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| ==Overview== | | ==Overview== |
| ==Pathophysiology== | | ==Pathophysiology== |
| The cause of fibromyalgia is unknown. In fact it is not be due to a singular factor at all, but r due to a multiplicity of causes. Fibromyalgia can, but most often does not, start as a result of some [[Physical trauma|trauma]] such as a traffic accident, major surgery, or disease. Some evidence shows that [[Lyme Disease]] may be a trigger of fibromyalgia symptoms.<ref>{{cite web | url = http://www.immunesupport.com/library/showarticle.cfm/ID/3579 | title = Late and Chronic Lyme Disease: Symptom Overlap with Chronic Fatigue Syndrome & Fibromyalgia}}</ref> Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic [[inflammation|inflammatory]] process to [[clinical depression]]<ref>http://www.springerlink.com/content/1271314042w8405g/ Mueller W, et al. The classification of fibromyalgia syndrome. Rheumatol Int. 2007 Jul 25</ref> | | The cause of fibromyalgia is unknown. In fact it is not be due to a singular factor at all, but r due to a multiplicity of causes. Fibromyalgia can, but most often does not, start as a result of some [[Physical trauma|trauma]] such as a traffic accident, major surgery, or disease. Some evidence shows that [[Lyme Disease]] may be a trigger of fibromyalgia symptoms.<ref>{{cite web | url = http://www.immunesupport.com/library/showarticle.cfm/ID/3579 | title = Late and Chronic Lyme Disease: Symptom Overlap with Chronic Fatigue Syndrome & Fibromyalgia}}</ref> Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic [[inflammation|inflammatory]] process to [[clinical depression]]<ref>http://www.springerlink.com/content/1271314042w8405g/ Mueller W, et al. The classification of fibromyalgia syndrome. Rheumatol Int. 2007 Jul 25</ref> |
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| === Genetics ===
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| By using self-reported "Chronic Widespread Pain" (CWP) as a surrogate marker for fibromyalgia, the [http://www.meb.ki.se/twinreg/index_en.html Swedish Twin Registry] found that a modest genetic contribution may exist:<ref name="PMID16646040">{{cite journal |author=Kato K, Sullivan P, Evengård B, Pedersen N |title=Importance of genetic influences on chronic widespread pain |journal=Arthritis Rheum. |volume=54 |issue=5 |pages=1682-6 |year=2006 | doi=10.1002/art.21798 |pmid=16646040}}</ref><ref name="PMID16908799">{{cite journal |author=Kato K, Sullivan P, Evengård B, Pedersen N |title=Chronic widespread pain and its comorbidities: a population-based study |journal=Arch. Intern. Med. |volume=166 |issue=15 |pages=1649-54 |year=2006 | url=http://archinte.ama-assn.org/cgi/content/full/166/15/1649 |pmid=16908799}}</ref>
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| * [[Monozygotic twins]] with CWP have a 15% chance that their twin sibling has CWP
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| * Dizygotic [[twins]] with CWP have a 7% chance that their twin sibling has CWP
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| === Stress ===
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| Studies have shown that [[Stress (medicine)|stress]] is a significant precipitating factor in the development of fibromyalgia,<ref>{{cite journal | author = Anderberg UM, Marteinsdottir I, Theorell T, von Knorring L | title=The impact of life events in female patients with fibromyalgia and in female healthy controls. | journal=Eur Psychiatry | month=Aug| year=2000 | pages=33-41 | volume=15 | issue=5 | id=PMID 10954873 }}</ref> and that [[PTSD]] is linked with fibromyalgia.<ref>{{cite journal | author= Amital D, Fostick L, Polliack ML, Segev S, Zohar J, Rubinow A, Amital H | title=Posttraumatic stress disorder, tenderness, and fibromyalgia syndrome: are they different entities? | journal=J Psychosom Res | month=Nov | year=2006 | pages=663-9 | volume=61 | issue=5 | id=PMID 17084145}}</ref><ref>{{cite journal | author= Raphael KG, Janal MN, Nayak S | title=Comorbidity of fibromyalgia and posttraumatic stress disorder symptoms in a community sample of women. | journal=Pain Med. | month=Mar| year=2004 | pages=33-41 | volume=5 | issue=1 | id=PMID 14996235}}</ref> The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.
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| A non-mainstream hypothesis that fibromyalgia may be a [[psychosomatic illness]] has been described by John E. Sarno's "[[tension myositis syndrome]]". He believes many cases of [[chronic pain]] result from changes in the body caused by the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, (and in some cases, psychotherapy) are treatments proposed to stop the brain from using that strategy.<ref>{{cite book |last=Sarno|first=Dr. John E,|authorlink=John E. Sarno|title=The Mindbody Prescription: Healing the Body, Healing the Pain |year=1998 |isbn=0-446-67515-6 |pages=76-78}}</ref><ref>{{cite book |last=Sarno|first=Dr. John E. et al,| title=The Divided Mind: The Epidemic of Mindbody Disorders |year=2006 |isbn=0-06-085178-3 |pages=21-22,235-237,294-298}}</ref> Robert G. Schwartz, MD has proposed an alternative view where in mind-body connections may play an important role in chronic disease (not just fibromyalgia). Through his program strategies to align incentives are offered.
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| ===Dopamine abnormality===
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| [[Dopamine]] is a [[catecholamine]] [[neurotransmitter]] perhaps best known for its role in the pathology of [[schizophrenia]], [[Parkinson's disease]] and [[addiction]]. As is the case with several of the neurotransmitters, there is evidence for a role of dopamine in [[restless leg syndrome]] <ref>[http://www.ncbi.nlm.nih.gov/pubmed/16816393?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Support for dopaminergic hypoactivity in restless ...[Brain. 2006] - PubMed Result<!-- Bot generated title -->]</ref>, which is a common co-morbid condition in patients with fibromyalgia. <ref>[http://www.bmj.com/cgi/content/full/312/7042/1339 Restless legs syndrome and leg cramps in fibromyalgia syndrome: a controlled study - Yunus and Aldag 312 (7042): 1339 - BMJ<!-- Bot generated title -->]</ref> Interestingly, patients with restless legs syndrome have also been demonstrated to have [[hyperalgesia]] to static mechanical stimulation.<ref>[http://brain.oxfordjournals.org/cgi/content/full/127/4/773 Static mechanical hyperalgesia without dynamic tactile allodynia in patients with restless legs syndrome - Stiasny-Kolster et al. 127 (4): 773 - Brain<!-- Bot generated title -->]</ref>
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| Fibromyalgia has been commonly referred to as a "stress-related disorder" due to its frequent onset and worsening of symptoms in the context of stressful events.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/16174484?ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of life stress in fibromyalgia. [Curr Rheumatol Rep. 2005] - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/12849719?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Chronic widespread pain and fibromyalgia: what we ...[Best Pract Res Clin Rheumatol. 2003] - PubMed Result<!-- Bot generated title -->]</ref> It was therefore proposed that fibromyalgia may represent a condition characterized by low levels of central dopamine that likely results from a combination of genetic factors and exposure to environmental stressors, including psychosocial distress, physical trauma, systemic viral infections or inflammatory disorders (e.g. [[rheumatoid arthritis]], systemic [[lupus erythematosus]]).<ref>[http://www.ncbi.nlm.nih.gov/pubmed/14975515?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Stress and dopamine: implications for the pathophy...[Med Hypotheses. 2004] - PubMed Result<!-- Bot generated title -->]</ref> This conclusion was based on three key observations: (1) fibromyalgia is associated with stress; (2) chronic exposure to stress results in a disruption of dopamine-related neurotransmission<ref>[http://www.ncbi.nlm.nih.gov/pubmed/9355111?ordinalpos=27&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The effects of stress on central dopaminergic neur...[Neurochem Res. 1997] - PubMed Result<!-- Bot generated title -->]</ref>; and (3) dopamine plays a critical role in modulating pain perception and central [[analgesia]] in such areas as the [[basal ganglia]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/7715939?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of the basal ganglia in nociception and p...[Pain. 1995] - PubMed Result<!-- Bot generated title -->]</ref> including the [[nucleus accumbens]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/10597883?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum The role of dopamine in the nucleus accumbens in a...[Life Sci. 1999] - PubMed Result<!-- Bot generated title -->]</ref>, [[insular cortex]]<ref>[http://www.jneurosci.org/cgi/content/full/19/10/4169 Dopamine Reuptake Inhibition in the Rostral Agranular Insular Cortex Produces Antinociception - Burkey et al. 19 (10): 4169 - Journal of Neuroscience<!-- Bot generated title -->]</ref>, [[anterior cingulate cortex]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/15327817?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Dopamine and NMDA systems modulate long-term nocic...[Pain. 2004] - PubMed Result<!-- Bot generated title -->]</ref>, [[thalamus]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/1611515?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Neurophysiological, pharmacological and behavioral...[Brain Res. 1992] - PubMed Result<!-- Bot generated title -->]</ref>, [[periaqueductal gray]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/15275769?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Opiate anti-nociception is attenuated following le...[Pain. 2004] - PubMed Result<!-- Bot generated title -->]</ref>, and [[spinal cord]]<ref>[http://www.ncbi.nlm.nih.gov/pubmed/6314870?ordinalpos=113&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Dopamine-containing neurons in the spinal cord: an...[Ann Neurol. 1983] - PubMed Result<!-- Bot generated title -->]</ref> <ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15975975 Direct inhibition of substantia gelatinosa neurones in the rat spinal cord by activation of dopamine D2-like receptors<!-- Bot generated title -->]</ref>.
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| ===Serotonin===
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| [[Serotonin]] is a [[neurotransmitter]] that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration and descending inhibition of pain. Accordingly, it has been hypothesized that the [[pathophysiology]] underlying the symptoms of fibromyalgia may be a dysregulation of serotonin metabolism, which may explain (in part) many of the symptoms associated with the disorder. This [[hypothesis]] is derived in part by the observation of decreased serotonin metabolites in patient [[plasma]] <ref>[http://www.ncbi.nlm.nih.gov/pubmed/1313504?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Platelet 3H-imipramine uptake receptor density and...[J Rheumatol. 1992] - PubMed Result<!-- Bot generated title -->]</ref> and [[cerebrospinal fluid]].<ref>[http://www.ncbi.nlm.nih.gov/pubmed/1374252?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Cerebrospinal fluid biogenic amine metabolites in ...[Arthritis Rheum. 1992] - PubMed Result<!-- Bot generated title -->]</ref> However, [[selective serotonin reuptake inhibitors]] (SSRIs) have met with limited success in alleviating the symptoms of the disorder, while drugs with activity as mixed [[serotonin-norepinephrine reuptake inhibitor]]s (SNRIs) have been more successful<ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16762044 Biology and therapy of fibromyalgia. New therapies in fibromyalgia<!-- Bot generated title -->]</ref>. Accordingly, [[duloxetine]] ([[Cymbalta]]), a SNRI originally used to treat depression and painful [[diabetic neuropathy]], has been demonstrated by controlled trials to relieve symptoms of some patients. Eli Lilly and Company, the manufacturer of duloxetine has submitted a supplementary new drug application (sNDA) to the [[FDA]] for approval of it use in the treatment of FM. The relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/17693607?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Serum serotonin levels are not useful in diagnosin...[Ann Rheum Dis. 2007] - PubMed Result<!-- Bot generated title -->]</ref> Ironically, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin [[5-HT3 antagonist]]s) actually block some of the effects of serotonin.<ref>[http://www.ncbi.nlm.nih.gov/pubmed/12122920?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Current experience with 5-HT3 receptor antagonists...[Rheum Dis Clin North Am. 2002] - PubMed Result<!-- Bot generated title -->]</ref>
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| ===Sleep disturbance===
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| [[Electroencephalography]] studies have shown that people with fibromyalgia lack [[slow-wave sleep]] and circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or [[anxiety]]) may cause or worsen the condition. According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The hypothesis supposes that stage 4 sleep is critical to the function of the [[nervous system]], as it is during that stage that certain neurochemical processes in the body 'reset'. In particular, pain causes the release of the [[neuropeptide]] [[substance P]] in the [[spinal cord]] which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound to become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect.
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| The sleep disturbance/substance P hypothesis could explain "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures. The hypothesis proposes that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. This hypothesis could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system. The sleep disturbance hypothesis could also provide a possible connection between fibromyalgia, [[chronic fatigue syndrome]] (CFS) and [[post-polio syndrome]] through damage to the ascending reticular activating system of the [[reticular formation]]. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.
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| Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.
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| ===Human growth hormone===
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| An alternate hypothesis suggests that stress-induced problems in the [[hypothalamus]] may lead to reduced sleep and reduced production of [[human growth hormone]] (HGH) during [[slow-wave sleep]]. People with fibromyalgia tend to produce inadequate levels of HGH. Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.
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| This view is supported by the fact that those hormones under the direct or indirect control of HGH, including [[IGF-1]], [[cortisol]], [[leptin]] and [[neuropeptide Y]] are abnormal in people with fibromyalgia,<ref>{{cite journal | last = Anderberg | first = UM | coauthors = Liu Z, Berglund L, Nyberg F | pmid = 10700334 | title = Elevated plasma levels of neuropeptide Y in female fibromyalgia patients. | journal = European Journal of Pain | volume = 3 | issue = 1 | year = 1999 | pages = 19-30}}</ref> In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep<ref> {{ cite journal | last = Jones | first = KD | coauthors = Deodhar P, Lorentzen A, Bennett RM, Deodhar AA | title = Growth hormone perturbations in fibromyalgia: a review. | journal = Seminars in Arthritis and Rheumatism | year = 2007 | volume = 36 | issue = 6 | pages = 357-79 | pmid = 17224178 }}</ref><ref>{{cite journal | last = Shuer | first = ML | title = Fibromyalgia: symptom constellation and potential therapeutic options | journal = Endocrine | volume = 22 | issue = 1 | pages = 67-76 | pmid = 14610300 }}</ref><ref>{{cite journal | last = Yuen | first = KC | coauthors = Bennett RM, Hryciw CA, Cook MB, Rhoads SA, Cook DM | journal = Growth hormone & IGF research | title = Is further evaluation for growth hormone (GH) deficiency necessary in fibromyalgia patients with low serum insulin-like growth factor (IGF)-I levels? | volume = 17 | issue = 1 | year = 2007 | pages = 82-8 | pmid = 17289417 }}</ref><ref>{{cite journal | last = Bennett | first = RM | coauthors = Cook DM, Clark SR, Burckhardt CS, Campbell SM. | pmid = 9228141 | title = Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia | | Journal of Rheumatology | volume = 24 | issue = 7 | pages = 1384-9 }}</ref> though there is disagreement about the proposition.<ref>{{cite journal | last = McCall-Hosenfeld | first = JS | coauthors = Goldenberg DL, Hurwitz S, Adler GK. | title = Growth hormone and insulin-like growth factor-1 concentrations in women with fibromyalgia | journal = Journal of Rheumatology | volume = 30 | issues = 4 | pages = 809-14 | pmid = 12672204 }}</ref>
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| ===Deposition disease===
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| The 'deposition hypothesis of fibromyaglia' poses that fibromyalgia is due to intracellular [[phosphate]] and [[calcium]] accumulations that eventually reaches levels sufficient to impede the [[Adenosine triphosphate|ATP]] process, possibly caused by a [[kidney]] defect or missing [[enzyme]] that prevents the removal of excess phosphates from the blood stream. Accordingly, proponents of this hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is required for the excess phosphate to enter the cells. The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.
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| The phosphate build-up hypothesis explains many of the symptoms present in fibromyalgiaand proposes an underlying cause. The guaifenesin treatment, based on this hypothesis, has received mixed reviews, with some practitioners claiming many near-universal successes and others reporting no success. Of note, guaifenesin is also a central acting [[muscle relaxant]] used in veterinary anaesthesia<ref>[http://www.ncbi.nlm.nih.gov/pubmed/2282545?ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Intravenous anesthesia. [Vet Clin North Am Equine Pract. 1990] - PubMed Result<!-- Bot generated title -->]</ref> that is structurally related to [[methocarbamol]], a property that might explain its utility in some fibromyalgia patients. A controlled trial of guaifenesin for the treatment of fibromyalgia demonstrated no evidence for efficacy of this medication. However, this study has been criticized by the chief proponent of the deposition hypothesis for not limiting salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method.<ref>{{cite journal | url = http://www.fibromyalgiatreatment.com/Research_Oregon.htm | title = A Response To The Oregon Study's Implication | accessdate = 2007-06-23 | first = R. Paul | last = St. Amand | journal = Clinical Bulletin of Myofascial Therapy | volume = 2 | issue = 4 | year = 1997 }}</ref> As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the hypothesis. It should be noted that ''nothing'' in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.
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| ===Other hypotheses===
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| Other hypotheses have been proposed related to various [[toxin]]s from the patient's environment, [[virus|viral]] causes such as the [[Epstein-Barr Virus]], [[growth hormone]] deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to [[intestinal bacteria]],<ref name="ClinExpDermatol2004-KendallSN">{{cite journal | author=Kendall SN | title=Remission of rosacea induced by reduction of gut transit time. | journal=Clin Exp dermatol. | month=May | year=2004 | pages=297-9 | volume=29 | issue=3 | pmid=15115515}}</ref><ref name="AnnRheumDis2004-PimentalM">{{cite journal | author=Pimental M, Wallace D, Hallegua D et .al | title=A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. | journal=Ann Rheum Dis. | month=April | year=2004 | pages=450-2 | volume=63 | issue=4 |pmid=15020342}}</ref> [[neurotransmitter]] disruptions in the [[central nervous system]], and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule.<ref name="Brown2001">{{cite journal | author=Brown SL, Pennello G, Berg WA, Soo MS, Middleton MS | title=Silicone gel breast implant rupture, extracapsular silicone, and health status in a population of women | journal=J Rheumatol | year=2001 | pages=996-1003 | volume=28 | issue=5 | pmid=11361228}}</ref><ref>{{cite web |title=Study of Silicone Gel Breast Implant Rupture, Extracapsular Silicone, and Health Status in a Population of Women |url=http://www.fda.gov/cdrh/breastimplants/extracapstudy.html |date=May 29, 2001 |publisher=FDA}}</ref> This association has not repeated in a number of related studies,<ref name=Lipworth>{{cite journal | author=Lipworth L, Tarone RE, McLaughlin JK.| title=Breast implants and fibromyalgia: a review of the epidemiological evidence.| journal=Ann Plast Surg. | year=2004 | pages=284-7| volume=52 | issue=3 |pmid=15156983}}</ref> and the US-FDA concluded "the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants."<ref>{{cite web |title=FDA Breast Implant Consumer Handbook 2004 |url=http://www.fda.gov/cdrh/breastimplants/handbook2004/diseases.html#1 |date=June 8, 2004 |publisher=FDA}}</ref> Due to the multi-systemic nature of illnesses such as fibromyalgia and [[chronic fatigue syndrome]] (CFS/ME), an emerging branch of medical science called [[psychoneuroimmunology]] (PNI) is looking into how the various hypotheses fit together.
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| Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from [[vasomotor]] dysregulation causing improper [[Blood vessel|vascular]]flow and [[hypoperfusion]] (decreased blood flow to a given tissue or organ).<ref name="pmid17376601">{{cite journal |author=Katz DL, Greene L, Ali A, Faridi Z |title=The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation |journal=Med Hypotheses. |volume=(Epub ahead of print) |issue= |pages= |year=2007 |month=19 Mar |pmid=17376601 |doi=10.1016/j.mehy.2005.10.037}}</ref>
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| ===Always a comorbid disease?===
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| Cutting across several of the above hypotheses is the proposition that fibromyalgia is almost always a [[comorbidity|comorbid]] disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are [[gluten sensitivity]] and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia,<ref name="pmid16042909">{{cite journal | author = Frissora CL, Koch KL | title = Symptom overlap and comorbidity of irritable bowel syndrome with other conditions | journal = Current gastroenterology reports | volume = 7 | issue = 4 | pages = 264-71 | year = 2005 | pmid = 16042909 | doi = }}</ref> and a large coeliac
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| support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurrence with chronic fatique.<ref name="pmid12741468">{{cite journal | author = Zipser RD, Patel S, Yahya KZ, Baisch DW, Monarch E | title = Presentations of adult celiac disease in a nationwide patient support group | journal = Dig. Dis. Sci. | volume = 48 | issue = 4 | pages = 761-4 | year = 2003 | pmid = 12741468 | doi = }}</ref>
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| According to this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery. In other cases the two disorders coexist. Since it can be extremely complex to treat the source of fibromyalgia, and since it is most probably a multifactoral disorder that is different from one afflicted patient to the next, the concept of [http://wehelpwhathurts.homestead.com/diseasemanagement.html Reducing Total Load] has been proposed. In this instance the total number of things that does not allow a patient to get well is treated, one at a time, taking into consideration the unique conditions of that individual patient.
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| ===Controversies===
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| The validity of fibromyalgia as a unique clinical entity is a matter of some contention among researchers in the field. For example, it has been proposed that the pathophysiology responsible for the symptoms that are collectively classified as representing "fibromyalgia" is poorly understood, thereby suggesting that the fibromyalgia [[phenotype]] which is the difference between an individual’s heredity and what that heredity produces, may result from several different disease processes that have global hyperalgesia - an increased sensitivity to pain - and allodynia in common, <ref>http://www.springerlink.com/content/1271314042w8405g/ Mueller W, et al. The classification of fibromyalgia syndrome. Rheumatol Int. 2007 Jul 25</ref><ref>The association or otherwise of the functional somatic syndromes.Psychosom Med. 2007 Dec;69(9):855-9. Review. PMID: 180400</ref><ref>Comorbidity of fibromyalgia and psychiatric disorders.Curr Pain Headache Rep. 2007 Oct;11(5):333-8. Review. PMID: 17894922</ref> an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other.<ref>An integrated model of group psychotherapy for patients with fibromyalgia.Int J Group Psychother. 2007 Oct;57(4):451-74</ref> Alternatively, there is evidence for the existence of differing pathophysiological - which is the study of the disturbance of normal mechanical, physical, and biochemical functions of the body - within the greater fibromyalgia construct<ref>[http://www.ncbi.nlm.nih.gov/pubmed/17084146?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum Psychophysiological responses in patients with fib...[J Psychosom Res. 2006] - PubMed Result<!-- Bot generated title -->]</ref><ref>[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16356200 Heterogeneity of psychophysiological stress responses in fibromyalgia syndrome patients<!-- Bot generated title -->]</ref>, which may be interpreted to represent evidence for the existence of biologically distinct "sub-types" of the disorder akin to conditions such as [[epilepsy]], [[schizophrenia]] and [[major depressive disorder]]. In a January 14, 2008 article in the New York Times, the controversy of the reality of the disease and its proposed cures are discussed, while citing that the [[American College of Rheumatology]], the [[Food and Drug Administration]] and insurers recognize fibromyalgia as a diagnosable disease. Drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.
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| ==References== | | ==References== |