Neural mechanisms of response inhibition impairments in patients with perimenopausal insomnia

This study aimed to investigate the neural mechanisms underlying impaired response inhibition in patients with perimenopausal insomnia (PMI) using event-related potentials (ERP) and resting-state functional connectivity (rsFC) approaches.

PMI patients and age-matched healthy controls (HCs) completed clinical assessments, electroencephalography (EEG), and functional magnetic resonance imaging. Response inhibition was evaluated using the stop signal task (SST). EEG data were analyzed for ERP components and event-related spectral perturbations (ERSP), and rsFC analyses were conducted using seed regions in the right inferior frontal cortex (IFC), including the ventral posterior (vpIFC) and anterior (aIFC) subregions. Correlation analyses were conducted among neurophysiological indices and clinical measures.

Compared to HCs, PMI patients exhibited prolonged stop signal reaction time, enhanced Stop-N2 amplitudes, and delayed Stop-P3 responses. ERSP analysis revealed reduced beta-band event-related desynchronization (ERD). RsFC analysis showed decreased connectivity between the vpIFC and inferior temporal gyrus (ITG), and increased connectivity between the aIFC and precuneus and posterior cingulate gyrus in PMI patients. Correlation analysis indicated that ERD power and rsFC alterations were significantly associated with hyperarousal and behavioral activation system traits.

This study confirms impaired response inhibition in PMI patients, primarily manifested through aberrant electrophysiological processes underlying inhibitory control. Altered rsFC between the IFC and both the default mode network and temporal network may represent the neural basis of impaired response inhibition. These findings highlight potential neural markers of inhibitory dysfunction in PMI and suggest that hyperarousal and motivational dysregulation may play a key role in its pathophysiology.