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==Pathophysiology== Fibromyalgia is a '''pain processing disorder''' involving altered pain processing in the [[central nervous system]] which causes widespread pain and a constellation of additional symptoms.<ref name="ScienceOfFibro" /> Neuroimaging and brain imaging studies have shown that the pain and other symptoms of fibromyalgia appear to be caused by neurochemical imbalances in the [[central nervous system]] that lead to a '''central amplification''' of pain perception (Clauw et al., 2011).<ref name="ScienceOfFibro" /> According to the CDC, there is no evidence that a single event "causes" fibromyalgia, instead it appears to be associated with many physical and/or emotional [[Stress|stressors]] and other [[#risk_factors|risk factors]] that may trigger or aggravate symptoms. These include certain [[Infection|infections]], such as a [[Viral infection|viruses]] or [[Lyme disease]], as well as emotional or physical [[trauma]] (injury)."<ref name="FibroBasics" /><ref name="CDC-complications" /> The widespread pain is severe, debilitating, and abnormal in processing its pain. [[Sleep dysfunction|sleep disturbance]] and [[fatigue]] are common symptoms.<ref name="omf">{{Cite news |url =https://www.omf.ngo/what-is-mecfs-old/fibromyalgia/ | title = What is Fibromyalgia?|work=Open Medicine Foundation|access-date=2018-08-09|language=en-US | last = | first = | date = |quote= | author-link = |archive-url=|archive-date=}}</ref> *May 2012, [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394355/ Fibromyalgia Syndrome: An Overview of Pathophysiology, Diagnosis and Management]<ref name="Firdous2012">{{Cite journal | last = Jahan | first = Firdous | last2 = Nanji | first2 = Kashmira | last3 = Qidwai | first3 = Waris | last4 = Qasim | first4 = Rizwan | date = 2012 | title = Fibromyalgia Syndrome: An Overview of Pathophysiology, Diagnosis and Management| url = https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3394355/|journal=Oman Medical Journal|volume=27|issue=3 | pages = 192–195|doi=10.5001/omj.2012.44|issn=1999-768X|pmid=22811766|via=}}</ref> ''See'' Table 1: "Conditions associated with fibromyalgia." Musculoskeletal, [[:Category:genitourinary signs and symptoms|genitourinary]], [[Gastrointestinal system|gastrointestinal]], and miscellaneous conditions often exist among fibromyalgia patients. <blockquote>Pathophysiology: Although the etiology remains unclear, characteristic alterations in the [[Sleep dysfunction|pattern of sleep]] and changes in neuroendocrine transmitters such as [[serotonin]], substance P, growth hormone and [[cortisol]] suggest that regulation of the [[Autonomic nervous system|autonomic]] and [[neuroendocrine system]] appears to be the basis of the syndrome. Fibromyalgia is not a life-threatening, deforming, or [progressive disease. [[Anxiety]] and [[depression]] are the most common association. Aberrant pain processing, which can result in [[chronic pain]], may be the result of several interplaying mechanisms. [[Central sensitization]], blunting of inhibitory pain pathways and alterations in [[neurotransmitter]]s lead to aberrant neurochemical processing of sensory signals in the CNS, thus lowering the threshold of pain and amplification of normal sensory signals causing constant pain." (Firdous et al, 2012)<ref name="Firdous2012" /></blockquote> <blockquote>The frequent co-morbidity of fibromyalgia with [[Mood swings|mood disorders]] suggests a major role for the stress response and for neuroendocrine abnormalities. The [[hypothalamic pituitary axis]] (HPA axis) is a critical component of the stress-adaptation response. In FMS, stress adaptation response is disturbed leading to stress induce symptoms. Psychiatric co-morbidity has been associated with FMS and needs to be identified during the consultation process, as this requires special consideration during treatment.<ref name="Firdous2012" /></blockquote> *May 2018, [https://www.chiropractic.ca/wp-content/uploads/2018/05/107243-2_Chiro_62_1d_Bourgaize.pdf A comparison of the clinical manifestation and pathophysiology of myofascial pain syndrome and fibromyalgia: implications for differential diagnosis and management] *Jun 2018, [https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0198625 SNPs in inflammatory genes] [[CCL11]], [[CCL4]] and [[MEFV]] in a fibromyalgia family study.<ref name="Zhang2018" /> <blockquote>SNPs with significant TDTs were found in 36% of the cohort for CCL11 and 12% for MEFV, along with a protein variant in CCL4 (41%) that affects CCR5 down-regulation, supporting an immune involvement for FM.</blockquote> *Jul 2018, [https://www.jrheum.org/content/early/2018/07/09/jrheum.180083 Primary and Secondary Fibromyalgia Are The Same: The Universality of Polysymptomatic Distress] <blockquote>Fibromyalgia can be considered either primary, or dominant, also known as idiopathic fibromyalgia, or secondary. In the primary form, the causes of the disorder are unknown, but in secondary fibromyalgia, the disorder usually occurs alongside other debilitating medical conditions, such as rheumatoid arthritis (RA), lupus, and multiple sclerosis.<ref>{{Cite journal | last = Wolfe | first = Frederick | last2 = Walitt | first2 = Brian | last3 = Rasker | first3 = Johannes J. | last4 = Häuser | first4 = Winfried | date = 2018-07-15 | title = Primary and Secondary Fibromyalgia Are The Same: The Universality of Polysymptomatic Distress |url =https://www.jrheum.org/content/early/2018/07/09/jrheum.180083|journal=The Journal of Rheumatology|volume =46|issue=2 | pages = 204-212|language=en|doi=10.3899/jrheum.180083|issn=0315-162X|pmid=30008459}}</ref></blockquote> ===Immune system research=== Dr. [[Jarred Younger]] believes an overactive [[immune system]] is the cause and will be conducting a study to test this hypothesis.<ref>{{Cite news |url =http://nationalpainreport.com/new-uab-study-could-radically-change-fibromyalgia-treatment-as-we-know-it-8833437.html | title = New UAB Study Could Radically Change Fibromyalgia Treatment As We Know It | last = Gregory Burch | first = Donna | date = 2017-04-24|work=National Pain Report|access-date=2018-08-09|archive-url=|archive-date=|language=en-US}}</ref><ref>{{Cite web | url = https://www.youtube.com/watch?v=8e5xKX036bE | title = Testing the fibromyalgia immune system with lipopolysaccharide (LPS) | last = Younger | first = Jarred | authorlink = Jarred Younger | date = May 24, 2017 | website = YouTube | archive-url=|archive-date=|access-date=|via=Younger Lab}}</ref> An overactive immune system can cause [[inflammation]] and [[chronic pain]].<ref>{{Cite news |url =https://www.epainassist.com/autoimmune/what-is-overactive-immune-system | title = What is Overactive Immune System {{!}} Causes {{!}} Symptoms {{!}} Treatment | last = Kerkar | first = Pramod | date = 2016-09-29|work=ePainAssist|access-date=2018-10-04|archive-url=|archive-date=|language=en-gb}}</ref><ref>{{Cite news |url =https://www.webmd.com/a-to-z-guides/autoimmune-diseases | title = Autoimmune Diseases|work=WebMD|access-date=2018-10-04|language=en-US}}</ref> Dr. William Pridgen's research of [[Herpes simplex virus#HSV-1|HSV-1]] (cold sore virus) as being involved in FM has conducted a successful Phase III clinical trial, which had been fast-tracked by the [[Food and Drug Administration]] (FDA), of a combination drug that suppresses this virus and also helps with pain. {{See also|Fibromyalgia drugs|Fibromyalgia drugs (see drug trials section for IMC-1)}} Recognizing FM may involve activation of the [[immune system]] researchers performed [[Whole exome sequencing|exome sequencing]] on [[chemokine]] genes in a region of chromosome 17 identified in a genome-wide family association study. Their conclusion: "SNPs with significant TDTs were found in 36% of the cohort for [[CCL11]] and 12% for [[MEFV]], along with a protein variant in CCL4 (41%) that affects CCR5 down-regulation, supporting an immune involvement for FM."<ref name="Zhang2018">{{Cite journal | last = Zhang | first = Zhifang | last2 = Feng | first2 = Jinong | last3 = Mao | first3 = Allen | last4 = Le | first4 = Keith | last5 = Placa | first5 = Deirdre La | last6 = Wu | first6 = Xiwei | last7 = Longmate | first7 = Jeffrey | last8 = Marek | first8 = Claudia | last9 = Amand | first9 = R. Paul St | date = 2018-06-21 | title = SNPs in inflammatory genes CCL11, CCL4 and MEFV in a fibromyalgia family study| url = http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0198625|journal=PLOS ONE|language=en|volume=13|issue=6| pages = e0198625|doi=10.1371/journal.pone.0198625|issn=1932-6203|pmid=29927949|via=}}</ref> Dr David Andersson from the Institute of Psychiatry, Psychology and Neuroscience at King's College London, led a new study into Fibromyalgia being an immune system disorder.<ref name="Goebel2021">{{Cite journal | last = Goebel | first = Andreas | last2 = Krock | first2 = Emerson | last3 = Gentry | first3 = Clive | last4 = Israel | first4 = Mathilde R. | last5 = Jurczak | first5 = Alexandra | last6 = Urbina | first6 = Carlos Morado | last7 = Sandor | first7 = Katalin | last8 = Vastani | first8 = Nisha | last9 = Maurer | first9 = Margot | date = 2021-07-07 | title = Passive transfer of fibromyalgia symptoms from patients to mice | url =https://www.jci.org/articles/view/144201?key=51bf6d85e305f6b62f87#SEC4|journal=The Journal of Clinical Investigation|language=en|volume=131|issue=13|doi=10.1172/JCI144201|issn=0021-9738}}</ref><blockquote>Andersson and his colleagues harvested blood from 44 people with fibromyalgia and injected purified antibodies from each of them into different mice. The mice rapidly became more sensitive to pressure and cold, and displayed reduced grip strength in their paws. Animals injected with antibodies from healthy people were unaffected.<ref name="Guardian2021">{{Cite web | url = http://www.theguardian.com/society/2021/jul/01/fibromyalgia-may-be-a-condition-of-the-immune-system-not-the-brain-study | title = Fibromyalgia may be a condition of the immune system not the brain – study | date = 2021-07-01 | website = The Guardian|language=en|access-date=2021-07-08}}</ref></blockquote><blockquote>Prof Camilla Svensson from the Karolinska Institute in Sweden, who was also involved in the study, said: “Antibodies from people with fibromyalgia living in two different countries, the UK and Sweden, gave similar results, which adds enormous strength to our findings.”<ref name="Guardian2021" /></blockquote> === Brain and spinal cord research === A 2004 study by Heffez et al. studied 270 patients with FM and found that 46% had [[cervical spinal stenosis]] and 20% [[chiari malformation]].<ref name="Heffez2004">{{Cite journal | last = Heffez | first = Dan S. | last2 = Ross | first2 = Ruth E. | last3 = Shade-Zeldow | first3 = Yvonne | last4 = Kostas | first4 = Konstantinos | last5 = Shah | first5 = Sagar | last6 = Gottschalk | first6 = Robert | last7 = Elias | first7 = Dean A. | last8 = Shepard | first8 = Alan | last9 = Leurgans | first9 = Sue E. | date = 2004-04-09 | title = Clinical evidence for cervical myelopathy due to Chiari malformation and spinal stenosis in a non-randomized group of patients with the diagnosis of fibromyalgia| url = https://link.springer.com/article/10.1007/s00586-004-0672-x|journal=European Spine Journal|language=en|volume=13|issue=6 | pages = 516–523|doi=10.1007/s00586-004-0672-x|issn=0940-6719|pmc=|pmid=15083352|via=}}</ref> In 2007, Heffez et al. saw significant improvement in physical and mental well-being was found in patients with cervical stenosis who received surgery.<ref name="Heffez2007">{{Cite journal | last = Heffez | first = Dan S. | last2 = Ross | first2 = Ruth E. | last3 = Shade-Zeldow | first3 = Yvonne | last4 = Kostas | first4 = Konstantinos | last5 = Morrissey | first5 = Mary | last6 = Elias | first6 = Dean A. | last7 = Shepard | first7 = Alan | date = 2007 | title=Treatment of cervical myelopathy in patients with the fibromyalgia syndrome: outcomes and implications |url =https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2200733/|journal=European Spine Journal|volume=16|issue=9 | pages = 1423–1433|doi=10.1007/s00586-007-0366-2|issn=0940-6719|pmc=2200733|pmid=17426987|quote=|via=}}</ref> A second study in 2007 by Andrew Holman found that 71% had cervical [[spinal cord]] compression.<ref name="Holman2008">{{Cite journal | date = 2008-07-01 | title = Positional Cervical Spinal Cord Compression and Fibromyalgia: A Novel Comorbidity With Important Diagnostic and Treatment Implications |url =https://www.sciencedirect.com/science/article/pii/S1526590008004379|journal=The Journal of Pain|language=en|volume=9|issue=7 | pages = 613–622|doi=10.1016/j.jpain.2008.01.339|issn=1526-5900 | last = Holman | first = Andrew|quote=|via=|pmc=|pmid=}}</ref> In the past many patients were misdiagnosed with FM when further testing would have revealed the correct diagnosis for the cause of their pain; the 2010 (updated in 2016) ACR criteria has helped curb misdiagnoses.<ref name="misdiagnosis">{{Cite news | title = Common Misdiagnoses of Fibromyalgia| url = https://www.webmd.com/fibromyalgia/guide/common-misdiagnoses-of-fibromyalgia#|work=WebMD|access-date=2018-11-26|language=en-US | last = | first = | date = |archive-url=|archive-date=}}</ref><ref name="Wolfe2018" /> Various types of brain imaging are being used to research FM. {{See also|Fibromyalgia notable studies}} In 2002, an [[Functional magnetic resonance imaging|fMRI]] study conducted by Richard Gracely and Daniel Claw found people with FM "have measurable pain signals in their brains, from a gentle finger squeeze that barely feels unpleasant to people without the disease."<ref name="anapsid2002">{{Cite web | url = http://www.anapsid.org/cnd/diagnosis/brainpain.html | title = Fibromyalgia Pain Isn't All In Patient's Heads, New Brain Study Finds|website= Melissa Kaplan's Chronic Neuroimmune Diseases| date = 2014 |access-date=2021-11-28}}</ref> A 2007 study by Borsook et al. found decreased gray matter density relative to controls in cingulate cortex (CC), medial prefrontal cortex (Med. PFC), parahippocampal gyrus (PHG) and insula.<ref name="Borsook2007">{{Cite journal | last = Borsook | first = David | last2 = Moulton | first2 = Eric A | last3 = Schmidt | first3 = Karl F | last4 = Becerra | first4 = Lino R | date = 2007-09-11 | title = Neuroimaging Revolutionizes Therapeutic Approaches to Chronic Pain | url =https://link.springer.com/article/10.1186/1744-8069-3-25|journal=Molecular Pain|language=en|volume=3|issue=1 | pages = 1744–8069-3-25|doi=10.1186/1744-8069-3-25|issn=1744-8069|pmid=17848191|via=}}</ref> In 2015, Loggia et al. imaged [[neuroinflammation]] due to [[Glial cell|glial]] activation using MR/PET imaging.<ref name="Loggia2015">{{Cite journal | last = Loggia | first = Marco L. | last2 = Chonde | first2 = Daniel B. | last3 = Akeju | first3 = Oluwaseun | last4 = Arabasz | first4 = Grae | last5 = Catana | first5 = Ciprian | last6 = Edwards | first6 = Robert R. | last7 = Hill | first7 = Elena | last8 = Hsu | first8 = Shirley | last9 = Izquierdo-Garcia | first9 = David | date = 2015-01-08 | title = Evidence for brain glial activation in chronic pain patients |url =https://academic.oup.com/brain/article/138/3/604/333527?searchresult=1|journal=Brain|language=en|volume=138|issue=3 | pages = 604–615|doi=10.1093/brain/awu377|issn=1460-2156}}</ref> In 2017, López-Solà et al. identified three [[brain]] patterns based on [[Functional magnetic resonance imaging|fMRI]] responses to pressure pain and non-painful multisensory stimulation. "These patterns, taken together, discriminate FM from matched healthy controls with 92% sensitivity and 94% specificity."<ref name="Lopez2017">{{Cite journal | last = López-Solà | first = Marina | last2 = Woo | first2 = Choong-Wan | last3 = Pujol | first3 = Jesus | last4 = Deus | first4 = Joan | last5 = Harrison | first5 = Ben J. | last6 = Monfort | first6 = Jordi | last7 = Wager | first7 = Tor D. | date = 2017 | title=Towards a neurophysiological signature for fibromyalgia| url = https://www.ncbi.nlm.nih.gov/pubmed/27583567|journal=Pain|volume=158|issue=1 | pages = 34–47|doi=10.1097/j.pain.0000000000000707|issn=1872-6623|pmid=27583567|via=}}</ref> In 2018, Albrecht et al used [[Positron emission tomography|PET]] scans to document [[Glial cell|glial]] activation.<ref name="Albrecht2018">{{Cite journal | last = Albrecht | first = Daniel S. | last2 = Forsberg | first2 = Anton | last3 = Sandstrom | first3 = Angelica | last4 = Bergan | first4 = Courtney | last5 = Kadetoff | first5 = Diana | last6 = Protsenko | first6 = Ekaterina | last7 = Lampa | first7 = Jon | last8 = Lee | first8 = Yvonne C. | last9 = Höglundi | first9 = Caroline Olgart | date = 2018-09-14|others=Catana, Ciprian; Cervenka, Simon; Akeju, Oluwaseun; Lekander, Mats; Cohen, George; Halldin, Christer; Taylor, Norman; Kim, Minhae; Hooker, Jacob M.; Loggia, Marco L. | title = Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation | url =https://www.sciencedirect.com/science/article/pii/S0889159118302423|journal=Brain, Behavior, and Immunity|language=en|volume= | pages = |doi=10.1016/j.bbi.2018.09.018|issn=0889-1591|via=}}</ref> Also in 2018, Martucci et al. found unbalanced activity between the ventral and dorsal cervical spinal cord. Ventral neural processes were increased and dorsal neural processes were decreased which may reflect the presence of [[central sensitization]] contributing to [[fatigue]] and other bodily symptoms in FM.<ref name="Martucci2018">{{Cite journal | last = Martucci | first = Katherine T | last2 = Weber | first2 = Kenneth A | last3 = Mackey | first3 = Sean C | date = 2018-10-03 | title = Altered Cervical Spinal Cord Resting State Activity in Fibromyalgia| url = https://onlinelibrary.wiley.com/doi/abs/10.1002/art.40746|journal=Arthritis & Rheumatology|language=en|doi=10.1002/art.40746|issn=2326-5191}}</ref> === Fibromyalgia is not the same as depression === * Oct 24, 2003, [https://www.webmd.com/depression/news/20031024/fibromyalgia-isnt-depression#1 Fibromyalgia Isn't Depression]<ref name="webmd-notdepress" /> <blockquote>[[Depression]] doesn't cause the pain of fibromyalgia, a new study shows.<ref name="webmd-notdepress" /></blockquote> <blockquote>"People still doubt fibromyalgia is a disease," Giesecke tells WebMD. "Previously, we found that fibromyalgia patients really do have increased central pain processing. Now we can show this is not affected by depression. Something is wrong here, and it is not at all connected with depression."<ref name="webmd-notdepress" /></blockquote> <blockquote>"Giesecke's group looked at [[brain]] responses to painful stimuli, and then checked to see if there was any difference between depressed and nondepressed fibromyalgia patients. They showed the activation of areas of the brain related to pain were not different in patients with and without depression." But there is a difference between people with and without fibromyalgia, he says.<ref name="webmd-notdepress" /> </blockquote><blockquote>The researchers use an imaging device called [[functional magnetic resonance imaging]], or fMRI, to look at how the brain responds to pain. Study participants get a mildly painful pressure on their thumb, which makes the brain's pain centers "light up" on the image. Thumb pressure -- at a level healthy people hardly feel -- sets off a firestorm in the pain centers of fibromyalgia patients' brains.<ref name="webmd-notdepress" /></blockquote> * 2013, Small fibre pathology in patients with fibromyalgia syndrome<ref name="brain-1857" /> :A study involving skin biopsies funds that fibromyalgia is neuropathic - and not a form of [[depression]] or a [[Psychosomatic illness|Psychosomatic Disorder]] <blockquote>The study authors stated, "This strengthens the notion that fibromyalgia syndrome is not a variant of depression, but rather represents an independent entity that may be associated with depressive symptoms". The findings also point "towards a neuropathic nature of pain in fibromyalgia syndrome... with regard to the persistent somatoform pain disorder that is sometimes assumed to be underlying in patients with fibromyalgia syndrome, our study shows a clear distinction to fibromyalgia syndrome: persistent somatoform pain disorder (ICD-10 F45.40) may be present in patients with fibromyalgia syndrome, however, in the majority of cases the definition of pain starting in connection with an emotional conflict situation or psycho-social stress strong enough to be taken as a crucial aetiological influence and pain in the course of a primary depressive disorder or schizophrenia in addition to chronic widespread pain lasting longer than 6 months is not fulfilled."<ref name="brain-1857">{{Cite journal | last = Üçeyler | first = Nurcan | last2 = Zeller | first2 = Daniel | last3 = Kahn | first3 = Ann-Kathrin | last4 = Kewenig | first4 = Susanne | last5 = Kittel-Schneider | first5 = Sarah | last6 = Schmid | first6 = Annina | last7 = Casanova-Molla | first7 = Jordi | last8 = Reiners | first8 = Karlheinz | last9 = Sommer | first9 = Claudia | date = 2013-03-09 | title = Small fibre pathology in patients with fibromyalgia syndrome | url =https://doi.org/10.1093/brain/awt053|journal=Brain|volume=136|issue=6 | pages = 1857–1867|doi=10.1093/brain/awt053|issn=1460-2156}}</ref></blockquote> ===Insulin resistance === In 2019 a small observation study by Pappolla et al. was published that found insulin resistance was associated with fibromyalgia, however the study was quickly retracted due to both criticisms of the methodology and issues with ethics approval requirements. Some of the same authors, including Pappolla, published a second observational study in 2021, again showing a likely association between having insulin resistance and fibromyalgia.<ref name="Fang2021">{{Cite journal | title = Insulin Resistance is Associated with Central Pain in Patients with Fibromyalgia | date = Mar 2021| url = https://www.painphysicianjournal.com/linkout?issn&vol=24&page=175|journal=Pain Physician|volume=24|issue=2 | pages = 175–184 | last = Pappolla | first = Miguel A. | author-link = | last2 = Manchikanti | first2 = Laxmaiah | authorlink2 = | last3 = Candido | first3 = Kenneth D. | authorlink3 = | last4 = Grieg | first4 = Nigel | authorlink4 = | last5 = Seffinger | first5 = Michael | authorlink5 = | last6 = Ahmed | first6 = Fauwad | authorlink6 = | last7 = Fang | first7 = Xiang | last8 = Andersen | first8 = Clark | last9 = Trescot | first9 = Andrea M.|doi=|pmc=|pmid=33740353|access-date=|issn=2150-1149|quote=|via=}}</ref>
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