The association of psychosocial factors and exercise‐induced hypoalgesia in healthy people and people with musculoskeletal pain: a systematic review

Background Exercise, a cornerstone in current treatments for people with musculoskeletal pain, elicits a phenomenon called exercise‐induced hypoalgesia (EIH), which may result in reduced pain intensity and/or increased pain thresholds. However, EIH can be impaired in patients with musculoskeletal pain, and psychosocial factors may play a mediating role in EIH. Objective The aim of this study was to systematically review the scientific literature regarding the association between psychosocial factors and EIH in healthy people and people with musculoskeletal pain. Methods An extensive search in databases including Medline Ovid, Embase, Web of Science, PsycINFO Ovid, and the Cumulative Index to Nursing and Allied Health Literature (CINAHL) EBSCOhost was carried out. Two reviewers independently carried out study selection, data extraction, and critical appraisal. Included studies analyzed the association or effect of psychosocial factors on EIH in adults with or without musculoskeletal pain. Results Nine cross‐sectional studies were included, 6 involving healthy people and 4 involving people with musculoskeletal pain; 1 study included both. Overall risk of bias was high. Different types of exercise bouts, psychosocial factors, and/or outcome measures were used across studies. In healthy people and people with musculoskeletal pain, most studies did not find an association between psychosocial factors and EIH. However, 1 study involving musculoskeletal pain and 2 studies with healthy people did find a significant association. Conclusion Due to poor quality and heterogeneity between studies, no conclusions can be drawn regarding whether psychosocial factors are associated with EIH or not. This review includes recommendations and directions for further research to investigate the role of psychosocial factors on EIH

Convergent validity of the central sensitization inventory in chronic whiplash-associated disorders; associations with quantitative sensory testing, pain intensity, fatigue, and psychosocial factors

Objective Central sensitization is present in different pain conditions, including chronic whiplash-associated disorders. In the absence of a gold standard method of assessment to determine the presence of central sensitization, quantitative sensory testing is currently understood as an optimal proxy. Laboratory sensory testing is, however, not feasible in clinical practice, and the Central Sensitization Inventory was developed as an alternative. The aim of the current study was to evaluate the convergent validity of the Central Sensitization Inventory in chronic whiplash-associated patients by determining the association between the Central Sensitization Inventory and quantitative sensory testing, pain intensity, fatigue, and psychosocial factors. Methods A total of 125 chronic whiplash-associated patients completed multiple questionnaires and were subjected to pressure pain thresholds and temporal summation. Results The Central Sensitization Inventory showed a strong association with constructs of general psychopathology, anxiety, distress, depression, and somatization in chronic whiplash-associated disorders. Moderate correlations were found with fatigue and intrusive and avoidant phenomena after a variety of traumatic events. No significant association was found between the Central Sensitization Inventory and pressure pain thresholds and temporal summation, nor between the Central Sensitization Inventory and other pain measurements. Conclusions Overall, we found that the Central Sensitization Inventory is better in identifying the psychosocial factors related to central sensitization in chronic whiplash-associated disorders than the central nervous system adaptations. Thus, the convergent validity of the Central Sensitization Inventory appears to be only partially present in chronic whiplash-associated disorders

The effect of visual feedback of the neck during movement in people with chronic whiplash-associated disorders: an experimental study

Study Design Controlled laboratory study. Background Chronic whiplash-associated disorder (WAD) is an important health issue associated with poor recovery outcomes. Sensorimotor incongruence (SMI), defined as a mismatch between the efference copy in the brain and afferent sensory feedback from the body, is proposed as a possible underlying cause of chronic pain. Objectives To determine whether SMI causes sensory disturbances or pain in people with chronic WAD and healthy controls. Methods Sixty-four participants (30 with chronic WAD and 34 healthy controls) participated in a visual feedback experiment involving the neck and a bimanual coordination experiment involving the arms. In both experimental setups, SMI was induced by modifying the visual feedback during movement. Sensory disturbances and pain were the primary outcomes. Results A statistically significant difference in perceived sensory disturbance between conditions was found in the WAD group (P<.001). Intensity scores were highest for induced SMI, but only for visual feedback of the neck and not for visual feedback of the arms. This effect was not present in the control group (P = .139). Sensorimotor incongruence did not affect pain in either group. Conclusion Persons with chronic WAD are more susceptible to sensory disturbances owing to SMI, and this effect is specific to the region affected by pain. The hypothesis that SMI causes pain was not substantiated by the results of the present study. J Orthop Sports Phys Ther 2017;47(3):190–199. Epub 3 Feb 2017. doi:10.2519/jospt.2017.689

Pain mechanisms in low back pain: a systematic review and meta-analysis of mechanical quantitative sensory testing outcomes in people with non-specific low back pain

Study Design Systematic review and meta-analysis. Background Quantitative mechanical sensory testing (QST) assesses sensory functioning and detects functional changes in (central) nociceptive processing. In the current low back pain literature it has been hypothesized that these functional changes might be apparent in people with non-specific low back pain (NSLBP), although the results are mixed. Objective The aim of this systematic review/meta-analysis was to appraise and summarize the literature about QST outcomes in people with subacute and chronic NSLBP and healthy controls (HC). Methods This systematic review and meta-analysis was reported using PRISMA guidelines. Five databases were searched for relevant literature. Studies comparing mechanical QST-measures involving people with subacute and chronic low back pain and HC were included if 1) pressure pain thresholds (PPTs), 2) temporal summation (TS) and/or 3) conditioned pain modulation (CPM) were reported. Risk of bias was assessed using the Newcastle-Ottawa quality assessment scale (NOS). If possible, the results from different studies were pooled. Results Twenty-four studies were included. NOS scores varied between one and six points. Meta-analysis showed that people with NSLBP, compared to HC have significantly lower PPTs at remote sites and increased TS at the lower back. For example, PPTs measured at the scapula, were significantly lower in patients with NSLBP than in HC (pooled mean difference (MD): 119.2, 95% confidence interval (CI): (91.8, 146.6), P<0.00001. Conclusion This meta-analysis found that overall PPT measurements at remote body parts are significantly lower in the group with NSLBP compared with HC. TS and CPM measurements demonstrated mixed outcomes. Level of Evidence Therapy, level 3a. J Orthop Sports Phys Ther, Epub 23 Aug 2019. doi:10.2519/jospt.2019.887

Exercise-induce hyperalgesia, complement system and elastase activation in myalgic encephalomyelitis/chronic fatigue syndrome : a secondary analysis of experimental comparative studies

Background and aims: The interaction between the immune system and pain has been thoroughly explored in the recent decades. The release of inflammatory mediators from immune cells has the capability of activating neurons and glial cells, in turn sensitizing the nervous system. Both immune system alterations and pain modulation dysfunctions have been shown in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) following exercise. However, no studies tried to explore whether these two phenomena are linked and can explain exercise-induced symptoms worsening in people with ME/CFS. We hypothesized that exercise-induced changes in descending pain modulation is associated to changes in immune system functions. We used complement system product C4a and elastase activity as indicators of immune system activity. Methods: The study design was a secondary analysis of controlled experimental studies. Twenty-two patients with ME/CFS and 22 healthy sedentary controls were enrolled. In experiment 1, subjects performed an aerobic submaximal exercise test; in experiment 2 they underwent a self-paced exercise test. One week of rest period were set between the two exercise tests. Before and after each experiment, subjects underwent clinical assessment, pain thresholds (PPTs) measurement, and blood sampling. Immune system function was assessed measuring complement system C4a products and elastase activity. Results: Changes in elastase activity were not associated to changes in PPTs. Associations were observed in the ME/CFS group between changes in PPTs and C4a products, following both types of exercise. After submaximal exercise, the change in C4a products was associated with the change in PPT at the thumb in patients (r = 0.669, p = 0.001). Similarly, after self-paced exercise the change in C4a products was associated witht the change in PPT at the calf in patients (r = 0.429, p = 0.047). No such correlations were found in healthy controls. Regression analysis showed that C4a changes after the submaximal exercise significantly predicted the change in PPTs (R2 = 0.236; p = 0.02). Conclusions: Moderate associations between exercise-induced changes in PPTs and immune system activity were found only in ME/CFS. The change in the complement system following submaximal exercise might be able to explain part of the change in patient's pain thresholds, providing evidence for a potential link between immune system alteration and dysfunctional endogenous pain modulation. These results have to be taken with caution, as only one out of three measures of PPTs was found associated with C4a changes. We cannot reject the hypothesis that C4a might therefore be a confounding factor, and changes during exercise might be mediated by other mechanism

Cortical mapping of painful electrical stimulation by quantitative electroencephalography: unraveling the time&ndash;frequency&ndash;channel domain

Lisa Goudman,1&ndash;3 Jorne Laton,4 Raf Brouns,4,5 Guy Nagels,4&ndash;6 Eva Huysmans,2,3,7,8 Ronald Buyl,7,9 Kelly Ickmans,2,3,10 Jo Nijs,2,3,10 Maarten Moens,1,2,4,11 1Department of Neurosurgery, Universitair Ziekenhuis Brussel, 2Pain in Motion International Research Group, 3Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education and Physiotherapy, 4Center for Neurosciences (C4N), Vrije Universiteit Brussel (VUB), 5Department of Neurology, Universitair Ziekenhuis Brussel, 6National MS Center, 7Department of Public Health (GEWE), Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, 8Interuniversity Centre for Health Economics Research (I-CHER), 9Department of Biostatistics and Medical Informatics, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, 10Department of Physical Medicine and Physiotherapy, 11Department of Radiology, Universitair Ziekenhuis Brussel, Brussels, Belgium Abstract: The goal of this study was to capture the electroencephalographic signature of experimentally induced pain and pain-modulating mechanisms after painful peripheral electrical stimulation to determine one or a selected group of electrodes at a specific time point with a specific frequency range. In the first experiment, ten healthy participants were exposed to stimulation of the right median nerve while registering brain activity using 32-channel electroencephalography. Electrical stimulations were organized in four blocks of 20 stimuli with four intensities &ndash; 100%, 120%, 140%, and 160% &ndash; of the electrical pain threshold. In the second experiment, 15 healthy participants received electrical stimulation on the dominant median nerve before and during the application of a second painful stimulus. Raw data were converted into the time&ndash;frequency domain by applying a continuous wavelet transform. Separated domain information was extracted by calculating Parafac models. The results demonstrated that it is possible to capture a reproducible cortical neural response after painful electrical stimulation, more specifically at 250 milliseconds poststimulus, at the midline electrodes Cz and FCz with predominant &delta;-oscillations. The signature of the top-down nociceptive inhibitory mechanisms is &delta;-activity at 235 ms poststimulus at the prefrontal electrodes. This study presents a methodology to overcome the a priori determination of the regions of interest to analyze the brain response after painful electrical stimulation. Keywords: electroencephalography, Parafac model, painful electrical stimulation, conditioned pain modulatio

Abnormal pain response to visual feedback during cervical movements in chronic whiplash: an experimental study

Whiplash-associated disorders (WAD) are a debilitating condition. In chronic WAD, sensorimotor incongruence exacerbates symptoms. Sensorimotor incongruence occurs when somatosensory input and predicted motor output are in conflict, which can trigger pain. On the other hand, there is evidence that visual feedback can decrease pain in certain chronic pain conditions. Therefore, the aim of this study was to examine the effect of visual feedback and sensorimotor incongruence on pain thresholds in chronic WAD

In the spine or in the brain?: recent advances in pain neuroscience applied in the intervention for low back pain

Conservative, surgical and pharmacological strategies for chronic low back pain (CLBP) management offer at best modest effect sizes in reducing pain and related disability, indicating a need for improvement. Such improvement may be derived from applying contemporary pain neuroscience to the management of CLBP. Current interventions for people with CLBP are often based entirely on a “biomedical” or “psychological” model without consideration of information concerning underlying pain mechanisms and contemporary pain neuroscience. Here we update readers with our current understanding of pain in people with CLBP, showing that CLBP is not limited to spinal impairments, but is also characterised by brain changes, including functional connectivity reorganisation in several brain regions and increased activation in brain regions of the so-called ‘pain matrix’ (or ‘pain connectome’). Indeed, in a subgroup of the CLBP population brain changes associated with the presence of central sensitisation are seen. Understanding the role of these brain changes in CLBP improves our understanding not only of pain symptoms, but also of prevalent CLBP associated comorbidities such as sleep disturbances and fear avoidance behaviour. Applying contemporary pain neuroscience to improve care for people with CLBP includes identifying relevant pain mechanisms to steer intervention, addressing sleep problems and optimising exercise and activity interventions. This approach includes cognitively preparing patients for exercise therapy using (therapeutic) pain neuroscience education, followed by cognition-targeted functional exercise therapy