Assessment of Tennis Elbow

Original Editor - Mariam Hashem

Top Contributors - Mariam Hashem, Tarina van der Stockt, Tony Lowe, Rachael Lowe and Kim Jackson  

Introduction and Epidemiology

Tennis Elbow, also known as Lateral Epicondylitis or Lateral Epicondylopathy, is described as pain over the lateral epicondyle of the humerus. Tennis Elbow is a common musculoskeletal presentation (4-7 out of 1000 MSK conditions annually [1], about 1-3% of the general population), often seen between 35-45 years of age in the dominant arm[1].

Smoking, obesity, manual work requiring repetitive loading of wrist extensors and being a tennis player are considered to be risk factors of Tennis Elbow[2].

Tennis Elbow has great effects on quality of life as well as participation in work, sports and leisure activities. Work absenteeism is documented in 30% of Tennis Elbow patients[3].

Despite the fact that tennis players represent 5-10% of the represented cases, the term Tennis Elbow is more widely recognized among physiotherapists, general practitioners and patients than Lateral Epicondylitis.[4]

Although up to 90% of presentations are self-limiting, not all experience full recovery and pain and discomfort can persist for up to a year. Recurrence is also common in Tennis Elbow, about 72% after receiving a corticosteroid injection compared to 9% with a ''wait and see'' approach[5], and around 5% need surgery[2].

Pathophysiology

Research has proven that structural pathology is not present in many clinical presentations of Tennis Elbow. This is true particularly if Tennis Elbow is considered to be related to tendon pathology. A multifactorial model has been proposed by researchers to contribute to the related development of pain and disability with psychological factors, central sensitization and/or other CNS-mediated factors potentially playing roles in the onset and prognosis of the condition[2].

Coombes et al [1] proposed a pathophysiological integrative model explaining the development of Tennis Elbow. The model hypothesizes an integration of local tendon pathology, changes in the pain system, and impairment in the motor system as the factors behind Tennis Elbow. This could impact on the clinical decisions and research field to understand the nature of the condition and facilitate patients' sub-grouping.

From a histological point of view, increased cellularity, an accumulation of ground substance, collagen disorganization, and neurovascular ingrowth are similar to those observed in any other tendinopathy. In the case of Tennis Elbow this was observed in the deep and anterior fibers of the extensor carpi radialis brevis (ECRB). In severe presentations, the ECRB is often merged with the lateral collateral ligament (LCL), which fuses with the annular ligament of the proximal radioulnar joint. These structural changes could be the result of overuse, underuse or a combination of different forces across the tendon insertion. Both very high strain and low strain levels predispose the tendon to structural changes[1].

Some studies found a link between stress, anxiety[6][7] and while others reported no association[8].

The presence of neurochemical pain mediators is evident and is believed to be one of the contributing factors to the reduced pain threshold in Tennis Elbow[1].

Muscle weakness is also found in Tennis Elbow. Pain free gripping was reduced by about 60% compared to non affected side[1], another study found bilateral weakness[6][9] and another reported weakness in the whole upper limb except for the metacarpophalangeal joint muscles[10]. The last finding suggests Tennis Elbow patients may maintain or increase strength of the finger extensors to compensate for weakness in the wrist extensors[1]. Tennis players with a Tennis Elbow had significantly less ECRB activities during the early acceleration phase, while greater at ball impact compared with uninjured players. ECRB also produced less activity in isometric wrist extension and gripping tasks which was reversed with the relief of symptoms suggesting a link between neuromuscular activity and symptoms[11].

Tennis Elbow and Central Sensitization

Mechanical hyperalgesia and cold hyperalgesia are evident in Tennis Elbow. Clinical ice pain test, a simple test that allows clinicians to examine pain sensitivity. Pain intensity of more than 5/10, after 10 seconds of ice application indicates 90% likelihood of cold hyperalgesia[12].

Central sensitization (CS) could be detected clinically starting with a thorough history taking and use of the LANSS pain scale. There are some information obtained in history relates to the presence of CS such as: hypersensitivity to: bright light, touch, noise, mechanical pressure, medication, temperature. Sometimes the patient report being uncomfortable to partner hug or wearing sunglasses in buildings can be valuable in detecting CS. Fatigue, sleep disturbances, unrefreshing sleep, concentration difficulties, swollen feeling (e.g. in limbs), tingling and numbness may be clues for CS, if non present CS is excluded. If any of these symptoms are present, the clinicians may take it further to examine pain thresholds, sensitivity to touch during manual palpation, sensitivity to vibration, sensitivity to heat and sensitivity to cold at sites removed from the symptomatic area. Also, assessment of pressure pain thresholds during and following exercise, assessment of joint end feel and Brachial plexus provocation test[12].

Examination

Pain provoking tests are the most utilized method of diagnosing Tennis Elbow. This could be through palpating the lateral epicondyle, resisted extension of the wrist, index finger, or middle finger; and having the patient grip an object[2]. Mill's Test and Cozen's test can also be used to diagnose the condition.

ROM of elbow, wrist and forearm should also be examined along with the accessory motion of the radioulnar, radiohumeral, and humeroulnar joints to detect any underlying stiffness or restriction. During examination, signs of elbow instability should be noted, such as clicking, loss of control and difficulty with pushing up with the forearm supinated[2].

The posterolateral rotary drawer test can be used if instability was suspected which may need to be further examined by imaging[2].

In the presence of arm pain or neck pain, the cervical and thoracic spines and the radial nerve should all be examined[2].

Also, examination of posture and motor control should be considered to understand the kinematic influence and tackle any abnormalities in the rehabilitation[2].

Outcome Measures

The pain-free grip test. It is is a reliable in monitoring recovery and sensitive measure, however, it should be noted that grip strength is not always impaired in Tennis Elbow and the test may exacerbate the symptoms.

Patient Rated Tennis Elbow Evaluation is also a good measure for categorizing pain and disability and also to track improvement.

The Patient-Specific Functional Scale (PSFS) is another validated and reliable measure that could measure disability in functional activities in general[2].

[13]

Differential Diagnosis

Diagnosing Tennis Elbow may be challenging for clinicians because it shares similar clinical presentations with other pathologies such as non specific arm pain, arthritis, radial tunnel syndrome and posterior interosseous nerve entrapment. Distinguishing Tennis Elbow from other conditions is crucial to prescribe the most appropriate treatment options or refer the patient to a relevant healthcare specialist[2].

Refer to the table in this research paper to learn about the key features of different upper limb conditions that should help in differential diagnosis.

Imaging

A literature review summarized the following[2]:

  • MRI is sensitive but not specific
  • Ultrasonography detected tendopathic changes on 90% affected and 50% unaffected tendons. It also detects tendon tears, calcification and bony irregularity.
  • Negative Ultrasound can be used to rule out Tennis Elbow.
  • If clicking or locking are present, MRI,CT or magnetic resonance arthrography can be used to detect other pathologies such as loose bodies articular cartilage damage, ligament injury, or elbow synovial fold (plica) syndrome
  • Tendon neovascularisation in LE has been detected with Doppler ultrasound and correlated with degenerative tissue on biopsy. The absence of both tendon neovascularity and grey-scale changes was shown to rule out Lateral Tennis Elbow as a diagnosis and should prompt further investigation. Neovascualrity wasn't associated with pain severity or function.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Coombes BK, Bisset L, Vicenzino B. A new integrative model of lateral epicondylalgia. British journal of sports medicine. 2009 Apr 1;43(4):252-8.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Coombes BK, Bisset L, Vicenzino B. Management of lateral elbow tendinopathy: one size does not fit all. journal of orthopaedic & sports physical therapy. 2015 Nov;45(11):938-49.
  3. Chesterton LS, Mallen CD, Hay EM. Management of tennis elbow. Open access journal of sports medicine. 2011;2:53.
  4. Blanchette MA, Normand MC. Impairment assessment of lateral epicondylitis through electromyography and dynamometry. The Journal of the Canadian Chiropractic Association. 2011 Jun;55(2):96.
  5. Bisset L, Beller E, Jull G, Brooks P, Darnell R, Vicenzino B. Mobilisation with movement and exercise, corticosteroid injection, or wait and see for tennis elbow: randomised trial. Bmj. 2006 Nov 2;333(7575):939.
  6. 6.0 6.1 Alizadehkhaiyat O, Fisher AC, Kemp GJ, Frostick SP. Pain, functional disability, and psychologic status in tennis elbow. The Clinical journal of pain. 2007 Jul 1;23(6):482-9.
  7. Garnevall B, Rabey M, Edman G. Psychosocial and personality factors and physical measures in lateral epicondylalgia reveal two groups of “tennis elbow” patients, requiring different management. Scandinavian journal of pain. 2013 Jul 1;4(3):155-62.
  8. Coombes BK, Connelly L, Bisset L, Vicenzino B. Economic evaluation favours physiotherapy but not corticosteroid injection as a first-line intervention for chronic lateral epicondylalgia: evidence from a randomised clinical trial. Br J Sports Med. 2016 Nov 1;50(22):1400-5.
  9. Bisset LM, Russell T, Bradley S, Ha B, Vicenzino BT. Bilateral sensorimotor abnormalities in unilateral lateral epicondylalgia. Archives of physical medicine and rehabilitation. 2006 Apr 1;87(4):490-5.
  10. Ljung BO, Lieber RL, Friden J. Wrist extensor muscle pathology in lateral epicondylitis. Journal of Hand Surgery. 1999 Apr;24(2):177-83.
  11. Coombes BK, Bisset L, Vicenzino B. A new integrative model of lateral epicondylalgia. British journal of sports medicine. 2009 Apr 1;43(4):252-8.
  12. 12.0 12.1 Nijs J, Van Houdenhove B, Oostendorp RA. Recognition of central sensitization in patients with musculoskeletal pain: application of pain neurophysiology in manual therapy practice. Manual therapy. 2010 Apr 1;15(2):135-41.
  13. Measuring Grip Strength. Available from: https://www.youtube.com/watch?v=phAC-VIWr5Q