Making Sense of the “Alphabet Soup” Lesions Associated with Anterior and Posterior Glenohumeral Instability

The anatomy of the glenohumeral joint allows for a wide range of motion. Unfortunately, the trade-off is instability, as it is the most commonly dislocated joint in the human body.^1-2 Shoulder instability is commonly encountered in patients presenting with acute and/or chronic shoulder pain. Glenohumeral joint instability can be classified in a number of ways including frequency (acute, chronic, recurrent), degree (subluxation or dislocation), etiology (traumatic, atraumatic, or repetitive microtrauma), and direction (anterior, posterior, inferior, multidirectional).² Instability of the glenohumeral joint may also be divided into the categories of macroinstability and microinstability.^3-4 Macroinstability can be further categorized as traumatic, unidirectional, Bankart, requiring surgery (TUBS) and atraumatic, multidirectional, often bilateral, requires rehabilitation as first-line therapy, inferior capsular shift (AMBRI) as the best alternative (surgical) therapy.^3-6 AMBRI typically results from acquired instability due to repeated forced abduction-external rotation of the upper extremity, as is often seen in overhead athletes. The most common type of glenohumeral joint instability is macroinstability due to traumatic anterior dislocation.^3,4,7,8 Microinstability may lead to injuries involving the superior labrum, middle glenohumeral ligament, rotator interval structures, or rotator cuff and has a reported incidence of 5% in patients with shoulder pain.² The structures of the coracoacromial arch help prevent superior macroinstability. Microinstability therefore leads to subluxation and, as a result, does not present with frank clinical instability. Multidirectional instability is more often due to congenital laxity of the joint and is often bilateral. It is usually treated conservatively with physical therapy to strengthen the rotator cuff muscles. When patients with multidirectional instability fail conservative therapy, surgical techniques such as a capsular shift are undertaken. A more in-depth discussion of multidirectional instability is beyond the scope of this article.

Diagnostic imaging plays an important role in directing the management of patients with glenohumeral joint instability. Anteroinferior, posterior, and superior labral lesions have been identified as the three main classes of labral injuries seen in the setting of glenohumeral instability.² In this review article, we will discuss the normal anatomy of the labroligamentous complex as well as pathologic lesions, with a primary focus on the “alphabet soup” lesions encountered in the setting of anterior and posterior glenohumeral joint instability.

Instability of the glenohumeral joint may result from the loss of function of the static and dynamic stabilizers. The static stabilizers of the glenohumeral joint include the osseous configuration of the glenoid and humeral head, the glenoid labrum, the glenohumeral joint capsule, and the glenohumeral ligaments. Dynamic stabilizers of the glenohumeral joint include the rotator cuff muscles and tendons as well as the long head of the biceps tendon.

The glenoid labrum is a fibrocartilaginous structure that may have a rounded, blunted, or triangular appearance. Due to most of its composition consisting primarily of type I collagen, the labrum typically appears dark on all MRI pulse sequences. The labrum contributes to the depth, surface area, as well as a vacuum phenomenon between the labrum and humeral head, thus adding stability to the glenohumeral joint.^2,9,10,11 It also serves as a site of attachment for the long head of the biceps tendon and the glenohumeral ligaments.

Methods differ as to how to describe the location of labral pathology on an MRI or MR arthrogram of the shoulder. The orthopedic literature generally subscribes to a clockface convention (Figure 1A) with the midsuperior labrum designated as the 12-o’clock position and the midinferior labrum as the 6-o’clock position. Much of the controversy related to the clockface convention revolves around the assignment of the 3- and 9-o’clock positions on right vs left shoulders. In general, most radiologists who utilize the clockface convention designate the anterior labrum as the 3-o’clock position regardless of whether they are interpreting a right or left shoulder MRI. Orthopedic surgeons typically designate the anterior labrum as 3 o’clock in the right shoulder and 9 o’clock in the left shoulder. Alternatively, and as employed by the musculoskeletal radiologists at the primary author’s institution, the location of labral pathology can be described as that found in any of eight anatomic regions (Figure 1B).^2,12 

The glenoid labrum is generally firmly attached to the oval- or pear-shaped glenoid rim with the exception of a few common congenital variants typically seen in the 12- to 3-o’clock positions. The anterosuperior region is where normal variants known as the superior labral recess, the sublabral foramen, and the Buford complex may be encountered. The superior labral recess, also known as the sublabral sulcus, occurs between the 11- and 1-o’clock regions. It is the most common labral variant (Figure 2) and has a reported prevalence of up to 73% in cadaver studies.² The sublabral foramen (not shown), with an incidence of 11% to 15%, and the Buford complex, with an incidence of 1.5%, are typically found in the 1- to 3-o’clock positions.⁹ The Buford complex consists of an absent anterosuperior glenoid labrum and a cord-like middle glenohumeral ligament (Figure 3). The radiologist should be familiar with these entities to avoid mistaking them for pathology in the form of labral tears. Linear signal intensity that is parallel to the articular cartilage along the superior margin of the glenoid is more likely to be a normal variant, whereas high-signal intensity that extends laterally, or in a nonparallel fashion to the glenoid articular cartilage, is more likely to be a superior labral tear extending from anterior to posterior (SLAP) (Figure 4). 

The anterior glenohumeral joint capsule has been shown to vary in its attachment to the glenoid. Mosely and Overgaard have classified the anterior glenohumeral capsular insertion into one of three types: Type I anterior capsular insertion inserts on the labrum, type II capsular insertion inserts within 1 cm of the glenolabral junction, and type III anterior capsular insertion inserts more than 1 cm medial to the glenolabral junction along the cortex of the glenoid neck. ¹³ Type III anterior capsular insertions are associated with anterior glenohumeral instability.³ Similar to the anterior-capsular insertion, the insertion of the posterior glenohumeral joint capsule has also shown variability at MRI and MR arthrography (MRA).¹⁴

The superior, middle, and inferior glenohumeral ligaments (IGHLs) serve as the primary passive stabilizers of the glenohumeral joint. The glenohumeral ligaments reinforce the glenohumeral joint capsule and appear as thick, low-signal intensity bands, which are best appreciated on MRA (Figure 5). The IGHL is considered the most important passive stabilizer of the glenohumeral joint.^3,7

Anterior glenohumeral instability most commonly occurs in the setting of a prior anterior dislocation of the glenohumeral joint. Signs of previous traumatic dislocation of the glenohumeral joint such as a Hill-Sachs and bony Bankart, soft-tissue Bankart, or a Bankart variant are often apparent at radiography, CT, MR, CT arthrography, or MRA in these situations. Sheer and impaction forces exerted by the humeral head upon the glenoid contribute to injury of the anteroinferior glenoid labrum resulting in a Bankart or Bankart-like variants.

Several anteroinferior and posterior labroligamentous injuries resulting from glenohumeral joint instability have been described in the literature. Most of these lesions require different forms of surgical repair and, as such, accurate preoperative characterization is paramount to the orthopedic surgeon.^15,16

Imaging Workup

The diagnostic imaging workup for shoulder instability begins with radiographs (Figure 6). Anteroposterior (AP), AP Grashey, and axillary views are preferred.³ MRI or MRA are typically the next step in the diagnostic workup. In situations in which patients have a relative or an absolute contraindication to MRI, CT and CT arthrography can be utilized. In the acute setting, the presence of a joint effusion may provide adequate intra-articular fluid for exclusion of pathology. MRA is particularly useful in evaluating for labroligamentous pathology, particularly in the subacute and chronic settings where there is often a lack of intra-articular fluid.

MRI and MRA provide the most comprehensive evaluation prior to diagnostic and surgical arthroscopy. In general, MRA is considered superior to conventional MR imaging in detecting labroligamentous pathology.^7,17-21 Indications for MRA typically include a history of instability and/or concern for labral pathology. MRA may be performed via direct or indirect methods. The direct method entails intra-articular needle placement followed by distension of the joint with a dilute gadolinium-based solution followed by MRI. An indirect approach typically entails intravenous administration of 0.1 mmol per kilogram of body weight of a gadolinium-based contrast agent. The patient is then asked to exercise the joint for 10 minutes, followed by MRI. At our institution, we typically perform direct MRA utilizing a mixture of 10 cc of sterile saline, 10 cc of Omnipaque 300 mg/mL, and 0.10 cc of gadolinium. The injection is typically done via sterile technique utilizing fluoroscopic guidance from an anterior approach through the rotator cuff interval with a 3.5-inch, 22-gauge spinal needle.²² The MR portion of the examination is ideally undertaken as soon as possible after the injection.

When tolerated by the patient, additional imaging is performed by moving the arm from the neutral position to abduction and external rotation (ABER) alongside the patient. This positioning places tension on the anterior band of the IGHL making lesions along the anteroinferior glenoid labrum more conspicuous at MRA as contrast will extend into any defects or tears along the anteroinferior labrocartilaginous interface. The scan plane is aligned along the long axis of the humeral shaft. This position is often difficult for patients to tolerate due to pain or apprehension. The anteroinferior labrum and the anterior band of the IGHL are best evaluated on an axial oblique sequence with the patient’s shoulder in abduction and external rotation.^23-24 The ABER position also allows for the evaluation of subtle undersurface fraying or articular surface rotator cuff tears, which will fill with contrast as the tension is reduced on the supraspinatus and infraspinatus tendons in this position. In general, when the planes of the ABER sequence are appropriately prescribed, the coracoid process can serve as a landmark to indicate the 2- to 3-o’clock position of the glenoid labrum. Scrolling inferiorly from this point allows for scrutiny of the 5- to 7-o’clock position of the anteroinferior labrum, which is the classic location for Bankart and Bankart-like variants. The normal anatomy of the ABER sequence is depicted in Figure 7.

Lesions Associated With Anterior Instability

Anteroinferior labral lesions occur in the setting of a previous anterior dislocation of the glenohumeral joint and typically result in a Bankart lesion or Bankart variant. A classic Bankart lesion is most common and consists of detachment of the anteroinferior labrum and the attached anterior band of the IGHL, usually in the 3- to 6-o’clock positions.^15,25-26 The lesion is termed a bony Bankart lesion if a portion of the anteroinferior glenoid rim is also detached along with the labrum. Of note, the anterior scapular periosteum is disrupted in both soft tissue and bony Bankart lesions (Figures 8, 9). Surgical repair of Bankart lesions is usually required due to their poor propensity to heal.

Bankart lesions are the most common injury following an anterior dislocation of the glenohumeral joint. They commonly occur in patients under age 35 who have dislocated their shoulder for the first time. Bankart lesions can be broken down into either soft-tissue (fibrocartilaginous) or bony (osseous) types. Soft-tissue Bankart lesions consist of avulsion of the anterior labroligamentous complex with rupture of the anterior scapular periosteum. Bony Bankart lesions include an additional anterior glenoid rim fracture. It is important to note that rupture of the anterior scapular periosteum is the key finding that separates soft-tissue and bony Bankart lesions from the remainder of the Bankart variants. Bony Bankart lesions can sometimes be quite subtle. Scrutiny of the expected pear-shaped glenoid on the sagittal sequences can often aid in differentiation between a fibrous and bony Bankart lesion (Figure 10). Glenoid bone loss may occur as comminuted or noncomminuted fragments in the acute post-traumatic setting or as erosive change due to chronic instability. On average, the glenoid is 24 mm wide and just 6 mm of glenoid bone loss equates to loss of nearly 25% of the articular surface of the glenoid. Since the osseous anatomy of the normal glenohumeral joint provides little osseous constraint from the get-go, bone loss can play a significant factor in magnifying the degree of clinical instability. Various methods with respect to the quantification of glenoid bone loss via CT and MRI have been described in the literature.^3,27-29 Glenoid bone loss of 25% is the generally accepted threshold for surgical correction. It is therefore vital for the imaging report to quantify the amount of glenoid bone loss as it directly impacts the orthopedic surgeon’s clinical decision-making as whether to proceed with an instability repair or a Bristow-Latarjet open coracoid transfer.

Hill-Sachs lesions result from impaction of the posterosuperior humeral head against the anterior glenoid during anterior dislocation of the glenohumeral joint. Hill-Sachs lesions are easy to miss when they are small. Scrutiny of the posterosuperior head on the first 2-3 axial images at and above the level of the coracoid process is necessary to diagnose a Hill-Sachs lesion. In the normal setting, this portion of the humeral head typically maintains a round shape. In the setting of a Hill-Sachs lesion, the posterosuperior aspect of the humeral head appears to be flattened or concave (Figure 11). Bone marrow edema may be absent on fluid-sensitive sequences in the setting of a chronic Hill-Sachs lesion. When sizeable, Hill-Sachs lesions can take on the appearance of a wedge-shaped defect along the posterosuperior aspect of the humeral head on axial, coronal, and sagittal sequences. Due to their frequent association with Bankart lesions, the presence of a Hill-Sachs lesion should prompt close evaluation of the anteroinferior glenoid labrum for Bankart and Bankart-like variants. As discussed, the combination of any degree of glenoid and humeral head bone loss often magnifies the degree of clinical instability and different methods of calculating the degree of bipolar bone loss in the preoperative setting via CT and MRI have been described.^3,27-29 Based on these quantification methods, Hill-Sachs lesions are classified as either on-track (nonengaging) or off-track (engaging) lesions. The glenoid track concept provides a method to predict which Hill-Sachs lesions are more likely to engage the anteroinferior rim of the glenoid when the shoulder is placed in the provocative position of abduction and external rotation at arthroscopy. By classifying a Hills-Sachs lesion using the glenoid track concept, the radiologist adds value to the imaging report by guiding the orthopedic surgeon in clinical decision-making in the preoperative setting. Hill-Sachs lesions may require bone grafting or remplissage.

The Perthes lesion consists of a nondisplaced detachment of the anteroinferior labrum with an intact anterior scapular periosteum.^15,30 Minimal stripping of the anterior scapsular periosteum may be encountered with a Perthes lesion. These lesions have a propensity to resynovialize in situ and thus are usually treated conservatively. Perthes lesions can be difficult to detect at arthroscopy and are best detected on the ABER sequence of an MR arthrogram (Figure 12).

Anterior labroligamentous periosteal sleeve avulsion (ALPSA) consists of a detachment of the anteroinferior labrum with an intact and stripped anterior scapular periosteum. The IGHL, labrum, and periosteum are stripped and medially displaced along the anterior neck of the scapula.¹⁵ Imaging of the patient in the ABER position can greatly increase the conspicuity of an ALPSA lesion, which can easily be overlooked on a routine MRI of the shoulder or on the standard axial sequence of an MRA. ALPSA lesions are typically encountered in more of a chronic setting in patients with a history of multiple prior dislocations. These lesions have a propensity to scar down medially in the chronic setting, thus complicating surgical repair (Figure 13). The treatment of ALPSA lesions includes mobilization of the lesion by completing the Bankart lesion followed by reconstruction of the anteroinferior glenoid labrum.

Glenolabral articular disruption (GLAD) lesions are a rare Bankart variant that typically result from forced adduction and subluxation of the shoulder (Figure 14). Impaction of the humeral head upon the glenoid results in a partial tear of the anteroinferior labrum along with a defect in the adjacent articular cartilage. The adjacent anterior scapular periosteum remains intact and tightly adherent to the scapula.¹⁶ Repair of the labral tear and debridement of the articular cartilage injury are typically undertaken to address a GLAD lesion.³¹

It is also not uncommon for patients to present with imaging findings due to a combination of Bankart variants (Figure 15). In such cases, it is best to make the imaging report as descriptive as possible.

Inferior Glenohumeral Ligament Complex Injuries

The IGHL complex is a hammock-like structure that extends from the humeral neck to the inferior glenoid and glenoid labrum. The anterior band originates from the 2- to 4-o’clock position of the glenoid. The posterior band originates from the 7- to 9-o’clock position of the glenoid. The axillary pouch resides between the anterior and posterior bands. The humeral insertion of the IGHL either consists of a collar-like attachment just below the articular margin or a V-shaped attachment whereby the anterior and posterior bands insert just below the articular margin and the axillary pouch inserts more distal to the articular margin. The IGHL helps prevent anterior and posterior translation of the humeral head.^7,10,32-36 The anterior band of the IGHL is the most important of the glenohumeral ligaments. IGHL complex injuries typically result from anterior dislocations of the shoulder, which lead to anterior instability of the glenohumeral joint. The IGHL may fail at its humeral or glenoid attachments, or along the axillary pouch. Failure at these sites results in humeral avulsion of the glenohumeral ligament (HAGL), bony humeral avulsion of the glenohumeral ligament (BHAGL), glenoid avulsion of the glenohumeral ligament (GAGL), and tears of the axillary pouch, respectively.³⁷

Humeral Avulsion of the Glenohumeral Ligament

Humeral avulsion of the glenohumeral ligament is an infrequent cause of anterior glenohumeral instability and can be challenging to diagnose accurately with MRI and MRA.³⁷ It is most often due to hyperabduction and external rotation of the glenohumeral joint and contributes to anterior instability. MRI findings associated with HAGL lesions have been classically described to include a J-shaped as opposed to a U-shaped IGHL and joint capsule as well as edema and extravasation of joint fluid or contrast along the medial aspect of the proximal humerus (Figure 16).^38-39 Case series have shown there can be a high instance of false-positive preoperative imaging findings in which these findings are present on imaging but no HAGL is encountered on follow-up arthroscopy.³⁷ These authors proposed that a J sign or fluid extravasation along the medial humeral neck be described as a defect in the IGHL complex rather than making the precise diagnosis of a HAGL lesion.

Bony Humeral Avulsion of the Glenohumeral Ligament

Bony avulsion at the attachment site of the IGHL along the medial cortex (Figure 17) occurs in a small percentage of HAGL lesions and can easily be overlooked at imaging, particularly on an MRI.³⁷ Bony avulsion of the humeral insertion of the glenohumeral ligament often results from an anterior shoulder dislocation and contributes to anterior instability of the glenohumeral joint. BHAGL lesions are often associated with a tear of the subscapularis tendon.

Glenoid Avulsion of the Glenohumeral Ligament

GAGL lesions can be quite difficult to diagnose preoperatively and are even more rare than their previously discussed counterparts. Glenoid avulsion of the glenohumeral ligament is similar to a HAGL lesion; however, the injury takes place along the glenoid attachment as opposed to the humeral attachment. The IGHL is either completely avulsed or is stripped off along with the scapular periosteum. It should be noted that in the setting of a GAGL lesion, the glenoid labrum remains attached to the glenoid while the IGHL complex becomes detached from the labrum and glenoid.⁴⁰ It is the intact labrum that differentiates the GAGL from the soft-tissue Bankart and Bankart-like variants.⁴⁰ As with the HAGL lesion, the diagnosis of a GAGL lesion is best made at arthroscopy.

Axillary Pouch Tears

Severe or repetitive trauma may result in a tear of the midsubstance of the axillary pouch. The clinical picture may present similar to adhesive capsulitis. Extravasation of contrast from the inferior axillary pouch is demonstrated on standard MRI and MRA with intact humeral and glenoid attachments of the anterior and posterior bands of the IGHL.

Posterior Glenohumeral Instability and Posterior Labral Lesions

Posterior instability accounts for approximately 10% of cases of glenohumeral instability.⁴¹ Recurrent posterior subluxation is the most common type of posterior shoulder instability.⁴¹ Posterior dislocations of the glenohumeral joint account for only 2% to 4% of all traumatic dislocations.⁹ Patients at risk for posterior instability and dislocation include football linemen and those with a history of seizures, electrocution, heavy weight-lifting, and military background. These activities impart repetitive posteriorly directed loads to the glenohumeral joint predisposing these patients to posterior instability. Patients with congenital or acquired dysplasia or retroversion of the glenoid > 5 to 10 degrees are also predisposed to developing posterior instability.⁴¹ Patients with glenoid retroversion of > 15 degrees are known to have high failure rates of primary soft-tissue repair and may require more extensive surgical repairs including bony reconstruction or augmentation of the posterior glenoid using a variety of techniques.⁴¹

The lightbulb sign is a classic radiographic finding of a posterior dislocation of the glenohumeral joint on AP views with internal and external rotation of the humerus (Figure 18). Reverse Hill-Sachs and Bankart lesions may be seen on axial radiographs, CT scans or MRI of the shoulder.

Reverse Hill-Sachs and Reverse Bony Bankart Lesions

Posterior dislocation of the shoulder results in reverse Hill-Sachs and Bankart lesions. The reverse Hill-Sachs lesion is also known as the trough sign. It is an impaction fracture of the anteromedial humeral head. On axillary radiographs, CT and MRI, reverse Hill-Sachs consist of a wedge-shaped defect along the anteromedial aspect of the humeral head (Figures 19, 20, 21).

Similar to its anterior counterpart, posterior dislocation of the glenohumeral joint results in reverse Bankart and Hill-Sachs lesions. The reverse Bankart lesion consists of detachment of the posterior labrum in the 6- to 10-o’clock regions with rupture of the posterior scapular periosteum and joint capsule. Reverse Bankart lesions may also be classified as soft-tissue (fibrocartilaginous) or bony lesions. A reverse Bankart lesion typically requires surgical repair.

Posterior GLAD Lesion

A posterior GLAD lesion is similar to its anterior counterpart. Posterior GLAD lesions consist of a cartilaginous injury and labral tear along the 7- to 9-o’clock positions of the glenoid (Figure 22).

Kim Lesion

Kim lesions are characterized by a subtle marginal crack along the junction between the posteroinferior glenoid and posterior labrum while the labrum remains nondisplaced (Figure 23). These lesions are thought to occur due to chronic, repetitive subluxation, often in the setting of slight retroversion of the glenoid. The administration of intra-articular contrast for an MRA often causes the deep, and often arthroscopically occult, portion of the lesion to fill with contrast. Surgical management of a Kim lesion consists of completion of the labral tear followed by reattachment with a suture anchor.²

Posterior Labrocapsular Periosteal Sleeve Avulsion Lesion

Recurrent posterior subluxation or dislocation of the glenohumeral joint or a locked posterior dislocation can result in detachment of the posterior labrum and stripping of the posterior scapular periosteum (Figure 24). The combination of such findings is termed a posterior labroligamentous periosteal sleeve avulsion, or POLPSA lesion. Similar to its anterior counterpart, a POLPSA lesion is differentiated from a reverse Bankart lesion based on the presence of an intact scapular periosteum. Surgical repair of a POLPSA lesion requires a reduction of the stripped periosteum prior to the labrum being reattached. Chronic POLPSA lesions can be associated with Bennett lesions that result from chronic repetitive stress and traction upon the posterior band of the IGHL insertion. Over time, calcification of the posterior band of the IGHL develops and can best be appreciated on an axillary radiograph or CT scan.

Summary

In summary, the list of acronyms associated with labral lesions in the setting of glenohumeral joint instability can be daunting. When encountering any of these lesions in daily practice, it is best to emphasize the essential pathoanatomic features of the lesion and any associated injuries in the imaging report rather than the alphabet soup designation it will be assigned. Accurate interpretation of key imaging findings and normal variants on preoperative MRI and MRA is of paramount importance in directing the orthopedic management of these lesions.

References

1. Tirman PFJ. Glenohumeral instability. In: Steinbach LS, Tirman PFJ, Peterfy CG, Feller JF, eds. Shoulder Magnetic Resonance Imaging. Lippincott-Raven;1998.
2. De Coninck T, Ngai S, Tafur M, Chung C. Imaging the glenoid labrum and labral tears. RadioGraphics 2016;36:1628-1647.
3. De Filippo M, Schiro S, Sarohia D, et al. Imaging of shoulder instability. Skeletal Radiol 2020;49:1505-1523.
4. Matsen FA 3rd, Harryman DT 2nd, Sidles JA. Mechanics of glenohumeral instability. Clin Sports Med 1991;10(4):783-788.
5. Gerber C, Nyffeler RW. Classification of glenohumeral joint instability. Clin Orthop Related Res. 2002;400:65-76.
6. Palmer W, Bancroft L, Bonar F, et al. Glossary of terms for musculoskeletal radiology. Skeletal Radiol 2020;49(Suppl 1):S1-S33.
7. Waldt S, Burkart A, Imhoff AB, et al. Anterior shoulder instability: accuracy of MR arthrography in the classification of anteroinferior labroligamentous injuries. Radiology 2005;237:578-583.
8. Bencardino JT, Gyftopoulos S, Palmer WE. Imaging in anterior glenohumeral instability. Radiology 2013;269:323-337.
9. Stoller DW. Chapter 8. Magnetic Resonance Imaging in Orthopedics and Sports Medicine. 3^rded. Lippincott Williams & Wilkins; 2006:1353.
10. Wolf EM, Cheng JC, Dickson K. Humeral avulsion of glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy 1995;11(5):600-607.
11. Howell SM, Galinat BJ. The glenoid-labral socket: a constrained articular surface. Clin Orthop Relat Res 1989;(243):122-125.
12. Chang D, Mohana-Borges A, Borso M, Chung CB. SLAP lesions: anatomy, clinical presentation, MR imaging diagnosis and characterization. Eur J Radiol 2008;68(1):72-87.
13. Mosely HF, Overgaard B. The anterior capsular mechanism in recurrent anterior dislocation of the shoulder. J Bone Joint Surg Br. 1962;44-B(4):913-920.
14. Park YH, Lee JY, Moon SH, et al. MR arthrography of the labral capsular ligamentous complex in the shoulder: Imaging variations and Pitfalls. Am J Roentgenol 2000;175:667-672.
15. Nevasier TJ. The anterior labroligamentous periosteal sleeve avulsion lesion: a cause of anterior instability of the shoulder. Arthroscopy 1993;9:17-21.
16. Nevasier TJ. The GLAD lesion: another cause of anterior shoulder pain. Arthroscopy 1993;9:22-23.
17. Beltran J, Bencardino J, Mellado J, Rosenberg ZS, Irish RD. MR arthrography of the shoulder: variants and pitfalls. RadioGraphics 1997;17(6):1403-1412.
18. Chloros GD, Haar PJ Loghran TP, Hayes CW. Imaging of glenoid labrum lesions. Clin Sports Med 2013;32(3):361-390.
19. Sheridan K, Kreulen C, Kim S, Mak W, Lewis K, Marder R. Accuracy of magnetic resonance imaging to diagnose superior labrum anterior-posterior tears. Knee Surg Sports Traumatol Arthrosc 2015;23(9):2645-2650.
20. Bancardino JT, Beltran J, Rosenberg ZS, et al. Superior labrum anterior-posterior lesions: diagnosis with MR arthrography of the shoulder. Radiology 2000;214(1):267-271.
21. Major NM, Browne J, Domzalski T, Cothran RL, Helms CA. Evaluation of the glenoid labrum with 3-T MRI: Is intraarticular contrast necessary? Am J Roentgenol 2011;196(5):1139-1144.
22. Dépelteau^, H et al. Arthrography of the shoulder: a simple fluoroscopically guided approach for targeting the rotator cuff interval. Am J Roentgenol. 2004;182:329-332. 10.2214/ajr.182.2.1820329.
23. Cvitanic O, Tirman PF, Feller JF, Bost FW, Minter J, Carroll KW. Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrographgy in revealing tears of the anterior glenoid labrum. Am J Roentgenol 1997;169:837-844.
24. Chung CB, Sorenson S, Dwek JR, Resnick D. Humeral avulsion of the posterior band of the inferior glenohumeral ligament: MR arthrography and clinical correlation in 17 patients. Am J Roentgenol 2004;183:355-359.
25. Bankart AS. The pathology and treatment of recurrent dislocation of the shoulder. Br J Surg 1938;9:17-21.
26. Bankart ASB. Recurrent or habitual dislocation of the shoulder joint. Br Med J 1923;2:1132-1133.
27. Gyftopoulos S, Beltran LS, Bookman J, Rokito A. MRI evaluation of bipolar bone loss using the on-track off-track method: a feasible study. Am J Roentgenol 2015;205:848-852.
28. Di Giacomo G, Itoi E, Burkhart SS. Evolving concept of bipolar bone loss and the Hill-Sachs lesion: from “engaging/non-engaging” lesion to “on-track/off-track” lesion. Arthroscopy 2014;30(1):90-98.
29. Itoi E. ‘On-track’ and ‘off-track’ shoulder lesions. EFFORT Open Rev 2017;2(8):343-351.
30. Perthes G. Ueber operationen bei habitueller Schulterluxationen. Deutsch Z Chir 1906;85:199-227.
31. Zlatkin MB, Sanders TG. Magnetic resonance imaging of the glenoid labrum. Radiol Clin North Am 2013;51:279-297.
32. Massengill AD, Seeger LL, Yao L, et al. Labrocapsular ligamentous complex of the shoulder: normal anatomy, anatomic variation, and pitfalls of MR imaging and MR arthrography. RadioGraphics 1994;14:1211-1223.
33. Streubel PN, Krych AJ, Simone JP, et al. Anterior glenohumeral instability: a pathology-based surgical treatment strategy. J Am Acad Orthop Surg 2014;22:283-294.
34. Wolf EM, Siparsky PN. Glenoid avulsion of the glenohumeral ligaments as a cause of recurrent anterior shoulder instability. Arthroscopy 2010;26:1263-1267.
35. Pagnani MJ, Warren RF. Stabilizers of the glenohumeral joint. J Shoulder Elb Surg 1994;3:173-190.
36. Field LD, Bokar DJ, Savoie III. Humeral and glenoid detachment of the anterior inferior glenohumeral ligament: a cause of anterior shoulder instability. J Shoulder Elb Surg 1997;6:6-10.
37. Melvin JS, MacKenzie JD, Nacke E, Sennett BJ, Wells L. MRI of HAGL lesions: four arthroscopically confirmed cases of false-positive diagnoses. Am J Roentgenol 2008;191:730-734.
38. Bui-Mansfield LTB, Banks KP, Taylor DC. Humeral avulsion of the glenohumeral ligaments: the HAGL lesion. Am J Sports Med 2007;35:1960-1966.
39. Stoller DW. MR arthrography of the glenohumeral joint. Radiol Clin North Am 1997; 35:97-116.
40. O’Reilly O, Andrews K, Siparsky P. Understanding the glenoid avulsion of the glenohumeral ligaments as a cause of shoulder instability: surgical and postsurgical management. Arthros Tech 2019; 8(10):e1153-1158.
41. Antosh IJ, Tokish JM, Owens BD. Posterior shoulder instability. Sports Health 2016;8(6):520-526.