Disorders of the Elbow: Lateral

Common Extensor Origin Epicondylalgia

The commonest cause of pain in the lateral aspect of the elbow is tendinopathy or enthesopathy of the common extensor origin (CEO). The term ‘tennis elbow’ originates from early descriptions of this condition and it has largely stuck, passing into common usage. Despite the name, the condition occurs much more commonly in nontennis players and a wide variety of occupations and sports have been implicated. It is more common in golfers than is golfer's elbow (common flexor origin tendinopathy).

The characteristic location of pain is over the lateral epicondyle. The patients may also note muscle weakness, particularly in grip strength.

Pathologically there is angiofibroplastic hyperplasia and mucoid degeneration of the CEO. The extensor carpi radialis brevis component shows the earliest involvement.

The ultrasound anatomy and examination techniques have been described previously. The characteristic findings in patients with CEO tendinopathy include loss of reflectivity and disorganization of the normal reticular fibre pattern within the involved tendons. The anterior part is affected more often than the posterior, and the deeper portions more than the most superficial. This pattern reflects the characteristic involvement of extensor carpi radialis brevis. As the disease progresses, ingrowth of abnormal vessels (neovascularization or angiogenesis) occurs and abnormal Doppler signal is commonly found ( Fig. 6.1 ). The degree of vascular ingrowth is so great in some patients, that it has been suggested that much of the high signal within the tendons identified on fat-suppressed T2-weighted MR images represents abnormal vessels. As tendon degeneration progresses, fibre disruption appears and areas of focal tendon delamination or partial tears are seen ( Fig. 6.2 ). The disease progresses to involve the adjacent tendons. Involvement of the radial collateral ligament may also occur and this is said to carry a poor prognosis for conservative management. With further progression, the tendon may begin to separate from its periosteal attachment ( Fig. 6.3 ) and ultimately rupture occurs. There appears to be a good correlation between active Doppler changes and areas of tendon delamination with patient symptoms ( Fig. 6.4 ).

Enthesopathy is the term used to describe pathological changes at the enthesis, the point where the tendon inserts into the lateral epicondyle. Occasionally this is distinct from tendinopathy but in practice the two coexist and often merge. Chronic enthesopathy is diagnosed when insertional bone changes are present at the tendon attachment. Such findings include calcification, which can assume several patterns: linear or conglomerates. With maturity the calcium deposits may ossify. Bony irregularity of the attachment site ( Fig. 6.5 ) leads to spur formation, visible on radiographs. It should be noted that bony changes at the enthesis may persist and become chronic and are, therefore, not necessarily associated with active symptoms. Active Doppler at the enthesis is a more helpful sign of an active problem.

Although in most cases the disease is due to disordered biomechanics (as outlined above), some cases may be secondary to systemic disease, drug therapy and crystal deposition, especially gout. Once the diagnosis is established, treatment revolves around identifying and managing the underlying cause. When pain is persistent, ultrasound can be used to guide dry needle therapy and autologous blood or platelet-rich plasma (PRP) injection ( Fig. 6.6 ). This is covered in more detail in the intervention chapter.

Radial Collateral Ligament and Plica

The radial collateral ligament runs from the lateral epicondyle deep to the CEO proximally, to the lateral aspect of the neck of the radius distally, where it inserts on the annular ligament ( Fig. 6.7 ). Apart from being simultaneously involved in patients with CEO tendinopathy and traumatic injury, there are relatively few disorders that affect the ligament in isolation and it is relatively uncommon that imaging is required. The radial collateral ligament is not as easy to identify as the ulnar collateral ligament but it can be found on the deep aspect of the common CEO.

Abnormal findings within the ligament include loss of the normal bright fibrillary structure, thickening and fibre disruption when tears or partial tears are present.

Occasionally lateral symptoms have been attributed to thickening of the lateral meniscus/flange, presumed to be secondary to impingement. Apart from pain, patients may present with clicking and snapping. Occasionally this condition can be associated with areas of chondromalacia of the radial head. If symptomatic, the flange is excised and histology has demonstrated synovitis associated with fibrosis. Posterolateral synovial plica (synovial flange) thickening is also described. Stability on the lateral side is predominantly due to the lateral collateral ligament; however, there is a greater contribution from the lateral musculotendinous structures (CEO) than on the medial side.