Pizzo Francesca, Roehri Nicolas, Catenoix Hélène, Medina Samuel, McGonigal Aileen, Giusiano Bernard, Carron Romain, Scavarda Didier, Ostrowsky Karine, Lepine Anne, Boulogne Sébastien, Scholly Julia, Hirsch Edouard, Rheims Sylvain, Bénar Christian-George, Bartolomei Fabrice
Inserm, Institut de Neurosciences des Systèmes (INS), Aix Marseille Univ, Marseille, France.
Department of Functional Neurology and Epileptology, Hospices Civils de Lyon (Lyon University Hospital), Hospital for Neurology and Neurosurgery Pierre Wertheimer, Lyon, France.
Epilepsia. 2017 Dec;58(12):2112-2123. doi: 10.1111/epi.13919. Epub 2017 Oct 6.
Defining the roles of heterotopic and normotopic cortex in the epileptogenic networks in patients with nodular heterotopia is challenging. To elucidate this issue, we compared heterotopic and normotopic cortex using quantitative signal analysis on stereoelectroencephalography (SEEG) recordings.
Clinically relevant biomarkers of epileptogenicity during ictal (epileptogenicity index; EI) and interictal recordings (high-frequency oscillation and spike) were evaluated in 19 patients undergoing SEEG. These biomarkers were then compared between heterotopic cortex and neocortical regions. Seizures were classified as normotopic, heterotopic, or normoheterotopic according to respective values of quantitative analysis (EI ≥0.3).
A total of 1,246 contacts were analyzed: 259 in heterotopic tissue (heterotopic cortex), 873 in neocortex in the same lobe of the lesion (local neocortex), and 114 in neocortex distant from the lesion (distant neocortex). No significant difference in EI values, high-frequency oscillations, and spike rate was found comparing local neocortex and heterotopic cortex at a patient level, but local neocortex appears more epileptogenic (p < 0.001) than heterotopic cortex analyzing EI values at a seizure level. According to EI values, seizures were mostly normotopic (48.5%) or normoheterotopic (45.5%); only 6% were purely heterotopic. A good long-term treatment response was obtained in only two patients after thermocoagulation and surgical disconnection.
This is the first quantitative SEEG study providing insight into the mechanisms generating seizures in nodular heterotopia. We demonstrate that both the heterotopic lesion and particularly the normotopic cortex are involved in the epileptogenic network. This could open new perspectives on multitarget treatments, other than resective surgery, aimed at modifying the epileptic network.
确定结节性异位患者中异位皮质和正常皮质在致痫网络中的作用具有挑战性。为阐明这一问题,我们使用立体脑电图(SEEG)记录的定量信号分析比较了异位皮质和正常皮质。
对19例接受SEEG检查的患者在发作期(致痫指数;EI)和发作间期记录(高频振荡和棘波)期间的临床相关致痫生物标志物进行了评估。然后在异位皮质和新皮质区域之间比较这些生物标志物。根据定量分析的各自值(EI≥0.3)将发作分为正常发作、异位发作或正常-异位发作。
共分析了1246个触点:异位组织(异位皮质)中有259个,病变同侧新皮质(局部新皮质)中有873个,远离病变的新皮质(远处新皮质)中有114个。在患者层面比较局部新皮质和异位皮质时,EI值、高频振荡和棘波率没有显著差异,但在发作层面分析EI值时,局部新皮质比异位皮质更具致痫性(p<0.001)。根据EI值,发作大多为正常发作(48.5%)或正常-异位发作(45.5%);只有6%是纯粹的异位发作。热凝和手术切断后只有两名患者获得了良好的长期治疗反应。
这是第一项定量SEEG研究,为结节性异位中发作产生的机制提供了见解。我们证明异位病变尤其是正常皮质都参与了致痫网络。这可能为旨在改变癫痫网络的多靶点治疗(而非切除性手术)开辟新的前景。