Pain
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Remembering an event partially reactivates cortical and subcortical brain regions that were engaged during its experience and encoding. Such reinstatement of neuronal activation has been observed in different sensory systems, including the visual, auditory, olfactory, and somatosensory domain. However, so far, this phenomenon of incidental memory has not been explored in the context of pain. ⋯ Moreover, the bilateral ventral striatum showed stronger responses for remembered pain-associated images as compared with tone-associated images, suggesting a higher behavioral relevance of remembering neutral pictures previously paired with pain. Our results support the biological relevance of pain in that only painful but not equally unpleasant auditory stimuli were able to "tag" neutral images during their simultaneous presentation and reactivate pain-related brain regions. Such mechanisms might contribute to the development or maintenance of chronic pain and deserve further investigation in clinical populations.
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Pain catastrophizing is associated with enhanced pain; however, the mechanisms by which it modulates pain are poorly understood. Evidence suggests that catastrophizing modulates supraspinal processing of pain but does not modulate spinal nociception (as assessed by nociceptive flexion reflex [NFR]). Unfortunately, most NFR studies have been correlational. ⋯ Although NFRs were not affected by the catastrophizing manipulation, temporal summation of NFR was reduced. However, this effect was not mediated by catastrophizing. These results indicate that reductions in catastrophizing lead to reductions in pain perception but do not modulate spinal nociception and provides further evidence that catastrophizing modulates pain at the supraspinal, not the spinal, level.
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Morphine and other opioid analgesics are potent pain-relieving agents routinely used for pain management in patients with cancer. However, these drugs have recently been associated with a worse relapse-free survival in patients with surgical cancer, thus suggesting that morphine adversely affects cancer progression and relapse. ⋯ Our studies further demonstrate that morphine, administered in the presence or absence of surgery-induced tissue damage, neither facilitates de novo metastatic dissemination nor promotes outgrowth of minimal residual disease after surgery. Together, these findings indicate that opioid analgesics can be used safely for perioperative pain management in patients with cancer and emphasize that current standards of "good clinical practice" should be maintained.
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The dorsal reticular nucleus (DRt) plays a key role in facilitation of nociceptive transmission at the spinal cord. In this study, we evaluated the mechanisms involved in GABA-mediated control of the DRt focusing on the role of local GABAB receptors. First, we used in vivo microdialysis to study the release of GABA in the DRt during the course of the formalin test. ⋯ For that purpose, we combined retrograde tract-tracing from the DRt with immunodetection of glutamate decarboxylase, the GABA-synthesizing enzyme. The higher numbers of retrogradely labelled glutamate decarboxylase-immunoreactive neurons were located at insular, somatosensory, and motor cortices. Collectively, the results suggest that GABA acting on GABAB receptors may enhance pain facilitation from the DRt during inflammatory pain.