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Source-level α periodic power in visual and default mode networks predicts topiramate treatment response in migraine

Siyuan Xie, Chenghui Pi, Kang Jin, Longteng Ma, Yunyun Huo, Miaomiao Hu, Xi Zhang, Suyuan Tai, Jiayin Lin, Shengyuan Yu, Ye Ran, Zhao Dong

The Journal of Headache and Pain July 17, 2026 DOI: 10.1186/s10194-026-02461-5 (opens in new tab) via OpenAlex

Summary

AI-generated from the abstract

Periodic alpha-band brain activity, measured with electroencephalography (EEG) before treatment, predicts how well patients with episodic migraine without aura will respond to the preventive drug topiramate. Higher alpha power in specific brain regions—the cuneus, pericalcarine cortex, medial orbitofrontal cortex, frontal pole, and precuneus—indicates a poorer clinical response. A predictive model using these features achieved an area under the receiver operating characteristic curve of 0.859 in identifying treatment responders. The visual network and default mode network together explained 26.1% of the variance in headache improvement. These findings suggest that baseline alpha activity is a strong neurobiological marker for personalizing migraine preventive therapy.

Study at a glance

Characteristics Observational cohort Peer reviewed
Sample size 112
Population Patients with episodic migraine without aura
Intervention Topiramate
Duration 3 months of topiramate treatment
Topics Default mode network
Keywords Topiramate Electroencephalography Receiver operating characteristic Feature linguistics
Key finding Higher periodic alpha-band power in the cuneus, pericalcarine cortex, medial orbitofrontal cortex, frontal pole, and precuneus predicts poorer response to topiramate preventive treatment.

Abstract

BACKGROUND: Migraine is highly heterogeneous, and patients exhibit substantial variability in their responses to preventive treatment. The dose-escalation strategy of topiramate further complicates early evaluation of therapeutic efficacy. Identifying neurobiological markers that can predict treatment response is therefore essential for individualized therapy. In this study, we constructed predictive models based on individualized periodic and aperiodic power features derived from source-reconstructed electroencephalography (EEG) to identify electrophysiological indicators associated with topiramate efficacy, thereby providing a foundation for personalized prediction in migraine prevention. METHODS: In total, 112 patients with episodic migraine without aura received baseline EEG assessment and subsequently completed 3 months of topiramate treatment. EEG signals were source-reconstructed, and periodic and aperiodic components were separated using FOOOF with adjustment by each participant's individual α frequency (IAF). Predictive models were developed using XGBoost, with stratified cross-validation and 0.632 + bootstrap used to estimate generalization performance. Shapley Additive exPlanations (SHAP) analysis quantified feature contributions. Correlation analysis and Leave-One-Out Cross-Validation (LOOCV) regression were subsequently performed to examine the relationships between key features and treatment outcomes. RESULTS: The model achieved an area under the receiver operating characteristic curve (AUROC) of 0.859 in identifying treatment responders. SHAP analysis indicated that the most influential features were periodic α-band power localized to the cuneus, pericalcarine cortex, medial orbitofrontal cortex, frontal pole, and precuneus. Principal component analysis (PCA) of the functional brain networks comprising these regions showed that the principal components of the visual network (VN) and default mode network (DMN) were significantly associated with headache improvement, and their joint inclusion in a LOOCV regression model explained 26.1% of the variance in treatment efficacy. CONCLUSION: Periodic α activity represents a strong predictive biomarker of topiramate efficacy, with higher α power indicating poorer clinical response. These findings provide an interpretable neurobiological basis for individualized prediction in migraine preventive therapy. CLINICAL TRIAL NUMBER: Not applicable.

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