Pain
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Musculoskeletal pain is common among adolescents, but little is known about the factors that affect seeking health care for the problem. We examined the care-seeking pattern among adolescents reporting musculoskeletal pain. The study consisted of adolescents aged 16 years from the 1986 Northern Finland Birth Cohort who responded to a mailed questionnaire in 2001 and reported musculoskeletal pain over the preceding 6 months (n=5052). ⋯ Reporting pain in other anatomical areas decreased the likelihood of seeking care for pain among both genders. In conclusion, relatively few adolescents with musculoskeletal pain had consulted a health professional for the problem. Being physically active (trauma), participating in organized sport (accessibility of care), and having other health problems may explain why an adolescent seeks care for musculoskeletal pain.
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Preliminary evidence suggests that pain catastrophizing in children may be important in understanding how parents respond to their child's pain. However, no study has investigated whether parental responses, in turn, moderate the impact of child's catastrophizing upon pain outcomes. The present study was designed to address this, and investigated the association of the child's catastrophizing with different types of parental responses (ie, solicitousness, discouragement and coping promoting responses) and the extent to which parental responses moderate the association between the child's catastrophizing and disability. ⋯ Findings also revealed a moderating impact of mothers' and fathers' promotion of their child's well behaviour/coping. Specifically, the detrimental impact of child catastrophizing upon disability was less pronounced when parents reported high promotion of their child's well behaviours/coping. The findings of the present study suggest the importance of assessing and targeting parental responses to their child's pain to alter the adverse impact of the child's pain catastrophizing on pain outcomes.
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Peripheral inflammation alters AMPA receptor (AMPAR) subunit trafficking and increases AMPAR Ca(2+) permeability at synapses of spinal dorsal horn neurons. However, it is unclear whether AMPAR trafficking at extrasynaptic sites of these neurons also changes under persistent inflammatory pain conditions. Using patch-clamp recording combined with Ca(2+) imaging and cobalt staining, we found that, under normal conditions, an extrasynaptic pool of AMPARs in rat substantia gelatinosa (SG) neurons of spinal dorsal horn predominantly consists of GluR2-containing Ca(2+)-impermeable receptors. ⋯ This increase was also accompanied by an inward rectification of AMPA-induced currents and enhancement of sensitivity to a highly selective Ca(2+)-permeable AMPAR blocker, IEM-1460. Electron microcopy and biochemical assays additionally showed an increase in the amount of GluR1 at extrasynaptic membranes in dorsal horn neurons 24h post-CFA. Taken together, our findings indicate that CFA-induced inflammation increases functional expression and proportion of extrasynaptic GluR1-containing Ca(2+)-permeable AMPARs in tonically firing excitatory dorsal horn neurons, suggesting that the altered extrasynaptic AMPAR trafficking might participate in the maintenance of persistent inflammatory pain.
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Facial expression is one of the most relevant nonverbal behaviors in the communication of pain. However, little is known about brain processing of pain expressions in comparison with other affective facial expressions. The present experiment aimed to examine the effects of pain expression intensity on affective ratings and brain dynamics by recording electroencephalography (EEG) from 20 female healthy volunteers 18-24 years of age. ⋯ EEG results further showed that facial expressions of pain elicited more enhanced amplitudes of the visual evoked potentials than anger and neutral faces in the latency between 350 and 550 milliseconds after stimulus onset; whereas anger faces elicited greater P200 amplitudes than pain and neutral faces. In addition, more increased theta activity in the latency of 200 to 400 milliseconds after stimulus onset was observed to high-intense as compared with low-intense facial expressions. These findings indicate that brain activity elicited by affective faces is modulated by the intensity of facial expressions and suggest the involvement of different brain mechanisms during the processing and recognition of facial expressions of pain and anger in healthy volunteers.
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Sensitization of primary afferent neurons is one of the most important components of pain hypersensitivity after tissue injury. Insulin-like growth factor 1 (IGF-1), involved in wound repair in injured tissue, also plays an important role in maintaining neuronal function. In the present study, we investigated the effect of tissue IGF-1 on nociceptive sensitivity of primary afferent neurons. ⋯ The IGF1R inhibitor successfully alleviated mechanical allodynia, heat hyperalgesia, and spontaneous pain behavior observed after plantar incision. Expression of phosphorylated Akt in DRG neurons significantly increased after plantar incision and was suppressed by IGF1R inhibition. These results demonstrate that increased tissue IGF-1 production sensitizes primary afferent neurons via the IGF1R/Akt pathway to facilitate pain hypersensitivity after tissue damage.