Materiały źródłowe

• #1 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8068842/

  Fibromyalgia is caused by a central sensitization phenomenon characterized by the dysfunction of neuro-circuits, which involves the perception, transmission and processing of afferent nociceptive stimuli, with the prevalent manifestation of pain at the level of the locomotor system. […] The main alterations observed in FM are dysfunctions in mono-aminergic neurotransmission, leading to elevated levels of excitatory neurotransmitters, such as glutamate and substance P, and decreased levels of serotonin and norepinephrine in the spinal cord at the level of descending anti-nociceptive pathways. […] Other factors that appear to be involved in the pathophysiology of FM are neuroendocrine factors, genetic predisposition, oxidative stress and environmental and psychosocial changes. […] Central sensitization refers to a neuronal signal amplification mechanism within the central nervous system that leads to a greater perception of pain.

• #2 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://www.mdpi.com/1422-0067/22/8/3891

  Fibromyalgia is a syndrome characterized by chronic and widespread musculoskeletal pain, often accompanied by other symptoms, such as fatigue, intestinal disorders and alterations in sleep and mood. […] It is known that fibromyalgia is caused by a central sensitization phenomenon characterized by the dysfunction of neuro-circuits, which involves the perception, transmission and processing of afferent nociceptive stimuli, with the prevalent manifestation of pain at the level of the locomotor system. […] In recent years, the pathogenesis of fibromyalgia has also been linked to other factors, such as inflammatory, immune, endocrine, genetic and psychosocial factors. […] The main alterations observed in FM are dysfunctions in mono-aminergic neurotransmission, leading to elevated levels of excitatory neurotransmitters, such as glutamate and substance P, and decreased levels of serotonin and norepinephrine in the spinal cord at the level of descending anti-nociceptive pathways.

• #2 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://www.mdpi.com/1422-0067/22/8/3891

  Other anomalies observed are dopamine dysregulation and altered activity of endogenous cerebral opioids. […] Taken together, these phenomena seem to explain the central physiopathology of FM. […] Peripheral abnormalities may contribute to increased nociceptive tonic supply in the spinal cord, which results in central sensitization. […] Other factors that appear to be involved in the pathophysiology of FM are neuroendocrine factors, genetic predisposition, oxidative stress and environmental and psychosocial changes. […] Central sensitization refers to a neuronal signal amplification mechanism within the central nervous system that leads to a greater perception of pain. […] For this reason, patients with FM present an increase in the receptive field of pain, allodynia and hyperalgesia.

• #3 Pathophysiology of Fibromyalgia | Encyclopedia MDPI

  https://encyclopedia.pub/entry/39160

  Fibromyalgia syndrome (FMS) is one of the most prevalent disorders that affects the muscles and is characterized by pain, stiffness, and soreness in the muscles, tendons, and joints. […] The exact pathophysiological mechanism behind fibromyalgia remains undefined, though it is likely multifactorial in origin including abnormal cortical processing, reductions in inhibitory pain modulatory mechanisms and molecular changes to the pain pathway. […] What is clear however is that patients with fibromyalgia have increased sensitivity to a variety of stimuli, including mechanical and ischemic pressure, heat, and cold. […] Studies have shown that compared to healthy controls, the stimulus intensity required to elicit a pain response in fibromyalgia patients is almost 50% lower. […] The pathophysiology of this heightened sensitivity (hyperalgesia and allodynia) has been studied and is thought to involve both impaired central cortical processing as well as dysregulation of the central nervous system (CNS) at the spinal cord level.

• #4 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8068842/

  For this reason, patients with FM present an increase in the receptive field of pain, allodynia and hyperalgesia. […] Although central sensitization plays an important role in FM, it is even more important to understand the initial cause, that is, the persistent nociceptive input associated with tissue damage, including peripheral sensitization. […] Taken together, these phenomena seem to explain the central physiopathology of FM. […] Patients with FM present a lower pain threshold that generates a condition of diffuse hyperalgesia and/or allodynia. […] These FM phenomena have been confirmed in clinical studies that used functional neuroimaging or measured alterations in neurotransmitter levels that influence sensory transmission and pain. […] Clinical studies based on functional magnetic resonance imaging (fMRI) have confirmed a central neuronal alteration in nociceptive processes.

• #5 Fibromyalgia | PM&R KnowledgeNow

  https://now.aapmr.org/fibromyalgia/

  Fibromyalgia (FM) is a clinical syndrome characterized by widespread chronic musculoskeletal pain, stiffness and tenderness in addition to a variety of physical and mental symptoms including fatigue, sleep/mood disturbances, depression, anxiety, cognitive dysfunction, headaches, and intestinal disorders. […] While genetic polymorphisms have been suggested to be contributory, the main alterations observed are thought to be mono-amine neurotransmission (serotonin and norepinephrine) pathways leading to elevated levels of excitatory neurotransmitters such as glutamate and substance P as well as decreased levels of serotonin and norepinephrine in the spinal cord. There are also abnormalities such as the dysregulation of dopamine and endogenous cerebral opioids. […] As we expand our knowledge about the etiologic factors that are contributory to this condition current research suggests that the cause is likely multifactorial with environmental, psychosocial, inflammatory/immune, endocrine, and genetic elements.

• #6 Fibromyalgia pathogenesis provides drug target clues

  https://www.drugtargetreview.com/article/14249/fibromyalgia-pathogenesis-target/

  In the cerebrospinal fluid (CFS) of FM patients increased concentrations of substance P (two to three-fold), endogenous opioids (three to four-fold), glutamine (twofold), nerve growth factor (four-fold) and brain-derived neurotrophic factor (two to four-fold) have been observed. […] The altered biochemistry of serotonin and noradrenaline in the CSF and serum is consistent with a decreased endogenous serotonergic and noradrenergic activity responsible for the reduced DNIC in FM patients. […] Thus, low-dose naltrexone (LDN), an opioid receptor antagonist, has been proposed as an effective treatment strategy in some FM patients. […] Pro-inflammatory factors released from microglia, which in FM may be abnormally sensitised, interact with CNS neurons leading to central facilitation of pain processing.

• #7 Fibromyalgia pathogenesis provides drug target clues

  https://www.drugtargetreview.com/article/14249/fibromyalgia-pathogenesis-target/

  Pharmacological treatments that simultaneously raise both serotonin and noradrenaline, for example, tricyclic antidepressants and serotonin noradrenaline reuptake inhibitors have gained interest and demonstrated efficacy in treating FM, further supporting the involvement of the low levels of these neurotransmitters in the pathogenesis of the disease. […] The enhanced wind-up and central sensitisation in FM has been associated with elevated excitatory CNS neurotransmitters. […] Glutamate levels in FM patients are elevated in key pain-processing areas of the brain and these levels change in response to successful treatment that attenuates the pain. […] In addition, a subset of FM patients responded to NMDA receptor antagonists (ketamine, dextromethorphan and memantine) which would be consistent with suppression of an increased glutamatergic activity.

• #8 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8068842/

  The use of fMRI has also been useful for examining the degree of connection between the various brain regions. […] Furthermore, pregabalin has been observed to reduce glutamatergic activity in the insula and functional connectivity between the default mode network and the insula in patients with FM. […] An important role in the excitability of neurons is played by the NR1 subunit of the NMDA receptor, which is necessary for the formation of the receptor itself and its insertion into the synapse. […] Taken together, these data provide evidence that NMDA glutamate receptors in the CNS play a central role in the induction and maintenance of widespread hyperalgesia. […] Over the years, researchers have searched for biomarkers that are capable of detecting these changes. […] Increasing evidence indicates that neurogenic-derived inflammatory processes occurring in the peripheral tissues, spinal cord and brain are also responsible for the pathophysiology of FM.

• #9 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://www.mdpi.com/1422-0067/22/8/3891

  Although central sensitization plays an important role in FM, it is even more important to understand the initial cause, that is, the persistent nociceptive input associated with tissue damage, including peripheral sensitization. […] According to Vierck, if peripheral pain generators can be blocked, the symptoms of FM should disappear or not even develop. […] However, sensitization is not a unitary phenomenon, and a distinction must be made between central, peripheral and psychosocial sensitization. […] The chronic pain typical of FM is due to alterations in central and peripheral sensitization. […] Over the years, researchers have searched for biomarkers that are capable of detecting these changes. […] Increasing evidence indicates that neurogenic-derived inflammatory processes occurring in the peripheral tissues, spinal cord and brain are also responsible for the pathophysiology of FM.

• #10 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://pmc.ncbi.nlm.nih.gov/articles/PMC8068842/

  Studies conducted in patients have confirmed that inflammation is involved in FM. […] It appears that immune cells such as mast cells, monocytes and neutrophils, as mediators of inflammation processes, may also have a function in defining an inflammatory substrate of fibromyalgia. […] Over the years, studies have shown the potential involvement of genetic factors in the onset of FM. […] The role of stress in the exacerbation of fibromyalgia symptoms has been widely described from an epidemiological point of view through both self-reports and clinical questionnaires. […] Sleep disorders are classically described within the symptomatic process of fibromyalgia. However, some recently reported data have generated the hypothesis that such disorders may be included among the causative factors of this pathology, rather than among its manifestations. […] The pathogenesis of fibromyalgia is not well known, and the diagnosis is only clinical at present. […] The chronic pain typical of FM is due to alterations in central and peripheral sensitization.

• #11 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://www.mdpi.com/1422-0067/22/8/3891

  Studies conducted in patients have confirmed that inflammation is involved in FM. […] The release of biologically active agents, such as chemokines and cytokines, leads to the activation of the innate and adaptive immune system. […] Therefore, pro-inflammatory cytokines could play a role in the generation of chronic muscle pain, including FM. […] Over the years, studies have shown the potential involvement of genetic factors in the onset of FM. […] The role of stress in the exacerbation of fibromyalgia symptoms has been widely described from an epidemiological point of view through both self-reports and clinical questionnaires. […] The hypothalamic–pituitary–adrenal axis, central to the stress response, was examined. […] The possible pathogenetic role of the growth hormone (GH)/insulin-like growth factor 1 (IGF-1) axis was also investigated.

• #12 Physiopathology of fibromyalgia | Reumatología Clínica

  https://www.reumatologiaclinica.org/en-physiopathology-fibromyalgia-articulo-S2173574320300605

  Pro-inflammatory and anti-inflammatory imbalance is found in patients with primary fibromyalgia, with more pro-inflammatory cytokines (TNF, IL-1, IL-6 and IL-8) and potential central neuro-inflammation. […] Intestinal dysbiosis has been described as a result rather than a cause of fibromyalgia; there is excessive bacterial growth in the small intestine (SIBO) and there is a clinical improvement after treatment. […] Studies of proteomics and fibromyalgia have found 5 dominant enriched routes: acute phase response signalling, LXR/RXR activation, FXR/RXR activation, coagulation system and complementary system.

• #13 Fibromyalgia: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/329838-overview

  Studies of the neuroendocrine aspects of fibromyalgia have found dysfunction of the HPA axis. The HPA axis is a critical component of the stress-adaptation response. […] Some authors have noted that 5 main measurable neuroendocrine abnormalities are associated with dysfunction of the HPA axis. […] In some studies, nerve growth factor was found to be 4 times higher in the CSF of patients with fibromyalgia than it was in the CSF of individuals without the condition. Nerve growth factor enhances the production of substance P in afferent neurons, increasing an individual’s sensitivity to or awareness of pain. […] A functional brain imaging study has demonstrated activation of glial cells in patients with fibromyalgia; these cells release inflammatory mediators that are thought to sensitize pain pathways and contribute to symptoms such as fatigue.

• #14 Fibromyalgia – Wikipedia

  https://en.wikipedia.org/wiki/Fibromyalgia

  Fibromyalgia can be viewed as a condition of nociplastic pain. […] Nociplastic pain has been referred to as „Nociplastic pain syndrome” because it is coupled with other symptoms including fatigue, sleep disturbance, cognitive disturbance, hypersensitivity to environmental stimuli, anxiety, and depression. […] Some suggest that fibromyalgia is caused or maintained by a decreased vagal tone, which is indicated by low levels of heart rate variability, signaling a heightened sympathetic response. […] Inflammation has been suggested to have a role in the pathogenesis of fibromyalgia. […] Neurogenic inflammation has been proposed as a contributing factor to fibromyalgia. […] A repeated observation shows that autoimmunity triggers, such as traumas and infections, are among the most frequent events preceding the onset of fibromyalgia. […] Though there is a lack of evidence in this area, it is hypothesized that gut bacteria may play a role in fibromyalgia. […] The gut-brain axis, which connects the gut microbiome to the brain via the enteric nervous system, is another area of research.

• #15 Azthena logo with the word Azthena

  https://www.news-medical.net/health/Brain-Inflammation-in-Patients-with-Fibromyalgia.aspx

  Several studies have now shown the presence of neuroinflammation in the brains of patients with fibromyalgia. […] This suggests that fibromyalgia has both neuroinflammation as well as systemic inflammation. […] A more recent brain imaging study of 31 patients and 27 controls (published in Brain, Behaviour and Immunity by Albrecht and colleagues in 2019), found that the patients had widespread microglial activation as measured by [11C]PBR28 signal using a PET scan. […] Activated microglia release pro-inflammatory mediators in the brain, sensitising nociceptive (pain) neural pathways in the brain. […] In summary, there is new evidence of neuroinflammation in patients with fibromyalgia. Knowing that neuroinflammation is seen in patients with fibromyalgia, novel therapeutic targets can be researched and developed to target the sensitisation of pain pathways in the brain that lead to the symptoms, including fatigue. Neuroinflammation is also seen in chronic fatigue syndrome. Blocking the inflammatory mediators released by activated microglia could in part reduce the overall symptoms of fibromyalgia.

• #16 S100 proteins: a new frontier in fibromyalgia research | Molecular Brain | Full Text

  https://molecularbrain.biomedcentral.com/articles/10.1186/s13041-024-01102-9

  S100 proteins, particularly S100A8 and S100A9, are significantly upregulated in inflammatory conditions and have been shown to mediate inflammatory responses and pain perception. Thus, S100 protein-mediated inflammation could be a key element in the pathophysiology of FM. […] The disruption of these S100 proteins in individuals diagnosed with fibromyalgia suggests that these proteins play a pivotal role in the pathogenesis of this disease. […] When released extracellularly, S100 proteins can act as damage-associated molecular patterns (DAMPs) and contribute significantly to inflammatory pain. […] It has been demonstrated that increased proinflammatory cytokines, such as IL-1, IL-6, IL-8, and TNF-, are associated with the development of neuropathic pain and fatigue. […] The pathophysiology of fibromyalgia involves a non-virtuous cycle between hyperalgesia, central sensitization, and S100 protein-mediated inflammation. This cycle significantly contributes to one of the most characteristic symptoms of fibromyalgia, which is chronic widespread pain. […] Concerning the role of S100 proteins on the pathophysiology of FM, it needs a deeper exploration from a molecular point of view; however, this initial information is important to guide future research.

• #17 Pharmacological treatment options for fibromyalgia – The Pharmaceutical Journal

  https://pharmaceutical-journal.com/article/research/pharmacological-treatment-options-for-fibromyalgia

  Fibromyalgia has a strong genetic predisposition — twin studies suggest the contribution is as high as 50%. […] In genetically susceptible individuals, symptoms tend to be triggered by a stressful event such as physical illness, trauma or psychological distress. […] The cerebrospinal fluid (CSF) of patients with fibromyalgia has been shown to have lower levels of biogenic amines, the metabolites of noradrenaline and serotonin, suggesting a deficiency of these neurotransmitters. […] Studies using murine models have shown that modulation of noradrenaline and serotonin in unison provides more effective analgesic effects than modulation of serotonin alone. […] However, there is no direct comparative study between SNRIs and selective serotonin reuptake inhibitors (SSRIs) in fibromyalgia.

• #18 Fibromyalgia Pathophysiology

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9776089/

  The enhanced pain sensitivity and persistence of widespread pain in people with fibromyalgia may be caused by changes in the central processing of sensory input and deficiencies in endogenous pain inhibition. […] Evidence of small fiber neuropathies in patients diagnosed with FMS indicate a connection between the two. […] The recent recognition of SFN in a significant subgroup of patients with FMS reinforces the dysautonomia-neuropathic hypothesis and validates fibromyalgia pain. […] Although numerous genes abnormalities have been identified in FMS their direct correlation or significance is yet to be seen. […] These differences could suggest several subgroups if not different disease processes under the FMS diagnosis.

• #19 Fibromyalgia | PM&R KnowledgeNow

  https://now.aapmr.org/fibromyalgia/

  The pathology behind FM is currently conceptualized as being due to an increased sensitization of the central nervous system (CNS) to pain, and a decrease in the function of the descending tracts that inhibit pain. Many research studies suggest an abnormal temporal summation of painful stimuli, indicating pain amplification at the level of the spinal cord and brain. […] Clinical studies based on functional magnetic resonance imaging (fMRI) have confirmed a central neuronal alteration in nociceptive processes. […] Recent studies reveal that neurogenic derived inflammatory processes can also be responsible for the pathophysiology of FM with the increased release of chemokines and cytokines that activate the immune system. […] Linkage studies over the years have revealed a 50% correlation rate between genetic variants and chronic pain which suggest the prevalence of FM has a genetic predisposition.

• #20 Fibromyalgia Facts & Information – Swing Care

  https://www.swing.care/blog/facts-information-on-fibromyalgia/

  Fibromyalgia is a complex, multifactorial syndrome, making it hard to determine an exact cause. A 2016 study conducted with twins suggests the development of fibromyalgia is partly related to your genes and partly related to your environment. […] While the exact genetic link has yet to be discovered, current research suggests this genetic component may be a genetic change related to the neurotransmitters in your brain. Neurotransmitters broadcast and receive pain signals, and having a genetic mutation in the genes that form neurotransmitters would change how your brain sends and receives these signals. […] Chronic stress is often associated with the development of fibromyalgia. Experts believe long-lasting stressors can increase cytokine levels. In turn, this may activate pain points and peripheral sensitization. Cytokines are part of your immune system and control immune system cell growth and activity. […] There is a strong correlation between fibromyalgia and physical or emotional traumas. One study found that a fibromyalgia diagnosis was highest among U.S. active duty servicemen who were also seeking treatment for post-traumatic stress disorder (PTSD).

• #21 Fibromyalgia: Pathogenesis, Mechanisms, Diagnosis and Treatment Options Update

  https://www.mdpi.com/1422-0067/22/8/3891

  The role of stress in the exacerbation of fibromyalgia symptoms has been widely described from an epidemiological point of view through both self-reports and clinical questionnaires. […] Studies published in recent years have described a bidirectional correlation between sleep disturbances and widespread musculoskeletal pain, and it even seems that insomnia tends to precede the onset of pain and has predictive value regarding its onset and its persistence. […] The chronic pain typical of FM is due to alterations in central and peripheral sensitization. […] The pathogenesis of fibromyalgia is not well known, and the diagnosis is only clinical at present. […] Numerous studies, however, provide insights into the pathophysiology of fibromyalgia.

• #22 Physiopathology of fibromyalgia | Reumatología Clínica

  https://www.reumatologiaclinica.org/en-physiopathology-fibromyalgia-articulo-S2173574320300605

  Characteristically in fibromyalgia there is dysfunction of the hypothalamus-hypophasis-suprarenal axis. This affects the adaptive response, with alterations in the levels of corticotrophin-releasing hormone, over-production of adrenocorticotrophic hormone (ACTH) and a fall in cortisol level. […] The central nociceptive processing by C fibres towards the spine causes abnormal recovery in the dorsal horn neurone, forming part of the central sensitisation secondary to active amplification, increasing the response to pain and recruiting low threshold sensory inputs which are able to activate the pain circuit. […] Several studies of fibromyalgia have shown high levels of oxidative stress markers; the accumulation of damaged mitochondrial DNA in cells leads to an innate inflammatory response; the mitochondrial DNA content in fibromyalgia correlates inversely with TNF levels.

• #23 Pathophysiology of Fibromyalgia | Encyclopedia MDPI

  https://encyclopedia.pub/entry/39160

  Physiological stress can lead to symptoms such as fatigue, decreased work capacity and insomnia. […] Patients with fibromyalgia frequently demonstrate abnormalities in the autonomic nervous system’s (ANS). […] Inappropriate immune responses and specifically IgG immunoglobulin has demonstrated the ability to cause pain without obvious inflammation or nerve damage.

• #24

  https://apcz.umk.pl/JEHS/article/view/JEHS.2020.10.09.038

  Pathogenesis of fibromyalgia is multifactorial. Genetic factors, in addition to environmental factors, such as psychical stress and various types of infection, are considered to be the triggers of the disease. Central sensitization became a commonly accepted hypothesis of the fibromyalgias pathogenesis. […] However, the newest finding of small fiber neuropathy in patients with fibromyalgia supports another hypothesis, in which the disease is presented as stress-related dysautonomia with neuropathic pain features. […] Understanding the pathogenesis of fibromyalgia is essential to provide the best care to the patients with fibromyalgia. Although there are multiple evidence for central sensitization hypothesis, new findings continue to emerge and question commonly accepted paradigm. Despite numerous findings on etiology of fibromyalgia, more studies are needed.

• #25 Fibromyalgia Pathophysiology

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9776089/

  This article examines the biological, genetic, and environmental aspects of fibromyalgia that may have an impact on its pathogenesis. […] Symptoms of fibromyalgia may be related to aberrations in the endogenous inhibition of pain as well as changes in the central processing of sensory input. […] Dysfunctional pain processing may also be influenced by exposure to physical or psychological stressors, abnormal biologic reactions in the autonomic nervous system, and neuroendocrine responses. […] The exact pathophysiological mechanism behind fibromyalgia remains undefined, though it is likely multifactorial in origin including abnormal cortical processing, reductions in inhibitory pain modulatory mechanisms and molecular changes to the pain pathway. […] What is clear however is that patients with fibromyalgia have increased sensitivity to a variety of stimuli, including mechanical and ischemic pressure, heat, and cold.

• #26 Fibromyalgia pathogenesis explained by a neuroendocrine multistable model | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0303573

  Fibromyalgia (FM) is a central disorder characterized by chronic pain, fatigue, insomnia, depression, and other minor symptoms. Knowledge about pathogenesis is lacking, diagnosis difficult, clinical approach puzzling, and patient management disappointing. We conducted a theoretical study based on literature data and computational analysis, aimed at developing a comprehensive model of FM pathogenesis and addressing suitable therapeutic targets. We started from the evidence that FM must involve a dysregulation of central pain processing, is female prevalent, suggesting a role for the hypothalamus-pituitary-gonadal (HPG) axis, and is stress-related, suggesting a role for the HP-adrenocortical (HPA) axis. Central pathogenesis was supposed to involve a pain processing loop system including the thalamic ventroposterolateral nucleus (VPL), the primary somatosensory cortex (SSC), and the thalamic reticular nucleus (TRN). For decreasing GABAergic and/or increasing glutamatergic transmission, the loop system crosses a bifurcation point, switching from monostable to bistable, and converging on a high-firing-rate steady state supposed to be the pathogenic condition. Thereafter, we showed that GABAergic transmission is positively correlated with gonadal-hormone-derived neurosteroids, notably allopregnanolone, whereas glutamatergic transmission is positively correlated with stress-induced glucocorticoids, notably cortisol. Finally, we built a dynamic model describing a multistable, double-inhibitory loop between HPG and HPA axes. This system has a high-HPA/low-HPG steady state, allegedly reached in females under combined premenstrual/postpartum brain allopregnanolone withdrawal and stress condition, driving the thalamocortical loop to the high-firing-rate steady state, and explaining the connection between endocrine and neural mechanisms in FM pathogenesis. Our model accounts for FM female prevalence and stress correlation, suggesting the use of neurosteroid drugs as a possible solution to currently unsolved problems in the clinical treatment of the disease.

• #27

  https://journals.lww.com/painrpts/fulltext/2025/02000/decoding_the_connection__unraveling_the_role_of.8.aspx

  The gut microbiome is emerging as a critical player in the pathophysiology of fibromyalgia, offering mechanistic insights as well as potential diagnostic and therapeutic applications. […] Recent studies have unveiled a promising avenue of investigation—the role of the gut microbiome in fibromyalgia. […] These alterations were independent of host and environmental factors such as diet, physical activity, medications, and other medical comorbidities. […] These experiments demonstrate that the gut microbiome is not only altered in fibromyalgia but that it may play a causal role in the syndrome. […] In recent years, increasing evidence highlights neuroinflammation as an important feature of fibromyalgia. […] The intricate cross-talk between the gut microbiome and the immune system makes it a possible candidate to mediate the effect of the environment on immunity.

• #28

  https://journals.lww.com/painrpts/fulltext/2025/02000/decoding_the_connection__unraveling_the_role_of.8.aspx

  In conclusion, current evidence suggests that gut microbiota may affect pain hypersensitivity in fibromyalgia both through immune activation and by the disrupted metabolism of bacterial-derived molecules. […] The intricate interplay between the gut microbiome and fibromyalgia is a burgeoning field of research that holds promise for unraveling the mysteries surrounding this complex disorder. […] Alterations in the gut microbial community appear to contribute to the immune activation and dysregulated circulating metabolite profile observed in patients with fibromyalgia.

• #29 Identification of unique genomic signatures in patients with fibromyalgia and chronic pain | Scientific Reports

  https://www.nature.com/articles/s41598-024-53874-8

  The presence of multiple subgroups within FM patients reflects the inherent clinical heterogeneity associated with FM and chronic pain disorders which explains the diagnostic difficulty often encountered in a clinical setting. The two major subgroups displayed distinct transcriptional profiles indicating two different etiologies that are grouped together under the same general diagnosis of FM. […] The differences observed among the patients suggest that different treatment approaches will be required for patients with FM.

• #30 Fibromyalgia pathogenesis provides drug target clues

  https://www.drugtargetreview.com/article/14249/fibromyalgia-pathogenesis-target/

  The mechanism(s) of action of the gabapentanoids, pregabalin and gabapentin appear to provide a unique, albeit limited, control of the neuronal hyperexcitability and central sensitisation associated with FM. […] Although inflammation has also been suggested to underlie the pathology in FM, literature on cytokines has been variable and the studies have several limitations that could influence the findings. […] Advances in the understanding of the pathophysiology of FM are providing clues as to underlying mechanisms as targets for new medications. […] Bioamine modulation and voltage-gated Ca2+ channel 2 subunits in addition to dopamine receptors, NMDA receptors, cannabinoid receptors and melatonin receptors are emerging as drug targets.

• #31 Azthena logo with the word Azthena

  https://www.news-medical.net/health/What-Conditions-Are-Similar-to-Fibromyalgia.aspx

  Fibromyalgia is a complex syndrome with a wide array of symptoms, including chronic widespread pain, fatigue, sleep disturbances, cognitive dysfunction, and psychological issues. The diagnosis and management of this condition remain challenging due to its multifaceted nature and the evolving understanding of its pathogenesis. […] However, the precise molecular mechanisms linking inflammation to pain amplification remain unclear. […] While the exact mechanisms underlying these associations remain unclear, it is evident that shared pathophysiological pathways, such as inflammation, immune dysfunction, and neurotransmitter imbalances, may contribute to the development and progression of all these conditions. […] Further research is needed to elucidate molecular mechanisms and develop targeted therapeutic interventions for fibromyalgia and its comorbidities.

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