Simons Myofascial Pain & Dysfunction-The Trigger Point Manual Vol 2-The Lower Extremities

Chapter 27 / Deep Intrinsic Foot Muscles 533 through the head of the talus. Blockage of exert sufficient pressure to penetrate deep tarsometatarsal joint movement may re- to the plantar aponeurosis with the toes strict rotation in either or both directions. slightly extended. Spot tenderness is usu- The second part tests pronation and supi- ally clearly definable, but one should not nation by swinging the forefoot back and expect to feel a taut band in this muscle. forth around the subtalar joint. Restric- tion of this motion indicates blockage of Flexor Hallucis Brevis. Because the joints proximal to the tarsometatarsal plantar aponeurosis covers much of the joints. If this screening test is positive, flexor hallucis brevis, the medial head of then the individual joints should be ex- this muscle is most effectively palpated amined for restriction of mobility.41 using flat palpation through the thinner skin along the medial margin of the sole Any patient with sore intrinsic foot of the foot (Fig. 27.6B). Lateral head TrPs muscles, particularly if associated with must be examined for spot tenderness by inflammation of the first MP joint (po- deep palpation through the plantar sur- dagra), should be checked for crystal dep- face of the foot. The tendon of the abduc- osition disease. tor hallucis should not be mistaken for a taut band in the flexor hallucis brevis. Oc- The feet should be examined for struc- casionally, the taut band of a TrP is palpa- tural deviations such as a Morton foot ble in the medial head of the flexor hal- structure (Chapter 20), hindfoot varus or lucis brevis against the underlying first valgus, forefoot varus or valgus, equinus, metatarsal bone. hypermobility or malposition of the first ray, excessively high arch, hallux valgus, Adductor Hallucis. To create a moderate and hammer toes. The presence and thick- stretch on the muscle, the great toe is ness of calluses are important. The pa- gently abducted passively during examina- tient's shoes should be examined for a tion. The adductor hallucis must be pal- tight vamp, a rigid distal sole, and abnor- pated through the plantar aponeurosis in mal wear that indicates distorted foot me- the distal forefoot proximal to the heads chanics. of the four lesser metatarsals. The trans- verse head of the muscle extends across The strength of MP flexion of the great the foot just proximal to the metatarsal toe tests the flexor hallucis brevis and, to heads (Fig. 27.6CC, fully rendered finger) and some extent, the abductor hallucis and the oblique head angles slightly across adductor hallucis muscles. This test is the instep from the bases of the second, performed by stabilizing the forefoot and third, and fourth metatarsals (Figs. 27.4B resisting flexion of the great toe at the and 27.6C, outlined finger). Only rarely is a proximal phalanx.39 Some examiners test taut band of either head palpable; how- the strength of the interossei by resisting ever, one can detect TrP tenderness. the patient's attempt to extend the IP joints40 of the four lesser toes, while stabi- Interossei. The interossei and lumbri- lizing the MP joints with the foot held in cals may be palpated between adjacent 20-30° plantar flexion. This test may be metatarsal bones using a bimanual tech- more an indication of lumbrical strength nique as illustrated in Figure 27.6D. This than of interosseus strength.33 Interosseus technique tends to separate these bones strength may be estimated by springing and to increase the stretch on the mus- the proximal phalanges of the toes both cles. The dorsal interossei are palpated by medially and laterally while the subject the finger of one hand with precise attempts to hold the toes spread apart. counter pressure applied on the plantar The examiner must keep in mind, how- surface by a finger of the other hand. ever, that many individuals cannot per- Then tenderness in the lumbricals and form these toe movements well. plantar interossei can be elicited by deep palpation through the plantar aponeuro- 9. TRIGGER POINT EXAMINATION sis against counter pressure applied to the (Fig. 27.6) dorsal surface by the other hand. One of- ten can palpate the taut bands of active Quadratus Plantae. To examine the TrPs in a dorsal interosseus muscle quadratus plantae for TrPs, the clinician against the adjacent metatarsal bone to must use deep palpation (Fig. 27.6A) and which it attacbes. In that case, one may

534 Part 3 / Leg, Ankle, and Foot Pain Figure 27.6. Examination of deep intrinsic muscles with dashed outline) using flat or deep palpation. D, of the right foot for active trigger points. A, quadratus interossei and lumbricals, bimanual technique that plantae using deep palpation. B, flexor hallucis brevis uses the finger of one hand for palpation while the fin- using flat palpation, C, adductor hallucis, transverse ger of the other hand provides counter pressure. head (fully rendered finger) and oblique head (finger elicit a local twitch response by snapping region and the only muscle being pal- palpation of an active TrP. However, one pated is the flexor digiti minimi brevis. In cannot distinguish between the lumbri- some patients, taut bands are palpable cals and plantar interossei by palpation and local twitch responses can be elicited through the plantar aponeurosis and/or in this fifth toe flexor. the oblique head of the adductor hallucis muscle. 10. ENTRAPMENTS Flexor Digiti Minimi Brevis. It is rarely No nerve entrapments have been identi- possible to distinguish by palpation the fied that were due to TrP tension in these flexor digiti minimi brevis from the ab- deep intrinsic foot muscles. ductor digiti minimi that lies beside it lat- erally. Usually, making the distinction is 11. ASSOCIATED TRIGGER POINTS not important. Both are palpated by pin- cer palpation along the lateral border of Single-muscle myofascial pain syn- the foot beside and plantar to the fifth dromes are sometimes seen in the feet (for metatarsal. Sometimes, the abductor dig- example, in the interossei). However, in iti minimi is essentially tendinous in this the complex chronic cases seen in the au-

Chapter 27 / Deep Intrinsic Foot Muscles 535 Figure 27.7. Stretch position and intermittent cold medial half of the plantar surface of the pattern (thin arrows) for a trigger point (X) in the right forefoot as the operator extends the great flexor hallucis brevis muscle. The great toe is ex- toe. The ankle in this case remains in the tended at the metatarsophalangeal joint (ankle posi- neutral position. If one wishes also to in- tion neutral). Intermittent cold with passive stretch of clude release of adductor hallucis TrPs, all short flexors of the toes may be combined (see Fig. the intermittent cold pattern is extended 26.6D) by simultaneously extending all five toes and to include all of the plantar surface of the applying parallel sweeps of the coolant to the plantar forefoot and the great toe is passively ab- surface of the entire forefoot. If hypermobility of the ducted as well as extended. tarsometatarsal region is present, the intermittent cold can be applied prior to the stretch, then the clinician's If the tarsometatarsal region of the foot other hand can be used to stabilize the midfoot. is hypermobile, that region should be sta- bilized by one hand while the other hand thors' practices, when one of these deep takes up slack in the muscles being intrinsic muscles of the foot is involved, lengthened. In this case, the intermittent several others are usually involved also. cold can be applied prior to, rather than during, the stretch. 12. INTERMITTENT COLD WITH STRETCH The remaining deep intrinsic muscles (Fig. 27.7) of the foot are not readily amenable to in- termittent cold with stretch as individual For lasting relief, any nypomobile joints muscles, but can be managed as a group. in the foot should be mobilized, either The technique illustrated in Figure 26.6C prior to or following inactivation of TrPs. (of the previous chapter) for releasing TrPs in the flexor digitorum brevis also The use of ice for applying intermittent releases TrPs in the quadratus plantae cold with stretch is explained on page 9 and flexor digiti minimi brevis. The ankle of this volume and the use of vapocoolant should not be dorsiflexed at the same spray with stretch is detailed on pages time, because tension in the flexor dig- 67-74 of Volume l . 7 3 Techniques that itorum longus would then block full augment relaxation and stretch are re- stretch of the quadratus plantae. viewed on pages 10-11 of this volume. It is important when treating groups of Myofascial TrPs in the flexor hallucis muscles in this way to devote a few min- brevis muscle respond to intermittent utes to their antagonists to prevent reac- cold with stretch applied as illustrated in tive cramping. In this case, one must con- Figure 27.7. With the patient in the side- sider the extensor digitorum brevis and lying position, parallel applications of va- the extensor hallucis brevis muscles. pocoolant spray or ice (using the dry edge The concept and prevention of reactive of a plastic-covered ice cube) cover the cramping (shortening activation) are re- viewed on page 19 of this volume. The complex actions of the interossei and lumbricals and their frequent inter- connections complicate efforts to release their TrPs by intermittent cold with stretch. It is possible to stretch a dorsal interosseous muscle between its two adja- cent metatarsals by moving one metatar- sal dorsally while moving the other in a plantar direction and, at the same time, separating the heads of the two metatar- sals transversely. Techniques of deep massage and injection may be more effec- tive for these muscles. Alternative meth- ods of treatment are reviewed on pages 9— 10 of this volume. Evjenth and Hamberg18 illustrate and describe clearly how to stretch each head of the flexor hallucis brevis by extending

536 Part 3 / Leg, Ankle, and Foot Pain the MP joint of the great toe. Using that the TrP tenderness is localized in this technique, an assistant could apply muscle (Fig. 27.8B). Since the proper dig- sweeps of the intermittent cold distal- ital nerve lies superficial to this muscle, ward over the muscle and its referred the needle enters the medial side of the pain pattern. Similarly, they present the foot to pass deep to the nerve and superfi- technique for stretching the lumbricals,19 cial to the first metatarsal bone into the for simultaneously stretching the second, flexor hallucis brevis.4 third, and fourth dorsal interossei, for stretching the flexor digiti minimi brevis To inject TrPs in the adductor hallucis with the abductor digiti minimi,21 and for muscle with the patient side lying as pre- stretching the adductor hallucis.20 viously described, the clinician localizes the point of maximum TrP tenderness by 13. INJECTION AND STRETCH deep palpation. After skin preparation, (Figs. 27.8 and 27.9) the clinician inserts the needle lateral to the TrP (Fig. 27.8C, syringe free) so that Before injection, the skin of the foot is the needle will angle medially in the di- carefully cleansed, as described in Chap- rection of the first metatarsal to reach the ter 26, page 515. Injection of these deep oblique head of the adductor hallucis muscles can readily result in a transient (Fig. 27.9). To inject the transverse head block of the plantar nerve, which lasts of this muscle, the operator inserts the only 15 or 20 minutes when 0.5% pro- needle distally, close to the heads of the caine solution has been injected. The pa- metatarsal bones (Fig. 27.8C, syringe in tient should be warned of this possibility hand). before injection of the TrPs. All interossei (dorsal and plantar) are For injection of these muscles, a 10-mL approached for injection through the dor- syringe is filled with 0.5% procaine solu- sal surface of the foot (Figs. 27.8D and tion that has been prepared by dilution 27.9). The patient lies supine with the with isotonic saline. A 38-mm (l1/2-in) 22- knee bent to place the foot nearly flat on gauge needle should be long enough to the examining table. After localizing TrP reach these deep intrinsic muscles. spot tenderness in the dorsal interossei by palpation, the clinician injects the muscle For injection of the quadratus plantae between the metatarsal bones. The fingers muscle, the patient lies on the side of the of one hand press upward from the plan- involved muscle and the clinician local- tar surface of the foot into the interos- izes the spot of tenderness in the quad- seous space being injected (as shown in ratus plantae by deep palpation through Figs. 27.6D and 27.8D). One must be care- the plantar aponeurosis and from the me- ful to explore both bellies of a dorsal in- dial border of the foot. The needle enters terosseous muscle in order to locate all of at the medial border of the sole (Fig. the TrPs on each side of the interosseous 27.8A), angled laterally to reach the quad- space (Fig. 27.5A). ratus plantae, between the medial and lat- eral plantar nerves.4 To reach a TrP in a plantar interosseous muscle that is localized by tenderness to The lumbricals are small muscles and deep bimanual pressure from the plantar are indistinguishable from the plantar in- side of the foot, the spot of tenderness is terossei by palpation. Their TrPs would fixed by the finger of one hand while the probably be included when injecting TrPs other hand manages the syringe. Figure in the plantar interossei as described later 27.9 shows why, in order to reach the first in this section. plantar interosseus muscle through a dor- sal approach, the needle must angle later- The flexor digiti minimi brevis may be ally between the second and third meta- indistinguishable from a distal belly of tarsal bones to probe the muscle that lies the abductor digiti minimi. Its TrPs are lo- on the medioplantar aspect of the third cated and injected essentially like those metatarsal. of the abductor digiti minimi as described in Chapter 26, on page 517. After injecting TrPs in one of these muscles, the clinician applies a few For injection of TrPs in the flexor hal- parallel sweeps of intermittent cold lucis brevis muscle, the patient again lies while gently stretching the muscle, as on the side of the involved muscle and

Chapter 27 / Deep Intrinsic Foot Muscles 537 Figure 27.8. Injection of trigger points in the deep in- the second metatarsal bone. The needle of the syringe trinsic foot muscles. A, quadratus plantae. B, flexor in hand is directed into the second dorsal interosseous hallucis brevis. C, adductor hallucis, transverse head muscle between the second and third metatarsals. To (syringe in hand) and oblique head (syringe free). D, reach the first plantar interosseous muscle, the needle first and second dorsal interossei. The free syringe must angle laterally and penetrate between the sec- shows the direction that must be probed to locate trig- ond and third metatarsal bones and reach deep to the ger points in the first dorsal interosseous muscle along third metatarsal (see Fig. 27.9). described in the previous section, to re- aged. Then TrPs that developed seconda- lease any residual TrPs that were rily can be inactivated, whereas they had missed by injection. The prompt appli- previously been refractory to local treat- cation of moist heat reduces the likeli- ment. hood of severe postinjection soreness. Several slow cycles of active range of Normal joint play and range of motion motion to the fully shortened and fully should be restored.41 lengthened positions help equalize sarcomere length and restore the full Appropriate supports should be used range of muscle function. in the shoes to compensate for struc- tural and mechanical problems of the 14. CORRECTIVE ACTIONS foot that cannot be otherwise corrected. This is especially important in patients Crystal deposition disease, such as gout, who are accustomed to running and jog- and other systemic conditions perpetuat- ging, who do extensive walking for ex- ing the TrPs must be diagnosed and man- ercise, or who must stand for long peri- ods of time.

538 Part 3 / Leg, Ankle, and Foot Pain Tendons of extensor 1 st metatarsal digitorum longus bone Tendons of extensor Adductor digitorum brevis hallucis, 5th metatarsal oblique bone head Abductor digiti minimi Abductor Flexor digiti minimi brevis Flexor hallucis hallucis Toe flexor tendons brevis Tendon of flexor Figure 27.9. Cross section through the foot just hallucis longus proximal to the metatarsal heads, viewed from the front. The dorsal interosseous muscles (D) are dark red; the plantar interossei (P) are light red; other muscles, uncolored. Adapted from Ferner and Staubesand.22 Corrective Posture and Activities also applicable to these deep intrinsic muscles. Walking and running should be done on even and level surfaces until TrP activity Home Therapeutic Program has been resolved and the patient is ready to start conditioning of the muscles. The self-stretch techniques described and illustrated in Chapter 26, pages 518-519 Shoes should fit well and should have a are equally useful for patients with in- firm heel counter and good arch support. volvement of the quadratus plantae, lum- The shoe should have a flexible sole, partic- bricals, flexor hallucis brevis, and the ularly in the metatarsal head region. The pa- short flexors of the toes. Stretching may tient should avoid shoes with high or spike be effectively done with the foot im- heels and pointed toes. He or she should be mersed in warm water, for example, encouraged to buy shoes with good shock when taking a tub bath. The methods de- absorption, including rubber heels, rubber scribed are the Toe Flexor Self-stretch Ex- soles, and resilient foam insoles. ercise (see Fig. 26.8) and the Golf-ball and Rolling-pin Techniques (see Fig. 26.9). Basford and Smith8 evaluated the effect of vis- coelastic polyurethane insoles in reducing back, References leg, and foot pain in 96 adult women. These sub- jects spent most of the workday on their feet and 1. Alfred RH, Bergfeld JA: Diagnosis and manage- were not under medical care. Twenty-five of the ment of stress fractures of the foot. Phys Sports- women found that the insole made their shoes too med 7 5 : 8 3 - 8 9 . 1987. tight for comfort and they discarded it. The re- maining subjects found the insoles comfortable 2. Anderson JE: Grant's Atlas of Anatomy, Ed. 8. Wil- and reported that their pain in all three regions liams & Wilkins, Baltimore, 1983 (Fig. 4-95). was reduced significantly.8 3. Ibid. (Fig. 4 - 9 8 ) . Corrective Exercises 4. Ibid. (Fig. 4 - 1 0 0 ) . 5. Ibid. (Fig. 4 - 1 0 2 ) . Conditioning and strengthening exercises 6. Ibid. (Fig. 4 - 1 0 3 ) . described in Section 14 of Chapter 26 are 7. Ibid. (Fig. 4 - 1 0 7 ) . 8. Basford JR, Smith MA: Shoe insoles in the work- place. Orthopedics 1 1 : 2 8 5 - 2 8 8 , 1 9 8 8 . 9. Basmajian JV, Deluca CJ: Muscles Alive, Ed. 5. Williams & Wilkins, Baltimore, 1985 (p. 3 5 1 - 352).

Chapter 27 / Deep Intrinsic Foot Muscles 539 10. Carter BL, Morehead J, Wolpert SM, et al.: Cross- 4 1 . Lewit K: Manipulative Therapy in Rehabilitation of Sectional Anatomy. Appleton-Century-Crofts, the Motor System. Butterworths, London, 1 9 8 5 New York, 1977 (Sects. 82-84). (pp. 136-137, 207-210). 11. Ibid. (Sects. 8 3 - 8 7 ) . 12. Ibid. (Sects. 85,86). 42. Mann R, Inman VT: Phasic activity of intrinsic 13. Ibid. (Sects. 8 5 - 8 7 ) . muscles of the foot. J Bone Joint Surg [Am]) 46: 14. Clemente CD: Gray's Anatomy of the Human Body, 469-481, 1964. American Ed. 30. Lea & Febiger, Philadelphia, 43. Manoli A II, Weber TG: Fasciotomy of the foot: 1985 (pp. 587-590, Fig. 6-83). an anatomical study with special reference to 15. Ibid. (p. 588, Fig. 6 - 8 9 ) . release of the calcaneal compartment. Foot Ankle 16. Ibid. (pp. 8 8 9 - 8 9 0 , Figs. 6 - 8 5 , 6 - 8 6 ) . 17. Duchenne GB: Physiology of Motion, translated by 70:267-275, 1990. E.B. Kaplan. J.B. Lippincott, Philadelphia, 1949 44. Manter JT: Variations of the interosseous mus- cles of the human foot. Anat Rec 9 3 : 1 1 7 - 1 2 4 , (pp. 375-377). 18. Evjenth O, Hamberg J: Muscle Stretching in Man- 1945. 4 5 . McGIamry ED (Ed.): Comprehensive Textbook of ual Therapy, A Clinical Manual. Alfta Rehab Ferlag, Foot Surgery, Vols. I and II. Williams & Wilkins, Alfta, Sweden, 1984 (pp. 153, 158, 159). Baltimore, 1987. 19. Ibid. (p. 157). 4 6 . McMinn RMH, Hutchings RT: Color Atlas of 20. Ibid. (p. 158). 21. Ibid. (p. 162). Human Anatomy. Year Book Medical Publishers, 22. Ferner H, Staubesand J: Sobotta Atlas of Human Chicago, 1977 (p. 289). Anatomy, Ed. 10, Vol. 2. Urban & Schwarzen- 47. Ibid. (p. 3 2 5 ) . 4 8 . Ibid. (p. 3 2 6 ) . berg, Baltimore, 1983 (Fig. 493). 4 9 . McMinn RMH, Hutchings RT, Logan BM: Color 23. Ibid. (Fig. 4 9 7 ) . 24. Ibid. (Fig. 500). Atlas of Foot and Ankle Anatomy. Appleton-Cen- 25. Ibid. (Figs. 501, 502). tury-Crofts, Connecticut, 1982 (p. 29). 26. Goldner JL, Ward WG: Traumatic horizontal 50. Ibid. (p. 56). 51. Ibid. (p. 64). deviation of the second toe: mechanism of de- 52. Ibid. (p. 65). formity, diagnosis, and treatment. Bull Hosp Jt 53. Ibid. (p. 66). Dis Orthop Inst 4 7 : 1 2 3 - 1 3 5 , 1987. 54. Ibid. (p. 67). 55. Ibid. (p. 74). 27. Hollinshead WH: Functional Anatomy of the Limbs 56. Ibid. (p. 75). and Back, Ed. 4. W.B. Saunders, Philadelphia, 57. Netter FH: The Ciba Collection of Medical Illustra- 1976 (p. 358, Table 20-1). tions, Vol. 8, Musculoskeletal System. Part I: 28. Hollinshead WH: Anatomy for Surgeons, Ed. 3., Anatomy, Physiology and Metabolic Disorders. Vol. 3, The Back and Limbs. Harper & Row, New Ciba-Geigy Corporation, Summit, 1987 (p. 105). York, 1982 (pp. 840-841). 58. Ibid. (p. 1 1 2 ) . 29. Ibid. (pp. 8 4 1 - 8 4 2 ) . 59. Ibid. (p. 115). 30. Ibid. (pp. 8 4 2 - 8 4 3 ) . 60. Ibid. (p. 116). 31. Ibid. (pp. 8 4 3 - 8 4 6 ) . 6 1 . Rasch PJ, Burke RK: Kinesiology and Applied Anat- 32. Inman VT, Ralston HJ, Todd F: Human Walking. omy, Ed. 6. Lea & Febiger, Philadelphia, 1 9 7 8 Williams & Wilkins, Baltimore, 1981 (p. 116). (pp. 324-325, 330, Table 17-2). 33. Jarret BA, Manzi JA, Green DR: Interossei and 62. Richardson EG: Injuries to the hallucal sesa- lumbricales muscles of the foot: an anatomical moids in the athlete. Foot Ankle 7 : 2 2 9 - 2 4 4 , 1 9 8 7 . and function study. J Am Podiatr Assoc 7 0 : 1 - 1 3 , 63. Rohen JW, Yokochi C: Color Atlas of Anatomy, Ed. 1980. 2. Igaku-Shoin, New York, 1988 (p. 425). 34. Jimenez AL, McGIamry ED, Green DR: Lesser 64. Ibid. (p. 4 2 7 ) . ray deformities, Chapter 3. In Comprehensive 6 5 . Ibid. (p. 4 2 8 ) . Textbook of Foot Surgery, edited by E.D. Mc- 66. Ibid. (p. 4 2 9 ) . 67. Ibid. (p. 4 5 6 ) . GIamry, Vol. 1. Williams & Wilkins, Baltimore, 1987 (pp. 5 7 - 1 1 3 , see pp. 6 5 - 6 7 ) . 68. Rondhuis JJ, Huson A: The first branch of the lateral plantar nerve and heel pain. Acta Morphol 35. Kalin PJ, Hirsch BE: The origins and function of Neerl-Scand 2 4 : 2 6 9 - 2 7 9 , 1 9 8 6 . the interosseous muscles of the foot. J Anat 152: 69. Ruch JA, Banks AS: Anatomical dissection of 83-91, 1987. the first metatarsophalangeal joint, Chapter 5, 36. Kellgren JH: A preliminary account of referred Part 3. In Comprehensive Textbook of Foot Surgery, pains arising from muscle. Br Med J 1:325-327, edited by E.D. McGIamry, Vol. 1. Williams & 1938. Wilkins, Baltimore, 1 9 8 7 (pp. 1 5 1 - 1 7 2 , see p. 37. Kellgren JH: Observations on referred pain aris- 159). ing from muscle. Clin Sci 3 : 1 7 5 - 1 9 0 , 1938 (see 70. Simons DG: Myofascial pain syndrome due to Fig. 8). trigger points, Chapter 4 5 . In Rehabilitation Medi- cine edited by J. Goodgold. C. V. Mosby Co., St. 38. Kelly M: The relief of facial pain by procaine Louis, 1 9 8 8 (pp. 6 8 6 - 7 2 3 , see p. 712, Fig. 4 5 - (novocaine) injections. J Am Geriatr Soc 1 1 : 5 8 6 - 9F). 596, 1963. 39. Kendall FP, McCreary EK: Muscles, Testing and 71. Simons DG, Travell JG: Myofascial pain syn- dromes, Chapter 2 5 . In Textbook of Pain, edited Function, Ed. 3. Williams & Wilkins, Baltimore, by P.D. Wall and R. Melzack, Ed 2. Churchill 1983 (p. 132). Livingstone, London, 1989 (pp. 368-385, see p. 40. Ibid. (pp. 1 3 6 - 1 3 7 ) . 378, Fig. 25.9H).

540 Part 3 / Leg, Ankle, and Foot Pain 72. Travell  JG:  Chronic  Myofascial  Pain  Syndromes.  74. Turner  RS:  Dynamic  post‐surgical  hallux  varus  after  Mysteries  of  the  History,  Chapter  6.  In  Myofascial lateral  sesamoidectomy:  treatment  and  prevention.  Pain and Fibromyalgia, Vol.  17  of  Advances in Pain Orthopedics 9:963‐969, 1986.  Research and Therapy, edited by J.R. Fricton and E.A.  Awad, Raven Press, New York, 1990 (pp. 129‐137).  75. Valvo P, Hochman D, Reilly C: Anatomic and clinical  significance  of  the  first  and  most  medial  deep  73. Travell  JG,  Simons  DG:  Myofascial Pain and Dys- transverse  metatarsal  ligament.  J Foot Surg function: The Trigger Point Manual. Williams  &  26:194‐203, 1987.  Wilkins, Baltimore, 1983.  76. Wood J: On some varieties in human myology. Proc R   Soc Lond 13:299‐303, 1864. 

CHAPTER 28 Management of Chronic Myofascial Pain Syndrome HIGHLIGHTS: In OVERVIEW, pain caused by pain and tenderness referred from TrPs in any myofascial trigger points (TrPs) may present as of the muscles in a region focus on one location; an acute, recurrent, or chronic pain syndrome. the post-traumatic hyperirritability syndrome, in In the presence of sufficiently severe perpetuat- which nociception and TrP irritability are greatly ing factors, an acute syndrome persists to be- enhanced following central nervous system come a chronic myofascial pain syndrome. For trauma; fibromyalgia, which has characteristics the complete DIAGNOSIS of a chronic myofas- that distinguish it from the chronic myofascial cial pain syndrome, the clinician must conduct a pain syndrome; and articular dysfunction, which thorough general medical history, complete a can interact strongly with myofascial TrPs. detailed trauma and pain history of each distin- TREATMENT, besides specific TrP inactivation, guishable pain area, and check for specific concentrates on teaching patients how to recog- symptoms that would identify systemic perpetu- nize and stretch the muscles responsible for ating factors. The history also examines the total their myofascial pain, and on the management life situation and the patient's orientation toward of muscle stress factors. Mechanical and sys- function or pain. In addition to a complete gen- temic perpetuating factors that are responsible eral physical examination, the clinician performs for the chronicity must be corrected. If patients a myofascial examination of each muscle sus- are pain oriented rather than function oriented, pected of harboring active or latent TrPs and a the reasons must be identified and addressed, thorough evaluation for postural and structural thus enabling them to take responsibility for the dysfunction that could perpetuate the patient's health of their muscles, including carrying out a TrPs. The object of this examination is to locate self-treatment program. Inadequate coping skills the individual active TrPs responsible for a spe- and depression require correction. Patients may cific part of the composite pain problem. DIF- have concomitant articular dysfunction or fibro- FERENTIAL DIAGNOSIS considers: the myo- myalgia, either of which also requires attention. fascial pain modulation disorder, in which the 1. OVERVIEW therefore, expects it to be self-limiting, like postexercise soreness. In the absence Recent studies indicate that myofascial of mechanical or systemic perpetuating pain is the most common single source of factors, a newly activated TrP sometimes musculoskeletal pain, and that myofas- spontaneously regresses to a latent TrP, if cial pain compares in severity with other the muscle remains moderately active but painful conditions that cause the patient is not overloaded. This residual myofas- to seek medical assistance.10, 15, 3,9 51 cial syndrome due to latent TrPs contin- ues to cause some degree of dysfunction, Myofascial pain due to active trigger but no pain.55 The individual muscle points (TrPs) can present as acute, recur- chapters of Volumes 1 and 2 of THE rent, or chronic. The patient with an TRIGGER POINT MANUAL deal primar- acute-onset myofascial pain syndrome ily with single-muscle myofascial pain usually associates the onset of pain with a syndromes. specific overload of the muscles and,

542 Myofascial Pain and Dysfunction: The Trigger Point Manual Active TrPs that spontaneously regress clusters of myofascial syndromes in sev- to the latent stage are readily susceptible eral regions of the body. to reactivation, and the patient may expe- rience recurrent episodes of the same 2. DIAGNOSIS pain problem. Again, the individual ex- pects each episode to be limited in dura- Patients with chronic myofascial pain are tion and, therefore, tolerates it until relief people who have suffered more than just becomes overdue. pain for many months or longer. The se- verity and chronicity of their \"untreat- However, in the presence of sufficiently able\" pain has often reduced their physi- severe perpetuating factors, the active cal activity, limited participation in social TrPs persist and may propagate as sec- activities, impaired sleep, induced a major ondary and satellite TrPs, leading to or minor degree of depression, caused loss a progressively severe and widespread of role in the family, led to loss of employ- chronic myofascial pain syndrome. ment, and deprived them of control of Chronic enigmatic pain, for which health their lives. Many have been depersonal- care providers have been unable to find ized by the ultimate indignity—the con- an organic cause, is a major unsolved viction that their pain is not \"real,\" but problem of the health care system in this psychogenic. Well-meaning practitioners country.23 Fields9 observed, \"The most sometimes have also convinced the pa- common persistent and disabling pains tients' families and friends that the pain is are those of musculoskeletal origin.\" not real, leaving many patients nowhere to Many times, this chronic pain of enig- turn for help. Several of the resulting con- matic origin is caused by myofascial TrPs, ditions listed previously may cause or aug- by fibromyalgia, by articular dysfunction, ment pain; all of them cause suffering. The or by some combination of the three that patients come to the clinician seeking re- has been overlooked. This chapter deals lief from their suffering, which they may primarily with TrP-induced chronic pain, present only in terms of pain. which is both diagnosable and treatable. When examining the patient who has When undiagnosed, interminable pain presented with chronic enigmatic pain, has, psychologically, a totally different the diagnostician must first conduct a impact than pain of limited duration. As thorough, time-consuming history and emphasized by Hendler,21 chronic pain physical examination to identify what con- creates psychological problems in a pre- ditions are contributing to tbe patient's viously well-adjusted individual, and pain and to determine whether there is a therefore, \"if the patient's response to significant myofascial component. Mater- pain is appropriate, but there are no ob- son34 presents a clearly written, in- jective physical findings, it is incumbent sightful, and detailed description of the upon the physician to keep looking for examination required. Hendler21 empha- the source of the patient's pain com- sizes how frequently a thorough examina- plaint.\"21 Gamsa16 concluded that emo- tion is bypassed once the patient has been tional disturbance in patients with labeled a \"chronic pain patient.\" If it ap- chronic pain is more likely to be the con- pears likely that tbe patient does have sequence than the cause of the pain. chronic myofascial pain syndrome, the diagnostic task becomes twofold. In addi- Since secondary and satellite TrPs usu- tion to identifying which TrPs, in which ally develop in functionally related mus- muscles, are causing what portion of the cles of the same region of the body as the patient's total pain complaint, the exam- primary TrP, the term chronic regional iner must determine what perpetuating myofascial pain syndrome may help distin- factors converted the initial acute myofas- guish the regional distribution of the cial pain syndrome to a chronic one. chronic myofascial pain syndrome from Myofascial TrPs may be perpetuated by the total-body painfulness of fibromy- mechanical (structural or postural) fac- algia. Because mechanical and systemic tors, by systemic factors, by associated perpetuating factors also increase the sus- medical conditions, and by psychological ceptibility of the muscles to the activation stress. What we call perpetuating factors, of primary TrPs, patients with severe per- petuating factors are likely to develop

Chapter 28 / Chronic Myofascial Pain Syndrome 543 Fricton refers to as contributing factors12 tinguish what makes it worse. Phase 2 or associated problems;13 he lists those (pain from less irritable TrPs that is per- commonly found in chronic myofascial ceived only on movement and not at rest) pain syndromes of the head and neck.13 is ideal for educating the patient as to which muscles and movements are re- Myofascial Pain History sponsible for the pain, and how to man- age it. In phase 3 (latent TrPs that are Above all, clinicians must believe that causing no pain), the patient still has their patients hurt as much and in the some residual dysfunction and is vulnera- way that they say they do. The patients ble to reactivation of the latent TrPs. are describing their suffering. The first author discovered and mapped the re- The first author has reviewed55 many ferred pain patterns by believing her pa- pitfalls in taking a myofascial pain his- tients, even though they described pain in tory and emphasized the importance of areas that were originally unexplainable. understanding the patient's daily routine We now know that the central nervous in detail, such as sleep positions, custom- system powerfully modulates pain input ary diet, and posture and movements in from the muscles in ways that can explain the work situation. A recent review49 in- referred pain and altered sensation from cluded a sample patient information TrPs.35,42 Referral of pain, tenderness, and questionnaire that is useful both as a pre- other altered sensation from muscles is liminary review instrument and as a no longer the enigma that it was in the check list when taking the initial and in- past 3 5 , 4 2 , 4 8 terval histories. The examiner begins locating the active Specific systemic perpetuating factors TrPs by taking a thorough pain history, that need to be considered in taking the precisely drawing on a body form each history are listed in a recent review47 and area of pain that the patient identifies. are considered in depth on pages 114-155 Each pain area can be numbered on the in Volume l.56 form in the chronological order of its first appearance, and its course and character- The specific functional losses in the pa- istics recorded, as its pattern is drawn. tient's life need to be identified as to kind The technique for doing this is described and degree. Whether the patient's orienta- in Volume 1, pages 4 6 - 5 0 . 5 6 One patient tion is toward function or toward pain may have many distinguishable areas of should be clarified promptly; if the orien- pain (some of which may be caused not tation is not toward function, the therapy by TrPs but by other conditions, such as team should explore why it is not. Most peripheral nerve entrapment). The distri- patients are function oriented and want bution of pain referred from myofascial nothing more than to obtain enough un- TrPs in these patients generally corre- derstanding to control their pain so that sponds to areas published in this and in they can return to a normal life-style. Pa- the first Volume56 of THE TRIGGER tients with poor coping skills learn to de- POINT MANUAL. Several active TrPs pend on pain to survive in life and need may contribute to the pain reported in counseling to deal with this additional one region if the referred pain patterns of suffering. Often, patients' involvement in the TrPs overlap. litigation regarding their pain is based ei- ther on their conviction that the medical It is critically important to delineate community has nothing more to offer clearly the margins of each pain area and them by way of pain relief and improved to identify its time of onset, any strain or function, or on the hope of receiving pay- trauma associated with its onset, events ment for accumulated medical bills. that aggravate it, and what relieves it. The latter two observations are influenced by Myofascial Physical Examination the phase of that myofascial pain syn- drome.55 In phase 1 (constant pain from Specific myofascial examination of the severely active TrPs), patients may al- muscles is undertaken following a com- ready have such intense pain that they do plete general physical examination. not perceive an increase and cannot dis- When searching for active TrPs that are responsible for the patient's pain, it is es-

544 Myofascial Pain and Dysfunction: The Trigger Point Manual sential to know the precise location of the 3. DIFFERENTIAL DIAGNOSIS pain and to know which specific muscles can refer pain to that location. Muscles Two variants of myofascial pain syn- that could be causing the pain are tested dromes should be recognized: the myo- for restriction of passive stretch range of fascial pain modulation disorder, which motion and for pain at the shortened end leads to diagnostic confusion, and of active range of motion, as compared the post-traumatic hyperirritability syn- with uninvolved contralateral muscles. drome, which complicates management. Suspected muscles are also tested for In addition, either fibromyalgia or articu- mild to moderate weakness either by con- lar dysfunction can confusingly mimic a ventional isometric strength testing or chronic myofascial pain syndrome. Each during a lengthening contraction. Such requires an additional specific examina- weakness is not associated with atrophy tion technique and its own treatment ap- of the muscle. proach. The muscles showing abnormalities in To help a patient with chronic enig- these tests are the ones most likely to matic pain, the examiner must find have the taut bands and spot tenderness sources of pain that have been over- of the TrP. The taut bands are located by looked, and that means conducting exam- palpation and then tested for a local inations that were not previously per- twitch response and reproduction of the formed. After the history, the first order of patient's pain complaint by digital pres- business is to conduct a time-consuming, sure on the TrP. One must try to distin- detailed, complete physical examination guish active TrPs from latent ones, which looking for well-known causes of pain can also respond positively to the tests that were missed.21,34 Such an examina- described but are not responsible for a tion is rarely performed when the exam- pain complaint. Active TrPs are more irri- iner expects to find that the patient's pain table than latent TrPs and show greater is \"all in the head.\" responses on examination. If inactivation of the suspected TrP does not relieve the Myofascial Pain Modulation Disorder pain, it may either have been a latent TrP or it may nor have been the only active TrP The term \"myofascial pain modulation referring pain to that area. disorder\",45 adapted from a term used by Moldofsky,36 identifies a relatively small Examination for mechanical perpetuat- group of myofascial pain patients who ing factors requires careful observation of show a remarkable distortion of their pain the patient's postures, body symmetry, referral patterns. Instead of each active and movement patterns. A recent review47 TrP projecting pain to its expected loca- lists many of these factors that need to be tion (reference zone), the referred pain considered; they are discussed in detail and tenderness from all TrPs in a region on pages 104-114 in Volume l 5 6 and in converge on one common location. This Section 7 (Activation and Perpetuation of location may not be the expected zone of Trigger Points) of the muscle chapters in pain reference for any of the involved both volumes of THE TRIGGER POINT muscles. Characteristically, the conver- MANUAL. Common mechanical factors gent focus is the site of previous trauma that can influence many muscles are the or intense pain prior to onset of the pain round-shouldered, head-forward posture modulation disorder. These features re- with loss of normal lumbar lordosis, and semble the experimental observations of body asymmetries including a lower Reynolds and Hutchins.38 limb-length inequality and a small hemi- pelvis. The postural factors are discussed It appears that the aberrant referral pat- in the following section on treatment, in terns are caused by a distortion of sensory Chapter 2 of this volume, and, as appro- modulation in the central nervous sys- priate, in individual muscle chapters. tem. Many of these patients had previ- Body asymmetries are presented in detail ously experienced trauma or painful im- in Chapter 4 of this volume. Tightness of pact at the focus of pain, but often not of the iliopsoas and hamstring muscles can such severity that it would be expected to also seriously disrupt balanced posture. cause structural damage to the central nervous system. The mechanism behind

Chapter 28 / Chronic Myofascial Pain Syndrome 545 this sensory nervous system dysfunction strong sensory input of almost any kind is not clear, but possible mechanisms are can activate non-specific motor activity being explored in current neurosensory for an extended period of time. Similarly, research. in these patients, a strong sensory input can increase the excitability of the noci- Post-traumatic Hyperirritability ceptive system for long periods. In addi- Syndrome tion, these patients may show lability of the autonomic nervous system with skin The term \"post-traumatic hyperirritabil- temperature changes and swelling that re- ity syndrome\" was introduced24,46 to iden- solve with inactivation of regional TrPs. tify a limited number of patients with Since routine medical examination of myofascial pain who exhibit marked these suffering patients fails to show any hyperirritability of the sensory nervous organic cause for their symptoms, they system and of existing TrPs. This syn- are often relegated to \"crock\" status. drome follows a major trauma, such as an automobile accident, a fall, or a severe Any additional fall or motor vehicle ac- blow to the body that is apparently suffi- cident that would ordinarily be consid- cient to injure the sensory modulation ered minor can severely exacerbate the mechanisms of the spinal cord or brain hyperirritability syndrome for years. Un- stem. The patients have constant pain, fortunately, with successive traumas, the which may be exacerbated by the vibra- individual may become increasingly vul- tion of a moving vehicle, by the slamming nerable to subsequent trauma. A frequent of a door, by a loud noise (a firecracker at finding is a series of motor vehicle acci- close range], by jarring (bumping into dents over a period of several years. something or being jostled), by mild thumps (a pat on the back), by severe pain Similar phenomena have been de- (a TrP injection), by prolonged physical scribed as the cumulative trauma disorder,5 activity, and by emotional stress (such as the stress neuromyelopathic pain syn- anger). Recovery from such stimulation is drome,33 and as the jolt syndrome.8 slow. Even with mild exacerbations, it may take the patient many minutes or Fibromyalgia hours to return to the baseline pain level. Severe exacerbation of pain may require Fibromyalgia, previously called fibrositis, days, weeks, or longer to return to base- is officially defined as causing WIDE- line. SPREAD pain for at least 3 months. Digi- tal palpation of the patient must elicit These patients almost always give a pain at 11 or more of 18 prescribed tender history of having coped well in life prior point sites.59 An older term, fibrositis, has to their injury, having paid no more atten- been used in many ways,37 and anyone tion to pain than did their friends and who delves into that literature can easily family. They were no more sensitive to be confused by it. Throughout this cen- these stimuli than other persons. From tury, prior to 1977, the published descrip- the moment of the initial trauma, how- tions of fibrositis had a closer resem- ever, pain suddenly became the focus of blance to myofascial pain syndromes than life. They must pay close attention to the to what is now known as fibromyalgia.45 avoidance of strong sensory stimuli; they In 1977, Smythe and Moldofsky52 rede- must limit activity because even mild to fined fibrositis in terms that were similar moderate muscular stress or fatigue inten- to what is now called fibromyalgia. The sifies the pain. Efforts to increase exercise term fibrositis (in the sense that Smythe tolerance may be self-defeating. Such pa- and Moldofsky used it) has now been offi- tients, who suffer greatly, are poorly un- cially replaced59 by the term fibromyalgia, derstood and, through no fault of their which was introduced in 1981.61 own, are difficult to help. Many authors,3,6,20,41,44,57,60 including the In these patients, the sensory nervous authors of this volume, consider myofas- system behaves much as the motor sys- cial pain syndrome and fibromyalgia as tem does when the spinal cord has lost two separate conditions that need to be supraspinal inhibition. In the latter, a distinguished clinically. Others believe that a myofascial pain syndrome and

546 Myofascial Pain and Dysfunction: The Trigger Point Manual fibromyalgia are different aspects of basi- The myofascial examination includes cally the same condition, with each diag- palpation of the suspected muscles for nosis representing the ends of a spectrum tender spots in taut bands, which, when of signs and symptoms. An acute single- compressed, refer pain to the area of the muscle myofascial pain syndrome is patient's pain complaint and, when easily distinguished from fibromyalgia. snapped transversely, produce a local However, it can be difficult to distinguish twitch response. To examine for fibromy- chronic myofascial pain syndromes from algia, the prescribed tender point loca- fibromyalgia. The distinctions are partic- tions are examined only for tenderness; a ularly blurred if the patient has both relationship between the location of the fibromyalgia and chronic widespread myo- tender points and the distribution of the fascial pain that involves multiple re- patient's pain is not an issue. gions. On palpation, the diffusely tender mus- A number of characteristics may be cles of patients with fibromyalgia feel soft helpful in distinguishing one condition and doughy (except in specific areas, if from the other. Patients with fibromyalgia they also have TrPs in taut b a n d s 3 2 , 5 0 ) , are predominantly female (73-88% in six whereas the muscles of patients with studies).57 Men and women are nearly myofascial pain feel tense and are non- equally likely to have myofascial pain tender except at TrPs and in reference syndromes, as the senior author and other zones. authors51,53 have found. The patient with an acute myofascial pain syndrome typi- Muscles that exhibit TrPs also exhibit cally can identify the onset precisely as to some weakness without atrophy, but they time and place. Usually the muscle was are not particularly fatigable. Generalized subjected to momentary overload, e.g. an severe fatigue, rather than weakness, is automobile accident, a near fall, a sudden characteristic of fibromyalgia.3 and vigorous movement (sports activity), moving a heavy box, reacbing over to pick The chronicity of myofascial pain syn- something up from the floor, or getting dromes is caused by perpetuating factors into an automobile, although there may that usually are correctable; the chronic- be a lag of several hours to a day after the ity of fibromyalgia is inherent to the dis- initiating event before pain appears. Pa- ease. This distinction is not evident at ini- tients with chronic myofascial pain may tial evaluation. have difficulty identifying the onset so clearly. These patients are likely to have Some features are confusingly common more than a single myofascial pain syn- to both conditions. Disturbed, non-restful drome. In contrast, the symptoms of fibro- sleep may occur in either, but is not re- myalgia typically develop insidiously; quired for diagnosis. Over half of the des- these patients usually can identify no ignated tender point locations are also specific moment in time when their common muscle TrP sites.45 By defini- symptoms began. Thus, the onset of myo- tion, a latent or an active TrP at one of fascial pain characteristically relates those tender point sites would be counted much more strongly to muscular activity as a tender point. Recent studies indicate and specific movements than does fibro- that taut bands may be found not only in myalgia. patients with myofascial pain and in pa- tients with fibromyalgia, but also in \"nor- The orientation of the patient examina- mal\" subjects.14,58 This finding may have tion is quite different for the two condi- unexplored implications as to the rela- tions. For the diagnosis of myofascial tionship between the taut band and its pain, the clinician painstakingly identi- TrP. Many patients with fibromyalgia also fies precisely the distribution of each have active myofascial TrPs.58 pain complaint, looks for dysfunctional postures and asymmetries, and examines At this time, no specific cause of either the muscles to determine which ones fibromyalgia or myofascial TrPs has been show a restricted stretch range of motion. established. However, clinically, myofas- Restriction of motion is not a part of the cial pain caused by TrPs is primarily a fo- diagnosis of fibromyalgia. cal dysfunction of muscle, whereas fibro- myalgia is a systemic disease7,40,45 that also affects the muscles.2,25

Chapter 28 / Chronic Myofascial Pain Syndrome 547 Articular Dysfunction If one starts by correcting obvious mechanical perpetuating factors, myofas- We think of articular dysfunction either cial TrP therapies that were previously as joint hypomobility (including loss of ineffective are then likely to provide sig- joint play) that requires manual move- nificant relief and to encourage the pa- ment, mobilization, or manipulation to tient. Each component myofascial pain restore normal function, or as hypermo- syndrome should be analyzed and man- bility that requires stabilization. The term aged as a single-muscle syndrome in the somatic dysfunction is now commonly context of other TrPs in the same region. used and includes skeletal dysfunctions For patients with chronic pain, a home that are often treated by mobilization and program of stretch exercises is extremely manipulation, as well as myofascial dys- important, probably even more so than functions that are frequently treated with for patients with a myofascial pain syn- myofascial release techniques.19 drome of only one or two muscles. An understanding of the interface be- Setting specific goals as described by tween myofascial pain syndrome and ar- Materson34 is critical for patients with ticular dysfunction is one of the great chronic myofascial pain. The primary voids in our current knowledge of manual goal is to teach patients how to recognize medicine. The early work of Korr et a l . 2 9 , 3 0 specific TrP syndromes, how to employ on segmental facilitation describes modu- appropriate body positioning, and which lation of referred tenderness, motor activ- stretcb techniques to use for relief. This ity, and skin conductance changes more puts the patients in control. If they want than it describes modulation of pain. more relief, they know how to obtain it. If The facilitation of motor responsiveness they prefer to trade a given level of pain caused by articular dysfunction is espe- for the time and effort required to relieve cially pertinent to the myofascial pain it, that is their decision. They learn that syndrome, but remains essentially unex- control of the pain is in their bands. They plored with modern instrumentation. come to understand what constitutes Janda,28 in association with others,27 has abuse of their muscles (that will aggravate examined distortion of the normal se- the pain) and what measures will reduce quence of coordinated motor activity as- unnecessary overload of the muscles. sociated with skeletal asymmetries and They learn to converse with and listen to muscular imbalance. Lewit31 has empha- their muscles. sized the close clinical relationship be- tween myofascial pain syndromes and ar- Travell55 emphasized the importance of ticular dysfunction. having the patients, at the end of the office visit, recollect and write down the recom- 4. TREATMENT mendations given them. Before leaving the office, they must perform their correc- A chronic myofascial pain syndrome be- tive stretching exercises under supervi- came chronic because of perpetuating fac- sion according to the instructions in hand. tors that were unrecognized or were inad- equately managed. An identifying char- Mechanical Perpetuating Factors acteristic of a chronic myofascial pain syndrome is the initially unsatisfactory If the clinician selects for initial treatment response to specific myofascial therapy. a myofascial pain syndrome that is a ma- Relief is usually only temporary, lasting a jor source of pain, is likely to respond to few hours or days. However, with correc- TrP therapy, and has a mechanical per- tion of the perpetuating factors, the involved petuating factor that is readily correctable muscles become increasingly responsive to (such as sitting posture or lower limb- therapy. Occasionally, severe perpetuating length inequality), the patient will see factors render the TrPs so irritable that immediate benefits and will develop con- even the most gentle attempts at therapy fidence in the treatment. Additional cause more distress than relief. As prog- mechanical perpetuating factors relevant ress is made in resolving the perpetuating to the patient's pain should also be cor- factors, the involved muscles become in- rected promptly. creasingly treatable.

548 Myofascial Pain and Dysfunction: The Trigger Point Manual Many mechanical factors have been re- ciple of raising the top of the head away viewed in detail on pages 104-114 in Vol- from the shoulders should also be applied ume l 5 6 and in another publication.49 when leaning forward to bathe or eat, Each muscle chapter in THE TRIGGER thereby avoiding rolling the shoulder up POINT MANUAL discusses relevant per- and forward and dropping the head. petuating factors in Section 7 (Activation and Perpetuation of TrPs). Faulty posture For good seated posture, one's feet is a mechanical perpetuating factor that is must reach the floor; when a person's legs becoming increasingly common and seri- are short or a seat is too high, a flexible ous with the proliferation of computer footrest (small firm pillow, bean bag, or terminals and computerized work sta- sand bag) may be used to support the feet. tions. A hard telephone book is less desirable, but can be temporarily useful. The arms Postural training should be one of the should be supported on armrests that are first parts, if not the first part, of the treat- high enough to allow the individual to sit ment program. Kendall and McCreary28 erect with the elbows supported. Forearm described ideal standing postural align- support extensions can be adapted for ment, identified several types of faulty desk work when typing. When one sits on standing posture, and suggested thera- a sofa or at a desk, arm support can be peutic procedures for correction of the provided by using a lap board placed on a malalignments. pillow. The common round-shouldered, head- An alternate sitting position is one of forward posture is discussed briefly in sitting toward the front edge of a chair Chapter 2, pages 19-20. Faulty posture seat, placing one foot back under the can aggravate TrPs in many regions of the chair and the other foot forward. This bal- body and can also increase the tenderness anced position promotes an erect posture of fibromyalgia tender points.22 Its impor- with a natural, but not excessive, lumbar tance has been emphasized and re-em- curve. Another way to promote good sit- phasized by Brugger.4 ting alignment witb little effort is to place a pad at the back of the chair seat, directly In the seated individual, the \"slumped under the ischial tuberosities (not under posture,\" or fatigue posture, is character- the thighs). The padding tilts the pelvis ized by a flattened lumbar spine (loss of forward slightly to induce normal lumbar normal lordosis), sometimes by an in- lordosis, whicb, in turn, facilitates good creased dorsal kyphosis, by protracted upper body alignment. Having two ways scapulae, and usually by a flattened cervi- of sitting with good posture can be partic- cal spine with the head forward. This ularly useful for someone working at a posture leads to multiple muscle and desk. Frequent changes of position are joint problems in the trunk, upper limbs, needed to promote health of the muscles neck, and head, as well as limited respira- and intervertebral discs. tory function. Most important is patient awareness of For the seated slumped position, the the problem, understanding of its signifi- patient can improve postural alignment cance, and willingness to practice sitting by consciously raising the top of the head and standing erect. Following appropriate upward, keeping it slightly forward.1 This postural training (both \"static\" and dy- simple maneuver lifts the chest to an opti- namic), the patient can take responsibility mum position for respiratory function. A for the management of the pain that re- comparable alignment can be accom- sults from chronic postural strain and plished by \"putting a hollow\" in the low many activities of daily living. As pa- back. Since this erect posture (sitting tients exercise increasing control, they \"tall\") cannot be actively held for long improve both physically and emotionally. periods, the individual can achieve this without effort by positioning the buttocks Systemic Perpetuating Factors against the back of the chair and then placing a small roll behind the lumbar Systemic perpetuating factors should be spine (waist level). \"Reaching\" upward corrected as they are identified when lab- with the top of the head can be done sev- oratory test results become available. eral times a day as an exercise. The prin-

Chapter 28 / Chronic Myofascial Pain Syndrome 549 These multiple factors are discussed in minimized, and effort should be concen- detail on pages 114-156 in Volume l 5 6 trated on teaching what can be done by and summarized in later publication.49 the patient. Systemic factors are commonly over- looked, can be difficult to manage, and of- Associated Conditions ten make the difference between a suc- cessful and unsuccessful therapeutic out- Articular dysfunction and TrP tension in come for the patient. related muscles can perpetuate each other; in which case, both conditions Vitamin inadequacy is probably the must be corrected to obtain lasting bene- most common systemic perpetuating fac- fit. tor, and it has been experimentally dem- onstrated as important in patients with Addressing the myofascial pain syn- chronic pain.43 drome in patients who also have fibromy- algia can significantly improve their con- Another frequently overlooked sys- dition; they will still have fibromyalgia temic factor is marginal or subclinical hy- and should receive therapy for it, too.17 pothyroidism. Like vitamin inadequacies, The extent to which these two conditions it is correctable.54 adversely affect each other is not yet clearly established. Psychological Aspects If the patient is function oriented and has References developed few pain behaviors, the pro- gram described previously can be suc- 1. Barker S: The Alexander Technique. Bantam cessful. If the patient has lost self-esteem, is pain oriented, and has developed pain Books, New York, 1978. behaviors, the clinician is faced with a complex web of problems that often re- 2. Bennett RM: Muscle physiology and cold reac- quires an interdisciplinary team that in- tivity in the fibromyalgia syndrome. In The cludes a professional counselor in order Fibromyalgia Syndrome, Rheumatic Disease Clinics to restore the patient to function. Elimina- of North America, Vol. 15, edited by R.M. Bennett, tion of the original myofascial TrP cause of the patient's pain is an essential part of D.L. Goldenberg. W.B. Saunders, Philadelphia, the program. However, the pain is often perpetuated by poor sleep, inactivity, and 1989 (pp. 135-147). hesitancy to undertake the necessary home-stretching program. Teaching the 3. Bennett RM: Myofascial pain syndromes and patient improved coping skills may be a necessary first step to eliminate reinforce- the fibromyalgia syndrome: a comparative anal- ment of pain behaviors by well-meaning, ysis, Chap. 2. In Myofascial Pain and Fibromyalgia, but over-protective, significant others. Advances in Pain Research and Therapy, Vol. 17, The principles for accomplishing this are clearly presented by Fordyce.11 edited by J.R. Fricton, E.A. Awad. Raven Press, The effectiveness of this multi-pronged New York, 1990 (pp. 43-65). approach with emphasis on patient edu- 4. Briigger A: Die Erkrankungen des Bewegungsap- cation and on elimination of their TrPs was eloquently demonstrated experimen- parates und seines Nervensystems. Gustav Fischer tally by Graff-Radford et al.18 Verlag, New York, 1980. If patients with chronic pain are de- pressed, it is necessary to relieve their de- 5. Burnette JT, Ayoub MA: Cumulative trauma dis- pression. Inactivity aggravates it and ac- orders. Part I. The problem. Pain Management 2: tivity that gives them a sense of accom- plishment improves it. A regular exercise 196-209, 1989. program is very important. Antidepres- sant medication may be necessary, espe- 6. Campbell SM: Regional myofascial pain syn- cially if sleep is impaired. Treatments dromes. In The Fibromyalgia Syndrome, Rheumatic that are done to the patient should be Disease Clinics of North America, Vol. 15, edited by R.M. Bennett, D.L. Goldenberg. W.B. Saun- ders, Philadelphia, 1989 (pp. 31-44). 7. Caro XJ: Is there an immunologic component to the fibrositis syndrome? In The Fibromyalgia Syn- drome, Rheumatic Disease Clinics of North America, Vol. 15, edited by R.M. Bennett, D.L. Golden- berg. W.B. Saunders, Philadelphia, 1989 (pp. 169-186). 8. Elson LM: The jolt syndrome. Muscle dysfunc- tion following low-velocity impact. Pain Man- agement 3 : 3 1 7 - 3 2 6 , 1 9 9 0 . 9. Fields HL: Pain. McGraw-Hill, New York, 1 9 8 7 (pp. 209-214). 10. Fishbain DA, Goldberg M, Meagher BR, et al.: Male and female chronic pain patients catego- rized by DSM-III psychiatric diagnostic criteria. Pain 2 6 : 1 8 1 - 1 9 7 , 1 9 8 6 . 1 1 . Fordyce WE: Behavioral Methods for Chronic Pain and Illness. C.V. Mosby, St. Louis, 1 9 7 6 .

550 Myofascial Pain and Dysfunction: The Trigger Point Manual 12. Fricton JR: Myofascial pain syndrome. Neurol malities of the musculoskeletal system. Acta Clin 7:413-427, 1 9 8 9 . Neurovegetativa 2 5 : 5 8 9 - 6 0 6 , 1964. 3 1 . Lewit K: Manipulative Therapy in Rehabilitation of 13. Fricton JR: Myofascial pain syndrome. Charac- the Motor System. Butterworths, London, 1985. teristics and epidemiology, Chapter 5. In Myo- fascial Pain and Fibromyalgia, Advances in Pain 32. Lewit K: Personal communication, 1989. Research and Therapy, Vol. 17, edited by J.R. Fricton, E.A. Awad. Raven Press, New York, 33. Margoles MS: Stress neuromyelopathic pain 1990 (pp. 107-127, see pp. 118-121). syndrome (SNPS): report of 333 patients. J 14. Fricton JR: Personal communication, 1991. Neurol Orthop Surg 4 : 3 1 7 - 3 2 2 , 1 9 8 3 . 15. Fricton JR, Kroening R, Haley D, Siegert R: Myo- 34. Materson RS: Assessment and diagnostic tech- fascial pain syndrome of the head and neck: A niques, Chapter 5. In Innovations in Pain Manage- review of clinical characteristics of 164 patients. ment, edited by R.S. Weiner, Vol. 1. Paul M. Oral Surg 6 0 : 6 1 5 - 6 2 3 , 1 9 8 5 . Deutsch Press, 1990 (pp. 5-3 to 5-25). 16. Gamsa A: Is emotional disturbance a precipita- tor or a consequence of chronic pain? Pain 42: 35. Mense S: Physiology of nociception in muscles, 183-195, 1990. Chapter 3. In Myofascial Pain and Fibromyalgia, Advances in Pain Research and Therapy, Vol. 17, 17. Goldenberg DL: Treatment of fibromyalgia syn- drome. In The Fibromyalgia Syndrome, Rheumatic edited by J.R. Fricton, E.A. Awad. Raven Press, Disease Clinics of North America, Vol. 15, edited by R.M. Bennett, D.L. Goldenberg. W.B. Saun- New York, 1990 (pp. 67-85). ders, Philadelphia, 1989 (pp. 61-71). 36. Moldofsky H, Tullis C, Lue FA: Sleep related 18. Graff-Radford SB, Reeves JL, Jaeger B: Manage- ment of chronic headache and neck pain: the ef- myoclonus in rheumatic pain modulation disor- fectiveness of altering factors perpetuating myo- der (fibrositis syndrome). J Rheumatol 7 3 : 6 1 4 - fascial pain. Headache 2 7 : 1 8 6 - 1 9 0 , 1987. 617, 1986. 19. Greenman PE: Principles of Manual Medicine. Wil- liams & Wilkins, Baltimore, 1989 (pp. 106-112). 37. Reynolds MD: The development of the concept of fibrositis. J Hist Med Allied Sci 3 8 : 5 - 3 5 , 1983. 20. Hench PK: Evaluation and differential diagnosis of fibromyalgia. Approach to diagnosis and 38. Reynolds OE, Hutchins HC: Reduction of cen- management. In The Fibromyalgia Syndrome, Rheumatic Disease Clinics of North America, Vol. tral hyper-irritability following block anesthesia 15, edited by R.M. Bennett, D.L. Goldenberg. of peripheral nerve. Am J Physiol 7 5 2 : 6 5 8 - 6 6 2 , W.B. Saunders Company, Philadelphia, 1989 (pp. 19-29). 1948. 39. Rosomoff HL, Fishbain DA, Goldberg M, et al.: 21. Hendler N: The psychiatrist's role in pain man- agement, Chapter 6. In Innovations in Pain Man- Physical findings in patients with chronic in- agement, Vol. 1, edited by R.S. Weiner. Paul M. Deutsch Press, Orlando, 1990 (pp. 6-1 to 6-36, tractable benign pain of the neck and/or back. see pp. 6 - 7 , 6 - 2 0 to 6 - 2 3 ) . Pain 3 7 : 2 7 9 - 2 8 7 , 1 9 8 9 . 22. Hiemeyer K, Lutz R, Menninger H: Dependence 4 0 . Russell IJ: Neurohormonal aspects of fibromy- of tender points upon posture—key to the un- algia syndrome. In The Fibromyalgia Syndrome, derstanding of fibromyalgia syndrome. J Man Rheumatic Disease Clinics of North America, Vol. Med 5 : 1 6 9 - 1 7 4 , 1 9 9 0 . 15, edited by R.M. Bennett, D.L. Goldenberg. 23. Institute of Medicine: Pain and Disability: Clinical, Behavioral and Public Policy Perspectives. Na- W.B. Saunders, Philadelphia, 1989 (pp. 1 4 9 - tional Academy Press, Washington, D.C., May 1987. 168). 24. Ibid. (p. 2 8 8 ) . 41. Scudds RA, Trachsel LC, Luckhurst BJ, Percy JS: 25. Jacobsen S, Danneskiold-Samsee B: Muscle A comparative study of pain, sleep quality and function in patients with primary fibromyalgia syndrome—an overview. J Man Med 5 : 1 5 5 - 1 5 7 , pain responsiveness in fibrositis and myofascial 1990. pain syndrome. J Rheumatol Suppl 7 9 : 1 2 0 - 1 2 6 , 26. Janda V: Muscle Function Testing. Butterworths, 1989. London, 1983. 42. Sessle BJ: Central nervous system mechanisms 27. Jull GA, Janda V: Muscles and motor control in of muscular pain, Chapter 4. In Myofascial Pain low back pain: assessment and management, and Fibromyalgia, Advances in Pain Research and Chapter 10. In Physical Therapy of the Low Back, Therapy, Vol. 17, edited by J.R. Fricton, E.A. edited by L.T. Twomey and J.R. Taylor. Church- ill Livingstone, New York, 1987 (pp. 253-278). Awad. Raven Press, New York, 1990 (pp. 8 7 - 28. Kendall FP, McCreary EK: Muscles, Testing and 105). Function, Ed. 3. Williams & Wilkins, Baltimore, 1983. 43. Shealy CN: Vitamin B6 and other vitamin levels in chronic pain patients. Clin J Pain 2 : 2 0 3 - 2 0 4 , 29. Korr IM, Thomas PE, Wright HM: Symposium on the functional implications of segmental fa- 1987. cilitation. J Am Osteopath Assoc 5 4 : 2 6 5 - 2 8 2 , 44. Sheon RP, Moskowitz RW, Goldberg VM: Soft 1955. Tissue Rheumatic Pain, Ed. 2. Lea & Febiger, Phil- 30. Korr IM, Wright HM, Chace JA: Cutaneous pat- terns of sympathetic activity in clinical abnor- adelphia, 1987. 45. Simons D: Muscular Pain Syndromes, Chapter 1. In Myofascial Pain and Fibromyalgia, Advances in Pain Research and Therapy, Vol. 17, edited by J.R. Fricton and E.A. Awad. Raven Press, New York, 1990 (pp. 1-41). 46. Simons DG: Myofascial pain syndrome due to trigger points, Chapter 4 5 . In Rehabilitation Medi- cine, edited by J. Goodgold. C.V. Mosby Co., St. Louis, 1988 (pp. 686-723). 47. Simons DG: Myofascial pain syndromes. In Cur- rent Therapy of Pain, edited by K.M. 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Chapter 28 / Chronic Myofascial Pain Syndrome 551 48. Simons  DG:  Symptomatology  and  clinical  patho‐ Pain and Fibromyalgia, Advances in Pain Research physiology  of  myofascial  pain.  Rheuma und Schmerz, State of the Art Lectures, edited  by  M.  and Therapy, Vol.  17,  edited  by  J.R.  Fricton,  E.A.  Zimmermann,  H.  Zeidler,  H.  Ehlers.  Verlag:  Awad. Raven Press, New York, 1990 (pp. 129‐137).  Ge‐sellschaft  zum  Studium  des  Schmerzes,  Heidel‐ 56. Travell  JG,  Simons  DG:  Myofascial Pain and Dys- berg,  pp.  29‐37,  1990.  (ISBN:  3‐980  1528‐1‐2).  Also,  Der function: The Trigger Point Manual. Williams  &  Schmerz 5[Suppl. 1/:S29‐S37, 1991.  Wilkins, Baltimore, 1983.  57. Wolfe F: Fibrositis, fibromyalgia, and musculoskeletal  49. Simons  DG,  Simons  LS:  Chronic  myofascial  pain  disease:  the  current  status  of  the  fibrositis  syndrome.  syndrome,  Chapter  42.  In  Handbook of Chronic Pain Arch Phys Med Rehabil 69:527‐531, 1988.  Management, edited  by  C.  D.  Tol‐lison.  Williams  &  58. Wolfe  F,  Simons D,  Fricton  J, et al.: The fibromyalgia  Wilkins, Baltimore, 1989 (pp. 509‐529).  and  myofascial  pain  syndromes:  a  study  of  tender  points and trigger points in persons with fibromyalgia,  50. Simons L: Personal communication, 1989.  myofascial  pain  syndromes  and  no  disease.  Arthritis 51. Skootsky  SA,  Jaeger  B,  Oye  RK:  Prevalence  of  Rheum 33 (Sup):Sl37, Abst. No. D22, 1990.  59. Wolfe  F,  Smythe  HA,  Yunus  MB,  et  al.: American  myofascial  pain  in  general  internal  medicine  practice.  College  of  Rheumatology  1990  Criteria  for  the  West J Med 151:157‐160, 1989.  Classification  of  Fibromyalgia:  Report  of  the  52. Smythe  HA,  Moldofsky  H:  Two  contributions  to  Multicenter  Criteria  Committee.  Arth Rheum 33: understanding  of  the  ʺfibrositisʺ  syndrome.  Bull 160‐172, 1990.  Rheum Dis 28:928‐931, 1977.  60. Yunus  M,  Kalyan‐Raman  UP,  Kalyan‐Raman  K:  53. Sola  AE,  Rodenberger  ML,  Gettys  BB:  Incidence  of  Primary  fibromyalgia  syndrome  and  myofascial  pain  hypersensitive  areas  in  posterior  shoulder  muscles.  syndrome:  clinical  features  and  muscle  pathology.  Am J Phys Med 34:585‐590, 1955.  Arch Phys Med Rehabil 69:451‐454, 1988.  54. Sonkin  LS:  Endocrine  disorders,  locomotor  and  61. Yunus M, Masi AT, Calabro JJ, Miller KA, Feigenbaum  temporomandibular  joint  dysfunction,  Chapter  6.  In  SL:  Primary  fibromyalgia  (fibrositis):  clinical  study  of  Clinical Management of Head, Neck and TMJ Pain 50  patients  with  matched  normal  controls.  Semin Arthritis Rheum 77:151‐171, 1981.  and Dysfunction, edited  by  H.  Gelb.  W.B.  Saunders  Company, Philadelphia, 1977 (pp. 158‐164).  55. Travell  JG:  Chronic  myofascial  pain  syndromes.  Mysteries  of  the  history,  Chapter  6.  In  Myofascial  

Appendix—Postexercise Muscle Soreness Reviews of postexercise (delayed-onset) Training Effect muscle soreness (not \"charley horse,\" muscle strain or tear, cramps, or chronic Training with mild slow eccentric exercise leg pain) were published as early as prior to vigorous eccentric contractions 190231 and, more recently, in 1983,19 in protects against postexercise soreness. In 1984,2 and in 1986.38 Hough31 in 1902 had addition, a vigorous bout of exercise per- not yet recognized the important differ- formed a week after a first vigorous bout ence between concentric (shortening) and caused significantly less muscle shorten- eccentric (lengthening) contractions. In ing, less creatine kinase release into the many ways, the soreness of muscles fol- blood, and less pain.11 A similar reduced lowing exercise is similar to a myofascial effect was also observed 2 weeks follow- pain syndrome, but in other ways, it is ing a strenuous bout of eccentric exer- different. Because postexercise muscle cise.42 The same was true when a modest soreness has been so well studied, under- exposure to eccentric exercise preceded standing the similarities and differences the strenuous test by 2 weeks.12 Although in the two conditions should help to bet- mild daily eccentric exercise for 1 or 2 ter understand myofascial trigger points weeks prior to strenuous exercise pro- (TrPs). The features of delayed-onset vided protection, the same work ex- muscle soreness are reviewed here and pended as concentric exercise did not.52 are related to TrPs as to features that are Another study found that training effect similar, those that are different, and those could still be seen 6 weeks following a that have an equivocal relationship. single bout of exercise, and that the train- ing effect is specific to eccentric exercise.9 Similarities Intensive progressive eccentric bicycle Muscle Shortening ergometry exercise for 8 weeks increased eccentric work capacity 375% with little In two separate studies,11,12 vigorous ec- change in maximal dynamic concentric centric exercise produced significant muscle strength.24 Biopsies taken before shortening of the biceps brachii muscle and immediately after a maximal eccen- on the day following, but not immedi- tric exercise stint showed increased num- ately following, the exercise. The muscle bers of type 2C fibers and selective glyco- gradually returned close to its baseline gen depletion of type 2B fibers. This indi- length during the next 4 days. Reduced cates that type 2 fibers were selectively ability to shorten the muscle fully on a affected by the exercise. Ultramicroscopi- voluntary basis followed a similar time cally, the fine structure was well pre- course. served. An increased volume density of mitochondria was seen with no change in Muscles with active or latent TrPs are Z-band widths.24 also restricted in stretch length and in ac- tive shortening, but these restrictions re- Vigorous eccentric contractions per- main as long as the TrPs are present. formed at long muscle length caused markedly greater weakness of the muscle 552 that lasted several times longer than the

Appendix 553 weakness caused by eccentric contrac- Clinical experience has shown that tions performed at short muscle length. postexercise stiffness may be prevented This occurred despite the fact that the or markedly reduced by 500 mg or more contractions performed at short muscle of vitamin C (preferably timed release) length were stronger (produced more taken so that it is available at the time of work) than those at long muscle the exercise. To our knowledge, this has length.34,44 not been tested in controlled experiments (see Volume 1, page 139).58 Conditioning of muscles also makes them more resistant to activation of myo- Differences fascial TrPs. Whether this protective ef- The sharpest contrasts between postex- fect against the development of TrPs is ercise muscle soreness and a myofascial equally specific to training by eccentric pain syndrome are in the location of the exercise has not been tested experimen- pain and tenderness, and in the time tally. course of symptoms. In addition, marked serum enzyme changes occur in associa- Resting Electromyographic Activity tion with postexercise muscle soreness Careful quantification of electromy- but not as a rule in myofascial pain syn- ographic (EMG) activity in the medial and dromes. The weakness of each apparently lateral heads of the gastrocnemius muscle stems from different causes. Static at 24, 48, and 72 hours after strenuous ec- stretching and warm-up exercises do not centric exercise showed no increase in prevent the muscle soreness from exhaus- average EMG activity in the 11 subjects tive eccentric exercise,30 but are helpful studied.6 Similarly, the biceps brachii32 in relieving pain and stiffness associated and other muscles33 were electrically si- with myofascial TrPs. lent at times when there was pain and re- striction of elbow extension following ec- Location of Pain and Tenderness centric exercise.32 During episodes of delayed-onset muscle soreness, pain and tenderness are often This demonstrates that neither the described as generalized throughout most shortening of the muscle, nor its painful- of the muscle belly.2 In other studies, the ness, are caused by true muscle spasm. tenderness is described as localized at the Similarly, tense muscles with myofascial region of the distal musculotendinous TrPs show no increased resting EMG ac- junction.2,47 tivity.22,53 In myofascial pain syndromes, the pain Response to Treatment is primarily referred, often to areas well beyond the muscle that harbors the re- Most (but not all) studies have shown that sponsible TrPs. Often, the patient is una- anti-inflammatory drugs provide little or ware of the TrP in the muscle that is caus- no relief of postexercise muscle soreness, ing the pain. In myofascial syndromes, weakness, and shortening.14,21,33,49 Because the local tenderness is most marked at the prostaglandin E2 may be important in TrP and extends with reduced intensity muscle repair, prostaglandin blockers, along the taut band associated with the such as aspirin, may be not only useless, TrP. Tenderness may extend to and in- but actually detrimental to restoration of clude the musculotendinous attachment the contractile elements.15 Similarly, aspi- of that band. Tenderness is also present in rin has not been found useful in the relief the pain reference zones of TrPs. of pain referred from myofascial TrPs.59 Time Course Vitamin E was ineffective in reducing Muscle soreness appears between 8 and the soreness, loss of range of motion, and 24 hours following eccentric exercise,57 weakness that resulted from exhausting increases in intensity to reach a peak at eccentric exercise;20 nor has it been found 24-72 hours, and is usually gone in 5-7 helpful, generally, in the management of myofascial pain syndromes except for some cases of nocturnal calf cramps asso- ciated with gastrocnemius TrPs.

554 Myofascial Pain and Dysfunction: The Trigger Point Manual days. Subjects often describe such exer- connective tissues than from damage to cised muscles as \"stiff\" and \"tender.\"2 the contractile elements. Soreness peaked at 24—48 hours follow- No increase in serum enzymes has been ing eccentric exercise depending on the found in association with chronic myo- age and training of the subjects and the fascial pain syndromes, unless the patient exercise protocol u s e d . 1 0 , 1 1 , 3 2 , 3 3 , 4 1 , 5 6 , 5 7 Vig- has some coincidental disease. Acute-on- orous exercise every 2 weeks produced set myofascial pain syndromes have not soreness that peaked in 48 hours after the been critically tested for these enzyme first bout and in 24 hours after subse- changes, partly because the effects of quent bouts.42 Soreness may not be gone trauma frequently associated with activa- until the fifth day,41,42 the seventh day,32 tion of the TrPs would confuse the issue. or until 2 weeks47 after vigorous eccentric exercise. Weakness The weakness caused by TrPs and that The histological damage from a severe caused by postexercise muscle soreness bout of eccentric exercise may take as appear to be caused by different mechan- long as 12 weeks for recovery.15 isms. Paavo and associates47 found that 40 minutes of vigorous eccentric exercise re- After sudden trauma, pain referred duced strength to 50% of baseline, from acute myofascial TrPs appears im- whereas corresponding concentric exer- mediately at the time of injury or within a cise reduced it only to 80% of baseline. few hours. In chronic myofascial pain Sargeant and Dolan50 reported that the re- syndromes due to repetitive overload and duction in maximum voluntary contrac- fatigue, the pain usually develops gradu- tion persisted up to 96 hours after eccen- ally over a period of days or weeks, some- tric exercise. In a study of bouts of exer- times months. After either type of onset, cise repeated every 2 weeks,42 it took 2 the myofascial pain may gradually re- weeks for strength to recover after the ini- solve spontaneously or run a chronic tial bout, and only one week or less after course. subsequent bouts. The weakness is not primarily due to inhibition by pain be- Response to Treatment cause it is most marked immediately fol- Two muscle-stretching techniques,41 myo- lowing the exercise, it is demonstrable by fascial manipulation and a muscle-energy direct electrical stimulation, and some re- technique, had no effect on the muscle covery from weakness may occur in 24 soreness, but stretch is effective for treat- hours, prior to the time of maximum sore- ment of myofascial pain. ness.42 The weakness of sustained maxi- mum isometric contraction is not due to Blood Indices neuromuscular junction failure.36 The Following vigorous eccentric exercise, weakness associated with postexercise some indicators of muscle damage peak soreness appears to stem from damage to in the blood much earlier than others. the contractile apparatus of the muscle as evidenced by so many enzyme changes. The concentration of plasma in- terleukin-1 (IL-1),16 total thiobarbituric Both active and latent TrPs characteris- acid-reactive substances,37 lactic dehydro- tically cause a modest degree of muscle genase (LDH),25,37,57 serum creatine phos- weakness that is not due to conscious phokinase (CPK),57 aspartate aminotrans- avoidance of pain. The weakness persists ferase (AST),37 and serum glutamic ox- as long as the TrPs remain. This mild per- aloacetic acid transaminase (SGOT)25,57 all sistent weakness caused by TrPs is proba- peaked within the first 24 hours. How- bly caused by reflex inhibition. ever, plasma creatine kinase (CK) concen- tration11,18,33,42,43 and muscle uptake of the Relationship Unclear radioisotope 99m technetium pyrophos- Swelling phate45 may not peak until 5 or 6 days af- Swelling appeared clinically in sore mus- ter exercise. Blood lactic acid was un- cles following strenuous eccentric exer- changed following eccentric exercise.51 Jones et al.33 concluded that the pain is more likely to arise from stress on the

Appendix 555 cise.47 An increase of 11% and 17% in Biopsies of human muscles exposed to weight caused by edema was observed in exhausting eccentric exercise27, 28 showed rabbit triceps surae muscles 24 and 48 no abnormality of fiber organization or re- hours, respectively, following vigorous generation at the cellular level. At the eccentric exercise, but not 6 days follow- subcellular level, severe disorganization ing exercise.7 Biopsies of human anterior of the striation pattern was seen within an tibial muscles 48 hours after eccentric hour following the exercise and at 2 and 3 work showed a significantly higher water days thereafter. Immediately after exer- content than contralateral muscles fol- cise, nearly half of the myofibrillar Z lowing concentric work.26 Volume bands (which join one sarcomere to the plethysmography of the leg on the side of next) showed marked broadening, stream- exercised triceps surae muscles showed ing (scattered broadening), and some- significant increase in calf volume 24, 48, times total disruption. Most remarkable and 72 hours following exercise, com- was the observation that sarcomeres near pared to the non-exercised contralateral the affected Z-bands were either super- leg.6 A comparison of tissue pressures contracted or disorganized and out of reg- and biopsy following eccentric exercise of ister with the Z-bands. Seven days after one tibialis anterior muscle and after con- the exercise, much recovery had oc- centric exercise of the other26 found mus- curred. Supercontraction is characteristic cle fiber swelling as a predominant fea- of a contraction knot, and one was illus- ture only after eccentric exercise. A trated.27 comparable study56 and an intramuscular pressure study33 of the forearm flexors Biopsies of the vastus lateralis muscle found no significant difference between taken before, and up to 6 days following, the control and exercised limbs. How- strenuous eccentric exercise were ob- ever, the forearm flexors are not prone to served for immunocytological changes. developing a compartment syndrome. Only the 3-day specimens showed re- markable changes. Intermediate filament The question as to whether the region protein responded with microscopic im- in the vicinity of myofascial TrPs is char- munofluorescence using an antibody spe- acterized by edema has not been clearly cific to desmin. The authors23 suggested resolved. Two reports4,8 of biopsies in fi- that the abundant longitudinal \"desmin\" brositis described the presence of intersti- extensions and strongly autofluorescent tial fluid. Their descriptions of \"fibrosi- granules represented an increased synthe- tis\" suggest that the authors were study- sis of desmin and reorganization of the ing persons with myofascial TrPs (rather cytoskeletal system in order to restructure than fibromyalgia as the latter is now per- the distorted myofibrillar elements. ceived by rheumatologists).5 Friden and co-workers,27,28 McCully,38 Histological Differences. The histological and Armstrong3 concluded that the pri- changes that appear after vigorous eccen- mary lesion in delayed-onset muscle sore- tric exercise indicate exposure of the ness was disruption of myofibrillar struc- muscle to the stress of that specific ture due to mechanical overload rather mechanical overload39 rather than to met- than to a metabolic disturbance. abolic distress. This is consistent with the much greater mechanical efficiency of ec- A subsequent biopsy study of severe ec- centric, as compared to concentric, exer- centric bicycle exercise46 showed myo- c i s e . 1 3 , 3 5 , 4 6 - 4 8 , 5 0 The net mechanical effi- fibrillar tearing and edema immediately ciency of concentric and eccentric work after exercise. In this study, after 10 days, was computed based on force-plate mea- there was myofibrillar necrosis, inflam- surement of mechanical work and analy- matory cell infiltration, and no evidence sis of expired air for energy expenditure.35 of myofibrillar regeneration. At that time, The mechanical efficiency of concentric muscle glycogen was still depleted in work averaged 19.4%. The efficiency of both type 1 and type 2 fibers. These eccentric work, in many instances, ex- changes cannot be attributed simply to in- ceeded 100%; eccentric work was pro- creased metabolic demand caused by duced with much less metabolic cost. muscular activity. No biopsy studies of acute myofascial TrPs are known. However, most reports of

556 Myofascial Pain and Dysfunction: The Trigger Point Manual fibrositis prior to 1977 fit the description metabolites, including phosphocreatine of chronic myofascial TrP syndromes and adenosine triphosphate (ATP). This much better than they fit the current defi- result could be attributed to a defect in nition of fibromyalgia.54 This terminology oxidative metabolism, to tissue necrosis issue is clarified in Chapter 28 of this associated with the ultramicroscopic le- volume, under Fibromyalgia. Several sions described previously, or to sarco- studies of fibrositis (using the pre-1977 lemmal damage that permitted influx of definition) have reported contraction inorganic phosphate.1 knots,29,40,55 and one describes disintegra- tion of the actin filaments where they No magnetic resonance imaging or connect to the Z-bands.17 spectroscopy studies of myofascial TrPs are known to us. The acute activation of myofascial TrPs is strongly, but not exclusively, related to These observations on muscle soreness overload caused by vigorous lengthening induced by vigorous eccentric exercise do contractions. Superimposed reflex con- not apply to the therapeutic value of a tractions may contribute additional over- limited number of slow eccentric contrac- load responsible for activating TrPs. In tions used to inactivate myofascial TrPs, these acute situations, the myofascial or to recondition muscles, as discussed TrP-inducing overload is an instantane- under Sit-ups and Sit-backs in Volume 1 ous one-time stress as compared to the (see Fig. 49.11).60 cumulative stress effects of prolonged ec- centric exercise. References A myofascial TrP may result from a 1. Aldridge R, Cady EB, Jones DA, et al.: Muscle more focal and severe mechanical disrup- pain after exercise is linked with an inorganic tion of the type described in muscle sore- phosphate increase as shown by P3 1 NMR. Biosci ness, but one that establishes a self-sus- Rep 6 : 6 6 3 - 6 6 7 , 1986. taining feedback loop through the central nervous system.53 2. Armstrong RB: Mechanisms of exercise-induced delayed onset muscular soreness: a brief review. Magnetic Resonance Findings. Magnetic Med Sci Sports Exerc 7 6 : 5 2 9 - 5 3 8 , 1984. resonance imaging18 of runners with post- exercise muscle soreness showed bright 3. Armstrong RB: Muscle damage and endurance rims around both heads of the gastrocne- events. Sports Med 3 : 3 7 0 - 3 8 1 , 1986. mius muscle and the soleus muscle im- mediately after vigorous exercise. How- 4. Awad EA: Interstitial myofibroses: hypothesis ever, after 24-72 hours, when pain and of the mechanism. Arch Phys Med 54:440—453, rhabdomyolysis had developed, signal in- 1973. tensity was markedly increased only at the medial head of the gastrocnemius 5. Bennett RM, Goldenberg DL (editors): The fibro- muscle. In trained athletes, imaging ab- myalgia syndrome. Rheum Dis Clin North Am 15: normalities tended to be located near the 1-191, 1989. attachments of the muscles, in the region of myotendinous junctions. Magnetic res- 6. Bobbert MF, Hollander AP, Huijing PA: Factors onance image abnormalities appeared in delayed onset muscular soreness of man. Med preceding other evidence of injury, in- Sci Sports Exerc 1 8 : 7 5 - 8 1 , 1 9 8 6 . cluding pain and histochemical changes, and lasted as long as 2 weeks following 7. Brendstrup P: Late edema after muscular exer- resolution of other changes. cise. Arch Phys Med Rehabil 4 3 : 4 0 1 - 4 0 5 , 1962. Spectra obtained by magnetic reso- 8. Brendstrup P, Jespersen K, Asboe-Hansen G: nance spectroscopy before and immedi- Morphological and chemical connective tissue ately after eccentric exercise showed nor- changes in fibrositic muscles. Ann Rheum Dis 16: mal resting phosphorylated metabolite 4 3 8 ^ 4 0 , 1957. levels and normal intracellular pH.1 How- ever, 24 hours later, when muscle sore- 9. Byrnes WC, Clarkson PM: Delayed onset muscle ness was apparent, inorganic phosphate soreness and training. Clin Sports Med 5 : 6 0 5 - levels were increased an average of 42%. 614, 1986. No significant changes occurred in other 10. Clarkson PM, Byrnes WC, McCormick KM, et al.: Muscle soreness and serum creatine kinase ac- tivity following isometric, eccentric, and con- centric exercise. Int J Sports Med 7 : 1 5 2 - 1 5 5 , 1986. 11. Clarkson PM, Dedrick ME: Exercise-induced muscle damage, repair, and adaptation in old and young subjects. J Gerontol 4 3 : M 9 1 - M 9 6 , 1988. 12. Clarkson PM, Tremblay I: Exercise-induced muscle damage, repair, and adaptation in humans. J Appl Physiol 6 5 : 1 - 6 , 1 9 8 8 . 13. Dick RW, Cavanagh PR: An explanation of the upward drift in oxygen uptake during prolonged

Appendix 557 sub-maximal downhill running. Med Sci Sports Tiengo ef al. Raven Press, Ltd., New York, 1987 Exerc 7 9 : 3 1 0 - 3 1 7 , 1987. (pp. 207-218). 14. Donnelly AE, McCormick K, Maughan RJ, et al.: 34. Jones DA, Newham DJ, Torgan C: Mechanical Effects of a non-steroidal anti-inflammatory influences on long-lasting human muscle fa- drug on delayed onset muscle soreness and in- tigue and delayed-onset pain. J Physiol 4 7 2 : 4 1 5 - dices of damage. Br J Sports Med 2 2 : 3 5 - 3 8 , 1 9 8 8 . 427, 1989. 15. Evans WJ: Exercise-induced skeletal muscle 35. Komi PV, Kaneko M, Aura O: EMG activity of damage. Phys Sportsmed 7 5 : 8 9 - 1 0 0 , 1987. the leg extensor muscles with special reference to mechanical efficiency in concentric and ec- 16. Evans WJ, Meredith CN, Cannon JG, et al.: Meta- centric exercise. Int J Sports Med (8 Suppl) 1 : 2 2 - bolic changes following eccentric exercise in 29, (Mar) 1987. trained and untrained men. J Appl Physiol 61: 1864-1868, 1986. 36. Kukulka CG, Russell AG, Moore MA: Electrical and mechanical changes in human soleus mus- 17. Fassbender HG: Pathology of Rheumatic Diseases. cle during sustained maximum isometric con- Springer-Verlag, New York, 1975 (Chapter 13, tractions. Brain Res 3 6 2 : 4 7 - 5 4 , 1 9 8 6 . pp. 303-314). 37. Maughan RJ, Donnelly AE, Gleeson M, et al.: 18. Fleckenstein JL, Weatherall PT, Parkey RW, ef Delayed-onset muscle damage and lipid perox- al.: Sports-related muscle injuries: evaluation idation in man after a downhill run. Muscle with MR imaging. Radiology 7 7 2 : 7 9 3 - 7 9 8 , 1989. Nerve 7 2 : 3 3 2 - 3 3 6 , 1 9 8 9 . 19. Francis KT: Delayed muscle soreness: a review. 38. McCully KK: Exercise-induced injury to skeletal J Orthop Sport Phys Ther 5 : 1 0 - 1 3 , 1983. muscle. Fed Proc 4 5 : 2 9 3 3 - 2 9 3 6 , 1 9 8 6 . 20. Francis KT, Hoobler T: Failure of vitamin E and 39. McCully KK, Faulkner JA: Injury to skeletal delayed muscle soreness. Ala Med 5 5 : 1 5 - 1 8 , muscle fibers of mice following lengthening 1986. contractions. J Appl Physiol 5 9 : 1 1 9 - 1 2 6 , 1 9 8 5 . 21. Francis KT, Hoobler T: Effects of aspirin on 40. Miehlke K, Schulze G, Eger W: Klinische und delayed muscle soreness. J Sports Med Phys Fit- experimentelle Untersuchungen zum Fibrositis- ness 2 7 : 3 3 3 - 3 3 7 , 1987. syndrom. Z Rheumaforsch 7 9 : 3 1 0 - 3 3 0 , 1 9 6 0 . 22. Fricton JR, Auvinen MD, Dykstra D, et al.: Myo- 41. Molea D, Murcek B, Blanken C, et al.: Evaluation fascial pain syndrome: electromyographic of two manipulative techniques in the treatment changes associated with local twitch response. of postexercise muscle soreness. J Am Osteopath Arch Phys Med Rehabil 6 6 : 3 1 4 - 3 1 7 , 1985. Assoc 8 7 : 4 7 7 - 4 8 3 , 1987. 23. Friden J, Kjorell U, Thornell L-E: Delayed mus- 42. Newham DJ, Jones DA, Clarkson PM: Repeated cle soreness and cytoskeletal alterations: an im- high-force eccentric exercise: effects on muscle munocytological study in man. Int J Sports Med pain and damage. J Appl Physiol 6 3 : 1 3 8 1 - 1 3 8 6 , 5:15-18, 1984. 1987. 24. Friden J, Seger J, Sjostrom M, et al.: Adaptive re- 4 3 . Newham DJ, Jones DA, Edwards RHT: Plasma cre- sponse in human skeletal muscle subjected to atine kinase changes after eccentric and concentric prolonged eccentric training. Int J Sports Med 4: contractions. Muscle Nerve 9 : 5 9 - 6 3 , 1986. 177-183, 1983. 44. Newham DJ, Jones DA, Ghosh G, et al.: Muscle 25. Friden J, Sfakianos PN, Hargens AR: Blood indi- fatigue and pain after eccentric contractions at ces of muscle injury associated with eccentric long and short length. Clin Sci 7 4 : 5 5 3 - 5 5 7 , 1 9 8 8 . muscle contractions. J Orthop Res 7 : 1 4 2 - 1 4 5 , 1989. 4 5 . Newham DJ, Jones DA, Tolfree SE, et al.: Skele- tal muscle damage: a study of isotope uptake, 26. Friden J, Sfakianos PN, Hargens AR, et al.: Re- enzyme efflux and pain after stepping. Eur J Appl sidual muscular swelling after repetitive eccen- Physiol 5 5 : 1 0 6 - 1 1 2 , 1 9 8 6 . tric contractions. J Orthop Res 6 : 4 9 3 - 4 9 8 , 1988. 46. O'Reilly KP, Warhol MJ, Fielding RA, et al.: Ec- 27. Friden J, Sjostrom M, Ekblom B: A morphologi- centric exercise-induced muscle damage im- cal study of delayed muscle soreness. Experientia pairs muscle glycogen repletion. J Appl Physiol 37:506-507, 1981. 63:252-256, 1987. 28. Friden J, Sjostrom M, Ekblom B: Myofibrillar 47. Paavo V, Komi PV, Rusko H: Quantitative evalu- damage following intense eccentric exercise in ation of mechanical and electrical changes dur- man. Int J Sports Med 4 : 1 7 0 - 1 7 6 , 1983. ing fatigue loading of eccentric and concentric work. Scand J Rehabil Med (Suppl.) 3 : 1 2 1 - 1 2 6 , 29. Glogowski G, Wallraff J: Ein beitrag zur Klinik 1974. und Histologie der Muskelharten (Myogelosen). Z Orthop 8 0 : 2 3 7 - 2 6 8 , 1 9 5 1 . 48. Romano C, Schieppati M: Reflex excitability of human soleus motoneurones during voluntary 30. High DM, Howley ET, Franks BD: The effects of shortening or lengthening contractions. J Physiol static stretching and warm-up on prevention of 90:271-281, 1987. delayed-onset muscle soreness. Res Quart Exer- cise Sport 6 0 : 3 5 7 - 3 6 1 , 1989. 49. Salminen A, Kihlstrom M: Protective effect of indomethacin against exercise-induced injuries 31. Hough T: Ergographic studies in muscle sore- in mouse skeletal muscle fibers. Int J Sports Med ness. Am J Physiol 7 : 7 6 - 9 2 , 1902. 8:46-49, 1987. 32. Jones DA, Newham DJ, Clarkson PM: Skeletal 50. Sargeant AJ, Dolan P: Human muscle function muscle stiffness and pain following eccentric following prolonged eccentric exercise. Eur J exercise of the elbow flexors. Pain 3 0 : 2 3 3 - 2 4 2 , Appl Physiol 5 6 : 7 0 4 - 7 1 1 , 1987. 1987. 51. Schwane JA, Watrous BG, Johnson SR, et al.: Is 33. Jones DA, Newham DJ, Obletter G, et al.: Nature lactic acid related to delayed-onset muscle sore- of exercise-induced muscle pain. In Advances in ness? Phys Sportsmed 7 7 : 1 2 4 - 1 3 1 , 1 9 8 3 . Pain Research and Therapy. Vol. 10, edited by M.

558 Myofascial Pain and Dysfunction: The Trigger Point Manual 52. Schwane JA, Williams JS, Sloan JH: Effects of in canine muscle. Am J Phys Med 5 5 : 6 5 - 8 8 , training on delayed muscle soreness and serum 1976. creatine kinase activity after running. Med Sci 56. Talag TS: Residual muscular soreness as influ- Sports Exerc 1 9 : 5 8 4 - 5 9 0 , 1987. enced by concentric, eccentric, and static con- tractions. Res Quart 4 4 : 4 5 8 - 4 6 9 , 1973. 53. Simons DG: Myofascial pain syndrome due to 57. Tiidus PM, Ianuzzo CD: Effects of intensity and trigger points, Chapter 4 5 . In Rehabilitation Medi- duration of muscular exercise on delayed sore- cine, edited by Joseph Goodgold. C.V. Mosby ness and serum enzyme activities. Med Sci Co., St. Louis, 1988 (pp. 686-723). Sports Exerc 1 5 : 4 6 1 - 1 6 5 , 1 9 8 3 . 54. Simons DG: Muscle pain syndromes, Chap. 1. In 58. Travell JG, Simons DG: Myofascial Pain and Dys- Myofascial Pain and Fibromyalgia, edited by J.R. function: The Trigger Point Manual. Williams & Fricton and E.A. Awad. Raven Press, New York, Wilkins, Baltimore, 1983. 1990 (pp. 1-41). 59. Ibid. (pp. 91). 55. Simons DG, Stolov WC: Microscopic features 60. Ibid. (pp. 6 8 0 - 6 8 1 , Fig. 4 9 . 1 1 ) . and transient contraction of palpable bands