Neural mechanisms of working memory dysfunction in patients with chronic insomnia disorder.

OBJECTIVE

This study aimed to investigate the neural mechanisms underlying working memory impairment in patients with chronic insomnia disorder (CID) using event-related potentials (ERP) and resting-state functional connectivity (rsFC) approaches.

METHODS

Participants, including CID patients and healthy controls (HCs), completed clinical scales and underwent electroencephalography (EEG) and functional magnetic resonance imaging (fMRI). EEG analysis compared reaction times, P3 amplitudes, event-related spectral perturbations (ERSP), and inter-trial phase synchronisation (ITPS) between CID patients and HCs. Subsequently, frontal regions (i.e., the Superior Frontal Gyrus [SFG] and Middle Frontal Gyrus [MFG]) corresponding to the EEG were selected as seeds for rsFC analysis. Correlation analyses were conducted to further investigate the relationship between functional connectivity abnormalities in brain regions and clinical symptom severity and P3 amplitude in CID patients.

RESULTS

Compared to HCs, CID patients exhibited slower reaction times across all working memory conditions, with the deficits becoming more pronounced as memory load increased. ERP analysis revealed increased P3 amplitude, theta wave power, and reduced inter-trial synchrony in CID patients. rsFC analysis showed decreased connectivity of SFG-posterior cingulated cortex (PCC), SFG-MFG, and MFG-frontal pole (FP), and increased connectivity of MFG- Middle Temporal Gyrus (MTG)in CID patients. Importantly, a significant correlation was found between the rsFC of SFG-MTG and P3 amplitude during 1-back.

CONCLUSION

This study confirms deficits in working memory capacity in patients with CID, specifically in the neural mechanisms of cognitive processing that vary depending on the level of cognitive load. Alterations in connectivity patterns within and between the frontal and temporal regions may be the neural basis of the cognitive impairment.