Alterations in resting-state control energy of limbic-to-subcortical networks in individuals with alcohol use disorder and comorbid sleep disturbances.
TL;DR
Comorbid sleep disturbance in AUD may reflect disrupted energetic regulation of limbic-subcortical state transitions, and network control energy provides a mechanistic framework for understanding sleep-brain interactions in addiction.
Abstract
Background
Alcohol use disorder (AUD) is frequently comorbid with sleep disturbances, yet the neural mechanisms through which sleep and AUD jointly shape brain organization remain unclear. Conventional resting-state analyses describe connectivity but not the energetic cost of transitions between large-scale network states.
Methods
Resting-state fMRI data from 93 individuals with AUD and 91 demographically matched healthy controls (HC) from the Human Connectome Project were analyzed. Sleep was assessed with the Pittsburgh Sleep Quality Index (PSQI). Static inter-network transition energies were computed across eight canonical networks using network control theory. Group × PSQI interactions were tested for directed transitions, with Bonferroni correction. Exploratory ROI analyses examined limbic-to-subcortical ROI pairs.
Results
Individuals with AUD showed greater sleep impairment than HC, particularly in sleep latency, efficiency, and nocturnal disturbances. A significant Group × PSQI interaction was observed for limbic-to-subcortical transition energy (Bonferroni-corrected p = 0.020). In HC, poorer sleep was associated with lower transition energy; this coupling was absent in AUD. Uncorrected effects converged on transitions targeting the subcortical network. Eleven ROI pairs survived correction, linking parahippocampal, amygdalar, and temporal regions to thalamic subnuclei.
Conclusion
Comorbid sleep disturbance in AUD may reflect disrupted energetic regulation of limbic-subcortical state transitions. Network control energy provides a mechanistic framework for understanding sleep-brain interactions in addiction.