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Curr Pain Headache RepDOI 10.1007/s11916-012-0289-4 MYOFASCIAL PAIN (RD GERWIN, SECTION EDITOR) # The Author(s) 2012. This article is published with open access at Springerlink.com Abstract Myofascial pain syndrome (MPS) is described as Keywords Etiology . Myofascial . Pain . Trigger points .
the sensory, motor, and autonomic symptoms caused by Muscle damage . Calcium . Sustained low-level contractions .
myofascial trigger points (TrPs). Knowing the potential causes of TrPs is important to prevent their developmentand recurrence, but also to inactivate and eliminate existingTrPs. There is general agreement that muscle overuse or direct trauma to the muscle can lead to the development ofTrPs. Muscle overload is hypothesized to be the result of Myofascial pain syndrome (MPS) is described as the senso- sustained or repetitive low-level muscle contractions, eccen- ry, motor, and autonomic symptoms caused by myofascial tric muscle contractions, and maximal or submaximal con- trigger points (TrPs). TrPs are defined as exquisitely tender centric muscle contractions. TrPs may develop during spots in discrete taut bands of hardened muscle that produce occupational, recreational, or sports activities when muscle local and referred pain, among other symptoms. A TrP is use exceeds muscle capacity and normal recovery is composed of numerous so-called contraction knots. An in- dividual contraction knot appears as a segment of a musclefiber with extremely contracted sarcomeres and an increaseddiameter. The integrated TrP hypothesis postulates that inmyofascial pain motor endplates release excessive acetyl-choline, which is evidenced histopathologically by the pres- ence of sarcomere shortening []. These areas of intense Scientific Institute for Quality of Healthcare, focal sarcomere contraction have been described in animals Radboud University Nijmegen Medical Centre,Nijmegen, The Netherlands An active TrP causes a clinical pain complaint. It is always tender and refers a patient-recognized pain on com- pression. It prevents full lengthening of the muscle, weakens Shoulder and Upper Extremity Disorders,Paulus Potterstraat 46, the muscle, and mediates a local twitch response of muscle fibers when adequately stimulated. When compressed with- in the patient’s pain tolerance, it produces referred motorand often autonomic phenomena, generally in its pain ref- J. D. DommerholtBethesda Physiocare Inc. and Myopain Seminars LLC, erence zone []. A latent TrP is “clinically quiescent with respect to spontaneous pain; it is painful only when palpat- ed. A latent TrP may have all the other clinical character-istics of an active TrP and always has a taut band that J. D. DommerholtUniversidad CEU Cardenal Herrera, increases muscle tension and restricts range of motion” TrPs are very common, although literature about theirprevalence is sparse Knowing the potential causes of TrPs is important to Shenandoah University,Winchester, VA, USA prevent their development and recurrence, but also to inactivate and eliminate existing TrPs. There is general Since oxygen and glucose are required for the synthesis of agreement that any kind of muscle overuse or direct trauma adenosine triphosphate (ATP), which provides the energy to the muscle can lead to the development of TrPs. Muscle needed for muscle contractions, sustained contractions may overload is thought to be the result of sustained or repetitive cause a local energy crisis due to the lack of oxygen. To low-level muscle contractions, eccentric muscle contrac- guarantee an adequate supply of ATP, the muscle can switch tions, and maximal or submaximal concentric muscle con- within a few seconds to anaerobic glycolysis. During the tractions []. Although muscle damage is not required for initial phase of glycolysis (sugar splitting) 1 glucose molecule the development of TrP, there may be a disruption of the cell is broken down into 2 pyruvic molecules releasing enough membrane, damage to the sarcoplasmic reticulum with a energy to form 2 ATP molecules. Under aerobic circumstan- subsequent release of high amounts of calcium-ions, and ces, oxygen reacts with pyruvic acid producing a high amount disruption of cytoskeletal proteins, such as desmin, titin, and of ATP (16 molecules per pyruvic acid molecule), carbon dystrophin. Ragged red (RR) fibers and increased numbers dioxide and water. Under anaerobic circumstances, however, of cytochrome-c-oxidase (COX) negative fibers are com- most of the pyruvic acid produced during glycolysis is con- mon in patients with myalgia, which are suggestive of an verted into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid diffuses out of the muscleinto the bloodstream; post-exercise lactic acid is washed outwithin 30 minutes after exercise. Unfortunately, when the Sustained Low-Level Contractions and Intramuscular capillary circulation is restricted, as in sustained low-level contractions, this process comes to a standstill.
Researchers at the US National Institutes of Health found Mechanical muscle overuse can be defined as the result of that in the direct environment of active TrPs, the pH may be muscle contractions that exceed muscle capacity. Since the well below 5, which is more than sufficient to excite muscle capillary blood pressure ranges from approximately 35 mm nociceptors, including acid-sensing ion channels (eg, ASIC Hg at the beginning (arterial side) to 15 mm Hg at the end of 1 and 3), and the transient receptor potential vanilloid re- the capillary beds (venous side), the capillary blood flow is ceptor TRPV1 , ]. Small increases of the H+ concen- temporarily obstructed during muscle contractions. The tration, as seen with inflammation, heavy muscle work, and blood flow recovers immediately with relaxation, which is ischemia, are sufficient to excite muscle group IV endings, consistent with its normal physiological mechanism. In dy- contributing to mechanical hyperalgesia and central sensiti- namic rhythmic contractions, intramuscular blood flow is zation ]. Furthermore, a low pH downregulates acetyl- enhanced by this contraction-relaxation rhythm, also known cholinesterase (AChE), increases the efficacy of as the muscular pump. During sustained muscle contrac- acetylcholine (ACh), and maintains the sarcomere (super-) tions, however, muscle metabolism is highly dependent contraction. It also triggers the release of several nociceptive upon oxygen and glucose, which are in short supply.
substances, such as calcitonin gene-related peptide (CGRP) Even contractions performed at only 10 % and 25 % of ], which can enhance the release of ACh from the motor capacity or maximum voluntary contraction (MVC) may endplate and simultaneously decrease the effectiveness of produce intramuscular pressures high enough to significant- AChE in the synaptic cleft. CGRP also upregulates the ly impair the intramuscular blood circulation. The associa- ACh-receptors (AChR) at the muscle and thereby creates tion of the percentage of MVC and intramuscular pressure more docking stations for ACh. Miniature endplate activity (IMP) is highly dependent upon the architecture of the depends on the state of the AChR and on the local concen- muscle. It has been postulated that the percentage of MVC tration of ACh, which is the result of ACh-release, reuptake, reported as the upper limit for localized muscle fatigue varies between muscles, because of the variation of IMP Relaxation within the muscle cells occurs when myosin- during a contraction. For example, 10 % of MVC of the actin cross-bridges detach. After ATP is attached to the supraspinatus muscle produces approximately 50 mm Hg of myosin molecule, the link between myosin and actin weak- IMP, while 25 % of MVC of the trapezius muscle is good for ens, and the myosin head detaches from actin. In other only 22 mm Hg of pressure. Even lower values of IMP may words, the cross-bridge between myosin and actin ‘breaks’.
affect muscle metabolism [The EMG signs of localized Simultaneously, the Ca2+ ion detaches from the troponin muscle fatigue did not recover until the muscle contraction molecule, which blocks tropomyosin. Under normal physi- pressure was below 20 mm Hg in the biceps muscle [].
ological circumstances, large amounts of free calcium-ions According to Otten, the increased pressure gradients during will reenter the sarcoplasmic reticulum by the Ca2+ pump low-level exertions may contribute to the development of (Calcium ATPase), which places a high demand on ATP pain ] and eventually to the formation of TrPs (personal during relaxation. In case of severe energy depletion, the sarcomeres may stay contracted, until enough ATP is available to resolve the intracellular Ca2+ accumulation.
Maximal or Submaximal Concentric Contractions High concentrations of intracellular Ca2+ are associated withsustained sarcomere contraction and muscle damage. Ca2+ During (sub-) maximal concentric contractions high amounts accumulation due to sustained motor unit activity has been of energy (ATP) are required. Initially, ATP is utilized from suggested to play a causative role in the development of storage depots within the muscle fibers itself. After about 4–6 seconds, the muscle shifts to direct phosphorylation In a preliminary study using Doppler ultrasound, Sikdar of ADP by creatine phosphate (CP). Phosphorylation produ- et al have shown that blood flow waveforms show signifi- ces ATP by coupling 1 phosphate group to an ADP molecule cant differences between active TrPs, latent TrPs and normal catalyzed by the enzyme creatine kinase. Stored ATP and CP sites. The flow waveforms near active sites showed in- provide enough energy for maximum muscle power for ap- creased systolic velocities and flow reversal with negative proximately 14–16 seconds. Hereafter, a short period of rest is diastolic velocities [•]. They identified 2 contributing needed to replenish the exhausted reserves of intracellular factors, namely an increase in the volume of the vascular ATP and CP. When ongoing ATP demands are within the compartment, and an increased outflow resistance. In- capacity of the aerobic pathway, muscular activity can contin- creased outflow resistance could be due to muscle contrac- ue for hours in well-conditioned individuals. However, when tures at the TrP that compress the capillary or venous bed.
the demands of exercise begin to exceed the ability of the Sustained low-level contractions are common in the work- muscle cells to carry out the necessary reactions quickly place where many occupations rely on prolonged postures, enough, anaerobe glycolysis will contribute more and more as seen in musicians, supermarket cashiers, computer oper- of the total generated ATP. Finally, the muscle will run out of ators, hairdressers, and dentists, among others.
ATP and sustained sarcomere contractions may occur, startingthe development of TrPs.
During normal activity muscles are often active while being Henneman, working with anesthetized cats, showed that in lengthened. This is referred to as an eccentric contraction response to increasing physiological excitation, motor neu- ]. Classic examples of this are walking, whereby the rons are recruited in order of increasing size. This fundamen- knee extensors are active while being lengthened just after tally important finding was verified in humans by Milner- heel strike while the knee flexes; placing an object gently Brown et al ] and is now generally accepted. Smaller motor downwards, whereby the arm flexors are active while being units have a smaller alpha-motor neuron cell body, smaller lengthened to control the rate of movement of the object. In axons and fewer muscle fibers to activate compared with other words, eccentric contractions are commonly used to larger ones. According to the size principle, small motor units control the rate of movement. In another scenario, the load innervating type I red colored, slow oxidative fibers are on the muscle may increase to the point where the external recruited first, followed by red to pink colored, fast oxidative force on the muscle is greater than the force that the muscle fibers, and finally by white colored, fast glycolytic fibers.
can generate. In that case, the muscle is forced to lengthen Furthermore, small type I muscle fibers are activated during prolonged tasks although a few studies have described There is no solid evidence that eccentric loading would some degree of motor unit substitution Hägg suggested lead to the development of TrPs, but as Gerwin et al sum- that the continuous activity of these motor units in sustained marized, there is much overlap between the mechanisms of contractions causes overuse muscle fiber damage, especially eccentric contraction and the development of TrPs ]. In to the Type I fibers during low-level activities, which he one study, Itoh et al found that healthy volunteers presented summarized in his Cinderella hypothesis []. It is conceiv- with tender ropy taut bands, which were painful on com- able that in sustained low-level contractions and in dynamic pression, immediately after 3 sets of eccentric exercises of repetitive contractions, ischemia, hypoxia and insufficient the middle finger extensor muscle ]. One day and 2 days ATP synthesis in type I motor unit fibers are responsible for after the exercises the findings were similar. After 7 days the increasing acidity, Ca2+ accumulation, and subsequently sar- muscles were recovered. While this study suggests that comere contracture. Furthermore, starting with the sarcomere eccentric loading does contribute to the development of (super-) contraction, the intramuscular perfusion slows down TrPs, the study also employed isometric loading in addition and ischemia and hypoxia will occur. This may lead to the to eccentric loading, which precludes definitive conclusions.
release of several sensitizing substances causing peripheral There is evidence from biopsy studies that during eccen- tric contractions disruption of the cytoskeletal structures occurs, especially of the protein desmin that interconnects the adjacent myofibrils [, ] and of titin, the largestprotein in the human body. Titin connects myosin filaments Eccentric contractions occur during all activities of daily to the Z-bands and is also linked to actin filaments , ].
life, but have been researched especially in sports. Overhead Microscopic research revealed increased sections of abnor- throwing, spiking in tennis and volleyball, javelin-throwing, mal fibers in eccentrically exercised muscles , ], which downhill running, jumping and running (landing phase) appeared to be approximately 4 times the normal size ].
involve eccentric activities. During the deceleration phase This was only observed with eccentric exercise, and not of throwing, the posterior shoulder muscles such as the with concentric exercise or passive stretching. Furthermore, infraspinatus, teres minor and major, posterior deltoid, and all enlarged fibers were exclusively of the fast glycolytic latissimus dorsi muscles, contract eccentrically not only to type or fast contracting type II fibers that are highly fatiga- decelerate horizontal adduction and internal rotation of the ble. It is hypothesized that early in the exercise period fast arm, but also to resist shoulder distraction and anterior glycolytic fibers fatigue as they are unable to regenerate subluxation forces. A shoulder compressive force slightly ATP and as a result they enter into a rigor or high stiffness greater than bodyweight is generated to resist shoulder state. Subsequent stretching of the stiff fibers mechanically distraction, while a posterior shear force of 40 %–50 % disrupts the fibers resulting in cytoskeletal and myofibrillar bodyweight is generated to resist shoulder anterior sublux- damage. There is also evidence that in eccentric exercised ation. Consequently, high activity is generated by the pos- muscles the intracellular concentration of calcium is in- terior shoulder musculature, in particular the rotator cuff creased, probably because of disruption of the sarcoplasmic muscles. The percentage of maximum voluntary isometric reticulum. As we have seen before high concentrations of contraction (MVIC) is calculated in studies using needle Ca2+ keep myosin and actin molecules together. Further- electromyography. For example, the teres minor exhibits more, increased Ca2+ has the potential for activating several its maximum activity (84 % of MVIC), the infraspinatus mechanisms that leads to further damage of the cell mem- 37 %, supraspinatus 51 %, posterior deltoid 69 %, latissimus 88 %, subscapularis 115 %, and triceps 89 % during the In contrast, Hocking has postulated that eccentric deceleration phase. Scapular muscles also exhibit high ac- loading does not provide a good model for the TrP tivity to control scapular elevation, protraction, and rotation pathogenesis. He suggested that sustained partial depo- during this phase. The lower trapezius muscle, which exerts larization or plateau depolarization of an α-motor neu- force on the scapula in the direction of depression, retraction ron dendrites leads to lasting alterations in the function and upward rotation, generated its highest activity during of the entire α-motor neuron [due to an upregula- the eccentric phase []. High EMG activity from gleno- tion of L- or N- type voltage dependent calcium chan- humeral and scapular musculature during eccentric contrac- nels and α1-adrenergic receptors and a downregulation tion illustrates the vulnerability of the posterior musculature of calcium-activated potassium channels, which would for developing TrPs in the overhead-throwing athlete.
lead to an increase in the motor terminal cytosolic Posterior shoulder pain is a common complaint of throw- calcium ion concentration (personal communication, ing athletes and is mostly explained by posterior impinge- 2012). He suspects that the increased calcium concen- ment []. Interestingly, stretching exercises have been tration triggers the spontaneous release of ACh. In other shown to assist in reducing the athlete’s pain and to normal- words, according to Hocking, the increased ACh release ize shoulder motion, particularly shoulder internal rotation would be the cause and not the result of the energy and horizontal adduction. It is common for the overhead crisis. Alpha-1-adrenergic receptors are linked to L-type thrower to exhibit loss of internal rotation of 20 ° or more, voltage dependent calcium channels, which would sug- referred to as “glenohumeral internal rotation deficit gest that sympathetic activity would increase the cyto- (GIRD).” This internal rotation deficit has been suggested solic calcium ion concentration and the excessive to be a cause of specific shoulder injuries. Wilk expressed release of Ach []. Rather than looking at overuse that loss of internal rotation is most often due to osseous mechanisms, Hocking maintains that persistent nocicep- adaptations of the humerus and posterior muscle tightness, tive input causes the formation of TrPs through central and not posterior capsular tightness. Stretching exercises, sensitization of the C-fiber nociceptive withdrawal reflex including the sleeper’s stretch and supine horizontal adduc- and plateau depolarization of withdrawal agonist alpha- tion with internal rotation, are advised to improve the flex- motor neurons and compensatory reticulospinal motor ibility of the posterior musculature, which may become tight facilitation of antigravity muscles and plateau depolar- because of the muscle contraction during the deceleration ization of withdrawal antagonist alpha-motor neurons phase of throwing TrPs can be found in many sports- [Future research in the underlying mechanisms of men, including elite volleyball players, swimmers, and 10. Jarvholm U, Palmerud G, Karlsson D, Herberts P, Kadefors R.
Intramuscular pressure and electromyography in 4 shouldermuscles. J Orthop Res. 1991;9:609–19.
In spite of a lack of well-designed studies, the best available 11. Palmerud G, Forsman M, Sporrong H, Herberts P, Kadefors R.
evidence supports that TrPs develop after muscle overuse.
Intramuscular pressure of the infra- and supraspinatus muscles in Several potential mechanisms may play a role, such as relation to hand load and arm posture. Eur J Appl Physiol.
eccentric overload, submaximal sustained, and (sub)-maxi- 12. Dommerholt J, Bron C, Franssen J. Myofascial trigger points: an mal concentric contractions. A key factor is the local ische- evidence-informed review. J Man Manip Ther. 2006;14:206–21.
mia, which leads to a lowered pH and a subsequent release 13. Shah JP, Phillips TM, Danoff JV, Gerber LH. An in vivo micro- of several inflammatory mediators in muscle tissue. Hock- analytical technique for measuring the local biochemical milieu of ing proposed an interesting counterargument, which human skeletal muscle. J Appl Physiol. 2005;99(5):1977–84. Epub2005/07/23.
deserves further exploration. Whether overuse mechanisms 14. Gautam M, Benson CJ, Sluka KA. Increased response of muscle are the crucial initiating factor or persistent nociceptive sensory neurons to decreases in pH after muscle inflammation.
input remains a point of debate and further study.
Neuroscience. 2010;170(3):893–900. Epub 2010/08/10.
15. Dommerholt J. Dry needling-peripheral and central considerations.
J Manual Manipul Ther. 2011;19:223–37.
16. Gissel H, Clausen T. Excitation-induced Ca2+ influx and skeletal No potential conflicts of interest relevant to this article muscle cell damage. Acta Physiol Scand. 2001;171:327–34. Epub 17. • Sikdar S, Ortiz R, Gebreab T, Shah JP. Understanding the Vascular Environment of Myofascial Trigger Points using Ultrasonic Imaging This article is distributed under the terms of the Creative and Computational Modeling. 32nd Annual International Conference Commons Attribution License which permits any use, distribution, and of the IEEE EMBS. 2010. This is an interesting paper presenting a reproduction in any medium, provided the original author(s) and the theoretical model to understand the role of vascular compression in 18. De Luca CJ, Contessa P. Hierarchical control of motor units in voluntary contractions. J Neurophysiol. 2012;107:178–95. Epub 19. Zennaro D, Laubli T, Krebs D, Klipstein A, Krueger H. Continuous, intermitted and sporadic motor unit activity in the trapezius muscle Papers of particular interest, published recently, have been during prolonged computer work. J Electromyogr Kinesiol.
20. Henneman E. Relation between size of neurons and their suscep- tibility to discharge. Science. 1957;126:1345–7. Epub 1957/12/27.
21. Hagg GM. Human muscle fibre abnormalities related to occupa- 1. Simons D. Review of enigmatic MTrPs as a common cause of tional load. Eur J Appl Physiol. 2000;83:159–65. Epub 2000/12/ enigmatic musculoskeletal pain and dysfunction. J Electromyogr 22. Hoyle JA, Marras WS, Sheedy JE, Hart DE. Effects of postural and 2. Simons D, Travell JG, Simons LS. Myofascial pain and dysfunction.
visual stressors on myofascial trigger point development and motor The trigger point manual. Upper half of body. 2nd ed. Baltimore: unit rotation during computer work. J Electromyogr Kinesiol.
Lippincott, Williams and Wilkins; 1999.
3. Fricton J, Kroening R, Haley D, Siegert R. Myofascial pain syn- 23. Lieber RL. Skeletal muscle structure, function, and plasticity. The drome of the head and neck: a review of clinical characteristics of physiological basis of rehabilitation. 3rd ed. Baltimore- 164 patients. Oral Surg Oral Med Oral Pathol. 1985;60:615–23.
Philadelphia: Lippincott, Williams & Wilkins; 2009.
24. Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons’ 4. Fishbain D, Goldberg M, Meagher B, Steele R, Rosomoff H. Male integrated hypothesis of trigger point formation. Curr Pain Head- and female chronic pain patients categorized by DSM-III psychi- ache Rep. 2004;8:468–75. Epub 2004/10/29.
atric diagnostic criteria. Pain. 1986;26:181–97. Epub 1986/08/01.
25. Itoh K, Okada K, Kawakita K. A proposed experimental model of 5. Skootsky SA, Jaeger B, Oye R. Prevalence of myofascial pain in myofascial trigger points in human muscle after slow eccentric exer- general internal medicine practice. West J Med. 1989;151:157–60.
cise. Acupunct Med. 2004;22:2–12. discussion–3. Epub 2004/04/14.
26. Barash IA, Peters D, Friden J, Lutz GJ, Lieber RL. Desmin 6. Gerwin R. A study of 96 subjects examined both for fibromyalgia cytoskeletal modifications after a bout of eccentric exercise in and myofascial pain. J Musculoskeletal Pain. 1995;3(Suppl 1).
the rat. Am J Physiol Regul Integr Comp Physiol. 2002;283: 7. Bron C, Dommerholt J, Stegenga B, Wensing M, Oostendorp R.
High prevalence of shoulder girdle muscles with myofascial trig- 27. Lieber RL, Shah S, Friden J. Cytoskeletal disruption after eccentric ger points in patients with shoulder pain. BMC Musculoskelet contraction-induced muscle injury. Clin Orthop Relat Res.
8. Gerwin R. Myofascial pain syndrome: here we are, where must we 28. Niederlander N, Raynaud F, Astier C, Chaussepied P. Regulation go? J Musculoskeletal Pain. 2010;18:329–47.
of the actin-myosin interaction by titin. Eur J Biochem.
9. Larsson B, Björk J, Henriksson K, Gerdle B, Lindman R. The 2004;271:4572–81. Epub 2004/11/25.
prevalence of cytochrome c oxidase negative and superpositive 29. Nagy A, Cacciafesta P, Grama L, Kengyel A, Malnasi-Csizmadia fibers and ragged-red fibers in the trapezius muscle of female A, Kellermayer MS. Differential actin binding along the PEVK cleaners with and without myalgia and of female healthy controls.
domain of skeletal muscle titin. J Cell Sci. 2004;117(Pt 24):5781–9.
30. Lieber RL, Friden J. Selective damage of fast glycolytic muscle 36. Myers J. Glenohumeral range of motion deficits and posterior fibres with eccentric contraction of the rabbit tibialis anterior. Acta shoulder tightness in throwers with pathologic internal impinge- Physiol Scand. 1988;133:587–8. Epub 1988/08/01.
ment. Am J Sports Med. 2005;34:385–91.
31. Lieber RL, Friden J. Muscle damage is not a function of muscle 37. McFarland E, Hsu C, Neira C, O'Neil O. Internal impingement of force but active muscle strain. J Appl Physiol. 1993;74:520–6.
the shoulder: a clinical and arthroscopic analysis. J Shoulder Elbow 32. Friden J, Lieber RL. Segmental muscle fiber lesions after repetitive 38. Wilk KE, Obma P, Simpson CD, Cain EL, Dugas JR, Andrews JR.
eccentric contractions. Cell Tissue Res. 1998;293:165–71. Epub Shoulder injuries in the overhead athlete. J Orthop Sports Phys 33. Hocking MJL. Trigger points and central modulation - a new 39. Osborne NJ, Gatt IT. Management of shoulder injuries using dry hypothesis. J Musculoskeletal Pain. 2010;18:186–203.
needling in elite volleyball players. Acupunct Med. 2010;28:42–5.
34. Wessler I, Dooley DJ, Osswald H, Schlemmer F. Differential blockade by nifedipine and omega-conotoxin GVIA of alpha 1- 40. Hidalgo-Lozano A, Fernandez-de-Las-Penas C, Calderon-Soto C, and beta 1-adrenoceptor-controlled calcium channels on motor Domingo-Camara A, Madeleine P, Arroyo-Morales M. Elite swim- nerve terminals of the rat. Neurosci Lett. 1990;108:173–8. Epub mers with and without unilateral shoulder pain: mechanical hyper- algesia and active/latent muscle trigger points in neck-shoulder 35. • Escamilla RF, Yamashiro K, Paulos L. Shoulder muscle activity muscles. Scand J Med Sci Sports. 2011. Epub 2011/05/14.
and function in common shoulder rehabilitation exercises. Sports 41. Fredericson M, Guillet M, Debenedictis L. Innovative solutions for Med. 2009. This is an interesting paper presenting the results of iliotibial band syndrome. Phys Sportsmed. 2000;28:53–68. Epub electromyography research in shoulder movements.

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