Pain
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Rodents and human studies indicate that the hippocampus, a brain region necessary for memory processing, responds to noxious stimuli. However, the hippocampus has yet to be considered a key brain region directly involved in the human pain experience. One approach to answer this question is to perform quantitative sensory testing on patients with hippocampal damage-ie, medial temporal lobe epilepsy. ⋯ Only left hippocampal volume was positively associated with mechanical pain sensitivity-the greater the hippocampal damage, the lower the sensitivity to mechanical pain. Hippocampal measures of functional integrity were not significantly associated with mechanical pain sensitivity, suggesting that the mechanisms of hippocampal pain processing may be different than its memory functions. Future studies are necessary to determine the mechanisms of pain processing in the hippocampus.
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Research has consistently suggested that media consumption plays a vital role in children's socialization, including the socialization of painful experiences. Past research examining young children's popular media revealed worrisome trends in media depictions of pain; it consisted of narrow depictions of pain, gender stereotypes, and an overwhelming lack of empathy from observers, which could contribute to pain-related stigma. Research has not yet examined how pain is portrayed in adolescent media, despite adolescence being the developmental period when chronic pain often emerges. ⋯ Furthermore, regardless of observed gender or "race," observers displayed a lack of empathy for sufferers and rarely engaged in prosocial behaviors. Popular media may serve as an agent of socialization in adolescence; thus, pain depictions may be a powerful force in propagating pain-related stigma and inequities. An opportunity exists to harness popular media to adaptively and accurately portray pain to adolescents.
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Repetitive transcranial magnetic stimulation (rTMS) is a promising technology to reduce chronic pain. Investigating the mechanisms of rTMS analgesia holds the potential to improve treatment efficacy. Using a double-blind and placebo-controlled design at both stimulation and pharmacologic ends, this study investigated the opioidergic mechanisms of rTMS analgesia by abolishing and recovering analgesia in 2 separate stages across brain regions and TMS doses. ⋯ In the DLPFC, double but not the first TMS session induced significant pain reduction in the saline condition, resulting in less pain compared with the naloxone condition. In addition, TMS over the M1 or DLPFC selectively increased plasma concentrations of β-endorphin or encephalin, respectively. Overall, we present causal evidence that opioidergic mechanisms are involved in both M1-induced and DLPFC-rTMS-induced analgesia; however, these are shaped by rTMS dosage and the release of different endogenous opioids.