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Background: Pain neuroscience education (PNE) has received increasing research attention demonstrating beneficial effects on pain‐related outcomes in adults. Conversely, studies on the effectiveness of PNE in children are scarce. Methods: This study investigated the effect of a pain educational video intervention on child pain‐related outcomes (i.e. experienced pain intensity, pain‐related fear and catastrophic worry about pain, pain threshold and pain knowledge) in healthy children undergoing an experimental pain task. Furthermore, the moderating role of children's demographic (i.e. sex and age) and psychological (i.e. baseline pain knowledge and anticipated pain intensity, pain‐related fear and catastrophic worry) characteristics was examined. Participants were 89 children (Mage = 11.85, SD = 1.78), randomly assigned to either a condition whereby they were instructed to watch a brief pain educational video (i.e. experimental group) or to a control condition whereby they did not watch any video. Results: Study findings revealed that accurate pain knowledge and pain threshold were higher amongst children in the experimental group compared to the control group. In contrast with expectations, no main effects of the video intervention were observed for experienced pain intensity, pain‐related fear and catastrophic worry. Moderation analyses indicated that the video intervention contributed, in comparison with the control condition, to higher levels of pain knowledge amongst younger children only and to higher pain thresholds amongst boys only. Conclusions: Further investigation is needed to optimize pain educational video interventions and to determine whether more beneficial outcomes can be found in clinical (i.e. non‐experimental) situations and in children with persistent or recurring pain problems. Significance: Examining the impact of pain educational interventions within a non‐clinical setting is deemed particularly important given that adaptive pain coping strategies likely play an important role in preventing the development and maintenance of future maladaptive pain‐related behaviour. Further, study findings provide preliminary evidence of baseline and demographic (i.e. age and sex) characteristics explaining differences in the effect of a pain educational video intervention in pain knowledge and pain‐related experiences during experimental pain. [ABSTRACT FROM AUTHOR]

Objective: The epigenetics of neurotrophic factors holds the potential to unravel the mechanisms underlying the pathophysiology of complex conditions such as chronic fatigue syndrome (CFS). This study was undertaken to explore the role of brain‐derived neurotrophic factor (BDNF) genetics, epigenetics, and protein expression in patients with both CFS and comorbid fibromyalgia (CFS/FM). Methods: A repeated‐measures study was conducted in 54 participants (28 patients with CFS/FM and 26 matched healthy controls). Participants underwent a comprehensive assessment, including questionnaires, sensory testing, and blood withdrawal. Serum BDNF (sBDNF) protein levels were measured using enzyme‐linked immunosorbent assay, while polymorphism and DNA methylation were measured in blood using pyrosequencing technology. To assess the temporal stability of the measures, participants underwent the same assessment twice within 4 days. Results: Repeated‐measures mixed linear models were used for between‐group analysis, with mean differences and 95% confidence intervals (95% CIs) shown. Compared to controls, serum BNDF was higher in patients with CFS/FM (F = 15.703; mean difference 3.31 ng/ml [95% CI 1.65, 4.96]; P = 0.001), whereas BDNF DNA methylation in exon 9 was lower (F = 7.543; mean difference −2.16% [95% CI −3.93, −0.83]; P = 0.007). BDNF DNA methylation was mediated by the Val66Met (rs6265) polymorphism. Lower methylation in the same region predicted higher sBDNF levels (F = 7.137, β = −0.408 [95% CI −0.711, −0.105]; P = 0.009), which in turn predicted participants' symptoms (F = 14.410, β = 3.747 [95% CI 1.79, 5.71]; P = 0.001) and widespread hyperalgesia (F = 4.147, β = 0.04 [95% CI 0.01, 0.08]; P = 0.044). Conclusion: Our findings indicate that sBDNF levels are elevated in patients with CFS/FM and that BDNF methylation in exon 9 accounts for the regulation of protein expression. Altered BDNF levels might represent a key mechanism explaining CFS/FM pathophysiology. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Chronic pain has a tremendous personal and socioeconomic impact and remains difficult to treat. Therefore, it is important to provide an update on the current understanding regarding lifestyle factors in people with chronic pain across the lifespan. Lifestyle factors such as physical (in)activity, sedentary behavior, stress, poor sleep, unhealthy diet, and smoking are associated with chronic pain severity and sustainment. This applies to all age categories, that is, chronic pain across the lifespan. Yet current treatment options often do not or only partly address the many lifestyle factors associated with chronic pain or attempt to address them in a standard format rather than providing an individually tailored multimodal lifestyle intervention. The evidence regarding lifestyle factors is available in adults, but limited in children and older adults having chronic pain, providing important avenues for future research. In conclusion, it is proposed that treatment approaches for people with chronic pain should address all relevant lifestyle factors concomitantly in an individually-tailored multimodal intervention. Ultimately, this should lead to improved outcomes and decrease the psychological and socioeconomic burden of chronic pain. Level of Evidence: IV. [ABSTRACT FROM AUTHOR]

Background 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. Methods Sixty-four participants (healthy controls and patients with chronic WAD) were subjected to six experimental conditions. Participants watched correct real-time or modified visual feedback of the neck or hand (without movement as well as during repetitive neck lateroflexion). Sensorimotor incongruence was induced by manipulating visual feedback. Pressure pain thresholds were measured at baseline and during each condition. Results Marked between-group differences were observed. Visual feedback of the neck-correct or modified-did not influence pain thresholds in chronic WAD. In contrast, healthy controls had significantly higher pain thresholds when provided with the correct or modified visual feedback. When a movement of the neck was added during visual feedback, patients with chronic WAD showed no significant difference in pain thresholds, while an increase in pain thresholds was found in the healthy control group. Conclusion In contrast to the healthy controls, visual feedback and sensorimotor incongruence did not alter pain thresholds in patients with chronic WAD. These findings suggest an abnormal pain response to visual feedback and somatosensory incongruence as well as failing mechanisms of pain inhibition in chronic WAD. [ABSTRACT FROM AUTHOR]

Objective Temporal summation ( TS) of pain, conditioned pain modulation ( CPM), and exercise-induced analgesia ( EIA) are often investigated in chronic pain populations as an indicator for enhanced pain facilitation and impaired endogenous pain inhibition, respectively, but interactions are not yet clear both in healthy controls and in chronic pain patients. Therefore, the present double-blind randomized placebo-controlled study evaluates pains cores, TS, and CPM in response to exercise in healthy controls, patients with chronic fatigue syndrome and comorbid fibromyalgia ( CFS/ FM), and patients with rheumatoid arthritis ( RA), both under placebo and paracetamol condition. Methods Fifty-three female volunteers - of which 19 patients with CFS/ FM, 16 patients with RA, and 18 healthy controls - underwent a submaximal exercise test on a bicycle ergometer on 2 different occasions (paracetamol vs. placebo), with an interval of 7 days. Before and after exercise, participants rated pain intensity during TS and CPM. Results Patients with rheumatoid arthritis showed decreased TS after exercise, both after paracetamol and placebo ( P < 0.05). In patients with CFS/ FM, results were less univocal. A nonsignificant decrease in TS was only observed after taking paracetamol. CPM responses to exercise are inconclusive, but seem to worsen after exercise. No adverse effects were seen. Conclusion This study evaluates pain scores, TS, and CPM in response to submaximal exercise in 2 different chronic pain populations and healthy controls. In patients with RA, exercise had positive effects on TS, suggesting normal EIA. In patients with CFS/ FM, these positive effects were only observed after paracetamol and results were inconsistent. [ABSTRACT FROM AUTHOR]

Background Chronic fatigue syndrome ( CFS) patients frequently complain of muscle fatigue and abnormally slow recovery, especially of the upper limb muscles during and after activities of daily living. Furthermore, disease heterogeneity has not yet been studied in relation to recovery of muscle function in CFS. Here, we examine recovery of upper limb muscle function from a fatiguing exercise in CFS patients with ( CFS+ FM) and without ( CFS-only) comorbid fibromyalgia and compare their results with a matched inactive control group. Design In this case-control study, 18 CFS-only patients, 30 CFS+ FM patients and 30 healthy inactive controls performed a fatiguing upper limb exercise test with subsequent recovery measures. Results There was no significant difference among the three groups for maximal handgrip strength of the non-dominant hand. A significant worse recovery of upper limb muscle function was found in the CFS+ FM, but not in de CFS-only group compared with the controls ( P < 0·05). Conclusions This study reveals, for the first time, delayed recovery of upper limb muscle function in CFS+ FM, but not in CFS-only patients. The results underline that CFS is a heterogeneous disorder suggesting that reducing the heterogeneity of the disorder in future research is important to make progress towards a better understanding and uncovering of mechanisms regarding the nature of divers impairments in these patients. [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2012; 42 (10): 1136-1144 Abstract Background Despite the large number of studies emphasizing the effectiveness of graded exercise therapy (GET) and cognitive behavioural therapy (CBT) for people with chronic fatigue syndrome (CFS), clinicians are left wondering how exactly to apply exercise therapy to their patients with CFS. The aim of this literature review is to identify the appropriate exercise modalities (i.e. exercise duration, mode, number of treatment sessions, session length, duration of treatment, exercise intensity and whether or not to apply home exercise program) for people with CFS. Materials and methods All studies that were identified through electronic databases (PubMed and PEDro) were assessed for methodological quality by using selection criteria (Delphi score). Results In this literature review, 12 studies fulfilled all study requirements. One study had a low methodological quality. The parameters used in the GET and CBT interventions were divided into subgroups: (i) time or symptom contingent, (ii) exercise frequency and (iii) exercise modality. Conclusion The lack of uniformity in outcome measures and CFS diagnostic criteria make it difficult to compare the findings across studies. Based on the available evidence, exercise therapy for people with CFS should be aerobic and must comprise of 10-11 sessions spread over a period of 4-5 months. A time-contingent approach is preferred over a symptom-contingent way of exercising. In addition, people with CFS can perform home exercises five times a week with an initial duration of 5-15 min per exercise session. The exercise duration can be gradually increased up to 30 min. [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2011 Abstract Background Central sensitisation entails several top-down and bottom-up mechanisms, all contributing to the hyperresponsiveness of the central nervous system to a variety of inputs. In the late nineties, it was first hypothesised that chronic fatigue syndrome (CFS) is characterised by hypersensitivity of the central nervous system (i.e. central sensitisation). Since then, several studies have examined central sensitisation in patients with CFS. This study provides an overview of such studies. Materials and Methods Narrative review. Results Various studies showed generalised hyperalgesia in CFS for a variety of sensory stimuli, including electrical stimulation, mechanical pressure, heat and histamine. Various tissues are affected by generalised hyperalgesia: the skin, muscle tissue and the lungs. Generalised hyperalgesia in CFS is augmented, rather than decreased, following various types of stressors like exercise and noxious heat pain. Endogenous inhibition is not activated in response to exercise and activation of diffuse noxious inhibitory controls following noxious heat application to the skin is delayed. Conclusions The observation of central sensitisation in CFS is in line with our current understanding of CFS. The presence of central sensitisation in CFS corroborates with the presence of several psychological influences on the illness, the presence of infectious agents and immune dysfunctions and the dysfunctional hypothalamus-pituitary-adrenal axis as seen in these severely debilitated patients. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusion Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) are comorbid disorders with overlapping symptoms. Research highlights autonomic dysfunction compared to healthy individuals, particularly involving the sympathetic branch. While past reviews focused on neurophysiological assessments, this systematic review summarises biological adrenergic markers, offering deeper insights into the observed sympathetic dysfunction in ME/CFS and FM aiming to identify targetable pathophysiological mechanisms.A systematic search was performed on PubMed, Web of Science, Embase and Scopus. Studies investigating peripheral biological markers of adrenergic function in patients with ME/CFS or FM compared to healthy controls at baseline were included. Meta‐analyses were performed using R statistical software.This meta‐analysis of 37 studies, encompassing 543 ME/CFS patients and 651 FM patients, compared with 747 and 447 healthy controls, respectively, revealed elevated adrenaline (SMD = .49 [.31–.67]; Z = 5.29, p < .01) and β1 adrenergic receptor expression (SMD = .79 [.06–1.52]; Z = 2.13; p = .03) in blood of ME/CFS patients at rest. Additionally, patients with ME/CFS had a greater increase in the expression of α2A adrenergic receptor (AR, SMD = .57 [.18–.97]; Z = 2.85, p < .01), β2 AR (SMD = .41 [.02–.81]; Z = 2.04; p = .04) and COMT (SMD = .42 [.03–.81]; Z = 2.11; p = .03) after exercise and an increased response of noradrenaline to an orthostatic test (SMD = .11 [−.47 to −.70]; Z = 2.10; p = .04), both found in blood. FM patients showed no significant differences at baseline but exhibited a diminished adrenaline response to exercise (SMD = −.79 [−1.27 to −.30]; Z = −3.14; p < .01).This systematic review and meta‐analysis revealed adrenergic dysfunction mainly in patients with ME/CFS. Higher baseline adrenaline levels and atypical responses to exercise in ME/CFS indicate that sympathetic dysfunction, underscored by adrenergic abnormalities, is more involved in the pathophysiology of ME/CFS rather than FM. [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2012; 42 (12): 1363-1365 [ABSTRACT FROM AUTHOR]

Eur J Clin Invest 2012; 42 (11): 1257-1258 [ABSTRACT FROM AUTHOR]