Pain
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Migraine is the third most common disease in the world (behind dental caries and tension-type headache) with an estimated global prevalence of 15%, yet its etiology remains poorly understood. Recent clinical trials have heralded the potential of therapeutic antibodies that block the actions of the neuropeptide calcitonin gene-related peptide (CGRP) or its receptor to prevent migraine. Calcitonin gene-related peptide is believed to contribute to trigeminal nerve hypersensitivity and photosensitivity in migraine, but a direct role in pain associated with migraine has not been established. ⋯ However, the nonsteroidal anti-inflammatory drug meloxicam failed to block the effect of CGRP. Interestingly, an apparent sex-specific response to treatment was observed with the antimigraine drug sumatriptan partially blocking the CGRP response in male, but not female mice. These results demonstrate that CGRP can induce spontaneous pain, even in the absence of light, and that the squint response provides an objective biomarker for CGRP-induced pain that is translatable to humans.
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We aimed to examine the effects of contextual factors (ie, observers' training background and priming texts) on decoding facial pain expressions of younger and older adults. A total of 165 participants (82 nursing students and 83 nonhealth professionals) were randomly assigned to one of 3 priming conditions: (1) information about the possibility of secondary gain (misuse); (2) information about the frequency and undertreatment of pain in the older adult (undertreatment); or (3) neutral information (control). Subsequently, participants viewed 8 videos of older adults and 8 videos of younger adults undergoing a discomforting physical therapy examination. ⋯ By contrast, priming observers with the misuse text attenuated their valence ratings towards younger patients. Finally, the undertreatment prime influenced observers' pain estimates indirectly through observers' valence towards patients. In summary, results add specificity to the theoretical formulations of pain by demonstrating the influence of patient and observer characteristics, as well as informational primes, on decoding pain expressions.
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Ongoing pain has been linked to ongoing activity (OA) in human C-fiber nociceptors, but rodent models of pain-related OA have concentrated on allodynia rather than ongoing pain, and on OA generated in non-nociceptive Aβ fibers rather than C-fiber nociceptors. Little is known about how ongoing pain or nociceptor OA is generated. To define neurophysiological alterations underlying nociceptor OA, we have used isolated dorsal root ganglion neurons that continue to generate OA after removal from animals displaying ongoing pain. ⋯ Can DSFs also be enhanced acutely to promote OA in neurons from uninjured animals? A low dose of serotonin failed to change resting membrane potential but lowered action potential threshold. When combined with artificial depolarization to model inflammation, serotonin also strongly potentiated DSFs and OA. These findings reveal nociceptor specializations for generating OA that may promote ongoing pain in chronic and acute conditions.