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Updated: Oct 17, 2026

Microstate and Omega Complexity Analyses of the Resting-state Electroencephalography
Published on: June 15, 2018
Abnormal resting-state EEG microstates correlate with objective sleep parameters in insomnia disorder
Qianqian Wu1, Linman Weng1, Xu Lei1
1Sleep and NeuroImaging Center, Faculty of Psychology, Southwest University, Chongqing, 400715, China; Key Laboratory of Cognition and Personality (Southwest University), Ministry of Education, Chongqing, 400715, China.
Background:
Insomnia is a common sleep disorder, and Electroencephalogram (EEG) microstates, which mirror transient cerebral cortical functional activity, are linked to sleep disorder pathophysiology. The microstate characteristics in insomnia patients and correlations with objective sleep parameters remain to be further explored.
Method:
This study enrolled 45 insomnia disorder (ID) patients and 48 healthy controls (HC), collecting awake resting-state EEG for microstate analysis; 27 ID and 13 H C participants additionally completed overnight polysomnography (PSG), and exploratory correlation analyses of microstate and PSG data performed for the ID group.
Results:
Compared with HC, ID patients had markedly shorter duration of microstate A and B, higher occurrence and contribution of microstate C, and reduced duration, occurrence and contribution of microstate D (p < 0.05). ID patients also showed significantly lower transition probabilities of A→D, B→D, D→A and D→B (p < 0.01), and higher probabilities of A→C, B→C, C→A and C→B (p < 0.05). Correlation analyses revealed that in the ID, microstate D occurrence was negatively correlated with rapid eye movement sleep proportion (REM Sleep%, r = -0.427, p = 0.026) and positively correlated with non-rapid eye movement sleep stage 1 proportion (S1%, r = 0.385, p = 0.047).
Conclusion:
ID patients present significant abnormalities in EEG microstates, and the occurrence of microstate D is correlated with objective sleep indicators of PSG. These findings suggest that EEG microstate parameters may reflect abnormalities in the sleep architecture of ID and may provide references for analyzing the cortical hyperarousal mechanism of chronic insomnia, constructing objective assessment schemes, and developing targeted neuroregulation interventions.
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