic zone network; FOp: frontal operculum; Hipp: anterior hippocampus; INS ant: anterior insula; INS post: posterior insula; L: left; OFC: orbitofrontal cortex; PNH: periventricular nodular heterotopia; PreM: premotor cortex; R: right; T: temporal; Tlant: anterior temporal lateral.

Another study examined the differences between TLE and T+ TLE epilepsy, defined based on the results of SEEG recordings [13]. The study highlights that auras and post-ictal symptoms are essential in differentiating these two types of epilepsy. While viscerosensitive auras and post-ictal amnesia orient towards TLE, gustatory auras, vestibular symptoms, auditory illusions, and post-ictal dysphoric states suggest T+ TLE. Additionally, T+ seizures are characterized by more complex motor manifestations, including ipsilateral tonic signs and contralateral version, as well as a tendency towards earlier loss of consciousness.

Temporal basal seizures are characterized by language disturbances (aphasia, jargonophasia, speech production),

motor phenomena (gestural automatisms, hyperkinetic behaviors), and cognitive symptoms (déjà vu, dreamy states), with fewer emotional and sensory signs compared to other temporal lobe epilepsies. However, due to overlapping features with other TLE subtypes, further studies are needed to improve the semiological knowledge of these seizures [12].

## 5. Conclusion

Understanding the diverse forms of temporal lobe epilepsy (TLE) and their associated epileptogenic networks (EZN) offers crucial insights for guiding surgical interventions. The precise
delineation of these networks using SEEG has not only deepened our knowledge of seizure genesis but also provided a robust foundation for tailoring surgical approaches [48]. Consequently, minimally invasive techniques such as laser interstitial thermal therapy (LITT) [79] and neuromodulation [80] have emerged as promising alternatives to conventional resective surgeries.

Detailed characterization of mesial, lateral, mesio-lateral, and temporal-plus subtypes improves the ability to target specific epileptogenic zones while preserving functional brain areas. For instance, LITT, with its precision and minimal collateral damage, is well-suited for the small, well-defined EZNs, typically observed in MTLE. Similarly, neuromodulation techniques, including responsive neurostimulation (RNS), vagus nerve stimulation (VNS) and deep brain stimulation (DBS), are more advantageous for addressing broader or multifocal networks, particularly in cases of temporal-plus epilepsy where resective surgery might be less effective or in cases of bitemporal epilepsies.

Finally, the network-based conceptualization of epilepto-
genesis underlines the importance of accurate SEEG inter-
pretation [33]. Understanding the dynamic interplay and
hierarchy between epileptogenic, propagation, and non-
involved networks is crucial for identifying optimal surgical
targets. The integration of advanced quantitative markers
further refines SEEG analysis and surgical planning, poten-
tially improving outcomes for patients with drug-resistant
epilepsy.

Funding source

There is no specific funding for this work.

Disclosure of interest

The authors declare that they have no competing interest.

REFERENCES

[1] Jehi L, Friedman D, Carlson C, Cascino G, Dewar S, Elger C, et al. The evolution of epilepsy surgery between 1991 and 2011 in nine major epilepsy centers across the United States, Germany, and Australia. Epilepsia 2015;56:1526-33. http://dx.doi.org/10.1111/epi.13116.

[2] Blümcke I, Thom M, Aronica E, Armstrong DD, Bartolomei F, Bernasconi A, et al. International consensus classification of hippocampal sclerosis in temporal lobe epilepsy: a Task Force report from the ILAE Commission on Diagnostic Methods. Epilepsia 2013;54:1315-29. http://dx.doi.org/10.1111/epi.12220.

[3] Kahane P, Bartolomei F. Temporal lobe epilepsy and hippocampal sclerosis: lessons from depth EEG recordings. Epilepsia 2010;51:59-62. http://dx.doi.org/10.1111/j.1528-1167.2009.02448.x.

[4] Lamberink HJ, Otte WM, Blümcke I, Braun KPJ, Aichholzer M, Amorim I, et al. Seizure outcome and use of antiepileptic drugs after epilepsy surgery according to histopathological diagnosis: a retrospective multicentre cohort study. Lancet

Neurol 2020;19:748-57. http://dx.doi.org/10.1016/S1474-4422(20)30220-9.

[5] Bartolomei F. Different anatomo-functional forms of temporal lobe seizures. Prat Neurol FMC 2012;3:143-8. http://dx.doi.org/10.1016/j.praneu.2012.01.015.

[6] Bartolomei F, Comments on: Usui N, Mihara T, Baba K, Matsuda K, Tottori T, et al. Intracranial EEG findings in patients with lesional lateral temporal lobe epilepsy. Epilepsy Res 2008;78:82-91. http://dx.doi.org/10.1016/j.eplepsyres.2008.08.009. Epilepsy Res 2009;83:94-5.

[7] Paredes-Aragon E, AlKhaldi NA, Ballesteros-Herrera D, Mirsattari SM. Stereo-encephalographic presurgical evaluation of temporal lobe epilepsy: an evolving science. Front Neurol 2022;27:1-18. http://dx.doi.org/10.3389/fneur.2022.867458.

[8] Bartolomei F. The epileptogenic network concept: applications in the SEEG exploration of lesional focal epilepsies. Neurophysiol Clin 2024;54:103023. http://dx.doi.org/10.1016/j.neucli.2024.103023.

[9] Bancaud J, Talairach J, Bonis A, Schaub C, Szikla G, Morel P, et al. La Stéréoencéphalographie dans l'épilepsie. Paris: Masson; 1965.

[10] Bartolomei F, Wendling F, Bellanger J-J, Régis J, Chauvel P. Neural networks involving the medial temporal structures in temporal lobe epilepsy. Clin Neurophysiol 2001;112:1746-60. http://dx.doi.org/10.1016/S1388-2457(01)00591-0.

[11] Chabardès S, Kahane P, Minotti L, Tassi L, Grand S, Hoffmann D, et al. The temporopolar cortex plays a pivotal role in temporal lobe seizures. Brain 2005;128:1818-31. http://dx.doi.org/10.1093/brain/awh512.

[12] Hadidane S, Lagarde S, Medina-Villalon S, McGonigal A, Laguitton V, Carron R, et al. Basal temporal lobe epilepsy: SEEG electroclinical characteristics. Epilepsy Res 2023;191. http://dx.doi.org/10.1016/j.eplepsyres.2023.107090.

[13] Barba C, Barbati G, Minotti L, Hoffmann D, Kahane P. Ictal clinical and scalp-EEG findings differentiating temporal lobe epilepsies from temporal “plus” epilepsies. Brain 2007;130:1957-67. http://dx.doi.org/10.1093/brain/awm108.

[14] Bartolomei F, Wendling F, Vignal J-P, Kochen S, Bellanger J-J, Badier J-M, et al. Seizures of temporal lobe epilepsy: identification of subtypes by coherence analysis using stereo-electro-encephalography. Clin Neurophysiol 1999;110:1741-54. http://dx.doi.org/10.1016/S1388-2457(99)00107-8.

[15] Wendling F, Chauvel P, Biraben A, Bartolomei F. From intracerebral EEG signals to brain connectivity: identification of epileptogenic networks in partial epilepsy. Front Syst Neurosci 2010;4. http://dx.doi.org/10.3389/fnsys.2010.00154.

[16] Bartolomei F, Cosandier-Rimele D, McGonigal A, Aubert S, Régis J, Gavaret M, et al. From mesial temporal lobe to temporoperisylvian seizures: a quantified study of temporal lobe seizure networks. Epilepsia 2010;51:2147-58. http://dx.doi.org/10.1111/j.1528-1167.2010.02690.x.

[17] Jobst BC, Bartolomei F, Diehl B, Frauscher B, Kahane P, Minotti L, et al. Intracranial EEG in the 21st Century. Epilepsy Curr 2020;20:180-8. http://dx.doi.org/10.1177/1535759720934852.

[18] Wendling F, Bartolomei F, Bellanger JJ, Chauvel P. Interpretation of interdependencies in epileptic signals using a macroscopic physiological model of the EEG. Clin Neurophysiol 2001;112:1201-18. http://dx.doi.org/10.1016/S1388-2457(01)00547-8.

[19] Spencer SS. Neural networks in human epilepsy: evidence of and implications for treatment. Epilepsia 2002;43:219-27. http://dx.doi.org/10.1046/j.1528-1157.2002.26901.x.

[20] Bartolomei F, Lagarde S, Wendling F, McGonigal A, Jirsa V, Guye M, et al. Defining epileptogenic networks:
contribution of SEEG and signal analysis. Epilepsia
2017;58:1131-47. http://dx.doi.org/10.1111/epi.13791.

[21] Lagarde S, Bénar C-G, Wendling F, Bartolomei F. Interictal functional connectivity in focal refractory epilepsies investigated by intracranial EEG. Brain Connect 2022;12:850-69. http://dx.doi.org/10.1089/brain.2021.0190.

[22] Wendling F, Bartolomei F, Senhadji L. Spatial analysis of intracerebral electroencephalographic signals in the time and frequency domain: identification of epileptogenic networks in partial epilepsy. Philos A Math Phys Eng Sci 2009;367:297-316. http://dx.doi.org/10.1098/rsta.2008.0220.

[23] Bartolomei F, Wendling F, Chauvel P. The concept of an epileptogenic network in human partial epilepsies. Neurochirurgie 2008;54:174-84. http://dx.doi.org/10.1016/j.neuchi.2008.02.013.

[24] Stefan H, Lopes da Silva FH. Epileptic neuronal networks: methods of identification and clinical relevance. Front Neurol 2013;4:8. http://dx.doi.org/10.3389/fneur.2013.00008.

[25] Bartolomei F, Wendling F, Régis J, Gavaret M, Guye M, Chauvel P. Pre-ictal synchronicity in limbic networks of mesial temporal lobe epilepsy. Epilepsy Res 2004;61:89-104. http://dx.doi.org/10.1016/j.epilepsres.2004.06.006.

[26] Courtens S, Colombet B, Trébuchon A, Brovelli A, Bartolomei F, Bénar CG. Graph measures of node strength for characterizing preictal synchrony in partial epilepsy. Brain Connect 2016;6:530-9. http://dx.doi.org/10.1089/brain.2015.0397.

[27] Guye M, Régis J, Tamura M, Wendling F, McGonigal A, Chauvel P, et al. The role of corticothalamic coupling in human temporal lobe epilepsy. Brain 2006;129:1917-28. http://dx.doi.org/10.1093/brain/awl151.

[28] Ponten SC, Bartolomei F, Stam CJ. Small-world networks and epilepsy: graph theoretical analysis of intracerebrally recorded mesial temporal lobe seizures. Clin Neurophysiol 2007;118:918-27. http://dx.doi.org/10.1016/j.clinph.2006.12.002.

[29] Gnatkovsky V, Schindler K. Computational EEG Analysis of Human Epileptogenic Networks. In: Avoli M, de Curtis M, Bernard C, Soltesz I, editors. Jasper's Basic Mechanisms of the Epilepsies. New York: Oxford University Press; 2024p. 387-8. http://dx.doi.org/10.1093/med/9780197549469.003.0019.

[30] Bartolomei F, Chauvel P, Wendling F. Epileptogenicity of brain structures in human temporal lobe epilepsy: a quantified study from intracerebral EEG. Brain 2008;131:1818-30. http://dx.doi.org/10.1093/brain/awn111.

[31] Makhalova J, Madec T, Medina Villalon S, Jegou A, Lagarde S, Carron R, et al. The role of quantitative markers in surgical prognostication after stereoelectroencephalography. Ann Clin Transl Neurol 2023. http://dx.doi.org/10.1002/acn3.51900.

[32] Wendling F, Koksal-Ersoz E, Al-Harrach M, Yochum M, Merlet I, Ruffini G, et al. Multiscale neuro-inspired models for interpretation of EEG signals in patients with epilepsy. Clin Neurophysiol 2024;161:198-210. http://dx.doi.org/10.1016/j.clinph.2024.03.006.

[33] Bartolomei F, Nica A, Valenti-Hirsch MP, Adam C, Denuelle M. Interpretation of SEEG recordings. Neurophysiol Clin 2018;48:53-7. http://dx.doi.org/10.1016/j.neucli.2017.11.010.

[34] Lagarde S, Buzori S, Trebuchon A, Carron R, Scavarda D, Milh M, et al. The repertoire of seizure onset patterns in human focal epilepsies: determinants and prognostic values. Epilepsia 2019;60:85-95. http://dx.doi.org/10.1111/epi.14604.

[35] Perucca P, Dubeau F, Gotman J. Intracranial electroencephalographic seizure-onset patterns: effect of underlying pathology. Brain 2014;137:183-96. http://dx.doi.org/10.1093/brain/awt299.

[36] Mercadal B, Lopez-Sola E, Galan-Gadea A, Al Harrach M, Sanchez-Todo R, Salvador R, et al. Towards a mesoscale

physical modeling framework for stereotactic-EEG recordings. J Neural Eng 2023;20:016005. http://dx.doi.org/10.1088/1741-2552/acae0c.

[37] Pizzo F, Roehri N, Giusiano B, Lagarde S, Carron R, Scavarda D, et al. The ictal signature of thalamus and basal ganglia in focal epilepsy: a SEEG study. Neurology 2021;96:e280-93. http://dx.doi.org/10.1212/WNL.0000000000011003.

[38] Soulier H, Pizzo F, Jegou A, Lagarde S, Garnier E, Makhalova J, et al. The anterior and pulvinar thalamic nuclei interactions in mesial temporal lobe seizure networks. Clin Neurophysiol 2023;150:176-83. http://dx.doi.org/10.1016/j.clinph.2023.03.016.

[39] Evangelista E, Bénar C, Bonini F, Carron R, Colombet B, Régis J, et al. Does the thalamo-cortical synchrony play a role in seizure termination? Front Neurol 2015;6. http://dx.doi.org/10.3389/fneur.2015.00192.

[40] Wendling F, Benquet P, Bartolomei F, Jirsa V. Computational models of epileptiform activity. J Neurosci Methods 2016;260:233-51. http://dx.doi.org/10.1016/j.jneumeth.2015.03.027.

[41] Proix T, Bartolomei F, Guye M, Jirsa VK. Individual brain structure and modelling predict seizure propagation. Brain 2017;140:641-54. http://dx.doi.org/10.1093/brain/awx004.

[42] Jirsa VK, Proix T, Perdikis D, Woodman MM, Wang H, Bernard C, et al. The virtual epileptic patient: individualized whole-brain models of epilepsy spread. Neuroimage 2017;145:377-88. http://dx.doi.org/10.1016/j.neuroimage.2016.04.049.

[43] Commission ILAE 1989. Proposal for revised classification of epilepsies and epileptic syndromes. Epilepsia 1989;30:389-99. http://dx.doi.org/10.1111/j.1528-1157.1989.tb05316.x.

[44] Gil-Nagel A, Risinger M. Ictal semiology in hippocampal versus extrahippocampal temporal lobe epilepsy. Brain 1997;120:183-92. http://dx.doi.org/10.1093/brain/120.1.183.

[45] Munari C, Talairach J, Bonis A, Szikla G, Bancaud J. Differential diagnosis between temporal and "Perisylvian" Epilepsy in a Surgical Perspective; 1980;97-101. http://dx.doi.org/10.1007/978-3-7091-8592-6_11.

[46] Isnard J, Guénot M, Ostrowsky K, Sindou M, Mauguière F. The role of the insular cortex in temporal lobe epilepsy. Ann Neurol 2000;48:614-23.

[47] Ryvlin P, Kahane P. The hidden causes of surgery-resistant temporal lobe epilepsy: extratemporal or temporal plus? Editorial review. Curr Opin Neurol 2005;18:125-7. http://dx.doi.org/10.1097/01.wco.0000162852.22026.6f.

[48] Sperling MR, Wu C, Kang J, Makhalova J, Bartolomei F, Southwell D. The temporal lobe club: newer approaches to treat temporal lobe epilepsy. Epilepsy Curr 2024;24:10-5. http://dx.doi.org/10.1177/15357597231213161.

[49] de la Vaissière S, Milh M, Scavarda D, Carron R, Lépine A, Trébuchon A, et al. Cortical involvement in focal epilepsies with epileptic spasms. Epilepsy Res 2014;108:1572-80. http://dx.doi.org/10.1016/j.epilepsres.2014.08.008.

[50] King D, Spencer SS, McCarthy G, Spencer DD. Surface and depth EEG findings in patients with hippocampal atrophy. Neurology 1997;48:1363-7. http://dx.doi.org/10.1212/WNL.48.5.1363.

[51] Gloor P. The temporal lobe and limbic system. New York-Oxford: Oxford University Press; 1997.

[52] Bonilha L, Yasuda CL, Rorden C, Li LM, Tedeschi H, De Oliveira E, et al. Does resection of the medial temporal lobe improve the outcome of temporal lobe epilepsy surgery? Epilepsia 2007;48:571-8. http://dx.doi.org/10.1111/j.1528-1167.2006.00958.x.

[53] Wieser HG, Siegel AM, Ya'argil GM. The Zürich amygdalo-hippocampectomy series: a short up-date. Neurosurgical aspects of epilepsy. Vienna: Springer Vienna; 1990: 122-7. http://dx.doi.org/10.1007/978-3-7091-9104-0_24.
[54] Wu C, Jermakowicz WJ, Chakravorti S, Cajigas I, Sharan AD, Jagid JR, et al. Effects of surgical targeting in laser interstitial thermal therapy for mesial temporal lobe epilepsy: a multicenter study of 234 patients. Epilepsia 2019;60:1171-83. http://dx.doi.org/10.1111/epi.15565.

[55] Catenoix H, Decaestecker K, Hermier M, Chochoi M, Guinet V, Montavont A, et al. The role of SEEG in the presurgical decision-making process in MRI-normal mesial temporal lobe epilepsy. Rev Neurol (Paris) 2024;180:1128-38. http://dx.doi.org/10.1010/j.neurol.2024.06.006.

[56] Le Van Quyen M, Adam C, Baulac M, Martinerie J, Varela FJ. Nonlinear interdependencies of EEG signals in human intracranially recorded temporal lobe seizures. Brain Res 1998;792:24-40. http://dx.doi.org/10.1016/S0006-8993(98)00102-4.

[57] van Mierlo P, Carrette E, Hallez H, Raedt R, Meurs A, Vandenberghe S, et al. Ictal-onset localization through connectivity analysis of intracranial EEG signals in patients with refractory epilepsy. Epilepsia 2013;54:1409-18. http://dx.doi.org/10.1111/epi.12206.

[58] Bartolomei F, Wendling F, Régis J, Gavaret M, Guye M, Chauvel P. Pre-ictal synchronicity in limbic networks of mesial temporal lobe epilepsy. Epilepsy Res 2004;61:89-104. http://dx.doi.org/10.1016/j.epilepsyres.2004.06.006.

[59] Bartolomei F, Khalil M, Wendling F, Sontheimer A, Régis J, Ranjeva J-P, et al. Entorhinal cortex involvement in human mesial temporal lobe epilepsy: an electrophysiologic and volumetric study. Epilepsia 2005;46(5):677-87.

[60] Maillard L, Vignal J-P, Gavaret M, Guye M, Biraben A, McGonigal A, et al. Semiologic and electrophysiologic correlations in temporal lobe seizure subtypes. Epilepsia 2004;45(12):1590-9.

[61] Usui N, Mihara T, Baba K, Matsuda K, Tottori T, Umeoka S, et al. Intracranial EEG findings in patients with lesional lateral temporal lobe epilepsy. Epilepsy Res 2008;78:82-91. http://dx.doi.org/10.1016/j.epilepsyres.2007.10.009.

[62] Balatskaya A, Roehri N, Lagarde S, Pizzo F, Medina S, Wendling F, et al. The “Connectivity Epileptogenicity Index” (cEI), a method for mapping the different seizure onset patterns in StereoElectroEncephalography recorded seizures. Clin Neurophysiol 2020;131:1947-55. http://dx.doi.org/10.1016/j.clinph.2020.05.029.

[63] Bottan JS, Suller Marti A, Parrent AG, MacDougall KW, McLachlan RS, Burneo JG, et al. Seizure freedom in temporal plus epilepsy surgery following stereo-electroencephalography. Can J Neurol Sci 2020;47:374-81. http://dx.doi.org/10.1017/cjn.2020.26.

[64] Blauwblomme T, David O, Minotti L, Job A, Chassagnon S, Hoffman D, et al. Prognostic value of insular lobe involvement in temporal lobe epilepsy: a stereoelectroencephalographic study. Epilepsia 2013;54:1658-67. http://dx.doi.org/10.1111/epi.12260.

[65] Bartolomei F, Cosandier-Rimele D, McGonigal A, Aubert S, Régis J, Gavaret M, et al. From mesial temporal lobe to temporoperisylvian seizures: a quantified study of temporal lobe seizure networks. Epilepsia 2010;51:2147-58. http://dx.doi.org/10.1111/j.1528-1167.2010.02690.x.

[66] Barba C, Rheims S, Minotti L, Guénot M, Hoffmann D, Chabardès S, et al. Temporal plus epilepsy is a major determinant of temporal lobe surgery failures. Brain 2016;139:444-51. http://dx.doi.org/10.1093/brain/awv372.

[67] Zhang X, Zhang G, Yu T, Xu C, Zhu J, Yan X, et al. Temporal-insular spreading time in temporal lobe epilepsy as a

predictor of seizure outcome after temporal lobectomy. Medicine 2022;101:e30114. http://dx.doi.org/10.1097/MD.00000000000030114.

[68] Makhalova J, Le Troter A, Aubert-Conil S, Giusiano B, McGonigal A, Trebuchon A, et al. Epileptogenic networks in drug-resistant epilepsy with amygdala enlargement: assessment with stereo-EEG and 7 T MRI. Clin Neurophysiol 2022;133:94-103. http://dx.doi.org/10.1016/j.clinph.2021.10.012.

[69] Vaugier L, Aubert S, McGonigal A, Trébuchon A, Guye M, Gavaret M, et al. Neural networks underlying hyperkinetic seizures of “temporal lobe” origin. Epilepsy Res 2009;86:200-8. http://dx.doi.org/10.1016/j.epilepsyres.2009.06.007.

[70] Mesulam M, Mufson EJ. Insula of the old world monkey. Architectonics in the insulo-orbito-temporal component of the paralimbic brain. J Comp Neurol 1982;212:1-22. http://dx.doi.org/10.1002/cne.902120102.

[71] Wu TQ, Kaboodvand N, McGinn RJ, Veit M, Davey Z, Datta A, et al. Multisite thalamic recordings to characterize seizure propagation in the human brain. Brain 2023;146:2792-802. http://dx.doi.org/10.1093/brain/awad121.

[72] Arthuis M, Valton L, Rgis J, Chauvel P, Wendling F, Naccache L, et al. Impaired consciousness during temporal lobe seizures is related to increased long-distance corticalsubcortical synchronization. Brain 2009;132:2091-101. http://dx.doi.org/10.1093/brain/awp086.

[73] Filipescu C, Lagarde S, Lambert I, Pizzo F, Trébuchon A, McGonigal A, et al. The effect of medial pulvinar stimulation on temporal lobe seizures. Epilepsia 2019;60:e25-30. http://dx.doi.org/10.1111/epi.14677.

[74] Salanova V, Sperling MR, Gross RE, Irwin CP, Vollhaber JA, Giftakis JE, et al. The SANTÉ study at 10 years of follow-up: effectiveness, safety, and sudden unexpected death in epilepsy. Epilepsia 2021;62:1306-17. http://dx.doi.org/10.1111/epi.16895.

[75] Rosenberg DS, Mauguière F, Catenoix H, Faillenot I, Magnin M. Reciprocal thalamocortical connectivity of the medial pulvinar: a depth stimulation and evoked potential study in human brain. Cereb Cortex 2009;19:1462-73. http://dx.doi.org/10.1093/cercor/bhn185.

[76] Pizzo F, Carron R, Laguitton V, Clement A, Giusiano B, Bartolomei F. Medial pulvinar stimulation for focal drug-resistant epilepsy: interim 12-month results of the PULSE study. Front Neurol 2024;15. http://dx.doi.org/10.3389/fneur.2024.1480819.

[77] Chandran AS, Joshi S, Suresh S, Savarraj J, Snyder K, Vasconcellos FDN, et al. Efficacy of neuromodulation of the pulvinar nucleus for drug-resistant epilepsy. Epilepsia 2025. http://dx.doi.org/10.1111/epi.18244.

[78] Bratu IF, Medina Villalon S, Garnier E, Bénar CG, Bartolomei F. How fast does the brain recover after an epileptic seizure? Ann Clin Transl Neurol 2024;11:1630-5. http://dx.doi.org/10.1002/acn3.52073.

[79] Alomar SA, Moshref RH, Moshref LH, Sabbagh AJ. Outcomes after laser interstitial thermal ablation for temporal lobe epilepsy: a systematic review and meta-analysis. Neurosurg Rev 2023;46:261. http://dx.doi.org/10.1007/s10143-023-02164-4.

[80] Fisher RS. Deep brain stimulation of thalamus for epilepsy. Neurobiol Dis 2023;179:106045. http://dx.doi.org/10.1016/j.nbd.2023.106045.