Sleep restriction does not potentiate nocebo‐induced changes in pain and cortical potentials

Abstract

Background The increased pain sensitivity following reduced sleep may be related to changes in cortical processing of nociceptive stimuli. Expectations shape pain perception and can inhibit (placebo) or enhance (nocebo) pain. Sleep restriction appears to enhance placebo responses; however, whether sleep restriction also affects nocebo responses remains unknown. The aim of the present study was to determine whether sleep restriction facilitates nocebo‐induced changes in pain and pain‐evoked cortical potentials. Methods In an experimental study with a crossover design, the sensitivity to electrically induced pain was determined in 53 nurses under two sleep conditions, after habitual sleep and after two consecutive nights at work. Nocebo was induced by conditioning one‐third of the pain stimuli. Pain‐elicited cortical event‐related potentials were recorded by electroencephalography (EEG). Data were analysed both in the time domain (N2P2 amplitude) and in the time–frequency domain (ERP magnitude). Sleepiness and vigilance were also assessed. Results Both nocebo alone and sleep restriction alone increased the sensitivity to electrically induced pain. However, no interaction effect was found. Moreover, the magnitude of the pain‐elicited responses increased after sleep restriction and decreased after nocebo expectation, suggesting that nocebo is probably not an underlying mechanism for the commonly observed hyperalgesia induced by sleep restriction. Conclusions The present work addresses whether sleep restriction, known to increase the sensitivity of the pain system, facilitates nocebo‐induced hyperalgesia. Our findings suggest that this is not the case, indicating that the increased sensitivity of the pain system following nocebo and sleep restriction are mediated by different cortical mechanisms.

Virtual reality hypnosis in the management of pain: Self‐reported and neurophysiological measures in healthy subjects

“…This was first illustrated by the modification of N100 and P200 ERPs components following painful stimulations, and further supported by the significant correlation between those ERPs component and the selfreported level of pain. The relevance of the N100-P200 as an objective measure of pain perception has similarly been highlighted in several studies investigating laserevoked EEG (Matre et al, 2015;Ree et al, 2020).…”

“…The Digitimer electrical stimulus generator device (DS7A) was kept at 500 μs with 300 V, meaning that the pulse duration was 0.5 ms with a maximum compliance of the stimulation set to 300 V. The electrical pulse intensity calibrated for each subject ranged from 4 to 8 mA. To deliver the first 30 automatically electrical pulse noxious stimuli, the following parameters were set in the electrical pulse generator device (DG2A): pulse mode = free run, repetition: 0.1 Hz (i.e., 10 s of inter‐stimulus interval), delay: 10 ms, output = OUT‐2 (i.e., to deliver the electrical stimulation as a double pulse) (Ree et al, 2020 ). For the last manually delivered electrical pulse noxious stimulation, the following parameters were set: pulse mode = train, delay: 10 ms, output = OUT‐2, and manual inter‐stimulus interval = 10–15 s (Matre et al, 2015 ).…”

Experimental sleep restriction increases latency jitter in pain elicited cortical responses

“…Previous studies have reported increased or unchanged pain ratings, combined with lowered or unchanged time-domain ERPs after sleep restriction compared to habitual sleep ( Matre et al., 2015 ; Odegard et al., 2014 ; Ree et al., 2019 ; Schuh-Hofer et al., 2015 ; Tiede et al., 2010 ). Our results indicate that increased latency jitter after sleep restriction may contribute to the attenuation of averaged ERPs after sleep restriction.…”

“…Recent studies of experimental sleep restriction and pain-elicited ERPs have shown that while laser-induced pain ratings were unchanged (Odegard et al, 2014) or increased after sleep restriction (Schuh-Hofer et al, 2015;Tiede et al, 2010), the corresponding ERP amplitude was reduced (Odegard et al, 2014;Schuh-Hofer et al, 2015;Tiede et al, 2010). However, for electrical stimuli, sleep restriction increased pain ratings, but did not change the ERP amplitude (Matre et al, 2015;Ree et al, 2019). These seemingly paradoxical differential effects of sleep restriction on psychophysical and neurophysiological outcome measures need attention.…”