Impingement is a clinical condition in which the subacromial soft tissues (bursa, biceps, and supraspinatus tendons) are compressed between the humeral head and the coracoacromial arch. Rotator cuff degeneration and tears can be a combination of intrinsic factors such as repetitive action, repetitive incidence trauma, and poor technique.

Primary impingement, in which there is impingement of the supraspinatus tendon on the coracoacromial arch, is fairly uncommon in young (athletic) individuals, but much more prevalent in older golfers (Tuite 2003).

In athletes the most frequent locations of rotator cuff tears are the anterior half of the supraspinatus tendon at 0.5–1 cm from the insertion, posterosuperior tears, and the undersurface area of the cuff attachment to the humeral head. The young athletic cuff is resistant to extensive tearing, and partial-thickness and interstitial partial tears are commonly encountered.

Ultrasound or MRI can be used to evaluate rotator cuff disease and cuff-related abnormalities. Ultrasound has the advantage of dynamic imaging, and it can be used in image-guided interventions.

On MRI, tendinosis is seen as intermediate- to high-signal intensity on T2-weighted images, frequently with mild to moderate thickening of the tendon. Ultrasound may demonstrate an enlarged, heterogeneous, or hypoechoic tendon. A tear in the tendon will appear as a fluid- or synovial-filled defect on ultrasound and as a hyperintense lesion within the tendon on T2-weighted images. Full-thickness tears extend across both the bursal and articular surfaces of the tendon; partial tears involve only one surface (Fig. 14.2).

Subacromial-subdeltoid bursal disease is more often depicted as thickening of the synovial lining rather than large quantities of bursal fluid (Fig. 14.3). The most common location is over the supraspinatus tendon where the bursa abuts the coracoacromial ligament, and dynamic shoulder assessment using ultrasound can be useful to detect a minimally enlarged bursa with arm movement. However, it should be appreciated that the ultrasound can be normal in patients with symptomatic bursal disease, highlighting a role for guided diagnostic injection.

A variety of internal impingement syndromes have been described, including posterosuperior, anterosuperior, and the anterior impingement syndromes. Although most commonly reported in baseball pitchers, posterosuperior impingement can also occur during other activities such as the golf swing or the overhead serve (Drakos et al. 2009).

There are many proposed pathomechanics for this syndrome. Golfers particularly encounter a combination of anterior capsular laxity and posterior capsular contraction. The mechanism behind this is similar to the development of glenohumeral internal rotation deficit as described by Burkhart et al. in the throwing athlete, where there is decreased internal rotation of the shoulder with the arm in abduction (Burkhart et al. 2003). In golfers, this is thought to be related to the follow-through and can lead to an abnormal range of movements and secondary impingement.

MRI features include irregularity and thickening of the posterior limb of the inferior glenohumeral ligament, microfractures/bone marrow changes of the posterosuperior glenoid and greater tuberosity of the humerus, and tears of the posterior superior labrum (Fig. 14.4a) (Giaroli et al. 2005). MRI arthrography has been used to demonstrate these lesions and in particular the use of the ABER (abduction external rotation) position. It is at this position that the supraspinatus tendon may be seen to impose between the posterosuperior glenoid rim and the greater tuberosity of the humerus, though repeated torsion of the tendon during repetitive action is thought to be more important. The supraspinatus lesion usually involves the posterior part of the tendon, in the junctional area between the supraspinatus and infraspinatus, on its joint surface, in contrast to subacromial impingement (Fig. 14.4b) (Woertler and Waldt 2006).

There is substantial overlap with the overhead throwing athlete, particularly in glenohumeral internal rotation deficit where thickening of the inferior capsule (posterior limb of the inferior glenohumeral ligament), partial or complete rotator cuff tears, and SLAP II lesions (thought to be a consequence of the “peel back” mechanism) can be encountered at MRI (Fig. 14.5).

Chronic repetitive loading of the acromioclavicular joint leading to osteoarthritis is typically seen in the lead shoulder in golfers. It is at the top of the back swing and at the end of the follow-through that the maximal force is applied across the joint. The chronic repetitive nature of this motion leads to excessive loading of the joint (Mallon and Colosimo 1995), resulting in chronic ligament injury, cartilage injury, and secondary osteoarthritis.

Osteoarthritis can be depicted on radiographs and on MRI. One should be cautious, however, in attributing pain to osteoarthritis, as the prevalence of osteoarthritis on MRI of asymptomatic individuals has been reported to be as high as 48 % (Needell et al. 1996).

Traditionally medial epicondylitis has been termed “golfer’s elbow” and lateral epicondylitis “tennis elbow.” These are misnomers as both varieties occur with equal frequency in the golfer and are the most common abnormality of the elbow (McCarroll 1996). Injury to the common flexor or extensor origin can be caused by repetitive strain, typically due to improper technique, or as the result of acute trauma injury such as striking a club or racquet against a fixed object. Deceleration during the downswing and impact phases strains the medial compartment but also causes forceful contractions at the medial and lateral lower arm musculature. This leads to strain on both the lateral and medial compartments and explains the equal frequency of both medial and lateral epicondylitis in golfers.

The term epicondylitis is misleading however since these are entities of misuse tendinosis and partial tearing of the common flexor and extensor origin (medial and lateral epicondylitis, respectively) caused by repetitive traction on the osteotendinous attachment. The term “epicondylitis” persists in common usage, although common flexor or extensor tendinopathy are better designations for this disorder.

Common extensor tendinopathy predominately involves the extensor carpi radialis brevis tendon. There is also variable involvement of the extensor digitorum communis, extensor carpi radialis longus, and extensor carpi ulnaris tendons (Hume et al. 2006). Common flexor tendinopathy involves the pronator teres and flexor carpi radialis tendons; less common sites include the flexor carpi ulnaris, palmaris longus, and flexor sublimis origins (Nirschl 1988).

Ultrasound remains the imaging modality of choice and offers a quick and focused examination of both areas. The main ultrasound findings of tendinosis include pre-insertional hypoechoic swelling of the tendon with focal or diffuse areas of decreased reflectivity in the tendon substance, loss of the normal fibrillary pattern, fluid adjacent to the common tendon, and ill-defined tendon margins (Connell et al. 2001) (Fig. 14.6a). In high-grade tendinosis, striking hypervascularity of the intratendinous hypoechoic areas can be seen on Doppler interrogation (Fig. 14.6b).

Involvement of the deep fibers particularly of the extensor carpi radialis brevis component is most common. Discriminating focal areas of tendinosis and a partial tear on ultrasound can be difficult, particularly on MRI. On ultrasound a well-defined anechoic focus with no fibers intact or discrete cleavage planes are more typical of partial tears (Fig. 14.7).

MRI can also be used for evaluation particularly in the assessment of nonspecific elbow pain and those recalcitrant to conservative management. Studies reporting greater accuracy of MRI over ultrasound have generally not used Doppler ultrasound, which assists in the identification of the disorder. MRI shows the normal common tendons as homogenous low signal T1 and T2 structures. Similar changes are seen both in medial and lateral epicondylitis with tendon thickening and increased signal intensity on both the T1- and T2-weighted images (Fig. 14.8). This corresponds histologically to mucoid degeneration and neovascularization. Partial tears are depicted as thinning or partial disruption of the tendon and increased T2-weighted signal within and adjacent to the tendon origin (Bancroft et al. 2007). In common extensor tendinopathy, involvement of the radial collateral ligament should be assessed, as the involvement denotes a more advanced stage of the disease.

Conservative treatment with rest, anti-inflammatory drugs and physiotherapy are the initial treatments. Percutaneous ultrasound dry needling supplemented with autologous blood or platelet-rich plasma therapy can be used for refractive cases. The role of corticosteroid injection is increasingly questioned. Surgery remains the final consideration with excision of the degenerated tissue, resection of the common tendon, and debridement of the common tendon origin.

Entrapment neuropathies can be difficult to differentiate from tendon disease particularly on the medial side where there is considerable overlap of symptoms between the conditions.

Ulnar neuropathy can be the result of compression or traction from valgus stress or in combination with chronic epicondylitis or ulnar collateral ligament insufficiency. Compression can occur due to a narrowed cubital tunnel, osteophytes from the ulnohumeral joint, muscle hypertrophy, or subluxation of the nerve. Subluxation can occur when the constraining Osborne ligament is injured or lax and is more likely when there is an enlarged or accessory medial head of the triceps. In itself, ulnar nerve subluxation is not always pathological, though its presence does render the nerve more prone to injury.

Entrapment of the posterior interosseous nerve, the motor branch of the radial nerve, causes lateral-side elbow pain and weakness, often confused with lateral epicondylitis. The nerve is most commonly compressed at the arcade of Frohse, a fibrous condensation at the leading edge of the superficial head of the supinator muscle. Other causes of posterior interosseous nerve and radial nerve compression include fibrous bands at either end of the radial tunnel and prominent vessels around the arcade of Henry.

Although uncommon, pronator teres syndrome has been described in racquet sports where entrapment of the median nerve occurs as the result of muscle hypertrophy of the dominant arm with entrapment between the 2 heads of the pronator teres (Frostick et al. 1999). Clinical manifestations include anterior pain and distal paresthesia worsened with resisted pronation. An accessory head of the pronator teres may also lead to neural compression.

The anterior interosseous nerve is a major branch of the median nerve and compression of this nerve causes Kiloh-Nevin syndrome. As the nerve is purely motor, compression leads to dysfunction of the flexor pollicis longus, pronator quadratus, and flexor digitorum profundus to the second and third digits and the inability to oppose thumb and index finger. The nerve can be compressed between the heads of the pronator teres muscle and the proximal edge of the flexor digitorum superficialis arch or due to anatomical variants such as Gantzer muscle, an anomalous head of the flexor pollicis longus.

Entrapment of the lateral cutaneous nerve of the forearm has been reported in racquet players (Retting and Patel 1995). The nerve is compressed between the distal biceps tendon and the brachialis muscle, probably secondary to repetitive elbow hyperextension (Cabrera and McCue 1986).