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Response Inhibition Deficits in Insomnia Disorder: An Event-Related Potential Study With the Stop-Signal Task

Background: Response inhibition is a hallmark of executive function, which was detected impaired in various psychiatric disorders. However, whether insomnia disorder (ID) impairs response inhibition has caused great controversy. Methods: Using the auditory stop-signal paradigm coupled with event-rel...

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Detalles Bibliográficos
Autores principales: Zhao, Wenrui, Gao, Dong, Yue, Faguo, Wang, Yanting, Mao, Dandan, Chen, Xinyuan, Lei, Xu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6090996/
https://www.ncbi.nlm.nih.gov/pubmed/30131753
http://dx.doi.org/10.3389/fneur.2018.00610
Descripción
Sumario:Background: Response inhibition is a hallmark of executive function, which was detected impaired in various psychiatric disorders. However, whether insomnia disorder (ID) impairs response inhibition has caused great controversy. Methods: Using the auditory stop-signal paradigm coupled with event-related potentials (ERPs), we carried out this study to examine whether individuals with ID presented response inhibition deficits and further investigated the neural mechanism correlated to these deficits. Twelve individuals with ID and 13 matched good sleepers (GSs) had participated in this study, and then they performed an auditory stop-signal task (SST) in the laboratory setting with high density EEG recordings. Results: The behavioral results revealed that compared to GSs, patients with ID presented significantly longer stop-signal reaction time (SSRT), suggesting the impairment of motor inhibition among insomniacs. Their reaction time in go trials, however, showed no significant between-group difference. Considering the electrophysiological correlate underlying the longer SSRT, we found reduced P3 amplitude in patients with insomnia in the successful stop trials, which might reflect their poor efficiency of response inhibition. Finally, when we performed exploratory analyses in the failed stop and go trials, patients with ID presented reduced Pe and N1 amplitude in the failed sop trials and go trials respectively. Discussion: Taken together, these findings indicate that individuals with ID would present response inhibition deficits. Moreover, the electrophysiological correlate underlying these deficits mainly revolves around the successful stop P3 component. The present study is the first to investigate the electrophysiological correlate underlying the impaired response inhibition among insomniacs.