IJSPT
CASE REPORT
SUBSCAPULARIS SYNDROME: A CASE REPORT Michael S. Thurner, PT, DPT, CSCS1 Robert A. Donatelli, PhD, PT1 Randa Bascharon, DO, ATC2
ABSTRACT Dysfunction of the subscapularis muscle is introduced in this case report as a potential factor for consideration in the etiology and/or consequential sequelae of subacromial impingement syndrome. Although dysfunction of the supraspinatus and infraspinatus are implicated as being most commonly involved with subacromial impingement pathology, the subscapularis is often overlooked and therefore undertreated. Identifying the subscapularis’ potential involvement in patients with subacromial impingement pathology may offer insight into shoulder impingement dysfunction and injury treatment options available to specifically address subscapularis dysfunction. In this manuscript, a case report is presented to highlight the signs and symptoms of subscapularis pathology concordant with subacromial impingement syndrome and provide a clinical rationale for treatment. The purpose of this case report is not to suggest a new approach to shoulder rehabilitation, but rather to prompt the consideration of subscapularis dysfunction when evaluating and treating patients with subacromial impingement pathology. Key words: Subcapularis, subscapularis syndrome, subacromial impingement Level of Evidence: 5
CORRESPONDING AUTHOR 1
Physiotherapy Associates Orthopedic & Sports Center, Las Vegas, NV, USA 2 Orthopedic & Sports Medicine Institute of Las Vegas, Las Vegas, NV, USA Acknowledgments We would like to thank the participants for their time. Funding for this project was provided by a grant from the United States National Institutes of Health; K12 HD055931
Michael S. Thurner, PT, DPT, CSCS Physiotherapy Associates Orthopedic & Sports Center 5920 South Rainbow Blvd. Suite 1 Las Vegas, NV 89118 Email: [email protected]
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INTRODUCTION Impingement syndrome is well defined in the literature as a pathological condition of the shoulder complex associated with a clinical manifestation of signs and symptoms altering normal motion and pain free function of the affected upper extremity.1,2,3 In this case report, the authors introduce the subscapularis muscle of the rotator cuff as a plausible factor for consideration as part of a cascade of potential causes and subsequent sequelae associated with subacromial impingement pathology. Relative scarcity of literature describing the relationship between subacromial impingement syndrome and subscapularis dysfunction combined with numerous clinical observations of improved outcomes with specific interventions prompt the senior author to refer to the subscapularis as the “hidden culprit” of the rotator cuff. There are several cardinal signs and symptoms that may implicate the subscapularis muscle of the rotator cuff as a contributing factor to dysfunction and functional limitations of the shoulder complex. Linking underlying subscapularis soft tissue restrictions to subacromial impingement syndrome with positive tests and measures may be helpful in gaining a more thorough and broad understanding of contributions to shoulder impingement pathology and also have implications for treatment to address subscapularis dysfunction. With early recognition and treatment, patients presenting with subacromial impingement and concurrent subscapularis impairments may be able to reduce time of recovery and enhance optimal outcomes. The subscapularis originates in the subscapular fossa on the costal surface of the scapula and courses anterior and laterally to insert on the lesser tuberosity of the humerus.4,5,6 (Figure 1) This is the largest of the four rotator cuff muscles with nearly three times the physiological cross sectional area as the remaining three posterior cuff muscles combined.7 The subscapularis muscle primarily functions as a humeral depressor and stabilizer along with its traditional role as an internal rotator of the humerus.8 The histologic architecture of the rotator cuff tendons fiber arrangement is composed of multiple layers, which consist of crossover and interlocking of the fiber layers.9,10 The tendon fibers blend with and reinforce the glenohumeral capsule.10 This protective overlap of interlocking
Figure 1. Anatomy of the Shoulder complex.
fibers may potentially preserve the functional integrity of the rotator cuff’s dynamic stabilization role in case of a partial tear or complete rupture due to this integrated anatomical relationship of the rotator cuff tendon fibers.9,11,12 Histologically, some fibers of the subscapularis and supraspinatus interlock and converge together as they course around and above the humeral head to their respective insertion sites on the greater tubercle, thereby anatomically preserving the depressive capability of the remaining cuff fibers.12 The force vectors of the subscapularis and the infraspinatus are biomechanically more optimally aligned to efficiently provide depression of the humeral head, compared with the supraspinatus.9,13,14 Specific exercises of the rotator cuff and scapular rotators eliciting high EMG activity of the targeted musculature are later described in the interventions section of this case report.8,15 Also, it is important to note when developing a comprehensive rehabilitation or strength and conditioning program for the cuff deficient patient or client, that the teres major and latissimus dorsi can also provide humeral depression forces secondary to their anatomical alignment.9,13 Therefore, in the case of rotator cuff dysfunction, the health care professional should carefully consider the development of an individualized program incorporating specific therapeutic strengthening exercises and stretching or soft tissue mobilization in order to promote function of the patient or client by offsetting the deficiency or weakness that is present.
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BACKGROUND & PURPOSE The glenohumeral joint is the most mobile joint present in the human body due to its osseous configuration.16,17 The articulation of the shallow glenoid cavity with the relatively large humeral head allows for extreme ranges of movement in all planes of motion, and thus inherently lacks stability.16,17 In the healthy shoulder, synchronous activation of the dynamic stabilizers (acting as a force couple) provide stability to this proximal link of the upper extremity chain. Proximal stability is crucial to influence distal functional mobility, allowing the hand to move freely in space. As a complement to dynamic stability, the ligamentous and capsular tissue architecture of the glenohumeral joint provide tension at the extremes of available motion offering inherent static stability relative to all planes of shoulder movement. Dynamic stabilization of the glenohumeral joint is affected by the rotator cuff and the scapulothoracic musculature. The rotator cuff muscles stabilize the glenohumeral joint by acting to depress and compress the humeral head within the glenoid concavity.8,9 The scapulothoracic muscles control scapular movements allowing for optimal length-tension relationships of the rotator cuff musculature by properly aligning the glenoid concavity relative to the humeral head.8 Neuromuscular control and adequate ratios of scapular muscle strength are essential to shoulder complex function because the scapula and humerus simultaneously move together in a complex yet coordinated fashion during shoulder movement, referred to as scapulohumeral rhythm.8 A disruption of this synergistic relationship may occur secondary to a muscle imbalance, altering the normal kinematics of this complex network of force couples.3 Compensatory movement patterns may subsequently present as scapular dyskinesis or concomitant scapular asymmetry.3,18 The inability of the rotator cuff to effectively offset the superior shear force of the deltoid may result in superior humeral head migration into the subacromial space.3,18 Consequently, this sequela of events may potentially lead to subacromial impingement. Subacromial impingement has been defined as mechanical compression of the soft tissue structures that pass beneath the coracoacromial arch as the shoulder is elevated.1,2,3 The structures subject to impingement are the rotator cuff tendons, long head of the biceps tendon and
the subacromial bursa.1,2,3 Subacromial impingement pathology commonly affects the posterior rotator cuff tendons, most notably the supraspinatus. This may induce a compensatory increase in activation of the subscapularis in order to accommodate for the deficient or inhibited ability of the affected muscles to sufficiently counteract the superior shear force of the humeral head as the deltoid muscle contracts during elevation of the arm.9 Although dysfunction of the supraspinatus and infraspinatus is commonly implicated as being associated with subacromial impingement pathology, it is the assertion of the authors that the subscapularis is often overlooked and therefore undertreated. Compensatory activation of the subscapularis may consequently lead to overuse over time secondary to repetitive microtrauma, eventually resulting in pathology of the muscle-tendon complex. Adaptive overuse without adequate healing time for the tissue to recover will ultimately result in fatty infiltration of the muscle belly and/or degenerative scarring of the tendon consistent with tendinosis pathology as may be evident through magnetic resonance imaging (MRI).4 Fibrosis or scarring of the subscapularis may present clinically as trigger points to palpation and adaptive shortening of the muscle belly and/or tendon, thus limiting shoulder external rotation in the adducted position.19,20,21,22,23 Cadaveric studies by Turkel et al indicate that the subscapularis muscle is the most influential stabilizing structure during passive external rotation of the glenohumeral joint at zero degrees of abduction in the frontal plane.22,23 Furthermore, the integrity of the muscle-tendon complex may continue to be compromised by adaptive shortening secondary to protective shoulder postures of immobilization in the adducted and internally rotated position. Travell and Simmons propose that a trigger point within the subscapularis muscle may sensitize adjacent muscles of the shoulder girdle presenting as secondary or satellite trigger points potentially leading to a heightened sensitization of pain and motion restrictions of the shoulder complex.21 (Figure 2) Resultant scapular malalignment as a result of restricted mobility of the subscapularis may subsequently cause poor length-tension relationships of the scapular musculature, further accentuating the muscle imbalance.
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Figure 2. Subscapularis Trigger Points (x’s) & projected referral pain pattern. The essential referred pain zone appears as solid red with the spillover zone illustrated as stippled.
Scapular malalignment or asymmetrical scapulae, often referred to as S.I.C.K. (Scapular malposition, Inferior medial border prominence, Coracoid pain, Scapular dyskinesia) scapula, may present as a protracted scapula on the side of the affected extremity in patients presenting with shoulder impingement.24 Through clinical observation, the author’s note adaptive shortening of the subscapualris often occurs in conjunction with an internally rotated scapular postural abnormality, associated with lengthened and subsequently weakened posterior rotator cuff and scapular musculature. Limited and painful active elevation of the shoulder in the plane of the scapula is a classic sign of subacromial impingement syndrome. This may be a consequence of a lack of disassociation between the scapula and the humerus and/or the diminished glenohumeral external rotational capacity preventing sufficient clearance of the greater tuberosity under the coracoacromial arch during elevation of the shoulder.19 The lack of disassociation will inherently disrupt the normal biomechanics of the shoulder complex and could potentially limit the depressive capability of the already compromised subscapularis muscle, resulting in superior migration of the humeral head, due to the previously described muscle imbalance in relation to the deltoid. Repetitive overhead activity may result in subacromial impingement pathology with the associated painful shoulder movement into positions of glenohumeral joint elevation. The Hawkins-Kennedy, Neer, and Yocum impingement tests will usually confirm
the diagnosis of impingement.25,26,27,28 Although anatomically the subscapularis does not pass under the subacromial region, it has been shown to limit glenohumeral external rotation, which may lead to subacromial impingement pathology as previously described.22,23 Secondary to the characteristic nature of overuse, the subscapularis muscle will usually present as weak and painful upon muscle testing illustrated by the belly press and/or lift-off test.26,29 The clinical presentation of limited external rotation in the adducted position, pain to palpation of trigger points within the subscapularis muscle belly and/ or tendon, and dysfunction of the subscapularis on strength testing should be considered in the etiology of subacromial impingement. The concept of labeling or categorizing specific shoulder impingement pathology helps identify the relationship between clinical findings and shoulder dysfunction. Identifying the subscapularis’ potential involvement in patients with subacromial impingement pathology may be helpful in gaining a greater insight into shoulder dysfunction, and expand intervention options to address subscapularis dysfunction. Further research is warranted to determine the cause and effect relationship between the subscapularis and subacromial impingement syndrome pathology. CASE REPORT Patient History A 22 year old right hand dominant female tennis player was sent to physical therapy with a physician diagnosis of right shoulder pain secondary to sub-
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acromial impingement. The patient reported a threemonth history of ‘deep’ shoulder pain without being able to identify specific physical boundaries. The pain was elicited when she was serving overhead or during the follow-through phase of a forehand swing. She reported an insidious onset of symptoms with no history of specific trauma to the right shoulder. Magnetic resonance imaging (MRI) results suggested tendinopathy of the supraspinatus and subscapularis tendon with a possible partial tear of the supraspinatus tendon. The Quick DASH outcome measure with the optional sports/performing arts module was completed at the initial evaluation and the patient scored fifty percent, and twenty-two percent disability/symptom scores in sport and overall function, respectively. Examination The patient tested positive on the Neer and Yocum impingement tests. An internally rotated right scapula, medial border prominence, and a mild lack of disassociation of the scapula and humerus were identified during active elevation of the arm in the plane of the scapula through visual observation in comparison with the opposite extremity. Passive external rotation (ER) at zero degrees of abduction was limited to 30 degrees with the total internal/external rotation arc of motion at 90 degrees of abduction equal to the left shoulder. (Figure 3) The opposite extremity was measured for comparison at zero degrees of abduction and was found to be within normal limits, at 75 degrees of external rotation. Prominent weakness (3-/5) and pain (7/10) were noted during manual muscle testing of both the
Figure 3. Restricted External Rotation in the Adducted Position.
Figure 4. Lift-off Test for the Subscapularis.
supraspinatus in the ‘full can’ position and the subscapularis while performing the lift-off test. (Figure 4) Mild deficits were also noted during testing of the infraspinatus and teres minor, which were graded with a 4/5 and 4-/5 respectfully. The serratus anterior, middle and lower trapezius were also tested via manual muscle testing and were graded as 4-/5, 4/5, and 4-/5 respectfully. Subjective complaints of pain 4/10 were noted during manual muscle testing of the lower trapezius. The authors note that the test position in question requires the test subject to abduct and externally rotate the glenohumeral joint, which also recruits the supraspinatus and may biomechanically result in impingement due to faulty mechanics of the injured shoulder, thus irritating the already compromised soft tissue structures. Trigger points were identified upon palpation of the superior and inferior lateral aspect on the anterior surface of the subscapularis muscle belly with the patient positioned in supine with the humerus supported in an abducted and externally rotated position. (Figure 5) At the conclusion of the physical examination, the identifying signs and symptoms were enough to suspect involvement of the subscapularis. Intervention & Outcome The focus of treatment was to re-establish scapulohumeral rhythm by improving strength and mobility of the shoulder complex allowing the patient/athlete to return to tennis unrestricted and symptom free. During the first four weeks of physical therapy, treatment consisted of a progressive resistive exercise (PRE) pro-
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Figure 5. Trigger Points to palpation of the Subscapularis Muscle Belly and/or Tendon.
gram to address weakness and postural adaptations of the rotator cuff and scapula rotator musculature, low-level laser therapy (LLLT) with deep sustained pressure to relieve trigger points in the subscapularis muscle belly, low load prolonged-duration (LLPS) stretching into external rotation and soft tissue mobilization to improve the mobility of the subscapularis. Therapeutic exercises were initiated using high repetitions (12-15 × 2-3 sets) and moderate to light weight with an emphasis on pain free motion in Phase I. The overall goal of therapeutic exercise in the initial phase was to stimulate appropriate muscle activation, promote muscular strength and endurance, and increase blood flow to the healing tissue in order to enhance the recovery process. The exercises were selected to target specific musculature identified during the examination as having less than optimal strength. Specific exercises of the rotator cuff and scapular rotators eliciting high EMG activity of the targeted musculature are illustrated in figures 610.8,15 (Figures 6-10) The exercises were progressed in Phase 2 using increased weight with fewer repetitions (8-12 reps × 3 sets) in order to transition to a more focal emphasis on muscular strengthening of the shoulder complex. LLLT was utilized in phases III using a pulsed (905 nm) laser with deep sustained pressure utilizing a laser probe for three sets of fiveminute cycles. (Figure 11) Pressure was applied over the trigger points identified in the examination and modified according to patient tolerance. Manual mobilization of the scapula was also initiated in the initial phase and progressed into phase II based on patient tolerance. The patient was positioned in a
Figure 6. Subscapularis Diagonal Exercise.
Figure 7. Dynamic Hug, using pulley system.
side-lying position with the upper extremity relaxed at the patient’s side. The physical therapist performs a distraction force to the scapula with a sustained hold to patient tolerance with oscillatory mobilizations performed intermittently between manual stretch holds at the therapist’s discretion. (Figure 12) A low-load prolonged stretch into glenohumeral external rotation was applied continuously for 20 minutes in phases I-II. The patient was positioned in the supine position with the shoulder supported on a foam wedge in zero degrees of abduction allowing gravity to produce the intended stretch into external rotation. (Figure 13) By the end of the fourth week of
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Figure 8. Biodex Eccentric Loading Internal/External Rotation.
Figure 11. Low Level Laser with Deep Sustained Pressure Over the Trigger Points.
Figure 9. Prone Horizontal Abduction with External Rotation @ 90 & 135 Degrees of Abduction.
Figure 12. Scapular Tilt & Distraction.
Figure 10. Prone External Rotation and Horizontal Abduction @ 90 Degrees of Abduction & Elbow Flexion.
Figure 13. Low Load Prolonged Stretch of the Subscapularis.
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treatment, the patient demonstrated full active elevation without evidence of compensatory movement patterns, symmetrical scapulae, pain free grades of 5/5 during manual muscle testing of the rotator cuff and scapular rotator musculature, improved passive range of motion to 75 degrees of external rotation at zero degrees of abduction, and no pain 0/10 to palpation of the subscapualris muscle belly or tendon.30 Table 1 highlights the clinical deficits present and the proposed corrective therapeutic exercise or treatment as depicted in figures 3-13. (Table 1) Table 2 identifies the prescription of therapeutic exercise and phase in which specific therapeutic interventions were implemented in relation to this case report. (Table 2)
in this phase to reintroduce the overhead movement including the tennis serve in a controlled environment. Lateral bounding and agility drills with sport cord resistance were incorporated with the tennis swing in order to enhance neuromuscular control and spatial awareness. Internal and external rotation performed above 90 degrees of abduction at varying speeds was also introduced in this phase to improve strength and power in the overhead position. Interval training using ten second intervals of high intensity lateral movement inter-dispersed with submaximal low intensity active rest for thirty seconds on the dynamic edge was also initiated at this time to progress the patient/athlete’s conditioning status.
Weeks 4-6 comprised of advancing the progressive resistive strengthening program using the principles of muscle strengthening established by ACSM guidelines.31 A return to sport program specific to tennis was also integrated at this time on order to optimally prepare the patient for return to play. The resistance of the therapeutic exercise targeting the rotator cuff and scapular rotators was increased accordingly to the patient’s tolerance and ability to demonstrate proper technique throughout the exercise. The emphasis of the Phase III, during weeks 4-6, was low repetition exercise (6-8 reps × 3 sets) with adequate resistance to enhance overall muscular strength. Sport specific exercises for the overhead athlete were also initiated
The Quick DASH was performed again, and the patient scored a zero percent disability/symptoms at discharge with no deficits or dysfunction reported. The patient/athlete was able to return to unrestricted tennis, symptom free, following the aforementioned six weeks of physical therapy. DISCUSSION Clinically, over the past 20 years the senior author has consistently observed a clinical relationship between a loss of glenohumeral external rotation in the adducted position and signs and symptoms of subacromial impingement pathology. Furthermore, these patients concurrently exhibited near
Table 1. Clinical presentation and proposed intervnetions.
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Table 2. Phased Intervention used during treatment of the subject in the case report.
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Table 2. Phased Intervention used during treatment of the subject in the case report. (continued)
equal (+/- 5 degrees) total internal/external arc of motion at 90 degrees of abduction when compared to uninvolved side. According to Turkel et al, the most influential stabilizing structure during passive glenohumeral external rotation at zero degrees of abduction is the subscapularis muscle.22 Thus, the authors of this case report believe that a restriction of external rotation at zero degrees of abduction with normal passive external rotation range of motion at 90 degrees of abduction may be indicative of the subscapularis as the primary restricting tissue. Elkstrom et al and Donatelli et al describe external rotation at zero degrees of shoulder elevation as the selective stretch or testing position for the subscapularis.20,32 A more recent cadaveric study suggests varying angles of abduction in conjunction with external rotation induce strain on different portions of distinct fiber arrangements within the subscapularis muscle.33 Turkel et al also note that no single structure solely stabilizes the glenohumeral joint in any one plane of motion, and the position and tightness of anterior structures vary with abduction and external rotation angles.22,32 This anatomical concept of stability has been well established in the literature although the contributions of specific stabilizing structures remains controversial. The authors of this case report acknowledge the anatomic variance of the orientation of fibers comprising the subscapularis muscle and thus promote stretching at multiple angles of elevation if the subscapularis is identified as the predominately restricted tissue structure. The subject of this case report presented with mobility
restrictions of the shoulder characteristic of the subscapularis’ involvement. Godges et al recently demonstrated a positive correlation between soft tissue mobilization with proprioceptive neuromuscular facilitation to the subscapularis muscle belly and an increase in external rotation and overhead reach.34 In the current case report, the treating clinicians utilized a deep pressure soft tissue mobilization technique in conjunction with LLLT, as illustrated in figure 11. LLLT is a modality treatment used to facilitate recovery by attempting to promote a healing response at the cellular level. Several authors suggest that LLLT with a high power level of impulse or biphasic dose response has the capacity to drive photons (light energy) to the target tissue at depths of up to 10-13 cm or 4-5 inches.35,36,37 The proposed healing effects revolve around improvement of microcirculation at an adequate depth of penetration to reach the targeted soft tissue structures and increase cell metabolism (which is proposed to influence ATP production or energy used to enhance recovery at a cellular level). This may may assist in returning the damaged cells to a stable, healthy state.38,39 LLLT has been cited as a safe and effective modality to accelerate pain relief and healing.38,39 Also, a subscapularis tilt and distraction soft tissue mobilization technique was used to provide oscillatory mobilization stretch in an attempt to alleviate any soft tissue restrictions present within the subscapularis muscle as illustrated in Figure 12. Low load prolonged-duration stretch (LLPS) has histori-
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cally been utilized in physical therapy as an effective means to induce lengthening of soft tissue.40 The emphasis of the stretching technique applied in this case report is to restore tissue length by way of gradual application of tension over time to produce a permanent or plastic remodeling of the connective tissues allowing increased range of motion over the course of time. LLPS was implemented at the onset of treatment to promote tissue lengthening without inducing pain. In this case, the patient was able to fully tolerate treatment and ultimately regained full mobility of the shoulder. The patient was also introduced to a progressive resistance exercise program early in the rehabilitation process in order to develop neuromuscular control, improve overall strength, and facilitate optimal ratios of strength of the rotator cuff and scapular rotator musculature for promotion of normal scapulohumeral rhythm. She responded well to physical therapy intervention progressing as appropriate under the discretion of the physical therapist, ultimately returning to tennis without residual pain or limitation. CONCLUSION Patients frequently present or are referred to physical therapy with a non-specific diagnosis relating to shoulder ‘pain’. Any patient presenting with shoulder pathology may present with some or all of the signs and symptoms that implicate the subscapularis as a part of the dysfunction. Manual therapy techniques and exercise prescription as illustrated in this case report may be implemented once a treatment plan is established based on the clinical examination. Further research is warranted in order to establish the degree of involvement of the subscapularis in the presentation of patient with subacromial impingement syndrome. Higher-level studies are needed to establish parameters for ‘significant’ external rotation range of motion loss, to objectively quantify strength deficits (perhaps using isokinetic dynamometry), and determine the effectiveness of interventions utilized to resolve subscapularis impairments. REFERENCES 1. Bigliani L, Levine W. Current concepts review: subacromial impingement syndrome. J Bone and Joint Surg. 1997;79:1854-1868. 2. Harrison A, Flatow E. Subacromial impingement syndrome. J Am Acad Orthop Surg. 2011;19(11):701-708.
3. Ludewig P, Reynolds J. The association of scapular kinematics and glenohumeral joint pathologies. J Orthop Sports Phys Ther. 2009;39(2):90-104. 4. Morag Y, Jamadar D, Miller B, et al. The subscapularis: anatomy, injury, and imaging. Skeletal Radiol. 2011;40:255-269. 5. Cleeman E, Brunelli M, Gothelf T, et al. Releases of subscapularis contracture: an anatomic and clinical study. J Shoulder Elbow Surg. 2003;12:231-6. 6. Warwick R, Williams P, Gray H. Gray’s Anatomy (35 ed). Philadelphia. Saunders Company. 1973;532-540. 7. Ward S, Hentzen E, Smallwood L, et al. Rotator cuff muscle architecture: implications for glenohumeral stability. Clin Orthop Relat Res. 2006;448:157-163. 8. Reinold M, Escamilla R, Wilk K. Current concepts in the scientific and clinical rationale behind exercises for glenohumeral and scapulothoracic musculature. J Orthop Sports Phys Ther. 2009;39 (2):105-117. 9. Millet P, Wilcox III R, O’Holleran J, Warner J. Rehabilitation of the rotator cuff: an evidence based approach. J Am Acad Orthop Surg. 2006;14(11):599609. 10. Cooper D, O’Brian S, Warren R. Supporting layers of the glenohumeral joint. An anatomic study. Clin Orthop Relat Res. 1993;289:144-155. 11. Sakurai G, Ozaki J, Tomitta Y, et al. Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus: cadaveric and clinical studies. J Shoulder and Elbow Surg. 1998;7(5):510-515. 12. Thompson W, Debski R, Boardman N III, et al. A biomechanical analysis of rotator cuff deficiency in a cadaveric model. Am J Sports Med. 1996;24:286-292. 13. Halder A, Zhao K, O’Driscoll S, Morrey B, et al. Dynamic contributions to superior shoulder stability. J Orthop Res. 2001;19:206-212. 14. Neuman D. Kinesiology of the musculoskeletal system. Foundations for physical rehabilitation. Shoulder Complex. St.Louis. Churchhill Livingstone. 2002:91-132. 15. Decker M, Tokish J, Ellis H, Torry M, Hawkins R. Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med. 2003;31:126-134. 16. Bigliani L, Kelkar R, Flatow E, et al. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;330:13-30. 17. Wilk K, Arrigo C, Andrews J. Current concepts: the stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther. 1997;25(6):364-379. 18. Kibler W, McMullen J. Scapular dyskinesias and its relation to shoulder pain. J Am Acad Orthop Surg. 2003;11:142-151.
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19. Donatelli, R. Physical therapy of the shoulder (5th ed). Functional anatomy and mechanics. St. Louis. Churchhill Livingstone. 2012:9-23. 20. Elkstrom R, Osborn R. Physical therapy of the shoulder (5th ed). Muscle length testing and electromyographic evidence for manual strength testing and exercises for the shoulder. St. Louis. Chrchhill Livingstone. 2012:329-350. 21. Travell J, Simons D. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams & Wilkins. 1983:410-424. 22. Turkel S, Panio M, Marshall J, Girgis F. Stabilizing Mechanisms Preventing Anterior Dislocation of the Glenohumeral Joint. J Bone Joint Surg Am. 1981;63(8):1208-1217. 23. Kelley MJ, Shaffer MA, Kuhn JE, et al. J Orthop Phys Ther. 2013;43(5):A1-31. 24. Burkhart S, Morgan C, Kibler W. The disabled throwing shoulder: spectrum of pathology Part III: The sick scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19(6):641-661. 25. Hawkins R, Kennedy J. Impingement syndrome in athletes. Am J Sports Med. 1980;8(3):151-157. 26. Magee D. Orthopedic Physical Assessment (5th ed). Shoulder. St. Louis. Churchhill Livingstone. 2008:231260. 27. Neer CS 2nd. Impingement Lesions. Clin Orthop Relat Res. 1983;173:70-77. 28. Yocum L. Assessing the shoulder. Clin Sports Med. 1983;2(2):281-289. 29. Gerber C, Krushell R. Isolated rupture of the tendon of the subscapularis muscle. Clinical features in 16 cases. J Bone Joint Surg. 1991;73-B(3):389-394.
30. Kibler W. The role of the scapula in athletic function. Am J Sports Med. 1998; 26:325-337. 31. American College of Sports Medicine position stand. Progression models in resistance training for healthy adults. Med Sci Sports Exerc. 2009;41(3):687-708. 32. Donatelli R, McMahon T. Physical therapy of the shoulder (5th ed). Manual therapy techniques. St. Louis. Churchhill Livingstone. 2012:305-327. 33. Muraki T, Aoki M, Uchiyama E, et al. A cadaveric study of strain on the subscapularis muscle. Arch Phys Med Rehabil. 2007;88:941-946. 34. Godges J, Mattson-Bell M, Thorpe D, Shah D. The immediate effects of soft tissue mobilization with proprioceptive neuromuscular facilitation on glenohumeral external rotation and overhead reach. J Orthop Sports Phys Ther. 2003;339(12):713-718. 35. Bjordal J, Coupe C, Chow R, et al. A systematic review of low level laser therapy with locationspecific doses for pain from chronic joint disorders. Aust J Physiother. 2003; 49(2):107-116. 36. Kneebone W. Laser therapy. Deep penetration therapeutic laser. Practical Pain Management. 2007;7(4):54-56. 37. Turner J, Hode L. The laser therapy handbook. Sweden. Prima Books. 2004:43. 38. Bjordal J, Couppe C, Ljunggren A. Low level laser therapy for tendinopathy: evidence of a doseresponse pattern. Phys Ther Rev. 2001;6:91-99. 39. Huang Y, Chen A, Carroll J, Hamblin M. Bi-phasic dose response in low level light therapy. Dose Response. 2009;7:358-383. 40. Neviaser A, Hannafin J. Adhesive capsulitis: a review of current treatment. Am J Sports Med. 2010;38(11):2346-2356.
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CASE REPORT
SUBSCAPULARIS SYNDROME: A CASE REPORT Michael S. Thurner, PT, DPT, CSCS1 Robert A. Donatelli, PhD, PT1 Randa Bascharon, DO, ATC2
ABSTRACT Dysfunction of the subscapularis muscle is introduced in this case report as a potential factor for consideration in the etiology and/or consequential sequelae of subacromial impingement syndrome. Although dysfunction of the supraspinatus and infraspinatus are implicated as being most commonly involved with subacromial impingement pathology, the subscapularis is often overlooked and therefore undertreated. Identifying the subscapularis’ potential involvement in patients with subacromial impingement pathology may offer insight into shoulder impingement dysfunction and injury treatment options available to specifically address subscapularis dysfunction. In this manuscript, a case report is presented to highlight the signs and symptoms of subscapularis pathology concordant with subacromial impingement syndrome and provide a clinical rationale for treatment. The purpose of this case report is not to suggest a new approach to shoulder rehabilitation, but rather to prompt the consideration of subscapularis dysfunction when evaluating and treating patients with subacromial impingement pathology. Key words: Subcapularis, subscapularis syndrome, subacromial impingement Level of Evidence: 5
CORRESPONDING AUTHOR 1
Physiotherapy Associates Orthopedic & Sports Center, Las Vegas, NV, USA 2 Orthopedic & Sports Medicine Institute of Las Vegas, Las Vegas, NV, USA Acknowledgments We would like to thank the participants for their time. Funding for this project was provided by a grant from the United States National Institutes of Health; K12 HD055931
Michael S. Thurner, PT, DPT, CSCS Physiotherapy Associates Orthopedic & Sports Center 5920 South Rainbow Blvd. Suite 1 Las Vegas, NV 89118 Email: [email protected]
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INTRODUCTION Impingement syndrome is well defined in the literature as a pathological condition of the shoulder complex associated with a clinical manifestation of signs and symptoms altering normal motion and pain free function of the affected upper extremity.1,2,3 In this case report, the authors introduce the subscapularis muscle of the rotator cuff as a plausible factor for consideration as part of a cascade of potential causes and subsequent sequelae associated with subacromial impingement pathology. Relative scarcity of literature describing the relationship between subacromial impingement syndrome and subscapularis dysfunction combined with numerous clinical observations of improved outcomes with specific interventions prompt the senior author to refer to the subscapularis as the “hidden culprit” of the rotator cuff. There are several cardinal signs and symptoms that may implicate the subscapularis muscle of the rotator cuff as a contributing factor to dysfunction and functional limitations of the shoulder complex. Linking underlying subscapularis soft tissue restrictions to subacromial impingement syndrome with positive tests and measures may be helpful in gaining a more thorough and broad understanding of contributions to shoulder impingement pathology and also have implications for treatment to address subscapularis dysfunction. With early recognition and treatment, patients presenting with subacromial impingement and concurrent subscapularis impairments may be able to reduce time of recovery and enhance optimal outcomes. The subscapularis originates in the subscapular fossa on the costal surface of the scapula and courses anterior and laterally to insert on the lesser tuberosity of the humerus.4,5,6 (Figure 1) This is the largest of the four rotator cuff muscles with nearly three times the physiological cross sectional area as the remaining three posterior cuff muscles combined.7 The subscapularis muscle primarily functions as a humeral depressor and stabilizer along with its traditional role as an internal rotator of the humerus.8 The histologic architecture of the rotator cuff tendons fiber arrangement is composed of multiple layers, which consist of crossover and interlocking of the fiber layers.9,10 The tendon fibers blend with and reinforce the glenohumeral capsule.10 This protective overlap of interlocking
Figure 1. Anatomy of the Shoulder complex.
fibers may potentially preserve the functional integrity of the rotator cuff’s dynamic stabilization role in case of a partial tear or complete rupture due to this integrated anatomical relationship of the rotator cuff tendon fibers.9,11,12 Histologically, some fibers of the subscapularis and supraspinatus interlock and converge together as they course around and above the humeral head to their respective insertion sites on the greater tubercle, thereby anatomically preserving the depressive capability of the remaining cuff fibers.12 The force vectors of the subscapularis and the infraspinatus are biomechanically more optimally aligned to efficiently provide depression of the humeral head, compared with the supraspinatus.9,13,14 Specific exercises of the rotator cuff and scapular rotators eliciting high EMG activity of the targeted musculature are later described in the interventions section of this case report.8,15 Also, it is important to note when developing a comprehensive rehabilitation or strength and conditioning program for the cuff deficient patient or client, that the teres major and latissimus dorsi can also provide humeral depression forces secondary to their anatomical alignment.9,13 Therefore, in the case of rotator cuff dysfunction, the health care professional should carefully consider the development of an individualized program incorporating specific therapeutic strengthening exercises and stretching or soft tissue mobilization in order to promote function of the patient or client by offsetting the deficiency or weakness that is present.
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BACKGROUND & PURPOSE The glenohumeral joint is the most mobile joint present in the human body due to its osseous configuration.16,17 The articulation of the shallow glenoid cavity with the relatively large humeral head allows for extreme ranges of movement in all planes of motion, and thus inherently lacks stability.16,17 In the healthy shoulder, synchronous activation of the dynamic stabilizers (acting as a force couple) provide stability to this proximal link of the upper extremity chain. Proximal stability is crucial to influence distal functional mobility, allowing the hand to move freely in space. As a complement to dynamic stability, the ligamentous and capsular tissue architecture of the glenohumeral joint provide tension at the extremes of available motion offering inherent static stability relative to all planes of shoulder movement. Dynamic stabilization of the glenohumeral joint is affected by the rotator cuff and the scapulothoracic musculature. The rotator cuff muscles stabilize the glenohumeral joint by acting to depress and compress the humeral head within the glenoid concavity.8,9 The scapulothoracic muscles control scapular movements allowing for optimal length-tension relationships of the rotator cuff musculature by properly aligning the glenoid concavity relative to the humeral head.8 Neuromuscular control and adequate ratios of scapular muscle strength are essential to shoulder complex function because the scapula and humerus simultaneously move together in a complex yet coordinated fashion during shoulder movement, referred to as scapulohumeral rhythm.8 A disruption of this synergistic relationship may occur secondary to a muscle imbalance, altering the normal kinematics of this complex network of force couples.3 Compensatory movement patterns may subsequently present as scapular dyskinesis or concomitant scapular asymmetry.3,18 The inability of the rotator cuff to effectively offset the superior shear force of the deltoid may result in superior humeral head migration into the subacromial space.3,18 Consequently, this sequela of events may potentially lead to subacromial impingement. Subacromial impingement has been defined as mechanical compression of the soft tissue structures that pass beneath the coracoacromial arch as the shoulder is elevated.1,2,3 The structures subject to impingement are the rotator cuff tendons, long head of the biceps tendon and
the subacromial bursa.1,2,3 Subacromial impingement pathology commonly affects the posterior rotator cuff tendons, most notably the supraspinatus. This may induce a compensatory increase in activation of the subscapularis in order to accommodate for the deficient or inhibited ability of the affected muscles to sufficiently counteract the superior shear force of the humeral head as the deltoid muscle contracts during elevation of the arm.9 Although dysfunction of the supraspinatus and infraspinatus is commonly implicated as being associated with subacromial impingement pathology, it is the assertion of the authors that the subscapularis is often overlooked and therefore undertreated. Compensatory activation of the subscapularis may consequently lead to overuse over time secondary to repetitive microtrauma, eventually resulting in pathology of the muscle-tendon complex. Adaptive overuse without adequate healing time for the tissue to recover will ultimately result in fatty infiltration of the muscle belly and/or degenerative scarring of the tendon consistent with tendinosis pathology as may be evident through magnetic resonance imaging (MRI).4 Fibrosis or scarring of the subscapularis may present clinically as trigger points to palpation and adaptive shortening of the muscle belly and/or tendon, thus limiting shoulder external rotation in the adducted position.19,20,21,22,23 Cadaveric studies by Turkel et al indicate that the subscapularis muscle is the most influential stabilizing structure during passive external rotation of the glenohumeral joint at zero degrees of abduction in the frontal plane.22,23 Furthermore, the integrity of the muscle-tendon complex may continue to be compromised by adaptive shortening secondary to protective shoulder postures of immobilization in the adducted and internally rotated position. Travell and Simmons propose that a trigger point within the subscapularis muscle may sensitize adjacent muscles of the shoulder girdle presenting as secondary or satellite trigger points potentially leading to a heightened sensitization of pain and motion restrictions of the shoulder complex.21 (Figure 2) Resultant scapular malalignment as a result of restricted mobility of the subscapularis may subsequently cause poor length-tension relationships of the scapular musculature, further accentuating the muscle imbalance.
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Figure 2. Subscapularis Trigger Points (x’s) & projected referral pain pattern. The essential referred pain zone appears as solid red with the spillover zone illustrated as stippled.
Scapular malalignment or asymmetrical scapulae, often referred to as S.I.C.K. (Scapular malposition, Inferior medial border prominence, Coracoid pain, Scapular dyskinesia) scapula, may present as a protracted scapula on the side of the affected extremity in patients presenting with shoulder impingement.24 Through clinical observation, the author’s note adaptive shortening of the subscapualris often occurs in conjunction with an internally rotated scapular postural abnormality, associated with lengthened and subsequently weakened posterior rotator cuff and scapular musculature. Limited and painful active elevation of the shoulder in the plane of the scapula is a classic sign of subacromial impingement syndrome. This may be a consequence of a lack of disassociation between the scapula and the humerus and/or the diminished glenohumeral external rotational capacity preventing sufficient clearance of the greater tuberosity under the coracoacromial arch during elevation of the shoulder.19 The lack of disassociation will inherently disrupt the normal biomechanics of the shoulder complex and could potentially limit the depressive capability of the already compromised subscapularis muscle, resulting in superior migration of the humeral head, due to the previously described muscle imbalance in relation to the deltoid. Repetitive overhead activity may result in subacromial impingement pathology with the associated painful shoulder movement into positions of glenohumeral joint elevation. The Hawkins-Kennedy, Neer, and Yocum impingement tests will usually confirm
the diagnosis of impingement.25,26,27,28 Although anatomically the subscapularis does not pass under the subacromial region, it has been shown to limit glenohumeral external rotation, which may lead to subacromial impingement pathology as previously described.22,23 Secondary to the characteristic nature of overuse, the subscapularis muscle will usually present as weak and painful upon muscle testing illustrated by the belly press and/or lift-off test.26,29 The clinical presentation of limited external rotation in the adducted position, pain to palpation of trigger points within the subscapularis muscle belly and/ or tendon, and dysfunction of the subscapularis on strength testing should be considered in the etiology of subacromial impingement. The concept of labeling or categorizing specific shoulder impingement pathology helps identify the relationship between clinical findings and shoulder dysfunction. Identifying the subscapularis’ potential involvement in patients with subacromial impingement pathology may be helpful in gaining a greater insight into shoulder dysfunction, and expand intervention options to address subscapularis dysfunction. Further research is warranted to determine the cause and effect relationship between the subscapularis and subacromial impingement syndrome pathology. CASE REPORT Patient History A 22 year old right hand dominant female tennis player was sent to physical therapy with a physician diagnosis of right shoulder pain secondary to sub-
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acromial impingement. The patient reported a threemonth history of ‘deep’ shoulder pain without being able to identify specific physical boundaries. The pain was elicited when she was serving overhead or during the follow-through phase of a forehand swing. She reported an insidious onset of symptoms with no history of specific trauma to the right shoulder. Magnetic resonance imaging (MRI) results suggested tendinopathy of the supraspinatus and subscapularis tendon with a possible partial tear of the supraspinatus tendon. The Quick DASH outcome measure with the optional sports/performing arts module was completed at the initial evaluation and the patient scored fifty percent, and twenty-two percent disability/symptom scores in sport and overall function, respectively. Examination The patient tested positive on the Neer and Yocum impingement tests. An internally rotated right scapula, medial border prominence, and a mild lack of disassociation of the scapula and humerus were identified during active elevation of the arm in the plane of the scapula through visual observation in comparison with the opposite extremity. Passive external rotation (ER) at zero degrees of abduction was limited to 30 degrees with the total internal/external rotation arc of motion at 90 degrees of abduction equal to the left shoulder. (Figure 3) The opposite extremity was measured for comparison at zero degrees of abduction and was found to be within normal limits, at 75 degrees of external rotation. Prominent weakness (3-/5) and pain (7/10) were noted during manual muscle testing of both the
Figure 3. Restricted External Rotation in the Adducted Position.
Figure 4. Lift-off Test for the Subscapularis.
supraspinatus in the ‘full can’ position and the subscapularis while performing the lift-off test. (Figure 4) Mild deficits were also noted during testing of the infraspinatus and teres minor, which were graded with a 4/5 and 4-/5 respectfully. The serratus anterior, middle and lower trapezius were also tested via manual muscle testing and were graded as 4-/5, 4/5, and 4-/5 respectfully. Subjective complaints of pain 4/10 were noted during manual muscle testing of the lower trapezius. The authors note that the test position in question requires the test subject to abduct and externally rotate the glenohumeral joint, which also recruits the supraspinatus and may biomechanically result in impingement due to faulty mechanics of the injured shoulder, thus irritating the already compromised soft tissue structures. Trigger points were identified upon palpation of the superior and inferior lateral aspect on the anterior surface of the subscapularis muscle belly with the patient positioned in supine with the humerus supported in an abducted and externally rotated position. (Figure 5) At the conclusion of the physical examination, the identifying signs and symptoms were enough to suspect involvement of the subscapularis. Intervention & Outcome The focus of treatment was to re-establish scapulohumeral rhythm by improving strength and mobility of the shoulder complex allowing the patient/athlete to return to tennis unrestricted and symptom free. During the first four weeks of physical therapy, treatment consisted of a progressive resistive exercise (PRE) pro-
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Figure 5. Trigger Points to palpation of the Subscapularis Muscle Belly and/or Tendon.
gram to address weakness and postural adaptations of the rotator cuff and scapula rotator musculature, low-level laser therapy (LLLT) with deep sustained pressure to relieve trigger points in the subscapularis muscle belly, low load prolonged-duration (LLPS) stretching into external rotation and soft tissue mobilization to improve the mobility of the subscapularis. Therapeutic exercises were initiated using high repetitions (12-15 × 2-3 sets) and moderate to light weight with an emphasis on pain free motion in Phase I. The overall goal of therapeutic exercise in the initial phase was to stimulate appropriate muscle activation, promote muscular strength and endurance, and increase blood flow to the healing tissue in order to enhance the recovery process. The exercises were selected to target specific musculature identified during the examination as having less than optimal strength. Specific exercises of the rotator cuff and scapular rotators eliciting high EMG activity of the targeted musculature are illustrated in figures 610.8,15 (Figures 6-10) The exercises were progressed in Phase 2 using increased weight with fewer repetitions (8-12 reps × 3 sets) in order to transition to a more focal emphasis on muscular strengthening of the shoulder complex. LLLT was utilized in phases III using a pulsed (905 nm) laser with deep sustained pressure utilizing a laser probe for three sets of fiveminute cycles. (Figure 11) Pressure was applied over the trigger points identified in the examination and modified according to patient tolerance. Manual mobilization of the scapula was also initiated in the initial phase and progressed into phase II based on patient tolerance. The patient was positioned in a
Figure 6. Subscapularis Diagonal Exercise.
Figure 7. Dynamic Hug, using pulley system.
side-lying position with the upper extremity relaxed at the patient’s side. The physical therapist performs a distraction force to the scapula with a sustained hold to patient tolerance with oscillatory mobilizations performed intermittently between manual stretch holds at the therapist’s discretion. (Figure 12) A low-load prolonged stretch into glenohumeral external rotation was applied continuously for 20 minutes in phases I-II. The patient was positioned in the supine position with the shoulder supported on a foam wedge in zero degrees of abduction allowing gravity to produce the intended stretch into external rotation. (Figure 13) By the end of the fourth week of
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Figure 8. Biodex Eccentric Loading Internal/External Rotation.
Figure 11. Low Level Laser with Deep Sustained Pressure Over the Trigger Points.
Figure 9. Prone Horizontal Abduction with External Rotation @ 90 & 135 Degrees of Abduction.
Figure 12. Scapular Tilt & Distraction.
Figure 10. Prone External Rotation and Horizontal Abduction @ 90 Degrees of Abduction & Elbow Flexion.
Figure 13. Low Load Prolonged Stretch of the Subscapularis.
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treatment, the patient demonstrated full active elevation without evidence of compensatory movement patterns, symmetrical scapulae, pain free grades of 5/5 during manual muscle testing of the rotator cuff and scapular rotator musculature, improved passive range of motion to 75 degrees of external rotation at zero degrees of abduction, and no pain 0/10 to palpation of the subscapualris muscle belly or tendon.30 Table 1 highlights the clinical deficits present and the proposed corrective therapeutic exercise or treatment as depicted in figures 3-13. (Table 1) Table 2 identifies the prescription of therapeutic exercise and phase in which specific therapeutic interventions were implemented in relation to this case report. (Table 2)
in this phase to reintroduce the overhead movement including the tennis serve in a controlled environment. Lateral bounding and agility drills with sport cord resistance were incorporated with the tennis swing in order to enhance neuromuscular control and spatial awareness. Internal and external rotation performed above 90 degrees of abduction at varying speeds was also introduced in this phase to improve strength and power in the overhead position. Interval training using ten second intervals of high intensity lateral movement inter-dispersed with submaximal low intensity active rest for thirty seconds on the dynamic edge was also initiated at this time to progress the patient/athlete’s conditioning status.
Weeks 4-6 comprised of advancing the progressive resistive strengthening program using the principles of muscle strengthening established by ACSM guidelines.31 A return to sport program specific to tennis was also integrated at this time on order to optimally prepare the patient for return to play. The resistance of the therapeutic exercise targeting the rotator cuff and scapular rotators was increased accordingly to the patient’s tolerance and ability to demonstrate proper technique throughout the exercise. The emphasis of the Phase III, during weeks 4-6, was low repetition exercise (6-8 reps × 3 sets) with adequate resistance to enhance overall muscular strength. Sport specific exercises for the overhead athlete were also initiated
The Quick DASH was performed again, and the patient scored a zero percent disability/symptoms at discharge with no deficits or dysfunction reported. The patient/athlete was able to return to unrestricted tennis, symptom free, following the aforementioned six weeks of physical therapy. DISCUSSION Clinically, over the past 20 years the senior author has consistently observed a clinical relationship between a loss of glenohumeral external rotation in the adducted position and signs and symptoms of subacromial impingement pathology. Furthermore, these patients concurrently exhibited near
Table 1. Clinical presentation and proposed intervnetions.
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Table 2. Phased Intervention used during treatment of the subject in the case report.
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Table 2. Phased Intervention used during treatment of the subject in the case report. (continued)
equal (+/- 5 degrees) total internal/external arc of motion at 90 degrees of abduction when compared to uninvolved side. According to Turkel et al, the most influential stabilizing structure during passive glenohumeral external rotation at zero degrees of abduction is the subscapularis muscle.22 Thus, the authors of this case report believe that a restriction of external rotation at zero degrees of abduction with normal passive external rotation range of motion at 90 degrees of abduction may be indicative of the subscapularis as the primary restricting tissue. Elkstrom et al and Donatelli et al describe external rotation at zero degrees of shoulder elevation as the selective stretch or testing position for the subscapularis.20,32 A more recent cadaveric study suggests varying angles of abduction in conjunction with external rotation induce strain on different portions of distinct fiber arrangements within the subscapularis muscle.33 Turkel et al also note that no single structure solely stabilizes the glenohumeral joint in any one plane of motion, and the position and tightness of anterior structures vary with abduction and external rotation angles.22,32 This anatomical concept of stability has been well established in the literature although the contributions of specific stabilizing structures remains controversial. The authors of this case report acknowledge the anatomic variance of the orientation of fibers comprising the subscapularis muscle and thus promote stretching at multiple angles of elevation if the subscapularis is identified as the predominately restricted tissue structure. The subject of this case report presented with mobility
restrictions of the shoulder characteristic of the subscapularis’ involvement. Godges et al recently demonstrated a positive correlation between soft tissue mobilization with proprioceptive neuromuscular facilitation to the subscapularis muscle belly and an increase in external rotation and overhead reach.34 In the current case report, the treating clinicians utilized a deep pressure soft tissue mobilization technique in conjunction with LLLT, as illustrated in figure 11. LLLT is a modality treatment used to facilitate recovery by attempting to promote a healing response at the cellular level. Several authors suggest that LLLT with a high power level of impulse or biphasic dose response has the capacity to drive photons (light energy) to the target tissue at depths of up to 10-13 cm or 4-5 inches.35,36,37 The proposed healing effects revolve around improvement of microcirculation at an adequate depth of penetration to reach the targeted soft tissue structures and increase cell metabolism (which is proposed to influence ATP production or energy used to enhance recovery at a cellular level). This may may assist in returning the damaged cells to a stable, healthy state.38,39 LLLT has been cited as a safe and effective modality to accelerate pain relief and healing.38,39 Also, a subscapularis tilt and distraction soft tissue mobilization technique was used to provide oscillatory mobilization stretch in an attempt to alleviate any soft tissue restrictions present within the subscapularis muscle as illustrated in Figure 12. Low load prolonged-duration stretch (LLPS) has histori-
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cally been utilized in physical therapy as an effective means to induce lengthening of soft tissue.40 The emphasis of the stretching technique applied in this case report is to restore tissue length by way of gradual application of tension over time to produce a permanent or plastic remodeling of the connective tissues allowing increased range of motion over the course of time. LLPS was implemented at the onset of treatment to promote tissue lengthening without inducing pain. In this case, the patient was able to fully tolerate treatment and ultimately regained full mobility of the shoulder. The patient was also introduced to a progressive resistance exercise program early in the rehabilitation process in order to develop neuromuscular control, improve overall strength, and facilitate optimal ratios of strength of the rotator cuff and scapular rotator musculature for promotion of normal scapulohumeral rhythm. She responded well to physical therapy intervention progressing as appropriate under the discretion of the physical therapist, ultimately returning to tennis without residual pain or limitation. CONCLUSION Patients frequently present or are referred to physical therapy with a non-specific diagnosis relating to shoulder ‘pain’. Any patient presenting with shoulder pathology may present with some or all of the signs and symptoms that implicate the subscapularis as a part of the dysfunction. Manual therapy techniques and exercise prescription as illustrated in this case report may be implemented once a treatment plan is established based on the clinical examination. Further research is warranted in order to establish the degree of involvement of the subscapularis in the presentation of patient with subacromial impingement syndrome. Higher-level studies are needed to establish parameters for ‘significant’ external rotation range of motion loss, to objectively quantify strength deficits (perhaps using isokinetic dynamometry), and determine the effectiveness of interventions utilized to resolve subscapularis impairments. REFERENCES 1. Bigliani L, Levine W. Current concepts review: subacromial impingement syndrome. J Bone and Joint Surg. 1997;79:1854-1868. 2. Harrison A, Flatow E. Subacromial impingement syndrome. J Am Acad Orthop Surg. 2011;19(11):701-708.
3. Ludewig P, Reynolds J. The association of scapular kinematics and glenohumeral joint pathologies. J Orthop Sports Phys Ther. 2009;39(2):90-104. 4. Morag Y, Jamadar D, Miller B, et al. The subscapularis: anatomy, injury, and imaging. Skeletal Radiol. 2011;40:255-269. 5. Cleeman E, Brunelli M, Gothelf T, et al. Releases of subscapularis contracture: an anatomic and clinical study. J Shoulder Elbow Surg. 2003;12:231-6. 6. Warwick R, Williams P, Gray H. Gray’s Anatomy (35 ed). Philadelphia. Saunders Company. 1973;532-540. 7. Ward S, Hentzen E, Smallwood L, et al. Rotator cuff muscle architecture: implications for glenohumeral stability. Clin Orthop Relat Res. 2006;448:157-163. 8. Reinold M, Escamilla R, Wilk K. Current concepts in the scientific and clinical rationale behind exercises for glenohumeral and scapulothoracic musculature. J Orthop Sports Phys Ther. 2009;39 (2):105-117. 9. Millet P, Wilcox III R, O’Holleran J, Warner J. Rehabilitation of the rotator cuff: an evidence based approach. J Am Acad Orthop Surg. 2006;14(11):599609. 10. Cooper D, O’Brian S, Warren R. Supporting layers of the glenohumeral joint. An anatomic study. Clin Orthop Relat Res. 1993;289:144-155. 11. Sakurai G, Ozaki J, Tomitta Y, et al. Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus: cadaveric and clinical studies. J Shoulder and Elbow Surg. 1998;7(5):510-515. 12. Thompson W, Debski R, Boardman N III, et al. A biomechanical analysis of rotator cuff deficiency in a cadaveric model. Am J Sports Med. 1996;24:286-292. 13. Halder A, Zhao K, O’Driscoll S, Morrey B, et al. Dynamic contributions to superior shoulder stability. J Orthop Res. 2001;19:206-212. 14. Neuman D. Kinesiology of the musculoskeletal system. Foundations for physical rehabilitation. Shoulder Complex. St.Louis. Churchhill Livingstone. 2002:91-132. 15. Decker M, Tokish J, Ellis H, Torry M, Hawkins R. Subscapularis muscle activity during selected rehabilitation exercises. Am J Sports Med. 2003;31:126-134. 16. Bigliani L, Kelkar R, Flatow E, et al. Glenohumeral stability. Biomechanical properties of passive and active stabilizers. Clin Orthop Relat Res. 1996;330:13-30. 17. Wilk K, Arrigo C, Andrews J. Current concepts: the stabilizing structures of the glenohumeral joint. J Orthop Sports Phys Ther. 1997;25(6):364-379. 18. Kibler W, McMullen J. Scapular dyskinesias and its relation to shoulder pain. J Am Acad Orthop Surg. 2003;11:142-151.
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19. Donatelli, R. Physical therapy of the shoulder (5th ed). Functional anatomy and mechanics. St. Louis. Churchhill Livingstone. 2012:9-23. 20. Elkstrom R, Osborn R. Physical therapy of the shoulder (5th ed). Muscle length testing and electromyographic evidence for manual strength testing and exercises for the shoulder. St. Louis. Chrchhill Livingstone. 2012:329-350. 21. Travell J, Simons D. Myofascial pain and dysfunction: the trigger point manual. Baltimore: Williams & Wilkins. 1983:410-424. 22. Turkel S, Panio M, Marshall J, Girgis F. Stabilizing Mechanisms Preventing Anterior Dislocation of the Glenohumeral Joint. J Bone Joint Surg Am. 1981;63(8):1208-1217. 23. Kelley MJ, Shaffer MA, Kuhn JE, et al. J Orthop Phys Ther. 2013;43(5):A1-31. 24. Burkhart S, Morgan C, Kibler W. The disabled throwing shoulder: spectrum of pathology Part III: The sick scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy. 2003;19(6):641-661. 25. Hawkins R, Kennedy J. Impingement syndrome in athletes. Am J Sports Med. 1980;8(3):151-157. 26. Magee D. Orthopedic Physical Assessment (5th ed). Shoulder. St. Louis. Churchhill Livingstone. 2008:231260. 27. Neer CS 2nd. Impingement Lesions. Clin Orthop Relat Res. 1983;173:70-77. 28. Yocum L. Assessing the shoulder. Clin Sports Med. 1983;2(2):281-289. 29. Gerber C, Krushell R. Isolated rupture of the tendon of the subscapularis muscle. Clinical features in 16 cases. J Bone Joint Surg. 1991;73-B(3):389-394.
30. Kibler W. The role of the scapula in athletic function. Am J Sports Med. 1998; 26:325-337. 31. American College of Sports Medicine position stand. Progression models in resistance training for healthy adults. Med Sci Sports Exerc. 2009;41(3):687-708. 32. Donatelli R, McMahon T. Physical therapy of the shoulder (5th ed). Manual therapy techniques. St. Louis. Churchhill Livingstone. 2012:305-327. 33. Muraki T, Aoki M, Uchiyama E, et al. A cadaveric study of strain on the subscapularis muscle. Arch Phys Med Rehabil. 2007;88:941-946. 34. Godges J, Mattson-Bell M, Thorpe D, Shah D. The immediate effects of soft tissue mobilization with proprioceptive neuromuscular facilitation on glenohumeral external rotation and overhead reach. J Orthop Sports Phys Ther. 2003;339(12):713-718. 35. Bjordal J, Coupe C, Chow R, et al. A systematic review of low level laser therapy with locationspecific doses for pain from chronic joint disorders. Aust J Physiother. 2003; 49(2):107-116. 36. Kneebone W. Laser therapy. Deep penetration therapeutic laser. Practical Pain Management. 2007;7(4):54-56. 37. Turner J, Hode L. The laser therapy handbook. Sweden. Prima Books. 2004:43. 38. Bjordal J, Couppe C, Ljunggren A. Low level laser therapy for tendinopathy: evidence of a doseresponse pattern. Phys Ther Rev. 2001;6:91-99. 39. Huang Y, Chen A, Carroll J, Hamblin M. Bi-phasic dose response in low level light therapy. Dose Response. 2009;7:358-383. 40. Neviaser A, Hannafin J. Adhesive capsulitis: a review of current treatment. Am J Sports Med. 2010;38(11):2346-2356.
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