ArticleCNS neuroscience & therapeutics2026
Altered Evening Aperiodic Activity and Microstate Dynamics in Insomnia Disorder: An OPM MEG Study.
Article in CNS neuroscience & therapeutics, 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
backgroundInsomnia disorder (ID) is characterized by hyperarousal, yet the relationship between cortical excitability and large-scale network dynamics remains incompletely understood. While fMRI studies indicate network alterations in ID, high-temporal-resolution characterization of these dynamics across the sleep-wake cycle is lacking.
methodsTwenty-six patients with ID and 29 healthy controls underwent eyes-closed resting-state OPM-MEG recordings during evening (pre-sleep) and morning (post-awakening) sessions. We analyzed the aperiodic spectral exponent to index cortical excitability and employed microstate analysis to quantify fast network dynamics. A mediation analysis was conducted to explore the associations between electrophysiological features and sleep quality.
resultsCompared to controls, patients with ID exhibited a significantly flatter aperiodic power spectrum in the evening, suggesting elevated cortical excitability. Microstate analysis revealed distinct spatiotemporal alterations: (1) an evening-specific increase in the coverage of a putative temporal-limbic microstate, and (2) a sustained elevation of a putative sensorimotor microstate observed in both evening and morning sessions. Mediation analysis indicated that the altered evening limbic microstate dynamics statistically mediated the association between the aperiodic exponent and subjective sleep disturbance measures.
conclusionsThese findings indicate that ID involves concurrent disruptions in aperiodic neural activity and microstate temporal organization. The study highlights distinct diurnal profiles for putative sensorimotor and limbic network alterations, suggesting that OPM-MEG can effectively capture the multifaceted electrophysiological signatures of the insomnia phenotype.
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