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

Abstract

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.

The Effects of Sleep Quality on Dream and Waking Emotions

“…This kind of mechanism was plausibly active in GS, whose negative emotions, excluded from waking consciousness in favor of positive ones, may have rebounded in the dream. The process of negative affect suppression could instead have been ineffective in PS, possibly due to the fact that disrupted sleep is linked to deficits in higher cognitive functions including inhibition (e.g., [ 19 , 76 , 77 ]). In line with Malinowski et al [ 78 ], who showed that successful suppression of thoughts and their rebound in the dream benefit the emotional response to pleasant and unpleasant thoughts, it may be hypothesized that, in good sleepers, the dream rebound of negative emotions reflects their effective processing in sleep, irrespective of the specific episodic memories (thoughts, events, etc.)…”

Altered brain activity related to inhibitory processing in youth with insomnia

“…The lack of P3 differences might be due to the different tasks being used and the varying levels of cognitive demands. The smaller effect size in our data might be related to the relatively shorter duration of insomnia in our sample, which consisted of younger participants with insomnia, as compared with the middle-aged sample in the earlier studies (Muscarella et al, 2019;Zhao et al, 2018). Our pattern of results was similar to that of a previous study based on a non-clinical sample, which reported that self-identified poor sleepers (as defined by a sleep disturbance index) had reduced N2 but not P3 in a Go/NoGo task (Breimhorst, Falkenstein, Marks, & Griefahn, 2008).…”

“…Our time-domain finding was generally in line with those of previous ERP studies conducted in the adults with insomnia. It was found that adult insomnia patients had reduced CNV, N2, and P3 components during the AX-continuous performance task (Muscarella et al, 2019) and reduced P3 during the Stop Signal Task (Zhao et al, 2018) than healthy sleepers (median to large effect size, η 2 = 0.13-0.21). These ERPs findings collectively suggested insomnia is associated with altered neural processing related to inhibitory control.…”

“…Inhibitory control is a key feature of executive functions that helps individuals to resist impulses, habitual responses, and ultimately impulsivity (Diamond, 2012). Previous studies that assessed the performance on inhibition task in individuals with insomnia were mostly conducted using adult samples and have yielded mixed findings, with some reporting a significant behavioral impairment (e.g., Zhao et al, 2018), while others showing no difference (e.g., Muscarella, Mairesse, Hughes, & Neu, 2019). On the other hand, functional neuroimaging studies found that prefrontal cortex, one of the key brain regions involved in inhibitory control (Swick, Ashley, & Turken, 2011), showed reduced activities during the wake time positron emission tomography scan (Nofzinger et al, 2004) and lower activation during category and letter fluency task (Altena et al, 2008) in patients with insomnia as compared with healthy sleepers.…”

“…One study found that although adults with insomnia disorder (N = 18, aged 20-53, Mean = 32) showed comparable performance as the healthy sleepers (N = 15, aged 21-53, Mean = 32) on the AX-continuous performance task assessing cognitive control, they showed altered neural activities of inhibitory functioning as indicated by reduced amplitudes of the P3 component and the contingent negative variation (CNV) component (Muscarella et al, 2019). Another study that assessed ERP during an auditory stop-signal task found that adults with insomnia disorder (N = 12, aged 18-65, Mean = 49) showed slower reaction time and reduced P3 amplitude as compared with healthy sleepers (N = 13, aged 18-65, Mean = 41) (Zhao et al, 2018). Collectively, these studies have provided preliminary evidence showing electrophysiological correlates of inhibitory deficits in insomnia.…”