In the late cocking phase of the overhead-throwing cycle, during extreme ABER, there may be repetitive impaction of the posterior greater tuberosity on the supraspinatus–infraspinatus junction and posterosuperior glenoid (Fig. 9.2). This common condition in handball players is called internal or posterosuperior glenohumeral impingement, which may lead to rotator cuff tears and posterosuperior labral tears (Jobe 1997) (Fig. 9.3). Internal impingement can be either primary (i.e., without evidence of glenohumeral instability) or, more commonly, secondary (due to increased anterior shoulder laxity and instability) (Ouellette et al. 2005). On MRI, posterior supraspinatus or supraspinatus–infraspinatus junction (posterior interval) tears are seen at up to 1 cm from the greater tuberosity insertion. The tendon tears are usually small and seen at the articular surface of the rotator cuff. Thus, internal impingement rotator cuff tears are better evaluated using MR or CT arthrography where they appear as a small undersurface linear contrast extension in the tendon. ABER positioning is important in these patients since relaxation of the posterior superior rotator cuff may allow contrast to seep into a subtle tear (Tirman et al. 1994). Moreover, these patients often have associated posterosuperior labral lesions (Fig. 9.3). Cysts and impaction deformities are also commonly found at the posterior greater tuberosity in handball players with internal impingement (Ouellette et al. 2005).

External impingement can be either primary or secondary (Ouellette et al. 2005). In primary external impingement, shoulder pain occurs following contact between the coracoacromial arch and the rotator cuff. The origin of the pain is the rotator cuff itself and irritation of the interposed subacromial bursa. The large inferior torque in the deceleration phase of the throwing cycle may result in subacromial impingement (Meister 2000) (Fig. 9.4). Posttraumatic deformity, downsloping acromion, acromioclavicular degenerative change, and congenital thickening of the coracoacromial arch and os acromiale may also increase the risk of impingement (Tuite 2003). On MRI, rotator cuff tendinosis and tears associated with primary external impingement are more commonly found in older handball players and usually involve the anterior half of the supraspinatus tendon up to 1 cm from its insertion (Tuite et al. 1998). Diagnosis of tendinosis is made when there is thickening of a rotator cuff tendon with increased intermediate signal. Tears are diagnosed when fluid signal intensity or gadolinium extends into a rotator cuff tendon (Ouellette et al. 2005).

Coracohumeral impingement syndrome is also an important cause of pain in handball players. A decreased distance between the lateral aspect of the coracoid and the lesser tuberosity of the humerus results in impingement of the anterior rotator cuff, causing pain (Kassarjian et al. 2004). A coracohumeral distance of less than 6 mm on MRI is suggestive of impingement (Ouellette et al. 2005). Patients with coracohumeral impingement syndrome usually do not have rotator cuff tears (Paulson et al. 2001), but the presence of coracohumeral impingement increases the likelihood of a subscapularis tear (Kassarjian et al. 2004).

Secondary external impingement results from glenohumeral joint instability. It is one of the most common causes of shoulder pain in handball players. Although glenohumeral instability is the underlying etiology, secondary external impingement is uncommonly secondary to glenohumeral joint dislocation. Rather, it is usually secondary to accentuated microinstability, which is in itself typically asymptomatic (Tuite 2003).

During the late cocking and early acceleration phases of throwing, there is significant shear force across the shoulder. Over time, the anterior capsule fails, giving rise to anterior glenohumeral joint laxity and increased anterior translation during throwing (Dillman et al. 1993). Handball players with superior labrum anterior to posterior (SLAP) tears or injury to the long head of the biceps are also susceptible to secondary impingement. On MRI, supraspinatus and infraspinatus abnormalities can be seen at any location (Tuite 2003). The imaging appearance of rotator cuff tendinosis and tears seen in secondary external impingement is similar to that of primary impingement.

Rotator cuff overuse syndrome (tensile overload) results from repetitive traction. Although axial tendon strength is greater than that of bone, a large amount of stress at the rotator cuff during the deceleration phase of the overhead-throwing cycle is eccentric and is thought to cause tensile overload tears in normal tendons (Blevins 1997). Repetitive stress encountered in handball players also accelerates the degenerative process of the rotator cuff, resulting in early tendinosis (Tuite 2003). Tendinosis weakens tendons and increases the risk of a superimposed rotator cuff tear. On MRI, rim-rent tears (which are articular surface partial tears at the humeral tendinous insertion) can be seen from tensile overload on a normal tendon. Rim-rent tears have high signal extending between the greater tuberosity tendon insertion and the tendon. High signal violates the very distal articular surface of the affected tendon. Other tensile overload tears may be seen at the articular surface of the supraspinatus and infraspinatus tendon. These tears are commonly small and best appreciated on MR arthrography in the ABER position as fluid intensity or as gadolinium transgressing the low-intensity line on the articular surface of rotator cuff tendons (Tuite 2003).

A Bennett lesion is a bony spur at the posterior inferior aspect of the glenoid (Ferrari et al. 1994). This lesion is most commonly seen in baseball pitchers, probably caused by traction of the posterior band of the inferior glenohumeral ligament that occurs during the deceleration and follow-through phases of throwing. Further growth of the lesion is likely due to posterior humeral impingement in the late cocking phase of overhead throwing. Bennett lesions are frequently associated with tears of the posterior labrum, teres minor, and infraspinatus tendons in symptomatic shoulders (Ferrari et al. 1994). Bennett lesions are usually asymptomatic, but large lesions may cause posterior shoulder pain (Nakagawa et al. 2006).

In the late cocking and early acceleration phases of overhead throwing, there is significant shear force across the shoulder. Over time, there is an increased load at the anterior capsule, often secondary to poor technique and fatigue of the external stabilizing musculature of the shoulder. The anterior capsule eventually fails with stress and accumulation of repetitive microtrauma, leading to anterior glenohumeral joint laxity (Dillman et al. 1993). Laxity of the anterior shoulder joint allows increased anterior translation of the humeral head during throwing, which in turn increases the risk of anterior labral lesions and SLAP tears.

Some players have generalized ligamentous laxity bilaterally, which may be accompanied by a hypoplastic labrum. These players also exhibit hyperextension of other joints such as elbows and knees and are capable of the highest-velocity throws and ball movements. They do, however, have a high level of risk for microtrauma and long-term injury secondary to throwing (Meister 2000).

Acute traumatic instability is uncommon in handball players. An acute traumatic event typically leads to a unidirectional pattern of instability of the glenohumeral joint (Matsen 2002) (Fig. 9.8).

The ulnar collateral ligament comprises three bands: the anterior, posterior, and transverse. The anterior band is the largest and is the major valgus stabilizing structure at the degree of flexion seen in throwing athletes (Hotchkiss and Weiland 1987; Morrey et al. 1991; Regan et al. 1991). The anterior band of the ulnar collateral ligament originates from the inferior aspect of the medial epicondyle and inserts on the sublime tubercle at the medial aspect of the coronoid process of the ulna. Repetitive tension on the medial ligaments during the acceleration phase of the throwing cycle may lead to ligamentous weakening, inflammation, and progressive laxity (Popovic and Lemaire 2002). Following repetitive stress, the anterior band of the ulnar collateral ligament may eventually tear, usually at its ulnar insertion at the sublime tubercle of the coronoid process. Less commonly, a small avulsion fracture of the sublime tubercle may occur (Glajchen et al. 1998).

Imaging diagnosis of ulnar collateral anterior band injuries is important because this structure is not well assessed arthroscopically (Field et al. 1995). There are indirect signs on radiography that may indicate ligamentous injury, i.e., heterotopic ossification of the ulnar collateral ligament and a variation of more than 0.5 mm at the medial joint on stress views, compared with nonstress images (Mulligan et al. 2000; Rijke et al. 1994). Contrast extending beyond the medial capsule on CT arthrography is sensitive and specific for partial and complete ligamentous tears (Timmerman et al. 1994). On MRI, the anterior band of the ulnar collateral ligament appears as a line of low signal intensity extending from the inferior medial epicondyle to the sublime tubercle of the coronoid. MRI features of acute injury include discontinuity of some or all fibers of the ligament and intraligamentous T2 hyperintensity. The ligament may be retracted if completely torn. MRI features of chronic injury include diffuse ligamentous T2 hyperintensity and thickening. MRI arthrography is the study of choice for ulnar collateral ligament injury (Wenzke 2013). It has been demonstrated that MR arthrographic sensitivity for partial tears is 86 % with a specificity of 100 % (Schwartz et al. 1995). In addition to the features of ligamentous tear seen on conventional MRI, extracapsular leakage of contrast indicates complete medial collateral ligamentous disruption or avulsion on MR arthrography (Cohen and Bruno 2001). Partial-thickness undersurface tears of the distal anterior band of the ulnar collateral ligament near the sublime tubercle insertion have been described as having the appearance of a “T,” hence the T sign (Schwartz et al. 1995) (Figs. 9.9 and 9.10).

Lateral elbow pain may result from osteochondral injuries and osteochondritis dissecans of the capitellum, probably caused by compressive forces at the radiocapitellar joint during late cocking and early acceleration of the throwing cycle. A subchondral lucency with variable marginal sclerosis and fragment attachment at the capitellum represents osteochondral injury on radiography and CT. CT and CT arthrography are useful for the detection of subtle osteochondral abnormalities or for the assessment of detached fragments (Ouellette et al. 2005) (Fig. 9.12).

MRI is also helpful in the assessment of subtle osteochondral injuries of the capitellum which may be radiographically occult (Wenzke 2013). MRI may demonstrate capitellar articular cartilage irregularity and fissuring. Osteochondral lesions show decreased signal intensity on T1-weighted and increased signal intensity on T2-weighted images within the capitellum. On contrast-enhanced T1-weighted images, complete enhancement of the fragment or incomplete craterlike fragment enhancement is associated with favorable clinical outcomes with conservative treatment. Fragment displacement or circumferential fluid surrounding the osteochondral fragment on MRI is indicative of fragment instability (Mesgarzadeh et al. 1987). MR arthrography is useful for visualization of intra-articular loose bodies and fragment stability determination.

One should be aware of a common diagnostic pitfall, so-called pseudodefect of the capitellum, which is seen at the junction between the anterolateral capitellum and posterolateral aspect of the lateral epicondyle (Ouellette et al. 2005). This should not be mistaken for an osteochondral injury. Pseudodefect of the capitellum can be easily recognized by its typical location. An apparent defect should be cross correlated with the sagittal view to distinguish between a true defect and a pseudodefect (Ouellette et al. 2005).

Because of valgus overload syndrome, handball players may develop posterior and posteromedial olecranon osteophytes, which are frequently symptomatic. Olecranon osteophytes may fracture and become intra-articular loose bodies (Ouellette et al. 2005). Symptomatic posterior olecranon impingement may require surgical therapy.

Fractures of the carpal bones are common in athletes, with the scaphoid the most commonly fractured (Rettig 2003). Triquetral fractures represent the second most common form of carpal bone fractures, far behind those of the scaphoid (Bonnin and Greening 1944; Hey et al. 2011). Most triquetral fractures result from falls from standing height onto the outstretched hand (Hey et al. 2011). Three types have been described in the literature: cortical dorsal (the most common), body, and cortical palmar (Hey et al. 2011; Smith and Murray 1996). Although triquetral fractures were first described in the literature more than 80 years ago (Thompson 1933), the exact mechanism of injury remains controversial. Two major theories have been suggested: ligament avulsion fracture (Bonnin and Greening 1944; Smith and Murray 1996) and ulnocarpal impaction (Levy et al. 1979; Garcia-Elias 1987). Other less common theories include direct trauma to the dorsum of the hand or sudden resistance against a twisting motion of the wrist (Bartone and Grieco 1956).

The prevalence of carpal bone fractures may be underestimated because they may be occult or overlooked on radiographs and consequently undiagnosed or misdiagnosed as wrist sprain (Becce et al. 2013). It has been shown that radiography has low sensitivity (30 %, for all carpal bones) for the detection of carpal bone fractures compared to CT (Welling et al. 2008), and thus, CT should be considered after a negative radiographic finding if clinically warranted. MRI is also an option for cross-sectional imaging (Mack et al. 2003; Fotiadou et al. 2011), but its relatively high cost may preclude routine use of MRI in clinical practice (Fig. 9.13).

The scapholunate ligament comprises volar, central, and dorsal components. Each of these has different histologic properties and biomechanical functions. The location of the injury and size of the lesion may have clinical implications regarding therapy and prognosis (Pappou et al. 2013). Injuries to the scapholunate (SL) interosseous are the most common ligamentous injuries in the wrist (Rettig 2003). The SL ligament is a key stabilizer of the proximal carpal row of the wrist, and its dorsal component is the most important (Kuo and Wolfe 2008). Scapholunate ligament injury typically occurs following a dorsiflexion injury, e.g., a fall on a pronated outstretched hand. In handball, this injury usually occurs as a result of excessive force applied to a hyperextended wrist in a player who sustains a fall (Lewis and Osterman 2001). The patient complains of dorsal wrist pain and swelling and may report a discernable popping sound with wrist motion. Patients may also experience a weakness of grip (Rosner et al. 2004). On clinical examination, there is tenderness to palpation 1 cm distal to the dorsoradial tubercle (Fufa and Goldfarb 2013).

A static increase in the scapholunate interval (scapholunate dissociation) and dorsiflexion of the lunate occur as a consequence of a complete tear of the scapholunate ligament associated with a tear of one or more extrinsic ligaments (Meade et al. 1990). In addition, rotatory subluxation (volar flexion) of the scaphoid occurs, and further dorsal and proximal translation of the capitate along with the distal carpal row will lead to a dorsal intercalated segment instability (DISI) deformity (Linscheid et al. 1972). DISI causes abnormal articular loading that leads to the degenerative changes known as scapholunate advanced collapse (SLAC) wrist (Crema et al. 2012).

Scapholunate ligament injury may be suspected with a widening of the SL interval of greater than 2 mm on AP radiograph. This widening can be exaggerated with an AP clenched fist view (Rosner et al. 2004). A common radiographic finding of scapholunate dissociation is the “cortical ring sign” which occurs due to abnormal orientation of the scaphoid with the scaphoid rotated and appearing foreshortened on the AP radiograph (Ritchie and Munter 1999).

MRI can depict partial or complete intrinsic ligament tears. The intrinsic ligaments are optimally visualized on coronal images. Complete tears appear as distinct areas of discontinuity of the ligament with fluid signal on T2/T2* contrast or STIR sequences (Fig. 9.14). Complete absence of the ligament is also indicative of a tear. In more advanced cases, there may be associated widening of the SL ligament interval similar to that seen on radiographs, particularly if two or more portions of the ligament are involved. Fluid pooling around the ligament, concomitant bone injury, and adjacent ganglia are other clues to underlying injury (Rosner et al. 2004). Depiction of disruption of the dorsal portion of the ligament is also important, as injury to the dorsal component means the loss of the most important stabilizer of the SL ligament (Timins et al. 1995; Rosner et al. 2004). MRI or MR arthrography can also demonstrate partial ligament disruptions. Partial disruptions frequently involve the volar portion of the ligament. MRI may depict a dysfunctional ligament that has healed with scarring (Rosner et al. 2004). A recent study showed, however, that conventional MRI is outperformed by CT or MR arthrography for imaging diagnosis of scapholunate ligament tears, with CT arthrography having the highest sensitivity, specificity, and accuracy for identifying which component of the scapholunate ligament was torn (Lee et al. 2013).

Multidetector CT (MDCT) arthrography accurately depicts partial or complete tears of the scapholunate ligament. Axial images are useful to evaluate partial or complete tears of the dorsal and volar components. Coronal images are useful to evaluate tears of the membranous (proximal) component. DISI can be evaluated on MDCT using sagittal images, from which the axis of the scaphoid, lunate, and capitate may be determined. For exact angle measurement, neutral positioning of the wrist is critical. As a result of scaphoid volar flexion and lunate dorsiflexion, the scapholunate angle is increased (normal angle, 30–60°). The capitolunate angle is also increased (normal angle, 0–30°) because of the lunate dorsiflexion (Crema et al. 2012).

The triangular fibrocartilage complex (TFCC) is a major stabilizer of the distal radioulnar and ulnocarpal joints. The TFCC consists of the following structures: (1) a triangularly shaped fibrocartilaginous articular disk, (2) a meniscal homologue, (3) the ulnar collateral ligament, (4) dorsal and volar radioulnar ligaments, and (5) the extensor carpi ulnaris tendon sheath. The TFCC also coalesces to form extrinsic ligaments that extend distally to insert on the triquetrum, hamate, and fifth metacarpal. The articular disk extends from the sigmoid notch of the radius to insert on the fovea and ulnar styloid. Lesions of the TFCC may be confined to the articular disk or involve one or more components of the TFCC (Rosner et al. 2004).

Patients present with ulnar wrist pain and tenderness exacerbated by wrist and forearm motion. Traumatic TFCC tears are more common in younger patients including athletes and in those with ulnar-negative variance. The most common mechanism of injury in the athlete involves rapid twisting of the wrist with ulnar-sided loading, which often occurs in racquet sports, golf, and gymnastics, as well as handball (Ko and Wiedrich 2012). Traumatic TFCC tears frequently occur close to the radial insertion. Fluid accumulation within the distal radial ulnar joint is an important secondary sign for a radial-sided TFCC tear (Rosner et al. 2004). Ulnar-sided TFCC injuries are more difficult to diagnose. Positive MRI findings include altered morphology of the ulnar attachments, linear fluid extending to the surface of the peripheral TFCC, and excessive fluid localizing to this region particularly if the fluid extends below the expected location of the prestyloid recess (Sofka and Potter 2001). Ulnar-sided TFCC injuries heal spontaneously or can be repaired (Rosner et al. 2004).

TFCC injuries can be classified according to the Palmer classification (Palmer 1989). Type 1 injuries are traumatic and further subclassified into 1A (central perforation), 1B (ulnar avulsion with or without distal ulnar fracture), 1C (distal avulsion of the TFCC attachments to the lunate or triquetrum), and 1D (radial avulsion with or without sigmoid notch fractures). Type 2 injuries are degenerative and represent progressive stages of ulnocarpal impaction syndrome. Type 2 injuries are also further subclassified: stage 2A is characterized by thinning and degeneration of the undersurface of the articular disk. Stage 2B indicates further TFCC degeneration with the addition of ulnolunate chondromalacia. Stage 2C represents TFCC perforation with ulnolunate chondromalacia. In stage 2D, TFCC perforation and ulnolunate chondromalacia are accompanied by lunotriquetral perforation. Stage 2E is characterized by each of the findings seen in stage D with the addition of ulnolunate arthritis (Rosner et al. 2004) (Figs. 9.15 and 9.16).