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Crohn's Disease Forum » Books, Multimedia, Research & News » Fibromyalgia and Irritable Bowel Syndrome: Is There a Connection?


07-15-2010, 02:40 PM   #1
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Fibromyalgia and Irritable Bowel Syndrome: Is There a Connection?

Afton L. Hassett, PsyD; Daniel J. Clauw, MD
CME/CE Released: 06/28/2010; Valid for credit through 06/28/2011

Introduction

Fibromyalgia is a disorder of the central nervous system characterized by the presence of chronic widespread pain. It affects at least 2% of the general population, primarily women.[1] Additional symptoms associated with fibromyalgia include fatigue, insomnia, nonrefreshing sleep, and cognitive "fogginess" (known as fibrofog). Patients with fibromyalgia are also likely to experience 1 or more co-occurring regional chronic pain syndromes, such as irritable bowel syndrome (IBS), interstitial cystitis, temporomandibular joint disorder, and tension headaches, over their lifetime.[2-4] For example, it has been estimated that between 32% and 70% of individuals with fibromyalgia also meet criteria for IBS.[5,6] Patients who experience multiple syndromes and/or comorbid conditions present a more complex clinical scenario that requires special consideration, and such patients tend to have worse outcomes.

This review focuses on the current knowledge regarding similarities and overlap between fibromyalgia and IBS and their treatment approaches as a basis for understanding the pathophysiology of pain.
Chronic Pain Syndromes Comorbidities

Chronic pain syndromes can co-occur with other diseases; for example, fibromyalgia has been observed in about 1 in 4 patients with rheumatoid arthritis, osteoarthritis, and systemic lupus erythematosus.[7] Wolfe[8] characterizes these patients as having varying degrees of "fibromyalgianess," characterized by varying degrees of multifocal pain, fatigue, insomnia, and memory difficulties that cannot be explained on the basis of the current understanding of the pathogenesis of their rheumatologic disorders. Similarly, IBS has been estimated to co-occur in 10%-20% of patients with inflammatory bowel disease, while 5%-33% of patients with enteric infections will subsequently go on to have chronic IBS symptoms (a condition known as postinfectious IBS).[9-11] Psychological factors such as depression and anxiety are associated with the presence of IBS-like symptoms in these patients.[12]

Psychiatric comorbidities, especially depression and anxiety, are common in chronic pain conditions, including fibromyalgia and IBS. In fibromyalgia, depression and/or anxiety are present in approximately 25% of patients,[13,14] while lifetime estimates of depression are well over 60%.[13-16] Similarly, psychiatric disorders have been identified in up to 50% of patients with functional abdominal pain.[17] The presence of psychiatric comorbidities, inadequate response to treatment, and a lack of objective evidence of disease (eg, positive lab tests and identification of a peripheral cause of pain) contributed to the belief that these pain syndromes are somatization disorders -- psychiatric in nature and a "fashionable" expression of psychological distress.[18] Terms such as "functional somatic syndromes" or "medically unexplained syndromes" have only reinforced the dualism that restricts research and treatment and can be stigmatizing for individuals affected by these illnesses.

Over the past decade, innovative research inspired by advances in the neuroscience of pain has markedly contributed to the understanding of the pathophysiology of conditions like fibromyalgia and IBS. These advances have allowed us to reliably demonstrate augmented central processing of pain and sensory information in fibromyalgia, IBS, interstitial cystitis, and temporomandibular joint disorder, resulting in new and more integrative ways of conceptualizing these conditions (characterized as "central sensitivity syndromes" or "central pain syndromes") and their treatment.[19]
Fibromyalgia and Irritable Bowel Syndrome: Understanding the Central Augmentation of Pain and Sensory Processing

There is a growing consensus among experts in the pain field that chronic pain is a disease and that the underlying mechanisms may be similar to those of fibromyalgia, regardless of whether pain is present throughout the body or localized to a specific area.[20,21] Realizing that the underlying pain was not caused by peripheral damage or inflammation, but was likely the product of central nervous system dysfunction, further increased our understanding of these disorders.

Experimental pain testing studies in fibromyalgia and IBS have also enhanced our understanding of the pathophysiology of pain and sensory processing. Although early fibromyalgia dolorimetry studies found that pain thresholds correlated with distress, expectancy, and hypervigilance,[1,22,23] recent studies using sophisticated experimental paradigms demonstrated that: (1) unlike tender-point and dolorimetry exams, the random measures of pressure pain threshold were not influenced by levels of distress of the individual; (2) patients with fibromyalgia were much more sensitive to pressure, even when these more sophisticated paradigms were used; (3) patients with fibromyalgia were not more "expectant" or "hypervigilant" than controls; and (4) pressure pain thresholds at any 4 points in the body highly correlated with the average tenderness at all 18 tender points and 4 "control points."[24,25]

In addition to heightened sensitivity to pressure, individuals with fibromyalgia and IBS also display decreased somatic thresholds to heat, cold, electrical, and sensory information other than somatic stimuli, such as auditory tones.[26-29] The notion that fibromyalgia and related syndromes like IBS might represent biological amplification of all sensory stimuli also has significant support from functional neuroimaging studies. In a seminal study using functional magnetic resonance imaging to evaluate neural processing in fibromyalgia, Gracely and colleagues[30] found that stimuli of equal pressure magnitude resulted in significant increases in the blood oxygen level-dependent signal in patients with fibromyalgia compared with control individuals. Affected areas included the primary and secondary somatosensory cortices, insula, and anterior cingulate. This finding has been replicated in fibromyalgia, and similar findings of a hyperalgesic state (including hyperreactivity of the insula) have been noted in a variety of chronic pain states, including IBS.[31] The insula plays a critical role in sensory integration; while the posterior insula is associated with sensory processing, the anterior insula is linked to the emotional processing of sensations.[32-34]

Besides the common observance of diffuse hyperalgesia/allodynia, attenuated activity of descending analgesic pathways (sometimes referred to as diffuse noxious inhibitory control [DNIC]) has been reported in several of these conditions and may contribute to pain sensitivity.[35-37] In animals and healthy humans, the repeated administration of an acutely painful stimulus typically results in a subsequent increase in pain threshold (ie, decrease of tenderness).[38] This phenomenon is known as DNIC because it involves the recruitment of descending analgesic pathways to address the painful stimulus. Diffuse noxious inhibitory control has been shown to be attenuated or absent in both fibromyalgia and IBS patients, suggesting a deficiency in descending analgesic systems.[35-37] Furthermore, in fibromyalgia and comorbid depression, the deficit in pain inhibition has been shown to be more pronounced.[39] A relative deficiency in DNIC thus appears to be one of the mechanisms of central pain augmentation and may eventually serve to help characterize subgroups of patients who might be differentially responsive to various treatment modalities.

Role of Neurotransmitters

Studies from a variety of sources support the analogy of an increased "volume control" or "gain" setting on pain and sensory processing.[20] Like essential hypertension, for which a variety of causes can result in elevated systemic blood pressure, these disorders can be characterized as "essential hypertension of pain and sensory processing pathways". As depicted in the Figure, in central pain syndromes elevated levels of neurotransmitters tend to be pro-nociceptive (left side of figure), while reduced levels of neurotransmitters that inhibit pain transmission have a tendency to increase volume control (right side of figure). To date, the endogenous opioid system is the only neurotransmitter system not found to be "out of line" in a direction that would cause augmented pain transmission. Drugs that block neurotransmitters or increase their activity typically are effective treatments for individuals with central pain syndromes.

Figure 1. Neural influences on pain and sensory processing. GABA = gamma-aminobutyric acid

fms.jpg

Last edited by David in Seattle; 07-15-2010 at 02:47 PM.
07-15-2010, 02:42 PM   #2
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Genetic and Environmental Factors

Several lines of evidence support a stress-diathesis etiology for the development of central pain syndromes. Family studies have shown that first-degree biological relatives of individuals with fibromyalgia display an 8-fold greater risk of developing fibromyalgia compared with the general population,[6] while family members of individuals with IBS have almost 3 times the odds of developing IBS.[40] Furthermore, compared with controls, family members of individuals with fibromyalgia tend to be more sensitive to pain and are more likely to have other central pain disorders, such as IBS, temporomandibular joint disorder, and headaches.[41] Findings from twin studies suggest that approximately half of the risk of developing chronic widespread pain is genetic, while the other half is environmental.[42]

Environmental factors may predispose and/or trigger central pain syndromes in some individuals. Although the retrospective analysis of childhood traumatic events is fraught with pitfalls, numerous studies have found elevated rates of these events reported in patients with central pain syndromes.[43] The reported presence of a history of early trauma has been associated with poor outcomes, including physiologic dysfunction.[44,45] Central pain syndromes can be triggered in approximately 5%-10% of individuals who experience peripheral pain syndromes, infections (eg, parvovirus, Epstein-Barr virus, Lyme disease, bacterial gastroenteritis), physical trauma (eg, automobile accidents), psychological trauma/distress, hormonal alteration, or catastrophic events.[46] Environmental factors have also been implicated in triggering fibromyalgia and related conditions.

Psychological and Behavioral Factors

As previously noted, depression and anxiety are common in central pain syndromes. In addition to psychiatric comorbidities, other psychological variables associated with poor outcomes have been frequently described in fibromyalgia and IBS, including pain catastrophizing and somatosensory amplification.[47-50] Similar to what is observed in almost every medical condition, psychological factors significantly contribute to symptom severity and treatment outcome in central pain syndromes. For example, in addition to the presence of mucosal inflammation, psychological distress at the time of enteric infection best predicted those who later developed postinfectious IBS.[51]

In fibromyalgia, such psychological factors occur on a continuum, from a high incidence of personality disorders in tertiary care patients[13] to psychological resilience, whereby patients have no psychiatric comorbidity and exhibit high levels of positive affect and significantly better functional outcomes.[52] Years of psychopathology-oriented research in fibromyalgia and IBS have shown that no single psychological factor accounts for the symptoms or behaviors of all individuals with these conditions in any given sample. It is possible that within subgroups of resilient patients, positive psychological and/or cognitive characteristics may buffer neurobiologic factors that result in pain and other symptoms.[52-54] Subgroups of patients may also present differently, respond differently to treatment, and/or require specific or "tailored" treatment strategies
Treatment of Fibromyalgia and Irritable Bowel Syndrome

The diagnosis, evaluation, and effective management of individuals with chronic pain is a complex process, due to tremendous heterogeneity with respect to the underlying cause of any given pain symptoms. Individuals with chronic pain can have varying involvement of peripheral nociceptive factors (eg, tissue damage and inflammation) and central non-nociceptive factors (eg, pain amplification and psychiatric comorbidity) contributing to their pain (Table 1).[55] Differential diagnosis of chronic pain involves identifying the degree to which these factors are present in a given individual so that the appropriate pharmacologic, procedural, and psychological therapies can be administered. The treatment strategies discussed below predominantly focus on addressing pain (most of the approved pharmacologic therapies for IBS are more effective at treating motility than pain). For management of IBS-specific symptoms, mainly diarrhea or constipation, the recommendations of the American College of Gastroenterology Task Force on IBS should be considered.[56]

Table 1. Mechanistic Characterization of Pain (any combination may be present in a given individual)

tbl 1.jpg
07-15-2010, 02:44 PM   #3
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Pharmacologic Treatment

Tricyclic antidepressants (TCAs). TCAs generally increase concentrations of serotonin and/or norepinephrine by directly blocking their reuptake. The efficacy of TCAs in treating pain, poor sleep, and fatigue in fibromyalgia patients is supported by several randomized controlled trials.[57] Furthermore, they have been found to be effective in a broad range of chronic pain states, including IBS.[57,58] Although tolerability can represent a problem, this issue can be improved by initiating treatment at very low doses.

Selective serotonin reuptake inhibitors (SSRIs). Given that they exhibit a better side-effect profile than TCAs, SSRIs have been evaluated in randomized, placebo-controlled trials in fibromyalgia[59-62] and IBS.[63-66] In general, the results of these studies paralleled those evaluating other pain conditions. Newer, highly selective SSRIs (eg, citalopram) seem less efficacious than the older SSRIs, which have some noradrenergic activity at higher doses.[67]

Serotonin norepinephrine reuptake inhibitors (SNRIs). SNRIs are pharmacologically similar to TCAs in their ability to inhibit the reuptake of serotonin and norepinephrine but lack significant activity at other receptor systems, resulting in diminished side effects and enhanced tolerability. Data on venlafaxine, the first agent of this class available for clinical investigation, support its use in the management of neuropathic pain and in the prophylaxis of migraine and tension headaches.[68] Although venlafaxine was ineffective in the management of fibromyalgia at 75 mg/day in a randomized controlled trial, it appeared effective at higher doses in 2 case reports.[59]

Duloxetine is an SNRI that was recently approved by the US Food and Drug Administration (FDA) for the treatment of fibromyalgia. Recent clinical trials have shown that duloxetine is effective in the management of pain and other symptom domains of fibromyalgia, as well as a number of other chronic pain states (eg, osteoarthritis and chronic low back pain), further supporting the involvement of central nervous system factors in these conditions.[69,70] To date, only 1 small open pilot study of duloxetine has been conducted in IBS, showing a significant reduction of pain.[71]

Milnacipran, another SNRI, may preferentially inhibit norepinephrine reuptake over serotonin, in contrast to duloxetine and other SNRIs.[72] In recent large, multicenter trials, milnacipran showed efficacy in the management of pain and other symptom domains of fibromyalgia, such as fatigue and physical functioning.[73] The benefits of milnacipran and duloxetine in fibromyalgia management have been shown to be independent of their effect on mood, suggesting that the analgesic and other beneficial effects of this class of drugs are not simply due to their antidepressant effects.[69,74]

Antiepileptic drugs. Several antiepileptic drugs are widely used in the treatment of various chronic pain conditions.[75] Pregabalin, an alpha(2)delta calcium channel ligand approved for the treatment of neuropathic pain, was the first pharmacologic agent approved by the FDA for the treatment of fibromyalgia. Recent randomized, double-blinded, placebo-controlled trials demonstrated efficacy of pregabalin against pain, sleep disturbances, and fatigue in fibromyalgia patients compared with placebo.[76-78] Similarly, in a small but thorough study, pregabalin was found to increase visceral pain threshold in IBS compared with placebo.[72] Gabapentin is a compound with similar pharmacology to pregabalin that has been indicated for the treatment of postherpetic neuralgia and studied in a variety of pain states, including fibromyalgia, IBS, and headache prophylaxis.[75,79,80]

Sedative-hypnotic compounds. Sedative-hypnotic compounds are widely used by fibromyalgia patients. A number of studies published on the use of nonbenzodiazepine hypnotics (ie, zopiclone and zolpidem) have suggested that although these agents can improve lack of sleep and possibly fatigue in fibromyalgia patients, they do not have significant effects on improving pain.[81,82] However, gamma-hydroxybutyrate (also known as sodium oxybate), a precursor of gamma-aminobutyric acid (GABA) with powerful sedative properties, was recently shown to be useful in improving fatigue, pain, and sleep architecture in fibromyalgia patients.[81] It is important to note that this agent is a scheduled substance due to its abuse potential.

Opioids. There have not been adequate randomized controlled clinical trials of opiates in fibromyalgia and IBS, and many practitioners in the field have not found this class of compounds to be effective. In fact, there is anecdotal evidence that some individuals with central pain states may develop opioid-induced hyperalgesia, and thus this class of drugs may make some individuals' conditions worse. Tramadol, a compound that exhibits opioid activity combined with serotonin/norepinephrine reuptake inhibition, appears to be somewhat efficacious in the management of fibromyalgia, both as monotherapy and as a fixed-dose combination with acetaminophen.[83]

Nonpharmacologic Treatment

For both fibromyalgia and IBS, multidisciplinary treatment is recommended.[84,85] Central to this approach is taking into consideration the unique characteristics of each patient and adding adjunctive nonpharmacologic interventions to the evidence-based use of medication. The importance of including exercise, patient education, and cognitive-behavioral therapy in the treatment of fibromyalgia and IBS has been substantiated in a number of studies.[86-89] Balneotherapy, hypnotherapy, and various forms of biofeedback have also demonstrated some degree of benefit.[90]

Exercise. Jones and Liptan[86] noted that over 80% of patients with fibromyalgia have below-average fitness levels and do not engage in aerobic exercise. Exercise studies conducted in central-pain populations almost always exhibit high attrition rates; however, they consistently demonstrate benefit for participants.[89,91] Persistence with an exercise regimen can be improved by participation in low-intensity, nonrepetitive exercise (eg, aquatic exercise), "starting slow and going slow" (eg, 15 minutes of exercise a day twice a week), and making it fun (eg, exercise with friends, walk in pleasant surroundings, engage in dance or yoga).

Education. Psychoeducation is viewed by most experts as useful, if not necessary, for the treatment of fibromyalgia.[84] A recent study in IBS also found a structured patient education program to be particularly effective for patients with this condition.[92] These educational programs aim to improve the understanding of the complex interactions between neurobiological processes, behavior, stress, and symptoms. Such programs have varied foci but typically target the stigma often attached to fibromyalgia, IBS, and similar disorders.

Cognitive-behavioral therapy. Cognitive-behavioral therapy interventions for fibromyalgia and IBS should target modification of maladaptive thoughts and expectations, how to better cope with pain, mood, perceived stress, and problem-solving, while including behavioral interventions (eg, activity pacing, sleep hygiene, and relaxation training) that address symptoms. The main goal of cognitive-behavioral therapy for chronic pain syndromes is to increase self-management and level of functioning.

For daily clinical practice, the principles of comprehensive nonpharmacologic pain management represented by the acronym ExPRESS (Table 2) can help guide intervention.[90] Many of the ExPRESS domains can be addressed by using a self-paced education, exercise, and cognitive-behavioral therapy program known as FibroGuide (www.knowfibro.com).

Table 2. ExPRESS Approach to Adjunctive, Nonpharmacologic Treatment for Patients With Chronic Pain Syndromes

tbl 2.jpg
07-15-2010, 02:45 PM   #4
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Summary

Data from various types of studies show a significant overlap between fibromyalgia and IBS in terms of symptom profile, underlying pathophysiologic processes, and response to treatment. A hallmark of both of these conditions is an "increased gain" in pain processing due in large part to central nervous system mechanisms. This phenomenon, also termed hyperalgesia, is being identified in a subset of individuals with nearly any chronic pain state, including conditions such as osteoarthritis, for which pain previously was thought to be due exclusively to peripheral nociceptive factors.[93,94] The most appropriate treatment for these hyperalgesic states includes choosing the appropriate pharmacologic therapy (ie, drugs that modify neurotransmitters involved in setting the gain on pain transmission rather than nonsteroidal anti-inflammatory drugs or opioids, which are more appropriate for treating peripheral pain) and combining it with the aggressive use of nonpharmacologic therapies, such as education, cognitive-behavioral therapy, and exercise.

Supported by independent educational grants from Forest Laboratories and Pfizer, Inc.

References

1. Wolfe F, Ross K, Anderson J, Russell IJ. Aspects of fibromyalgia in the general population: sex, pain threshold, and fibromyalgia symptoms. J Rheumatol. 1995;22:151-156. Abstract
2. Aaron LA, Burke MM, Buchwald D. Overlapping conditions among patients with chronic fatigue syndrome, fibromyalgia, and temporomandibular disorder. Arch Intern Med. 2000;160:221-227. Abstract
3. Hudson JI, Hudson MS, Pliner LF, Goldenberg DL, Pope HG Jr. Fibromyalgia and major affective disorder: a controlled phenomenology and family history study. Am J Psychiatry. 1985;142:441-446. Abstract
4. Arnold LM, Hudson JI, Hess EV, et al. Family study of fibromyalgia. Arthritis Rheum. 2004;50:944-952. Abstract
5. Sperber AD, Atzmon Y, Neumann L, et al. Fibromyalgia in the irritable bowel syndrome: studies of prevalence and clinical implications. Am J Gastroenterol. 1999;94:3541-3546. Abstract
6. Veale D, Kavanagh G, Fielding JF, Fitzgerald O. Primary fibromyalgia and the irritable bowel syndrome: different expressions of a common pathogenetic process. Br J Rheumatol. 1991;30:220-222. Abstract
7. Clauw DJ, Katz P. The overlap between fibromyalgia and inflammatory rheumatic disease: when and why does it occur? J Clin Rheumatol. 1995;1:335-342. Abstract
8. Wolfe F. Fibromyalgianess. Arthritis Rheum. 2009;61:715-716. Abstract
9. Bayless TM, Harris ML. Inflammatory bowel disease and irritable bowel syndrome Inflammatory bowel disease and irritable bowel syndrome. Med Clin North Am. 1990;74:21-28. Abstract
10. Saito YA, Schoenfeld P, Locke GR. The epidemiology of irritable bowel syndrome in North America: a systematic review. Am J Gastroenterol. 2002;97:1910-1915. Abstract
11. Thabane M, Marshall JK. Post-infectious irritable bowel syndrome. World J Gastroenterol. 2009;15:3591-3596. Abstract
12. Kurina LM, Goldacre MJ, Yeates D, Gill LE. Depression and anxiety in people with inflammatory bowel disease. J Epidemiol Community Health. 2001;55:716-720. Abstract
13. Hassett AL, Radvanski DC, Buyske S, Savage SV, Sigal LH. Psychiatric comorbidity and other psychological factors in patients with "chronic Lyme disease." Am J Med. 2009;122:843-850. Abstract
14. Epstein SA, Kay G, Clauw D, et al. Psychiatric disorders in patients with fibromyalgia. A multicenter investigation. Psychosomatics. 1999;40:57-63. Abstract
15. Arnold LM, Hudson JI, Keck PE, Auchenbach MB, Javaras KN, Hess EV. Comorbidity of fibromyalgia and psychiatric disorders. J Clin Psychiatry. 2006;67:1219-1225. Abstract
16. Raphael KG, Janal MN, Nayak S, Schwartz JE, Gallagher RM. Psychiatric comorbidities in a community sample of women with fibromyalgia. Pain. 2006;124:117-125. Abstract
17. Drossman DA, Creed FH, Olden KW, Svedlund J, Toner BB, Whitehead WE. Psychosocial aspects of the functional gastrointestinal disorders. Gut. 1999;45:25-30.
18. Ford CV. Somatization and fashionable diagnoses: illness as a way of life. Scand J Work Environ Health. 1997;23:7-16.
19. Yunus MB. Central sensitivity syndromes: a new paradigm and group nosology for fibromyalgia and overlapping conditions, and the related issue of disease versus illness. Semin Arthritis Rheum. 2008;37:339-352. Abstract
20. Williams DA, Clauw DJ. Understanding fibromyalgia: lessons from the broader pain research community. J Pain. 2009;10:777-791. Abstract
21. Tracey I, Bushnell MC. How neuroimaging studies have challenged us to rethink: is chronic pain a disease? J Pain. 2009;10:1113-1120. Abstract
22. Wolfe F. The relation between tender points and fibromyalgia symptom variables: evidence that fibromyalgia is not a discrete disorder in the clinic. Ann Rheum Dis. 1997;56:268-271. Abstract
23. Gracely RH, Grant MA, Giesecke T. Evoked pain measures in fibromyalgia. Best Pract Res Clin Rheumatol. 2003;17:593-609. Abstract
24. Petzke F, Clauw DJ, Ambrose K, Khine A, Gracely RH. Increased pain sensitivity in fibromyalgia: effects of stimulus type and mode of presentation. Pain. 2003;105:403-413. Abstract
25. Petzke F, Khine A, Williams D, Groner K, Clauw DJ, Gracely RH. Dolorimetry performed at 3 paired tender points highly predicts overall tenderness. J Rheumatol. 2001;28:2568-2569. Abstract
26. Wilder-Smith CH, Robert-Yap J. Abnormal endogenous pain modulation and somatic and visceral hypersensitivity in female patients with irritable bowel syndrome. World J Gastroenterol. 2007;13:3699-3704. Abstract
27. Gracely RH. A pain psychologist's view of tenderness in fibromyalgia. J Rheumatol. 2007;34:912-913. Abstract
28. Geisser ME, Glass JM, Rajcevska LD, Clauw DJ, Williams DA, Kileny PR. A psychophysical study of auditory and pressure sensitivity in patients with fibromyalgia and healthy controls. J Pain. 2008;9:417-422. Abstract
29. Geisser ME, Strader Donnell C, Petzke F, Gracely RH, Clauw DJ, Williams DA. Comorbid somatic symptoms and functional status in patients with fibromyalgia and chronic fatigue syndrome: sensory amplification as a common mechanism. Psychosomatics. 2008;49:235-242. Abstract
30. Gracely RH, Petzke F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 2002;46:1333-1343. Abstract
31. Mayer EA, Naliboff BD, Craig AD. Neuroimaging of the brain-gut axis: from basic understanding to treatment of functional GI disorders. Gastroenterology. 2006;131:925-942. Abstract
32. Craig AD. Interoception: the sense of the physiological condition of the body. Curr Opin Neurobiol. 2003;13:500-505. Abstract
33. Craig AD. Human feelings: why are some more aware than others? Trends Cogn Sci. 2004;8:239-241. Abstract
34. Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. Neuron. 2007;55:377-391. Abstract
35. Julien N, Goffaux P, Arsenault P, Marchand S. Widespread pain in fibromyalgia is related to a deficit of endogenous pain inhibition. Pain. 2005;114:295-302. Abstract
36. Heymen S, Maixner W, Whitehead WE, Klatzkin RR, Mechlin B, Light KC. Central processing of noxious somatic stimuli in patients with irritable bowel syndrome compared with healthy controls. Clin J Pain. 2010;26:104-109. Abstract
37. King CD, Wong F, Currie T, Mauderli AP, Fillingim RB, Riley JL 3rd. Deficiency in endogenous modulation of prolonged heat pain in patients with irritable bowel syndrome and temporomandibular disorder. Pain. 2009;143:172-178. Abstract
38. Le Bars D, Villanueva L, Bouhassira D, Willer JC. Diffuse noxious inhibitory controls (DNIC) in animals and in man. Patol Fiziol Eksp Ter. 1992;4:55-65. Abstract
39. de Souza JB, Potvin S, Goffaux P, Charest J, Marchand S. The deficit of pain inhibition in fibromyalgia is more pronounced in patients with comorbid depressive symptoms. Clin J Pain. 2009;25:123-127. Abstract
40. Saito YA, Petersen GM, Larson JJ, et al. Familial aggregation of irritable bowel syndrome: a family case-control study. Am J Gastroenterol. 2010;105:833-841. Abstract
41. Kato K, Sullivan PF, Evengard B, Pedersen NL. Chronic widespread pain and its comorbidities: a population-based study. Arch Intern Med. 2006;166:1649-1654. Abstract
42. Kato K, Sullivan PF, Evengård B, Pedersen NL. A population-based twin study of functional somatic syndromes. Psychol Med. 2009;39:497-505. Abstract
43. Goldberg RT, Pachas WN, Keith D. Relationship between traumatic events in childhood and chronic pain. Disabil Rehabil. 1999; 21:23-30. Abstract
44. Weissbecker I, Floyd A, Dedert E, Salmon P, Sephton S. Childhood trauma and diurnal cortisol disruption in fibromyalgia syndrome. Psychoneuroendocrinology. 2006;31:312-324. Abstract
45. McLean SA, Williams DA, Harris RE, et al. Momentary relationship between cortisol secretion and symptoms in patients with fibromyalgia. Arthritis Rheum. 2005;52:3660-3669. Abstract
07-15-2010, 02:46 PM   #5
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46. Ablin K, Clauw DJ. From fibrositis to functional somatic syndromes to a bell-shaped curve of pain and sensory sensitivity: evolution of a clinical construct. Rheum Dis Clin North Am. 2009;35:233-251. Abstract
47. Hassett AL, Cone JD, Patella SJ, Sigal LH. The role of catastrophizing in the pain and depression of women with fibromyalgia syndrome. Arthritis Rheum. 2000;43: 2493-2500. Abstract
48. Lackner JM, Quigley BM. Pain catastrophizing mediates the relationship between worry and pain suffering in patients with irritable bowel syndrome. Behav Res Ther. 2005;43: 943-957. Abstract
49. Jones MP, Wessinger S, Crowell MD. Coping strategies and interpersonal support in patients with irritable bowel syndrome and inflammatory bowel disease. Clin Gastroenterol Hepatol. 2006;4:474-481. Abstract
50. Sayar K, Barsky AJ, Gulec H. Does somatosensory amplification decrease with antidepressant treatment? Psychosomatics. 2005;46:340-344. Abstract
51. Gwee KA, Leong YL, Graham C, et al. The role of psychological and biological factors in postinfective gut dysfunction. Gut. 1999;44:400-406. Abstract
52. Hassett AL, Simonelli LE, Radvanski DC, Buyske S, Savage SV, Sigal LH. The relationship between affect balance style and clinical outcomes in fibromyalgia. Arthritis Rheum. 2008;59:833-840. Abstract
53. Giesecke T, Williams DA, Harris RE, et al. Subgrouping of fibromyalgia patients on the basis of pressure-pain thresholds and psychological factors. Arthritis Rheum. 2003;48:2916-2922. Abstract
54. Thieme K, Spies C, Sinha P, Turk DC, Flor H. Predictors of pain behaviors in fibromyalgia syndrome. Arthritis Rheum. 2005;53:343-350. Abstract
55. Clauw DJ. Fibromyalgia: an overview. Am J Med. 2009;122:S3-S13.
56. Moayyedi P, Ford AC, Quigley EM, et al. The American College of Gastroenterology irritable bowel syndrome monograph: translating systemic review data to clinical practice. Gastroenterology. 2010;138:789-791. Abstract
57. Kroenke K, Krebs EE, Bair MJ. Pharmacotherapy of chronic pain: a synthesis of recommendations from systematic reviews. Gen Hosp Psychiatry. 2009;31:206-219. Abstract
58. Arnold LM, Keck PE Jr, Welge JA. Antidepressant treatment of fibromyalgia. A meta analysis and review. Psychosomatics. 2000;41:104-113. Abstract
59. Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA. 2004;292:2388-2395. Abstract
60. Anderberg UM, Marteinsdottir I, von Knorring L. Citalopram in patients with fibromyalgia -a randomized, double-blind, placebo-controlled study. Eur J Pain. 2000;4:27-35. Abstract
61. Norregaard J, Volkmann H, Danneskiold-Samsoe B. A randomized controlled trial of citalopram in the treatment of fibromyalgia. Pain. 1995;61:445-449. Abstract
62. Capaci K, Hepguler S. Comparison of the effects of amitriptyline and paroxetine in the treatment of fibromyalgia syndrome. The Pain Clinic. 2002;14:223-228.
63. Vahedi H, Merat S, Rashidioon A, et al. The effect of fluoxetine in patients with pain and constipation-predominant irritable bowel syndrome: A double-blind randomized controlled study. Aliment Pharmacol Ther. 2005;22:381-385. Abstract
64. Kuiken SD, Tytgat GNJ, Boeckxstaens GEE. The selective serotonin reuptake inhibitor fluoxetine does not change rectal sensitivity and symptoms in patients with irritable bowel syndrome: A double-blind, randomized, placebo-controlled study. Clin Gastroenterol Hepatol. 2003;1:219-228. Abstract
65. Tabas G, Beaves M, Wang J, et al. Paroxetine to treat irritable bowel syndrome not responding to high fiber diet: A double-blind placebo-controlled trial. Am J Gastroenterol. 2004;99:914-920. Abstract
66. Tack J, Broekaert D, Fischler B, et al. A controlled crossover study of the selective serotonin reuptake inhibitor citalopram in irritable bowel syndrome. Gut. 2006;55:1095-1103. Abstract
67. Fishbain D. Evidence-based data on pain relief with antidepressants. Ann Med. 2000;32:305-316. Abstract
68. Adelman LC, Adelman JU, Von Seggern R, Mannix LK. Venlafaxine extended release (XR) for the prophylaxis of migraine and tension-type headache: A retrospective study in a clinical setting. Headache. 2000;40:572-580. Abstract
69. Arnold LM, Lu Y, Crofford LJ, et al. A double-blind, multicenter trial comparing duloxetine with placebo in the treatment of fibromyalgia patients with or without major depressive disorder. Arthritis Rheum. 2004;50:2974-2984. Abstract
70. Chappell AS, Ossanna MJ, Liu-Seifert H, et al. Duloxetine, a centrally acting analgesic, in the treatment of patients with osteoarthritis knee pain: a 13-week, randomized, placebo-controlled trial. Pain. 2009;146:253-260. Abstract
71. Brennan BP, Fogarty KV, Roberts JL, Reynolds KA, Pope HG Jr, Hudson JI. Duloxetine in the treatment of irritable bowel syndrome: an open-label pilot study. Hum Psychopharmacol. 2009;24:423-428. Abstract
72. Vaishnavi SN, Nemeroff CB, Plott SJ, Rao SG, Kranzler J, Owens MJ. Milnacipran: a comparative analysis of human monoamine uptake and transporter binding affinity. Biol Psychiatry. 2004;55:320-322. Abstract
73. Geisser ME, Clauw DJ, Strand V, Gendreau RM, Palmer R, Williams DA. Contributions of change in clinical status parameters to Patient Global Impression of Change (PGIC) scores among persons with fibromyalgia treated with milnacipran. Pain. 2010;149:373-378. Abstract
74. Vitton O, Gendreau M, Gendreau J, Kranzler J, Rao SG. A double-blind placebo-controlled trial of milnacipran in the treatment of fibromyalgia. Hum Psychopharmacol. 2004;19:S27-S35. Abstract
75. Wiffen P, McQuay H, Carroll D, Jadad A, Moore A. Anticonvulsant drugs for acute and chronic pain. Cochrane Database Syst Rev. 2000;3:CD001133.
76. Crofford LJ, Rowbotham MC, Mease PJ, et al. Pregabalin for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 2005;52:1264-1273. Abstract
77. Arnold LM, Goldenberg DL, Stanford SB, et al. Gabapentin in the treatment of fibromyalgia: a randomized, double-blind, placebo-controlled, multicenter trial. Arthritis Rheum. 2007;56:1336-1344. Abstract
78. Arnold LM, Russell IJ, Diri EW, et al. A 14-week, randomized, double-blinded, placebo-controlled monotherapy trial of pregabalin in patients with fibromyalgia. J Pain. 2008;9:792-805. Abstract
79. Redillas C, Solomon S. Prophylactic pharmacological treatment of chronic daily headache. Headache. 2000;40:83-102. Abstract
80. Lee KJ, Kim JH, Cho SW. Gabapentin reduces rectal mechanosensitivity and increases rectal compliance in patients with diarrhoea-predominant irritable bowel syndrome. Aliment Pharmacol Ther. 2005;22:981-988. Abstract
81. Scharf MB, Baumann M, Berkowitz DV. The effects of sodium oxybate on clinical symptoms and sleep patterns in patients with fibromyalgia. J Rheumatol. 2003;30:1070-1074. Abstract
82. Russell IJ, Perkins AT, Michalek JE. Sodium oxybate relieves pain and improves function in fibromyalgia syndrome: a randomized, double-blind, placebo-controlled, multicenter clinical trial. Arthritis Rheum. 2009;60:299-309. Abstract
83. Bennett R. Pharmacological treatment of fibromyalgia. J Funct Syndr. 2001;1:79-92.
84. Carville SF, Arendt-Nielsen S, Bliddal H, et al. EULAR evidence-based recommendations for the management of fibromyalgia syndrome. Ann Rheum Dis. 2008;67:536-541. Abstract
85. American College of Gastroenterology Task Force on Irritable Bowel Syndrome; Brandt LJ, Chey WD, Foxx-Orenstein AE, et al. An evidence-based position statement on the management of irritable bowel syndrome. Am J Gastroenterol. 2009;104:S1-S35.
86. Jones KD, Liptan GL. Exercise interventions in fibromyalgia: clinical applications from the evidence. Rheum Dis Clin North Am. 2009;35:373-391. Abstract
87. Burckhardt CS, Bjelle A. Education programmes for fibromyalgia patients: description and evaluation. Baillieres Clin Rheumatol. 1994;8:935-955. Abstract
88. Williams DA. Psychological and behavioural therapies in fibromyalgia and related syndromes. Best Pract Res Clin Rheumatol. 2003;17:649-665. Abstract
89. Daley AJ, Grimmett C, Roberts L. The effects of exercise upon symptoms and quality of life in patients diagnosed with irritable bowel syndrome: a randomised controlled trial. Int J Sports Med. 2008;29:778-782. Abstract
90. Hassett AL, Gevirtz RN. Nonpharmacologic treatment for fibromyalgia: patient education, cognitive-behavioral therapy, relaxation techniques, and complementary and alternative medicine. Rheum Dis Clin North Am. 2009;35:393-407. Abstract
91. Busch AJ, Schachter CL, Overend TJ, Peloso PM, Barber KA. Exercise for treating fibromyalgia syndrome. Cochrane Database Syst Rev. 2007;4:CD003786.
92. Ringström G, Störsrud S, Posserud I, Lundqvist S, Westman B, Simrén M. Structured patient education is superior to written information in the management of patients with irritable bowel syndrome: a randomized controlled study. Eur J Gastroenterol Hepatol. 2010;22:420-428. Abstract
93. Clauw DJ, Witter J. Pain and rheumatology: thinking outside the joint. Arthritis Rheum. 2009;60:321-324. Abstract
94. Gwilym SE, Keltner JR, Warnaby CE, et al. Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients. Arthritis Rheum. 2009;61:1226-1234. Abstract
07-17-2010, 05:40 AM   #6
soupdragon69
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Join Date: Dec 2006
David,

I have just read this thread and it is spot on! Thanks so very much for posting it!!

I am due to start a 4 week residential course on 29th November which follows the above principles. The have asked to me to buy a book to read between now and then which is what most of their programme is based on.

It is called Practical and Positive Ways of Adapting to Chronic Pain - Manage your Pain

The authors are Nicholas, Molloy, Tonkin and Beeston. I bought it on Amazon during the week and looking forward to finding out more about it.

Thanks again!
__________________
Jan

IF YOU DON'T JUMP YOU WONT EVER LEARN TO FLY





Brittle asthma 1996, Hypothyroidism 1998, Severe Crohns ileitis 2006 , Severe IBS 2007, Inflammatory/Rheumatoid Arthritis 2008, Sebhorreic Eczema and Folliculitis 1992, Roseca, steroid induced acne and Hidradenitis Suppurativa 2008, Multiple allergies and food intolerances diagnosed from 2003. Newly diagnosed fibromyalgia Dec 2009. Newly diagnosed calcific tendonitis Jan 2010. Chronic Pain diagnosed Dec 2010.
07-18-2010, 03:36 AM   #7
David in Seattle
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Jan - I'm glad you found the article helpful. Best of luck!

David
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