Research-Based 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, especially the supraspinatus.  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.

Research-Based 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; (2) the shape of the acromion (e.g., curved or overhanging edge); (3) the slope of the acromion (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 (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). (3)

Research-Based Classification of Shoulder Impingement and Rotator Cuff Tears

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 (2):

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

Stage 2: Fibrosis and tendinitis but no radiographic findings nor irreversible 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. (2)

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 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.

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.

Subscapularis Muscle Tendon Tear

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).

Teres Minor Muscle Tendon Tear

Biceps Tendinitis and Tenosynovitis

Biceps tenosynovitis, or inflammation of the synovial sheath that surrounds the bicep tendon, is most frequently a degenerative process, with inflammation occurring in the bicipital groove.  When located in the intra-articular or extra-articular portions of the tendon, it may be a result of trauma.  MR images frequently display increased fluid, nonspecific for inflammation, in the bicipital synovial sheath.  Since communication between the joint capsule and the biceps tendon synovial sheath is normal, intrinsic hyperintensity or tendon thickening may be a more specific finding for biceps tendonitis, inflammation of the biceps tendon.  The Yergason test, in which forced supination produces pain in the biceps groove, is helpful in distinguishing biceps tendinitis from rotator cuff impingements.  The biceps tendon lies within its groove, which makes it difficult to palpate; in fact, it is impossible to palpate the tendon in its intracapsular, intraarticular portion.

Biceps tenodesis in the bicipital groove is the treatment of choice in biceps tendinitis.  Because the long head of the biceps tendon (through the biceps labral complex) is known to contribute to both superior and anterior stability of the glenohumeral, there is some concern that this fixation may compromise the stabilizing aspect of the glenohumeral ligament labral complex.  However, since chronic biceps tendinitis generally occurs in older patients who are not prone to recurrent instability, the use of biceps tenodesis is not usually contraindicated. 

Now that we have examined the pathology associated with rotator cuff syndrome, we will see how therapeutic massage can have a place in healing and restored function.

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