The Shoulder Girdle: Kinesiology Review Pamela K Levangie, PT, DSC, and Ellen Cook Humphrey, PT, MAPT, OCS, ATC

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1 The Shoulder Girdle: Kinesiology Review Pamela K Levangie, PT, DSC, and Ellen Cook Humphrey, PT, MAPT, OCS, ATC Objectives After reading this continuing education (CE) article and reviewing shoulder girdle anatomy, you should be able to meet the following objectives: Describe the intra-articular and capsuloligamentous structure of the sternoclavicular, acromioclavicular, and glenohumeral joints and the osteokinematic and arthrokinematic movements that take place at each joint. Describe the interrelationship among the scapulothoracic, sternoclavicular, and acromioclavicular joints, including the roles of the coracoclavicular and costoclavicular ligaments and the muscles that act on these joints. Explain the structural components and synergy of muscles necessary to stabilize and complete a full range of active elevation of the arm at the glenohumeral joint. Identify factors that may place a shoulder at increased risk for an impingement problem. Explain how a given capsuloligamentous or muscular restriction to motion of the clavicle, scapula, or humerus can affect normal movement of the arm. Identify factors that may increase the risk of shoulder girdle hypomobility in a patient who had a mastectomy with adjuvant radiation. Pamela K Levangie, PT, DSc, is associate professor, Physical Therapy Program, Sacred Heart University, Fairfield, Connecticut. Ellen Cook, PT, MAPT, OCS, ATC, was instructor, Department of Physical Therapy and Human Movement Sciences, Northwestern University Medical School, Chicago, Illinois. Introduction In the May 2000 issue of PT, Davies and Durall discussed rotator cuff impingement, focusing on recognizing atypical symptoms. This month s continuing education offering focuses on shoulder girdle kinesiology in a case involving a patient who has shoulder dysfunction secondary to a bilateral mastectomy, high-dose chemotherapy, and breast implant surgery. Management of patients with any type of shoulder dysfunction poses a particular challenge to clinicians, because they must recall and apply their knowledge of shoulder girdle kinesiology. Given the complex mobility and stability components that support shoulder function, knowledge of anatomy alone is insufficient to understand the potential sources of pain and dysfunction in the interdependent joints of the shoulder girdle, cervical spine, and rib cage. Through this case example, we will review the biomechanics of the joints of the shoulder girdle that may be implicated when a patient has shoulder pain and hypomobility. We will first discuss the history and systems review that provide a snapshot of the case; then, we will review the kinesiologic considerations that contribute to the subsequent selection of tests and measures. The initial examination and the evaluation of examination data follow. For the purpose of this case, the interdependent issues of joint integrity and muscle performance for the shoulder girdle are emphasized in the examination. Because the primary objective of this case is to review shoulder girdle kinesiology, we will review prognosis and intervention only briefly. Knowledge of muscle anatomy (attachments, innervation, and basic functions) and of joint configurations (osteology and arthrology) is assumed. Readers who want to review these elements are encouraged to refer to a basic anatomy text, such as Gray s Anatomy 1 or Clinically Oriented Anatomy. 2 Examination History JD is a 50-year-old woman who has been referred to a physical therapist by her primary care physician for management of right shoulder pain. She is a high school science teacher. Married with two adult children, she lives in and cares for her own two-story home, commutes to work 1 hour by car, and walks 2 miles each day. JD reports intermittent right antero-superior shoulder pain that began 5 months ago, apparently in connection with breast implant reconstruction. Symptoms were exacerbated recently (with no identifiable precipitating factor), leading her to seek medical attention. JD describes her pain as dull and aching, with an occasional sharp twinge aggravated by lifting and reaching above shoulder level (7/10 on a verbal pain scale [VPS]). She is independent in activities of daily living (ADL), but she reports fatigue and pain (5/10 on a VPS) with blowdrying her hair, household cleaning, or spending any

2 amount of time at the blackboard at school, and she reports an inability to fasten her bra behind her back. Symptoms are relieved to 2/10 on a VPS with rest, ibuprofen, and ice. JD reports that she is unable to sleep on her right side because of pain. She is right-hand dominant. Prior to the fall of 1997, JD indicated that she was active and in good health, with only occasional bouts of low back pain. In the fall of 1997, she had a stage III malignancy removed from her right breast. Two weeks later, she underwent a bilateral mastectomy, with prophylactic removal of the left breast. She opted for implant reconstruction at the time of her surgery. The left tissue expander was put into place, but the right tissue expander was withheld because the lymph nodes were positive for cancer, indicating a need for adjuvant radiation. JD received 4 months of high-dose chemotherapy, which was completed in March Treatment concluded in June 1998 after 6 weeks of routine radiation to the right chest wall and axilla. In October, JD had a tissue expander inserted for stage I reconstruction of the right breast mound. Despite slow tissue expansion over 6 months, the postradiation fibrotic tissue changes resulted in the extrusion of the expander through the healed incision. The expander was removed, and a saline implant was inserted. After 3 weeks, the sutures were removed, and the incision reopened 12 hours later. The implant was removed. Incision healing from the last surgery was compromised, and complete wound closure took 3 months, with one wound infection that was treated successfully. JD reports that a recent set of bone and computed tomography scans was negative for metastatic disease. She is currently taking tamoxifen. Systems Review The physical therapist performs a systems review as part of the examination process before determining the complete battery of tests and measures that will be used to examine JD. Cardiovascular/pulmonary system. No impairments were noted in the cardio-vascular/pulmonary system. Integumentary system. The physical therapist notes that the right anterior chest wall incision is 3 inches long, puckered, and extends diagonally into the axilla. There is a pronounced anterior axillary fold. The skin over and around the surgical scar appears to adhere to the underlying tissue and bone, and the ribs beneath the scar appear to be depressed relative to the surrounding ribs. The scar and surrounding tissue are completely immobile and appear to adhere to the thorax. Limited skin mobility extends into the axilla. The left chest wall shows a wellhealed 4-inch horizontal scar over the implanted breast mound. Musculoskeletal system. The physical therapist observes that the right scapula is protracted and tipped forward and that the right arm is slightly medially rotated. There is a moderate increase in the cervico-thoracic kyphosis, and the cervical spine is in mild lateral flexion to the right and rotation on the left. There is a mildly increased lumbar lordosis. JD has pain and hypomobility of the right shoulder girdle. She reports discomfort (4/10 on a VPS) with active shoulder abduction. Horizontal adduction do not increase discomfort; however, JD reports a pulling sensation at the anterior chest wall. JD does not perceive hyperextension as painful, but it exacerbates the pulling sensation. JD is able to just reach the back of her head on the right (2/10 on a VPS) and is able to put her right hand in the small of her back, but she cannot lift her hand off her back in that position without pain. Range of motion (ROM) on the left appears to be adequate for JD s usual activities. With JD in a standing position as she performs the motions, the physical therapist uses visual observation to estimate active ROM for the shoulder girdle as 135 degrees of flexion, 70 degrees of abduction, and 30 degrees of extension. At JD s maximal active shoulder abduction, horizontal adduction is estimated to be 110 degrees, and horizontal abduction is estimated to be 10 degrees from the frontal plane. Neuromuscular system. No impairments were noted in the neuromuscular system. With this picture of JD in mind, we will now review the joint structures of the shoulder girdle that may be associated with JD s pain and limited ROM. Kinesiology: The Shoulder Girdle The function of the shoulder girdle is to move the long lever of the upper extremity though a large frame of space for the placement of the hand. Concomitantly, the shoulder girdle must provide a stable base from which hand function can be performed. The structurally contradictory mobility and stability demands on the shoulder are met by distributing motion through a set of open- and closed-chain linkages that contribute in different ways to the dynamic stability requirements. Interference with the active or passive components of any one of the bony interfaces can, and commonly does, change the 2

3 dynamic at one or more of the other interfaces. Closer examination of the functional demands of the linkages is necessary to understand the possible sources of pain and hypomobility experienced by JD. Scapulothoracic joint. Clinicians must know the components that contribute to scapulothoracic (ST) position and motion in order to understand how the glenoid fossa moves to receive the rotating humeral head and how the scapula adjusts to maintain the proper length tension in the muscles that move the humerus. The ST joint is a functional joint and does not have the fibrous, cartilaginous, or capsular connections that characterize anatomic joints. The scapula is attached to the thorax anatomically by the articulation between the acromion of the scapula and the lateral end of the clavicle and by the articulation between the clavicle and the manubrium of the sternum. Consequently, the functional ST joint forms a closed chain with the acromioclavicular (AC) and sternoclavicular joints (SC), and the motion of the scapula on the thorax depends on the other two articulations. The scapula normally sits on the thorax between the second and seventh ribs, with the medial border approximately 2 inches from the midline. 3 Given the curvature of the thorax, the scapula typically does not lie in the frontal plane but rests 30 to 40 degrees anterior to the frontal plane (medially rotated or winged) and tipped 8 to 20 degrees anteriorly from vertical.4 The ST joint is capable of the interdependent motions of superior translation (elevation), inferior translation (depression), protraction and retraction, and upward and downward rotation. These motions cannot occur, however, unless there is adequate integrity of the AC and SC joints. Together, the ST, AC, and SC joints normally contribute 60 degrees to the elevation of the arm. For our purposes, elevation is defined as movement of the upper extremity from the side anywhere between the frontal and sagittal planes. The ST joint contributes to elevation by upwardly rotating the glenoid fossa (upward rotation of the scapula). There is a consensus that the trapezius and serratus anterior muscles each make important contributions to producing the upward rotation of the scapula that is required for elevation (both flexion and abduction) of the arm; however, there is some disagreement about relative contributions and sequencing. 4-7 These muscles are particularly important because there are no other muscles capable of upwardly rotating the scapula and, therefore, no possibilities for substitution. Acromioclavicular joint. The acromion of the scapula is joined to the lateral clavicle at the AC joint. The AC joint is essentially a plane joint, with variablity among individuals as to which surface is concave and which is convex.1 The angle of inclination of the articulating surfaces also varies considerably from person to person. 8 The angle of inclination of the articulating surfaces varies considerably from person to person. 8 There also may be a fibrocartilaginous disk, depending on the individual s age and the degree of degeneration in the joint. 9 The joint is supported by a relatively weak capsule and stronger superior and inferior ligaments that are reinforced superiorly by aponeurotic fibers of the trapezius and deltoid muscles. 9,10 The coracoclavicular ligament is composed of two bands (the conoid and trapezoid) that firmly join the coracoid process of the scapula to the clavicle, thus maintaining a relatively fixed relationship between the scapula and the clavicle and enhancing the stability of the AC joint. The coracoclavicular ligament plays a critical role in the interdependence of the ST, AC, and SC joints. The AC joint would appear to allow 3 degrees of freedom for the scapula. The first 2 degrees of freedom are not often appreciated as part of normal function but are key to keeping the scapula against the rib cage as the scapula moves around the medial-lateral and superior-inferior convexity of the thorax. 10,11 Terminology for these motions is used inconsistently in the literature. For the purposes of this article, the first degree of freedom is described as medial/lateral rotation of the scapula (motion of the glenoid fossa around a vertical axis through the AC joint). Medial rotation at the AC joint allows the scapula to round the substantial medial-lateral curvature of the rib cage during scapular protraction. As a result of the medial rotation of the scapula, the glenoid fossa faces anteriorly rather than laterally during flexion of the arm and remains behind the flexed humeral head. The second degree of freedom at the AC joint is the anterior and posterior tipping of the superior scapula (motion around a side-to-side axis through the AC joint). The third degree of freedom for the AC joint is the traditionally described scapular motion of upward and downward rotation, which appears to occur around an anteroposterior axis at the AC joint. Under normal conditions, however, little if any upward rotation actually occurs at the AC joint. True upward rotation at the AC joint requires that the coracoid process of the scapula move inferiorly and away from the clavicle. The separation of the coracoid process and clavicle is prevented by the coracoclavicular ligament that binds these two bony segments together. The ligament maintains a relatively constant angle between the clavicle and the superior border of the scapula (the scapuloclavicular angle). As long as the coracoclavicular ligament is intact, the scapula cannot upwardly rotate around an anteroposterior axis at the AC joint (Fig. 1). Upward rotatory forces applied to the scapula by the trapezius and serratus anterior muscles, therefore, produce the motion not at the AC joint but at the next available linkage in the chain that is, at the SC joint. 3

4 Given that upward rotation of the scapula relative to the clavicle cannot occur at the AC joint, it appears that the primary role of the AC joint is to allow the scapula to adjust to the changing contour of the thorax through medial/lateral rotation and anterior/posterior tipping. Injury to or degenerative changes in the AC joint are common and increase with age. Pathology of the AC joint may, in the acute stages, result in pain and hypomobility secondary to that pain. However, persistent subluxation and dislocation (hypermobility) or fixation and fusion (hypomobility) does not appear to result in long-term functional limitations Sternoclavicular joint. The SC joint is an incongruent, saddle-shaped joint with three degrees of freedom. Its congruence and stability are substantially enhanced by a fibrocartilaginous joint disk that diagonally transects the joint space (from the superior clavicular facet to the inferior manubrial facet). The joint is further supported by a strong capsuloligamentous structure. Elevation and depression of the clavicle at the SC joint requires the large medial end of the clavicle (convex vertically) 1 to glide in a direction opposite to the motion of the lateral end of the clavicle. Protraction and retraction require the shallow antero-posterior concavity of the medial clavicle1 to glide in the same direction as the movement of the end of the clavicle. When active elevation of the arm is initiated, activity in the upper trapezius muscle will pull the acromion and lateral end of the clavicle up while the other segments of the trapezius and the serratus anterior muscles exert an upward rotatory force on the scapula. The scapula cannot upwardly rotate at the AC joint, as already noted, because the coracoclavicular ligament maintains a fixed scapuloclavicular angle. Rather, the upward rotatory forces of the trapezius and serratus anterior on the scapula are dissipated at the next available joint: the SC joint. The trapezius and serratus anterior muscles produce upward rotation of the scapula not by rotating the AC joint but by elevating the clavicle at the SC joint. As the clavicle elevates, the superior border of the scapula tilts upwardly, as does the glenoid fossa (Fig. 2a). Clavicular elevation created by the trapezius and serratus anterior muscles produces the first 30 degrees of upward rotation of the scapula and its glenoid fossa. When the costoclavicular ligament becomes taut, elevation at the SC joint is complete. There still remains, however, an additional 30 degrees of upward rotation of the scapula that must be provided to complete a full range of elevation of the arm. The final 30 degrees of scapular upward rotation that are needed to complete the ST joint s contribution to elevation of the upper extremity is provided through rotation of the clavicle around its longitudinal axis. As the trapezius and serratus anterior muscles continue to exert an upward rotatory force on the scapula, the coracoclavicular ligament still prevents upward rotation at the AC joint. The upward rotatory force on the scapula can no longer be dissipated through SC joint elevation, however. As the active muscles attempt to pull the coracoid process away from the clavicle, tension in the coracoclavicular ligament (especially the conoid portion15) builds to the point at which the posteroinferior attachment of the ligament on the clavicle is drawn toward the coracoid process. As the inferiorly located ligament is drawn toward the coracoid process, the inferior surface of the clavicle is drawn anteriorly, rotating the clavicle around its longitudinal axis into what might be termed posterior rotation. Given the crank or S shape of the clavicle, the rotation of the clavicle causes the acromial end of the clavicle to flip up (Fig. 2, inset). When the lateral end of the clavicle flips up, it carries the attached scapula with it, further tilting the glenoid fossa upwardly through another 30 degrees (Fig. 2b). Longitudinal rotation of the clavicle presumably requires mobility at both the AC and the SC joints. However, fixation of the AC joint does not appear to result in long-term restrictions to clavicular motion We can conclude that mobility at the SC joint is mandatory for full scapular ROM as long as the coracoclavicular ligament is intact. The need for AC mobility is less clear, but restriction at either the AC or the SC joint, regardless of the reason, typically will result in hypermobility of the other joint as long as that joint is not otherwise restricted. 15 In summary, the following four factors are necessary to achieve the normal 60 degrees of ST contribution to elevation of the arm: SC joint mobility to allow the clavicular elevation and rotation necessary to swing the glenoid fossa of the scapula upwardly. AC joint mobility to allow anterior and posterior tipping and medial and lateral rotation of the scapula to maintain appropriate contact of the scapula with the thorax. Trapezius and serratus anterior muscle activity to drive the scapula into upward rotation. Extensibility of other scapular and clavicular muscles to allow normal ST motion as well as clavicular elevation and rotation. Glenohumeral joint. The articulation of the large humeral head with the smaller glenoid fossa and differences in the radii of curvature of the two surfaces make the glenohumeral (GH) joint incongruent. The glenoid labrum (a fibrous structure with a fibrocartilaginous transition zone at its attachment to the periphery of the glenoid fossa16) increases the depth of the glenoid fossa. 17 The joint capsule is large and loose and is reinforced by several ligaments, including the superior, middle, and inferior GH ligaments as well as the coracohumeral ligament. 4

5 The superior capsule, superior GH ligament, and coracohumeral ligament appear to be interconnected. 18,19 Harryman et al 19 found that the interconnected ligaments bridged the gap between the supraspinatus and subscapularis tendons and also had fibrous connections to those tendons and to the sheath surrounding the long head of the biceps tendon. This complex of interconnected tendons and ligaments is referred to as the rotator interval capsule The passive components of the rotator interval capsule provide the necessary support for preventing inferior subluxation of the humeral head on the shallow glenoid fossa in the neutral or dependent position (0 degrees). When the arm is in the dependent position with no load or a moderate load, the passive structures alone can support the humeral head against the downward pull of gravity without active contributions from surrounding muscles. 22,23 As the upper extremity is elevated, the superior structures at the GH joint become slack as GH end-range is approached, and the inferior GH ligament complex (with its anterior band, posterior band, and axillary pouch 24 ) becomes more important in limiting inferior translation of the humeral head. 17,21,24 In the middle of the glenohumeral ROM, the capsuloligamentous complex is largely slack, 21 allowing as much as a 2- to 3-mm distraction of the joint. 1 Concomitant medial or lateral rotation of the humerus affects the relative contributions of these passive structures as well. The close-packed position of a joint is the point in the joint ROM where the capsuloligamentous structures are maximally taut and the joint surfaces are drawn together. The close-packed position of the GH joint is considered to be full abduction and lateral rotation. 1 Controversy surrounds what are considered to be the available ranges for elevation at the GH joint. These ranges apparently vary from person to person, which is not surprising, given what appear to be substantial individual and side-to-side differences in articular surfaces and in capsuloligamentous contributions. The GH joint is most commonly considered to have 120 degrees of abduction (frontal plane); however, reports of normal ranges as small as 90 degrees are not uncommon. 3,25,26 Glenohumeral flexion and elevation in the plane of the scapula (so-called scaption 27 ) are more consistently estimated at 120 degrees, but smaller ranges also have been reported for this plane of movement. 28,29 Full GH abduction requires simultaneous lateral rotation of the humerus, which is necessary to prevent the greater tubercle from making contact with the coracoacromial arch. If sufficient lateral rotation cannot be provided, the greater tubercle will impinge on the coracoacromial arch by 60 degrees of GH motion. 9,25 Although scaption presumably allows elevation to proceed without the necessity of clearing the greater tubercle, 35 to 40 degrees of lateral rotation has been found to typically accompany a full range of scaption The articulation of the large humeral head with the smaller glenoid fossa requires the humeral head to glide in a direction opposite to the motion of the distal humerus in order for full GH ranges to be completed. These accessory motions are required to keep the large humeral head centered in the glenoid fossa. The accessory motions include translatory glides and rotation of the bone around its long axis. This rotation around the long axis is referred to as conjunct rotation1, 23 rather than medial and lateral rotation, because the motion does not add an additional degree of freedom to the humerus; rather, the motion serves to minimize migration of the humeral head on the fossa. Although some of the accessory glides and conjunct rotations may vary with individual differences in articular and periarticular influences, it is necessary to center the humeral head as much as possible during abduction and scaption because unopposed upward rolling of the humeral head on the fossa could result in an impingement of the humeral head into the overhanging coracoacromial arch. The potential for upward migration of the humeral head is accentuated by the direction of pull of the three components of the deltoid muscle that serve as primary movers for abduction and scaption. When abduction or scaption is initiated, the deltoid generates a nearly vertical upward pull on the humerus that, if unopposed, would superiorly translate the humeral head into the coracoacromial arch. Although flexion also tends to translate the humeral head superiorly on the fossa, the coracoacromial arch is not in the way, and the primary movers for flexion (anterior deltoid, coracobrachialis, and clavicular pectoralis major muscles) produce a more oblique and, therefore, smaller superiorly directed force. The muscles of the rotator cuff provide the active forces needed to offset upward rolling of the humeral head, to offset the upward translatory pull of the deltoid, and to center the humeral head on the glenoid fossa. Checks to superior translation cannot be provided by the passive structures because the rotator interval capsule is slack when the arm is elevated and because the inferior GH ligament complex can restrain inferior but not superior translations. The capsular structures (along with muscles) do seem to contribute to the conjunct rotations that accompany GH motion and to minimize translatory motions within the joint. 17,19,31 Rotator cuff muscles. The supraspinatus, infraspinatus, teres minor, and subscapularis muscles form the rotator cuff and are credited with providing dynamic stability to the GH joint. The combined line of pull of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles is nearly perpendicular to the humerus and directed into the glenoid fossa, making these muscles strong and effective compressors and stabilizers of the GH joint. 32 The stabilizing function is enhanced by the fibrous connections of the cuff tendons to the GH capsule. 10 Furthermore, the infraspinatus, teres minor, and

6 subscapularis muscles have a line of pull that is slightly downward (caudal), allowing the muscles to produce downward gliding of the humeral head on the fossa. 33 The role of the supraspinatus muscle differs somewhat from that of the infraspinatus, teres minor, and subscapularis muscles, because its line of pull would effect gliding of the humeral head superiorly (cephalad) rather than inferiorly. 34 The supraspinatus muscle also is capable of abducting the GH joint independently of the deltoid muscle and makes an active contribution to resisting inferior translation of the humeral head when the arm is at the side and has a heavy load. 23 The long head of the biceps brachii muscle passes through a tunnel formed by the coracohumeral ligament to reach the supraglenoid tubercle and has connections through its sheath to the rotator interval capsule as well as to the glenoid labrum. It is considered by some to be part of the rotator cuff mechanism. 20 The long head of the biceps muscle, when active, may augment stability of the GH joint at lower levels of elevation by centering the humeral head on the glenoid fossa. 35 Although the long head of the biceps does not appear to be able to contribute directly to downward gliding of the humeral head, 35,36 its role as a secondary stabilizer of the GH joint is supported by observations of hypertrophy of the long head in the presence of rotator cuff tears. 35, 37 The supraspinatus, infraspinatus, teres minor, and subscapularis muscles work during active flexion, scaption, and abduction of the GH joint to offset the upward pull of the deltoid muscle, stabilize the GH joint, and augment the rotatory force of the deltoid. The supraspinatus muscle may be called upon to assist with limiting inferior translation of the humeral head by gravitational forces. The infraspinatus and teres minor (and perhaps, to a lesser extent, the supraspinatus) muscles make an additional contribution to GH abduction by providing the lateral rotation necessary to clear the greater tubercle. As a result of the multi-dimensional roles of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles, chronic overuse results in degenerative changes that increase with age even if such changes are not symptomatic. 9,10,38 The supraspinatus muscle is particularly vulnerable because it is either active (in elevation activities) or passively stretched (with the arm in the dependent position) during a large portion of a person s waking hours. The position of the supraspinatus muscle and tendon below the coracoacromial arch also contributes to increased risk for impingement and degenerative changes. Coracoacromial arch. The coracoacromial arch is an osteoligamentous vault consisting of the coracoid process, the coracoacromial ligament, and the acromion process. It serves the functions of preventing superior dislocation of the humeral head and protecting the humeral head from downwardly directed forces at the lateral shoulder. The suprahumeral space between the humeral head and the arch contains the subacromial bursa, the supraspinatus muscle and tendon, the superior GH capsule, and part of the tendon of the long head of the biceps brachii muscle. When the suprahumeral space is reduced, the potential for painful impingement and compromise of these structures exists. Anatomic factors that may narrow the space include, but are not limited to, the shape and orientation of the inferior acromion, 17 changes in the growth epiphysis of the acromion, acromial spurs, AC osteophytes, and a large coracoacromial ligament.20 The space also can be narrowed dynamically if the superior translatory pull of the deltoid muscles during attempted elevation of the arm is not sufficiently offset by the inferior pull of the infraspinatus, teres minor, and subscapularis muscles. When the rotator cuff and the deltoid are working in appropriate synergy, the humeral head remains relatively centered on the glenoid fossa, and little superior displacement occurs. 30,39 There is still evidence, however, that the pressures in the subacromial bursa increase with elevation of the loaded upper extremity. These pressure increases may be attributable to the increased volume of the supraspinatus muscle as it contracts during the activity and occupies more of the suprahumeral space. Cailliet 9 notes that subacromial bursitis and supraspinatus tendinitis often occur simultaneously (primary subacromial bursitis is rare) because the inferior portion of the subacromial bursa is the outer sheath of the supraspinatus muscle and tendon. Inflammation of the supraspinatus tendon can therefore create secondary subacromial bursitis. Total scapulohumeral motion. In addition to considering the individual structures of the shoulder, physical therapists should consider the coordinated interaction of the ST and GH joints in producing elevation of the upper extremity. Medial rotation and lateral rotation of the arm primarily are functions of the GH joint. Full scaption and abduction of the arm require not only 90 to 120 degrees of GH motion but also 60 degrees of upward rotation of the scapula that must involve the SC joint and, to a lesser extent, the AC joint. Flexion of the arm has requirements similar to those of abduction but includes the additional requirement of scapular protraction that must accompany upward rotation. Various researchers have conducted extensive investigations of the ratio of GH to ST movements. A substantial variability in ratios of GH to ST movements has been found between individuals and under different load conditions. 40,41 The rhythm or timing of GH and ST movements essentially is irrelevant to clinical examination, however, because any interference with any component of the movement at the various linkages will alter the sequencing and ratio of the movement. Every patient will 6

7 use whatever motion is available, regardless of ratios and proportions. For instance, if only GH motion is available, the patient still should be able to achieve 90 to 120 degrees of elevation (subject to the position of the scapula). Correspondingly, if the GH joint is immobilized by fusion or adhesive capsulitis, the scapula still can achieve its full 60 degrees of upward rotation and the arm still can move 60 degrees from the side (assuming neutral GH positioning). Partial contributions from each joint also can occur if both joints encounter restrictions. On the other hand, hypermobility of one component may develop in response to mobility restrictions elsewhere in the complex. The only mandatory sequence in movement of the shoulder girdle linkages is at the SC joint. The costoclavicular ligamentous restriction of clavicular elevation (contributing the first 30 degrees to scapular upward rotation) must be reached before tension in the coracoclavicular ligament will be sufficient to rotate the clavicle (contributing the final 30 degrees to scapular upward rotation). Hyperextension of the arm is accomplished largely through GH mobility (with some scapular tipping). Motions such as horizontal abduction and adduction of the arm, however, require both GH motion and scapular retraction and protraction, respectively (including mandatory SC contributions). Tests and Measures As JD s examination proceeds, the physical therapist must choose tests and measures to identify impairments of normal function in these kinematic and kinetic components of the shoulder that may contribute to JD s clusters of signs, symptoms, and impairments. The physical therapist will then evaluate the examination findings and, based on the evaluation, form a diagnosis and prognosis and select appropriate interventions. Sensory integrity. Although sensory integrity is examined commonly in patients with shoulder dysfunction to determine whether there is cervical nerve involvement, patients who have had surgery for breast cancer frequently have sensory changes that need to be identified before proceeding with other components of the hands-on examination. JD is insensitive to light touch and pinprick in a 1- to 2- inch margin around the scar and in an area extending into the axilla and posteromedially down the right arm almost to the elbow (Fig. 3). This distribution is indicative of deficits of the right intercostobrachial and medial brachial cutaneous nerves. Range of motion. To begin differentiating between GH and ST limitations, the therapist decides to use passive ROM with overpressure as described by Kaltenborn, 42 accessory mobility, and goniometric measurements. The therapist also wants to explore the nature of the limitation at the involved joints; that is, to explore whether the dysfunction appears to be consistent with contractile or passive (inert) structures. 43 The goniometric measurement of total active and passive ROM, as well as ROM with a manually stabilized scapula (GH ROM), are shown in the Table. ROM values and passive end-feels for the joints of the left shoulder girdle are within normal limits. 44 Overpressure for right passive extension and horizontal adduction have firm end-feels, with resistance encountered before pain. Overpressure for right medial rotation, lateral rotation, and horizontal abduction have firm end-feels, again with resistance encountered before pain. The end-feels for abduction and flexion are limited by spasms, with pain reported before onset of resistance. These observations would appear to be consistent with a GH capsular pattern that will need to be explored with joint integrity and mobility testing. 43 A comparison of total passive ROM values for right shoulder flexion and abduction to the values obtained with the scapula stabilized suggests both GH and ST limitations of motion. Although GH flexion is close to the normal range of 120 degrees, combined GH and ST (total) flexion suggests a primary limitation in the ST contribution to the motion in flexion. Glenohumeral abduction is substantially less than the 90 to 120 degrees that the therapist would expect for that joint alone. When the ST contribution is added (for total ROM), only an additional 30 degrees of range is obtained, suggesting both GH and ST limitations. Medial rotation and lateral rotation, primarily GH motions, are both limited. The substantial limitation to lateral rotation can account for much of the restriction in GH abduction, because an inability to laterally rotate the humerus will result in early impingement of the greater tubercle into the coracoacromial arch and is consistent with the pain experienced by JD with both active and passive abduction. Glenohumeral flexion does not require lateral rotation to clear the greater tubercle, and JD shows little or no restriction of GH flexion. The therapist hypothesizes that the primary limitation to GH abduction is related to the lateral rotation limitation. Both flexion and abduction show a restriction of approximately 30 degrees of ST motion. The therapist reasons that, because both motions normally require 60 degrees of upward rotation of the scapula, a restriction of upward rotation should be considered. An essentially normal finding for horizontal adduction ROM indicates that the contributing components of GH adduction and scapular protraction are within normal limits. Horizontal abduction, however, is sufficiently limited that both the GH contribution and ST retraction need to be investigated 7

8 further. The therapist proceeds to examine joint integrity and mobility as a way to narrow down the involved structures and test these hypotheses. Joint integrity and mobility. Examination of joint mobility is based on the conceptual framework that osteokinematic restrictions may be related to arthrokinematic restrictions. Evidence of an association between arthrokinematic and osteokinematic restrictions, however, is largely empirical, and reliability of judgment of joint glides has not been demonstrated in the literature. Although not definitively diagnostic, suspected limitations of arthrokinematic glides and atypical end-feels have the potential to contribute to our hypotheses about affected structures and tissues that need intervention. The therapist therefore links the arthrokinematic findings to other examination findings. Accessory glides of a joint are tested where the GH capsule is as loose as possible. For JD, accessory glides of the right GH joint are restricted (estimated to be grade 2 on a scale from 0 to 642), with capsular end-feels and resistance before pain in the inferior, anterior, and posterior directions. Accessory glides of the left GH joint appeared to be within normal limits and reasonably symmetric (estimated to be grade 3), with capsular endfeels and resistance before pain. These observations lead the therapist to hypothesize that the right GH restrictions observed during the ROM examination may have had a capsuloligamentous component in addition to a possible limitation in the extensibility of muscular and other extracapsular tissues. Long-axis traction applied to the humerus is limited (estimated to be grade 2) by spasm. This finding suggests inflammation of the superior GH structures (rotator interval capsule and passive supraspinatus muscle). Imposing an inferior glide on the humerus (as is done with longitudinal traction) would be expected to place tension on the superior GH structures (evoking pain if inflammation is present), whereas during other passive GH joint motions, these structures would generally become more slack. Manual glides of the right AC joint (anterior, posterior, cephalad, and caudal) are slightly limited (estimated to be grade 2) compared with those of the left (estimated to be grade 3), all with capsular end-feels and resistance before pain. Manual glides of the left SC joint are within normal limits (estimated to be grade 3), with capsular end-feels and resistance before pain), whereas those of the right are estimated to be grade 3 for anterior, grade 2 for caudal and cephalad, and grade 1 for posterior glides (all with capsular end-feels). In the saddle-shaped SC joint, a restriction in posterior glide may be associated with a limitation in clavicular (and scapular) retraction, because the anteroposterior concavity of the medial end of the clavicle is expected to move in the same direction as the lateral end of the clavicle. Restrictions in cephalad and caudal glides may be associated with limitations in clavicular (and scapular) depression and elevation, respectively, because the vertical convexity of the medial end of the clavicle is expected to glide in a direction opposite to the motion of the lateral end of the clavicle. The therapist would expect joint glide (arthrokinematic) restrictions at the SC joint to be consistent with decreased scapular motion. Manual movements of the scapula on the thorax on the left are within normal limits. On the right, with the patient in a prone position, the scapula is observed to be protracted and anteriorly tipped, as was found when JD was in the standing position. Manual movements of the scapula on the thorax are estimated to be grade 3 for lateral glide (protraction) and grade 2 for caudal glide and for downward rotation, each with firm end-feels and resistance before pain. Manual movements of the scapula cephalad (elevation), medially (retraction), and into upward rotation are estimated to be grade 1, with firm end-feels and resistance before pain. The findings for the scapula are consistent with those for arthrokinematics of the SC joint, and they lead the therapist to expect limitations in scapular elevation, retraction, and upward rotation. Although SC restrictions may be the primary cause of ST limitations, it also is possible that some other factor may be limiting scapular mobility and producing secondary adaptive shortening of the capsuloligamentous structure of the SC joint. None of the SC, AC, or ST glides reproduces JD s pain. The therapist decides to examine the contractile elements. Muscle performance. All shoulder girdle musculature on the left appear to be within normal limits (5/5), as estimated by manual muscle testing. 45 Right shoulder extensors are 5/5, and horizontal adductors are 4/5, with mild discomfort described as a pulling sensation. Flexors and medial rotators are 5/5 within the available range. The positions for horizontal abduction and lateral rotation are modified because of range limitations, with resistance from horizontal adduction and medial rotation, respectively. Right horizontal abductors are measured as 5/5, lateral rotators measured as 4/5, and abductors measured as 3+/5, with both of these resisted motions reproducing JD s pain symptoms. The right serratus anterior muscle is measured as 5/5, and the upper trapezius and the levator scapula muscles are measured as 5/5 within the available range. Positional modification for testing of the middle trapezius, lower trapezius, and rhomboid muscles is required. The therapist places JD in the prone position, with her right shoulder brought over the edge of the table. Because her arm cannot be brought overhead for testing of the lower 8

9 trapezius, JD is instructed to actively depress the scapula against manual resistance. Some weakness (estimated to be 4/5) is evident. When the patient is placed in the starting position for testing of the middle trapezius and rhomboids, no further scapular retraction actively or passively is available. Manual resistance on the scapula against retraction with downward rotation at JD s end-range indicates weakness (estimated to be 4/5). Manual muscle testing of the muscles of the GH joint indicates pain and weakness with both abduction and lateral rotation. Scapulothoracic muscle testing confirms limitations of motion, but the identified muscle weaknesses are minimal and are more likely to be secondary to positional faults rather than causative. The impingement sign 46 and the supraspinatus test 47 yield positive results. The apprehension, relocation, Speed s, and Yergason s tests 47 yield negative results. Evaluation JD s pattern, degree, and location of pain (anterosuperior shoulder pain) with active, passive, and resisted abduction; resisted lateral rotation; and passive longitudinal traction are consistent with a grade II acute supraspinatus tendinitis and subacromial bursitis. The pain at 70 degrees of active abduction occurs at the beginning of the 60- to 120-degree painful arc that is typical of supraspinatus inflammation, 9 although JD s range limitation precludes a true positive finding. Pain in this range from supraspinatus inflammation is thought to occur because the supraspinatus muscle normally shows peak activity (and, therefore, peak tension) through this range, whereas the suprahumeral space in which the tendon lies is simultaneously being reduced as the greater tubercle approaches the coracoacromial arch. 9 Pain with passive longitudinal traction on the humerus is consistent with supraspinatus inflammation because this action places stress on the supraspinatus muscle and tendon. The pain experienced by JD with overpressure on abduction may indicate additional involvement of the subacromial bursa just above the supraspinatus muscle. Results of the special tests for the shoulder appear to confirm supraspinatus tendinitis and rule out GH instability. Although supraspinatus tendinitis is considered multifactorial and can occur without a significant history, 9, 20 the physical therapist must determine whether JD s other biomechanical limitations are contributing to or potentially causing the problem. JD does not have passive lateral rotation beyond the neutral position. Capsuloligamentous restrictions found on examination might have contributed to restricted lateral rotation. The comparative mobility of medial rotation and flexion at the joint, however, would appear to argue against capsuloligamentous restriction as a sole source of the restriction in lateral rotation. The therapist believes that JD s history might provide some clues to additional causes. JD had surgery and radiation involving the anterior chest wall and axilla. Radiation is known to result in fibrotic changes and potential vascular compromise to the skin and underlying tissues. 48,49 JD also had a tissue expander inserted under the pectoralis major muscle, as is typically done in implant reconstruction. There is evidence that the expansion process alone (without adjuvant radiation) can result in muscle fiber degeneration and interstitial fibrosis. 50 The subsequent failure of the skin expansion in JD s case is consistent with more severe fibrotic changes than might be considered typical. The potential for radiation- and expansion-induced soft tissue changes might have been further accentuated by the subsequent surgeries when the right implant extruded. There is little or no skin mobility in the area of the scar, and the skin appears to adhere to the underlying thorax. The sternal portion of the pectoralis major muscle, however, should lie between the skin and the thorax. On the right, the therapist could not trace the pectoralis major muscle inferiorly from the superior margin of the scar. These findings might indicate that the sternal portion of the muscle is atrophied and completely adherent to the skin above and the thorax below. Fibrosis and lack of extensibility of the sternal pectoralis major muscle could produce the limitation of lateral rotation in JD. A limitation of lateral rotation (and possibly of accompanying conjunct rotation) could lead to supraspinatus tendon impingement, because the greater tubercle cannot clear the coracoacromial arch in abduction of the arm. The pectoralis minor muscle is found deep to the pectoralis major. Both the pectoralis major and minor muscles are separately enveloped by the clavipectoral fascia. The clavipectoral fascia and pectoralis minor muscle also might be involved in the fibrotic changes resulting from radiation and surgery and, consequently, contribute to the findings. JD s scapular resting position of protraction and anterior tipping is consistent with pectoralis minor muscle tightness, as are the active and passive limitations of scapular retraction, elevation, and upward rotation. Tightness of the pectoralis minor muscle and the resulting faulty scapular posture can change the position of the acromion, narrow the suprahumeral space, and increase the likelihood of impingement, even in the absence of the other pathology presented by JD. 4,9 9

10 The clavipectoral fascia surrounds the pectoralis muscles, attaches to the lateral clavicle and coracoid process, and blends with the axillary fascia. 1 If it also has been subjected to fibrotic changes as might be anticipated, given its location lack of extensibility in this fascia could restrict clavicular motion. Although the shortening of or fibrotic changes in the pectoralis minor muscle and clavipectoral fascia alone theoretically can account for a substantial portion of the scapular limitation of motion, JD had axillary node dissection and axillary radiation. Either of these procedures may create fibrotic changes in the axillary soft tissues and in the underlying serratus anterior muscle that could further compromise scapular mobility. 49 To explore the clinical hypothesies of tissue fibrosis, the therapist asks JD to repeat the active motions of scapular elevation, depression, and retraction and to report altered sensation. The patient reports a stretching or pulling sensation in the axilla or its margins with all test movements. The stretching or pulling is consistent with, although not necessarily a definitive indication of, fibrosis in the anterior chest wall and in the axilla. Diagnosis JD has impaired joint mobility and integrity, impaired muscle performance, and impaired range of motion impairments that are consistent with dynamic subacromial impingement in the right shoulder, 31 an acute stage II supraspinatus tendinitis, 45 and probable subacromial bursal involvement. JD s functional limitations include restrictions in her ability to perform ADL. Based on the framework used in the Guide to Physical Therapist Practice (Guide), the physical therapist makes a diagnosis of Impaired Joint Mobility, Motor Function, Muscle Performance, and Range of Motion Associated With Localized Inflammation. 51 Hypothesized shortening and fibrotic changes in the glenohumeral capsule, pectoralis major and pectoralis minor muscles, clavipectoral fascia, and axillary soft tissues appear to be limiting ST and GH joint mobility. Additional or secondary limitations to SC and AC joint mobility appear to be contributing to altered scapulohumeral mechanics and increasing the risk of impingement. Prognosis According to the Guide, it is estimated that 80% of all patients in the chosen diagnostic pattern will demonstrate a return to premorbid level of function within 8 to 16 weeks, with physical therapy ranging from 6 to 24 visits. 51 The physical therapist expects the prognosis for JD to be atypical compared with that of other patients in this diagnostic pattern. Because of the anticipated fibrotic tissue changes, the potential for vascular compromise of the affected tissues, and the increased risk of lymphedema in a patient who has undergone lymph node dissection and 10 axillary radiation, the therapist expects a delay in goal achievement and limitations in the outcome. Plan of care. With JD, the therapist identifies the following main goals to address pathology/pathophysiology, impairments, functional limitations, disabilities, risk factor reduction/secondary prevention, and patient satisfaction: Joint integrity and mobility of shoulder are improved. Muscle performance (strength, power, endurance) in shoulder is increased. Lymphedema is prevented. Range of motion is increased. Risk of secondary impairments (eg, subacromial impingement) is reduced by improving posture. Tolerance of positions and activities is increased. Ability to perform movement tasks is increased. Pain is decreased. Joint and soft-tissue swelling, inflamation, or restriction related to supraspinatus tendinitis is reduced. Intervention As noted, the emphasis of this CE offering is on the review of kinesiology of the shoulder girdle in a patient with pain and hypomobility. However, because the purpose of any examination and evaluation is to guide intervention, we will discuss how the findings might influence the physical therapist s clinical decisions. Therapeutic Exercise As a passive stretching program is initiated, faulty postural alignment also must be addressed to reduce the risk of impingement. The patient must be educated to improve cervical, cervicothoracic, and shoulder girdle alignment. An adjunct program of strengthening of key muscle groups can begin during the acute phase with isometric scapular and GH stabilization in all directions. Submaximal resistance to painful motions should be used until the motions are pain free. As acute inflammation subsides, a home program of resisted GH and ST motions can be added Manual Therapy Techniques (Including Mobilization and Manipulation) JD s hypomobility has both extra-articular and capsular components. The GH, SC, and AC capsular restrictions indicate a need for joint mobilization. The direction and degree of force applied during joint mobilization are suggested by end-feels and by the pain/resistance sequence. 43 The scapula also appears to require mobilization of the restricted muscles and soft tissues. The

11 therapist begins with mobilization of the scapula while the acute inflammation at the GH joint is addressed. The acute inflammation suggested by the findings might be managed through anti-inflammatory medications prescribed by JD s surgeon, rest/relief positions, accessory mobilizations for longitudinal distraction, and physiological mobilizations for abduction. The shortened and fibrotic extra-articular tissues of the right anterior chest wall and axilla indicate the need for scar mobilization and soft tissue mobilization. Scar mobilization must proceed carefully, given the absence of pain sensation and the possible compromised vascularity indicated by the patient history. The target muscles for soft tissue mobilization should be those showing evidence of fibrotic changes or those anticipated to be in the radiation field. 52, 53 Shortening of these same muscles suggests the need for passive stretching of the muscles, but this action should not be initiated until end-ranges no longer produce acute pain or spasm. When the patient is ready, passive stretching with an emphasis on flexion, abduction, external rotation, and horizontal abduction of the arm can be taught as part of a home program. Electrotherapeutic Modalities and Physical Agents and Mechanical Modalities The physical therapist may select electrotherapeutic modalities and supportive taping to help reduce pain and minimize tension on potentially inflamed structures. Cautions Several cautions unrelated to shoulder mechanics and specific to JD should be noted. Any soft tissue mobilization techniques or attempts to lengthen the involved muscles must be performed with consideration of the hypothesized fibrotic tissues, the potential for vascular compromise of the tissues, and JD s sensory deficits. There is some evidence that sound agents (ultrasound) may increase tumor growth. 54 Furthermore, because of concerns about increasing blood flow in the vicinity of tumors, some texts of physical agents caution against the use of sound and thermal agents in areas where there is or may be malignancy JD has not shown signs of lymphedema to date. The risk, however, is long-term (up to decades later) and is compounded by the combination of axillary node dissection, axillary radiation, and surgery in the radiated area. 58 Lymphedema precautions include avoiding the following in the involved arm 59 : Tissue trauma that could lead to local swelling or inflammation (including routine injections or blood draws). Exposure to extreme temperatures. 11 Circumferential tissue constriction. Heavy lifting or vigorous repetitive movements against resistance. 59 The last precaution is particularly important as the physical therapist formulates an exercise program for the patient. Finally, consideration should be given to possible entrapment of components of the brachial plexus in the fibrotic tissues below the clavicle. 60 Each of these precautions argues for proceeding cautiously with treatment and for careful and consistent communication with the patient regarding her perceptions of pain, stretching, exertion, or neuropathic symptoms. The case discussed here is complex and certainly not typical of patients with supraspinatus tendinitis. JD s history and findings provide a particular challenge both to our understanding of shoulder girdle kinesiology and to the planning of intervention strategies. References 1. Williams P. Gray s Anatomy. New York, NY: Churchill Livingstone; Moore K, Dalley AI. Clinically Oriented Anatomy. Philadelphia, Pa: Lippincott Williams & Wilkins; Kapandji I. The Physiology of the Joints. Vol 1. Edinburgh, United Kingdom: Churchill Livingstone; Ludewig PM, Cook TM, Nawoczenski DA. Threedimensional scapular orientation and muscle activity at selected positions of humeral elevation. J Orthop Sports Phys Ther. 1996;24: Bull M, defreitas V, Vitti M. Electromyographic study of the trapezius (pars superior) and serratus anterior (pars inferior) in free movements of the arm. Anat Anz. 1990;171: Inman B, Saunders J, Abbott L. Observations of function of the shoulder joint. J Bone Joint Surg Br. 1944;26:1. 7. Saha A. Theory of Shoulder Mechanism: Descriptive and Applied. Springfield, Ill: Charles C Thomas; Depalma A. Degenerative Changes in Sternoclavicular and Acromioclavicular Joints in Various Decades. Springfield, Ill: Charles C Thomas; Cailliet R. Shoulder Pain. Philadelphia, Pa: FA Davis; Pratt N. Anatomy and biomechanics of the shoulder. J Hand Ther. 1994;7: Morris J. Joints of the shoulder girdle. Australian Journal of Physiotherapy. 1978;24(6): Bargien JH, Erlanger S, Dick HM. Biomechanics and comparison of two operative methods of treatment of complete acromioclavicular separation. Clin Orthop. 1978;130: MacDonald PB, Alexander MJ, Frejuk J, Johnson GE. Comprehensive functional analysis of shoulders

12 following complete acromioclavicular separation. Am J Sports Med. 1988;16: Post M. Current concepts in the diagnosis and management of acromioclavicular dislocations. Clin Orthop. 1985;200: Pronk GJ, van der Helm FC, Rozendaal LA. Interaction between the joints of the shoulder mechanism: the function of the costoclavicular, conoid and trapezoid ligaments. Proc Inst Mech Eng [H]. 1993;207: Cooper DE, Arnoczky S, O Brien SJ, et al. Anatomy, histology, and vascularity of the glenoid labrum: an anatomical study. J Bone Joint Surg Am. 1992;74: Bigliani LU, Kelkar R, Flatow EL, et al. Glenohumeral stability: biomechanical properties of passive and active stabilizers. Clin Orthop. 1996;330: Cooper D, O Brien J, Arnoczky S. The structure and function of the coracohumeral ligament: an anatomic and microscopic study. J Shoulder Elbow Surg. 1993;2: Harryman DT II, Sidles JA, Harris SL, Matsen FA II. The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am. 1992;74: Soslowsky LJ, Carpenter JE, Bucchieri JS, Flatow EL. Biomechanics of the rotator cuff. Orthop Clin North Am. 1997;28: Warner JJP, Deng XH, Warren RF, Torzilli PA. Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am J Sports Med. 1992;20: Basmajian J, Bazant F. Factors preventing downward dislocation of the adducted shoulder. J Bone Joint Surg Am. 1959;41: MacConaill M, Basmajian J. Muscles and Movement: A Basis for Human Kinesiology. Baltimore, Md: Williams & Wilkins; O Brien SJ, Schwartz RS, Warren RF, Torzilli PA. Capsular restraints to anterior-posterior motion of the abducted shoulder: a biomechanical study. J Shoulder Elbow Surg. 1995;4: Lucas DB. Biomechanics of the shoulder joint. Arch Surg. 1973;107: Steindler A. Kinesiology of the Human Body. Springfield, Ill: Charles C Thomas; McMahon PJ, Jobe FW, Pink MM, et al. Comparative electromyographic analysis of shoulder muscles during planar motions: anterior glenohumeral instability versus normal. J Shoulder Elbow Surg. 1996;5: Freedman L, Munro RR. Abduction of the arm in the scapular plane: scapular and glenohumeral movements, a roentgenographic study. J Bone Joint Surg Am. 1966;48: Doody SG, Freedman L, Waterland JC. Shoulder movements during abduction in the scapular plane. Arch Phys Med Rehabil. 1970;51: Soslowsky LJ, Flatow EL, Bigliani LU, et al. Quantitation of in situ contact areas at the 12 glenohumeral joint: a biomechanical study. J Orthop Res. 1992;10: Wilk K. The shoulder. In: Malone TR, McPoil TG, Nitz AJ, eds. Orthopedics and Sports Physical Therapy. Chicago, Ill: Mosby-Year Book Inc, Wuelker N, Korell M, Thren K. Dynamic glenohumeral joint stability. J Shoulder Elbow Surg. 1998;7: Sharkey NA, Marder RA. The rotator cuff opposes superior translation of the humeral head. Am J Sports Med. 1995;23: Wuelker N, Plitz W, Roetman B, Wirth CJ. Function of the supraspinatus muscle: abduction of the humerus studied in cadavers. Acta Orthop Scand. 1994;65: Pagnani MJ, Deng XH, Warren RF, et al. Role of the long head of the biceps brachii in glenohumeral stability: a biomechanical study in cadavera. J Shoulder Elbow Surg. 1996;5: Kumar VP, Satku K, Balasubramaniam P. The role of the long head of biceps brachii in the stabilization of the head of the humerus. Clin Orthop. 1989;244: Sakurai G, Ozaki J, Tomita Y, et al. Morphologic changes in long head of biceps brachii in rotator cuff dysfunction. J Orthop Sci. 1998;3: Ferrari DA. Capsular ligaments of the shoulder: anatomical and functional study of the anterior superior capsule. Am J Sports Med. 1990;18: Poppen NK, Walker PS. Normal and abnormal motion of the shoulder. J Bone Joint Surg Am. 1976;58: McQuade KJ, Smidt GL. Dynamic scapulohumeral rhythm: the effects of external resistance during elevation of the arm in the scapular plane. J Orthop Sports Phys Ther. 1998;27: Hogfors C, Peterson B, Sigholm G, Herberts P. Biomechanical model of the human shoulder joint, II: the shoulder rhythm. J Biomech. 1991;24: Kaltenborn F. Manual Mobilization of the Extremity Joints: Basic Examination and Treatment Techniques. Oslo, Norway: OPTP; Cyriax J. Diagnosis of Soft Tissue Lesions. Baltimore, Md: WB Saunders; Textbook of Orthopedic Medicine; vol Norkin C, White D. Measurement of Joint Motion: A Guide to Goniometry. 2nd ed. Philadelphia, Pa: FA Davis, Hislop HR, Montgomery J. Daniels and Worthingham s Muscle Testing: Techniques of Manual Examination. Philadelphia: WB Saunders; Neer CS II, Welsh RP. The shoulder in sports. Orthop Clin North Am. 1977;8: Hawkins RJ, Bokor DJ. Clinical evaluation of shoulder problems. In: Rockwood CA, Matsen FA, eds. The Shoulder. Vol 1. Philadelphia, Pa: WB Saunders; 1990.

13 48. Borger JA, Kemperman H, Smitt HS, et al. Dose and volume effects on fibrosis after breast conservation therapy. Int J Radiat Oncol Biol Phys. 1994;30: Ryttov N, Holm NV, Qvist N, Blichert-Toft M. Influence of adjuvant irradiation on the development of late arm lymphedema and impaired shoulder mobility after mastectomy for carcinoma of the breast. Acta Oncol. 1988;27: Gur E, Hanna W, Andrighetti L, Semple JL. Light and electron microscopic evaluation of the pectoralis major muscle following tissue expansion for breast reconstruction. Plast Reconstr Surg. 1998;102: Guide to Physical Therapist Practice. Alexandria, Va: American Physical Therapy Association; Sugden EM, Rezvani M, Harrison JM, Hughes LK. Shoulder movement after the treatment of early stage breast cancer. Clin Oncol. 1998;10: Ryttov N, Holm NV, Qvist N, Blichert-Toft M. Influence of adjuvant irradiation on the development of late arm lymphedema and impaired shoulder mobility after mastectomy for carcinoma of the breast. Acta Oncol. 1998;27: Sicard-Rosenbaum L, Dannoff JV, Guthrie JA, Eckhaus MA. Effects of energy-matched pulsed and continuous ultrasound on tumor growth in mice. Phys Ther. 1988;78: Whitney SL. Physical agents: heat and cold modalities. In: Scully RM, Barnes MR, eds. Physical Therapy. Philadelphia, Pa: JB Lippincott, Kahn J. Physical agents: electrical, sonic, and radiant modalities. In: Scully RM, Barnes MR, eds. Physical Therapy. Philadelphia, Pa: JB Lippincott, Cameron M. Physical Agents in Rehabilitation. Philadelphia, Pa: WB Saunders; Harpham W. After Cancer: A Guide to Your New Life. New York, NY: WW Norton; 1994: Lymphedema: eighteen steps to prevention for upper extremities National Lymphedema Network. Accessed: October 29, Box R. Rehabilitation after breast cancer. In: Sapsford R, Bullock-Saxton J, Markwell S, eds. Women s Health: A Textbook for Physiotherapists. London, United Kingdom: WB Saunders;

14 Figure 1. Figure 2a 2b. 14

15 Figure 3. Table. 15