Guest guest Posted August 15, 2006 Report Share Posted August 15, 2006 Pamela wrote: <<Water therapy helps tremendously. I am monitoring the pain levels after workouts so I can relate to the people who come to me (in the future) for FM water workouts. I want to be able to tell them how much it will or will not hurt them and encourage them to keep working out. I've been fighting with disability. A lot of people with FM get on disability but I think if we keep working through this, we can come out the other side, healthier and in better control of our bodies and our pain & fatigue levels. So, my question to this group is; is there anyone out there that is dealing with fibromyalgia patients and if so, who? How is their routine laid out? Is there anyone I may contact for more info on getting back into working out in spite of the pain and fatigue? Thank you all, Group! Sincerely, ~Pamela WA State [Mod: Please sign all letters with full name and city of residence, thanks] >> **** Pamela I think that your approach to fibromyalgia is not only the right one but admirable. You need to have a positive attitude that you will overcome this condition. I have seen patients who just throw up their hands and use fibromyalgia as a reason to decrease physical activity and these individuals become truly disabled. I have also seen patients who refuse to let fibromyalgia get in the way of living their life. As a Gastroenterologist I treat many patients with Irritable bowel syndrome (IBS). IBS shares some common pathophysiologic aspects with fibromyalgia and many patients with Irritable bowel syndrome also suffer from fibromyalgia. While I don’t see patients specifically for fibromyalgia many of the patients I do treat also have have fibromyalgia. Generally Rheumatoloigists deal specifically with fibromyalgia. And most of the medical research is found in the Rheumatology literature. In our community there is one Rheumatologists who specializes in the treatment of this condition and most of the other physicians and Rheumatologists refer their patients to him. I have included excerpts from several sources which I think should be the beginning of your search for some meaningful answers to your condition. Over the last several years there has been quite a bit of research into the pathophysiology of chronic conditions such as irritable bowel syndrome and fibromyalgia and therefore a better understanding in the approach and treatment of these conditions. Although all the answers as to cause, and treatment I believe the research is making great progress in understanding these conditions. While there is no cure for these conditions nevertheless there is better understanding of possible treatments which can allow patients a means to better deal with these conditions. For many years the very existence of the fibromyalgia was doubted because the muscles appeared to be perfectly normal. Lab tests and muscle biopsies, electromyograms are normal in the patient with fibromyalgia. There was no evidence that there was anything wrong with the muscles. In fact if you read the full articles I have cited below you will see that in fact fibromyalgia is not a muscle disease but rather caused by neuro-endocrinoligical abnormality. <<Fibromyalgia is a common disorder of unclear etiology that is characterized by chronic widespread pain and several nonspecific symptoms, such as anxiety, depression, fatigue, unrefreshing sleep, and gastrointestinal complaints. Patients seem to have a generalized abnormality in pain perception, with a decline in pain threshold and tolerance to an assortment of stimuli, such as pressure, cold, and heat [1], [2], [3], [4]. It was suggested that the pathogenesis of fibromyalgia involves aberrations in central nervous system function that result in abnormal pain perception [5], [6] Rheumatic Diseases Clinics of North America Volume 31 • Number 1 • February 2005 Copyright © 2005 W. B. Saunders Company >> <<Studies have shown that several hormonal axes controlled by the hypothalamus are disrupted in FMS patients.[100] [117] 100. Neeck G, Crofford LJ: Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North Am 26:989–1002, 2000. 117. Neeck G: Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 113:8–12, 2000. >> How and why these changes occur in a given individual is still unclear but just as with Irritable bowel syndrome there are probably several different mechanisms by which an individual develops this condition. Not knowing your complete history I will not even begin to suggest how or why you developed this condition. There are many suggested treatments for this condition and only a practitioner who knows your medical history in detail would be in a position to recommend an appropriate course of action. Not only is exercise not contraindicated for fibromyalgia, but if the approach is done properly, exercise can help make fibromyalgia manageable. <<Subjects who have fibromyalgia who actively participate in a low-intensity aerobic exercise program may show improvement in fitness and improvement in symptoms of fibromyalgia [99], [100], [101]. (Hypothalamic–Pituitary–Adrenal and Autonomic Nervous System Functioning in Fibromyalgia Gail K. Adler, MD, PhD a, * Rinie Geenen, PhD>> <<EXERCISE Aerobic exercise is one of the best validated treatments for fibromyalgia and CFS.[180] [181] [182] Unfortunately, it is a difficult task to get patients to agree to exercise training when they are experiencing severe pain, fatigue, or both. It is advisable to reassure them that exercise is safe and effective for patients with their condition and to advise them to start slowly and increase duration or intensity only slowly. It is important to acknowledge the difficulty patients will have following the exercise program while expressing the hope that they will benefit from perseverance. s Kelley's Textbook of Rheumatology, 7th ed. Pg 531 >> It is important to understand that for reasons which are not well understood your body no longer responds to pain and stress the way it did prior to your becoming ill. You have become extremely sensitive to pain from even the slightests of stimuli. Discomfort which most of us would judge as a 2 or 3 on a scale of 10 is interpreted by your nervous system and feels like a 8-10 out of 10. Stress while not the cause of your condition tends to worsen the pain of fibromyalgia. Any therapy which is aimed at lowering stress will help with management. Meditation, Relaxation therapay are also helpful and there are studies which indicate that Accupuncture may also be helpful <<COGNITIVE BEHAVIORAL THERAPY Cognitive behavioral therapy (CBT) is a process that examines a patient's way of reacting to experiences and attempts to restructure maladaptive coping habits into effective coping skills. CBT has been shown to be effective in reducing disability and increasing function in patients with OA, RA, and CFS.[183] [184] [185] [186] [187] A few studies of CBT in fibromyalgia have been done, with most showing an improvement.[188] Most experts suggest that CBT works by allowing patients to experience a greater locus of control over their symptoms and their illness. It has been shown to improve patients' compliance with other aspects of their care, such as exercise programs Kelley's Textbook of Rheumatology, 7th ed. Pg 531>> You seem to have already started some these therapies. Hydrotherapy can be considered an excellent tool. Moving away may have helped in easing some previous stresses. Properly paced exercise can and should be the basis of starting your recovery. Just be patient and don’t over do it. .. I would agree with your therapist who suggested that you start and exercise program even if it is only 5 minutes at a time several times a day. I would recommend that each day you extend your exercise time just a little. Start simply by walking, or swimming, hydrotherapy etc. Avoid initially trying to do too much. With time you will be able to increase your volume of exercise (time) and intensity. Be patient and don’t over do it. If you wish to communicate with me through personal email feel free to do so. Perhaps I can be more specific in answering some of your questions. I would suggest that you read the excepts of the article below and if possible get the entire article. You should be able to obtain copies of the articles or the books through your local Hospital Library. I would also recommend that you see a Rheumatologist who specializes in the treatment of Fibromyalgia. ragiarn@... Ralph Giarnella MD Southington, CT <<<Rheumatic Diseases Clinics of North America Volume 31 • Number 1 • February 2005 Copyright © 2005 W. B. Saunders Company Hypothalamic–Pituitary–Adrenal and Autonomic Nervous System Functioning in Fibromyalgia Fibromyalgia is a common disorder of unclear etiology that is characterized by chronic widespread pain and several nonspecific symptoms, such as anxiety, depression, fatigue, unrefreshing sleep, and gastrointestinal complaints. Patients seem to have a generalized abnormality in pain perception, with a decline in pain threshold and tolerance to an assortment of stimuli, such as pressure, cold, and heat [1], [2], [3], [4]. It was suggested that the pathogenesis of fibromyalgia involves aberrations in central nervous system function that result in abnormal pain perception [5], [6] Disturbances in neuroendocrine and ANS function can result in many symptoms that are observed commonly in fibromyalgia, including fatigue, weakness, and orthostatic intolerance. Several recent reviews have described, in detail, studies of neuroendocrine and autonomic dysfunction in fibromyalgia [8], [9], [10], [11].. In response to a stressful event, the neuroendocrine and autonomic nervous systems function in a coordinated fashion. The stress response varies depending on the specific stress and stress history of the individual. In healthy individuals, pre-exposure to an acute stress [34], [35] reduces the neuroendocrine and ANS responses to a subsequent acute stress. Chronic stress also may result in impaired neuroendocrine and ANS responses to an acute stress. .. Drugs alter the stress response. Caffeine consumption increases exercise-induced activation of the HPA axis and sympathoadrenal system [42]. These increases are postulated [42], [43] to account for the delayed fatigue and increased exercise performance that are associated with caffeine ingestion [44], [45]. Gender also influences the stress response; women have smaller increases in corticotropin in response to a brief psychosocial stress [46] and smaller increases in plasma catecholamines in response to exercise than men [47]. Even after taking gender into account, baseline ANS and neuroendocrine function vary between individuals. For example, baseline corticotropin levels are higher in male marathon runners than in healthy men who exercise moderately [48]. Individuals can be categorized as high or low corticotropin responders; this categorization seems to be maintained across different types of stress [49]. Thus, the neuroendocrine and ANS response to a specific stress vary based on a wide range of factors, including inherent differences between individuals, gender, physical fitness, drugs, and acute or chronic stresses. The extent of the neuroendocrine and ANS response to stress seems to be important. Enhanced responses may be associated with increased exercise performance and reduced fatigue [42], [43], whereas reduced neuroendocrine and ANS stress responses may result in inadequate physiologic responses, as occurs in patients who have HAAF [39], [40]. Furthermore, the neuroendocrine and ANS systems function in concert, so that mild impairments in multiple systems may have profound effects. Therefore, in examining stress responses in individuals, it is important to examine multiple aspects of this response. THE ORIGIN OF CHANGED STRESS RESPONSIVENESS A major dilemma exists in interpreting the source of altered ANS and HPA stress responsiveness [11], [75]. It may reflect an impairment that is constitutional or acquired by being exposed to severe trauma in the past; however, it also is possible that reduced stress responsiveness reflects the current consequences of stress, low physical fitness, sleep disturbance, or pain. Fig. 1 presents a model for understanding the possible interactions between stress, the stress response, and symptoms of fibromyalgia. SUMMARY The small numbers of studies that have examined coordinated HPA axis and ANS functioning in fibromyalgia showed hyporeactivity to applied stress. This altered neuroendocrine responsiveness seems to be due to changes in hypothalamic function, not to a primary adrenal defect. It is unknown whether these neuroendocrine alterations are involved in the pathophysiology of fibromyalgia and contribute to its ongoing symptomatology or are a consequence of pain and its associated symptoms (eg, fatigue, low physical fitness, sleep and mood disorder) or both. The changes in HPA axis function do not meet set criteria for hormone deficiency; hormone supplementation therapy is not recommended. Subtle impairments in multiple systems function in concert and together may result in more intense and clinically significant alterations in the response to stress. If so, factors that improve HPA and ANS responses to stress may be beneficial; this may explain why exercise can be helpful for patients who have fibromyalgia. REFERENCES: [1] Mikkelsson M., Latikka P., Kautiainen H., Muscle and bone pressure pain threshold and pain tolerance in fibromyalgia patients and controls. Arch Phys Med Rehabil (1992) 73 : pp 814-818. Abstract [2] Berglund B., Harju E.L., Kosek E., Quantitative and qualitative perceptual analysis of cold dysesthesia and hyperalgesia in fibromyalgia. Pain (2002) 96 : pp 177-187. Abstract [3] Granges G., Littlejohn G., Pressure pain threshold in pain-free subjects, in patients with chronic regional pain syndromes, and in patients with fibromyalgia syndrome. Arthritis Rheum (1993) 36 : pp 642-646. Abstract [4] McDermid A.J., Rollman G.B., McCain G.A., Generalized hypervigilance in fibromyalgia: evidence of perceptual amplification. Pain (1996) 66 : pp 133-144. Abstract [5] Clauw D.J., Chrousos G.P., Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation (1997) 4 : pp 134-153. Abstract [6] Weigent D.A., Bradley L.A., Blalock J.E., Current concepts in the pathophysiology of abnormal pain perception in fibromyalgia. Am J Med Sci (1998) 315 : pp 405-412. Abstract [6] Weigent D.A., Bradley L.A., Blalock J.E., Current concepts in the pathophysiology of abnormal pain perception in fibromyalgia. Am J Med Sci (1998) 315 : pp 405-412. Abstract [7] Henriksson K.G., Fibromyalgia–from syndrome to disease. Overview of pathogenetic mechanisms. J Rehabil Med (2003) : pp 89-94. [8] Petzke F., Clauw D.J., Sympathetic nervous system function in fibromyalgia. Curr Rheumatol Rep (2000) 2 : pp 116-123. Abstract [9] ez-Lavin M., Management of dysautonomia in fibromyalgia. Rheum Dis Clin North Am (2002) 28 : pp 379-387. Abstract [10] Adler G.K., Manfredsdottir V.F., Creskoff K.W., Neuroendocrine abnormalities in fibromyalgia. Curr Pain Headache Rep (2002) 6 : pp 289-298. Abstract [11] Geenen R., s J.W., Bijlsma J.W., Evaluation and management of endocrine dysfunction in fibromyalgia. Rheum Dis Clin North Am (2002) 28 : pp 389-404. Abstract 34] S.N., Mann S., Galassetti P., Effects of differing durations of antecedent hypoglycemia on counterregulatory responses to subsequent hypoglycemia in normal humans. Diabetes (2000) 49 : pp 1897-1903. Abstract [35] S.N., Tate D., Effects of morning hypoglycemia on neuroendocrine and metabolic responses to subsequent afternoon hypoglycemia in normal man. J Clin Endocrinol Metab (2001) 86 : pp 2043-2050. Full Text [42] t D., Schneider K.E., Prusaczyk W.K., Effects of caffeine on muscle glycogen utilization and the neuroendocrine axis during exercise. J Clin Endocrinol Metab (2000) 85 : pp 2170-2175. Full Text [43] Adler G.K., Exercise and fatigue—is neuroendocrinology an important factor?. J Clin Endocrinol Metab (2000) 85 : pp 2167-2169. Citation [44] Dodd S.L., Herb R.A., Powers S.K., Caffeine and exercise performance. An update. Sports Med (1993) 15 : pp 14-23. Abstract [45] Jackman M., Wendling P., Friars D., Metabolic catecholamine, and endurance responses to caffeine during intense exercise. J Appl Physiol (1996) 81 : pp 1658-1663. Abstract [46] Kirschbaum C., Kudielka B.M., Gaab J., Impact of gender, menstrual cycle phase, and oral contraceptives on the activity of the hypothalamus-pituitary-adrenal axis. Psychosom Med (1999) 61 : pp 154-162. Abstract [47] S.N., Galassetti P., Wasserman D.H., Effects of gender on neuroendocrine and metabolic counterregulatory responses to exercise in normal man. J Clin Endocrinol Metab (2000) 85 : pp 224-230. Abstract [48] Wittert G.A., Livesey J.H., Espiner E.A., Adaptation of the hypothalamopituitary adrenal axis to chronic exercise stress in humans. Med Sci Sports Exerc (1996) 28 : pp 1015-1019. Abstract [49] Singh A., Petrides J.S., Gold P.W., Differential hypothalamic-pituitary-adrenal axis reactivity to psychological and physical stress. J Clin Endocrinol Metab (1999) 84 : pp 1944-1948. Abstract [75] Masi A.T., White K.P., Pilcher J.J., Person-centered approach to care, teaching, and research in fibromyalgia syndrome: justification from biopsychosocial perspectives in populations. Semin Arthritis Rheum (2002) 32 : pp 71-93. Abstract >>>> ======== Goldman: Cecil Textbook of Medicine, 22nd ed., Copyright © 2004 W. B. Saunders Company ============ ====== DISORDERED STRESS RESPONSE AND ENDOCRINE OR HORMONAL FACTORS : Kelley's Textbook of Rheumatology, 7th ed., Copyright © 2005 Saunders References 1. Wolfe F, Smythe HA, Yunus MB, et al: The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia: Report of the Multicenter Criteria Committee. Arthritis Rheum 33:160–172, 1990. 2. Stockman R: The causes, pathology, and treatment of chronic rheumatism. Edinburgh Med J 134:107, 1904. 3. Osler W: The Principles and Practice of Medicine. New York, D. Appleton, 1900, p 406. 4. Kellgren JH: Observations on referred pain arising from muscles. Clin Sci 3:42–46, 1938. 5. Kellgren JH: On distribution of pain arising from deep somatic structures, with charts of segmental pain areas. Clin Sci 4:126–130, 1939. 6. T, Kellgren JH: Observations relating to referred pain, visceromotor reflexes, and other associated phenomena. Clin Sci 4:131–135, 1939. 7. RM: Fibrositis. In Kelley WN, ED Jr, Ruddy S, Sledge CB (eds): Textbook of Rheumatology. Philadelphia, W.B. Saunders, 1989, pp 541–553. 8. Comroe: Fibrositis. Arthritis and Allied Conditions. Philadelphia, Lea & Febiger, 1944, pp 679–701. 9. Fukuda K, Nisenbaum R, G, et al: Chronic multisymptom illness affecting Air Force veterans of the Gulf War. JAMA 280:981–988, 1998. 10. Yunus M, Masi AT, Calabro JJ, et al: Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls. Semin Arthritis Rheum 11:151–71, 1981. 11. SM, S, Tindall EA, et al: Clinical characteristics of fibrositis. I. A " blinded, " controlled study of symptoms and tender points. Arthritis Rheum 26:817–824, 1983. 12. Wolfe F, Hawley DJ, Cathey MA, et al: Fibrositis: Symptom frequency and criteria for diagnosis: An evaluation of 291 rheumatic disease patients and 58 normal individuals. J Rheumatol 12:1159–1163, 1985. 13. Clauw DJ, Chrousos GP: Chronic pain and fatigue syndromes: overlapping clinical and neuroendocrine features and potential pathogenic mechanisms. Neuroimmunomodulation 4:134–153, 1997. 14. White KP, Harth M, Speechley M, Ostbye T: A general population study of fibromyalgia tender points in noninstitutionalized adults with chronic widespread pain. J Rheumatol 27:2677–682, 2000. 15. Gowin KM: Diffuse pain syndromes in the elderly. Rheum Dis Clin North Am 26:673–682, 2000. 16. Wolfe F, Ross K, J, et al: The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum 38:19–28, 1995. 17. White KP, Speechley M, Harth M, Ostbye T: The London Fibromyalgia Epidemiology Study: The prevalence of fibromyalgia syndrome in London, Ontario. J Rheumatol 26:1570–1576, 1999. 18. Wessely S, Chalder T, Hirsch S, et al: The prevalence and morbidity of chronic fatigue and chronic fatigue syndrome: A prospective primary care study. Am J Public Health 87:1449–1455, 1997. 19. Steele L, Dobbins JG, Fukuda K, et al: The epidemiology of chronic fatigue in San Francisco. Am J Med 105:83S–90S, 1998. 20. Buchwald D, Garrity D: Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Arch Intern Med 154:2049–2053, 1994. 21. White KP, Speechley M, Harth M, Ostbye T: Co-existence of chronic fatigue syndrome with fibromyalgia syndrome in the general population: A controlled study. Scand J Rheumatol 29:44–51, 2000. 22. Wysenbeek AJ, Shapira Y, Leibovici L: Primary fibromyalgia and the chronic fatigue syndrome. Rheumatol Int 10:227–229, 1991. 23. LA, Burke MM, Buchwald D: Overlapping conditions among patients with chronic fatigue syndrome, fibromyalgia, and temporomandibular disorder. Arch Intern Med 160:221–227, 2000. 24. Hudson JI, Goldenberg DL, Pope HG Jr, et al: Comorbidity of fibromyalgia with medical and psychiatric disorders. Am J Med 92:363–367, 1992. 25. Yunus MB, Inanici F, Aldag JC, Mangold RF: Fibromyalgia in men: comparison of clinical features with women. J Rheumatol 27:485–490, 2000. 26. Sivri A, Cindas A, Dincer F, Sivri B: Bowel dysfunction and irritable bowel syndrome in fibromyalgia patients. Clin Rheumatol 15:283–286, 1996. 27. Gomborone JE, Gorard DA, Dewsnap PA, et al: Prevalence of irritable bowel syndrome in chronic fatigue. J R Coll Physicians Lond 30:512–513, 1996. 28. Triadafilopoulos G, Simms RW, Goldenberg DL: Bowel dysfunction in fibromyalgia syndrome. Dig Dis Sci 36:59–64, 1991. 29. Goldenberg DL, Simms RW, Geiger A, Komaroff AL: High frequency of fibromyalgia in patients with chronic fatigue seen in a primary care practice. Arthritis Rheum 33:381–387, 1990. 30. Romano TJ: Coexistence of irritable bowel syndrome and fibromyalgia. W V Med J 84:16–18, 1988. 31. Sperber AD, Atzmon Y, Neumann L, et al: Fibromyalgia in the irritable bowel syndrome: Studies of prevalence and clinical implications. Am J Gastroenterol 94:3541–3546, 1999. 32. 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 30:220–222, 1991. 33. Slotkoff AT, Radulovic DA, Clauw DJ: The relationship between fibromyalgia and the multiple chemical sensitivity syndrome. Scand J Rheumatol 26:364–367, 1997. 34. sson PO, Lindman R, Stal P, Bengtsson A: Symptoms and signs of mandibular dysfunction in primary fibromyalgia syndrome (PSF) patients. Swed Dent J 12:141–149, 1988. 35. Plesh O, Wolfe F, Lane N: The relationship between fibromyalgia and temporomandibular disorders: Prevalence and symptom severity. J Rheumatol 23:1948–1952, 1996. 36. Buchwald D, Pearlman T, Kith P, Schmaling K: Gender differences in patients with chronic fatigue syndrome. J Gen Intern Med 9:397–401, 1994. 37. s RK, Ahmed M, Wearden AJ, et al: The role of depression in pain, psychophysiological syndromes and medically unexplained symptoms associated with chronic fatigue syndrome. J Affect Disord 55:143–148, 1999. 533 38. LA, RR, Kennedy CL: Chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities in a community-based sample of persons with chronic fatigue syndrome-like symptoms. Psychosom Med 62:655–663, 2000. 39. Holmes GP, Kaplan JE, Gantz NM, et al: Chronic fatigue syndrome: a working case definition. Ann Intern Med 108:387–389, 1988. 40. Komaroff AL, Buchwald DS: Chronic fatigue syndrome: an update. Annu Rev Med 49:1–13, 1998. 41. Rau CL, IJ: Is fibromyalgia a distinct clinical syndrome? Curr Rev Pain 4:287–294, 2000. 42. LA, Buchwald D: A review of the evidence for overlap among unexplained clinical conditions. Ann Intern Med 134:868–881, 2001. 43. McBeth J, Silman AJ: The role of psychiatric disorders in fibromyalgia. Curr Rheumatol Rep 3:157–164, 2001. 44. Winfield JB: Pain in fibromyalgia. Rheum Dis Clin North Am 25:55–79, 1999. 45. Monti DA, Herring CL, Schwartzman RJ, Marchese M: Personality assessment of patients with complex regional pain syndrome type I. Clin J Pain 14:295–302, 1998. 46. Zagari MJ, Mazonson PD, Longton WC: Pharmacoeconomics of chronic nonmalignant pain. Pharmacoeconomics 10:356–377, 1996. 47. Skevington SM, Carse MS, AC: Validation of the WHO-QOL-100: Pain management improves quality of life for chronic pain patients. Clin J Pain 17:264–275, 2001. 48. LA, Bradley LA, Alarcon GS, et al: Psychiatric diagnoses in patients with fibromyalgia are related to health care-seeking behavior rather than to illness. Arthritis Rheum 39:436–445, 1996. 49. Kersh BC, Bradley LA, Alarcon GS, et al: Psychosocial and health status variables independently predict health care seeking in fibromyalgia. Arthritis Rheum 45:362–371, 2001. 50. Sotgui ML: Descending influence on dorsal horn neuronal hyperactivity in a rat model of neuropathic pain. Neuroreport 4:21–24, 1993. 51. Honore P, SD, Schwei MJ, et al: Murine models of inflammatory, neuropathic and cancer pain each generates a unique set of neurochemical changes in the spinal cord and sensory neurons. Neuroscience 98:585–598, 2000. 52. Apkarian AV, Gelnar PA, Krauss BR, Szeverenyi NM: Cortical responses to thermal pain depend on stimulus size: A functional MRI study. J Neurophysiol 83:3113–3122, 2000. 53. Kwiatek R, Barnden L, Tedman R, et al: Regional cerebral blood flow in fibromyalgia: single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis Rheum 43:2823–2833, 2000. 54. Mountz JM, Bradley LA, Modell JG, et al: Fibromyalgia in women. Abnormalities of regional cerebral blood flow in the thalamus and the caudate nucleus are associated with low pain threshold levels. Arthritis Rheum 38:926–938, 1995. 55. Wolfe F, J, Harkness D, et al: A prospective, longitudinal, multicenter study of service utilization and costs in fibromyalgia. Arthritis Rheum 40:1560–1570, 1997. 56. Wolfe F, J, Harkness D, et al: Work and disability status of persons with fibromyalgia. J Rheumatol 24:1171–1178, 1997. 57. Alagiri M, Chottiner S, Ratner V, et al: Interstitial cystitis: Unexplained associations with other chronic disease and pain syndromes. Urology 49:52–57, 1997. 58. Holmes GP, Kaplan JE, JA, et al: A cluster of patients with a chronic mononucleosis-like syndrome: Is Epstein-Barr virus the cause? JAMA 257:2297–2302, 1987. 59. Hellinger WC, TF, Van Scoy RE, et al: Chronic fatigue syndrome and the diagnostic utility of antibody to Epstein-Barr virus early antigen. JAMA 260:971–973, 1988. 60. J, de Diego A, Trinchet M, Monforte A: Fibromyalgia-associated hepatitis C virus infection. Br J Rheumatol 36:981–985, 1997. 61. Kennedy M, Felson DT: A prospective long-term study of fibromyalgia syndrome. Arthritis Rheum 39:682–685, 1996. 62. Park JH, Niermann KJ, Olsen N: Evidence for metabolic abnormalities in the muscles of patients with fibromyalgia. Curr Rheumatol Rep 2:131–140, 2000. 63. Henriksson KG: Muscle pain in neuromuscular disorders and primary fibromyalgia. Eur J Appl Physiol Occup Physiol 57:348–352, 1988. 64. Kalyan-Raman UP, Kalyan-Raman K, Yunus MB, Masi AT: Muscle pathology in primary fibromyalgia syndrome: a light microscopic, histochemical and ultrastructural study. J Rheumatol 11:808–813, 1984. 65. Bengtsson A, Henriksson KG, Larsson J: Muscle biopsy in primary fibromyalgia: Light-microscopical and histochemical findings. Scand J Rheumatol 15:1–6, 1986. 66. Drewes AM, sen A, Schroder HD, et al: Pathology of skeletal muscle in fibromyalgia: A histo-immuno-chemical and ultrastructural study. Br J Rheumatol 32:479–483, 1993. 67. Lindh M, Johansson G, Hedberg M, et al: Muscle fiber characteristics, capillaries and enzymes in patients with fibromyalgia and controls. Scand J Rheumatol 24:34–37, 1995. 68. Yunus MB, Kalyan-Raman UP, Masi AT, Aldag JC: Electron microscopic studies of muscle biopsy in primary fibromyalgia syndrome: A controlled and blinded study. J Rheumatol 16:97–101, 1989. 69. sen S, Bartels EM, Danneskiold-Samsoe B: Single cell morphology of muscle in patients with chronic muscle pain. Scand J Rheumatol 20:336–343, 1991. 70. Elert JE, Rantapaa-Dahlqvist SB, Henriksson-Larsen K, et al: Muscle performance, electromyography and fibre type composition in fibromyalgia and work-related myalgia. Scand J Rheumatol 21:28–34, 1992. 71. Kravis MM, Munk PL, McCain GA, et al: MR imaging of muscle and tender points in fibromyalgia. J Magn Reson Imaging 3:669–670, 1993. 72. de Blecourt AC, Wolf RF, van Rijswijk MH, et al: In vivo 31P magnetic resonance spectroscopy (MRS) of tender points in patients with primary fibromyalgia syndrome. Rheumatol Int 11:51–54, 1991. 73. sen S, Jensen KE, Thomsen C, et al: 31P magnetic resonance spectroscopy of skeletal muscle in patients with fibromyalgia. J Rheumatol 19:1600–1603, 1992. 74. Norregaard J, Bulow PM, Danneskiold-Samsoe B: Muscle strength, voluntary activation, twitch properties, and endurance in patients with fibromyalgia. J Neurol Neurosurg Psychiatry 57:1106–1111, 1994. 75. Lund N, Bengtsson A, Thorborg P: Muscle tissue oxygen pressure in primary fibromyalgia. Scand J Rheumatol 15:165–173, 1986. 76. Bengtsson A, Henriksson KG, Larsson J: Reduced high-energy phosphate levels in the painful muscles of patients with primary fibromyalgia. Arthritis Rheum 29:817–821. 1986. 77. Mengshoel AM, Forre O, Komnaes HB: Muscle strength and aerobic capacity in primary fibromyalgia. Clin Exp Rheumatol 8:475–479, 1990. 78. Sietsema KE, DM, Caro X, et al: Oxygen uptake during exercise in patients with primary fibromyalgia syndrome. J Rheumatol 20:860–865, 1993. 79. Norregaard J, Bulow PM, Lykkegaard JJ, et al: Muscle strength, working capacity and effort in patients with fibromyalgia. Scand J Rehabil Med 29:97–102, 1997. 80. RM, SR, Goldberg L, et al: Aerobic fitness in patients with fibrositis: A controlled study of respiratory gas exchange and 133xenon clearance from exercising muscle. Arthritis Rheum 32:454–460, 1989. 81. Mense S: Descending antinociception and fibromyalgia. Z Rheumatol 57(Suppl 2):23–26, 1998. 82. Mense S: Neurobiological concepts of fibromyalgia: the possible role of descending spinal tracts. Scand J Rheumatol Suppl 113:24–29, 2000. 83. Rainville P, Bushnell MC, Duncan GH: Representation of acute and persistent pain in the human CNS: Potential implications for chemical intolerance. Ann N Y Acad Sci 933:130–141, 2001. 84. Bell IR, Baldwin CM, Russek LG, et al: Early life stress, negative paternal relationships, and chemical intolerance in middle-aged women: Support for a neural sensitization model. J Womens Health 7:1135–1147, 1998. 85. Bell IR, Baldwin CM, Schwartz GE: Illness from low levels of environmental chemicals: Relevance to chronic fatigue syndrome and fibromyalgia. Am J Med 105:74S–82S, 1998. 534 86. Garland EM, on D: Chiari I malformation as a cause of orthostatic intolerance symptoms: a media myth? Am J Med 111:546–552, 2001. 87. Kosek E, Ekholm J, Hansson P: Sensory dysfunction in fibromyalgia patients with implications for pathogenic mechanisms. Pain 68:375–83, 1996. 88. McDermid AJ, Rollman GB, McCain GA: Generalized hypervigilance in fibromyalgia: Evidence of perceptual amplification. Pain 66:133–144, 1996. 89. Lorenz J: Hyperalgesia or hypervigilance? An evoked potential approach to the study of fibromyalgia syndrome. Z Rheumatol 57(Suppl 2):19–22, 1998. 90. IJ, Orr MD, Littman B, et al: Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum 37:1593–1601, 1994. 91. Vaeroy H, Sakurada T, Forre O, et al: Modulation of pain in fibromyalgia (fibrositis syndrome): Cerebrospinal fluid (CSF) investigation of pain related neuropeptides with special reference to calcitonin gene related peptide (CGRP). J Rheumatol Suppl 19:94–97, 1989. 92. Vaeroy H, Helle R, Forre O, et al: Elevated CSF levels of substance P and high incidence of Raynaud phenomenon in patients with fibromyalgia: New features for diagnosis. Pain 32:21–26, 1988. 93. Wallace DJ, Linker-Israeli M, Hallegua D, et al: Cytokines play an aetiopathogenetic role in fibromyalgia: A hypothesis and pilot study. Rheumatology (Oxford) 40:743–749, 2001. 94. Maes M, Libbrecht I, Van Hunsel F, et al: Lower serum activity of prolyl endopeptidase in fibromyalgia is related to severity of depressive symptoms and pressure hyperalgesia. Psychol Med 28:957–965, 1998. 95. Schwarz MJ, Spath M, Muller-Bardorff H, et al: Relationship of substance P, 5-hydroxyindole acetic acid and tryptophan in serum of fibromyalgia patients. Neurosci Lett 259:196–198, 1999. 96. Helme RD, Littlejohn GO, Weinstein C: Neurogenic flare responses in chronic rheumatic pain syndromes. Clin Exp Neurol 23:91–94, 1987. 97. Littlejohn GO, Weinstein C, Helme RD: Increased neurogenic inflammation in fibrositis syndrome. J Rheumatol 14:1022–1025, 1987. 98. Sann H, Pierau FK: Efferent functions of C-fiber nociceptors. Z Rheumatol 57(Suppl 2):8–13, 1998. 99. Gibson SJ, Littlejohn GO, Gorman MM, et al: Altered heat pain thresholds and cerebral event-related potentials following painful CO2 laser stimulation in subjects with fibromyalgia syndrome. Pain 58:185–193, 1994. 100. Neeck G, Crofford LJ: Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North Am 26:989–1002, 2000. 101. Bradley LA, McKendree- NL, Alberts KR, et al: Use of neuroimaging to understand abnormal pain sensitivity in fibromyalgia. Curr Rheumatol Rep 2:141–148, 2000. 102. Lekander M, Fredrikson M, Wik G: Neuroimmune relations in patients with fibromyalgia: a positron emission tomography study. Neurosci Lett 282:193–196, 2000. 103. Offenbaecher M, Bondy B, de Jonge S, et al: Possible association of fibromyalgia with a polymorphism in the serotonin transporter gene regulatory region. Arthritis Rheum 42:2482–2488, 1999. 104. Bondy B, Spaeth M, Offenbaecher M, et al: The T102C polymorphism of the 5-HT2A-receptor gene in fibromyalgia. Neurobiol Dis 6:433–439, 1999. 105. Gursoy S, Erdal E, Herken H, et al: Association of T102C polymorphism of the 5-HT2A receptor gene with psychiatric status in fibromyalgia syndrome. Rheumatol Int 21:58–61, 2001. 106. Skeith KJ, Hussain MS, Coutts RT, et al: Adverse drug reactions and debrisoquine/sparteine (P450IID6) polymorphism in patients with fibromyalgia. Clin Rheumatol 16:291–295, 1997. 107. Moldofsky H, Warsh JJ: Plasma tryptophan and musculoskeletal pain in non-articular rheumatism ( " fibrositis syndrome " ). Pain 5:65–71, 1978. 108. IJ, Michalek JE, Vipraio GA, et al: Platelet 3H-imipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol 19:104–109, 1992. 109. IJ, Michalek JE, Vipraio GA, et al: Serum amino acids in fibrositis/fibromyalgia syndrome. J Rheumatol Suppl 19:158–163, 1989. 110. Yunus MB, Dailey JW, Aldag JC, et al: Plasma tryptophan and other amino acids in primary fibromyalgia: a controlled study. J Rheumatol 19:90–94, 1992. 111. IJ, Vaeroy H, Javors M, Nyberg F: Cerebrospinal fluid biogenic amine metabolites in fibromyalgia/fibrositis syndrome and rheumatoid arthritis. Arthritis Rheum 35:550–556, 1992. 112. Wolfe F, IJ, Vipraio G, et al: Serotonin levels, pain threshold, and fibromyalgia symptoms in the general population. J Rheumatol 24:555–559, 1997. 113. Klein R, Bansch M, Berg PA: Clinical relevance of antibodies against serotonin and gangliosides in patients with primary fibromyalgia syndrome. Psychoneuroendocrinology 17:593–598, 1992. 114. Klein R, Berg PA: A comparative study on antibodies to nucleoli and 5-hydroxytryptamine in patients with fibromyalgia syndrome and tryptophan-induced eosinophilia-myalgia syndrome. Clin Investig 72:541–549, 1994. 115. Klein R, Berg PA: High incidence of antibodies to 5-hydroytryptamine, gangliosides and phospholipids in patients with chronic fatigue and fibromyalgia syndrome and their relatives: Evidence for a clinical entity of both disorders. Eur J Med Res 1:21–26, 1995. 116. Werle E, Fischer HP, Muller A, et al: Antibodies against serotonin have no diagnostic relevance in patients with fibromyalgia syndrome. J Rheumatol 28:595–600, 2001. 117. Neeck G: Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. Scand J Rheumatol Suppl 113:8–12, 2000. 118. McCain GA, Tilbe KS: Diurnal hormone variation in fibromyalgia syndrome: A comparison with rheumatoid arthritis. J Rheumatol Suppl 19:154–157, 1989. 119. Griep EN, Boersma JW, de Kloet ER: Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. J Rheumatol 20:469–474, 1993. 120. Crofford LJ, Pillemer SR, Kalogeras KT, et al: Hypothalamic-pituitary-adrenal axis perturbations in patients with fibromyalgia. Arthritis Rheum 37:1583–1592, 1994. 121. Griep EN, Boersma JW, Lentjes EG, et al: Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and low back pain. J Rheumatol 25:1374–1381, 1998. 122. Maes M, Lin A, Bonaccorso S, et al: Increased 24-hour urinary cortisol excretion in patients with post-traumatic stress disorder and patients with major depression, but not in patients with fibromyalgia. Acta Psychiatr Scand 98:328–335, 1998. 123. Riedel W, Layka H, Neeck G: Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 57(Suppl 2):81–87, 1998. 124. Adler GK, Kinsley BT, Hurwitz S, et al: Reduced hypothalamic-pituitary and sympathoadrenal responses to hypoglycemia in women with fibromyalgia syndrome. Am J Med 106:534–543, 1999. 125. Torpy DJ, Papanicolaou DA, Lotsikas AJ, et al: Responses of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis to interleukin-6: A pilot study in fibromyalgia. Arthritis Rheum 43:872–880, 2000. 126. Korszun A, Young EA, Engleberg NC, et al: Follicular phase hypothalamic-pituitary-gonadal axis function in women with fibromyalgia and chronic fatigue syndrome. J Rheumatol 27:1526–1530, 2000. 127. Catley D, Kaell AT, Kirschbaum C, Stone AA: A naturalistic evaluation of cortisol secretion in persons with fibromyalgia and rheumatoid arthritis. Arthritis Care Res 13:51–61, 2000. 128. Lentjes EG, Griep EN, Boersma JW, et al: Glucocorticoid receptors, fibromyalgia and low back pain. Psychoneuroendocrinology 22:603–614, 1997. 129. Kirnap M, Colak R, Eser C, et al: A comparison between low-dose (1 microg), standard-dose (250 microg) ACTH stimulation tests and insulin tolerance test in the evaluation of hypothalamo-pituitary-adrenal axis in primary fibromyalgia syndrome. Clin Endocrinol (Oxf) 55:455–459, 2001. 535 130. AJ, Wessely S, Cleare AJ: The neuroendocrinology of chronic fatigue syndrome and fibromyalgia. Psychol Med 31:1331–1345, 2001. 131. RM, SR, SM, Burckhardt CS: Low levels of somatomedin C in patients with the fibromyalgia syndrome: A possible link between sleep and muscle pain. Arthritis Rheum 35:1113–1116, 1992. 132. RM, Cook DM, SR, et al: Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia. J Rheumatol 24:1384–1389, 1997. 133. Bagge E, Bengtsson BA, Carlsson L, Carlsson J: Low growth hormone secretion in patients with fibromyalgia: A preliminary report on 10 patients and 10 controls. J Rheumatol 25:145–148, 1998. 134. Older SA, Battafarano DF, Danning CL, et al: The effects of delta wave sleep interruption on pain thresholds and fibromyalgia-like symptoms in healthy subjects: Correlations with insulin-like growth factor I. J Rheumatol 25:1180–1186, 1998. 135. Leal-Cerro A, Povedano J, Astorga R, et al: The growth hormone (GH)-releasing hormone-GH-insulin-like growth factor-1 axis in patients with fibromyalgia syndrome. J Clin Endocrinol Metab 84:3378–81, 1999. 136. sen S, Main K, Danneskiold-Samsoe B, Skakkebaek NE: A controlled study on serum insulin-like growth factor-I and urinary excretion of growth hormone in fibromyalgia. J Rheumatol 22:1138–1140, 1995. 137. Buchwald D, Umali J, Stene M: Insulin-like growth factor-I (somatomedin C) levels in chronic fatigue syndrome and fibromyalgia. J Rheumatol 23:739–742, 1996. 138. Griep EN, Boersma JW, de Kloet ER: Pituitary release of growth hormone and prolactin in the primary fibromyalgia syndrome. J Rheumatol 21:2125–2130, 1994. 139. Dinser R, Halama T, Hoffmann A: Stringent endocrinological testing reveals subnormal growth hormone secretion in some patients with fibromyalgia syndrome but rarely severe growth hormone deficiency. J Rheumatol 27:2482–2488, 2000. 140. Gursel Y, Ergin S, Ulus Y, et al: Hormonal responses to exercise stress test in patients with fibromyalgia syndrome. Clin Rheumatol 20:401–405, 2001. 141. RM: Disordered growth hormone secretion in fibromyalgia: a review of recent findings and a hypothesized etiology. Z Rheumatol 57(Suppl 2):72–76, 1998. 142. ez-Lavin M: Is fibromyalgia a generalized reflex sympathetic dystrophy? Clin Exp Rheumatol 19:1–3, 2001. 143. Tougas G: The autonomic nervous system in functional bowel disorders. Can J Gastroenterol 13(Suppl A):15A–17A, 1999. 144. Meggs WJ: Neurogenic switching: A hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity. Environ Health Perspect 103:54–56, 1995. 145. Visuri T, Lindholm H, Lindqvist A, et al: Cardiovascular functional disorder in primary fibromyalgia: a noninvasive study in 17 young men. Arthritis Care Res 5:210–215, 1992. 146. Hubbard DR, Berkoff GM: Myofascial trigger points show spontaneous needle EMG activity. Spine 18:1803–1807, 1993. 147. ez-Lavin M, Hermosillo AG, s M, Soto ME: Circadian studies of autonomic nervous balance in patients with fibromyalgia: A heart rate variability analysis. Arthritis Rheum 41:1966–1971, 1998. 148. Anderberg UM, Liu Z, Berglund L, Nyberg F: Elevated plasma levels of neuropeptide Y in female fibromyalgia patients. Eur J Pain 3:19–30, 1999. 149. Wachter KC, Kaeser HE, Guhring H, et al: Muscle damping measured with a modified pendulum test in patients with fibromyalgia, lumbago, and cervical syndrome. Spine 21:2137–2142, 1996. 150. Cohen H, Neumann L, Alhosshle A, et al: Abnormal sympathovagal balance in men with fibromyalgia. J Rheumatol 28:581–589, 2001. ======= NEUROPLASTICITY OR CENTRAL NERVOUS SYSTEM PAIN-PROCESSING PATHWAY DYSFUNCTION : Kelley's Textbook of Rheumatology, 7th ed., Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.