Pain
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The present study examined the value of a measure of catastrophizing as a predictor of activity intolerance in response to delayed onset muscle soreness (DOMS). A sample of 50 (17 men, 33 women) sedentary undergraduates participated in an exercise protocol designed to induce muscle soreness and were asked to return 2 days later to perform the same physical maneuvers. Participants performed five strength exercises that emphasized the eccentric component of the muscle contraction in order to induce DOMS. ⋯ Regression analyses revealed that catastrophizing predicted reductions in weight lifted even after controlling for pain and negative mood. These findings extend previous research in demonstrating that catastrophizing is associated with objective indices of activity intolerance associated with pain. Implications of these findings for understanding pain-related disability are addressed.
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There is extensive evidence that spinal excitatory amino acids (EAAs) like glutamate (Glu) and aspartate (Asp) are important in the processing of nociceptive behaviors caused by incisions. To better understand EAA-induced dorsal horn sensitization caused by surgery, we examined the time course and extent of spinal amino acid (AA) release during and after a plantar incision utilizing in vivo microdialysis. We also examined the role of primary afferent input and axonal conduction by measuring spinal EAAs in rats after hindpaw denervation and in rats treated with spinal tetrodotoxin (TTX). ⋯ The concentrations of AAs returned to baseline by 1h. The percentage increase is in some cases less and for a shorter period of time compared to other models of persistent pain, perhaps because the incision injury is less severe compared to others models. This profile of EAA release further explains why models of inflammation and chemical irritation do not translate well to human postoperative pain.
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This paper reports an experimental investigation of engagement with and disengagement from a threatening cue of pain. As most paradigms in pain research only provide an overall index of attentional deployment by pain-related information, a new paradigm was developed that allowed an independent investigation of engagement with and disengagement from pain cues. Forty pain-free volunteers performed a cueing task in which they had to detect pain targets and tone targets as quickly and as accurately as possible. ⋯ However, when pain was cued and did not occur, there was retardation in disengagement from the pain cue. This retardation was more pronounced and extended across time in those high in catastrophic thinking about pain. On examination it appeared that catastrophic thinking about pain may operate by a protection of the belief that the cue for pain is a valid one, despite experience to the contrary.
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Although known primarily for its role in neuronal development, brain-derived neurotrophic factor (BDNF) has also recently been implicated in processes mediated by the adult nervous system, such as spinal nociception. Peripheral inflammation increases expression of BDNF preferentially in dorsal root ganglion cells that contain substance P and/or calcitonin gene-related peptide, known nociceptive transmitters for which synthesis is also increased during inflammatory states. Expression of the tyrosine kinase receptor that selectively binds BDNF, trkB, is increased in the spinal dorsal horn during inflammation as well. ⋯ FL-mediated mechanism, the i.t. administration of another trkB ligand, neurotrophin-4/5, also produces hyperalgesia while the trkC agonist neurotrophin-3, which weakly cross-reacts with trkB, has little effect. Finally, with the accumulating evidence linking BDNF to synaptic plasticity, we investigated whether BDNF-induced hyperalgesia in normal mice involves the N-methyl-D-aspartate (NMDA) receptor. Interestingly, i.t. co-administration of the NMDA receptor antagonist D(-)-2-amino-5-phosphonovaleric acid (D-APV) with BDNF dose-dependently inhibits BDNF-induced hyperalgesia, suggesting that BDNF induces acute hyperalgesic responses and affects central sensitization in a process dependent on NMDA receptor activation.