Pain
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Multicenter Study Comparative Study
How do children with autism spectrum disorders express pain? A comparison with developmentally delayed and typically developing children.
There is a lack of knowledge about pain reactions in children with autism spectrum disorders (ASD), who have often been considered as insensitive to pain. The objective of this study was to describe the facial, behavioral and physiological reactions of children with ASD during venipuncture and to compare them to the reactions of children with an intellectual disability and nonimpaired control children. We also examined the relation between developmental age and pain reactions. ⋯ Moreover, we observed a significant decrease in pain expression with age in nonimpaired children, but no such effect was found regarding children with ASD. The data reveal that children with ASD displayed a significant pain reaction in this situation and tend to recover more slowly after the painful experience. Improvement in pain assessment and management in this population is necessary.
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While group 1 metabotropic glutamate receptors (mGluRs) and ionotropic N-methyl-d-aspartate (NMDA) receptors regulate nociception, the precise molecular mechanism(s) contributing to glutamate signaling in chronic pain remain unclear. Here we not only confirmed the key involvement of Homer proteins in neuropathic pain, but also distinguished between the functional roles for different Homer family members and isoforms. Chronic constriction injury (CCI) of the sciatic nerve induced long-lasting, time-dependent increases in the postsynaptic density expression of the constitutively expressed (CC) isoforms Homer1b/c and/or Homer2a/b in the spinal dorsal horn and supraspinal structures involved in nociception (prefrontal cortex, thalamus), that co-occurred with increases in their associated mGluRs, NR2 subunits of the NMDA receptor, and the activation of downstream kinases. ⋯ Thus, nerve injury-induced increases in CC-Homers expression promote pain in pathological states, but IEG-Homer induction protects against both the development and maintenance of neuropathy. Additionally, exacerbated pain hypersensitivity in transgenic mice with reduced Homer binding to mGluR5 supports also an inhibitory role for Homer interactions with mGluR5 in mediating neuropathy. Such data indicate that nerve injury-induced changes in glutamate receptor/Homer signaling contribute in dynamic but distinct ways to neuropathic pain processing, which has relevance for the etiology of chronic pain symptoms and its treatment.
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Pain is known to play an important role in the pathway to becoming work disabled, in particular for award of disability pensions (DP) due to musculoskeletal diagnoses (MSD). This prospective cohort study investigated MSD-related pain stability and/or changes as predictors for DP during a 23-year follow-up. Additionally confounding factors were examined to elucidate whether familial effects (including genetics and family background) or socioeconomic status, other pain, or use of medication would affect the associations between pain and DP. ⋯ Musculoskeletal pain impairing work ability both measured at 1 time point and 6 years apart, and either 1 pain location or multiple locations, predicted increased risk for DP due to MSD, OA, and LBD. The associations were independent of familial confounding factors and of several influential background factors, including headache; migraine; use of analgesics, hypnotics, or tranquillizers; life satisfaction; and education and marital status. This study concluded that musculoskeletal pain impairing work ability is an early and direct predictor for DP due to MSD, OA, and LBD.