Aberrant Effective Connectivity Within and Between the Default Mode, Executive Control, and Salience Networks in
Todor Georgiev1, Rositsa Paunova2,3, Anna Todeva-Radneva2,3
1Department of Pathophysiology, Medical University of Plovdiv, 4002 Plovdiv, Bulgaria.
None:
Background: Chronic insomnia (CID) is a highly prevalent sleep disorder, yet the precise mechanisms underlying it remain incompletely understood. The aim of this study is to analyze effective connectivity between key regions of the default mode network (DMN), executive control network (ECN), and salience network (SN) in patients with CID as potential neurologic correlates of the hyperarousal state. Methods: Thirty-one CID patients and 24 healthy controls (HC) were recruited. All the subjects filled out the Insomnia severity index scale (ISI), Beck depression inventory (BDI), and Epworth sleepiness scale (ESS), underwent polysomnography, and were scanned on functional magnetic resonance imaging. Statistical Parametric Mapping 12 was used to analyze the results. Spectral dynamic causal modeling was applied to the chosen regions of interest. Results: There were three significant connections present in the CID group-inhibitory from the dorsolateral prefrontal cortex (DLPFC) to the right hippocampus (Hippocamp R); excitatory from the dorsomedial prefrontal cortex to the ventromedial prefrontal cortex; and excitatory from the common medial prefrontal cortex to the right anterior insula (AIR). Two statistically significant excitatory connections were lacking in the patients' group-from the posterior cingulate cortex (PCC) to AIR, and from precuneus to PCC. CID patients scored higher on the ISI and BDI. Significant negative correlations between DLPFC-Hippocamp R connectivity and both ISI and BDI scores were identified. Conclusions: Disruptions within the DMN and between the DMN, SN, and ECN reflect an impaired ability to appropriately shift between internally and externally directed cognitive states-an imbalance that potentially underlies the hyperarousal state of CID.
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