Rotator Cuff Disease 

Updated: Aug 30, 2018
Author: André Roy, MD, FRCPC; Chief Editor: Stephen Kishner, MD, MHA 



In 1834, Smith wrote the first description of a rupture of the rotator cuff tendon. Since then, with the work of such authors as Duplay, Von Meyer, Codman, and Neer, degenerative changes to the rotator cuff have been better characterized; however, the exact mechanisms leading to the degeneration of the rotator cuff still are debated today.[1, 2, 3, 4, 5, 6, 7, 8] Moreover, despite numerous trials, questions still exist about the efficacy of different therapeutic modalities for rotator cuff disease.[9] With the help of better methodology for studies, more successful treatment of degenerative rotator cuff disease can be expected. See the images below.

Normal plain radiograph of the shoulder in interna Normal plain radiograph of the shoulder in internal, external, and neutral positions.
This image depicts the channel between the articul This image depicts the channel between the articular capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear.
Even if the channel cannot be always identified, t Even if the channel cannot be always identified, the presence of contrast medium in the subdeltoid-subacromial bursa signs the presence of a complete rotator cuff tear.


The pathophysiology of rotator cuff degeneration is a controversial topic that still is not fully understood. Two hypotheses (ie, extrinsic, intrinsic) coexist and are supported by different authors.[10]

The extrinsic hypothesis

In this theory, the lesion results mainly from repeated impingement of the rotator cuff tendon against different structures of the glenohumeral joint. The following 3 distinct impingement syndromes have been described:

The anterosuperior impingement syndrome

Impingement of the rotator cuff beneath the coracoacromial arch is an established cause of chronic shoulder pain. In 1972, Neer, in a landmark article, described and popularized the term impingement syndrome.[3] Observations from cadaver studies and surgery gave evidence that impingement occurs against the under surface of the anterior third of the acromion, the coracoacromial ligament, and at times, the acromioclavicular joint. Located anterior to the coracoacromial arch in the neutral position, the supraspinatus tendon insertion to the greater tuberosity and the bicipital groove must past beneath the arch with forward flexion of the shoulder, especially if internally rotated, causing an impingement. His works showed that degenerative tendinitis and tendon ruptures were centered in the supraspinatus tendon, extending at times to the anterior part of the infraspinatus tendon and the long head of the biceps tendon.

Neer believed that 95% of tears of the rotator cuff were initiated by impingement wear, rather than circulatory impairment or trauma. He observed proliferative traction spurs at the undersurface of the anterior acromion that he explained by the repeated impingement of the cuff (see the image below). He stated that the variation in shape and slope of the acromion could make people more susceptible to impingement and tear, making it appear logical to perform an anterior acromioplasty at the time of every cuff repair.

Presence of a bony spur on the inferior surface of Presence of a bony spur on the inferior surface of the acromion.

Later, the shape of the acromion was studied in cadavers and roentgenographically. Biglianni described 3 different shapes of acromia in cadavers, according to the anterior slope[11] :

  • Type 1 - Flat

  • Type 2 - Curved

  • Type 3 - Hooked

Only 3% of tears are associated with a type 1 acromion. Although there is a strong association between cuff tears and hook acromia, it is unclear whether the shape is the cause or the result of the cuff tear or simply the result of aging; however, Ozaki et al's study on cadavers showed that the undersurface of the acromion was normal when the incomplete tear was on the articular side.[12] On the other hand, when the incomplete tear was on the bursal side of the cuff tendon, pathological changes of the under surface of the acromion were observed, suggesting that a hooked acromion is the result of the cuff tear on the bursal side of the tendon and not the cause. Nevertheless, curved and hooked acromia appear to be due to a degenerative process with formation of the osteophyte-enthesophyte complex at the acromion-coracoacromial ligament junction that is increasingly prevalent with age. See the image below.

Slight hyperintensity signal within the tendon wit Slight hyperintensity signal within the tendon without transsectional hyperintensity throughout the tendon is compatible with tendinopathy without complete tear. Additionally, note the presence of the hyperintensity signal in the region of the subdeltoid-subacromial bursa, which indicates bursitis.

Neer described impingement lesions in the following 3 progressive stages:

  • In stage 1, edema and hemorrhage result from excessive overhead use and are observed in patients younger than 25 years.

  • In stage 2, fibrosis and tendinitis affect the bursa and the cuff following repeated episodes of mechanical inflammation in patients aged 25-40 years.

  • In stage 3, bone spurs and incomplete and complete tears of the rotator cuff and long head of the biceps tendon are found almost exclusively in patients older than 40 years.

Clinical course and treatment vary according to the stage of the disease process. Neer's picture of the impingement syndrome may explain tears on the bursal (superficial) side of the tendon. However, partial tears most commonly involve the articular (deep) side of the tendon, as observed by many investigators. Other etiologies, then, must be considered to explain the rotator cuff degeneration.

The posterosuperior impingement syndrome

In 1991, Walch et al described, from arthrographic observations, an impingement occurring between the articular side of the supraspinatus tendon and the posterosuperior edge of the glenoid cavity.[13] With the shoulder held at 120° of abduction, retropulsion, and in extreme external rotation (similar to the late cocking phase in throwers), the labrum moves away from the glenoid and the glenoid rim comes in contact with the deep surface of the tendon, producing repeated microtrauma and leading to partial tears. This process has been confirmed by MRI studies and may explain some of the articular side tears, especially in overhead sport athletes; however, it does not account for all the tears observed in older patients.

The anterointernal impingement syndrome

In 1985, Gerber described, from CT scan studies and from surgery observations, impingement of the cuff in the coracohumeral interval. He demonstrated that, when the shoulder is held in flexion and internal rotation, the coracohumeral distance is reduced from 8.6 mm when the arm is at the side to 6.7 mm. In this position, the lesser tuberosity, and also the biceps tendon and the supraspinatus tendon, become closer to the coracoid process, creating subcoracoid impingement and cuff lesions. Subcoracoid impingement can be idiopathic (eg, large coracoid tip), iatrogenic (eg, following a Trillat procedure) or following a fracture (eg, humeral head or neck fracture).

The intrinsic hypothesis

In this theory, the lesions result from progressive age-related degeneration of the tendon. Von Meyer was probably the first to introduce the concept that degeneration of the tendon plays a major role in the production of cuff lesions. Many histologic studies show the age-related degeneration of the cuff tendon; however, it is not the purpose of this article to describe those numerous changes. Observations from various sources (eg, cadaver, surgical, MRI, ultrasonographic, arthrographic studies) show that cuff tears rarely are seen in patients before age 40 years and that the number observed after the patient has reached 50 years increases progressively.

In 1934, Codman introduced the concept that most tears originate on the articular side of the tendon. Since that time, many authors have come to support that theory from cadaver, surgery, and MRI observations. Most of the tears have been observed on the articular surface of the tendon, near its insertion on the greater tuberosity, in an area Codman called the critical zone. This zone appears to be at greater risk of developing a tear. To explain why the critical zone is more prone to tearing, some investigators have suggested that it is a poorly vascularized area. Histologic, cadaver, and Doppler studies show that the articular side of the tendon, near its insertion on the tuberosity, is relatively avascular when compared to the remainder of the cuff.

By contrast, some other authors did not support these observations and found no difference in vascularity when the critical zone was compared to the other parts of the cuff. On the other hand, Rathbun suggested that the relative avascularity of the cuff is position-dependent and observed a poor filling only when the shoulder is in adduction.[14] Finally, Nixon stated that the critical zone is an area of anastomoses between the muscular vessels and the osseous vessels.[15] The most recent studies suggest that the critical zone is not an avascular area. The normal degenerative process associated with aging, then, is the main factor to explain the lesions of the articular side of the cuff.

In all probability, the intrinsic and the extrinsic theories coexist and explain the pathophysiology of rotator cuff degeneration. Nevertheless, this degeneration is the result of a continuum that is beautifully described by Matsen, Arntz, and Lippitt.[16, 17] The lesion starts where the load is presumably the greatest (eg, on the articular side of the anterior insertion of the supraspinatus tendon, near the tendon of the long head of the biceps muscle). Tendon fibers fail when the load exceeds their strength. The fibers tend to retract because they are under tension, causing rupture. Fiber failure causes at least the following 4 complications:

  • Increases the load on the neighboring, yet intact, fibers

  • Detaches muscle fibers from the bone, diminishing the force that the cuff muscles can deliver

  • Compromises the tendon fibers' blood supply by distorting the anatomy, contributing to progressive local ischemia

  • Exposes increasing amounts of the tendon to joint fluid containing lytic enzymes, which remove any hematoma that could contribute to tendon healing

The scar tissue of the healing tendon lacks the normal resilience of tendon and, therefore, is under increased risk for failure. In the absence of repair, the degenerative process tends to continue through the substance of the supraspinatus tendon to produce a full thickness defect in the anterior supraspinatus tendon. The full thickness tear tends to concentrate loads at its margin, facilitating additional fiber failure with smaller loads than those that produced the initial defect.

Once a supraspinatus tendon defect is established, it typically propagates posteriorly through the remainder of the supraspinatus tendon, then into the infraspinatus tendon. With the increasing defect of the cuff tendon, the spacer effect of the cuff tendon is lost (as well as its stabilizing effect), allowing the humeral head to displace superiorly, placing increased load on the biceps tendon (see the image below).[18] As a result, the breadth of the long head tendon of the biceps is often greater in patients with cuff tears in comparison with uninjured shoulders. In chronic cuff deficiency, the long head tendon of the biceps frequently is ruptured.

Superior migration of the humeral head in chronic, Superior migration of the humeral head in chronic, complete rotator cuff tear. Note the reduced space between the acromion and the humeral head.

Further propagation of the cuff defect crosses the bicipital groove to involve the subscapularis tendon, starting at the top of the lesser tuberosity and extending inferiorly. As the defect extends across the bicipital groove, it may be associated with rupture of the transverse humeral ligament and destabilization of the long head tendon of the biceps, allowing its medial displacement. The concavity compression mechanism of glenohumeral stability is compromised by cuff disease. Beginning with the early stage of cuff fiber failure, the compression of the humeral head becomes less effective in resisting the upward pull of the deltoid.

A partial thickness cuff tear causes pain on muscle contraction. This pain produces reflex inhibition of the muscle action. In turn, the combination of reflex inhibition and loss of strength from fiber detachment makes the muscle less effective for balance and stability; however, as long as the glenoid cavity is intact, the compressive action of the residual cuff may stabilize the humeral head. When the weakened cuff cannot prevent the humeral head from rising under the pull of the deltoid, the residual cuff becomes squeezed between the humeral head and the coracoacromial arch, contributing to further cuff degeneration.

Degenerative traction spurs develop in the coracoacromial ligament, which is loaded by pressure from the humeral head. Upper displacement of the humeral head also wears on the upper lip of the glenoid rim and labrum, reducing the effectiveness of the upper glenoid concavity. Further deterioration of the cuff allows the tendon to slide down below the center of the humeral head, producing a boutonnière deformity. The cuff tendons become humeral head elevators, rather than head compressor-depressors. Just as in the boutonnière deformity of the fingers, the shoulder with a buttonholed cuff is affected by the conversion of balancing forces into unbalancing forces.

This theoretical model on the continuum of the cuff degeneration demonstrates the result of many years of overuse, but this process is also the consequence of the phenomenon that happened when human beings first stood erect. That development led to the use of the glenohumeral joint in a biomechanically unusual way (eg, repetitive overhead activities, arm length activities, throwing). The extremely long lever arm of the upper limb leads the short lever arm cuff muscles to produce extremely high forces in order to stabilize the joint, in opposition to the upward pull of the humeral head by the deltoid and preventing the impingement of the cuff, but at the expense of overload and degeneration.

In summary, the pathophysiology of rotator cuff degeneration may be explained by a combination of extrinsic, intrinsic, and biomechanical factors; however, it is not understood why in some individuals those pathological changes cause pain, but not in some others. This question should keep investigators busy for many years to come.



United States

Shoulder pain is the third most common cause of musculoskeletal disorder after low back pain (LBP) and cervical pain. Estimates of the cumulative annual incidence of shoulder disorders vary from 7-25% in Western general population. The annual incidence is estimated at 10 cases per 1000 population, peaking at 25 cases per 1000 population in the age category of 42-46 years. In the population aged 70 years or more, 21% of persons were found to have shoulder symptoms, most of which were attributed to the rotator cuff.

In cadaver studies, the incidence of full thickness tears varies from 18-26%. The incidence of partial thickness tears varies from 32-37% after age 40 years. Before 40, tears rarely are observed. In MRI studies, tears have been observed in 34% of asymptomatic individuals of all ages. After 60 years, 26% of patients have partial thickness tears, and 28% demonstrate full thickness tears.


The above data are derived from international literature. No known regional variation exists for the frequency of this disease.


As mentioned before, shoulder pain is the third most common cause of musculoskeletal disorder after low back and neck pain. Although considered a benign condition, according to a study on the long-term outcome of rotator cuff tendinitis, 61% of the patients were still symptomatic at 18 months, despite receiving what was considered sufficient conservative treatment. Moreover, 26% of patients rated their symptoms as severe. Musculoskeletal disorders are the primary disabling conditions of working adults. The prevalence of rotator cuff tendinitis has been found to be as high as 18% in certain workers who performed heavy manual labor.

Webster and Snook estimated that the mean compensation cost per case of upper extremity work-related musculoskeletal disorder (MSD) was $8070 in 1993; the total US compensable cost for upper extremity, work-related MSDs was $563 million in the 1993 workforce. The compensable cost is limited to the medical expenses and indemnity costs (lost wages). When other expenses (eg, full lost wages, lost production, cost of recruiting and training replacement workers, cost of rehabilitating the affected workers) are considered, the total cost to the national economy becomes much greater. The impact of rotator cuff disease on the quality of life (QOL) is even more difficult to assess than its cost. Further studies using valid methods like the Medical Outcomes Study (MOS) 36-item short-form health survey (SF-36), measuring the impact of the disorder on the general health should assess this issue.


No known race variation associated with rotator cuff disease is cited in the literature.


In one study, there is a predominance of male patients (66%) seeking consultation for rotator disease, but, in other studies, the male-to-female ratio is 1:1.


Rotator cuff disease is more common after age 40 years. The average age of onset is estimated at 55 years.




Without a good knowledge of the anatomy and biomechanics of the shoulder complex (see the image below), the probability that a systematic history and physical examination leads to the correct diagnosis is reduced.[19] The following paragraphs review these topics.

Normal plain radiograph of the shoulder in interna Normal plain radiograph of the shoulder in internal, external, and neutral positions.

Focused anatomy

The shoulder joint is a complex structure comprising not 1, but 5 joints (ie, 3 synovial joints [sternoclavicular, acromioclavicular, glenohumeral joints] and 2 physiologic joints [scapulothoracic joint, subdeltoid joint]). The latter are called physiologic joints because they are not true anatomic joints with the usual joint characteristics (eg, capsule, ligament). Instead, they are gliding structures that play an important role in the biomechanics of the shoulder by positioning and stabilizing the shoulder complex.[20] The 5 joints fall into the following 2 groups:

  • First group

    • Glenohumeral joint, a true joint

    • Subdeltoid joint, a physiologic joint

  • Second group

    • Sternoclavicular joint, a true joint

    • Acromioclavicular joint, a true joint

    • Scapulothoracic joint, a physiologic joint

In both groups, true joints are linked mechanically to physiologic joints and work simultaneously to produce movement.

The sternoclavicular joint

This joint represents the only bony connection between the trunk and the upper limb. The sternoclavicular joint is a synovial saddle-shaped joint composed of a capsule, the sternal side of the clavicle, the sternoclavicular joint surface, an articular disk, the costoclavicular ligament, the anterior and posterior sternoclavicular ligaments, and the interclavicular ligament. The fibrous capsule surrounds the joint and is attached around the clavicular and sternochondral articular surfaces. The concave clavicular surface fits snugly on the convex sternocostal surface similar to how a rider sits on a saddle and the saddle fits on the back of a horse.

The fibrocartilaginous articular disk increases the capacity for movement, cushions forces transmitted from the shoulder, improves the congruity of the surfaces, and resists upward dislocation of the clavicle. This costoclavicular ligament is a short flat band of fibers running between the cartilage of the first rib and the costal tuberosity on the undersurface of the clavicle. This ligament is the principal stabilizer of the sternoclavicular joint, opposing the upward pull of the sternocleidomastoid muscles, and it also resists the elevation of the clavicle.

The anterior sternoclavicular ligament is a broad anterior band linking the upper and anterior borders of the sternal end of the clavicle and the upper anterior surface of the manubrium of the sternum. Reinforced by the tendinous origin of the sternocleidomastoid muscle, it stabilizes the joint anteriorly. The posterior sternoclavicular ligament has similar origin and insertion and stabilizes the joint posteriorly. The interclavicular ligament attaches on the upper border of both clavicles and the sternum, strengthening the capsule above.

Acromioclavicular joint

The acromioclavicular joint is a synovial plane joint composed of a capsule, the lateral end of the clavicle, the medial border of the acromion, an articular disk, the acromioclavicular ligaments, the coracoclavicular ligaments, and the coracoacromial ligament. The joint stability is maintained by the surrounding ligaments rather than by the bony configuration of the joint. The plane joint surfaces slope downward and medially, favoring displacement of the acromion downward and under the clavicle. The articular capsule encloses the joint, attaching at the articular margins. The capsule is reinforced by the fibers of the deltoid and the upper trapezius muscles and the powerful superior acromioclavicular ligament superiorly, and the anterior, inferior, and posterior acromioclavicular ligaments. The wedge-shaped articular disk dips into the joint from the superior part of the capsule and makes the articular surfaces more congruent.

The coracoclavicular ligaments, although separated medially from the joint, are the primary joint stabilizers. Its 2 parts, named for their shape, are the posteromedial conoid ligament and the anterolaterally placed trapezoid ligament. The 2 ligaments lie in 2 planes, more or less at right angles to each other. A third part, the medial coracoclavicular ligament, is described inconsistently in anatomy textbooks. The coracoclavicular ligaments act to resist superior and, to a lesser extent, anterior dislocation of the acromioclavicular joint, resist axial compression at the distal clavicle, and indirectly limit excess rotation of the joint. The conoid ligament is fan-shaped with its apex lying inferiorly. This ligament inserts on the "tip of the elbow" of the coracoid process and the undersurface of the medial third of the clavicle.

During abduction and external rotation, the angle between the scapula and the clavicle widens and the conoid ligament is stretched, transmitting the force to the clavicle and, ultimately, to the strong acromioclavicular ligaments, preventing dislocation. The trapezoid ligament inserts on the medial border of the upper surface of the coracoid process and runs superiorly and laterally to attach on the undersurface of the clavicle. During adduction, the angle between the scapula and the clavicle is closed and the trapezoid ligament is stretched, preventing the dislocation of the acromioclavicular joint by the same force-transmission mechanism. In summary, the vertical stability of the acromioclavicular joint is provided mainly by the coracoclavicular ligaments, and the anteroposterior stability is provided mainly by the acromioclavicular ligament-capsule complex.

The scapulothoracic joint

The scapulothoracic joint is not a true anatomic joint because it lacks the usual joint characteristics. Except for its attachment to the axial skeleton at the acromioclavicular joint and with the coracoclavicular ligaments, the scapulothoracic joint is free gliding without any ligament restraint. Although it is not a true joint, the scapulothoracic joint plays an important role in the biomechanics of the shoulder complex. The scapula represents a mobile platform from which the upper limb operates.

The main role of the scapula is to orient the glenoid fossa in an optimal position to receive the humeral head and to provide a stable base of support for the controlled movement of the articular surface of the humeral head. It also allows increased shoulder mobility. In the resting position, the scapula lies between the second and seventh rib, over the serratus anterior and the subscapularis muscles. The superomedial angle corresponds to the first thoracic vertebra; the inferior angle corresponds to the seventh thoracic vertebra. The scapula runs obliquely, mediolaterally, and posteroanteriorly, forming an angle of 30° open anterolaterally with the frontal plane.

Five muscles directly control the scapula (trapezius, rhomboids, levator scapulae, serratus anterior, and, to a lesser extent, the pectoralis minor). These muscles act in a synchronous way to position the glenoid fossa.

The glenohumeral joint

The glenohumeral joint is a multiaxial ball and joint socket that is the most mobile and the least stable of all the joints. This joint is composed of a capsule, the head of the humerus, the glenoid fossa, the glenoid labrum, the glenohumeral ligaments, the coracohumeral ligament, and the transverse humeral ligament. The glenohumeral joint also is stabilized externally by the tendons of the rotator cuff muscles and the long head of the biceps tendon.

The joint capsule is a loose thin redundant sleeve that contributes to the mobility of the joint, but also to its instability. On the humeral head, the capsule attaches on the anatomic neck, immediately medial to the tuberosities, and then it extends onto the medial surface of the shaft, slightly below the articular head. The capsule has 2 openings. The upper end opening allows the passage of the long head of the biceps tendon; the anterior opening allows a communication between the joint cavity and the subscapular bursa. On the glenoid side, the capsule attaches to the labrum and, less frequently, to the scapular neck. Because of its laxity, the joint capsule is 2 times larger than the humeral head, and assistance is needed to stabilize the glenohumeral joint. This assistance is provided partly by the glenohumeral ligaments and the coracohumeral ligament.

Three intrinsic, yet distinct, capsular ligaments provide anterior stability to the joint. The anterior inferior, middle, and superior glenohumeral ligaments form a Z in front of the joint capsule. These ligaments become taut and restrict certain motions of the humerus. They are the last structures that provide stability after other static and dynamic stabilizers have been involved. The thin superior glenohumeral ligament arises from the anterosuperior edge of the glenoid and attaches to the top of the lesser tuberosity of the humerus, limiting inferior dislocation in the adducted shoulder and providing secondary restraint to posterior dislocation.

The middle glenohumeral ligament arises from the supraglenoid tubercle and the superior labrum, next to the superior ligament and attaches medially to the base of the lesser tuberosity, beneath the subscapularis tendon. The primary role of the middle glenohumeral ligament is to limit external rotation at 45° of abduction. This ligament also provides a secondary restraint to anterior dislocation.

The inferior glenohumeral ligament complex arises from the anteroinferior labrum and the glenoid border and attaches to the lesser tuberosity, just inferior to the middle ligament. This ligament is a hammock-shaped structure that consists of 3 parts, the axillary pouch and the anterior and posterior bands. The anterior and posterior bands reciprocally tighten as the humeral head is rotated. The anterior band is the primary restraint to anterior dislocation and external rotation at 90° of abduction. The loss of integrity of this ligament is a major cause of anterior instability in the throwing athlete.

The coracohumeral ligament is a broad band that arises from the lateral border of the horizontal arm of the coracoid process and attaches to the top of the greater and lesser tuberosities and the transverse humeral ligament. The primary role of this ligament is to stabilize the adducted shoulder and resist inferior subluxation of the humeral head.

The transverse humeral ligament stretches from the greater to the lesser tuberosity. The primary role of this ligament is to stabilize the long head of the biceps tendon in the bicipital groove.

The humeral head and glenoid fossa

The large humeral head articulates with the slender and shallow glenoid fossa, only a little more than one third its size. The axis forms an angle of 135° with the shaft and an axis of 30° with the frontal plane (retroversion angle). The head faces superiorly, medially, and posteriorly; the glenoid points anteriorly, laterally, and slightly superiorly. The concavity of the humeral head is irregular and less marked than the convexity of the humeral head. The irregular minimal bony contact between those 2 joint surfaces explains the lack of joint stability and the necessity for other mechanisms of stabilization.

The glenoid labrum is a rim of fibrocartilage that surrounds the glenoid fossa. This labrum serves many important functions for the glenohumeral joint, including the following:

  • Provides an extension to the concavity of the glenoid fossa and deepens the glenoid by 50%

  • Provides an increase in depth and, to a lesser extent in width, resulting in an increased stabilization against translating forces

  • Serves as an articular surface to the humeral head

  • Serves as an attachment for the capsule, the ligaments, and the long head of the biceps tendon

Rotator cuff muscles and the long head of the biceps tendon

The rotator cuff is made up of 4 interrelated muscles arising from the scapula and attaching to the tuberosities. Their tendons form a continuous cuff around the head that allows the cuff muscles to provide an infinite variety of moments to rotate and adjust the humeral head in the glenoid fossa, providing the optimal muscle balance for precise coordinated movements.

The supraspinatus muscle arises from the medial two thirds of the supraspinous fossa of the scapula. This muscle passes under the acromion and acromioclavicular joint and inserts onto the superior aspect of the greater tuberosity and joint capsule. The supraspinatus muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize the head of the humerus in the glenoid fossa and to abduct the shoulder.

The infraspinatus muscle arises from the medial two thirds of the infraspinous fossa of the scapula and inserts on the middle facet of the greater tuberosity and joint capsule. This muscle is innervated by the suprascapular nerve (C4-C5-C6). Its primary role is to stabilize and externally rotate the head of the humerus.

The teres minor muscle arises from the upper two thirds of the dorsal aspect of the lateral border of the scapula and inserts onto the lower facet of the greater tuberosity and joint capsule. Its primary role is to stabilize and externally rotate the head of the humerus.

The subscapularis muscle arises from the subscapular fossa of the scapula and inserts to the lesser tuberosity and joint capsule. This muscle is innervated by the upper and lower subscapular nerve (C5-C6-C7). Its primary role is to stabilize and externally rotate the head of the humerus.

The long head of the biceps tendon arises from the supraglenoid tubercle of the scapula, runs between the supraspinatus and subscapularis muscles, exits the shoulder through the bicipital groove under the transverse humeral ligament, and inserts onto the tuberosity of the radius. The long head of the biceps is innervated by the musculocutaneous nerve (C5-C6). Its primary role is to stabilize and flex the humeral head and flex the elbow.

The subdeltoid joint

Like the scapulothoracic joint, the subdeltoid joint is not a true anatomic joint. The subdeltoid is composed of the undersurface of the acromion, the coracoacromial ligament, the subacromiodeltoid bursa, the rotator cuff, and the long head of the biceps tendon. Like the glenoid fossa, they form a concave structure that matches with the convex humeral head. Many authors have stressed the importance of this joint and have described it as the fifth joint of the shoulder. The subdeltoid joint serves the following 2 major roles:

  • Provides a gliding surface for the head of the humerus, especially during abduction and flexion

  • Resists the upward pull of the humeral head during abduction and flexion and provides superior stability

Degenerative changes observed on the undersurface of the acromion and coracoacromial ligament tend to confirm the involvement of this physiologic joint in shoulder motion.

Biomechanics of shoulder elevation

Most glenohumeral motion, especially in overhead activities, occurs around the plane of the scapula, which is approximately 30-45° anterior to the frontal plane. Any time the arm is raised in flexion or abduction, movements from the scapula and the clavicle accompany the glenohumeral joint. In the first 30° of abduction or 45-60° of flexion, the scapula moves either toward or away from the spine to seek a position of stability on the thorax. Consequently, the scapulothoracic joint does not participate in the early elevation of the arm, and the movement of the first 30° comes from the glenohumeral joint. After stabilization has been achieved, the scapula moves laterally, anteriorly, and superiorly, causing an upward rotation of the scapula and glenoid fossa. This scapular rotation serves the following 2 purposes:

  • Maintains the glenoid fossa in an optimal position to receive the head of the humerus, thus increasing the range of motion (ROM)

  • Permits the muscles acting on the humeral head to maintain a satisfactory length-tension relationship

Beyond the first 30° of abduction (or 45-60° of flexion), scapulothoracic motion occurs and contributes to the scapulohumeral rhythm. As the abduction progress, according to widely accepted belief, there is a 2:1 ratio of motion between the glenohumeral and scapulothoracic motion. Toward the end of the elevation, the scapula contributes more motion and the humerus less.

In total, the glenohumeral joint contributes 90-120° to shoulder abduction and the scapulothoracic joint supplies 60°. The contributing joint actions to the scapular motions are 20° produced by the acromioclavicular joint, 40° produced at the sternoclavicular joint, and 50° of clavicle elevation and 30° of posterior rotation. For the glenohumeral joint to realize 120° of abduction, external rotation of the humerus must occur. When internally rotated, the humerus can abduct to approximately 90° before the greater tuberosity hits the coracoacromial arch; however, when externally rotated, the greater tuberosity and cuff tendons avoid the coracoacromial arch, and 120° of abduction can be obtained. Full abduction cannot be achieved without trunk extension and contralateral flexion.

The muscle actions

The muscles contributing to shoulder abduction and flexion are similar. The glenohumeral abduction is performed primarily by the deltoid and the supraspinatus. Initially, it was assumed that the abduction was initiated by the supraspinatus and continued by the deltoid; however, studies in which selective nerve blocks were used to inhibit the deltoid and supraspinatus muscles showed that complete abduction still occurs, but with a 50% loss in power, when one muscle or the other is inhibited.

The contribution of the supraspinatus is greater at the initiation of abduction. As the abduction increases, the contribution of the deltoid increases because this muscle is more active through 90-180°. Therefore, the supraspinatus can be viewed not as an initiator of abduction, but as a useful and effective component of movement, particularly at the start of abduction. Simultaneous nerve blocks of both these muscles result in the inability to raise the arm.

In summary, each muscle can abduct the arm in a full ROM; each is more active in a certain ROM, but there is a loss of 50% in power if only 1 muscle is involved. As abduction occurs, the rotator cuff muscles act to stabilize the humeral head in the glenoid fossa.

In the early stages of abduction, the teres minor is active to depress and stabilize the humeral head and the muscle force of the teres minor is equal and opposite to that of the deltoid, forming a force couple. The subscapularis and the infraspinatus join a little later to assist the teres minor in the stabilization of the humeral head. The latissimus dorsi contracts eccentrically to assist the stabilization and increases in activity as the angle progresses. Above 90°, the rotator cuff force decreases, making the joint more susceptible to injury. The supraspinatus remains a major contributor to stabilization above 90°. As the arm is abducted, the scapula moves laterally, anteriorly, and superiorly to cause an upward rotation of the scapula. The serratus anterior and, to a lesser degree, the trapezius are responsible for this movement. Both muscles, along with the rhomboid muscles, stabilize the scapula on the thoracic wall and prevent winging of the scapula.


A complete medical history should be obtained in order to direct the physical examination and make the right diagnosis. Most of the time, the diagnosis can be made following a systematic history. Relevant past history, treatments, and test results should complement the history of the present injury. Sometimes, relevant social and family histories are necessary.

Patients with degenerative rotator cuff disease are almost always aged more than 40 years. Fifty percent of patients have a progressive onset of shoulder pain, whereas the other 50% can identify a specific event responsible for the onset of pain. The evolution of rotator cuff disease is characterized by variable episodes of recurrence following more intensive shoulder activities, followed by remission with rest or treatment.

As the disease progresses, shoulder pain becomes more constant. Overhead and arm-length activities typically increase the pain. Discomfort and night pain also can be present. With time, the individual can notice some weakness during shoulder elevation. Crepitus also can be noted. With the evolution of the disease, shoulder pain can be accompanied by cervical and mid back pain.

The following questions should help the physician in assessing the patient:

  • What is the patient's age?

    • Shoulder pain in young overhead athletes suggests underlying shoulder instability.

    • In older patients, degenerative rotator cuff disease or frozen shoulder is suggested by shoulder pain.

  • What is the patient's occupation or sport? Repetitive overhead activities and sports predispose to rotator cuff tendinitis.

  • What was the mechanism of injury?

    • A fall on an outstretched arm could indicate a dislocation of the glenohumeral joint or a fracture of the humeral neck.

    • Repetitive overhead motions can cause tendinitis and, in the long run, chronic degenerative changes.

    • A fall or a trauma on the tip of the shoulder can result in an acromioclavicular sprain.

  • What was the onset?

    • Insidious slow onset may suggest tendinitis or osteoarthritis.

    • Sudden onset usually is due to a trauma causing a fracture, dislocation, or a rotator cuff tear.

  • Where is the pain located?

    • Pain located on the superior or lateral aspect of the shoulder suggests rotator cuff tendinitis.

    • Pain on the anterior aspect of the shoulder may result from bicipital tendinitis, an acromioclavicular sprain, or anterior instability.

    • Neck pain and radicular pain or paresthesias suggest a cervical spine disorder.

  • What is the severity of the pain?

    • An acute burning pain could indicate an acute bursitis.

    • An intermittent dull pain may be due to a degenerative rotator cuff disease.

  • What is the type of pain?

    • Sharp burning pain suggests a neurologic origin.

    • Bone and tendon pain is deep, boring, and localized.

    • Muscle pain is dull and aching, not localized, and may be referred to other areas.

    • Vascular pain is aching, cramplike, poorly localized, and may be referred to other areas.

  • What is the duration of the symptoms?

    • Frozen shoulder goes through 3 stages that can last up to 3-4 years.

    • Acute bursitis has a short-term evolution and responds well to nonsteroidal anti-inflammatory drugs (NSAIDs).

  • What is the timing of the pain?

    • Predominantly night pain suggests frozen shoulder.

    • Morning pain and stiffness improved by activity may be caused by a synovitis.

    • Pain that increases with activity is usually the result of a rotator cuff tendinitis.

  • Which activities/positions increase the pain?

    • Pain increased by overhead activities or arm-length activities suggests rotator cuff tendinitis.

    • Pain increased when throwing is likely to be due to anterior instability.

    • Pain increased by lying on the affected shoulder may be caused by an acromioclavicular sprain.

  • Which activities/positions relieve the pain?

  • Is there any weakness or paresthesias in the upper extremities? Neurologic symptoms are caused by a cervical radiculopathy or peripheral nerve entrapment/lesion.

  • Are the symptoms constant or intermittent?

    • Intermittent symptoms usually result from soft tissues or joint disorders.

    • Constant symptoms suggest a neurologic lesion.

  • Are there any joint motion restrictions?

    • Passive and active joint restriction in all directions of ROM is caused by a frozen shoulder or glenohumeral synovitis.

    • Restriction in internal rotation suggests an impingement syndrome due to rotator cuff tendinitis.

    • Inability to perform active abduction suggests a rotator cuff tear or a frozen shoulder.

  • Is some crepitus noted?

    • Crepitus is the result of degenerative rotator cuff changes.

    • Crepitus is not a normal finding in the shoulder.

  • Are there any changes in the color of the arm?

    • Color changes may be due to ischemia secondary to vascular insufficiency.

    • Reflex sympathetic dystrophy (also called complex regional pain syndrome, type 1) can cause skin color changes.

  • Has the patient had any treatments like oral medication, injections, or physical therapy to date?

  • Has the patient had any diagnostic tests performed to date?

  • What is the evolution of the symptoms?

    • Has the pain changed?

    • Has the pain spread or moved?

    • Has the pain subsided or increased?

The last 3 questions help in deciding the appropriate treatment and management.

The importance of obtaining a systematic detailed history cannot be overemphasized. Any attempt to shortcut the process leads to a nonfocused physical examination and inaccurate diagnosis. Remember that a study assessing the interobserver agreement of a diagnostic classification of shoulder disorders based on history and physical examination showed only moderate agreement between experienced observers.


A systematic examination of the shoulder region includes a careful observation, the palpation of the bones and soft tissues, passive and active ROM, impingement and topographic tests complemented, as needed, by instability tests, labrum tests, and special tests. The examination is completed by a cervical spine examination, along with neurologic and vascular examination.


The observation begins from the moment the patient enters the room. The smoothness and symmetry of the shoulders and the movements of the upper extremities are evaluated, as well as the patient's gait. The examiner must be aware of any signs of painful posturing and irregularity of motion of the affected shoulder. Bilateral examination allows for comparison of the affected shoulder with the unaffected one.

The patient then must be asked to get suitably undressed so that an appropriate assessment of the bone and soft tissues can be performed. The shoulder, cervical region, and the entire upper extremity must be assessed. The examiner should assess bones and joints for possible asymmetry or deformities, as well as soft tissue changes suggesting vasomotor abnormalities, like swelling, erythema, white shiny skin, loss of hair, or atrophy. Scars and abrasions also must be noted. The observer should assess bony contours first and then soft tissues. Observation of the patient must be completed from the front, side, and back.

Anterior observation

Looking at bony contours, the examiner makes a general assessment. The dominant side may be lower than the nondominant one; the head and neck should be in the mid line; the clavicle should be symmetric without any deformity of the acromioclavicular joint and sternoclavicular joint.

Each of these parts is examined then in more detail. Because of its superficial location, a fracture of the clavicle or a subluxation or dislocation of both ends is easy to identify. A step deformity of the acromioclavicular or sternoclavicular joint, with the clavicle side of the joint migrating superiorly, is due to a dislocation of those joints.

Observation of the soft tissues is directed first at the contours of the deltoid. The mass of the deltoid should be round with the anterior and posterior aspects symmetrical. Flattening of the muscle suggests an atrophy of the deltoid usually due to a neurologic lesion like an axillary nerve neuropathy, an upper trunk brachial plexopathy (Erb palsy) or a C5-C6 radiculopathy. An anterior dislocation of the glenohumeral joint produces a flattening of the deltoid with a bulging of the anterior aspect of the muscle due to the dislocated head of the humerus, with the patient holding the shoulder in slight adduction and across the trunk. A bulge may be observed in the middle third of the belly of the biceps, when the elbow is flexed, suggesting a rupture of the long head of the biceps tendon.

Lateral observation

The side view allows the examiner to assess thoracic spine kyphosis, a protraction of the head or the shoulders. Deltoid atrophy also can be observed.

Posterior observation

Looking at bony contours, the examiner seeks evidence of a scoliosis of the thoracolumbar spine and then observes the scapulae. The scapula extends from the spinous process of T2 (superomedial angle) to the spinous process of T7 (inferomedial angle). Both scapulae should be at the same height and at the same distance from the spine. The examiner should check for a winging of the scapula (ie, a displacement of the medial side of the scapula away from the thorax). When the winging takes place with a medial displacement of the scapula toward the spine, a serratus anterior muscle palsy is suggested. This palsy usually is due to a long thoracic nerve injury. When the winging takes place with a lateral displacement of the scapula, a trapezius muscle palsy or, more rarely, a rhomboid muscle palsy must be suspected.

The trapezius muscle palsy can be due to a spinal accessory nerve (cranial nerve XI) injury, and the rhomboid muscle palsy can be due to a dorsal scapular nerve injury. A prominent spine of the scapula may be due to a supraspinatus and infraspinatus muscle atrophy caused by a suprascapular nerve injury in the suprascapular notch or a rotator cuff tear.

Observation of the soft tissues is directed at the posterior aspect of the deltoid muscle. The trapezius muscle then is observed. Atrophy resulting from palsy of the muscle has been discussed previously. Because the rhomboid is overlapped by the trapezius, atrophy of the rhomboids is more difficult to assess.


Like observation, palpation must be performed in an orderly manner, beginning with the anterior structures and finishing with the posterior structures. Palpation must include bony structures and soft tissues. Irregular joint surfaces, swelling, heat, crepitus, pain, tenderness, and muscle tension and spasms must be looked for. Palpation can be performed more conveniently with the patient standing. In this position, it is easier for the examiner to move around the patient. The examiner should stand behind the patient for the palpation.

Beginning with the anterior structures, the examiner palpates the sternoclavicular joint. Superior migration of the medial end of the clavicle is palpated if there is a dislocation of the joint. The examiner must remember that the clavicle is superior to the manubrium. Always compare the affected side with the contralateral side. The sternocleidomastoid muscle also must be palpated, looking for tension and spasms. The muscle contracts to turn the head on the contralateral side. The muscle is easier to identify and palpate in this position. The sternal and clavicular heads of the muscle must be palpated. Hands can be moved medially to palpate the suprasternal notch. The first rib, the costochondral joints, and the sternum also should be assessed.

The clavicle should be palpated along its whole length, looking for bumps (suggesting callus formation resulting from fracture), loss of continuity, and crepitus. The acromioclavicular joint is a common site of pain and must be palpated with care. Because the acromioclavicular joint is a superficial joint, swelling and synovial thickening, as well as crepitus, can be felt under the fingers. Step deformities with superior migration of the lateral end of the clavicle, seen in dislocation or subluxation are easily palpable.

The coracoid process can be palpated approximately 2.5 cm (1 in) inferior and just medial to the acromioclavicular joint. The coracoid process is the site of origin of the short head of the biceps tendon, the coracobrachialis muscle, and the insertion of the pectoralis minor. The pectoralis major and minor also must be palpated. Muscle tension and spasms frequently are associated with shoulder disorders.

The acromion and subacromial space are palpated. The subacromiodeltoid bursa can be palpated indirectly in the subacromial space. Because it is overlapped by the deltoid muscle, the bursa cannot be felt under the fingers; however, the examiner, through pressure on the deltoid muscle, applies indirect pressure on the inflamed bursa, causing pain.

The examiner follows by palpating the greater tuberosity, the long head of the biceps tendon, and the lesser tuberosity. These structures can be identified easily in a lean patient by an experienced examiner. This identification may be more difficult in an overweight patient or one with abundant muscle mass. By rotating the shoulder medially (eg, by putting the dorsal aspect of the hand on the buttock), the examiner can feel the greater tuberosity on the anterior aspect of the shoulder, just inferior to the acromion. The supraspinatus, infraspinatus, and teres minor tendons all insert into this structure and, when inflamed, can produce pain on palpation of the greater tuberosity.

Keeping the fingers on the greater tuberosity, the examiner rotates the shoulder laterally. The fingers feel the bicipital groove where the long head of the biceps tendon can be palpated. Pain or thickening of the tendon sheet indicates an inflamed tendon, whereas its absence suggests a rupture or dislocation. By rotating the shoulder more laterally, the examiner can palpate the lesser tuberosity. The tendon of the subscapularis inserts on that structure and, when it is inflamed, the tendon is painful on palpation. With the shoulder back to a neutral position, extension of the shoulder allows the palpation of the subacromiodeltoid bursae under the anterior edge of the acromion.

All these structures must be palpated gently because they may be tender. Any painful palpation must be compared with the contralateral shoulder. A positive finding is when pain is more significant on the affected side compared with the contralateral shoulder. Any excessive pain caused by a vigorous palpation makes the examination less sensitive.

The biceps muscle should be palpated, looking for any bulging that indicates a long head of the biceps tendon rupture. The deltoid muscle also must be palpated to look for painful spasm or tension. Tone and atrophy also are assessed.

The examination is continued by palpation of the posterior structures. Bony structures can be rapidly assessed because they are rarely a source of pain. The spine of the scapula is palpated, followed by the palpation of the superior medial angle of the scapula. The levator scapulae muscle that inserts on this angle is a common site of pain. The medial border of the scapula then is palpated from the superior to the inferior medial angle. The bony palpation is completed by the palpation of the spinous processes of the dorsal and cervical spine.

Because muscle spasm and tension frequently are associated with a rotator cuff disease, the posterior muscles must be palpated with care to identify and treat those muscles. The superior trapezius is commonly tense and painful and must be palpated from its cervical and occipital origin to its insertion on the spine of the scapula and the acromion. Under this muscle, lying in the supraspinatus fossa, the supraspinatus muscle also should be palpated.

The rhomboid muscles, originating from C7 to T5, run downward to attach on the medial border of the scapula. These muscles, often a source of pain, are difficult to distinguish from the overlying middle trapezius muscle. The rhomboid muscles can be identified by asking the patient to put his/her hand behind the back, with the shoulder internally rotated and the elbow flexed, and to push posteriorly against a resistance. The muscle belly of the rhomboid muscles then becomes palpable. Muscle palpation is completed by assessing the infraspinatus and teres major and minor, as well as the latissimus dorsi muscles.

Range of motion

Both active and passive ROM must be evaluated. Although some authors suggest that there is no need to assess passive ROM if the patient is able to perform a complete active ROM without pain, passive ROM must be assessed systematically. Some patients with glenohumeral ROM restrictions have learned to compensate with increased scapulothoracic mobility and seem to have near normal active range. The following movements (with the normal ranges provided) should be assessed:

  • Abduction (70-180°)

  • Adduction (30-45°)

  • Flexion (160-180°)

  • Extension (45-50°)

  • External rotation (80-90°)

  • Internal rotation (90-110°)

Active movements are evaluated first. With the observer behind the patient who is standing, active abduction is performed. The reader is referred to the above section Biomechanics of Shoulder Elevation for a detailed description of the abduction.

The scapulohumeral rhythm is observed. If a painful arc (ie, pain or inability to abduct because of pain) is observed between 45-120°, a subacromial impingement syndrome is suggested. If the pain is greater after 120°, when full elevation is reached, an acromioclavicular joint disorder is suggested.

If a reverse scapulohumeral rhythm (ie, an abduction initiated by the scapulothoracic joint rather than by the glenohumeral joint) is observed, a frozen shoulder is suggested. Look for a winging of the scapula caused by a trapezius or rhomboid muscle weakness. Active flexion also is evaluated. In the presence of a subacromial impingement syndrome, this movement also can be painful. Active flexion also can elicit a winging of the scapula caused by a serratus anterior weakness.

Other motions can be evaluated through a combination of active movements. The Apley scratch test is probably the most well known of all. This test combines internal rotation and adduction of one shoulder with external rotation and abduction of the other.

Passive range of motion

The evaluation can be performed with the patient standing, sitting, or lying down. For practical purposes, the examination is performed with the patient standing. Passive abduction is assessed with the observer behind the patient. Full abduction is performed first to evaluate the combination of scapulothoracic and glenohumeral motion. Then, the scapulothoracic joint is locked by putting one hand over the scapula and the clavicle to resist any motion of this joint. This maneuver allows for a more selective evaluation of the glenohumeral joint (90-120°).

The same procedure can be used to evaluate full flexion that combines scapulothoracic and glenohumeral motion and flexion performed selectively by the glenohumeral joint. This maneuver is followed by the evaluation of the adduction. The external rotation is tested with the elbow held close to the waist and flexed at 90°. Then the arm is rotated externally. The examination is followed by an evaluation of the extension and an assessment of the internal rotation. The full range of internal rotation is achieved with the forearm passing behind the trunk with the shoulder slightly extended.

Impingement tests

Positive impingement tests result from the reproduction of the impingement of the rotator cuff tendon by different provocative maneuvers. In the case of an anterosuperior impingement syndrome, the impingement takes place underneath the coracoacromial arch; in the case of the posterosuperior impingement syndrome, the impingement is on the posterosuperior border of the glenoid cavity, whereas, in the case of the anterointernal impingement syndrome, the impingement takes place in the subcoracoid space or in the coracohumeral interval. For a better understanding of those syndromes, the reader is referred to the Pathophysiology section.

A study on cadaveric shoulders has showed that some provocative impingement tests, the Neer and Hawkins-Kennedy tests, appear to elicit contact consistent with impingement.

  • The Neer impingement test

    • With the examiner standing behind the patient, the shoulder is flexed passively. Although not originally described by Neer, the shoulder is positioned in internal rotation by this author.

    • When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the anterior third of the undersurface of the acromion and the coracoacromial ligament, as well as by contact of the articular side of the tendon with the anterosuperior glenoid rim.

    • A positive test suggests an anterosuperior impingement syndrome.

    • The sensitivity of this test, assessed by operatively observed anatomic lesions, is 89%

  • The Hawkins-Kennedy test

    • With the examiner standing behind the patient, the shoulder is flexed passively to 90°, followed by repeated internal rotation.

    • When positive, this test produces pain that is caused by the contact of the bursal side of the rotator cuff on the coracoacromial ligament and by the contact between the articular surface of the tendon and the anterosuperior glenoid rim.

    • Contact between the subscapularis tendon and the coracoid process also is observed.

    • A positive test suggests an anterosuperior or an anterointernal impingement test.

    • This author uses a modified version of this test with the shoulder positioned initially at 90° of abduction and 30° of flexion, in the plane of the scapula. Along with repeated internal rotation motion, the shoulder is brought progressively to 90° of flexion.

    • If pain is present when the shoulder is flexed at 30°, it is caused by an anterosuperior impingement syndrome.

    • If the pain is present only when the shoulder is brought to 90° of flexion, reducing the coracohumeral interval, an anterointernal impingement syndrome is suggested.

    • The sensitivity of this test is 87%.

  • The Yocum test

    • With the examiner standing behind the patient, the hand on the ipsilateral side of the examined shoulder is placed on the contralateral shoulder.

    • The elevation of the elbow is resisted by the examiner.

    • When positive, this test produces pain caused by the contact of the bursal side of the cuff tendon with the coracoacromial ligament and possibly the undersurface of the acromioclavicular joint.

    • A positive test suggests an anterosuperior or an anterointernal impingement syndrome.

    • The sensitivity of this test is only 78%; however, the sensitivity of the 3 tests together is 100%, which justifies that the 3 tests should be systematically performed together.[21]

  • The posterior impingement test

    • With the patient lying down, the shoulder is positioned at 90-100° of abduction and maximally externally rotated.

    • When positive, this test produces pain in the posterior aspect of the shoulder that is caused by the impingement of the articular side of the cuff tendon between the greater tuberosity and the posterosuperior glenoid rim and labrum.

    • The relocation of the humeral head, performed by applying a posteriorly directed force to the humeral head, causes a reduction in pain.

    • The sensitivity of this test is 90%.

    • Impingement tests confirm an impingement syndrome; however, they do not determine the location of the rotator cuff lesion.

Topographic tests

Using resisted isometric contraction of specific muscles of the rotator cuff, it is possible to identify the location of the tendon lesion causing the impingement.

The supraspinatus tendon

See the list below:

  • The Jobe test

    • The shoulder is placed at 90° of abduction and 30° of flexion in the plane of the scapula.

    • Shoulder elevation is resisted.

    • The test is positive if pain is noted. When compared with surgical observations, the sensitivity of this test is 86%, and its specificity is 50%.

    • The positive predictive value (the ratio of true positive tests on all the positive tests) of the Jobe test is 96%, and its negative predictive value (the ratio of all the negative tests on all the negative tests) is 22%.

  • The full can test

    • The shoulder is placed at 90° of flexion and 45° of external humeral rotation (thumb pointing upward, like someone holding a full can, right-side-up).

    • Shoulder elevation is resisted.

    • The test is positive if it produces pain.

    • An electromyographic (EMG) study showed that this test results in the greatest supraspinatus activation with the least activation from the infraspinatus.

The infraspinatus tendon

See the list below:

  • The infraspinatus isolation test

    • The shoulder is positioned at 0° of elevation (elbows against the waist flexed at 90°) and 45° of internal rotation.

    • Shoulder external rotation is resisted.

    • The test is positive if it produces pain.

    • EMG shows that this is the optimal infraspinatus isolation test.

  • The Patte test

    • The shoulder is placed at 90° of abduction, neutral rotation, and in the plane of the scapula.

    • The examiner holds the elbow of the patient and the external rotation is resisted.

    • The test is positive if it produces pain.

    • The sensitivity of the test is 92%, but its specificity is only 30%.

    • The positive predictive value is 29%, and its negative predictive value is 93%.

A palsy of the external rotator also can be tested.

See the list below:

  • With the elbow held against the waist, the shoulder is positioned passively in external rotation.

  • The test is positive when the patient is unable to maintain the shoulder in external rotation, suggesting a full tear of the external rotators.

The teres minor tendon

See the list below:

  • No specific teres minor isolation tests exist.

  • The same tests used to test the infraspinatus tendon serves for the teres minor.

The subscapular tendon

See the list below:

  • The Gerber lift-off test[22]

    • The shoulder is placed passively in internal rotation and slight extension by placing the hand 5-10 cm from the back with the palm facing outward and the elbow flexed at 90°.

    • The test is positive when the patient cannot hold this position, with the back of the hand hitting the patient's back.

    • The sensitivity and specificity of this test are 100% when there is a full tear of the subscapularis.

  • The Gerber push with force test

    • The shoulder is placed in the same position as the lift-off test; however, the patient has to keep his hand away from the back and resists a push in the palm of the hand.

    • EMG shows that this is the optimal subscapularis isolation test with minimal activation of the pectoralis and latissimus dorsi muscles.

The long head of the biceps tendon

See the list below:

  • The Speed palm up test

    • The shoulder is placed at 90° of flexion with the elbow in extension and the forearm in supination, bringing the palm of the hand up.

    • The flexion of the shoulder is resisted.

    • The test is positive if it produces pain.

    • The sensitivity of this test is 63%, but its specificity is only 35%.

    • The positive predictive value is 43%, and its negative predictive value is 55%.

  • The Yergason test: In this author's opinion, this test is technically difficult and ineffective, and, therefore, it is not described in this article.

Generally, the topographic tests are sensitive but not specific, except for the Gerber's lift-off test. The combination of the impingement and topographic tests make up the rotator cuff tests that allow determination of whether or not a patient's symptoms are caused by rotator cuff disease. As mentioned before, the examination must be completed by instability and labrum tests, special tests (eg, thoracic outlet syndrome tests), a cervicothoracic spine examination, and a neurologic and vascular examination, but it is not the purpose of this section to describe them.


Rotator cuff disease may result from a variety of causes. Damage to the rotator cuff commonly is caused by degeneration associated with aging. Other causes of injury to the rotator cuff may include tendinitis, bursitis, or arthritis. These injuries are particularly common in individuals who perform repetitive overhead activities at work or through involvement in sports. Throwing athletes are prone to this problem secondary to the repetitive stress and trauma to the rotator cuff. Rotator cuff disease also may be the result of a traumatic injury (eg, a fall onto the shoulder, motor vehicle accident).





Laboratory Studies

See the list below:

  • Laboratory studies are not necessary for diagnosing rotator cuff disease.

Imaging Studies

See the list below:

  • A wide variety of radiological examinations are offered to image the rotator cuff. Each of them has advantages and limitations. To prescribe the most useful examination, one must start with a good clinical history and physical examination. Imaging should be used to confirm the anomaly, describe its extension and the associated findings. The following paragraphs briefly explain the indications, the technique, and the findings for each modality available to image the rotator cuff in radiology.

  • Plain film radiography

    • Indication

      • Plain films are not very specific or sensitive to rotator cuff disease, but they remain the first examination to perform.

      • Radiographs give a gross evaluation of the mineralization of the bone, the alignment, posttraumatic changes, the normal variant of the acromion shape, the presence of degenerative changes, and the presence of fine soft tissue calcifications that could be missed otherwise by other modalities.

      • This is most useful test in trauma or chronic complete tear.

      • In the last stage of complete chronic rotator cuff tear, it could be the only imaging modality needed to confirm the diagnosis.

    • Technique: Plain films are acquired routinely in 3 planes (ie, neutral, internal, external rotation; see the image below). Additional views, like the Neer profile, can be performed to better characterize the shape of the acromion.

      Normal plain radiograph of the shoulder in interna Normal plain radiograph of the shoulder in internal, external, and neutral positions.
    • Findings (see Table 1, below)

      • Rotator cuff tendinitis: Signs of chronic tendinitis without tear include subchondral sclerosis of humeral head (see the first image below), flattening and geode of the greater tuberosity, sclerosis of the acromion, calcifications located in the presumed area of rotator cuff tendon (see the second image below), acromion spurs (see the third image below), or a type 2 or 3 acromion.[23]

        Subchondral sclerosis of the humeral head as seen Subchondral sclerosis of the humeral head as seen in chronic tendinopathy.
        Calcification at the insertion of the rotator cuff Calcification at the insertion of the rotator cuff, another sign of chronic tendinopathy.
        Presence of a bony spur on the inferior surface of Presence of a bony spur on the inferior surface of the acromion.
      • Partial rotator cuff tear: All of the above can be present, but no specific signs can help in the diagnosis of a partial tear, as tendons are not visible on plain film.

      • Complete rotator cuff tear: In acute tears, the presence of synovial effusion or hemorrhage can subluxate the humeral head caudally. On the other hand, if the tear is chronic, the humeral head migrates superiorly as the rotator cuff loses its ability to stabilize the humeral head in the glenoid cavity. Radiographically, an acromiohumeral space less than 6 mm, with or without erosion, on the inferior aspect of the acromion is a good semiologic landmark for chronic complete tear. All the signs of tendinitis also can be found in complete chronic tears.

Table 1: Radiological Findings on Plain Film (Open Table in a new window)



Partial Tear

Complete Tear





Soft tissue calcification(s)




Greater tuberosity flattening or hypertrophy




Humeral head cysts




Acromial sclerosis




Acromial spurs




Acromion type 2 and 3




Acromioclavicular osteoarthritis




Upward migration of humeral head ( < 6 mm)




See the list below:

  • Arthrography

    • Indication

      • The main indication of arthrography is to identify complete rotator cuff tears and intra-articular infiltration of corticoid.

      • As a diagnostic tool, it is combined generally with arthro-CT.

    • Technique: Arthrography is performed by injecting iodine contrast medium or air or both into the glenohumeral joint. Eight to twelve milliliters of contrast (or 3-4 mL of contrast and 10-12 mL of air) are injected to distend the joint capsule. If air and contrast are injected the term double contrast study is used. Then, plain films are taken in different positions, such as external rotation, internal rotation, and subacromial views before and after motions. The image below shows an intact capsule.

      Normal double-contrast arthrography of the shoulde Normal double-contrast arthrography of the shoulder.
    • Findings: In the presence of a complete tear, the contrast floods from the glenohumeral joint into the subacromial-subdeltoid bursa (see first 2 images below). With a partial tear, the contrast is seen as a line or small filled cavity within the tendon but without contrast in the subacromial-subdeltoid bursa. This finding is more difficult to demonstrate than in a complete tear. Intratendon tears and tears on the superior aspect of the tendon (bursal side) are not visualized with this technique. Arthrography also can provide some information about the long portion of the biceps tendon, loose bodies, and synovial disorders, such as inflammatory synovitis (see the third image below), osteochondromatosis, or villonodular pigmented synovitis.

      This image depicts the channel between the articul This image depicts the channel between the articular capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear.
      Even if the channel cannot be always identified, t Even if the channel cannot be always identified, the presence of contrast medium in the subdeltoid-subacromial bursa signs the presence of a complete rotator cuff tear.
      Complete rotator cuff tear with presence of contra Complete rotator cuff tear with presence of contrast medium in the subacromial-subdeltoid bursa. Also note the multiple irregularities in the synovial fluid showed as multiples filling defects.
  • CT-arthrography

    • Indication: This study, although very accurate (100% sensibility, 100% specificity) in depicting complete rotator cuff tears, is limited in the evaluation of tendinitis and partial tears where its sensitivity drops to 17-43%. On the other hand, this test gives more information than arthrography about the joint itself and the soft tissues around it. The ability to evaluate the labrum, the glenohumeral ligaments, the long head of the biceps tendon, and the bony structures, as well as the presence of loose bodies, makes this a useful study.

    • Technique: CT-arthrography is performed exactly like a double contrast (air and iodine contrast) arthrography but followed by tomodensitometry imaging (CT scan). For this examination, the shoulder is imaged in the axial plan in internal and external rotation. Thin slices as small as 2-3 mm are acquired throughout the entire joint. With new CT scan technology, it has become easy to reformat images in multiple planes.

    • Findings

      • The semiologic signs of rotator cuff tears are essentially the same as seen on conventional arthrography. The presence of contrast in the subacromial-subdeltoid space confirms the diagnosis of complete rotator cuff tears (see the image below). The contrast also can facilitate determination of the size and location of the tear to help the surgeon plan the surgery. Degenerative findings such as osteophytes, geodes, sclerosis, and articular space narrowing also are well depicted.

        Computed tomography (CT)-arthrography scan of the Computed tomography (CT)-arthrography scan of the shoulder in the axial plane. Note the presence of air and contrast in the subacromial-subdeltoid bursa.
    • In addition to conventional arthrography, this technique can identify labral and glenohumeral ligament tears. The presence of contrast between the labrum and the articular space indicates the presence of a tear. The axial views also permit a good visualization of the long head of the biceps tendon in its groove. Therefore, subluxation of this tendon, or rupture, also can be diagnosed. Finally, the shape of the acromion can be evaluated on the oblique sagittal reformatted study that requires a special acquisition.

  • Magnetic resonance imaging

  • Indication

    • Magnetic resonance imaging (MRI) is the state-of- the-art diagnostic tool for a full evaluation of the shoulder. MRI allows a fine evaluation of the bone marrow, tendons, muscles, ligaments, capsules, bursae, and labrum. MRI combines the advantage of visualization of the bony structures, as well as all the soft tissues about the shoulder and in any plane desirable. With this imaging modality, it is now possible to diagnose the full continuum of rotator cuff disease, from simple tendinosis, to complete tear. MRI is much more powerful than the previous modalities to identify partial tears, and it also can identify intratendon tears or tears on the bursal aspect of the tendon. As with CT scan and plain film, the bone structures resulting or contributing to the impingement syndrome can be evaluated.

    • MRI also can give information about retraction of the muscle, atrophy, bursitis, and bone marrow abnormalities (such as edema or contusion), which all are associated findings in rotator cuff disease.

    • MRI is somewhat limited in the evaluation of the labrum and glenohumeral ligaments. MRI arthrography is the study of choice for the evaluation of labrum and glenohumeral ligaments.

  • Technique: This technique takes advantage of the properties of hydrogen protons submitted to a magnetic field and RF waves. Therefore, there is no radiation exposure for the patient. Multiple sequences are available to highlight different substances such as water, fat, blood, or solid structures. Mainly spin echo T1, spin echo T2, and gradient echo sequences, in axial, sagittal, and coronal oblique plans, are acquired in different combinations. Inversion recovery, fat saturation, and injection of gadolinium (IV or intra-articular) can be added if necessary.

  • Findings

    • MRI shows great detail of the anatomy in multiple plans. MRI also allows seeing the nature of a structure or an anomaly better, according to its intrinsic property. Therefore, the examiner should know some characteristics of the MRI signals for the most common structures. Fat, methemoglobin, melamine, gadolinium, and some forms of calcium all are hyperintense in T1-weighted images. On the contrary, water appears at low signal intensity. In T2-weighted images or in gradient echo, the liquids are hyperintense, as are most lesions, meaning that edema, inflammatory processes, tumors, tendinitis, and tendon tears are hyperintense in T2-weighted images and hypointense in T1-weighted images.

    • Therefore, the presence of fluid in a bursa or articular joint is hyperintense in T2 or gradient echo, and indicates inflammatory or posttraumatic fluid. A full thickness tear of the tendon is demonstrated by a hypersignal intensity in T2 that extends throughout the tendon (see the image below).[24]

      Full-thickness tear of the supraspinatus seen as a Full-thickness tear of the supraspinatus seen as a hyperintensity line through the full thickness of the tendon (as viewed in a flash 2-dimensional magnetic resonance imaging [MRI] sequence in the coronal oblique plane).
  • Tendinitis is recognized as a grey signal in the tendon (see the first image below). Finally, calcification, as well as cortical bone, appears hypointense in all sequences (see the second image below).

    Slight hyperintensity signal within the tendon wit Slight hyperintensity signal within the tendon without transsectional hyperintensity throughout the tendon is compatible with tendinopathy without complete tear. Additionally, note the presence of the hyperintensity signal in the region of the subdeltoid-subacromial bursa, which indicates bursitis.
    Calcifications are seen as hypointense foci in fla Calcifications are seen as hypointense foci in flash 2-dimensional.
  • Arthro-MRI follows the same principle as arthro-CT. This modality can help to identify labral tears (see the image below) and glenohumeral tears.

    Arthro–magnetic resonance imaging (MRI) can help t Arthro–magnetic resonance imaging (MRI) can help to identify labral tears, as seen in this image. The contrast medium penetrates between the labrum and the articular surface.
  • Tables 2 and 3 summarize the possible findings. Resnick and Kang is suggested for further reading.

Table 2: Radiological Findings on MRI (Open Table in a new window)


Soft tissues

Bone structures

Thickening of rotator cuff tendon (RCT)

Intra-articular effusion

Greater tuberosity flattening or hypertrophy

Grey signal intensity within the RCT

Subacromial-subdeltoid bursal effusion

Humeral head cysts

Fluid-filled gap across the tendon

Muscle atrophy

Acromial sclerosis


Thickening of coracoacromial ligament

Anterior acromial spur

Grey signal intensity in the long head of biceps tendon


Acromion type 2 and 3

Acromioclavicular osteoarthritis

Rupture of the long head of the biceps tendon


Upward migration of humeral head

Os acromiale

Calcifications in the supraspinatus, infraspinatus or teres minor


Bone edema


Table 3: Radiological Signs of Specific Disorders (Open Table in a new window)



Partial Tear

Complete Tear

Thickening of RCT




Grey signal intensity within the RCT




High signal intensity crossing only 1 surface of the tendon




Fluid-filled gap across the tendon








Grey signal intensity in the long head of the biceps tendon




Rupture of the long head of the biceps tendon




Calcifications in the supraspinatus, infraspinatus or teres minor tendon




Intra-articular effusion




Subacromial-subdeltoid bursa effusion




Muscular atrophy




Thickening of coracoacromial ligament




Greater tuberosity flattening or hyper-trophy




Humeral head cysts




Acromial sclerosis




Anterior acromial spur




Acromion type 2 and 3




Acromio-clavicular osteoarthritis




Upward migration of humeral head




See the list below:

  • Ultrasonography

    • Indication: The main purpose of ultrasonography is to study the soft tissues. In experienced hands, ultrasonography has a sensitivity of 93-100% and a respective specificity of 85-97% for complete tear and a sensitivity of 69-93% for partial tear. These results are comparable to MRI.

    • Technique

      • Ultrasonography is a technique that uses the same principles as radar. The images are created using a high- resolution transducer that first sends a sound signal and then receives the echo produced when the sound hits the different structures at different depths.

      • The advantages of this technique reside in its low cost, high availability, and high resolution. Ultrasonography is a dynamic study for demonstrating impingement syndrome.

      • The disadvantages are that it is time consuming for the radiologist and is operator-dependent. Ultrasonography cannot study bone structures, as sound does not penetrate bone very well.

    • Findings

      • With ultrasonography, the normal tendon is an echoic structure, whereas the cartilage and fluids are hypoechoic (see Table 4, below). All the tendons, bony landmarks (eg, humerus, greater tuberosity) and intra-articular or intrabursal effusion are recognized easily. Tendinitis is diagnosed when the tendon loses its echogenicity and becomes diffusely hypoechoic. Calcifications appear as bright foci within the tendon, accompanied by a posterior shadowing, as the sound cannot pass through the calcium.

      • The main, and most sensitive, sign of a complete rotator cuff tear is an interruption in the tendon that fills with fluid, producing a hypoechogenic foci extending from the cartilage surface to the subdeltoid-subacromial bursa (see the image below). The secondary signs include the uncovered cartilage (cartilage appears hyperechoic at the site of the tear), bursa herniation, loss of convexity of the tendon and bursa, and effusion within the glenohumeral articulation and the subacromial-subdeltoid bursa.

        Ultrasonography is another modality that can demon Ultrasonography is another modality that can demonstrate a complete rotator cuff tear. This image reveals a gap of more than 2 cm between both extremities of the torn tendon.
    • The diagnosis of a partial rotator cuff tear is made when the hypoechoic or bursal herniation does not cross the full width of the tendon. The use of ultrasonography also allows the operator to demonstrate in real time the impingement of the supraspinatus tendon on the acromion when the arm is positioned in internal rotation and moved in abduction or flexion.

Table 4: Ultrasonographic Signs of Rotator Cuff Disease (Open Table in a new window)

Primary signs

Accessory findings

Focal interruption of tendon

Retraction of the muscle

Presence of fluid in the gap

Synovial cysts in the humeral head

Lost of convexity of the tendon and bursa

Hyperechoic foci + shadowing (calcium)

Uncovered cartilage sign

Fluid effusion in the bursa

Diffusely hypoechoic tendon articulation

Fluid effusion in the Ganglion cysts


See the list below:

  • Nuclear medicine imaging: Bone scintigraphy is not used routinely in the rotator cuff disease imaging.



Rehabilitation Program

Physical Therapy

Physical therapy can be a useful adjunct in the conservative treatment of patients with degenerative rotator cuffs. Although there are numerous studies on the conservative treatment and surgical approach of the painful shoulder and, more specifically, the rotator cuff, the conclusions of a review of randomized controlled trials of interventions for painful shoulder were that little evidence supports or refutes the efficacy of common interventions for shoulder pain. Lack of definition and strict diagnostic criteria for the different painful shoulder conditions, valid randomization procedures, blinding, valid scales for outcome measurement, and heterogeneous populations are among the reasons why it is difficult to draw firm conclusions about the efficacy of any of these interventions.

In his/her approach to conservative treatment, the clinician must be critical and try to use an evidence-based medicine approach as much as possible when planning the patient's treatment. The clinician also must use a combination of experience and intuition to compensate for the lack of scientific evidence supporting the different therapeutic modalities to be prescribed.

The conservative treatment of the degenerative rotator cuff[25, 26]

  • Pain relief

    • Avoidance of painful motions and activities

    • Simple analgesics

    • Nonsteroidal anti-inflammatory drugs

    • Physical modalities

    • Manual physical therapy

    • Subacromial corticosteroid injection

    • A new promising procedure called the bupivacaine suprascapular nerve block

  • Restoration of motion

    • Stretching of the glenohumeral capsule and muscles

    • Manual physical therapy of the glenohumeral, scapulothoracic, acromioclavicular, and sternoclavicular joints and the parascapular and scapula-stabilizer muscles

    • Normal scapulohumeral rhythm must be restored.

    • Manual therapy of the cervicodorsal spine, because of its close relationship with the shoulder, often is necessary. Restoration of strength and function: Restoration of strength is achieved by strengthening of the rotator cuff muscles, the scapula-stabilizer muscles and the long humeral depressor muscles (latissimus dorsi and pectoralis major).

  • Proprioception: In a young individual who has premature degenerative rotator cuff changes because of shoulder instability, proprioceptive exercises must complement strengthening exercises.

  • Sport-specific rehabilitation

    • In a young individual or athlete, sport-specific exercises must be included before resuming normal sport activities.

    • With the aging of the active population, this aspect of the rehabilitation, combined with progressive return to sport activities should not be omitted.

A study by Collin et al indicated that in patients with massive, irreparable rotator cuff tears, rehabilitation outcomes are more successful in those with isolated posterior tears than in patients with anterior tears or tears in three or more tendons. In the study, which involved 45 patients, anterior shoulder elevation of over 160° was achieved in 24 individuals, with frequent treatment failures occurring in those with anterior tears or tears in a minimum of three tendons.[27]

A study by Jain et al of patients with rotator cuff tears indicated that nonoperative treatment is more likely to reduce shoulder pain and disability in patients who are married, have at least a college education, have a partial-thickness tear, use alcohol at least once or twice per week, and engage in light or no shoulder-associated manual labor during daily work activities, and in whom symptom duration has been shorter and fatty infiltration of the rotator cuff is absent.[28]

Physical modalities for rotator cuff disease

Physical modalities are used widely in the treatment of rotator cuff disease. Physical therapists should be diligent in choosing the modalities and their parameters to be used for treatment. Some excellent review articles have been published on the different therapeutic modalities for the painful shoulder. Van der Heijden, Grauer, and Green did a systematic review of randomized clinical trials on the therapeutic effects of physical modalities on painful shoulder disorders. These authors concluded that there is insufficient evidence to prove or disprove the efficacy of most therapies for the treatment of various shoulder pain syndromes.

Based on these review studies, it appears that ultrasound therapy, transcutaneous electrical nerve stimulation (TENS), magnetotherapy, and different methods of thermotherapy are not effective in the treatment of shoulder disorder. Pulsed electromagnetic field therapy and low power laser could have short-term efficacy as compared with placebo. The lack of proof of efficacy of the different physical modalities was due to small sample sizes and the unsatisfactory methodology of most trials; however, some other trials have shown otherwise.

  • Ultrasound

    • Ebenbichler et al showed in a randomized, double-blind, placebo-controlled study that the use of pulsed ultrasound performed 5 times a week for 15 minutes (0.89 MHz frequency, 2.5 watts per square centimeter, pulsed mode 1:4) significantly resolves calcification of the shoulder, decreases pain, and improves the short-term quality of life (QOL).[29] Long-term follow-up did not show significant differences; however, in the long term, the symptoms of calcifying tendinitis may be self-limiting and may improve independently from the resolution of the calcium deposit.

    • This theory may explain why the use of ultrasound is only significantly effective in the short term. The short-term efficacy of ultrasound therapy has been demonstrated only in calcifying tendinitis. Its efficacy in other shoulder disorders has not been shown. Extracorporeal shock wave therapy

    • Another modality that looks promising is extracorporeal shock wave therapy. Passing a strong electric current through a flat coil inducing a magnetic field generates shock waves. Shock waves were used first for the treatment of delayed and nonunion fractures by stimulating osteogenesis. In an uncontrolled study, shock wave therapy (1500 impulses of 0.28 mj/mm2) reportedly disintegrated calcium deposits partially or completely in 62% of patients, and 75% had significant improvement in pain, power, ROM, and shoulder function. The authors of the study concluded that a larger scale placebo-controlled trial should be conducted to analyze the benefits of this modality.

    • A subsequent prospective, randomized, controlled study by Loew, using valid functional shoulder scale, showed the efficacy of extracorporeal shock wave therapy. At 3-6 months, there was a significant improvement in pain and function. At 6 months, there was radiological disappearance or disintegration of calcium deposits in up to 77% of patients. Comparing different regimens of shock waves, they concluded that the improvement in pain and function, as well as the radiological disintegration of calcification was dose-dependent. Thus, extracorporeal shock wave therapy appears to be a promising treatment for calcifying tendinitis. Like ultrasound, its efficacy in other shoulder conditions has not been established.

  • Iontophoresis

    • Some randomized controlled studies have shown the efficacy of topical steroids, NSAIDs, and acetic acid iontophoresis compared with a placebo in different musculoskeletal disorders; however, those studies were not specifically on rotator cuff disease. Moreover, a later trial did not show any difference in outcomes between no treatment and treatment with acetic acid iontophoresis followed immediately by 9 sessions of ultrasound therapy in a constant mode (0.8 W/cm2 at a frequency of 1 MHz for 5 minutes) over a period of 3 weeks. Some authors could not show any effect of iontophoresis on steroid migration through in vivo and in vitro studies, whereas others did. Thus, it is not possible to draw any conclusions on the efficacy of iontophoresis in the treatment of rotator cuff disease.


Publications on rotator cuff disease are rare. Despite the fact that the effectiveness of nonoperative treatment was recognized many years ago and that many authors have emphasized its importance, only 1 randomized controlled study has been published. In a landmark study, Brox compared the efficacy of supervised exercises with arthroscopic surgery and placebo laser. At 6 months, there was a significant difference between the exercise group and the placebo group in terms of pain reduction, function, and increased ROM. However, there was no significant difference between the exercise group and the arthroscopic surgery group.

Other studies on the nonoperative treatment of rotator disease have shown satisfactory and unsatisfactory results, but they were all retrospective uncontrolled trials. Therefore, on the basis of the Brox study, a supervised exercise program should be part the conservative treatment of rotator cuff disease.

It is this author's opinion that an exercises program is the basis of the conservative treatment and no therapeutic modality will provide long-term relief of pain and increased functional status unless it is complemented by an exercise program. The goal of this program is to restore shoulder ROM, enhance glenohumeral and scapulothoracic function to normalize the scapulohumeral motion, and improve the shoulder stability. However, more randomized controlled studies are necessary to support this author's opinion, as well as the findings of the Brox study. The reader is referred to an excellent work by Wilk on shoulder rehabilitation for more information.[30]

Manual therapy

Most of the trials on manual therapy study its efficacy in frozen shoulder. Manual therapy has been compared with no intervention, corticosteroid injection, and cold therapy, and it has not shown any superiority over these modalities. As for exercises, trials on manual therapy in rotator cuff disease are rare. A randomized clinical trial by Graver showed that manual therapy combined with supervised shoulder exercise was superior to supervised shoulder exercise alone for decreasing pain, increasing strength, and improving function at 2 months.[31]

A study by Gutiérrez-Espinoza et al indicated that in patients over age 60 years with a massive, irreparable rotator cuff tear, manual therapy can improve pain and function. Following a 12-week program of manual therapy and specific exercises, study patients demonstrated a 24.9-point increase in the Constant-Murley score; a 28.7-point reduction in the Disabilities of the Arm, Shoulder, and Hand (DASH) score; and a 3.6-cm decrease in the visual analogue scale score.[32]

Thus, manual therapy may be a useful adjunct to exercises and other therapeutic modalities in the treatment of rotator cuff disease. Of course, further randomized controlled studies are needed to support its efficacy.

Postsurgical therapy

A meta-analysis of randomized trials by Chan et al indicated that following arthroscopic rotator cuff repair, early motion therapy has no significant benefits over delayed therapy in terms of functional outcome. At the same time, the study found no statistically significant difference in the risk of postsurgical retear between the early and delayed-motion groups. There was, compared with delayed motion therapy, a statistically significant improvement in forward elevation following early passive motion rehabilitation, but the investigators stated that the difference probably had no clinical importance.[33]

In another meta-analysis, by Chang et al, patients who underwent early passive ROM exercises demonstrated greater improvement in forward flexion than those who had delayed rehabilitation, but the investigators also found a greater retear rate associated with early ROM in patients who had undergone surgery for large tears.[34]

According to a consensus statement from the American Society of Shoulder and Elbow Therapists on rehabilitation after arthroscopic rotator cuff repair, a 2-week immobilization period should be followed by the staged introduction, from the second to the sixth postoperative week, of protected, passive ROM. Active ROM should then be restored, with postoperative week 12 marking the start of progressive strengthening. The patient should undergo a functional progression, when appropriate, to allow resumption of athletic or demanding job activities.[35]

Surgical Intervention

Surgery is not part of the conservative treatment and is not discussed here. Readers are referred to the work of Matsen on that topic.


When symptoms persist after an initial treatment, the primary care physician should refer the patient to a specialist. A consultation in physiatry, orthopedic surgery, or rheumatology should be arranged. Because physiatrists are rehabilitation specialists and because most patients are treated conservatively, the author suggests a consultation in physiatry.

Other Treatment

Subacromial corticosteroid injection

As with NSAIDs, there are many studies with poor methodological quality on the efficacy of corticosteroid injection in various shoulder conditions. Green, Van Der Heijden, and Sibilia did a systematic review of all the randomized clinical trials on corticosteroid injection. Although the trials selected were essentially the same in the three studies, their conclusions differ because of the different assessment methods. Two of these articles suggested that corticosteroid injection may be superior to placebo in the short-term treatment of rotator cuff tendinitis, whereas one suggested that there is no conclusive evidence about the efficacy of corticosteroid injection.[36]

Subacromial corticosteroid and local anesthetic agent injection also appears to be more effective than an injection of a local anesthetic alone, although some authors disagree. Corticosteroid injection also appears to be significantly more effective than NSAIDs. Therefore, subacromial corticosteroid injection appears indicated when pain persists after simple analgesic and NSAIDs have been used.

  • Number of injections: Because some authors have reported poorer surgical outcome in patients who have had 3 or more corticosteroid injections, it is recommended that no more than 2 injections are given.

  • Route of injection: No trials compare the different routes of corticosteroid injection, so the physician should select his or her preferred route.

  • Type of corticosteroid: No trial exists comparing the efficacy of different corticosteroids. Triamcinolone acetonide is the agent most frequently studied.

  • Action mechanism: Inhibition of prostaglandin formation by inhibiting more selectively the COX-2 activity is the mechanism of action.

  • Dose: The optimal dose has not been evaluated. Recommended doses vary from 20-80 mg in the different trials. This author recommends 20-40 mg of triamcinolone acetonide.

  • Side effects: Side effects can be local or systemic.[37] Although systemic side effects can occur following a subacromial injection, only local side effects are discussed here, including the following:

    • Dermal atrophy

    • Necrosis and loss of pigmentation

    • Synovitis

    • Septic arthritis

    • Hemarthroses

    • Cartilage damage and degeneration

    • Tendon rupture

    • Charcot arthropathy

Bupivacaine suprascapular nerve block

The bupivacaine suprascapular nerve block is a relatively unknown, although effective, method to treat different painful shoulder disorders. Few randomized controlled trials have shown its efficacy in painful shoulder of rheumatoid arthritis patients, chronic rotator cuff disease, and frozen shoulder. Preliminary data of a study on chronic impingement syndrome conducted at the Montreal Rehabilitation Institute show its efficacy as compared with placebo. At 3 months, a significant improvement in pain and function measured by a valid functional shoulder scale was observed. Supported by randomized controlled studies, this procedure appears to be a very promising new approach in the treatment of rotator cuff disease.

The technique for nerve block is very inexpensive, simple and safe, and consists of injecting 10 mL of bupivacaine 0.5% in the supraspinatus fossa of the scapula to produce an indirect suprascapular nerve block. In rotator cuff disease, 2 injections are administered 4 weeks apart.

Edetate disodium (disodium EDTA)

Cacchio et al investigated the effectiveness of disodium EDTA treatment for calcific tendinitis of the shoulder, administering the drug to 40 patients with the condition and evaluating them against 40 patients with calcific tendinitis who did not receive the therapy.[38] By 1-year follow-up, the calcifications had completely cleared up in 62.5% of the patients who received disodium EDTA and had partially disappeared in 22.5% of them. Among patients in the control group, none of the calcifications vanished completely, although partial disappearance occurred in 15% of these individuals. The investigators suggested that disodium EDTA therapy offers a safe and effective treatment for calcific tendinitis of the shoulder.



Medication Summary

Oral medications for the treatment of degenerative rotator cuff disease include simple analgesics and nonsteroidal anti-inflammatory drugs. Because rotator cuff disease is a chronic condition, opioid analgesics are not recommended.

Simple analgesics

Class Summary

While NSAIDs are known to be effective in reducing pain and improving function and ROM, they may exert their effect through their analgesic rather than their anti-inflammatory properties. One study with poor methodological quality did not show short-term superiority of NSAIDs as compared to acetaminophen in the treatment of painful shoulder syndrome. Long-term and short-term studies comparing the efficacy of NSAIDs with acetaminophen in osteoarthritis of the knee exist and showed similar efficacy. Moreover, even the presence of inflammatory signs did not predict a better response to treatment with NSAIDs than acetaminophen, suggesting that improvements are not necessarily dependent on an anti-inflammatory effect.

Considering the toxicity of NSAIDs, the need for an analgesic rather than anti-inflammatory effect, the lower cost of a simple analgesic, and the chronicity of degenerative rotator cuff disease, it is indicated to prescribe acetaminophen (APAP) as an initial treatment.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

Analgesic effect of acetaminophen is mediated by prostaglandin inhibition.

Nonsteroidal anti-inflammatory drugs

Class Summary

Numerous studies on the efficacy of NSAIDs for different shoulder conditions have been published; however, because of the factors previously mentioned, most of them have poor methodological quality and, therefore, no conclusions can be drawn about the efficacy of NSAIDs.

Recent review articles, using strict inclusion criteria based on the quality of the methodology, concluded that the trials with the best methodology show a superior short-term efficacy (2 weeks) of NSAIDs compared with placebo; however, at 4 weeks, results did not show any statistical differences. Therefore, it is indicated to prescribe a short course of 10-14 days of NSAIDs as a second-line treatment. No evidence supports a longer use. In case of persistent pain, other therapeutic modalities should be sought. Comparison between different types of NSAIDs didn't show evidence of the superiority of one NSAID with respect to efficacy. Therefore, NSAIDs with the fewest side effects like the newer Cox-2 selective molecules or NSAID with a combination of prostaglandin E1 analog (diclofenac/misoprostol) should be the drug of choice.

In an aging population taking additional medication that may interact with NSAIDs, drug interactions must be avoided. Forty to sixty percent of drugs consumed are over-the-counter (OTC) medications, most often analgesics and NSAIDs, increasing the risk of potential gastrointestinal side effects. The patient should be asked whether he/she is taking any medications concomitantly, such as anticoagulants (hemorrhage), corticosteroids (peptic ulcer), diuretics and antihypertensives (decreased blood pressure control), ACE inhibitors (acute renal failure), high dose methotrexate (increased MTX toxicity), lithium, digoxin, aminoglycosides (decreased renal clearance), phenytoin (decreased albumin binding), and antacids (decreased NSAID levels). NSAIDs should be avoided, if possible, in elderly patients with congestive heart failure or renal or hepatic dysfunction and who are taking other medications.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased. Seek lowest dose of celecoxib for each patient.



Further Outpatient Care

See the list below:

  • A follow-up visit should be scheduled 6-8 weeks following the initial evaluation. During this time period, prescribed tests should have been performed and results received. Effectiveness of the initial treatment should be assessed and, if necessary, modifications made.

  • Following visits depend on the responsiveness to the treatment. Recommend 2 months of follow-up visits until the condition has improved or stabilized.


See the list below:

  • No medication or homeopathic agent is known to prevent tendon degeneration.

  • Avoidance of highly repetitive activities or sustained shoulder posture with greater than 60° of flexion or abduction is probably the best prevention.

Patient Education

See the list below:

  • For excellent patient education resources, visit eMedicineHealth's Osteoporosis Center. Also, see eMedicineHealth's patient education articles Shoulder and Neck Pain and Chronic Pain.