High cognitive load may prevent the development of nociceptive hypersensitivity

Abstract

Whether, how, and which cognitive factors modulate the development of secondary hypersensitivity/hyperalgesia following central sensitization is not fully understood. Here we tested, in 60 healthy volunteers, whether being engaged in non-pain related cognitive demanding tasks: i) lessens the amount of hypersensitivity developed after an experimental procedure sensitizing nociceptive pathways; ii) modulates cortical responses to somatosensory stimuli (measured by electroencephalography, EEG). In the first experiment we validated a novel model in humans using low frequency stimulation (LFS) of the skin and demonstrated that it was able to successfully induce hypersensitivity to mechanical pinprick stimuli in the area surrounding the sensitized site. In the second and third experiments we engaged participants in tasks of increasing difficulty (the Eriksen Flanker Task in experiment 2, and a modified N-back task in experiment 3). We observed that hypersensitivity to mechanical stimuli still developed in experiment 2, i.e. the pinprick stimuli applied on the sensitized arm were perceived as more intense after LFS. In contrast, no such effect was observed in experiment 3, indicating that, at the group level, being engaged in high-cognitive load task may interfere with the development of mechanical hypersensitivity. Contrary to previous studies, which have used different methods to induce sensitization, we did not observe any increase in the cortical response to somatosensory stimuli applied on the sensitized arm. We conclude that i) the development of hyperalgesia partly depends on attention, and ii) the enhancement of cortical responses to somatosensory stimuli is related to the method used to induce central sensitization

The influence of a manipulation of threat on experimentally-induced secondary hyperalgesia

“…Threat manipulations are known to induce “weak…concerns about the pain stimulus” in experimental pain studies ( Vlaeyen et al, 2009 )—perhaps because participants know the pain will be short-lived and because ethical review provides implicit reassurance. Threat manipulations that give participants threatening information about the experimental procedures have been successful in previous studies ( Jackson et al, 2005 ; Torta et al, 2019 ; Van Damme et al, 2008 ; Wiech et al, 2010 ). However, our early piloting of a strategy in which we provided participants with threatening information about the HFS procedure (rather than the integrity of the skin at the induction site) was ineffective in eliciting threat of tissue damage (see File S1 : Piloting procedure).…”

“…Experimental induction of secondary hyperalgesia uses safe stimulation to induce a short-lived expression of secondary hyperalgesia under controlled conditions, in a laboratory. The induction can use stimuli such as high-frequency electrical stimulation (HFS) ( Klein et al, 2004 ), low-frequency electrical stimulation ( Torta et al, 2019 ), intradermal capsaicin injection ( Baron et al, 1999 ), topical capsaicin application ( You, Creech & Meagher, 2016 ) and burn injury ( Wahl et al, 2019 ). In this study, we used high-frequency electrical stimulation to induce experimental secondary hyperalgesia.…”

The Effect of High Versus Low Cognitive Load on the Development of Nociceptive Hypersensitivity: The Roles of Sympathetic Arousal, Sex, and Pain-Related Fear

“…The literature shows mixed findings, with Rolke et al (2006) indicating that females show lower pain thresholds before sensitization and enhanced hypersensitivity after sensitization than males, whereas another study could not confirm this (Jensen & Petersen, 2006). Torta et al (2020) did not find evidence for a role of sex in the cognitive modulation of hypersensitivity, but their sample size was limited, and results await replication.…”

“…Our knowledge about whether, how, and which cognitive factors affect the development of secondary hyperalgesia (Kóbor et al, 2009;Matre et al, 2006;Torta et al, 2020;Wiech et al, 2005) is limited.…”

“…Secondary hyperalgesia 1 is considered as an indirect measure of central sensitization (Ali et al, 1996, Baumann et al, 1991Klein et al, 2004;LaMotte et al, 1991;Raja et al, 1984;Simone et al, 1991;Woolf, 2011), contributing to persistent pain (Arendt-Nielsen et al, 2018;Woolf et al, 2011) (however see Cayrol et al, 2020;van den Broeke, 2018;van den Broeke et al, 2019 for a debate regarding the use of the term central sensitization), and can be experimentally induced using Low Frequency electrical Stimulation (LFS) of the skin (Torta et al, 2020). Torta et al (2020) showed that performing a high cognitive load task during LFS results in less hypersensitivity, whereas this was not the case for a low cognitive load task. The robustness of this cognitive modulation, the conditions in which it appears, and the underlying mechanisms remain to be confirmed and elucidated.…”