The journal of pain : official journal of the American Pain Society
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Pain catastrophizing is one of the most powerful predictors of poor outcomes in youth and adults with pain; however, little is known about differential effects of pain catastrophizing on outcomes as a function of age. The current study examined the predictive value of pain catastrophizing on pain interference and pain intensity across children, adolescents, and 2 age groups of young adults with chronic pain. Cross-sectional data are presented from the adult and pediatric Collaborative Health Outcomes Information Registry (CHOIR), including measures of pain catastrophizing, pain intensity, pain interference, and emotional distress from 1,028 individuals with chronic pain. Results revealed that age moderated the relation between pain catastrophizing and pain interference, with the strength of these effects declining with age. The effect of pain catastrophizing on pain interference was strongest in adolescents and relatively weak in all 3 other groups. Emotional distress was the strongest predictor of pain interference for children, whereas pain intensity was the strongest predictor for both adult groups. Pain catastrophizing was found to predict pain intensity and, although age was a significant moderator, statistical findings were weak. Developmental considerations and clinical implications regarding the utility of the construct of pain catastrophizing across age groups are discussed. ⋯ This article explores differences in pain catastrophizing as predictors of pain interference and pain intensity across cohorts of children, adolescents, and 2 age groups of young adults. This work may stimulate further research on chronic pain from a developmental perceptive and inform developmentally tailored treatment interventions that target catastrophizing, emotional distress, and pain intensity.
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Dysfunction of biological stress systems and adverse life events, independently and in interaction, have been hypothesized to predict chronic pain persistence. Conversely, these factors may hamper the improvement of chronic pain. Longitudinal evidence is currently lacking. ⋯ The number of adverse life events were assessed at baseline and 2-year follow-up using the List of Threatening Events Questionnaire. We showed that hypothalamic-pituitary-adrenal axis, immune system, and autonomic nervous system functioning and adverse life events were not associated with the improvement of chronic multisite musculoskeletal pain, either as a main effect or in interaction. This longitudinal study could not confirm that biological stress system dysfunction and adverse life events affect the course of chronic multisite musculoskeletal pain.
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It is not uncommon for patients chronically treated with opioids to exhibit opioid-induced hyperalgesia, and this has been widely reported clinically and experimentally. The molecular substrate for this hyperalgesia is multifaceted, and associated with a complex neural reorganization even in the periphery. For instance, we have recently shown that chronic morphine-induced heat hyperalgesia is associated with an increased expression of GluN2B containing N-methyl-D-aspartate receptors, as well as of the neuronal excitatory amino acid transporter 3/excitatory amino acid carrier 1, in small-diameter primary sensory neurons only. ⋯ The selective TRPM8 antagonist RQ-00203078 blocked cold hyperalgesia in morphine-treated rats. Also, TRPM8 knockout mice failed to develop cold hyperalgesia after chronic administration of morphine. Our results show that chronic morphine upregulates TRPM8 channels, which is in contrast with the previous finding that acute morphine triggers TRPM8 internalization.
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Chronic inflammation, which changes the neurotransmitter metabolism and kindles neuroendocrine system dysfunction in the central nervous system, might cause fibromyalgia (FM) formation. In FM patients without traditional FM risk factors, such as hypertension, hyperlipidemia, diabetes, sleep disorder, depression, and anxiety, the chronic inflammatory process is a possible risk factor for FM. Thus, we investigated whether chronic osteomyelitis (COM), a disease characterized by chronic inflammation, increases FM risk. ⋯ Younger people had an even greater risk (age younger than 35 years: aHR = 1.58, 95% CI, 1.03-2.44; age 60 years or older: aHR = 1.03, 95% CI, .78-1.36). To our knowledge, this is the first study to link COM to an enhanced risk of FM development. The results imply that COM is a predictor of FM, suggesting that close follow-up for patients with COM is required to prevent FM, especially in younger populations.