Pain
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Placebo effects can act as powerful pain relievers. Although the ethics of therapeutic placebo use are highly controversial, recent evidence suggests that medical providers frequently utilize placebo treatments and patients may be open to these interventions in certain contexts. This investigation used a patient-centered approach to answer essential questions about placebo treatment acceptability. ⋯ Also, an analgesic placebo response mitigated the negative consequences of deception by improving provider trust and decreasing negative mood. These findings suggest that, contrary to popular belief, patients may be rather pragmatic in their appraisals of placebo treatment acceptability, and may consider a variety of treatments/contexts as ethically permissible for managing their pain. This is the first study of its kind to quantify perceptions of placebo analgesia knowledge and efficacy among individuals with chronic pain, and to assess the role of different medical contexts in treatment acceptability.
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Activity pacing is a widely used self-management strategy, but we lack a clear understanding of its nature and usefulness. One source of confusion is a lack of clarity about the use of pacing in everyday life (ie, naturalistic pacing) in people not trained on how to pace activities. It is unknown whether people engage in more pacing when pain is high (pain-contingent) or when fatigue is high (fatigue-contingent). ⋯ Contrary to our hypothesis, increased pacing was associated with higher subsequent levels of pain and fatigue. Naturalistic pacing seems symptom-contingent and not reinforced by symptom reduction. Naturalistic pacing may be distinct from trained or programmatic pacing in terms of outcomes, and further research into naturalistic pacing may provide an important foundation for how best to deliver activity pacing interventions.
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Two-pore domain background K(+) channels (K2p or KCNK) produce hyperpolarizing currents that control cell membrane polarity and neuronal excitability throughout the nervous system. The TREK2 channel as well as the related TREK1 and TRAAK channels are mechanical-, thermal- and lipid-gated channels that share many regulatory properties. TREK2 is one of the major background channels expressed in rodent nociceptive neurons of the dorsal root ganglia that innervate the skin and deep body tissues, but its role in somatosensory perception and nociception has remained poorly understood. ⋯ TREK2 is also involved in mechanical pain perception and in osmotic pain after sensitization by prostaglandin E2. TREK2 is involved in the cold allodynia that characterizes the neuropathy commonly associated with treatments with the anticancer drug oxaliplatin. These results suggest that positive modulation of the TREK2 channel may have beneficial analgesic effects in these neuropathic conditions.
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Fast Conducting Mechanoreceptors Contribute to Withdrawal Behavior in Normal and Nerve Injured Rats.
Fast-conducting myelinated high-threshold mechanoreceptors (AHTMR) are largely thought to transmit acute nociception from the periphery. However, their roles in normal withdrawal and in nerve injury-induced hyperalgesia are less well accepted. Modulation of this subpopulation of peripheral neurons would help define their roles in withdrawal behaviors. ⋯ This suggests that AHTMR neurons play a role not only in threshold-related withdrawal behavior in the normal animal, but also in sensitized states after nerve injury. This is the first time this subpopulation of neurons has been reversibly modulated to test their contribution to withdrawal-related behaviors before and after nerve injury. This technique may prove useful to define the role of selective neuronal populations in different pain states.
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Endometriosis, the most common cause of chronic pelvic pain, is an estrogen-dependent disease in which classic estrogen receptors (ERα, ERβ) play an important role. Although recent evidence suggests that the novel G protein-coupled estrogen receptor (GPR30) also plays a key role in the progression of endometriosis, whether it is also involved in endometriosis pain is still unknown. Here we tested the hypothesis that GPR30 expressed by nociceptors contributes to endometriosis pain. ⋯ Finally, intralesional injection of the GPR30 antagonist G-36 also inhibited the mechanical hyperalgesia at the site of ectopic uterine tissue. We conclude that local GPR30 agonists produce persistent mechanical hyperalgesia in naive female rats, whereas local GPR30 antagonists inhibit mechanical hyperalgesia in a model of endometriosis pain. Thus, GPR30 expressed by nociceptors innervating ectopic uterine lesions might play a major role in endometriosis pain.