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Several studies have shown that the retroinsular and posterior parietal operculum regions play a central role in vestibular processing. Electrical stimulations performed during stereoelectroencephalography (SEEG) in patients with focal drug-resistant epilepsy could contribute to the analysis of this area. Among the 264 SEEGs performed in both an adult and a paediatric epilepsy surgery centre, we retrospectively identified 24 patients (9%) reporting vertigo during electrical stimulations (ES). In seven of them (29% of patients experiencing vertigo during ES), it was evoked by stimulating the retroinsular region. The reported responses were mostly not rotatory sensations but actually illusions of body, limb or limb segment movement. The involved area is limited. Moreover, two patients reported having the same symptoms at the beginning of their seizures starting in the same region. Our case study confirms the pivotal role of the retroinsular and posterior parietal operculum areas in vestibular responses, and we therefore advise the exploration of this region when patients report an illusion of body movement at the beginning of their seizures., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Objective: Electrical stimulations performed in awake patients identified dura mater, venous sinuses, and arteries as pain-sensitive intracranial structures. However, cephalic pain has been only occasionally reported in patients with epilepsy undergoing stereo-electroencephalography (SEEG) stimulations., Methods: The aim of our study was to investigate whether headache can be triggered by SEEG stimulations and might be related to specific cortical areas. Data were gathered from 16 050 stimulations collected in 266 patients who underwent a SEEG as part of a presurgical assessment of their drug-resistant epilepsy., Results: Two-hundred and eight stimulations (1.3%) evoked headaches. Pain was more frequently described as bilateral (42.31%) than ipsilateral (16.83%) or contralateral (14.42%) to the stimulated hemisphere. Headache was more frequently elicited during stimulation of the insulo-limbic regions such as the anterior and medial cingulate gyrus, the mesial part of temporal lobe, and the insula., Conclusion: This study shows that cortical stimulation can evoke headache, mostly during stimulation of the temporo-frontal limbic regions. It suggests that brief epileptic headache can be an epileptic symptom caused by a cortical discharge involving somatic or visceral network and does not reflect only trigemino-vascular activation. Although not specific, the occurrence of a brief epileptic headache may point to a seizure origin in the temporo-frontal limbic regions., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objective: Few data are available about the functionality of type II focal cortical dysplasia (FCD). Identification of high-frequency activities (HFAs) induced by cognitive tasks has been proposed as an additional way to map cognitive functions in patients undergoing presurgical evaluation using stereoelectroencephalography (SEEG). However, the repetitive subcontinuous spiking pattern which characterizes type II FCD might limit the reliability of this approach, and its feasibility in these patients remains to be evaluated., Methods: Seven patients whose magnetic resonance imaging (MRI) data, SEEG data, and/or pathological data were consistent with the diagnosis of type II FCD were included. All patients performed standardized cognitive tasks specifically designed to map task-induced increase of HFA (50 Hz to 150 Hz) at the recorded sites. Electrode contacts which showed an interictal SEEG pattern typical of type II FCD were considered to be localized within the FCD. A site was considered responsive if it was significantly different from baseline in at least one cognitive task., Results: Three of the seven patients (43%) had significant task-induced increase of HFA in the FCD for a total of 15 sites with an interictal SEEG pattern typical of type II FCD. These sites were always localized at the external border of the FCD whereas no HFA response was in the core of FCD. In three of the four other patients, a significant task-induced increase of HFA was observed in a cortical site immediately adjacent to the dysplastic cortex., Significance: Detection of task-induced HFA remains feasible despite the repetitive subcontinuous spiking pattern which characterizes type II FCD. Depending on the localization of the FCD, some sites of the dysplastic cortex were included in large-scale functional networks. However, these sites were always those closest to the nondysplastic cortex suggesting that persistence of cortical functions might be restricted to a limited part of the FCD., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Four patients with refractory epilepsy and hypermotor seizures (HMS) benefited from an intracerebral investigation after a presurgical evaluation and demonstrated an ictal onset zone primarily involving the posterior cortex, specifically the posterior cingulate gyrus in two patients. At seizure onset, these two patients reported a falling sensation, followed by HMSs characterized by swinging movements of the trunk with intense grasping of the bed railing. The two other patients with lateral parietal seizure onset reported blurred vision and dizziness, followed by a mixed pattern of the previously described type 1 and 2 HMSs. Three patients have been operated on, including two class I of Engel after 36 and 52months of follow-up. One patient developed a postoperative infection and continues to suffer seizures. Pathological findings disclosed a type IIa focal cortical dysplasia in all the patients. The last patient is awaiting surgery. Posterior cortex epilepsies, including those originating from the posterior cingulate cortex, can be responsible for HMSs., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Interictal spikes are a hallmark of cortical epileptogenicity; their spatial distribution in the cortex defines the so-called 'irritative' zone or spiking volume (SV). Delineating the SV precisely is a challenge during the presurgical evaluation of patients with epilepsy. Magnetoencephalography (MEG) recordings enable determination of the brain sources of epileptic spikes using source localization procedures. Most previous clinical MEG studies have relied on dipole modeling of epileptic spikes, which does not permit a volumetric estimation of the spiking cortex. In the present study, we propose a new source modeling procedure, Volumetric Imaging of Epileptic Spikes (VIES). In VIES, the SV is identified as the 3D region where sources of the high frequency activities (>20 Hz) associated with epileptic spikes are distributed. We localized these sources using a beamforming approach (DICS, Dynamic Imaging of Coherent Neural Sources). To determine the optimal parameters and accuracy of the method, we compared the SV obtained by VIES with the SV defined by the invasive gold standard, intracranial stereotactic EEG recordings (SEEG), in 21 patients with focal epilepsy. Using rigorous validation criteria based on the exact anatomical location of SEEG contacts, we found that the overall sensitivity of VIES for detecting spiking SEEG contacts was 76% and its specificity for correctly identifying non-spiking SEEG contacts was 67%, indicating a good agreement between VIES and SEEG. Moreover, we found that classical dipole clustering was not informative in 9/21 patients, while VIES enable to delineate the SV in all patients. For the 12 patients having a SV delineated both with VIES and dipole clustering, VIES method had higher sensitivity and lower specificity. This proof-of-concept study shows that VIES is a promising approach to non-invasive estimation of the SV in focal epilepsy., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Ictal vomiting is a rare manifestation most often associated with right temporal lobe epilepsy. The implication of the anterior insula in the occurrence of this symptom has been suggested based on the role of this region in swallowing and on the observation that electrical insular stimulation can elicit nausea and vomiting. We report the first case, to our knowledge, of a patient presenting with ictal vomiting who underwent bilateral intracranial exploration including insular depth electrodes. The seizure onset zone was localized in the left temporomesial structures, but the occurrence of ictal vomiting correlated in time with a discharge affecting exclusively the anterior part of both insular lobes. It is concluded that the occurrence of ictal vomiting reflects a propagation of the discharge to the insular cortex. Observation of this symptom at the very onset of the seizures in a patient with temporal lobe epilepsy is highly suggestive of an insular seizure onset zone.

Experimental data in animals show that 5-HT(1A) receptors are predominantly located in limbic areas and suggest that serotonin, via these receptors, mediates an antiepileptic and anticonvulsant effect. In this PET study, we used an antagonist of the 5-HT(1A) receptor, [(18)F]MPPF, to assess the extent of 5-HT(1A) receptor binding changes in a group of seven temporal lobe epilepsy (TLE) patients with hippocampal ictal onset demonstrated by intracerebral EEG recording. On the basis of MRI-measured hippocampal volumes (HV), patients were classified into "normal HV" or "hippocampal atrophy" (HA). Voxel-based analyses (SPM99) were performed to objectively assess the differences in [(18)F]MPPF binding potential (BP) between patients (taken as a group or as individuals) and a database of 48 controls subjects. In the full group of patients, a significant decreased BP was detected ipsilateral to the epileptogenic zone in the hippocampus, temporal pole, insula, and temporal neocortex. This result was confirmed in the subgroup of patients with HA. In patients with normal HV, the BP decrease was restricted to the temporal pole. TLE patients also demonstrated an increased BP in various regions contralateral to the epileptogenic zone. These data suggest that in TLE patients with hippocampal seizure onset, the decrease in 5-HT(1A) receptor binding partly reflects hippocampal neuronal loss, but is also observed in various regions involved in temporo-limbic epileptogenic networks that appeared normal on MRI. Further studies are warranted to evaluate the clinical usefulness of [(18)F]MPPF-PET as compared to other established PET tracers in drug resistant TLE.