Advanced Clinical Pathology: The Shoulder (Page 3)

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 (Slide 1, Slide 2).

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 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 can be classified as either partial articular or bursal surface lesions.  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 of Rotator Cuff Tears

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.

Paralabral Cysts

When synovial-filled ganglion cysts (sometimes called paralabral cysts because the term paralabral cyst better describes the relationship between the cyst and the glenoid labrum) involve the spinoglenoid notch they can produce atrophy of the infraspinatus and/or the supraspinatus muscle, secondary to suprascapular nerve entrapment.  Isolated infraspinatus atrophy is associated with more posteriorly located ganglion cysts and dorsal suprascapular nerve entrapment.  Supraspinatus and infraspinatus muscle atrophy are seen in association with anteriorly located masses and proximal nerve entrapment.  In the initial stage of suprascapular nerve compression, edematous changes in the infraspinatus muscle are characterized by low to intermediate signal intensity on T1 weighted images and hyperintensity on T2, fat-suppressed T2 fast spin-echo, or gradient-echo T2* weighted images.  Chronic compression may lead to the development of fatty muscle atrophy.

There is a high correlation between paralabral cysts, which have a posterior location, and posterosuperior labral tears. These cysts may communicate and undermine the posterosuperior glenoid labrum and they may extend medially in the spinoglenoid notch.  Anterior inferior paralabral cysts may be identified in communication with tears of the anterior inferior glenoid labrum.  These small tears of the anterior inferior glenoid labrum may not be appreciated on routine axial MR images and require the use of an abduction external rotation view to display the inferior glenohumeral ligament labral complex.  SLAP type II lesions may be visualized with fluid signal intensity communicating with a superiorly located paralabral cyst.  Anterior extension of a paralabral cyst through a labral tear can involve the subcoracoid space superior to the subscapularis bursa.

The posterosuperior paralabral cyst is thus a common location for a cyst seen in association with posterior capsulolabral injuries, including SLAP lesions.  The location of these cysts should be carefully described.  They usually involve the spinoglenoid notch, which is located posterior to the suprascapular notch and is the location for the suprascapular nerve after it turns around the lateral edge of the scapular spine.  The inappropriate use of the term suprascapular notch to describe the location of all superior paralabral cysts may result in surgical exploration which is far anterior to the correct location of the cyst within the spinoglenoid notch.  Most superior paralabral cysts originate in the spinoglenoid notch.  The spinoglenoid ligament (inferior transverse scapular ligament) is variably present and is located superior to the suprascapular nerve.  Initial treatment of a paraglenoid cyst is conservative, progressing to cyst aspiration or surgical release of the suprascapular ligament in symptomatic patients.  Cyst aspiration, which can be performed with CT guidance, may relieve some of the patient's symptoms obviating the need for arthroscopy.  The associated labral tear, however, may remain symptomatic.

Most paralabral cysts, including but not limited to posterosuperior cysts, communicate with a labral tear.  The paralabral cyst may be confined to the spinoglenoid notch or it may demonstrate anterior extension into the suprascapular notch as seen on anterior coronal oblique or axial MR images with the cyst identified anterior to the supraspinatus muscle.  Superior and posterosuperior paralabral cysts are commonly seen in association with SLAP type II lesions and the associated labral tear is identified on both axial and coronal oblique T2 weighted images.

Calcific Tendinitis

Calcification of the rotator cuff most commonly occurs in the supraspinatus tendon, but can occur in any of the tendons of the rotator cuff.  Hydroxyapatite deposits can be seen in various views on conventional radiographs.  Formation of calcific deposits in the tendinous portion of the rotator cuff is a degenerative process.  The calcific build up can be extremely painful and act almost as an internal furuncle.  In the initial subclinical or silent phase, calcific deposits are limited to the tendons of the rotator cuff.  In the mechanical or clinical phase, the foci of calcification increase in size and there may be elevation of the subacromial bursa.  Subbursal and intrabursal rupture may subsequently develop, with the extrusion of calcific deposits into the subacromial-subdeltoid bursa.

Coracoid Impingement

Coracohumeral impingement is thought to occur secondary to narrowing of the space between the coracoid process and the humeral head, and may be associated with interval measurements less than 11 mm.  Narrowing may be most evident in the position of internal rotation.  MR findings of impingement may include signal inhomogeneity as well as thickening and fluid within the subcoracoid bursa.  This type of impingement, which may encroach on the subscapularis, does not involve the supraspinatus tendon or cause outlet impingement.

Subacromial-subdeltoid bursitis  (Magnetic Resonance Appearance in Shoulder Impingement)

The changes in the subacromial bursa are generally thought to be secondary to tendon degeneration or tendinopathy as part of impingement.  Normally, the subacromial-subdeltoid bursa is small, with a flat and noninflamed synovial lining.  Identification of this structure, and of signal intensity within the peribursal fat, can be used to describe subacromial bursitis on MR images.  Bursal inflammation is seen as decreased signal intensity – or loss of peribursal fat – on T1 weighted images and as increased signal intensity – from associated fluid, inflammation, and/or bursal proliferative disease – on conventional T2 or fat-suppressed T2 fast spin-echo sequences.  Although the changes of subacromial bursal inflammation are usually associated with tendinitis or cuff tear, small amounts of subacromial bursal fluid may be found without abnormal cuff morphology or signal intensity alterations.  The finding of low signal intensity within a thickened subacromial bursa on T1 and T2 weighted images indicates a proliferative process in chronic bursitis, and is also associated with rotator cuff disease.  In our experience, the presence or absence of subacromial fat is a variable finding in both asymptomatic volunteers and in various stages of impingement.  In both partial and complete rotator cuff tears, the subacromial bursa may be distended with fluid.  It is unusual to see a fluid-filled bursa in the presence of a normal cuff.

Biceps Tenosynovitis and Related Pathology

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. 

Biceps tendinitis and tenosynovitis are the earliest phases of biceps disease.  Eventually, the biceps tendon may rupture and produce a classic "Popeye" muscle in the upper arm.  Rupture of the long head of the biceps occurs in the bicipital groove.  Biceps subluxations, although rare, can be seen in disease processes in which loss of the integrity of the rotator cuff has occurred or in which the biceps tendon loses the support structures (such as the transverse ligament) that maintain it in its groove.  The dislocated biceps tendon is usually identified medial to the bicipital groove and can be seen on anterior coronal oblique, axial, and sagittal oblique images.  Associated findings may include a shallow bicipital groove and tears of the coracohumeral ligament, subscapularis tendon, and supraspinatus tendon.  The biceps tendon is located medial and anterior to the subscapularis tendon, with disruption of the transverse ligament and an intact subscapularis.  The biceps tendon dislocates beneath the subscapularis when there is associated tearing or degeneration of the subscapularis tendon insertion to the lesser tuberosity.

Quadrilateral and triangular spaces

The long head of triceps passes between teres minor and major, producing a small triangular space medially and a larger quadrilateral (quadrangular) space laterally.  The triangular space is bounded by the long head of triceps laterally, the lower border of teres minor above and the upper border of teres major below.  The quadrangular space is bounded by the lower border of teres minor above, the upper border of teres major below, long head of triceps medially and the surgical neck of humerus laterally.  The axillary nerve passes through the quadrangular space with the posterior circumflex humeral artery.  The nerve may be compromised as it traverses this restricted space.  The triangular space transmits circumflex scapular vessels. 


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