Fibromyalgia symptoms are mediated by neuroplasticity
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Peer-reviewed literature indicates that neuroplasticity processes, including central sensitization and cortical inhibition changes, contribute to the pathophysiology and mediation of fibromyalgia symptoms.
Background: Major depressive disorder (MDD) and fibromyalgia (FM) present overlapped symptoms. Although the connection between these two disorders has not been elucidated yet, the disruption of neuroplastic processes that mediate the equilibrium in the inhibitory systems stands out as a possible mechanism. Thus, the purpose of this cross-sectional exploratory study was: (i) to compare the motor cortex inhibition indexed by transcranial magnetic stimulation (TMS) measures [short intracortical inhibition (SICI) and intracortical facilitation (ICF)], as well as the function of descending pain modulatory systems (DPMS) among FM, MDD, and healthy subjects (HS); (ii) to compare SICI, ICF, and the role of DPMS evaluated by the change on Numerical Pain Scale (NPS) during the conditioned pain modulation test (CPM-test) between FM and MDD considering the BDNF-adjusted index; (iii) to assess the relationship between the role of DPMS and the BDNF-adjusted index, despite clinical diagnosis. Patients and Methods: A cohort of 63 women, aged 18 to 75 years [FM (n = 18), MDD (n = 19), and HC (n = 29)]. Results: The MANCOVA analysis revealed that the mean of SICI was 53.40% larger in FM compared to MDD [1.03 (0.50) vs. 0.55 (0.43)] and 66.99% larger compared to HC [1.03 (0.50) vs. 0.34 (0.19)], respectively. The inhibitory potency of the DPMS assessed by the change on the NPS during CPM-test was 112.29 % lower in the FM compared to MDD [0.22 (1.37) vs. −0.87 (1.49)]. The mean of BDNF from FM compared to MDD was 35.70% higher [49.82 (16.31) vs. 14.12 (8.86)]. In FM, the Spearman’s coefficient between the change in the NPS during CPM-test with the SICI was Rho = −0.49, [confidence interval (CI) 95%; −0.78 to −0.03]. The BDNF-adjusted index was positively correlated with the disinhibition of the DPMS. Conclusion: These findings support the hypothesis that in FM a deteriorated function of cortical inhibition, indexed by a higher SICI parameter, a lower function of the DPMS, together with a higher level of BDNF indicate that FM has different pathological substrates from depression. They suggest that an up-regulation phenomenon of intracortical inhibitory networks associated with a disruption of the DPMS function occurs in FM.
Neuroplasticity mechanisms in the pathophysiology of chronic pain.
2012 · cited by 34
Chronic pain is a widespread healthcare problem with great impact on mental health, professional and family life of the patient. It can be a consequence of many disorders; however, its pathogenesis has not yet been fully understood. Neuroplasticity is the ability of the nervous system to adapt to different changes and it is present throughout life, not only in prenatal period, infancy and childhood. However, in the pathophysiology of chronic pain, neuroplasticity shows its "dark side". Due to the central sensitization process, noxious stimuli can produce chronic pain or misinterpretation of non-noxious stimuli (secondary hyperalgesia and allodynia). These changes occur at the level of brain cortex as well at peripheral nerves and receptors. This review summarizes a significant portion of literature dealing with neuroplasticity processes in well known chronic pain conditions such as migraine, chronic posttraumatic headache, low back pain, fibromyalgia, and others. The relevance of this topic lies in providing a new insight in the pathophysiology of chronic pain, while also offering a possibility of new therapeutic approaches including not only pharmacological agents.
Fibromyalgia syndrome (FMS) is a chronic musculoskeletal disorder with unclear pathogenesis and a lack of targeted therapies. Central sensitization has emerged as a key mechanism that drives its pathophysiology. Although clinical studies support the efficacy of acupressure (ACP) in alleviating FMS symptoms, its underlying mechanisms remain poorly understood. This study investigates how ACP modulates central sensitization and inflammatory pathways in a rat model of FM. An FM rat model was developed to evaluate the efficacy of ACP therapy. Pain sensitivity and emotional distress were assessed using behavioral tests. Molecular analyses, including Western blot and immunofluorescence, were used to measure MAPK pathway activity (phosphorylation of p38 MAPK and JNK MAPK), glial cell activation (microglia and astrocytes), and inflammatory cytokine levels (TNF-ɑ, IL-6). Post-translational modifications were analyzed to explore anti-inflammatory mechanisms. ACP therapy significantly reduced pain sensitivity in FM rats. Mechanistically, ACP inhibited phosphorylation of p38 MAPK and JNK MAPK, suppressed glial cell activation, reduced pro-inflammatory cytokine release, and eventually attenuated central sensitization. The anti-inflammatory effects were mediated primarily by regulating post-translational modifications rather than altering protein synthesis or degradation. Additionally, ACP restored muscle function and demonstrated therapeutic effects on somatic manifestations of FMS. ACP exerts multimodal therapeutic effects on FMS through dual modulation of MAPK signaling, which targets central sensitization and inflammation through precision-driven post-translational regulation. Its ability to alleviate physical symptoms highlights its potential as a targeted intervention for FMS. These findings provide mechanistic insights into ACP’s clinical efficacy and support its integration into FMS management strategies.
Introduction Central sensitization explains the mismatch between structural damage or inflammation and pain intensity in chronic musculoskeletal diseases. It defines the phenotype of fibromyalgia and contributes to persistent pain in osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Objective To characterize the role of central sensitization in nociplastic pain in fibromyalgia, osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. Materials and Methods A structured search of PubMed, Scopus, Web of Science, and Google Scholar (1990–2025) identified open-access, evidence-based publications addressing pain pathophysiology, diagnosis, and treatment in these conditions. Results Central sensitization manifests as hyperalgesia, allodynia, expanded receptive fields, and impaired endogenous pain inhibition. It predominates in fibromyalgia and contributes to persistent pain in osteoarthritis and rheumatoid arthritis that may not correlate with inflammation or structural damage. Screening tools such as the Widespread Pain Index and Symptom Severity Scale, together with quantitative sensory testing and algometry, help identify nociplastic pain features. Neuroimmune mechanisms, including microglial activation and imbalance between excitatory and inhibitory neurotransmission, may contribute to the mismatch between pain intensity and clinical findings. Conclusion Chronic pain reflects inflammatory, mechanical, and nociplastic mechanisms in rheumatoid arthritis, osteoarthritis, and fibromyalgia, respectively. Recognition of central sensitization improves assessment and supports mechanism-based management.
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