Epilepsy & behavior : E&B · 2025
Connectivity-based localization and mapping of central epilepsy semiology.
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Zhu Min, Song Jianping, Shi Xianjun, Shen Kaifeng, Wang Lukang, Wang Zhiji, Liu Lihong, Wu Yahua, Guo Yao, Yang Xiaolin, Liu Shiyong, Yang Hui, He Xiju, Zhang Chunqing
Аннотация
OBJECTIVE: Semiology-based preoperative anatomical hypotheses are necessary, yet comprehensive reports on the semiology and its correlation with central subregions in central epilepsy has still lacked. We wished to identify semiologic subgroups and their correlations with central subregions.
METHODS: We retrospectively included 21 patients with central epilepsy identified by stereoelectroencephalography (sEEG). The central region was segmented into 12 subregions using the Human Brainnetome Atlas, and both sEEG data and semiology underwent quantitative analysis.
RESULTS: We defined three patient groups based on semiologic pattern similarities. Several intriguing anatomical-electroclinical correlations were initially observed, including the involvement of paracentral lobule (PCL) subregion 2 in upper-limb sensations, PCL1 in autonomic signs, and notably, postcentral gyrus (PoG) 2 in orofacial motor signs and precentral gyrus (PrG) 1 in hand sensations, which may be explained by the overlap among motor and sensory cortices, suggesting a reexamination of traditional localizations of somatosensory or motor signs to the PoG or PrG. Furthermore, anatomic structures initiating ictal signs constructed specific early spread networks. While all patient groups exhibited propagation to the parietal (P) and cingulate cortices (CG), ictal discharges originating from the superior, the posterior-inferior (near the lateral sulcus), and the middle-inferior aspects tended to propagate anteriorly toward the frontal lobe, in a superior direction and to the adjacent insula, and in a bidirectional manner-that is, towards the middle-front and the posterior regions, respectively.
CONCLUSION: Localizing semiology to central subregions and mapping clinical patterns to early spread networks allowed central epilepsy dynamics to be realized and helped define the range of epileptogenic anomalies preoperatively.
METHODS: We retrospectively included 21 patients with central epilepsy identified by stereoelectroencephalography (sEEG). The central region was segmented into 12 subregions using the Human Brainnetome Atlas, and both sEEG data and semiology underwent quantitative analysis.
RESULTS: We defined three patient groups based on semiologic pattern similarities. Several intriguing anatomical-electroclinical correlations were initially observed, including the involvement of paracentral lobule (PCL) subregion 2 in upper-limb sensations, PCL1 in autonomic signs, and notably, postcentral gyrus (PoG) 2 in orofacial motor signs and precentral gyrus (PrG) 1 in hand sensations, which may be explained by the overlap among motor and sensory cortices, suggesting a reexamination of traditional localizations of somatosensory or motor signs to the PoG or PrG. Furthermore, anatomic structures initiating ictal signs constructed specific early spread networks. While all patient groups exhibited propagation to the parietal (P) and cingulate cortices (CG), ictal discharges originating from the superior, the posterior-inferior (near the lateral sulcus), and the middle-inferior aspects tended to propagate anteriorly toward the frontal lobe, in a superior direction and to the adjacent insula, and in a bidirectional manner-that is, towards the middle-front and the posterior regions, respectively.
CONCLUSION: Localizing semiology to central subregions and mapping clinical patterns to early spread networks allowed central epilepsy dynamics to be realized and helped define the range of epileptogenic anomalies preoperatively.