ArticleBrain sciences2026
Repeated Continuous Theta-Burst Stimulation Modulates Resting-State EEG Microstate Dynamics in Athletes with Chronic Insomnia.
Article in Brain sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic insomnia can impair recovery and performance in athletes. Continuous theta-burst stimulation (cTBS) is a brief neuromodulatory intervention, but its effects in athletes with chronic insomnia remain unclear. This study evaluated whether right dorsolateral prefrontal cTBS improves sleep quality and athletic performance and alters resting-state EEG microstate dynamics.
methodsIn this randomized, sham-controlled trial, 35 male athletes with chronic insomnia received active cTBS or sham stimulation once daily for 7 days; usable EEG data were obtained from 32 participants. Sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). Countermovement jump, 50 m sprint, and Illinois Agility Test performance were assessed before and after intervention. Resting-state electroencephalography (EEG) microstate temporal parameters and directional transition probabilities were analyzed.
resultsActive cTBS produced a greater reduction in PSQI global score than sham stimulation. Active stimulation increased microstate C duration and contribution and reduced microstate A occurrence. Directional transitions among microstates B, C, and D were also altered, with largely concordant findings in ΔTM sensitivity analyses. Active cTBS improved countermovement jump height, 50 m sprint performance, and agility, whereas sham stimulation improved sprint performance only.
conclusionsA 7-day course of right dorsolateral prefrontal cTBS improved subjective sleep quality and sport-related performance in athletes with chronic insomnia. These improvements were accompanied by selective changes in resting-state EEG microstate temporal parameters and transition probabilities. Given the exploratory nature of the EEG findings, these microstate changes should be interpreted as potential electrophysiological correlates of treatment response rather than evidence of a causal mechanism.
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