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Nocebo hyperalgesia refers to increases in perceived pain that putatively result from negative expectations regarding a nocebo stimulus (eg, an inert treatment, compared with no treatment). The precise cognitive-emotional factors contributing to the origins of nocebo effects are poorly understood. We aimed to test the effects of experimentally induced pain-related fear on the acquisition and extinction of nocebo hyperalgesia in healthy participants (N = 72). Acquisition and extinction of nocebo hyperalgesia were compared between a group receiving standard nocebo conditioning (Control group) and 2 groups receiving distinct fear inductions: high intensity of pain stimulations (High-pain group) or a threat manipulation (High-threat group). During nocebo acquisition, the Control and High-threat groups were administered thermal pain stimulations of moderate intensity paired with sham electrical stimulation (nocebo trials), whereas high pain intensity was administered to the High-pain group. During extinction, equivalent pain intensities were administered across all trials. Pain-related fear was measured by eyeblink startle electromyography and self-report. Nocebo hyperalgesia occurred in all groups. Nocebo effects were significantly larger in the High-pain group than those in the Control group. This effect was mediated by self-reported fear, but not by fear-potentiated startle. Groups did not differ in the extinction rate. However, only the High-pain group maintained significant nocebo responses at the end of extinction. Anticipatory pain-related fear induced through a threat manipulation did not amplify nocebo hyperalgesia. These findings suggest that fear of high pain may be a key contributor to the amplification of nocebo hyperalgesia, only when high pain is experienced and not when it is merely anticipated.
Learn More >Background and aims Few studies have reported the long-term impact of chronic pain on health care utilization. The primary aim of this study was to investigate if chronic musculoskeletal pain was associated with health care utilization in the general population in a 21-year follow-up of a longitudinal cohort. The secondary aim was to identify and describe factors that characterize different long-term trajectories of health care utilization. Methods A prospective cohort design with a baseline sample of 2,425 subjects (aged 20-74). Data were collected by self-reported questionnaires, and three time points (1995, 2007, and 2016) were included in the present 21-year follow up study. Data on health care utilization were dichotomized at each time point to either high or low health care utilization. High utilization was defined as >5 consultations with at least one health care provider, or ≥1 consultation with at least 3 different health care providers during the last 12 months. Low health care utilization was defined as ≤5 consultations with one health care provider and <3 consultations with different health care providers. The associations between baseline variables and health care utilization in 2016 were analyzed by multiple logistic regression. Five different trajectories for health care utilization were identified by visual analysis, whereof four of clinical relevance were included in the analyses. Results Baseline predictors for high health care utilization at the 21-year follow-up in 2016 were chronic widespread pain (OR: 3.2, CI: 1.9-5.1), chronic regional pain (OR:1.8, CI: 1.2-2.6), female gender (OR: 2.0, CI: 1.4-3.0), and high age (OR: 1.6, CI:0.9-2.9). A stable high health care utilization trajectory group was characterized by high levels of health care utilization, and a high prevalence of chronic pain at baseline and female gender (n = 23). A stable low health care utilization trajectory group (n = 744) was characterized by low health care utilization, and low prevalence of chronic pain at baseline. The two remaining trajectories were: increasing trajectory group (n = 108), characterized by increasing health care utilization, chronic pain at baseline and female gender, and decreasing trajectory group (n = 107) characterized by decreasing health care utilization despite a stable high prevalence of chronic pain over time. Conclusions The results suggest that chronic pain is related to long-term health care utilization in the general population. Stable high health care utilization was identified among a group characterized by female gender and a report of chronic widespread pain. Implications This cohort study revealed that chronic widespread pain predicted high health care utilization over a 21-year follow-up period. The results indicate the importance of early identification of musculoskeletal pain to improve the management of pain in the long run.
Learn More >Background and aims Evidence for analgesic effects of oral alcohol consumption on heat pain has recently been documented in a placebo-controlled, randomized and double-blind design. We aimed at further investigating these effects and now set the focus on pain threshold and the ratings of supra-threshold pain to cover most of the pain range. Moreover, we now firstly evaluated sex differences in these effects. Methods We investigated 41 healthy participants (22 females) in a randomized, double-blind and placebo-controlled design and targeted two different moderate breath-alcohol levels of 0.06% and 0.08%. Before and after an alcoholic or placebo drink, contact heat was applied at the forearm. Subjects evaluated pain threshold (method of adjustment) and rated pain intensity and pain unpleasantness of supra-threshold stimuli (intensity: threshold +3 °C; duration: 5 s). Results Analgesic effects taking the form of increased pain thresholds were found after both alcohol doses, surprisingly with more pronounced effects for the lower dose. While the high alcohol dose exerted small analgesic effects on pain intensity ratings (i.e. decrease), slightly increased ratings of pain intensity and pain unpleasantness after the low alcohol dose rather suggest pain enhancement. Alcohol did not affect intensity vs. unpleasantness ratings differentially. We found no evidence for sex differences in any of these effects. Conclusions Overall, acute alcohol effects on pain were subtle. Our findings suggest that while low alcohol doses already exert analgesic effects on pain threshold, stronger doses are required for pain reduction on supra-threshold pain levels. Furthermore, sex differences could not be detected within our experimental paradigm but should be further explored in future research. Implications Analgesic effects of sub-toxic alcohol doses – as normally occurring during social drinking – might be weak; however, susceptibility to pain relieving effects of alcohol might be a risk factor for the use of alcohol as self-medication in acute pain states.
Learn More >Rheumatoid arthritis (RA) is characterized by chronic inflammation of the synovial tissue, joint dysfunction, and damage. Epoxyeicosatrienoic acids (EETs) are endogenous anti-inflammatory compounds, which are quickly converted by the soluble epoxide hydrolase (sEH) enzyme into a less active form with decreased biological effects. The inhibition of the sEH enzyme has been used as a strategy to lower nociception and inflammation. The goal of this study was to investigate whether the peripheral treatment with the sEH enzyme inhibitor 1- trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU) could prevent the hypernociception and inflammation in the albumin-induced arthritis model in rats' temporomandibular joint (TMJ). After the induction of experimental arthritis, animals were assessed for nociceptive behavior test, leukocyte infiltration counts and histologic analysis, ELISA to quantify several cytokines and Western blotting. The peripheral pretreatment with TPPU inhibited the arthritis-induced TMJ hypernociception and leukocyte migration. Moreover, the local concentrations of proinflammatory cytokines were diminished by TPPU, while the anti-inflammatory cytokine interleukin-10 was up-regulated in the TMJ tissue. Finally, TPPU significantly decreased protein expression of iNOS, while did not alter the expression of MRC1. This study provides evidence that the peripheral administration of TPPU reduces hypernociception and inflammation in TMJ experimental arthritis.
Learn More >Occipital nerve stimulation (ONS) is shown to be effective in treating various forms of headache. Most studies describe the treatment of occipital neuralgia (ON), but in many patients, the clinical description could also correspond to cervicogenic headache (CGH) or occipital migraine (OM). These different entities (ON, CGH, and OM) may be grouped together under the term occipital headaches.
Learn More >The external validity of randomized controlled trials (RCTs) is critical for the relevance of trial results in a clinical setting. We aimed to assess the external validity of RCTs investigating postoperative pain treatment after total hip and knee arthroplasty (THA and TKA) by comparing patient characteristics in these trials with a clinical cohort. Further, we assessed the use of exclusion criteria of the included RCTs.
Learn More >Medical cannabis (MC) is currently being used as an adjunct to opiates given its analgesic effects and potential to reduce opiate addiction. This review assessed if MC used in combination with opioids to treat non-cancer chronic pain would reduce opioid dosage.
Learn More >Neuropathic pain is related to the sustained activation of neuroglial cells and the production of proinflammatory cytokines in the spinal dorsal horn. However, the clinical efficacy of currently available treatments is very limited. The transcription factor nuclear factor κB (NF-κB) is a ubiquitously expressed protein family and considered to be crucial in autoimmunity. Thus, our study aimed to examine the influence of NF-κB p65 in chronic constriction injury (CCI)-induced neuropathic pain as well as its underlying mechanism.
Learn More >Post-traumatic headache (PTH) is one of the most frequent symptoms following mild traumatic brain injury (mTBI). Neuroimaging studies implicate hypothalamic function connectivity (FC) disruption as an important factor in pain disorders. However, it is unknown whether there are alterations in the hypothalamus-based resting state FC within PTH following mTBI at the acute stage and its relationship with headache symptom measurement.
Learn More >Clinical trials are a key component of the evidence base for the treatment of headache disorders. In 1991, the International Headache Society Clinical Trials Standing Committee developed and published the first edition of the . Advances in drugs, devices, and biologicals, as well as novel trial designs, have prompted several updates over the nearly 30 years since, including most recently the (2018), the (2019), and (2019). The present update incorporates findings from new research and is intended to optimize the design of controlled trials of preventive pharmacological treatment of episodic migraine in adults. A guideline for clinical trials with devices will be published separately.
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