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Background: The biopsychosocial-spiritual model recognizes the impact of religious factors in modulating the experience of pain. Religious beliefs are factors that can influence perceptions, emotions, and behavior, all of which have important implications on health, pain experience, and treatment outcomes., Objectives: The aim of the present study was to identify if and how religious beliefs and attitudes can influence pain intensity, pain interference, pain-related beliefs and cognitions, emotions, and coping among patients with chronic musculoskeletal pain., Study Design: Systematic review., Methods: This systematic review was conducted and reported, following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines (PRISMA). An electronic search was conducted in 4 online databases (PubMed, Embase, Web of science, and PsychArticles) and complemented with a hand search (PROSPERO registry: CRD42020161289). Two reviewers independently performed eligibility screening, risk of bias assessment, and data extraction. The risk of bias of the included studies was assessed using the Newcastle Ottawa Scale., Results: Nine cross-sectional studies and one case-control study were included in the review. The methodological quality of the included studies ranged from low to high. The results gathered regarding the association between religiosity and pain intensity, disability, or pain interference were found to be conflicting. Limited evidence suggests that religiosity is positively associated with worse pain-related beliefs and cognitions, worse pain-related emotion, and better pain acceptance. There is insufficient data available to support the claim that religiosity is negatively associated with physical functioning and pain-related self-efficacy in people with chronic musculoskeletal pain., Limitations: The number of included studies was small, with a low level of evidence, and a possible risk of bias., Conclusion: This systematic review shows low evidence and conflicting results for the presence of associations between religiosity and different pain domains such as pain intensity, disability, and pain-related cognitions or emotions in people with chronic musculoskeletal pain.

Background: Pain can be influenced by several factors, including stress. Stress can have various reactions on pain. These reactions are influenced by several internal factors such as gender, age, and experience with stress or pain., Objectives: To determine the effect of acute stress on mechanical hyperalgesia (with pressure pain thresholds [PPT]), endogenous pain facilitation (measured by temporal summation [TS]), and inhibition (measured by conditioned pain modulation [CPM]) in healthy people and to determine which factors are responsible for this stress result., Study Design: Pre-posttest design., Setting: Healthy volunteers from Belgium., Methods: One hundred and one healthy pain-free patients underwent a modified Trier Social Stress Test. Prior and following the stress manipulation, PPT, TS, and CPM efficacy were determined in the mm. trapezius and quadriceps and overall. Furthermore, possible explanatory factors, such as fear of pain, pain catastrophizing, pain hypervigilance, and daily activity levels, were assessed using questionnaires., Results: We found a significant stress result on widespread pain sensitivity, with an increase of PPT (P < 0.001), unchanged TS (P > 0.05), and a decrease in CPM efficacy (P < 0.001). Factors associated with the stress result were age, previous surgery, attentional focus on the conditioning stimulus during CPM, fear of pain, and daily activity levels., Limitations: The efficacy of the stress manipulation was not examined, and the lack of a control group prevented to examine a real stress-effect. Furthermore, no physiologic parameters were measured as possibly influencing internal factors for the stress-result., Conclusions: The increase in PPT was not a clinically significant change, whereas the decrease in CPM was meaningful. None of the factors predicted the stress result in all experimental pain measurements, and the predictions that were observed only explained a small proportion of the observed effects.

Background: Offset analgesia (OA) is an increasingly described phenomenon to measure endogenous pain inhibition, in which a greater decrease in pain intensity is experienced than would be predicted by the decrease in painful stimulation. The temporal filtering in this OA phenomenon differs from the spatial filtering in the commonly described conditioned pain modulation (CPM). Yet, the knowledge on the efficacy of OA in chronic pain patients is scarce, compared to CPM efficacy., Objective: This systematic review has been conducted to provide an overview of the current knowledge regarding OA, and to compare it to CPM., Study Design: A systematic review of research studies that investigated the application or mechanisms of OA., Setting: The present study took place at Ghent University and the University of Antwerp., Methods: This systematic review follows the PRISMA guidelines. The electronic databases Pubmed and Web of Science were searched in January 2015. Full text clinical reports addressing OA were included. The checklists for randomized controlled trials, case-control studies, and cohort-studies provided by the Dutch Institute for Healthcare Improvement and the Dutch Cochrane Centre were used to assess methodological quality. The articles received a level of evidence A1, A2, B, C, or D, based on study design and risk of bias. These levels were used to determine the strength of conclusion (level 1 to 4)., Results: Seventeen articles met the inclusion criteria. Sixteen studies used quantitative sensory testing to provoke OA; however, differences in protocols are present. OA can function as a non-opioid mediated assessment tool for endogenous pain inhibition, and activates brain regions such as periaqueductal gray (PAG), dorsolateral prefontral cortex, insula, medulla, pons and cerebellum, indicating strong brain derived pain modulation. The primary somatosensory cortex is, conversely, less activated during OA. OA is decreased in neuropathic patients. Nonetheless, evidence for the influence of individual factors on OA is limited. OA and CPM seem to rely on different mechanisms., Limitations: Search strategy was taken wide, wherefore a large variety of research perspectives were included., Conclusions: This systematic review displays OA as a temporal filtering mechanisms that is more brain-derived compared to the spatial assessment method CPM. There is strong evidence for reduced OA in neuropathic patients, however, evidence regarding OA in (sub)acute and central sensitization patients, and the influence of personal factors on OA is currently scarce and needs further investigation.

Background: Compelling evidence has demonstrated that impaired central pain modulation contributes to persistent pain in patients with chronic whiplash associated disorders (WAD) and fibromyalgia (FM). However, there is limited research concerning the influence of stress and relaxation on central pain modulation in patients with chronic WAD and FM., Objectives: The present study aims to investigate the effects of acute cognitive stress and relaxation on central pain modulation in chronic WAD and FM patients compared to healthy individuals., Study Design: A randomized crossover design was employed., Setting: The present study took place at the University of Brussels, the University Hospital Brussels, and the University of Antwerp., Methods: Fifty-nine participants (16 chronic WAD patients, 21 FM, 22 pain-free controls) were enrolled and subjected to various pain measurements. Temporal summation (TS) of pain and conditioned pain modulation (CPM) were evaluated. Subsequently, participants were randomly allocated to either a group that received progressive relaxation therapy or a group that performed a battery of cognitive tests (= cognitive stressor). Afterwards, all pain measurements were repeated. One week later participant groups were switched., Results: A significant difference was found between the groups in the change in TS in response to relaxation (P = 0.008) and cognitive stress (P = 0.003). TS decreased in response to relaxation and cognitive stress in chronic WAD patients and controls. In contrast, TS increased after both interventions in FM patients. CPM efficacy decreased in all 3 groups in response to relaxation (P = 0.002) and cognitive stress (P = 0.001)., Limitations: The obtained results only apply for a single session of muscle relaxation therapy and cognitive stress, whereby no conclusions can be made for effects on pain perception and modulation of chronic cognitive stress and long-term relaxation therapies., Conclusions: A single relaxation session as well as cognitive stress may have negative acute effects on pain modulation in patients with FM, while cognitive stress and relaxation did not worsen bottom-up sensitization in chronic WAD patients and healthy persons. However, endogenous pain inhibition, assessed using a CPM paradigm, worsened in chronic WAD and FM patients, as well as in healthy people following both interventions.

Background: The awareness is growing that central sensitization is of prime importance for the assessment and management of chronic pain, but its classification is challenging clinically since no gold standard method of assessment exists., Objectives: Designing the first set of classification criteria for the classification of central sensitization pain., Methods: A body of evidence from original research papers was used by 18 pain experts from 7 different countries to design the first classification criteria for central sensitization pain., Results: It is proposed that the classification of central sensitization pain entails 2 major steps: the exclusion of neuropathic pain and the differential classification of nociceptive versus central sensitization pain. For the former, the International Association for the Study of Pain diagnostic criteria are available for diagnosing or excluding neuropathic pain. For the latter, clinicians are advised to screen their patients for 3 major classification criteria, and use them to complete the classification algorithm for each individual patient with chronic pain. The first and obligatory criterion entails disproportionate pain, implying that the severity of pain and related reported or perceived disability are disproportionate to the nature and extent of injury or pathology (i.e., tissue damage or structural impairments). The 2 remaining criteria are 1) the presence of diffuse pain distribution, allodynia, and hyperalgesia; and 2) hypersensitivity of senses unrelated to the musculoskeletal system (defined as a score of at least 40 on the Central Sensitization Inventory)., Limitations: Although based on direct and indirect research findings, the classification algorithm requires experimental testing in future studies., Conclusion: Clinicians can use the proposed classification algorithm for differentiating neuropathic, nociceptive, and central sensitization pain.

Background: Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis, and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established (i.e. evidence based), it is currently unclear whether exercise has positive effects on the processes involved in chronic pain (e.g. central pain modulation)., Objectives: Reviewing the available evidence addressing the effects of exercise on central pain modulation in patients with chronic pain., Methods: Narrative review., Results: Exercise activates endogenous analgesia in healthy individuals. The increased pain threshold following exercise is due to the release of endogenous opioids and activation of (supra)spinal nociceptive inhibitory mechanisms orchestrated by the brain. Exercise triggers the release of beta-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively. The hypothalamus, through its projections on the periaqueductal grey, has the capacity to activate descending nociceptive inhibitory mechanisms. However, several groups have shown dysfunctioning of endogenous analgesia in response to exercise in patients with chronic pain. Muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalised pain sensitivity in fibromyalgia patients. In patients having local muscular pain (e.g. shoulder myalgia), exercising non-painful muscles activates generalized endogenous analgesia. However, exercising painful muscles does not change pain sensitivity either in the exercising muscle or at distant locations., Limitations: The reviewed studies examined acute effects of exercise rather than long-term effects of exercise therapy., Conclusions: A dysfunctional response of patients with chronic pain and aberrations in central pain modulation to exercise has been shown, indicating that exercise therapy should be individually tailored with emphasis on prevention of symptom flares. The paper discusses the translation of these findings to rehabilitation practice together with future research avenues.