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This study examined whether a modified version of biofeedback (ie, Conditioned Biofeedback) that incorporated placebo analgesia-like manipulations could promote anti-nociception in healthy, pain-free participants. During Conditioned Biofeedback (n=28), sympathetic arousal level was displayed visually and participants were asked to reduce it while they received painful electric stimulations that were surreptitiously controlled by their arousal level. Thus, electric pain decreased as arousal decreased to associate successful arousal-reduction/relaxation with pain relief, and to promote expectations for future pain relief. A Biofeedback Only group (n=24) controlled for the general effects of biofeedback/relaxation. A Biofeedback+Shock group (n=21) controlled for the effects of practicing biofeedback during painful shocks. Nociceptive flexion reflex (NFR) threshold and temporal summation of pain (TS-pain) were used to assess changes in spinal nociception and pain facilitation, respectively. Results indicated all groups showed pre- to post-biofeedback increases in NFR threshold, but only the Conditioned Biofeedback group showed pre- to post-biofeedback reductions in TS-pain. Moreover, Conditioned Biofeedback resulted in a persistent (pre-biofeedback) increase in NFR threshold across sessions, whereas Biofeedback Only resulted in a persistent (pre-biofeedback) decrease in TS-pain. In sum, Conditioned Biofeedback may promote anti-nociception in healthy participants thus reducing risk for chronic pain. The study was registered prospectively on ClinicalTrials.gov (TU1560). PERSPECTIVE: A modified version of biofeedback that employs placebo analgesia manipulations was successful in increasing descending inhibition and reducing pain facilitation in healthy volunteers. As a result, it may be an effective means of reducing risk of future chronic pain onset by promoting an anti-nociceptive pain profile.
Learn More >Opioid-induced hyperalgesia (OIH) is a phenomenon whereby opioids increase patients' pain sensitivity, complicating their use in analgesia. We explored practitioners' attitudes towards, and knowledge concerning diagnosis, risk factors, and treatment of OIH.
Learn More >Endogenous Pain Modulation (EPM) impairment is a significant contributor to chronic pain. Conditioned pain modulation (CPM) testing assesses EPM function. Osteoarthritic (OA) dogs are good translational models, but CPM has not been explored. Our aim was to assess EPM impairment in OA dogs compared to controls using CPM. We hypothesized that CPM testing would demonstrate EPM impairment in OA dogs compared to controls. Dogs with stifle/hip OA and demographically-matched controls were recruited. The pre-conditioning test stimulus, using mechanical/thermal quantitative sensory testing (MQST or TQST), were performed at the metatarsus. A 22N blunt probe (conditioning stimulus) was applied to the contralateral antebrachium for 2 minutes, followed by MQST or TQST (post-conditioning test stimulus). The threshold changes from pre to post-conditioning (∆MQST and ∆TQST) were compared between OA and control dogs. Twenty-four client-owned dogs (OA, n = 11; controls, n = 13) were recruited. The ∆MQST(p < 0.001) and ∆TQST(p < 0.001) increased in control dogs but not OA dogs (∆MQST p = 0.65; ∆TQST p = 0.76). Both ∆MQST(p < 0.001) and ∆TQST(p < 0.001) were different between the OA and control groups. These are the first data showing that EPM impairment is associated with canine OA pain. The spontaneous OA dog model may be used to test drugs that normalize EPM function.
Learn More >The legalization of cannabis in some states has intensified interest in the potential for cannabis and its constituents to lead to novel therapeutics for pain. Our understanding of the cellular mechanisms underlying cannabinoid actions in the brain have lagged behind opioids; however, the current opioid epidemic has also increased attention on the use of cannabinoids as alternatives to opioids for pain, especially chronic pain that requires long-term use. Endogenous cannabinoids are lipid signaling molecules that have complex roles in modulating neuronal function throughout the brain. In this review, we discuss cannabinoid functions in the descending pain modulatory pathway, a brain circuit that integrates cognitive and emotional processing of pain to modulate incoming sensory inputs. In addition, we highlight areas where further studies are necessary to understand cannabinoid regulation of descending pain modulation.
Learn More >Treating neuropathic pain is challenging and novel non-opioid based medicines are needed. Using unbiased receptomics, transcriptomic analyses, immunofluorescence and in situ hybridization, we found the expression of the orphan GPCR (oGPCR) Gpr160 and GPR160 increased in the rodent dorsal horn of the spinal cord (DH-SC) following traumatic nerve injury. Genetic and immunopharmacological approaches demonstrated that GPR160 inhibition in the spinal cord prevented and reversed neuropathic pain in male and female rodents without altering normal pain response. GPR160 inhibition in the spinal cord attenuated sensory processing in the thalamus, a key relay in the sensory discriminative pathways of pain. We also identified cocaine- and amphetamine-regulated transcript peptide (CARTp) as a GPR160 ligand. Inhibiting endogenous CARTp signaling in spinal cord attenuated neuropathic pain, whereas exogenous intrathecal (i.th.) CARTp evoked painful hypersensitivity through GPR160-dependent ERK and cAMP response element-binding protein (CREB). Our findings de-orphanize GPR160, identify it as a determinant of neuropathic pain and potential therapeutic target, and provide insights to its signaling pathways. CARTp is involved in many diseases including depression, reward and addiction, de-orphanization of GPR160 is a major step forward understanding the role of CARTp signaling in health and disease.
Learn More >Chronic inflammation increases the production of cytokines and activates pro-inflammatory pathways which may lead to non-specific low back pain (LBP). We systematically reviewed the literature to investigate whether inflammatory biomarkers are associated with non-specific LBP.
Learn More >The transient receptor potential (TRP) ion channel TRPM3 functions as a noxious heat sensor and plays a key role in acute pain sensation and inflammatory hyperalgesia in rodents. Despite its potential as novel analgesic drug target, little is known about the expression, function and modulation of TRPM3 in the human somatosensory system.
Learn More >Scientific progress requires transparency and openness. The ability to critique, replicate and implement scientific findings depends on the transparency of the study design and methods, and the open availability of study materials, data and code. Journals are key stakeholders in supporting transparency and openness. This study aimed to evaluate 10 highest ranked pain journals' authorship policies with respect to their support for transparent and open research practices. Two independent authors evaluated the journal policies (as at 27 May 2019) using three tools: the self-developed Transparency and Openness Evaluation Tool, the Centre for Open Science (COS) Transparency Factor and the International Committee of Medical Journal Editors (ICMJE) requirements for disclosure of conflicts of interest. We found that the journal policies had an overall low level of engagement with research transparency and openness standards. The median COS Transparency Factor score was 3.5 (IQR 2.8) of 29 possible points, and only 7 of 10 journals' stated requirements for disclosure of conflicts of interest aligned fully with the ICMJE recommendations. Improved transparency and openness of pain research has the potential to benefit all that are involved in generating and using research findings. Journal policies that endorse and facilitate transparent and open research practices will ultimately improve the evidence base that informs the care provided for people with pain.
Learn More >Irritable bowel syndrome (IBS) is a common functional disease characterized by chronic abdominal pain and changes in bowel movements. Effective therapy for visceral hypersensitivity in IBS patients remains challenging. This study investigated the roles of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) and the effect of ANA-12 (a selective antagonist of TrkB) on chronic visceral hypersensitivity in an IBS-like rat model.
Learn More >The major symptoms of irritable bowel syndrome (IBS) are changes in bowel habits and abdominal pain. Psychological stress is the major pathophysiological components of IBS. Corticotropin-releasing factor (CRF) is a well-known integrator in response to psychological stress. In this study, a novel CRF1 receptor antagonist T-3047928 was evaluated in stress-induced IBS models of rats to explore its potency for IBS.
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