Epilepsia · 2025
Common network related to hyperkinetic seizures revealed by functional lesion network mapping.
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Yang Bowen, Yao Chen, Xu Jinping, Li Ningfei, Hu Wenhan, Wang Xiu, Zhao Baotian, Mo Jiajie, Zheng Zhong, Shao Xiaoqiu, Zhang Jianguo, Horn Andreas, Zhang Chao, Zhang Kai
Аннотация
OBJECTIVE: This study aims to determine whether the anatomically heterogeneous lesions that cause hyperkinetic seizures (HKS) are connected to a common functional network.
METHODS: We identified patients from the Beijing Tiantan-Fengtai Epilepsy Center with HKs as the primary ictal semiology. These included patients had focal seizure-onset zone, here referred to as a "lesion." The network of brain regions functionally connected to each lesion was identified using whole-brain functional connectivity from a functional magnetic resonance imaging (fMRI) dataset of healthy participants (n = 1000). Network maps were overlapped to identify regions functionally connected to most lesions. Specificity was evaluated using a case-control design. Therapeutic relevance was assessed using a cohort that underwent deep brain stimulation to the anterior nucleus of the thalamus to improve seizure control.
RESULTS: Lesion locations for patients with HKS (n = 50) and patients without HKS (n = 47 for automatisms; n = 53 for elementary motor signs) were included. Based on the lesion brain network, the most sensitive and specific region with HKS was the anterior cingulate cortex (ACC) (>90% overlap). Reversed connectivity patterns between the ACC and the whole brain encompassed most lesion locations that caused HKS (47/50, 94%). In addition, the functional connectivity between ACC and deep brain stimulation sites was associated with improved seizure control (r = .49, p < .01) in 27 patients with drug-resistant epilepsy.
SIGNIFICANCE: These findings indicated that HKS might be a symptom of brain network disruption that resulted from lesions in various brain regions commonly connected to ACC, emphasizing the ACC as a potential target for therapeutic intervention in HKS.
METHODS: We identified patients from the Beijing Tiantan-Fengtai Epilepsy Center with HKs as the primary ictal semiology. These included patients had focal seizure-onset zone, here referred to as a "lesion." The network of brain regions functionally connected to each lesion was identified using whole-brain functional connectivity from a functional magnetic resonance imaging (fMRI) dataset of healthy participants (n = 1000). Network maps were overlapped to identify regions functionally connected to most lesions. Specificity was evaluated using a case-control design. Therapeutic relevance was assessed using a cohort that underwent deep brain stimulation to the anterior nucleus of the thalamus to improve seizure control.
RESULTS: Lesion locations for patients with HKS (n = 50) and patients without HKS (n = 47 for automatisms; n = 53 for elementary motor signs) were included. Based on the lesion brain network, the most sensitive and specific region with HKS was the anterior cingulate cortex (ACC) (>90% overlap). Reversed connectivity patterns between the ACC and the whole brain encompassed most lesion locations that caused HKS (47/50, 94%). In addition, the functional connectivity between ACC and deep brain stimulation sites was associated with improved seizure control (r = .49, p < .01) in 27 patients with drug-resistant epilepsy.
SIGNIFICANCE: These findings indicated that HKS might be a symptom of brain network disruption that resulted from lesions in various brain regions commonly connected to ACC, emphasizing the ACC as a potential target for therapeutic intervention in HKS.