MR imaging in sports-related glenohumeral instability

Particularly in athletes, MR arthrography has been advocated for accurate depiction of labro-ligamentous injuries as well as rotator cuff pathology [5, 7‐11]. With the exception of examinations following acute shoulder dislocation, where joint effusion or hemorrhage serve as “natural” contrast media, at our institution MR arthrography is performed on a routine basis in individuals with clinical evidence of shoulder instability and in athletes with unclear shoulder pain. For intraarticular injection of contrast media, several different techniques have been described that can all successfully be employed in MR arthrography [9]. We inject 12–20 ml of a 2.5 mmol/l solution of a gadolinium chelate following fluoroscopically guided puncture of the glenohumeral joint via a classic anterior approach and verification of the intraarticular position of the needle tip by application of a small amount of iodinated contrast media. With the use of a dedicated shoulder coil transverse, coronal oblique, and sagittal oblique T1-weighted spin-echo (SE) sequences are then obtained. Fat-suppression is routinely applied in the coronal oblique plane, but not necessarily in the transverse and sagittal oblique planes. The examination is supplemented by acquisition of a coronal oblique intermediate weighted (echo time=33–45 ms) turbo spin-echo (TSE) sequence with spectral fat-saturation. In patients with anterior instability or suspected posterosuperior glenoid impingement we generally add a T1-weighted SE and/or an intermediate weighted TSE sequence in the ABER (abduction and external rotation) position, achieved by transverse oblique orientation of the images along the long axis of the humerus after flexing the elbow and placing the patient’s hand behind his head or neck (Fig. 1) [5, 9, 12]. Geometric parameters are identical for all pulse sequences with a section thickness of 3 mm and an in plane resolution of 0.4×0.3–0.5 mm.

The non-enhanced MR imaging protocol performed after acute shoulder dislocation includes a coronal oblique T1-weighted SE sequence, coronal oblique and transverse intermediate weighted TSE sequences with fat-saturation, and a sagittal oblique T2-weighted TSE sequence with the same geometric parameters as mentioned above.

Traumatic glenohumeral instability is typically initiated by a specific traumatic event, followed by other episodes of dislocation or subluxation with a unidirectional pattern [2, 7]. In the vast majority of athletes traumatic instability occurs in an anteroinferior direction when a sudden force overwhelms the anterior capsular structures while the athlete’s arm is in an abducted, externally rotated, and extended position [13]. The resulting combination of injuries represents the source of chronic instability, particularly those involving the inferior glenohumeral ligament (IGHL), which, according to the current opinion, is the most important passive stabilizer of the shoulder joint. The IGHL is formed by an anterior and a posterior band, which represent condensations of the capsule running from the inferior labrum to the humeral neck. The anteroinferior labrum and the anterior band of the IGHL together form the anteroinferior labro-ligamentous complex. The labrum is thought to serve more as an insertion site for the IGHL than to provide stability to the glenohumeral joint by deepening the glenoid fossa [13‐15]. Although generally common in sports, this type of instability is rarely observed in throwers or overhead athletes, but, if present, can cause secondary damage to the rotator cuff and the superior and posterior labrum [2].

Atraumatic glenohumeral instability is typically multidirectional and usually evident in individuals with congenital hypermobility syndrome. The diagnosis is predominantly based on the clinical examination, which uncovers bilateral affection of the shoulders in association with generalized hyperlaxity of ligaments and joints [1, 2, 35, 46]. The increased baseline laxity of the shoulder seen in athletes with generalized hypermobility is advantageous for several types of sports, but at the same time harbors a high risk of long-term injury with damage of intra- and periarticular structures [1, 2]. If conservative management fails, multidirectional instability is usually treated surgically by inferior capsular shift and closure of the rotator interval [6].

There are no specific findings to diagnose atraumatic glenohumeral instability by MR imaging or MR arthrography [46]. In most non-athletic AMBRII patients, MR arthrography shows an increased capsular volume but no or little substantial alterations of the intraarticular structures. In athletes, laxity of the capsule is frequently associated with secondary damage to the labrum and the rotator cuff [2]. The labrum may be hypoplastic or torn, but can as well appear swollen and increased in signal intensity due to more or less extensive degenerative change (Fig. 11). Further morphologic alterations can involve the biceps anchor and the articular surface of the rotator cuff [2]. MR arthrography can help with therapeutic decisions by identification or exclusion of significant intraarticular pathology that might represent an indication for surgical repair in addition to capsular reduction.

Microtraumatic glenohumeral instability is thought to result from chronic traumatization of the capsular structures in throwers and overhead athletes, such as tennis players, swimmers, and handball players. In contrast to atraumatic glenohumeral instability, microinstability is typically seen unilaterally only in the dominant shoulder of the athlete. Whereas repetitive abduction and external rotation cause microtrauma of the anterior capsule and thus can provoke anterior instability, repetitive overhead activity with abduction, flexion, and internal rotation might give rise to posterior microinstability as a result of injury to the posterior labro-ligamentous elements [4, 7, 9, 35, 46].

Structural abnormalities consecutive to microtraumatic glenohumeral instability can be depicted by MR arthrography and include laxity of the anterior or posterior capsule, labral injuries ranging from degeneration and fraying to tearing and detachment, SLAP (superior labral anteroposterior) lesions, and tears of the rotator cuff caused by secondary impingement [2].

SLAP lesions of the shoulder are common injuries in athletes which represent tears of the superior glenoid labrum that extend in an anterior to posterior direction [55, 56]. Four different types of SLAP lesions have been described in the original classification by Snyder:

This classification has been expanded with several further types of lesions, which mainly represent combinations of the most common form, the SLAP type 2 lesion, with other injuries of the labrum, medial glenohumeral ligament, or rotator cuff. However, only the Snyder classifications have found wide acceptance, and most institutions categorize these injuries as type 1–4 with or without asscociated lesions. Whereas type 1 and 2 lesions are typically caused by repetitive torsion of the biceps anchor (the so-called “peelback mechanism”) in throwers and overhead athletes, types 3 and 4 lesions are thought to occurr more often after a fall onto an outstretched arm or onto a flexed elbow [3, 55, 56]. Furthermore, type 2 lesions are frequently observed in athletes with traumatic anterior shoulder instability, where they develop in association with lesions of the anteroinferior labro-ligamentous complex (most often a classic Bankart lesion). In these cases, the labro-ligamentous avulsion can be considered as the main lesion, with the SLAP lesion being an associated injury [55]. Surgical treatment is indicated in all types of SLAP lesions except type 1 lesions which are usually of no clinical relevance. Since type 2 and 4 lesions impair the stabilizing function of the biceps insertion and therefore can provoke glenohumeral instability, secondary impingement, and rotator cuff lesions, they are commonly treated by refixation. Type 3 bucket-handle tears are usually not surgically reattached but treated by simple debridement [55, 56].

MR arthrography has proved to be superior to conventional MR imaging with regard to the identification of SLAP lesions and has been shown to be reliable in assessment of the stability of the biceps anchor and the detection of associated injuries [55, 57‐59]. However, its ability to correctly classify the different types of lesions is limited [55].

Most SLAP lesions are best depicted on MR arthrograms oriented in the coronal oblique plane (Fig. 13). Increased signal intensity and/or surface irregularity of the superior labrum can be seen in type 1 lesions which, however, can only infrequently be diagnosed by MR imaging. Type 2 lesions are characterized by linear extension of contrast media into the superior labrum and the biceps anchor. This most common type of SLAP lesion also represents the most problematic in terms of differential diagnosis. False positive and false negative diagnoses of a SLAP type 2 lesion can be caused by misinterpretation of a sublabral recess as a tear and vice versa [55]. The sublabral recess (Fig. 14) is a very common anatomic variant with an incidence of >70% in cadaveric studies [26, 60]. It represents a variably sized synovialized cleft between the superior labrum and the bony glenoid which is typically oriented medially and points at the supraglenoidal tubercule [26, 55, 60]. The most important criterion for the presence of a SLAP type 2 lesion rather than a sublabral recess therefore is lateral or superior extension of the tear. If the tear extends medially (like a sublabral recess) it often shows irregular margins and/or a relatively wide separation between the labrum and the glenoid. In individuals with traumatic anterior instability the type 2 lesion often originates from an anteroinferior tear of the labro-ligamentous complex that extends cranially up into the superior labrum and the biceps anchor (Fig. 15) [55]. Type 3 lesions are characterized by a vertical and an additional horizontal contrast interface which separate the avulsed superior labrum as a triangular-shaped fragment from the intact biceps tendon. In Type 4 lesions the horizontal component of the tear additionally extends into the long head of biceps tendon. The bucket-handle fragment therefore is composed of the superior labrum as well as a portion of the tendon and might be more or less displaced from the superior glenoid [55, 59].