The Shoulder

By admin Last updated Jul 6, 2023

8 – The Shoulder

Chapter 8

The Shoulder

David W. Stoller

Eugene M. Wolf

Arthur E. Li

Wesley M. Nottage

Philip F. J. Tirman

Many imaging modalities have been used to assess the shoulder, most commonly:

Conventional radiology
Contrast arthrography
Contrast computed arthrotomography
Ultrasonography
Magnetic resonance (MR) imaging

Although each modality has advantages and disadvantages, MR imaging provides the most comprehensive and accurate assessment of the shoulder.

Conventional radiographic techniques demonstrate the osseous structure of the shoulder girdle but provide only limited evaluation of soft tissue anatomy, including the rotator cuff, the ligamentous attachments of the glenoid labrum capsule, and the subacromial space. Routine radiographs do not allow direct visualization of the rotator cuff tendons, their defects and abnormalities, or their relationship to their undersurface of the acromion and the acromioclavicular (AC) joint. As a result, impingement disorders are difficult to characterize on plain-film radiographic studies.

With single- and double-contrast arthrography, the extension of contrast into the subacromial-subdeltoid bursa, superior and lateral to the greater tuberosity, depicts complete tears of the rotator cuff.¹ However, arthrography is limited in assessing the size and morphology of cuff tears and is even less well suited for displaying partial tears, especially those involving the superior bursal surface of the supraspinatus tendon. In addition, the degree of retraction of the cuff tendons or the status of cuff musculature cannot be assessed with arthrography.

With the intra-articular injection of air and contrast, contrast computed arthrotomography has been used to visualize the glenoid labrum and capsule.²^,⁴ However, limited soft tissue contrast and spatial resolution in reformatted scans restrict the usefulness of this technique for routine assessment of the rotator cuff and subacromial space in impingement disorders.

Ultrasonography has also been used to visualize the subacromial-subdeltoid bursa and areas of increased echogenicity in the rotator cuff.⁵^,¹¹ This technique, however, is operator-dependent, requiring

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high-end equipment used by an experienced examiner.¹³ In addition, the individual tendons of the rotator cuff are poorly delineated, and as a result a comprehensive assessment of the shoulder is not provided. In our review of 100 consecutive requests for imaging evaluation to rule out rotator cuff tears, almost half the patients had non–cuff-related pathology.¹² The majority of non-cuff pathology was caused by labral tears, a condition not easily identified on ultrasound studies. Although conflicting results have been reported for the usefulness of ultrasonography in differentiating partial- and full-thickness tears,⁹^,¹¹^,¹⁴^,¹⁵ our direct comparison of MR imaging and ultrasound in both cadavers and patients showed ultrasound to be grossly inadequate in identifying labral tears and paralabral cysts.

MR imaging affords visualization of both soft tissue and osseous pathology of the shoulder, which is not possible with conventional arthrography or computed tomography (CT). MR of the rotator cuff provides direct coronal oblique images parallel with the course of the supraspinatus tendon as localized on axial plane images (Fig. 8.1).¹⁶^,³⁰ Axial plane images through the glenohumeral joint display capsular and labral anatomy. Sagittal oblique images demonstrate acromial anatomy, display the coracoacromial and coracohumeral ligaments, and show the relationships of the capsulolabral complex. Two- and three-dimensional GRE (GRE) images provide axial coverage from the AC joint through the glenohumeral joint. Axial images should include a fat-suppressed (FS) proton-density (PD) fast spin-echo (FSE) sequence

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in addition to GRE T2*-weighted images. Contrast enhancement with intra-articular gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) may increase diagnostic conspicuity in partial articular surface tears of the rotator cuff, helps distinguish severe tendinitis from rotator cuff tears, and improves visualization of the capsulolabral anatomy of the glenohumeral joint.¹⁶^,²⁶^,²⁹^,³¹ T1-weighted Gd-DTPA images also minimize the effect of magnetic susceptibility seen with GRE images in the postoperative cuff. With or without gadolinium enhancement, MR arthrography is not required for routine studies when there is access to phased-array shoulder coils and appropriate imaging sequences are used.

FIGURE 8.1 ● (A) Axial cross-sectional illustration showing a steeper (greater slope) obliquity of the supraspinatus tendon relative to the supraspinatus muscle. Coronal oblique MR images are correctly prescribed using image locations parallel to the supraspinatus tendon. Images improperly obtained parallel to the supraspinatus muscle and not the tendon will foreshorten the supraspinatus tendon in the coronal plane and lead to a potential misdiagnosis of a rotator cuff tear. (B) A T1-weighted coronal oblique MR arthrogram shows the continuity between the supraspinatus muscle and tendon (long white arrow), biceps labral complex (BLC), biceps tendon (b), and coracoacromial ligament (small white arrow).

Imaging Protocols for the Shoulder

Pearls and Pitfalls

Routine Protocols

Position arm in partial external rotation.
Coronal oblique images are performed parallel to the course of the supraspinatus tendon.
FS PD FSE coronal oblique images are sensitive to rotator cuff degeneration and fluid signal, and T2 FSE coronal images are required to distinguish between tendinosis and tear.
Axial FS PD FSE images are sensitive for the detection of small paralabral cysts as markers for labral tears.
Rotator cuff tears should be measured in the coronal and sagittal planes.
The glenoid fossa is evaluated in the sagittal plane for patterns of glenoid rim and fossa sclerosis associated with instability and osteoarthritis.
ABER (abduction external rotation) images in conjunction with MR arthrography are helpful in evaluating the postoperative labrum and nondisplaced (e.g., Perthes) labral tears.

Improvements in surface coil design, including the development of custom-curved coils that conform to the shoulder apex and coils that are mounted with a fixed platform (free of transmitted respiratory artifact), have resulted in more uniform signal intensity than was possible with a planar circular coil placed posterior to the shoulder. Quadrature and phased array coils (four- and eight-channel design) permit the acquisition of high-resolution images of both the rotator cuff and the glenohumeral joint and capsule. Off-axis (offset) capability is required to eliminate the requirement for positioning the shoulder isocenter with respect to the magnet. Also, direct coronal oblique images replace the need to bolster the affected shoulder to align the supraspinatus tendon parallel with the coronal imaging plane. The entire length of the supraspinatus muscle and tendon is shown in the coronal oblique plane. Direct coronal images result in foreshortening of the supraspinatus muscle and give a false appearance of discontinuity between the supraspinatus muscle and tendon.

Patient Positioning

The patient is placed in the supine position with the shoulder and arm placed alongside and parallel to the body, positioned in neutral to mild external rotation. Internal rotation should be avoided because it causes the anterior capsular structures to appear more lax and less sharply defined, and analysis in this position may be more difficult. Most patients cannot tolerate the position of extreme or full external rotation, which results in muscle spasms producing motion artifacts. Also, exaggerated external rotation makes it more difficult to follow the course of the biceps tendon, which is located more laterally, near the supraspinatus tendon attachment, in this position. In addition, bicipital tendon fluid may be mistaken for a rotator cuff in this position.³² Stabilizing the hand in partial external rotation with the use of small sandbags and tape will reduce shoulder motion artifact secondary to upper extremity muscle spasms.

Routine shoulder evaluations are performed with an axial localizer to identify the anatomic area of the AC joint through the glenohumeral joint. PD-weighted axial images demonstrate the normal high signal intensity of bony glenoid marrow fat, which may be useful in identifying osseous Bankart lesions. The low-signal-intensity tendon of the supraspinatus muscle can be identified on axial images between the AC joint and the superior aspect of the glenohumeral joint.

Imaging Planes

The coronal oblique plane (descriptions of images as coronal imply the use of the coronal oblique plane) is parallel to the supraspinatus tendon in this location. The tendon, and not the muscle of the supraspinatus (the tendon and muscle frequently have different degrees of obliquity), is used to prescribe coronal oblique images. Accurate cuff diagnosis may be limited if this technique is not carefully followed. Coronal oblique images are obtained with the following protocols:

A combination of FS PD-weighted FSE and T2-weighted (without FS) FSE sequences (Fig. 8.2), at 3- to 4-mm slice thickness, with a 256 to 512 (frequency) × 256 (phase) imaging matrix and a 12- to 14-cm field of view (FOV)³³
A conventional spin-echo sequence with PD and T2-weighted contrast (although this protocol can be used to evaluate the rotator cuff, increased imaging times limit its usefulness)
FS PD-weighted FSE scans (these images are more sensitive to subacromial bursal fluid, periarticular fluid, and rotator cuff tendinosis compared to non-FS T2-weighted FSE or conventional T2-weighted images)
Non-FS coronal oblique images (recommended to complement the FSE PD FSE sequence)
T2 FSE contrast images (these images improve specificity for distinguishing between tendinosis and partial rotator cuff tears)

Image blurring with PD-weighted FSE techniques can be reduced by keeping the echo train short and using a higher-resolution

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matrix and longer echo time (TE) values. To maximize signal-to-noise in FS PD-weighted FSE images, TE values are usually between 40 and 50 msec and repetition times (TRs) are between 3000 and 4000 msec. These parameters provide adequate coverage and maximum signal-to-noise. We do not use T2*-weighted coronal oblique images to evaluate the rotator cuff. Although GRE techniques adequately demonstrate bursal and articular cuff outlines, areas of increased signal intensity may be seen in both cuff degeneration and tears, making the distinction between tendinopathy or tendinosis and rotator cuff tear difficult. T2*-weighted axial images are, however, used to evaluate the glenohumeral capsule and labrum, at a FOV of 10 cm. GRE techniques provide good visualization of intralabral degeneration and tears, whereas FS PD FSE images are more sensitive to paralabral cysts and the articular cartilage labral interface. Magnetic susceptibility artifacts (signal void) are prominent with GRE techniques, especially when evaluating the postoperative shoulder. This susceptibility may be useful in identifying loose bodies or foci of calcific tendinitis. Coronal plane images are also used to quantify the medial-to-lateral dimension of a rotator cuff tear.

FIGURE 8.2 ● Rotator cuff tendon on coronal FS PD FSE (A) and T2 FSE (B) images using an eight-channel phased-array coil.

Axial images, obtained with a 10- to 14-cm FOV, are routinely included in the evaluation of the shoulder:

T2* GRE images (10-cm FOV) are used to evaluate intralabral pathology, subscapularis tendinosis, and calcific tendinitis (Fig. 8.3).
A separate FS PD-weighted FSE sequence is used to increase sensitivity to fluid and to identify paralabral cysts, articular cartilage labral avulsions, and muscle edema (Fig. 8.4). FSE sequences are less sensitive to intralabral signal intensity in the spectrum of degenerations or tears unless there is imbibed fluid. FSE (FS PD FSE) images, however, are superior for the demonstration of labral morphology in cases of avulsions or contour abnormalities.

We have not found the second echo of a conventional T2-weighted sequence to provide enough tissue contrast for the evaluation of the glenoid labrum in relationship to adjacent soft tissue structures and fluid. A common mistake in imaging protocols is to rely on GRE images as the sole axial sequence,

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without a FS PD FSE sequence to improve sensitivity for fluid and subtle labral tearing at the glenoid rim attachment.

FIGURE 8.3 ● Glenohumeral joint contrast on axial T2* GRE image. Axial GRE images optimize visualization of intralabral signal and subscapularis tendinosis. FS FSE images are more sensitive to fluid collections, paralabral cysts, and articular cartilage.

FIGURE 8.4 ● (A) Axial FS PD FSE image shows intact and congruous humeral head and glenoid articular cartilage surfaces (arrows), separate from the high-signal-intensity intra-articular contrast. (B) PD FSE contrast without FS is shown in an axial image of a Bankart lesion. Chondral surfaces are not as well demonstrated. (C) Excellent contrast is shown between the avulsed anterior labrum and the anterior glenoid rim on the corresponding sagittal FS PD FSE image.

T2-weighted FSE sagittal oblique plane images have become important in evaluating the conjoined insertion of the supraspinatus and infraspinatus tendons and in characterizing the anteroposterior size and location of rotator cuff tears initially detected or suspected from coronal plane images. For example, tears of the supraspinatus tendon located in a far anterior position are frequently easier to identify on sagittal oblique images, which do not have the partial volume effect seen on anterior coronal oblique images. The entire coracoacromial arch, including the rotator cuff and glenohumeral joint capsule relationships, is displayed in the sagittal oblique plane. External rotation may produce a normal pseudothickening of the infraspinatus tendon cross-section on sagittal images, which should not be mistaken for tendon retraction (Fig. 8.5). A FS PD FSE sagittal sequence is also used to improve contrast between joint fluid and capsular structures, including the inferior glenohumeral ligament labral (IGHLL complex).

MR Arthrography

MR arthrography was introduced in the 1990s as a natural extension of CT arthrography. Advantages of this modality include:

Joint distention, outlining intra-articular structures such as the labrum and capsular ligaments
Improved detection of rotator cuff tears, including partial tears
Demonstration of communication between the joint and extra-articular abnormalities (e.g., paralabral cysts, bursae, and other fluid-containing masses or potential spaces)

FIGURE 8.5 ● Pseudo-thickening of the infraspinatus tendon resulting from external glenohumeral joint rotation. This is not a cuff tear with retraction. (A) Sagittal PD image. (B) Axial FS PD FSE image.

Disadvantages include risks associated with needle placement into the joint, including infection, hemorrhage, synovitis, reaction to iodinated contrast material, and loss of signal if improper dilution is used.

MR arthrography is frequently used for shoulder evaluation in the following circumstances:

The athlete with chronic shoulder pain and an equivocal routine MR examination
Postoperative evaluation of repaired labral capsular structures and/or strictures, recurrent rotator cuff tears or partial tears, and displaced hardware
The patient with chronic shoulder pain and negative routine MR examination

Techniques of MR Arthrography

MR arthrography with intraarticular contrast is performed using either a paramagnetic contrast agent such as Gd-DTPA (Fig. 8.6) or saline to facilitate capsular distention and to improve the contrast between fluid and the rotator cuff and glenohumeral joint capsule.³⁴ When gadolinium is used, a preinjection T2-weighted FSE coronal oblique and a T2*-weighted axial sequence are performed to identify pathology that may not be appreciated on post-contrast images, including:

A bursal surface tear or intrasubstance degenerative cuff changes
A paralabral cyst that does not directly communicate with the joint (on T2* axial images) and may not be appreciated on post–intra-articular paramagnetic contrast injection FS T1-weighted images
Preexisting fluid secondary to an effusion or hemorrhage

FIGURE 8.6 ● Routine MR arthrography with FS T1-weighted (A) coronal oblique, (B) axial, and (C) sagittal oblique (at the level of the glenohumeral joint) images. s, supraspinatus tendon; b, biceps tendon; SL, superior labrum; arrow, conjoined origin of the superior and middle glenohumeral ligaments; AP, axillary pouch; al, anterior labrum; PL, posterior labrum; MGL, middle glenohumeral ligament; sub, subscapularis tendon; c, coracoid; BLC, biceps labral complex; small arrows, superior glenohumeral ligament.

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Fluid in the subacromial-subdeltoid bursa may be secondary to impingement or may be caused by a rotator cuff, which allows direct communication between the glenohumeral joint and subacromial-subdeltoid bursa. The finding of fluid within the shoulder joint may eliminate or obviate the need to perform an intra-articular injection.

Because of imaging time limitations, MR protocols frequently employ only post-MR arthrography sequences. In this situation it is important to maintain FS PD FSE and T2 FSE coronal images and FS PD FSE axial and sagittal images. The mistake of using a protocol with only FS T1-weighted post-arthrographic images results in decreased accuracy for rotator cuff bursal and intrasubstance pathology and paralabral cyst identification.

When gadolinium contrast is used, the gadolinium is diluted (0.4 cc into 100 cc of saline), and approximately 12 to 16 cc is then injected into the joint.³⁵ The injection of a nondiluted paramagnetic contrast agent produces an unacceptable susceptibility artifact and may serve as a synovial irritant. Although not currently approved by the U.S. Food and Drug Adminis-tration (FDA) for intra-articular use, most academic and private centers use and have accepted this technique to improve the accuracy of specific shoulder evaluations.

Since lack of access to fluoroscopy may make gadolinium MR arthrography difficult in certain outpatient centers, an alternative option is to use intra-articular saline, which does not require a patient consent form and can potentially be performed without fluoroscopy. The intraarticular injection of saline can be performed via a posterior approach. Saline MR arthrography requires T2 (conventional or FS FSE) and T2*-weighted sequences.

A routine MR arthrography protocol may include any of the following sequences:

FS T1-weighted coronal images (to distinguish contrast from subacromial subdeltoid fat in full-thickness rotator cuff tears)
FS PD FSE coronal images (to identify extraarticular noncommunicating fluid collections, intraosseous bone

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marrow abnormalities, and interstitial noncommunicating rotator cuff tears)
PD-weighted sagittal images, including the medial aspect of the shoulder (to evaluate the belly of the supraspinatus for atrophy and osseous acromion outlet morphology)
FS PD FSE sagittal images (to assess the AC joint and intraarticular biceps abnormalities)
FS T1-weighted axial images (for high-resolution labral evaluation)
FS PD FSE axial images (for labral and glenoid articular cartilage evaluation)
PD FSE abduction external rotation (ABER) oblique sagittal images (to evaluate the anterior labrum, the undersurface of the rotator cuff, and the position of the humeral head)

Most commonly, FS T1-weighted images at a 3-mm slice thickness in at least one plane, usually the coronal oblique, are used. Fat suppression helps to avoid mistaking areas of normal fat from high-signal-intensity contrast, increasing the conspicuity of the paramagnetic contrast agent. Sagittal images display the entire labral complex on a single 3-mm sagittal oblique image.

Rotator Cuff

MR arthrographic evaluation of the rotator cuff outlines the surfaces of the rotator cuff, with imbibition of contrast indicating surface fraying or tendinosis. Contrast also insinuates into partial tears from the articular surface side.³⁶ T2-weighted or FS PD-weighted images are needed for bursal surface evaluation. In full-thickness tears of the supraspinatus, contrast extends into the subacromial subdeltoid bursa.

Labrum

MR arthrography outlines the anatomy of the glenoid labrum, identifies partial articular or full-thickness tears of the rotator cuff, and demonstrates glenohumeral capsular ligaments not adequately appreciated in the nondistended joint capsule. Distention will sometimes “pull” on the labral attachment, revealing detachment. Healing changes or fibrosis may prevent this pulling away and therefore prevent visualization of lesions. In this instance the ABER technique (see below) may be helpful. FS PD FSE images may show granulation tissue or underlying bone reactive changes indicative of labral abnormalities. Except for subtle cases of a humeral avulsion of the glenohumeral ligament (HAGL) or reverse HAGL, adherent Perthes lesion, or postoperative Bankart repair, MR arthrography is not required if properly optimized MR studies with high signal-to-noise and adequate spatial resolution have been used.

Biceps

Contrast outlines the biceps and the biceps labral complex in cases where a paucity of joint fluid prevents optimal visualization, aiding in the detection and characterization of superior-labral anterior-to-posterior (SLAP) lesions. In addition, ligamentous anatomy may be demonstrated at the biceps anchor origin, permitting evaluation of the middle glenohumeral ligament (MGHL). Arthrography helps to differentiate a cord-like glenohumeral ligament from a displaced labral fragment and to distinguish a torn MGHL in the setting of a type 7 SLAP lesions from synovitis. Arthrography is also useful in visualization of the superior glenohumeral ligament (SGHL) and the coracohumeral ligament (CHL), aiding in the detection and characterization of microinstability lesions.

ABER Technique

ABER imaging was originally developed for evaluating glenohumeral anterior instability and multidirectional instability and to assess tears or laxity of the anterior band of the inferior glenohumeral ligament (IGHL). O—Brien et al.³⁷ have reclassified the bands of the IGHL into anterior and posterior, and the band formerly termed superior is now referred to as the anterior band.

For ABER imaging, the arm is placed in abduction to tighten the inferior glenohumeral ligament labral complex (IGLLC) (Fig. 8.7). This technique places stress on the labral ligamentous complex to help reveal detachments that may not be seen on routine MR exams if the bulk of the subscapularis prevents displacement. It also relieves tension on the undersurface of the rotator cuff, thus revealing nondisplaced undersurface flap tears of the supraspinatus and helping to characterize the horizontal component of a partial articular side rotator cuff tear.³⁸ In SLAP lesions in throwing athletes, ABER positioning produces decentering of the humeral head, revealing biceps anchor detachment (the posterior peel-back subcategory of type 2 SLAP lesions). In subtle shoulder instability, ABER imaging may also reveal decentering of the humeral head from the normal central point of rotation.

ABER images were initially used to confirm IGHL tightening in the position of abduction and external rotation (Fig. 8.8). As presently used, ABER imaging is usually performed in conjunction with MR arthrography (Fig. 8.9). In routine imaging there is a greater reliance on coronal images to show the IGLLC without using ABER MR arthrography. Non-arthrographic imaging in the ABER position, although less common, can still be used to evaluate the taut IGL and anterior band.³⁹

Marrow Imaging

Metaphyseal marrow inhomogeneity of the proximal humerus may represent a normal pattern of conversion from red to yellow marrow as a function of age-related changes in marrow distribution in the shoulder (Fig. 8.10). Red marrow may also extend medially and proximal to the physeal scar.⁴⁰ Red marrow has a characteristic intermediate signal intensity on T2-weighted images and is not associated with aggressive characteristics such as cortical bone erosion or a soft tissue mass. When there is both medial and lateral extension of red marrow proximal to the physis, further evaluation for a marrow disorder is warranted (see Fig. 8.10).

Brachial Plexus

On axial images, the brachial plexus (Fig. 8.11) can be identified adjacent to the subclavian vessels, which are used as landmarks for off-axis coronal images. Axial STIR (including fast STIR techniques) or T2-weighted images of both upper extremities are obtained to demonstrate any extrinsic effacement

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of the brachial plexus (from either soft tissue or osseous encroachment) or secondary increased signal intensity from an area of trauma.

FIGURE 8.7 ● (A) Normal central point (red cross) of glenohumeral rotation with arm positioned in abduction and external rotation. This position of function is achieved by placing the hand behind the head with the patient in the supine position. (B) Axial oblique ABER (abduction and external rotation) anatomy illustrated at the level of the IGHL labral complex posterior to the ABER section through the supraspinatus tendon. The MGHL and conjoined rotator cuff tendon are visualized superior to this section, whereas the inferior labrum and teres minor tendon are demonstrated inferior to this section in the ABER sequence.

FIGURE 8.8 ● Functional anatomy of the inferior glenohumeral ligament (IGL). (A) A coronal localizer obtained with the arm placed in 90° of abduction (i.e., the position of function of the IGL) and external rotation. (B) The corresponding axial image through the glenohumeral joint shows a taut IGL (small straight arrows) and intact anterior labrum (curved arrow).

FIGURE 8.9 ● ABER MR arthrogram showing sequential images from superior to inferior. (A) Superior axial oblique image at the level of the biceps labral complex and the long head of the biceps tendon. (B) Anterosuperior axial oblique image at the level of the subscapularis tendon and supraspinatus footprint. (C) Mid-axial oblique image at the level of the conjoined insertion of the supraspinatus and infraspinatus tendons and the spinoglenoid notch. (D) Anteroinferior axial oblique image at he level of the IGL and infraspinatus tendon. (E) Inferior axial oblique image at the level of the inferior labrum and teres minor tendon.

Related Muscles

The relevant muscles about the shoulder include the deltoid (Fig. 8.12), subscapularis (Fig. 8.13), supraspinatus (Fig. 8.14), infraspinatus (Fig. 8.15), teres minor (Fig. 8.16), and teres major (Fig. 8.17). The relevant upper arm muscles are the coracobrachialis (Fig. 8.18) and biceps brachii (Fig. 8.19). The brachialis and triceps brachii are discussed in Chapter 9 on the elbow. The muscles that connect the upper extremity to the anterior and lateral thoracic walls include the pectoralis major (Fig. 8.20), pectoralis minor (Fig. 8.21), subclavius (Fig. 8.22), and serratus anterior (Fig. 8.23). The muscles that connect the upper extremity to the vertebral column are the trapezius (Fig. 8.24), latissimus dorsi (Fig. 8.25), rhomboid major (Fig. 8.26), rhomboid minor (Fig. 8.27), and levator scapulae (Fig. 8.28).

MR Anatomic Atlas of the Shoulder

Coronal Images (Fig. 8.29)

For rotator cuff evaluation, supraspinatus tendon anatomy is best displayed on coronal plane images:

On anterior and midcoronal oblique images, the supraspinatus muscle and its central tendon are seen in continuity. The low-density supraspinatus tendon is defined at its insertion on the greater tuberosity. The subacromial bursa is interposed between the rotator cuff and the acromion. A fibrofatty layer lies between the acromion, the AC joint, and the superior bursal layer.
On anterior coronal images, the subscapularis muscle fibers and multitendinous fibers can be identified where they converge on the lesser tuberosity. Anterior coronal oblique images display the coracohumeral and coracoacromial ligaments as thin black structures.
In a neutral position and with internal rotation of the humeral head, the long head of the biceps tendon is seen in the bicipital groove on anterior coronal oblique images. The long head of the biceps tendon enters the capsule inferior to the supraspinatus tendon and can be traced to its insertion on the superior rim of the glenoid at the biceps labral complex (BLC).
The coracoclavicular ligaments are also displayed on anterior coronal oblique images. The anatomy of the AC articulation is best displayed at the level of the supraspinatus tendon. When present, AC joint fluid may represent an asymptomatic manifestation of osteoarthritis.⁴¹
The inferior glenoid labrum and axillary pouch are clearly demonstrated on these oblique images. Subscapularis bursal fluid may extend inferior and medial to the inferior glenoid on anterior coronal images.
On midcoronal images, the muscle belly of the supraspinatus extends laterally beyond the glenoid before its central tendon reaches the musculotendinous junction of the rotator cuff. The axillary pouch of the IGHL, with its attachment to the anatomic neck of the humerus and the inferior pole of the glenoid, can also be seen on these images. It is not unusual to see variable

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amounts of fluid in the axillary pouch in the presence of a joint effusion. Otherwise, the axillary pouch is collapsed. The presence of a glenohumeral joint effusion is associated with osteoarthritis and rotator cuff disease.⁴² The axillary pouch can be followed from anterior to posterior on coronal oblique images through the shoulder.
On midcoronal to posterior coronal sections, there is a subtle transition between the supraspinatus and the conjoined insertion of the infraspinatus tendon. Posterior to the AC joint, the supraspinatus tendon forms a conjoined attachment to the greater tuberosity with the infraspinatus tendon. On more posterior sections, the infraspinatus tendon may be mistaken for the supraspinatus tendon, which may be out of the plane of section. Humeral head articular cartilage, intermediate in signal intensity on T1-weighted images, is interposed between the low-signal-intensity supraspinatus tendon superiorly and the cortex inferiorly. The posterior circumflex humeral artery and the axillary nerve are identified medial to the coracobrachialis, the latissimus dorsi, and the teres major muscles and tendons.
The teres minor muscles and tendons are shown on more posterior coronal oblique images at the level of the scapular spine, where the teres minor attaches to the greater tuberosity.

FIGURE 8.10 ● (A) Coronal PD FSE image showing normal hypointense red marrow signal distal to the proximal humeral physeal scar. Red marrow may partially exist in subchondral locations of the proximal humeral epiphysis, providing characteristic T1 and T2 signal intensities. (B, C) Marrow reconversion in polycythemia vera, a myeloproliferative disorder. Red marrow signal intensity is apparent proximal to the physeal scar. Red marrow demonstrates lower signal intensity than fat on coronal PD-weighted images (B) and is hyperintense relative to fat signal on coronal FS PD FSE images. (C). Red marrow associated with pathologic conditions tends to image with greater hyperintensity than normal areas of persistent red marrow. (D) Abnormal hyperintense marrow replacement in chronic lymphocytic leukemia (CLL) on a sagittal FS PD FSE image. CLL is not associated with high-dose radiation or benzene exposure.

FIGURE 8.11 ● The components of the brachial plexus. The veins and most of the axillary artery have been removed.

FIGURE 8.12 DELTOID ● The deltoid abducts the arm and represents the largest of the glenohumeral muscles. The deltoid is multipennate, with an anterolateral raphe, and is important in any form of arm elevation. It is active throughout the entire arc of glenohumeral abduction, even if the supraspinatus muscle is inactive.

FIGURE 8.13 Subscapularis ● The subscapularis muscle represents the anterior compartment of the rotator cuff. It internally rotates and flexes the humerus. The superior two thirds of the muscle has a tendinous distribution dispersed within the muscle belly, converging into a single large tendon laterally. The inferior third of the subscapularis is muscular throughout its course. The subscapularis forms the upper border of both the quadrilateral and triangular spaces.

FIGURE 8.14 Supraspinatus ● The supraspinatus initiates abduction of the arm and is active during the entire arc of scapular plane abduction. The parallel independent collagen fascicles permit differential excursion of segments of the tendon. The supraspinatus exerts maximal effort at approximately 30° of abduction and functions with the rotator cuff as a humeral head depressor.

FIGURE 8.15 Infraspinatus ● The infraspinatus functions with the teres minor to externally rotate and extend the humerus. The infraspinatus is more active with the arm in the adducted position and accounts for up to 60% of external rotation force. The infraspinatus contributes to the humeral head depressor action of the rotator cuff.

FIGURE 8.16 Teres Minor ● The teres minor functions with the infraspinatus to externally rotate and extend the humerus. The teres minor is active with the shoulder in 90° of elevation.

FIGURE 8.17 Teres Major ● The teres major internally rotates and adducts the arm. The axillary nerve and posterior humeral circumflex artery pass superior to the upper border of the teres major through the quadrilateral space. The quadrilateral space is also bordered by the teres minor, the triceps, and the humerus. The teres major functions with the latissimus dorsi muscle in humeral extension, internal rotation, and adduction.

FIGURE 8.18 Coracobrachialis ● The coracobrachialis flexes and adducts the arm. The coracobrachialis and the short head of the biceps have a conjoined tendon origin at the coracoid.

FIGURE 8.19 Biceps Brachii ● The biceps brachii functions to flex and supinate the forearm. The long head of the biceps tendon (LHBT) has origins at both the superior pole of the glenoid and the posterosuperior labrum of the biceps labral complex. The LHBT extends within the synovial sheath of the glenohumeral joint. The long and short head muscle bellies join at the level of the deltoid insertion on the humerus.

FIGURE 8.20 Pectoralis Major ● The pectoralis major muscle adducts the arm and internally rotates the humerus. The pectoralis major has an upper clavicular and a lower sternocostal head. The clavicular head contributes to the anterior lamina of the broad flat tendon insertion to the humerus, whereas the more distal and deep sternocostal head fibers form the posterior lamina of the tendinous insertion.

FIGURE 8.21 Pectoralis Minor ● The pectoralis minor and major are internal rotators and flexors of the shoulder joint. The pectoralis minor helps stabilize the scapula.

FIGURE 8.22 Subclavius ● The subclavius muscle functions to depress the clavicle.

FIGURE 8.23 Serratus Anterior ● The serratus anterior muscle holds the scapula to the chest wall, protracting and allowing for upward rotation. The serratus anterior originates from the outer surface of the first eight or nine ribs. Injury to the long thoracic nerve with absence of serratus function produces a winged scapula with forward flexion of the arm.

FIGURE 8.24 Trapezius ● The trapezius muscle functions as a scapular retractor by elevating and rotating the scapula.

FIGURE 8.25 Latissimus Dorsi ● The latissimus dorsi, which adducts, extends, and internally rotates the humerus, forms the posterior axillary fold. The thoracodorsal nerve arises from the posterior cord and innervates the muscle.

FIGURE 8.26 Rhomboid Major ● The rhomboid major muscle adducts the scapula, participating in its retraction and elevation.

FIGURE 8.27 Rhomboid Minor ● The rhomboid minor and the rhomboid major both retract the scapula and participate in elevation of the scapula.

FIGURE 8.28 Levator Scapulae ● The levator scapulae elevates the scapula. In conjunction with the serratus anterior, the levator scapulae produces upward rotation of the scapula. Innervation is from the cervical plexus and occasionally the dorsal scapular nerve. Levator scapulae insertional pain may be caused by a SICK scapula.

FIGURE 8.29 ● (A) Coronal T1- or PD-weighted images are used to evaluate the distal acromion. (B) Coronal FS PD-weighted images show the majority of the cranial-to-caudal extent of the subscapularis tendon. This image is used to triangulate on subscapularis tears suspected on other planes. Most commonly, tears of the subscapularis begin in the superior articular margin of the tendon. (C) In the setting of supraspinatus tears, coronal T1- or PD-weighted images at or near this image slice are best for assessment of supraspinatus atrophy. (D) Coronal FS PD-weighted images display two important anatomic structures. The first is the anterior-most portion of the distal supraspinatus tendon (also called the “anterior leading edge”), which is seen attaching at the greater tuberosity. This location is the most common starting point for tears of the supraspinatus tendon. The second is the LHBT as it turns 90° around the lesser tuberosity within the proximal portion of the bicipital groove. This is a common location for tendinosis of the biceps tendon. In addition, medial subluxation is visualized in this location, not uncommonly associated with tears of the distal superior supraspinatus tendon. (E) Coronal T1- or PD-weighted images are used to depict the undersurface spurring of the acromion and lateral downsloping of the acromion, both of which are associated with impingement. (F) Coronal FS PD-weighted images show the superior labrum (the anterior superior quadrant). Areas of linear increased signal are normal at this image location, due to fluid/synovium interposed between the multitude of structures coursing toward the superior labrum, including the biceps tendon and the superior glenohumeral ligament. Linear high signal visualized in the labrum is more likely to be due to a tear anterior or posterior to the 12-o—clock position on the glenoid. (I) Coronal T1- or PD-weighted images display the Hill-Sachs lesion, which is visualized as flattening and impaction of the posterior lateral humeral head. This lesion should be differentiated from the extremely common presence of subcortical cystic changes in the posterior lateral humeral head. (J) Coronal FS PD-weighted images are used to display subacromial/subdeltoid fluid. Even in the absence of a rotator cuff tear, fluid in the subacromial/subdeltoid tendon should be described because subacromial/subdeltoid bursitis may mimic the symptoms of a rotator cuff tear and can be a secondary sign of impingement. (K) Coronal T1- or PD-weighted images are used for assessment of infraspinatus muscle atrophy in the setting of rotator cuff tears. This coronal image location is preferred over sagittal plane images because medial retraction of the infraspinatus muscle from a tendon tear can appear falsely atrophic on sagittal images. (L) Coronal FS PD-weighted images demonstrate the insertion of the infraspinatus tendon on the posterior superior portion of the humeral head. Because the insertion is oblique, small tears of the infraspinatus can be difficult to assess in the coronal plane, and infraspinatus pathology in the coronal plane is cross-referenced with sagittal images.

Axial Images (Fig. 8.30)

On superior axial images, the normal oblique course of the supraspinatus muscle is displayed with intermediate signal intensity. The supraspinatus tendon, from its insertion on the capsule and greater tuberosity posterior to the bicipital groove, to the supraspinatus fossa of the scapula, is displayed with low signal intensity. The supraspinatus muscle appears intermediate in signal intensity on T2-weighted and FS PD-weighted FSE images, demonstrating low signal intensity within its tendinous fibers. High-signal-intensity marrow fat is present in the acromion, seen lateral to and parallel with the supraspinatus muscle. In the adducted position, the tendon of the supraspinatus projects lateral to the acromion.
At the level of the superior coracoid process, the long axis of the infraspinatus originates from the posteroinferior surface of the scapula, crosses the glenohumeral joint posterior to the supraspinatus, and inserts on the lateral aspect of the greater tuberosity. As it approaches the greater tuberosity posterolaterally, the low-signal-intensity supraspinatus tendon merges with the low-signal-intensity cortex of the humerus. The spine of the scapula separates the supraspinatus and infraspinatus muscles.
The teres minor is posterolateral to the infraspinatus, originating at the axillary border of the scapula and inserting on the inferior facet of the greater tuberosity.
In cross-section, the tendon of the long head of the biceps is seen as a low-signal-intensity structure within the bicipital groove and is sometimes associated with a small amount of high-signal-intensity fat.
The suprascapular artery and nerve are located posterior and medial to the superior glenoid rim. The dark, low-signal-intensity labrum is located at the level of the glenohumeral articulation, inferior to the coracoid. Normally, the anterior and posterior labrum have well-defined triangular shapes. The posterior labrum may be smaller and more rounded than the anterior labrum. With internal rotation, however, the anterior labrum appears to be larger than the posterior labrum.
Glenohumeral articular cartilage follows the concave shape of the glenoid cavity and demonstrates intermediate signal intensity on T1-weighted images and bright signal intensity on T2*-weighted images. Articular cartilage of the glenoid margin of the anterior labrum may be mistaken for a tear. Articular cartilage of the glenohumeral joint is better evaluated on FS PD-weighted FSE sequences.
Anteromedial to the glenoid, the subscapularis muscle arises from the subscapularis fossa and inserts on the lesser tuberosity. The low-signal-intensity subscapularis can then be identified anterior to the apex of the anterior glenoid labrum. The subscapularis tendon is present at the level of the middle and superior glenohumeral joint.
The MGHL is identified as a low-signal-intensity thin band or cord anterior to the anterior labrum, and the anterior band of the IGHL is between the anterior labrum and the subscapularis tendon. The MGHL may be closely applied to the anterior aspect of the anterior labrum or plastered against the subscapularis tendon, indistinguishable from the low-signal-intensity subscapularis without the benefit of intra-articular contrast. The SGHL is identified at the level of the coracoid and the biceps tendon.
With the arm abducted by the patient—s side, axial images through the inferior glenohumeral joint display the IGHL as a lax structure. The axillary pouch of the IGHL is identified inferior to the level of the bony glenoid and requires axial sections that extend inferior to the glenohumeral joint. The subacromial-subdeltoid bursa and the deltoid muscle can be identified between the rotator cuff and the acromion.

Sagittal Images (Fig. 8.31)

The muscle groups of the deltoid, supraspinatus, infraspinatus, teres minor, teres major, subscapularis, and coracobrachialis are defined on sagittal plane MR images:

On midsagittal and lateral sagittal images, the supraspinatus, infraspinatus, and the conjoined cuff tendons demonstrate low signal intensity between the acromion and the superior articular surfaces of the humeral head. The thickened tendon seen in the anterior

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half of the sagittal images is the supraspinatus component, whereas the flatter tendon that arches over the posterior half of the humeral head is the infraspinatus component.
The long head of the biceps tendon is identified anterior and inferior to the supraspinatus tendon on lateral sagittal images and can be followed to its attachment to the BLC at the level of the glenohumeral joint.
Toward the glenoid, the coracoacromial ligament is seen as a low-signal-intensity band that arches over the anterior aspect of the rotator cuff from the acromion and coracoid.
Medial sagittal sections display the clavicle and AC joint in profile. The oblique transversely oriented physis is also delineated on sagittal images. Marrow inhomogeneity, seen frequently as red-to-yellow marrow conversion, may not be complete distal to the physis in the metadiaphyseal region.⁴³
The low-signal-intensity glenoid labrum is also defined on sagittal images that transect the glenohumeral joint. The anterior band of the IGHL can be seen extending anterior and superior to become the anterior labrum. The MGHL is seen anterior to the anterior labrum. The subscapularis tendon is located anterior to the MGHL. This relationship is constant, even though the MGHL may be variable in size and shape. The MGHL may also be absent. The axillary pouch extends between the anterior and posterior bands of the IGHL.
Medial sagittal images demonstrate the coracoclavicular ligaments. The low-spin-density tendon of the supraspinatus is identified in the anterior portion of the supraspinatus muscle. The pectoralis minor and coracobrachialis muscles are anterior to the coracoid process. The axillary artery, vein, and brachial plexus are anterior to the subscapularis muscle, deep to the pectoralis minor. The subscapularis muscle and tendon are anterior to the capsule of the glenohumeral joint. The long head of the biceps tendon enters the joint capsule superiorly, anterior and inferior to the supraspinatus tendon. The SGHL lies anterior to the humeral head and glenoid and inferior to the long head of the biceps tendon. The MGHL is anterior to the medial humeral head or lateral glenoid. The thick inferior glenoid labrum is seen as a low-signal-intensity structure along the inferior aspect of the glenoid.

FIGURE 8.30 ● Axial images through the AC joint should be obtained on all shoulder MR examinations. (A) Axial T1- or PD-weighted images at this location are used to identify fractures of the distal clavicle and to demonstrate an os acromiale. (B) Axial FS PD-weighted images show cartilage covering the distal aspect of the clavicle and the medial aspect of the acromion at the AC joint. Cartilage defects and thinning, as well as subchondral bone marrow edema and cystic change, are evaluated on axial images through the AC joint. These degenerative changes can mimic the symptoms of a rotator cuff tear. (C) Axial T1- or PD-weighted images demonstrate the Hill-Sachs lesion of the humeral head, usually visualized as focal flattening or concave deformities in the posterolateral humeral head. The Hill-Sachs lesions is identified on the first or second superior axial image through the humeral head. Subcortical cystic change is more commonly visualized in the posterolateral humeral head and is usually an incidental finding in asymptomatic patients. (D) Axial FS PD-weighted images depict the biceps tendon coursing across the anteromedial aspect of the humeral head, within the rotator interval. This image location serves as a starting point for following the remainder of the biceps tendon into the bicipital groove on successive axial images moving from cranial to caudal. Tears of the supraspinatus and infraspinatus tendons are also identified at this image location on axial images. (E) Axial T1- or PD-weighted images allow evaluation of subcoracoid impingement. (F) In this location, thickening and increased signal in the superior glenohumeral ligament and coracohumeral ligament on an axial FS PD-weighted image may indicate adhesive capsulitis, particularly when accompanied by thickening and increased signal within the inferior glenohumeral ligament. (G) Axial T1- or PD-weighted images are used to identify subcortical cystic change in the greater and lesser tuberosity. This finding is commonly an indirect indication of abnormality or tearing in the overlying distal supraspinatus and subscapularis tendons, respectively. (H) Axial FS PD-weighted images through the proximal bicipital groove are used to identify “hidden lesions,” which are diagnosed when the biceps tendon is medially subluxing out of the bicipital groove, usually into a distal subscapularis tear or anterior to the lesser tuberosity. A degenerated biceps tendon may appear flattened and elongated as it rounds the lesser tuberosity into the proximal bicipital groove. Commonly, only the medial “tail” of the flattened degenerated biceps tendon subluxes out of the groove; the remainder of the flattened biceps tendon stays within the groove. (I) Axial T1- or PD-weighted images display the osseous glenoid subchondral surface, which should appear flat. Osseous glenoid remodeling, hypertrophy, deformity, subchondral cystic change, and edema are commonly identified as indirect evidence of overlying chronic cartilage degeneration or prior trauma. Posterior glenoid spurring may completely replace a degenerated or markedly attenuated posterior labrum. (J) Axial FS PD-weighted images are optimal for displaying the glenoid and humeral head cartilage. Chondral fissures, thinning, and defects are visualized when viewing successive cranial-to-caudal images through the glenohumeral joint. The anterior and posterior labrum are also optimally visualized and are normally firmly adherent to the glenoid and glenoid articular cartilage. (K) Axial T1- or PD-weighted images are used to identify bony Bankart lesions. These lesions are seen on inferior axial images through the glenohumeral ligament as oblique fracture lines extending through the anterior inferior glenoid. (L) Axial FS PD-weighted images show the prominent anterior band of the IGHL, which is occasionally mistaken for a tear of the anterior inferior labrum when fluid is interposed between the anterior band and the normal labrum.

FIGURE 8.31 ● (A) Sagittal T1- or PD-weighted images show the coracoclavicular ligament extending from the anterosuperior aspect of the coracoid process to attach onto the undersurface of the distal clavicle. Sagittal images through the plane of the ligament are optimal for diagnosing coracoclavicular tears or sprains in cases of suspected AC joint separation. (B) Sagittal FS PD-weighted images are used to demonstrate intramuscular ganglion cysts, which are commonly visualized along the myotendinous junction of the supraspinatus and infraspinatus muscles, often at or medial to the level of the glenoid. These ganglion cysts can be followed laterally on successive sagittal images to the level of the distal rotator cuff tendon, where they commonly communicate with partial articular-side tendon tears. These ganglions may be caused by imbibition of joint fluid into the muscle through a partial tendon tear via a one-way check valve at the tear. (C) Sagittal T1- or PD-weighted images are used to assess the shape of the glenoid, which should normally appear somewhat pear-shaped. Chronic erosion of the anterior-inferior glenoid from repetitive trauma may result in an abnormal “inverted-pear” shape, which can predispose to recurrent dislocations. In addition, bony Bankart fractures are diagnosed on the sagittal image through the glenoid as an oblique fracture line extending across the anterior-inferior glenoid. (D) Sagittal FS PD-weighted images through the level of the labrum are useful for confirming labral tears suspected from viewing labral abnormalities in other planes. High signal is often visualized on sagittal images within the labrum or in an arc just superficial to the torn labrum, possibly from perilabral inflammation. Sagittal images are also useful in the identification of associated paralabral cysts and localizing their origin. (E) Sagittal T1- or PD-weighted images medial to or at the level of the glenoid can be used to diagnose rotator cuff muscle atrophy. However, in the setting of a rotator cuff tear with significant retraction, the muscle of interest may be retracted medially, sometimes medial to the sagittal plane that is being used for making the atrophy assessment. Since sagittal plane images used alone may falsely suggest atrophy, confirmation of atrophy should be obtained on the coronal plane images. (F) Sagittal FS PD-weighted images through the glenohumeral joint optimally display the anterior and posterior bands of the IGHL and are useful for confirming adhesive capsulitis, sprains, or tears of the IGHL. Further confirmation of adhesive capsulitis is obtained when the changes of capsular increased signal and thickening involve not only the axillary pouch, but also the joint capsule within the rotator interval, best identified in the sagittal plane. (G) Sagittal T1- or PD-weighted image sectioning through the AC joint. In cases of significant degenerative joint disease, hypertrophic changes, including inferior spurring of the anterior acromion or distal clavicle, are visualized in this location. Inferior spurring pressing into the supraspinatus muscle is associated with impingement and may mimic pain from a rotator cuff tear. (H) Sagittal FS PD-weighted images at this location show the LHBT in cross-section coursing through the rotator interval. Sagittal images are useful in the identification of tendinosis of the biceps tendon within the rotator interval. In the case of complete biceps tendon tear from the biceps labral anchor with distal retraction, the rotator interval appears empty, with no biceps tendon identified. (I) Sagittal T1- or PD-weighted images through the acromion are used for identification of broad-based osteophytic spurring along the undersurface of the acromion from anterior to posterior. Spurring is associated with impingement. (J) Sagittal FS PD-weighted images at this location display tears of the distal subscapularis tendon as high signal within the tendon, most commonly beginning at the superior margin of the tendon. When a tear of the subscapularis is identified, the biceps tendon should be examined for any evidence of medial subluxation into the subscapularis tear. (K) Sagittal T1- or PD-weighted images are used to examine the multiple slips of the deltoid muscle, which fan out from the acromion and clavicle, for strain, tear, or denervation. In patients who have had acromioplasty, the deltoid attachments to the acromion are examined to exclude dehiscence or detachment. (L) Sagittal FS PD-weighted images at this location show the biceps tendon as it turns 90° from the rotator interval to descend vertically within the bicipital groove. This is a common location for biceps tendinosis. (M) Sagittal T1-weighted images are used to evaluate the humeral head physis. In children and adolescent throwing athletes, subtle widening and irregularity may suggest a chronic physeal stress injury, called “Little Leaguer—s shoulder.” (N) Sagittal FS PD-weighted images display the distal supraspinatus, infraspinatus, and teres minor tendons where they insert on the lateral aspect of the humeral head. Sagittal images through the distal tendon insertions can localize tears. The anterior-to-posterior dimension of tendon tears is measured on sagittal images.

Imaging Checklist for the Shoulder

The checklist for reviewing a shoulder MR examination includes the following elements:

Acromion and acromioclavicular joint
Rotator cuff
Biceps tendon and pulley
Labrum
Glenohumeral joint cartilage and osseous structures
Capsular ligaments

These structures are evaluated in all three planes, and the degree of confidence in a diagnosis of common shoulder pathology (including rotator cuff tears, labral tears, biceps subluxation, chondromalacia, and adhesive capsulitis) is increased by visualizing the abnormality in more than one plane.

Coronal Plane Checklist

(1) Rotator Cuff (Fig. 8.32)

To locate the anterior-most aspect of the supraspinatus tendon, identify the image showing the anterior aspect of the humeral head and locate the long head of the biceps tendon as it takes a 90° turn along the proximal aspect of the bicipital groove. One to two images posterior to this, the hypointense fibers of the normal anterior leading edge of the supraspinatus are visualized, attaching to its footprint along the greater tuberosity. This is the most common site for supraspinatus tears, which are identified by fluid signal intensity along the footprint instead of normal hypointense tendon. Tears often begin anteriorly and propagate posteriorly. Continuing posteriorly, the remainder of the supraspinatus tendon is visualized. Just posterior to the level of the acromioclavicular joint, the supraspinatus transitions to a region of shared supraspinatus and infraspinatus fiber insertions known as the conjoined tendon. Beyond the posterior aspect of the humeral head, the infraspinatus tendon fibers are identified coursing posterior-superior to the humeral head to attach to the posterior aspect of the greater tuberosity. Triangulating on rotator cuff pathology in the sagittal plane aids in determining which components of the rotator cuff are involved by tears or tendinosis.

(2) Acromioclavicular Joint (Fig. 8.33)

The AC joint courses posteromedially on consecutive coronal images from anterior to posterior. AC joint arthrosis is similar to arthrosis in any other joint of the body, with cartilage loss, subchondral edema, subcortical cystic change, and osseous-spurring. Inferior spurring of the distal clavicle and medial acromion, as well as lateral undersurface spurring of the acromion (usually at or near the insertion of the coracoacromial ligament), can narrow the supraspinatus outlet and impress upon the supraspinatus muscle. A low-lying or laterally downsloping acromion may also narrow the outlet. The presence of subacromial-subdeltoid bursal fluid and bursitis (in which AC joint and acromial spurring contribute to the etiology) are identified on coronal images. Traumatic injury, including distal clavicle fractures, AC joint capsular sprain/tearing, and coracoclavicular ligament tears, are also identified on coronal images.

FIGURE 8.32 Rotator Cuff.

FIGURE 8.33 Acromioclavicular Joint.

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(3) Biceps Tendon (Long Head) (Fig. 8.34)

The biceps tendon is identified on coronal images that scan through the anterior humeral head. The first part of the tendon visualized on anterior-most images is the curved portion, seen within the proximal bicipital groove. The horizontal portion of the tendon in the rotator interval takes a 90° turn to course vertically in the bicipital groove. On consecutive posterior images both the horizontal and vertical portions of the tendon are visualized. The horizontal portion of the tendon courses posteromedially within the rotator interval to insert at the biceps-labral anchor and superior glenoid. The vertical portion is visualized descending within the bicipital groove along the proximal humeral shaft. The biceps tendon frequently demonstrates degeneration at the level of the proximal bicipital groove. As the tendon degenerates, it appears either thickened with increased signal, or attenuated and flattened. With dysfunction of the biceps pulley mechanism, the biceps tendon subluxes medially over the lesser tuberosity, often seen as flattening and attenuation of the medial portion of the biceps tendon, with the flattened portion of the tendon fanning out medially over the lesser tuberosity. Medial biceps subluxation and dislocation are visualized in both coronal and axial planes. If the horizontal portion of the biceps tendon is not visualized in the rotator interval, the tendon is probably torn and retracted distally into the bicipital groove. The retracted tendon may be either thickened and frayed, or thinned and chronically attenuated. Tenodesis is another possible explanation for absence of the biceps tendon within the rotator interval.

FIGURE 8.34 Biceps Tendon.

(4) Labrum (Fig. 8.35)

The coronal plane is optimal for evaluating the superior and inferior labrum. However, there are multiple pitfalls in evaluating the anterior superior quadrant of the labrum. In addition to the large number of normal variants in this area, the superior and middle glenohumeral ligament and the long head of the biceps tendon course toward the superior glenoid labrum in the anterior superior quadrant. In this location, normal joint fluid interposed between these structures can mimic labral tears and labral detachment. A simple rule of thumb is to find the coronal image on which the inferior glenoid tip is most prominent. This coronal image approximates the 12 o—clock position of the superior glenoid and the 6 o—clock position of the inferior glenoid. On this image, and any images posterior to it, the superior labrum is normally firmly attached to the glenoid, without superimposition of the glenohumeral ligaments or biceps tendon. Tears within the substance of the labrum and detachment from the glenoid are identified with a higher degree of confidence on these images. The presence of paralabral cysts is a clue to the presence of a labral tear. If a paralabral cyst is present but no tear is visualized, there is still a high likelihood of an adjacent tear that has either resynovialized and healed, or is not visualized as fluid-filled on the MR examination.

FIGURE 8.35 Labrum.

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(5) Inferior Glenohumeral Ligament (Axillary Pouch) (Fig. 8.36)

To find the IGHL or IGL, identify the inferior glenoid on any coronal slice. The IGHL is a hypointense band of fibers that extends inferolaterally from the inferior glenoid and then sweeps superolaterally upward to insert on the medial humeral neck. This U-shaped course of the IGHL forms the axillary pouch. The IGHL is composed of both an anterior band and a posterior band, arising from the anterior and posterior glenoid, respectively. As a result, on coronal images, the entire inferior glenoid and medial inferior humeral neck from anterior to posterior are enveloped by the IGHL, which can be identified on many consecutive coronal images. In patients with adhesive capsulitis, the IGHL becomes thickened and demonstrates increased signal. This appearance is nonspecific, however, and may be seen in a capsular sprain after trauma or with capsular scarring. The diagnosis of adhesive capsulitis, therefore, needs to be correlated with clinical history. In cases where the IGHL is thickened and adhesive capsulitis is suspected, the capsular structures within the rotator interval should be inspected, since the rotator interval is commonly involved in adhesive capsulitis. Tears of the IGHL from either the humerus attachment (HAGL), the glenoid attachment (glenoid avulsion of the glenohumeral ligaments), or midportion are also visualized on coronal images.

(6) Glenohumeral Joint Cartilage (Fig. 8.37)

Cartilage covering the superior and medial portions of the humeral head and the opposing glenoid surface are well displayed on coronal images. Chondromalacia and chondral defects can be characterized as to the depth, extent, and exact location of the cartilage pathology, and any subchondral bone marrow edema can also be identified. If there are significant cartilage abnormalities, the joint spaces should be scrutinized in all three planes for the presence of loose bodies. Chondral or osteochondral bodies are commonly found in the axillary pouch and can also migrate outside of the glenohumeral joint proper and be found in the subscapularis recess (between the coracoid and humeral head) and in the biceps tendon sheath.

(7) Osseous Structures (Humeral Head, Glenoid, Scapula, Suprascapular Notch) (Fig. 8.38)

Common fractures of the proximal humerus can be identified on coronal images, including fractures of the greater tuberosity and of the humeral neck. The degree of displacement and cortical step-off in greater tuberosity fractures can also be measured. Hill-Sachs deformities of the posterolateral humeral head are also visualized, as are glenoid fractures, particularly bony Bankart fractures. However, both Hill-Sachs deformities and Bankart fractures are probably more easily identified in the axial plane. Neoplasms and metastatic disease to the humerus or scapula are also visualized. The suprascapular notch is seen on coronal images as a U-shaped notch medial to the superior glenoid. Mass lesions, including paralabral cysts and tumors causing suprascapular nerve compression and supraspinatus and infraspinatus denervation, are occasionally visualized in the suprascapular notch.

FIGURE 8.36 IGL.

FIGURE 8.37 Glenohumeral Joint.

FIGURE 8.38 Osseous.

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(8) Supporting Muscles (Deltoid) (Fig. 8.39)

The deltoid muscle origin is extensive, with muscle and tendon slips depicted anteriorly at the distal clavicle, all along the anterior, lateral, and posterior acromion, and posteriorly along the scapular spine. The deltoid muscle can be strained or torn, or may demonstrate changes of denervation in the setting of neuropathies.

Axial Plane Checklist

(1) Acromioclavicular Joint (Fig. 8.40)

Axial MR scans through the shoulder should include the AC joint, since examination of AC joint chondral surfaces, which cover both the distal clavicle and medial acromion, is optimally performed on axial images. Subjacent subchondral bone marrow edema and cystic change is also evaluated on axial images. The presence of an os acromiale, with or without stress-related edema across the synchondrosis, is also visualized on axial images. Severe AC joint arthrosis is occasionally the primary pain generator and can mimic symptoms of a rotator cuff tear. Inferior spurring, however, is better evaluated on sagittal and coronal images.

FIGURE 8.39 Deltoid Muscle.

(2) Subscapularis Tendon and Biceps Tendon (Fig. 8.41)

On axial images, the superior margin of the horizontally oriented subscapularis tendon is identified at the level where the biceps tendon enters the proximal bicipital groove. Another useful landmark is the coracoid process, since axial images through the inferior aspect of the coracoid process include the superior margin of the subscapularis muscle coursing horizontally to attach on the lesser tuberosity. The tendon has a broad footprint on the lesser tuberosity. Partial tendon tears are commonly located along the deep margin of the superior aspect of the tendon. Interstitial tears of the distal tendon are also common. Tears of the distal superior subscapularis tendon are associated with medial subluxation of the biceps tendon and are seen on both axial and coronal images. On axial images the appearance of medial subluxation of the biceps tendon into an interstitial tear of the distal subscapularis tendon has been described as resembling a football (the biceps tendon in cross-section) being placed into a quarterback—s hands (the split subscapularis tendon). Medial dislocation of the biceps tendon can also be seen on axial images, often associated with full-thickness tears of the subscapularis tendon. Sometimes, all or part of the subscapularis tendon is completely

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stripped from its lesser tuberosity attachment. However, because of an intact connection with the transverse humeral ligament, which connects the subscapularis tendon to the greater tuberosity, the tendon fibers appear to course in continuity without retraction. Proximal biceps tendon and subscapularis tendon pathology commonly coexist, since the pathogenesis of tendinosis and tears of both tendons are interrelated.

FIGURE 8.40 Acromioclavicular Joint.

Any subscapularis and/or biceps tendon pathology (tears or tendinosis) detected in the axial plane should be confirmed and further characterized in the sagittal and coronal planes.

FIGURE 8.41 Subscapularis and Biceps.

(3) Labrum (Fig. 8.42)

The entire labrum, from the superior to the inferior aspects, is evaluated on consecutive axial images from cranial to caudal, starting superiorly at the biceps labral anchor. Tears and detachments of the superior labrum are further characterized on axial images, particularly the anterior or posterior extension of SLAP tears. In patients with shoulder dislocation, the axial plane is best for identification of Bankart lesions in the anterior inferior quadrant of the labrum. Posterior labral tears are also identified on axial plane images, as are associated findings such as adjacent chondral defects or periosteal stripping.

FIGURE 8.42 Labrum.

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(4) Joint Capsule Structures (Fig. 8.43)

On images depicting the superior and middle of the joint, the MGHL is identified coursing anterior to the labrum. The anterior and posterior bands of the IGHL are seen at and below the level of the inferior glenoid labrum. Capsular thickening, associated with adhesive capsulitis, is confirmed in the axial plane. The location of capsular tears is also further characterized in the axial plane.

(5) Glenohumeral Joint Cartilage (Fig. 8.44)

The cartilage covering the glenoid and medial humeral head is well displayed on axial plane images. Chondromalacia (often more severe in the posterior glenoid) can be localized and characterized using both axial and coronal images.

(6) Osseous Structures (Fig. 8.45)

Hill-Sachs deformities are identified as impaction deformities of the posterolateral humeral head, with an irregular flattening or concave appearance to the normally rounded or convex posterolateral humeral head on superior axial images. The presence of bone marrow edema adjacent to a Hill-Sachs deformity suggests recent shoulder dislocation. Subcortical cystic change is commonly identified in the posterolateral humeral head and may be associated with internal impingement. The glenoid is evaluated for fractures, particularly bony Bankart fractures, and for subchondral bone marrow edema suggestive of overlying chondral degeneration. The coracoid process is evaluated for fractures and for elongation of the coracoid process resulting in narrowing between it and the humerus, causing subcoracoid impingement. The spinoglenoid notch is examined for the presence of mass lesions that may impinge on the suprascapular nerve.

(7) Supraspinatus and Infraspinatus Tendons (Fig. 8.46)

The horizontal portion of the supraspinatus tendon is identified on axial scans one or two images inferior to the acromion and is seen directly beneath the acromion. Over the next one or two images inferiorly, the curved portion of the distal supraspinatus tendon inserts onto the greater tuberosity and can be identified as a semicircle of dark tendon tissue marginating the edge of the greater tuberosity. Posteriorly, and on further consecutive inferior images, the infraspinatus tendon is seen sweeping horizontally, posterior to the humeral head, to insert posterolaterally. Axial images thus provide further characterization or confirmation of supraspinatus and infraspinatus pathology seen in other planes.

(8) Supporting Muscles (Fig. 8.47)

The pectoralis major muscle is best evaluated using a dedicated pectoralis muscle protocol, with coronal plane images obtained parallel to the pectoralis muscle. Occasionally, however, tears of the pectoralis major tendon insertion on the humerus are depicted on the inferior-most axial images of a

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routine shoulder MR examination, when edema and hemorrhage are seen adjacent to the biceps tendon along the proximal humeral shaft. The large arc of muscle bundles making up the deltoid muscle are visualized on axial images anterior, lateral, and posterior to the humeral head and rotator cuff muscles.

FIGURE 8.43 Capsule.

FIGURE 8.44 Glenohumeral Joint Cartilage.

FIGURE 8.45 Osseous.

Sagittal Plane Checklist

(1) Rotator Cuff (Fig. 8.48)

The muscle bellies of the supraspinatus, infraspinatus, subscapularis, and teres minor muscles are well displayed starting on the medial-most sagittal images, and muscle atrophy associated with tendon tears or denervation can be identified on these images. It is not uncommon for atrophy of the teres minor to occur in isolation, without a tendon tear (often with no mass seen in the quadrilateral space). In the presence of supraspinatus, infraspinatus, and subscapularis tendon tears, the muscles may appear falsely atrophic on sagittal images due to retraction of the normal muscle belly medial to the plane of imaging. Therefore, any apparent atrophy on sagittal images should be confirmed on coronal and axial images, and the degree of retraction should be taken into consideration when evaluating the appearance of the muscle on sagittal images. Sagittal images are also useful for detecting and characterizing rotator cuff muscle strains and tears, and the presence of intramuscular cysts. Intramuscular cysts are analogous to paralabral and parameniscal cysts in that they are highly associated with

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tendon tears and may result from fluid entering the muscle via a one-way valve mechanism through a partial-thickness tendon tear.

FIGURE 8.46 Rotator Cuff.

FIGURE 8.47 Muscle.

The rotator cuff muscles are identified on medial sagittal images. Examination of consecutive images laterally shows transition of the muscles into myotendinous junctions and finally into the tendons proper. Tendon tears are seen as fluid signal on lateral sagittal images at the attachment sites of the cuff tendons on the greater tuberosity (supraspinatus anteriorly, and infraspinatus posteriorly) and lesser tuberosity (subscapularis). A fluid-filled tear of the rotator cuff seen on a lateral image can be precisely localized to the supraspinatus (anterior), conjoined (middle), or infraspinatus (posterior) tendon by identifying a tear distally at the greater tuberosity insertion and then following the level of the tear on consecutive lateral-to-medial images back to the myotendinous junction. When the rotator cuff is torn, both the anterior-to-posterior dimension (measured on sagittal images) and the medial-to-lateral dimension (measured on coronal images) of the tear are measured. Triangulating on supraspinatus, infraspinatus, and subscapularis tendon tears in all three planes is critical to proper identification and characterization of tears.

FIGURE 8.48 Rotator Cuff.

(2) Acromion/AC Joint (Figs. 8.49 and 8.50)

Spurring of the acromion and distal clavicle is identified on both the sagittal and coronal planes. Narrowing of the supraspinatus outlet between the acromion/clavicle and humeral head is caused by inferior distal clavicle spurring and anterior inferior acromial spurring. The most common acromial spurs are inferior spurs, arising from the anterior margin of the acromion at or near the coracoacromial ligament attachment,

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and broad-based undersurface spurs that extend along the majority of the acromial undersurface area. Inferior spurring of the distal clavicle from AC joint arthrosis can also narrow the outlet and impress upon the superior surface of the supraspinatus, leading to rotator cuff impingement and pain. Fluid and bursitis in the subacromial/subdeltoid space, often the result of impingement, are also characterized on sagittal images.

FIGURE 8.49 AC Joint.

The acromial shape (Bigliani types I–III; see discussion on Acromial Morphology and Impingement below) is determined on sagittal images. As a general rule, sagittal slices that show the insertion of the coracoacromial ligament on the anterior inferior acromion can be used to make this determination.

FIGURE 8.50 Acromion.

(3) Rotator Interval/Biceps Tendon (Including Coracohumeral Ligament and SGHL) (Figs. 8.50, 8.51, and 8.52)

On sagittal images through the glenoid, the biceps tendon origin at the biceps labral anchor is identified at or near the 12 o—clock position on the glenoid. The proximal biceps tendon is then followed distally from its superior glenoid origin by viewing consecutive images moving laterally through the rotator interval. The biceps tendon is visualized in cross-section just inferior to the supraspinatus tendon. Near the lateral aspect of the humeral head, the biceps tendon turns 90° and descends within

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the bicipital groove. The sagittal plane is useful in identification of tendinosis of the proximal biceps tendon both within the rotator interval and at the proximal bicipital groove. Complete tears with retraction of the biceps tendon into the bicipital groove are displayed as absence of the biceps tendon within the rotator interval.

FIGURE 8.51 Biceps Tendon.

Two other structures to identify in the rotator interval are the CHL and SGHL or SGL. The CHL originates at the lateral base of the coracoid and travels superior to the biceps tendon in the rotator interval. The SGHL originates at the anterior superior glenoid and courses along the inferior aspect of the biceps. Injuries to the CHL and SGHL manifest with thickening and increased signal. In the setting of acute injury, this appearance is compatible with CHL and SGHL sprain or tear. In the setting of chronic pain and limited range of motion, thickening of the CHL and SGHL suggests adhesive capsulitis, usually accompanied by thickening of the axillary pouch. Since the CHL and SGHL form a portion of the anterior superior portion of the joint capsule, they may be involved by capsulitis.

FIGURE 8.52 CHL and SGL.

(4) Glenoid Fossa (Fig. 8.53)

The most lateral sagittal image through the glenoid demonstrates the teardrop-shaped labrum marginating the circumference of the glenoid. When a labral tear is suspected from findings on axial and/or coronal images, high signal within the labrum on sagittal images is commonly visualized and is helpful in localizing and further characterizing the tear. Paralabral cysts are also depicted on sagittal images, and a neck of fluid signal extending from the cyst toward the labral tear is commonly

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identified. In patients with a history of recurrent dislocations, a sagittal image through the glenoid demonstrates deficiency of the anterior inferior glenoid, manifested as bony Bankart fractures through the anterior inferior glenoid or remodeling and attrition of the anterior inferior glenoid, resulting in an “inverted pear” appearance. Subchondral cystic changes in the glenoid are seen as focal high-signal areas within the glenoid, suggesting overlying chondromalacia.

FIGURE 8.53 Glenoid Fossa.

(5) Capsule (MGHL and IGHL) (Fig. 8.54)

The MGHL or MGL is identified on sagittal images intermediate between the glenoid and humeral head. The MGHL is visualized as a dark band of linear fibers just anterior to and paralleling the anterior labrum and inferior to the biceps tendon. The MGHL can be thickened and cord-like as part of the Buford complex. Superior labral tears occasionally extend into the MGHL, which has been termed a type 7 SLAP lesion. In addition, the anterior and posterior bands of the IGHL are visualized on the sagittal images that show the transition between the glenoid and humerus at the inferior aspect of the joint. Thickening and increased signal in the IGHL are indicative of capsular sprain or adhesive capsulitis.

FIGURE 8.54 MGL and IGL.

FIGURE 8.55 Sample Case.

Sample MRI Report, Shoulder Injury

Clinical Information: Shoulder pain, evaluate for rotator cuff tear

Technique: Fat-suppressed FSE proton-density coronal, sagittal, and axial scans; T2 non-fat-suppressed FSE coronal and sagittal images, GRE axial images

Findings: There is an interstitial tear of the posterior supraspinatus tendon extending into the conjoined portion of the tendon and anterior aspect of the infraspinatus tendon (Fig. 8.55A and B). At the anterior margin of the tear there is extension to the articular surface (Fig. 8.55C). On sagittal images, the interstitial tear measures 1.7 cm anterior to posterior (Fig. 8.55D), and on coronal images the interstitial tear measures 1.7 cm medial to lateral (see Fig. 8.55A). There is no evidence of supraspinatus or infraspinatus muscle atrophy (Fig. 8.55E).

There is a longitudinal oblique tear of the superior labrum extending preferentially into the posterior superior labrum, representing a posterior type 2 SLAP lesion (Fig. 8.55C and F). The remainder of the labrum is intact. The glenohumeral joint cartilage is intact. The joint capsule is normal.

The subscapularis tendon and biceps tendon are intact. There is no evidence of fracture. There is moderate subcortical

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cystic change in the posterior greater tuberosity subjacent to the rotator cuff tear (Fig. 8.55G).

There is mild cartilage thinning across the acromioclavicular joint compatible with degenerative arthrosis (Fig. 8.55H). There is a type 3 hooked acromion with a developing anterior inferior acromial spur containing mild reactive bone marrow edema (Fig. 8.55I and J). There is an os acromiale, without degenerative changes across the synchondrosis (Fig. 8.55K). There is mild subacromial/subdeltoid bursitis (see Fig. 8.55J).

Impression:

Interstitial tear extending from the posterior supraspinatus tendon to the anterior infraspinatus tendon. The anterior margin of the tear extends to the articular surface.
Type 2 SLAP tear extending primarily into the posterior superior labrum
Anterior inferior acromial spurring, os acromiale, and mild subacromial/subdeltoid bursitis

Normal Anatomy of the Shoulder

The shoulder girdle articulations include the glenohumeral joint, the AC joint, the scapulothoracic joint, and the sternoclavicular joint. The humeral head articulates with the relatively shallow glenoid fossa of the scapula and is dependent on muscular, ligamentous, and labral integrity for its stability (Fig. 8.56).

Osteology of the Shoulder

Several key structures make up the relevant osseous anatomy of the shoulder:

The clavicle connects the axial and appendicular skeletons of the upper extremity.⁴⁴ It is S-shaped in configuration, with a convex anterior border medially and a concave

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anterior border laterally. It is flattened and narrowed laterally and has a thicker cylindrical configuration medially. The clavicle articulates with the sternoclavicular joint medially and with the AC joint laterally (Fig. 8.57). The surfaces of the sternoclavicular joint are covered by fibrocartilage, and a fibrocartilaginous articular disk divides the joint into separate recesses.⁴⁵
The scapula consists of the scapular body, the scapular spine, the scapular neck, the acromion, the glenoid fossa, and the coracoid process.⁴⁴ The subscapular fossa represents the costal concave surface of the scapula. The dorsal convex surface of the scapula is separated into supraspinous and infraspinous fossae divided by the spine of the scapula. The suprascapular nerve is located in the supraspinous or spinoglenoid notch, at the superior border of the supraspinous fossa. Compression of the suprascapular nerve by a ganglion or entrapment, secondary to thickening of the suprascapular ligament, occurs in this location.
The tip of the coracoid projects anterior and lateral to the glenoid, with its origin superior and medial on the scapular neck. The coracoid is an important surgical landmark because neurovascular structures travel along its inferomedial surface.
The acromion is classified into several types according to its morphology:
- Type 1 (a flat or straight undersurface with a high angle of inclination)
- Type 2 (a curved arc and decreased angle of inclination)
- Type 3 (hooked anteriorly with a decreased angle of inclination)
- Type 4 (upward convexity of the inferior surface) (see also the discussion of the etiology of shoulder impingement syndrome)

FIGURE 8.56 ● A superior view of the scapula and the upper end of the humerus. The acromion and the coracoacromial ligament prevent upward displacement of the humeral head.

FIGURE 8.57 ● The hypointense articular disc is attached to the capsule and separates the two articular surfaces. Degenerative changes at the disc are associated with fibrillation, degeneration, or erosion of the joint articular cartilage.

The angle of inclination is formed by the intersection of a line drawn from the posteroinferior aspect of the acromion and the anterior margin of the acromion with a line formed by the posteroinferior aspect of the acromion and the inferior tip of the coracoid process.

At the lateral angle of the scapula is the glenoid cavity (glenoid fossa) with its supraglenoid and infraglenoid tuberosities. The glenoid version angle varies and may contribute to instability patterns of the shoulder.
The proximal humerus consists of the head, anatomic neck, and the greater and lesser tuberosities. The intertubercular or bicipital groove is located between the greater and lesser tuberosities along the anterior surface of the humerus. A decrease in the height of the medial wall of the lesser tuberosity and the presence of a supratubercular ridge of bone projecting from the superolateral aspect of the lesser tuberosity may predispose to instability of the biceps tendon within the groove, but dislocation or subluxation of the biceps tendon is extremely rare in the absence of a massive rotator cuff tear.

Glenohumeral Joint and Capsular Gross Anatomy

Pearls and Pitfalls

Glenohumeral Joint and Capsule

The BLC is classified as type 1, 2, or 3.
Type 1 BLC has the superior labrum firmly attached to the superior pole of the glenoid.
The superior labral sulcus in BLC types 2 and 3 should not be mistaken for the more anterior (anterosuperior quadrant) sublabral foramen (also known as the sublabral hole).
The IGHL contributes to the anterior labrum through its anterior band. The anterior band may be prominent and overlay a small or even absent anterosuperior labrum as a normal variation.
The MGHL may be cord-like, absent, thin, or redundant on MR.
The superior glenohumeral and coracohumeral ligaments stabilize the long head of the biceps tendon by forming the biceps pulley or sling in the rotator cuff interval.

The anatomic configuration of the glenohumeral joint allows a greater range of motion than any other joint in the body. Glenohumeral motion depends on the congruity of the humeral head, the glenoid, the rotator cuff mechanism, and the deltoid

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muscle. Glenohumeral joint version or humeral retroversion projects the axis of the humeral head joint surfaces 25° to 40° from the coronal plane, whereas the glenoid surface is retroverted 4° to 12° with respect to the scapula.⁴⁶ The glenoid labrum, wedge-shaped in cross-section, is a ring of fibrous tissue with transitional fibrocartilage attached to the margin of the glenoid cavity.⁴⁷ Labral tissue deepens the depression of the glenoid fossa and enlarges the glenohumeral socket contact area (Figs. 8.58 and 8.59).

Glenoid Labrum

The glenoid labrum is the fibrous attachment of the glenohumeral ligaments and capsule to the glenoid rim (Fig. 8.60).⁴⁸ It is ovoid, conforming to the essentially kidney-shaped glenoid rim. The normal glenoid labrum is 3 mm high and 4 mm wide, but its size, shape, and configuration vary considerably. The anterior glenoid labrum provides the major area of attachment for the anterior band of the IGHL.³⁷ The MGHL is considerably more variable but may also contribute fibers to the more superior aspects of the anterior glenoid labrum as it approaches the biceps tendon.

FIGURE 8.58 ● The lateral aspect of the scapula shows the pear-shaped glenoid fossa. The positions of the supraspinatus, infraspinatus, and subscapular fossae are shown.

The glenoid fossa and rim are divided into six quadrants (Fig. 8.61). Because sagittal images may be obtained from either the right or the left shoulder, only descriptive locations should be used, as indicated in Figure 8.61A and B. The superior pole is often referred to as the 12 o—clock position and the inferior pole as the 6 o—clock position, because these positions remain constant for both right and left shoulders. The articular cartilage of the central glenoid is normally thin and should not be confused with chondromalacia.⁴⁹^,⁵⁰

FIGURE 8.59 ● The scapular component of a disarticulated shoulder joint. The relations and internal features of the joint are seen.

FIGURE 8.60 ● Glenohumeral capsular anatomy. A, acromion; AB, anterior band of IGHL; AL, anterior labrum; AP, axillary pouch of IGHL; B, biceps tendon; C, coracoid; IGLC, IGHL complex; MGL, middle glenohumeral ligament; PC, posterior capsule; PL, posterior labrum; S, supraspinatus tendon; SGL, superior glenohumeral ligament; Sub, subscapularis tendon.

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Biomechanics and Vascularity of the Labrum

The glenoid labrum makes up approximately 50% of the total depth of the glenoid socket.⁵¹^,⁵² It also increases the glenoid surface in the vertical and horizontal planes to better accommodate the humeral head. The strength of the attachment between the fibrous labrum and the bony glenoid increases with age, and in cases of acute dislocations disruption of the labral glenoid connection (Bankart lesion) is more likely to occur in younger individuals (under 25 years of age).

In a cadaveric study by Karzel et al., the posteroinferior labrum was shown to absorb the majority of load in 90% of shoulder abduction with an applied compressive load.⁵²^,⁵³ This may explain why the posterior labrum is strong and usually more triangular in shape compared with the anterior labrum. Jobe demonstrated posterior superior labral impingement in cadaver shoulders in 70° of abduction and maximum external rotation.⁵⁴

Vascularity in the superior and anterosuperior labrum segments is decreased in comparison with the posterosuperior and inferior segments. This decreased vascularity may be responsible for the development of superior labral degeneration with increasing age and may make the labrum more susceptible to SLAP lesions.⁵⁵

In general, the labrum is more firmly attached inferior to the epiphyseal line and is continuous with the cartilaginous surface of the glenoid. De Palma demonstrated that with increasing age and degeneration, separation of the fibrous labrum from the cartilaginous glenoid surface occurs throughout the periphery of the glenoid.⁵⁶ This is evident on arthroscopy in older patients. Subtle tears of the anterior inferior labrum are best demonstrated on MR scans performed with the shoulder abducted and in external rotation, which displays the IGHL and IGLLC.

FIGURE 8.61 ● Six quadrants of the glenoid. MR units may default to a display of sagittal images of the shoulder from a left-shoulder perspective even if the right shoulder was imaged. It is accepted practice to describe a lesion by its quadrant. The description of the superior pole as 12 o—clock and the inferior pole as 6 o—clock is accurate for both right and left shoulders. To avoid mistaking right for left, however, use of the 3-o—clock or 9-o—clock positions should be avoided. (A) Illustration using a right-shoulder perspective. (B) Left-shoulder perspective. S, superior; AS, anteroposterior; AI, anteroinferior; I, inferior; PS, posterosuperior; PI, posteroinferior.

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Labral Types

There are several normal variations in labral morphology. Initially, Detrisac and Johnson described five types:⁴⁸

A superior wedge labrum with the labrum firmly attached anteriorly, posteriorly, and inferiorly. Separation (a sublabral foramen) between the glenoid and superior anterior labrum occurs as a normal variation (Fig. 8.62).
A posterior wedge-shaped labrum in which the superior labrum is smaller and more firmly attached to the superior glenoid. The posterior labrum overlaps the articular surface of the glenoid and has a free central border (Fig. 8.63).
An anterior wedge labrum, which is characterized by a large anterior band of the IGHL that replaces or covers a small anterior labrum (e.g., the Buford complex) (Fig. 8.64)
A labrum with the characteristics of both a superior and anterior wedge labrum (Fig. 8.65)
A meniscal or meniscoid labrum, which has a circumferential free central margin with relatively symmetric anterior and posterior labral tissue on cross-section above the epiphyseal line (Fig. 8.66). Although a meniscoid labrum may be seen at the level of the biceps labral complex, it is unusual. An unattached labral free edge also present at the level of the inferio labrum is rare.

This original classification was subsequently simplified into two labral types:⁵²

A labrum that is attached to the glenoid in its periphery through a fibrocartilaginous transitional zone. Above the physeal line or equator, the labrum may be mobile along its central border, with a meniscoid appearance.
A labrum that is entirely secured to the glenoid both peripherally and centrally

Although a meniscoid-like labrum has been reported with a 10% incidence below the equator, the anterior inferior glenoid labrum is rarely visualized on MR images with fluid undermining its glenoid attachment.⁵⁷ A classification of anterior labral anatomy has also been proposed based on the relative contribution of the glenohumeral ligaments.⁵⁸ In this classification, a type 1 labrum (incidence of 34%) is the IGHL labrum. A type 2 labrum (11%) is the SGHL and MGHL labrum, and a type 3 labrum (55%) represents the combined glenohumeral ligament labrum. We recommend classifying the labrum according to the three different types of attachment of the BLC, as discussed below.

Hypertrophy of the posterior glenoid labrum is associated with posterior glenoid (rim) hypoplasia (Fig. 8.67). Posterior humeral subluxation and an eccentric posterior glenoid fossa wear pattern may develop. Posterior glenoid dysplasia may be graded as mild, moderate, or severe. Retroversion of the osseous glenoid is greater than seen with measurements performed at the chondrolabral portion of the glenoid, the reverse of the normal shoulder glenohumeral joint. Posterior subluxation is a function of the glenoid retroversion, which cannot be compensated for by an enlarged or hypertrophied labrum. This excessive retroversion produces posterior instability.

Long Head of the Biceps Tendon and Biceps Labral Complex

The long head of the biceps tendon (LHBT) attaches to the superior glenoid at the supraglenoid tubercle. It exits the shoulder joint through a hiatus between the subscapularis and supraspinatus tendons. The LHBT, with the BLC (Fig. 8.68), centralizes and stabilizes the joint, as does the rotator cuff. Multiple fine synovial bands, referred to as the vincula biceps (Fig. 8.69), may surround the LHBT at the proximal entrance of the intertubercular groove and pass from the biceps tendon to the surrounding synovium and capsule.⁵⁰

The LHBT has four attachments (Fig. 8.70):

The supraglenoid tubercle
The posterior superior labrum
The anterior superior labrum
Extra-articular fibers that attach to the lateral edge of the base of the coracoid process

Rarely, the biceps presents with a large synovial mesentery attached to the articular side of the supraspinatus tendon. Another rare variation is the bifid biceps (Fig. 8.71), in which one portion of the biceps attaches to the supraglenoid tubercle (the normal attachment) and the second portion attaches to the rotator cuff cable or ridge. The rotator cuff cable is a capsular tissue thickening of articular side cuff tissue that is oriented perpendicular to the biceps tendon.

Above the epiphyseal line (i.e., the junction of the upper and middle thirds of the glenoid body fossa), the attachment of the glenoid labrum is variable. The superior labrum does have a role in the stability of the glenohumeral joint and functions in conjunction with the biceps tendon (Figs. 8.72 and 8.73), with which it is contiguous (the BLC). Inferior to the epiphyseal line the labrum is continuous with the glenoid articular cartilage and serves as the insertion site for the IGHL. It is the superior and anterosuperior portions of the labrum that can be variably attached to the glenoid.⁵⁹ There are three different types of attachment of the BLC to the glenoid (Fig. 8.74):

Type 1 BLC (see Fig. 8.74A; Fig. 8.75): The BLC is firmly adherent to the superior pole of the glenoid. There is no sublabral foramen in the anterosuperior quadrant. This type of BLC attachment corresponds to the morphology of the BLC in the posterior wedge or type B labrum.
Type 2 BCL (see Fig. 8.74B; Fig. 8.76): The BLC is attached several millimeters medial to the sagittal plane of the glenoid. The superior pole of the glenoid continues its hyaline cartilage surface under the labrum. This configuration has a small sulcus at the superior pole of the glenoid that may be continuous with the more anterior variation of a sublabral foramen and communicate with the subscapularis bursa.⁶⁰ This type of BLC

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attachment, with a triangular superior labrum and a free central edge, is associated with both the superior wedge labrum and the combined superior and anterior wedge labrum.
Type 3 BLC (see Fig. 8.74C; Fig. 8.77): The labrum is very meniscoid in shape and has a large sulcus that projects under the labrum and over the cartilaginous pole of the glenoid. It is seen in the meniscal or meniscoid (type E) labrum.

FIGURE 8.62 ● (A) The superior wedge labrum is characterized by a firm attachment of the anterior, posterior, and inferior labrum to the glenoid articular surfaces, with no free central edge. The superior labrum is, however, triangular in cross-section and its central free edge is separated and overlaps the articular cartilage at the biceps labral complex. An associated anterosuperior sublabral foramen is common in this labral type. (B) A superior wedge labrum is shown firmly attached to the anterior and posterior glenoid rim. The anterior band of the IGL blends with the labrum to form one structure near the equator of the anterior glenoid rim. A sublabral foramen may exist in the anterosuperior quadrant in a superior wedge labrum. (C) A superior wedge labrum in which the free central edge of the superior labrum forms the biceps labral sulcus of the biceps labral complex type 2. A sublabral foramen is an associated finding in the anterosuperior quadrant. Note the firm attachment of the anterior labrum (below the equator), posterior labrum, and inferior labrum.

FIGURE 8.63 ● (A) The posterior wedge labrum is characterized by a posterior wedged-shaped labrum attached only at its periphery. A probe can be passed between the articular cartilage and the overlapping posterior labrum. When present, a well-defined posterior band of the IGL may overlap a relatively small posterior labrum, analogous to the anterior wedge labrum that occurs with a prominent anterior band. Anteriorly, superiorly, and inferiorly the labrum is firmly attached to the glenoid so that a probe cannot be passed between the glenoid articular surface and the labrum. The superior labrum is smaller than in the superior wedge labrum and is more firmly attached to the articular cartilage of the superior glenoid, as seen in the type 1 biceps labral complex (BLC 1). (B) A prominent or thick posterior band of the inferior glenohumeral ligament (IGL). This may be associated with a posterior wedge labrum. Normally the posterior band is not as well defined as the anterior band of the IGL. The posterior labrum may be relatively small underneath a prominent posterior band. Sagittal FS PD FSE image. (C) A posterior wedge labrum with free central edge of posterior labrum overlapping the posterior glenoid rim. From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999.

FIGURE 8.64 ● (A) The anterior wedge labrum is firmly attached to the glenoid articular surface inferiorly, posteriorly, and superiorly. The anterior band (AB) of the IGHL, however, is thick and prominent and covers or overlaps the anterior labrum anterior to the anterior glenoid rim. The anterior wedge labrum may be further defined into two subtypes. The first subtype has a small anterior superior labrum, as already described, whereas the second subtype has an absent anterosuperior labrum underneath or deep to the prominent anterior band. Deep to the prominent anterior band of the IGHL, the anterior rim articular cartilage may taper and become thin peripherally. (B) The anterior band of the IGHL overlapping a small anterior labrum. Axial T1-weighted MR arthrogram.

FIGURE 8.65 ● (A) Another labral variation is a combination of features of the superior wedge labrum and the anterior wedge labrum. A prominent or large anterior band of the IGL overlaps and may replace a small anterosuperior labrum. Superiorly the labrum has a free central margin and overlaps the glenoid articular cartilage, unlike the firmly attached superior labrum found in the anterior wedge labrum. There are three subtypes of this variant. In the first subtype there is no anterosuperior labrum. The second subtype has a small anterosuperior labrum firmly attached to the glenoid articular cartilage. In a third subtype the superior labrum and the anterior band of the IGL may blend together to form a free margin. This unattached free margin extends from the posterosuperior glenoid to the anteroinferior glenoid without an associated sublabral foramen anterosuperior. (B) Unattached free margin of superior labrum in a combination-type labrum.

FIGURE 8.66 ● Meniscoid labrum with a circumferential free edge. This configuration is rare, and it is unusual to visualize an attached free margin involving the inferior labrum on MR studies. Fluid between the inferior labrum and glenoid articular cartilage on coronal MR images thus represents labral tearing. (A) Lateral color illustration with probing of the free labral margin and (B) corresponding gross specimen of meniscoid labrum.

FIGURE 8.67 ● (A) Color axial section of normal posterior glenoid rim (top) compared to severe dysplastic posterior glenoid rim (bottom) with compensatory posterior labral hypertrophy. Axial T1 FSE (B) and axial FS PD FSE (C) images with severe posterior glenoid hypoplasia with thickened glenoid articular cartilage and posterior glenoid labral hypertrophy.

FIGURE 8.68 ● The biceps tendon (BT) contributes to the superior anterior labrum (AL) and the superior posterior labrum (PL) in the BLC. One component of the LHBT attaches to the supraglenoid tubercle. Extra-articular fibers attach to the lateral edge of the base of the coracoid process. The intra-articular portion of the LHBT is oriented at an approximate right angle to the surface of the glenoid (G). HH, humeral head; SGL, superior glenohumeral ligament.

FIGURE 8.69 ● Vincula biceps extending anterior to the biceps tendon. Axial FS PD FSE image.

FIGURE 8.70 ● Origin of the long head of the biceps with idealized attachments to the posterior labrum, supraglenoid tubercle, anterior glenoid labrum, and base of the coracoid. (Based on

Detrisac DJ, Johnson LL. Biceps and subscapularis tendons. In: Detrisac DJ, Johnson LL eds. Arthroscopic shoulder anatomy: pathologic and surgical implications. Thorofare, NJ: Slack, 1986:21-34.

)

Rodosky et al.⁶⁰ have demonstrated that tension placed on the biceps tendon stabilizes the humeral head. Although significant lesions of the BLC have been noted in traumatic dislocations, an incomplete or meniscoid attachment of the superior labrum may represent a variation of normal anatomy. Type 2 and type 3 BLC attach primarily to the supraglenoid tubercle, creating a synovium-lined sulcus (the biceps labral sulcus) at the superior aspect of the glenoid.⁵⁹^,⁶¹ This normal sulcus should not be mistaken for a SLAP lesion (Fig. 8.78). The biceps labral sulcus is located superiorly, whereas a sublabral foramen is positioned in the anterosuperior quadrant between the equator of the glenoid anteriorly and the superior pole of the glenoid.

Glenohumeral Ligaments

The glenohumeral ligaments (superior, middle, and inferior) are thickened bands of the anterior joint capsule with attachments to both glenoid margins and the proximal humerus (Fig. 8.79).⁴⁸ The normally lax glenohumeral ligaments can be thought of as check reins on extremes of motion for the glenohumeral joint.⁴⁶ The importance of joint compression and stabilization by the rotator cuff, as well as the maintenance of congruency and adhesion of the glenohumeral surfaces, cannot be overemphasized.

Inferior Glenohumeral Ligament

The IGHL or IGL is the largest and most important of the glenohumeral ligaments. The IGHL consists of anterior and posterior bands and an axillary

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pouch that attaches to the inferior two thirds of the entire circumference of the glenoid by means of the labrum (Figs. 8.80 and 8.81).³⁷^,⁶² The IGHL is lax in adduction and taut in abduction and external rotation (Fig. 8.82). As it tightens with increasing abduction, the anterior and posterior bands move superiorly with respect to the humeral head. At 90° of abduction, the IGHL is the primary restraint for anterior and posterior dislocations.⁶³ The axillary pouch is located between the anterior and posterior bands and, like the anterior and posterior bands, is lax with the arm by the patient—s side in the adducted position. The axillary pouch extends inferior to the body of the glenohumeral joint as a redundancy of thickened capsular tissue best visualized on coronal oblique images.

FIGURE 8.71 ● (A) Double biceps with two tendons inserting into the supraglenoid tubercle. (From

DePalma AF. Surgery of the shoulder, 3rd ed. Philadelphia: JB Lippincott, 1983.

) A bifid biceps tendon is shown in its extra-articular course on an axial T1-weighted arthrogram (B) and a corresponding gross dissection (C).

FIGURE 8.72 ● (A) Removal of part of the shoulder joint capsule reveals the intracapsular but extrasynovial tendon of the long head of the biceps brachii. (B) Corresponding anterior coronal (coronal oblique) FS MR arthrogram shows the course of the LHBT.

FIGURE 8.73 ● (A) The biceps origin can be located on a T2*-weighted coronal image. The glenoid origin of the long head of the biceps (b) is shown, as are the attachments to the anterior labrum (l) and superior glenoid (g). The biceps courses laterally and exits the joint between the supraspinatus (s) and subscapularis tendons. The axillary pouch (ap) of the IGHL is indicated. The tendon of the long head of the biceps enters the intertubercular groove under the transverse ligament. (B) Gross dissection demonstrates the anterior band (AB) and posterior band (PB) of the IGHL complex. This surgical view is from the perspective of viewing inferiorly into the axillary pouch. The anterior (A), posterior (P), and humeral head (HH) are indicated. Both the biceps tendon and posterior band contribute to the posterior labrum.

The IGLC originates from either the glenoid labrum or glenoid neck and inserts onto the humeral neck at the periphery of the articular margin.⁵⁹ In the right shoulder, the origin of the anterior band is located near the 3 o—clock (2 to 4 o—clock) position on the glenoid, and the origin of the posterior band is near the 9 o—clock (7 to 9 o—clock) position. The anterior band forms the anterior labrum at the medial attachment of the IGHL to the glenoid. Because of the important role of the IGLC in forming the anterior labrum, this relationship has also been referred to as the inferior glenohumeral ligament labral complex (IGLLC). The posterior band contributes to the formation of the posterior labrum. The IGLC inserts onto the anatomic neck of the humerus in one of two configurations, either as a collar-like attachment or as a V-shaped attachment.³⁷^,⁶¹ The IGLC functions as a hammock, cradling the humeral head with increasing abduction. Different portions of the complex support the humeral head both anteriorly and posteriorly during 90° of abduction with internal and external rotation. With internal rotation of the abducted arm, the posterior band of the IGLC fans out and supports the humeral head posteriorly, with the anterior band moving under the humeral head. When the abducted arm is in external rotation, the anterior band of the IGLC fans out and supports the humeral head anteriorly, while the posterior band stabilizes the joint inferiorly. Thus, the IGLC has a role in anterior-posterior and superior-inferior stability, as represented by the function of its two bands and intervening axillary pouch. The IGLC and its components (the anterior band, axillary pouch, and posterior band) have been shown to be histologically present in all specimens studied by O—Brien et al.³⁷ As discussed earlier, the anterior and posterior bands can be accentuated by external and internal rotation of the arm, respectively.

Middle Glenohumeral Ligament

The MGHL or MGL attaches to the anterior aspect of the anatomic neck of the humerus, medial to the lesser tuberosity (Fig. 8.83).⁴⁸ It arises from the glenoid by way of the labrum and scapular neck. It passes across the subscapularis tendon and can be identified between the subscapularis tendon and the anterior labrum or anterior band of the IGHL (Fig. 8.84). The foramen of Weitbrecht is located between the superior and middle glenohumeral ligaments, and the foramen of Rouviere is located between the middle and inferior glenohumeral ligaments (Fig. 8.85). Of the three glenohumeral ligaments, the MGHL demonstrates the greatest variation in size and thickness.⁵⁹ Wall and O—Brien⁶¹ found that it was absent in up to 27% of specimens, a finding consistent with the work of De Palma,⁵⁶ who originally described a poorly defined or absent MGHL in 30% of shoulders studied. The MGHL, which may present as thin ligamentous tissue or appear cord-like and as thick as the biceps tendon, has a role in the stability

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of the shoulder joint from 0° to 45° of abduction.⁵⁹ Along with the subscapularis tendon and the superior part of the IGHL, the MGHL contributes to anterior stability at 45° of abduction.⁶⁴ In the lower and middle ranges of abduction, the MGHL limits external rotation. The MGHL has also been shown to have a secondary role in anterior stability of the shoulder in 90° of abduction when the anterior band of the IGHL is cut.⁶⁵ Inferior translation of the abducted and externally rotated shoulder is limited as a secondary restraint function of the MGHL. With internal rotation the MGHL demonstrates a more vertical orientation, and with external rotation it assumes a more horizontal orientation (elongation of the MGHL).

FIGURE 8.74 ● Biceps labral complex (blc) attachments. (A) In type 1, the BLC is firmly attached to the superior pole of the glenoid. m, middle glenohumeral ligament; ca, coracoacromial ligament. (B) In type 2, the biceps is attached to the superior labrum lateral to the superior glenoid. A fluid-filled sublabral sulcus (black arrow) is formed at the superior pole of the glenoid. Intermediate-signal-intensity cartilage (white arrow) of the glenoid extends medially over the superior glenoid surface. (C) Meniscoid labrum (large arrow) associated with a large sulcus (small arrow), which extends underneath the meniscoid superior labrum. FS T1-weighted coronal oblique MR arthrography images.

FIGURE 8.75 ● (A) Type 1 BLC with superior labrum firmly attached to the superior pole of the glenoid. The type 1 BLC may be seen in the posterior wedge labrum and the anterior wedge labrum. (B) Coronal FS PD FSE image showing a type 1 BLC with a firm attachment of the superior labrum to the articular cartilage of the superior pole of the glenoid.

FIGURE 8.76 ● (A) Type 2 BLC with a normal sulcus or separation of the free edge of the superior labrum from the superior pole of the glenoid. A type 2 BLC would be seen in the superior wedge labrum and combination superior and anterior wedge labrum. (B) Type 2 BLC with a fluid-filled sulcus separating the superior labrum from the adjacent articular cartilage of the glenoid. The superior labrum is triangular in cross-section. The sulcus may become more prominent with external rotation; however, its medial-to-lateral separation should not exceed 5 mm. Coronal MR arthrogram.

FIGURE 8.77 ● (A) Type 3 BLC with meniscoid superior labrum and a free central margin. (B) Coronal PD FSE image illustrating a large meniscoid superior labrum in a type 3 BLC.

Capsular Insertion Types (Relative to Ighl and Mghl)

Zlatkin et al. identified three types of capsular insertions: type 1 inserts near the anterior labrum, and types 2 and 3 insert more broadly or medially on the scapular neck.⁶⁶ These types of insertions represent normal variations in the size and morphology of the subscapularis recess and are dependent on the rotation of the shoulder. They are not the result of stripping of the capsule (Fig. 8.86). With internal rotation, the recess is large and the capsule appears to insert more medially on the scapular neck. Although it is unlikely that the anterior pouch in a type 3 capsular insertion predisposes to anterior humeral subluxation or dislocation in a created potential space, there may be stretching of the capsular complex in patients with a history of anterior dislocations. However, on MR images it may be difficult to appreciate stretching of the IGHL in the absence of tear or avulsion. Sperer and Wredmark,⁶⁷ using saline infusions and pressure/volume measurements during arthroscopic shoulder surgery, have shown that capsular elasticity and joint volume do not contribute to anterior shoulder instability.⁶⁷ Recurrent dislocations do not produce irreversible capsular distention.

The key components of the IGHL are, in fact, assessed below the level of the subscapularis recess on axial images. The MGHL, however, is visualized at the mid-glenohumeral joint level posterior to the subscapularis tendon.

Superior Glenohumeral Ligament

The SGHL or SGL is the smallest of the glenohumeral capsular structures.⁴⁸ The SGHL originates from the upper pole of the glenoid cavity and base of the coracoid process and is attached to the MGHL, to the biceps tendon, and to the labrum (Fig. 8.87). It inserts just superior to the lesser tuberosity in the region of the bicipital groove.⁵⁹ A normal foramen or opening exists between the SGHL and MGHL, allowing communication with the subscapularis bursa.⁶⁸ The SGHL has been reported to be present in 90% to 97% of shoulders.³⁷^,⁵⁶ The size of the SGHL varies, ranging from a thin thread-like thickening of the capsule to a more substantial ligament. The SGHL is closely related to the extra-articular coracohumeral ligament. The coracohumeral ligament (see below) originates in the lateral aspect of the coracoid and inserts on the greater tuberosity. The SGHL and the coracohumeral ligament contribute to the stabilization of the glenohumeral joint and prevent posterior and inferior translation

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of the humeral head. Warner et al. showed that the SGHL was well developed in 50% of shoulders.⁶⁹ When present and well formed (developed), the SGHL represents the primary capsuloligamentous restraint to inferior translation of the unloaded, abducted shoulder joint.⁵⁹^,⁶⁹ Both the SGHL and the CHL have an important role in forming the biceps pulley of the rotator cuff interval.

FIGURE 8.78 ● Type 2 BLC with normal superior sulcus on coronal FS PD (A) and axial PD (B) images with intra-articular contrast. (C) Corresponding axial color cross-section demonstrating the sulcus of a type 2 BLC. This sulcus should not be mistaken for detachment of the superior labrum.

FIGURE 8.79 ● (A) An oblique anterior view of the scapula and lateral part of the clavicle. The bones have been separated to show the articular surfaces of the AC joint and the sites of attachment of the coracoclavicular ligament. (B) The glenoid attachments of the anterior capsular ligaments including the superior glenohumeral ligament (SGHL or SGL), the middle glenohumeral ligament (MGHL or MGL), the anterior band of inferior glenohumeral ligament (IGHL or IGL), and the axillary pouch of IGHL. (C) Glenohumeral capsular and ligament attachments in anterior, posterior, and medial humeral projections. (A–C: Based on

Detrisac DJ, Johnson LL. Biceps and subscapularis tendons. In: Detrisac DJ, Johnson LL eds. Arthroscopic shoulder anatomy: pathologic and surgical implications. Thorofare, NJ: Slack, 1986:21–34.

)

FIGURE 8.80 ● (A) The axillary pouch of the IGHL is seen on a T1-weighted sagittal MR arthrogram. Arrows and ap, axillary pouch of IGHL; b, biceps tendon; s, supraspinatus tendon; sub, subscapularis tendon. (B) The IGHL complex. An arthroscopic photograph shows the anterior band (AB) and axillary pouch (AP) components of the inferior glenohumeral ligament (IGL) complex. The inferior pole of the glenoid (IP) and the anatomic neck attachments of the IGL complex (AN) are shown as viewed from the axillary pouch. HH, humeral head.

FIGURE 8.81 ● (A) The anterior band (ab) and posterior band (pb) of the IGHL (curved arrows) extend from the glenoid origin to the humeral attachment, as seen on an enhanced T1-weighted sagittal (oblique) image. C, coracoid; H, humeral head. (B) On a gross shoulder specimen, the superior course of the anterior band (AB) of the IGHL is identified (triangular marker). The glenoid (G) and humeral head (HH) are also identified.

FIGURE 8.82 ● A gross shoulder specimen illustrates the structure of the inferior glenohumeral ligament (IGL) complex. With abduction of the humerus, the IGL structures are more prominent and taut in position. Coronal oblique MR images routinely show the lax axillary pouch of the IGL when the humerus is in the adducted position. Curved arrow, axillary pouch; AB, anterior band; AL, anterior labrum; HH, humeral head; PB, posterior band; PL, posterior labrum.

FIGURE 8.83 ● T2*-weighted axial images at (A) and below (B) the level of the subscapularis show the normal middle glenohumeral ligament (MGL; curved arrows), its medial origin from the glenoid and neck of the scapula, and its attachment to the lesser tuberosity. Small straight arrows, anterior labrum. (C) A T1-weighted sagittal oblique arthrogram shows the attachment of the MGL (mgl) to the anterior superior glenoid labrum (asl). The MGL arises from the labrum below the superior glenohumeral ligament and from the neck of the scapula. The humeral attachment of the MGL is located medial to the lesser tuberosity. Normal variants of the MGL include the ligament arising only from the labrum or having no attachment to it. pb, posterior band of IGL; s, supraspinatus tendon. (D) Arthroscopic view of the middle glenohumeral ligament (MGL) anterior to the anterior labrum (AL) and posterior to the subscapularis tendon (Sub). An anterior superior quadrant sublabral foramen (curved arrow) exists as a normal variant. HH, humeral head.

FIGURE 8.84 ● An arthroscopic photograph shows the anterior band (AB) of the IGHL. The subscapularis tendon (arrow) is located beneath the middle glenohumeral ligament (MGL) and is not directly seen. G, glenoid; HH, humeral head.

FIGURE 8.85 ● Normal foramen of Weitbrecht (solid curved arrow) is shown between the middle glenohumeral ligament (MGL) and the superior glenohumeral ligament. The foramen of Rouviere (open curved arrow) is located between the MGL and the inferior glenohumeral ligament (IGL).

FIGURE 8.86 ● Normal variation in morphology of the subscapularis bursa is seen with (A) internal rotation and (B) external rotation on gadolinium-enhanced T1-weighted axial images. The subscapularis bursa has the appearance of a type 3 capsular insertion (long black curved arrow) in internal rotation (short black curved arrow) and a type 1 capsular insertion (long curved white arrow) in external rotation (short black curved arrow). Gadolinium contrast between the posterior band of the IGHL and the posterior labrum (large straight black arrow) and gadolinium contrast lateral to the humeral head in the subacromial bursa (small straight black arrows) are indicated. (C) A transverse section at the level of the humeral head shows the relations of the glenohumeral joint.

FIGURE 8.87 ● (A) The superior glenohumeral ligament (SGHL) is seen on an enhanced T1-weighted axial image above the level of the coracoid. The extra-articular coracohumeral ligament (CH) and intra-articular SGHL are closely related. The middle portion of the CH crosses the SGHL. The SGHL is oriented perpendicular to the middle glenohumeral ligament (MGL) as shown. BT, biceps tendon; G, glenoid; H, humeral head. (B) Arthroscopic photograph (posterior view) showing the lateral location of the biceps (B) relative to the superior glenohumeral ligament (SGHL). HH, humeral head; Sub, subscapularis tendon.

Synovial Recesses

De Palma described six anatomic types of the capsule, based on the topographic arrangements of the synovial recesses with respect to the glenohumeral ligaments (Fig. 8.88).³⁷^,⁵⁶ MGHL morphology determines the type of synovial recess (see Fig. 8.85 and 8-88; Fig. 8.89).⁶¹ The six types of synovial recesses are best assessed on sagittal oblique images in which the MGHL and IGHL can be identified (Figs. 8.90 and 8.91).

Other Capsuloligamentous Structures

Coracohumeral Ligament

The CHL, which originates on the lateral aspect of the base of the coracoid inferior to the origin of the coracoacromial ligament, courses in a horizontal or transverse direction to its insertion on the greater tuberosity on the lateral aspect of the bicipital groove (Fig. 8.92).⁵⁹ At the anterior superior aspect of the shoulder, the coracohumeral ligament overlies and is superficial to the SGHL (Fig. 8.93). The CHL has been reported to contribute, along with the SGHL, to the restraint of inferior translation in external rotation in the abducted shoulder. However, Cooper et al.⁷⁰ have characterized it as a folded portion of the glenohumeral joint capsule in the interval between the subscapularis and supraspinatus, without contribution to glenohumeral joint stability.⁷⁰ The CHL has both medial and lateral fibers. The medial fibers contribute to the biceps pulley and assist in the stabilization of the LHBT (Fig. 8.94).⁷¹ Sagittal images through the mid-portion of the rotator interval demonstrate the initial formation of the biceps pulley with a T-shaped junction between the CHL (forming the roof) and SGHL (forming the floor) of the pulley or biceps sling (Fig. 8.95). The anterior aspect of the biceps sling represents the confluence of the CHL and SGHL, which provides the restraint to medial subluxation of the biceps tendon.

Posterior Capsule

The posterior capsule includes the capsule posterior to the biceps tendon and superior to the posterior band of the IGHL. This represents the thinnest portion of the capsule. The posterior capsule has a role in limiting both posterior and anterior translation of the glenohumeral joint.⁵⁹^,⁷² With an intact anterior

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capsule, posterior dislocation does not occur even with division of the posterior capsule. The posterior capsule is torn in reverse HAGL lesions.⁷³

FIGURE 8.88 ● Six arrangements of synovial recesses (i.e., joint capsule variations, arrows) are described by DePalma. Type 1: One synovial recess exists above the middle glenohumeral ligament. Type 2: One synovial recess exists below the middle glenohumeral ligament. Type 3: Two synovial recesses exist, with a superior subscapular recess above the middle glenohumeral ligament and an inferior subscapular recess below the middle glenohumeral ligament. Type 4: No middle glenohumeral ligament is present, and one large synovial recess exists above the inferior glenohumeral ligament. Type 5: The middle glenohumeral ligament exists as two small synovial folds. Type 6: Complete absence of synovial recesses. (From

DePalma AF. Surgery of the shoulder. Philadelphia: JB Lippincott, 1983.

)

FIGURE 8.89 ● (A) Small synovial recesses above and below the middle glenohumeral ligament. (B) Large synovial recess above the middle ligament. This recess may be interpreted erroneously as a rent in the capsule. (From

DePalma AF. Surgery of the shoulder, 3rd ed. Philadelphia: JB Lippincott, 1983

, with permission.)

FIGURE 8.90 ● A single type 4 synovial recess. T1-weighted sagittal oblique arthrogram displays absence of the middle glenohumeral ligament, resulting in one large synovial recess above the inferior glenohumeral ligament. S, supraspinatus tendon; SR, synovial recess; s, subscapularis tendon.

FIGURE 8.91 ● Sagittal MR image with two synovial recesses. Synovial recesses are present above and below the middle glenohumeral ligament. SR, synovial recess; S, subscapularis; mgl, middle glenohumeral ligament; ab, anterior band; straight arrow, subscapularis tendon; small curved arrow, superior course of mgl; large curved arrow, superior course of anterior band.

FIGURE 8.92 ● Coronal PD-weighted images showing (A) the lateral band of the coracohumeral ligament inserting on the greater tuberosity and anterior border of the supraspinatus and (B) the medial band of the coracohumeral ligament inserting on the lesser tuberosity, the superior fibers of the subscapularis, and the transverse ligament.

FIGURE 8.93 ● The coracohumeral ligament (CHL) inserts on either side of the bicipital groove rotator interval. The CHL and the superior glenohumeral ligament help stabilize the biceps tendon by forming a biceps pulley.

Rotator Cuff

The supraspinatus, infraspinatus, teres minor, and subscapularis muscles constitute the rotator cuff (Figs. 8.96, 8.97, 8.98). Their primary function is to centralize the humeral head, limiting superior translation during abduction. The rotator cable, a condensation of articular side capsular tissue, extends from anterior to posterior across the supraspinatus and infraspinatus insertions (Fig. 8.99).⁵⁰ The rotator crescent, which spans the conjoined tendon insertion lateral to the cable, is the area at risk for most rotator cuff tears. The supraspinatus, infraspinatus, and teres minor tendons insert on the greater tuberosity, whereas the subscapularis tendon inserts on the lesser tuberosity:

The infraspinatus muscle (Fig. 8.100) is bipennate and has a median raphe,⁷⁴ which at surgery may be mistaken for the border between the infraspinatus and teres minor.
The subscapularis tendon lies on the anterior aspect of the anterior capsule of the glenohumeral joint, and its superior portion is intra-articular.⁴⁸ The subscapularis bursa lies between the subscapularis tendon and the scapula. The subscapularis muscle may be the cause of recurrent instability as it becomes attenuated from repeated dislocations.⁴⁴
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 SGHL. A hidden lesion of the rotator interval has been attributed to pathology of the CHL–SGHL confluence, which forms the biceps sling or pulley. Surgical closure of the interval appears to eliminate excessive inferior translation.⁵⁹
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 LHBT, and the medial border of the humerus.⁴⁴

Coracoacromial Arch

Coracoacromial Ligament

The coracoacromial ligament is the key structure of the coracoacromial arch and plays an important role in the spectrum of impingement disorders of the shoulder (Fig. 8.101). This ligament, a triangular band of two fascicles, originates from the lateral aspect of the coracoid and attaches to the anterior, lateral, and

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inferior surfaces of the acromion. The coracoacromial arch stabilizes the humeral head and prevents superior ascent (Fig. 8.102). The subacromial bursa is located between the acromion, the coracoacromial ligament, and the rotator cuff.⁴⁴ The bursa runs from the AC joint medially, under the anterior third of the acromion and coracoacromial ligament, to a line that extends approximately 4 cm anterior and lateral to the anterolateral margins of the acromion. Anterior acromial spurs, caused by chronic irritation from the humerus in contact with this ligamentous structure, may form within the acromial portion of the coracoacromial ligament.⁴⁶ Frequently, anterior acromial spurs are identified adjacent to the acromial attachment of the coracoacromial ligament. The normal low-signal-intensity acromial attachment of the coracoacromial ligament is frequently mistaken for an anterior acromial spur on coronal oblique MR images. The additive thickness of the coracoacromial ligament and the inferior acromial cortex produces this pseudospur (Fig. 8.103). In acromioplasty performed for chronic impingement, the coracoacromial ligament and the anterior inferior margin of the acromion are resected.

FIGURE 8.94 ● (A) The biceps pulley complex is sectioned in the sagittal plane at the level of the proximal, middle, and distal rotator cuff interval. The confluence of the CHL and SGHL occurs at the middle and distal aspects of the rotator interval. A T-shaped junction is formed between the SGHL and CHL at the mid-interval, superior to the humeral head. An anterior U-shaped sling is shown at the distal interval at the entrance to the bicipital groove. (B) An anterior coronal FS PD FSE image demonstrates the biceps tendon contained between the CHL and SGHL components of the biceps pulley.

FIGURE 8.95 ● Sagittal MR arthrograms. (A) The anterior biceps sling is formed by the confluence of the CHL and SGHL anterior to the LHBT. (B, C) The T-shaped junction of the SGHL and CHL at the midportion of the rotator cuff interval.

FIGURE 8.96 ● A superior view of the supraspinatus tendon after removal of the acromion of the scapula.

FIGURE 8.97 ● An anterior view of the subscapularis. The attachment of the serratus anterior to the medial border of the scapula has been excised.

FIGURE 8.98 ● The posterior aspect of the shoulder joint. The acromion and parts of the rotator cuff muscles have been excised to reveal the joint capsule.

FIGURE 8.99 ● (A) The rotator cable and crescent shown from a posterior view. The cable represents thickened capsular tissue from the articular side of the cuff connecting the anterior and posterior tendon edges of the tendinous portion of the rotator cuff. An extension of the coracohumeral ligament contributes to the cable. The rotator crescent, especially the lateral portion of the supraspinatus peripheral to the cable, represents the concave portion of the cuff at risk for pathology. (B) A superior view of the rotator cuff ridge or cable.

FIGURE 8.100 ● The bipennate infraspinatus muscle.

FIGURE 8.101 ● (A) The coracoacromial ligament extends from the inferior surface of the acromion to the lateral aspect of the coracoid. The humeroscapular motion interface represents a relationship between the rotator cuff, the humeral head, the biceps, the coracoacromial arch, and the deltoid and the coracoid muscles. Contact and load transfer occur between the rotator cuff and coracoacromial arch. (B) Coronal FS PD FSE image demonstrates the course of the coracoacromial ligament to the undersurface of the acromion. The lateral slip of the deltoid extends between the coracoacromial ligament and the rotator cuff. (C) Gross specimen highlighting the anatomy of the coracohumeral ligament (CHL) and coracoacromial ligament (CAL). The coracobrachialis (C), the short head of the biceps (SH), and the acromion (A) are indicated.

FIGURE 8.102 ● (A) The anterior undersurface of the acromion and the coracoacromial ligament form the coracoacromial arch. The subacromial subdeltoid bursa facilitates the passage of the rotator cuff and proximal humerus under the coracoacromial arch. (B) A superior axial image shows the anterior-to-posterior extent of the coracoacromial (CA) ligament perpendicular to the supraspinatus tendon. The fluid in the subacromial-subdeltoid bursa represents fluid between two serosal surfaces in contact with each other. One serosal surface is contributed by the undersurface of the coracoacromial arch and deltoid, and the other serosal surface is on the bursal side of the cuff.

FIGURE 8.103 ● Pseudospur. The normal broad attachment of the coracoacromial ligament to the inferior surface of the acromion is shown on (A) T1-weighted coronal oblique and (B) sagittal oblique images. The low-signal-intensity acromial cortex (black arrows) and adjacent coracoacromial ligament and lateral slip of the deltoid attachment (white arrows) give the false impression of a small subacromial spur in the coronal plane. This pseudospur should not be misinterpreted as impingement; otherwise, unnecessary acromioplasties may be performed on patients with a normal coracoacromial ligament attachment and no associated acromial spurs.

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The LHBT attaches to the supraglenoid tubercle and exits the joint in the bicipital groove in the hiatus between the subscapularis and supraspinatus tendons.⁴⁸ Fibers of the biceps contribute to the posterior and anterior superior labrum. The LHBT, with the BLC, centralizes and stabilizes the joint, as does the rotator cuff. The biceps tendon has a synovial sheath as an extension of the synovial lining of the glenohumeral joint.

Subacromial Bursa

The subacromial bursa extends under the acromion and coracoacromial ligament. Laterally, the bursa lies over the superior surface of the supraspinatus and infraspinatus tendons and extends beyond the lateral and anterior aspects of the acromion, under the deltoid. The bursa, which represents sliding serosal surfaces lubricated by synovial fluid (Fig. 8.104), serves as a gliding mechanism between the rotator cuff and coracoacromial arch.⁷⁵ Although communication exists between the subacromial and subcoracoid bursae, there may be no communication between the subcoracoid and subscapularis bursae (Fig. 8.105).⁷⁶^,⁷⁷ Therefore, if MR contrast medium or saline is inadvertently injected into the subcoracoid bursa, visualization of capsular structures will not occur because the subscapularis bursa is not distended. In this situation, gadolinium contrast in the subacromial bursa is not related to rotator cuff pathology. An obliterated peribursal fat plane has been used as an ancillary sign of shoulder disease. Fibrous bands may be seen within the subacromial bursa.⁴⁸

Acromioclavicular Joint

The AC joint is a synovial joint with articular surfaces covered by fibrocartilage similar to that in the sternoclavicular joint.⁷⁸ The articular capsule is reinforced by superior and inferior AC ligaments. The articular surfaces are separated by a wedge-shaped articular disc. The coracoclavicular ligament, with its conoid and trapezoid components, provides major stability to the joint. The coracoclavicular ligament assists in controlling vertical stability, and the AC ligament restrains posterior translation of the clavicle.⁴⁴

Pathology of the Shoulder

Shoulder Impingement Syndrome

Pearls and Pitfalls

Shoulder Impingement

Impingement syndrome, a clinical diagnosis, is characterized by a range of MR findings from tendinosis to rotator cuff tears.
Intrinsic impingement is associated with shoulder instability.
Primary extrinsic impingement is associated with abrasion of the rotator cuff against the inferior surface of the acromion.

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Subacromial keel spurs are located on the anteroinferior lateral portion of the acromion.
Acromial thickness is important in planning subacromial decompression procedures.
The AC joint may hypertrophy, but it is not responsible for true impingement.
The imaging reference to hypertrophy of the coracoacromial ligament correlates with fraying or fragmentation of the ligament in association with impingement.
A symptomatic os acromiale is associated with marrow edema on either side of the synchondrosis.
Degenerative tendinopathy or intrinsic tendon degeneration associated with eccentric tensile overload may be the primary pathology in impingement.
Rotator cuff tendinosis is most conspicuous on FS PD FSE images. It does not demonstrate hyperintensity on T2 FSE images. Partial- and full-thickness tears are hyperintense on both FS PD FSE and T2 FSE sequences unless associated with chronic scarring or granulation tissue.

FIGURE 8.104 ● The subacromial bursa extends over the insertion of the supraspinatus superiorly and over the infraspinatus and teres minor posteriorly. The superior surface of the bursa is in contact with the undersurface of the acromion, the coracoacromial ligament, and the origin of the mid-portion of the deltoid muscle. The superior surface of the bursa extends medially adjacent to the deep surface of the acromioclavicular joint.

FIGURE 8.105 ● (A) After separate contrast injections into the subcoracoid (SC) and subscapularis (S) bursae, the subcoracoid and subacromial bursae are seen to communicate, whereas no communication occurs between the subacromial and subscapularis bursae. C, coracoid. (B) T2*-weighted sagittal oblique gadopentetate-saline subcoracoid bursagram demonstrates filling of the subcoracoid bursa anterior to the subscapularis tendon (straight arrow) and posterior to the conjoined tendon of the coracobrachialis and short head of the biceps (curved arrow). C, coracoid.

The shoulder impingement syndrome consists of a continuum from mild tendinosis to massive rotator cuff tears. With the exception of throwing injuries in athletes, rotator cuff impingement or impingement syndrome is a condition of middle age. There is an insidious onset of pain with overhead activities, usually without a history of a specific injury. There may also be stiffness, catching, and local or referred pain to the deltoid insertion. Night pain and weakness are usually associated with rotator cuff tears and not impingement.

Clinical assessment of shoulder impingement includes evaluation for atrophy and range of motion as well as direct palpation.⁷⁹ In Neer's impingement test, pain is elicited by forcible elevation of the arm and is caused by impingement of the critical area of the supraspinatus tendon on the anteroinferior acromion. Injection of lidocaine into the subacromial space relieves or decreases the pain. The impingement reinforcement or Hawkins' test is performed by flexing the humerus 90° and then forcibly internally rotating the shoulder until pain is reproduced by cuff impingement. Weakness is evaluated in the supraspinatus (weakness with abduction), subscapularis (weakness with internal rotation), and infraspinatus (weakness with external rotation).

Related Anatomy

The coracoacromial arch includes the coracoid, the coracoacromial ligament, and the anterior inferior acromion.⁷⁴ These structures can impinge on the subacromial bursa, the LHBT, the rotator cuff (especially the supraspinatus), and the proximal humerus. Anterior inferior acromial spurs and to a lesser extent acromioclavicular osteophytes are related to impingement. The supraspinatus and superior aspect of the infraspinatus are most frequently involved in impingement-related rotator cuff tears.

Pathogenesis

Impingement is caused by degenerative changes that develop where the tendinous fibers of the rotator cuff attach to the greater tuberosity, most often in the area of the insertion of the supraspinatus tendon. This tendon—anatomically confined, under tension, and compressed between bony structures at both its inferior and superior surfaces—is at risk for both acute injury and chronic wear. Bursal inflammation and tendinitis produced by compression may cause pain, leading to disuse atrophy of the supraspinatus and infraspinatus in the subacromial space. A hooked type 3 acromion and muscle weakness lead to loss of the centralizing forces, and increased compression can be a further negative factor. The chronic compressive and irritative forces cause changes in the coracoacromial ligament, producing an anterior spur that may contribute to further impingement in the subacromial space.

Rotator cuff tears also play a part in the development of chronic impingement,⁸⁰^,⁸¹^,⁸²^,⁸³^,⁸⁴ although there is controversy 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 (Fig. 8.106).

The relationship among the rotator cuff, the LHBT, the subacromial bursa, the AC joint, the acromion, and the humeral head is also important in the spectrum of impingement disorders.⁷⁵^,⁸⁵ The most common location for impingement is between the anterior third of the acromion and the underlying tendons. Painful impingement syndrome is the most common presenting picture in rotator cuff lesions. The importance of the lateral edge of the acromion has been minimized, and the posterior portion of the acromion is no longer thought to be implicated in impingement. 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.⁸⁶

Etiology

A variety of causes of the painful shoulder impingement syndrome have been proposed,⁸⁷^,⁸⁸ including:

Hypovascularity in the supraspinatus tendon
Mechanical wear
Acute trauma
Repetitive microtrauma from overuse (this is especially common in throwing athletes or those whose work activities emphasize overhand motions)

Factors contributing to bony supraspinatus outlet compromise include:⁷⁵^,⁸⁹^,⁹⁰

Anterior acromial spurs
Acromion shape (a curved or overhanging edge)
The slope of the acromion (a flat or decreased angle)
The morphology of the AC joint (hypertrophic bone, callus formation)

FIGURE 8.106 ● (A) Rotator cuff tendinosis is seen as collagen degeneration without the influx of inflammatory cells. The thickened distal cuff tendon is viewed in an anterior coronal perspective. Moderate to severe rotator cuff tendinosis demonstrates hyperintensity on a coronal FS PD FSE image (B) and intermediate signal intensity on a coronal T2 FSE image (C).

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Less frequent mechanisms of impingement (non-outlet impingement) include:

Prominence of the greater tuberosity (fracture, malunion, nonunion)
Loss of humeral head depressors,⁹¹ as seen in rotator cuff tears and biceps tendon rupture
Loss of the glenohumeral joint fulcrum function from articular surface destruction or ligamentous laxity
Impaired scapular rotation from trapezius paralysis or AC joint disruption
Lesions of the acromion, including an unfused anterior acromial epiphysis (apophysis)
Fracture malunion or nonunion
Subacromial bursal thickening (chronic bursitis or cuff thickening in calcific tendinitis)

Differential Diagnosis and Etiologic Classifica-tion

The shoulder-related differential diagnosis for impingement syndrome includes AC joint arthrosis, adhesive capsulitis, biceps tendinitis (tendinosis), and glenohumeral arthrosis.

The causes of rotator cuff impingement can be grouped into structural and dynamic factors. Structural etiologies lead to mechanical obstruction and decreased space for rotator cuff clearance within the supraspinatus outlet. Mechanical obstruction abrades the rotator cuff and is associated with tendon degeneration and tears. Dynamic etiologies of impingement are associated with superior migration of the humeral head during arm elevation, which leads to abatement of the greater tuberosity against the coracoacromial arch, resulting in rotator cuff tendon injury. Dynamic imbalance is attributed to rotator cuff dysfunction and fatigue. Dynamic impingement related to glenohumeral instability may require operative stabilization to center the humeral head within the glenoid fossa.

Structural causes of subacromial pathology include abnormal acromial morphology; calcific tendinitis (thickening of the rotator cuff); severe AC joint arthrosis with hypertrophy and osteophytes; coracoacromial ligament degeneration (hypertrophy);

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os acromiale; inflammatory bursitis, malunion of the greater tuberosity, distal clavicle or acromion; and partial- or full-thickness tears of the rotator cuff. Dynamic causes of subacromial pathology include scapular dysfunction, primary tendon overload, glenohumeral instability, repetitive microtrauma, and an imbalance of shoulder musculature.

Intrinsic and Extrinsic Impingement

Impingement may also be classified as intrinsic or extrinsic to the glenohumeral joint, although the clinically described discomfort is similar in both conditions. Intrinsic impingement (also referred to as secondary extrinsic impingement) is associated with instability and represents secondary or non-outlet impingement. It includes the following:

Posterior peel-back
Microinstabilities of the glenohumeral joint
Scapular dyskinesia
Greater tuberosity malunion
Loss of humeral head depressor function

Primary extrinsic impingement is the painful abrasion of the rotator cuff against the underside of the acromion with arm elevation. Subcoracoid impingement is caused by a separate mechanism and is related to narrowing of the space between the coracoid process and the humeral head. Anterosuperior impingement is discussed below in the sections on the rotator cuff interval and biceps pulley lesions.

Primary extrinsic impingement may be caused by any of the following:

Variations in anterior acromial shape
Slope of the acromion (lateral or anterior downsloping)
A low-lying acromial position
AC joint osteophytes
Anterior inferior acromial spurs
Coracoacromial ligament thickness
Os acromiale

Non-impinged shoulders have proper contact and load transfer between the rotator cuff and the coracoacromial arch. There is a normal sliding contact between the superior cuff and the coracoacromial arch. Although there is a strong association among aging, the presence of cuff tears, and alterations of acromial contour, it has not been established whether the change in acromial shape was caused by or resulted from the cuff defect or whether both are consequences of aging. Neer⁸³ determined that rotator cuff disease causes characteristic changes on the undersurface of the coracoacromial arch.

Ozaki⁹² correlated the histology of the acromial undersurface with the status of the rotator cuff in 200 cadaver shoulders. Cuff tears that did not extend to the bursal surface were associated with normal acromial histology. Cuff tears that extended to the bursal surface, however, were associated with pathologic changes in the acromial undersurface. Ozaki concluded that most tears were related to tendon degeneration and that acromial changes were secondary to pathology of the bursal side of the cuff. Although it is normal to have subacromial contact with shoulder motion, the process is considered pathologic when the sliding motion becomes an impaction motion. Tendon dysfunction and not bony changes are the cause of both impingement and rotator cuff tears. These findings differ from the teachings of Neer, who indicated that the acromion would abrade through the cuff to produce a tear.

Pathogenesis of extrinsic impingement

Since there is normally no gap between the superior cuff and the coracoacromial arch, the slightest degree of superior translation compresses the cuff tendon between the humeral head and the arch.⁷⁴ Superior displacement is opposed by a downward force exerted by the coracoacromial arch through the cuff tendon to the humeral head. Ziegler et al.⁹³ demonstrated that when the cuff tendon is excised, a superiorly directed humeral load of 80 N increased superior humeral displacement from 1.7 mm to 5.4 mm. In extrinsic impingement, the superior surface of the rotator cuff abrades the undersurface of the acromion during elevation and/or overhead motion. It should not be assumed, however, that shoulder pain with elevation is always caused by extrinsic impingement. Severe biceps tendinitis, for example, may mimic impingement.

Acromial Morphology in impingement

Shape of the acromion

The shape of the acromion as seen on sagittal oblique MR images or on an 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 et al.:⁸⁹

The type 1 acromion (Fig. 8.107) has a flat or straight undersurface.
The type 2 acromion (Fig. 8.108) has a smooth, curved inferior surface that approximately parallels the superior humeral head in the sagittal oblique plane.
The type 3 acromion (Fig. 8.109) has an anterior hook or beak. The acromiohumeral distance is narrowed relative to the remainder of the acromion at the site of the hook. It is the type 3 acromion that 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). In the clinical series of Morrison and Bigliani,⁹⁴ 80% of patients with rotator cuff tears had type 3 acromions.
The type 4 acromion, described by Vanarthos and Mono⁹⁵ (Fig. 8.110), has a convex inferior contour. Although there may be partial narrowing of the subacromial space near the midposterior aspect of the distal acromion, there is no correlation between a type 4 acromion and impingement.

Fukuda et al.⁹⁶ showed that the site of bursal side partial cuff tears corresponds to anterior inferior acromial impingement and correlates with histologic changes of degeneration.⁹⁶ Neer proposes that the majority of rotator cuff tears are caused by mechanical impingement leading to tendinitis, fibrosis, bursal surface pathology (partial tears), and eventual full-thickness cuff tears.⁷⁵^,⁹⁷

Type 1 and 2 acromions are more common than type 3 in the general population. The morphologic changes seen in type

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2 and 3 acromions may be acquired rather than developmental.⁹⁸ Most acromial hooks lie within the coracoacromial ligament and may be traction spurs (analogous to the traction spur or enthesophyte seen in the plantar ligament at its attachment to the calcaneus). The traction loads producing such hooks may result from loading of the arch by the cuff. In the presence of cuff degeneration, dependence on the coracoacromial arch for superior stability increases, and so may the traction loads. The hypothesis that the hook is a traction phenomenon was first put forward by Neer.⁸³^,⁹⁹ Putz and Reschelt⁹⁹ reported that three quarters of operative specimens of the coracoacromial ligament showed chondroid metaplasia near the acromial insertion. This metaplastic area becomes the acromial hook by enchondral bone formation.¹⁰⁰ Because the hook lies within the coracoacromial ligament and points toward the coracoid, it may not directly affect or jeopardize the passage of the cuff beneath the coracoacromial arch, as previously thought.

FIGURE 8.107 ● (A) Type 1 acromion with flat acromial undersurface. (B) Type 1 acromion with straight inferior margin as seen on a sagittal T2 FSE image.

FIGURE 8.108 ● (A) Type 2 acromion with a curved convex inferior surface that parallels the contour of the humeral head. (B) Type 2 curved acromion on a corresponding sagittal PD FSE image.

FIGURE 8.109 ● (A) Type 3 acromion with an inferiorly directed beak or hook, which contributes to narrowing of the supraspinatus outlet for the supraspinatus tendon. (B) Sagittal PD FSE image of the type 3 or anterior hooked acromion. The type 3 acromion is assessed at least one to two images lateral to the AC joint.

FIGURE 8.110 ● (A) Color illustration and (B) sagittal PD FSE image of a type 4 acromion with upward or superior convexity of its inferior border. There is no association with cuff impingement.

A subacromial keel (Fig. 8.111) is an aggressive inferior acromial spur shaped like the keel of a sailboat.¹⁰¹ The acromial keel spur can be found on the anterior edge between the lateral border of the acromion and the AC joint, continuing posteriorly to midway under the acromion. The subacromial keel spur is seen in young and middle-aged women and may result in severe damage to the bursal surface of the cuff.

Thickness of acromion

Consideration of the thickness of the osseous acromion is as important as understanding acromial morphology when performing subacromial decompression.¹⁰¹ Measurement of the thickness of the bone helps prevent inadvertent acromial fracture caused by overly aggressive burring. Snyder¹⁰¹ has developed the following classification of acromial thickness assessed at the posterior margin of the AC joint:

Type A acromion: thin, less than 8 mm
Type B acromion: 8 to 12 mm
Type C acromion: thick, more than 12 mm

FIGURE 8.111 ● Coronal FS PD FSE image showing an acromial “keel” spur associated with a full-thickness rotator cuff tear with retraction.

In one third of female patients with a Bigliani type 3 acromion, the acromion was also found to be thin (<8 mm), putting these patients at risk for acromial fracture during arthroscopic or open decompression.

Acromial slope

The normal acromial slope approximates the horizontal plane or slopes superiorly from posterior to anterior. Anterior downsloping of the acromion is assessed in the sagittal plane. Lateral downsloping of the anterior acromion may narrow the supraspinatus outlet and contribute to impingement. A low-lying acromion relative to the distal clavicle is also demonstrated in the coronal plane at the level of the AC joint and may predispose to impingement and degenerative changes of the acromion.

Acromioclavicular Joint Disease in Impingement

Extrinsic impingement can be produced by many causes, all of which cause the humeral head to no longer be centered or contained on the glenoid fossa.⁷⁴ The unbalanced elevating force of the deltoid then pulls the superior cuff into contact with the anterior acromial undersurface. True impingement with the undersurface of the AC joint does not usually exist. AC osteophytes are usually sufficiently medial that they do not compromise the rotator cuff (Fig. 8.112). This may explain why AC joint hypertrophy or osteophytes are not specific for impingement and these findings are frequently identified in the asymptomatic population. A symptomatic AC joint, however, may require resection.¹⁰² Useful tests to identify the symptomatic AC joint include:

Cross-est adduction (increasing symptoms)
Adduction, internal rotation, and extension (to isolate posterior AC facet pain)
Direct superior tenderness reproducing the pain
Tenderness on anteroposterior translation
Localized pain in the AC joint with impingement testing

Coracoacromial Ligament and Arch in Impinge-ment

When associated with significant impingement, the coracoacromial ligament (Fig. 8.113) is usually frayed and fragmented, with surrounding synovitis. Increased contact and abrasion occur with upward displacement of the humeral head, as the rotator cuff is squeezed against the acromion and the coracoacromial ligament. The result is a traction spur in the coracoacromial ligament. Further upward displacement of the humeral head is associated with abrasion of humeral head articular cartilage and rotator cuff tear arthropathy.⁷⁴

Os Acromiale in Impingement

Os acromiale is failure of the acromial ossification centers to fuse (normally complete by 22 years of age). The pre-, meso-, meta-, or basiacromion may fail to fuse¹⁰³ (Fig. 8.114). Meso- and

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meta-acromion failure (failure of fusion of the mesoacromion to the meta-acromion) is more common. The synchondrosis-like articulation may contain fibrous tissue, periosteum, or synovium. The os acromiale may be relatively mobile with shoulder abduction causing impingement.¹⁰³ Degenerative changes across the os acromiale, including edema, also contribute to impingement. An unstable degenerative os acromiale is often associated with AC joint degeneration. The coracoacromial ligament inserts onto the os acromiale, and thus the os acromiale is susceptible to instability. Failure to recognize an os acromiale is associated with a failed acromioplasty.

FIGURE 8.112 ● (A) Although AC arthrosis may be concurrent with impingement, it is the more lateral acromial spurs that are directly associated with symptomatic bursal-side cuff damage. (B) AC joint degenerative disease with hypertrophic inferior acromial side spur.

FIGURE 8.113 ● (A) Arthroscopic view from the subacromial space shows the fascicles of the coracoacromial ligament as they attach to the inferior aspect of the acromion. The coracoacromial ligament attaches to the anterior, lateral, and inferior surfaces of the acromion and originates as a triangular band of two fascicles from the lateral aspect of the coracoid. (B) The corresponding coracoacromial ligament has been cut, with the acromial attachment intact. (A, B: From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.)

FIGURE 8.114 ● Superior view of os acromiale subtypes from distal to proximal. These unfused ossification centers include pre-, meso-, meta-, and basiacromion based on the location of the articulation. The mesoacromion-meta-acromion type is most common.

Clinical Classification of Impingement

Neer proposed a three-stage classification system for the impingement syndrome.⁸³^,¹⁰⁴ In this system, subacromial impingement is presented as a mechanical process of progressive wear (i.e., a pretear impingement lesion) that causes 95% of rotator cuff tears.⁸⁰^,⁸¹^,⁸²^,⁸³^,⁸⁴^,⁸⁵ Degeneration, thinning, and full-thickness tears of the supraspinatus may extend to involve the long head of the biceps and infraspinatus tendons. The stages in Neer's classification system are:

Stage 1: Tendon edema and hemorrhage
Stage 2: Fibrosis and tendinitis
Stage 3: Partial or complete rupture or tear of the rotator cuff, often in association with anterior acromial spurring 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.

At surgery, rotator cuff tendons display areas appearing gray, dull, edematous, and friable.⁹⁷ Degenerative changes, including angiofibroblastic hyperplasia without inflammatory cells, can be seen on correlative histologic examination. Because leukocyte infiltration of the rotator cuff tendons is rare, the tendinitis or inflammation of the cuff (especially in the later stages of rotator cuff pathology) as described in Neer's classification has not been adequately documented.⁸⁶

Arthroscopic visualization of the rotator cuff from the articular and bursal surfaces has provided new perspectives on the progression of this disease process. A complete diagnostic arthroscopic evaluation of the entire glenohumeral joint allows evaluation of articular damage, labral tears, biceps labral lesions, and loose bodies, as well as articular surface tears of the rotator cuff. Similarly, the subacromial space can be inspected for erosive “kissing” lesions of the coracoacromial ligament and rotator cuff. The bursal view allows better evaluation of the extent and amenability to repair of full-thickness rotator cuff tears. Thus, the progressive stages of impingement might be more accurately described as follows:

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, partial tears of the rotator cuff involving the articular surface of the rotator cuff adjacent to the tendon insertion are more commonly seen.⁸⁶^,¹⁰⁵ Articular cuff lesions may be the result of tensile strength failure from overuse, whereas bursal cuff lesions are more closely associated with impingement.¹⁰⁰^,¹⁰⁵ Because a direct mechanical cause of impingement is frequently not found in patients with suspected impingement syndrome, intrinsic tendon degeneration (degenerative tendinopathy), and not mechanical impingement, may be the primary pathology in the development of most rotator cuff disorders.⁹⁷ Rotator cuff tendinitis has been attributed to repeated eccentric tensile overload of the rotator cuff tendons. Nirschl found acromial spurs in only 10% of patients referred for surgery for rotator cuff tendinitis.¹⁰⁶

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Rotator cuff degeneration has also been observed in the absence of anteroinferior acromial spurs.¹⁰⁰ Ozaki et al.⁹⁰ found that bursal side and full-thickness rotator cuff tears correlated with degenerative changes of the coracoacromial ligament and anterior third of the inferior acromion. Articular surface partial tears, however, were associated with normal acromial morphology and histology. Most tears of the rotator cuff were thus attributed to degenerative lesions that were associated with increasing age, and the acromial changes present were secondary. Athletes may demonstrate both degenerative rotator cuff tendinitis and primary mechanical impingement.¹⁰⁵

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.⁹⁷^,¹⁰⁷ The area of avascularity may be dependent on arm position, with decreased vascular perfusion when the arm is in the abducted position and normal perfusion with the arm adducted.⁸⁸

In the Neer classification system 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.

FIGURE 8.115 ● Coronal FS PD FSE image showing severe tendinosis with greater bursal-side involvement and an anterior inferior acromial spur.

MR Appearance

The spectrum of MR changes in shoulder impingement have been characterized and documented.²⁹^,⁴⁷^,⁸²^,⁸⁴^,¹⁰⁸ Rotator cuff disease is evaluated on the basis of tendon morphology and changes in the observed signal intensity within the specific cuff tendons. In addition, pathologic processes in the coracoacromial arch, including the acromion, the AC joint, and the subacromial-subdeltoid bursa, may be identified in the spectrum of findings in impingement lesions.

MR Appearance of Subacromial-Subdeltoid Bursitis

Changes in the subacromial bursa are generally thought to be secondary to tendon degeneration or tendinopathy as part of impingement.¹⁰⁹^,¹¹⁰ Normally, the subacromial-subdeltoid bursa is small, with a flat and noninflamed synovial lining.¹¹¹ Identification of this structure, and of signal intensity within the peribursal fat, can be used to describe subacromial bursitis on MR images.⁸⁴^,¹¹² Bursal inflammation is seen as decreased signal intensity (or loss of peribursal fat) on T1 or PD-weighted images and increased signal intensity (from associated fluid, inflammation, or bursal proliferative disease) on conventional T2 or FS PD-weighted FSE sequences (Fig. 8.115). Although the changes of subacromial

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bursal inflammation are usually associated with tendinitis or cuff tears, small amounts of subacromial bursal fluid may be seen without abnormal cuff morphology or signal intensity alterations. Low signal intensity within a thickened subacromial bursa on T1- and T2-weighted images indicates a proliferative process in chronic bursitis, also associated with rotator cuff disease.¹¹³ Subacromial bursal thickening occurs in Neer's stage 2 impingement, although the subacromial bursa may not show any surgical signs of scarring in chronic impingement.⁸⁶^,¹¹⁴ The presence or absence of subacromial fat, however, is a variable finding in asymptomatic volunteers and in the various stages of impingement. FS PD-weighted FSE images are more sensitive than conventional T2 or non-FS PD-weighted FSE sequences in identifying small amounts of subacromial bursal fluid on coronal oblique or axial images. The subacromial bursa may be distended with fluid in both partial and complete rotator cuff tears. It is unusual to see a fluid-filled bursa in the presence of a normal cuff. FS PD FSE images have a high sensitivity for small amounts of fluid, making assessment of loss of peribursal fat no longer relevant.

MR Appearance of Impingement Lesions of the Rotator Cuff

Pitfalls of interpretation of rotator cuff degeneration

The normal rotator cuff tendons display low signal intensity on T1, conventional T2, PD-weighted FSE, FS PD-weighted FSE, STIR, and T2* GRE sequences. Areas of intermediate signal intensity or signal inhomogeneity, especially in the distal extent of the supraspinatus tendon on T1- and PD-weighted images, can be seen in both cadaver cuffs and asymptomatic volunteers.¹¹⁵^,¹¹⁶ These changes have been variously attributed to a magic-angle phenomenon, partial volume averaging of the distinct components of the supraspinatus muscle and tendon, or histologic degeneration (eosinophilic, fibrillar, and mucoid).¹¹⁷

In the magic-angle phenomenon, tendon orientation at the magic angle of 55° to B₀ contributes to increased signal intensity in the supraspinatus tendon on short-TR/TE sequences.¹¹⁸ These signal effects may also be seen on GRE and FS images. The routine use of T2-weighted images and observation of cuff morphology should minimize misinterpretation of these affected segments of the rotator cuff. It may be difficult, however, to distinguish between a magic-angle effect and early changes of cuff degeneration.

A partial volume averaging effect of tendon, muscle, connective tissue, or fat has not been well accepted as an explanation for 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. Persistent cuff signal intensity has been shown independent of different imaging orientations along the axis of the supraspinatus tendon and muscle.¹¹⁹ Interposed muscle has not been described in or near cuff insertions.¹²⁰^,¹²¹

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,¹¹⁹ including the anterior fusiform portion, containing the dominant tendon of the supraspinatus, and a strap-like posterior portion. The orientation of the tendon differs from the main muscle by 10°. The pseudogap signal is not related to fat and is thought to represent a focal difference in tissue relaxation parameters.

In cuff tendon degeneration, there are areas of intermediate signal intensity on T1- and PD-weighted images, which display intermediate to high signal intensity on T2*, FS PD-weighted FSE, and STIR sequences in both asymptomatic and symptomatic patients. On heavily weighted T2 or T2-weighted (non-FS) FSE images, however, these regions of altered signal intensity are diminished or remain unchanged and are used to increase specificity in differentiating between tendon degeneration and partial tears.

Additional pitfalls to be avoided in the interpretation of MR findings include the following:

Although the subacromial peribursal fat plane is usually preserved on T1- or PD-weighted images in the early stages of impingement, it may be effaced by bursal surface inflammation in the absence of a rotator cuff tear.⁸⁴
An area of increased signal intensity on T2-weighted (long TR/long TE) sequences may be caused by the injection of long-acting steroids and local anesthetics used in the diagnosis and treatment of impingement. Prior use of this technique should be taken into consideration to decrease false-positive diagnoses.⁸²
In addition to articular and bursal tendon degeneration, intrasubstance degeneration may also be associated with intrasubstance tears without bursal or articular surface extension. Although intrasubstance cuff pathology can be identified on MR images, these changes are usually not confirmed on arthroscopic surface evaluations. Conventional and Gd-DTPA–enhanced MR images are also negative for intrasubstance degeneration and tear.

Rotator cuff degeneration in impingement

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 PD- or T2-weighted or T2-weighted FSE sequences. Evaluation is best accomplished with coronal oblique and sagittal oblique planar images. The axial plane may be used secondarily to evaluate specific sites or locations of abnormal tendon signal intensity.

In rotator cuff degeneration, there is intermediate signal intensity on PD-weighted images, with no increase in signal intensity on T2- or T2-weighted FSE images (Fig. 8.116). FS PD-weighted FSE sequences (TEs 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* GRE 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. Changes of tendon degeneration

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are seen as an age-related phenomenon in older patients and in normal asymptomatic volunteers. More severe changes of degeneration may be characterized by intermediate to increased signal intensity on short-TE or T1- and PD-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 short- and long-TE images (conventional T2 and FSE T2), with a further increase in signal intensity between T1 or PD and T2-weighted images, is associated with a partial- or full-thickness tear. Differentiating severe tendinitis and 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 T2-weighted images in areas of severe degeneration or tear obliterated by scar tissue or tendon remnants.¹²² Fraying of the cuff may be appreciated as a surface contour irregularity involving either the articular or bursal surface (Fig. 8.117).

FIGURE 8.116 ● (A) Infraspinatus tendinosis appears hyperintense on this FS PD FSE coronal image. (B) Corresponding T2 FSE coronal image shows intact bursal and articular cuff surfaces. Note that cuff degeneration is visualized as intermediate signal intensity, thus increasing the specificity of this imaging sequence. (C) A separate area of infraspinatus tendinosis that may be mistaken for a partial articular-side tear is displayed on this FS PD FSE image. (D) A coronal T2 FSE image demonstrating tendinosis with no hyperintensity of cuff fibers.

The signal-intensity changes described in degeneration are the result of macromolecular collagen changes.¹⁰⁵ In the normal tendon, there is no significant molecular motion of water, which is tightly bound to collagen macromolecules. Damage to collagen fibers is associated with an increase in absorbed water. The increased amount of absorbed water increases T2 relaxation times, resulting in hyperintensity from water molecules on short-TE images. In severe degeneration and tears, there is a greater amount of free water within tendon defects, resulting in a long T2 and high signal intensity on long-TE or T2-weighted spin-echo images. The increased signal intensity detected on T2-weighted sequences reflects significant macromolecular disruption, as would be seen in severe tendon degeneration or tears.

FIGURE 8.117 ● (A) Articular surface fraying of the supraspinatus in a gymnast. (B) Coronal FS PD FSE MR arthrogram in a separate case of articular surface fraying.

These imaging characteristics are used by Seeger et al.⁸⁴ in their classification of impingement lesions. In this system, impingement lesions are grouped into several types based on coronal plane MR images:⁸⁴

Type 1 impingement is characterized by the presence of subacromial bursitis, and signal intensity in the supraspinatus may remain normal. Isolated subacromial bursitis is an infrequent finding on MR images; however, it is usually associated with tendinitis. This is substantiated by postmortem and histologic studies from the surgical literature.¹²³^,¹²⁴^,¹²⁵^,¹²⁶^,¹²⁷
In Seeger's type 2 impingement, the supraspinatus tendon demonstrates increased signal intensity on T1-weighted images. Increased signal intensity on T2-weighted images is considered a type 2b change and may represent a partial tear.
Type 3 impingement is characterized by a complete tear of the rotator cuff, with or without supraspinatus retraction. Complete tears exist only in type 3 impingement, and in this classification system high signal intensity of the supraspinatus tendon on conventional T2-weighted images is considered pathognomonic for a tear.

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In Zlatkin's grading system (grades 0 to 3) for characterization of the rotator cuff tendons, tendinitis with normal morphology (grade 1) is differentiated from tendinitis or tendon degeneration with abnormal morphology (grade 2).³⁰ Associated tendinous enlargement, which may be seen in the more acute stages of impingement, is still considered normal morphology (normal tendon outlines). In both grade 1 and grade 2 tendons, there is increased signal intensity on T1- and PD-weighted images, without any further increase in signal intensity on T2-weighted images. A grade 3 tendon demonstrates both morphologic changes (a tendinous defect) and signal-intensity changes (increased signal intensity on T2-weighted images). This increased signal intensity is related to corresponding T1-weighted (short TR/TE) and PD-weighted (long TR/short TE) images and is seen within the tendon defect as bright signal intensity from fluid. A grade 3 tendon represents a rotator cuff tear. Because Zlatkin specifically uses the term “degeneration” to designate surface morphologic changes (i.e., thinning or irregularity) of the tendon, separate from histologic findings of degeneration, a grade 2 tendon with abnormal morphology by definition may represent tendinitis with superficial tendon degeneration or a partial rotator cuff tear. Thus, a rotator cuff tear may exhibit abnormal morphology (attenuation) but not increased signal intensity on T2-weighted images. In addition, the association of small amounts of fluid in the subacromial bursa and loss of the subacromial-subdeltoid fat plane on T1-weighted images are not reliable secondary signs for distinguishing between degeneration and tears. The increased sensitivity of FS PD FSE images in detecting increases in tendon signal intensity may be secondary to increased PD or prolonged T1 or T2 values. Careful evaluation of bursal and articular surfaces is necessary to identify the possible development of a partial tear. High-resolution imaging techniques combined with the appropriate use of both FS PD FSE and T2 FSE coronal images are more accurate than protocols that use coronal PD images instead of T2 FSE images. PD FSE contrast thus may not be as accurate in distinguishing between tendinosis and partial cuff tears.

Histologically, the inflammation and mucoid degeneration seen on tendon biopsy specimens are thought to correlate with increased signal intensity on T1- and PD-weighted images.⁸² Both Raffi et al. and Kjellin et al. propose that areas of increased signal intensity in the supraspinatus tendon on PD-weighted images represent degeneration (eosinophilic, fibrillar, and mucoid) and scarring, and not active inflammation.¹¹⁵^,¹²² This is consistent with the fact that leukocytic infiltration of the rotator cuff tendons is rare. These studies support our observations of increased signal intensity in the supraspinatus tendon in some asymptomatic patients on short-TR/TE, PD, and T2*-weighted images.¹¹⁶^,¹²⁸

Raffi et al.¹²² also suggest that tendinous enlargement associated with homogeneous or nonhomogeneous increased signal intensity is a more specific finding in symptomatic shoulders with tendinitis. Tendinous enlargement, or the increased signal intensity of tendon degeneration, may also characterize the reparative process and healing of an interstitial tear.

It seems that the common usage of the term “tendinitis,” which implies active inflammation, without histologic confirmation, may be imprecise in characterizing tendon signal-intensity alterations. Kjellin et al. suggest the use of the term tendinosis or tendinopathy in such cases.¹¹⁵ Since the term “tendinosis” is widely accepted (compared to tendinitis), it is acceptable to characterize an area of increased signal intensity on intermediate-weighted images and intermediate signal intensity on T2-weighted images as tendon degeneration. Impingement, however, is a clinical diagnosis, not a radiologic or MR diagnosis.¹²⁹ The tendon findings or osseous changes seen in the impingement syndrome may be identified and described on MR images when patients are referred for study to determine whether these findings, in conjunction with the patient's clinical presentation, are consistent with impingement syndrome.

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 (pretear tendinosis), 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.

Arthroscopic Classification of Impingement

Arthroscopy allows identification of all structures involved in the impingement syndrome and determination of the cause and effect of the pathology in each case. Arthroscopic classification also allows more precise communication among clinicians, which has contributed to the development of a well-defined approach to treatment. One proposed classification system based on arthroscopic findings is as follows:

Type 1 impingement is characterized by signs of tendon wear or degeneration on the articular or bursal surface, with associated fraying or irregularity of either articular or bursal structures. Type 1 impingement is subdivided into type 1a (articular) and type 1b (bursal). Type 1 impingement also includes any signs of wear or degeneration of any of the structures in the bursa (e.g., coracoacromial ligament erosion or fraying). In addition to articular (type 1a) and bursal (type 1b) tendon degeneration, intrasubstance degeneration, which we refer to as type 1c, may be associated with intrasubstance partial tears (Fig. 8.118). Such intrasubstance degeneration is not detected and cannot be confirmed on arthroscopic surface evaluations. Conventional and gadolinium-enhanced MR images are negative in type 1 impingement.
In type 2 impingement, in addition to tendon wear or degeneration, there are partial-thickness tears, of the articular surface in type 2a (Fig. 8.119) or the bursal surface in type 2b (Fig. 8.120). Type 2 impingement lesions are also characterized on MR images as partial articular

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(type 2a) or bursal (type 2b) tears. In the presence of a surface tear, it may be difficult and redundant to classify associated intrasubstance changes, whether secondary to degeneration or intrasubstance tearing. Cadaveric histopathologic studies have shown that partial tears may originate from regions of tendon degeneration without associated inflammation, as discussed earlier.¹¹⁵ Coronal oblique MR images show increased signal intensity in the distal supraspinatus tendon on T1-, intermediate-, T2-, T2*-, and T2-weighted FSE images. Increased-signal-intensity fluid within the bursal or articular surface of the cuff is characteristic of this lesion. Small amounts of fluid may be seen in the subacromial bursa, especially in bursal surface type 2b lesions, in the absence of a full-thickness or complete tear. In addition to a partial-thickness tear, in type 2 impingement associated tendon thinning and fraying may be present. Well-defined, linear high signal intensity on T2-weighted images, or an area of increased signal intensity on long-TR/TE images, that does not extend to either the articular or bursal surfaces may represent intrasubstance partial tears. Morphologic tendon changes, such as tendon irregularities or thinning, help support the diagnosis.
Type 3 impingement is characterized by a full-thickness tear of the rotator cuff. Without retraction of the cuff, the tear is classified as type 3a; with retraction of the cuff, it is classified as type 3b. MR imaging may depict a complete tear of the rotator cuff (type 3a impingement) or a tear with proximal tendon retraction (type 3b impingement). Without demonstration of a defined defect, retraction of the muscle belly, or extension of fluid across the supraspinatus tendon into the subacromial-subdeltoid bursa, a complete tear cannot be unequivocally diagnosed. Increased signal intensity within the tendon on T2-weighted images in the presence of normal tendon morphology is not diagnostic of a rotator cuff tear. Therefore, the presence of small amounts of fluid within the subacromial-subdeltoid bursa should not be used as a primary sign of rotator cuff tear, unless associated with a direct communication of fluid from the glenohumeral joint into the subacromial-subdeltoid bursa.

FIGURE 8.118 ● (A) Subacromial impingement with subacromial bursal inflammatory changes and development of a bursal-side partial tear of the rotator cuff. (B) Articular-side partial tear in subacromial impingement. Bursal inflammatory changes may be present with both bursal and articular side pathology. (C) Surgically confirmed intrasubstance tear (arrows) with intact bursal and articular cuff surfaces on an FS T1-weighted coronal oblique MR arthrogram. The biceps tendon (b) and supraspinatus tendon (s) are identified.

FIGURE 8.119 ● (A) Articular-side partial-thickness supraspinatus tendon tear. Arthroscopic view from the glenohumeral joint using the posterior portal. (Based on

Johnson TS, Warren RF. Arthroscopic subacromial decompression and rotator cuff debridement. In: Craig EV, editor. The shoulder, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2004:3–20.

) (B) Partial articular surface tear (straight arrow) is hyperintense on FS PD-weighted FSE coronal oblique image. A corsinosis is indicated (curved arrow).

FIGURE 8.120 ● Partial-thickness bursal-side rotator cuff tear as viewed from a posterior arthroscopic portal. (Based on

Johnson TS, Warren RF. Arthroscopic subacromial decompression and rotator cuff debridement. In: Craig EV, ed. The shoulder, 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2004:3–20.

)

MR Appearance of the Acromion in Impingement

When present, an anterior acromial spur can be identified on MR images and acromial morphology and slope (potential risk factors for anterior acromial impingement) can be characterized (Fig. 8.121). An anterior acromial spur, or enthesophyte, extends from the anteroinferior surface of the acromion in a medial and inferior direction. These spurs may also be seen on

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anteroposterior (outlet view) radiographs. They arise in or adjacent to the acromial attachment to the coracoacromial ligament and are thought to represent traction osteophytes.⁷⁵ Acromial spurs containing marrow fat demonstrate high signal intensity on T1-weighted images. They may, however, blend with the adjacent acromial cortex on FS PD-weighted images, obscuring their identification. Anterior acromial spurs are intermediate in signal intensity and may be overlooked on conventional T2 and T2-weighted FSE sequences. The anterior and inferior location of the spur is best shown on sagittal oblique images. Larger spurs are evident on coronal oblique images. Spurs are composed of primary cortical bone and are low in signal intensity on all pulse sequences. It is important not to misinterpret the normal inferior acromial attachment of the coracoacromial ligament or lateral deltoid attachment as an acromial spur. An area of suspected cortical thickening on the inferior acromial surface, as identified on coronal oblique images, should be verified on corresponding sagittal oblique images. Anterior inferior acromial spurs, although less common than AC joint osteophytes, have a higher predictive value for rotator cuff pathology.

FIGURE 8.121 ● (A) Coronal PD FSE image illustrates a true acromial “keel” spur associated with cuff impingement. Keel spurs are considered aggressive with respect to their potential to cause damage to the bursal side of the cuff if not removed. (B) Complete chronic rotator cuff tear associated with anterior inferior acromial “keel” spur. The associated hypertrophic AC joint is not as important in the pathogenesis or progression of impingement to cuff tear.

The importance of acromial shape in impingement and its classification by Bigliani were described earlier under the section on Acromial Morphology and Impingement. As mentioned, it is the type 3, or hooked, acromion that is associated with a greater predisposition to rotator cuff tears (i.e., tears involving the critical zone immediately proximal to the greater tuberosity insertion on the supraspinatus tendon). A true hook, however, is rare and represents a variant in the development of the preacromial epiphysis. The influence of the hook is related to the slope of its attached acromion.⁹⁵ The type 4 acromion (distal convex undersurface), described by Vanarthos and Mono,⁹⁵ was found in 7% of the patient population studied by MR imaging in 30 patients. The significance of this acromial shape with respect to the incidence of rotator cuff disease is still under study. The appearance of the acromial arch shape is sensitive to the MR section selected on oblique sagittal images.¹³⁰ For example, more medial sections closer to the AC joint may falsely produce the shape of a hooked anterior acromion, which has a flat undersurface on more peripheral sagittal oblique images. It is important, therefore, that sagittal MR review be performed lateral to the AC joint for the determination of acromial shape.¹³¹ MR imaging should not be used as a substitute for the supraspinatus outlet view.²⁴^,¹³⁰

The slope of the acromion can also be assessed on sagittal oblique images (Fig. 8.122). A line drawn tangential to the acromial surface can be used to estimate narrowing of the supraspinatus outlet by a decrease or flattening of the acromial angle.¹³² A flat angle is associated with a higher incidence of impingement in rotator cuff tears in cadavers. An anterior downsloping acromion (see Fig. 8.122) is present when the

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anterior inferior cortex of the acromion is more inferiorly located relative to its posterior cortex as assessed in the sagittal oblique plane. The normal acromion is usually shown as nearly horizontal in its lateral aspect on sagittal oblique images. As discussed in the case of the flat or decreased acromial angle, an anterior downsloping acromion is thought to be associated with an increased risk for anterior acromial impingement.¹³²

FIGURE 8.122 ● (A) Normal upward-oriented acromial slope. (B) Anterior downsloping acromion with narrowed supraspinatus outlet. (C) Anterior downsloping acromion on sagittal PD FSE image.

A lateral downsloping of the acromion, which narrows the acromiohumeral distance, can be appreciated on coronal oblique images (Fig. 8.123). The inferior surface of the distal acromion is inferior or caudally located, relative to the inferior surface of the more proximal aspect of the acromion, which is adjacent to the AC joint (Fig. 8.124). This lateral downsloping of the acromion may be associated with impingement of the supraspinatus tendon near its attachment to the greater tuberosity. The acromion may also appear inferiorly offset relative to the distal clavicle, even in the presence of a normal acromial slope (Fig. 8.125).

Acromial erosion and eburnation are chronic osseous changes of impingement that occur on the undersurface of the anterior third of the acromion. This irregularity on the inferior surface of the acromion is identified on both coronal and sagittal oblique images and may contribute to the further progression of rotator cuff disease.

As mentioned earlier, os acromiale (Fig. 8.126) may also be linked to the development of impingement and rotator cuff tears.¹³³ The os acromiale is visualized in all imaging planes and should not be mistaken for the AC joint. Four types of os acromiale have been described: preacromion, mesoacromion, meta-acromion, and basiacromion. Articulation of the synchondrosis is common between the preacromion and mesoacromion (Fig. 8.127) or mesoacromion and meta-acromion,¹³⁴ and a movable unfused segment of the acromion may result in impingement. Axial images best display the morphology and size of the os acromiale unfused segment. Osteophytic lipping at the margins of the acromial gap may cause direct impingement on the rotator cuff, and contraction of the deltoid muscle, secondary to the downward pull on the os acromiale, has also been implicated in impingement. An unstable os acromiale is also associated with AC joint degeneration.

We have observed increased signal intensity in adjacent portions of the acromial marrow on either side of the fusion defect on both STIR and FS PD-weighted FSE sequences (Fig. 8.128). This hyperintensity may correlate with degenerative changes or instability in symptomatic patients (Fig. 8.129). It is important that impingement not be solely attributed to an os acromiale, because some patients with shoulder impingement who have undergone arthroscopic decompression of the os acromiale have shown subsequent development of recurrent symptoms.¹³⁵ Attempts at epiphysiodesis may result in considerable morbidity with mixed results. Arthroscopic excision of even the largest os acromiale, however, does not produce any deltoid defects or weakness of elevation. All causes of impingement syndrome, including os acromiale, should be carefully evaluated preoperatively and correlated with the patient—s symptoms.

MR Appearance of Acromioclavicular Joint Disease

As previously indicated, arthrosis of the AC joint (Fig. 8.130), including callus and osteophytes, may contribute to impingement, although it now appears to be less important than inferioracromial spurs. The AC joint may encroach on the supraspinatus outlet and cause an extrinsic indentation on the bursal surface of the musculotendinous junction of the supraspinatus. MR imaging is more accurate than conventional radiography in demonstrating the morphology and degree of AC joint enlargement and its relationship to soft tissue structures under the coracoacromial arch (the rotator cuff). The portion of the cuff inferior to the AC joint is not as rigidly confined as the critical zone of the supraspinatus, which is more frequently affected by pathologic impingement at the location of the anterior inferior acromion. Even when the contour of the supraspinatus muscle or tendon is deformed by the AC joint, patients may be asymptomatic.

Although AC joint arthrosis may be described by the radiologist, the diagnosis of impingement remains a clinical one. Marginal osteophytes of the AC joint may precede the presence of anterior acromial erosion. The MR characteristics of degenerative changes in the AC joint may be evaluated in all three imaging planes. The coronal oblique and sagittal oblique planes are more useful in showing the relationship of the callus and osteophyte to the subacromial space and bursal cuff surface. Low-signal-intensity sclerosis, erosions, subchondral cysts, and marrow hyperemia (bright signal on T2, STIR, and FS T2-weighted FSE sequences) are characteristic.

MR Appearance of Humeral Head Changes

Degenerative cysts and sclerosis of the greater tuberosity can be seen on MR scans in shoulder impingement. Humeral head cysts may present adjacent to an area of rotator cuff tendinosis or tear. Greater tuberosity cysts are more common posterior at the greater tuberosity or at its junction with the humeral head adjacent to the capsular insertion.¹³⁴ Degenerative cysts also occur more superiorly or anteriorly.¹³⁴ Squaring and sclerosis of the greater tuberosity are best seen on coronal and sagittal oblique images. Glenohumeral joint degeneration and rotator cuff tears represent the end stage in the spectrum of impingement.⁸⁷^,¹³⁶ Loss of the acromiohumeral distance is also a finding in the later stages of impingement. Rounding of the greater tuberosity also occurs in advanced impingement and is usually associated with corresponding changes of bone erosion or sclerosis on the inferior acromial surface.

The posterior aspect of the rotator cuff is attached adjacent to the bare area of the humeral head. The posterior cuff insertion may be fenestrated with arthroscopically visible openings in the superficial layers. The bare area of the humeral head is adjacent to the posterolateral rotator cuff insertion of the infraspinatus. The normal bare area of the

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humeral head can vary from a few millimeters to up to 2 or 3 cm in diameter. There is a normal absence of articular cartilage in this region. The bare area is associated with either indentations or deep holes representing vascular access channels to the subchondral bone. In comparison, the Hill-Sachs lesion is located more medially and is surrounded by otherwise normal articular cartilage.⁷³

FIGURE 8.123 ● Lateral downsloping acromion as viewed on coronal section.

FIGURE 8.124 ● Lateral downsloping acromion assessed on coronal FSE image.

FIGURE 8.125 ● Inferior projection of the acromion relative to the distal clavicle. Mild arthrosis is also shown on this coronal T2 FSE image.

FIGURE 8.126 ● Asymptomatic os acromiale (arrow) without associated marrow changes on T1-weighted coronal (oblique) image.

FIGURE 8.127 ● Preacromion without degenerative changes. (A) The synchondrosis and the AC joint are shown together on this axial PD FSE image. (B) On this sagittal PD FSE image the synchondrosis could be mistaken for an AC joint.

FIGURE 8.128 ● A mesoacromion with degenerative change and osseous edema across the synchondrosis is shown on an axial color illustration (A) and an axial FS PD FSE image (B).

FIGURE 8.129 ● (A) A painful mesoacromion synchondrosis in a basketball player. (B) Subsequent severe inflammation of the os acromiale after 6 weeks of intensive weight lifting. Axial FS PD FSE images.

FIGURE 8.130 ● AC joint arthrosis with subchondral cystic changes (A) and edema (B) of the distal clavicle and adjacent acromion.

MR examination performed at maximal elevation of the glenohumeral joint has shown abutment of the acromion against the humerus distal to the rotator cuff insertion. Abutment of the undersurface of the supraspinatus tendon against the superior glenoid rim, however, occurs at the extremes of motion. In throwing athletes, subchondral cystic changes are thought to occur with humeral head non-articular contact with the posterior superior glenoid rim. These changes typically occur posterior and deep to the infraspinatus tendon or posterior supraspinatus attachment and have been attributed to internal impingement.

Coracoacromial Ligament

The coracoacromial ligament has a trapezoid shape and attaches to the undersurface of the acromion in a broad or wide insertion. It varies in thickness from 2 to 5.6 mm¹³⁷ and twists in a helical orientation inferiorly to its narrower coracoid insertion. Arthroscopically, the coracoacromial ligament may present in a plane almost perpendicular to the anterior aspect of the supraspinatus tendon as viewed from above. Variation in the size of the coracoacromial ligament may explain the MR observation of ligament hypertrophy. The variable size and thickness of the wide portion of the ligament, inferior to the acromion, may contribute to narrowing of the supraspinatus outlet. Arthroscopic findings of impingement include erosive changes in the acromial attachment of the coracoacromial ligament. Edelson and Luchs have shown enthesopathic transformations of the coracoacromial ligament into bone at its acromial insertion in cadaveric specimens.¹³⁸ These various enthesopathic bone changes can produce different configurations of the hooks and spurs on the inferior surface of the acromion. Although the coracoacromial ligament attachment can be detached from the overlying anterior deltoid muscle, the coracoacromial ligament blends with the deltoid muscle fascia along the lateral acromion, demarcating the anterior from the middle deltoid fibers.

MR Appearance of Coracoid Impingement

Coracohumeral or subcoracoid impingement is thought to occur secondary to narrowing of the space between the coracoid process and the humeral head (Figs. 8.131 and 8.132). The narrowing may be most evident in the position of internal rotation. Bonutti et al.¹³⁹ reported that the normal interval between the coracoid process and the lesser tuberosity is greater than 11 mm in internal rotation as assessed on axial images. Coracohumeral impingement is thought to be associated with interval measurements less than 11 mm. MR findings of impingement may include signal inhomogeneity as well as thickening and fluid within the subcoracoid bursa.¹³⁹ This type of impingement, which may encroach on the subscapularis, does not involve the supraspinatus tendon or cause outlet impingement.⁴⁶ Developmental enlargement of the coracoid process (so that the coracoid projects more laterally) may contribute to subcoracoid impingement when the humeral head is in forward flexion and internal rotation.

FIGURE 8.131 ● Subcoracoid impingement with narrowing of the space between the coracoid and the insertion of the subscapularis tendon on the lesser tuberosity. Hyperintense subscapularis tendinosis is shown on this axial T2* GRE image.

Treatment of Impingement Disorders

Treatment for the different types of impingement disorders depends on the age and activity level of the patient.⁷⁵^,⁸⁷ In general, most patients are treated with conservative therapy for a period of 6 months before surgical intervention is deemed necessary.

Conservative Treatment

In the acute phase, analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and steroid injection are the most effective forms of treatment. In less acute situations, conservative therapy may also include physical therapy, in particular strengthening of the rotator cuff musculature with abduction and external rotation exercises. Internal rotation exercises for the subscapularis are also recommended.

Subacromial bursal injections of steroidal anti-inflammatory agents are effective, but the effect is often temporary, and steroids may be associated with painful postinjection flares. These flares can last as long as 48 hours and produce significant distress. Repeated steroid injections in and about the rotator cuff tendons may have a destructive effect. In general, not more than two or three injections should be used in this area during a 12-month period. Oral NSAIDs may be effective when combined with a reduced activity level. Regardless of the specific treatment, more than 6 months of pain or dramatically decreased activity

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and sleep levels are often unacceptable to the patient. Therefore, if pain reduction through conservative measures is not achieved, an arthroscopic approach is warranted.

FIGURE 8.132 ● Coracoid impingement with narrowing (curved arrows) between the coracoid process (CP) and humeral head. Associated subscapularis tendon degeneration (straight arrow) and subchondral cystic change of the anteromedial humeral head (curved arrow) are shown on (A) T1 and (B) T2*-weighted axial images. LT, lesser tuberosity

Acromioplasty

Arthroscopic subacromial decompression (ASD) is now the method of choice for the treatment of chronic outlet impingement. It is rapidly replacing open acromioplasty⁷⁵^,⁸⁷ because it does not violate the deltoid and overlying deltotrapezial fascia. Arthroscopic anterior acromioplasty, as part of ASD, is indicated for alleviation of pain secondary to the impingement of the anterior inferior surface of the acromion. In ASD, the coracoacromial ligament is detached from the anterior inferior acromial surface, and inflamed or frayed cuff tissue is débrided. A bur is used to perform the anterior acromioplasty.

Patients with early impingement, demonstrating degenerative irregularities of the articular bursal surface of the rotator cuff, are treated by ASD only. Arthroscopic findings usually include not only fraying of the articular or bursal surface but also evidence of fraying of the coracoacromial ligament as it attaches to the anterior and lateral borders of the anterior inferior surface of the acromion. Kissing lesions are irregularities of the bursal surfaces of the cuff found opposite irregularities or fraying of the coracoacromial ligament. Subacro-mial decompression produces good to excellent results in 85% of patients.

Partial-thickness tears involving either the articular or bursal surfaces of the rotator cuff are treated with subacromial decompression and débridement of the partial-thickness tear. Results of treatment of these lesions depend on the extent of the rotator cuff tear: the deeper and more extensive the cleavage planes and the larger the flap of cuff produced by the tear, the greater the likelihood that a simple subacromial decompression will be insufficient and either an arthroscopic or an open repair of the more significantly damaged partially torn cuff will be necessary. Nonetheless, a good number of these patients respond positively to subacromial decompression alone, and because of its minimal morbidity, this procedure can be tried prior to reconstructive procedures.

Full-thickness lesions of the rotator cuff are more difficult treatment dilemmas. In general, patients with full-thickness tears of the rotator cuff require an open procedure, although arthroscopic-assisted rotator cuff repairs, and even purely arthroscopic repairs, are possible. The present standard of care is a deltoid-splitting approach, without significant detachment of the deltoid from the acromial edge, to close the tear following an ASD.

The information provided by MR imaging is helpful in preoperative planning. If MR images show a small tear with minimal retraction, a less invasive arthroscopic approach can be used. If MR images show significant retraction of the tendon to the level of the superior pole of the glenoid, a more extensive approach is necessary. In patients with severe tendon retraction and MR evidence of fiber changes (e.g., fibrosis or atrophy), the prognosis for cuff repair is less optimistic, and the cuff may be irreparable. These patients may be best served with a simple ASD. For patients with evidence of rotator cuff arthropathy with proximal humeral migration, the likelihood of a successful repair is remote. These patients are often older and their main complaint is pain; therefore, ASD alone produces satisfactory results (i.e., pain relief) in approximately 50% of cases.

Associated Arthroscopic Procedures

During subacromial decompression, the entire glenohumeral joint is evaluated, and associated lesions are often noted and appropriate procedures undertaken. Resection of the coracoacromial ligament is always performed in addition to the acromioplasty.

Patients with significant degenerative changes in the AC joint need additional preoperative diagnostic testing, particularly local injections of lidocaine (Xylocaine), to distinguish between pain emanating from a degenerative AC joint and impingement pain produced by spurs. If joint pain is associated

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with impingement, it is necessary to perform an arthroscopic Mumford procedure (i.e., resection of the distal 2 cm of the clavicle) at the same time as the ASD. If a degenerative prominence of the AC joint is producing extrinsic compression of the muscle belly of the supraspinatus, it can also be removed by resecting the distal clavicle.

The biceps tendon, a component of the rotator cuff, must also be arthroscopically evaluated intraoperatively. The tendon is pulled into the joint so that the part of the tendon that lies within the bicipital groove can be assessed. If it is significantly frayed or attenuated, it is resected from its insertion at the glenohumeral tubercle, a deltoid-splitting incision is made, and a tenodesis is performed in the bicipital groove (Fig. 8.133).

FIGURE 8.133 ● T1-weighted (A) coronal oblique and (B) axial images show biceps tenodesis (arrow). (C) The corresponding T2*-weighted axial image shows an absence of the biceps tendon in the bicipital groove (arrow).

Rotator Cuff Tears

Pearls and Pitfalls

Rotator Cuff Tears

Partial-thickness rotator cuff tears are articular, bursal, or interstitial (intrasubstance).
The PASTA lesion is a partial articular-sided supraspinatus tendon avulsion and corresponds to the articular surface delamination tears visualized on MR.
The bursal puddle sign of localized hyperintense fluid signal on coronal oblique MR images correlates with a bursal-side rotator cuff tear.
Intramuscular rotator cuff cysts communicate with partial- or full-thickness cuff tears.

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Coronal images identify an intact stump of cuff tendon attaching to the greater tuberosity in cuff tears proximal to the tendinous footprint.
A wavy contour (“cuff wave sign”) of the retracted cuff tendon is associated with an easier cuff reattachment as the tissue is more compliant and less scarred.
Sagittal images are used to evaluate far anterior supraspinatus tendon tears.
Retracted rotator cuff tears are associated with an increase in cross-sectional diameter on sagittal images.
The normal (without atrophy) supraspinatus muscle nearly occupies the suprascapular fossa as assessed on sagittal images.
The biceps tendon may be medially subluxed or dislocated anteriorly, deep or within the substance of a torn distal subscapularis tendon.
Rotator cuff tendon retears may be associated with partial or complete tendon retraction and/or granulation tissue at the tear site simulating apparent cuff continuity.

No two rotator cuff tears are alike, making their evaluation and treatment protocols complicated. The tears can be characterized as either partial or complete.⁸⁰^,⁸¹ 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. A massive rotator cuff tear involves at least two of the rotator cuff tendons. MR images, particularly in the coronal and sagittal oblique planes, are able to demonstrate partial rotator cuff tears that escape arthrographic detection.¹⁴⁰ In middle-aged and older patients, traumatic tears from a single episode are more commonly found, as are tears associated with acute dislocations.⁷⁸

Partial Tears

Partial-thickness bursal-side rotator cuff tears are most frequently associated with an impingement-type syndrome,¹⁴¹ whereas articular-side cuff tears may be associated with an underlying instability of the shoulder. Partial cuff tears present as fraying without complete disruption of the tendon. Throwers with posterior peel-back lesions have partial-thickness articular-side tears usually located posteriorly at the junction of the supraspinatus and infraspinatus tendons or involving the anterior infraspinatus tendon. Anterior partial cuff articular-side tears are associated with superior labrum-anterior cuff (SLAC) lesions, which demonstrate the anterior labral components of a type 2 SLAP tear. Both location and severity can be used to classify partial tears.¹⁰¹

The location of rotator cuff tears is identified as:

A: At the articular surface
B: At the bursal surface
C: A complete tear, connecting A and B tears

The severity of partial rotator cuff tears (A and B partial tears) has been classified by Snyder¹⁰¹ as:

0: Normal
I: Minimal superficial bursal or synovial irritation or mild capsular fraying in a small localized area (< 1 cm)
II: Fraying and failure of some rotator cuff fibers plus synovial bursal or capsular injury (< 2 cm)
III: Fraying and fragmentation of tendon fibers usually involving the whole surface of a cuff tendon, most commonly the supraspinatus (< 3 cm)
IV: Severe tear with tendon fraying, fragmentation, and a sizable flap tear involving more than a single tendon

The depth of tendon fiber involvement is also used as a criterion for grading of partial tears:¹³⁴^,¹⁴²

Grade 1: Less than 3 mm deep
Grade 2: 3 to 6 mm deep and less than 50% of the cuff thickness involved
Grade 3: A high-grade partial tear more than 6 mm deep with more than 50% of the rotator cuff thickness involved

Partial rotator cuff tears involving the midsubstance are intrasubstance or interstitial tears. As those tears do not extend to either the bursal or articular surface, they may not be detected at arthroscopy. Intratendinous tears tend not to heal over time. The term rim rent tear describes a partial-thickness articular or deep surface tear of the rotator cuff at its attachment to the greater tuberosity (Fig. 8.134). Rotator cuff lesions start where loads are greatest, at the articular surface of the anterior insertion of the supraspinatus adjacent to the LHBT. Cuff tendon fibers fail when the applied load exceeds their strength.

Partial articular supraspinatus tendon avulsions (PASTA lesions)¹⁴³ are delamination tears of the articular surface of the supraspinatus tendon (Fig. 8.135). The term “PASTA lesion” is used to describe partial tears as a III or a IV using the Snyder classification. PASTA lesions demonstrate significant tendon fragmentation or have a flap component that can be arthroscopically repaired. PASTA lesions are more common in repetitive overhead sports and in patients less than 45 years of age. Selective delamination of the opposite or bursal surface of the cuff is also possible (“reverse PASTA”). In cases of bursal surface tearing, continuity of articular fibers is maintained in an attenuated peripheral cuff (see Fig. 8.135). Repair of PASTA lesions is performed with at least 25% good-quality bursal tendon remaining.

MR Appearance of Partial Tears

MR imaging characteristics can be used to classify partial rotator cuff tears as described above, as either partial articular (Fig. 8.136) or bursal (Fig. 8.137) surface lesions. Intrasubstance partial tears do not communicate with either the bursal or articular surface (Fig. 8.138). Cadaveric histopathologic studies have shown that partial tears may originate from regions of tendon degeneration

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(Fig. 8.139). Partial articular surface tears occur more frequently than partial bursal surface or intrasubstance tears.¹⁴⁴ Partial or incomplete tears are thought to be twice as common as complete or full-thickness tears of the rotator cuff.¹¹⁷ Partial tendon tears are distinct from muscle–tendon unit (MTU) strains. MTU strains demonstrate partial muscle group hyperintensity proximal to the conjoined tendon of the rotator cuff (Fig. 8.140). On coronal oblique MR images, partial tears demonstrate low to intermediate signal intensity on T1-weighted images, intermediate to high signal intensity on PD-weighted images, and bright signal intensity on conventional T2-weighted, T2-weighted FSE, and FS PD-weighted FSE sequences. Because severe degeneration and partial tears demonstrate similar regions of increased signal intensity on T2*-weighted images, we do not advocate the routine use of GRE sequences for the detection of rotator cuff disease.

FIGURE 8.134 ● (A) Partial-thickness articular-side tear with adjacent osseous reaction on coronal FS PD FSE image. (B) Coronal FS PD FSE image illustrating a separate case of a rim rent partial articular-side cuff tear with adjacent greater tuberosity edema and erosion. (C) Articular surface irregularity on the undersurface of the cuff. The LHBT is intact. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.)

FIGURE 8.135 ● (A) Delamination of the articular surface of the rotator cuff that creates a substantial flap tear retracted from the remaining tendon is referred to as the PASTA (partial articular supraspinatus tendon avulsion) lesion. (B) PASTA tear with approximately 25% to 30% of the supraspinatus footprint still attached to the greater tuberosity. Retracted or avulsed articular surface fibers are retracted medially underneath the acromion. (C) A “reverse PASTA” involves partial bursal-side (rather than articular-side) delamination.

FIGURE 8.136 ● (A) Partial-thickness articular-side tear of the rotator cuff. (B) Intra-articular contrast extension into a partial-thickness tear of the rotator cuff.

Increased signal intensity due to tracking of fluid within the bursal or articular surface of the cuff is characteristic of partial tears on T2 spin-echo or T2-weighted FSE sequences. Because fat suppression increases the conspicuity of fluid in the subacromial bursa and in a tear site, the addition of fat suppression to the PD-weighted FSE sequence can be useful. T2*-weighted images may also show fluid, which displays higher signal intensity than associated degeneration. Identification of bursal or articular surface defects on these images requires careful evaluation of tendon morphology. Small amounts of fluid may be seen in the subacromial bursa, especially in bursal surface lesions, in the absence of a full-thickness or complete tear (Fig. 8.141). In addition to a partial-thickness tear, there may be associated tendon thinning and fraying. On T2 spin-echo or T2-weighted FSE images, well-defined linear high-signal-intensity changes that do not extend to either the articular or bursal surfaces may represent an intrasubstance partial tear.

As mentioned, partial-thickness tears are characterized by increased signal intensity extending to either the bursal or articular surfaces on coronal oblique or sagittal oblique T2-weighted images, or FSE images perpendicular to the long axis of the tendon (Fig. 8.142). Alternatively, a partial tear may be associated with a more linearly oriented area of degeneration or an intrasubstance tear parallel to the long axis of the supraspinatus or infraspinatus tendon. Some partial-thickness tears are seen in association with an attenuated or thickened cuff and surface morphologic irregularities with variable changes in tendon signal intensity¹¹⁷ (Fig. 8.143). These tears may be difficult to evaluate without an intra-articular paramagnetic MR contrast agent or saline to improve visualization of tendon contours. Fat-suppression techniques, used in conjunction with T2-weighted FSE imaging, and STIR techniques may be more sensitive to fluid signal intensity within small partial tears than conventional spin-echo T2-weighted sequences.

Because of the T1-shortening effects of gadolinium, MR arthrography with intra-articular Gd-DTPA administration is useful in highlighting small, partial tears involving the articular surface. Partial articular surface tears not seen on conventional arthrograms may be identified using MR arthrography, especially in areas of granulation tissue in chronic tears. Tears are bright on T1-weighted post-injection images.¹⁴⁵

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The addition of fat suppression improves the visualization of the hyperintense fluid while suppressing the normal bright signal from fat.¹⁴⁶ This technique helps to avoid mistaking areas of fat, especially linear streaks of fat, for gadolinium contrast extending into a partial tear site. The detection of partial articular surface tears can also be improved by using MR arthrography with the arm positioned in abduction and external rotation.¹⁴⁷

FIGURE 8.137 ● (A) Bursal surface partial-thickness rotator cuff tear. (B) High-grade or severe partial rotator cuff tear of the bursal surface. A sizable flap tear involving both the supraspinatus and conjoined portions of the cuff is demonstrated. (C) This sagittal image lateral to the articular fibers demonstrates fluid between torn bursal fibers and the greater tuberosity.

FIGURE 8.138 ● (A) Intrasubstance or interstitial tear of the supraspinatus without bursal or articular surface extension. (B) Coronal FS PD FSE image demonstrates the hyperintense interstitial tear without loss of continuity of the corresponding bursal or articular surfaces.

FIGURE 8.139 ● (A) Degenerative cuff pathology with initial failure of the rotator cuff occurring along the articular surface of the supraspinatus adjacent to its greater tuberosity insertion. (Based on

Matsen F III, Titelman R, Lippitt S, et al. Rotator cuff, Chapter 15. In: Rockwood CA Jr., Matsen FA III, Wirth MA, et al, eds. The shoulder, 3rd ed. Philadelphia: Saunders, 2004:791–878.

) (B) Partial articular surface tear (arrow) involving the conjoined portion of the rotator cuff. The bursal surface is intact and no fluid is identified in the subacromial-subdeltoid bursa. The tear is hyperintense on this FS PD-weighted FSE coronal (oblique) image.

FIGURE 8.140 ● Superior surface muscle–tendon unit strain of the supraspinatus demonstrates hyperintense muscle edema superior to the tendinous expansion of the cuff on coronal FS PD FSE (A) and sagittal FS PD FSE (B) images.

In patients with tendinosis or tendon degeneration alone, there is no extension of contrast on post-injection images, and the supraspinatus tendon can be seen to be intact. In addition, intra-articular contrast is not helpful in the identification of partial bursal surface tears and does not enhance intrasubstance tears. A preliminary T2-weighted spin-echo or T2-weighted FSE sequence is performed to evaluate these areas. Intraven-ous use of an MR contrast agent may prove to be helpful in enhancing synovium and granulation tissue in partial bursal surface tears.

Since MR arthrography is not routinely used in uncomplicated evaluations of the rotator cuff, the detection of partial tears can also be optimized by using fat suppression in conjunction with conventional or FSE T2-weighted sequences without the use of intra-articular contrast.

Full-Thickness Tears

Rotator cuff disruption may be characterized as partial- or full-thickness, acute or chronic, and traumatic or degenerative.⁷⁴ The mechanism of cuff tears usually involves an attritional tear of the rotator cuff tendons with or without subacromial impingement. A cuff tear as a result of a traumatic injury occurs in the setting of preexisting tendon degeneration. Contributing factors to cuff disruption, therefore, include trauma, attrition, ischemia, and subacromial abrasion. Partial-thickness tears progress to full-thickness lesions (Fig. 8.144). The rotator cuff is subjected to traction, compression, contusion, subacromial abrasion, inflammation, and, most importantly, age-related degeneration. Rotator cuff tendon fibers may fail a few at a time or en masse. Torn tendon fibers retract because they are under load even with the arm at rest. Healing cuff scar tissue lacks normal tendon resilience and may be at an increased risk of failure with subsequent loading. Because of the marked ability of the cuff to repair itself, the degeneration process continues and propagates until a full-thickness anterior supraspinatus tendon defect is produced. Because the full-thickness tendon defect concentrates loads at its margin, additional tendon fiber failure may subsequently occur with even smaller applied loads (Fig. 8.145). A supraspinatus defect will propagate posteriorly through the remainder of the supraspinatus and may then involve the infraspinatus. Intramuscular cysts ¹⁴⁸ may dissect along the path of the torn rotator cuff tendon (Fig. 8.146). The supraspinatus is prone to both mucoid degeneration with interstitial tendon extension as well as communicating intramuscular cysts. AC joint cysts may communicate with an extensive rotator cuff tear and present as a superior pseudotumor of the shoulder.¹⁴⁹ Once the apron effect of the rotator cuff is lost, the humeral head displaces superiorly, placing increased loads on the biceps tendon. The LHBT is

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frequently ruptured in chronic rotator cuff deficiency. As the rotator cuff defect propagates, the tear may destabilize the LHBT and involve the subscapularis tendon. Biceps pulley lesions are associated with medial displacement of the biceps tendon, especially when both the anterior articular surface of the supraspinatus tendon and superior deep fibers of the subscapularis tendon are involved (also see discussion on Biceps Pulley Lesions). Rotator cuff arthropathy develops with failure and abrasive contact between the chondral surface of the humeral head and the coracoacromial arch, causing degenerative joint disease.

FIGURE 8.141 ● Bursal puddle sign associated with an adjacent bursal-side rotator cuff tear as seen on a color coronal section (A) and a coronal T2 FSE image (B). If this localized collection of subacromial fluid is identified without a full-thickness tear, then the diagnosis of bursal-side fraying or partial-thickness tear must be assumed. (C, D) A partial-thickness bursal surface tear (arrow) in communication with the subacromial-subdeltoid bursa. Fluid is hyperintense on intermediate weighted (C) and T2-weighted (D) FSE coronal oblique images.

FIGURE 8.142 ● Partial-thickness articular surface tear requiring both coronal and sagittal images to assess the area of involvement (size of tear). (A) Coronal T2 FSE image. (B) Sagittal FS PD FSE image.

FIGURE 8.143 ● Partial tear with abnormal attenuation (arrow) of the distal conjoined supraspinatus and infraspinatus cuff tendons. Fluid is hyperintense and cuff degeneration is intermediate in signal intensity. There is no direct communication of fluid between the glenohumeral joint and subacromial-subdeltoid bursa on this FS PD-weighted FSE coronal oblique image.

FIGURE 8.144 ● A complete tear connecting articular and bursal sides of the rotator cuff can be seen on this coronal FS T1-weighted MR arthrogram.

FIGURE 8.145 ● The notch phenomenon occurs when stress forces on the cuff tendon are directed toward the margin of the defect. Increased retraction forces result in further fiber failure, enlarging the area of the tear. (A) Posterosuperior view color illustration and (B) axial PD FSE image.

FIGURE 8.146 ● (A) Coronal FS PD FSE and (B) sagittal FS PD FSE images depict a hyperintense intramuscular cyst dissecting proximally into the supraspinatus muscle from the side of tendinous disruption.

After minimal débridement, chronic complete rotator cuff tears are assessed at their greatest point of retraction for muscle changes, including:

Atrophy¹⁵⁰
Fatty degeneration
Retraction
Loss of excursion

Tear size is assessed on MR examination as the size of the fluid-filled gap or retraction from medial to lateral in the coronal plane and anterior to posterior in the sagittal plane. Cuff size and quality of muscle and tendon, including atrophy, rupture of the biceps tendon, and shoulder weakness, are important prognostic factors in determining surgical outcome. Cuff tendon retraction can be staged in the coronal plane as stage 1 (adjacent to the tendon insertion), stage 2 (retraction superior to the humeral head), or stage 3 (proximal retraction to the glenoid margin).

Isolated infraspinatus full-thickness tears are uncommon.¹³⁴ These tears may be found in the throwing athlete with involvement of the articular surface of the supraspinatus–infraspinatus junction or anterior infraspinatus articular surface. Although tears of the teres minor are unusual, the superior fibers of the teres minor may be involved with a massive rotator cuff tear. Teres minor tears may also occur in association with infraspinatus tendon tears and posterior capsular trauma in posterior dislocation. The rotator cuff tendon edges may be good, fair, or poor. Atrophy is also graded in a similar fashion as mild, moderate, or severe.

Snyder¹⁵¹ has classified complete rotator cuff tears based on size and complexity into the following categories:

0: Tear lacks full-thickness communication between the bursal and articular surfaces, even if partial tears exist on both.
I: A small complete tear (puncture)
II: A moderate (< 2 cm) tear involving one tendon without retraction
III: A large (3 to 4 cm) complete tear involving an entire tendon with minimal retraction of the torn edge
IV: A massive cuff tear involving two or more cuff tendons, usually with associated retraction and scarring of the remaining tendon ends. Tears in this group may be subclassified or determined to be irreparable

MR Appearance of Full-Thickness Tears

Complete (full-thickness) tears of the rotator cuff, with or without proximal retraction, can be depicted clearly with MR imaging.¹⁴⁶^,¹⁵²^,¹⁵³^,¹⁵⁴^,¹⁵⁵^,¹⁵⁶^,¹⁵⁷ The combination of FS PD-weighted FSE and T2-weighted FSE sequences improves the characterization of tear morphology. The exclusive use of FS PD-weighted FSE images, however, may produce a false-positive result because areas of degeneration may be misinterpreted as hyperintense partial tears. The FS PD-weighted FSE sequence thus is typically used in conjunction with a non-FS T2-weighted FSE sequence. Many protocols, however, still use only PD and FS PD FSE without taking advantage of the increased specificity of T2 FSE coronal images.

According to Neer—s classification, 95% of all rotator cuff tears are impingement tears caused by outlet impingement.⁸⁰ Together, traumatic tears and rotator interval tears account for only 5% of all cuff tears. MR imaging confirms the gross anatomic finding that most tears of the supraspinatus involve its anterior attachment to the greater tuberosity. In critical zone tears (tears immediately proximal to the greater tuberosity insertion of the supraspinatus tendon), a small remnant of tendon may be still attached to the greater tuberosity. In patients older than 40 years of age, rotator cuff tendon tears are frequently associated with acute glenohumeral dislocations. Infrequent traumatic tears in younger individuals may avulse a segment of the greater tuberosity.

The size of a rotator cuff tear can be determined by measuring its long diameter in centimeters. A small cuff tear measures less than 1 cm, a medium cuff tear measures 1 to 3 cm, a large cuff tear is 3 to 5 cm, and a massive tear is greater than 5 cm. The number of tendons involved, and their level of retraction, is of more clinical significance than size, however.

MR findings have been divided generally into two categories, primary and secondary.

Primary signs

Primary signs of full-thickness rotator cuff tears include:

Visualization of a tendon defect or tendinous gap, which is seen as an interruption or loss of continuity of the normally low-signal-intensity tendon
Tendon retraction, which is best assessed in the coronal plane. The torn cuff edge is located near the greater tuberosity insertion in stage 1 (Fig. 8.147), superior to the humeral head in stage 2 (Fig. 8.148), or retracted to the level of the glenoid margin in stage 3 (Fig. 8.149).
Joint fluid or granulation tissue at the cuff tear site, which is seen as areas of intermediate to increased signal intensity on T1-weighted and PD-weighted images. Depending on the complexity of the tear and the degree of retraction of the supraspinatus, a large fluid-filled gap may not be seen on sagittal images, especially if there is a delamination component to the cuff tear. Fluid signal appearing superior, anterior, and inferior along the undersurface of the supraspinatus tendon is characteristic of a complete tear (Fig. 8.150). On T2 spin-echo, T2-weighted FSE, and FS PD-weighted FSE sequences, these areas demonstrate markedly increased signal intensity.

FIGURE 8.147 ● (A) Color coronal section and (B) coronal FS PD FSE image show a stage 1 full-thickness cuff tear with the torn cuff edge adjacent to the greater tuberosity.

FIGURE 8.148 ● (A) Coronal color section, (B) coronal T2 FSE image, and (C) sagittal FS PD FSE image of a stage 2 full-thickness rotator cuff tear with supraspinatus tendon retraction superior to the humeral head.

FIGURE 8.149 A ● Coronal color section, (B) coronal T2 FSE image, and (C) axial PD FSE image show a stage 3 full-thickness rotator cuff tear with tendon retraction to the level of the glenoid.

FIGURE 8.150 ● (A) Sagittal T2 FSE and (B) coronal FSE images display hyperintense fluid signal intensity surrounding the anterior, bursal, and articular surfaces of the anterior cuff.

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Although PD-weighted images are sensitive to changes in signal intensity in cuff tendons, in comparison with T2-weighted images these sequences are limited in differentiating small or partial cuff tears from severe tendinosis. T1- or PD-weighted images are, however, useful in demonstrating associated fatty atrophy in the supraspinatus muscle or alterations in the AC joint with osteophytes and subchondral sclerosis. 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). Sagittal oblique images provide additional information, allowing identification of articular and bursal surface extension and the location and size of the tear in the anteroposterior direction.

Acute rotator cuff tears are often associated with muscle and MTU edema in addition to retraction of the involved tendons of the rotator cuff (Fig. 8.151). Superior ascent of the humeral head occurs with loss of the depressor action of the torn cuff and may occur with acute multitendon (massive) cuff tears (see Figs. 8.149 and 8-151; Fig. 8.152). Massive cuff tears may involve the supraspinatus, the infraspinatus, and the subscapularis tendons. The LHBT is also frequently disrupted in massive cuff tears. Nonacute cuff tears require evaluation of the integrity and loss of continuity of torn tendon edges. In subacute tears, FS PD FSE images may actually be more useful than T2 FSE studies because the relative hyperintensity of granulation tissue and synovium helps to define the tendon edges (Fig. 8.153).

Isolated infraspinatus tears are identified on posterior coronal and sagittal images (Fig. 8.154). The increased cross-sectional diameter sign of the retracted tendon may be helpful in more subtle cases of subacute supraspinatus or infraspinatus tendon tears (Fig. 8.155).

Preoperative MR imaging studies provide important information about the size of the cuff tear, the degree of proximal or medial retraction, and the quality of the associated muscle tissue. Complete absence of the rotator cuff indicates a major tendinous disruption and is typical of rotator cuff arthropathy in which the proximal head is in direct contact with the undersurface of the acromion (Fig. 8.156). 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 (Fig. 8.157). Patients with complete tears complicated by cuff arthropathy, tendon retraction, and muscle atrophy may not be candidates for surgical repair.

Retraction of the supraspinatus or infraspinatus tendon is best seen on coronal oblique images that demonstrate the medial and lateral extension of the cuff tear. The retracted cuff tendon may be seen as far medially as the level of the bony glenoid rim. The retracted cuff margins may be thickened in response to healing or attenuated in more chronic tears. The uninvolved areas of the tendon adjacent to the tear site may demonstrate degenerative changes or partial-thickness tear. Less frequently, the remaining tendon demonstrates normal signal intensity or morphology. T2-weighted sagittal oblique images are used to identify the anteroposterior extent of the cuff tear. Subscapularis and infraspinatus tendon tears are evaluated on both sagittal

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oblique and axial plane images. The tendinous gap and high-signal-intensity fluid seen in large supraspinatus tendon tears can be shown on axial images superior to the glenohumeral joint.

FIGURE 8.151 ● (A) Coronal FS PD FSE and (B) sagittal FS PD FSE images of hyperintense muscle–tendon signal intensity associated with a large full-thickness acute rotator cuff tear. There is secondary superior ascent of the humeral head.

FIGURE 8.152 ● (A) Posterosuperior view color graphic showing a massive rotator cuff tear involving the supraspinatus, infraspinatus, and subscapularis tendons. (B) Coronal FS PD FSE image showing the wave sign of a retracted supraspinatus tendon as a sign of a reparable acute cuff tear without associated scarring.

FIGURE 8.153 ● Coronal images depicting a nonacute supraspinatus tendon tear. The tears shows residual hyperintensity at the tear site on FS PD FSE images (A) and intermediate signal intensity on T2 FSE images (B).

FIGURE 8.154 ● An isolated infraspinatus tendon tear shown on (A) a posterior superior color illustration, (B) a posterior coronal FS PD FSE image, and (C) a sagittal FS PD FSE image.

FIGURE 8.155 ● Increased cross-sectional diameter “sign” of a retracted infraspinatus tendon in an isolated tendon tear of the rotator cuff is seen on (A) sagittal FS PD FSE and (B) coronal FS PD FSE images. Increased tendon diameter is useful as a secondary sign of supraspinatus or infraspinatus tendon retraction.

FIGURE 8.156 ● Coronal FS PD FSE (A) and T2 FSE (B) images showing chronic cuff arthropathy with superior ascent of the humeral head, contact and remodeling of the undersurface of the acromion, greater tuberosity cystic change, and fatty atrophy of the supraspinatus.

FIGURE 8.157 ● (A) Chronic rotator cuff fatty atrophy associated with proximal retraction. (B) Coronal PD FSE image showing supraspinatus atrophy with increased fat signal intensity superior to the retracted rotator cuff tendon. (C) Sagittal PD FSE image showing decreased supraspinatus muscle bulk with circumferential fat signal intensity extending from the supraspinatus fossa to the supraspinatus outlet.

Secondary signs

Secondary signs of rotator cuff tears were previously used in conjunction with primary signs to help in the diagnosis of cuff tears. The use of secondary signs, however, has been mostly supplanted by identification of the primary diagnostic criteria of tendon signal and morphology depicted by using higher-resolution images, the combination of FS PD FSE and T2 FSE coronal images, and MR arthrography when indicated. Recognition of these secondary signs, however, is still important in the interpretation of routine shoulder MR studies.

Secondary signs of full-thickness tears include:

Subacromial-subdeltoid bursal fluid, which should be readily identifiable, especially when there is a large volume of articular and bursal fluid associated with a complete tear. However, fluid in the subacromial bursa may also be present in impingement or in a partial bursal surface tear without communication with the glenohumeral joint. Subacromial-subdeltoid bursal fluid is also seen in asymptomatic individuals and in cases of isolated bursitis.¹¹⁷
Retraction of the supraspinatus musculotendinous junction may be seen in full-thickness cuff tears but is not observed with small cuff tears. The normal location of the supraspinatus musculotendinous junction is at approximately the 12 o—clock position, superior to the center of the humeral head. The location of this junction may vary within a 30° radius (15° either medial or lateral to the 12 o—clock position).¹¹⁶ The location of the musculotendinous junction may change with the position of the arm in internal or external rotation. Although this finding, even without a defined cuff defect, may indicate an increased probability for a tear, it is still a secondary finding.
Tears with granulation tissue may not demonstrate bright signal intensity on spin-echo or FSE T2-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.
Rarely a massive synovial reaction (hyperintense on FS PD FSE) may develop and fill the gap of a rotator cuff tear (Fig. 8.158). The biceps tendon may be difficult to find at surgery if it is encased in concentric layers of hypertrophied gelatinous synovium. Inflammatory arthropathy and even infection may present with similar imaging characteristics. Rice bodies (discrete synovial fronds) or subcutaneous edema, however, is not associated with this type of synovial response.
Subacromial and subdeltoid peribursal fat changes may also be considered secondary signs of cuff pathology. Because peribursal fat may be replaced by either low-signal-intensity granulation tissue or scar or bright-signal-intensity fluid, which is often limited to the site of the cuff tear, we use this abnormality as a secondary to tertiary sign when a cuff tear is not clearly visualized.
Fatty atrophy of the rotator cuff muscle is usually associated with more chronic complete tears. Fatty replacement is best demonstrated on T1- or PD-weighted images, which display high-signal-intensity (equal to fat) horizontal streaks parallel to the long axis of the supraspinatus. The changes of supraspinatus muscle atrophy are not conspicuous on GRE, FS PD-weighted FSE, or STIR sequences.

Alterations in the peribursal fat plane and proximal musculotendinous junction are present in up to 92% of complete tears. With the use of fat-suppression techniques, Mirowitz¹⁵⁸ has shown that many of the established secondary criteria for diagnosis of rotator cuff tears, including obliteration of the subacromial-subdeltoid fat plane and fluid in the subacromial-subdeltoid bursa, are routinely found in asymptomatic populations.¹⁵⁸

Subscapularis Tendon Tears

The subscapularis muscle forms the anterior cuff. The inferior third of the subscapularis insertion on the humerus is primarily muscular with minimal intervening tendinous tissue¹⁵⁹ (Fig. 8.159). The supraspinatus is multipennate and is dually innervated by the upper and lower subscapular nerves. The axillary neurovascular bundle, including the axillary nerve, is located in proximity to the anterior inferior surface of the muscle as it passes around the inferior border of the subscapularis to enter the quadrilateral space. The axillary nerve is at risk in operative repair of subscapularis tendon avulsions if the retracted tendon and localized hemorrhage obscure the course of the nerve. The axillary nerve may be incarcerated in scar tissue with the subscapularis tendon stump.

Isolated avulsion of the subscapularis is associated with severe external rotation or hyperextension of the shoulder (Fig. 8.160). Repair of isolated subscapularis tears is often performed with a tenodesis or tenotomy of the biceps tendon to improve shoulder function.¹⁶⁰ Anterior dislocation of the shoulder may be associated with subscapularis avulsion in patients over 30 years of age. Anterior shoulder pain and pain with forward flexion and external rotation may accompany weakness. Painful popping occurs secondary to coexisting biceps tendon subluxation. Anterior instability may also coexist with subscapularis rupture. Increased passive external rotation of the affected shoulder and a positive lift-off test are observed on physical examination. In the lift-off test the patient starts with the back of the hand placed behind the back and is asked to push away from the lumbar spine under resistance. The inability to push the hand away from the back during the lift-off test indicates a subscapularis tendon tear.

MR Appearance of Subscapularis Tendon Tears

Most subscapularis tendon tears occur in association with

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tears of the supraspinatus and infraspinatus tendons. How-ever, injury to the subscapularis may occur as an isolated partial tear independent of any other cuff pathology.¹⁵⁴ Subscapularis tendon injuries range from small corner tears at the superior edge, adjacent to the bone tendon junction, to chronic massive retracted tears with fatty atrophy of the muscle (Fig. 8.161). Partial tears may be associated with thickening of the subscapularis tendon in conjunction with regions of fiber discontinuity.

FIGURE 8.158 ● Hyperintense hypertrophic synovium occupying the tendinous gap of a full-thickness rotator cuff tear on a coronal FS PD FSE image (A) and sagittal FS PD FSE image (B). (C) The biceps tendon is encased in a massive thickened synovial envelope on this axial FS PD FSE image.

FIGURE 8.159 ● Inferior muscle belly partial tear of the subscapularis on (A) axial FS PD FSE and (B) sagittal PD FSE images.

FIGURE 8.160 ● (A) Isolated subscapularis tendon tear without associated biceps tendon dislocation. (B) Subscapularis tendon tear with involvement of anterior or superficial fibers. Subscapularis tendon tears are associated with biceps tendon instability with laxity or disruption of the CHL–SGHL sling. SGHL tears are frequently associated with superior distal subscapularis tendon disruptions. Axial FS PD FSE image.

Although increased signal intensity on T2-weighted images can be observed on coronal oblique and sagittal oblique images through the subscapularis, it is the axial plane that is most important and specific for the evaluation of subscapularis tendon tears. MR in the axial plane documents partial tearing or degenerative fraying, which may involve only the leading edge (Fig. 8.162). A partial tear of the attachment of the subscapularis to the lesser tuberosity is associated with a deficiency in the superior aspect of the tendon insertion onto the lesser tuberosity just inferior to the coracoid process. Complete detachment from the lesser tuberosity is associated with fluid signal intensity extending anterior to the retracted tendon. Avulsion fractures of the lesser tuberosity are uncommon and usually occur in younger patients.¹⁶¹ Associated biceps tendon abnormalities, including medial dislocation, may also be present (Fig. 8.163). A full-thickness tear of the subscapularis tendon may be retracted, with the torn anterior capsule proximal to the lesser tuberosity to the level of the anterior glenoid rim.¹⁶² The location of the biceps relative to the intertubercular groove, the status of the remaining rotator cuff tendons, and the finding of degenerative joint changes are assessed prior to surgery. Patients with chronic instability may have a tag of anterior capsule attached to the torn or ruptured subscapularis tendon. A retracted and atrophied subscapularis may never regain function even if reattached to the humerus. Partial tears may show fraying at the attachment site of the tendon to the lesser tuberosity. Splitting along the superior rolled border of the tendon edge is also seen with partial tears. Interstitial tears may extend along a segment of the distal subscapularis and can usually be visualized both on axial and sagittal images.

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Because of the multipennate morphology of the subscapularis, the diagnosis of partial tears on sagittal images should always be confirmed in the axial plane.

FIGURE 8.161 ● Axial PD FSE (A) and FS PD FSE (B) images showing a subscapularis tendon tear with deep fiber osseous avulsion from the lesser tuberosity in a wrestler.

FIGURE 8.162 ● Degenerative fraying and tendinosis of the distal leading edge of the subscapularis tendon.

FIGURE 8.163 ● Biceps dislocation associated with rupture of the distal subscapularis tendon and tearing of the CHL–SGHL sling.

Teres Minor Tendon Tears

Tears of the teres minor tendon, either in association with massive cuff tears or as an isolated injury, are uncommon (Fig. 8.164). Large or massive rotator cuff tears involving the infraspinatus and teres minor tendons are associated with either the inability to externally rotate the shoulder with the arm at 90° of abduction or the inability to actively maintain a passive position of external rotation with the arm at 90° of abduction (horn blower—s sign).¹⁶³ A suprascapularis nerve palsy may also be present. 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) (Fig. 8.165).¹⁶⁴ These changes are visualized on sagittal oblique FS PD FSE images as hyperintensity of the teres minor. More chronic, fatty replacement of the muscle is best visualized on non-FS images. Osteophytes or paralabral cysts may also cause neurapraxia involving the teres minor branch of the axillary nerve (Fig. 8.166). MR signs of denervation include areas of hyperintensity on T2 or FS images. Changes in fatty atrophy, however, do not show an increase in signal intensity on FS T2-weighted or STIR images.

Accuracy of MR Imaging in Rotator Cuff Tears

MR imaging is both sensitive and specific for rotator cuff tears. Zlatkin et al.³⁰ reported MR sensitivity and specificity for imaging of partial- and full-thickness tears of 91% and 88%, respectively, with 89% accuracy. Preoperative assessment of the size of the rotator cuff tear compared favorably with surgical findings in 95% of cases. In another study, using arthroscopic or surgical correlation in complete cuff tears in 91 patients, MR imaging had a sensitivity of 100% and a specificity of 95%.¹⁶⁵ Burk et al. reported comparable findings in the diagnosis of rotator cuff tears: 92% sensitivity and 100% specificity for MR compared to 63% sensitivity and 50% specificity for ultrasound.¹⁶ Raffi et al., in a study of 37 documented full-thickness tears, reported a sensitivity of 97% and a specificity of 94%. Of 16 partial tears, 14 were diagnosed accurately with MR imaging.¹²²

Fat-suppression techniques improve the detection of both complete and partial rotator cuff tears when compared with conventional spin-echo techniques.¹⁵⁶ It is the combination of both FS PD FSE and T2 FSE, however, that produces the highest detection rates. These protocols have been reported to have a combined accuracy rate of 93% (with a sensitivity of 84% and a specificity of 97%) in the detection of complete and partial tears of the rotator cuff.¹⁵⁵ Muscle inflammation, infection,

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or strain is also more accurately displayed with greater conspicuity on FS PD FSE images (Fig. 8.167).

FIGURE 8.164 ● Isolated teres minor muscle–tendon unit overload/strain on (A) axial and (B) sagittal FS PD FSE images.

FIGURE 8.165 ● Isolated fatty atrophy of the teres minor muscle in quadrilateral space syndrome on (A) sagittal and (B) coronal PD FSE images.

FIGURE 8.166 ● On this sagittal T2 FSE image, space-occupying inferior osteophytes associated with partial fatty replacement of the teres minor muscle are seen encroaching into the quadrilateral space.

The addition of fat suppression to MR arthrography increases the sensitivity and specificity of this technique from 90% and 75%, respectively, to 100% for both sensitivity and specificity for the identification of full- and partial-thickness cuff tears.¹⁴⁶ FS images are also sensitive to the intratendinous imbibition of contrast material in regions of associated tendon swelling, fraying, and friability.

FIGURE 8.167 ● Infraspinatus myositis secondary to injection on an axial FS PD FSE image.

MR Findings in Asymptomatic Shoulders

In a study of 96 asymptomatic individuals, Sher et al. found tears of the rotator cuff in 34%.¹⁶⁶ The frequency of both full- and partial-thickness tears increases with age, and in asymptomatic individuals over 60 years of age, 54% had a tear of the rotator cuff. Partial tears (24%) were more common than full-thickness tears (4%) in younger individuals (40 to 60 years of age). Among 19- to 39-year-old patients, partial-thickness tears were found in 4%, but no full-thickness tears were found. Miniaci et al. found similar results and reported no full-thickness tears in 20 asymptomatic volunteers ranging in age from 17 to 49, with a mean age of 29.¹⁶⁷ It is clear that MR findings of rotator cuff disease must be considered in a clinical context and should never be used as the only basis for operative intervention.¹⁶⁶ Positive MR findings for a rotator cuff tear may not be concordant with a patient—s symptoms or lack thereof.

MR Appearance of Postoperative Rotator Cuff

MR imaging has also been used for postoperative evaluation of rotator cuff repairs.¹⁶⁸ Because GRE sequences frequently show increased magnetic susceptibility artifacts, the repair site may not be clearly visualized on the scans. Conventional T1 and T2 spin-echo and FSE sequences minimize these low-signal-intensity artifacts and allow visualization of increased signal intensity in cuff defects. Postoperative MR arthrography, using an FS 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 (Fig. 8.168) and include:

Persistent changes from impingement (including tendon degeneration, partial tear, and retear [Fig. 8.169], a rough undersurface of the acromion, or residual AC joint callus or osteophytes)
Deltoid attachment instability (Fig. 8.170)
Nerve damage

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 diagnose a failed repair or retear of the rotator cuff. Relative increased cuff signal intensity on FS PD FSE images may also be seen in the postoperative cuff repair without retear. 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

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of fluid signal intensity on T2-weighted or FS PD-weighted FSE sequences is diagnostic for a retorn repair. A retracted or nonvisualized section of the rotator cuff also represents a full-thickness tear. Because rotator cuff contours may be irregular in the postsurgical cuff, the distinction between a partial-thickness tear and an intact repair site may be difficult. Owen et al.¹⁵³ reported a 90% accuracy for the detection of full-thickness tears in the postoperative shoulder. Sagittal T2-weighted images are particularly useful in the evaluation of the anterior portion of the supraspinatus tendon. They minimize the partial volume effect of subacromial-subdeltoid fluid anteriorly and demonstrate portions of the cuff that may be difficult to discern on coronal oblique images because of a micrometallic or suture artifact.

FIGURE 8.168 ● (A) Partial anterior acromioplasty. The coracoacromial ligament (CA) should be released from the acromion and not resected from under the deltoid in order to allow the ligament to reattach to the acromion and reconstitute the anterior arch. (B) Subacromial decompression performed for a partial-thickness rotator cuff tear. In cuff impingement the coracoacromial ligament is frayed and fragmented and associated with synovitis. Decompression results in a flat undersurface of the acromion and release of the CA ligament. The inferior lip of the distal clavicle is also removed if it extends inferior to the flattened acromion. Coplaning the distal clavicle avoids a step-off between the acromion and clavicle.

FIGURE 8.169 ● Massive retear of the rotator cuff tendons after repair. The retracted supraspinatus and infraspinatus tendons are shown on coronal PD FSE (A) and sagittal FS PD FSE (B) images.

FIGURE 8.170 ● Postoperative deltoid avulsion. In the presence of a symptomatic AC joint, an undersurface claviculoplasty is performed, which protects and preserves the deltoid origin. Although these avulsions may not be painful, they can be repaired along with a re-repair of the cuff to allow the patient to lift the arm with a functioning deltoid.

FIGURE 8.171 ● A Mumford or arthroscopic distal clavicle resection (ADCR) is performed for symptomatic AC joints. Coplaning or the “mini-Mumford” is also an option to remove inferior AC joint spurs. (A) Axial FS PD FSE and (B) axial T2 FSE images.

Surgical Management

The repair procedure of choice begins with an arthroscopic subacromial decompression, followed by a deltoid-splitting approach to gain access to the torn cuff.⁸⁰ 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. As mentioned earlier, a Mumford procedure (Fig. 8.171) may be performed when AC degeneration is evident.

The rotator cuff is usually repaired with nonabsorbable sutures (Fig. 8.172) or suture anchors (used in arthroscopic repairs) (Figs. 8.173) to reattach the avulsed tendon to a denuded bed of bone. With the deltoid-splitting approach, drill holes in the acromion are not necessary, and proper subperiosteal reflection of the deltoid at the acromion permits a side-to-side closure. If extensive dissection of the deltoid from the acromion is carried out, drill holes are necessary to repair the deltoid, which is reflected during surgery. This approach has a higher rate of morbidity, and postoperative deltoid defects are more common. Most repairs can be achieved through a more limited deltoid-splitting approach.

Suture anchors can be used to repair more massive cuff tears as well as isolated supraspinatus injuries (Fig. 8.174). The suture anchors should be located lateral to the edge of the humeral

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head articular cartilage and directed medial and inferiorly into subchondral bone. The deltoid-sparing aspect of the arthroscopic repair represents an advantage over open procedures. Postoperative inflammation usually resolves by 6 weeks. As mentioned above, postoperative MR examination should document healing of the repaired cuff with a reestablished supraspinatus tendon footprint over the greater tuberosity.¹⁶⁹

FIGURE 8.172 ● Tendon-to-bone rotator cuff repair with suturing of the edge of the distal cuff into a prepared humeral head trough.

FIGURE 8.173 ● (A) The majority of torn rotator cuffs can be repaired arthroscopically. Suture anchor fixation of the rotator cuff tear to bone is shown. One or two sutures can be used in each suture anchor. The arthroscopic technique allows for an enhanced fixation of the cuff tendon, which can be performed with side-to-side suture anchors. (B) Coronal FS PD FSE image showing the suture anchors (two or three anchors may be needed) located lateral to the edge of the articular cartilage and directly obliquely and medial into subchondral bone. There is residual cuff tendinosis and subacromial bursal fluid.

FIGURE 8.174 ● Suture anchor repair of both the supraspinatus and subscapularis tendons. Suture anchors do not preclude postoperative MR assessment. Arthroscopy spares damage to the deltoid and allows an ideal subacromial decompression.

Complications

Arthroscopic repair of an isolated supraspinatus full-thickness tear usually results in complete tendon healing. However, lower healing rates have been observed in patients over 65 years of age, in cases of associated delamination of the subscapularis, and in infraspinatus tears.¹⁷⁰ Superior ascent of the humeral head, remodeling of the undersurface of the acromion, and fatty atrophy of the rotator cuff are all indicators of a difficult direct cuff repair. A soft tissue grasper may be used at arthroscopy to test the mobility of the cuff and to assess the need for a capsule release or interval slide.¹⁷¹ Scar tissue is removed to expose a retracted supraspinatus (Fig. 8.175). A rotator cuff may adhere to or retract from the undersurface of the acromion with no tendinous attachment to the humeral head. Cuff atrophy may be minimal in this scenario, since there is a fixation point to bone by scar tissue. The supraspinatus tendon must be mobilized and peeled off the inferior acromial surface and reattached to the greater tuberosity. Suture anchors should be evaluated for retraction (superior displacement relative to the humeral head contour) (Fig. 8.176).¹⁷² A rotator cuff washer may be displaced on a failed cuff repair. If it migrates into the subacromial bursa, it is visualized as hypointense, thin, and convex (Fig. 8.177).

Microinstability

The term microinstability was developed to characterize the spectrum of pathologic processes that occur in the upper half of the shoulder joint. The structures involved in microinstability lesions (Fig. 8.178) include:

Superior structures:
- The biceps and its associated pulley (CHL and SGHL)
- The biceps root attachment/superior labrum (SLAP lesions)
- The rotator cuff
Anterior structures:
- Rotator interval, including the SGHL in the anterior superior portion and the MGHL inferior to the SGHL

At arthroscopy the rotator interval is directly visualized between the intra-articular biceps, superior labrum, MGHL, and humeral head. Cadaveric sectioning of the rotator interval has been demonstrated to produce increased inferior and posterior humeral head translation. There is increased anterior translation of the humeral head at 60° of flexion characterized as microinstability.¹⁷³ The spectrum of pathologic changes in microinstability pathology includes:

SGHL avulsion or laxity
MGHL avulsion producing straight anterior laxity
SLAP lesions (types 1–10). A type 10 SLAP lesion is a type 2 SLAP tear with extension into the rotator interval.
Posterior peel-back SLAP tears
Interval defects or biceps pulley lesions
Articular side cuff lesions (partial-thickness and typically non-crescentic in location). These articular side tears may occur from abrasion of the rotator cuff on the glenoid either anteriorly or posteriorly.

The estimated incidence of microinstability is 6%. The etiology is repetitive stress or acute injury. The clinical diagnosis of microinstability is made based on findings from the history and physical examination. MR and arthroscopic findings confirm the diagnosis.

Clinical symptoms of microinstability include:

Rotator cuff tendinitis (tendinosis) or pain
A subjective feeling of slipping of the shoulder when not abducted and externally rotated. (This slipping is perceived by the patient as an abnormal or uncomfortable motion or laxity between the glenoid and humeral head.)
Easy fatigue of the shoulder muscles or parascapular pain
Impingement-like pain, which may mimic rotator cuff disease

The various mechanisms of injury in microinstability determine the location of the involved structures as indicated:

The application of traction forces in the overhead position may produce a SLAP or SLAC lesion.
A seat belt across the involved shoulder (roll-around seat belt on impact) is associated with SLAC lesions.
A fall on the abducted arm is associated with the classic and SLAP variants.
“Throwing out” of the shoulder may produce a MGHL injury.
Overhead repetitive work or sports activity and professional throwing athletes may present with posterior peel-back SLAP with posterior superior instability due to glenohumeral internal rotation deficit (GIRD).
No trauma history may be associated with biceps pulley lesions.

There is no one specific clinical test (Jobe, Load and Shift, O—Brien, or Speed) that is reliably positive for confirmation of the diagnosis of instability. Support for a clinical diagnosis can be obtained with routine MR studies performed with proper sequences

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and optimized signal-to-noise or MR arthrograms using the ABER position. MR examinations are important in identifying partial-thickness articular surface tears of the rotator cuff and peel-back lesions. MR examinations in microinstability include:

Posterior coronal images and sagittal and axial images display peel-back lesions with posterosuperior labral tears. Axial and sagittal images may further show an early pattern of eccentric sclerosis or wear as a pre-posterior peel-back lesion.
Coronal plane images are used to distinguish a type 2 or 3 BLC with a normal biceps labral sulcus from a SLAP lesion.
MR arthrography optimizes depiction of biceps pulley lesions, with improved appreciation of the degree of injury to the CHL and SGHL.
Non-contrast studies are satisfactory for characterization of gross subluxation of the biceps.
Partial-thickness articular surface tears are seen as a detachment of cuff fibers at their footprint attachment to the greater tuberosity both on ABER MR arthrograms and routine phased-array coil imaging of the shoulder.

FIGURE 8.175 ● (A) Adherence of the retracted rotator cuff to the coracohumeral ligament. (B) Coronal FS PD FSE image showing the thickened coracohumeral ligament associated with torn and retracted supraspinatus. (C) A corresponding arthroscopic view shows the articular surface of the avulsed supraspinatus tendon (S; arrow). B, biceps tendon; HH, humeral head; Sub, subacromial space.

FIGURE 8.176 ● A coronal FS PD FSE image after rotator cuff repair shows a proud suture anchor superficial to the humeral head contour.

Arthroscopic findings of microinstability include:

Superior labral detachment and extensions (synovial reaction and chondral erosions may be associated findings)
Capsular (SGHL and MGHL) tears and laxity
Laxity of the rotator interval
Non-crescentic articular-side partial-thickness rotator cuff lesions
The attachment of the CHL at the bicipital groove (lateral lip or greater tuberosity side) (the CHL is a bursal structure and cannot be visualized from the articular surface)
Biceps pulley lesions with either biceps subluxation on dislocation

FIGURE 8.177 ● Coronal FS PD FSE image showing a cuff retear with subacromial displacement of a linear cuff washer with attached suture. The washer was used to gain greater cuff surface purchase.

Surgical options for microinstability include imbrication of capsular laxity in the rotator interval if laxity is present. If detached, the anterior superior labrum is reattached. The anatomic attachment of the SGHL and/or MGHL is repaired if displaced, especially if these structures are scarred and in an abnormal position. SLAP tears are repaired, as is the biceps anchor if detached. Tenotomy/tenodesis is performed if there is a severe disruption of the biceps pulley. The subscapularis or supraspinatus tendons are also repaired when associated with the biceps pulley lesion.

SLAC Lesions

FIGURE 8.178 ● Potential sites of involvement in microinstability, including the anterior supraspinatus and anterior component of a SLAP 2 in the SLAC lesion; the posterior cuff and posterior component of a SLAP 2 in the posterior peel-back lesion; the classic anterior-to-posterior SLAP 2 lesion; anterosuperior impingement (ASI) involving the superior subscapularis, CHL–SGHL complex, the anterior supraspinatus and anterosuperior labrum, and the middle glenohumeral ligament (MGL) in anterior laxity.

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The SLAC lesion (Fig. 8.179) represents an injury to the anterior-superior glenoid labrum that involves the insertion of the SGHL and the anterior portion of the biceps tendon.¹⁷⁴ Because of the resultant anterosuperior instability, the articular surface of the anterior supraspinatus tendon contacts the anterior superior labrum (the anterior component of a type 2 SLAP lesion) and glenoid. Severe contact can result in a partial-thickness rotator cuff tear on the articular side of the supraspinatus tendon. The term “SLAC lesion” refers to the combination of the labral and cuff injuries.

The attachment of the MGHL may also be involved in a SLAC lesion. The mechanism of injury represents either a repetitive overhead activity or a traumatic event. The trauma, including falls and motor vehicle accidents, involves an anterior superior subluxation episode. In overhead activity, the patient—s dominant arm is commonly affected. In motor vehicle accidents the arm on the side of the shoulder strap is frequently involved.

The SLAC lesion is primarily an instability problem. The anterior rotator cuff component is different from the lesion that impingement or traumatic injury causes. Contact between the cuff and the anterior superior glenoid labrum results from increased anterior-superior translation. Corrective treatment addresses the underlying instability and not just the rotator cuff.

Rotator Cuff Interval

The rotator interval (Fig. 8.180) is a triangular area of tissue that functions to allow rotational motion around the coracoid process.⁷¹ The rotator interval is defined by the supraspinatus tendon above, the leading edge of the subscapularis tendon below, the base of the coracoid process medially, and the transverse humeral ligament (overlying the intertubercular groove) laterally.¹⁷⁵ The biceps pulley is composed of both the medial portion (limb) of the coracohumeral ligament

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and the SGHL. The rotator interval contains a bursal layer and an articular layer:

The bursal layer of the interval is the CHL.
The articular layer of the interval is the SGHL.
The CHL and SGHL become confluent at their attachment to the greater and lesser tuberosities.

FIGURE 8.179 ● (A) Coronal FS PD FSE image of a SLAC lesion with partial articular-side supraspinatus tendon tear and anterior SLAP lesion. Sagittal color section (B) and FS PD FSE image (C) demonstrate labral separation of the anterior component of a SLAP 2 lesion.

FIGURE 8.180 ● The rotator cuff interval, demonstrating the confluence of CHL and SGHL (SGL) to form the biceps pulley or sling at the entrance of the intertubercular groove. (A) The superior aspect of the glenohumeral joint capsule is windowed to reveal the contribution of the CHL to the roof and the SGHL to the floor of the biceps pulley. (Based on

Habermeyer P, Magosch P, Pritsch M, et al. Anterosuperior impingement of the shoulder as a result of pulley lesions: a prospective arthroscopic study. J Shoulder Elbow Surg 2004;13(1):5.

) Consecutive coronal oblique FS PD FSE images show the transition from the CHL and SGHL anteriorly (B) to the CHL one image posteriorly (C) and to the intra-articular biceps one more image posterior (D). The CHL (which forms the roof of the biceps pulley) and the SGHL (which forms the floor of the biceps pulley) are visualized anterior to the biceps in their proximal course through the rotator cuff interval.

The boundaries of the rotator interval are:

The anterior edge of the supraspinatus tendon at the superior edge
The superior edge of the subscapularis tendon at the inferior edge
The transverse ligament over bicipital groove at the apex
The humeral head cartilage at the floor
The capsule of the rotator interval at the roof

At the level of the coracoid and BLC, the origin of the coracohumeral ligament can be seen on the lateral aspect of the base of the coracoid (see Fig. 8.180). In this proximal portion of the rotator cuff interval, the SGHL is anterior to the biceps tendon. The CHL forms a roof over both the SGHL and proximal biceps tendon in this location.

At the mid-portion of the rotator cuff interval, the T-shaped link or junction is formed when the SGHL changes direction to create an anterior floor for the biceps pulley and intersects the undersurface of the overlying CHL (Figs. 8.181 and 8.182).⁷¹ The SGHL can be seen between the biceps and subscapularis tendons. The CHL bridges the gap between the supraspinatus and subscapularis tendons. Corresponding coronal images (Fig. 8.183) demonstrate the oblique path of the SGHL, which can be seen coursing lateral to the MGHL to contact the inferior surface of the CHL, forming the biceps pulley proximal to the intertubercular groove.

In the distal portion of the rotator cuff interval, the anterior confluence of the CHL and SGHL form a U-shaped sling (see Fig. 8.181C).⁷¹ At the entrance of the bicipital groove, the open portion of the U-shaped sling is directed posteriorly toward the greater tuberosity. The SGHL inserts onto the lesser tuberosity in the distal portion of the rotator cuff interval at the entrance of the intertubercular groove.

The lateral band of the CHL inserts on both the greater tuberosity and on the anterior border of the supraspinatus.¹⁷⁵ The smaller medial portion crosses anteriorly, over the intra-articular biceps, to insert on the lesser tuberosity, the superior fibers of the subscapularis, and the transverse ligament. Thus, tears of the anterior supraspinatus may involve the lateral band of the CHL, whereas tears of the superior distal fibers of the subscapularis tendon may involve both the SGHL and the medial band of the CHL. Both the distal insertional fibers of the supraspinatus and subscapularis are intimately associated with and blend with the lateral and medial bands of the CHL respectively.

FIGURE 8.181 ● (A) Coronal 3D perspective of the rotator cuff interval. The formation of the biceps pulley or sling is shown from proximal, middle, and distal sections through the confluence of the CHL and SGHL. There is a T-shaped junction between the SGHL and CHL at the mid-interval, and a more U-shaped anterior sling is formed distally at the entrance of the intertubercular groove. A perpendicular junction between the SGHL and CHL medial to the formation of the more U-shaped biceps pulley developed in the distal portion of the rotator cuff interval. Corresponding sagittal PD FSE MR arthrograms, mid-interval (B) and distal interval (C).

FIGURE 8.182 ● (A) Sagittal color section illustrating the proximal biceps pulley with the CHL forming the roof and the SGHL forming the floor, which envelops the LHBT. Note the T-shaped junction between the CHL/roof and the SGHL/floor at the level of the mid-rotator cuff interval. (B, C) Sagittal MR arthrograms of the proximal rotator cuff interval demonstrate the initial parallel course of the CHL and SGHL at the more lateral T-shaped junction of the biceps pulley formed between the CHL and SGHL at the mid-rotator cuff interval, superior to the medial humeral head. (D, E) Sagittal FS PD FSE images show comparison with complete disruption of the biceps pulley with abnormal laxity and thickening of the CHL–SGHL complex medially (D) and complete absence of the SGHL at the mid-rotator cuff interval in the expected location of the T junction between the CHL and SGHL (E).

FIGURE 8.183 ● (A) The proximity of the CHL to the anterior border of the supraspinatus and its relationship to the SGHL and MGHL (MGL) are shown on this anterior coronal MR arthrogram. (B) CHL, SGHL, and intra-articular biceps are visualized on one image posterior to (A). (C) Coronal FS PD FSE image shows comparison in a separate case with a torn and medially retracted SGHL in the rotator cuff interval in a case of biceps instability and medial subluxation. (D) Coronal FS PD FSE image demonstrates discontinuity of the CHL in conjunction with an anterior supraspinatus.

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The intra-articular biceps tendon (the long head of the biceps brachii tendon) traverses the rotator cuff interval from the medially located BLC to the intertubercular (bicipital) groove. The formation of the biceps pulley by the medial portion of the CHL and the SGHL and the superior fibers of the subscapularis prevents medial subluxations and dislocations by stabilizing the biceps tendon in a sling.

The rotator cuff interval capsule provides stability, resisting inferior and posterior glenohumeral translation through the direct contribution of the CHL and secondarily by the negative pressure that it maintains in the glenohumeral joint.⁷¹^,¹⁷⁵ The LHBT functions as an anterior stabilizer of the glenohumeral joint by increasing resistance to torsional forces in abduction and external rotation and by reducing stress on the IGHL. In the acute setting, a rotator interval tear associated with trauma may be the result of either extension of the anterior supraspinatus tearing to involve the lateral CHL or extension of the superior subscapularis tendon tearing to involve the SGHL and medial CHL.

A pulley tear may occur initially as an isolated lesion (Fig. 8.184) prior to secondary involvement of the rotator cuff.¹⁷⁵ Approximately half of subscapularis tendon tears involve both the SGHL and CHL. In chronic lesions the rotator interval capsule and ligaments may become thickened and scarred (appearing hypointense on MR images) (Fig. 8.185). Intermediate signal intensity is visualized with synovial hypertrophy or granulation tissue. There is an association between adhesive capsulitis and recess, synovitis and scarring of the rotator interval. In shoulders with multidirectional instability, the rotator interval may be larger than would normally be found.

Biceps Pulley Lesions

Pearls and Pitfalls

Biceps Pulley Lesions

Biceps pulley lesions are associated with tearing of the deep fibers of the distal subscapularis and articular surface of the distal supraspinatus tendon.
The medially dislocated biceps tendon is displaced either intra-articularly, between the coracohumeral ligament and the subscapularis tendon, or extra-articularly.
Intra-articular dislocation is associated with disruption of both the lesser tuberosity attachment of the subscapularis tendon and the SGHL–CHL complex.
Extra-articular subluxation is associated with an anterolateral supraspinatus tendon tear with extension into the lateral coracohumeral ligament.

As described earlier, the SGHL and the CHL blend together at the entrance of the sulcus to form the U-shaped section of the biceps pulley or sling (Fig. 8.186). A biceps pulley lesion is defined as an interruption of the surrounding sheath of the LHBT with an intact rotator cuff.¹⁷⁶ Biceps tendon instability is also associated with abnormalities of the rotator cuff (the subscapularis and supraspinatus components).¹⁷⁷

FIGURE 8.184 ● Type 1 (isolated) biceps pulley lesion with tear of the anterior CHL–SGHL sling shown on a sagittal FS PD FSE image. The articular surface of the supraspinatus and deep fibers of the subscapularis are intact.

The superior insertion fibers of the subscapularis tendon are intimately associated with the proximal opening to the bicipital groove. The medial wall of the bicipital sheath is composed

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of the SGHL–medial CHL complex. Tears of this complex may occur with or without associated tearing of the distal subscapularis tendon fibers and result in biceps tendon subluxation. This occult bicipital instability represents the hidden lesion described by Walch.¹⁷⁸ The CHL normally inserts with the fibers of the subscapularis and traverses the intertubercular groove to contribute to the lateral aspect of the biceps sheath and supraspinatus. The medial CHL, the key anatomic portion, prevents medial subluxation of the biceps and contributes directly to the root and anterior superior aspect of the biceps tendon. The lateral CHL attaches more posteriorly to the greater tuberosity.

FIGURE 8.185 ● Thickened SGHL and CHL components of the biceps pulley seen at the mid-rotator interval on sagittal T2 FSE (A) and coronal FS PD FSE (B) images.

FIGURE 8.186 ● Biceps pulley formed by the CHL and SGHL. A 2D sagittal section of the subscapularis and a 3D perspective of the supraspinatus are shown in proximity to the pulley. Note the intimate relationship between the CHL (roof of the biceps pulley) and the anterior leading edge of the supraspinatus tendon. The medial CHL primarily contributes to the pulley, whereas the lateral CHL stabilizes the biceps (LHBT) through its attachment to the greater tuberosity. These lateral fibers are at a risk for injury with anterior and far lateral supraspinatus tears.

FIGURE 8.187 ● (A) The Habermeyer classification of biceps pulley lesions groups them into four subtypes. Type 1 lesions are isolated pulley lesions with an intact supraspinatus and subscapularis tendon. Type 2 represents a pulley lesion and a partial articular surface supraspinatus tendon tear. Type 3 is a pulley lesion with partial medial subluxation of the biceps tendon associated with a partial articular or deep surface tear of the superior distal fibers of the subscapularis tendon. Type 4 combines the pulley lesion with partial articular surface tears of both the supraspinatus and subscapularis tendons. There is frank medial subluxation of the LHBT as both the contributions of the CHL (roof of the sling) and SGHL (floor of the sling) are affected. (B) Arthroscopic view of type 3 biceps pulley lesion with disruption of the CHL–SGHL sling and medial subluxation of the biceps tendon associated with deep surface tearing of the subscapularis.

FIGURE 8.188 ● A type 1 biceps pulley lesion with a torn anterior CHL–SGHL sling. The biceps tendon (LHBT), although unstable, has not undergone subluxation.

Clinical signs of biceps pulley failure are not accurate (50% positive correlation), and two thirds of patients have no history of trauma. Bennett¹⁷⁸^,¹⁸⁰ and Habermeyer¹⁸¹^,¹⁸² have classified the arthroscopic findings of biceps pulley lesions based on a combination of findings in lesions of the subscapularis tendon, the SGHL–medial CHL complex, and the lateral CHL. The Habermeyer classification of biceps pulley lesions is divided into four subtypes (Fig. 8.187):

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A type 1 lesion is restricted or limited to an isolated surface of the pulley without involvement of the supraspinatus or subscapularis tendons (see Fig. 8.184; Fig. 8.188).
The type 2 pulley lesion involves articular side tearing of the supraspinatus tendon in association with pulley failure and mild medial subluxation of the biceps tendon.
The type 3 pulley lesion demonstrates partial deep surface tearing of distal subscapularis tendon fibers. The biceps undergoes medial subluxation, partially extending beyond the containment of the CHL–SGHL sling.
The type 4 lesion represents a dislocation of the biceps tendon (Fig. 8.189). In the type 4 lesion there is partial tearing of both the supraspinatus and subscapularis tendons in association with the medially displaced biceps tendon, which is located anterior to the lesser tuberosity. The supraspinatus and subscapularis tears are more extensive than those observed in type 2 and 3 lesions respectively.

FIGURE 8.189 ● A type 4 biceps pulley disruption with biceps tendon medial subluxation anterior to the lesser tuberosity is shown on an axial FS PD FSE image (A) and sagittal FS PD FSE images from lateral to medial (B). Associated tears of both the supraspinatus and subscapularis are present.

Although this classification addresses only partial tears of the supraspinatus and subscapularis tendons, complete tears are also associated with biceps subluxations and dislocations.

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Management of type 1 lesions may require a suture repair of the lax pulley. Treatment of type 2 lesions involves débridement of the supraspinatus with a transtendon repair. Subscapularis and biceps tendon stabilizations are performed in a type 3 pulley lesion. Type 4 biceps pulley lesions are managed by repair of both the subscapularis and supraspinatus tendons plus a biceps tenodesis/tenotomy.

Biceps tendon instability patterns have also been classified as either intra-articular dislocations (between the coracohumeral ligament and the subscapularis tendon) or extra-articular dislocations:¹⁷⁵

FIGURE 8.190 ● Intra-articular dislocation of the biceps tendon (LHBT) with complete disruption of the SGHL on a coronal color illustration (A) and on coronal (B) FS PD FSE images. Both the insertion of the subscapularis tendon and the SGHL component of the CHL–SGHL complex are disrupted. Intra-articular dislocation of the biceps tendon (LHBT) with complete disruption of the SGHL on a coronal color illustration on axial (C) FS PD FSE image. Both the insertion of the subscapularis tendon and the SGHL component of the CHL–SGHL complex are disrupted. (D) Sagittal FS PD FSE image in a separate case demonstrates avulsion of the SGHL attachment associated with an intra-articular biceps tendon dislocation.

Intra-articular dislocation (Fig. 8.190) of the LHBT with the biceps displaced medially and anterior to the

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glenohumeral joint space occurs in association with disruption of both the insertion of the subscapularis tendon and the SGHL–medial CHL complex.
Disruption of the SGHL–medial CHL complex with an intact lateral band (Fig. 8.191) of the coracohumeral ligament is associated with biceps subluxation anterior to the subscapularis but deep to the lateral band.
Extra-articular subluxation (Fig. 8.192) exists when there is an anterolateral supraspinatus tendon tear with extension into the lateral coracohumeral ligament. This permits the biceps tendon to subluxate in a medial direction (anterior to the lesser tuberosity), superficial to both the coracohumeral ligament and subscapularis tendon.
Delamination of the deep surface of the subscapularis (Fig. 8.193) produces injury to the SGHL–medial CHL complex. The biceps tendon is subluxated directly into the substance of the subscapularis tendon at the location of the delamination tear.

An isolated subscapularis tendon tear without disruption of the biceps pulley may demonstrate a normal position of the biceps tendon in the groove without subluxation or dislocation (Fig. 8.194). The pulley ligaments may become thickened and scarred with plastic deformation of the medial portion of the ligamentous biceps sling (SGHL–medial CHL complex).

Anterosuperior Impingement

Anterosuperior impingement (ASI) represents an internal impingement developing as a result of pulley lesions, including partial tears of the subscapularis and supraspinatus tendons.¹⁸² The progressive lesions of the biceps pulley lead to instability of the biceps, which in turn results in an increased passive anterior translation and superior ascent of the humeral head, leading to the development of ASI. A partial articular-side subscapularis and supraspinatus tendon tear further contributes to the condition of ASI. Impingement of the biceps pulley occurs at the undersurface of the reflection formed by the confluence of the CHL and SGHL. In horizontal adduction and internal rotation of the arm, both the pulley and subscapularis

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tendon impinge against the anterosuperior aspect of the glenoid rim (Fig. 8.195). The probability of ASI increases with subscapularis tendon involvement and secondarily with supraspinatus tearing. The addition of a partial articular-side tear or a lesion of the deep subscapularis to an existing pulley lesion is required for the development of ASI. A partial articular-side supraspinatus tear in the absence of subscapularis tendon involvement does not result in ASI. The frequency of an anterosuperior labral lesion as part of ASI is greater with the involvement of the biceps pulley, subscapularis, and supraspinatus (Fig. 8.196). Normally the LHBT is an anterior stabilizer of the glenohumeral joint during rotation of the arm. This anterior stabilizing effect on the glenohumeral joint is lost as the LHBT undergoes medial subluxation because of the pulley tear. The subluxation of the LHBT and decentralization of the humeral head represent the initial steps of the progressive cascade concluding in ASI. The superior fibers of the articular surface of the subscapularis are most frequently affected, and the tearing of deep fibers of the subscapularis is caused by the medial subluxation of the LHBT. Deep surface tears of the subscapularis tendon allow further anterior superior translation of the humeral head and potentiate ASI. The incidence of a symptomatic AC joint is higher in ASI, although the mechanism of injury has not been elucidated. There is also an association with symptomatic AC arthritis and posterior capsular injuries. We have observed an increased frequency of posterior SLAP 2 lesions and hypertrophic AC joints that demonstrate edema of the distal clavicle and adjacent acromion.

FIGURE 8.191 ● (A) Coronal color illustration showing medial subluxation of the biceps tendon anterior to the subscapularis tendon and deep to the CHL. This pathology is made possible by disruption of the anterior sling with intact lateral fibers of the CHL. The medial fibers of the CHL that directly contribute to the CHL–SGHL complex are torn in conjunction with the SGHL. (B) Axial PD FSE image showing medial subluxation of the biceps anterior to the subscapularis tendon and deep to the CHL.

FIGURE 8.192 ● Extra-articular subluxation on (A) coronal color illustratio and, (B) coronal FS PD FSE image. The extra-articular subluxation is seen with the biceps perched anterior to the lesser tuberosity and anterior to both the coracohumeral ligament and the subscapularis tendon. The lateral band of the coracohumeral ligament is torn as a result of the anterior extension from an anterior and lateral supraspinatus tear. Extra-articular subluxation on (C) axial T2* GRE image. The extra-articular subluxation is seen with the biceps perched anterior to the lesser tuberosity and anterior to both the coracohumeral ligament and the subscapularis tendon. The lateral band of the coracohumeral is torn as a result of the anterior extension from an anterior and lateral supraspinatus tear. (D) Sagittal FS PD FSE image demonstrates disruption of the lateral fibers of the coracohumeral ligament in a separate case.

FIGURE 8.193 ● Dislocation of the biceps tendon (LHBT) directly into a delamination of the subscapularis tendon on (A) axial color illustration and (B) axial FS PD FSE image. Dislocation of the biceps tendon (LHBT) directly into a delamination of the subscapularis tendon on (C) coronal FS PD FSE image and (D) sagittal FS PD FSE image. The subscapularis tendon is visualized imbedded within the substance of the subscapularis tendon. An associated SGHL tear with reactive osseous erosion is shown in the sagittal plane (D).

FIGURE 8.194 ● A T2*-weighted axial image illustrates a subscapularis tendon tear with proximal retraction (arrow) to the level of the lesser tuberosity. There is free communication of fluid between the glenohumeral joint subscapularis bursa and the subcoracoid bursa anterior to the subscapularis tendon.

FIGURE 8.195 ● Anterosuperior impingement occurring with an internal rotation and adduction mechanism. Medial subluxation of the LHBT is associated with disruption of the biceps pulley system and partial tears of the articular surface of the subscapularis and supraspinatus tendons. Medial subluxation of the LHB causes the deep or articular surface tear of the subscapularis tendon. (A) Color graphic of a tennis player in position of shoulder adduction and internal rotation. (B) Superolateral view color illustration demonstrating the association of a grade 4 biceps pulley lesion and the corresponding pathomechanics of humeral adduction and internal rotation in anterosuperior impingement. (A, B: Based on

Habermeyer P, Magosch P, Pritsch M, et al. Anterosuperior impingement of the shoulder as a result of pulley lesions: a prospective arthroscopic study. J Shoulder Elbow Surg 2004;13(1):5.

) (C) An axial FS PD FSE image demonstrating biceps instability and an associated anterosuperior labral tear. There is tearing of the distal fibers of the subscapularis tendon.

FIGURE 8.196 ● (A) Color graphic of the glenohumeral joint as viewed from a superolateral exposure with the humerus adducted and internally rotated. In anterosuperior impingement (ASI), an anterosuperior labral tear occurs as the humeral head migrates into the anterosuperior quadrant against the anterior glenoid rim. The normal posterior and compressive joint retraction function of the LHB is lost in ASI secondary to the unstable medially subluxed LHB. (Based on

Habermeyer P, Magosch P, Pritsch M, et al. Anterosuperior impingement of the shoulder as a result of pulley lesions: a prospective arthroscopic study. J Shoulder Elbow Surg 2004;13(1):5.

) (B) Axial FS PD FSE image shows ASI with medial subluxation of the biceps tendon, partial distal tearing of the subscapularis tendon, and an associated anterosuperior labral tear. (C) Corresponding sagittal PD FSE image with sclerosis of the anterior superior glenoid rim.

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Throwing Shoulder

Pearls and Pitfalls

Throwing Shoulder

A SLAP 2 or posterior SLAP 2 lesion causes the dead arm.
Repetitive tensile loading during follow-through results in a tight posterior band of the IGHL.
The tight posterior band bowstrings the humeral head in the late cocking phase, resulting in a posterosuperior shift of the glenohumeral contact point.
Glenohumeral internal rotation deficit (GIRD) is an acquired loss of internal rotation resulting from the tight posterior band of the IGL.
Peel-back posterior SLAP 2 lesions and posterior articular surface tears of the supraspinatus represent the net effect of the shift of the glenohumeral rotation contact point with a loss of internal rotation and gain of external rotation.
Pseudolaxity of the anterior IGHL results from a reduced cam effect of the proximal humerus, which allows for an even greater degree of external rotation.
On sagittal MR images, eccentric posterior glenoid rim sclerosis may precede the development of the peel-back labral lesion.

The disabled throwing shoulder represents a pathologic cascade that culminates in the “dead arm” (Fig. 8.197).¹⁸³^,¹⁸⁵ There is a sudden onset of mechanical pain with the development of a posterior type 2 SLAP lesion.¹⁸⁵ Prior to the development of the posterior type 2 SLAP tear, there may be a prodromal phase or pre-SLAP stage where the thrower describes posterior shoulder tightness. At this stage MR studies frequently demonstrate eccentric posterior glenoid rim sclerosis without a SLAP lesion. There may also be associated remodeling of the posterior glenoid rim.

Dead Arm

The dead arm is defined as a pathologic shoulder condition characterized by the sudden loss of the ability to throw a fastball. Sharp pain and discomfort occur as the arm moves forward during the late cocking or early acceleration phase of throwing. A posterior type 2 SLAP lesion (Fig. 8.198) or a combined anteroposterior type 2 SLAP lesion causes the dead arm. Internal shoulder impingement, which occurs in the position of 90° of abduction and 90° of external rotation (the 90°–90° position), was at one time thought to describe entrapment of the rotator cuff between the greater tuberosity and the posterosuperior glenoid in abduction and external rotation of the shoulder (Fig. 8.199). It is now appreciated as a normal phenomenon that occurs in all shoulders. The pathology in the disabled throwing shoulder involves contraction or tightening of the posterior band of the IGHL and not, except in the older elite thrower, internal impingement. Additionally, earlier descriptions of the normal anteroinferior pseudolaxity associated with posterior type 2 SLAP lesions led to the inappropriate use of the term “microinstability” for this disorder.

Glenohumeral Internal Rotation Deficit

Repetitive tensile loading occurring during the follow-through phase of throwing predisposes to the development of a tight or contracted posterior band of the IGHL (see discussion below) (Fig. 8.200).¹⁸³ Glenohumeral internal rotation deficit (GIRD) is an acquired loss in the degree of glenohumeral internal rotation. This loss of internal rotation in abduction is the most important pathologic process that occurs in throwers and is the result of posteroinferior capsular contracture of the tight posterior band of the IGHL evident in the late cocking phase of throwing. The majority of throwers with symptomatic GIRD (>25°) respond to posteroinferior capsular stretching.

Posterior Band of IGHL

The tight posterior band of the IGHL acts as a tether and shifts the glenohumeral contact point posterosuperiorly during abduction and external rotation (Fig. 8.201).¹⁸³ The arc of motion of the greater tuberosity is also shifted posterosuperiorly and, in the position of abduction and external rotation, no longer abuts the expected posterosuperior glenoid contact area described in internal impingement. Because of the increased clearance of the greater tuberosity (tuberosity clearance provides additional external rotation of the shoulder), the posterosuperior shift of the glenohumeral contact point preserves hyperexternal rotation and also reduces the cam effect of the humeral head and proximal humeral calcar, creating a relative redundancy of the anterosuperior capsule (Fig. 8.202). This pseudolaxity or redundancy of the anteroinferior capsule produces functional lengthening of the anterior IGHL and also contributes to a secondary increase in external rotation. The tight posteroinferior capsule thus facilitates hyperexternal rotation of the humerus by a shift in the glenohumeral contact point posterosuperiorly before internal impingement can occur and by minimizing the cam effect of the proximal humerus on the anterior inferior capsule. Internal impingement is avoided because the posterosuperior shift of the glenohumeral contact point occurs before the greater tuberosity contacts the posterior glenoid. Increased retroversion in the dominant or throwing shoulder is associated with increased external rotation (hyperexternal rotation) at 90° of abduction and corresponds with both a decrease in the cam effect and increased tuberosity clearance. Whereas hyperexternal rotation may be due to functional lengthening of the IGHL (caused by a tight posterior band and posterosuperior shift of the glenohumeral contact point), chronic hyperexternal rotation associated with a protracted scapula may partially stretch the IGHL directly.

In the older elite thrower, hyperexternal rotation may lead to chronic failure of the anteroinferior capsule in the Bankart zone.¹⁸³ IGHL disruption, however, is not typically seen in the younger pitcher presenting with dead arm. Hyperexternal rotation in the older pitcher/thrower may contribute to the pseudolaxity associated with combined internal impingement. It is only considered pathologic, however, in the older elite thrower in whom excessive hyperexternal rotation in the late phase of cocking causes abrasion of the undersurface of the cuff against the posterosuperior glenoid. Increased posterolateral humeral cystic changes may also be seen in this group of elite throwers (see Fig. 8.202).¹⁸⁶ These older elite throwers achieve maximal external rotation in excess of 130°. Cystic lesions of the posterosuperior

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region of bare area of the humeral head were shown by Jin et al. to be lined with collagen and connective tissue and are connected to the joint space.¹⁸⁷ Since internal impingement is a normal phenomenon, it is not surprising that humeral head cystic changes are seen in asymptomatic patients as a normal variation. These bare area cysts are more extensive in older elite throwers, and it appears that internal impingement becomes a pathologic process because excessive hyperexternal glenohumeral rotation produces abrasion of the cuff and bare area against the posterosuperior glenoid. Walch¹⁸⁸ reported finding osteochondral lesions of the humeral head, superior to the classic Hill-Sachs lesion, that were less than 1 cm in size and only a few millimeters in depth. Although impaction on the posterosuperior glenoid was postulated, it could not be demonstrated at arthroscopy.¹⁸⁸ In the younger throwing athlete the greater tuberosity usually has clearance over the posterosuperior glenoid rim through a greater arc of external rotation before internal impingement occurs.⁷⁹ Hyperexternal rotation also results in repetitive hypertwisting of the rotator cuff fibers, causing torsional overload and shear failure of articular-side cuff fibers (Fig. 8.203). The external rotation proprioceptive set-point of high-level pitchers is referred to as “the slot,” and it allows for high-velocity throws of a baseball at speeds above 90 mph. The shift of the glenohumeral contact point with a tight posterior band of the IGHL allows the pitcher to more effectively externally rotate back to the set point.

FIGURE 8.197 ● Initial steps of the pathologic cascade of changes in the throwing shoulder. (A) Abduction and external rotation with a tight and thickened posterior band of the inferior glenohumeral ligament. Thickened cross-section of the posterior band of the inferior glenohumeral ligament on sagittal (B) and axial (C) FS PD FSE images. (D) Posterosuperior shift of the glenohumeral contact point.

FIGURE 8.198 ● Dead arm with the development of a posterior SLAP 2 lesion. (A, B) Color illustrations of glenohumeral joint from lateral perspective. Hypertwisting and torsion of the intra-articular biceps are shown on (A), and a peel-back posterosuperior labral tear is shown on (B). (C) Sagittal PD FSE image of posterosuperior glenoid rim sclerosis associated with both the posterosuperior cam shift and the posterior SLAP 2 or peel-back lesion. The peel-back may extend to involve the posterior labrum contiguous with the posterosuperior quadrant.

FIGURE 8.199 ● Internal impingement of the articular surface of the rotator cuff between the posterior superior glenoid and the greater tuberosity is appreciated as a normal mechanism in the position of shoulder abduction and external rotation. Therefore, internal impingement is usually not responsible for the pathologic cascade in the throwing shoulder.

FIGURE 8.200 ● Repetitive tensile loading during the follow-through phase of throwing is the primary mechanism responsible for the development of the tight posteroinferior capsule. Large distraction forces must be resisted by the posteriorly rotated IGL during follow-through. (Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: Patho-anatomy and biomechanics. Arthroscopy 2003;19(4):404.

)

FIGURE 8.201 ● (A) A color graphic illustrating hyperabduction and external rotation in the late cocking phase of throwing. In the late cocking phase of throwing the posterior band of the IGHL is bowstrung underneath the humeral head, causing a posterosuperior shift in the glenohumeral contact or rotation point. An acquired tight or contracted posterior band of the IGHL thus initiates the pathologic cascade (evident in abduction and external rotation causing GIRD). A posterosuperior shift of the humeral head causes increased shear and peel-back forces to the posterosuperior glenoid labrum, increased greater tuberosity clearance, and scapular protraction. (Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 2003;19(4):404.

) (B) The thickened posterior band of the IGL with mild posterior glenoid rim sclerosis in a baseball pitcher capable of throwing 100 miles an hour on a sagittal PD FSE MR arthrogram. (C) Corresponding posterior subluxation of the humeral head secondary to early changes of posterior glenohumeral wear and a tight posteroinferior capsule on an axial PD MR arthrogram.

FIGURE 8.202 ● (A) Internal impingement, a normal phenomenon in all shoulders, is demonstrated with abduction and external rotation of the shoulder. The greater tuberosity abuts against the posterosuperior glenoid, which entraps the rotator cuff between these two osseous structures. In throwers the posterosuperior shift of the glenohumeral contact point produces a reduction of the cam effect as the space-occupying effect of the proximal humerus on the anteroinferior capsule (IGL) is reduced. (B) The resultant relative laxity (shown here) or redundancy of the IGL should not be misinterpreted as anteroinferior instability. Hyperexternal rotation of the rotator cuff results in repetitive hypertwisting with torsional overload and shear failure of cuff fibers. A partial-thickness articular surface tear then develops in the posterior supraspinatus or anterior infraspinatus tendon. (A, B: Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology Part I: Pathoanatomy and biomechanics. Arthroscopy 2003;19(4):404.

) (C) Axial FS PD FSE image in abduction and external rotation confirms the relative laxity of the IGL and posterior shift of the humeral head. Note the proximity of the greater tuberosity to the rotator cuff. The nonarticular humeral erosion has been attributed to posterosuperior glenoid rim contact in internal impingement. (D) Axial PD FSE image of posterolateral humeral head cyst changes in a 30-year-old elite baseball player. The subchondral sclerosis and erosions are posterior to the greater tuberosity deep to the distal infraspinatus and involve the bare area of the humeral head. Associated posterosuperior glenoid rim remodeling is characteristic.

Peel-Back Lesion

The peel-back phenomenon occurs with the shoulder in abduction and external rotation (Fig. 8.204).¹⁸³ Pitchers with a tight posteroinferior capsule and GIRD throw with deranged mechanics and are at risk for increased peel-back and shear forces on the superior labrum.

There is a posterior shift of the biceps vector and twist at the base of the biceps in the late cocking phase of throwing. Increased torsional force is transmitted to the posterior aspect of the BLC and results in a posterior type 2 SLAP or peel-back lesion. This lesion, sometimes called “thrower—s” SLAP, is treated with a suture anchor to resist torsional forces generated in the peel-back mechanism. In abduction and external rotation, acceleration of the arm occurs in the late cocking phase and produces a type 2 or posterior type 2 SLAP lesion as the biceps and superior labral complex are peeled (medial rotation of the superior labrum onto the posterosuperior scapular neck and medical shift of the biceps root relative to the supraglenoid tubercle).

A protracted scapula will potentiate the pathologic cascade initiated by the acquired capsular contracture (tight posterior band of the IGHL); with the development of the SLAP or posterior peel-back lesion, the posterosuperior shift and hyperexternal rotation components of the cascade are further emphasized, and thus the pathologic cascade continues. The associated partial-thickness articular surface rotator cuff tears occur in the posterior portion of the rotator crescent posterior to the supraspinatus contribution to the cuff. The posterior type 2 SLAP lesions produce a break in the labral ring contributing to posterosuperior subluxation of the humerus, which in turn produces high tensile forces in the posterosuperior cuff (Fig. 8.205).

Sick Scapula

The SICK scapula ¹⁸⁵ (S capular malposition, I nferior medial border prominence, C oracoid pain and malposition, and dysK inesis of scapular movement) is an overuse muscular fatigue syndrome seen in the throwing athlete who presents with dead arm (Fig. 8.206). It represents an extreme form of scapular dyskinesis.

The type I (inferior medial scapular border prominence) and type II (medial scapular border prominence) patterns are associated with posterosuperior labral lesions, whereas the type III pattern (prominence of the superomedial border of the scapula) is associated with impingement and rotator cuff lesions. Clinical presentation in the SICK scapula syndrome is of an apparent “dropped” scapula in the dominant shoulder of a thrower, subsequent to initial scapular protraction (tilting). There is associated coracoid tenderness on the medial aspect of the coracoid tip, corresponding to the insertion of the pectoralis minor tendon. In the scapular retraction test the scapula is manually repositioned in retraction and posterior tilt by the examiner. Full forward flexion without coracoid pain is diagnostic of the SICK scapula syndrome. As the scapula tilts anteriorly, it protracts and abducts and displaces up and over the top of the thorax. Impingement-like symptoms are associated with anteroinferior angulation of the acromion secondary to scapular protraction. Traction and pain related to the levator scapulae muscle result from the tilt and lateral rotation of the scapula. The combination of a SICK scapula and GIRD may result in injury to the posterosuperior labrum, the articular surface of the posterior supraspinatus, and the anterior inferior capsular structures.

Summary of the Throwing Shoulder and Dead Arm

The throwing athlete often presents with a sudden onset of mechanical pain caused by a posterior type 2 or type 2 SLAP lesion.¹⁸⁵ Prior to the development of the peel-back tear, there may be a prodromal phase or pre-SLAP stage of posterior shoulder tightness. At this stage MR studies frequently demonstrate eccentric posterior glenoid rim sclerosis and sometimes associated remodeling of the posterior glenoid rim. The shoulder at risk for dead arm symptoms exhibits mild to moderate GIRD and/or a malpositioned SICK scapula. When GIRD exceeds the external rotation gain (ERG), the GIRD/ERG ratio is greater than 1. A posterosuperior shift of the glenohumeral rotation point then follows, with abduction and external rotation during the late cocking phase of throwing. The SICK scapula syndrome is an extreme form of scapular dyskinesis. In a thrower with a dropped elbow, the upper arm hyperangulates posterior to the plane of the scapula (Fig. 8.207). Hyperangulation of the humerus on the glenoid and poor throwing mechanics may further contribute to increased humeral external rotation and the peel-back effect.

The dead arm is characterized by the following pathologic changes:

A tight posterior band of the IGHL (a response to the follow-through phase of throwing)
GIRD

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A posterosuperior shift in glenohumeral rotation point, which results in:
- Increased clearance of the greater tuberosity over the glenoid
- Reduced humeral head cam effect on the anterior inferior capsule
- Hyperexternal rotation of the humerus relative to the scapula
Peel-back forces in late cocking phase, which cause a posterior type 2 SLAP lesion
Scapular protraction

FIGURE 8.203 ● (A) Color coronal graphic of hyperexternal rotation during cocking phase of throwing, causing hypertwisting of the rotator cuff fibers. (Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 2003;19(4):404.

) (B) Coronal FS PD FSE image with articular side-cuff hyperintensity and posterosuperior labral tear in a pitcher. (C) Sagittal FS PD FSE image in a separate case with posterior articular side-cuff overload. This may occur in the posterior supraspinatus or anterior portion of the infraspinatus. Hyperintensity is demonstrated in the infraspinatus musculotendinous junction tearing.

FIGURE 8.204 ● (A) Posterior superior view of the biceps labral complex at the resting position (top illustration). In abduction and external rotation there is a dynamic peel-back phenomenon as the biceps vector shifts posteriorly, with twisting at the base of the biceps (bottom illustration). (Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part I: Pathoanatomy and biomechanics. Arthroscopy 2003;19(4): 404.

) (B) Color illustration of glenoid labrum with lateral perspective. The peel-back mechanism is associated with either posterior SLAP 2 or combined anteroposterior SLAP 2 (classic SLAP 2) lesions.

FIGURE 8.205 ● Pseudolaxity of the anterior inferior capsule secondary to a break in the labral ring associated with a posterior SLAP 2 lesion is shown on a sagittal color graphic (A) and a sagittal FS PD FSE image (B). (C) Moderate posterior glenoid rim sclerosis associated with mild anteroinferior rim sclerosis. The anteroinferior rim changes may be the initial changes of anteroinferior labral injury in the older elite pitcher or may be anterior rim wear secondary to pseudolaxity of the anteroinferior capsule.

FIGURE 8.206 ● SICK scapula associated with scapular abduction and protraction. Tension on the superomedial scapular insertion of the levator scapulae produces a painful tendinopathy between the medial angle and root of the scapular spine. (Based on

Burkhart SS, Morgan CD, Kibler WB. The disabled throwing shoulder: spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 2003;19(6): 641.

)

FIGURE 8.207 ● (A) Proper throwing mechanics with abduction of the arm in the plane of the scapula. Note the upper arm is maintained above the horizontal plane with the elbow positioned high. (B) Improper mechanics with a dropped elbow position and hyperangulation of the upper arm (humerus) posterior to the plane of the scapula. (Based on

)

Glenohumeral Joint Instability

The stability of the glenohumeral joint depends on the stabilizing musculotendinous structures of the rotator cuff as well as almost all the muscles of the shoulder girdle. A discussion of the importance of the IGLLC and particularly the IGHL, can be found in the paper by Turkel et al.¹⁸⁹

Anterior Instability

The most common of all glenohumeral joint instabilities is anterior instability, particularly that produced by lesions of the IGHL–labral complex (Fig. 8.208). The anterior band of the IGHL, which forms the anterior labrum, has been shown by Turkel et al. to be the primary restraint to anterior translation of the humeral head at 90° of abduction.¹⁸⁹ It is best demonstrated on sagittal oblique MR images and is routinely seen on MR arthrography in this plane.

Avulsion of the IGLLC from the glenoid rim, known as a Bankart lesion (Fig. 8.209), involves the detachment of the anterior labrum and the IGLC from the anterior glenoid rim. Rowe¹⁹⁰ has developed a classification system for Bankart lesions based on the detachment of the labrum and capsule from the anterior glenoid. A Bankart lesion can involve labral avulsion without a bony inferior glenoid rim fracture. Bankart lesions are discussed in greater detail below.

The IGL complex (Fig. 8.210) can also tear at its midportion or be avulsed from its humeral insertion. A HAGL lesion can be demonstrated arthroscopically and in some cases is solely responsible for shoulder instability (Fig. 8.211).¹⁹¹ HAGL lesions are also discussed in greater detail below. Pollock and Bigliani have shown that pathology or defects in the IGLLC are found at the humeral origin and within the substance of the ligament more commonly than was previously appreciated.¹⁹² It is therefore important to evaluate the IGLLC from its humeral origin throughout its course to its labral insertion.

FIGURE 8.208 ● Anterior labral avulsion from the anterior glenoid rim (arrows). a, acromion; ab, anterior band of inferior glenohumeral ligament; al, anterior labrum; ap, axillary pouch of inferior glenohumeral ligament; c, coracoid; pb, posterior band of inferior glenohumeral ligament; s, supraspinatus tendon; sgl, superior glenohumeral ligament; sub, subscapularis tendon; b, biceps tendon; mgl, middle glenohumeral ligament.

Pollock and Bigliani have also studied IGHL thickness and report that the anterior band is the thickest region, followed by the anterior and posterior aspects of the axillary pouch.¹⁹² Failure of the IGHL can occur at the glenoid insertion site (40%), in the ligament substance (35%), and at the humeral insertion site (25%). Avulsions occur more frequently in the anterior band and the anterior aspect of the axillary pouch, whereas ligament substance tears are more common in the posterior aspect of the axillary pouch. Bankart avulsions represent failure of the IGHL at the glenoid insertion, and IGHL capsule laxity represents intrasubstance ligament failure. The tensile properties of the IGHL allow for significant stretching before failure; therefore, redundancy of the IGHL may be as important as avulsions of the glenoid insertion at the IGHL in producing glenohumeral instabilities.

Operative stabilization for anterior instability includes the following procedures:

Tightening of the anterior structures to limit external rotation (Magnuson-Stack and Putti-Platt procedure) (Fig. 8.212)
Coracoid transfer procedures (Bristow operation) to provide a bony block and a tenodesis effect to prevent anterior translation of the humeral head over the anterior glenoid rim
Osteotomies of the glenoid or humerus

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Reconstruction of the avulsed or stretched IGLC structures (Bankart procedure and its modifications)

FIGURE 8.209 ● Bankart lesion. (A) A tear (large curved arrow) of the inferior glenoid and labral attachment of the inferior glenohumeral ligament (IGL) is present. Scarred muscle of the subscapularis is shown along the inferior glenoid neck (small curved arrow). The humeral head (HH) is subluxed inferiorly. G, glenoid. (B) The arthroscopic view from inferior to anterior is seen with the scope in the axillary pouch, oriented toward the anterior inferior pole of the glenoid. Note the avulsed labrum from the glenoid rim (G) and torn inferior pole attachment (large curved arrow) of the IGL. HH, humeral head. Scarred tearing of subscapularis muscle from the scapular neck is also identified (small curved arrow). (C) Avulsed anterior glenoid labrum (L; curved arrow) and IGL attachment are shown on a T2*-weighted coronal oblique image. Fluid extension (straight arrows) is identified between the inferior glenoid neck, detached labrum, and subscapularis muscle (S).

FIGURE 8.210 ● Inferior glenohumeral ligament labral complex. (A) Enhanced T2*-weighted GRE coronal oblique images demonstrate the normal inferior glenoid pole attachment of the axillary pouch (ap) of the inferior glenohumeral ligament (straight arrow). Note gadolinium contrast in normal inferior extension of subscapularis bursa (curved arrow). (B) An enhanced T1-weighted axial image displays the subscapularis bursa (curved arrow) and glenoid origin (straight arrow) of the inferior glenohumeral ligament complex (IGLC). The IGLC may originate from the glenoid, the labrum (L), or the neck of the glenoid immediately adjacent to the labrum. There is no anterior lateral tear on this image. (C) An enhanced T1-weighted axial image below the level of the glenoid displays the normal axillary pouch (ap) of the inferior glenohumeral ligament. (D) An enhanced T1-weighted axial image in a different patient identifies the anterior band (ab) of the IGLC and its continuation as the anterior labrum (al). Gadolinium contrast is shown in the subscapularis bursa (s) anterior to the anterior band. There is no tear of the anterior inferior labrum.

FIGURE 8.211 ● (A, B) Anterior coronal oblique images display an abnormally capacious axillary pouch (straight arrows) secondary to avulsion of the IGL humeral insertion (curved arrows). (C) An arthroscopic image also shows the avulsed humeral attachment of the IGL (curved arrows). AB, anterior band; HH, humeral head; IL, torn inferior labrum; S, subscapularis muscle.

FIGURE 8.212 ● Axial FS PD FSE image showing a failed Putti-Platt with recurrent anterior instability and deficiency of the anterior inferior glenoid rim. In the Putti-Platt procedure the subscapularis tendon is divided. The lateral stump of the subscapularis is attached to soft tissue along the anterior rim of the glenoid and the medial stump is lapped over the lateral stump to the greater tuberosity to effect shortening of the capsule and subscapularis muscle.

Indications for open surgery include:

Anterior rim glenoid fracture (>20%)
Large posterior humeral head defect
Severe ligament damage (previous capsular shrinkage with failure or HAGL lesion)

Arthroscopic stabilization procedures¹⁹³ involve a capsular plication combined with reattachment of the IGLLC (arthroscopic Bankart repair) (Fig. 8.213). Arthroscopic stabilization can be used in the following circumstances:

First-time traumatic dislocations, such as Hill-Sachs, Bankart, or Perthes lesions, without hyperlaxity
Recurrent posttraumatic dislocation with or without hyperlaxity
Injuries not involving compromise of IGHL and MGHL competence
Injuries without osteochondral lesions
Symptomatic subluxation

Arthroscopic stabilization is contraindicated in the following situations:

Osseous or bony Bankart lesions
Labral hypoplasia
Severe injury of the IGHL or MGHL
HAGL lesions
Injuries with concomitant cuff lesions
Voluntary instability and multidirectional instability

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Posterior instability
Nondisplaced fracture of the greater tuberosity

FIGURE 8.213 ● Arthroscopic repair of the anterior and posterior labrum help centralize an anteriorly dislocated humeral head as viewed from the level of the biceps tendon. (A) Frayed posterior labrum (pl) and anterior labrum (al) associated with a Hill-Sachs (HS) fracture of the humeral head are identified. g, glenoid. (B) Repair begins with the posterior inferior capsule sutured to the posterior labrum (pl). hh, humeral head; g, glenoid. (C) Anteriorly placed sutures (arrow) complete the arthroscopic stabilization centralizing the humeral head (hh) on the glenoid (g).

Classification of Anterior Instability

Eighty-five percent of dislocations are anterior, and of anterior dislocations, subcoracoid dislocations, caused by abduction, extension, and external rotation, are the most common. Other types of anterior dislocation include:

Subglenoid
Subclavicular
Intrathoracic
Retroperitoneal

Anterior shoulder instability can be classified as either traumatic or nontraumatic.¹⁹⁴^,¹⁹⁵ Any severe trauma, such as fracture of the greater tuberosity or rotator cuff avulsions, may cause anterior instability. Unidirectional (anterior) traumatic dislocation, accounting for 95% of shoulder instability, is referred to as traumatic unidirectional instability treated with Bankart surgery (TUBS). Multidirectional atraumatic subluxation is referred to as atraumatic multidirectional and bilateral instability (AMBRI) or multidirectional instability (MDI). MDI is discussed in greater detail later in the chapter. This instability is often bilateral and is treated with rehabilitation or reconstruction of the rotator interval capsule–coracohumeral ligament mechanism and an inferior capsular shift. Patients may have a combination of TUBS and AMBRI (MDI).

TUBS patients present in pain with anterior prominence of the humeral head. There is usually a history of an anterior force applied to an abducted, externally rotated arm. This force results in the shoulder “popping out of its socket.” AMBRI patients are often difficult to diagnose; many report a sensation of their shoulder sliding forward or their arm going numb.

In true MDI of the glenohumeral joint, force applied distally in the upper extremity with the patient—s arm abducted causes inferior subluxation of the humeral head. This produces a visible sulcus (i.e., the sulcus sign) between the prominence of the acromion and the inferior subluxed humeral head.¹⁹⁶ In classic MDI, the ligament laxity is bilateral and atraumatic. The index of suspicion should be high in young patients, especially young female patients with generalized joint laxity and complaints referable to the shoulders. These patients are best treated with physical therapy. Specific muscle rehabilitation, with particular attention to the shoulder compressors, helps to provide stability to the lax joints.

No visible ligament labral lesions are seen in patients with true MDI of the glenohumeral joint. The capsular ligaments are redundant, and the labrum is often hypoplastic. Some patients with multidirectional laxity, however, present with unidirectional pathology and experience dislocation predominantly in only one direction. Intra-articular arthroscopic findings confirm the direction of the instability.

Related Injuries

Injuries associated with anterior ligament and capsule dislocations include:¹⁹⁵

Avulsion of the anterior inferior glenohumeral ligament (AIGHL) and capsule from the glenoid (more common in younger individuals)
HAGL lesion with or without bone flecks
Fractures of the glenoid, humeral head, tuberosities, or coracoid process
Cuff tears associated with anterior and inferior glenohumeral dislocation (30% incidence in patients less than 40 years of age and 80% incidence in patients over 60 years of age)
Vascular injury, which may occur during dislocation or reduction and is more common in elderly patients. The structures at risk include the axillary artery or vein or branches of the axillary artery—the thoracoacromial, subscapular, circumflex, and less commonly the long thoracic.
Neurovascular injuries, usually affecting the brachial plexus and axillary nerves

MR Findings in Anterior Instability

Bankart Lesions

The Bankart lesion and anterior labral variants (plus the posterior labrocapsular periosteal sleeve avulsion [POLPSA] lesion shown for comparison) are illustrated in Figure 8.214. Anterior labral pathology in the anteroinferior quadrant may vary based on the degree of involvement of the anterior inferior labrum, the scapular periosteum, the IGHL, the osseous glenoid rim, and the articular cartilage of the anterior inferior glenoid and displacement of the anterior labrum.¹⁹⁷ The mechanism of subcoracoid dislocation (Fig. 8.215), the most common form of anterior dislocation, is usually a combination of shoulder abduction, extension, and external rotation. MR examination in a fixed dislocation demonstrates displacement of the humeral head anterior to the glenoid and inferior to the coracoid process. The humeral head is impacted on the anterior inferior glenoid rim, producing Hill-Sachs posterolateral humeral head fractures.

MR studies¹⁹⁸^,²⁰¹ are used to distinguish between soft tissue (labral only) and osseous (labrum and glenoid rim) Bankart lesions:

In soft tissue Bankart lesions (Fig. 8.216), the anteroinferior labrum is avulsed without fracture, deformity, or blunting of the anteroinferior glenoid rim. There may be only minimal subchondral edema of the anteroinferior glenoid.
The osseous or bony Bankart lesion (Fig. 8.217) presents with a small to large anterior inferior glenoid rim fracture that may extend anterior and superior to the equator.

MR is also used to describe associated rotation of the fractured glenoid rim (Fig. 8.218) and to quantify associated medial displacements of the IGHL underneath the glenoid (Fig. 8.219). Superior extension of a Bankart lesion into a SLAP tear represents a SLAP 5 (SLAP 2 or 3 plus Bankart) lesion (Fig. 8.220).

FIGURE 8.214 ● (A) Normal anterior inferior labrum and capsule. (B) Classic or soft tissue Bankart with disruption of scapular periosteum. (C) Bony or osseous Bankart with a double labral lesion. (D) Double labral lesion with labral disruption from both the glenoid rim and adjacent IGHL. (E) Perthes avulsion of the labrum and IGHL from the anterior scapular neck without periosteal disruption. (F) Triple labral lesion with disruption of the labrum from the glenoid rim and IGHL, with additional tearing of the IGHL from the scapular neck. (G) A GLAD lesion (glenoid labrum articular disruption) is also known as a GARD lesion (glenoid articular rim divot). These lesions involve a partial tear of the anterior inferior glenoid labrum with adjacent articular cartilage defect in clinically stable patients. (H) The ALPSA lesion is an anterior labroligamentous periosteal sleeve avulsion. (I) The POLPSA lesion (posterior labrocapsular periosteal sleeve avulsion).

FIGURE 8.215 ● (A) Coronal and (B) sagittal T2 FSE images showing fixed anterior subcoracoid dislocation with a large posterolateral humeral head Hill-Sachs fracture.

FIGURE 8.216 ● (A) Sagittal color graphic illustrating a soft tissue Bankart lesion. (B) Axial FS PD FSE image of anterior displaced anterior inferior labrum (Bankart lesion).

FIGURE 8.217 ● (A) Sagittal color graphic illustrating an osseous Bankart lesion. (B) Axial PD FSE MR arthrogram shows an anteroinferior osseous Bankart with avulsion of the labrum and involvement of the anterior glenoid rim. (C) Sagittal FS PD FSE MR arthrogram shows the extent of an anteroinferior glenoid rim fracture from the equator to the inferior pole.

FIGURE 8.218 ● Sagittal FS PD FSE image demonstrates rotation of an anteroinferior osseous Bankart fracture.

FIGURE 8.219 ● Coronal FS PD FSE image displays medial displacement of the anterior inferior labrum and axillary pouch of the IGHL in a Bankart lesion.

FIGURE 8.220 ● Coronal FS PD FSE image showing a SLAP 5 lesion. A type 5 SLAP is a combination of a type 2 or 3 SLAP and a Bankart lesion.

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Sagittal MR images are used to accurately assess the entire area of glenoid fossa involved in the fracture between the equator and the inferior pole of the glenoid. Coronal images often underestimate the size of the osseous Bankart fracture. The anterior labral tear usually extends superior to the fracture site on axial MR images. Axial T1-weighted images show subchondral bone changes, including low-signal-intensity sclerosis or marrow hyperemia at the fracture site. T2*-weighted images are useful in demonstrating the morphology of the labrum and associated tear pattern, but FS PD FSE axial images provide increased contrast for identification of fluid edema and paralabral cysts. Coronal oblique images show avulsion of the anterior inferior labrum and its relationship to the axillary pouch, which is lax when the arm is adducted (Fig. 8.221). Axial oblique images perpendicular to the long axis (12 o—clock to 6 o—clock) of the glenoid are more sensitive in detecting anteroinferior labral tears on axial images (Fig. 8.222). The region of the anteroinferior labrum may be obscured by partial volume averaging on axial images obtained inferior to the equator.

The ABER technique, although not routinely used, is helpful in postoperative assessment of labral repair, properly displaying the labral scar complex in abduction and external rotation (Fig. 8.223).

Sagittal oblique images define the size of the anterior inferior glenoid fracture and the extent of the labral tear, both anterosuperiorly and superoinferiorly. The relationship of the anterior band of the IGHL to the avulsed labrum is identified at the level of the glenoid fossa. Medial displacement of the

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avulsed labrum, when it occurs, is secondary to medial and inferior pull from the anterior band of the IGHL. A linear area of hyperintensity is seen in the area of stretching or plastic deformation across the axillary pouch of the IGHL. This is better visualized with the arm positioned in abduction and external rotation to tighten the IGHL complex.

FIGURE 8.221 ● In the absence of the rare circumferential meniscoid labral variant, no contrast should extend between the inferior labrum and adjacent glenoid articular cartilage. Coronal FS PD FSE image.

FIGURE 8.222 ● Soft tissue Bankart lesion on coronal (A) and axial (B) FS PD FSE images. Note detection of contrast between the inferior labrum and glenoid inferior pole articular cartilage on the coronal image (A). An anteroinferior labral tear can be seen at the inferior glenoid pole using an axial oblique acquisition. This technique matches the anteroinferior glenoid rim with the corresponding posterior inferior glenoid rim and thus minimizes partial volume effects in evaluating anterior inferior labral tears.

It is important to differentiate between acute and chronic Bankart lesions (Fig. 8.224). In acute lesions, there is increased signal intensity in the subchondral bone of the glenoid on T2, FS T2-weighted FSE, or STIR images. In athletes, there may be acute trauma superimposed on a chronic Bankart lesion that does not need to be clinically repaired. This is especially likely in high-level amateur and professional athletes who perform despite a previous history of shoulder trauma or dislocation. A chronic osseous Bankart frequently heals with hypertrophic bone, producing a convex “beer-gut” contour anterior to the anterior inferior glenoid rim on sagittal images (Fig. 8.225).

Recurrent instability is more likely to occur in patients who are under the age of 20 years at the time of the initial dislocation.¹⁹⁵ There is a lower incidence (as low as 10%) of recurrence in patients between 30 and 40 years of age. Most recurrences occur within 2 years following the first traumatic dislocation. The recurrence rate of instability is lower when a first-time dislocation is associated with a greater tuberosity fracture. However, an associated greater tuberosity fracture is

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up to three times more common in patients over 30 years of age. It occurs in less than 10% of patients under 30 years of age (Fig. 8.226). Older patients who stretch the IGHL complex or sustain a greater tuberosity fracture are more likely to heal with a static shoulder than younger patients who have nonhealing injuries, including IGHL avulsions and posterolateral humeral head fracture defects (Hill-Sachs defects). Recurrence is high in atraumatic instability because there is no traumatic lesion to heal.

FIGURE 8.223 ● Retear of the anteroinferior labrum, difficult to appreciate on an axial PD MR arthrogram (A), is easily identified on the corresponding abduction external rotation (ABER) sequence (B).

A Hill-Sachs posterolateral compression fracture (Fig. 8.227) can be seen in patients with subluxation and single or multiple episodes of dislocation.²⁰² The compression defect is identified on the posterolateral humeral head. There is a normal bare area of bone where the capsule attaches laterally to the anatomic neck of the humerus posteriorly. This bare area shows normal flattening of the posterior aspect of the humeral head in its inferior portion and should not be mistaken for a Hill-Sachs defect. Normal posterolateral cysts or erosions may also occur in the region of the bare area and extend deep to the distal fibers of the infraspinatus tendon posterior to the greater tuberosity. Posterolateral bone contusions, without humeral head indentation, may also be identified on MR images.²⁰³

Treatment of posttraumatic anterior instability must address:

The Bankart lesion
Anterior labroligamentous periosteal sleeve avulsion (ALPSA)
HAGL
Capsular laxity

Bankart repair

Bankart labral detachment, the primary lesion after initial traumatic dislocation, is associated with coexistent capsular redundancy or laxity at the time of the initial dislocation. With chronic recurrent instability there is even further capsule attenuation.¹⁹⁵ A Bankart repair and capsular shifting or plication may be required to restore and maintain stability. Metallic devices such as staples, rivets, or screws are no longer used because of high instability recurrence rates. Techniques commonly used to achieve repair include:

Bioabsorbable tacks
Transglenoid sutures
Suture anchors (used for both soft tissue and osseous Bankart repair)²⁰⁴

The goal of repair procedures is to fix the detached labrum to the anterior glenoid rim. Capsular shift techniques involve advancing redundant anteroinferior capsular tissue proximally and medially and then attaching the capsule to the glenoid rim. Arthroscopic Bankart repair may be used in acute anterior instability in patients with first-time traumatic dislocation, especially in younger patients, who have an 80% to 90% recurrence rate.

In cases of chronic instability with recurrent dislocation and capsular laxity, a Bankart repair and inferior capsular shift are performed simultaneously. Arthroscopic capsular imbrication is used to reduce capsular volume in patients with small amounts of capsular redundancy. Thermal capsulorrhaphy, using a heat probe with radiofrequency heat energy to reduce

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capsular laxity, has been associated with high failure rates and tissue necrosis. AMBRI (MDI) patients undergo rehabilitation for at least 3 to 6 months after repair.

FIGURE 8.224 ● Chronic Bankart lesion (arrow) in an injured football player is seen on T2* (A), FS PD FSE (B), and axial CT (C) images. On the FS PD FSE image there is a lack of bone marrow edema at the fracture site or in adjacent glenoid subchondral bone marrow. Sclerotic changes are seen in the anterior inferior glenoid rim on the corresponding CT scan (C).

FIGURE 8.225 ● Sagittal PD FSE image showing a chronic healed osseous Bankart lesion with prominent convex anterior inferior glenoid rim contour (the “beer gut sign”).

FIGURE 8.226 ● Coronal FS PD FSE image of a greater tuberosity fracture and a Bankart lesion. The association of a greater tuberosity fracture is more common in patients over 30 years of age.

FIGURE 8.227 ● (A) Posterolateral Hill-Sachs deformity with flattening of the posterior humeral head contour on a sagittal FS PD FSE image. (B) Arthroscopic view of Hill-Sachs fracture.

FIGURE 8.228 ● Stages of engaging Hill-Sachs lesion with posterolateral humeral head defect contacting the posterior glenoid rim (A, B) and subsequently engaging the anterior rim (C, D). The engaging Hill-Sachs reproduces the anterior inferior instability event with humeral head displacement. (A, C) Superior axial views illustrating stages of engagement. (B, D) Axial PD FSE images in external rotation.

Complications of operative management of anterior instability include:

Infection
Recurrent instability
Loss of external rotation
Neurovascular injury
Hardware migration

For experienced arthroscopists, the results of arthroscopic repairs approximate the results of open Bankart repair and capsular shift. A poor prognosis for repair is associated with osseous deficiency of the glenoid, which may be found in cases of an ongoing engaging Hill-Sachs lesions on the humeral side and an inverted-pear deformity on the glenoid side.²⁰⁵ In the engaging Hill-Sachs defect at the posterolateral humeral head, the humeral head may contact the anterior glenoid rim in abduction and external rotation (Fig. 8.228). The inverted-pear glenoid (Fig. 8.229) is created by an anterior inferior glenoid rim fracture (an osseous Bankart lesion), which results in an inferior glenoid fossa that is

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narrower than the superior glenoid. The inverted-pear glenoid has less shearing resistance and decreased resistance to humeral axial forces. The effective glenoid available for humeral rotation is therefore shortened secondary to loss of bone.

FIGURE 8.229 ● (A) Sagittal color illustration and (B) sagittal FS T1-weighted MR arthrogram illustrate an inverted-pear deformity with loss of the anterior inferior glenoid rim bone stock in an osseous Bankart lesion. L, labrum; curved arrows, deficient anteroinferior glenoid rim.

The engaging Hill-Sachs lesion can be treated by an open capsular shift. The inverted-pear glenoid is treated by lengthening the glenoid and by restoring the glenoid bone stock (e.g., Latarjet reconstruction using a coracoid graft).

MR sagittal images are used to identify tacks or suture anchors (Fig. 8.230) at the level of the glenoid fossa. All three imaging planes are used to identify labral detachment (Fig. 8.231) and displaced tacks (Fig. 8.232). MR images in the axial plane are used to characterize and differentiate granulation/scar tissue from fluid undermining the labral repair. ABER MR arthrography may be required to differentiate an unstable labral repair from the anterior glenoid rim when placed under tension in abduction and external rotation.

Perthes Lesions

The Perthes lesion (Fig. 8.233) is a labral ligamentous avulsion with an intact scapular periosteum.²⁰⁶ The periosteum is stripped medially from the anterior glenoid without medial displacement of the labral periosteal complex. The IGHL and labrum are positioned normally relative to the underlying glenoid. Perthes lesions often occur after the initial dislocation. In chronic cases there may be fibrosis and resynovialization of the labrum and periosteum. FS PD FSE images demonstrate a subtle increased signal intensity at the base of a usually minimally displaced labrum (sublabral hyperintensity). Bankart and Hill-Sachs fractures may be associated findings. Although ABER MR arthrography may improve visualization of Perthes lesions, optimized FS PD FSE coronal and axial images should be accurate in most cases.

ALPSA Lesions

Anterior labroligamentous periosteal sleeve avulsion (ALPSA lesion) is an avulsion of the IGHL through its anterior band attachment to the anterior labrum, similar to the Bankart lesion.²⁰⁷ An ALPSA lesion differs from a Bankart lesion, however, in that an ALPSA lesion has an intact anterior scapular periosteum that allows the labroligamentous structures to displace medially and rotate inferiorly on the scapular neck (Fig. 8.234). In a Bankart lesion, the anterior scapular periosteum ruptures, resulting in displacement of the labrum and attached ligaments anterior to the glenoid rim. After the ALPSA lesion heals, there may be recurrent anterior dislocations secondary to IGHL incompetence. Arthroscopically, an ALPSA lesion is converted to a Bankart lesion to allow reconstruction of the anterior inferior structures of the capsule (capsulorrhaphy). Neviaser identified ALPSA lesions in four of eight patients with primary anterior shoulder dislocations.²⁰⁷ The mechanism of injury is the same for both Bankart and ALPSA lesions.

On axial MR images, the anterior labrum with stripped periosteum can be seen to be displaced medially and rotated inferiorly on the neck of the glenoid (see Fig. 8.234). Sagittal images at the level of the glenohumeral joint are used to identify medial displacement of the anterior band relative to the neck of the glenoid (Fig. 8.235). In comparison, a Bankart lesion usually is shown with a space or gap between the anterior rim of the bony glenoid and displaced anterior glenoid. This gap is the result of rupture of the glenoid neck periosteum and is frequently filled with fluid signal intensity.

FIGURE 8.230 ● (A) Illustration of a Bankart repair with anterior inferior suture anchors shown. Anterior capsule and posterior-inferior capsule plication are further techniques used to improve surgical success for anterior-inferior reconstructions. The goal is to restore anterior and posterior capsular integrity and rebuild the anterior labral wedge. Associated SLAP lesions and middle glenohumeral ligament detachments are also repaired. The reattached anterior inferior labrum is seen from the equator to the inferior pole of the glenoid on sagittal FS PD FSE image (B) and axial FS PD FSE image (C).

FIGURE 8.231 ● Axial FS PD FSE MR arthrogram (A) shows labral detachment superior to the Bankart repair shown in (B), a PD FSE MR arthrogram.

FIGURE 8.232 ● (A) Coronal FS PD FSE and (B) axial T2 FSE images show displaced tacks located posterior to the supraspinatus muscle after extensive Bankart repair. These dislodged tacks may lead to degenerative glenohumeral arthrosis and synovitis. The axillary recess, subscapularis, and bursa are common locations.

FIGURE 8.233 ● (A) Axial color graphic, (B) axial FS PD FSE image, (C) axial T1 MR arthrogram (in a separate case), and (D) corresponding gross dissection in Perthes lesion, a labral ligamentous avulsion with intact but medially stripped periosteum along the anterior glenoid neck.

FIGURE 8.234 ● (A) ALPSA axial (transverse plane) color illustration, (B) axial FS PD FSE image, (C) coronal color illustration, and (D) coronal FS PD FSE image of an ALPSA lesion (anterior labroligamentous periosteal sleeve avulsion) with medial and inferior rotation of the anteroinferior labroligamentous complex. The ALPSA is also referred to as a medialized Bankart lesion.

FIGURE 8.235 ● (A, B) Sagittal PD FSE MR arthrograms demonstrate progressive (B is medial to A) medialization of the displaced and rotated inferior glenohumeral ligament labral complex. (C) Corresponding arthroscopic view of a displaced ALPSA lesion. The labrum and fibrous tissue may resynovialize anterior to the neck of the glenoid.

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GLAD Lesions

As described by Neviaser,²⁰⁸ the glenolabral articular disruption (GLAD) results from a forced adduction injury occurring from the position of abduction and external rotation of the shoulder (Fig. 8.236). There is a superficial anterior inferior labral tear associated with an anterior inferior glenoid articular cartilage injury. There are no signs of clinical or surgical anterior instability. Identification of anterior inferior labral tears may require imaging of the shoulder with the arm positioned in external rotation and abduction. The use of intra-articular contrast helps to visualize small tears at the level of the anterior inferior glenoid rim. Articular cartilage lesions are best demonstrated with FS PD-weighted FSE sequences or FS MR arthrography at smaller FOVs (8 to 12 cm). The anterior labrum and glenoid articular cartilage often demonstrate normal morphology one image superior to the GLAD lesion (Fig. 8.237).

Capsular-Related Lesions

In addition to anterior dislocation associated with failure of the IGHL at the inferior glenoid attachment, the IGHL may fail at other locations (Fig. 8.238), causing the following lesions:²⁰⁹

Failure at the anatomic neck of the humerus causes HAGL and bony HAGL lesions.
Failure at both the humerus and glenoid causes AIGHL lesions.

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Posterior capsular detachment and failure of the posterior band attachment to the humerus causes reverse HAGL lesions.
Failure of the IGHL glenoid attachment without labral avulsion causes glenoid avulsion of the glenohumeral ligaments (GAGL) lesions.
Medial displacement of the IGHL associated with a Bankart causes an inferior ALPSA lesion.
Mid-axillary pouch tears
Axillary pouch sprain and scarring of the IGHL at the glenoid attachment (partial or healed GAGL)

FIGURE 8.236 ● (A) Axial color section, (B) axial FS PD FSE MR arthrogram, and (C) arthroscopic view of a GLAD (glenolabral articular disruption) or GARD (glenoid articular rim divot) lesion with a flap tear of the anterior inferior labrum and chondral defect of the adjacent articular cartilage.

FIGURE 8.237 ● Axial FS PD FSE images show a GLAD lesion anteroinferiorly (A) with intact anterior labrum directly superiorly (B). There was no associated glenohumeral instability.

HAGL Lesions

Humeral avulsion of the glenohumeral ligament (HAGL lesion) is significantly less frequent than the classic Bankart lesion as a cause of anterior shoulder instability. Wolf et al.¹⁹¹ identified HAGL lesions in 9.3% of 64 shoulders preoperatively evaluated by arthroscopy for anterior instability and in 35% of shoulders that were unstable without labral pathology at the level of the glenoid rim. Thus, the HAGL lesion may exist in patients with anterior instability with or without an associated anterior labral tear.²¹⁰

Identification of the humeral detachment of the IGHL on MR images usually requires the presence of a joint effusion or the use of MR arthrography. The axillary pouch is converted from a fluid-distended U-shaped structure to a J-shaped structure as the IGHL drops inferiorly (Fig. 8.239). The direct extension of fluid or contrast can be identified between the humerus and the avulsed IGHL. On sagittal oblique images, the retracted or redundant IGHL appears as a mass of low-signal-intensity tissue. Coronal images display HAGL lesions as either partial (Fig. 8.240) or complete (Fig. 8.241), with primary involvement of the attachment of the anterior capsule (centered on the anterior band of the IGHL) to the humerus (see Fig. 8.238).

Bony humeral avulsion of the glenohumeral ligaments (BHAGL) lesions are also associated with traumatic anterior dislocation but are relatively rare compared to HAGL.²¹¹ In bony HAGL lesions there is a small avulsed osseous fragment attached to the torn end of the humeral attachment of the IGHL. Repair consists of excising the fragment and reattaching the IGHL to the anatomic neck of the humerus.

In a reverse HAGL lesion (Fig. 8.242)⁷³ (discussed in detail under posterior instability), there is detachment of the posterior capsule or reverse humeral avulsion of the glenohumeral ligament.

In open surgical repair for shoulder instability, the HAGL lesion may be overlooked or mistaken for an iatrogenic defect of the anterior capsule during dissection of the subscapularis tendon from the anterior capsule. Although the mechanism of injury for HAGL lesions is similar to that of other traumatic dislocations resulting in anterior instability, the HAGL lesion is produced by external rotation of the abducted shoulder (compared to the Bankart lesion, which is produced by external rotation of the abducted shoulder with simultaneous compression). At arthroscopy the HAGL lesion is found in the anterior

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inferior quadrant of the humeral origin of the IGHL. The goal of arthroscopic HAGL repair is to mobilize and suture the avulsed capsular edge; therefore, HAGL lesions are treated by surgical reattachment of the glenohumeral ligament to its humeral insertion.

FIGURE 8.238 ● Capsular IGL lesions illustrated in the coronal plane include: (A) HAGL (humeral avulsion of the glenohumeral ligament), (B) BHAGL (bony humeral avulsion of the glenohumeral ligament), (C) AIGHL (anterior inferior glenohumeral ligament), (D) RHAGL (reverse HAGL), (E) GAGL (glenohumeral avulsion of the glenohumeral ligaments), (F) inferior ALPSA (anterior labroligamentous periosteal sleeve avulsion), (G) mid-axillary pouch (AP) tear, (H) IGHL sprain, (I) IGLLC (inferior glenohumeral ligament labral complex) scarring.

FIGURE 8.239 ● Stages of a displaced HAGL tear in the anterior atomic neck attachment of the IGHL(IGL). (A) Coronal illustration with partial IGLinferior displacement. (B) Coronal illustration of a J-shaped or inferiorly displaced IGL. (C) Arthroscopic view of a torn subscapularis tendon (short arrow) and humeral avulsion of the IGL (double-headed long arrow) creating the J-shaped axillary pouch.

FIGURE 8.240 ● HAGL lesion on coronal color graphic (A) and coronal T1-weighted MR arthrogram (B). Arthroscopic view (C) demonstrates avulsion of the anterior capsule.

FIGURE 8.241 ● HAGL lesion wth avulsion of the humeral attachment of the inferior glenohumeral ligament (arrow) on FS PD-weighted FSE coronal oblique (A) and T2-weighted FSE sagittal oblique (B) images. Corresponding arthroscopic photograph (C) shows suturing with coaptation of the detached portion of the IGHL. HH, humeral head.

FIGURE 8.242 ● (A) Axial FS T1 MR arthrogram, (B) sagittal FS T1MR arthrogram, and (C) sagittal FS T1-weighted image showing reverse humeral avulsion of the glenohumeral ligaments (RHAGL) associated with both posterior capsular avulsion and rupture of the posterior band of the IGL. There is extension of contrast between the torn posterior capsule and teres minor.

FIGURE 8.243 ● Coronal FS PD FSE image of floation anterior inferior glenohumeral ligament (AIGL) with unattached glenoid (Bankart) and humeral (HAGL) components.

FIGURE 8.244 ● (A) Coronal FSPD FSE and (B) sagittal PD FSE images show glenoid avulsion of the glenohumeral (GAGL) with intact anterior inferior labrum.

Floating Anterior Inferior Glenohumeral Liga-ment Lesions

The “floating” anterior inferior glenohumeral ligament (AIGHL) lesion (see Fig. 8.238; Fig. 8.243) is a rare injury that involves both disruption of the IGHL attachment at the inferior pole of the glenoid (Bankart component) and tearing of the IGHL from its attachment to the anatomic neck of the humerus (HAGL component).²¹² Restoration of function requires reattachment of the humeral and glenoid capsular disruptions. Although it is unusual to see disruptive forces produce both HAGL and Bankart lesions, we have observed ALPSA lesions with associated tearing of the anterior attachment of the IGHL to the anatomic neck of the humerus. These compound ALPSA lesions also demonstrate a greater degree of medial IGHL displacement associated with the labral or Bankart component. Coronal plane images are required to identify both the humeral and glenoid IGHL involvement or a single image. FS PD FSE images show the greatest conspicuity of fluid at the interface of the torn capsule (IGHL).

GAGL Lesions

Glenoid avulsion of the glenohumeral ligament (GAGL)(Fig. 8.244) are uncommon; there is avulsion of the

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IGHL from the inferior pole of the glenoid without associated disruption of the inferior labrum. The Bankart lesion is more common at the location of the inferior pole with involvement of both the anteroinferior labrum and medial capsular displacement.

Inferior ALPSA Lesions

In inferior ALPSA or cul-de-sac lesions, there is medial displacement of both the anterior inferior labrum and the IGHL underneath the inferior neck of the glenoid (see Fig. 8.238; Fig. 8.245). Involvement of the anterior inferior labrum establishes the existence of a Bankart lesion. The additional displacement of the labrum and IGHL represents a variation of the Bankart lesion. Coronal MR images characteristically demonstrate greater medial displacement of the capsule relative to the anterior inferior labrum. There is complete absence of labral fibrocartilage in the 6-o—clock position of the glenoid at the expected location of the labral glenoid–chondral interface.

Axillary Pouch Midligament Tears, Sprains, and Scarring

Mid-ligament (midportion of the IGHL) tears (Fig. 8.246) are less common than axillary pouch sprains. Coronal MR images demonstrate disruption or discontinuity centered in the middle third of the IGHL. Posttraumatic IGHL sprains (Fig. 8.247) are characterized by partial or diffuse hyperintensity and thickening of the IGHL as an isolated finding or in association with other IGHL-related lesions, including the Bankart lesion. Adhesive capsulitis, more common than posttraumatic axillary pouch sprain, may present with identical findings, including IGHL thickening and hyperintensity on FS PD FSE images. Scarring of the IGHL attachment to the anterior inferior labrum and/or inferior glenoid (Fig. 8.248) may represent a partial or healed GAGL lesion. MR demonstrates intermediate signal intensity at the IGHL junction, best visualized on coronal PD FSE images. The scar tissue may not be appreciated on FS PD FSE images because there is an insufficient contrast differential between scar tissue and the IGHL. A focal chondral lesion (a small Hill-Sachs lesion without osteochondral impaction) of the posterolateral humeral head may be associated with isolated complete capsular tears, including mid-ligament and HAGL lesions.²⁰⁹

FIGURE 8.245 ● Coronal T1-weighted MR arthrogram of inferior ALPSA with medial displacement of both the anterior inferior labrum and IGHL (IGL) underneath the inferior pole of the glenoid and along the inferior neck.

Posterior Instability

Posterior instability (Fig. 8.249) may occur after trauma and presents with pain and apprehension on examination with forward flexion and adduction of the shoulder.²¹³ The jerk-test (a jerking motion on posterior shoulder displacement near the midline or as the shoulder reduces anteriorly) is used to demonstrate the instability or apprehension. Documentation of a posterior dislocation is unusual. A redundant posterior capsule, posterior labral tearing, and osteochondral defects (including reverse Hills-Sachs and Bankart lesions) may be found. Posterior inferior instability occurs as a component of MDI. Additional findings in MDI include abnormal anterior and inferior laxity. Global pathology in MDI thus includes the labrum, the capsule (IGHLC), and the rotator cuff interval.

The posterior band of the IGLC is primarily responsible for capsuloligamentous restraint to posterior translation in 90° of abduction.⁶⁵^,²¹⁴ The anterior-superior capsule, or rotator interval capsule, has also been shown to be important in limiting posterior and inferior translation. Posterior dislocation occurs only with combined dysfunction of the posterior capsule and anterior superior capsule.²¹⁵ The incidence of posterior instability has been reported to be between 2% and 4% of patients with shoulder instability.

Acute posterior dislocation may occur secondary to indirect forces (such as electric shock procedure) that produce adduction, flexion, and internal rotation. A fall on the outstretched hand with the arm abducted is another mechanism of injury in posterior instability. These same mechanisms, including a direct posterior force on an anteriorly flexed, abducted, and internally rotated arm (e.g., football pass blocking), may also produce acute posterior shoulder subluxation. Posterior

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instability may also occur as an operative complication in patients with MDI after a misdirected anterior capsular procedure. With arthroscopy it is possible to assess associated intra-articular lesions, including labral tears, avulsions, and articular surface rotator cuff, SLAP, and biceps lesions.²¹⁵

FIGURE 8.246 ● Mid-axillary pouch tear of the IGHL (IGL) on a coronal color graphic centered on the axillary pouch (A) and a coronal FS PD FSE image (B). (C) Abduction external rotation (ABER) T1-weighted MR arthrogram in a separate case. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999.

)

FIGURE 8.247 ● Coronal FS PD FSE image of axillary pouch hyperintensity after traumatic injury with abduction and external rotation component.

Posterior instability should be suspected in the presence of posterior labral disruption or fragmentation.²¹⁶ A detailed examination with the patient under anesthesia (EUA) is critical in identifying this type of instability. EUA must be conducted in a lateral decubitus position with the patient—s arm adducted, forward flexed, and in internal rotation. Stabilization of the scapula allows the examiner to appreciate the degree of posterior translation and relocation of the humeral head with abduction and external rotation. The results of the EUA, and the findings on diagnostic arthroscopy, determine the choice of surgical procedure for management.

MR Findings in Posterior Instability

MR examinations in posterior instability may yield the following findings:²¹⁷

FIGURE 8.248 ● Intermediate-signal-intensity scarring of the IGL attachment to the inferior labrum and inferior pole of the glenoid without labral disruption on a coronal PD FSE image.

A reverse Hill-Sachs lesion (notch sign or trough lesion) in the anteromedial humeral head (Fig. 8.250)
Fractures of the posterior glenoid margin (reverse osseous Bankart lesion) associated with a posterior labral tear (Fig. 8.251)
Deficiency of the posterior glenoid rim (see Fig. 8.251)²¹⁸
Fractures of the lesser tuberosity associated with a posterior dislocation secondary to the pull of the supra-scapularis tendon insertion with or without tears of the subscapularis tendon and teres minor tendon
Fracture of the acromion/distal clavicle (Fig. 8.252)
A posterior labrocapsular periosteal sleeve avulsion (POLPSA) (Fig. 8.253).²¹⁷ Normally the posterior capsule attaches directly to the posterior aspect of the posterior labrum. The posterior labrum is secured to the glenoid by the posterior scapular periosteum. Stripping of the posterior labrum produces the POLPSA lesion.
A posterior capsular tear (Fig. 8.254) with an intact posterior labrum (the opposite or reverse of the GAGL lesion of the anterior inferior glenoid)
Reverse HAGL with or without associated posterior labral tear (Fig. 8.255)
Posterior superior labral tears as part of a posterior SLAP 2 (posterior peel-back lesion) or posterosuperior to posterior labral tear in association with a paralabral cyst (Fig. 8.256)
Posterior labral tears in the throwing athlete at the mid-glenohumeral joint level as a posterior continuation of a posterior peel-back lesion (especially if associated with posterior humeral subluxation and a posterior eccentric glenohumeral wear pattern)
Isolated posterior labral tears (less common)

The association of a posterior labral tear (reverse Bankart lesion, see Fig. 8.251; Fig. 8.257) with an anteromedial superior humeral head impaction (a reverse Hill-Sachs lesion) can be identified on all three MR imaging planes. The posterior

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labrum disruption is identified directly on axial or sagittal images. Axial images may display fluid undermining the base of a torn posterior labrum or show abnormal laxity (redundancy) of a torn posterior capsule. In posterior instability, the humeral head is often subluxed posteriorly relative to the glenoid fossa. In addition, MR arthrography demonstrates the posterior extension of contrast or fluid in the plane between the posterior labrum, the capsule, and the infraspinatus muscle. A lax posteroinferior capsule may show preferential distention with contrast on an axial MR arthrogram.²¹⁹

FIGURE 8.249 ● Posterior instability and labral tear. (A) Posterior instability with anterior rotation of the scapula after dislocation. (B) FS T1-weighted sagittal oblique MR arthrogram with posterior labral avulsion and discontinuity (arrows). (C) Posterior labral tear centered on the posterior quadrant of the glenoid fossa.

FIGURE 8.250 ● Reverse Hill-Sachs with hyperintense marrow edema and associated posterior labral tear (reverse Bankart) on an axial FS PD FSE image. Traumatic posterior instability is less common than anterior instability and is more frequently seen with multidirectional instability or as a component of a complex laxity pattern associated with anterior dislocation.

The same arthroscopic capsulorrhaphy and anchor fixation can be used to treat posterior shoulder subluxations when there is a detachment of the posterior or superior capsule and/or labrum. An open posterior capsular plication with capsular shift has a high success rate in the management of posterior shoulder instability.

Reverse HAGL

Posterior instability is sometimes associated with a complete avulsion of the posterior attachment of the shoulder capsule from the posterior humeral neck (reverse HAGL lesion) (see Fig. 8.255; Fig. 8.258).⁷³ Both the posterior band and the posterior capsule of the IGHL may be disrupted, and there may also be an associated posterior labral tear (see Fig. 8.242). Humeral avulsion of the posterior band of the IGHL (PHAGL lesion) has been described using MR arthrography.²²⁰ In these lesions there is a discontinuous avulsed posterior capsule that can be identified on axial images. At arthroscopy the posterior capsule appears absent and the muscle of the posterior cuff is visualized. The MR equivalent is seen on sagittal images, where fluid or contrast forms an irregular outline of the anterior surface of the teres minor muscle or infraspinatus muscle. Frequently there is extension of fluid through a capsular defect anterior to the junction between the infraspinatus and teres minor muscles. The laxity of the medial retracted posterior capsule is evident on axial images. The reverse HAGL lesion is repaired with anchors and side-to-side sutures to close the remaining capsular flap.

Bennett Lesion

The Bennett lesion (Fig. 8.259), an extra-articular posterior ossification associated with posterior labral injury and posterior articular surface rotator cuff damage, is believed to be the result of a posterior capsular avulsion secondary to traction of the posterior band of the IGHL (during the deceleration phase of pitching, for example) or to the posterior subluxation that occurs during cocking of the arm.²²¹

Although the Bennett lesion is frequently asymptomatic, a fracture in the spur or a fibrous union at its base may interfere with the throwing motion. The calcification itself can contribute to posterior inferior capsular contracture. The crescentic extra-articular ossification, which extends from the posterior inferior medial glenoid posterior to the posterior labrum, can be demonstrated on CT or MR scans (Fig. 8.260). There may be associated reactive posterior inferior glenoid rim sclerosis. MR findings include low-signal-intensity calcification, posterior humeral subluxation, and a posterior labral tear. Ferrari et al.²²¹ reported on a study of seven elite baseball players, all of whom had an associated posterior labral tear on arthroscopic examination. The ossification cannot be identified arthroscopically because of its extra-articular location. Posterior labral tears are most frequent in the posterior superior quadrant of the glenoid labrum. The Bennett lesion may represent a further progression on the spectrum of concentric glenoid wear or posterior glenoid fossa sclerosis associated with a posterosuperior cam shift of the humeral head in the throwing athlete (Fig. 8.261). However, this lesion is usually located directly posteriorly and not posterosuperiorly.

Multidirectional Instability

Pearls and Pitfalls

Multidirectional Instability

Referred to as either MDI (multidirectional instability) or AMBRI (atraumatic multidirectional instability, bilateral treated with rehabilitation or inferior capsular shift)
MDI must include a component of inferior instability (anteroinferior or posteroinferior).
MR findings in MDI may include subtle anterior and posterior glenoid rim sclerosis or static humeral head subluxation in the axial plane.
A pancapsular plication is used to selectively tighten lax ligaments.

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As discussed earlier, shoulder instability can be grouped into the Bankart lesions (patients with TUBS) and atraumatic MDI. MDI is also referred to as atraumatic multidirectional instability, bilateral treated with rehabilitation or inferior capsular shift) (AMBRI).

FIGURE 8.251 ● (A) Axial FS PD FSE and (B) sagittal FSE PD FSE images of posterior labral tear with associated glenoid rim fracture. This represents a reverse bony Bankart lesion. (C) Axial FS PD FSE image shows increased glenoid version associated with a posterior labral tear and mild posterior subluxation. Patients with posterior instability frequently have pain exacerbated by activities that posteriorly load the glenohumeral joint in shoulder adduction.

FIGURE 8.252 ● Sagittal FS PD FSE image shows an acromion fracture associated with a posterior shoulder dislocation. The posterior dislocation findings may be overlooked on conventional radiographs.

MDI/AMBRI may be seen in both athletic and nonathletic individuals with excessive capsular laxity, and the incidence is higher in females than in males. Etiologies range from anatomic defects to neuromuscular or biochemical abnormalities.²²² Although a structural lesion is not usually found, the IGHLC is suspect, since all MDI patients have a component of inferior instability, whether anteroinferior or posteroinferior.²²³ The glenoid labrum and rotator cuff interval are also potential anatomic sites of pathology. In athletic patients MDI may result from overuse and present as instability after minor trauma. Symptoms may also appear after minimal trauma in patients with preexistent laxity. Rarely, MDI presents in patients with genetic or inheritable hypermobility syndromes (e.g., Ehlers-Danlos syndrome or Marfan syndrome).

The primary direction of instability can usually be determined. An MR arthrogram may demonstrate an increased capsular volume and capsular or ligamentous injury. In the case of posteroinferior MDI, increased chondrolabral and osseous retroversion and variable capsular stretching may be identified.²²⁴ Loss of chondrolabral containment of the glenoid and an associated decrease in posterior labral height is a consistent finding in shoulders with atraumatic posteroinferior MDI.

FIGURE 8.253 ● Axial PD FSE image of a posterior labrocapsular periosteal sleeve avulsion (POLPSA) with stripping of the posterior labrum and capsule with separation from the posterior glenoid rim.

On MR images, the retroversion of the chondrolabral portion of the glenoid is seen to be greater than the osseous glenoid at the level of the inferior glenohumeral joint. MR is also useful for assessing static subluxation of the humeral head (Fig. 8.262). Eccentric glenoid fossa (rim) sclerosis is directly visualized on sagittal images, even in the absence of an overlying chondral or lateral lesion (Fig. 8.263). These patterns of sclerosis or wear may correlate with the direction of underlying laxity.

Surgical treatment is indicated if an extended course of rehabilitation for involuntary MDI fails. Earlier intervention may be justified in cases of MR-documented IGHLC injury in association with a physical examination for instability. Wolf²²³ uses a triad repair for MDI addressing the posterior-inferior capsule, anterior repair or shift of IGHLC, and superior capsular closure. Snyder²²⁵ recommends arthroscopic pancapsular plication (Fig. 8.264). Advantages of Snyder—s technique include:

Selective tightening of lax ligaments
Widening of the surface area of the labrum and thus the weight-bearing capacity of the glenoid
Augmentation of the “chock block” effect of the labrum by deepening the relative concavity of the glenoid fossa
Closing of the rotator interval, providing a temporary internal splint (the SGHL and MGHL do not heal together) by reducing forces on the inferior capsule and limiting external rotation and inferior subluxation in the early postoperative period

FIGURE 8.254 ● (A) Posterior capsular tear with firmly attached posterior labrum shown on an axial FS T1-weighted MR arthrogram. (B) Corresponding surgical exposure of torn posterior capsule. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.)

FIGURE 8.255 ● (A) FS T1-weighted MR arthrogram of reverse humeral head avulsion of the glenohumeral ligaments (RHAGL). There is discontinuity of the humeral attachment of the posterior capsule (curved arrow) with extravasation (large straight arrow) of contrast and associated tears of the anterior (Perthes) and posterior labrum (small arrow). Repair of both the posterior labrum and RHAGL is required. (B) Arthroscopic view of posterior labral repair. The RHAGL repair uses two or three anchors and several side-to-side sutures for closure of the capsular flap and reattachment of the capsule to the humeral head.

FIGURE 8.256 ● Axial FS PD FSE image showing association of a posterior labral tear with a paralabral cyst. These posterior para-labral cysts should also be evaluated on sagittal images since they may be extensive and reach from the BLC to the inferior glenohumeral ligament labral complex.

FIGURE 8.257 ● A reverse Bankart lesion with anteromedial humeral head impaction (curved arrow), anterior labral avulsion, and posterior labral tear. Note fluid undermining the posterior labrum (straight arrow) and anterior fracture fragment (open arrow). The anteromedial defect creates the notch sign or trough lesion.

FIGURE 8.258 ● (A) Posterior coronal color view of RHAGL with avulsion of the posterior humeral attachment of the shoulder capsule. (B) Axial FS PD FSE image shows posterior humeral detachment of the posterior capsule associated with capsular laxity or a wavy contour. (C) A characteristic dimple or defect in the posterior capsule between the infraspinatus and teres minor on a sagittal FS PD FSE image. (D) Direct extension of fluid outlining the anterior muscle of the infraspinatus secondary to posterior capsular rupture can be seen on this sagittal FS PD FSE image.

FIGURE 8.259 ● (A) Extra-articular ossification of a Bennett lesion on posterior coronal view (color illustration). The Bennett lesion is associated with injury to the posterior superior labrum in the throwing athlete. (B) Axial T2*-weighted GRE image with linear crescentic ossification corresponding to the course of the posterior capsule. This ossification is usually in contact with the posterior glenoid neck. (C) Corresponding sagittal FS PD FSE image with hypertrophic buildup or ossification along the posterior rim. The Bennett lesion usually occurs in the location of greatest posterior glenoid rim wear or sclerosis and inferior to the posterosuperior peel-back lesion.

FIGURE 8.260 ● Bennett lesion with posterior extra-articular ossification (straight arrows) on FS T1-weighted axial arthrographic image (A), axial CT (B), and 3D CT rendering (C).

FIGURE 8.261 ● Posterior glenoid rim sclerosis can be seen on this sagittal FS PD FSE image prior to the development of a posterior peel-back labral tear or Bennett's ossification. This pitcher has a fastball velocity of over 100 mph.

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Labral Pathology

Normal Variations

Pearls and Pitfalls

Normal Variations

The sublabral foramen is located in the anterosuperior quadrant of the glenoid fossa. The biceps labral sulcus is identified at the level of the superior pole of the glenoid in the 12-o—clock position.
The MGL may be cord-like, thin, or absent.
When cord-like, the MGL presents as an isolated variation or in conjunction with a prominent anterior band of the IGL or as part of the Buford complex.
Since there is no anterosuperior labrum in the Buford complex, a sublabral foramen cannot exist. In the presence of a prominent anterior band of the IGHL and a Buford complex, the anterior band may form an apparent or pseudo-sublabral foramen above the equator.

Sublabral Foramen

There is considerable variation in the attachment and morphology of the glenoid labrum. The most significant variation is the relative attachment, or lack thereof, to the glenoid rim in the anterior superior quadrant above the epiphyseal line (Fig. 8.265). There is frequently a sublabral foramen between the labrum and the glenoid rim, which is often the cause for misinterpretation of anterior labral disruptions or tears. Although the glenoid labrum in the superior one third of the glenoid above the epiphyseal line can be firmly fixed in its periphery, De Palma has shown that there is considerable variation in the anterior superior bursa and labral foramen of the complex.⁵⁶ Although the resulting differential bursal configurations produce MR images that appear to demonstrate superior and anterior labral tears, these are normal anatomic variations.

FIGURE 8.262 ● Axial FS PD FSE image of posterior subluxation of the humeral head in a 20-year-old swimmer with a clinical “loose” shoulder. An episode of trauma may aggravate a shoulder with a preexisting or mild underlying laxity.

A normal anterosuperior sublabral foramen or hole has been reported in up to 11% of individuals.⁶¹^,²²⁶ The anterosuperior labrum is firmly attached to the glenoid rim in up to 88% of cases.⁵⁷ Cooper and coworkers reported the presence of a sublabral foramen as a normal vari
ant in 17% of specimens.⁵⁵ Care must be taken not to mistake a sublabral foramen, which can vary in size from a few millimeters up to the entire anterosuperior quadrant above the level of the subscapularis tendon,⁶¹ for a SLAP lesion or a Bankart lesion. Hyperintense fluid, which undermines the anterosuperior labrum, may be over-read as a SLAP lesion. In contrast to a Bankart lesion, the sublabral foramen is seen superior to the anterior glenoid notch or above the physeal line representing the superior one third of the glenoid. The Bankart lesion usually involves a labral tear or avulsion at or below the level of the subscapularis tendon on axial MR images. This is below the physeal line or equator. (The physeal line divides the bony glenoid into an upper one third and lower two thirds, corresponding to the two glenoid ossification centers. It is also referred to as the equator, as identified at the region of the anterior glenoid notch.⁶¹) Direct communication between the sublabral foramen and the subscapularis bursa can be seen on MR arthrography. A sublabral foramen may be seen with a type 2 or type 3 BLC. The sublabral foramen is anterior to the biceps labral sulcus when viewed in the coronal plane (Fig. 8.266).

Middle Glenohumeral Ligament Variations

In almost two thirds of cases studied, the MGHL is identified as a folded thickening of the anterior capsule between the anterior labrum and subscapularis tendon, inserting on the labrum or

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near the glenoid rim (Fig. 8.267).⁵⁷^,⁶¹ In 19% of cases, the MGHL has a cord-like morphology, compared with the more normal sheet-like appearance of ligamentous tissue (Fig. 8.268). An attenuated or thin variation of the MGHL is observed in 5% of shoulders. Complete absence of the MGHL may be associated with a congenitally lax anterior capsule.

FIGURE 8.263 ● Four types of glenoid fossa sclerosis. (A ₁, upper left) Anterosuperior impingement (ASI) pattern. (A ₂, upper right) Multidirectional instability (MDI). (A ₃, lower left) Posterior glenoid rim wear in the throwing athlete. (A ₄, lower right) Osteoarthritis pattern with central glenoid fossa and posterior glenoid wear. (B) Sagittal FS PD FSE image showing MDI wear with anterior and posterior glenoid rim sclerosis. (C) Osteoarthritis in a 70-year-old patient with posterior wear and central glenoid sclerosis. The initial change of inferior rim sclerosis can also be seen. (D) Similar osteoarthritis pattern in the older elite pitcher with central and posterior rim sclerosis without the degenerative changes of the inferior pole. Central or posterosuperior glenohumeral fossa sclerosis is an unusual finding in the younger throwing athlete; instead, wear is initially limited to the posterior rim.

FIGURE 8.264 ● Arthroscopic pancapsular plication for treatment of multidirectional instability with the IGL and capsule folded to the labrum from the posteroinferior quadrant to the anteroinferior quadrant. The rotator interval is closed, and the final result is to have the humeral head centralized within the glenoid fossa.

The cord-like MGHL i s best demonstrated on axial and sagittal MR images. The thick and low-signal-intensity cord-like MGHL may be mistaken for a detached anterior labrum above the epiphyseal line (Bankart lesion). The prominent MGHL on multiple axial images, distinct from the normal anterior inferior glenoid labrum below the level of the subscapularis tendon, excludes the presence of a Bankart lesion. The direct course of the MGHL as it crosses the superior border of the subscapularis is shown on sagittal images. The cord-like MGHL can also be identified as a distinct structure on sagittal images anterior to the anterior band and anterior labrum, and should not be misdiagnosed as a torn or avulsed anterior labrum. The filamentous extension or attachment may be identified between the cord-like MGHL and the anterior labrum (Fig. 8.269). An attenuated MGHL may be either very thin or fibrous in appearance with no ligamentous thickening.⁵⁰ This variation, as well as the absent MGHL, is frequently associated with a prominent anterior band of the IGHL (Fig. 8.270).

Buford Complex

In the normal labrum a thin MGHL is identified anterior to the anterior labrum. The normal anterior labrum is found above and below the equator. In contrast, the Buford complex (Fig. 8.271) consists of three defining elements:

A cord-like MGHL
An MGHL that attaches directly to the superior labrum anterior to the biceps (at the base of the biceps anchor)
An absent anterosuperior labrum⁵²^,⁵⁸

Of 200 shoulder arthroscopies reviewed by Williams and Snyder et al.,⁵²^,⁵⁸ the Buford complex was found in 1.5% and a sublabral foramen, located between the anterosuperior glenoid quadrant and the articular surface of the anterior glenoid, was found in 12%. In 75% of patients who demonstrated a sublabral foramen, a cord-like MGHL was also present. This cord-like MGHL attaches directly to the superior labrum. The additional finding of an absent anterosuperior labrum places patients into the subgroup of the Buford complex.

Several key MR findings help to avoid misinterpretation of the absence of anterosuperior labral tissue as a sublabral foramen or a Bankart lesion. These findings include:

An absent anterior labrum at and above the level of the subscapularis tendon as assessed on axial images. A sublabral foramen can only exist in the presence of an anterior superior labrum.
The anterior inferior glenoid labrum below the level of the subscapularis tendon is firmly attached to the glenoid with normal morphology.
A cord-like MGHL must be identified anterior to the glenoid rim.
There may be remnant or hypoplastic anterosuperior labral tissue identified on axial images at the level of the subscapularis tendon.

It is easy to distinguish a Bankart lesion from the Buford complex because in the former the anterior inferior labrum is torn or avulsed and does not appear firmly attached to the anteroinferior glenoid rim.

The sagittal oblique plane demonstrates the course of the cord-like MGHL attaching directly to the superior labrum at the anterior base of the biceps tendon. Although the Buford complex may be mistaken for a large sublabral foramen, a sublabral foramen or hole does not exist since there is no anterior superior labral tissue present. It is important to remember that a cord-like MGHL with an associated sublabral hole beneath a normal anterior superior labrum is more common than a cord-like MGHL in association with a deficient anterior superior labrum. Intra-articular MR arthrography can be used to improve visualization of the cord-like MGHL distinct from the bare anterior glenoid rim. However, this complex can be recognized without the routine use of an MR contrast agent. If the Buford complex is associated with a SLAP lesion, the cord-like MGHL may be incompetent since it is attached to a lax or loose superior labrum (the superior labrum pulls away from the glenoid under traction).²²⁷

Failure to recognize the Buford complex may result in the inappropriate surgical attachment of the cord-like MGHL directly to the anterior glenoid. This fixation leads to limitation of shoulder elevation and external rotation.

Prominent Anterior Band of the IGHL

A prominent anterior band of the IGHL is sometimes found anterior to the

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anterior labrum on axial images above the equator. Below the equator the prominent anterior band may appear to be adherent to the anteroinferior labrum and is thus indistinguishable. In the presence of a prominent or thickened anterior band, the anterosuperior labrum is either attenuated (hypoplastic) or absent. Demonstration of the course of the anterior band deep to the MGHL on corresponding axial images prevents the misdiagnosis of a labral tear. In this case the anterior band of the IGHL effectively functions as an anterior labrum and attaches superiorly at the BLC. The following variations can exist with a prominent anterior band of the IGHL:

FIGURE 8.265 ● (A) An arthroscopic photograph of a normal anatomic variant of the sublabral foramen with a missing anterior labrum attachment above the epiphyseal line of the glenoid (curved arrow). AL, anterior labrum; BT, biceps tendon; G, glenoid; HH, hum-eral head; MGL, middle glenohumeral ligament; RCI, rotator cuff interval or Weitbrecht's foramen; S, subscapularis tendon. (B) Sublabral foramen (arrow) shown above the equator (above the anterior glenoid notch) on an FS T1-weighted sagittal oblique MR arthrogram. Contrast extends between the anterosuperior labrum and the glenoid rim as a normal variant. MGL, middle glenohumeral ligament; al, anterior labrum; pl, posterior labrum. (C) Lateral view color graphic of a sublabral foramen beneath the anterior superior labrum.

FIGURE 8.266 ● The sublabral foramen is present in 14% of shoulders and can range in size from a few millimeters to the entire anterosuperior quadrant between the superior pole and the equator. The sublabral foramen should not be mistaken for a Bankart labral detachment or a SLAP lesion of the biceps labral complex. The sublabral foramen is often associated with a cord-like middle glenohumeral ligament. This assumes that the cord-like MGL is not associated with a Buford complex, since a sublabral foramen cannot exist in this variation (because the anterosuperior labrum is absent). (A) Coronal T1 MR arthrogram with a large anterosuperior sublabral foramen. (B) Corresponding axial T1 MR arthrogram demonstrating the subscapularis, the middle glenohumeral ligament (MGHL), the anterior labrum, the sublabral foramen, and the anterior glenoid as visualized from anterior to posterior.

FIGURE 8.267 ● Normal middle glenohumeral ligament (MGHL or MGL) on axial FS PD FSE (A) and sagittal FSE (B) images. The MGL is the most variable in morphology of all the anterior glenohumeral capsular ligaments. In the most common appearance (70% of cases) the MGL represents a folded anterior capsular thickening that crosses the subscapularis tendon at a 45° angle. The MGL inserts onto the anterosuperior glenoid neck at the level of or just medial to the labrum. The MGL, superior glenohumeral ligament, and anterosuperior labrum thus converge at the anterior superior pole of the glenoid. This ligament configuration creates one opening into the subscapularis recess anterior to the leading edge of the MGL.

FIGURE 8.268 ● The cord-like middle glenohumeral ligament (MGL) represents the most common variation of MGL anatomy and is seen in up to 20% of normal shoulders. The cord-like MGL has a smooth rope-like or round cross-section instead of the more linear sheet-like morphology. The cord-like MGL attaches either to the neck of the glenoid superiorly or directly to the anterosuperior labrum. The cord-like MGL may be associated with a sublabral pole in cases where it attaches directly to the anterosuperior labrum. This variation does not represent a labral detachment or Buford complex. (A) Lateral color illustration of the cord-like MGL. (B) Enhanced T1-weighted axial images showing a cord-like or hypertrophied MGL (small black arrows) that simulates an avulsion of the anterior labrum. (C) A corresponding enhanced T1-weighted sagittal image displays a normal anterior labrum (curved arrows) and anterior band of the IGL (AB). A thick, cord-like MGL and subscapularis tendon (S) can also be identified. Intra-articular gadolinium contrast is shown in the axillary pouch (AP) of the inferior glenohumeral ligament and in a synovial recess (SR) below the MGL.

FIGURE 8.269 ● Cord-like middle glenohumeral ligament (MGL) on T1-weighted enhanced axial images at the level of the coracoid (A) and inferior to the coracoid at the level of the subscapularis tendon (B). Curved arrow, filamentous attachment to cord-like MGL; large straight arrow, cord-like portion of MGL; small straight arrows, thin portion of MGL; AGL, anterior glenoid labrum. (C) Corresponding T1-weighted enhanced sagittal oblique image showing the relationship of the MGL to the anterior band of the IGL (AB; straight arrow), the anterior glenoid labrum (AGL; curved arrow), the middle glenohumeral ligament (MGL), and the subscapularis tendon (S). The MGL is located in the plane between the subscapularis tendon and the anterior band of the IGL or anterior glenoid labrum.

FIGURE 8.270 ● (A) Normal MGL morphology on lateral glenoid exposure. (B) Sagittal T1-weighted MR arthrogram demonstrating a thin (with no area of thickening) linear MGL (arrows) anterior to the anterior labrum (al). In 10% of shoulders the MGL is a thin attenuated structure or completely absent. The anterior band of the IGL may be inversely prominent in association with an attenuated or fibrous MGL variation. b, biceps; al, anterior labrum.

FIGURE 8.271 ● (A) Lateral color illustration of a Buford complex with cord-like MGL attached to superior labrum just anterior to the base of the biceps anchor, and absent anterosuperior labrum above the equator. (B) Thick cord-like middle glenohumeral ligament (mgl) attaching directly to the superior labrum (sl) on an FS T1-weighted sagittal oblique arthrogram. (C) Corresponding FS T1 axial image displays the cord-like middle glenohumeral ligament (m) with an absent anterior superior labrum as a normal variant. Note that the posterior labrum (p) is present. (D) Corresponding gross specimen demonstrates the cord-like MGL, which attaches directly to the superior labrum. (E) An arthroscopic view of cord-like MGL in a Buford complex. The anterior superior glenoid edge (black arrows) shows an absence of the labrum as a normal variant in association with prominent MGL. The MGL originates from the anteromedial humeral neck and attaches medially on the glenoid (G) and the neck of the scapula. Open arrow, subscapularis recess; BT, biceps tendon; HH, humeral head; PL, posterior labrum.

Prominent anterior band plus a small anterosuperior labrum (Fig. 8.272)
Prominent anterior band plus an absent anterosuperior labrum (Fig. 8.273)
Prominent anterior band plus a cord-like MGHL (Fig. 8.274) (associated with an absent or small anterosuperior labrum)

At arthroscopy the prominent anterior band may appear to create a sublabral foramen if the anterosuperior labrum is absent. In fact, in many cases the diagnosis of sublabral foramen may represent a prominent anterior band with an absent anterosuperior labrum. This appearance could be included in the Buford complex if the original description were expanded to include a prominent anterior band associated with an absent anterosuperior labrum and cord-like MGHL. However, referring to the relationship of the anterior band to the anterosuperior glenoid rim as forming a sublabral foramen could lead to confusion since, by definition, there is no sublabral foramen in the Buford complex because the anterior superior labrum is absent.

A biceps labral sulcus may be seen on one image posterior (in the coronal oblique plane) through the junction of the biceps and labrum in association with either a Buford complex or a prominent anterior band of the IGHL. This normal capsulolabral variation above the equator should not be mistaken for a SLAP tear.

Labral Tears

The labrum can be arbitrarily divided into six areas:⁵²

The superior labrum
The anterosuperior (superior to the mid-glenoid notch) labrum
The anteroinferior labrum
The inferior labrum
The posteroinferior labrum
The posterosuperior labrum

Labral tear patterns may be:⁵²

Degenerative lesions
Flap tears
Vertical split nondetached tears
Bucket-handle tears
SLAP lesions

Degenerative Labrum

Degenerative lesions show fraying of the labrum, probably as part of the spectrum of degenerative glenohumeral joint disease. De Palma et al. have described degenerative tears of the superior labrum associated with advancing age.⁵⁶^,²²⁸ The degenerative roughened labrum may contribute to the process of joint degeneration by creating an abrasive articular interface in addition to humeral head chondromalacia. Degenerative labral tears are treated with arthroscopic resection of damaged tissue.

Flap Tears

Flap tears represent a frequent labral tear pattern in acute or subacute injuries.⁵² These tears may occur in any location but are frequently identified in the posterosuperior segment of the labrum. Flap tears may occur secondary to chronic shear stress,²²⁹ as seen in repetitive subluxation in throwing or overhead athletes. An unstable flap tear may cause mechanical symptoms of joint clicking, catching, and popping, and mimic instability. Treatment of these tears involves arthroscopic resection of the unstable tissue.

Vertical Split and Bucket-Handle Labral Tears

Vertical split labral tears are the least frequent labral tear pattern.⁵² A complete vertical split labrum may be associated with a displaceable fragment and present as a bucket-handle tear. A vertical split labrum is seen in the meniscoid-type labrum, which is most commonly observed in the superior quadrant. A type 3 SLAP lesion is a bucket-handle tear of the superior labrum (see SLAP Tears below). Although a vertical split may occur in the anterior and posterior labrum, this tear pattern is unusual in the inferior labrum. The mechanism of injury is thought to be intra-articular compression from a fall on the outstretched arm or extensive humeral rotation associated with anterior or posterior labral compression. Symptoms include pseudosubluxation with locking, catching, and popping. Associated clinical instability, however, is uncommon in this lesion. Treatment is directed at producing a stable meniscal rim by excision or repair of the tear.

Superior Labral Tears

Anterosuperior labral tears with avulsion and fraying of the labrum have been described in throwing athletes.²³⁰ There may be involvement of the biceps and associated partial rotator cuff tears. Traction by the LHBT on the anterosuperior labrum occurs during the deceleration phase of throwing. Treatment is arthroscopic débridement of the frayed labrum, cuff, and biceps tendon.

Slap Tears

Pearls and Pitfalls

SLAP Tears

A biceps labral sulcus greater than 5 mm is abnormal.
Superior paralabral cysts that often extend into the spino-glenoid notch communicate with SLAP 2 or posterior SLAP 2 (peel-back) lesions.

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Inferior displacement of the superior labrum (relative to the biceps labral junction) is associated with bucket-handle SLAP morphology.
SLAP tears are grouped into 10 subtypes. Four primary types were initially described and six further types were subsequently characterized.
The SLAP 2 or classic SLAP lesion is further subdivided into anterior SLAP 2 in the SLAC lesion and posterior SLAP 2 in the posterior peel-back lesion.
A SLAP fracture is a posterosuperior medial humeral head chondral fracture in association with a SLAP lesion.

FIGURE 8.272 ● Prominent or superior (above the equator) attachment of the anterior band of the inferior glenohumeral ligament coursing anterior to a small anterosuperior labrum and attaching at the level of the superior labrum. (A) Lateral color illustration. (B) Sagittal PD-weighted MR arthrogram. (C) Inferior axial PD-weighted MR arthrogram at the inferior edge of subscapularis tendon. (D) Axial PD-weighted MR arthrogram at the level of superior edge of subscapularis tendon above the equator.

FIGURE 8.273 ● (A) Prominent anterior band of the IGHL with absent anterosuperior labrum. This is not a Buford complex, since the MGL is not cord-like. (B –D) If the anterosuperior labrum is absent, as in the case of a prominent anterior band, Buford complex, or Buford variant (cord-like MGL plus a prominent anterior band), there may be a normal sulcus between the superior labrum and superior pole of the glenoid. This biceps labral sulcus may be seen one image posterior to the biceps labral junction in association with the Buford complex or prominent anterior band of the IGL. (B) Sagittal T1-weighted MR arthrogram. (C) Axial T1-weighted MR arthrogram. (D) Coronal FS PD FSE MR arthrogram.

Snyder et al.²³¹ have described SLAP (superior labrum from anterior to posterior, relative to the biceps tendon anchor) lesions, which vary from simple fraying and fragmentation of the BLC, to a bucket-handle tear, to a tricorn bucket-handle tear in which one rim of the tear actually extends up into the biceps tendon, splitting it as the tear goes up toward the bicipital groove.²³¹ One proposed mechanism of injury is a fall on the outstretched abducted arm with associated superior joint compression and a proximal subluxation force.⁵²^,²³² Another mechanism is sudden contraction of the biceps tendon that avulses the superior labrum. Less severe, repetitive stress acting through the biceps tendon may also produce SLAP lesions, as may instability of the glenohumeral joint. The normal biceps labral sulcus should not be mistaken for a SLAP lesion. This sulcus may become more prominent in external rotation of the arm (Fig. 8.275).

Guidelines for SLAP tear detection

Useful guidelines for improving the accuracy of SLAP tear detection on MR include:

A biceps labral sulcus measurement of less than 5 mm is within a normal range, although the biceps labral sulcus is most commonly less than 3 mm on coronal MR images (see Fig. 8.275). A sulcus of greater than 5 mm is abnormal.²²⁷
On review of coronal oblique images at or posterior to the osseous anteroinferior pole of the glenoid, there should not be hyperintense signal intensity located between the intra-articular biceps tendon and the superior labrum (Fig. 8.276).
There is frequently a normal lateral oblique cleft of fluid signal intensity between the biceps tendon and the superior labrum anterior to the biceps labral junction (Fig. 8.277). A firmly attached connection between the intra-articular biceps and the superior labrum prevents increased signal intensity between the biceps tendon and the superior labrum.
A paralabral cyst adjacent to the superior labrum usually communicates with a classic SLAP 2 or the posterior component of a SLAP 2 lesion (see Fig. 8.276).
Inferior displacement of the superior labrum separated from its biceps connection is associated with bucket-handle SLAP morphology (Fig. 8.278).
Fragmentation or splitting of the superior labrum into separate fragments is associated with bucket-handle SLAP tear patterns. This SLAP tear pattern should not

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be mistaken for the normal biceps labral sulcus.²³³ Avulsion of the superior labrum from the superior pole of the glenoid will result in an enlarged biceps labral sulcus (Fig. 8.279).
SLAP tears occur either centrally or eccentrically with the superior labrum at the biceps labral junction. Eccentric tears are located adjacent to either the glenoid (Fig. 8.280) or humerus (Fig. 8.281).
SLAP tears are usually parallel to the long axis of the posterosuperior labrum posterior to the biceps tendon (Fig. 8.282).²³⁴
Superior displacement (Fig. 8.283) of the biceps labral complex relative to the superior pole of the glenoid on sagittal images is associated with SLAP 2 lesions.
Common patterns of SLAP tears demonstrate a spectrum of lesions from detachment at the biceps labral junction to splitting and fragmentation of the labrum (Fig. 8.284).
A SLAP tear occurs commonly in one of three locations:
- Between the biceps tendon and the superior labrum
- Within the superior labrum
- Between the superior labrum and the superior pole of the glenoid
Visualization of three distinct hypointense structures (the biceps tendon and the split superior labrum) on sagittal images through the BLC correlates with bucket-handle morphology (Fig. 8.285).
Complex or extended SLAP lesions (SLAP 5 through SLAP 10) may be associated with SLAP 2 or SLAP 3 lesions.
A biceps labral sulcus may be seen one image posterior to the biceps labral junction in association with the Buford complex or prominent anterior band of the IGHL.

FIGURE 8.274 ● A prominent anterior band associated with a cord-like MGL and absent anterosuperior labrum on a lateral view color illustration (A), a sagittal PD MR arthrogram (B), and an axial FS PD FSE MR arthrogram (C). Because the MGL is cord-like, this could be considered a Buford variant. The original description of the Buford complex did not include the variant of a prominent anterior band. (D) Axial FS PD FSE image in a separate case demonstrating a combination of a cord-like MGL, a prominent anterior band, and hypoplastic anterior labrum.

FIGURE 8.275 ● Coronal FS PD FSE image showing a normal biceps labral sulcus. The medial to lateral measurement is 2.5 mm with the shoulder positioned in neutral to external rotation.

FIGURE 8.276 ● Linear signal between the intra-articular biceps and superior labrum is abnormal if visualized on a coronal oblique image posterior to an established firm attachment between the superior labrum and biceps tendon. Linear hyperintensity can be seen between the biceps tendon and superior labrum, representing posterior extension of the SLAP tear.

FIGURE 8.277 ● Coronal PD FSE MR arthrogram displays the normal cleft between the intra-articular biceps and the superior labrum anterior to the 12-o—clock position of the biceps labral complex.

FIGURE 8.278 ● Coronal FS PD FSE image showing inferior displacement (relative to the biceps anchor) of the superior labrum in a type 3 SLAP lesion with bucket-handle morphology.

FIGURE 8.279 ● (A) Coronal FS PD FSE and (B) axial FS PD FSE images show an avulsed superior labrum from the superior pole of the glenoid. The chemical shift artifact of the superior pole articular cartilage may be mistaken for a small labral fragment.

Classification of SLAP tears

SLAP tears were initially divided into four distinct but related lesions:²³⁵

Type 1 SLAP lesions (Fig. 8.286) are characterized by a frayed and degenerative superior labrum with a normal (stable) biceps tendon anchor.
Type 2 SLAP lesions (Fig. 8.287) have similar labral fraying but also have detachment of the superior labrum and biceps anchor, making them unstable. A type 2 lesion may appear similar to the normal free edge of the meniscoid-like superior labrum. In the latter, however, the articular cartilage of the superior glenoid extends to the attachment of the labrum. In a type 2 SLAP lesion there is usually a space or gap between the glenoid articular cartilage and the attachment of the superior labrum and biceps anchor (Fig. 8.288). Displacement of the labrum from the superior glenoid of more than 3 to 4 mm is usually associated with an abnormal superior labrum and biceps anchor attachment. A type 2 SLAP lesion may also be associated

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with anterior glenohumeral joint dislocation. Tearing of the superior labrum biceps anchor may contribute to anteroinferior capsule and labral stress in the development of anterior instability. The classic SLAP 2 lesion has been subdivided into anterior and posterior SLAP 2 lesions (Fig. 8.289):
- The anterior SLAP 2 lesion (the anterior component of a SLAP 2 lesion) is associated with an anterior supraspinatus articular-side partial cuff tear in the SLAC (superior labrum anterior cuff) lesion (Fig. 8.290).
- The posterior SLAP 2 lesion (posterosuperior labral tear) is the posterior peel-back lesion in the throwing athlete (Fig. 8.291).
Type 3 SLAP lesions involve a bucket-handle tear of the superior labrum without extension into the biceps tendon. The biceps anchor is stable and the remaining labrum is intact (Fig. 8.292). Multiple hypointense structures on sagittal images represent the biceps tendon and split superior labrum and are associated with a bucket-handle SLAP tear (Fig. 8.293).²³⁶ Type 3 SLAP lesions are commonly associated with anterior labral tears, creating a type 5 SLAP lesion (see below). The inferiorly displaced superior labrum may become entrapped within the superior glenohumeral joint (Fig. 8.294).

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Type 4 SLAP lesions (Fig. 8.295) also involve a bucket-handle tear of the superior labrum, but in this case with extension into the biceps tendon. A ruptured biceps tendon represents completion of the biceps tendon tear extension, resulting in a proximal biceps stump (Fig. 8.296). A partially torn biceps tendon may displace the superior labral flap into the joint.

FIGURE 8.280 ● Eccentric superior labral tear with type 2 SLAP lesion occurring adjacent to the glenoid on (A) a coronal FS PD FSE image and (B) a sagittal FS PD FSE image.

FIGURE 8.281 ● Eccentric humeral side SLAP tear. If a fragment of the superior labrum is absent or displaced, a type 3 SLAP lesion should be considered. Coronal FS PD FSE image.

FIGURE 8.282 ● (A) Coronal FS PD FSE image shows characteristic SLAP 2 linear oblique signal intensity of the posterior superior labrum posterior to the biceps anchor attachment to the superior labrum. (B) Corresponding sagittal FS PD FSE image.

FIGURE 8.283 ● Coronal T1-weighted MR arthrogram of superior displacement of the biceps anchor and superior labrum (a type 2 SLAP lesion). This may be a difficult MR pattern to distinguish from a normal biceps labral sulcus. Correlation with sagittal images confirms superior displacement of the labrum. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.)

FIGURE 8.284 ● Common SLAP tear variants include labral fragmentation, vertical split, inferior displacement, and eccentric tears (humeral or glenoid side). A fragmented labrum with gross displacement or absence of labral tissue is associated with bucket-handle morphology. A split of the labrum into separated triangles (double triangle sign) is also associated with a bucket-handle tear pattern. Inferior displacement of the entire superior labrum or a portion of the labrum indicates displacement of a bucket-handle tear. Linear signal without loss of labral tissue or labral displacement/fragmentation is associated with SLAP 2 lesions. There may also be complete superior labral separation from the superior pole with a widened biceps labral sulcus (seen in Fig. 8.279).

FIGURE 8.285 ● Type 4 SLAP lesion with the torn biceps stump superior to the two components of the fragmented labrum on (A) a sagittal FS PD FSE image and (B) a coronal FS PD FSE image. In a separate case, a type 3 SLAP bucket-handle tear with an intact biceps tendon and a separate inferiorly displaced labral fragment is visualized on a coronal FS T1-weighted MR arthrogram (C) and a sagittal T1-weighted MR arthrogram (D).

FIGURE 8.286 ● (A) Lateral color illustration of a type 1 SLAP lesion with fraying of the free edge and intrasubstance degeneration of the superior labrum. This is considered a normal finding in the aging labrum, similar to grade 1 or 2 signal intensity within the degenerative meniscus. This is not considered a symptomatic lesion. (B) Corresponding coronal FS PD FSE image with diffuse intralabral signal intensity without a defined tear, split, fragmentation, or displacement.

FIGURE 8.287 ● (A) Type 2 SLAP tear with detached superior labrum and biceps anchor. The labral tear extends from anterior to posterior and may occur within the substance of the labrum or with complete detachment of the biceps and labrum from the superior pole of the glenoid. (B) Type 2 SLAP lesion on a corresponding gross dissection identifying superior labral and biceps tendon detachment. The term “biceps expansion” is more accurate and should be used instead of “torn biceps anchor,” since the origin of the biceps tendon from the supraglenoid tubercle is not involved. The biceps tendon has a separate expansion or attachment directly to the anterior and posterior glenoid labrum. Except for the frayed appearance of the superior labrum, this SLAP lesion could be mistaken for a prominent biceps labral sulcus on coronal oblique MR images. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.) (C) Coronal FS PD FSE image of a type 2 SLAP lesion defined by linear hyperintensity extending across the superior labrum. The associated biceps labrum sulcus is a normal finding. With an intact coapted triangular outline of the superior labrum, the tear represents a type 2 SLAP and not a bucket-handle tear.

FIGURE 8.288 ● Type 2 SLAP lesion. (A) Separation of the superior labrum and biceps anchor (b) from the underlying anterior glenoid rim. Hyperintense fluid (arrows) fills the detachment on this FS T1-weighted coronal oblique MR arthrogram. (B) Posterior extension of the tear is shown as a linear hyperintensity through the posterior superior labrum (arrow) on this FS T1-weighted coronal oblique MR arthrogram. Corresponding FS T1-weighted sagittal oblique (C) and axial (D) images display the avulsion (arrows) of the BLC (C) and anterior-to-posterior extension (arrows) of the superior labral tear (D).

FIGURE 8.289 ● Location of anterior SLAP 2 (blue) and posterior SLAP 2 (green) subtypes. Hemorrhage is highlighted in red. A classic type 2 SLAP lesion would involve both anterior and posterior components.

FIGURE 8.290 ● Coronal FS PD FSE image of an anterior SLAP lesion combined with an articular-side supraspinatus partial tear in a superior labrum anterior cuff (SLAC) lesion.

The extended or complex SLAP lesion may consist of a combination of two or more types, usually types 2 and type 4. Six extended tear types have been characterized in addition to the original types 1 through 4:²³⁷

Type 5 SLAP lesion (Fig. 8.297) is a SLAP 2 or 3 lesion plus superior extension of a Bankart lesion. A Hill-Sachs posterolateral humeral head fracture and inferiorly displaced superior labrum may be seen on superior axial images through the glenohumeral joint (Fig. 8.298).
Type 6 SLAP lesions (Figs. 8.299 and 8.300) are flap tears of the superior labrum.
Type 7 SLAP lesions are SLAP 2 or SLAP 3 lesions with extension into the middle glenohumeral ligament (Fig. 8.301). Extension into the MGHL is difficult to assess on MR in the presence of the numerous normal variants and laxity (redundant folding) of the MGHL.
Type 8 SLAP lesions (Fig. 8.302) are SLAP 2 or SLAP 3 lesions plus a posterior labral tear.

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Type 9 SLAP lesions (Fig. 8.303) are circumferential labral tears with anterior and posterior labral involvement. SLAP 9 tears are best appreciated on axial images, with superior and inferior labral involvement shown on coronal images. The entire circumference of the torn labrum is often displayed on a single sagittal image with associated degenerative changes of the adjacent glenoid rim.
Type 10 SLAP lesions (Fig. 8.304) are SLAP 2 or 3 lesions with extension into the rotator cuff interval through the superior glenohumeral ligament.

FIGURE 8.291 ● Coronal FS PD FSE (A) and T2 FSE (B) images of posterior peel-back lesion with a tear of the posterosuperior labrum associated with an articular-side posterior cuff partial tear.

FIGURE 8.292 ● Lateral color illustration of a type 3 SLAP lesion with bucket-handle tear. The superior labrum may be meniscoid. The biceps tendon attachment is intact. The bucket fragment may be split into two fragments and/or inferiorly displaced from the biceps anchor on MR images.

FIGURE 8.293 ● The “three structure sign” corresponding to the biceps tendon superior to the two bucket-handle components of the superior labrum on (A) a coronal FS PD FSE MR arthrogram and (B) a sagittal PD FSE MR arthrogram.

FIGURE 8.294 ● (A, B) Intra-articular displacement of a bucket-handle superior labral tear in a SLAP 3 associated with a Bankart lesion (a SLAP 5 equivalent). (A) Coronal FS PD FSE. (B) Sagittal FS PD FSE. (C) Arthroscopic view of type 3 SLAP tear at the superior pole of the glenoid. There is separation from the biceps anchor at the probe site in this bucket-handle tear.

FIGURE 8.295 ● (A) Lateral color graphic illustrating a SLAP 4 lesion with a split or bucket-handle tear of the superior labrum that continues into the biceps tendon. (B) Coronal FS PD FSE image with bucket-handle tear and split of the intra-articular biceps. (C) Arthroscopic view of type 4 SLAP with extension of the superior labral tear into the biceps root.

FIGURE 8.296 ● (A) Coronal FS PD FSE and (B) sagittal FS PD FSE images of a SLAP 4 lesion with associated rupture of the intra-articular biceps. The intra-articular biceps stump is visible superior to the superior labrum.

FIGURE 8.297 ● Type 5 SLAP lesion with superior extension of a Bankart lesion into a superior SLAP lesion. The superior labral lesion may be type 2 or 3. (A) Lateral color illustration with anterosuperior and anteroinferior SLAP 5 extension. (B) Sagittal PD FSE image showing an extensive anterior labral tear. (C) Coronal PD FSE image of inferior displacement of the superior labrum. (D) Axial FS PD FSE image of an anterior labral soft tissue Bankart lesion.

FIGURE 8.298 ● An axial FS PD FSE image displaying a SLAP 5 lesion with an associated posterolateral Hill-Sachs humeral head fracture. Superior glenohumeral joint entrapment of bucket-handle labral fragments is visualized in the same axial section.

Clinical presentation and diagnosis of SLAP tears

The clinical diagnosis of SLAP lesions may be difficult. Symptoms are often nonspecific and include pain associated with locking, snapping, and pseudosubluxation. Patient history may suggest a differential diagnosis that includes impingement syndrome, biceps tendinitis, or glenohumeral joint instability. Some characteristics of specific SLAP lesions include:

SLAP 1 lesions are a normal finding.
SLAP 2 lesions occur in traction injuries with forced extension on a flexed forearm.
In 31% of cases, SLAP 3, 4, or 5 lesions are associated with a fall on an outstretched hand.
Anterior dislocation is often associated with SLAP 5 lesions.

Patients usually present after trauma, and approximately one third have symptoms referable to the biceps tendon.²²⁷ Rotator cuff pain is common in type 2 or type 2 subtype SLAP lesions. Bicipital groove tenderness is assessed with Speed—s test (resisted forward flexion of a supinated arm) or Yergason—s test (resisted supination with the elbow in 90° of flexion). In a positive crank or clunk test there is pain and/or popping with compression and rotation. O—Brien—s active compression test for SLAP lesions elicits pain with resisted elevation with the forearm fully pronated. A positive Jobe relocation test indicates a posterior SLAP lesion. SLAP tears are associated with microinstability, including rotator cuff interval lesions.

Pathologic findings in SLAP tears

Pathologic changes found in SLAP lesions include:

A bare labral footprint
A sublabral sulcus greater than 5 mm (measured between the superior labrum and the superior pole of the glenoid)
A displaceable biceps (biceps root rolls over the glenoid)
Associated effects of SLAP lesions include:
- Biceps anchor disruption between the intra-articular biceps and the superior labrum with or without associated intralabral tearing (The superior labrum may be directly avulsed from the superior glenoid articular cartilage in a type I BLC.)
- Increased humeral head translation in microinstability
- Strain of humeral head restraints
- Glenohumeral laxity and/or instability
- Paralabral cysts (commonly associated with type 2 SLAP lesion)
- SLAP fracture²²⁷ with a superior humeral head chondral fracture and a SLAP (Fig. 8.305) lesion
- SLAP fracture avulsion (Fig. 8.306) from the superior pole of the glenoid (rare)

Treatment of SLAP lesions

Treatment of SLAP lesions is based on the type of labral lesion present. Properly used and optimized, MR imaging is accurate in identifying the spectrum of SLAP lesions (see discussion of MR Appearance of Labral Tears below). SLAP tears, including associated para-labral cysts, however, are not well displayed on ultrasound studies.

Treatment is as follows:

A type 1 SLAP lesion is treated with arthroscopic débridement of the degenerative labrum.
Treatment of a type 2 SLAP lesion (which involves detachment of the superior labrum and biceps anchor) addresses the avulsed labrum and reattachment of the detached biceps anchor to the superior glenoid (Fig. 8.307). A suture anchor technique, for example, may be used for a type 2 SLAP tear.
Since there is no involvement of the biceps anchor in a type 3 SLAP lesion (a bucket-handle tear and a meniscoid-type superior labrum), arthroscopic débridement of the loose labral fragment may be sufficient to relieve symptoms of catching and snapping.

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A type 4 SLAP lesion, which also involves a bucket-handle tear associated with a meniscoid-type superior labrum, additionally extends into the biceps tendon. Treatment of type 4 lesions ranges from resection of torn tissue to suture repair for bucket-handle tears associated with more extensive involvement of the biceps tendon.
Types 5 through 10 SLAP lesions require restoration of normal anatomy, including the MGHL and IGHLC. The labrum is stabilized and reattached.

FIGURE 8.299 ● (A) Lateral color illustration, (B) sagittal FS PD FSE image, and (C) coronal FS PD FSE image of posterior-based superior flap SLAP 6 lesion. The sagittal plane is required for direct visualization of the flap morphology; otherwise, the coronal MR appearance is similar to a bucket-handle tear.

FIGURE 8.300 ● (A) Lateral color graphic, (B) sagittal FS PD FSE image, and (C) coronal FS PD FSE of anterior-based superior flap tear of a SLAP 6 lesion.

FIGURE 8.301 ● (A) Lateral color illustration of a SLAP 7 lesion with extension of a superior SLAP 2 or 3 into the middle glenohumeral ligament (MGL). (B) Coronal FS PD FSE image demonstrates anterior extension of a SLAP tear toward the MGL. (C) Axial T2*-weighted GRE image with fragmentation of the MGL. Normal MGL laxity with ligament redundancy may falsely appear as a torn ligament on axial images. Therefore, confirmation of pathology requires proper correlation with sagittal images. (D) Confirmation of MGL involvement on a sagittal FS PD FSE image.

FIGURE 8.302 ● (A) Lateral (sagittal) color illustration of a type 8 SLAP with extension of a SLAP 2 to involve the posterior labrum. (B) Coronal FS PD FSE image with a SLAP 2 component and paralabral cyst as part of the SLAP 8 lesion. (C) Axial FS PD FSE image documents posterior labral tear extension from the biceps labral complex.

FIGURE 8.303 ● (A) Lateral color graphic of a type 9 SLAP lesion with circumferential labral tearing of all glenoid quadrants. (B) Coronal FS PD FSE image with a type 2 SLAP at the BLC and an inferior labral tear at the 6-o—clock position of the inferior pole. (C) Corresponding axial FS PD FSE image with anterior and posterior labral tears. (D) Sagittal PD FSE image of circumferential labral tear (around the entire glenoid “clock” tear). There is usually associated glenoid rim sclerosis.

FIGURE 8.304 ● (A) A SLAP 10 lesion with associated rotator cuff interval involvement shown with extension in the superior glenohumeral ligament on a lateral glenoid color illustration. (B) Coronal FS PD FSE image with SLAP 2 component of the SLAP 10 lesion. (C) Sagittal FS PD FSE image with associated rupture of the superior glenohumeral ligament.

FIGURE 8.305 ● (A) Coronal color illustration and (B) coronal FS PD FSE image of a SLAP fracture with a chondral divot of the superior humeral head. This type of injury is caused by impaction, often occurring in the setting of a fall onto an outstretched arm that drives the humeral head against the superior labrum and biceps anchor. These chondral fractures are more anterior and medial than the posterolateral Hill-Sachs anterior instability lesion. The SLAP fracture is frequently associated with a type 3 or 4 SLAP lesion, especially in the presence of a meniscoid-type superior labrum, which is more susceptible to injury.

FIGURE 8.306 ● Coronal FS PD FSE image showing the unusual SLAP 2 avulsion fracture. This type of fracture is seen with osseous avulsion of the biceps and labrum from the superior glenoid as the biceps tendon is stretched over the humeral head during a fall onto an outstretched arm. The avulsion-type fracture is rare relative to the humeral head dome chondral “SLAP fracture.”

Although not all SLAP 2 lesions are symptomatic, patients with bucket-handle lesions (including type 3 or 4 SLAP tears, which produce a displaced labral fragment into the superior glenohumeral joint) benefit from early identification by MR or MR arthrography. Snyder²²⁷ uses a single-anchor, double-suture (SADS) technique to repair a type 2 SLAP lesion. This technique creates a sling anterior and posterior to the biceps anchor point, allowing for stability and healing of the biceps labral complex. Posterior peel-back lesions may require an additional suture anchor in the posterosuperior corner.

FIGURE 8.307 ● (A) Coronal FS PD FSE and (B) sagittal PD FSE images of a SLAP lesion treated with superior quadrant suture anchors. SLAP lesions have also been treated by a single-anchor, double-suture SLAP repair to form a sling around the biceps anchor. Techniques that drill across the glenoid or through the acromion or use an absorbable tacking device are less successful and may lead to implant failure, synovitis, and intra-articular loose fragments.

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MR Appearance of Labral Tears

Pearls and Pitfalls

MR of Labral Tears

The coronal oblique plane is used to assess both the superior labrum at the superior pole of the glenoid and the IGLLC at the inferior pole of the glenoid.
The sagittal oblique plane is useful in identifying normal variations in the MGHL and the anterior band of the IGHL relative to the corresponding morphology of the anterior labrum in the axial plane. The sagittal oblique plane demonstrates bucket-handle SLAP tear patterns.
The labrum usually tears in an entire quadrant on more than one image location.

MR imaging has proved to be a sensitive, specific, and accurate modality for evaluating the glenoid labrum, including SLAP tears.¹⁹⁸^,²⁰⁰^,²⁰¹^,²³⁸^,²³⁹^,²⁴⁰^,²⁴¹^,²⁴² In MR studies of labral tears with surgical or arthroscopic correlation, sensitivity was reported to be 88% and specificity 93%.¹⁶⁵^,²⁴³ These statistics compare favorably with air-contrast CT arthrography,²⁴⁴^,²⁴⁵ and in addition MR imaging provides superior visualization of associated capsular structures and the IGHL.²⁴⁶ The glenoid labrum is routinely evaluated in all three imaging planes. Axial plane images, however, provide the most diagnostic information.

Routinely, axial images are obtained using a T2*-weighted 2D or 3D FT sequence as well as an FS PD-weighted FSE sequence. When MR arthrography with a paramagnetic contrast agent is used, post-contrast T1-weighted FS axial and coronal oblique images are obtained. Post-MR arthrography sequences must also include routine MR protocols using FS PD FSE and T2 FSE to accurately assess tendon pathology, paralabral cysts, articular cartilage, and edema of both osseous and soft tissue (including muscle structures). MR studies using intravenous contrast enhancement can be used to enhance joint fluid and synovium but will not create the capsular distention seen with MR arthrography.¹⁹⁷ Sagittal and coronal plane images are also routinely obtained to supplement axial images in the assessment of labral and capsulolabral anatomic abnormalities.²⁴⁷ The coronal oblique plane demonstrates the humeral and inferior glenoid attachment to the IGHL and displays the anatomy of the BLC, especially helpful in the diagnosis of SLAP lesions.²⁴⁸ The sagittal oblique plane is used to view the relationship between the IGLLC and the anterior and posterior labrum relative to the anterior and posterior bands of the IGHL. The MGHL and anterior labrum are frequently best visualized on sagittal oblique images.

Anatomic variations in the anterosuperior aspect of the glenoid labrum (e.g., a sublabral foramen, a cord-like MGHL, and the Buford complex) may influence glenohumeral biomechanics (changes associated with increased internal rotation), but

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they are not directly related to nor do they contribute to shoulder instability. Complex labral tears and the location of the labral segments involved can be correlated between sagittal oblique and axial images.

The intact fibrous labrum demonstrates low signal intensity on all pulse sequences (T1, T2, T2*, and T2-weighted FSE). We have not found the radial MR sequence helpful in routine evaluations of the labrum.²⁴⁹ The inferior labrum, however, should be carefully evaluated on coronal MR images, which may be more accurate than the inferior-most axial images through the glenohumeral joint. The IGLLC and the anterior inferior glenoid labrum are also shown when scans are performed with the arm positioned in abduction and external rotation. The low-signal-intensity labrum circles the glenoid articular surface and is usually triangular in cross-section on axial plane images. The peripheral attachment of the labrum joins the capsule and glenohumeral ligaments, creating the capsulolabral complex. This capsulolabral or labral ligamentous complex is best appreciated on sagittal oblique MR images, on which the BLC anatomy and the IGHL labral anatomy are responsible for the formation of the superior one third and inferior two thirds of the glenoid labrum, respectively. The central attachment of the labrum blends with the articular cartilage surface of the glenoid. A meniscoid appearance usually involves the superior labrum and is characterized by a free inner or central edge of the labrum.⁵²

Intralabral signal intensity

Loredo et al.²⁴⁰ have correlated the MR finding of intralabral signal intensity with histology showing mucoid or eosinophilic degeneration of fibrovascular tissue. An anterior sublabral band of intermediate signal intensity corresponds with a transition zone of fibrocartilage. These findings correlate with those of Detrisac and Johnson, who showed the labrum to be composed of bundles of fibrous tissue with a thin transitional zone of fibrocartilage between the labrum and articular cartilage.⁴⁸ This transitional zone may be only a few cells in width and is variably visualized in Detrisac and Johnson—s five types of variations of labral anatomy. Without the use of MR arthrography, with either intra-articular MR contrast or saline, this thin transitional cartilage may be over-read as a sublabral foramen or potentially as a SLAP lesion.

GLOM sign

A glenoid ovoid mass (GLOM sign),²⁵⁰ used by some as an indication of a labral tear, has not been used in our practice. In fact, a low-signal-intensity mass anterior to the glenoid rim may represent a cord-like MGHL and should not be interpreted as a tear or avulsed anterior labrum.

IGHL tears

Tears of the IGHL or IGL are usually associated with traumatic dislocation or subluxation.⁴⁸^,²⁵¹ Labral tissue may be interposed between the humeral head and glenoid rim, most often due to a labral tear with a relatively discoid and hypermobile biceps labral configuration. As the labrum becomes more meniscoid in shape, the likelihood of meniscal bucket-handle tears increases, and tissue may become interposed between the humeral head and glenoid surface. Posterolateral Hill-Sachs lesions and anterior inferior glenoid rim fractures can be seen on MR images in all three imaging planes. Subacute or chronic bony Bankart lesions are best identified on T1-weighted axial images, which show low-signal-intensity sclerosis in contrast to higher-signal-intensity marrow fat. A vacuum phenomenon, visualized as circular or linear areas of low signal intensity within the glenohumeral joint on GRE MR sequences, should not be misdiagnosed as a displaced labral fragment. This appearance is caused by intra-articular gas and is associated with positioning the arm in external rotation.²⁵²

SLAP tears

Care must be taken not to overdiagnose SLAP lesions on MR images, especially in the case of SLAP type 1 and 2 tears:

Type 1 SLAP lesion. Superior labral degeneration in a SLAP 1 lesion may be difficult to appreciate. The degeneration and fraying display increased signal intensity in T2*-weighted images, and morphologic irregularities may be appreciated with MR arthrography with intra-articular contrast. There is no labral detachment in SLAP 1 lesions.
Type 2 SLAP lesions demonstrate increased signal intensity, which undermines the superior labral base, on FS PD FSE images or MR arthrography. This may communicate with a superior glenoid labral cyst. Separation of the superior labrum from the glenoid rim increases the specificity of differentiating a type 2 SLAP lesion from a sublabral foramen. A sublabral foramen is located more anteriorly within the anterior superior quadrant, in comparison with the more superior position of the SLAP lesion, which is centered on the superior pole of the glenoid in the region of the BLC. Sagittal oblique images may be helpful in confirming fluid signal intensity crossing the base of the superior labrum or biceps anchor. Associated synovitis with effacement of fat may be seen between the coracoid and the anterior superior glenoid rim in acute or subacute SLAP lesions. A sublabral foramen should not demonstrate associated synovitis. We have observed intravenous MR contrast enhancement of synovial tissue and fat anterior to the superior labrum in cases of capsular strain without associated labral pathology. The SLAP 2 lesion should be carefully inspected for true anterior-to-posterior extension.²⁵³ For example, a posterior subtype of SLAP 2 (posterior peel-back lesion) does not demonstrate anterior extension within the superior labrum of the BLC. The SLAP lesion may occur within the labrum at the biceps tendon–labrum attachment or between the labrum and the superior pole of the glenoid in cases of type 1 BLC (the BLC is firmly adherent to the articular cartilage of the superior pole of the glenoid). Under forcible excessive humeral rotation, a normal preexisting biceps labral sulcus can develop into a pathologic type 2 SLAP lesion.²⁵⁴

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Distinguishing between a normal sulcus and a type 2 SLAP requires consideration of secondary and associated findings of a SLAP tear, including:
- Superior displacement of the labrum
- Increased depth of the sulcus
- Synovitis
- Adjacent labral and chondral fraying
- Micro-paralabral (early) cyst formation
Type 3 and type 4 SLAP lesions and bucket-handle tears. Sagittal images are particularly useful in identifying bucket-handle lesions and types 3 and 4 SLAP lesions with a bucket-handle tear. Extension of the tear into the biceps anchor (type 4) is best depicted in the sagittal oblique plane. Displaced labral tissue in types 3 and 4 SLAP lesions is seen as low-signal-intensity fragments within the glenohumeral joint on both axial and coronal oblique images. A bucket-handle type labral tear is characterized by a torn superior labrum, visualized as two separate sections on coronal images through the BLC. The MR visualization of fluid between two fragments of the superior labrum lateral to the biceps labral sulcus has been referred to as the double “Oreo cookie” configuration.²³⁷ However, we recommend avoiding this terminology. Inferior displacement of the superior labrum, or a portion of the superior labrum, from its biceps attachment is associated with a displaced bucket-handle tear. Signal intensity seen between the biceps tendon and labrum indicates the presence of a SLAP lesion. Type 3 and type 4 SLAP tears demonstrate an additional hypointense labral structure on sagittal images through the biceps labral complex (the triple structure sign of a displaced SLAP tear). Three separate and distinct structures may also be appreciated on coronal images when there is fluid between the biceps tendon and the superior labrum and fluid between two separated labral fragments.
Type 5 SLAP lesions. In type 5 SLAP the anterior labrum is torn in continuity with the SLAP tear (associated type 2 or type 3). The Bankart component is identified on axial images, whereas the SLAP region is visualized in the coronal plane.
Type 6 SLAP lesions. The type 6 SLAP is best identified on coronal images, although sagittal images are required to appreciate the flap component.
Type 7 SLAP lesions. Caution should be used in diagnosing a type 7 SLAP lesion because on axial images the two separate portions of a normal lax MGHL may mistakenly appear like a torn ligament.
Type 8 SLAP lesions. Type 8 SLAP lesions involve the posterosuperior and posteroinferior labrum in continuity with a SLAP 2 tear. Axial and sagittal images display the extent of posterior labral involvement.
Type 9 SLAP lesions. Coronal images display superior and inferior labral tearing in type 9 SLAP. Axial images demonstrate anterior and posterior labral tearing, and sagittal images show circumferential tearing with or without associated glenoid rim sclerosis.
Type 10 SLAP lesions. The type 10 SLAP tear presents as a SLAP lesion plus injury to the biceps pulley associated with medial subluxation of the biceps tendon (medial relative to the bicipital groove). Sagittal images demonstrate pathology of the superior glenohumeral ligament, whereas axial images are used to assess medial subluxation (instability) of the biceps tendon.

Zlatkin et al. have devised a four-category system of classification for abnormal labral signal intensity:¹⁰⁸^,²⁴³

In type 1, there is increased signal intensity within the labrum but no surface extension. Type 1 corresponds to internal labral degeneration without tear.
In type 2, the blunted or frayed labrum demonstrates normal dark signal intensity.
In type 3, T1-weighted or T2*-weighted images demonstrate increased signal intensity that extends to the surface, indicating a labral tear.
In type 4, a labral tear is depicted by a combination of abnormal morphology with type 2 features and increased signal intensity extending to the surface of the labrum with type 3 features.

Large tears and detachments may demonstrate a more diffuse increase in signal intensity, whereas discrete tears maintain linear morphology.¹¹²^,²³⁹^,²⁴⁶^,²⁵⁵ It is not unusual, however, for avulsed labral tissue to demonstrate low signal intensity, especially in chronic injuries. Normal labral outlines, blunting, and avulsion of the labrum from the underlying bone are also seen. Articular cartilage, of intermediate signal intensity on T1- and T2-weighted images and increased signal intensity on T2*-weighted images, may undermine the base of anterior labral tissue and should not be mistaken for an oblique labral tear. Fluid undermining the anterior labrum below the level of the coracoid or subscapularis tendon is a pathologic finding that represents labral tearing. The normal sublabral foramen does not usually extend below the level of the coracoid process. Labral tears may involve more than one quadrant. Careful inspection of the BLC and IGLLC on coronal images and the anterior and posterior labrum on axial and sagittal images will improve detection of extensive labral tears.²⁵⁶

Linear tears and fragmentation of the posterior labrum are less common and can be seen in patients with posterior instability and recurrent posterior subluxation.²⁵⁷^,²⁵⁸ Associated osseous findings include an impaction fracture or a defect on the anteromedial humeral head (reverse Bankart lesion), as well as fractures involving the posterior glenoid margin or lesser tuberosity.¹⁰⁸ Eccentric wear of the glenohumeral joint is frequently displayed as low-signal-intensity posterior glenoid subchondral sclerosis, which may be associated with fatty marrow conversion. The eccentric wear pattern may also be demonstrated by asymmetric attenuation of articular cartilage in the posterior aspect of the glenohumeral joint.

Intra-articular gadolinium or saline distends the joint capsule and facilitates imaging of the glenohumeral ligaments.³¹^,¹⁹⁸^,²⁰⁰^,²⁰¹^,²³⁸^,²⁴¹^,²⁵⁹ Without knowledge of glenohumeral ligament anatomy, these structures may be mistaken

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for detached labral fragments. Gadolinium-enhanced MR imaging allows the spatial detection of avulsed labral tissue relative to the glenoid rim. Labral tears are usually highlighted on FS T1-weighted images following intra-articular gadolinium administration. A synovial shelf in the subscapularis bursa is a normal finding sometimes seen on enhanced studies.²⁶⁰ Normal intermediate-signal-intensity fibrocartilage at the base of the anterior labrum does not show extension of contrast with MR arthrography. MR arthrography has also been shown to be accurate in the evaluation of chronic labral tears.²⁶¹

Paralabral Cysts and Suprascapular Nerve Entrapment

Pearls and Pitfalls

Paralabral Cysts

Paralabral cysts frequently communicate with a SLAP 2 or posterior-type SLAP 2 lesion.
A paralabral cyst usually coexists with a labral tear but may be associated with degenerative arthritis.
Suprascapular notch cysts are associated with edema or atrophy of the supraspinatus and infraspinatus.
Spinoglenoid notch cysts are associated with edema or atrophy of the infraspinatus.
Inferior paralabral cysts are associated with isolated denervation of the teres minor muscle.

Paralabral cysts, previously known as synovium-filled ganglion cysts, usually communicate with a labral tear. Paralabral cysts may occur in any of the following locations:

Associated with the biceps labral complex in continuity with a SLAP 2 or posterior peel-back type SLAP 2 lesion involving the posterior superior labrum
The anterior labrum
The posterior labrum
The inferior labrum (Fig. 8.308)
Complex (anterior and posterior) paralabral cysts may be associated with multiple locations (Fig. 8.309).
Paralabral cysts that extend to the spinoglenoid notch can produce atrophy of the infraspinatus and/or the supraspinatus muscles secondary to suprascapular nerve entrapment (see discussion below).²⁶²^,²⁶³^,²⁶⁴

FIGURE 8.308 ● (A) Coronal FS PD FSE and (B) sagittal FS PD FSE images of an inferior paralabral cyst communicating with an anteroinferior-to-inferior labral tear.

Intramuscular hemorrhage may mimic the appearance of a synovial ganglion. There is a high correlation between para-labral cysts, which have a posterior location, and posterosuperior labral tears.²⁶⁴^,²⁶⁵ These cysts may communicate with 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 may not be appreciated on routine axial images and an abduction external rotation view may be necessary to display the IGLLC. As discussed earlier, SLAP type 2 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.

Posterosuperior paralabral cysts are thus commonly seen in association with posterior capsulolabral injuries, including SLAP lesions.²⁶⁴^,²⁶⁵ 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.²⁶³ The inappropriate use of the term “suprascapular notch” to describe the location of all superior paralabral cysts may result in surgical exploration that 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

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(inferior transverse scapular ligament) is variably present and is located superior to the suprascapular nerve.

FIGURE 8.309 ● Axial FS PD FSE image showing anterior and posterior paralabral cysts communicating with their respective labral tears.

At the level of the suprascapular fossa, the suprascapular nerve has passed through the suprascapular notch.²⁶⁶ As a result, paralabral cysts that extend to the spinoglenoid notch can produce atrophy of the infraspinatus and/or the supraspinatus muscles secondary to suprascapular nerve entrapment (Fig. 8.310).²⁶²^,²⁶³^,²⁶⁴ Isolated infraspinatus atrophy is associated with more posteriorly located paralabral cysts of the spinoglenoid notch or occurs with spinoglenoid ligament entrapment. More proximal suprascapular nerve entrapment occurs with cysts located in the anterior suprascapular notch (Fig. 8.311). Suprascapular nerve entrapment at the suprascapular notch also occurs secondary to a thickening or scarring of the transverse scapular ligament in conjunction with a tight, bony notch, or by repetitive-use injuries at the shoulder.

The suprascapular nerve has two motor branches that innervate the supraspinatus, in addition to sensory branches to the glenohumeral and acromioclavicular joints. Since the supra-scapular nerve does not have a cutaneous sensory component, patients with isolated compression at the more posterior- and inferior-located spinoglenoid notch may experience painless muscle wasting of the infraspinatus. In contrast, compression of the suprascapular nerve proximally, at the suprascapular notch, is frequently associated with nonspecific shoulder pain involving both the supraspinatus and infraspinatus. This painful paralysis of both the supraspinatus and infraspinatus muscles occurs as the sensory fibers of the posterior glenohumeral joint capsule arise at the level of the suprascapular notch. The suprascapular nerve terminates by contributing two to four motor branches to the infraspinatus. Posterosuperior labral tears frequently develop paralabral cysts that extend into the spinoglenoid notch. These cysts are located in proximity to the motor branches to the infraspinatus. The suprascapular nerve is thus potentially constrained in one or two locations, the suprascapular notch (fixed by the transverse scapular ligament) and the spinoglenoid notch (fixed by the spinoglenoid ligament) (Fig. 8.312).²⁶⁷

Paralabral cysts develop along the path of least resistance and therefore dissect along the fibrofatty tissue overlying the suprascapular nerve toward the spinoglenoid notch between the supraspinatus and infraspinatus muscles.²⁶⁶ They arise from interruptions in the integrity of the joint such as labral tears, capsular tears, or capsular diverticula. A paralabral cyst should be assumed to communicate with an adjacent labral tear (see discussion below) unless it is far removed from the labrum.²⁶⁸

As a result of compression of the suprascapular nerve, supraspinatus and infraspinatus muscle atrophy is seen in association with anteriorly located masses and proximal nerve entrapment. In the initial stage of suprascapular nerve compromise, edematous changes in the infraspinatus muscle are characterized by low to intermediate signal intensity on T1-weighted images and hyperintensity on T2, FS PD-weighted FSE, or GRE T2*-weighted images. Chronic compression may lead to the development of fatty muscle atrophy.

As mentioned, most paralabral cysts, including but not limited to posterosuperior cysts, communicate with a labral tear. The cyst may be confined to the spinoglenoid notch or it may demonstrate anterior extension into the suprascapular notch, as seen on anterior coronal oblique MR images or axial images with the cyst identified anterior to the supraspinatus muscle. Superior and posterosuperior paralabral cysts are commonly seen in association with SLAP type 2 lesions, and the associated labral tear is identified on both axial and coronal oblique T2-weighted images. Documentation of direct communication of the paralabral cyst with the glenohumeral joint is possible with MR arthrography (Fig. 8.313). MR arthrography, however, must also be performed in conjunction with routine FS PD FSE sequences to identify non-contrast-filling paralabral cysts.

Paralabral cysts that are not directly related to the labrum may be associated with degenerative arthritis of the shoulder. They may also be associated with a symptomatic labral tear without nerve compression. The clinical profile of paralabral cysts includes:

Suprascapular nerve compression syndrome (pain and weakness of supraspinatus and infraspinatus muscles)
SLAP lesions with associated anterosuperior, posterosuperior, or combined paralabral cysts
Posterosuperior labral tears associated with spinoglenoid notch cysts, presenting as a deep ache or muscle tightness in the shoulder with progressive weakness
Axillary nerve compression (weakness of the deltoid and teres minor associated with axillary nerve denervation), when the cyst extends inferiorly and dissects into the quadrilateral space

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Isolated teres minor muscle denervation (when the teres minor branch of the axillary nerve, which is closest in proximity to the axillary pouch of IGHL, is compressed by an inferior paralabral cyst; also see discussion of the quadrilateral space syndrome below)
Clicking or catching with pain in the cocking and acceleration phase of throwing (a deep ache in the posterior shoulder with progressive weakness indicates nerve compression)

FIGURE 8.310 ● (A) Posterior coronal color illustration, (B) sagittal FS PD FSE image, and (C) coronal FS PD FSE image illustrate a spinoglenoid notch cyst in communication with a SLAP 2 tear and causing compression of the suprascapular nerve.

FIGURE 8.311 ● (A)Posterior coronal color graphic illustrating the combined denervation of the supraspinatus and infraspinatus muscles associated with paralabral cyst involvement affecting both the suprascapular notch anteriorly and the spinoglenoid notch posteriorly.MR characteristics can be seen on sagittal FS PD FSE images at the level of the suprascapular notch(B)and the spinoglenoid notch(C 0)

FIGURE 8.312 ● Selective or isolated infraspinatus denervation secondary to compression by a thickened spinoglenoid ligament. The suprascapular nerve and artery enter the supraspinatus fossa through the scapular notch by passing deep to the transverse scapular ligament. The suprascapular nerve enters the infraspinatus fossa by coursing lateral to the spinoglenoid notch. The lateral margin of the spinoglenoid notch is created by the fibrous band called the spinoglenoid ligament. The suprascapular nerve is relatively immobile in this area and thus susceptible to injury or compression by paralabral cysts. In extreme abduction and external rotation (in the throwing athlete, for example), the medial tendinous margin of the supraspinatus and infraspinatus can impinge against the lateral edge of the scapular spine. This results in compression of the infraspinatus branch of the suprascapular nerve. Painless atrophy of the infraspinatus muscle in volleyball players (attribu-ted to contraction of the infraspinatus muscle during the volleyball serving action) involves neuropathy of the inferior branch of the supra-scapular nerve.

FIGURE 8.313 ● T1 FS axial MR arthrograms of paralabral cyst. (A) Partial filling (curved arrow) of a spinoglenoid notch cyst (small straight arrows) with intra-articular contrast. (B) Communication of the cyst with a SLAP type 2 lesion. The superior labrum is torn from anterior to posterior (arrows) as assessed on the axial image through the most superior aspect of the glenohumeral joint.

The mechanisms of injury in paralabral cysts associated with SLAP tears include:

Trauma with a fall on the shoulder
Traction injury
Weightlifting (which is also associated with traction injury to the teres minor nerve branch of the axillary nerve, even in the absence of an inferior paralabral cyst)
Sports emphasizing an overhead motion

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.

Quadrilateral Space Syndrome

Pearls and Pitfalls

Quadrilateral Space Syndrome

The posterior branch of the axillary nerve courses adjacent to the inferior pole of the glenoid and inferior joint capsule and then divides into a branch to the teres minor muscle and a superolateral brachial cutaneous nerve branch.
The quadrilateral space syndrome is more commonly associated with denervation edema or atrophy restricted to the teres minor muscle, although the teres minor and deltoid are both supplied by the axillary nerve.

The quadrilateral space syndrome is an entrapment (compression) neuropathy of the axillary nerve in the quadrilateral space.²²²^,²⁶⁹ Increased signal intensity within the teres minor and deltoid muscle indicates denervation on FS PD FSE or STIR images. Chronic fatty atrophy is best appreciated on T1- or PD-weighted images (Fig. 8.314). Compression of the distal branch of the axillary nerve and involvement of the posterior humeral circumflex artery is associated with:

Proximal humeral and scapular fractures
Posttraumatic fibrous bands
Masses, including teres minor hypertrophy and lipomas (Fig. 8.315)

The axillary nerve normally innervates the teres minor, deltoid, and posterolateral cutaneous area of the upper arm and shoulder. Compression of the nerve and artery can result in ischemia and denervation. In the early and subacute phase there may be an edematous muscle belly. Fatty atrophy of the deltoid and teres minor develops in the chronic phase. Athletes with pain on abduction and external rotation in the age range of 22 to 35 years are frequently affected. Associated abnormalities include:

Inferior labral tears with dissecting paralabral cysts
Lipomatous masses
Enlarged veins extending into the quadrilateral space

MR appearance

The MR finding of chronic fatty atrophy of the teres minor and deltoid is not the most common presentation of imaging findings for quadrilateral space syndrome. In the absence of an associated quadrilateral space mass, selective involvement (denervation or atrophy) of both the teres minor and deltoid muscles could occur in Parsonage-Turner syndrome.

The posterior branch of the axillary nerve courses directly inferior and in close association with the inferior pole of the glenoid and shoulder joint capsule (Fig. 8.316). The posterior branch divides into the nerve supplying the teres minor and a superolateral brachial cutaneous nerve branch. The posterior branch of the axillary nerve is not only at risk for injury during capsular plication or internal shrinkage procedures, but is also susceptible to compression by inferior paralabral cysts and axillary pouch pathology, including adhesive capsulitis and stretch injuries to the IGHL (Fig. 8.317). This explains the selective involvement of the teres minor with either denervation edema or fatty atrophy, including cases attributed to quadrilateral space syndrome. Involvement of the superolateral brachial cutaneous nerve is associated with loss of sensation over the deltoid muscle. Isolated teres minor denervation²⁷⁰ may also be associated with nonstructural (relative to the axillary neurovascular structures) lesions, including rotator cuff injuries and traction of the axillary nerve of the teres minor branch resulting from a glenohumeral joint translational episode.²⁷¹

The treatment for neurapraxia (a transient episode of motor paralysis with little or no sensory or autonomic dysfunction) is conservative. Relief of compression due to mass or fibrous bands, however, may be necessary.

Parsonage-Turner Syndrome

The Parsonage-Turner syndrome is an acute brachial neuritis (acute shoulder pain described as intense and burning) or

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nontraumatic neuropathy involving an idiopathic denervation syndrome of the shoulder girdle musculature.²⁷² More than one nerve distribution may be involved, with denervation typically affecting mainly the lower motor neurons of the brachial plexus and/or individual nerves or nerve branches. The etiology is related to an immune-mediated inflammatory reaction against nerve fibers. Infection, surgery, trauma, childbirth, vaccinations, and systemic illness are all possible causes. In an associated rare digital form, the forearm, wrist, and hand may be involved. Denervation and swelling within the affected muscles are found in the early and subacute phase, which lasts 3 to 6 months. Fatty atrophy is seen in the chronic phase. Age range spans from 3 months to 74 years, with the majority of cases lasting up to 1 year. There is a 2 to 4:1 male predominance. Bilateral involvement may occur in up to one third of patients. Residual denervation is present in 10% to 20% of cases after 2 years.

FIGURE 8.314 ● Quadrilateral space syndrome with denervation and fatty atrophy of the teres minor and deltoid in the throwing athlete. (A) Coronal illustration of teres minor and deltoid fatty atrophy. The axillary nerve is susceptible to entrapment by fibrous bands in the quadrilateral space when the arm is abducted externally rotated. Selective involvement of the teres minor with posterior pain and tenderness may be present. (B) Coronal PD FSE image of fatty atrophy of both the deltoid and teres minor muscle groups.

FIGURE 8.315 ● Sagittal PD FSE image of the quadrilateral space syndrome with isolated fatty atrophy of the teres minor associated with a space-occupying lipoma demonstrating fat signal intensity. The quadrilateral space, which contains the axillary nerve and posterior circumflex humeral artery, is bordered by the inferior border of the teres minor superiorly, the teres major inferiorly, the long head of the triceps brachii muscle medially, and the diaphysis of the humerus laterally.

FIGURE 8.316 ● The normal course of the posterior branch of the axillary nerve, which divides into the nerve to the teres minor and a superolateral cutaneous nerve branch.

MR examination of affected muscle groups demonstrates the following patterns:

Supraspinatus and infraspinatus muscles affected, indicating suprascapular nerve involvement (Fig. 8.318)
Supraspinatus, infraspinatus, and deltoid muscles affected, indicating suprascapular and axillary nerve involvement (Fig. 8.319)

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Infraspinatus and teres minor muscles affected, indicating suprascapular and axillary nerve involvement (Fig. 8.320)

FIGURE 8.317 ● (A) Teres minor denervation related to inferior capsular adhesive capsulitis. The thickened and inflamed inferior capsule is adjacent to the posterior branch of the axillary nerve. (B) Inferior paralabral cyst associated with teres minor hyperintensity on a sagittal FS PD FSE image.

FIGURE 8.318 ● (A) Parsonage-Turner syndrome with denervation of the supraspinatus and infraspinatus muscles. (B) Sagittal FS PD FSE image with uniform supraspinatus and infraspinatus denervation without any associated suprascapular notch mass. The involvement of the supraspinatus and infraspinatus in idiopathic denervation is a common presentation of Parsonage-Turner. (C) Brachial plexus neuritis with hyperintensity of the upper and middle trunks. The suprascapular nerve is derived from the upper (superior) trunk. The upper or superior trunk is formed by the upper two roots (C5, C6). The brachial plexus network originates from the anterior primary rami of the C5 to T1 spinal nerves. (D) Corresponding coronal FS PD FSE sequence shows supraspinatus and infraspinatus denervation related to Parsonage-Turner syndrome as an acute brachial neuritis.

FIGURE 8.319 ● (A) Color posterior coronal illustration of Parsonage-Turner variation with denervation of the supraspinatus, infraspinatus, and deltoid (suprascapular and axillary nerve innervation). Sagittal (B) and coronal (C) FS PD FSE images showing subtle changes of Parsonage-Turner syndrome with denervation hyperintensity of the deltoid, supraspinatus, and infraspinatus muscles (B) and the deltoid muscle (C).

FIGURE 8.320 ● Chronic Parsonage-Turner syndrome with history of bilateral involvement. Fatty atrophy is demonstrated in the infraspinatus and teres minor on this sagittal PD FSE image. Parsonage-Turner syndrome is not usually associated with muscle fatty infiltration but more commonly demonstrates muscle atrophy with decreased muscle bulk.

In the acute and subacute phase, FS PD FSE and STIR images are helpful in identifying hyperintense diffuse muscle edema affecting the supraspinatus and infraspinatus muscles (suprascapular nerve involvement) and the deltoid muscle (axillary nerve involvement). Chronic muscle changes may result in an overall decrease in muscle bulk in addition to fatty changes and/or atrophy within the muscle proper. Rarely, denervation of the supraspinatus, infraspinatus, and teres minor muscles is caused by direct neurapraxia associated with a traumatic posterior dislocation (Fig. 8.321), and this possibility should also be considered in the differential diagnosis of unilateral Parsonage-Turner syndrome.

FIGURE 8.321 ● Posterior dislocation with suprascapular neurapraxia affecting the supraspinatus and infraspinatus muscles is seen on sagittal (A) and axial (B) FS PD FSE images. The MR appearance of supraspinatus and infraspinatus distribution could mimic Parsonage-Turner syndrome. The axillary nerve is usually at risk in anterior dislocations.

Biceps Tendon

Pearls and Pitfalls

Biceps Tendon

The biceps tendon origin includes the posterosuperior labrum and supraglenoid tubercle medial to the BLC.
The CHL-SGHL complex and not the transverse humeral ligament provides the stability of the biceps tendon in the intertubercular sulcus (groove).
Intra-articular biceps tendinosis may be overestimated on sagittal images secondary to the magic-angle effect.
Biceps tenosynovitis is visualized with hyperintense fluid or intermediate to hyperintense signal in the presence of thickened synovium.
Biceps tendon ruptures occur at the biceps anchor or within the rotator cuff interval.

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Related Anatomy

The origin of the biceps tendon is most commonly at the posterosuperior glenoid labrum, although a variable portion may also be attached directly to the supraglenoid tubercle.²⁷³ The primary attachment of the intra-articular biceps is to the superior portion of the labrum (at the BLC), prior to its attachment to the supraglenoid tubercle. Although the biceps tendon usually has a significant posterior superior labral attachment at the BLC, there are variations (Fig. 8.322) in which the biceps may be attached equally to both the anterior and posterior aspects of the superior labrum or may have a major contribution to the anterosuperior labrum. These variations may affect the relative anterior-to-posterior extent of the biceps labral sulcus when viewed on coronal MR images.²⁷⁴

The tendon of the long head of the biceps is divided into two zones, a traction zone of normal tendon and a sliding zone, which is the fibrocartilaginous portion of the biceps tendon in contact with the bicipital groove. The vascularity of the biceps tendon is decreased in the sliding zone, which has no vessels on the humeral side.

A mesotendon may be present, arising from the posterolateral aspect of the groove, which is associated with the extra-articular biceps tendon. The position of the arm determines the extent of the intra-articular portion of the biceps tendon. In adduction and extension the maximal amount of biceps tendon is located intra-articularly. With the arm in extreme abduction, the least amount of biceps tendon is located within the joint.

The rotator interval between the supraspinatus and subscapularis tendons contains both the coracohumeral (CHL) and superior glenohumeral (SGHL) ligaments. The intra-articular biceps tendon is stabilized (preventing medial biceps dislocation) by the pulley or sling created by the CHL–SGHL complex (Fig. 8.323). The CHL attachments include an origin from the lateral border of the coracoid and two bands of insertion: a lateral band that extends to the anterior edge of the supraspinatus and greater tuberosity and a medial band that extends to the superior edge of the subscapularis, transverse humeral ligament, and lesser tuberosity.

The SGHL attachments include an origin from the superior labrum, adjacent to the supraglenoid tubercle, and an insertion into the superolateral aspect of the lesser tuberosity, blending with the medial fibers of the CHL in the anterior aspect of the biceps sling. The SGHL also crosses the floor of the interval, whereas the CHL forms the roof or bursal side of the rotator interval. Both the supraspinatus and subscapularis tendons contribute to the formation of a sheath that surrounds the biceps at the proximal aspect of the bicipital groove.

In the intertubercular sulcus, the transverse humeral ligament is either absent or too weak to provide stability to the biceps. The transverse humeral ligament is not a distinct identifiable structure; instead, it represents a continuation of fibers of the subscapularis tendon with contributions from the supraspinatus tendon and the coracohumeral ligaments.²⁷⁵ Within the groove itself the falciform ligament, which is a tendinous expansion of the sternocostal portion of the pectoralis major muscle, helps to contain the biceps tendon.

Interstitial splitting of a bifid biceps tendon may result in the appearance of three structures in the bicipital groove (Fig. 8.324). The LHBT may end in two or, in rare cases, three tendons inserting onto the supraglenoid tubercle. The biceps brachii may also have three muscle bellies: the long head, the short head, and the third head.

FIGURE 8.322 ● Variation in the biceps tendon contribution to the BLC. These variations include an exclusive contribution to the posterosuperior labrum (A); a primary contribution to the posterosuperior labrum and secondary involvement of the anterosuperior labrum (B); equal contribution to the anterosuperior and posterosuperior labrum (C); and a primary contribution to the anterosuperior labrum and secondary contribution to the posterosuperior labrum (D).

FIGURE 8.323 ● Coracohumeral and superior glenohumeral ligaments coursing laterally toward the entrance of the intertubercular groove, forming the stabilizing biceps pulley within the rotator cuff interval as seen on a coronal T2 FSE image.

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Biceps Tendinosis and Tenosynovitis

Degeneration of the LHBT may occur as a result of chronic microtrauma or acute traumatic injury.²⁷³ FS PD FSE images typically show thickening and increased signal intensity of the biceps tendon within the rotator interval or bicipital groove (Fig. 8.325). Associated tenosynovitis may lead to an altered gliding mechanism of the biceps tendon sheath. Tenosynovitis is characterized by intermediate to hyperintense fluid signal intensity surrounding the biceps tendon in its extra-articular course (Fig. 8.326). Intermediate signal or heterogeneity of signal intensity corresponds to synovial thickening or pannus-like tissue. In tenosynovitis there is a disproportionate increase in the amount of fluid in the bicipital sheath relative to the volume of glenohumeral fluid.

Tenosynovitis of the biceps is associated with a variety of inflammatory or infectious processes of the glenohumeral joint, including:

Rheumatoid arthritis
Osteoarthritis (or osteochondromatosis of the shoulder and biceps tendon sheath)
Hemodialysis arthropathy
Crystalline arthritis (Fig. 8.327)

Biceps tendinosis accompanies rotator cuff disease, especially impingement. When the anterior cuff is torn, the biceps is impinged upon by exposure to the acromion through the rotator cuff tear gap. Biceps tendon degeneration may occur in conditions that cause biceps instability (the spectrum of pulley lesions of the rotator cuff interval) and in the throwing athlete with chronic microtrauma and shearing forces. Tendinosis of the biceps is associated with the following lesions:

FIGURE 8.324 ● Axial FS PD FSE image showing the bifid biceps tendon with interstitial split of the posterior extra-articular component.

Pulley lesions of the rotator interval
Anterosuperior impingement (ASI)
Posterior peel-back lesions in throwing athletes
SLAP lesions
Biceps tenosynovitis

Increased intratendinous signal within the rotator cuff interval may be a function of the obliquity of the biceps tendon (the magic-angle effect) and should be correlated with tendon thickening or intratendinous signal in multiple imaging planes. Patients with biceps tendinosis present with upper arm pain or shoulder pain often radiating into the upper arm, especially in overhead athletes. The typical complaint is of dull anterior shoulder pain especially with lifting and elevated pushing or pulling. Impingement signs are often positive. Pain can often be reproduced on physical examination with tests such as Yergason—s test (bicipital groove pain with resisted supination), Speed—s bicipital resistance test, and O—Brien—s test (an active compression test to entrap the anterosuperior labrum and demonstrate SLAP lesions).

Biceps lesions have been classified into three types based on their pathoanatomy:²⁷³

FIGURE 8.325 ● (A) Biceps tendinosis with thickening and increased signal intensity within the substance of the intra-articular biceps can be seen on this coronal FS PD FSE image. (B) Extra-articular biceps tendon with interstitial degeneration is seen on this axial FS PD FSE image.

FIGURE 8.326 ● (A) Biceps tenosynovitis with inflammation of the proximal biceps tendon sheath. A positive Speed—s test (downward force applied to the arm with the elbow extended and forearm supinated) with upper anterior arm and shoulder pain is associated with biceps tendon inflammation. (B) Axial FS PD FSE image showing thickened intermediate synovium with hyperintense fluid surrounding the biceps tendon in severe tenosynovitis.

FIGURE 8.327 ● Calcium hydroxyapatite deposition involving the proximal biceps sheath. Calcific tendinitis may involve the biceps at its attachment to the superior pole of the glenoid or distal to the glenohumeral joint at the junction of the tendon and muscle. Small deposits are characteristic at the level of the proximal humeral diaphysis and occur anterior, medial, or lateral to the biceps tendon, as seen on this axial T2* GRE image.

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Type A is impingement tendinitis.
Type B is subluxation and/or dislocation of the biceps tendon.
Type C is attritional tendinitis.

Impingement tendinitis is associated with impingement syndrome and rotator cuff disease. The biceps is exposed to the rigid coracoacromial arch in the presence of a full-thickness rotator cuff tear. Impingement tendinitis is the most common cause of biceps tendinitis (tendinosis). Lesions of the rotator cuff interval that involve the CHL–SGHL complex (as isolated disorders or in combination with tears of the supraspinatus and subscapularis tendons) are associated with subluxation and dislocation of the biceps tendon. Inflammation and fraying of the biceps tendon occur with the spectrum of pulley lesions associated with biceps instability. Attrition tendinitis is rare and represents a primary biceps tendon lesion that occurs within the bicipital groove. Stenosis of the bicipital groove results in attrition and degeneration of the biceps tendon. Inflammation of the biceps sheath is associated with hypertrophic spurs and further narrowing of a tight canal.

Biceps lesions have also been classified based on their anatomic location, including:

The biceps origin
The rotator interval
The rotator cuff (lesions associated with rotator cuff tears)

Biceps origin lesions include SLAP tears, which may be associated with extension into the biceps tendon (type 4). Interval lesions have been subdivided into biceps instability lesions and isolated rupture of the biceps. Both subluxation and dislocation (no contact between the LHBT and the bicipital groove) of the biceps tendon can occur in association with rotator cuff tears, in addition to tendinitis and tendon rupture.

Biceps Tendon Rupture

Biceps tendon rupture occurs at the top of the bicipital groove, usually in patients older than 40 years of age, and is related to the spectrum of shoulder impingement. Pure musculotendinous junction ruptures are rare and are associated with violent trauma. Biceps rupture may also occur as a complication of proximal humeral fractures, especially if impingement occurs at the osseous bicipital groove. Although biceps tendon tears are most common in the rotator interval, they may also occur adjacent to the biceps anchor (Fig. 8.328). There may be a proximal stump extending from the supraglenoid tubercle. The biceps tendon tear may be associated with retraction of the tendon (Fig. 8.329) and absence of both the intra-articular portion and proximal extra-articular portion of the biceps on coronal and axial MR images. The status of the biceps tendon with the rotator interval is also evaluated on sagittal MR images using FS PD FSE images. Interstitial tearing and an extra-articular course are most accurately assessed on axial images (Fig. 8.330).

Posterior dislocation and entrapment of the long head of the biceps tendon (Fig. 8.331) is rare and is associated with anterior shoulder dislocation.²⁷⁶ Tears of the supraspinatus, infraspinatus, and subscapularis tendons allow the biceps to displace in a lateral direction over the greater tuberosity and posterior to the humeral head. The entrapped biceps tendon may prevent reduction of the humeral head.

Neer classifies ruptures of the long head of the biceps tendon into three types:

Type 1 is tendon rupture without retraction.
Type 2 is tendon rupture with partial recession.
Type 3 is a self-attaching rupture without retraction.

Clinical diagnosis of a self-attaching long head rupture without retraction is difficult, and these types of injuries are usually identified at the time of rotator cuff repair. Absence of the biceps tendon on axial images through the bicipital groove or on sagittal images is diagnostic. A bifid biceps tendon may be mistaken for a tear that splits the biceps tendon longitudinally. A bifid biceps tendon is more likely to be visualized throughout all axial images in the glenohumeral joint and extends below the bony glenoid. A longitudinally split biceps tendon is more commonly restricted to a segment of the superior biceps tendon. Sagittal oblique MR images are used to confirm a normal BLC associated with a bifid biceps tendon. A bucket-handle tear of the labrum is not visualized in the presence of a normal BLC.

FIGURE 8.328 ● (A) Coronal anterior view color illustration of rupture of the intra-articular biceps at the BLC adjacent to the biceps anchor. (B) Coronal FS PD FSE image with biceps rupture at the supraglenoid tubercle.

FIGURE 8.329 ● Rupture of the biceps with retraction. The edge of the torn biceps tendon is visualized as a redundant structure in the groove. Coronal T2 FS MR is especially useful in distinguishing between retraction and partial recession (retraction) from a self-attaching but non-retracted biceps.

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Treatment of Biceps Lesions

Biceps tenodesis in the bicipital groove is the treatment of choice in biceps tendinitis. The criteria for biceps tenodesis²⁷⁷^,²⁷⁸ include:

Reversible tendon change with less than 25% partial-thickness tear from a normal width biceps tendon. The biceps tendon size and groove location are normal.
Irreversible tendon change with partial-thickness tear or fraying of greater than 25% of the normal biceps tendon width. There is associated biceps subluxation and disruption of the bicipital groove osseous or ligamentous anatomy.

If tenodesis is performed prior to rupture, the tendon and muscles are fixed under proper tension and the function of the biceps muscle as well as the LHBT is maintained. The contribution of the LHBT (through the BLC) to both superior and anterior stability of the glenohumeral joint is well documented,⁶⁰^,²⁷⁹ and 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. The micrometallic artifact from a proximal tenodesis

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and the discontinuity of the intra-articular biceps tendon can be displayed on MR images (Fig. 8.332).

FIGURE 8.330 ● (A) Severe interstitial split of the biceps tendon involving the extra-articular course of the tendon split is hyperintense on this axial FS PD FSE image. (B) Biceps tendon rupture and retraction associated with chronic proximal humeral surgical neck fracture are seen on a coronal FS PD FSE image.

FIGURE 8.331 ● Axial FS PD FSE image of posterior dislocation of the biceps tendon posterior to the humeral head and biceps labral complex. There is an associated complete rupture of the rotator cuff. The bicipital groove is empty and the biceps tendon is posteriorly directed relative to the humeral head and entrapped.

Adhesive Capsulitis

Pearls and Pitfalls

Adhesive Capsulitis

Acute adhesive capsulitis demonstrates a hyperintense and thickened IGHL on coronal FS PD FSE images. Associated synovial hypertrophy is shown as intermediate signal intensity and occupies the space created by the axillary pouch.
Residual or chronic thickening of the axillary pouch does not demonstrate hyperintensity on coronal FS PD FSE images.
Adhesive capsulitis may coexist with synovitis in other joint locations, including the rotator cuff interval and subscapularis recess.
The axillary nerve is susceptible to injury during transection of the axillary pouch in arthroscopic treatment of adhesive capsulitis. Arthroscopic capsular release should be considered when conservative management or manipulation is unsuccessful.

Adhesive capsulitis is a clinical syndrome of pain and severely restricted joint motion (frozen shoulder) secondary to thickening and contraction of the joint capsule and synovium (Fig. 8.333).²⁸⁰^,²⁸¹^,²⁸² It produces painful restriction of active and

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passive shoulder and scapulothoracic motion. Symptoms are usually present for at least 1 month, and the clinical course can be divided into stable or progressive categories. Adhesive capsulitis is either primary (idiopathic), with no predisposing history or cause, or secondary, with an antecedent event such as trauma or previous surgery. Inflammation of the inferior shoulder capsule also causes a limited range of motion or a frozen shoulder. The association of adhesive capsulitis with other shoulder disorders, such as impingement, represents secondary adhesive capsulitis. The etiology of secondary adhesive capsulitis can be further subdivided into the following causes:²⁸³

FIGURE 8.332 ● Management with arthroscopic biceps tenodesis is based on the ability to also repair an associated rotator cuff tear. Either a suture-only or suture anchor-to-bone fixation technique can be used. Anchor-to-bone fixation is used when the rotator interval tissues are deficient. Sagittal PD FSE image.

FIGURE 8.333 ● Adhesive capsulitis or frozen shoulder with thickened inflamed IGHL and synovial thickening within the axillary pouch. Idiopathic adhesive capsulitis is more common than posttraumatic or secondary adhesive capsulitis, which occurs in only 10% of cases.

Trauma
Surgery
Degenerative disease
Intrinsic rotator cuff and biceps tendinitis/tear
Inflammatory disease
Metabolic disease (including diabetes mellitus)

An autoimmune theory is supported by increased C-reactive protein levels and the presence of HLA-B27 in adhesive capsulitis. In addition, 10% to 20% of patients with diabetes (36% of those with type 1 or insulin-dependent diabetes) are affected. The incidence estimate of 3% of the general population may be low, based on the more frequent MR finding of a thickened and hyperintense axillary pouch of the IGHL on coronal images (Fig. 8.334).

On arthrography, there is a decreased capacity to inject contrast material in a tight or resistant joint.¹¹⁷ The subscapularis bursa and axillary pouch may be small and thickened. Emig et al.²⁸⁰ reported that joint capsule and synovial thickness greater than 4 mm, as assessed at the level of the axillary recess, is a useful MR criterion for the diagnosis of adhesive capsulitis.²⁸⁰ Articular fluid volumes are unreliable in the identification of adhesive capsulitis. Other MR findings in adhesive capsulitis include:

Synovitis (intermediate signal intensity)
Capsular contraction, which may require validation with MR arthrography to appreciate loss of capsular volume and compliancy.

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Effusion
A hyperintense thickened IGHL and intermediate-signal-intensity synovial hypertrophy within the confines of the axillary pouch in symptomatic or active adhesive capsulitis (see Fig. 8.333)
A thickened IGHL without hyperintensity on FS PD FSE images (Fig. 8.335) in post-inflammatory changes or scarring of the axillary pouch

FIGURE 8.334 ● Coronal PD FSE (A) and FS PD FSE (B) and axial FS PD FSE (C) images of adhesive capsulitis. The thickened, hyperintense axillary pouch produces a soft tissue fullness in the anteroinferior capsule. Primary adhesive capsulitis has a 5:1 female-to-male prevalence. Patients may present with spontaneous insidious pain following a mild or trivial traumatic event including extension or lifting.

Intravenous contrast MR imaging, used to enhance the acute changes of adhesive capsulitis, shows a hyperintense thickened IGHL (Fig. 8.336). There is also thickening of the CHL and joint capsule in the rotator cuff interval and obliteration of the fat triangle between the CHL and the coracoid process (subcoracoid triangle sign).²⁸⁴ Synovitis may be also observed at the superior border of the subscapularis tendon. Arthroscopic findings range from proliferative synovitis to capsular and intra-articular subscapularis tendon thickening to fibrosis. MR identification of adhesive capsulitis should always be reported and should not be assumed to be posttraumatic. In fact, posttraumatic adhesive capsulitis is not common and is seen in only 10% of cases. A small percentage of patients may have persistent symptoms after conservative treatment, including physical therapy and passive range-of-motion exercises.²⁸¹ Other treatment options include:

Brisement or distention arthrography leading to capsular rupture
Manipulation under anesthesia
Arthroscopic capsular release

Adhesive capsulitis is frequently underdiagnosed, although MR findings are usually present. The assessment of painful and restrictive passive and active range of shoulder motion with rotator cuff disease should always be assessed at clinical presentation.

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.²⁸⁵^,²⁸⁶ The involved tendons, from most to least likely, are:²⁸⁷

Supraspinatus
Infraspinatus
Teres minor
Subscapularis

FIGURE 8.335 ● Coronal PD FSE (A) and FS PD FSE (B) images show the chronic phase of adhesive capsulitis with a thickened IGHL without hyperintensity on the FS PD FSE image (B). MR arthrography is required to demonstrate loss of the inferior capsular recess with scarring.

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Periarticular soft tissues, including the capsule, ligaments, and bursae (Fig. 8.337), are also potential sites of involvement. The size of the deposition varies from a few millimeters to several centimeters. 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.

FIGURE 8.336 ● Intravenous enhancement of the axillary pouch in adhesive capsulitis on a coronal FS T1-weighted MR image. Associated retear of the rotator cuff repair is seen.

There are several staging systems for calcific tendinitis. In one, it is staged as being in one of four phases:

The formation phase
The resting phase (no enlargement of deposit)
The resorptive phase (inflammation with cells resorbing calcium)
The post-calcific phase (reconstruction of tendon integrity)

In another it is considered to be in one of three phases:

An asymptomatic silent phase (Fig. 8.338), with calcium salts deposited in the critical zone of the tendon
A mechanical phase (Fig. 8.339) of enlarging deposits causing intratendinous stress pain associated with intrabursal or subbursal rupture
Adhesive periarthritis (Fig. 8.340)

Adhesive periarthritis is associated with adhesive bursitis as a complication of tendinous calcific deposits. The bursitis is an acute inflammatory reaction to the crystal deposits in a semiliquid state and demonstrates a more heterogeneous hyperintensity with associated scattered foci of signal void on T2, FS PD FSE, or T2*-weighted images.

The microscopic features of calcific tendinitis include:

Crystalline hydroxyapatite in the tendon
Influx of inflammatory cells, especially in the resorptive phase
Macrophages and multinuclear giant cells
Fibroblasts, in the post-calcific phase

FIGURE 8.337 ● (A) Sagittal FS PD FSE and (B) axial T2* GRE images of calcific tendinitis subscapularis bursal variant with intermediate-signal-intensity paste-like thickening deep to the subscapularis tendon. GRE images are required to appreciate the susceptibility and hypointensity of the calcium hydroxyapatite crystals.

FIGURE 8.338 ● (A) Coronal 3D color perspective of the silent or subclinical phase of calcium deposition within the substance of the rotator cuff tendons. (B) Transition from the silent phase to the early mechanical phase is characterized by mild elevation of the subacromial bursal floor. Localized hyperintensity of the adjacent subacromial bursa can be seen on this coronal FS PD FSE image.

FIGURE 8.339 ● Coronal PD FSE (A) and FS PD FSE (B) images show the mechanical phase of intrabursal rupture with the bulk of the calcific deposit occupying the subacromial-subdeltoid bursal space. The mechanical phase is characterized by bursal floor elevation, subbursal rupture, or intrabursal rupture.

FIGURE 8.340 ● Adhesive periarthritis demonstrates intratendinous calcific deposits associated with adhesive bursitis and distension of the subacromial bursa. The subacromial subdeltoid bursa may be thickened with areas of intermediate signal intensity. Coronal 3D perspective with 2D coronal section inset in color.

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The hydroxyapatite deposits can be seen in various views on conventional radiographs. On MR examination calcium hydroxyapatite deposition disease located within the rotator cuff tendons is visualized as a globular area of decreased signal intensity or a mass on all pulse sequences. The globular morphology may be hood-like, linear, angular, or round. T2* GRE images demonstrate the greatest degree of hypointensity and are thus more sensitive and specific for the diagnosis. GRE images are also useful in the identification of the liquefied form of the disease within a bursa or recess, which may display a more intermediate and inhomogeneous signal on FS PD FSE images without the use of a T2*-weighted sequence. The calcific deposit may be occult on MR examination.

Hyperintense perilesional edema and subacromial-subdeltoid fluid are seen on FS PD FSE images. There is no direct involvement of articular cartilage. Tendinosis or a partial rotator cuff tear are associated findings. Areas of rotator cuff tendon necrosis, however, do not occur until the deposit increases in size, causing pressure on adjacent tissue and vascular elements. Cuff tendon fiber injury occurs as the calcium hydroxyapatite infiltrates and replaces damaged tissue.

Treatment of calcific tendinitis usually consists of a subacromial decompression, along with excision and removal of the calcific deposits by dissection and debridement.

Pectoralis Major Tear

Pectoralis major tears may involve disruption of the pectoralis myotendinous unit or the humeral insertion site.²⁸⁸ The broad, bilaminar tendon of the pectoralis major inserts into the lateral lip of the bicipital groove. It is formed from the two heads of the pectoralis major muscle: the sternocostal head and the clavicular head. The upper clavicular head of the pectoralis forms the anterior insertion and the sternocostal head forms the posterior tendon insertion. The sternocostal head produces the rounded anterior axillary fold prominence with spiral layering

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of muscle fibers. The most inferior fibers of the sternocostal head insert superiorly and the superior fibers insert inferiorly. The sternocostal head is more susceptible to avulsion than the clavicular head. The pectoralis major is innervated by the medial and lateral pectoral nerves from the medial and lateral cords of the brachial plexus. The pectoralis major functions in adduction and medial rotation of the humerus.

The most common causes of pectoralis major tears are:

Resisted forced abduction and external rotation
Forceful contraction with the arm adducted, flexed, and internally rotated
Tendon rupture in bench-press weightlifting (muscle failure associated with bench-press lifting is secondary to either overload of the short inferior fibers in the eccentric phase of lifting [sternal head failure] or from a direct blow [sternoclavicular head failure])

Most injuries involve the musculotendinous junction (Fig. 8.341) or the distal tendon insertion (Fig. 8.342).²⁸⁹ Partial tears are the most common presentation, with combined sternal and clavicular head injuries more frequent than individual head injuries (Fig. 8.343). Silent injuries of the pectoralis muscle may occur in the elderly. In acute rupture pain is severe and weakness is present in internal rotation. Deformity is also present, especially with attempted muscle contraction. The weightlifter usually has a history of injury during humeral extension at the beginning of a lift. A hematoma then develops in the proximal medial arm or chest wall. Tendinous avulsions from the humerus are associated with ecchymosis.

FIGURE 8.341 ● (A) Coronal color illustration of musculotendinous junction injury involving clavicular and sternal head tendon contributions. (B) Axial FS PD FSE image with hyperintensity and retraction of the pectoralis major in a musculotendinous junction injury with intact remaining stump of tendon insertion.

MR findings on FSE PD FSE images include:

Hyperintense edema in the clavicle, sternum, or ribs
Increased signal intensity at the humeral insertion in the proximal humeral diaphysis (lateral lip of bicipital groove)
Hyperintense edema and hemorrhage within the muscle tear site, perifascial zone, and subcutaneous fat

The normal myotendinous unit is hypointense on T1- and T2-weighted images. Coronal oblique images are prescribed parallel to the muscle and with large FOV. Axial images demonstrate side-to-side pectoralis asymmetry and complement small-FOV dedicated pectoralis major muscle images of the affected side.

A complete tear of the pectoralis major may retract and undergo fibrosis, causing a visible deformity of the chest wall. In more than 90% of cases, both primary and delayed repair successfully restore strength and function. Complete rupture of the pectoralis major tendon is an indication for immediate surgical repair. These injuries usually occur in young active individuals who would have persistent weakness without repair. Chronic ruptures have also been successfully repaired in symptomatic athletes. Complications of pectoralis major injuries are:

Hematoma with pseudocyst
Infection
Rupture at the musculotendinous junction

FIGURE 8.342 ● (A) Axial FS PD FSE image shows complete avulsion of the tendon–bone interface with localized hemorrhage. The pectoralis major muscle may be injured at the tendon–bone interface or the tendon–musculotendinous junction, or intramuscularly. Hematoma and periosteal stripping are associated with primary tendon avulsion. (B) Axial PD FSE image of normal pectoralis major tendon insertion shown for comparison. The hypointense pectoralis major tendon is located directly anterior to the coracobrachialis muscle.

FIGURE 8.343 ● Partial tear involving both the clavicular and sternal head with preservation of the distal tendon insertion on axial FSE PD (A) and coronal oblique FS PD FSE (B) images. There is greater disruption of clavicular head muscle fibers appreciated on the coronal oblique image of the pectoralis muscle.

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Mature scar tissue formation in a failed repair can be used to perform a delayed repair of the avulsed tendon stump.

Acromioclavicular Separations

AC injuries range from separations (direct trauma) to distal clavicle osteolysis (overuse injury in weightlifters). A direct fall onto the shoulder may result in either a distal clavicle fracture or an AC separation.²⁹⁰ The relevant anatomy of the AC joint (Fig. 8.344) is used to classify these injuries. The distal clavicle is stabilized in the anteroposterior direction by the AC ligament (capsule) and in the superior-to-inferior direction by the coracoclavicular ligaments (the cone-shaped conoid and the broad trapezoid ligament).

FIGURE 8.344 ● Anterior view coronal color perspective of the normal trapezoid and conoid ligaments, which function as a single coracoclavicular ligament. The conoid is posterior and medial, whereas the trapezoid is anterior and lateral.

The coracoacromial ligament can be used as a ligament substitute when transferred to the end of a recessed distal clavicle and thus functions as a coracoclavicular ligament.

AC separations are classed into six different types based on the degree of displacement and the location of the distal clavicle:²⁹¹

Type I: AC ligamentous sprain
Type II: AC joint disruption with intact coracoclavicular ligaments
Type III: AC joint and coracoclavicular ligament disruption. The coracoclavicular interspace is widened 25% to 100% (Fig. 8.345) and the distal clavicle is mobile in both superior to inferior and anteroposterior directions.
Type IV: Posterior displacement of the clavicle into or through the trapezius (Fig. 8.346)
Type V: Type III separation with greater displacement (100% to 300% compared to the contralateral side) between the coracoid and clavicle (Fig. 8.347)
Type VI: Inferior dislocation of the clavicle inferior to the acromion (subacromial) or coracoid (subcoracoid)

MR studies in the coronal and sagittal planes are used to quantify the edema and degree of tearing of the coracoclavicular

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ligaments. The relative position of the distal clavicle to the acromion is also assessed. Associated fractures of the coracoid, acromion, midclavicle, and/or distal clavicle with extension into the AC joint are also evaluated. It is important to establish the integrity of the coracoacromial ligament to determine whether allograft reconstruction may be required. Indications for surgical intervention include types IV, V, and VI dislocations. Treatment options for types I and III AC dislocations are more controversial and are often based on activity requirements (i.e., needs of an athlete compared to those of a laborer or someone with a more sedentary lifestyle).

FIGURE 8.345 ● (A, B) Type III AC separation with complete disruption of both the AC and CC ligaments. The distal clavicle is above the superior border of the acromion. The CC interspace is usually widened by 25% to 100%. The space between the coracoid and clavicle is normally between 1.1 and 1.3 cm. (A) Sagittal FS PD FSE image. (B) Coronal FS PD FSE image.

FIGURE 8.346 ● Type IV AC separation with the distal clavicle displaced posteriorly into the trapezius. There is a fluid-filled gap between the torn and separated CC ligaments and widening of the AC joint space in the coronal plane. Sagittal FS PD FSE image.

Arthritis

Pearls and Pitfalls

Arthritis

Central and posterior glenoid wear with sclerosis and cartilage loss is typically seen in osteoarthritis.
Loose bodies are frequently located in the subscapularis recess.
Coronal images demonstrate the medial and inferior projection of humeral head osteophytes. Spurring is also present directed from the inferior pole of the glenoid.
Severe glenohumeral osteoarthritis may be associated with reactive subchondral marrow edema.
Rheumatoid-related synovial hypertrophy or pannus is intermediate in signal intensity on FS PD FSE images and will enhance with intravenous contrast.

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Rotator cuff tears are commonly seen in association with rheumatoid arthritis.
Rice bodies are hypointense on FS PD FSE images and represent detached fibrotic synovial villi.

FIGURE 8.347 ● (A, B) Type V AC separation with complete disruption of the AC and CC ligaments and severe superior displacement of the distal clavicle. The deltoid and trapezius aponeurosis is avulsed from the distal clavicle and the distal clavicle is displaced subcutaneously, with the CC interspace widened 100% to 300%. (A) Coronal PD FSE image. (B) Sagittal PD/T2 FSE image.

Osteoarthritis

Osteoarthritis is characterized by chondral erosions, osteophyte formation, subchondral cysts and sclerosis, and synovitis.²⁹² Degenerative arthritis may be primary, caused by chronic microtrauma, or secondary, related to predisposing events of previous trauma, congenital deformity, infection, or metabolic disorder. The shoulder is predisposed to unique instabilities because of its non-weight-bearing anatomy. Compression of weakened bone occurs with subchondral fracture. Loose bodies are seen with fragmentation of osteochondral surfaces (Fig. 8.348). Synovial hypertrophy and synovial fluid production correlate with joint pain and increased intra-articular pressure.

MR is accurate in identifying both posterior glenoid wear (Fig. 8.349) and posterior humeral subluxation in primary degenerative joint disease. Hypointense glenoid sclerosis is associated with loss of posterior glenoid articular cartilage on axial PD and FS PD FSE images. Although anterior capsular contracture may be more difficult to visualize, with appropriate sequences it can be seen as hypointense thickening of the anterior capsule. Rotator cuff tears are uncommon in primary degenerative joint disease.²⁹³ Humeral head sclerosis and cartilage loss are usually central or superior in glenohumeral osteoarthritis. Peripheral osteophytes projecting from the humeral head are directed inferiorly on coronal images (Fig. 8.350). Subchondral cysts are seen in both the humeral head and glenoid. Glenoid cartilage loss and sclerosis is usually central or posterior, and there can be complete loss of the glenoid chondral surface. Glenoid peripheral osteophytes involve the lower two thirds of the glenohumeral joint. The inferior capsule may be enlarged and the anterior capsule contracted. Loose bodies occur within the glenohumeral joint or subscapularis bursa (Fig. 8.351). Advanced glenoid arthrosis demonstrates subchondral erosions of the glenoid fossa on sagittal images in the posterosuperior, posteroinferior, inferior, and anteroinferior quadrants (see Fig. 8.351). A secondary chondromatosis is associated with full-thickness chondral loss of the humerus or glenoid (Fig. 8.352). An intraosseous ganglion (Fig. 8.353) is a less common finding in degenerative osteoarthritis and may be mistaken for an intraosseous hemangioma or infectious tract.

If conservative treatment with physical therapy and NSAIDs is not successful, total shoulder replacement is considered. The major diagnostic indications for total shoulder replacement include rheumatoid arthritis, osteoarthritis (primary and secondary), old trauma, prosthetic revision, arthritis after

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recurrent dislocation, and rotator cuff arthropathy (see discussion below).

FIGURE 8.348 ● Coronal T2 FSE (A) and axial FS PD FSE (B) images of osteoarthritis with glenohumeral chondral loss, inferomedial osteophytes, and subscapularis bursa loose bodies.

Degenerative osteoarthritis of the AC joint (Fig. 8.354) is also categorized as either primary or secondary (e.g., AC separation). We have noted an association between moderate AC joint arthrosis (hypertrophy with hyperintense edema of the distal clavicle and acromion) and posterosuperior labral tears. Weightlifters and triathlon athletes (primarily from activities during the swimming phase of the competition) are subject to AC joint and posterosuperior labrum stress and are prone to this combination of arthrosis and posterosuperior labral tears. MR findings of AC capsular hypertrophy have been used to predict the success of intra-articular injection for pain relief.²⁹⁴

Rheumatoid Arthritis

Rheumatoid arthritis is a systemic inflammatory arthritic condition.²⁹³ The glenoid articular cartilage is eroded medially, in contrast to the eccentric wear pattern of degenerative joint disease. The erosions of rheumatoid arthritis involves both cartilage and subchondral bone.²⁹² Osteopenic changes may be seen as patchy areas of hyperintensity on FS PD FSE images. The superolateral articular surface of the humerus is commonly affected by erosive involvement. The glenohumeral, AC, and sternoclavicular shoulder articulations may be affected simultaneously. Bilateral disease and separate involvement of the elbow, wrist, and hand are not uncommon.

Rheumatic disease of the shoulder is associated with full-thickness rotator cuff tears (Fig. 8.355) in up to 50% in patients requiring total shoulder arthroplasty. Inflammation, fibrosis, and synovial hypertrophy involve both the subdeltoid bursa and synovial joint lining. In addition, osseous erosions, resorption, sclerosis, and cysts (Fig. 8.356) may be found. The synovial hypertrophy is often accompanied by decreased-signal-intensity rice bodies (Fig. 8.357) within the intermediate to hyperintense fluid/synovial complex. These rice bodies are detached fibrotic synovial villi. Uniform joint space narrowing often results. The shoulder capsule may become thinned or stretch.

Inflamed synovium enhances with intravenous MR contrast. PD- or T1-weighted images demonstrate distal clavicle resorption. Elevation or superior ascent of the humeral head is associated with rotator cuff defects. The surgical treatment of rheumatoid arthritis includes synovectomy, arthroplasty, arthrodesis, and osteotomy.

Fractures of the Proximal Humerus and Osteochondral Lesions

Pearls and Pitfalls

Fractures of the Proximal Humerus and Osteochondral Lesions

Proximal humeral fractures have been grouped into involvement of the anatomic neck, greater tuberosity, lesser tuberosity, and surgical neck.
Fracture displacement and angulation requires correlation of coronal and axial images.
A chondral SLAP fracture involves the posteromedial superior humeral head.
In acute fractures, T2* GRE images may be useful if hyperintense marrow edema obscures fracture site morphology or if a number of segments are involved.

Neer classifies upper humeral fractures (Fig. 8.358) into four types:²⁹⁵

FIGURE 8.349 ● (A) Axial color section illustrating posterior or eccentric wear pattern of osteoarthritis with loss of posterior glenohumeral joint articular cartilage. Axial PD FSE (B) and coronal FS PD FSE (C) images showing posterior glenoid eccentric wear with subchondral fracture, chondral delamination, and joint space narrowing. MR is used to assess the wear pattern and glenoid bone stock, important in planning the resurfacing of the glenoid.

FIGURE 8.350 ● Advanced changes of osteoarthritis of the glenohumeral joint. Articular cartilage loss with sclerosis and subchondral cystic change is greatest in the area of the humeral head in contact with the glenoid between 60° and 100° of abduction. Characteristic large peripheral osteophytes develop inferiorly and limit rotation by effectively enlarging the diameter of the humeral head. (A) Coronal color section of degenerative osteoarthritis of the glenohumeral joint. (B) Coronal FS PD FSE image with full-thickness glenohumeral articular cartilage loss, inferior osteophytes, and labral tearing shown at the BLC and inferior glenohumeral ligament labral complex. (C) Axial PD FSE with posterior glenoid wear advancing to involve the entire glenohumeral joint. Posterior glenoid wear is associated with an internal rotation contracture and posterior subluxation of the humeral head.

FIGURE 8.351 ● Loose bodies, glenoid erosions, and soft tissue contractures all limit active and passive range of motion in osteoarthritis, although the rotator cuff is usually intact. (A) Sagittal FS PD FSE image with subscapularis bursa loose bodies. (B) Sagittal FS PD FSE image of diffuse glenoid rim erosions of osteoarthritis. (C) Sagittal PD FSE image for comparison with multidirectional instability in a 20-year-old wrestler. In contrast to osteoarthritis, the anterior and posterior rim sclerosis of MDI is shown without chondral wear or subchondral cystic erosion. This instability may eventually be associated with glenohumeral arthritis but should be identified and differentiated at this stage.

FIGURE 8.352 ● Secondary chondromatosis associated with full-thickness chondral loss of the humeral head on a sagittal FS PD FSE image.

FIGURE 8.353 ● Atypical manifestation of osteoarthritis with intraosseous ganglion extending into the proximal humeral diaphysis as seen on a coronal PD FSE image (A) and a coronal FS PD FSE image (B).

FIGURE 8.354 ● (A) Coronal FS PD FSE image showing AC joint with hyperintense edema of the distal clavicle and adjacent acromion in a weightlifter. Repetitive microtrauma is associated with posttraumatic arthritis, including osteolysis. The “weightlifter's clavicle” represents subchondral injury with microfractures and resorptive osteolysis. (B) Coronal PD FSE image showing AC joint arthrosis associated with rotator cuff impingement. Characteristic AC joint hypertrophy, greater tuberosity squaring, inferior acromial spurs, and full-thickness rotator cuff tear are shown.

FIGURE 8.355 ● Rheumatoid arthritis targets the glenohumeral joint but may involve all synovial-lined joints, including the acromioclavicular and sternoclavicular joints. Marginal erosions and subchondral cysts may involve large areas of the humeral head. Glenoid destruction is associated with central or peripheral erosions. Sclerosis and osteophytosis are not common and represent the development of secondary osteoarthritis. Chondral loss, subchondral erosions, and synovial pannus are shown on this color coronal illustration. Erosion with tapering of the distal clavicle is also indicated.

FIGURE 8.356 ● Coronal PD FSE (A) and FS PD FSE (B, C) images showing rheumatoid arthritis with severe proliferative granulation tissue or pannus destroying articular cartilage and invading subchondral bone of the greater tuberosity. The pannus has destroyed the distal clavicle and has attached to the joint capsule and torn cuff tendons.

FIGURE 8.357 ● Intermediate-signal rice bodies or detached fibrotic villi of rheumatoid arthritis shown on axial PD FSE (A) and FS PD FSE (B) images.

FIGURE 8.358 ● (A) Division of the proximal humerus into four separate fragments based on anatomic lines of epiphyseal union. These distinct fragments are the greater tuberosity, the lesser tuberosity, the anatomic head, and the diaphysis. (B) Coronal PD FSE image with fracture fragments involving the greater tuberosity anatomic head, shaft, and lesser tuberosity identified.

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Those involving the anatomic neck of the humerus (Fig. 8.359)
Those involving the greater tuberosity (Fig. 8.360)
Those involving the lesser tuberosity (Fig. 8.361)
Those involving the shaft or surgical neck of the humerus (Fig. 8.362)

A one-part fracture has either no or minimal displacement or angulation of any of the segments. A two-part fracture involves displacement of one segment. A three-part fracture involves displacement of two segments with an associated unimpacted surgical neck fracture with rotatory displacement. A four-part fracture is characterized by displacement of all four segments.²⁹⁶ Displacement is defined by fracture segment displacement of greater than 1 cm or angulation of more than 45°. Eight percent of proximal humeral fractures have minimal or no displacement and are held together by the rotator cuff, capsule, and periosteum.

MR imaging is particularly useful in identifying one-part or nondisplaced fractures not detected on conventional radiographs. MR images also display multiple fracture lines within any given segment. The axial plane is important in assessing the location of the humeral head in more complex fracture–dislocations and in determining involvement of the glenohumeral joint. STIR images are more sensitive than T2*-weighted protocols for the detection of areas of hemorrhage. FS PD-weighted FSE images can also be used to demonstrate areas of subchondral marrow hyperemia. T1-weighted images, however, adequately demonstrate the morphology of fracture segments and the continuity of articular cartilage surfaces.

Chondral lesions of the posteromedial superior humeral head are associated with SLAP tears and are referred to as SLAP fractures (Fig. 8.363).²²⁷ These chondral injuries should not be mistaken for the more posterolateral Hill-Sachs deformity of the humeral head.²⁹⁷ There may be a relative lack of subchondral edema in shearing chondral injuries. True osteochondral fractures extend into subchondral bone and are frequently associated with loose bodies (Fig. 8.364).

Avascular Necrosis

Avascular necrosis (AVN) may occur in association with three- and four-part fractures in which the main arterial supply (Fig. 8.365) to the humeral head is at risk from injury to a branch of the anterior humeral circumflex artery²⁹⁸ and its intraosseous anastomoses. This may occur even in the absence of humeral head displacement.²⁹⁶ Nontraumatic AVN of the humeral head (Fig. 8.366) may be either idiopathic or secondary to a variety of systemic conditions, including:²⁹⁶

Steroid use, including post-transplantation therapy
Dysbaric disorders
Vasculitis
Alcoholism
Sickle cell disease
Hyperuricemia
Gaucher disease
Pancreatitis
Familial hyperlipidemia
Lymphoma

AVN of the humeral head can usually be differentiated from osteoarthritis by the involvement of subchondral low-signal-intensity ischemia limited to the humerus, without associated glenoid involvement (i.e., sclerosis) (Fig. 8.367). AVN demonstrates a serpiginous pattern of involvement that may be identified in both metaphyseal and subarticular locations. A double line sign (a hyperintense inner border and a hypointense peripheral border on T2-weighted images) and an extended pattern of marrow edema are associated findings. AVN can be visualized on MR within 3 months after proximal humeral head fractures (Fig. 8.368).

The Neer classification for AVN of the humeral head is similar to the Ficat staging for hip osteonecrosis:²⁹⁹

Stage 1: Asymptomatic; conventional radiographs produce negative results, whereas MR imaging results are positive for alterations in subchondral marrow (Fig. 8.369).
Stage 2: Clinically characterized by pain; the humeral head retains its specific shape, although mild depression of the articular cartilage may be present in an area of subchondral bone.
Stage 3: Subchondral collapse or fracture with overlying articular cartilage irregularity is seen. No involvement of the glenohumeral joint articular cartilage is found.
Stage 4: Incongruity of the glenohumeral joint

Paget—s disease of the humerus (Fig. 8.370) also produces marrow changes, especially in the paratrabecular endosteal areas, which may be mistaken for ischemic disease.

Infection

Pearls and Pitfalls

Infection

T1-weighted images in at least one plane provide yellow marrow fat contrast relative to the patchy hypointensity of osseous osteomyelitis.

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T2* GRE images, although not sensitive for infection, can increase specificity in the diagnosis of osteomyelitis if areas of trabecular hyperintensity are shown. A non-marrow-sensitive sequence that demonstrates hyperintensity in association with joint sepsis is consistent with the spread or extension of osteomyelitis.
Intravenous contrast, although not specific for osteomyelitis, is used to enhance soft tissue tracts and abscesses, which may communicate with adjacent osseous erosions.

FIGURE 8.359 ● (A) Fracture of the anatomic neck as the articular segment. (A one-part fracture has no or minimal displacement or angulation. A two-part fracture has one segment displaced. A three-part fracture has two segments displaced with one tuberosity in continuity with the head. A four-part fracture has three segments displaced.) (B) Coronal PD FSE image of a displaced two-part fracture of the anatomic neck with proximal displacement of the diaphysis relative to the medial articular segment. (C) Axial PD FSE image showing the three-fragment sign of the shaft, anatomic neck, and glenoid visualized on a single axial image.

FIGURE 8.360 ● (A) Nondisplaced greater tuberosity fracture. Fractures of the greater tuberosity are associated with anterior dislocations. A greater tuberosity fracture usually reduces into a acceptable anatomic position but may displace underneath the acromial process or be directed posteriorly by the pull of the rotator cuff muscles. Impacted greater tuberosity fracture without superior displacement on coronal PD FSE (B) and FS PD FSE (C) images.

FIGURE 8.361 ● Axial FS PD FSE image showing a lesser tuberosity fracture associated with a posterior labral tear and dislocation. A fracture of the lesser tuberosity may be pulled anteriorly and medially by the subscapularis muscle.

FIGURE 8.362 ● (A) Surgical neck fracture with no displacement. Surgical neck fracture with minimal angulation on coronal PD FSE (B) and FS PD FSE (C) images. A fall onto the outstretched hand is the most common mechanism for a proximal humerus fracture.

FIGURE 8.363 ● (A) Coronal FS T1-weighted MR arthrogram of the posteromedial location of a SLAP fracture of the articular surface of the superior humeral head caused by a fall onto an outstretched arm. A chondral divot can be seen in the superior dome of the humeral head. (B) Corresponding gross dissection of the SLAP fracture. (From

Stoller DW. MRI, arthroscopy, and surgical anatomy of the joints. Philadelphia: Lippincott-Raven, 1999

, with permission.)

FIGURE 8.364 ● Focal osteochondral lesion involving the chondral and subchondral bone of the superior humeral head. Loose bodies are demonstrated in the axillary pouch on this coronal FS PD FSE image.

FIGURE 8.365 ● Coronal color graphic view of the blood supply of the humeral head. The major or primary vascular supply to the humeral head is from the anterior humeral circumflex artery. The arcuate artery, a continuation of the ascending branch of the anterior humeral circumflex, supplies the humeral head, including the greater and lesser tuberosities. A secondary or smaller contribution to the humeral head blood supply is derived from branches of the posterior circumflex artery and the tendinous–osseous anastomoses of the vascular rotator cuff.

FIGURE 8.366 ● Localized nontraumatic AVN associated with systemic lupus erythematosus. Lupus patients who are not on glucocorticoids or immunosuppressive drugs are at increased risk for septic arthritis and osteonecrosis. Osteonecrosis occurs in 4% to 15% of lupus patients and affects the humeral head in 80% of cases. (A) Color coronal illustration anterior view of osteonecrosis with subchondral fracture. Corresponding coronal PD FSE (B) and FS PD FSE (C) images demonstrate AVN prior to subchondral collapse. The double line sign of osteonecrosis consists of a hyperintense inner border and a hypointense outer margin on the FS PD FSE image (C).

FIGURE 8.367 ● Nondisplaced surgical neck and greater tuberosity fracture with humeral head AVN on coronal PD FSE (A) and FS PD FSE (B) images.

Intra-articular sepsis³⁰⁰ of the shoulder is classified as:

Hematogenous
Secondary to contiguous spread from osteomyelitis
Secondary to trauma, surgery, or intra-articular injection (Fig. 8.371)

Osteomyelitis of the humerus may extend to involve the joint directly. Septic arthritis of the shoulder commonly affects the glenohumeral joint (Fig. 8.372). Sarcoidosis of the shoulder frequently demonstrates a hypertrophic synovial inflammatory reaction simulating infection (Fig. 8.373). Hematogenous osteomyelitis is more frequent (80% to 90%) in children. In adults contiguous spread of osteomyelitis is usually secondary to surgery or direct inoculation (Figs. 8.374 and 8.375).

Clinical or imaging follow-up is recommended to exclude continuing infection and the development of osseous spread. In the shoulder, the humerus is the most frequently involved bone. In injection drug users the clavicle may be involved secondary to hematogenous seeding. MR findings include synovial fluid inhomogeneity and non-rheumatoid-type synovial hypertrophy. Subtle osseous erosions of the humerus with adjacent reactive marrow edema are seen in the initial stages of osteomyelitis. Inhomogeneous or patchy areas of hypointense humeral head and glenoid marrow involvement frequently require a T1-weighted sequence to appreciate osseous involvement. Hyperintensity of marrow visualized on T2* GRE images is suspicious for involvement of osteomyelitis in the presence of intra-articular sepsis. Since GRE imaging is not a marrow-sensitive technique, any signs of destruction of trabecular bone and/or influx of free water are more serious indicators of contiguous spread. FS PD FSE and STIR images may be sensitive but are not nonspecific with respect to marrow hyperintensity and distinguishing reactive edema from infection. Enlarged axillary lymph nodes (Fig. 8.376) may be seen in malignancy and infection and are best assessed on sagittal images. Metastatic disease may be mistaken for infection. In metastatic disease there is bone marrow involvement with trabecular destruction and less tissue reaction. Fibrous dysplasia may present in multiple locations in the polyostotic form (Fig. 8.377).

Shoulder Replacement

Glenohumeral arthroplasty ²⁹³ includes nonprosthetic arthroplasty, prosthetic humeral hemiarthroplasty, and total glenohumeral arthroplasty. Prosthetic humeral hemiarthroplasty is often used in cases of combined arthritis and cuff deficiency, whereas total shoulder arthroplasty is recommended in osteoarthritis and rheumatoid arthritis when the rotator cuff is intact. MR evaluation is useful in selecting the most appropriate type of procedure by quantifying the rotator cuff integrity, fatty atrophy, and fracture union. Further, MR evaluation of the deltoid muscle is important, since shoulder prostheses cannot function if the deltoid is atrophied.

A reverse shoulder replacement (Fig. 8.378)³⁰¹^,³⁰² has been designed for cases of deficient rotator cuff and arthritis (rotator cuff tear arthropathy), complex fractures, or revision

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of a failed joint replacement with a chronically torn and atrophied rotator cuff. In the reverse shoulder replacement, the glenoid socket is replaced with an artificial ball and the humeral head is replaced by a socket implant. This configuration thus reverses the normal relationship of the humeral head to the glenoid.

FIGURE 8.368 ● Development of humeral head AVN 3 months after anatomic neck fracture with involvement of the greater tuberosity. This pattern of deep subchondral ischemia demonstrates morphologic features of a bone infarct. (A) Coronal PD FSE at initial fracture. (B) Coronal PD FSE 3 months after fracture. (C) Coronal FS PD FSE 3 months after fracture.

FIGURE 8.369 ● A minimally (<1 cm) displaced surgical neck fracture with AVN of the humeral head on coronal PD FSE (A) and sagittal PD FSE (B) images.

FIGURE 8.370 ● Coronal PD FSE image showing increased osseous resorption and bone formation, characteristic changes of Paget—s disease. The osseous appearance may mimic fracture and metastatic carcinoma. The three phases of Paget—s disease are lytic, mixed lytic and blastic, and blastic phases. Pagetoid marrow contains new bone formation and fibrovascular tissue and is at an increased risk for fracture.

FIGURE 8.371 ● Axial FS PD FSE image of osteomyelitis secondary to injection of steroids with focal posterior humeral head erosion and soft tissue hyperintense complex fluid collection.

FIGURE 8.372 ● Septic shoulder with a hyperintense outline of inflammatory fluid within the axillary pouch as seen on coronal PD FSE (A) and FS PD FSE (B) images. There is no osseous involvement at this stage.

FIGURE 8.373 ● Sarcoid inflammatory reaction may be mistaken for a septic joint. Inflammatory arthropathy is a common feature of sarcoidosis.

FIGURE 8.374 ● Sagittal FS PD FSE image of an inflammatory tract with myositis that developed as a reaction to a flu inoculation.

FIGURE 8.375 ● Rarely, infectious myositis is complicated by a muscle infarction. Fibrotic myopathy, which usually involves the deltoid and quadriceps, may produce similar muscle hypointensity as a complication of direct intramuscular injection of drugs, as seen on this axial FS PD FSE image.

FIGURE 8.376 ● Sagittal FS PD FSE image showing enlarged axillary lymph nodes in chronic lymphocytic leukemia.

FIGURE 8.377 ● Osseous involvement of the glenoid and clavicle in polyostotic fibrous dysplasia, which may be mistaken for infection or metastatic disease, is seen on this sagittal FS PD FSE image.

FIGURE 8.378 ● (A) Reverse shoulder replacement optimizes the force of the deltoid (by increasing the lever arm) and stabilizes the glenohumeral articulation by moving the center of rotation of the glenohumeral joint medially and inferiorly. This provides an increased mechanical advantage for raising the arm overhead. Non-union of a surgical neck fracture complicated by humeral head AVN on a coronal FS PD image (B) and a corresponding sagittal PD FSE image (C). The sagittal plane image demonstrates severe supraspinatus atrophy with a rotator cuff deficient shoulder, fracture non-union, and humeral head AVN. Reverse prostheses may be used to direct forces through the glenosphere, converting centrifugal or outward forces into centripetal or inward forces.

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