The most common pain syndrome in the world.                                        Read The Flame within a guide to prevent & treat autoimmune diseases by Dr Imran Khan                        

Managing Myofascial Pain Syndrome

Sorting Through the Diagnosis and Honing Treatment

James M. Daniels, MD, MPH; Tim Ishmael, MD; Robert M. Wesley, MA

THE PHYSICIAN AND SPORTSMEDICINE - VOL 31 - NO. 10 - OCTOBER 2003

In Brief: Musculoskeletal complaints are among the leading reasons for visits to physicians, and about one third of these patients meet diagnostic criteria for myofascial pain syndrome (MPS). Although MPS was identified more than a century ago, debate over its existence as a separate clinical entity continues. Physicians who learn to identify characteristic symptoms can differentiate MPS from fibromyalgia and provide effective treatment. Key to treatment is identification of trigger points that when stimulated produce patterns of pain throughout a limb or region. Treatment modalities for MPS include trigger point injection, shiatsu, and the spray and stretch technique. Prognosis for MPS is better than that for fibromyalgia, and treatment usually follows an individualized regimen.

The musculoskeletal system comprises more than 400 individual muscles and is the largest organ system by weight in the human body.¹ A recent study² identified musculoskeletal complaints as one of the leading causes for patients to visit a primary care provider. As many as one third of these patients had symptoms that met the diagnostic criteria for myofascial pain syndrome (MPS).¹

Although MPS has been described variously in the literature since 1843,³ the debate over its existence continues. Whether one takes the position that it is a subset of fibromyalgia or a separate entity, treatment for MPS differs from that of fibromyalgia, as does its prognosis. Patients who have MPS often have regional pain symptoms after a relatively minor trauma or muscle overuse.

Describing and Distinguishing the Pathology

Simons et al¹ have defined regional MPS as a condition in which the patient has "hyperirritable spots" or "trigger points" within taut bands of skeletal muscle or fascia that are painful on compression and can give rise to characteristic referred pain, tenderness, and autonomic nervous system symptoms. Pain from MPS can be described as deep and achy, and it is occasionally accompanied by a sensation of burning or stinging. Patients may also report restricted range of motion in the area affected. MPS is limited to one area or quadrant of the body.¹

Differentiating the disorders. In 1990, the American College of Rheumatology developed criteria for the diagnosis of fibromyalgia,⁴ a condition that can sometimes be confused with MPS. MPS can be distinguished from fibromyalgia in a number of ways (table 1). Fibromyalgia is a disorder of sleep that affects areas throughout the body,⁴ while MPS is a disorder of muscle physiology, affecting only one region or extremity. In addition, MPS has a much better prognosis than fibromyalgia.^5,6

Some clinicians are skeptical that MPS is a distinct disorder and believe that the condition is a subset of fibromyalgia.⁷ The early literature on these conditions uses the two diagnoses interchangeably. Much of the controversy centers around differentiating the "tender points" found in patients with fibromyalgia and the "trigger points" found in patients with MPS. The trigger point may be associated with a local "jump response" or "jump sign." Thus, when physicians palpate the affected muscle, they feel a "knotted" or "doughy" area, and the patient may instinctively recoil or jump when the area is identified. A tender point associated with fibromyalgia may not be detected when palpated and may represent only an area of maximum tenderness within a sore muscle. Tender points are not associated with referred pain patterns, jump signs, or the motor endplates of the muscle-nerve interface.

One study⁷ employed clinical experts to perform tender point examinations on three groups of patients. A small number of patients were prediagnosed with either fibromyalgia or MPS. These patients were compared with 80 "healthy" patients. The experts found taut bands of muscle and muscle twitches in both healthy controls and in patients with either of the conditions. A liberal definition of "trigger points" by these investigators produced overlap between the fibromyalgia group and the MPS group, and local areas of tenderness or "tender spots" were found in both groups.⁷ A second study⁸ of similar design found that dolorimetry and palpation were very reliable in discriminating between control patients and those with MPS or fibromyalgia.

Muscle Basics, Trigger Points, and Pain Patterns

A review of structural and physiologic principles of muscle contraction helps address syndrome etiology and provides tips on trigger point identification.

Muscle structure and contraction. Skeletal muscle is an assembly of fascicles, each of which is a bundle of roughly 100 muscle fibers. Each muscle fiber or cell encloses approximately 1,000 to 2,000 myofibrils. Myofibrils consist of chains of sarcomeres connected serially, end-to-end. Individual sarcomeres are basic contractile units of skeletal muscle connected by z-lines, often described as "links in a chain" when visualized under the microscope. Each sarcomere is composed of actin and myosin molecules that form cross-bridges in the presence of ionized calcium.

When adenosine triphosphate (ATP) is bound to myosin, the actin-myosin cross-bridge remains relaxed (not attached). Hydrolysis of ATP into adenosine diphosphate (ADP) results in the interaction or crossbridging of the actin and myosin proteins. ADP then dissociates from the myosin, causing it to bend or "cock," thus pulling on the actin and shortening the sarcomere. Reattachment of another ATP releases the cross-bridge and uncocks the myosin, allowing the process to start over. As these cycles are repeated, the muscle contracts. When calcium is removed, the contraction is terminated. Without additional ATP input, the cross-bridges remain attached, myosin stays cocked, and the muscle is stiff, as in rigor mortis.⁹

It is key that the muscle can continue to expend energy in the presence of calcium when the muscle is at its shortest length and that maximum overlap exists between actin and myosin fibers. A deficit in calcium metabolism at the sarcoplasmic reticulum can cause a "trigger point" in a resting muscle.

The muscle fibers normally receive their nerve supply from a motor neuron via a motor end plate. Calcium release through the sarcoplasmic reticulum is controlled through the release of acetylcholine at the motor end plate.⁹ Clinically, it is important to understand that end plates are usually located in the center of the muscle fiber. Since trigger points characteristic of MPS are intimately involved with these motor end points, the orientation of the muscle fibers within the muscles affects the pain pathway.

In MPS, palpating the muscle is painful. The pain is relieved by stretching the sarcomere and restoring the muscle to its normal length by removing the overlap between the actin and myosin filaments.¹⁰ Such stretching is exquisitely painful and requires temporarily blocking pain receptors while the involved muscle is stretched. This phenomenon is the reason that spray and stretch, local injection, and acupressure—all of which inhibit pain and motor reflex—are employed in treatment as the muscle is stretched to length.

Although many theories responsible for MPS have been postulated,^5,11 no clear causal factors have been identified. Clinical studies have shown some association between MPS and prolonged static postures, lack of exercise, sleep disturbance, and emotional stress.⁵ With minimal training, clinicians can identify this syndrome based solely on history and physical examination findings.

Identifying trigger points. The recommended criteria for identifying trigger points consist of essential criteria and confirmatory observations (table 2).¹ Using pain diagrams, examiners can compare patient trigger points identified with those known from published drawings (figure 1).^5,10,12,13

Trigger points are subdivided into two groups. Active trigger points cause referred pain and usually have predictable patterns specific to each muscle. These trigger points are rarely located where the patient reports the pain. The pain pattern does not usually follow a specific dermatomal pattern. The suspected muscle should be palpated until a band or feeling of tightness is located. This finding is often described as a ropiness or nodularity in the muscle. Clinicians should then apply pressure until they find the "spot of maximum tenderness" along the length of the taut band of muscle fiber.¹⁴

When the trigger point is palpated, the patient may localize the discomfort and involuntarily withdraw from contact (jump sign).¹ Such a finding is a strong indication of a trigger point. Sustained digital pressure on a trigger point usually evokes the same referred pain pattern that brought the patient into the clinic. Occasionally, anatomically controlled phenomena, such as a change in skin temperature, color, or perspiration, may occur.

The second type of myofascial trigger point that Travell¹⁵ describes is the latent trigger point. On exam, the patient may have a nodular area that, while associated with a taut band of muscle, does not reproduce pain. This finding, along with increased muscle tension and a restricted range of motion, separates this particular myofascial trigger point from the tender points that are characteristic of fibromyalgia.

Treating Trigger Points

After identifying the characteristic trigger points of MPS and ruling out other diagnoses, various treatment protocols can be implemented in an office setting.

Trigger point injections. Various compounds have been described^16,17 for use in injections, including 3% promethazine-hydrochloride, 0.5% procaine hydrochloride, 1% lidocaine hydrochloride without vasoconstrictors, and 0.25% lidocaine with normal saline. Indications for trigger point injections are a limited number of tender spots coinciding with the patient's complaint that produce the jump sign in response to pressure.¹⁸ Several contraindications for injections have been proposed (table 3).¹⁸

The International Association for the Study of Pain has made suggestions for training to identify trigger points and has published recommended standards for injecting trigger points.¹⁷ Many experienced primary care physicians are skilled in performing injections, but physicians should be aware of the following caveats:

• To avoid pneumothorax, never aim the needle at an intercostal space. (Even with proper training and patient informed consent, we do not advocate injection in this area for outpatients.)
• Use a needle long enough to keep the hub well above the skin surface during injection.
• Never inject the needle to the hub, because, if the needle breaks, complications can arise.
• Be aware of the tip of the needle at all times and avoid placing any sideward pressure on the syringe that could bend the needle and deflect the tip.
• Check for a needle that has a rough tip surface, which may create a "drag" upon injection; the impact of the tip of such a needle produces a fish-hook burr, causing unnecessary bleeding.¹⁷ Needles can be replaced if a rough tip is found, even after the syringe is filled.

Shiatsu. This technique has many names, including ischemic acupressure and mild therapy. To perform the technique, the clinician uses the thumb to apply a slow, gentle, firm pressure to the trigger point. It is very important that light pressure be applied initially and slowly intensified over approximately 1 minute; application of sudden forceful pressure will actually aggravate the patient's symptoms. A second minute of maximal pressure is applied, at which time the examiner's thumb is slowly released from the trigger point. Clinicians familiar with this technique often describe a feeling of the muscle "giving way" beneath their fingers during this second minute. Once pressure is released, the skin blanches briefly, and a reactive hyperemia follows that may last several hours. This technique has no known complications other than local ecchymosis in some patients.¹⁹

Spray and stretch. Not all patients can tolerate ischemic acupressure, so some practitioners may employ a spray and stretch technique with vapocoolant.¹⁷ The pain signal sent by the stretched muscle is overridden by a nerve impulse to the posterior horn of the spinal column. Following identification of the trigger point, the physician places the patient in a comfortable, relaxed position. To prepare the patient, physicians may often use a heating pad or moist heat on the area for approximately 5 to 10 minutes. One end of the muscle is anchored either by one of the examiner's hands or by immobilizing the patient's distal appendage. The skin is then sprayed with repeated parallel sweeps of vapocoolant over the length of the muscle in the direction of the pain pattern (figure 2). It is important that the vapocoolant container be held approximately 12 in. (30 cm) from the skin at a 30° angle to the plane of the skin. Parallel sprays are made using unidirectional sweeps over the most tightly stretched muscle fibers and then over the rest of the muscle. Sweeps should be slow and even and cover about 4 in./sec (10 cm/sec). The spray should be overlapped slightly, but no more than two passes should be made over the same area.²⁰

After the first sweep of spray, pressure is applied to take up muscle slack; this pattern is continued as additional sweeps of spray are applied. The sweeps are extended to cover the referred pain pattern of the muscle. These steps are repeated two or three times until the skin becomes cold to the touch or when range of motion reaches its maximum. Reapplication of heat is followed by several cycles of full range of motion of that muscle. Some physicians suggest using the vapocoolant over a slightly larger area than that of the referred pain pattern. If the patient says the spray is too cold, the dispenser can be held closer to the skin than the usual 12 in. (30 cm). If a colder than usual spray is desired, distance can be increased to 18 in. (46 cm). The skin should be transiently cooled and not the underlying muscle. Passive stretching is gradually applied to get the joint to extend to its full range of motion, but the muscle should not be overstretched. The muscle should then be promptly returned to its shortened length.²¹

Coolant use and ice stroking. In the past, the most widely used vapocoolant was ethyl chloride, but this has been replaced by fluoromethane, which is nontoxic, is nonflammable, and does not irritate the skin. Unfortunately, fluorocarbons have been implicated in degradation of the upper atmosphere ozone layer and will no longer be manufactured. A temporary medical exception was granted for fluoromethane until a suitable substitute is developed, and one such spray is available (Fluori-Methane Spray and Stretch, Gebauer, Cleveland, 1-800-321-9348). The concentrated stream from a vapocoolant dispenser is far superior to the usual diffuse spray from a standard spray can. Physicians should be careful when using fluoromethane. Although the spray will not damage most tissues that are accidentally sprayed, the conjunctiva may be damaged if the spray hits a patient's eye.

Some patients with cold-induced asthma or other respiratory conditions may not tolerate vapocoolant spray near the face unless the clinician covers the patient's nose with a small cloth or hand.²² This difficulty has led to the development of a technique called ice stroking, which may replace spray for these patients. Water is frozen in a plastic or paper cup with a stirring stick, such as a tongue depressor, placed in the cup to provide a handle to hold the ice. The bottom of the cup is then torn back and an edge of ice is applied to the skin in a unidirectional stroke following the same patterns as for the spray. The patient's skin must remain dry, because dampness alters the rate of change in skin temperature. Some clinicians cover the ice with thin plastic wrap or have an assistant follow along with a small towel to blot the skin. It is imperative to move along at a rate so that the ice cools just the skin and not the underlying tissues.¹

These techniques can be easily mastered in a short time. The only contraindications to these methods would be if the patient has Raynaud's phenomenon, cold urticaria, or hypersensitivity to one of the cooling agents.

Battling Underdiagnosis

MPS is a common disorder that may be underdiagnosed. It is imperative that the physician has determined that the patient has no other condition that mimics MPS. Some of the simple techniques described for treating MPS can be easily learned by patients to provide pain relief and restore function without the additional cost of supervised physical therapy and medications.

References

1. Simons DG, Travell JG, Simons LS, et al: Travell & Simons' Myofascial Pain and Dysfunction: The Trigger Point Manual, ed 2. Baltimore, Williams & Wilkins, 1999, p 132
2. Skootsky SA, Jaeger B, Oye RK: Prevalence of myofascial pain in general internal medicine practice. West J Med 1989;151(2):157-160
3. Kellgren JH: A preliminary account of referred pains arising from muscle. BMJ 1938;1:325-327
4. 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(2):160-172
5. Han SC, Harrison P: Myofascial pain syndrome and trigger-point management. Reg Anesth 1997;22(1):89-101
6. Jaeger B, Reeves JL: Quantification of changes in myofascial trigger point sensitivity with the pressure algometer following passive stretch. Pain 1986;27(2):203-210
7. Wolfe F, Simons DG, Fricton J, et al: The fibromyalgia and myofascial pain syndromes: a preliminary study of tender points and trigger points in persons with fibromyalgia, myofascial pain syndrome and no disease. J Rheumatol 1992;19(6):944-951
8. Tunks E, McCain GA, Hart LE, et al: The reliability of examination for tenderness in patients with myofascial pain, chronic fibromyalgia and controls. J Rheumatol 1995;22(5):944-952
9. Mountcastle VB (ed): Medical Physiology, ed 14. St Louis, Mosby-Yearbook, 1980, pp 82-119
10. Fricton JR, Auvinen MD, Dykstra D, et al: Myofascial pain syndrome: electromyographic changes associated with local twitch response. Arch Phys Med Rehabil 1985;66(5):314-317
11. Fine PG, Milano R, Hare BD: The effects of myofascial trigger point injections are naloxone reversible. Pain 1988;32(1):15-20
12. Rachlin ES: History and physical examination for regional myofascial pain syndrome, in Rachlin ES (ed): Myofascial Pain and Fibromyalgia: Trigger Point Management. St Louis, Mosby-Yearbook, 1994, pp 159-172
13. Simons DG, Travell JG: Myofascial origins of low back pain: 1. Principles of diagnosis and treatment. Postgrad Med 1983;73(2):66-77
14. Price DD, McGrath PA, Rafii A, et al: The validation of visual analogue scales as ratio scale measures for chronic and experimental pain. Pain 1983;17(1):45-56
15. Travell J: Identification of myofascial trigger point syndromes: a case of atypical facial neuralgia. Arch Phys Med Rehabil 1981;62(3):100-106
16. Wolf SL, Minkwitz JA: Topical anesthetics: effects on the Achilles tendon and H-reflexes. 2. Stroke patients. Arch Phys Med Rehabil 1989;70(9):673-677
17. Fields HL (ed): Core curriculum for professional education in pain: a report of the Task Force on Professional Education of the International Association for the Study of Pain. Seattle, IASP Press, 1995
18. McClaflin RR: Myofascial pain syndrome: primary care strategies for early intervention. Postgrad Med 1994;96(2):56-73
19. Chan P: Finger Acupressure: Treatment for Many Common Ailments from Insomnia to Impotence by Using Finger Massage on Acupuncture Points. New York City, Ballantine Books, 1975
20. Nielsen AJ: Spray and stretch for myofascial pain. Phys Ther 1978;58(5):567-569
21. Halkovich LR, Personius WJ, Clamann HP, et al: Effect of Fluori-Methane spray on passive hip flexion. Phys Ther 1981;61(2):185-189
22. Mense S, Simons DG, Russell IJ: Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment. Philadelphia, Lippincott Williams & Williams, 2001, p 299

Dr Daniels is associate professor of family and community medicine in Southern Illinois University School of Medicine's family practice residency program and program director of the care sports medicine fellowship program in Quincy, Illinois. He has a certificate of added qualifications in primary care sports medicine. Dr Ishmael is a family practice physician in private practice in Litchfield, Illinois. Mr Wesley is director of research and program development in the department of family and community medicine at the Southern Illinois University School of Medicine in Springfield, Illinois. Address correspondence to James M. Daniels, MD, MPH, 612 N 11th St, Suite B, Quincy, IL 62301;

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