Exploring the potential role of mesocorticolimbic circuitry in motivation for and adherence to chronic pain self-management interventions

Abstract

Adherence to pain self-management strategies is associated with favorable psychobehavioral outcomes among individuals with chronic pain. Substantive adherence to treatments teaching these adaptive skills often proves challenging, resulting in poor individual and societal outcomes. Evidence demonstrates motivation for behavior change as a key predictor of treatment adherence. Despite behavioral techniques that target motivation, however, nonadherence persists as a barrier to positive clinical outcomes in chronic pain. Understanding the neurobiological mechanisms underlying treatment motivation might highlight novel avenues for augmentative therapies. The purpose of this review is to present theory and evidence that the mesocorticolimbic system (i.e., brain circuitry associated with reward processing and motivation) contributes to treatment motivation among chronic pain patients, ultimately influencing adherence. We review evidence for motivation as a key adherence determinant, detail neuroimaging findings relating mesocorticolimbic circuitry and motivation, and discuss data supporting mesocorticolimbic dysfunction among chronic pain patients. We propose a neurobehavioral model for adherence to pain self-management interventions, listing testable hypotheses. Finally, we discuss potential research and intervention implications from the proposed model.

Keywords: Behavioral pain management; Chronic pain; Mesocorticolimbic system; Motivational Model for Pain Self-Management; Treatment adherence.

Figure 1.

Motivation Circuitry: A forward-inference functional activation statistical map of regions consistently activated across 135 neuroimaging studies that load highly on the key term “motivation” (Neurosynth: http://neurosynth.org/). Results indicate that activated areas include mesolimbic (green arrows), corticolimbic (yellow arrows), and paralimbic (blue arrow) structures. This meta-analysis emphasizes mesocorticolimbic circuitry’s involvement in motivated behaviors across studies. Abbreviations: medial prefrontal cortex (mPFC), orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), ventral tegmental area (VTA), anterior insula (aIns), and nucleus accumbens (NAc)

Figure 2.

A Neurobehavioral Model of Pain, Mesocorticolimbic Circuitry, and Treatment Adherence: The present model demonstrates how neurobiological factors might contribute to the Motivational Model for Pain Self-Management. First, previous evidence has demonstrated altered functioning among brain circuitry related to hedonic processing and motivation (i.e., mesocorticolimbic system), reflecting changes in reward and motivational processes in a chronic pain state (a.). As a result, pain self-management strategies might seem less important (b.1.) or the individual might have poorer self-efficacy to implement such strategies (b.2.). Motivation for behavior change/treatment adherence occurs across a gradient based on these factors (c.), and movement through these stages ultimately leads to initiation of self-management strategies (d.1.). If enough reinforcement from pain relief is processed via mesocorticolimbic circuitry (e.), initiation and subsequent adherence are increased. However, if reinforcement from relief is not sufficient, or if competing reinforcers maintain pain behaviors (f), then nonadherence is the primary outcome.