One of the most common upper extremity overuse problems is lateral epicondylitis (LE), commonly referred to as tennis elbow. LE affects roughly 1–3 percent of the general population in the United States each year. Despite its common name of tennis elbow, only about five percent of the people with LE developed the condition from playing tennis.1
The dramatic increase of repetitive motions in numerous occupations has led to a surge of epicondylitis over the last several decades. Due to the nature of our work, LE is a common problem affecting massage therapists.
There are also heavy socioeconomic burdens associated with this condition. These burdens include lost productivity for employers, lost or diminished wages for employees, long periods of pain, and significant workers’ compensation claims. This article will focus on lateral epicondylitis, but the same principles hold for medial epicondylitis, which is a similar condition affecting the wrist flexor muscles.

Anatomical Background

Lateral epicondylitis affects the common wrist extensor tendon near the elbow. This proximal tendon is a conjoined tendon shared by the extensor carpi radialis brevis, extensor digitorum, extensor digiti minimi, and extensor carpi ulnaris (Image 1). The main tendon affected in most cases of LE is the extensor carpi radialis brevis (ECRB). It’s not immediately clear why this tendon is affected more than the others, except that its anatomical arrangement and line of pull are likely putting the greatest load on this portion of the tendon.
This common tendon inserts into the lateral epicondyle of the humerus. When the tendon is overused, tenderness can be felt in the tendon, as well as where the tendon blends into the periosteum of the bone. The periosteum is a thin membrane covering the bone and is one of the most pain-sensitive tissues in the body. That is one reason why constant pulling from an overused tendon produces pain at the tendon attachment site.

The Pathology

LE is most commonly associated with repetitive overuse actions of the wrist extensor muscles. These actions could include repetitive or forceful wrist extension, long periods of gripping objects, or movements that include forearm supination or radial deviation. Repetitive eccentric loading on the wrist extensors is also a primary cause. A repetitive eccentric load would be one where the wrist extensors are trying to prevent the wrist from moving into flexion while slowly resisting that motion (Image 2).
In addition to repetitive motion, long periods of isometric contraction of the wrist extensors may also lead to LE. For example, grasping tools or implements during occupational activities might not involve repetitive motion as much as constant contraction to hold the implement in a certain position. Computer users who spend much time operating a mouse develop epicondylitis for this reason. It’s not so much that there is a repetitive wrist extension movement as much as the wrist extensors and flexors are both in a chronic degree of isometric activity when holding and manipulating the mouse. Because both muscle groups, flexors and extensors, are overused at the same time, it is common to develop either medial or lateral epicondylitis from long periods using a computer mouse.
Other factors play a role in developing epicondylitis. Body mass index, history of rotator cuff disease, de Quervain’s tenosynovitis, carpal tunnel syndrome, and a history of smoking are all correlated with a higher incidence of lateral epicondylitis. It may be that some of these factors developed from the same mechanical stressors and just happened to occur simultaneously. The relationship between these corresponding factors is an important distinction. Just because those conditions occur together doesn’t mean that one of them caused the other.
The name of this condition, epicondylitis, would indicate that there is a primary inflammatory component because of its suffix, -itis. The original theories of epicondylitis suggested that it resulted from micro-tearing and inflammatory reactions within the extensor tendons. However, further investigations with increasingly sophisticated diagnostic instruments over the last several decades have revealed that epicondylitis, like most chronic overuse tendon disorders, is not an inflammatory condition caused by fiber tearing. Instead, the primary dysfunction appears to be collagen degeneration within the tendon.2 We have a better understanding of the actual physiology of tendon breakdown in these conditions now, but still don’t have a good understanding of why the collagen degeneration occurs.
There may still be some minor inflammatory activity at certain stages of the problem. However, framing the condition as one of fiber tearing and inflammation encourages a problematic treatment strategy. One of the primary treatment methods for reducing inflammation in soft tissues is corticosteroid injections. Unfortunately, corticosteroids have detrimental effects on long-term collagen synthesis within soft tissues and are a known factor in tendon weakening. The corticosteroid injections are effective at pain relief, which gives them the impression of healing the condition, but are detrimental in the long run.
Jill Cook, one of the most prolific researchers into tendon pathology, authored a paper along with her colleagues in 2009 that presented a new model for chronic tendon dysfunction such as epicondylitis.3 In this paper, they propose that tendon dysfunction exists on a continuum consisting of three essential stages of breakdown: reactive tendinopathy, tendon disrepair (failed healing), and degenerative tendinopathy. Each of these different stages has different physiological characteristics and responses to treatment. One reason that many overuse tendon pathology treatments seem effective is that one treatment is applied to conditions that are at different stages of the continuum. How different treatment strategies match up with the tendon dysfunction continuum is explained further in the treatment section below.
As with other soft-tissue pathologies, there is not a direct correlation between the amount of pain and the level of tissue degeneration/damage to the tendon. In some cases, there is a significant degree of tissue damage/degeneration with very little pain. In other cases, there is only a minor degree of damage and a great deal of pain. It is feasible that chronic overuse tendon pain may have more to do with certain biochemical processes in the tissue that irritate nociceptors than a measure of dysfunctional load on the tissues.

Assessment

Identifying lateral epicondylitis is usually pretty easy. The tissues are superficial, and the indicators that lead to this are often clearly identified within the client history. Initial intake usually reveals some history of repetitive motion or constant isometric load affecting the wrist extensor group. The client may also complain of grip strength loss. Their pain is usually around the lateral aspect of the elbow but may also extend down into the forearm. The pain is commonly described as a dull aching sensation. Palpating the involved tendons usually increases the pain significantly.
Because the wrist extensor muscles are involved, it seems likely that any motions of active wrist extension should reproduce the pain. However, simply moving the wrist in extension with no additional resistance often does not reproduce any pain. Just lifting the wrist is only minimal resistance, so very little load is on the tendon in active motion with no additional resistance. If, however, there is resistance throughout the range, reproduction of the client’s pain is more likely.
Pain at the lateral elbow region is also common with resisted wrist extension. The pain is likely to be even greater if the various extensor tendons are palpated just distal to their attachment site during the resisted wrist extension. Palpating the tendon during resisted wrist extension is called the tennis elbow test (Image 3).

Treatment

There is no gold standard treatment for lateral epicondylitis. As noted earlier, the wide variability in treatment effectiveness may be more about the stage of tendon dysfunction than the actual success or failure of a particular treatment approach across the board.
The most common traditional medical treatments for LE are various conservative treatment strategies. Symptoms generally resolve with these conservative treatments within a few months to around a year in some resistant cases. The most common strategies employed include physical therapy, nonsteroidal anti-inflammatory drugs (NSAID), shockwave therapy, kinesiology taping, biologics, or corticosteroid injections.
Biologics is a general term used to refer to several new treatment techniques, such as autologous blood transfusion (the collection of blood from the patient and re-transfusion of that same blood back into the patient). Platelet-rich plasma (PRP) injection therapy is another approach in this category. PRP injections use a method where platelets, which play a major role in tissue repair, are extracted from the individual and reinjected to stimulate tissue repair processes. It is also surprising that corticosteroid injections are still used as a treatment strategy even though their potential danger and damage of tendon tissue has been well documented for decades. They aren’t used anywhere near as often as they used to be, but they are still used in some cases.
For determining the most effective treatments, the tendon dysfunction continuum model mentioned earlier is divided into two main categories. Reactive tendinopathy and early tendon disrepair is the first stage. The second stage is late tendon disrepair and degenerative tendinopathy. Following are some recommended treatment strategies at the different stages.
Stage 1
• Pharmacologic interventions like NSAID
• Tendon load management (reducing the offending load and rest from offending activities)
Stage 2
• Biologic therapies
• Shockwave therapy
• Exercise (emphasizing eccentric loading on the muscle-tendon unit)
• Ultrasound
• Massage

So what role does massage play in epicondylitis treatment? One of the most commonly used massage treatment strategies is deep transverse friction (DTF). Originally it was thought that the primary benefit of DTF was helping to realign scar tissue from the torn tendon fibers. However, that idea has now fallen out of favor as it has become clear that torn tendon fibers rarely play a role in epicondylitis. Also, it’s not clear that realigning scar tissue fibers with thumb friction is even possible because of the multiple tissues between the thumb and the damaged tissue.
Some research studies that have looked into friction massage have shown that there appears to be some degree of enhanced fibroblast proliferation as a result of the pressure and movement of the friction massage. So in LE, pressure and movement on the impaired extensor tendons could be encouraging rebuilding of the damaged collagen structure within the tendon.
Another possibility is that the key benefits of friction massage are not only mechanical (pressure and movement), but also help in pain reduction through neurological processes. There is a neurological principle called conditioned pain modulation (CPM), which suggests that in certain cases, a low to moderate pain stimulus can essentially act as a distractor and reduce other pain sensations.4 Friction massage is usually performed at a level that can be somewhat uncomfortable, so its benefit in pain reduction could be at least partially due to CPM.
An important aspect of reducing the tendon load to encourage healing is to decrease chronic hypertonicity in the associated muscles. Reducing hypertonicity is another important role that massage can play in treating epicondylitis. A wide variety of techniques can be effective at helping reduce hypertonicity in the wrist extensor muscles. Superficial applications that appear particularly effective are good compressive effleurage and broad sweeping cross-fiber applications.
As treatment progresses, deeper longitudinal stripping methods, especially those with a small contact surface like a thumb, fingertip, or pressure tool, are very effective. Active engagement lengthening techniques appear to bring good results as well. In this technique, the practitioner applies a deeper longitudinal stripping technique to the wrist extensor muscles while they are engaged in an eccentric (lengthening) action (see video). Engaging the muscle in an eccentric contraction involves greater neurological input along with the massage technique. This greater neurological input may serve to enhance a pain-reducing process called descending modulation. We know this treatment is particularly effective, and it may be that much of this effect is due to the enhanced descending modulation.
Lateral epicondylitis can become a debilitating condition, and because it is often related to occupational injuries, the condition can provoke significant anxiety. It may appear as if a person, such as a massage therapist, will no longer be able to continue performing their chosen occupation. When caught early, activity modification and reduction of the mechanical load can halt the progression of the condition. If it has progressed further, massage is an ideal intervention for enhancing physiological change, as well as managing psychological and social impacts of this common malady.

Notes

1. Wilson C. Lai et al., “Chronic Lateral Epicondylitis: Challenges and Solutions,” Open Access Journal of Sports Medicine 9 (October 2018): 243–51, https://doi.org/10.2147/Oajsm.S160974.
2. Evelyn Bass, “Tendinopathy: Why the Difference Between Tendinitis and Tendinosis Matters,” International Journal of Therapeutic Massage and Bodywork 5, no. 1 (March 2012): 14–17.
3. J. L. Cook and C. R. Purdam, “Is Tendon Pathology a Continuum? A Pathology Model to Explain the Clinical Presentation of Load-Induced Tendinopathy,” British Journal of Sports Medicine 43, no. 6 (June 2009): 409–16, https://doi.org/10.1136/Bjsm.2008.051193.
4. D. Yarnitsky, “Conditioned Pain Modulation (The Diffuse Noxious Inhibitory Control-Like Effect): Its Relevance for Acute and Chronic Pain States,” Current Opinion in Anaesthesiology 23, no. 5 (October 2010): 611–15, https://doi.org/10.1097/ACO.0b013e32833c348b.