Cerebral and Spinal Modulation of Pain by Emotions and Attention

Fig. 3.1

Model of emotions’ and attention’s effects on nociception, pain sensation, and pain’s primary and secondary affect. Neural structures likely to have a role in these dimensions are shown by abbreviations in adjacent parentheses. PC parietal cortex, S1–S2 primary and secondary somatosensory cortices, pINS posterior insula, ACC anterior cingulate cortex, aMCC anterior midcingulate cortex, aINS anterior insula, amy amygdala, PFC prefrontal cortex, Nacc nucleus accumbens, PAG periaqueductal gray, hyp hypothalamus, LPFC lateral prefrontal cortex, MPFC medial prefrontal cortex

Although the supraspinal mechanisms engaged by attention and emotions may substantially differ, their effects on pain-evoked activations appear to be difficult to disentangle due to the highly integrated nature of the pain-processing system. It has been suggested that one potential point of separation could be that attention preferentially affects the cerebral structures underlying the sensory dimension of pain, but recent neuroimaging findings are not perfectly congruent with this hypothesis (Villemure and Bushnell 2009; Ploner et al. 2011). It is also important to note that because of the partially sequential relationship between pain sensation and affect (Price 2000), modulation of pain sensation should also indirectly impact the affective dimension of pain, thereby blurring the boundaries between attentional and emotional effects. Another potential point of separation between attentional and emotional effects could be that emotions preferentially modulate pain affect, either directly or indirectly through a modulation of pain-related appraisals. However, distraction away from pain could also impact the affective dimension by interfering with the appraisal processes underlying pain’s primary and secondary affect, which would be consistent with recent reports of selective effects of attention on aINS activity (Ploner et al. 2011). Finally, emotions could also influence pain perception through modulation of autonomic activity, which could be misattributed to pain (Schachter and Wheeler 1962), although this possibility has yet to be formally tested.

Moreover, emotional states can also alter the direction of attention (Salovey 1992) and be associated with different spinal and supraspinal effects that can either work synergistically or antagonistically. Therefore, in order to identify the origins of emotional effects on pain-related brain activity, it is necessary to try to probe as much as possible the various levels of pain processing by combining several methodologies, including NFR recordings, measures of autonomic activity, fMRI, EEG, etc. One interesting avenue for future imaging studies could be the use of cross-validated multivariate pain “signatures” in order to further characterize the nature of the modulatory effects of various interventions (Wager et al. 2013). Hopefully, a better understanding of the psychological factors that influence pain will lead to a better understanding of pain itself, including how it may become dysregulated in chronic pain syndromes.

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