The journal of pain : official journal of the American Pain Society
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Cognitive biases that emphasize bodily harm, injury, and illness could play a role in the maintenance of chronic pain by facilitating fear and avoidance. Whereas extensive research has established attention, interpretation, and memory biases in adults with chronic pain, far less is known about these same biases in children and adolescents with pain. Studying cognitive biases in attention, interpretation, and memory in relation to pain occurring in youth is important because youth is a time when pain can first become chronic, and when relationships between cognitive biases and pain outcomes emerge and stabilize. ⋯ In this article, we summarize the growing corpus of data that have measured cognitive biases in relation to pediatric pain. We conclude that although biases in attention, interpretation, and memory characterize children and adolescents with varying pain experiences, questions regarding the direction, magnitude, nature, and role of these biases remain. We call for independent extension of cognitive bias research in children and adolescents, using well powered longitudinal studies with wide age ranges and psychometrically sound experimental measures to clarify these findings and any developmental trends in the links between cognitive biases and pain outcomes.
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Increased HCN Channel Activity in the Gasserian Ganglion Contributes to Trigeminal Neuropathic Pain.
Orofacial neuropathic pain caused by trigeminal nerve injury is a debilitating condition with limited therapeutic options. Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability and are involved in the development and maintenance of chronic pain. However, the effect of HCN channel activity in the Gasserian ganglion on trigeminal neuropathic pain has not been examined. We evaluated nociceptive behaviors after microinjection of the HCN channel blockers ZD7288 or ivabradine into the Gasserian ganglion in rats with trigeminal nerve injury. Both blockers dose-dependently ameliorated evoked and spontaneous nociceptive behavior in rats with trigeminal neuropathic pain. Moreover, the clinically available HCN channel blocker ivabradine showed a prolonged antinociceptive effect. In the Gasserian ganglion, HCN1 and HCN2 are major HCN isoforms. After trigeminal nerve injury, the counts of HCN1 as well as HCN2 immuno-positive punctae were increased in the ipsilateral Gasserian ganglions. These results indicate that the increased HCN channel activity in the Gasserian ganglion directly contributes to neuropathic pain resulting from trigeminal nerve injury. ⋯ Trigeminal nerve damage-induced orofacial pain is severe and more resistant to standard pharmacological treatment than other types of neuropathic pain. Our study suggests that targeting HCN channel activities in the Gasserian ganglion may provide an alternative treatment of trigeminal neuropathy including trigeminal neuralgia.
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Musculoskeletal pain changes how people move. Although experimental pain is associated with increases in the variability of motor output, it is not clear whether motor-evoked pain in clinical conditions is also associated with increases in variability. In the current study, we measured jaw force production during a visually guided force paradigm in which individuals with chronic jaw pain and control subjects produced force at 2% of their maximum voluntary contraction (low target force level) and at 15% of their maximum voluntary contraction (high target force level). ⋯ We showed that the chronic jaw pain group exhibited greater force variability compared with controls irrespective of the force level, whereas the accuracy of force production did not differ between groups. Furthermore, predictors of force variability shifted from trait measures of pain intensity and pain interference at the low force level to state measures of pain intensity at the high force level. Our observations show that motor-evoked jaw pain is associated with increases in force variability that are predicted by a combination of trait measures and state measures of pain intensity and pain interference.
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Breast cancer metastasizes to bone, diminishing quality of life of patients because of pain, fracture, and limited mobility. Cancer-induced bone pain (CIBP) is characterized as moderate to severe ongoing pain, primarily managed by mu opioid agonists such as fentanyl. However, opioids are limited by escalating doses and serious side effects. ⋯ U50,488 blocked this pain without altering tumor-induced bone loss or tumor growth. Follow-up studies in human cancer cell lines confirmed that KOR agonists do not affect cancer cell proliferation. These studies suggest that KOR agonists could be a new target for cancer pain management that does not induce cancer cell proliferation or alter bone loss.
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Multicenter Study
Within-Person Pain Variability and Mental Health in Older Adults With Osteoarthritis: An Analysis Across 6 European Cohorts.
Pain is a key symptom of osteoarthritis (OA) and has been linked to poor mental health. Pain fluctuates over time within individuals, but a paucity of studies have considered day-to-day fluctuations of joint pain in relation to affective symptoms in older persons with OA. This study investigated the relationship of pain severity as well as within-person pain variability with anxiety and depression symptoms in 832 older adults with OA who participated in the European Project on OSteoArthritis (EPOSA): a 6-country cohort study. ⋯ Moreover, older-old participants experienced fewer symptoms of anxiety (ratio = .85, 95% confidence interval [CI], .77-.94), depression (ratio = .90, 95% CI, .82-.98), and total affective symptoms (ratio = .87, 95% CI, .79-.94) if their pain fluctuated more. No such association was evident in younger-old participants (65-74.0 years). These findings imply that stable pain levels are more detrimental to mental health than fluctuating pain levels in older persons.