Soft tissue mechanisms of pain in osteoarthritis

Soft Tissue Mechanisms

of Pain in Osteoarthritis

By John L. Merritt INDEX WORDS: Osteoarthritis; pain: soft tissue.

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HIS ARTICLE discusses the mechanisms by which soft tissues (capsules, ligaments, attachments, tendons, bursae, and muscles) contribute to pain in osteoarthritis (OA).im6 EFFECT OF SOFT TISSUES ON JOINTS

The Effect of Limited Motion

Joint stiffness may be explained by the following: (1) contractures of muscle, joint capsules, and ligaments; (2) capsular distention from effusion or synovitis; (3) intra-articular free bodies from meniscus tears, villonodular synovitis, synovial plica, etc; (4) joint surface incongruity; and (5) pain inhibition. ‘-‘I In OA, contractures and pain are early principal factors, but intraarticular free bodies (torn menisci, joint mice, etc) and surface incongruity are important in more advanced disease. Absence of motion has profound effects on the joint. Studies of joint immobilization have reported cartilage fibrillation, erosion, loss of metachromasia, degeneration, and necrosis of chrondrocytes.12 Immobilization experiments emphasize the need of motion for maintenance of articular cartilage health. How much loss of motion is required to adversely affect articular cartilage, however, remains unknown. Muscle Contraction Muscle contraction may effect intra-articular pressure, especially if accompanied by effusion. Sustained muscle contractions, isometric in character, due to muscle spasm, or muscle contractures that develop may produce sustained elevations of intra-articular pressure.5v13”4Capsular and pericapsular contractions may further affect intra-articular pressure and may be a source of pain. Pain due to elevated intra-articular pressure may enhance muscle spasm, further limiting joint motion and further increasing intra-articular pressure. The long-term effects of sustained intra-articular pressure remain unknown. The Eflect of Joint Instability

Soft tissue integrity is necessary to provide joint stability and cartilage health. Joint stability Seminars in Arthritis andflheumetism,

is provided mainly by ligaments and muscles. Muscle weakness and stretched ligaments (degenerative or traumatic), alone or in combination, result in joint instability in primary or secondary axes. Instability causes abnormal mechanical stress on cartilage. This field has been researched through models of cruciate ligament sectioning or meniscectomy that have shown degenerative changes of cartilage similar to those in patients with cruciate rupture or meniscectomy.‘2 Muscles and ligaments must be strong and balanced. Muscle weakness is frequent in OA. Whether it precedes OA or is a consequence of it, muscle weakness affects function and activities of daily living and contributes to further stress on the articular cartilage. Knee OA and Quadriceps Strength

Case reports that described the stabilization effect of progressive quadriceps strengthening in patients with severe OA of the knee and knee instability were reported in 1955 by Anderson.” Major improvement was noted in mediolateral stability during active quadriceps contraction, with resultant significant improvement in pain during ambulation and distance of ambulation. Quadriceps strengthening has since been a mainstay of the nonoperative treatment of OA of the knee.16 Quadriceps strengthening has been extended to milder forms of OA of the knee with less instability, including chondromalacia patella. Muscle imbalance in the extensor mechanism has been implicated as a cause of chondromalacia patella. I2 Relative weakness of the vastus medialis appears to allow lateral patellar tracking with excessive lateral pressure. Quadriceps weakness may result in patellar

From the Mayo Clinic, Mayo Medical School, Rochester, MN. John L. Merritt, MD, FACP: Associate Profissor, Physical Medicine and Rehabilitation, Mayo Clinic, Mayo Medical School. Address reprint requests to John L. Merritt, MD, FACP, Mayo Clinic, Mayo Medical School, 200 1st St SW, Rochester, MN 55905. 0 1989 by W.B. Saunders Company. 0049-0172/89/1804-2010$5.00/O

Vol 18, No 4, SuppI (May), 1989:pp 5 l-56

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dysfunction, mediolateral instability, and other mechanical alterations. During midstance the knee should be maintained by a strong quadriceps contraction in slight flexion. Relative quadriceps weakness may be due to obesity and/or actual muscle weakness. The weakness may allow the knee to “give way” a few degrees during midstance, producing undue patellar compression and shear on the tibiofemoral joint. To prevent this “give-way” sensation, one may lock the knee during midstance. This is a frequent observation in obese and elderly patients. Axial loading during midstance with a fully extended locked knee reduces the shock-absorbing function of the quadriceps muscle, resulting in increased impact loading and cumulative trauma on the intra-articular cartilage and subchondral bones. The clinical observation that muscle weakness accompanies OA is further supported by pathology.” There are two distinct types of muscle fibers, plus an intermediate.18 Type I muscle fibers are red and small, have a high oxidative metabolism, and fatigue slowly. They are the fibers of high-repetition, low-resistance, endurance activities. Type II fibers are white and glycolytic, fatigue rapidly, and are of large diameter. Type II fibers are associated with highresistance, low-repitition, “strength’‘-related activities. Type II fibers are responsible for most of the muscle hypertrophy seen in resistance training. Selective atrophy of type I (red) fibers is present in immobilization of animals and humans. Biopsies of hip group muscles in severe OA patients by Sirca and Susec-Michieli revealed a preferential atrophy of type II (white) fibers, similar to the atrophy seen in general muscle deconditioning. ” This type of fiber atrophy is different from the type I (red) atrophy of complete joint immobilization or tenotomy. The rehabilitation implication is that light activities and “gentle quadriceps strengthening” are inadequate. Progressive resistance exercises (PRE) are needed to develop adequate quadriceps power. Customary quadriceps programs often use only 5 to 10 lb of weights when normal quadriceps strength is >40 lb in women and >50 lb in men.” Proper technique is important if normal strength is to be restored. Strength is propor-

JOHN L. MElWIlT

tional to resistance applied during training. Commonly prescribed “quad sets” do not provide a strong enough resistance to achieve significant strengthening. Effective resistance is a product of weight applied times lever arm length. If a weight is applied at the ankle and the straight leg is raised, the greatest torque will be on the iliopsoas at the hip. A much smaller resistance is applied against the quadriceps to maintain an extended knee. If a lo-lb weight is lifted by straight leg raising and the iliopsoas-to-ankle distance is 2.6 ft, the torque on the iliopsoas (an inherently weaker muscle) will be 10 lb x 2.6 ft = 26 ft lb; but for the quadriceps it may be only 10 lb x 1.3 ft = 13 ft lb. Knight et al studied the electromyogram (EMG) signal and the maximal lift during knee extension and straight leg raising. l9 Their results point out that limited tension is possible on the quadriceps muscle with straight leg raising techniques. Therefore, full quadriceps power cannot be obtained with traditional straight leg raising. Isotonic and isokinetic PREs may not develop maximal strength because they may be associated with joint pain which will inhibit maximal muscle contraction. Isometric techniques that stress the quadriceps mechanism properly must be prescribed. In principle, such isometric PRE methods are the same as those described in Anderson’s 1955 report.7*‘5V’8It should also be noted that Anderson strengthened the quadriceps to a much higher level (10 RMs of ~40 lb) than is common practice today. The ineffectiveness of quadriceps strengthening in many cases of chrondromalacia patella and OA of the knee may be due to ineffective strengthening regimens. Joint stability requires optimal muscle strength, including type II fiber hypertrophy. High-resistance exercises increase muscle bulk by hypertrophy of type II (white) fibers (the type which is most atrophied in OA), whereas low-resistance, endurance exercises increase type I (red) fiber size and do not appreciably increase muscle bulk.‘4*‘5 Ligament stability is also important to joint stability. Orthotic stabilization and avoidance of overstretching may be needed. There are little data on the concept that injured or overstretched ligaments can be strengthened by progressive, measured resistance. Prolotherapy, a technique

SOFT TISSUE MECHANISMS

OF PAIN IN OA

of attempting to strengthen ligamentous tissue by hypertonic injections, remains controversial.*’ PAIN FROM SOFT TISSUES

Tendonitis Common sites of tendonitis include supraspinatus, infraspinatus, biceps, pectoralis, triceps, lateral epicondyle, medial epicondyle, abductor pollicis longus/extensor pollicis brevis (DeQuervain), hip adductor, periformis, patellar, popliteal, iliotibial, peroneal, and Achilles tendons. Inflammation usually includes the tendon sheath, ie, tenosynovitis. Tendonitis is not often attributed to known inflammation and may require surgical correction. Present concepts of tendon degeneration emphasize vascular mechanisms, whether due to OA, cumulative trauma, or strain.4 Tendons receive their arterial supply by an osseous and a muscular component and supplementary small vessels via the paratenon and tendon sheath microvessels. Muscular and osseous branches converge near a central “watershed” region that depends on both major branches for optimal vascular succor. When tension is imposed by external loading and/or muscular contraction, the arterial input is temporarily impeded, resulting in local ischemia. Relief of tension allows resumption of flow and a reactive hyperemia. Prolonged tension, and hence prolonged ischemia, may result in local tissue necrosis. The “inflammatory” response that follows becomes a repair response with cellular infiltration. During the cellular infiltration period, further tension, shear, or ischemia may result in further tendon necrosis, calcification, and possibly tendon rupture. Degenerative tendonitis of the rotator cuff is one such example. Local ischemia is frequent in several dynamic functions of the body. An analogy is the relative ischemia in skin during compression over bony prominences with prolonged sitting. Relief of pressure is followed by a reactive vasodilation, a clearing of glycolytic metabolites, and resumption of normal local metabolic processes. However, prolonged unrelieved pressure will produce local necrosis and pressure sores. Although tendons have less immediate metabolic needs than skin and require less blood flow, tendons need vascular support for remodeling, repair, and maintenance of strength and function.

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In such a scenario, injections of corticosteroids may be deleterious, delaying healing. On the other hand, they may reduce local edema and congestion, allow better blood flow, and promote healing. The appropriateness and efficacy of corticosteroid injections is still controversial. Cumulative trauma, such as prolonged or rapidly repetitive tendon tension that may involve friction or shearing stresses, may also impair tendon blood flow and produce tendon degeneration. Bursitis Bursae are thin sacs containing a film of low-friction fluid, located in more than 200 regions of potentially high-friction areas adjacent to muscles, tendons, ligaments, skin, and fascia. The pathogenesis of bursitis is poorly understood. Overuse and friction appear to be predisposing factors. Bursitis is common in bursae adjacent to arthritic joints and may be caused by direct inflammatory involvement of the bursa wall and/or to abnormal mechanical forces from the arthritis. Bursitis is frequent and is one cause of pain in OA. Therefore, treatment of bursitis associated with OA may result in substantial improvement of symptoms and function. Palpation may reveal bursitis in the subacromial, olecranon, ileocostalis, gluteus medius, greater trochanteric, ischial, iliopectineal, pes anserine, prepatellar, and infrapatellar bursae. Ligaments Ligaments are strong and relatively avascular. They provide joint and spine stability and absorb mechanical stress. Most ligaments have abundant nerve supplies, and provide proprioceptive input into the CNS. They are synergistic with muscle and are important in posture, balance, and muscle activity. **Tension on ligaments may result in inhibition or facilitation of muscle agonists or antagonists, enhancing muscle reflex activity and responsiveness. Joint pathology and altered biomechanics may result in pain from excessive tension on supporting ligaments. Muscle weakness associated with OA can also contribute to undue ligament stress. Strengthening muscles may reduce stress on ligaments. Strengthening muscles about joints with OA may provide pain relief.i5 Ligaments can elongate and weaken with pro-

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longed excessive stretching. Conversely, they may shorten and thicken when the distance between attachments is chronically reduced. Both enlongated and thickened ligaments may become painful. Of additional significance, proprioceptive input from such ligaments may be altered, adversely affecting muscle tone, responsiveness, and posture. These neurologically mediated alterations in biomechanics may further increase joint, ligament, and muscle stress5 Joint Capsules

Joint capsule contractures are a major cause of limited joint motion and can be a significant direct source of pain. If a joint is not moved through a full range of motion regularly, the joint capsule becomes thickened, contracted, and painful. By mechanisms that are poorly understood, inflammation can occur with cellular infiltration, edema, and further thickening of the capsule. Contiguous tendons, ligaments, and bursae may become involved with the inflammation and adhere to the capsule, adding to pain and limitation of motion. The most frequent example of such an inflammatory capsulitis is adhesive capsulitis of the shoulder.23 It may follow immobilization alone. Cumulative trauma, especially from rapid repetitious rotation and abduction, may play a role. Vascular compromise similar to tendonitis is possible in the pathogenesis of inflammatory capsulitis. Inflammation may be part of the remodeling process. The common denominator of capsulitis appears to be reduced motion or immobilization. Lack of aggressive joint mobilization is followed by additional capsule inflammation and thickening, often with permanent remodeling of paraarticular structures and significant disability. Experience with adhesive capsulitis of the shoulder indicates that once fully developed, permanent structural changes occur within the capsule; the syndrome never completely resolves and easily relapses. The normal compliant web structure of the capsule is often permanently lost. A contracted low-volume capsule becomes permanently tender and painful, aggravated by trauma or immobilization. Ganglions are mucoid-filled cysts that arise from incompetent joint capsules or tendon sheaths and occur most often on the dorsal surfaces of the

wrist, fingers, or foot. They may be painful and contribute to pain and limitations of the associated joints.24 Joint Play and Pain

“Joint play” is a small gliding joint movement not controlled by voluntary muscle action that contributes to smooth and full joint motion. This independent action occurs during active muscle contraction. Although there is no doubt about the presence of joint play in normal joints, its significance is not yet well established. Loss of joint play appears early in OA and is most noticeable in finger and wrist joints. Mennell and others hypothesize that much joint and soft tissue pain is due to a loss of normal joint play.25P26 Muscle

Several types of muscle pain have been described: (1) following unaccustomed heavy eccentric exercise, deep muscle ache and soreness that may develop 6 to 24 hours after the exercise; (2) pain and fatigue, from repetitious low-resistance muscle overuse, occurring during the activity and improving with rest; (3) myalgia-morning or static posture muscle soreness that decreases with motion and activity; and (4) muscle cramps and spasms-intense, sustained nonvoluntary muscle contractions following marked muscle fatigue or in response to local pain. Muscle spasm is a persistant muscular contraction not under voluntary control that is tender to palpation.27‘29 Muscle spasm by definition is inherently painful and not to be confused with postural guarding. Muscle contractures are frequent in OA. Contractures from impaired mobility occur primarily in the muscle contractile tissue and not in associated tendons. Contractures may develop from persistent muscle spasm, resulting from painful sources within the muscle or from adjacent anatomical structures. Muscle contractures themselves can be painful during muscle contraction and joint motion. Chronically contracted muscles often develop tender, painful nodules within or adjacent to the muscle belly. These nodules are of two types. One is transient and disappears with pressure, massage, and relaxation. Segmental muscle spasm is suggested to be underlying this type. The second type persists despite pressure and massage and

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OF PAIN IN OA

may represent a localized muscle contracture, inflammatory nidus, or intrafascicular scar. Pathological studies are conflicting and may reflect different etiologies. Tension Myalgia (Fibromyalgia)

Central factors are well known to initiate and amplify peripheral pain.30S31Pain due to central amplification and psychological factors is well discussed elsewhere. However, one amplification mechanism that must be mentioned in the context of OA pain is tension myalgia. Tension myalgia as a “pain-spasm cycle” mechanism is a state of persistent muscle contraction resulting in muscle and trigger point pain, secondary either to other sources of pain (eg, OA) or to CNS muscle excitation. The latter may include psychological stress, sleep disorders, poor posture, and habitual muscle contraction. Other names for this syndrome include fibrositis, tension myositis, fibromyalgia, and muscle attachment syndrome.32-39 Tension myalgia is a name chosen to reflect muscle or muscle attachment pain coupled with muscle and/or psychological tension. Pelvic floor myalgia is one form of this that is localized to the pelvic floor. It may mimic lower back pain,

sciatica, or hip pain but responds readily to pelvic floor muscle reeducation and relaxation.40 Chronic, untreated tension myalgia may increase muscle and joint contractures and can affect joint mobility and possibly intra-articular pressure in a manner similar to muscle spasms. I3 Tenderness in multiple trigger points is characteristic.41S43 Many of these trigger points correlate well with findings from scanning EMG biofeedback, supporting a muscular tension mechanism for at least some sites. Simms studied the pressure required to produce tenderness (dolorimeter method) in 75 sites in patients with diagnosis of fibromyalgia and in normal subjects and identified 19 sites where there was a significant difference in pressure required to produce pain.34 These tender points were not studied in OA, rheumatoid arthritis (RA), or other conditions. Whether these sites are or are not the same “tender points” associated with localized pain in OA, RA, or lower back pain needs further study. Central pain amplification mechanisms must be considered in all cases of chronic pain, including OA, but are not as well studied in peripheral OA as in chronic back and neck pain syndromes. Techniques to identify pain amplification are available and can be incorporated into clinical examinations.33

REFERENCES 1. Wall PA: Mechanisms of acute and chronic pain. Adv Pain Res Ther 6:95- 104, 1984 2. Iggo A, Guilbaud G, Tegner R: Sensory mechanisms in arthritic rat joints. Adv Pain Res Ther 6:83-93,1984 3. Sheon RP, Moskowitz RW, Goldberg VM (eds): Soft Tissue Rheumatic Pain, Recognition, Management, Prevention (ed 2). Philadelphia, Lea SKFebiger, 1987, pp 16-22 4. Calliet R: Soft Tissue Pain and Disability. Philadelphia, Davis, 1977 5. Harkness JAL, Higgs, Dieppe PA: Osteoarthritis, in Wall PD, Melzack R (eds): Textbook of Pain. New York, Churchill Livingtone, 1984, pp 215-224 6. Wu W: Pain Management, Assessment and Treatment of Chronic and Acute Syndromes. New York, Human Sciences, 1987, pp 2 l-44 7. Merritt JL: Arthritis, in Sinaki (cd): Basic Clinical Rehabilitation Medicine. Philadelphia, Decker, 1987, pp 225-24 1 8. Johansson 0: Pain, motility, neuropeptides, and the human skin: Immunohistochemical observations, in Tiengo M, Cue110 AC, Eccles J, et al (eds): Advances in Pain Research and Therapy, vol 10. New York, Raven, 19Xx, pp 31-44 9. Peretti G: Pain as the cause of limitation of joint movement in degenerative lesions of arthrosis, in Tiengo M,

Cue110AC, Eccles J, et al (eds): Advances in Pain Research and Therapy, vol 10. New York, Raven, 19Xx, pp 123-126 10. Vecchiet L, Giamberardino MA, Marini I: Immediate muscular pain from physical activity, in Tiengo M, Cuello AC, Eccles J, et al (eds): Advances in Pain Research and Therapy, vol 10. New York, Raven, 19Xx, pp 193-206 10a. Joynt RL: Therapeutic exercise, in DeLisa JA (ed): Rehabilitation Medicine Principles and Practice. Philadelphia, JB Lippincott, 1988, pp 347-371 11. Wells P: Movement education and limitation of movement, in Wall PD, Melzack R (eds): Textbook of Pain. New York, Churchill Livingstone, 1984, pp 741-750 12. Moskowitz RW, Howell DS, Goldberg VM, et al (eds): Osteoarthritis, Diagnosis and Management. Philadelphia, Saunders, 1984, pp 93-146 13. Hicks JE, Gerber LH: Rehabilitation of the patient with arthritis and connective tissue disease, in DeLisa JA (ed): Rehabilitation Medicine, Principles and Practice. Philadelphia, Lippincott, 1988, pp 765-794 14. Gerber LH, Hicks JE: Rehabilitation in the management of patients with osteoarthritis, in Moskowitz RW, Howell DS, Goldberg VM, et al (eds): Osteoarthritis, Diagnosis and Management. Philadelphia, Saunders, 1984, pp 287-315

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15. Anderson TP: Management of degenerative joint diseaseof the knee. Arch Phys Med Rehabil36:154-159, 1955 16. Turek SL: The knee, in Orthopaedics, Principles and Their Application (ed 4). Philadelphia, Lippincott, 1984, pp 1269- 1406 17. Sirca A, Susec-Michieli M: Selective type II fiber muscular atrophy in patients with osteoarthritis of the hip. J NeurolSci44:149-158, 1980 18. Joynt RL: Therapeutic exercise, in DeLisa JA (ed): Rehabilitation Medicine, Principles and Practice. Philadelphia, Lippincott, 1988, pp 347-37 1 19. Knight KL, Martin JA, Londeree BR: EMG comparison of quadriceps femoris activity during knee extension and straight leg raises. Am J Phys Med 58:57-69, 1979 20. Hackett GS: Ligament and Tendon Relaxation (Skeletal Disability) Treated by Prolotherapy (Fibro-osseous Proliferation) (ed 3). Springfield, IL, Thomas, 1958, pp 51-103 21. Curwin S, Stanish WD: Tendinitis: Its Etiology and Treatment. Lexington, KY, Collamore, 1984, pp 20-34 22. Solomonow M, Baratta R, Zhou BH, et al: The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am J Sports Med 15:207-213,19Xx 23. Bateman JE, Fornasier VL: The Shoulder and Neck. Philadelphia, Saunders, 1978, pp 242-314,367-372 24. McCarty DJ: Arthritis and Allied Conditions, a Testbook of Rheumatology (ed 10). Philadelphia, Lea & Febiger, 1985, pp 1212-1217 25. Mennell JM: Joint Pain. Boston, Little, Brown, 1964, pp l-15.154-159 26. Merritt JL, Sinaki M: Examination of joints, in Sinaki (ed): Basic Clinical Rehabilitation Medicine. Philadelphia, Decker, 1987, pp 30-62 27. Jones DA, Newham DJ, Obletter G, et al: Nature of exercise-induced muscle pain, in Tiengo M, Cue110 AC, Eccles J, et al (eds): Advances in Pain Research and Therapy, ~0110. New York, Raven, 19Xx, pp 207-218 28. Newham DJ: The consequences of eccentric contractions and their relationship to delayed onset muscle pain. Eur J Appl Physiol57:353-359, 1988 29. Little JW, Merritt JL: Spasticity and associated abnormalities of muscle tone, in DeLisa JA (ed): Rehabilitation Medicine, Principles and Practice. Philadelphia, Lippincott, 1988, pp 430-447

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30. Edwards RH: Hypotheses of peripheral and central mechanisms underlying occupational muscle pain injury. Eur J Appl Physiol57:275-281, 1988 3 1. Ursin H, Endresen M, Ursin G: Psychological factors and self-reports of muscle pain. Eur J Appl Physiol 57: 282-290, 1988 32. Sinaki M: Tension myalgia, in Sinaki (ed): Basic Clinical Rehabilitation Medicine. Philadelphia, Decker, 1987, pp 246-250 33. Hanson TJ, Merritt JM: Rehabilitation of the patient with lower back pain, in DeLisa JA (ed): Rehabilitation Medicine, Principles and Practice. Philadelphia, Lippincctt, 1988, pp 726-748 34. Simons DG: Myofascial pain syndromes due to trigger points, in Osterweis M, Kleinman A, Mechanic D (eds): Pain and Disability. Washington, DC, National Academy, 1987, pp 189-210,285-292 35. McCain GA, Bell DA, Francois MM, et al: A controlled study on the effects of a supervised cardiovascular fitness training program on the manifestations of primary fibromyalgia. Arthritis Rheum 31:1135-l 141, 1988 36. Smythe H: “Fibrositis” and other diffuse musculoskeleta1 syndromes, in Kelly WN, Harris ED, Ruddy S, et al (eds): Textbook of Rheumatology (ed 2). Philadelphia, Saunders, 1985, pp 1212-1218 37. Henriksson KG: Muscle pain in neuromuscular disorders and primary fibromyalgia. Eur J Appl Physiol 57: 348-352,1988 38. McCain GA, Scudds RA: The concept of primary fibromyalgia (fibrositis): Clinical value, relation and significance to other chronic musculoskeletal pain syndromes. Pain 33:273-287, 1988 39. Simons DG, Travel1 JG: Myofascial pain syndromes, in Wall PD. Melzack R (eds): Textbook of Pain. New York, Churchill Livingstone, 1984, pp 263-276 40. Sinaki M, Merritt JL, Stillwell GK: Tension myalgia of the pelvic floor. Mayo Clin Proc 52:717-722,1977 41. Wolfe F, Cathey MA: The epidemiology of tender points: A prospective study of 1520 patients. J Rheum 12:1164-1168, 1985 42. Lee P, Helewa A, Smythe HA, et al: Epidemiology of musculoskeletal disorders (complaints) and related disability incanada. JRheum 12:1169-1173,1985 43. Simms RW, Goldenberg DL, Felson DT, et al: Tenderness in 75 anatomical sites, distinguishing fibromyalgia patients from controls. Arthritis Rheum 31:182-187, 1988