Search

Fibromyalgia Syndrome (FMS), Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Long COVID (LC) are similar multisymptom clinical syndromes but with difference in dominant symptoms in each individual. There is existing and emerging literature on possible functional alterations of the central nervous system in these conditions. This review aims to synthesise and appraise the literature on resting-state quantitative EEG (qEEG) in FMS, ME/CFS and LC, drawing on previous research on FMS and ME/CFS to help understand neuropathophysiology of the new condition LC. A systematic search of MEDLINE, Embase, CINHAL, PsycINFO and Web of Science databases for articles published between December 1994 and September 2023 was performed. Out of the initial 2510 studies identified, 17 articles were retrieved that met all the predetermined selection criteria, particularly of assessing qEEG changes in one of the three conditions compared to healthy controls. All studies scored moderate to high quality on the Newcastle-Ottawa scale. There was a general trend for decreased low-frequency EEG band activity (delta, theta, and alpha) and increased high-frequency EEG beta activity in FMS, differing to that found in ME/CFS. The limited LC studies included in this review focused mainly on cognitive impairments and showed mixed findings not consistent with patterns observed in FMS and ME/CFS. Our findings suggest different patterns of qEEG brainwave activity in FMS and ME/CFS. Further research is required to explore whether there are phenotypes within LC that have EEG signatures similar to FMS or ME/CFS. This could inform identification of reliable diagnostic markers and possible targets for neuromodulation therapies tailored to each clinical syndrome., (Copyright © 2024 International Federation of Clinical Neurophysiology. Published by Elsevier B.V. All rights reserved.)

'Non-inflammatory' pain, pain that is not associated with measures of inflammation, is common in patients with inflammatory arthritis including RA. One important cause of non-inflammatory pain is concomitant fibromyalgia. Systematic review has shown that fibromyalgia is common in inflammatory arthritis including RA affecting 1 in 5 patients and is associated with higher disease activity scores due to inflated tender joint count and patient global assessment. Consequently, many patients with RA and concomitant fibromyalgia may fail to reach treatment target and switch to alternate disease modifying drugs frequently. European Alliance of Association for Rheumatology has highlighted that concomitant fibromyalgia is an important consideration in assessing difficult-to-treat RA. The incidence and prevalence of fibromyalgia are higher in RA than the general population, raising the possibility that fibromyalgia may be 'secondary' to RA rather than a concomitant disease. The precise mechanisms whereby patients with RA develop fibromyalgia are unknown. In this review, we discussed fibromyalgia in RA, its clinical impact and epidemiology as well as data suggesting fibromyalgia might be 'secondary'. Lastly, we reviewed potential pathogenic mechanisms which included inflammatory cytokines sensitizing nociceptive neurones, temporal summation, also known as windup, from chronic pain and impaired coping from poor quality sleep and mental well-being. Deciphering the exact mechanisms may lead to treatment strategies that prevent development of secondary fibromyalgia and will address a common factor associated with difficult-to-treat RA., (© The Author(s) 2022. Published by Oxford University Press on behalf of the British Society for Rheumatology.)

Fibromyalgia is characterised by widespread musculoskeletal pain, which may present with fatigue, depression, anxiety, sleep and cognitive disturbances. It is the second most prevalent rheumatic disease. An accurate diagnosis is challenging, since its symptoms may resemble diverse conditions such as carpal tunnel syndrome, Raynaud syndrome, Sjögren syndrome, amongst others. Neuropathic pain and autonomic dysfunction in fibromyalgia suggest the involvement of the nervous system. Ion channels, neurotransmitters and neuromodulators may play a role. Small fibre neuropathy (SFN) may also cause chronic widespread pain. SFN may occur in 50% of fibromyalgia patients, but its role in the disease is unknown. Despite several efforts to synthesise the evidence on the mechanisms for pain in fibromyalgia, there are few studies applying an integrative perspective of neurochemical, immunological, and neuroanatomical characteristics, and their relevance to the disease. This protocol aims to clarify the mechanisms of the central and peripheral nervous system associated with pain in fibromyalgia. We will retrieve published studies from Web of Science, MEDLINE, Scopus, EBSCOhost, Ovid and Google Scholar. All clinical studies or experimental models of fibromyalgia reporting imaging, neurophysiological, anatomical, structural, neurochemical, or immunological characteristics of the central or peripheral nervous systems associated with pain will be included. Exclusion criteria will eliminate studies evaluating pain without a standardised measure, studies written in languages different from Spanish or English that could not be appropriately translated, and studies whose full-text files could not be retrieved after all efforts made. A narrative synthesis will be performed., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Introduction: The pathophysiology of fibromyalgia (FM) is related to central sensitisation (CS) to pain. Algometry allows assessing CS based on dynamic evoked pain. However, current algometrýs protocols require optimising, unifying and updating., Objectives: 1) identify the dynamic pain measures used most frequently to effectively assess CS processes in FM, and 2) consider the future of the algometry assessing CS in these patients., Methods: Cochrane Collaboration guidelines and PRISMA statements were followed. The protocol was registered in PROSPERO database (ID: CRD42021270135). The selected articles were evaluated using the Cochrane risk of bias (ROB) assessment tool. The PubMed, Scopus, and Web of Science databases were searched., Results: Thirty-four studies were selected, including measures such as temporal summation of pain (TSP), aftersensations (AS), spatial summation of pain (SSP), the noxious flexion reflex (NFR) threshold, conditioned pain modulation (CPM), cutaneous silent period (CuSP), and slowly repeated evoked pain (SREP); and evoked pain combined with neuroimaging. Each measure offered various advantages and limitations. According to ROB, 28 studies were of low quality, 3 of moderate quality, and 3 of high quality., Conclusions: Several pain indicators have been demonstrated to successfully examine CS involvement in FM in the last years. Algometry, especially when it involves diverse body sites and tissues, might provide further insight into (1) the evaluation of psychological factors known to influence pain experience, (2) new dynamic pain indicators, and (3) the simultaneous use of certain neuroimaging techniques. Further research clarifying the mechanisms underlying some of these measures, and homogenisation and optimisation of the algometrýs protocols, are needed. KEY MESSAGESAlgometry allows for assessing Central Sensitisation by applying dynamic evoked pain.The future of algometry could relapse in its combination with neuroimaging.Recently-emerged pain indicators should be considered for algometrýs new protocols.

Introduction: Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both complex conditions that are challenging to treat. This may be related to an incomplete understanding of their pathophysiology, itself obfuscated by their heterogeneity. The symptomatic overlap between them and their common comorbidity suggests a shared vulnerability, which might be explained by central sensitisation., Methods: 19 CFS cases, 19 FM cases and 20 age and sex matched healthy controls (HC) were recruited primarily from secondary care clinics in London. Those with other pain disorders, psychiatric diagnoses and those taking centrally acting or opiate medications were excluded. Participants were asked to abstain from alcohol and over the counter analgaesia 48 h prior to assessment by static and dynamic quantitative sensory tests, including measures of temporal summation (TS) and conditioned pain modulation (CPM)., Results: CS, as defined by the presence of both enhanced TS and inefficient CPM, was present in 16 (84%) CFS cases, 18 (95%) FM cases, and none of the HC (p < 0.001). Pressure pain thresholds were lower in CFS (Median222kPaIQR 146-311; p = 0.04) and FM cases (Median 189 kPa; IQR 129-272; p = 0.003) compared to HC (Median 311 kPa; IQR 245-377). FM cases differed from HC in cold-induced (FM = 22.6 °C (15.3-27.7) vs HC = 14.2 °C (9.0-20.5); p = 0.01) and heat-induced (FM = 38.0 °C (35.2-44.0) vs HC = 45.3 °C (40.1-46.8); p = 0.03) pain thresholds, where CFS cases did not., Conclusion: Central sensitisation may be a common endophenotype in chronic fatigue syndrome and fibromyalgia. Further research should address whether central sensitisation is a cause or effect of these disorders., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Purpose: To translate and cross-culturally adapt the English version of the Central Sensitisation Inventory (CSI) into Thai (CSI-Thai) and to evaluate its psychometric properties in individuals with chronic non-specific neck pain. Materials and methods: Cross-cultural translation and adaptation of the CSI were performed according to standard guidelines. A total of 340 participants were invited to complete the CSI-Thai, Visual Analogue Scale (pain intensity), Neck Disability Index, Fear-Avoidance Beliefs Questionnaire, Pain Catastrophising Scale (PCS), and Short Form-36. Psychometric evaluation included confirmatory factor analysis, internal consistency, test-retest reliability, agreement, and construct validity. Results: Dimensionality analyses indicated that a bifactor model, comprising one general factor plus four orthogonal factors, fit the CSI structure better than unidimensional and the four-factor models. The general factor showed substantial reliability (Cronbach α=0.91, Omega ω=0.94, and omega hierarchical x-h=0.91). The intraclass correlation coefficient was 0.90, representing excellent stability over a 48 h interval. Moderate-to-strong correlations and acceptable-to-excellent discriminations were found between the CSI-Thai and all questionnaires. The exception was the PCS (no correlation and discrimination). The standard error of measurement and minimal detectable change of the CSI-Thai were 2.33 and 6.47, respectively. Conclusions: The translation and cross-cultural adaptation of the CSI-Thai were successful, with satisfactory reliability and construct validity. [ABSTRACT FROM AUTHOR]

Introduction The pathophysiology of fibromyalgia (FM) is related to central sensitisation (CS) to pain. Algometry allows assessing CS based on dynamic evoked pain. However, current algometrýs protocols require optimising, unifying and updating.Objectives 1) identify the dynamic pain measures used most frequently to effectively assess CS processes in FM, and 2) consider the future of the algometry assessing CS in these patients.Methods Cochrane Collaboration guidelines and PRISMA statements were followed. The protocol was registered in PROSPERO database (ID: CRD42021270135). The selected articles were evaluated using the Cochrane risk of bias (ROB) assessment tool. The PubMed, Scopus, and Web of Science databases were searched.Results Thirty-four studies were selected, including measures such as temporal summation of pain (TSP), aftersensations (AS), spatial summation of pain (SSP), the noxious flexion reflex (NFR) threshold, conditioned pain modulation (CPM), cutaneous silent period (CuSP), and slowly repeated evoked pain (SREP); and evoked pain combined with neuroimaging. Each measure offered various advantages and limitations. According to ROB, 28 studies were of low quality, 3 of moderate quality, and 3 of high quality.Conclusions Several pain indicators have been demonstrated to successfully examine CS involvement in FM in the last years. Algometry, especially when it involves diverse body sites and tissues, might provide further insight into (1) the evaluation of psychological factors known to influence pain experience, (2) new dynamic pain indicators, and (3) the simultaneous use of certain neuroimaging techniques. Further research clarifying the mechanisms underlying some of these measures, and homogenisation and optimisation of the algometrýs protocols, are needed. KEY MESSAGESAlgometry allows for assessing Central Sensitisation by applying dynamic evoked pain.The future of algometry could relapse in its combination with neuroimaging.Recently-emerged pain indicators should be considered for algometrýs new protocols.

Abstract Background Autistic adults, particularly women, are more likely to experience chronic ill health than the general population. Central sensitivity syndromes (CSS) are a group of related conditions that are thought to include an underlying sensitisation of the central nervous system; heightened sensory sensitivity is a common feature. Anecdotal evidence suggests autistic adults may be more prone to developing a CSS. This study aimed to investigate the occurrence of CSS diagnoses and symptoms in autistic adults, and to explore whether CSS symptoms were related to autistic traits, mental health, sensory sensitivity, or gender. Methods The full sample of participants included 973 autistic adults (410 men, 563 women, mean age = 44.6) registered at the Netherlands Autism Register, who completed questionnaires assessing autistic traits, sensory sensitivity, CSS, physical and mental health symptoms. The reliability and validity of the Central Sensitization Inventory (CSI) in an autistic sample was established using exploratory and confirmatory factor analyses. Chi2 analyses, independent t-tests, hierarchical regression and path analysis were used to analyse relationships between CSS symptoms, autistic traits, measures of mental health and wellbeing, sensory sensitivity, age and gender. Results 21% of participants reported one or more CSS diagnosis, and 60% scored at or above the clinical cut-off for a CSS. Autistic women were more likely to report a CSS diagnosis and experienced more CSS symptoms than men. Sensory sensitivity, anxiety, age and gender were significant predictors of CSS symptoms, with sensory sensitivity and anxiety fully mediating the relationship between autistic traits and CSS symptoms. Limitations Although this study included a large sample of autistic adults, we did not have a control group or a CSS only group. We also could not include a non-binary group due to lack of statistical power. Conclusions CSS diagnoses and symptoms appear to be very common in the autistic population. Increased awareness of an association between autism and central sensitisation should inform clinicians and guide diagnostic practice, particularly for women where CSS are common and autism under recognised.

Background: Autistic adults, particularly women, are more likely to experience chronic ill health than the general population. Central sensitivity syndromes (CSS) are a group of related conditions that are thought to include an underlying sensitisation of the central nervous system; heightened sensory sensitivity is a common feature. Anecdotal evidence suggests autistic adults may be more prone to developing a CSS. This study aimed to investigate the occurrence of CSS diagnoses and symptoms in autistic adults, and to explore whether CSS symptoms were related to autistic traits, mental health, sensory sensitivity, or gender. Methods: The full sample of participants included 973 autistic adults (410 men, 563 women, mean age = 44.6) registered at the Netherlands Autism Register, who completed questionnaires assessing autistic traits, sensory sensitivity, CSS, physical and mental health symptoms. The reliability and validity of the Central Sensitization Inventory (CSI) in an autistic sample was established using exploratory and confirmatory factor analyses. Chi2 analyses, independent t-tests, hierarchical regression and path analysis were used to analyse relationships between CSS symptoms, autistic traits, measures of mental health and wellbeing, sensory sensitivity, age and gender. Results: 21% of participants reported one or more CSS diagnosis, and 60% scored at or above the clinical cut-off for a CSS. Autistic women were more likely to report a CSS diagnosis and experienced more CSS symptoms than men. Sensory sensitivity, anxiety, age and gender were significant predictors of CSS symptoms, with sensory sensitivity and anxiety fully mediating the relationship between autistic traits and CSS symptoms. Limitations: Although this study included a large sample of autistic adults, we did not have a control group or a CSS only group. We also could not include a non-binary group due to lack of statistical power. Conclusions: CSS diagnoses and symptoms appear to be very common in the autistic population. Increased awareness of an association between autism and central sensitisation should inform clinicians and guide diagnostic practice, particularly for women where CSS are common and autism under recognised. [ABSTRACT FROM AUTHOR]

The common chronic pain syndromes of fibromyalgia, regional pain syndrome, and complex regional pain syndrome have been made to appear separate because they have been historically described by different groups and with different criteria, but they are really phenotypically accented expressions of the same processes triggered by emotional distress and filtered or modified by genetics, psychology, and local physical factors.

Introduction: Pain is considered to be one of a number of idiosyncratic, context-dependent 'protective actions' projected into the conscious domain by the central nervous system (CNS), as a result of a series of complex interactions in response to perceived threat. A model is described which proposes chronic pain and a variety of long-term, systemic functional neurological conditions to be a consequence of significant dysregulation of these protection systems. The Model: Previous research has demonstrated that a cognitive–behavioural model, first described in 1995 by Surawy et al., for chronic fatigue has been successful in predicting the transition from acute to chronic states in a number of conditions. This model includes predisposing, precipitating and perpetuating biopsychosocial factors. This article discusses the potential role of these factors in affecting descending inhibition in the CNS, significantly altering its ability to modulate the threat detection system. The development of 'central sensitisation' is considered in this context. Conclusion: This model proposes that chronic pain, chronic fatigue and other so-called functional neurological phenomena can, perhaps, be more helpfully seen as the actions of a dysregulated neurological protection system, rather than symptoms of an untreatable and deteriorating medical condition. Recommendations are made for the development of appropriate therapeutic interventions indicated by this model. [ABSTRACT FROM AUTHOR]

Hereditary neuropathy with liability to pressure palsy (HNPP) has historically been considered a pain-free condition, though some people with HNPP also complain of pain. This study characterised persistent pain in people with HNPP. Participants provided cross-sectional demographic data, information on the presence of neurological and persistent pain symptoms, and the degree to which these interfered with daily life. The painDETECT and Central Sensitization Inventory questionnaires were used to indicate potential neuropathic, central sensitisation and musculoskeletal (nociceptive) pain mechanisms. Additionally, participants were asked if they thought that pain was related to/part of HNPP. 32/43 (74%) subjects with HNPP had persistent pain and experience this pain in the last week. Of those with pain, 24 (75%) were likely to have neuropathic pain and 27 (84%) were likely to have central sensitisation. All 32 participants felt that their pain could be related to/part of their HNPP. Significant negative impact of the pain was common. Pain characterisation identified neuropathic pain and/or central sensitisation as common, potential underlying processes. Pain may plausibly be directly related to the underlying pathophysiology of HNPP. Further consideration of including pain as a primary symptom of HNPP is warranted. [ABSTRACT FROM AUTHOR]

Fibromyalgia (FM) is the most commonly encountered chronic widespread pain (CWP) condition in rheumatology. In comparison to inflammatory arthritis (IA), it can seem ill defined with no clear understanding of the pathology and therefore no specific targeted treatment. This inevitably raises controversies and challenges. However, this is an outdated view perpetuated by poor teaching of pain at undergraduate and postgraduate levels, and the perennial problem of advances in relevant cross-speciality knowledge penetrating speciality silos. Research has provided a better understanding of the aetiopathology and FM is now regarded as a centralized pain state. Effective treatment is possible utilizing a multidisciplinary approach combining nonpharmacologic and pharmacologic treatments rooted in a biopsychosocial model. This article will provide a review of the mechanisms, diagnosis and treatment of FM, focus on some ongoing contentious issues and propose a change to the diagnostic terminology. [ABSTRACT FROM AUTHOR]

Rheumatic pain and, in particular, rheumatoid arthritis, osteoarthritis and fibromyalgia, are common and debilitating chronic pain syndromes. Recently, human functional neuroimaging, for example EEG, fMRI, and PET has begun to reveal some of the crucial central nervous system mechanisms underlying these diseases. The purpose of this review is to summarise current knowledge on the brain mechanisms of rheumatic pain revealed by functional neuroimaging techniques. The evidence suggests that two mechanisms may be largely responsible for the clinical pain associated with these rheumatic diseases: abnormalities in the medial pain system and/or central nervous system sensitisation and inhibition. If we can understand how functioning of the central nociceptive system becomes altered, even in the absence of peripheral nociceptive input, by using functional neuroimaging techniques, in the future we may be able to develop improved, more effective treatments for patients with chronic rheumatic pain. [ABSTRACT FROM AUTHOR]

Abstract: During the past decade, scientific research has provided new insight into the development from an acute, localised musculoskeletal disorder towards chronic widespread pain/fibromyalgia (FM). Chronic widespread pain/FM is characterised by sensitisation of central pain pathways. An in-depth review of basic and clinical research was performed to design a theoretical framework for manual therapy in these patients. It is explained that manual therapy might be able to influence the process of chronicity in three different ways. (I) In order to prevent chronicity in (sub)acute musculoskeletal disorders, it seems crucial to limit the time course of afferent stimulation of peripheral nociceptors. (II) In the case of chronic widespread pain and established sensitisation of central pain pathways, relatively minor injuries/trauma at any locations are likely to sustain the process of central sensitisation and should be treated appropriately with manual therapy accounting for the decreased sensory threshold. Inappropriate pain beliefs should be addressed and exercise interventions should account for the process of central sensitisation. (III) However, manual therapists ignoring the processes involved in the development and maintenance of chronic widespread pain/FM may cause more harm then benefit to the patient by triggering or sustaining central sensitisation. [Copyright &y& Elsevier]

Abstract: Objective: Psychosocial stress is a risk factor for musculoskeletal pain, but how stress affects musculoskeletal pain is poorly understood. We wanted to examine the relationship between low-grade autonomic activation and stress-related pain in patients with fibromyalgia and localised chronic shoulder/neck pain. Methods: Twenty-three female patients with fibromyalgia, 29 female patients with chronic shoulder–neck pain, and 35 healthy women performed a stressful task lasting 60min. With a blinded study design, we recorded continuous blood pressure, heart rate, finger skin blood flow and respiration frequency before (10min), during (60min) and after (30min) the stressful task. The physiological responses were compared with subjective reports of pain. Results: The increase in diastolic blood pressure and heart rate in response to the stressful task were smaller in fibromyalgia patients compared with the healthy controls. Furthermore, fibromyalgia patients had reduced finger skin blood flow at the end of the stressful task compared to healthy controls. We also found an inverse relationship between the heart rate response and development and recovery of the stress-related pain in fibromyalgia patients. Conclusion: We found abnormal cardiovascular responses to a 60min long stressful task in fibromyalgia patients. Furthermore, we found a negative association between the heart rate response and the pain which developed during the stressful task in the fibromyalgia group, possibly a result of reduced stress-induced analgesia for fibromyalgia patients. [Copyright &y& Elsevier]

Previous studies have shown that repeated injections of acidic saline, given into the lateral gastrocnemius muscle of rats, results in a bilateral reduction in withdrawal threshold to tactile stimulation of the hindpaws. We have now characterised this model of muscoskeletal pain pharmacologically, by evaluating the antinociceptive effects of various analgesics after systemic administration. The μ-opioid receptor agonist morphine (3 and 6 mg/kg) produced a particularly prolonged antiallodynic effect. The glutamate receptor antagonists ([8-methyl-5-(4-(N,N-dimethylsulfamoyl)phenyl)-6,7,8,9,-tetrahydro-1H-pyrrolo[3,2-h]-iso-quinoline-2,3-dione-3-O-(4-hydroxybutyric acid-2-yl)oxime] NS1209 and ketamine (6 and 15 mg/kg, respectively), the KCNQ K+ channel openers retigabine and flupirtine (10 and 20 mg/kg, respectively) and the Na+ channel blocker mexiletine (37.5 mg/kg) also significantly increased paw withdrawal threshold, although to a lesser degree than morphine. In contrast, the anticonvulsant lamotrigine (30 mg/kg), the cyclooxygenase-2 inhibitor carprofen (15 mg/kg) and the benzodiazepine diazepam (3 mg/kg) were ineffective. All antinociceptive effects were observed at nonataxic doses as determined by the rotarod test. These results suggest that in this model, muscle-mediated pain can be alleviated by various analgesics with differing mechanisms of action, and that once established ongoing inflammation does not appear to contribute to this process. [Copyright &y& Elsevier]