Fibromyalgia

2019 ◽  
Author(s):  
Daniel Joseph Clauw

Clinicians often encounter individuals who present with pain that they cannot adequately explain based on the degree of damage or inflammation noted in peripheral tissues. This typically prompts an evaluation looking for a cause of the pain. If no cause is found, these individuals are often given a diagnostic label that merely connotes that the patient has chronic pain in a region of the body, without an underlying mechanistic cause. Fibromyalgia (FM) is merely the current term for widespread musculoskeletal pain for which no alternative cause can be identified. This review covers the epidemiology, etiology/genetics, pathophysiology and pathogenesis, diagnosis, differential diagnosis, treatment, and complications and prognosis of FM. Figures show underlying mechanisms that can cause chronic pain; an individual’s “set point” or “volume control setting” for pain as set by a variety of factors, including the levels of neurotransmitters that either facilitate pain or reduce pain transmission; the 2011 Fibromyalgia Survey Criteria; symptoms and syndromes frequently seen in individuals with FM; the distribution of the 2011 Fibromyalgia Survey scores in a large cohort of individuals undergoing joint replacement surgery; and an algorithm showing the importance of dually focused treatment for FM and other chronic pain conditions. Tables list clinical characteristics of centralized pain, pharmacologic therapies for FM, and nonpharmacologic therapies for FM. This review contains 6 figures, 9 tables, and 78 references. Keywords: Fibromyalgia, chronic low back pain, headache, temporomandibular joint disorder, gastrointestinal disorder, irritable bowel syndrome (IBS), nonulcer dyspepsia, or esophageal dysmotility,  interstitial cystitis, chronic prostatitis, vulvodynia, vulvar vestibulitis, and endometriosis


2019 ◽  
Author(s):  
Daniel Joseph Clauw

Clinicians often encounter individuals who present with pain that they cannot adequately explain based on the degree of damage or inflammation noted in peripheral tissues. This typically prompts an evaluation looking for a cause of the pain. If no cause is found, these individuals are often given a diagnostic label that merely connotes that the patient has chronic pain in a region of the body, without an underlying mechanistic cause. Fibromyalgia (FM) is merely the current term for widespread musculoskeletal pain for which no alternative cause can be identified. This review covers the epidemiology, etiology/genetics, pathophysiology and pathogenesis, diagnosis, differential diagnosis, treatment, and complications and prognosis of FM. Figures show underlying mechanisms that can cause chronic pain; an individual’s “set point” or “volume control setting” for pain as set by a variety of factors, including the levels of neurotransmitters that either facilitate pain or reduce pain transmission; the 2011 Fibromyalgia Survey Criteria; symptoms and syndromes frequently seen in individuals with FM; the distribution of the 2011 Fibromyalgia Survey scores in a large cohort of individuals undergoing joint replacement surgery; and an algorithm showing the importance of dually focused treatment for FM and other chronic pain conditions. Tables list clinical characteristics of centralized pain, pharmacologic therapies for FM, and nonpharmacologic therapies for FM. This review contains 6 figures, 9 tables, and 78 references. Keywords: Fibromyalgia, chronic low back pain, headache, temporomandibular joint disorder, gastrointestinal disorder, irritable bowel syndrome (IBS), nonulcer dyspepsia, or esophageal dysmotility,  interstitial cystitis, chronic prostatitis, vulvodynia, vulvar vestibulitis, and endometriosis



2019 ◽  
Author(s):  
Daniel Joseph Clauw

Clinicians often encounter individuals who present with pain that they cannot adequately explain based on the degree of damage or inflammation noted in peripheral tissues. This typically prompts an evaluation looking for a cause of the pain. If no cause is found, these individuals are often given a diagnostic label that merely connotes that the patient has chronic pain in a region of the body, without an underlying mechanistic cause. Fibromyalgia (FM) is merely the current term for widespread musculoskeletal pain for which no alternative cause can be identified. This review covers the epidemiology, etiology/genetics, pathophysiology and pathogenesis, diagnosis, differential diagnosis, treatment, and complications and prognosis of FM. Figures show underlying mechanisms that can cause chronic pain; an individual’s “set point” or “volume control setting” for pain as set by a variety of factors, including the levels of neurotransmitters that either facilitate pain or reduce pain transmission; the 2011 Fibromyalgia Survey Criteria; symptoms and syndromes frequently seen in individuals with FM; the distribution of the 2011 Fibromyalgia Survey scores in a large cohort of individuals undergoing joint replacement surgery; and an algorithm showing the importance of dually focused treatment for FM and other chronic pain conditions. Tables list clinical characteristics of centralized pain, pharmacologic therapies for FM, and nonpharmacologic therapies for FM. This review contains 6 figures, 9 tables, and 78 references. Keywords: Fibromyalgia, chronic low back pain, headache, temporomandibular joint disorder, gastrointestinal disorder, irritable bowel syndrome (IBS), nonulcer dyspepsia, or esophageal dysmotility,  interstitial cystitis, chronic prostatitis, vulvodynia, vulvar vestibulitis, and endometriosis



2018 ◽  
Author(s):  
Axel Davies Vittersø ◽  
Monika Halicka ◽  
Gavin Buckingham ◽  
Michael J Proulx ◽  
Mark Wilson ◽  
...  

Representations of the body and peripersonal space can be distorted for people with some chronic pain conditions. Experimental pain induction can give rise to similar, but transient distortions in healthy individuals. However, spatial and bodily representations are dynamic, and constantly update as we interact with objects in our environment. It is unclear whether induced pain disrupts the mechanisms involved in updating these representations. In the present study, we sought to investigate the effect of induced pain on the updating of peripersonal space and body representations during and following tool-use. We compared performance under three conditions (pain, active placebo, neutral) on a visuotactile crossmodal congruency task and a tactile distance judgement task to measure updating of peripersonal space and body representations, respectively. We induced pain by applying 1% capsaicin cream to the arm, and for placebo we used a gel that induced non-painful warming. Consistent with previous findings, the difference in crossmodal interference from visual distractors in the same compared to opposite visual field to the tactile target was less when tools were crossed than uncrossed. This suggests an extension of peripersonal space to incorporate the tips of the tools. Also consistent with previous findings, estimates of the felt distance between two points (tactile distance judgements) decreased after active tool-use. In contrast to our predictions, however, we found no evidence that pain interfered with performance on either task when compared to the control conditions. This suggests that the updating of peripersonal space and body representations is not disrupted by induced pain. Therefore, acute pain does not account for the distorted representations of the body and peripersonal space that can endure in people with chronic pain conditions.



2020 ◽  
Author(s):  
Vishwas Tripathi ◽  
Amaresh Mishra ◽  
Yamini Pathak ◽  
Aklank Jain ◽  
Hridayesh Prakash

Fibromyalgia (FM) or Fibromyalgia Syndrome (FMS) is a neurodegenerative disorder causing musculoskeletal pain, tenderness, stiffness, fatigue, and sleep disorder in the body. It is one of the most common chronic pain conditions, affecting about 6% of the world population. Being refractory, till date, no specific treatment of this disease is available. Accumulating evidences over the last few decades indicate that proinflammatory macrophages, cytokines, & chemokines as the key players in this disease. Recent findings suggest activation of Microglial cells and associated pro-inflammatory signals as one of the major causes of chronic pain in patients suffering from fibromyalgia. Increased density of iNOs/CD68+ M1 effector macrophages has been associated with neuropathic pain models. In light of this, depletion of these pro-inflammatory macrophages has been shown to reduce sensitivity to neuropathic pain. On the other hand, modulating pattern of AGEs (Advanced Glycation End-Products) can also contribute to inactivation of macrophages. These findings strongly suggest that macrophages are critical in both inflammatory and neuropathic pain. Therefore, this chapter highlights the impact of macrophage plasticity in various immunopathological aspects of fibromyalgia.



2005 ◽  
Vol 10 (3) ◽  
pp. 145-152 ◽  
Author(s):  
David K Lam ◽  
Barry J Sessle ◽  
Brian E Cairns ◽  
James W Hu

The purpose of the present review is to correlate recent knowledge of the role of peripheral ionotropic glutamate receptors in the temporomandibular joint and muscle pain from animal and human experimental pain models with findings in patients. Chronic pain is common, and many people suffer from chronic pain conditions involving deep craniofacial tissues such as temporomandibular disorders or fibromyalgia. Animal and human studies have indicated that the activation of peripheral ionotropic glutamate receptors in deep craniofacial tissues may contribute to muscle and temporomandibular joint pain and that sex differences in the activation of glutamate receptors may be involved in the female predominance in temporomandibular disorders and fibromyalgia. A peripheral mechanism involving autocrine and/or paracrine regulation of nociceptive neuronal excitability via injury or inflammation-induced release of glutamate into peripheral tissues that may contribute to the development of craniofacial pain is proposed.



2020 ◽  
Author(s):  
Daniele Di Lernia ◽  
Marco Lacerenza ◽  
Vivien Ainley ◽  
Giuseppe Riva

Chronic pain (CP) severely disrupts the daily life of millions. Interoception (i.e., the sensing of the physiological condition of the body) plays a pivotal role in the aetiology and maintenance of CP. Given that pain is inherently an interoceptive signal, interoceptive frameworks provide important, but currently under-utilised, approaches to this condition. Here we first investigated three facets of interoceptive perception in CP, compared with pain-free healthy controls. We then introduce a novel interoceptive treatment and demonstrate its capacity to reduce pain severity in CP, thus potentially providing effective complementary analgesic treatments. Study 1 measured ‘interoceptive accuracy’, ‘interoceptive confidence’ and ‘interoceptive sensibility’ in patients (N=60) with primary, secondary musculoskeletal, and neuropathic CP. Compared with matched pain-free controls, CP participants exhibited significantly lower interoceptive accuracy and interoceptive confidence. Pain severity was positively predicted by interoceptive accuracy, anxiety and depression, but negatively predicted by interoceptive confidence. In Study 2 we tested a promising new interoceptive treatment for CP, in a single-blind between-subjects design (N=51) with primary, secondary musculoskeletal, and neuropathic CP patients. The treatment specifically activates the C-Tactile system, by means of controlled stimulation of interoceptive unmyelinated afferents, at 3cm/s with a force of 2.5mN. This treatment led to significant pain reduction (mean 23%) in the CP treatment group, while CP controls who received comparable but non-interoceptive stimulation reported no change in pain intensity. Together, these two studies highlight the importance of interoceptive approaches to CP and demonstrate the potential of this novel method of C-Tactile fibre stimulation to reduce pain severity.



2020 ◽  
Vol 10 (4) ◽  
pp. 201
Author(s):  
Daniele Di Lernia ◽  
Marco Lacerenza ◽  
Vivien Ainley ◽  
Giuseppe Riva

Chronic pain (CP) severely disrupts the daily life of millions. Interoception (i.e., sensing the physiological condition of the body) plays a pivotal role in the aetiology and maintenance of CP. As pain is inherently an interoceptive signal, interoceptive frameworks provide important, but underutilized, approaches to this condition. Here we first investigated three facets of interoceptive perception in CP, compared with pain-free controls. We then introduce a novel interoceptive treatment and demonstrate its capacity to reduce pain severity in CP, potentially providing complementary analgesic treatments. Study 1 measured interoceptive accuracy, confidence and sensibility in patients (N = 60) with primary, secondary musculoskeletal, and neuropathic CP. Compared with matched controls, CP participants exhibited significantly lower interoceptive accuracy and interoceptive confidence. Pain severity was predicted positively by interoceptive accuracy, anxiety and depression, and negatively by interoceptive confidence. Study 2 tested a promising new interoceptive treatment for CP, in a single-blind between-subjects design (N = 51) with primary, secondary musculoskeletal, and neuropathic CP patients. The treatment specifically activates the C-Tactile system, by means of controlled stimulation of interoceptive unmyelinated afferents, at 3 cm/s with a force of 2.5 mN. This treatment led to significant pain reduction (mean 23%) in the CP treatment group after only 11 min, while CP controls who received comparable but non-interoceptive stimulation reported no change in pain intensity. These studies highlight the importance of interoceptive approaches to CP and demonstrate the potential of this novel method of C-Tactile stimulation to provide complementary analgesic treatments.



2021 ◽  
Vol 12 ◽  
Author(s):  
Yi-Shang Yan ◽  
Zihao Qu ◽  
Dan-Qing Yu ◽  
Wei Wang ◽  
Shigui Yan ◽  
...  

ObjectiveSex steroids are thought to contribute to the pathogenesis of osteoarthritis (OA). This study investigated the causal role of sex steroids in site- and sex-specific OA and risk of joint replacement surgery using the Mendelian randomization (MR) method.MethodsInstrumental variables for estradiol, dehydroepiandrosterone sulfate, testosterone (T), and dihydrotestosterone (DHT) were selected. We used the inverse variance weighting (IVW) approach as the main MR method to estimate causal effects based on the summary-level data for OA and joint replacement surgery from genome-wide association studies (GWAS).ResultsA positive causal association was observed between serum T level and risks of hip OA (odds ratio [OR]=1.558, 95% confidence interval [CI]: 1.193–2.034; P=0.001) and hip replacement (OR=1.013, 95% CI: 1.008–1.018; P=2.15×10−8). Serum DHT level was also positively associated with the risk of hip replacement (OR=1.011, 95% CI: 1.006–1.015; P=4.03×10−7) and had potential causality with hip OA (OR=1.398, 95% CI: 1.054–1.855; P=0.020).ConclusionsSerum T and DHT levels may play causal roles in the development of hip OA and contribute to the risk of hip replacement, although the underlying mechanisms require further investigation.



Genes ◽  
2021 ◽  
Vol 12 (8) ◽  
pp. 1226
Author(s):  
Maria Carla Gerra ◽  
Cristina Dallabona ◽  
Lars Arendt-Nielsen

Prescription opioids are used for some chronic pain conditions. However, generally, long-term therapy has unwanted side effects which may trigger addiction, overdose, and eventually cause deaths. Opioid addiction and chronic pain conditions have both been associated with evidence of genetic and epigenetic alterations. Despite intense research interest, many questions about the contribution of epigenetic changes to this typology of addiction vulnerability and development remain unanswered. The aim of this review was to summarize the epigenetic modifications detected in specific tissues or brain areas and associated with opioid prescription and misuse in patients who have initiated prescribed opioid management for chronic non-cancer pain. The review considers the effects of opioid exposure on the epigenome in central and peripheral tissues in animal models and human subjects and highlights the mechanisms in which opioid epigenetics may be involved. This will improve our current understanding, provide the basis for targeted, personalized pain management, and thus balance opioid risks and benefits in managing chronic pain.



2021 ◽  
Vol 15 ◽  
Author(s):  
Xiaorong Huai ◽  
Yingfu Jiao ◽  
Xiyao Gu ◽  
Huichen Zhu ◽  
Lingke Chen ◽  
...  

Background: Although major joint replacement surgery has a high overall success rate, postoperative cognitive dysfunction (POCD) is a common complication after anesthesia and surgery, increasing morbidity and mortality. Identifying POCD risk factors would be helpful to prevent and decrease the occurrence of POCD. We hypothesized that preoperative chronic pain increases the risk of POCD.Methods: A single-center, observational, prospective cohort study was conducted from January 2018 to March 2020. All consecutive elderly patients (>65 years) who underwent elective total hip arthroplasty or hemiarthroplasty with general anesthesia by the same surgeon were enrolled. The patients underwent neuropsychological testing preoperatively and at 7 days and 2 months after surgery. To determine POCD, a nonsurgical control group was recruited from the general community.Results: Of the 141 patients who finished the neuropsychological testing 7 days after surgery, 61 (43.2%) had preoperative chronic pain. Of the 61 patients, 17 (27.9%) developed POCD; of the 79 patients with no chronic pain, 10 (12.7%) had developed POCD by 7 days after surgery. Multivariate logistic regression analysis identified preoperative chronic pain as a risk factor of POCD assessed 7 days after surgery (odds ratio 6.527; P = 0.009). There was no significant difference in the POCD incidence 2 months after surgery between patients with and without preoperative chronic pain.Conclusion: Preoperative chronic pain was a risk factor of developing POCD within 7 days after surgery in elderly patients following hip joint replacement surgery.Clinical Trial Registration: [www.ClinicalTrials.gov], identifier [NCT03393676].



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