Resting-State Functional Connectivity Alterations in Insomnia Disorder: A Systematic Review of Studies Published from 2020 to July 2025
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
Abstract Insomnia disorder is increasingly linked to abnormalities in resting-state functional connectivity (rsFC). We systematically synthesized rs-fMRI studies published from January 2020 to July 2025 to characterize disorder-related connectivity patterns and methodological limitations. Twenty-four study reports met the eligibility criteria; reported sample sizes summed to 1,229 participants with insomnia disorder and 1,077 healthy controls, although some cohorts may overlap across publications. Alterations involved the default mode, salience, executive-control, emotion, and sensorimotor systems and sleep–wake regulatory hubs, including the thalamus and hypothalamus. The overall pattern is compatible with hyperarousal, but both increased and decreased connectivity were reported; diagnostic definitions, sex, symptom severity and duration, medication exposure, acquisition conditions, and seed-based versus data-driven analyses may moderate direction and magnitude. A formal study-level appraisal with the JBI analytical cross-sectional checklist identified predominantly low risk or some concerns, most often related to confounding control. Because all included comparisons were cross-sectional, rsFC alterations cannot be interpreted as causes rather than consequences or correlates of insomnia. Methodological heterogeneity precluded quantitative pooling. Standardized phenotyping, medication control, acquisition and preprocessing, preregistered longitudinal studies, and external val
Abstract
Abstract Insomnia disorder is increasingly linked to abnormalities in resting-state functional connectivity (rsFC). We systematically synthesized rs-fMRI studies published from January 2020 to July 2025 to characterize disorder-related connectivity patterns and methodological limitations. Twenty-four study reports met the eligibility criteria; reported sample sizes summed to 1,229 participants with insomnia disorder and 1,077 healthy controls, although some cohorts may overlap across publications. Alterations involved the default mode, salience, executive-control, emotion, and sensorimotor systems and sleep–wake regulatory hubs, including the thalamus and hypothalamus. The overall pattern is compatible with hyperarousal, but both increased and decreased connectivity were reported; diagnostic definitions, sex, symptom severity and duration, medication exposure, acquisition conditions, and seed-based versus data-driven analyses may moderate direction and magnitude. A formal study-level appraisal with the JBI analytical cross-sectional checklist identified predominantly low risk or some concerns, most often related to confounding control. Because all included comparisons were cross-sectional, rsFC alterations cannot be interpreted as causes rather than consequences or correlates of insomnia. Methodological heterogeneity precluded quantitative pooling. Standardized phenotyping, medication control, acquisition and preprocessing, preregistered longitudinal studies, and external validation are required before connectivity markers can be used clinically.