Distal Attachment - It passes laterally, forming a broad tendon which inserts on the lesser tuberosity, shoulder joint capsule, and the front of the upper shaft of the humerus. Some of the superficial fibers blend with the transverse humeral ligament.

Nerve Supply - Subscapularis is innervated by both subscapular nerves (C5, 6 ,7).

Actions - Subscapularis is an adductor and medial rotator of the humerus.

The rotator cuff is formed by four scapulohumeral muscles, subscapularis, supraspinatus, infraspinatus, and teres minor. Tendons of these four muscles blend closely with each other and the shoulder joint capsule. Their primary function is to centralize the humeral head, limiting superior translation during abduction.

Rotator cuff

The rotator cuff consists of the tendinous insertions of the subscapularis, supraspinatus, infraspinatus, and teres minor muscles. These tendons form a hood, that surrounds the head of the humerus anteriorly, superiorly and posteriorly. Co-contraction of these muscles stabilizes the glenohumeral joint during normal activities. In particular, abduction in the plane of the scapula will be accomplished principally by action of the deltoid muscle, but this acts nearly vertically when the humerus is still close to the side of the body, and so tends to sublux the head of the humerus superiorly. The rotator cuff muscles act more horizontally, and their tensions combine with that of the deltoid to direct the resultant joint force vector into the superior concavity of the glenoid, which is normally a stable state. Conversely, rotator cuff deficiency leads to superior subluxation of the head of the humerus, leading to impingement against the coracoacromial ligament, accompanied by abduction weakness and loss of motion.

The complex anatomical structure of the rotator cuff means that the reasons for the frequency of cuff degeneration, which is most often in the supraspinatus tendon, are not fully understood. It is known, for example, that there are distinct layers with different histological and mechanical properties, so this can lead to shearing between the layers, and this also applies to the zone of overlap of the supraspinatus and infraspinatus tendons. The tendons are also subjected to compression forces onto their surfaces, either due to the wrapping around the glenoid and head of the humerus, or from superior impingement beneath the acromion. Finally, humeral rotation will tense and slacken the edges of the supraspinatus tendon.

The Rotator Cuff

The rotator cuff is formed by four scapulohumeral muscles, subscapularis, supraspinatus, infraspinatus and teres minor . Tendons of these four muscles blend closely with each other and the shoulder joint capsule. Their primary function is to centralize the humeral head, limiting superior translation during abduction. The supraspinatus, infraspinatus, and teres minor tendons insert on the greater tuberosity, whereas the subscapularis tendon inserts on the lesser tuberosity. The subscapularis tendon lies on the anterior aspect of the anterior capsule of the glenohumeral joint, and its superior portion is intraarticular. The subscapularis bursa lies between the subscapularis tendon and the scapula. As the subscapularis muscle becomes attenuated from repeated episodes of dislocation, it may be the source of recurrent instability. The rotator cuff interval is located between the superior aspect of the subscapularis tendon and the inferior aspect of the supraspinatus tendon. This interval contains the coracohumeral ligament and the superior glenohumeral ligament. The rotator interval lesion has been attributed to a possible deficiency of the superior glenohumeral ligament. Surgical closure of the interval appears to eliminate excessive inferior translation.

The triangular space through which the scapular circumflex vessels travel is formed by the teres major, the lower border of the teres minor, and the long head of the triceps. Lateral to the triangular space, the quadrilateral space (through which the axillary nerve and posterior humeral circumflex artery travel) is formed by the lower border of the teres minor, the upper border of the teres major, the lateral border of the long head of the biceps, and the medial border of the humerus.

Pathogenesis of Shoulder Impingement

The pathogenesis of rotator cuff tears includes acute trauma, chronic impingement, or both. Some controversy exists as to whether chronic mechanical impingement precedes the development of complete rotator cuff lesions or whether primary degeneration of the cuff results in tears leading to chronic impingement syndrome.

There is an important relationship among the rotator cuff, the long head of the biceps, the subacromial bursa, the AC joint, the acromion, and the humeral head in the spectrum of impingement disorders. The most common location for impingement is between the anterior one-third of the acromion and the underlying tendons. A decrease in the subacromial space secondary to anatomic or pathologic changes is usually associated with a large tear that has compromised the centralizing ability of the cuff, allowing proximal humeral migration.

Etiology of Shoulder Impingement

A variety of causes of the painful shoulder impingement syndrome has been proposed, including hypovascularity in the supraspinatus tendon, mechanical wear, acute trauma, or repetitive microtrauma from overuse. Factors that contribute to bony supraspinatus outlet compromise include (1) anterior acromial spurs (image) ; (2) the shape of the acromion (e.g., curved or overhanging edge); (3) the slope of the acromion (image) (e.g., flat or decreased angle); and (4) the morphology of the AC joint (e.g., hypertrophic bone, callus formation). Less frequent mechanisms of impingement (not outlet impingement) include (1) prominence of the greater tuberosity (e.g., fracture malunion or nonunion); (2) loss of humeral head depressors, as seen in rotator cuff tears and biceps tendon rupture; (3) loss of the glenohumeral joint fulcrum function from articular surface destruction or ligamentous laxity; (4) impaired scapular rotation from trapezius paralysis or AC joint disruption; (5) lesions of the acromion including an unfused anterior acromial epiphysis (image) (apophysis); (6) fracture malunion or nonunion; and (7) subacromial bursal thickening (chronic bursitis or cuff thickening in calcific tendinitis). The shape of the acromion, as seen on sagittal oblique MR images or on the outlet view on plain film radiographs, is also thought to be a factor in the etiology of impingement syndrome. Acromial morphology has been classified into three different types by Bigliani. The type 1 acromion has a flat undersurface; the type 2 acromion has a smooth, curved, inferior surface; and the type 3 acromion has an anterior hook or beak. It is the type 3 acromion which is thought to be associated with a greater predisposition to rotator cuff tears (i.e., tears involving the critical zone immediately proximal to the greater tuberosity insertion of the supraspinatus tendon).

Neer developed a three-stage classification system for impingement in which subacromial impingement is presented as a mechanical process of progressive wear (i.e., a pretear impingement lesion) that causes 95% of rotator cuff tears. The degeneration, thinning, and full thickness tears of the supraspinatus may extend to involve the long head of the biceps and infraspinatus tendons. The three stages of Neer’s classification are as follows:

Stage 1: Tendon edema and hemorrhage but no radiographic findings nor reversible changes

Stage 2: Fibrosis and tendinitis but no radiographic findings nor reversible changes

Stage 3: Partial or complete rupture or tear of the rotator cuff, often in association with anterior acromial spurs or greater tuberosity excrescence.

When present, radiographic changes include greater tuberosity sclerosis and hypertrophic bone formation. Bursal thickening, fibrosis, and partial tears of the superficial rotator cuff may be present.

Rotator cuff tendons examined at surgery display areas appearing gray, dull, edematous, and friable. Histologic examination reveals degenerative changes such as angiofibroblastic hyperplasia without inflammatory cells. Because leukocyte infiltration of the rotator cuff tendon is rare, the tendinitis or inflammation of the cuff as described in Neer's classification (especially in the later stages of rotator cuff pathology) has not been adequately documented.

Arthroscopic visualization of the rotator cuff from the articular and bursal surfaces has provided new insight into the progression of this disease process and the progressive stages of impingement might be more accurately described as:

Type 1: Rotator cuff degeneration or tendinosis without visible tears of either surface
Type 2: Rotator cuff degeneration or tendinosis with partial thickness tears of either articular or bursal surfaces
Type 3: Complete thickness rotator cuff tears of varying size, complexity, and functional compromise.

Most rotator cuff tears do not begin at the bursal surface of the tendon, as tears secondary to impingement had originally been described. In fact, it is more common to find partial tears of the rotator cuff involving the articular surface of the rotator cuff adjacent to the tendon insertion. Articular cuff lesions may be the result of tensile strength failure from overuse, whereas bursal cuff lesions are more closely associated with impingement. Frequently, no direct mechanical cause of impingement can be found in patients suspected of having impingement syndrome. It is not unlikely, therefore, that intrinsic tendon degeneration (degenerative tendinopathy), and not mechanical impingement, may be the primary pathology in the development of most rotator cuff disorders. Rotator cuff tendinitis has been attributed to repeated eccentric tensile overload of the rotator cuff tendons. Rotator cuff degeneration has also been observed in the absence of anteroinferior acromial spurs. Ozaki and colleagues found a correlation between bursal-sided and full-thickness rotator cuff tears and degenerative changes in the coracoacromial ligament and anterior third of the inferior acromion. Articular surface partial tears, however, were associated with normal acromial morphology and histology. Most rotator cuff tears, therefore, seem to be attributable to degenerative lesions associated with increasing age, and the acromial changes present are secondary. Athletes may demonstrate both degenerative rotator cuff tendinitis and primary mechanical impingement. Relative rotator cuff hypovascularity in the critical zone of the supraspinatus (the distal 1 cm) may be associated with tendon degeneration or may exacerbate changes associated with mechanical impingement.

In the Neer classification of well-defined stages of impingement (edema, hemorrhage, fibrosis, and tendinitis leading to spur formation), cuff tears may be more correctly viewed as part of a progression of tendon degeneration leading to tendinopathy, with the subsequent development of a partial or complete rotator cuff tear and associated secondary changes.

Rotator cuff degeneration and pitfalls of MR interpretation

Normal rotator cuff tendons display low signal intensity on T1, conventional T2, T2 fast spin-echo, fat-suppressed T2 fast spin-echo, STIR, and T2* gradient-echo sequences. Areas of intermediate signal intensity or signal inhomogeneity can sometimes be seen on T1 and proton density weighted images in both cadaver cuffs and asymptomatic volunteers, especially in the distal extent of the supraspinatus tendon. This appearance has been variously attributed to a "magic-angle phenomenon," partial volume averaging of the distinct components of the supraspinatus muscle and tendon, or to histologic degeneration (eosinophilic, fibrillar, and mucoid).

In the "magic-angle phenomenon," increased signal intensity in the supraspinatus tendon on short TR/TE sequences is a result of tendon orientation at the magic-angle of 55º to Bo. However, there is no evidence of a partial volume averaging effect of tendon, muscle, connective tissue, or fat, and this explanation has not been accepted as the cause of areas of intermediate signal intensity within the asymptomatic cuff on short TR/TE weighted images with the shoulder in a neutral position or in external rotation.

The pseudogap is a zone of increased signal intensity seen adjacent to the supraspinatus tendon attachment in asymptomatic subjects. The pseudogap has been attributed to distinct portions of the supraspinatus muscle, including the anterior fusiform portion, which contains the dominant tendon of the supraspinatus, and a strap-like posterior portion.

In cuff tendon degeneration there are areas of intermediate signal intensity on T1 and proton density weighted images. On T2*, fat-suppressed T2 fast spin-echo, and STIR sequences these areas display intermediate to high signal intensity in both asymptomatic and symptomatic patients. On heavily weighted T2 or T2 fast spin-echo images, however, these regions of altered signal intensity are diminished or remain unchanged.

Impingement lesions of the rotator cuff (magnetic resonance appearance)

The MR signal intensity changes described in degeneration are the result of macromolecular collagen changes. MR findings in degeneration and partial tears may overlap, and tendon pathology must be evaluated on the basis of bursal, intrasubstance, and articular surface morphology, and on signal intensity changes on T1, proton density, T2, or T2 fast spin-echo sequences.

In rotator cuff degeneration, there is intermediate signal intensity in cuff degeneration on T1 or proton density weighted images, with no increase in signal intensity on T2 or T2 fast spin-echo images. Fat-suppressed T2 fast spin-echo sequences (TE's of 40 to 50 msec) are sensitive to changes of degeneration, and, in the absence of a partial or complete rotator cuff tear, display areas or regions of hyperintensity. T2* gradient-echo images in either the coronal oblique or sagittal oblique plane are not routinely used in the evaluation of the rotator cuff, because these images produce signal intensity which may be difficult to distinguish from that seen in degenerations and partial tears. More severe changes of degeneration may be characterized by intermediate to increased signal intensity on short TE or T1 and proton density weighted images which persist without further increase in signal intensity on T2 weighted images. These tendons may appear gray on long TE sequences. Increased signal intensity on images with short and long TE sequences (conventional T2 and fast spin-echo T2), with a further increase in signal intensity between T1 or proton density and T2 weighted images, is associated with a partial or full thickness tear. Differentiation of severe tendinitis from partial tears may require careful attention to the continuity of the bursal and articular surfaces of the cuff as well as the increased signal intensity observed on both short and long TE images. Secondary findings of musculotendinous retraction and atrophy of the supraspinatus muscle are seen with complete cuff tears. Low signal intensity may be identified on T1 and T2 weighted images in areas of severe degeneration or tear obliterated by scar tissue or tendon remnants.

In arthroscopic correlations of MR imaging and findings, degenerative tendon wear may be identified on the bursal or articular surface of the rotator cuff. Not all cuff tears are initiated on the bursal surface as a result of impingement. Most tears begin in the articular surface of the rotator cuff, adjacent to the tendon insertion on the greater tuberosity. In early impingement (pre-tear tendinitis), there is relative preservation of articular bursal tendon surface outlines. In addition, arthroscopic evaluation of impingement sometimes reveals tendon wear (degeneration with or without associated degenerative changes of the acromion and the coracoacromial ligament proximally) and not active inflammation.

Because the term tendinosis is not widely accepted, the phrase tendon degeneration is often used to describe an area of increased signal intensity on intermediate weighted images which does not increase in signal intensity on T2 weighted images. Impingement is a clinical diagnosis, not a radiologic or MR diagnosis. The tendon findings or osseous changes seen in the impingement syndrome may be identified and described on MR when patients are referred for study to determine whether these findings, in conjunction with the patient's clinical presentation, are consistent with impingement syndrome.

Posterior Superior Glenoid Impingement

Posterior superior glenoid impingement is a recently recognized mechanism of injury producing repetitive impingement of the inferior surface of the rotator cuff in the athlete who uses a throwing motion. Five structures are at risk from this mechanism of injury: the superior labrum, the rotator cuff tendon, the greater tuberosity, the inferior glenohumeral ligament or labrum, and the superior bony glenoid. Jobe found that damage to more than one of these structures resulted in posterior superior glenoid impingement. This mechanism of injury represents superior or posterior-superior angulation in the position of abduction and external rotation (the position of throwing). MR arthrography, performed with the arm positioned in abduction and external rotation, is the modality of choice for demonstration of associated cuff and labral pathology.

Treatment of Impingement Disorders

Treatment for the different types of impingement disorders depends on the age and activity level of the patient. In general, most patients are treated with conservative therapy for a period of six months prior to surgical intervention. If surgery is necessary, arthroscopic subacromial decompression (ASD) is the method of choice for the treatment of chronic outlet impingement. It is rapidly replacing open acromioplasty because it does not violate the deltoid and overlying deltotrapezial fascia. In ASD, the coracoacromial ligament is detached from the anterior inferior acromial surface, and inflamed or frayed cuff tissue is debrided. Arthroscopic anterior acromioplasty, as part of ASD, is indicated for alleviation of pain secondary to impingement of the anterior inferior surface of the acromion. A burr is used to perform the anterior acromioplasty.

Rotator Cuff Tears

Every rotator cuff tear (image) is unique, making evaluation and development of treatment protocols complicated. In general, tears can be characterized as either partial or complete. Partial tears may involve the articular or bursal surfaces in varying degrees of depth and extension into the tendon. Intratendinous lesions may not communicate with either bursal or articular surfaces. Complete rotator cuff tears, which extend through the entire thickness of the rotator cuff, allow direct communication between the subacromial bursa and the glenohumeral joint.

Partial Tears

Using MR imaging characteristics, partial rotator cuff tears ( Slide 1 (image) , Slide 2 (image) ) can be classified as either partial articular or bursal surface lesions (image) . Partial articular surface tears occur more frequently than partial bursal surface or intrasubstance tears. Partial or incomplete tears of the rotator cuff are thought to be twice as common as complete or full-thickness tears. On coronal oblique MR images, partial tears demonstrate low to intermediate signal intensity on T1 weighted images, intermediate to high signal intensity on proton density weighted images, and bright signal intensity on conventional T2, T2 fast spin-echo, and fat-suppressed T2 fast spin-echo sequences.

Full Thickness Tears

Complete (full thickness) tears of the rotator cuff , with or without proximal retraction, can be depicted clearly with MR imaging.

Primary signs: one of the primary signs of a full thickness rotator cuff tear is visualization of a tendon defect. This defect, or tendinous gap, is seen as an interruption or loss of continuity of the normally low signal intensity tendon. Joint fluid or granulation tissue at the cuff tear site is seen as areas of intermediate to increased signal intensity on T1 weighted and proton density weighted images. On T2 spin-echo, T2 fast spin-echo, and fat-suppression T2 fast spin-echo sequences, these areas demonstrate markedly increased signal intensity. A complete tear cannot be unequivocally diagnosed without visualization of either a defined tendon defect or indication of direct communication between the glenohumeral joint and the subacromial bursa (i.e., extension of the joint line, by even a small amount, across the cuff tendons into the subacromial-subdeltoid bursa). Involvement of the infraspinatus or subscapularis tendons may be seen in massive rotator cuff tears. Preoperative MR imaging can also identify associated muscle atrophy in chronic tears. Patients with complete tears complicated by cuff arthropathy, tendon retraction, and muscle atrophy may not be candidates for surgical repair.

Secondary signs: secondary signs of rotator cuff tears can be used in conjunction with the primary assessment of changes in tendon signal intensity and morphology to help in the diagnosis of cuff tears. Subacromial-subdeltoid bursal fluid should be readily identifiable, especially when there is a large volume of articular and bursal fluid associated with a complete tear. Retraction of the supraspinatus musculotendinous junction is another secondary sign that may be seen in full thickness cuff tears. Tears with granulation tissue or hypertrophied synovium may not demonstrate bright signal intensity on T2 (spin-echo or fast spin-echo) weighted images. However, these low signal intensity cuff tears may be identified by careful evaluation of tendon contour abnormalities and associated secondary signs of cuff disease. Fatty atrophy of the rotator cuff muscle is usually associated with more chronic complete tears. Alterations in the peribursal fat plane and proximal musculotendinous junction are present in up to 92% of complete tears.

Rotator Interval Tears

The rotator interval is the space between the supraspinatus and superior border of the subscapularis tendons. The rotator interval is formed from thin elastic, membranous tissue. This tissue is reinforced by the coracohumeral ligament and the superior glenohumeral ligament and capsule. Longitudinal interval tears, with or without extension to the subscapularis tendon, are often seen in association with acute glenohumeral dislocations, especially in patients over 40 years of age. In younger patients, under 35 years of age, an interval tear may also be associated with anterior and multidirectional laxity, secondary to repetitive trauma. T2 weighted images in the sagittal oblique plane may show the anterior extension of fluid across the rotator cuff interval. This finding may be more easily demonstrated by MR arthrography.

Subscapularis Tendon Tears

Most subscapularis tendon tears occur in association with tears of the supraspinatus and infraspinatus tendons. Rarely, however, they may occur as an isolated injury. Partial tears may be associated with thickening of the subscapularis tendon in conjunction with regions of fiber discontinuity. Complete detachment from the lesser tuberosity is associated with fluid signal intensity extending anterior to the retracted tendon. Associated biceps tendon abnormalities, including medial dislocation, may also be present.

Teres Minor Tendon Tear

Tears of the teres minor tendon, either in association with massive cuff tears or as an isolated tear, are uncommon. Edema and atrophy of the teres minor may be associated with impingement or denervation of the axillary nerve in the quadrilateral space (the quadrilateral space syndrome).

Surgical Management

Chronic impingement leads to complete rotator cuff tears. The repair procedure of choice begins with an ASD, followed by a deltoid-splitting approach to gain access to the torn cuff. The supraspinatus most commonly tears at its insertion on the greater tuberosity. Therefore, primary repairs are fixed directly to the bone with drill holes or suture anchors. A Mumford procedure may be performed when AC degeneration is evident.

Postoperative Rotator Cuff

MR imaging has been used for evaluation of the rotator cuff after surgical repair. Because gradient-echo sequences frequently show increased magnetic susceptibility artifacts, the repair site may not be clearly visualized on these scans. Conventional T1 and T2 spin-echo and fast spin-echo sequences minimize these low signal intensity artifacts, and allow visualization of increased signal intensity in cuff defects. Postoperative MR arthrography, using a fat-suppressed short TR/TE T1 weighted sequence, also minimizes surgical artifacts. Changes caused by acromioplasty, resection of the distal end of the clavicle, and division of the coracoacromial ligament, are also displayed on MR images. The rotator cuff interval between the supraspinatus and subscapularis tendons may be interrupted at surgery, allowing communication of contrast with the subacromial-subdeltoid bursa, even though the rotator cuff repair is intact. The isolated finding of subacromial-subdeltoid fluid is not sufficient to make the diagnosis of a failed or retorn repair of the rotator cuff. Some retears may be associated with granulation tissue and adhesions, and may appear as a low signal intensity tear on T2 weighted images without associated fluid signal intensity at the tear site or in the subacromial-subdeltoid bursa. The presence of a gap or defined defect in the cuff associated with extension of fluid signal intensity on T2 weighted or fat-suppressed T2 fast spin-echo sequences is diagnostic for a retorn repair.