Pain
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Following nociceptive heat or laser stimulation, an early contralateral and later vertex potential can be recorded. Although more indicative of the nociceptive input, the acquisition of the contralateral N1 after contact heat stimulation (contact heat-evoked potentials [CHEPs]) remains difficult. An advantage of contact heat is that the baseline skin temperature preceding peak stimulation can be controlled. ⋯ Based on standard averaging, N2/P2 amplitudes were also significantly increased with and without an accompanying change in the rating of perceived pain when the baseline temperature was increased (P<.05). In contrast, automated single-trial averaging revealed no significant difference in N2 amplitude when the baseline temperature was increased to 42°C and the peak temperature reduced. These findings suggest that 2 mechanisms underlie the improved acquisition of CHEPs: increased synchronization of afferent volley, yielding larger-amplitude evoked potentials in response to the same rating of intensity; and reduced inter-trial variability.
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Recent evidence indicates that pain-related fear can be acquired through associative learning. In the clinic, however, spreading of fear and avoidance is observed beyond movements/activities that were associated with pain during the original pain episode. One mechanism accounting for this spreading of fear is stimulus generalization. ⋯ These data illustrate that spreading of pain-related fear is fostered by previously acquired movement-pain contingencies. Based on recent advances in anxiety research, we proposed an innovative approach conceptualizing predictable pain as a laboratory model for fear of movement in regional musculoskeletal pain, and unpredictable pain generating contextual pain-related fear as a prototype of widespread musculoskeletal pain. Consequently, fear generalization might play an important role in spreading of pain-related fear and avoidance behavior in regional and widespread musculoskeletal pain.
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Crossing the hands over the midline impairs the ability to correctly judge the order of a pair of tactile stimuli, delivered in rapid succession, one to each hand. This impairment, termed crossed-hands deficit, has been attributed to a mismatch between the somatotopic and body-centred frames of reference, onto which somatosensory stimuli are automatically mapped. ⋯ We observed that crossing the hands over the midline significantly decreases the ability to determine the stimulus order when a pair of nociceptive stimuli is delivered to the hands, and that this crossed-hands deficit has a temporal profile similar to that observed for tactile stimuli. These findings suggest that similar mechanisms for integrating somatotopic and body-centred frames of reference underlie the ability to localise both nociceptive and tactile stimuli in space.
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Inflammatory pain severely affects the quality of life of millions of individuals worldwide. Prostaglandin E2 (PGE2), a pain mediator enriched in inflamed tissues, plays a pivotal role in nociceptor sensitization and in the genesis of inflammatory pain. Its EP4 receptor mainly mediates its role in inflammatory pain. ⋯ Intraplantar injection of complete Freud's adjuvant increases both total and cell-surface EP4 levels of L4-6 DRG neurons, an event suppressed by a cyclooxygenase-2 inhibitor or a selective EP4 antagonist, suggesting that PGE2/EP4 signalling in inflamed paw contributes to EP4 synthesis and export in DRG neurons, thus sensitizing nociceptors during inflammation. We conclude that PGE2/EP4 signalling-induced EP4 externalization in DRG neuron is a novel mechanism underlying nociceptor sensitization and inflammatory pain. Blocking EP4 externalization could open a novel therapeutic avenue to treat inflammatory pain.