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How Does Fibromyalgia Affect The Nervous System

5 min read

How Does Fibromyalgia Affect The Nervous System – Fibromyalgia syndrome (FMS) is a chronic, generalized muscle pain disorder associated with sleep disturbance, fatigue, and cognitive dysfunction. Apart from central pain pathways, there is no definitive pathogenesis. We previously reported elevated levels of the neuropeptide substance P (SP) and its structural analog hemokinin-1 (HK-1) ​​and the pro-inflammatory cytokines IL-6 and TNF in FMS patients compared to sedentary controls. We hypothesize that thalamic mast cells promote inflammation and pain by secreting neurosensitive molecules including histamine, IL-1β, IL-6, and TNF, as well as calcitonin-related peptide (CGRP), HK-1, and SP. These molecules can directly stimulate thalamic nociceptive neurons or stimulate microglia in the diencephalon. As a result, preventing mast cell stimulation may be used as a new approach to reduce pain and FMS symptoms.

Fibromyalgia syndrome is a disease associated with chronic generalized muscle pain, stiffness, general fatigue, sleep disturbances (Klauw et al., 2011; Schmidt-Wilke and Klauw, 2011; Klauw, 2014) and cognitive problems (Theocharides et al.; 2015b). Houser et al., 2019) was evaluated by the FSQ (Ferrari and Russell, 2013), which has a sensitivity of approximately 93% and a specificity of 92% (Clau, 2014). FMS affects approximately 5% of adults, primarily women aged 20–60 (Branco et al., 2010) and belongs to a complex family of conditions known as CSS (Table 1) (Younes, 2007; Theocharides, 2013). Central sensitization is recognized as the underlying mechanism (Woodman, 2013) and allodynia, pain from otherwise painless stimuli (Russell and Larson, 2009) and hyperalgesia (Staudt et al., 2001). response to painful stimuli (Wolf, 2011). The pathogenesis of FMS remains unclear and without objective diagnostic criteria (McBeth and Mulvey, 2012; Wolfe and Valit, 2013). FMS patients have reduced pain tolerance, particularly to heat and cold (Desmeules et al., 2003). There is substantial evidence of altered pain network circuitry (Jensen et al., 2012; Flodin et al., 2014) and abnormal pain processing (Staud, 2011) in FMS.

How Does Fibromyalgia Affect The Nervous System

The PubMed database was searched from 1960 to 2018 using the terms fatigue, fibromyalgia, hypothalamus, inflammation, mast cells, pain, and stress. Only articles in English are included.

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Here, we discuss how brain mast cell release of neurosensitive mediators in the thalamus leads to focal inflammation and contributes to FMS pathogenesis.

It has recently been suggested that FMS may involve localized inflammation in the hypothalamus (Theocharides et al., 2015c). Elevation of inflammatory chemokines/cytokines can negatively affect symptoms (Bazzichi et al., 2007; Carvalho et al., 2008; Nugraha et al., 2013) through sensitization of peripheral and central nociceptors (Uceyler et al., 2011; Behm et al., 2012; Hornig et al., 2015). Increased levels of the inflammatory chemokine IL-8 (CXCL8) in serum and CSF have been reported in patients with FMS (Ross et al., 2010; Cadetoff et al., 2012; Rodriguez-Pinto et al., 2014). Chemokines facilitate nociception by directly acting on chemokine receptors present in the pain pathway (Abbadi, 2005; Charo and Ransokhov, 2006).

The cytokines TNF and IL-17 mediate the inflammatory response (Romero-Sanchez et al., 2011; Griffin et al., 2012). In patients with FMS, IL-17 plasma levels were increased and correlated with TNF levels (Pernambuco et al., 2013). CSF and serum IL-17 are also positively associated with pain (Meng et al., 2013) and anxiety (Liu et al., 2012). Mast cells themselves can secrete IL-17; In addition, IL-6 and TGFβ promote the development of Th-17 cells from mast cells (Kenna and Brown, 2013).

Fibromyalgia syndrome is exacerbated by stress (Genen et al., 2002), which increases pain responses (Bote et al., 2012, 2013). Plasma concentrations of cortisol increase in the evening, indicating a disruption of the circadian rhythm (Crawford et al., 2004). Serum levels of CRH, secreted under stress, are increased in patients with FMS (Illioni et al., 2016). CRH in the CSF of such patients was also increased and correlated with pain severity (McLean et al., 2006). Physiological stress has been reported to be the most common trigger in patients with systemic mastocytosis (SM) (Jennings et al., 2014), which is frequently encountered in FMS (Theocharides et al., 2015d, 2019). We reported increased CRH levels in the serum of a patient with systemic mastocytosis (Theocharides et al., 2014). CRH can induce human mast cells to secrete VEGF without histamine or tryptase (Cao et al., 2005). CRH also has a synergistic effect on NT-stimulating VEGF release. As a result, skin permeability increases and the blood-brain barrier (BBB) ​​is damaged (Esposito et al., 2002; Donelan et al., 2006; Theoharides and Konstantinidou, 2007). Stress also disrupts the gut-blood barrier (Theocharides et al., 1999; Vallon et al., 2008), allowing molecules associated with the gut microbiome, such as propionate (Minerby et al., 2019), to enter and contribute to the brain. allows focusing on inflammation These results suggest that mast cells may act as an “immune barrier for the brain” (Theocharides, 1990; Ribatti, 2015).

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Neuropeptide SP (Russell, 1998) and NGF (Giovengo et al., 1999) levels are elevated in the CSF of FMS patients. NGF has been reported to enhance nociception and hyperalgesia (Maren, 2017). The SP receptor NK-1 has been implicated in the pathophysiology of pain (Greenwood-Wan et al., 2014). We reported increased levels of SP, its structural analog Hemokinin-1 (HK-1), and TNF in FMS patients (Illioni et al., 2016). SP (Theocharides et al., 2010a, b) and NGF (Levi-Montalcini, 1987) can stimulate mast cells. In addition, SP expressed CRHR-1 in mast cells (Scholzen et al., 2001). Cerebrovascular mast cells are stimulated by CGRP (Reiner-Reboufel et al., 1994; Ottosson and Edvinsson, 1997), which is well established to be involved in the pathophysiology of headache (Edvinsson, 2018). In addition to neuropeptides, sex hormones can also affect the reactivity of mast cells. For example, estradiol enhances immune (Kovats, 2015) and allergic (Hawks et al., 2015) processes. Specifically, we reported expression of estrogen receptors in rodent mast cells (Pang et al., 1995). We also reported that 17β-estradiol further enhanced mast cell stimulation by SP ( Theocharides et al., 1993 ). Findings like these may help explain why FMS is more common in women.

In addition to allergic responses, mast cells contribute to innate immunity, (Galli et al., 2011) autoimmunity (Rottem and McCoury, 2005) and inflammation (Theocharides et al., 2010a).

Increasing evidence supports a role for mast cells in FMS (Lucas et al., 2006; Pollack, 2014) and comorbid disorders (Theocharides, 2013) and other inflammatory (Gally et al., 2008; Theocharides et al., 2010a) and pain. conditions (Heron and Dubayl, 2013; Chatterjee and Martynov, 2014), as well as neuroimmune interactions (Skaper et al., 2017) (Figure 1). Chronic urticaria involving stimulation of skin mast cells is common in FMS (Torresani et al., 2009). In addition, mast cells are significantly increased in the papillary dermis of FMS patients (Blanco et al., 2010). The chemokines monocyte chemoattractant protein-1 (MCP-1/CCL2) and eotaxin (CCL-11) are elevated in the plasma of FMS patients ( Zhang et al., 2008 ). MCP-1 is a potent mast cell chemoattractant (Conti et al., 1998) and also induces mast cell recruitment in rodents (Conti and Theocharides, 1994). MKP-1 induced chronic muscle hyperalgesia in mice via activation of the high-affinity receptor, CC Chemokine receptor 2 (CCR2), in peripheral nerve terminals (Alvarez et al., 2014). Myoblasts treated with MCP-1 secreted IL-1β, a key inflammatory cytokine ( Zhang et al., 2008 ). C-reactive protein (CRP) is now considered a marker of chronic inflammation. CRP may be useful in the diagnosis of FMS (and depression/anxiety often accompanying FMS), although there is no direct correlation (De Berardis et al., 2006, 2017; Orsolini et al., 2018).

Figure 1. Schematic diagram illustrating the involvement of mast cells in pain generation in FMS. Mast cells of the thalamus (purple) secrete inflammatory and neurosensitive mediators (CRH, histamine, IL-6, HK-1, SP, TNF, Tryptase). These mediators may then activate microglia in the thalamic nuclei or regulate nociceptive pathways that produce pain. Natural molecules that can inhibit stimulated mast cells and/or microglia are flavonoids such as luteolin or tetramethoxyluteolin (Metlut).

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Mast cells originate from the bone marrow and mature in response to SCF acting through the tyrosine kinase KIT receptor on the cell surface ( Halli et al., 2011 ). Mast cell lineages migrate in all tissues. As a result, mast cell mediators affect all organs and can cause many symptoms. Mast cells are located near blood vessels and nerve endings; in the brain, mast cells are located in the thalamus, hypothalamus, and midbrain (Edvinson et al., 1976; Lambracht-Hall et al., 1990; Theocharides et al., 2015d).

Mast cells are stimulated by IgE through activation of a unique surface receptor (FcεRI) (Rivera et al., 2008). Mast cells can also be stimulated through TLRs (Ibrahim and St. John, 2010; Zhang et al., 2010). Stimulated mast cells secrete several vasoactive, inflammatory and neurosensory molecules (Galli et al., 2008; Theocharides et al., 2010a). Mast cell stimulation can be enhanced by the cytokine IL-33, (Fux et al., 2014), VEGF, (Theocharides et al., 2010b) and TNF (Tarakanova et al., 2010b). 2017) or IL-1β (Tarakanova et al., 2018). Whom

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