Regulatory Effects of Transcutaneous Electrical Acupoint Stimulation on EEG Power in 36-Hour Sleep Deprivation-Induced Cognitive Decline
Abstract
Transcutaneous Electrical Acupoint Stimulation (TEAS), as a non-invasive peripheral neuromodulation technique, has been shown to improve cognitive function. However, its neurophysiological mechanisms underlying cognitive regulation remain unclear. This study aims to investigate the intervention effects of TEAS on sleep deprivation-induced cognitive brain activity and its associated neural mechanisms based on electroencephalographic (EEG) frequency domain analysis. Twenty-five healthy male volunteers were recruited as subjects, and a 36-hour sleep deprivation protocol was used to establish a cognitive decline model. Following sleep deprivation, the subjects received TEAS intervention targeting the acupoints of Neiguan, Waiguan, and Shenmen. Subjects completed the improved Go/NoGo task before and after intervention, with simultaneous EEG recording. The study focused on analyzing power spectral density (PSD) changes across five frequency bands in different electrodes. Results indicate that PSD changes following TEAS intervention exhibit state-frequency-region specificity. Alpha band activity was significantly increased in frontal and centroparietal regions in Go conditions. Meanwhile, theta band power showed widespread activation across frontal, central, centroparietal, and parietal regions in NoGo conditions. This finding suggests that TEAS may partially reverse sleep deprivation-induced cognitive impairment at the neurophysiological level by selectively activating alpha rhythms associated with response execution and theta rhythms involved in inhibitory control. The study provides electrophysiological evidence at the EEG frequency domain level for non-invasive interventions targeting sleep deprivation-related cognitive decline, demonstrating the regulatory effectiveness of peripheral electrical neuromodulation.
Keywords: Cognitive Function, Transcutaneous Electrical Acupoint Stimulation, EEG, Sleep Deprivation
DOI: 10.54941/ahfe1007395
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