Pain
-
Theoretical accounts of chronic pain hypothesize that attentional bias towards pain-related information is a maintaining or exacerbating factor, fuelling further pain, disability, and distress. However, empirical research testing this idea is currently lacking. In the present study, we investigated whether attentional bias towards pain-related information predicts daily pain-related outcomes in a sample of chronic pain patients (n=69; M(age)=49.64 years; 46 females). ⋯ Results indicated that, although an attentional bias towards pain-related information was associated with the current level of disability and pain severity, it had no additional value above control variables in predicting daily pain severity, avoidance, distractibility, and disability. Attentional bias towards pain-related information did, however, moderate the relationship between daily pain severity and both daily disability and distractibility, indicating that, particularly in those patients with a strong attentional bias, increases in pain were associated with increased disability and distractibility. The use of interventions that diminish attentional bias may therefore be helpful to reduce daily disability and the level of distraction from current tasks despite the presence of pain in chronic pain patients.
-
Fatty acid ethanolamides (FAEs), which include palmitoylethanolamide (PEA) and oleoylethanolamide (OEA), are endogenous agonists of peroxisome proliferator-activated receptor-α (PPAR-α) and important regulators of the inflammatory response. They are degraded in macrophages by the lysosomal cysteine amidase, N-acylethanolamine acid amidase (NAAA). Previous studies have shown that pharmacological inhibition of NAAA activity suppresses macrophage activation in vitro and causes marked anti-inflammatory effects in vivo, which is suggestive of a role for NAAA in the control of inflammation. ⋯ ARN077 reversed these biochemical effects. The results identify ARN077 as a potent inhibitor of intracellular NAAA activity, which is active in vivo by topical administration. The findings further suggest that NAAA regulates peripheral pain initiation by interrupting endogenous FAE signaling at PPAR-α.