Reprinted from FMOnline

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. (Used with permission)

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 socioeconomic 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).

nterestingly 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 to 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, coworkers 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 four 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 psychosocial 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 fifteen 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 unproved 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.  Gurus 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 gurus 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 rewiring 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 multidimensional 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, retraining 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 a.m. 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 ù the classical medical model;  (3) pain evaluation requires a thorough understanding of a multifaceted 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.


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