Chibany Léa, Nicollin Elena, Courtin Edouard, Bar Claire, Michel Véronique, Penchet Guillaume, Aupy Jérôme
Institute for Neurodegenerative Diseases, Unité Mixte de Recherche, Centre National de la Recherche Scientifique, University of Bordeaux, Bordeaux, France.
Department of Clinical Neurosciences, Bordeaux University Hospital, Bordeaux, France.
Epilepsia. 2025 Jun 18. doi: 10.1111/epi.18510.
We investigated the interdependency between striatal activity and the electrophysiological dynamics of the cortical epileptogenic zone using intracerebral stereoelectroencephalographic recordings in patients with drug-resistant epilepsy. We performed both qualitative and quantitative analyses of ictal striatal activity and its synchronization with the cerebral cortex to gain deeper insight into the striatal contribution to seizure regulation.
Thirty-one patients were retrospectively included. The Epileptogenicity Index (EI) was computed, high EI values corresponded to structures in the epileptogenic zone (EZ), and brain regions with sustained discharge during the seizure were defined as the propagation zone network (PZN). To study the functional and directed connectivity between the striatum and the broader network, a nonlinear correlation coefficient (h) and an index Dᵪᵧ that provides quantitative information about the direction of couplings between neuronal populations were computed.
We analyzed 31 subjects and 68 seizures. We found that 84% (n = 57) of seizures spread to the ipsilateral striatum. This spread was mainly late during seizure evolution (69.12%, n = 47) and was mostly present in seizures characterized by a focal slow spread pattern (33.82%, n = 23). Striatal epileptogenicity was overall low, with only 4.41% (n = 3) of seizures exhibiting a striatal EI ≥ .4. Interestingly, the positive correlation between striatal epileptogenicity and the PZN (r = .4193, p = .0004) indicates that higher striatal epileptogenicity is associated with the recruitment of a greater number of brain regions within the PZN. Moreover, striatal functional connectivity with the broader network was the lowest during the background period and progressively increased during ictal and postictal phases (p < .001), with directed connectivity shifting from the EZ to the striatum in the preictal and termination phases.
These findings provide a framework for future research investigating the potential of basal ganglia-targeted therapies in epilepsy management.
我们利用脑内立体脑电图记录，研究耐药性癫痫患者纹状体活动与皮质致痫区电生理动力学之间的相互依赖性。我们对发作期纹状体活动及其与大脑皮层的同步性进行了定性和定量分析，以更深入地了解纹状体对癫痫发作调节的作用。
回顾性纳入31例患者。计算致痫指数（EI），高EI值对应致痫区（EZ）中的结构，发作期间持续放电的脑区定义为传播区网络（PZN）。为了研究纹状体与更广泛网络之间的功能和定向连接，计算了非线性相关系数（h）和指数Dᵪᵧ，该指数提供了有关神经元群体之间耦合方向的定量信息。
我们分析了31名受试者和68次癫痫发作。我们发现84%（n = 57）的癫痫发作扩散到同侧纹状体。这种扩散主要发生在癫痫发作演变的后期（69.12%，n = 47），并且大多出现在以局灶性缓慢扩散模式为特征的癫痫发作中（33.82%，n = 23）。纹状体致痫性总体较低，只有4.41%（n = 3）的癫痫发作表现出纹状体EI≥0.4。有趣的是，纹状体致痫性与PZN之间的正相关（r = 0.4193，p = 0.0004）表明，较高的纹状体致痫性与PZN内更多脑区的参与有关。此外，纹状体与更广泛网络的功能连接在背景期最低，在发作期和发作后期逐渐增加（p < 0.001），定向连接在发作前期和终止期从EZ转移到纹状体。
这些发现为未来研究调查基底神经节靶向治疗在癫痫管理中的潜力提供了一个框架。
