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Individuals exposed to trauma, especially those who develop posttraumatic stress disorder (PTSD), are at a higher risk of suffering from chronic pain as well as altered pain perception and modulation. However, the underlying mechanisms of these processes are yet to be established. Recent findings have indicated that trauma survivors tend to personify chronic pain that is developed after the exposure, in a way that resonates with the traumatic experience. The aim of this study was to test whether pain personification plays a significant role in explaining the long-term links between trauma, PTSD and pain.
Learn More >Previous attempts to develop a pragmatic human model for testing new anti-migraine drugs, have failed. Calcitonin gene-related peptide (CGRP) induces a mild headache in healthy volunteers and migraine-like headache in migraine patients. The induced headache must respond to already established migraine treatment for validation. Thus, the objective of the study was to test the effect of sumatriptan against CGRP-induced symptoms in an attempt to validate CGRP-induced headache as a model for drug testing.
Learn More >Endocannabinoids are showing great promise as effective mediators for controlling joint inflammation and pain. One strategy that could be harnessed to promote endogenous cannabinoid function is to inhibit the enzymatic break down of endocannabinoids locally in the joint. KML29 is an inhibitor of monoacylglycerol lipase (MAGL) activity which has been shown to promote increased 2-arachodonylglycerol (2-AG) levels in the circulation and in peripheral tissues. It is also known that 2-AG can be metabolised via the cyclo-oxygenase-2 (COX-2) pathway leading to the production of pro-inflammatory prostaglandins, which may counteract the effects of 2-AG. Therefore, this study examined the effect of KML29 alone as well as in combination with low-dose celecoxib (CXB) on joint pain and inflammation in the monoiodoacetate (MIA) model of osteoarthritis (OA) pain.
Learn More >This cross-sectional study examined, for the first time, a large cohort of patients with trigeminal neuralgia, to ascertain the occurrence of familial cases, providing a systematic description of clinical features of familial disease. Since there is evidence linking hyperexcitability of trigeminal ganglion neurons to trigeminal neuralgia, we also carried out an exploratory genetic analysis of the neuronal electrogenisome in these patients.
Learn More >Children's experience of chronic pain is influenced by the psychological and behavioural responses of their parents. However, the vast majority of research has been cross-sectional, precluding examination of how these dynamic relationships unfold over time. This study used a micro-longitudinal design to examine the daily relationships between parent mood and protective responses and child chronic pain. We also examined the moderating roles of child and parent pain catastrophizing to determine how the affective-motivational context may alter the influence of parent factors. Participants included 95 youth with idiopathic chronic pain (Mage=14.08; 71.6% female) and their parents. At baseline, parents and youth reported on their catastrophic thinking about child pain. For 7 consecutive days, parents completed daily assessments of their mood and protective responses, while youth completed assessments of their pain intensity, unpleasantness, and interference. Multi-level path analyses were conducted. At a daily level, greater parent protectiveness significantly predicted higher youth pain unpleasantness, interference, and intensity; more negative parent mood significantly predicted higher youth pain intensity and unpleasantness. Higher baseline youth pain catastrophizing predicted a stronger daily association between parent mood and youth pain unpleasantness and intensity. Higher baseline parent pain catastrophizing predicted a weaker daily association between parent protectiveness and youth pain interference. Findings suggest that parent mood and protective responses are dynamic, daily predictors of child pain. Findings also underscore the importance of addressing parents' daily mental health and protectiveness, among youth with chronic pain, and suggest different intervention targets depending on levels of child and parent catastrophizing.
Learn More >N-methyladenosine (mA) modification in RNA has been implicated in diverse biological processes. However, very little is currently known about its role in nociceptive modulation. Here, we found that the level of spinal mA modification was significantly increased in a mouse model of Complete Freund's Adjuvant (CFA)-induced chronic inflammatory pain, which was accompanied with the augmentation of methyltransferase-like 3 (METTL3) expression in the spinal cord. Knockdown of spinal METTL3 prevented and reversed CFA-induced pain behaviors and spinal neuronal sensitization. In contrast, overexpression of spinal METTL3 produced pain behaviors and neuronal sensitization in naive mice. Moreover, we found that METTL3 positively modulated the pri-miR-65-3p processing in a microprocessor protein DiGeorge critical region 8-dependent manner. Collectively, our findings reveal an important role of METTL3-mediated mA modification in nociceptive sensitization and provide a novel perspective on mA modification in the development of pathological pain.
Learn More >Sensory neurons and immune cells share a common microenvironmental niche for surveying tissue integrity. The immune and nervous systems both sense deviations in homeostasis and initiate protective responses and, upon malfunction, also jointly contribute to disease. Barrier tissues are heavily innervated by nociceptors, the sensory neurons that detect noxious stimuli, leading to pain and itch. The same tissues are also home to diverse immune cells that respond to infections and injury. The physical proximity of nociceptors and immune cells allows for direct local interactions between the two, independent of the CNS. We discuss in this study their ligand-receptor-based interactions and propose the need to shift from studying individual neuroimmune interactions to exploring the reciprocal neuroimmune interaction network in its entirety: the "neuroimmune interactome." Identification of the nature of the interactome in health and its plasticity in disease will unravel the functional consequences of interactions between nociceptors and immune cells.
Learn More >Recent research has shown that placebos can be effective even if they are openly prescribed to participants. Yet, it is unclear how such "open-label placebos" (OLPs) compare to deceptive placebo (DP) and what the mechanisms of actions are. In this study, we therefore compared 2 versions of OLP to DP and no treatment (NT).
Learn More >The evolution of peripheral and central changes following a peripheral nerve injury imply the onset of afferent signals that affect the brain. Changes to inflammatory processes may contribute to peripheral and central alterations such as altered psychological state and are not well characterized in humans. We focused on four elements that change peripheral and central nervous systems following ankle injury in 24 adolescent patients and 12 age-sex matched controls. Findings include (a) Changes in tibial, fibular, and sciatic nerve divisions consistent with neurodegeneration; (b) Changes within the primary motor and somatosensory areas as well as higher order brain regions implicated in pain processing; (c) Increased expression of fear of pain and pain reporting; and (d) Significant changes in cytokine profiles relating to neuroinflammatory signaling pathways. Findings address how changes resulting from peripheral nerve injury may develop into chronic neuropathic pain through changes in the peripheral and central nervous system.
Learn More >To review the effect of patient decision aids for adults making treatment decisions regarding the management of chronic musculoskeletal pain.
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