PATHOPHYSIOLOGY

Cyriax⁹ in 1936 recognized that the origin of extensor carpi radialis brevis (ECRB) was the primary site of injury. Other muscles involved are the extensor carpi radialis longus, extensor carpi ulnaris extensor digitorum communis (in at least 50% of cases) and the supinator muscle (Fig. 21-1). The condition also requires detailed evaluation and consideration to exclude neuropathy, such as radial tunnel syndrome, posterior interosseous nerve (PIN) compression, or both.¹⁰ The radial nerve can be entrapped at several sites (Fig. 21-2): by fibrous bands in front of the radial head, by the recurrent radial vessels (leash of Henry), at the arcade of Frohse (proximal thickened edge of superficial head of supinator muscle), and at the tendinous margin of the ECRB.

FIGURE 21-1 Anatomy of the lateral elbow.

(Adapted with permission from Bishai SK, Plancher KD: The basic science of lateral epicondylosis: Update for the future. Tech Orthop 21:250–255, 2006.)

FIGURE 21-2 Anatomy of the radial tunnel.

In chronic cases of lateral epicondylitis, it has been shown that there are little to no inflammatory cells, hence the term tendonitis is inappropriate because -itis implies inflammation. Nirschl¹¹ rather described it as “tendinosis” or “angiofibroblastic hyperplasia,” reflecting the degenerative changes based on histopathologic diagnosis. A review of histologic, immunohistochemical, and electron microscopy suggests that the condition is degenerative^12,13 with increased fibroblasts, vascular hyperplasia, proteoglycans and glycosaminoglycans, and disorganized and immature collagen. This is in keeping with current thinking about tendon pathology in general.^14,15

Many names have been proposed for this condition—tennis elbow, radial or lateral epicondylalagia,¹⁶ extensor tendinopathy, or epicondylitis lateralis humeri. The primary argument against lateral epicondylalgia (algia means “pain”) is that lateral elbow pain can also result from PIN entrapment (radial tunnel syndrome) and from compression of the nerves of the cervical spine; therefore, this is probably too general a term for diagnosis. The term extensor tendinopathy is not inclusive enough because often more than the wrist extensor tendons are involved (ECRB and sometimes the supinator muscle). Some authors¹⁷ have suggested that it is most appropriately termed lateral elbow tendinopathy, a painful overuse tendon condition in the area of lateral epicondyle. For purposes of consistency in the remainder of this review, however, the term lateral epicondylitis is used.

CLINICAL DIAGNOSTIC CRITERIA

Lateral epicondylitis is characterized by a corroborating history of injury and is a localized tenderness in the area where the common wrist extensors (especially ECRB) attach to the lateral epicondyle of the humerus.¹⁸ Functional use, such as gripping or lifting heavy objects, exacerbates symptoms. Differential diagnoses include radial nerve entrapment (or rarely, lateral antebrachial cutaneous neuropathy), elbow joint disease (osteochondral desiccans, intra-articular loose bodies, osteoarthrosis), partial or complete tear of the tendon, and extrinsic causes (cervical dysfunction and nerve root compression).¹⁹ Infrequently seen are degeneration or stenosis of the orbicular ligament, chronic impingement of the redundant synovial fold between the humerus and radial head, traumatic periostitis of the lateral epicondyle, and chondromalacia of the radial head and capitellum.

Clinical examination should include visual inspection of the elbow for alignment (varus or valgus angulation), muscle bulk, and obvious bruising or swelling; however, none of these is diagnostic. Elbow range of motion is sometimes decreased; one study found a decrease of 10% in supination and 15% in pronation in 25 patients with chronic unilateral epicondylosis.²⁰ Previous cortisone injections may leave residual skin discoloration or lack of pigmentation. Neurovascular examination of the distal extremity is also necessary.

The diagnosis of lateral epicondylitis is substantiated by tenderness over the ECRB or common extensor origin. The therapist or physician should be able to reproduce the typical pain by the following methods: (1) digital palpation on the facet of the lateral epicondyle, (2) resisted wrist extension (Fig. 21-3) or resisted middle-finger extension with the elbow in extension (Fig. 21-4), or (3) having the patient grip an object. In addition to pain, patients almost always have decreased function. In radial tunnel syndrome²¹ (which may coexist with lateral epicondylitis in up to 5% of cases), the pain is more diffuse and localized to the extensor mass, 3 to 4 cm distal to the lateral epicondyle. It may be provoked with supinator stress testing or resisted extension of the middle finger. Weakness of the distal muscle groups innervated by the PIN may also be present.

FIGURE 21-3 Resisted wrist extension.

FIGURE 21-4 Resisted extension of the middle finger.

Other tests have been described,^22,23 including Cozen’s test (with the elbow flexed and the forearm pronated, the patient is asked to make a fist and radially deviate and extend the wrist against resistance) (Fig. 21-5). Mill’s test (Fig. 21-6) refers to pain (on resisted wrist extension) with the elbow extended and wrist flexed and pronated with radial deviation.²⁴ Coonrad and Hooper²⁴ have also described the “coffee cup test,” where picking up a cup of coffee is painful. Another useful clinical tool is the “chair test” (Fig. 21-7), where the patient is asked to pick up a chair with the elbow extended and the wrist ulnarly deviated with the hand in palmar flexion.²⁵ One group studied a standardized and calibrated system to simulate the chair pick-up.²⁶ They demonstrated excellent reliability (inter-rater intraclass correlation coefficients [ICCs] ranging from 0.80–0.93 and intrarater ICCs ranging from 0.9–0.97) and reproducibility of results. Measurements in a group of 16 patients with MRI-confirmed diagnosis suggested that this test could be valid for monitoring patients with lateral epicondylosis. Other researchers²⁷ used an extensor grip test (where pain on resisted wrist extension was diminished by the examiner gripping the patients arm just below the elbow with an estimated 10–N pressure) to prospectively predict which patients would respond best to bracing. The validity (specifically the sensitivity and specificity) of the majority of these clinical tests has not yet been determined. This area is ripe for research, with a significant need for well-designed studies,²⁸ such as recently published for diagnosis of carpal tunnel syndrome.²⁹ Tests can also be validated against tissue observations of pathology or imaging studies.

FIGURE 21-5 Cozen’s test for lateral epicondylitis.

FIGURE 21-6 Mill’s test for lateral epicondylitis.

FIGURE 21-7 The “chair test.”

OUTCOME MEASURES

A variety of specific outcome measures has been used to assess the effects of therapy. None is specifically diagnostic, and they are mainly used to quantify the severity of elbow injury and to monitor effectiveness of rehabilitation protocols. In some cases, they can help distinguish a patient population with the disease from healthy control subjects. Measures of pain include pain threshold test (dolorimeter), size of pain drawing, and visual analogue scales (VASs), but only pressure pain is associated with pain on palpation, grip strength, and manual tests.³⁰ Both maximal grip strength and pain free grip strength have been utilized,³¹ and the latter has been shown to be moderately reliable.^32,33 Assessment of mean and maximal grip strength is done with an instrument such as a Jamar hydraulic hand dynamometer, with the elbow in 90 degrees of flexion and the elbow fully extended in front of patient. An average of multiple measurements is recommended, and from multiple sessions rather than from increasing the repetitions in a single test session. Dorf and colleagues³⁴ examined the sensitivity and specificity of grip strength in these positions in a population of 81 patients with lateral epicondylitis. In 41 patients, the affected side only was tested, whereas 40 had bilateral measurements done. The affected extremity was 29% stronger in flexion than in extension. The authors suggest that loss of grip strength between flexion and extension in a single extremity should be considered as a test to distinguish an extremity with lateral epicondylitis from a pain-free extremity. With a 5% decrease in grip strength between flexion and extension, the sensitivity was 83% and specificity 80%; with a 10% decrease, sensitivity was 78% and specificity 90% (Fig. 21-8). DeSmet and colleagues^35,36 had similar findings: a statistically significant mean grip strength loss of 43% from flexion to extension for the pathologic side in 55 consecutive patients with lateral epicondylitis compared with a less than 2% difference for the control side. In their studies, grip strength in both elbow extension and flexion significantly improved after surgery and correlated with a good clinical outcome.

FIGURE 21-8 Sensitivity/specificity of a test of difference in grip strength to distinguish an extremity with lateral epicondylitis from a pain-free extremity.

(Adapted from Dorf ER, Chhabra AB, Golish SR, et al: Effect of elbow position on grip strength in the evaluation of lateral epicondylitis. J Hand Surg [Am] 32A:882–886, 2007 with permission of Elsevier.)

Forearm muscle imbalance or shoulder muscle pathology may also be important in the development of tennis elbow. It has been suggested that there is a greater fatigability of wrist extensors compared with wrist flexors.³⁷ Alizadehkhaiyat and coworkers³⁸ actually developed an extension/flexion dynamometer type instrument to measure this (Fig. 21-9), but no other systematic studies have been done on this wrist-forearm-shoulder segment. Isokinetic dynamometer measurements have shown peak torque at a radial velocity of 90 degrees/sec, and work in wrist flexion reduced by 17% in lateral epicondylitis and 13% in medial epicondylitis.