While chronic pain is considered by some to be a CNS disease, little is understood about underlying neurobiological mechanisms. Addiction models have heuristic value in this regard, because both pain and addictive disorders are characterized by impaired hedonic capacity, compulsive drug seeking, and high stress. In drug addiction such symptomatology has been attributed to reward deficiency, impaired inhibitory control, incentive sensitization, aberrant learning, and anti-reward allostatic neuroadaptations. Here we propose that similar neuroadaptations exist in chronic pain patients.
Keywords: amygdala; analgesia; catastrophizing; corticotropin-releasing factor; deficient or excessive reward dysfunction; delay discounting; dopamine; dynorphin; effectors; habenula; hedonostat; homeostasis; nucleus accumbens; opioid; opponent; prediction error; regulators; therapeutic dependence.
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