Pain
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Regional decreases in grey matter volume as detected by magnetic resonance imaging-based volumetry have been reported in several clinical chronic pain cohorts. Here, we used voxel-based morphometry in a nonclinical cohort to investigate whether grey matter alterations also occur in older individuals (aged 40-85 years) from the general population. Based on self-report of pain, we identified 31 pain-free controls, 45 subjects with ongoing pain (low back pain, headache, or lower extremity joint pain) who had at least moderate pain on more than 3 days/month, and 29 individuals with past pain (stopped for >12 months). ⋯ No grey matter volume decreases were found in the group with pain that had stopped for >12 months. These results show that pain-related grey matter volume decreases are present in individuals from the general population. The lack of morphometric anomalies in subjects with past pain supports recent evidence suggesting that pain-related grey matter changes are reversible after cessation of 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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Parent responses to the experiences of adolescents with chronic pain are deemed important. At the same time the best ways to conceptualize, measure, and intervene with these are unclear. The purpose of the present study was to develop a measure of parent responses based on the approach proposed in Acceptance and Commitment Therapy (ACT), an approach that focuses on psychological flexibility. ⋯ It was also positively correlated with adolescent acceptance of pain and negatively correlated with measures of pain-related impact on their social, emotional, family, and developmental functioning. Additional analyses showed that the PPFQ yields significant unique information about adolescent functioning independent of age and gender and beyond that provided by another well-established measure of parent responses. There is increasing evidence for the effectiveness of ACT in the treatment of a range of behavior problems in adults and young people and in training for persons without identified "disorders." It seems potentially applicable for parent training in the context of adolescent chronic pain.
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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.
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Voltage-gated ion channels are implicated in pain sensation and transmission signaling mechanisms within both peripheral nociceptors and the spinal cord. Genetic knockdown and knockout experiments have shown that specific channel isoforms, including Na(V)1.7 and Na(V)1.8 sodium channels and Ca(V)3.2 T-type calcium channels, play distinct pronociceptive roles. We have rationally designed and synthesized a novel small organic compound (Z123212) that modulates both recombinant and native sodium and calcium channel currents by selectively stabilizing channels in their slow-inactivated state. ⋯ In vivo experiments demonstrate that oral administration of Z123212 is efficacious in reversing thermal hyperalgesia and tactile allodynia in the rat spinal nerve ligation model of neuropathic pain and also produces acute antinociception in the hot-plate test. At therapeutically relevant concentrations, Z123212 did not cause significant motor or cardiovascular adverse effects. Taken together, the state-dependent inhibition of sodium and calcium channels in both the peripheral and central pain signaling pathways may provide a synergistic mechanism toward the development of a novel class of pain therapeutics.