Neural Emotion Regulation Circuitry Underlying Anxiolytic Effects of Perceived Control over Pain

Abstract

Anxiolytic effects of perceived control have been observed across species. In humans, neuroimaging studies have suggested that perceived control and cognitive reappraisal reduce negative affect through similar mechanisms. An important limitation of extant neuroimaging studies of perceived control in terms of directly testing this hypothesis, however, is the use of within subjects-designs, which confound participants' affective response to controllable and uncontrollable stress. To compare neural and affective responses when participants were exposed to either uncontrollable or controllable stress, two groups of participants received an identical series of stressors (thermal pain stimuli). One group (“controllable”) was led to believe they had behavioral control over the pain stimuli while another (“uncontrollable”) believed they had no control. Controllable pain was associated with decreased state anxiety, decreased activation in amygdala and increased activation in nucleus accumbens (NAcc). In participants who perceived control over the pain, reduced state anxiety was associated with increased functional connectivity between each of these regions and ventral lateral/ventral medial prefrontal cortex (PFC). The location of PFC findings is consistent with regions found to be critical for the anxiolytic effects of perceived control in rodents. Furthermore, interactions observed between PFC and both amygdala and NAcc are remarkably similar to neural mechanisms of emotion regulation through reappraisal in humans. These results suggest that perceived control reduces negative affect through a general mechanism involved in the cognitive regulation of emotion.

Affect dysregulation, psychoform dissociation, and adult relational fears mediate the relationship between childhood trauma and complex posttraumatic stress disorder independent of the symptoms of borderline personality disorder

“…Although the link between childhood trauma and positive symptoms of somatoform dissociation (e.g. medically unexplained pain) was tenuous in the current study, there is evidence that childhood trauma is associated with physical as well as emotional pain (Nelson, Cunningham, & Kashikar-Zuck, 2017; Sachs-Ericsson, Sheffler, Stanley, Piazza, & Preacher, 2017) and that perceived control over pain is associated with reduced anxiety and enhanced emotion regulation (Salomons, Nusslock, Detloff, Johnstone, & Davidson, 2015). Therefore, assessment of somatoform dissociation appears warranted as a precaution when clinically treating adults with CPTSD/DESNOS.…”

Pain: A Precision Signal for Reinforcement Learning and Control

“…The fact that attention and controllability reliably modulate pain (Eccleston and Crombez, 1999;Wiech et al, 2006;Yoshida et al, 2013;Salomons et al, 2007Salomons et al, , 2015Taylor et al, 2017;Br€ ascher et al, 2016), beyond that which can be explained by mechanisms above, suggests that factors intrinsic to learning and control specifically modulate pain. Although the goal of RL is to learn to minimize pain as an objective function, performance can be enhanced by intrinsically modulating pain according to its informational value in learning.…”

Deficits in autonomic indices of emotion regulation and reward processing associated with prescription opioid use and misuse

“…Among chronic pain patients, maladaptive emotion regulation strategies like emotion suppression have been shown to exacerbate pain under stressful conditions (Burns 2006) by increasing physiological reactivity to pain and stress (Burns et al 2011). Neuroimaging research has suggested that the regulation of pain and emotion share overlapping neural substrates, including cortico-limbic-striatal circuits (Salomons et al 2014) which partially overlap with the central autonomic network thought to govern HRV. These studies suggest a linkage between emotion regulatory capacity and pain, yet it is unclear whether chronic pain patients who use and misuse opioids evidence emotion regulation deficits.…”