Fibromyalgia syndrome (FMS) is characterized by chronic musculoskeletal aches and pains as well as multiple tender points on palpation by an examiner. It is more common in women than men; about 90% of patients are women. The most common age of presentation is between 30 and 60 years.1-3 However, FMS has been well described among juveniles.4,5
FMS is a common condition. It is encountered among 2.1%, 5%, and 10% to 20% of patients seen in a family practice, internal medicine clinic, and rheumatic disease clinic, respectively.6 The prevalence of FMS in a community was found to be between 2% in Wichita, Kan,7 and 3.3% in London, Ontario.8 The prevalence increases with age until 65 to 79 years.7,8 More than 7% of women had FMS in the 55 to 64 age group in a Canadian study8 and in the 60 to 79 age group in a US study.7
The term "primary fibromyalgia" is used when a significant underlying or concomitant condition that may contribute to pain is absent. FMS may be classified as "concomitant" when another condition, such as rheumatoid arthritis (RA), osteoarthritis, or hypothyroidism is present and may contribute to pain or fatigue of FMS. However, currently the term FMS, or fibromyalgia, is collectively applied to both primary and concomitant types.
We describe clinical features, diagnosis, and pathophysiology in this article. Management is discussed in a future article.
Symptoms. Besides widespread pain, patients complain of many other symptoms, such as fatigue, poor sleep, a subjective swelling of soft tissues (and sometimes of the joints), paresthesia, cognitive dysfunction, and symptoms of other associated conditions, such as irritable bowel syndrome (IBS), headaches, restless legs syndrome, and temporomandibular dysfunction (Table 1).2,3,9 There is no significant correlation between subjective swelling or subjective numbness and psychological status.9 Common sites of pain or stiffness are low back, neck, shoulder region, arms, hands, knees, hips, thighs, legs, and feet. Chest pain is not uncommon and is accompanied by tender points in the chest wall (also see differential diagnosis). Fatigue is common in FMS and may be the presenting feature in some cases because of its severity. Several factors may contribute to, or aggravate, fatigue and pain in FMS, such as nonrestorative sleep, deconditioning, overwork, psychological factors, and poor coping skills.10 Patients are also sensitive to environmental stimuli, such as noise.9
Signs. Patients with FMS look healthy, but often they seem fatigued and in pain. Examination of the joints shows no objective swelling (unless there is concomitant arthritis), but some patients have marked joint tenderness on palpation. Despite neurologic symptoms, such as weakness and numbness, neurologic examination in FMS perseis normal. The most significant physical finding in FMS is the presence of multiple tender points in a widespread distribution. For the purpose of diagnosis (see below), one needs to examine 18 specified sites (Box, Figure 1), by application of a force of approximately 4 kg (roughly the pressure one needs to whiten the nail bed when pressing against a firm surface), using the index finger or the thumb. Note that the proper way of examining a tender point needs to be learned, as in the case of examining other physical signs in medicine, such as hepatomegaly or splenomegaly. An underestimation of the number of tender points in a patient with FMS is the most important reason for missing a diagnosis of this disorder.
The American College of Rheumatology
|2. Pain in 11+ of 18 tender point sites on digital palpation with an approximate force of 4 kg
Definition: Pain (mild or greater) on digital palpation must be present in at least 11 of the following 18 tender point sites:</P><P><em>Occiput:</em>bilateral, at the suboccipital muscle insertions.
Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-7.
Trapezius: bilateral, at the midpoint of the upper border.
Supraspinatus: bilateral, at origins above the scapula spine near the medial border.
Second rib: bilateral, at the second costochondral junctions, just lateral to the junctions on upper surfaces.
Lateral epicondyle: bilateral, 2 cm distal to the epicondyles.
Gluteal: bilateral, in upper outer quadrants of buttocks in anterior fold of muscle.
Greater trochanter: bilateral, posterior to the trochanteric prominence.
Knee: bilateral, at the medial fat pad proximal to the joint line.
|FMS, fibromyalgia syndrome.
*For classification purposes, patients will be said to have FMS if both criteria (1 and 2) are satisfied. The presence of a second clinical disorder does not exclude the diagnosis of FMS. From Wolfe F et al. Arthritis Rheum. 1990.2
It may surprise many physicians to learn that a diagnosis of FMS does not require any specific laboratory testing, since "ruling out" does not apply to FMS. Laboratory tests, including radiology, should be requested only if another concomitant condition is suspected by careful history taking and physical examination.There is no reason to order tests of antinuclear antibodies or rheumatoid factor unless clinically indicated. However, a complete blood count and a chemistry panel with blood urea nitrogen, creatinine, and hepatic enzymes are useful to monitor side effects of drugs either for FMS or a concomitant condition. Although the prevalence of hypothyroidism does not seem increased in FMS compared with the normal population, we obtain T4 and thyroid-stimulating hormone levels in patients with significant fatigue, even in the absence of other features of hypothyroidism.
Despite a common notion, diagnosis of FMS is disarmingly simple. It can, and should, be diagnosed by its own characteristics of widespread pain and multiple tender points; another concomitant condition, such as arthritis or hypothyroidism, does not exclude the diagnosis of FMS, as stated by the American College of Rheumatology (ACR) criteria.2 Putting it another way, if a patient has FMS as well as RA, this patient has both FMS and RA. Although the ACR criteria (see Box, Figure 1) were developed for classification of FMS (so that researchers can use a uniform set of criteria for patient selection), these criteria have been found to be very useful for the diagnosis of FMS in clinical practice. A patient with FMS may have many symptoms, but he or she needs only present with widespread pain (as defined in the Box) and 11 or more tender points among the 18 sites specified in ACR criteria. Note that a patient with FMS may be tender in many more sites (including bones) besides these 18. Some patients have diffuse tenderness "everywhere" on palpation. Such a phenomenon does not necessarily imply high psychological distress. Such diffuse tenderness on palpation or a significant psychiatric disease does not influence a diagnosis of FMS (as long as a patient satisfies the ACR criteria).
Now, a frequent question we hear from practicing physicians is: "Should one diagnose FMS if a patient has widespread pain but not 11 tender points?" For a clinical purpose, we suggest that a patient who has otherwise characteristic symptoms of FMS (eg, fatigue, poor sleep, morning fatigue, and 1 or more associated conditions; see Table 1), but only 6 to 10 tender points, should be treated for FMS.
1. Yunus M, Masi AT, Calabro JJ, et al. Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls. Semin Arthritis Rheum. 1981;11:151-171.
2. 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. 1990;33:160-172.
3. Yunus MB, Masi AT, Aldag JC. A controlled study of primary fibromyalgia syndrome: clinical features and association with other functional syndromes. J Rheumatol Suppl. 1989;19:62-71.
4. Yunus MB, Masi AT. Juvenile primary fibromyalgia syndrome. A clinical study of thirty-three patients and matched normal controls. Arthritis Rheum. 1985; 28:138-145.
5. Siegel DM, Janeway D, Baum J. Fibromyalgia syndrome in children and adolescents: clinical features at presentation and status at follow-up. Pediatrics. 1998;101:377-382.
6. Wolfe F. Fibromyalgia: the clinical syndrome. Rheum Dis Clin North Am. 1989;15:1-18.
7. Wolfe F, Ross K, Anderson J, et al. The prevalence and characteristics of fibromyalgia in the general population. Arthritis Rheum. 1995;38:19-28.
8. White KP, Speechley M, Harth M, Ostbye T. The London Fibromyalgia Epidemiology Study: the prevalence of fibromyalgia syndrome in London, Ontario. J Rheumatol. 1999;26:1570-1576.
9. Yunus MB, Inanici F. Clinical characteristics and biopathophysiological mechanisms of fibromyalgia syndrome. In: Baldry PE, ed. Myofascial Pain and Fibromyalgia Syndromes: A Clinical Guide to Diagnosis and Management. London: Churchill Livingstone; 2001:351-378.
10. Yunus MB, Arslan S. Fibromyalgia syndrome: can it be treated? Consultant. In press.
11. Simms RW. Fibromyalgia is not a muscle disorder. Am J Med Sci. 1998;315:346-350.
12. Coderre TJ, Katz J, Vaccarino AL, Melzack. Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence. Pain. 1993;52:259-285.
13. Bennett RM. Emerging concepts in the neurobiology of chronic pain: evidence of abnormal sensory processing in fibromyalgia. Mayo Clin Proc. 1999;74: 385-398.
14. Staud R, Vierck CJ, Cannon RL, et al. Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain. 2001;91:165-176.
15. Arroyo JF, Cohen ML. Abnormal responses to electrocutaneous stimulation in fibromyalgia. J Rheumatol. 1993;20:1925-1931.
16. 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. 1995;38:926-938.
17. Graceley RA, Petzka F, Wolf JM, Clauw DJ. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 2002;46:1333-1343.
18. Russell IJ. Advances in fibromyalgia: possible role for central neurochemicals. Am J Med Sci. 1998; 315:377-384.
19. Crofford LJ. Neuroendocrine abnormalities in fibromyalgia and related disorders. Am J Med Sci. 1998;315:359-366.
20. Bennett RM. Disordered growth hormone secretion in fibromyalgia: a review of recent findings and a hypothesized etiology. Z Rheumatol. 1998; 57(suppl 2):72-76.
21. Roizenblatt S, Moldofsky H, Benedito-Silva AA, Tufiq S. Alpha sleep characteristics in fibromyalgia. Arthritis Rheum. 2001;44:222-230.
22. Affleck G, Urrows S, Tennen H, et al. Sequential daily relations of sleep, pain intensity, and attention to pain among women with fibromyalgia. Pain. 1996;68:363-368.
23. Yunus MB. Psychological aspects of fibromyalgia syndrome: a component of the dysfunctional spectrum syndrome. Baillieres Clin Rheumatol. 1994;8: 811-837.
24. Buskila D, Neumann L, Hazanov I, Carmi R. Familial aggregation in the fibromyalgia syndrome. Semin Arthritis Rheum. 1996;26:605-611.
25. Bondy B, Spaeth M, Offenbaecher, et al. The T102C polymorphism of the 5-HT2A-receptor gene in fibromyalgia. Neurobiol Dis. 1999;6:433-439.
26. Yunus MB, Khan MA, Rawlings KK, et al. Genetic linkage analysis of multicase families with fibromyalgia syndrome. J Rheumatol. 1999;26:408-412.
27. Yunus MB. Primary fibromyalgia syndrome: current concepts. Compr Ther. 1984;10:21-28.