Elbow Tendinopathies: Clinical Presentation and Therapist’s Management of Tennis Elbow


  • A comprehensive examination should be performed to allow an adequate differential diagnosis of lateral elbow pain.

  • The patient’s age, duration of symptoms, exposure to risk factors, and number of recurrences are associated with degenerative changes to the common extensor tendon.

  • There are no optimal guidelines for selecting therapy interventions such as physical agents and exercise.

  • Patient education to avoid aggravating activity is essential to resolution of symptoms.

There is a great likelihood that an elbow tendinopathy will develop in individuals between the ages of 35 and 55, particularly if they have a high activity level that includes repetitive upper extremity motion. , This includes workers in a variety of occupations and athletes, particularly those that play tennis or golf. However, a single event, such as lifting a heavy object or performing an awkward grasping movement, can develop into a tendinopathy. The dominant arm is most commonly affected.

The incidence of medial elbow tendinopathy is much lower than lateral elbow tendinopathy. Tendinopathies of the biceps and triceps are rare, including ruptures. Chapters 83 and 84 offer additional information on the less common elbow tendinopathies. This chapter focuses on examination and therapeutic management of lateral elbow tendinopathy, but these principles generally apply to the management of medial elbow tendinopathy also.

Various names including tendinitis, tendinosis, paratenonitis , and peritendinitis have been used to represent the clinical condition of tendinopathy, depending on the status of the tendon tissue at different stages of healing. The common extensor tendon inserts onto the lateral epicondyle, which explains the use of the clinical terms lateral epicondylitis , lateral epicondylosis , and lateral epicondylalgia to describe what the layperson calls “tennis elbow.” The use of the suffix “itis” may be misleading because it assumes that there is an acute inflammatory state within the injured tendon. The suffixes “osis” and “algia” indicate a degenerative condition or pain, respectively. Although the term tennis elbow does not reveal the state of the tendon tissue, it is also not an appropriate term because most patients referred to hand therapy do not get the condition from playing tennis. The term lateral elbow tendinopathy encompasses all states of healing or lack of tendon healing, but the reality of this academic discussion is that our patients, most clinicians, and the general public refer to the condition as tennis elbow. As a search phrase for electronic literature databases, tennis elbow and lateral epicondylitis reveal significantly more citations (about 1300 each) than any of the other terms. Lateral epicondylosis only revealed 15 citations followed by 62 for lateral epicondylalgia, and 67 for lateral elbow tendinopathy. For consistency, tennis elbow is used in this chapter.

Tendon Structure and Function

Tendons serve as the interface between bone and muscle to transmit muscle force to the bone to create joint movement. The composition of tendon is primarily collagen, ground substance, and tenocytes. An aggregate of collagen fibrils form a collagen fiber that is the basic unit of a tendon. A network of thin reticular connective tissue known as the endotenon binds collagen fibers together to form the primary (subfascicle), secondary (fascicle), and tertiary bundles that compose the tendon ( Fig. 82-1 ). In addition to binding collagen fibrils together, the endotenon surrounds each of the collagen bundles. Tendons that are not enclosed in a tendon sheath are surrounded by two connective tissues layers called the epitenon and the paratenon . Together these two layers are known as the peritendon . The paratenon, a layer of loose areolar connective tissue, is the outermost layer and serves as an elastic sleeve to allow gliding of the tendon within the surrounding tissues. It is composed of type I and III collagen fibrils, elastic fibrils, and synovial cells that line the inner surface of the paratenon that interfaces with the endotenon. The epitenon is sandwiched between the paratenon and the tendon and consists of a dense network of collagen fibrils. The orientation of these fibrils is varied including longitudinal, oblique, and transverse to withstand loads applied from various directions. ,

Figure 82-1

Tendon structure with connective tissue. The collagen fibril is the smallest unit of tendon that can be mechanically tested. An aggregate of collagen fibrils form a collagen fiber. Collagen fibers are bound together by the endotenon to form the primary, secondary, and tertiary bundles. The epitenon and paratenon are the outermost layers of connective tissue and together are known as the peritendon.

(Modified from Jozsa LG, Kannus P. Human Tendons: Anatomy, Physiology, and Pathology . Champaign, IL: Human Kinetics, 1997.)

Tendons receive innervation, primarily sensory, from surrounding nerve fibers in the muscle or skin. The peritendinous tissues (paratenon and epitenon) are richly innervated with free nerve endings that function as pain receptors. Other nerve fibers penetrate through the connective tissue sheaths to the surface of the tendon and terminate on sensory nerve endings. The sensory end-organs are thought to play a role in coordination, motor control, and pain mediation. Neurokinin-1 receptor, a primary receptor for substance P, has been observed in the proximal extensor carpi radialis brevis (ECRB) tendon. Substance P, a neuropeptide, is a recognized pain modulator.

The vascularity of tendons arises from three distinct locations including the myotendinous junction, osseotendinous junction, and the paratenon. Tendons enclosed in a sheath have a more distinct vascular supply that arises from the vincula and mesotenon. In general, the vascularity of a mature tendon is poor and even absent in some regions of the tendon. This may contribute to the poor healing potential of some tendon injuries. , Neovascularization is present with tendon grafts, acute tendon injuries, and chronic tendinopathies. Although the increased capillary infiltration at the level of the chronic tendon lesion is not associated with tissue repair, it is not clear what role vascularity may play in the degenerative process of tendinosis. Abnormal vascularity may contribute to pain mediation.

Histopathology of Tendinopathies


The etiology associated with degenerative tendon changes is not well understood, but is described extensively in the literature for the Achilles tendon, patellar tendon, and the ECRB tendon. The term tendinosis has been used to describe the histopathologic findings identified in an overuse injury to a tendon. The findings include absence of inflammatory infiltrates; tenocyte or fibroblast hyperplasia and morphology; endothelial cell hyperplasia; microvascular thrombosis; hyaline, fatty, mucoid, calcified, fibrous infiltrates within the tendon substance; and cell necrosis.

Nirschl and Kraushaar , described four stages of tendinosis that may assist the therapist in determining what type of intervention to provide the patient. Stage 1 is described as a peritendinous inflammation. This stage is actually what most clinicians refer to as tendinitis. Crepitus is usually palpable over the common extensor tendon. Stages 2, 3, and 4 refer to the presence of angiofibroblastic degeneration, with stage 4 being the most severe. Because of fibrosis, stage 3 may lead to tendon rupture and stage 4 to calcification.

Despite the absence of cell-mediated inflammation, patients with tennis elbow still present with pain, particularly with aggravating activity. The reason for this distinct pain in patients with tendinosis is not well understood. Also, tendinosis has been observed via tissue analysis after excision of the involved tendon. Staging a patient’s tendinosis via clinical examination remains a challenge.

Neurogenic Inflammation

Despite the absence of inflammation, patients with tennis elbow still present with pain, particularly with abusive or aggravating activity. Tissue studies have identified the presence of neurochemicals within the tendon of the ECRB. , Significant levels of substance P and calcitonin gene-related peptide were reported within the ECRB tendon in patients with chronic tennis elbow with an average duration of symptoms of 22.7 months. Alfredson and colleagues investigated the use of a microdialysis technique to determine the local concentrations of glutamate, an excitatory neurotransmitter for pain, and prostaglandin E 2 , an inflammatory mediator in the ECRB tendon of patients with tennis elbow for at least 6 months. The results of the study yielded statistically significant differences in mean concentration levels of glutamate in the tennis elbow patients compared with the control subjects. No significant differences were noted in prostaglandin levels between groups. Similar findings have been found in the Achilles tendon and patellar tendon. Glutamate via N-methyl-d-aspartate receptor 1, a glutamate receptor, immunoreactivity has been observed within neural structures of excised Achilles tendons and patellar tendons in patients with respective chronic tendinopathies. , The presence of significant levels of glutamate, substance P, and calcitonin gene-related peptide in tendinosis may provide an alternative mechanism for pain mediation in tennis elbow as well as other chronic tendinopathies.

It is not known whether the neurochemical response is present in a tendinopathy with symptom duration of 6 months or less and if there are concurrent inflammation or degenerative changes within the tendon because the human subject studies were only performed on tendons of patients with chronic tendinopathies at the time of surgery. Animal models must be used to determine whether there is an early neurochemical response associated with tennis elbow and other tendinopathies. A chemically induced experimental model of tennis elbow in Sprague-Dawley rats revealed that substance P is abundant during an acute inflammatory response in the ECRB compared with similar tissue samples in the control group. Messner and colleagues examined immunoreactivity for substance P in the endotenon and paratenon tissues in the hindlimb triceps muscle after repetitive eccentric muscle contractions in a controlled kicking rat model. Neurofilament labeling was evident within the epitenon and paratenon of the trained tendons, but only sparsely apparent in the control tendons. Immunoreactivity for substance P was intensive in the experimental limbs of the trained animals and sparse in the contralateral limbs of the trained animals and control animal limbs. Substance P immunoreactivity was determined using bioquantification techniques in a volitional rat model of repetitive forceful motion. Substance P increases in peritendon tissue in forelimb tendons that have been exposed to highly repetitive and forceful tasks. The response is also dependent on task exposure, with the greatest response at 12 weeks. Degenerative changes to the tendon tissue was also observed. These animal studies suggest that at least substance P is present in acute overuse tendon conditions such as tennis elbow.

The ECRB is more commonly implicated in tennis elbow than other wrist or finger extensor muscles that share the common extensor tendon. Greenbaum and colleagues demonstrated that the ECRB and extensor digitorum share a common tendon and cannot be separated with gross dissection or histologic methods. The vascularity of the ECRB is compromised on its volar surface in the zone between the enthesis and the musculotendinous junction. This may add to its vulnerability to degenerative changes. Muscle biopsy specimens from the proximal and distal portions of the ECRB muscle were obtained from 20 patients with chronic tennis elbow and compared with those from controls. Abnormalities such as moth-eaten fibers, fiber necrosis, and muscle fiber regeneration had a higher incidence in the patient group than in the control group. The researchers theorized that the morphologic changes in the muscle might be attributed to a cumulative effect of mechanical or metabolic overload.

It is difficult to determine morphologic changes in the ECRB during a clinical examination. Palpable nodules, common in Achilles and patellar tendinopathies , are not common or readily palpable in the ECRB. The worst case scenario for a degenerative tendinopathy is a full-thickness tear of the tendon. Ruptures of the Achilles, patellar, and biceps tendons are easily identified. This may be attributed to the location of the rupture within the midsubstance of the tendon away from the point of insertion. Tears in the ECRB may not be identified with a clinical examination because the tear occurs at the enthesis or osseous-tendinous junction and it may not be a full-thickness tear due to the shared common tendon. The patient may only present with slight wrist extension weakness because the other common extensors, the extensor carpi radialis longus, would remain intact. The mild weakness may be attributed to pain if it is present.

Differential Diagnosis

Therapists should perform a thorough examination of a patient referred with lateral elbow pain. Because tennis elbow is such a common condition, many physicians are quick to label nontraumatic elbow pain “tennis elbow” despite the multiple sources of lateral elbow pain. Table 82-1 illustrates the numerous local and remote sources that may generate lateral elbow pain. A differential diagnosis should be developed with a thorough clinical examination. It is important to rule out proximal sources of elbow pain, such as cervical radiculopathy, proximal neurovascular entrapment, and radial tunnel syndrome. Referred pain from proximal upper quarter structures should be ruled out through patient interview, upper quarter screen, cervical examination, shoulder examination, and neurodynamic assessment as described by Butler and Elvey (see Chapter 9 , Chapter 10 , Chapter 53 , Chapter 55 , Chapter 118 ). The common signs and symptoms of other conditions that present with lateral elbow pain may help with the differential diagnosis. For example, if the pain is associated with a cervical radiculopathy or proximal nerve entrapment, active or resisted wrist extension or gripping activities should not be painful.

Table 82-1

Local and Remote Sources of Lateral Elbow Pain

Local Sources Remote Sources
Common extensor tendon Cervical discs (C5–C7)
Radial nerve Facet joints (C5–C7)
Posterior interosseous nerve Nerve roots (C5–C7)
Musculocutaneous nerve Brachial plexus (upper trunk)
Radial head Spinal cord connective tissues (dura)
Distal humerus Neuroplastic changes in CNS
Radiohumeral joint * Glenohumeral joint pathology
Superior radioulnar joint Wrist complex pathology
Fascia Remote nerve entrapment
Vascular Trigger points

CNS, central nervous system.

* Posterolateral plicae syndrome.

Once proximal sources of elbow pain are ruled out, local sources may be addressed. Radiologic studies may be used to rule out osseous conditions at the elbow or involvement of the cervical spine. Injury to the lateral collateral ligament complex may result in posterolateral rotatory instability (PLRI) and is also a source of lateral elbow pain. Patients with PLRI typically report a history of recurrent painful clicking, snapping, clunking, and locking, especially when extending the elbow with the forearm supinated. Careful patient interview may reveal a history of a “sprain” or prolonged crutch walking. There is an apprehension test that may be performed with stability testing of the elbow, but it is typically done under a local anesthetic. There is no evidence to suggest that PLRI leads to the development of tennis elbow due to increased hypermobility. However, a zealous ECRB surgical “release” may damage the lateral ulnar collateral ligament and precipitate PLRI.

The presence of posterolateral plicae in the radiocapitellar joint is another source of lateral elbow pain that is often mistaken for tennis elbow. These patients typically fail therapy for tennis elbow. Clinical examination reveals exquisite point tenderness posterior to the lateral epicondyle and centered at the posterior radiocapitellar joint. Patients frequently report a painful click or snap with terminal extension and forearm supination without instability. Analgesic injections to the lateral epicondyle may confirm this diagnosis because the pain does not subside. Elbow arthroscopy is used to diagnose and manage (remove) posterolateral plicae.

Another common painful condition that causes lateral elbow pain is radial tunnel syndrome. Chapter 52 discusses the signs and symptoms commonly associated with radial tunnel syndrome. It is often difficult to differentiate between tennis elbow and radial tunnel syndrome in an acutely painful elbow. Clinical examination techniques used to provoke symptoms of each condition usually stress the same tissues. An important clinical feature for differential assessment is the location of point tenderness. If a patient has pain from inflammation or degeneration of the common extensor tendon, the point tenderness would most likely be located on or near the lateral epicondyle. If radial nerve entrapment or irritation is more likely, the point tenderness will be approximately 2 to 3 cm dorsal and distal to the lateral epicondyle within the extensor muscle mass. , Pain (dull ache) will be referred to the dorsal wrist capsule because it is innervated by the posterior interosseous nerve. Figure 82-2 illustrates these areas of point tenderness.

Figure 82-2

Areas of point tenderness to differentiate between tennis elbow (LE) and radial tunnel syndrome (RT).

Clinical Presentation


Pain is the primary sign of tennis elbow; it is usually centered near the lateral epicondyle but may radiate proximally or distally depending on the severity of the condition. Palpation may reveal point tenderness directly on the lateral epicondyle or slightly anterior or up to 5 mm distal to it. Point tenderness along the lateral supracondylar ridge may suggest involvement of the extensor carpi radialis longus. Patients often report increased aching in the evening and elbow stiffness in the morning. In addition to pain at rest, functional use of the involved upper extremity, especially gripping activities, usually exacerbates pain symptoms. Pain is elicited with resisted wrist extension, radial deviation, finger extension, or forearm supination. All or some of these movements may be painful, depending on the irritation of the tissues. Resisted range-of-motion (ROM) movements may be more painful with the elbow extended. , Active wrist extension may be limited secondary to pain.


Initially, the age of the patient should help the therapist correlate the clinical findings to determine the appropriate clinical diagnosis. The incidence of tennis elbow is greatest from 35 to 55 years of age. Lateral elbow pain in patients younger than 35 years should be screened for other causes. The age of the patient also helps the therapist determine the prognosis or outcome after conservative management. Buckwalter and colleagues described age-related morphologic changes in tendons that appear to make tendons more susceptible to injury and more difficult to heal because of decreased vascular perfusion. Mechanical properties of the tendon diminish with age because of changes in cell function (especially fibroblasts) and the collagen fiber matrix, particularly with decreased tissue hydration.


Although commonly an overuse problem, many patients can relate the initial onset to a particular event. , Hotchkiss suggested that patients who can provide definitive information about onset will respond more successfully to treatment than patients who describe a slow, gradual onset. The number of previous episodes may help therapists determine tissue status (symptomatic degenerative state), prognosis for therapy, and predict outcome. At a minimum, this information would direct clinicians to emphasize patient education and neuromuscular conditioning in an attempt to reduce recurrence rates.

Occupation and Avocational Activities

Tennis elbow is considered the most prevalent work-related musculoskeletal disorder at the elbow, and sufficient evidence exists for a strong association between the prevalence of epicondylitis and a combination of physical risk factors including force, repetition, and posture. , Information gathered about work duties and avocational activities can help therapists determine potential causes of tennis elbow. Physical workplace demands such as force, repetition, and awkward upper extremity postures are not only risk factors for the development of tennis elbow, but also indicators of poor prognosis for medical intervention. Job modification to reduce physical demands during recovery may be more important than passive medical interventions. Interventions such as ergonomic counseling, sports modifications, and other lifestyle changes to reduce aggravating activity during the current episode and prevent recurrent episodes are key components of patient education.

Components of the Clinical Examination

The examination components presented in this section are based on evidence in the literature germane to the examination and intervention for tennis elbow. The results of these examination procedures should assist the therapist in collecting information about the patient’s impairments, help to confirm a therapy diagnosis, and aid in making an assessment about the prognosis or outcome of therapeutic management.

The clinical examination cannot confirm the tissue status of the tendon, inflammatory versus degenerative. This author believes that the index of suspicion is directed toward a degenerative condition if the patient (1) is between 35 and 55 years old, (2) has a duration of symptoms longer than 3 months, (3) has had more than one episode of tennis elbow in the same arm, and (4) has exposure to risk factors (repetitive, forceful, awkward movements). Research is needed to examine the use of clinical tests and measures as diagnostic tools and prognostic indicators for resolution of the condition.

Radiologic Findings

Most patients will not require radiologic studies, but if therapy fails or there is evidence that the signs and symptoms are not characteristic of tennis elbow, radiologic studies may be indicated to be sure that other diagnoses have not been overlooked.

Therapists should ask their patients whether any radiologic studies were performed. Diagnostic ultrasound is becoming the imaging technique of choice for tennis elbow. Plain radiographs may be used to rule out injuries to the radial head, radiohumeral joint, and proximal radioulnar joint such as radiocapitellar arthritis. , Plain radiographs may also reveal calcification in the soft tissue or osteophyte formation on the lateral epicondyle. Bone scans should rule out the presence of bone tumors in patients with uncharacteristic elbow pain. Magnetic resonance imaging studies may determine the severity of a common extensor tendon tear and associated conditions such as posterolateral instability of the elbow. However, if a tear is not evident on magnetic resonance imaging, the increased signal intensity indicates increased metabolic activity, but the tissue status cannot be determined.

Patient-Rated Tennis Elbow Evaluation (PRTEE)

Overend and colleagues demonstrated high test-retest reliability of the patient-rated forearm evaluation questionnaire and its two subscales, pain and function, in patients with tennis elbow. It was modified slightly, renamed the PRTEE, and validated as an outcome measure for tennis elbow patients. , Either form is a one-page self-report questionnaire that allows clinicians to quickly assess pain and function in patients with tennis elbow. Because tennis elbow is primarily a pain problem, other pain assessment tools may be used (see Chapter 114 ), but the PRTEE is easy to use and score.

Clinical Examination

Pressure Pain Threshold

Numerous authors have reported the reliable use of a pressure algometer to quantify the amount of pressure necessary to produce point tenderness as reported by the patient’s report of pain with pressure. Lower algometer scores would indicate increased point tenderness or pain. Higher pressure-tolerance scores would indicate less pain. Klaiman and colleagues used standard algometry technique over the area of maximal point tenderness in patients diagnosed with tendinopathy (see Fig. 114-6 ). Visual analog scale scores may be recorded when the therapist directly palpates the lateral epicondyle. Reliability may not be established, but the pressure algometer does not conform well to the lateral epicondyle.


In general, ROM of the upper extremity, especially the elbow, forearm, and wrist, is not significantly impaired. Secondary to pain, active or passive ROM may be limited in wrist extension or flexion and elbow extension. Solveborn and Olerud demonstrated that patients with tennis elbow had impaired ROM in the involved limb as compared with the symptom-free limb. In this study, most subjects had right elbow symptoms. The results indicated that with right arm symptoms, all measured active or passive motions of the elbow and wrist were limited except for passive supination. Patients with left arm symptoms had restrictions in active and passive wrist flexion, active and passive supination, and active elbow extension. These investigators argue that ROM measurements can be precisely measured in symptomatic patients and that these ROM impairments support the use of stretching in the rehabilitation of patients with tennis elbow. The measurement differences were so small that despite statistical significance, the changes may be difficult to measure with a standard clinic goniometer; however, the use of stretching may be indicated with the perception of tightness.

Grip Strength

Several studies demonstrated that grip strength will vary with shoulder, elbow, and wrist positions using a standard grip dynamometer. Therefore, therapists should use a consistent position for measurement. De Smet and Fabry demonstrated decreased grip strength with the elbow extended compared with the elbow flexed in patients with tennis elbow. They found that an increase in grip strength with the elbow extended significantly correlated with a satisfactory clinical outcome.

Pain-free grip strength can be measured on a standard grip dynamometer in the standard seated testing position with an average of three trials. The patient is instructed to squeeze the handle to the point where the pain starts and then stop. This method of grip strength testing is a commonly used outcome measure and more sensitive to change than maximal grip strength in tennis elbow patients.

Because patients with tennis elbow commonly report pain with gripping activities and pain reports are often influenced by many factors, grip strength may be used to assess treatment response. Grip strength can be measured maximally with elicited pain noted or no pain with a submaximal performance. , The expectation is that as symptoms resolve with treatment, submaximal grip strength will improve and maximum grip strength will be less painful.

Special Tests

It is important to keep in mind that special tests are not pathognomonic of a particular condition. To date, common special tests that have been described in the literature for tennis elbow have not been tested for their sensitivity or specificity. Each of the described special tests stresses other soft tissue located in the lateral elbow region, especially the radial nerve. Therefore, it is important to correlate the results of the special tests performed with the rest of the clinical examination. Because each special test is targeted to examine the same soft tissue, with appropriate rest, the ability to differentiate between structures should improve.

Tennis Elbow Test

The tennis elbow test, the traditional test used to assess tennis elbow, is sometimes referred to as Cozen’s test. Figure 82-3 shows that the patient’s elbow is stabilized by the examiner’s thumb, which rests on the patient’s lateral epicondyle. The patient actively makes a fist with the forearm in a pronated position. The patient actively extends the wrist and radially deviates while the examiner resists the motion. A positive finding is sudden, severe pain in the area of the lateral epicondyle of the humerus.

Figure 82-3

Tennis elbow test or Cozen’s test used to reproduce pain of the common extensor tendon.

Mills’ Tennis Elbow Test

In 1937, Mills originally described this test as a manipulation technique for patients with lateral elbow pain and limited elbow extension with the forearm pronated. He indicated that the limited elbow extension might be slight and have only a springy resistance to movement not evident on the noninvolved extremity. Mills deduced that some “tense bands,” which were painful upon stretch, were ruptured with the manipulation. It is not clear what structures in the lateral elbow region may be associated with the tense bands. Mills clearly stated that this technique should not be used on patients with muscular pain in the region. He recommended that the manipulation be performed only if there was a limitation in elbow extension.

In current practice, many clinicians do not perform the manipulation maneuver, but they use the extremity positions to provoke symptoms associated with tennis elbow. While palpating the lateral epicondyle or the most tender point near the lateral epicondyle, the examiner pronates the patient’s forearm and fully flexes the wrist as the elbow is gradually brought into full extension from the flexed position, as shown in Figure 82-4 . Although the original description by Mills does not indicate shoulder position, the test is usually performed with the arm at the side to avoid tension on radial nerve. A positive sign is exacerbation of pain over the lateral epicondyle, which may be accompanied by a slight limitation in elbow extension with a springy end-feel. The Mills’ test position is often used during the rehabilitation phase as a stretching technique. ,

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Apr 21, 2019 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Elbow Tendinopathies: Clinical Presentation and Therapist’s Management of Tennis Elbow

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