Comparaison du métabolisme cérébrale de la TEP cérébrale au 18F-FDG aux zones d’épileptogénicité de la SEEG chez les patients opérés pour épilepsie pharmacorésistante

Introduction Le bilan pré-chirurgical des patients épileptiques souffrant d’une forme réfractaire au traitement médical a pour objectif de délimiter la zone épileptogène (zone minimale à réséquer pour obtenir une disparition complète des crises). Il comprend une IRM cérébrale, une électroencéphalographie (EEG) voire une stéréo-EEG (SEEG), une TEP-TDM cérébrale au 18F-FDG et un bilan neuropsychologique. La SEEG est un examen invasif comprenant certains risques (chirurgicaux, infectieux, hémorragiques…). Des études ont trouvé des concordances entre l’hypométabolisme cérébral de la TEP au 18F-FDG à l’échelle d’une aire cérébrale et les résultats de la SEEG. Nous avons comparé le métabolisme de la TEP cérébrale au 18F-FDG en regard de chaque plot d’électrode de la SEEG situé dans la substance grise aux zones d’épileptogénicité décrites à la SEEG chez 15 patients opérés pour épilepsie réfractaire au traitement médical, afin d’évaluer si les variations fines du métabolisme étaient liées à ces zones. Matériels Parmi tous les patients opérés à Strasbourg pour épilepsie réfractaire au traitement médical entre février 2014 et décembre 2016, nous avons inclus les 15 patients qui avaient réalisé une TEP cérébrale au 18F-FDG, une IRM cérébrale et pour lesquels nous avons obtenu une relecture complète de la SEEG. Le suivi postopératoire était d’au moins un an. Le schéma des électrodes de SEEG a été fusionné avec l’IRM cérébrale et la TEP cérébrale au 18F-FDG. Pour chaque groupement de plots d’électrodes (GPE) situé dans la substance grise, le métabolisme de la TEP a été noté sur une échelle de 1 à 4 (hypométabolisme intense, hypométabolisme modéré, métabolisme normal, hypermétabolisme) et l’épileptogénicité a été analysée sur la SEEG et classée en 4 catégories (zone d’initiation, zone irritative, zone de propagation, zone saine). Un test de régression logistique a comparé le métabolisme de la TEP et les zones SEEG. Résultats/Conclusion La comparaison du métabolisme des 486 GPE aux zones d’épileptogénicité a permis de mettre en évidence une association entre la présence d’un métabolisme pathologique et la localisation des GPE dans les zones d’initiation et irritative et entre un métabolisme normal et la localisation des GPE dans la zone saine, avec des anomalies métaboliques progressivement plus présentes et plus intenses à proximité de la zone d’initiation. Les GPE hypermétaboliques ne semblaient pas être liées à une zone particulière décrite à la SEEG

Atonic seizures in children with surgically remediable epilepsy: a motor system seizure phenotype?

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Atonic seizures in children with surgically remediable epilepsy: a motor system seizure phenotype?

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High Frequency Oscillations and spikes running down after SEEG-guided thermocoagulations in the epileptogenic network of periventricular nodular heterotopia

International audienceObjective: Epilepsy associated with Periventricular Nodular Heterotopia (PNH) is characterized by complex relationships between the heterotopic and the normotopic cortex during the interictal state and at seizure onset. High frequency oscillations (HFO) have been proposed as a marker of epileptogenicity that might reflect disease activity. The effects of thermocoagulations on epileptogenicity in this context remain unknown. We aimed to investigate the interictal HFO-and spike profiles of different cortical structures before and after two consecutive SEEG-guided thermocoagulations, in correlation with seizure outcome, in a patient with PNH-related drugresistant epilepsy. Methods: The epileptogenic zone (EZ) was defined by SEEG analysis based on the Epileptogenicity Index. Interictal spikes, ripples (80-250Hz) and fast ripples (FR, 250-330Hz) were analyzed within the heterotopia, the temporal neocortex and the hippocampus. Results: The SEEG recordings revealed a distributed EZ involving the heterotopia and the posterior temporal neocortex. Both structures were targeted by thermocoagulations. Background spikes, ripples and FR-rates were significantly higher in PNH compared to the normotopic cortex. A drastic reduction of spikes (by over 80%) and absence of FR were demonstrated both in the PNH and in the neocortex during the second SEEG exploration 6 months after the first thermocoagulation, whereas no significant difference was observed in the posterior hippocampus. Ripples were significantly reduced by the first and suppressed by the second thermocoagulation within the three structures. Seizures relapsed after two months but decreased in frequency after the first thermocoagulation. Sustained seizure-freedom was achieved only after the second procedure. Conclusions: Our data demonstrate the running down of interictal HFO and spikes within the epileptogenic network following thermocoagulations of heterotopic and normotopic sites involved at seizure onset. This dynamics was in good correlation with significantly improved seizure control. Significance: Combination of ictal and different interictal markers of epileptogenicity, including HFO and spike analysis, is important to get the full picture of the epileptogenic zone and could help to evaluate the disease activity

Towards a definition of the "practical" epileptogenic zone: a case of epilepsy with dual pathology.

International audiencePresurgical evaluation for patients with drug-resistant epilepsy requires the definition of various zones that have a variable spatial relationship with the epileptogenic zone. All the available methods to directly measure the actual seizure-onset zone and to define "the minimum amount of cortical tissue that must be resected to produce seizure-freedom" have significant limitations.We report on the case of a patient with dual pathology (hippocampal sclerosis and a post-traumatic scar) and discuss the contribution of the various presurgical investigations that led to surgery and seizure-freedom

Illusory own body perceptions mapped in the cingulate cortex—An intracranial stimulation study

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Remarkable effect of transdermal nicotine in children with CHRNA4- related autosomal dominant sleep-related hypermotor epilepsy

Objective Autosomal dominant sleep-related hypermotor epilepsy (ADSHE) is characterized by hypermotor seizures and may be caused by gain-of-function mutations affecting the nicotinic acetylcholine receptor (nAChR). Benefit from nicotine consumption has been reported in adult patients with this disorder. For the first time, the effect of transdermal nicotine is evaluated in children. Methods Transdermal nicotine was applied to three boys, two aged 10 years (7 mg/24 h) and one six years (3.5 mg/24 h). Autosomal dominant sleep-related hypermotor epilepsy was caused by the p.S280F-CHRNA4 (cholinergic receptor, nicotinic, alpha polypeptide 4) mutation. The children suffered from frequent, persistent nocturnal seizures and had developed educational and psychosocial problems. Seizure frequency and cognitive and behavioral parameters were assessed before and after treatment. Results A striking seizure reduction was reported soon after treatment onset. Hypermotor seizures disappeared; only sporadic arousals, sometimes with minor motor elements, were observed. Psychometric testing documented improvement in cognitive domains such as visuospatial ability, processing speed, memory, and some areas of executive functions. Significance Nicotine appears to be a mechanistic treatment for this specific disorder, probably because of desensitization of the mutated receptors. It may control seizures resistant to conventional drugs for epilepsy and impact socioeducational function in children. This mode of precision therapy should receive more attention and should be available to more patients with uncontrolled CHRNA4-related ADSHE across the age span

Can histologically normal epileptogenic zone share common electrophysiological phenotypes with focal cortical dysplasia? SEEG-based study in MRI-negative epileptic patients

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