Pain
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Randomized Controlled Trial
Longitudinal change in parent and child functioning after internet-delivered cognitive-behavioral therapy for chronic pain.
Theoretical models of pediatric chronic pain propose longitudinal associations between children's pain experiences and parent and family factors. A large body of cross-sectional research supports these models, demonstrating that greater parent distress and maladaptive parenting behaviors are associated with greater child disability. Family-based cognitive-behavioral therapy interventions have been developed for youth with chronic pain which aim to improve child disability and reduce maladaptive parenting behaviors. ⋯ These findings indicate that parent distress may increase the risk of poor response to psychological pain treatment among youth with chronic pain. At present, parent distress is not routinely targeted in psychological interventions for pediatric chronic pain. Research is needed to determine optimal strategies for targeting parent and family factors in the treatment of pediatric chronic pain.
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Child and parent pain catastrophizing are reported preoperative risk factors for children's acute and persistent postsurgical pain. This study examined dyadic relations between child and parent pain catastrophizing and child and parent ratings of child pain prior to (M = 4.01 days; "baseline") and following surgery (M = 6.5 weeks; "acute follow-up"), as well changes in pain catastrophizing during this time in 167 youth (86% female; Mage = 14.55 years) undergoing spinal fusion surgery and 1 parent (89% mothers). Actor-partner interdependence models assessed cross-sectional and longitudinal intra- and interpersonal effects. ⋯ Baseline child and parent pain catastrophizing did not predict child pain at acute follow-up. In conclusion, child, not parent, pain catastrophizing was associated with children's pre- and postsurgical pain, and showed significantly less stability over time. There is a need to better understand contributors to the stability or changeability of pain catastrophizing, the prospective relation of catastrophizing to pain, and contexts in which child vs parent pain catastrophizing is most influential for pediatric postsurgical pain.
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Offset analgesia (OA) represents a disproportionately large decrease of pain perception after a brief, temporary increment of thermal pain stimulus and was reported attenuated in patients with neuropathic pain. We examined whether OA depends on the increment duration before offset, and whether individual features of OA distinguish patients with chronic pain and healthy controls. We used a Peltier-type thermal stimulator and OA paradigms including 5-, 10-, or 15-s duration of 1°C-increment (T2) over 45°C. ⋯ Maximum VAS latency was longer in patients than in controls and negatively correlated with [INCREMENT]OA in patients. An OA index ([INCREMENT]OA/[maximum VAS latency]) proved diagnostic of chronic pain with an area under the receiver operating characteristic curve at 0.897. Patients with chronic pain showed impairment of OA and reduced temporal sharpening of pain perception, which might imply possible disturbance of the endogenous pain modulatory system.
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The magnitude of antinociception elicited by intrathecal endomorphin 2 (EM2), an endogenous mu-opioid receptor (MOR) ligand, varies across the rat estrous cycle. We now report that phasic changes in analgesic responsiveness to spinal EM2 result from plastic interactions within a novel membrane-bound oligomer containing estrogen receptors (mERs), aromatase (aka estrogen synthase), metabotropic glutamate receptor 1 (mGluR1), and MOR. During diestrus, spinal mERs, activated by locally synthesized estrogens, act with mGluR1 to suppress spinal EM2/MOR antinociception. ⋯ Finally, spinal neurons were observed not only to coexpress MOR, mERα, aromatase, and mGluR1 but also be apposed by EM2 varicosities. This suggests that modulation of spinal analgesic responsiveness to exogenous EM2 likely reflects changes in its endogenous analgesic activity. Analogous suppression of spinal EM2 antinociception in women (eg, around menses, comparable with diestrus in rats) as well as the (pathological) inability to transition out of that suppressed state at other menstrual cycle stages could underlie, at least in part, the much greater prevalence and severity of chronic pain in women than men.