Shoulder anatomy and biomechanics

Phys Med Rehabil Clin N Am 15 (2004) 313–349

Shoulder anatomy and biomechanics Barry Goldstein, MD, PhD VA Puget Sound Health Care System, 1660 South Columbian Way, SCI-128, Seattle, WA 98108-1532, USA

Disorders of the shoulder are among the most frequent causes of musculoskeletal pain and disability [1]. Shoulder pain is the third most common cause of musculoskeletal disorder after low back pain and cervical pain. Estimates of the cumulative annual incidence of shoulder disorders vary from 7% to 25% in the Western general population. Degeneration, infection, inflammation, arthritic changes, injury, vascular disease, tumor, neuropathic disorders, and referred pain can cause painful shoulder disorders. Shoulder disorders represent a continuum ranging from a rotator cuff tear, which has relatively clear diagnostic criteria and pathophysiology, to undiagnosable, undefinable problems. From a clinical and epidemiologic perspective, these latter cases present challenges similar to the challenges of low back pain. Accurate diagnosis and treatment of shoulder disorders are essential for a successful return to full function. Proper diagnoses require a thorough knowledge of the anatomy and biomechanics of all the shoulder structures and the pathophysiology and mechanical problems of injury and disease. This article is divided into three major sections. First, the anatomy, biomechanics, and function of the shoulder are described. This section is presented in a regional manner with a focus on musculoskeletal structures of the shoulder. There is a particular emphasis on function and clinically relevant topics. Because of space constraints, other structures relevant to the surrounding anatomy and the development of a differential diagnosis of shoulder pain (eg, radiculopathy and referred pain) are mentioned only in passing. The second section is on the application of this information to the clinical evaluation of the patient. In the third section, applied anatomy and illustrative case studies are provided to highlight major shoulder problems.

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Anatomy, biomechanics, and function of the shoulder Anatomy and physiology of the joints To understand pain and loss of shoulder function, it is necessary to have a thorough knowledge of the anatomy and biomechanics of the region. To understand fully complaints about the shoulder, interrelationships between the shoulder, thorax, and cervical spine should be mastered. Surrounding neural and vascular structures also need to be studied. This article focuses primarily on the complex articulations of the shoulder, the integrated function of soft tissues relating to the shoulder, and five distinct articulations. The articulations consist of three synovial joints (ie, cartilage-to-cartilage articulations) and two movement interfaces (scapulothoracic and humeroacromial). Bones and joints of the pectoral girdle All vertebrates have limbs that are connected to the axial skeleton by way of a limb girdle. The human pelvic and pectoral girdles are designed in a way that reflects the overall function of the respective limb. In contrast with the lower limb, with its weight-bearing and locomotive functions, the pectoral girdle is built for mobility and does not have a bony junction with the vertebral column at all. Rather the girdle articulates with the thoracic cage at the sternoclavicular (SC) joint, permitting a wide range of motion (ROM) for placement of the hand. The clavicle, as it articulates with the sternum, acts as a bony strut, stabilizing the upper limb on the thorax, particularly with adduction activities (eg, a gymnast performing the iron cross). All mammals that develop full abduction and powerful adduction (ie, flying, burrowing, swimming, and climbing mammals) have a pectoral girdle designed in this manner. The pectoral girdle consists of two bones (scapula and clavicle), two synovial joints (SC and acromioclavicular [AC]), and two movement interfaces (scapulothoracic and humeroacromial). The humeroacromial interface is discussed with the glenohumeral joint. Clavicle. The S-shaped clavicle is a long bone, superficial and horizontal throughout most of its course. The medial two thirds is rounded and convex forward to clear the neurovascular bundle of the upper limb at the apex of the axilla. Its sternal end is expanded and fits into the notch on the manubrium at the SC joint. The lateral one third is flat, and its sternal end is expanded as it curves back to meet the scapula at the AC joint (Fig. 1). Clavicle fractures are more common in children but also occur in adults, representing about 4% to 10% of all adult fractures and 35% to 45% of all fractures that occur in the shoulder girdle area. A visible and palpable deformity usually is present because the clavicle is subcutaneous. These fractures usually are classified into thirds; the most frequent site of injury is at the middle third. Distal fractures may present similar to an AC separation with a prominence close to the AC joint. A force directly onto the shoulder

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Fig. 1. Anterior (A) and posterior (B) views of the shoulder identifying the various bones and joints and the sites of pathologic processes that produce pain and tenderness. (1) Subacromial space, which can be involved with calcific tendinitis, rotator cuff tendinitis/impingement syndrome, and rotator cuff tear; (2) bicipital groove, which can be involved in bicipital tendinitis and biceps tendon subluxation and tear; (3) acromioclavicular joint, which can be involved with degenerative and infectious processes; (4) anterior glenohumeral joint, which can be the site of glenohumeral arthritis, osteonecrosis, glenoid labial tears, and adhesive capsulitis; (5) sternoclavicular joint, which can be the site of pain due to infection, degenerative changes, or trauma; (6) posterior edge of the acromion, which can contribute to rotator cuff tendinitis, calcific tendinitis, and rotator cuff tear; (7) suprascapular notch, which can be the site of suprascapular nerve entrapment; and (8) quadrilateral space, which can be the site of axillary nerve entrapment.

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and a fall onto the outstretched hand are the typical injuries that result in clavicle fracture. A complete neurovascular examination is imperative because the brachial plexus and subclavian vessels traverse an area between the clavicle and first rib. The excellent collateral circulation to the upper extremity may mask injury to the subclavian artery. More proximal fractures may injure the apex of the lung and cause pneumothorax. Scapula. The scapula, or shoulder blade, is a remarkably thin (when held up to the light, the dried scapula is translucent) and triangular bone that is attached to the thorax via muscular attachments and to the clavicle by way of the AC joint (see Fig. 1). It possesses three borders and three angles. The three borders are the superior, medial (vertebral), and lateral (axillary). The three angles are the superior, inferior, and lateral. The scapula has costal (anterior) and posterior surfaces with its anterior surface in contact with the thoracic cage (ie, the scapulothoracic interface). From the upper part of the posterior surface, the spine of the scapula projects laterally, terminating in the acromion, which forms the lateralmost tip of the shoulder. The lateral angle of the scapula is thick and strong, with an expanded large, shallow glenoid fossa, facing slightly forward and upward, ready to receive the head of the humerus. Just medial to the glenoid fossa is the coracoid process as it projects upward from the neck of the scapula. The coracoid process serves as an attachment site for several important ligaments and muscles. Sternoclavicular joint. The only bony articulation between the upper limb and axial skeleton occurs between the clavicle and the manubrium at the SC joint. The entire pectoral girdle moves about the clavicle braced on the thorax at this saddle-shaped joint. The medial end of the clavicle is concave and fits over the convexity of the much larger sternocostal surface (Fig. 2). An articular disk between the sternum and clavicle divides the joint into two spaces and provides a greater congruence of surfaces than the bony articulation alone. Stability of the joint is provided by a strong, lax capsule and is enhanced by ligaments superiorly (interclavicular ligament) and posteriorly (posterior SC ligament). The major stabilizing factor of the SC joint is the strong costoclavicular ligament, attached from the first rib to the undersurface of the clavicle (see Fig. 2). This ligament limits elevation and rotation of the clavicle. It also serves as the fulcrum of movements at the SC joint. The joint is weakest anteriorly, where an effusion (eg, infection) tends to present. Rheumatoid arthritis (RA) and osteoarthritis may affect the SC joint. Subluxation and actual dislocation of the joint may occur, particularly in the setting of RA. The SC joint has two axes and two degrees of freedom, corresponding mechanically to a universal joint. Some axial rotation also occurs at this joint. These movements are described subsequently with discussion of pectoral girdle movements. Acromioclavicular joint. The overriding lateral end of the clavicle meets the medial border of the acromion at this small, flat joint of the plane variety.

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Fig. 2. Anatomy of the sternoclavicular joints viewed from front. (Adapted from Clement CD. Gray’s anatomy of the human body. 30th edition. Philadelphia: Lea & Febiger; 1985. p. 366– 367; with permission.)

The normal ‘‘stepoff’’ between the two bones often is appreciated on physical examination. The joint capsule is lax and not strong. It is strengthened superiorly by the AC ligament, a quadrilateral band of parallel fibers extending between the acromial end of the clavicle and the adjoining part of the acromion. The major stabilizing structure at this joint is the unyielding coracoclavicular ligament (Fig. 3). The conoid portion of this ligament is fan-shaped with its apex lying inferiorly and lies in the frontal plane. It is attached from the ‘‘elbow’’ of the coracoid process to the apex of the posterior arc of the distal clavicle and serves as a vertical axis for scapular rotation. The trapezoid portion inserts into the medial border of the upper surface of the coracoid process and runs superiorly and laterally. It has a more horizontal course and attaches from the upper aspect of the coracoid to the clavicle. The trapezoid ligament serves as a hinge for scapular motion about a horizontal axis. Normally, only a small amount of movement occurs at the AC joint before the conoid and trapezoid ligaments are stretched and limit further movement. When the ligaments are taut, the clavicle and scapula move as a unit. Most of the pectoral girdle movement occurs at the SC joint and at the scapulothoracic interface rather than the AC joint. A fall on the point of the shoulder may cause partial or complete disruption of the coracoclavicular ligament, resulting in separation of the AC joint. Injuries to the joint are graded as follows: Grade I involves minor stretching to the ligaments and joint capsule without ligament disruption, grade II involves subluxation of the joint with stretching and possibly a partial tear of the coracoclavicular ligaments, and grade III involves complete disruption of the coracoclavicular ligaments. After more severe AC separations, shoulder abduction and forward flexion often are limited

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Fig. 3. Anatomy of the shoulder joint. (A) Anterior view of ligaments of the left shoulder. (B) Coronal section through the head of the left humerus and shoulder joint, anterior half viewed from behind. (C) Interior of the right shoulder viewed from its lateral aspect. (Adapted from Clement CD. Gray’s anatomy of the human body. 30th edition. Philadelphia: Lea & Febiger; 1985. p. 368–372; with permission.)

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Fig. 4. In the left half of this horizontal section through the thorax, the space between the scapula and serratus anterior is seen at (1). The space between the thoracic wall and serratus anterior is seen at (2). The right half of the section shows that the scapula runs obliquely, forming an angle of 30 with the frontal plane. The clavicle also runs obliquely, forming an angle of 60 with the scapula. (Adapted from Kapankji IA. The physiology of the joints, vol. 1: upper limb. 5th edition. Edinburgh: Churchill Livingstone; 1982. p. 39; with permission).

because there is excessive movement between the scapula and clavicle, disrupting the stabilizing role of the clavicle on the sternum. AC joint involvement often is found in RA and may be the prime source of shoulder pain. Osteoarthritis commonly affects the AC joint as well. AC joint injury frequently leads to osteoarthritis; however, in most cases, the development of degenerative joint disease is not preceded by injury. Scapulothoracic interface. Scapulothoracic movements are of a gliding nature and occur at an interface between the ventral surface of the scapula and the rib cage. The contacting surfaces involve the subscapularis and bare areas of the scapula with the serratus anterior overlying the second through the seventh ribs. Although the scapula has no bony or ligamentous connections with the thorax, numerous muscles hold the scapula in close opposition to the chest wall (eg, serratus anterior, trapezius, rhomboids). Weakness or paralysis of these same three muscles results in winging of the scapula. With the upper limb in a neutral position and at rest, inspection can lead to the anatomic diagnosis of scapular winging. Weakness of the rhomboids results in a resting position where the scapula is directed laterally (ie, protracted) and rotated upward (think about the antagonist muscles pulling without opposition). Likewise, weakness of the serratus anterior results in a retracted scapula (directed medially) and rotated downward. Weakness of trapezius results in a protracted scapula (directed laterally) and rotated downward. Normally the scapula is set obliquely on the thorax at an angle of 30 , open anterolaterally, and moves along a curved thoracic surface during protraction and retraction (Fig. 4). The position of the scapula during active

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upper limb use is important to the stability and forces at the glenohumeral joint; this is discussed later. Movements and kinetics. Movements of the pectoral girdle include elevation-depression, protraction-retraction, and upward-downward rotation (Fig. 5). Muscles that move the pectoral girdle attach to the thorax, arm, and forearm (Fig. 6, Table 1). The fulcrum of movements is through the costoclavicular ligament. As the lateral end of the clavicle moves, the medial end moves in the opposite direction. During elevation, the scapula and lateral extremity of the clavicle are raised, while the medial aspect of the clavicle slides inferiorly. During depression, the scapula and lateral aspect of the clavicle are depressed, and the medial part of the clavicle is raised. Crutch walking is a good example of an activity in which active depression of the pectoral girdle occurs. Protraction, a movement that occurs during pushing activities, involves forward movement of the scapula and lateral clavicle, accompanied by retraction of the medial clavicle (these movements can be felt). Rotation of the pectoral girdle occurs with movements of the shoulder above the horizontal plane. The clavicle and the scapula rotate. Upward rotation of the scapula (the glenoid cavity moves superiorly) is required for full abduction and forward flexion of the shoulder (Fig. 7). The prime movers for upward rotation are the trapezius (upper and lower fibers) and the serratus anterior. Axial rotation of the clavicle follows this movement passively when the capsule and ligaments of the AC joint are put on tension. Downward rotation of the pectoral girdle usually is passive and assisted by gravity. For adequate stabilization and long-term health of the glenohumeral joint, proper positioning of the glenohumeral joint is imperative. Many shoulder treatment programs also focus on the orientation of the glenohumeral joint. The position of the scapula on the thorax is crucial to understand. When the vertebral border of the scapula moves medially (as in squaring the shoulders), it comes to lie more and more in a frontal plane. The glenoid cavity faces more directly laterally, and the lateral extremity of the clavicle moves medially and posteriorly. The angle between the scapula and the clavicle tends to open out (Fig. 8, right side). Conversely, when the scapula moves laterally, it comes to lie more in a sagittal plane. The glenoid cavity faces more directly anteriorly. The lateral extremity of the clavicle moves laterally and anteriorly, and its long axis tends to lie in a frontal plane. The angle between clavicle and scapula tends to close (Fig. 8, left side). The positioning of the scapula is discussed in greater detail as it applies to glenohumeral balance. Several large muscles move and stabilize the pectoral girdle. The trapezius and serratus anterior are powerful muscles that attach the pectoral girdle to the thorax. Deltoid and pectoralis major are thought of as muscles that move the humerus on the pectoral girdle. With a closed kinetic chain, however, these large, forceful muscles can move and stabilize

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Fig. 5. All views are seen from behind. (Top) Lateral (left) and medial (right) movements of the scapula are seen (retraction-protraction). (Center) Elevation (left) and depression (right) of the scapula. (Bottom) Upward rotation (left) and downward rotation (right) of the scapula.

the pectoral girdle as well. In the setting of weakness or instability of the shoulder, therapy directed at these large muscles and stable alignment of the glenohumeral joint is crucial. Glenohumeral joint The glenohumeral joint is a synovial joint of the ball-and-socket type (Fig. 9), linking the free limb through the ball (head of the humerus) to the socket of the pectoral girdle (glenoid cavity of the scapula). The head of the humerus is approximately one third of a sphere, and it is about four times larger than the socket on the scapula. In anatomic position, the head faces superiorly, medially, and posteriorly with the lesser tuberosity in front and the greater tuberosity pointing laterally (see Fig. 7). The rotator cuff muscles attach to the tuberosities. The long head of the biceps runs in a groove between the tuberosities called the intertubercular, or bicipital groove.

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Fig. 6. The muscles of the shoulder girdle and arm. Anterior views show the superficial muscles (A) and deep muscles (B). Posterior views show the superficial muscles (C) and deep muscles (D).

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Table 1 Prime movers of the pectoral girdle Elevation

Trapezius (upper fibers) Rhomboids Levator scapuale

Depression

Latissimus dorsi Pectoralis major (costal fibers) Trapezius (lower fibers)

Protraction

Serratus anterior Pectoralis minor Pectoralis major

Retraction

Trapezius Rhomboids

Upward rotation

Trapezius Serratus anterior

Downward rotation

Rhomboids

Fig. 7. The muscles that rotate the scapula upward during abduction of the arm. The upper part of the trapezius, which is attached to the outer part of the scapular spine, pulls upward, and the lower part of the serratus anterior, attached to the lower part of the scapula, pulls the inferior angle laterally, while the lower portion of the trapezius, attached to the medial part of the scapular spine, pulls downward. (From Hollinshead WH. Anatomy for surgeons, vol. 3: the back and lower limbs. 3rd edition. New York: Harper & Row; 1982. p. 321.)

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Fig. 8. Right side of the figure shows medial movement (retraction) of the scapula where the bone lies in a more frontal plane. The orientation of the glenoid cavity is directed laterally. The angle between the scapula and clavicle opens out. On the left side of the figure, lateral movement (protraction) occurs where the scapula lies in a more sagittal plane. The glenoid cavity faces more anteriorly, and the angle between the clavicle and scapula tends to close.

Fig. 9. The articular surfaces of the glenohumeral joint are typical of a ball-and-socket joint, which has three axes and three degrees of freedom. The head of the humerus faces superiorly, medially, and posteriorly. It corresponds to a third of a sphere 3 cm in radius. Its axis forms with the axis of the shaft an angle of 135 and with the frontal plane an angle of 30 . It is separated from the rest of the superior epiphysis of the humerus by the anatomic neck, which makes an angle of 45 with the horizontal plane. The glenoid cavity of the scapula lies at the superolateral angle of the scapula and points laterally, anteriorly, and slightly superiorly. The glenoid cavity is much smaller than the head of the humerus but is deepened by a ring of fibrocartilage, the glenoid labrum. This ring is attached to the margin of the glenoid cavity and deepens it appreciably so as to make the articular surfaces more congruent. (Adapted from Kapankji IA. The physiology of the joints, vol. 1: upper limb. 5th edition. Edinburgh: Churchill Livingstone; 1982. p. 23; with permission).

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The margin of the shallow, pear-shaped glenoid cavity is slightly raised and attaches to a ring of fibrocartilage, the glenoid labrum (see Fig. 7). The labrum deepens the socket significantly and is an important factor in the overall stability of the joint. Two small tubercles above and below the cavity (supraglenoid and infraglenoid) serve as attachments for the long head of the biceps and triceps. These two attachments help stabilize the head of the humerus, particularly the long head of the triceps, in preventing downward displacement. The capsule of the joint is thick and strong but lax, especially inferiorly, to allow great range of movement (see Fig. 3). It is attached to the humerus around the articular margins of the head except inferiorly, where it is attached to the surgical neck, enclosing a portion of the epiphyseal line. The capsule encompasses the joint completely and is attached to the scapula just beyond the glenoid labrum. With the arm hanging loosely at the side, there is a loose recess inferiorly, sometimes called the axillary fold, to allow space for the head of the humerus during full abduction (see Fig. 3). Conditions in which there are contractures or fibrosis of the capsule result in restriction of glenohumeral motion. Thickenings of the anterior capsule are named (superior, middle, and inferior glenohumeral ligaments) and strengthen the anterior and inferior capsule. The coracohumeral ligament attaches from the coracoid process to both of the tuberosities (anterior band to the lesser tuberosity and posterior band to the greater tuberosity). These bands are strong and limit extension and flexion, respectively. The capsule and ligaments are a significant stabilizing factor at the end ranges of motion. Deficiencies in these ligaments are important in the development of instability. The coracoacromial ligament extends from the undersurface of the acromion to the coracoid process (see Fig. 3). Along with the acromion and the coracoid process, it may act as a large articulating surface for the head of the humerus, particularly in the setting of a high-riding humerus. The synovial membrane lines the capsule and is in continuity (through the foramen of Weitbrecht in the anterior aspect of the capsule) with the subscapularis bursa [2]. Synovium also invests the long head of the biceps as it courses beneath the transverse ligament, the latter being a thickened part of the capsule that bridges the gap from the greater to lesser tuberosity (eg, over the upper end of the bicipital groove). The synovial cavity does not normally communicate with the subacromial bursa. Movements. At the glenohumeral joint, the ball-and-socket configuration allows relatively free movements of flexion-extension, abduction-adduction, and medial-lateral rotation (see Fig. 9). The prime movers are listed in Table 2 (Fig. 10). In general, the descriptions of these movements are oversimplified because in reality the pectoral girdle moves in concert with the glenohumeral joint. Protraction of the pectoral girdle occurs with flexion, retraction occurs with extension, and so on.

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Table 2 Prime movers of the glenohumeral joint Flexion

Pectoralis major (clavicular head) Deltoid (anterior fibers)

Extension

Latissimus dorsi Deltoid (posterior fibers)

Internal rotation

Pectoralis major Latissimus dorsi Teres major Subscapularis

External rotation

Infraspinatus Teres minor Deltoid (posterior fibers)

Abduction

Deltoid Supraspinatus

Adduction

Pectoralis major Latissimus dorsi Teres major Subscapularis

Rotation of the humerus on the glenoid fossa can be performed in any position. It is limited by the extent of articular surface on the humerus and by restrictions from the usual checkreins (ie, capsule and ligaments). Adduction and extension are straightforward. Adduction is produced by the great upper limb muscles of the thorax (pectoralis major and latissimus dorsi) along with several short rotators (subscapularis, infraspinatus, teres major, teres minor). The prime movers for extension include the latissimus dorsi, posterior fibers of deltoid, short muscles (teres major and minor), and long head of the triceps. Flexion and abduction of the shoulder require study and are discussed subsequently in the section on movement and stability of the shoulder. Flexion and abduction of the glenohumeral joint (in contrast to the shoulder) also are straightforward, however. The distinction is that flexion and abduction at the glenohumeral joint are limited. Prime movers for flexion include pectoralis major, the anterior fibers of deltoid, and the long head of the biceps. Prime movers for abduction include the supraspinatus and deltoid. For full range of flexion and abduction, however, pectoral girdle rotation is necessary (see subsequent discussion). Humeroacromial interface. The humeroacromial or subdeltoid interface is between the undersurface of the acromion and coracoacromial arch with the head of the humerus. The significance of this interface in the healthy shoulder is uncertain, and its physiologic role during normal shoulder motion still is debated. There has been speculation that abduction of the internally rotated shoulder may result in mechanical impingement between

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Fig. 10. Muscles that move the shoulder and arm: flexors (A), extensors (B), adductors (C), abductors (D), and rotators (E). (Adapted from Hollinshead WH. Anatomy for surgeons, vol. 3: the back and lower limbs. 3rd edition. New York: Harper & Row; 1982. p. 325–330.)

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the humeral head and the overhanging arch. The theory of impingement has fallen out of favor, however, with many clinicians. Between the head of the humerus and the acromion lies the supraspinatus tendon and the subacromial bursa. This close anatomic relationship between the rotator cuff and bursa makes differentiation between rotator cuff tendinitis and subacromial bursitis difficult. In many cases, involvement of the bursa and the tendon is thought to occur concurrently. This belief may exist, however, because little is known about the sensitivity and specificity of the physical examination and diagnostic tests in differentiating between the two. The humerus is in contact with the coracoacromial arch when there is upward displacement of the humeral head (eg, rotator cuff weakness or tears) (Fig. 11). Compression of the supraspinatus tendon and bursa results in progressive injury of the rotator cuff. In the setting of large rotator cuff tears, the coracoacromial arch provides superior stability to the humeral head. In this setting, acromioplasty may result in superior instability during abduction activities. Movement and stability of the shoulder Mobility Full range of shoulder movement includes motion of the glenohumeral joint and the pectoral girdle. Limitations of any part of this complex impair the whole. Raising the arm above the head into flexion or abduction is brought about by a combined action of the glenohumeral joint and of the pectoral girdle (Fig. 12). Abduction and forward flexion without any girdle movement are limited to approximately 90 . Further abduction is made possible by way of external rotation of the humerus, providing further articulating surface. Three phases of abduction are described. In the first phase, glenohumeral abduction occurs by way of deltoid and supraspinatus contraction. At approximately 90 , movement stops or locks. This locking is a result of the greater tuberosity hitting the superior margin of the glenoid; in other words, there is no further articular surface on the humeral head in this position (look at a humerus and this will make sense). External rotation adds articular surface and facilitates abduction. In the second phase, upper rotation of the glenoid cavity results in another 60 of abduction. The way in which the glenoid cavity is rotated upward is by rotation of the entire pectoral girdle. Trapezius (upper and lower fibers) and serratus anterior rotate the scapula (the clavicle follows) so that the glenoid cavity face superiorly. As the scapula rotates initially, there is movement at the AC joint until the ligaments are taut, then there is axial rotation along the clavicle. The third phase of abduction involves lateral flexion of the trunk. This flexion provides the last few degrees of abduction to reach the vertical position. Forward flexion follows these same three phases. These three phases are not strictly sequential; the various movements overlap. This conception is not strictly of interest to anatomists. Anything

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Fig. 11. With progressive cuff fiber failure, the head moves upward against the coracoacromial arch. (A) Normal relationships of the cuff and the coracoacromial arch. (B) Upward displacement of the head, squeezing the cuff against the acromion and the coracoacromial ligament. (C) Greater contact and abrasion, giving rise to a traction spur in the coracoacromial ligament. (D) Still greater upward displacement, resulting in abrasion of the humeral articular cartilage and cuff tear arthropathy. (Adapted from Matsen FA. Practical evaluation and management of the shoulder. Philadelphia: WB Saunders; 1994. p. 123.)

that interferes with any of these movements would impair abduction and forward flexion. Paralysis of serratus anterior results in abduction to 90 . Deltoid paralysis does not allow the movement to be initiated, but pectoral girdle rotation and trunk movements result in limited abduction. Limited scapular mobility also limits full abduction and forward flexion (eg, kyphotic posture interferes with scapular protraction and rotation). Stability Compared with the hip, the shoulder is seen as a remarkably mobile but inherently unstable structure. Although this comparison between shoulder

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Fig. 12. Biomechanics of the glenohumeral movements of arm abduction. (A) Normal position of the head and shaft of the humerus. The circle in the head of the humerus indicates the center of rotation. (B) Humerus abducted 45 and the scapula beginning upward rotation. The upper panel shows that the incongruity of the articulating surface of the head of the humerus and the surface of the glenoid cavity causes the greater tuberosity of the humerus to impinge on the coracoacromial ligament. The upper panel in (C) shows that to allow the greater tuberosity to pass under the coracoacromial hood during arm abduction, the humeral head is depressed (depicted by downward movement of the center of rotation) and the humeral head rotated (indicated by the thin arrow). The abduction movement of the arm is accomplished in a smooth coordinated movement during which for each 15 of arm abduction, 10 of motion occurs at the glenohumeral joint and 5 occurs due to scapular rotation on the thorax. As noted in (C), abduction of the arm to 90 is accomplished by 60 rotation of the humerus and 30 rotation of the scapula. Full abduction of the arm, as shown in (D), is accomplished by 120 of rotation at the glenohumeral joint and 60 rotation of the scapula. (Modified from Cailliet R. Shoulder pain. 2nd edition. Philadelphia: FA Davis; 1981.)

and hip is undoubtedly true, stability of the shoulder often is underrated. Most athletes and workers stress the shoulder in remarkable ways yet most never have problems with instability. Individuals with a spinal cord injury live for decades (some World War II veterans are now in their 80s and have been living with a spinal cord injury for >50 years) using their upper extremities for support, reaching, and wheelchair mobility without stability problems. To understand shoulder-stabilizing mechanisms better, stability at mid range and end range require study. End-range stability. End-range stability involves different mechanisms than mid-range stability at the shoulder. Three factors are important in end-range stability—bony, ligamentous, and muscular. Bony factors at the shoulder are significant, although not the major factor; the size and shape of the glenoid fossa is especially important. In comparison, an intrinsically more stable, deep ball-and-socket joint centers the hip joint. The small arc of the glenoid captures relatively little of the humeral head. Stability within the glenoid is precarious, and there is little margin of error. Many anatomic variants that compromise the glenoid may result in instability. A flat or small glenoid fossa

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often results in an intrinsically unstable joint, resulting in subluxation or frank dislocation. The integrity of the glenoid labrum is essential in enhancing bone surface congruity. Ligamentous factors, including the articular capsule, are crucial for end-range stability (see Fig. 3). In contrast to other joints with shallow sockets (eg, knee, interphalangeal joints), isometric articular ligaments do not stabilize the shoulder. To allow ample movement, the capsule and ligaments of the glenohumeral joint are slack in most of the joint’s positions until end range is reached. Then these tissues act as checkreins at the limits of motion. Finally, muscles and their associated tendons provide endrange stability. As the muscle-tendon structure reaches its elastic limit, it also acts as a checkrein. Muscles’ contractile properties provide a dynamic element to this stabilization process; this is considered in the discussion of mid-range stability. Mid-range stability. Different mechanisms provide mid-range stability (eg, limited joint volume and adhesion-cohesion), although only the dynamic mechanisms are discussed here because these can be enhanced and extended by exercises and therapy. Two mechanisms are discussed: glenohumeral positioning and concavity compression [3]. Glenohumeral positioning (ie, glenohumeral alignment, glenohumeral balance) is the most important mechanism of shoulder stability and warrants careful attention. Frequently, correcting poor glenohumeral alignment can ameliorate shoulder pain and dysfunction. Glenohumeral alignment refers to the relative position of the scapula to the humerus and the net humeral joint reaction force (Fig. 13). Because the scapula and the humerus are mobile, optimal alignment is not a simple matter. Consider the example of someone who is doing a press-up against a wall. Standing in front of the wall, a push-up motion is performed. Although the placement of the hands and position of the arms is relatively straightforward, the position of the shoulder is not. Identical humerothoracic positions are possible using different glenohumeral positions (Figs. 14 and 15). In the first example, the scapula is protracted (directed laterally) so that it lies in a more sagittal plane (see Fig. 14). The glenoid cavity faces more directly anteriorly, and the angle between the clavicle and scapula closes. In this position, the humerus is aligned closely with the glenoid centerline (see Fig. 13). Little in the way of muscular factors is necessary for stability in this position. This position also is independent of force magnitude. The joint remains stable with increasing forces because the bony alignment is stable. As forces increase, there is no need for additional muscular work. In the second example, the scapula is retracted (directed medially) so that it lies in a more frontal plane. The glenoid cavity faces more directly lateral, and the angle between the clavicle and scapula opens. In this position, the humerus is aligned poorly with the glenoid centerline (see Fig. 15). In this position, forceful muscular work must be exerted to maintain stability of the joint. This position is not independent of force magnitude. With increasing

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Fig. 13. Glenohumeral balance is a stabilizing mechanism in which the glenoid is positioned so that the net humeral joint reaction force passes through the glenoid fossa. (Adapted from Matsen FA. Practical evaluation and management of the shoulder. Philadelphia: WB Saunders; 1994. p. 62.)

forces, additional muscular work must be generated to maintain stability. This may seem to be a trivial point, but the forces are considerable. People who lift heavy loads (eg, welders, heavy laborers), high-performance athletes, individuals with physical disabilities (who rely on their upper limbs for transfers and wheelchair propulsion), and people who do activities that require prolonged static shoulder postures bear the greatest loads and are at the highest risk for problems. The importance of good glenohumeral alignment in people with spinal cord injury is discussed in the article by Hastings and Goldstein elsewhere in this issue. Glenohumeral positioning also is important in people with shoulder problems, such as a rotator cuff tear. When there is shoulder weakness, proper alignment of the glenohumeral joint decreases the mechanical load on soft tissues and the rotator cuff. Scapular strengthening often is targeted with the goal of alignment rather than compensating for weakness of the rotator cuff. This is a frequent misconception of shoulder strengthening in the setting of rotator cuff disease. Concavity compression keeps the head of the humerus pressed against the glenoid cavity in all positions of the shoulder (Fig. 16); this also has been called coaptation of the glenohumeral joint. Stability is related to the magnitude of force that comes from periarticular muscles compressing the head of the humerus into the glenoid cavity. Fundamentally, these muscles act as dynamic ligaments, relaxing to allow movement, then contracting again to stabilize the head of the humerus into the glenoid. As the glenohumeral

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Fig. 14. The scapula is protracted (directed laterally) so that it lies in a more sagittal plane.

joint is moved from one position to the next, the muscles relax, then tighten again to stabilize the joint in the new position (see Fig. 11). The periarticular muscles are in the best mechanical position to maintain coaptation of the articular surfaces at the glenohumeral joint. These muscles include the rotator cuff muscles (subscapularis, supraspinatus, infraspinatus, and teres minor). The tendon of the long head of the biceps assists in concavity compression by forcing the humeral head medially during contraction. Larger muscles (eg, pectoralis major and latissimus dorsi) also may help pull together the humeral head and glenoid fossa, although these muscles usually are acting as prime movers of the humerus. Coaptation is required at rest and during work. At rest, the rotator cuff muscles and long muscles of the arm are tonically active and prevent infraglenoid subluxation of the humeral head. If there is flaccid paralysis of

Fig. 15. The scapula is retracted (directed medially) so that it lies in a more frontal plane.

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the upper limb muscles, subluxation of the glenohumeral joint occurs. During active movement, periarticular muscles work in conjunction with prime movers to maintain coaptation. During abduction of the glenohumeral joint, supraspinatus and deltoid abduct the humerus. They also would exert an upward pull on the humerus, however, if not for the downward pull of teres minor and major. Simultaneously the subscapularis and infraspinatus compress the head into the glenoid fossa and prevent upward displacement. Severe rotator cuff tears that extend into the subscapularis or infraspinatus frequently result in significant weakness, and the humerus migrates superiorly. Another important factor in concavity compression is the depth of the glenoid fossa. In the case of a congenitally small, flat glenoid cavity, increased compressive forces need to be applied to prevent translation (ie, slippage) of the humeral head. This factor also would explain the need for higher compressive forces after injuries to the glenoid labrum. Rotator cuff strengthening exercises can enhance concavity compression.

Clinical evaluation of the patient In musculoskeletal medicine, the history and physical examination provide most of the key information required for diagnosis, assessment,

Fig. 16. (A–C) Short, periarticular muscles run transversely across the joint providing dynamic stability to the joint in all positions by pressing the humeral head against the glenoid cavity. Five muscles are illustrated as follows: (1) supraspinatus, (2) subscapularis, (3) infraspinatus, (4) teres minor, and (5) long head of the biceps. (Adapted from Kapankji IA. The physiology of the joints, vol. 1: upper limb. 5th edition. Edinburgh: Churchill Livingstone; 1982. p. 35; with permission).

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and treatment. The history provides crucial data about the pathologic processes involved and the functional consequences of the disorder, whereas the physical examination sorts out the anatomic structures involved and the specific mechanical impairments associated with the underlying pathology. When assessing a patient with shoulder complaints, the history and physical examination are an extension of the practitioner’s understanding of shoulder anatomy and biomechanics. A brief overview of the history and physical examination is presented here, then specific details of each are reconsidered within specific clinical conditions. History The history is the patient’s story. The initial ‘‘open’’ phase of the history is followed by specific questions. The most important presenting symptoms in mechanical disorders of the shoulder include pain, stiffness, instability, weakness, difficulty moving, roughness, and fatigue. Details about the characteristics of pain are essential, including onset, location, duration, quality, intensity, precipitating factors, and relieving factors. A patient with a rotator cuff tear may present with the abrupt onset of weakness, whereas the pain of degenerative glenohumeral arthritis is usually of insidious onset, chronic, and associated with stiffness after inactivity. Associated symptoms are helpful in differentiating between musculoskeletal and neurologic etiologies. Cervical radiculopathy may present with the abrupt onset of shoulder pain and weakness, but paresthesias also may be present. No sensory symptoms are associated with a rotator cuff tear. The location and type of pain are important historical elements. Pain from rotator cuff pathology usually is felt at the outer aspect of the upper arm or lateral deltoid region. The posterior deltoid or glenoid humeral area often is related to glenohumeral joint pathologies. AC and SC joint disorders are well localized over the involved joint. Pain from the cervical spine and radiculopathy often is parascapular (particularly in a C6 or C7 root lesion) across the back of the shoulder girdle and down the arm. Radiation of pain is common in radiculopathy and with other compressive neuropathies, brachial neuritis, and other cervical pathologies. Adhesive capsulitis tends to cause an intense aching deep in the shoulder. Night pain that interferes with sleep may be common with rotator cuff disease and adhesive capsulitis. The mechanism of an injury is important in making an accurate diagnosis. A fall onto an outstretched arm can cause instability in a younger person or a rotator cuff tear in an older person. A fall onto the point of the shoulder may result in injury to the clavicle or AC joint. Throwing injuries tend to injure the capsule and ligaments of the glenohumeral joint. Shoulder pain may be seen in association with several medical conditions and may be referred from the neck, thorax, and abdomen. A history of comorbid conditions, such as diabetes, Raynaud’s phenomenon, cervical spondylosis, cerebrovascular disease, and cardiac disease, needs careful review.

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A full history of the functional impact of the shoulder disorder is important. In this regard, self-assessment questionnaires have become an important part of musculoskeletal and orthopedic histories. Many different types of selfassessment questionnaires for people who have shoulder pain are available, including the simple shoulder test, American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, American Shoulder and Elbow Surgeons Shoulder Index, UCLA Shoulder Score, Constant-Murley Scale, Western Ontario Shoulder Instability Index, and Disabilities of the Arm, Shoulder and Hand Module (DASH questionnaire) [2–7]. These selfassessments often are given in conjunction with general health assessments (eg, SF-36) to monitor treatment and outcomes. Physical examination An examination of the neck, thorax, and shoulder should be conducted in all patients who have shoulder pain. Only a brief description of the obligatory parts of the shoulder examination are included here. Inspection should detect any gross abnormalities, such as Sprengel’s deformity (congenitally undescended scapula) or an absent clavicle as in cleidocranial dysostosis, asymmetries, atrophy (particularly deltoid, supraspinatus, and infraspinatus muscles), erythema, bruising, skin changes such as scars, or otherwise abnormal anatomy (scapular winging). Scapulohumeral and scapulothoracic rhythm during elevation and abduction should be assessed, and any asymmetry should be noted. Postural abnormalities, such as forward-rolled or drooped shoulder, should be noted. Postural abnormalities of the cervical spine also are noted. Determining cervical ROM is important, with particular attention to extension and rotation to the symptomatic side. Exacerbation of shoulder pain with these movements may indicate radiculopathy because these maneuvers narrow the intervertebral foramina. Palpation should assess the presence of tenderness and swelling to the AC, SC, and glenohumeral joints. Major tendons and muscular attachments are located and palpated; however, many normal individuals have tenderness of these structures (eg, biceps tendon, coracoid process). Crepitus and roughness should be noted during passive and active movement. Crepitus over the AC and SC joints is felt easily because the joints are subcutaneous. Glenohumeral crepitus is palpated best posteriorly just beneath the angle of the acromion as the adducted arm is rotated. Scapulothoracic crepitus is appreciated easily over the scapula (particularly the superior medial border) when the shoulder is elevated or protracted. Neck, shoulder, and distal upper limb joints should be evaluated for stiffness and impaired ROM. Matsen et al [3] recommended four parameters to evaluate range of shoulder motion: (1) forward elevation, (2) external rotation, (3) internal rotation, and (4) cross-body adduction. Basic pectoral girdle mobility can be assessed by active ROM, although measurement has

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not been well standardized. Isolating movements to a particular joint is important because compensation occurs when there is stiffness and impaired ROM. Commonly, there is increased scapular mobility in glenohumeral stiffness. Also, forearm supination and pronation compensate for a more proximal restriction (eg, limitation of shoulder rotation). Various stress tests and special maneuvers have been described for the shoulder for impingement, glenohumeral laxity, bicipital provocation, and specific muscle testing. In general, these maneuvers attempt to reproduce pain or elicit cardinal mechanical deficits (eg, stiffness, instability, weakness, or roughness). Several tests for impingement (Neer, Hawkins/Kennedy) have been described, although many clinicians no longer attribute shoulder pain to the mechanical impingement of the rotator cuff between the humeral head and coracoacromial arch. The impingement tests approximate the greater tuberosity and the acromion (or coracoacromial arch), then evaluate if symptoms have been provoked. Speed’s test, Yergason’s test, bicipital provocation test, and others are used to reproduce symptoms from the long head of the biceps (either pain from tendinitis or subluxation of the biceps tendon out of the intertubercular groove). Because many tests that require active movement or resistance exacerbate shoulder pain, some maneuvers use a strategy for muscles that cross two joints where the distal limb segment (eg, elbow flexion) is tested to see if proximal pain at the shoulder is reproduced (eg, Yergason’s test). There also are many tests for instability (apprehension, relocation, posterior stress test, sulcus sign with the inferior instability test, load and shift). Asymmetry, reproduction of symptoms, and apprehension are possible signs of instability. Just the presence of laxity in the absence of these signs has not been found to be a sensitive or specific sign of instability. Strength impairments are common in neurologic and musculoskeletal conditions, but the distribution and associated signs usually are different. A large rotator cuff tear manifests with abduction and external rotation weakness. A C5 radiculopathy also may lead to abduction (deltoid, supraspinatus) and external rotation (infraspinatus, teres minor, posterior deltoid) weakness because all of the prime movers for these two movements have a large component of C5. A C5 radiculopathy also leads to weakness of elbow flexion, sensory changes, and a depressed biceps reflex. Diagnostic testing In most cases, a standard series of shoulder radiographs in conjunction with a careful history and physical examination is sufficient to establish a working diagnosis and treatment plan. Radiographs typically are used to establish, or exclude, the diagnoses of arthritis, calcification, dislocation, high-riding humerus, tumor, and old trauma. Ultrasound, CT, MRI, arthrography, and arthroscopy all have been used to evaluate various shoulder conditions. A discussion of the appropriate use, sensitivity, and specificity of these tests is beyond the scope of this article.

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Differential diagnosis Two diagnoses are required to establish a treatment plan for shoulder disorders. First, pathophysiologic diagnoses are specified to elucidate fully mechanisms involved in the development of the shoulder problem (eg, inflammatory, infectious, autoimmune). Treatment to cure or stabilize the underlying condition is important (eg, disease-modifying antirheumatic drugs). A classification scheme and general approach to this topic are discussed in the next section. Second, mechanical impairments are identified. The four basic mechanical impairments of the shoulder are stiffness, instability, weakness, and roughness. Treatment of mechanical impairments includes interventions such as stretching (for stiffness) and strengthening (for weakness or instability). Descriptions and a case study for each type of mechanical problem are presented in the next section. Shoulder disorders: applied anatomy There are many different classification schemes for shoulder disorders. This section uses a pathophysiologic approach and discusses common mechanical problems. Case studies are used as typical examples of mechanical impairments that occur with shoulder complaints. Epidemiology Shoulder pain is one of the most common musculoskeletal complaints. Several studies have attempted to determine the prevalence of shoulder disorders in specific populations (eg, workers, and athletes). Since the 1970s, shoulder problems have increased dramatically, particularly occupational shoulder problems. Whether the increase is the result of ergonomic changes in industry (eg, automation or computerization) or whether it is the result of increased awareness, prevalence rates are remarkably high. In several countries, work-related shoulder complaints exceed low back complaints, whereas in other countries, shoulder pain is second or third to back and neck pain [8–11]. Organizational approach and definitions Many organizational schemes are useful in assisting the clinician to arrive at a diagnosis in patients with shoulder pain or dysfunction. A useful structure is to determine the following: (1) chronicity, (2) etiology (atraumatic versus traumatic), (3) anatomic location, and (4) mechanical impairments. Chronicity is separated into acute onset (hours) or longer (days). Traumatic and atraumatic disorders may manifest as mechanical problems and may be related to a mechanical etiology. Here the term traumatic refers to a single traumatic event in contrast to a condition, such a repetitive motion disorder. The anatomic location of shoulder pain can be organized into SC, AC,

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generalized, or specific locations about the shoulder (anterior, posterior, and lateral) [12]. Many specific problems already have been discussed (eg, clavicular fractures in the section on the clavicle, AC separations in the section on the AC joint). Acute atraumatic generalized pain In acute atraumatic generalized pain, the patient presents with relatively sudden onset of pain that is generalized about the glenohumeral joint (see Fig. 1). The acute onset of glenohumeral joint pain is characteristic of infectious arthritis, although several other arthropathies may have an acute presentation. Other examples of conditions with an acute onset include crystal-related arthropathies, rheumatic fever, and palindromic rheumatism. RA and psoriatic arthritis sometimes present with a sudden onset, although an insidious presentation is more common. Infectious arthritis is discussed as a typical example of an acute monarthritis. Infectious arthritis Bacterial arthritis of the shoulder usually presents with a painful, swollen joint, although a child may present with a high fever and other systemic signs. When the shoulder is involved, acute bacterial and nonpyogenic arthritides most commonly affect the SC and glenohumeral joint. Pain often is present at rest and is exacerbated by movement. The joint capsule typically is distended and warm and is held in the neutral position to give maximal compliance and avoid higher intrasynovial pressure. When shoulder effusions develop, they appear anteriorly below the acromion. The diagnosis requires analysis of joint fluid. Joint fluid should be drained completely because some agents (eg, Staphylococcus aureus and gram-negative bacilli) cause rapid cartilage and bone destruction. A delay in treatment beyond 2 to 3 days may result in significant joint destruction in septic arthritis [13]. Several bacterial and nonbacterial agents have been found as the cause of infectious arthritis. Neisseria gonorrhoeae and S aureus are the most common causes. Most cases of infectious arthritis are the result of injection, infected wounds, open fractures, penetrating injuries, hematogenous spread, or adjacent osteomyelitis. In immunosuppressed individuals, nongonococcal arthritis and nonbacterial arthritis occur more commonly. The incidence of tuberculosis continues to increase and may be the source of upper extremity infectious arthritis. Although uncommon, prosthetic joint infections of the shoulder may occur. If an infection presents soon after surgery, staphylococci and streptococci are more common, and the symptoms are more apparent. In the late postoperative period or later on, general symptoms may be more subtle, and local signs may be unimpressive as well. A prosthetic joint infection is always serious, associated with high morbidity and mortality. Prompt

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diagnosis and treatment are crucial. Treatment consists of early and aggressive drainage of the joint and administration of appropriate antibiotics.

Subacute or chronic atraumatic generalized pain Chronic pain, stiffness, and loss of function occur in a variety of rheumatologic diseases. These conditions typically are not localized to a specific shoulder structure and are a result of a diffuse synovitis. The major differential diagnoses to consider are degenerative arthritis, RA and other synovial disorders, crystal-related arthropathies, amyloidosis, seronegative spondyloarthropathies (although much less common than involvement of lower limb joints), and connective tissue disorders.

Rheumatoid arthritis RA is a chronic, systemic, inflammatory disease that affects approximately 2.5 million people in the United States. Genetic and environmental factors are involved in this autoimmune disease. The mean age at onset is 35 to 55 years, and there is an insidious onset in 70%. More women than men develop RA by a ratio of approximately 3:1. Involvement of the shoulder in RA often is found in patients who have progressive disease. Synovitis leads to erosion of the humeral head and glenoid fossa; however, symptoms may not be recognized until the disease has become advanced due to distal adaptation (eg, use of forearm pronation-supination rather than shoulder internal-external rotation). Local symptoms and signs involve joint pain, morning stiffness, and warm swollen joints. Constitutional symptoms include fatigue, anorexia, weight loss, depression, generalized weakness, malaise, lymphadenopathy, and lowgrade fever. Morning stiffness usually lasts longer than 1 hour, along with extra-articular symptoms, such as achiness. Pain occurs at rest and with movement, often disturbing sleep. Shoulder effusions may develop, and subacromial bursal swelling may occur. The long head of the biceps also may rupture in patients with RA (Fig. 17). The AC joint frequently is involved in RA with symptoms and signs easily identified over the joint. Age at presentation of patients with RA and glenohumeral involvement is often younger than the age of patients with degenerative joint disease. RA affects most of the joints in the upper limbs, and the associated disability is great. Nine out of 10 people with RA have significantly reduced function after 10 years. Less than 50% are able to continue to work after living with RA for 15 years [14]. RA interferes with most shoulder functions, including reaching, lifting, throwing, activities of daily living, and sleeping comfortably. Loss of motion, weakness, and roughness are the common mechanical manifestations of RA.

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Fig. 17. Infectious arthritis of the shoulder.

Pain that is not mechanical If the disorder is not mechanical, other diagnoses must be investigated. Referred pain to the shoulder can occur with neurologic, cervical, thoracic, and abdominal disorders. Neurologic disorders that cause referred pain to the shoulder include brachial neuritis, entrapment neuropathies, cervical radiculopathies, myopathies, and syringomyelia. Common cervical problems, such as degenerative joint disease, diskogenic pain, and facet joint pain, may cause referred pain to the shoulder or girdle musculature. Thoracic and abdominal pathologies, such as Pancoast’s tumor of the lung and subphrenic processes, also may cause referred pain to the shoulder. In general, these conditions result in shoulder pain that is unaffected by passive ROM, active movement, and resisted maneuvers, although this is not entirely true if there is associated muscle tightness or myofascial pain. Radiculopathy frequently results in muscular pain about the shoulder and may present as mechanical pain. Thus, a complete history and physical examination are required to differentiate between musculoskeletal and neurologic etiologies. Mechanical shoulder pain Mechanical shoulder pain includes conditions that are a result of major trauma, minor repetitive trauma, and chronic conditions. Common types of mechanical shoulder pain are reviewed here [3]. The identification of mechanical impairments is essential in establishing an effective treatment program. Four basic mechanical abnormalities occur at the shoulder: stiffness, instability, weakness, and roughness. These parameters have been discussed with respect to the basic design of shoulder joints and interfaces. This information is applied to four cases; each case is representative of a type of mechanical problem. Case 1 The patient is a 55-year-old merchant marine with complaints of progressively more severe pain and stiffness of the right shoulder for the past 3 weeks. Past medical history is unremarkable. There is no history of trauma

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or surgery. The patient complains that he is unable to lift or use his arm. Physical examination is remarkable for limited glenohumeral motion in all directions. There is pain with passive and active movement. Scapulothoracic movement is normal. Radiographs are normal.

Diagnoses. Mechanical diagnosis is shoulder stiffness. Pathologic diagnosis is idiopathic capsulitis (frozen shoulder). Impairment of shoulder motion. Shoulder movement is determined by motion at the glenohumeral joint and scapulothoracic interface. In the absence of trauma, glenohumeral movement may be restricted by capsulitis (idiopathic), arthritis, infection, or avascular necrosis. Limitations of scapulothoracic movement involve pathologies that affect the pectoral girdle (eg, SC arthritis, AC arthritis), pathologies that affect the thorax (posture, rib pathology), tumor, or trauma. In the setting of a normal scapulothoracic interface and radiographically normal glenohumeral joint, the mechanical restriction of motion is usually from contracture of the periarticular soft tissues surrounding the glenohumeral joint. In the absence of trauma, the condition is called frozen shoulder or idiopathic capsulitis. Contractures typically are localized or generalized. Generalized idiopathic capsulitis first was recognized as being distinct from glenohumeral arthritis in 1872 and is characterized by unknown etiology, painful restriction of all shoulder movements, and prominent reduction in the glenohumeral range of movement [15]. Adhesive capsulitis typically has been classified into two forms—primary and secondary. In the primary or idiopathic form, no known precipitating event can be identified. The secondary form is associated with or attributable to other illnesses or events, such as trauma, cardiac disease, pulmonary disease, neurologic disorders, rheumatologic disorders, and endocrine diseases. The cause of adhesive capsulitis is unknown. The necessary and sufficient diagnostic criteria for this diagnosis include functionally significant restriction of shoulder motion, absence of injury or surgery, limited glenohumeral motion on examination, and no radiographic changes in the cartilaginous joint space. Idiopathic adhesive capsulitis tends to affect women more than men, occurs in middle-aged to older individuals, does not show a particular preference for handedness, and occasionally can become bilateral (10%) [16]. The natural history has been well described and points toward good recovery in most people. Many have mild residual signs and symptoms years after the onset of disease. Half of patients have mild but detectable loss of external rotation and abduction, but usually these restrictions do not limit work or avocational activities. Most of these patients are unaware of their motion limits, but 20% might have residual pain without loss of motion. A small proportion (5–10%) are left with persistent significant pain, loss of motion, and disability.

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Treatments include rest, analgesia, passive ROM, passive mobilization, active ROM, ultrasound, oral prednisone, corticosteroid injection, capsular distention, manipulation under anesthesia, and surgical capsular release. Studies that compare interventions are lacking. Many reports are small and do not employ statistical analyses. Also, most reports are case series or convenience samples. In light of the natural history of this disorder, gentle ROM exercises performed several times per day while avoiding joint trauma are recommended by many experts. Case 2 The patient is a 32-year-old lawyer who describes an episode in which she was reaching back with her right arm to put a briefcase in the backseat and her shoulder ‘‘popped out of place.’’ As she pulled her arm back it popped back into place. She has no recent history of trauma. Her review of systems is unremarkable. The musculoskeletal and neurologic examinations are normal. Range of shoulder motion and laxity tests are symmetric. The patient is able to demonstrate a position in which her shoulder feels as if it will dislocate. Radiographs are normal. Diagnoses. Mechanical diagnosis is instability. Pathologic diagnosis is atraumatic instability. Impairment of shoulder stability. Atraumatic instability at the shoulder is a relatively common, bilateral condition affecting shoulder function. The cause of atraumatic instability is biomechanical and relates to failure of one or more of the stability mechanisms discussed earlier. Excessive mobility of the glenohumeral joint is present in all directions, although there may be a predominance of one direction, typically anteroinferior or posteroinferior. An estimated 5% of shoulder dislocations are atraumatic. Minor injuries, such as an awkward lift, may be the provocative event. Some people can dislocate or sublux their shoulder by putting their arm into a certain position. AMBRI (atraumatic, multidirectional, bilateral, rehabilitation, and inferior capsular shift) or ‘‘born loose’’ describes the condition in which the joint is unstable without any trauma and dislocates predominantly in one direction but can sublux or translate significantly in other directions as well. It is often bilateral and should be treated conservatively, although surgery may be necessary in selected cases. There are many causes of atraumatic instability relating to the numerous mid-range and end-range stability mechanisms. A small or flat glenoid fossa, poor glenohumeral alignment, weak rotator cuff muscles, neuromuscular disorders, or a redundant capsule may limit glenohumeral balance, concavitycompression, adhesion-cohesion, or the glenoid suction-cup phenomena that stabilize the shoulder. Atraumatic instability commonly occurs in individuals with generalized hyperlaxity due to connective tissue disorders such as EhlersDanlos syndrome and Marfan syndrome [11].

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The diagnosis of atraumatic instability is primarily by history. The necessary and sufficient criteria for atraumatic instability include a history of functionally significant subluxations or dislocations, spontaneous reduction of dislocations, absence of trauma, demonstration on examination of specific positions that reproduce symptoms, diminished resistance to translation in all planes, and absence of traumatic lesions on shoulder radiographs. Most people with shoulder instability improve with nonsurgical treatment. Initial treatment focuses on strengthening of the dynamic components of shoulder stability (the rotator cuff and the scapular stabilizers). Scapular positioning is a major part of therapy to optimize glenohumeral balance. For the few patients who still are not satisfied after therapy, surgery may offer advantages. The prognosis generally is good. Case 3 The patient is an active, right-handed, 56-year-old man who caught a large tree branch that fell toward him. He experienced sudden onset of left shoulder weakness and pain. He has had left shoulder pain ‘‘off and on’’ for years. He denies other trauma. Review of systems is unremarkable. Mild atrophy of the supraspinatus is noted. The left shoulder has normal passive ROM. The patient complains of weakness (forward flexion, abduction, and external rotation) and pain during active range of motion. He is able to forward flex the shoulder to approximately 150 . Impingement sign is negative. There is no tenderness in the bicipital groove. Radiographs show acromial spurring, but the humeral head is in anatomic position. Diagnoses. Mechanical diagnosis is weakness. Pathologic diagnosis is partial-thickness rotator cuff tear. Impairment of strength: partial-thickness rotator cuff tear. Weakness of the shoulder can result from disuse, immobilization, neurologic disorders, or various musculoskeletal problems. Shoulder strength is determined by the position, length, and strength of shoulder muscles. Because muscles are strongest near the middle of their length, poor scapular position and postural abnormalities also can affect overall strength. Rotator cuff tears are a common cause of shoulder weakness [17,18]. With advancing age, tears occur more commonly. Rotator cuff tears before age 40 are unusual and almost always associated with significant trauma. In cadaver studies, the incidence of full-thickness tears varies from 18% to 26%, whereas the incidence of partial-thickness tears varies from 32% to 37%. After age 60 years, 26% of patients have partial-thickness tears, and 28% have full-thickness tears. In contrast to many shoulder problems, rotator cuff tears are relatively well defined. After large rotator cuff tears, symptoms of pain and strength impairments on physical examination lead to a working diagnosis. Necessary and sufficient criteria for a partial-thickness rotator cuff tear include the

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following: pain and impaired function during activities that require rotator cuff function; diagnosis is supported if there was an unanticipated load; weakness of elevation and external rotation; diagnosis is supported by highriding humerus (radiographs) and subacromial spurring; diagnosis is confirmed by MRI, arthrography, or arthroscopy. The pathophysiology of rotator cuff degeneration is still a controversial topic that has been reviewed extensively in the literature. Many investigators still believe there is physical impingement between the humerus and the undersurface of the coracoacromial arch, particularly with flexion and internal rotation (extrinsic etiology). Others do not believe that physical impingement occurs until later in rotator cuff disease after the humeral head migrates upward against the coracoacromial arch. These investigators believe that mechanical loads (rather than physical impingement) cause damage to the rotator cuff tendons and eventually lead to small tears that progress (intrinsic etiology). This latter theory is based on observations in which the supraspinatus tendon has been found to have relatively little vascularity as it approaches the insertion onto the greater tuberosity. Although discussed as pathologic, this observation is relatively common in normal tendons. In several animals, including humans, tendons that sustain loads other than purely longitudinal-tensional forces are relatively avascular (e.g., supraspinatus, flexor pollicis longus, flexor hallucis longus, tibialis posterior, Achilles tendon). Decreased vascularity occurs in locations where the tendon experiences transverse-compressive and frictional forces (e.g., where tendons change direction as they wrap around bone, pass through a pulley, or are impinged on by nearby structures). This is an adaptive, not a pathologic, response. An adaptive response ensues in these areas, and fibrocartilage replaces the usual collagenous tissue typically found in tendon. Fibrocartilage is ideally suited for compressive forces. In experimental settings, the adaptability of these tissues has been shown. In similar areas where fibrocartilage is found along a tendon, when compressive forces were removed, collagenous tissue replaced fibrocartilage. If the compressive forces were added again, fibrocartilage was synthesized again and replaced the collagenous tissue. Tendons that are subjected to compressive or frictional forces adapt by producing more of a cartilaginous tissue. Fibrocartilage has a paucity of blood supply; this could predispose the tendon to degenerative changes and eventual rupture. This predisposition should be taken into account when contemplating any therapies that may decrease the blood supply further (eg, corticosteroid injections). The pathophysiologic mechanisms that affect these avascular areas have been discussed. Many authors believe that extrinsic compression leads to inflammation; many treatments are directed at blocking inflammatory mechanisms. There is a growing body of evidence, however, that the pathophysiologic process in these areas of fibrocartilage is primarily degenerative

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rather than inflammatory (similar observations have been made for lateral epicondylitis, de Quervain’s tenosynovitis, and Achilles tendinitis). Accommodating the extrinsic and the intrinsic theories in a treatment plan is straightforward. Avoiding impingement-prone postures and making environmental modifications usually are straightforward and relatively easy. Strengthening the muscles that depress the head of the humeral head (eg, teres minor and major) prevents the upward movement of the head against the coracoacromial arch. To minimize high-magnitude loads within the rotator cuff muscles, glenohumeral alignment should be assessed and corrected carefully. With good alignment, loads on soft tissues are minimized. Case 4 The patient is a right-handed, 50-year-old welder with complaints of grinding and roughness at both shoulders. He denies previous trauma or surgery to either shoulder. Review of systems is unremarkable. He was a baseball pitcher for 20 years on a local minor league club. In the left shoulder, grinding began in his teens, is not associated with pain, and has become progressively worse. The location is described as the back of the shoulder. On examination, the patient reproduces the roughness by protracting and retracting the shoulder. Palpation localizes the roughness to the superior medial border of the spine of the scapula. Left shoulder radiographs are normal. In the right shoulder, progressively more severe pain and roughness started approximately 5 years ago. Pain is associated with stiffness and more difficulties raising the arm and throwing a ball overhand. On examination, there is crepitance with glenohumeral movement. ROM is mildly decreased in all planes. Right shoulder radiographs show joint space narrowing and periarticular sclerosis. Diagnoses. Mechanical diagnosis is roughness. Pathologic diagnosis is left snapping scapula, right glenohumeral osteoarthritis. Impairment of shoulder smoothness. Problems with the quality of movement and smoothness of motion are relatively easy to diagnose at most joints. The shoulder has three synovial joints and two movement interfaces, however; a patient with a problem at any one of these areas may present with roughness and have impaired function of the whole shoulder complex. Degenerative, inflammatory, infectious, crystalline, metabolic, neoplastic, traumatic, and congenital processes may result in roughness at synovial joints. Common problems at the shoulder include osteoarthritis, RA, avascular necrosis, and rotator cuff tear arthropathy. Causes of roughness at the movement interfaces are different, however, because there is no synovial joint. Bone contact, neoplasm, alterations in postural relationships, trauma, and congenital problems may cause malalignment or roughness of the sliding surfaces. Finally, roughness may describe the quality of movement rather than a physical roughness between movement interfaces. Pain, weakness, and

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neurologic problems may interfere with normal smooth movements of the pectoral girdle and shoulder. The scapulothoracic interface may be the site of roughness. Snapping scapula is a tactile, acoustic, or painful condition due to an anomalous relationship between the anterior surface of the scapula and the thoracic wall. In some cases, a specific cause is found, such as osteochondromata, hypertrophic callus, or calcified spur [19]. No specific pathologic etiology is found in most cases, however. Many hypotheses have been made when no obvious cause is found. Anatomic differences such as length variability and excessive forward curve of the superomedial angle of the scapula posture, and excessive scapular movement have been suggested as possible reasons for snapping scapula. The diagnosis usually follows the history and physical examination. Careful attention should be paid to past history of trauma, other shoulder problems (eg, compensation for impaired glenohumeral motion may result in increased scapulothoracic excursion), or postural changes. The ‘‘snap’’ or ‘‘clunk’’ is typically low-pitched, in contrast to higher pitched crepitance of the subacromial interface or glenohumeral joint. Radiographs usually are normal, although in some case series, neoplasms and other correctable causes accounted for 50% of the cases [20]. Treatment of idiopathic cases is usually nonsurgical. Correction of posture and the relationship between the scapula and thorax is the mainstay of treatment. This correction requires stretching (in restricted scapular motion) and strengthening of scapular stabilizers. If there is concomitant impairment of glenohumeral motion, stretching of the glenohumeral joint also is indicated. The disease process in glenohumeral osteoarthritis is similar to that of other joints. Primary shoulder degenerative joint disease develops in the absence of trauma, surgery, or other processes known to cause osteoarthritis (eg, avascular necrosis). Secondary shoulder osteoarthritis occurs after one of these known causes. Progressive asymmetric narrowing of the joint space and fibrillation of the articular cartilage occur. Subchondral sclerosis and osteophyte formation follow. In later stages, complete loss of articular cartilage occurs, with bony destruction following. The diagnosis of osteoarthritis is made based on history, physical examination, and standard radiographs. The most common symptom of arthritis of the shoulder is pain, which is aggravated by activity and progressively worsens. If the glenohumeral shoulder joint is affected, the pain is centered in the back of the shoulder. This pain, which is described as vague and diffuse rather than sharp and localized, often is present at rest and is exacerbated by movement and activity. Limited motion and subsequent functional problems occur as the disease progresses (eg, place something on a shelf, activities of daily living). Eventually, night pain is common, and sleeping frequently is interrupted. Physical examination often shows painful restricted motion and crepitus. Weakness is common.

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Radiographs show joint space narrowing, osteophytes, cysts, and subchondral sclerosis. Later stages show glenoid erosions, which usually involve the posterior glenoid and posterior displacement of the humeral head. The necessary and sufficient diagnostic criteria of shoulder roughness caused by glenohumeral osteoarthritis include the following: history of impaired motion and function; limited glenohumeral motion on examination; diagnosis is supported by crepitance; radiographs show joint space narrowing; periarticular sclerosis; and osteophytes. Crepitance of the glenohumeral joint often is palpated posteriorly beneath the acromion and has a grating quality. The shoulder with glenohumeral osteoarthritis often has several mechanical impairments. Contractures and adhesions result in stiffness and restricted ROM. Weakness results from disuse. Instability may present with posterior subluxation. Roughness results from degeneration of the articular cartilage. Nonsurgical treatment is directed at the mechanical impairments found on physical examination. Summary The evaluation of shoulder disorders is challenging because of anatomic and biomechanical complexities. The shoulder comprises three synovial joints and two movement interfaces. The following principles are important to establish an accurate anatomic diagnosis and to develop a treatment plan: (1) perform a careful history and physical examination; (2) determine whether or not the problem is mechanical; (3) for mechanical problems, establish pathophysiologic and mechanical diagnoses; and (4) use mechanical impairments as the basis for therapeutic interventions. Further readings D’Ambrosia RD. Musculoskeletal disorders: regional examination and differential diagnosis. 2nd edition. Philadelphia: JB Lippincott; 1986. Dequeker J, Dieppe P. Disorders of bone, cartilage and connective tissue. In: Klippel JH, Dieppe PA, editors. Rheumatology. 2nd edition. London: Mosby; 1998. p. 8.2.1–8.2.10. Ellis H. Clinical anatomy: a revision and applied anatomy for clinical students. 5th edition. Oxford: Blackwell Scientific Publications; 1971. Hollinshead WH. Anatomy for surgeons, vol. 3: the back and limbs. 2nd edition. New York: Harper & Row; 1969. Kapandji IA. The physiology of the joints, vol. 1: upper limb. 5th edition. Edinburgh: Churchill Livingstone; 1995. Last R. Anatomy: regional and applied. 7th edition. Edinburgh: Churchill Livingstone; 1984. Rokito AS, Cuomo F, Gallagher MA, Zuckerman JD. Long-term functional outcome of repair of large and massive chronic tears of the rotator cuff. J Bone Joint Surg Am 1999;81: 991–7. Rosse C, Gaddum-Rosse P. Hollinshead’s textbook of anatomy. 5th edition. Philadelphia: Lippincott-Raven; 1997. Snell RS. Clinical anatomy for medical students. Boston: Little, Brown; 1973. Warwick R, Williams PL. Gray’s anatomy 35th British edition. Philadelphia: WB Saunders; 1973.

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