Baroreceptor activation attenuates attentional effects on pain-evoked potentials

Abstract

Focused attention typically enhances neural nociceptive responses, reflected electroencephalographically as increased amplitude of pain-evoked event-related potentials (ERPs). Additionally, pain-evoked ERPs are attenuated by hypertension and baroreceptor activity, through as yet unclear mechanisms. There is indirect evidence that these two effects may interact, suggesting that baroreceptor-related modulation of nociception is more than a low-level gating phenomenon. To address this hypothesis, we explored in a group of healthy participants the combined effects of cue-induced expectancy and baroreceptor activity on the amplitude of pain-evoked ERPs. Brief nociceptive skin stimuli were delivered during a simple visual task; half were preceded by a visual forewarning cue, and half were unpredictable. Nociceptive stimuli were timed to coincide either with systole (maximum activation of cardiac baroreceptors) or with diastole (minimum baroreceptor activation). We observed a strong interaction between expectancy and cardiac timing for the amplitude of the P2 ERP component; no effects were observed for the N2 component. Cued stimuli were associated with larger P2 amplitude, but this effect was abolished for stimuli presented during baroreceptor activation. No cardiac timing effect was observed for un-cued stimuli. Taken together, these findings suggest a close integration of cognitive–affective aspects of expectancy and baroreceptor influences on pain, and as such may cast further light on mechanisms underlying mental and physiological contributions to clinical pain.

Forebrain organization representing baroreceptor gating of somatosensory afferents within the cortical autonomic network

“…Second, as observed previously in smaller animal models, the present data provide evidence of measurable but reflex-specific baroreceptor gating of somatosensory inputs in humans. As such, these observations add to previous observations with respect to the interactions of baroreflex inputs on nociception and small-diameter type III and type IV somatosensory afferents (Edwards et al 2008;Gray et al 2010;Potts et al 2003;Quest and Gebber 1972).…”

“…Furthermore, Gray and colleagues (2009) have demonstrated an involvement of the insula, amygdala, and brain stem nuclei in the integration of somatosensory stimuli presented either before or during early cardiac systole in humans, showing that baroreceptor activity across the cardiac cycle influences the cortical processing of somatosensory stimuli (Gray et al 2009). The concept of baroreceptor modulation also extends to the gating of other sensory responses including nociception (Edwards et al 2008;Gray et al 2010). Thus, we sought to examine the sympathetic response and cortical representation of baroreflex gating of somatosensory afferent inputs.…”

The neural subjective frame: from bodily signals to perceptual consciousness

“…Evidence is less clear-cut in the case of cutaneous stimuli: sensitivity to cutaneous stimuli either at threshold for perception [75] or around pain threshold [76] was found to increase when the stimulus was presented about 300 ms after the R peak of the ECG. However, cardiac phase had no effect on pain ratings of nociceptive cutaneous stimuli above pain threshold [77].…”

Blood pressure and pain sensitivity in children and adolescents

“…Resting SBP has been convincingly linked to experimental pain manipulation, but the relationship with DBP is less consistent, with several adult studies finding no relation regardless of the pain task (Bruehl, Carlson, & McCubbin, ; Guasti, Zanotti et al., ; Helfer & McCubbin, ; Myers et al., ; Page & France, ). Relatedly, an emerging literature has used PRES to consider how timing and duration of baroreceptor activity during cardiac systole leads to changes in the neural signatures of pain processing (Gray et al., ). One key finding to explain how stable resting BP is linked to diminished pain sensitivity, in light of the mechanisms of baroreceptor resetting following prolonged blood pressure elevations, is the degree of phasic , rather than tonic, stimulation in relation to the cardiac cycle (Bruehl & Chung, ).…”