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Fibromyalgia and the Disability Dilemma: 
A new era in understanding a complex multidimensional pain syndrome  

Taken from: Bennett, R.M.  Fibromyalgia and the disability dilemma: new concepts in understanding a complex multidimensional pain syndrome.  Published in Arthritis and Rheumatism Volume 39: pages 1627-1634, 1996.

Fibromyalgia (FM) is a common syndrome of chronic pain that is increasingly seen in rheumatology practice (1-6).  According to a recent epidemiology survey from Kansas, FM affects 2% of the total population; 3.4% of all women and 0.5% of men (7).  Most FM patients report that chronic pain and fatigue adversely affect the quality of their life and negatively impact their ability to be competitively employed (8-10).  The extent of reported disability in FM varies greatly from country to country (11-14) – probably reflecting differences in political philosophies and socio-economic realities.  A recent survey of the work and disability status of 1,668 FM patients from 7 centers in the USA reported that 25.3% had received disability payments (14.8% were from Social Security Disability) (15).  Interestingly less than 25% of the SSD awards were specifically for the diagnosis of FM.  The majority of patients who considered themselves disabled were receiving disability payments.  On the other hand 66% of FM patients reported that they could work on all or most days. 

Rheumatologists when asked assess disability issues in FM patients, have difficulty in distinguishing between their FM patients who continue to work and the patients who claim disability.  It seems that it is only the patient's self-perception of disability that distinguish the able from the would-be disabled. There is often a mismatch between what we find on clinical examination and the amount of alleged dysfunction.  Instinctively we suspect that there is nothing really wrong with the patient – FM patients usually look normal.  Thus the problem must be in the psyche.  Is there some hidden agenda for these claims?  Is the patient getting some secondary gain for this behavior?  Maybe they are escaping the stresses of a boring job, receiving more attention, getting an early pension or are they just bucking the system?  Such invidious thoughts are not only the province of health care providers; family members, co-workers and friends often harbor the same suspicions.  Are FM patients ever truly disabled and if so, what is the nature of their impairment? 

Can Pain cause Disability?

            Most FM patients cite pain as a major cause for disability.  Chronic widespread pain is a common finding (7,16).  The valid assessment of disability in chronic pain states is notoriously difficult (17,18).  The problems that are encountered in assessing the chronic pain patient are largely related to 4 issues:  1)  pain is a purely subjective sensation which is usually interpreted in an emotional context,  2) chronic pain cannot be fully understood in terms of the classical model of disease that equates pathogenesis with tissue damage or dysfunction,  3)  many “non-sick” people have persistent pain but are not disabled, and 4) disability due to pain results from a complex interplay between past experiences, education, income level, work related self-esteem, motivation, psychological distress, fatigue, personal value systems, ethno-cultural background and the availability of financial compensation.  Rheumatologists are usually more confident of reliably assessing disability in patients with rheumatoid arthritis and osteoarthritis; yet important determinants of dysfunction in both of these diseases are psychosocial issues such as coping style, symptom focus, anxiety and depression (19,20).  It is increasingly evident that dysfunction in chronic pain states is poorly correlated with the severity of pain (18,21,22).  Disabled pain patients usually link impaired functioning to having persistent pain and cannot conceive of living a normal life as long as they are in pain (23,24).  Thus they pursue a fruitless search for a cure which is never realized -- thus rationalizing their continued disability.  In the process they not only remain dysfunctional, but also over-utilize medical care and develop increasing personal distress.  Interestingly it is the belief that pain is the major cause of disability, that seems to determine the actual degree of dysfunction, rather than the absolute level of pain (25).  These psycho-social and behavioral issues are clearly relevant to some FM patients seeking disability, but should not be generalized.  Each patient has to be thoughtfully evaluated according to their unique set of circumstances. 

The Diagnosis of Fibromyalgia:  Is this the problem?

            Fibromyalgia was not a frequent diagnosis prior to 1980 and seldom a prominent topic in rheumatology training programs.  Some 15 years later FM is one of the commonest diagnoses made by rheumatologists.  To some this is a cause for dismay: “we have created a monster and now it is up to us to make amends” (26).  It has been suggested that the very act of giving patients a name for their pain state legitimizes unproven pathophysiological theories in ways that are counterproductive to effective management (27).  In this view physicians are part of the problem.  Otherwise healthy individuals experience a string of transient discomforts throughout their lifetime: headaches, back pain, post exertional pain, fatigue, insomnia, stiffness, constipation, colds and depression.  At least one such symptom occurs in any month (28).  Some individuals have an increased predilection to attribute such symptoms to serious disease and repeatedly seek medical attention – this is the underlying basis of somatization (29).  "Medicalization" is the provision of a “chronic” medical diagnosis to a minor transient discomfort and its resulting treatment.  Guru’s of chronic pain research have averred that Western medicine’s increasing proclivity for medicalization is one of the causes for the current epidemic of chronic pain.  While maintaining that the patient has "real" pain, they minimize any pathophysiological explanations by maintaining that chronic pain states reflect the overwhelming stress engendered by the individuals failure to cope with the demands of industrialized society (22).  The general experience with FM patients does not fit the somatization concept.  A formal diagnosis of somatization can only be made in 14% to 23% of FM patients (30,31).  Whereas lifetime psychiatric disorders are more prevalent in FM patients than FM non-patients, they are not intrinsically related to the pathophysiology of the FM syndrome.  However they do seem to partly determine who becomes a patient with FM (31).  Furthermore psychological distress in FM patients appears to be mainly a result of symptom severity (31,32).  Most studies have reported that FM symptomatology is remarkably persistent and pervasive over many years (12,33,34), despite many patients being reassured that this is not a crippling condition.  Furthermore, providing a diagnosis and engaging the patient in a program of cognitive restructuring and aerobic conditioning has been shown to result in long term improvement (30).  If FM turns out to be primarily a behavioral disorder rheumatologists have done society a disfavor.  If the behavioral aspect of FM is largely secondary to persistent pain and fatigue, then pain guru's have pursued a narrow minded and self serving agenda. 

Why do fibromyalgia patients hurt?

            It is difficult to rationalize decisions regarding disability in FM patients without having a conceptual framework as to symptom generation. The cardinal symptom of FM is widespread body pain (35).  The cardinal finding is the presence of focal areas of hyperalgesia, the tender points (35).  Tender points imply that the patient has a local area of reduced pain threshold – suggesting a focal pathology (36).  In general tender points occur at muscle tendon junctions, a site where mechanical forces are most likely to cause micro-injuries (37).  Many, but not all FM patients, have tender skin and a overall reduction in pain threshold (38).  These latter observations suggest that some FM patients have a generalized pain amplification state.  There has been a recent plethora of experimental studies apposite to the pathophysiological basis of central pain states.  As the confident assessment of disability is aided by an understanding of relevant pathophysiology, a synopsis of this scientific evidence is now given. 

 

Peripheral Factors.
           
It is now apparent that there is no global defect of muscle in FM patients (39), but there are several clinical observations that indicate the focal muscle origin of pain.  (1) Most patients cite muscle as the source of their discomfort.  (2) FM patients experience increased pain during repetitive muscular activity -- which improves on cessation.  Interestingly, there is a rebound of pain 24-48 hours after unaccustomed activity -- as seen in normal individuals. (3). Fibromyalgia patients are tender over focal areas of muscle, usually at musculotendinous junctions (35,40).  (4) There is an improvement of pain after these locations are injected with local anesthetics (41).  Indeed, the very act of injection provides evidence for a focal muscle pathology.  The muscle adjacent to the tender points is relatively unresponsive to needling, whereas there is a sudden increase in pain when the tender point is needled (42).  5). Bengtsson et al. performed sequential epidural installations of saline, fentanyl, naloxone and lidocaine in FM patients (43).  The saline had no effect, the fentanyl caused a significant improvement (which was partly reversed by naloxone) and lidocaine totally abolished both pain and tender points.  These results are not compatible with the notion that FM pain is solely central in origin.  It is more likely that peripheral nociceptive input is required to maintain a state of central pain sensitization -- as envisaged in the concept of neuroplasticity (see below).  What is the nature of this continuing nociceptive input?  Elert et al. made the interesting observation that fibromyalgia patients were less able to relax their muscles in the short pauses between isokinetic muscle contractions and had increased muscle fatiguability compared to healthy controls (44).  These observations may be relevant to continuing nociceptive input on the basis of impaired central coordination of muscle activity predisposing to mechanical muscle damage -- as envisaged by Edwards (45).  

Central Factors
           
An objective demonstration that FM patients have a generalized increase in pain sensitivity was provided by Gibson et al (46).  They reported an increased nociceptive evoked EEG somatosensory response in 10 FM patients compared to 10 matched controls following CO2 laser stimulation of the skin.  Arroyo and Cohen, using the technique of electrocutaneous stimulation, found that the upper limbs of FM patients could be characterized as regions of secondary hyperalgesia (47).  Primary hyperalgesia is the normal perception of pain from nociceptor stimulation in an injured tissue.  Secondary hyperalgesia refers to pain elicited from uninjured tissues (48).  This results in normally non-noxious impulses (e.g. light touch) being perceived as painful; the elegant experiments of Torebjork et al have convincingly demonstrated this phenomenon in humans (49).  The pathophysiological basis for this phenomenon is an activation of NMDA  (N-methyl D-aspartate) receptors (50).  Synergism between substance P and NMDA receptors play a major role in the perpetuation of secondary hyperalgesia (51).  A recent study from Sweden has provided some evidence that secondary hyperalgesia may be relevant to pain in FM patients -- Sorensen et al reported  that intravenous ketamine (an NMDA receptor antagonist) attenuates pain and pain threshold, as well as improving muscle endurance in FM patients (52).  The finding of increased cerebrospinal fluid levels of substance-P in FM patients is consonant with the notion that secondary hyperalgesia is relevant to understanding FM pain (53).

The possibility that pain related functional CNS changes can be demonstrated by imaging techniques has been pursued by Mountz et al (54).  They reported that FM patients, characterized by low pain thresholds, had a decreased regional cerebral flow compared to healthy controls The decreased perfusion was particularly prominent in the thalamic and caudate nuclei (structures involved in the processing of nociceptive stimuli).  A similar finding has been reported in patients with chronic neuropathic pain, using O-15 positron emission tomography (55).

The term given to functional changes within the CNS is "neuroplasticity". The classical example of neuroplasticity is the phenomenon of phantom limb following an amputation.  Neuroplasticity refers to a re-wiring of the synaptic connections which, if prolonged, can result in a pain state in the absence of peripheral input.  An increased understanding of this phenomenon has been instrumental in providing a new conceptual framework for understanding chronic pain states. 

The Fibromyalgia Syndrome
                 Fibromyalgia is more than a muscle pain syndrome (56).  The central pain sensitization state, as outlined above, would account for the symptom magnification that is seen in the fibromyalgia associated conditions of irritable bowel syndrome, skin tenderness, headaches, restless legs syndrome, irritable bladder and premenstrual tension syndrome.  The continued barrage of noxious impulse from these associated conditions could be perpetuating factors for the maintenance of the neuroplastic changes -- resulting in the chronicity of fibromyalgia symptomatology.  The multi-dimensional features of fibromyalgia can be explained by persistent pain causing a variable chronic stress response which drives several feedback loops that amplify and perpetuate the chronic pain state (57,58)-- see figure 1. Some of these feedback loops have been identified:  altered behavior (e.g. deconditioning (59)), depression (32), high levels of psychological distress (31), sleep disturbance (60) and hypothalamic-pituitary dysfunction (61,62).  Secondary hyperalgesia and stress feedback loops probably account for the prominent "somatization" of some FM patients. 

What is the cause of disability in fibromyalgia patients?

            The World Health Organization defines disability as a limitation of function that compromises an individual's ability to perform an activity within the range appropriate considered normal (63).  Disability is the result of an impairment. There is seldom a good linear relationship between impairment and disability – this is particularly true in chronic pain states.  Impairment is defined as the anatomical/physiological loss or a psychological impediment that results in disability.  Impairment relates to disorders of function at the organ level (e.g. a left sided hemiplegia -an anatomic problem,  epilepsy – a physiologic problem,  schizophrenia – a psychological problem).  Disability is an integrated concept that views impairment in a multidimensional context; to wit: age, sex, educational level, psychological profile, past attainments, job satisfaction, motivation, re-training prospects, social support systems, economic consequences and the potential for being competitive in the workforce.  Work disability, which is the subject of this review, is the inability or diminished potential for engaging in full time gainful employment.  The problems that FM patients cite as being instrumental in their disability are: difficulty in sustaining repetitive motor tasks (due to both increasing pain and fatigue), reduced physical efficiency (as they take longer to accomplish tasks), loss of mental sharpness, fear of poor performance, difficulty in conforming to usual working hours (FM patients describe a diurnal variation in energy level and alertness that is different from healthy individuals, citing a "window of opportunity" for constructive work that typically extends from about 10 am to 2 p.m.(64)), prolonged sitting or standing and workplace stressors (coldness, excessive noise, rigid time/performance expectations) (9,65).  The net result of these problems may make an individual non-competitive in the work force due to erratic performance and frequent absences; these issues are themselves a potent cause for increased stress. 

            There are a few studies that have documented functional impairment in FM patients.  Cathey et al. used a computerized workstation to physically stress shoulders, cervical/thoracic/lumbar spine, wrists and elbows in a simulated work environment (66).  FM patients (#28) were compared to RA patients (#26) and healthy controls (#11).  As expected RA patients had a limited work capacity and could only perform 59% of the work done by healthy controls.  However FM patients were equally impaired and were only able to perform 62% of the healthy control workload.  There was a strong correlation between objective performance and the HAQ disability index (67).  FM patients decreased their rate of performance or stopped the test mainly due to increasing pain.  Hidding et al. compared self report measures of disability with a blinded evaluation of observed disability (by grading a videotape of 9 selected activities) in patients with RA, AS and FM (68).  The observers reported similar levels of disability in all 3 groups.     Cognitive dysfunction is a self perceived cause of impairment in many FM patients.  Sletvold et al. employed a comprehensive series of neuropsychological tests to evaluate information processing in FM (#25), major depression (#22) and healthy controls (#18) (69).  Both FM and major depression patients processed information less effectively than controls.  The defects included purely mental tasks as well as psychomotor performance. The results were not explainable by a subset of FM patients having depression. FM patients may be told that they are "just out of sorts" and should get on with their lives (70).  This advice is based on the concept that a major component of the FM dilemma is perceived helplessness and poor pain coping mechanisms.  Nicassio et al. analyzed the factor structure of the Coping Strategies Questionnaire(CSQ) with several measures of pain outcome (pain behavior, pain reporting, depressive symptoms and quality of well-being) in 122 FM patients (71).  There was strong correlation between high levels of passive coping (e.g.  perceived ability to control pain and absence of catastrophizing) and low levels in pain outcomes – as is also seen in patients with RA.  Quite unexpectedly high levels of active coping (e.g.  ignoring pain in the accomplishment of goals) was associated high levels in pain outcomes – this is the opposite of what is found in RA.  It was surmised that these findings reflect a fundamental difference between RA and FM.  The results indicate that "active coping in FM may unwittingly exacerbate muscular and other physiological mechanisms that contribute to FM pain" (71).  Though FM patients do need to "get on with their lives", such flip-advice is not a constructive substitute for management advice based on a careful analysis of each patients dysfunctional profile.

How can Disability be assessed in Fibromyalgia patients?

            Let me start by stating a truism: gainful employment is a powerful force in fulfilling one's obligations to society, maintaining self esteem and achieving financial security.  It should be the aim of rheumatologists to minimize disability in FM patients (72).  In utopia no one with FM will seek disability.  However in real life we are all faced with disability forms which ask for defensible opinions.

There are 3 excellent reviews that expertly pinpoint the dilemma faced by physicians as well as FM patients involved in the process of disability evaluation (52,73,74).  Hadler has provided eloquent essays on the role of the diagnostic process and disability evaluation as a prescription for reinforcement of illness behavior (75,76).  These concepts are clearly relevant to some FM patients – but such generalizations are seldom constructive when considering the complexities of the human dilemma.

There are no validated instruments for assessing disability in FM patients.  The most useful practical resource is the American Medical Association Guides to the Evaluation of Permanent Impairment (77).  Chapter 15 provides a balanced approach to assessing impairment in patients with chronic pain states.  As an overview to the problem it states: (1) pain evaluation does not lend itself to strict laboratory standards of accuracy;  (2) the evaluation of chronic pain cannot be made on the basis of the degree of tissue damage – the classical medical model;  (3) pain evaluation requires a thorough understanding of a multi-faceted biopsychosocial model of disease (78);  (4) the physicians judgment of impairment represents a blend of the art and science of medicine, and judgment must be characterized not so much by scientific accuracy as by procedural regularity.  It acknowledges that physicians are often uncomfortable in evaluating chronic pain states, but notes that they regularly make decisions on the basis of probabilities backed up by experience and stated in terms of reasonable medical probability.

A uniform approach to gathering data on which to base judgments of reasonable medical probability is required.  Goldenberg et al. have recently provided a model to assess the severity and impact of FM (79).  Out of 15 factors analyzed they found the following to be significantly associated with severity and impaired functional status: pain level, self-assessed disability, psychological distress, pending litigation, educational level, helplessness and poor coping strategies.   A suggested flowchart for the assessment of disability in FM is provided in figure 2.  It is recommended that patients have an independent psychological evaluation and occupational therapy evaluation (where available), and that assessors use validated questionnaires that have proven useful in evaluating FM.  Such instruments include: the Health Assessment Questionnaire (HAQ) (67),  the Fibromyalgia Impact Questionnaire (FIQ) (80), the Coping Strategies Questionnaire (CSQ) (81), the Beck Depression Inventory (82,83) and the Quality of Life Scale (84). 

Disability evaluation in FM patients can only be made in terms of the biopsychosocial model of disease (78) and stated in terms of reasonable probability. Some physicians will feel always uncomfortable in the assessment of chronic pain (85), others will not have acquired the broad knowledge base necessary for understanding the biopsychosocial concept of disease.  It is preferable that both groups excuse themselves from the disability process.    

References 

1. Marder WD, Meenan RF, Felson DT, Reichlin M, Birnbaum NS, Croft JD, Dore RK, Kaplan H, Kaufman RL, Stobo JD: Editorial:  The present and future adequacy of rheumatology manpower:  A study of health care needs and physician supply. Arth Rheum 34:1209-1217, 1991 

2. Prescott E, Kj:ller M, Jacobsen S, B:ulow PM, Danneskiold-SamsĂ« B, Kamper-J:rgensen F: Fibromyalgia in the adult Danish population: I. A prevalence study. Scand J Rheumatol 22:233-237, 1993 

3. Forseth KO, Gran JT: The prevalence of fibromyalgia among women aged 20-49 years in Arendal, Norway. Scand J Rheumatol 21:74-78, 1992 

4. Makela M, Heliovaara M: Prevalence of primary fibromyalgia in the Finnish population. BMJ 303:216-219, 1991 

5. Middleton GD, McFarlin JE, Lipsky PE: The prevalence and clinical impact of fibromyalgia in systemic lupus erythematosus. Arthritis Rheum 37:1181-1188, 1994 

6. Borenstein D: Prevalence and treatment outcome of primary and secondary fibromyalgia in patients with spinal pain. Spine 20:796-800, 1995 

7. Wolfe F, Ross K, Anderson J, Russell IJ, Hebert L: The prevalence and characteristics of fibromyalgia in the general population. Arth Rheum 38:19-28, 1995 

8. Henriksson C, Gundmark I, Bengtsson A, Ek AC: Living with fibromyalgia.  Consequences for everyday life. Clin J Pain 8:138-144, 1992 

9. Henriksson CM: Living with continuous muscular pain--patient perspectives. Part I: Encounters and consequences. Scand J Caring Sci 9:67-76, 1995 

10. Hawley DJ, Wolfe F: Pain, disability, and pain/disability relationships in seven rheumatic disorders:  a study of 1,522 patients. J Rheumatol 18:1552-1557, 1991 

11. Bengtsson A, Henriksson KG, Jorfeldt L, K~agedal B, Lennmarken C, Lindstrom F: Primary fibromyalgia. A clinical and laboratory study of 55 patients. Scand J Rheumatol 15:340-347, 1986 

12. Ledingham J, Doherty S, Doherty M: Primary fibromyalgia syndrome--an outcome study. Br J Rheumatol 32:139-142, 1993 

13. McCain GA, Cameron R, Kennedy JC: The problem of longterm disability payments and litigation  in primary fibromyalgia: The Canadian perspective. J Rheumatol 16 Suppl. 19:174-176, 1989 

14. Bruusgaard D, Evensen AR, Bjerkedal T: Fibromyalgia--a new cause for disability pension. Scand J Soc Med 21:116-119, 1993 

15. Wolfe F, Anderson J, Harkness D, Bennett RM, Caro X, Goldenberg DL, Russell IJ, Yunus MB: The work and disability status of persons with fibromyalgia. in review 1996 

16. Croft P, Rigby AS, Boswell R, Schollum J, Silman A: The prevalence of chronic widespread pain in the general population. J Rheumatol 20:710-713, 1993 

17. Mendelson G: Chronic pain, compensation and clinical knowledge. Theor Med 12:227-246, 1991 

18. Tait RC, Margolis RB, Krause SJ, Liebowitz E: Compensation status and symptoms reported by patients with chronic pain. Arch Phys Med Rehabil 69:1027-1029, 1988 

19. Fifield J, Reisine ST, Grady K: Work disability and the experience of pain and depression in rheumatoid arthritis. Soc Sci Med 33:579-585, 1991 

20. Dekker J, Boot B, van der Woude LH, Bijlsma JW: Pain and disability in osteoarthritis: a review of biobehavioral mechanisms. J Behav Med 15:189-214, 1992 

21. Anonymous: Report of the Commission on the Evaluation of Pain. Soc Secur Bull 50:13-44, 1987 

22. Loeser JD: What is chronic pain? Theor Med 12:213-225, 1991 

23. Reesor KA, Craig KD: Medically incongruent chronic back pain: physical limitations, suffering, and ineffective coping. Pain 32:35-45, 1988 

24. Talo S, Hendler N, Brodie J: Effects of active and completed litigation on treatment results: workers' compensation patients compared with other litigation patients. J Occup Med 31:265-269, 1989 

25. Riley JF, Ahern DK, Follick MJ: Chronic pain and functional impairment: assessing beliefs about their relationship. Arch Phys Med Rehabil 69:579-582, 1988 

26. Carette S: Fibromyalgia 20 years later: what have we really accomplished? [editorial]. J Rheumatol 22:590-594, 1995 

27. Hadler NM: A critical reappraisal of the fibrositis concept. Am J Med 81:26-30, 1986 

28. Benjamin S, Bridges K: The special needs of chronic somatizers, Liason psychiatry: defining needs and planning services. Edited by S Benjamin, A House, P Jenkins. London, England, Gaskell Press, 1994  

29. Barsky AJ, Borus JF: Somatization and medicalization in the era of managed care. JAMA 274:1931-1934, 1995 

30. Bennett RM, Burckhardt CS, Clark SR, O'Reilly CA, Wiens AN, Cambell SM: Group treatment of fibromyalgia: description and results of a 6 month out patient program. J  Rheumatol 23:521-528, 1996 

31. Aaron LA, Bradley LA, Alarcon GS, Alexander RW, Triana-Alexander M, Martin MY, Alberts KR: Psychiatric diagnoses in patients with fibromyalgia are related to health care seeking behavior rather than illness. Arth Rheum 39:436-445, 1996 

32. Yunus MB: Psychological aspects of fibromyalgia syndrome: a component of the dysfunctional spectrum syndrome. Baillieres Clin Rheumatol 8:811-837, 1994 

33. Felson DT, Goldenberg DL: The natural history of fibromyalgia. Arth Rheum 29:1522-1526, 1986 

34. Bengtsson A, Backman E, Lindblom B, Skogh T: Long term follow-up of fibromyalgia patients: clinical symptoms, muscular function, laboratory tests - an eight year comparison study. Journal of Musculoskeletal Pain 2:67-80, 1994 

35. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P, Fam AG, Farber SJ, Fiechtner JJ, Franklin CM, Gatter RA, Hamaty D, Lessard J, Lichtbroun AS, Masi AT, McCain GA, Reynolds WJ, Romano TJ, Russell IJ, Sheon RP: The American College of Rheumatology 1990 criteria for the  classification of fibromyalgia: Report of the Multicenter  Criteria Committee. Arth Rheum 33:160-172, 1990 

36. Bennett RM: The origin of myopain: An integrated hypothesis of focal muscle changes and sleep disturbance in patients with the fibromyalgia syndrome. J Musculoskeletal Pain 1:95-112, 1993 

37. Armstrong RB, Warren GL, Warren JA: Mechanisms of exercise-induced muscle fibre injury. Sports Med 12:184-207, 1991 

38. Cohen ML, Quintner JL: Fibromyalgia syndrome, a problem of tautology. Lancet 342:906-909, 1993 

39. Bennett RM, Jacobsen S: Muscle function and origin of pain in fibromyalgia. Bailliere's Clinical Rheumatology 8:721-746, 1994 

40. Bennett RM: Fibromyalgia:  The Commonest Cause of Widespread Pain. Comprehensive Therapy 21:269-275, 1995 

41. Jaeger B, Skootsky SA: Double blind, controlled study of different myofascial trigger point injection techniques. Pain 31:S2921987 

42. Travell JG, Simons DG: Myofascial pain and dysfunction: the trigger point manual. Baltimore, Williams & Wilkins, 1983 

43. Bengtsson M, Bengtsson A, Jorfeldt L: Diagnostic epidural opioid blockade in primary fibromyalgia  at rest and during exercise. Pain 39:171-180, 1989 

44. Elert JE, Rantapäa Dahlqvist SB, Henriksson-Larsen K, Gerdle B: Increased EMG activity during short pauses in patients with primary fibromyalgia. Scand J Rheumatol 18:321-323, 1989 

45. Edwards RH, Newham DJ, Jones DA, Chapman SJ: Role of mechanical damage in pathogenesis of proximal myopathy  in man. Lancet 1:548-552, 1984 

46. Gibson SJ, Littlejohn GO, Gorman MM, Helme RD, Granges G: Altered heat pain thresholds and cerebral event-related potentials following painful CO2 laser stimulation in subjects with fibromyalgia syndrome. Pain 58:185-193, 1994 

47. Arroyo JF, Cohen ML: Abnormal responses to electrocutaneous stimulation in fibromyalgia. J Rheumatol 20:1925-1931, 1993 

48. Koltzenberg M, Torebjork HE, Wahren LK: Nociceptor modulated central sensitization causes mechanical hyperalgesia in acute chemogenic and chronic neuropathic pain. Brain 117:579-591, 1994 

49. Torebjork HE, Lundberg LER, Lamotte RH: Central changes in processing of mechanoreceptive input in capsaicin-induced secondary hyperalgesia in humans. J Physiol 448:765-780, 1992 

50. Dickenson AH, Sullivan AF: NMDA receptors and central hyperalgesic states. Pain 46:344-345, 1991 

51. Dougherty PM, Willis WD: Enhancement of spinothalamic neuron responses to chemical and mechanical stimuli following combined micro-iontophoretic application of N-methyl-D-aspartic acid and substance P. Pain 47:85-93, 1992 

52. Wolfe F, Aarflot T, Bruusgaard D, Henriksson KG, Littlejohn G, Moldofsky H, Raspe H, Vaeroy H: Fibromyalgia and disability. Report of the Moss International Working Group on medico-legal aspects of chronic widespread musculoskeletal pain complaints and fibromyalgia. Scand J Rheumatol 24:112-118, 1995 

53. Russell IJ, Orr MD, Littman B, Vipraio GA, Alboukrek D, Michalek JE, Lopez Y, MacKillip F: Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum 37:1593-1601, 1994 

54. Mountz JM, Bradley LA, Modell JG, Alexander RW, Triana-Alexander M, Aaron LA, Stewart KE, Alarcon GS, Mountz JD: 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. Iadarola MJ, Max MB, Berman KF: Unilateral decrease in thalamic activity observed in positron emission tomography in patients with chronic neuropathic pain. Pain 63:55-64, 1995 

56. Clauw DJ: Fibromyalgia: more than just a musculoskeletal disease. Am Fam Physician 52:843-51, 853-4, 1995 

57. Yunus MB: Towards a model of pathophysiology of fibromyalgia: aberrant central pain mechanisms with peripheral modulation [editorial]. J Rheumatol 19:846-850, 1992 

58. Bennett RM: The contribution of muscle to the generation of fibromyalgia symptomatology. J Musculoskeletal Pain 1996 

59. Bennett RM, Clark SR, Goldberg L, Nelson D, Bonafede RP, Porter J, Specht D: Aerobic fitness in patients with fibrositis. A controlled study  of respiratory gas exchange and 133xenon clearance from  exercising muscle. Arth Rheum 32:454-460, 1989 

60. Branco J, Atalaia A, Paiva T: Sleep cycles and alpha-delta sleep in fibromyalgia syndrome. J Rheumatol 21:1113-1117, 1994 

61. Crofford LJ, Pillemer SR, Kalogeras KT, Cash JM, Michelson D, Kling MA, Sternberg EM, Gold PW, Chrousos GP, Wilder RL: Hypothalamic-pituitary-adrenal axis perturbations in patients with fibromyalgia. Arthritis Rheum 37:1583-1592, 1994 

62. Bennett RM, Clark SR, Campbell 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 

63. World Health Organization: The international classification of impairments, disabilities, and handicaps. World Health Organization 1980 

64. Moldofsky H: Chronobiological influences on fibromyalgia syndrome: theoretical and therapeutic implications. Baillieres Clin Rheumatol 8:801-810, 1994 

65. Waylonis GW, Ronan PG, Gordon C: A profile of fibromyalgia in occupational environments. Am J Phys Med Rehabil 73:112-115, 1994 

66. Cathey MA, Wolfe F, Kleinheksel SM, et al. Functional ability and work status in patients with fibromyalgia. Arthritis Care Res 1:85-98, 1988 

67. Fries JF: Measurement of patient outcome in arthritis. Arth Rheum 23:137-145, 1980 

68. Hidding A, van Santen M, De Klerk E, Gielen X, Boers M, Geenen R, Vlaeyen J, Kester A, van der Linden S: Comparison between self-report measures and clinical observations of functional disability in ankylosing spondylitis, rheumatoid arthritis and fibromyalgia. J Rheumatol 21:818-823, 1994 

69. Sletvold H, Stiles TC, Landro NI: Information processing in primary fibromyalgia, major depression and healthy controls. J Rheumatol 22:137-142, 1995 

70. Hadler NM: The danger of the diagnostic process, Occupational Musculoskeletal Disorders. Edited by NM Hadler. New York, NY, Raven Press, 1993 16 - 33 

71. Nicassio PM, Schoenfeld-Smith K, Radojevic V, Schuman C: Pain coping mechanisms in fibromyalgia: relationship to pain and functional outcomes. J Rheumatol 22:1552-1558, 1995 

72. Reilly PA: Fibromyalgia in the workplace: a 'management' problem. Ann Rheum Dis 52:249-251, 1993 

73. White KP, Harth M, Teasell RW: Work disability evaluation and the fibromyalgia syndrome. Semin Arthritis Rheum 24:371-381, 1995 

74. Wolfe F: Disability and the dimensions of distress in fibromyalgia. J Musculoskeletal Pain 1:65-87, 1993 

75. Hadler NM: Regional musculoskeletal diseases of the low back. Cumulative trauma versus single incident. Clin Orthop 33-41, 1987 

76. Hadler NM: Disability determination in America, Occupational Musculoskeletal Disorders. Edited by NM Hadler. New York, NY, Raven Press, 1993 249 

77. Anonymous: Guides to the Evaluation of Permanent Impairment. 4th edition. American Medical Association, 1993 

78. Engel GL: A clinical application of the Biophysical Model. Am J Psychiatry 137:535-544, 1980 

79. Goldenberg DL, Mossey CJ, Schmid CH: A model to assess severity and impact of fibromyalgia. J Rheumatol 22:2313-2318, 1995 

80. Burckhardt CS, Clark SR, Bennett RM: The fibromyalgia impact questionnaire: development and validation. J Rheumatol 18:728-733, 1991 

81. Rosenthiel AK, Keefe FJ: The use of coping strategies in chronic low back pain patients: Relationship to patient characteristics and current adjustment. Pain 17:33-44, 1983 

82. Beck AT, Rush AJ, Shaw BF, Emery G: Cognitive Therapy of Depression. Guilford Press, New York, 1979 

83. Burckhardt CS, O'Reilly CA, Wiens AN, Clark SR, Campbell SM, Bennett RM: Assessing depression in fibromyalgia patients. Arthritis Care Res 7:35-39, 1994 

84. Burckhardt CS, Woods SL, Schultz AA, Ziebarth DM: Quality of life of adults with chronic illness: a psychometric study. Res Nurs Health 12:347-354, 1989 

85. Diamond EL, Graver K: The physicians reactions to patients with chronic pain. Am Family Phys 34:117-122, 1986

 

 

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