Assessment of Tennis Elbow

Original Editor - Mariam Hashem

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Tennis Elbow, also known as Lateral Epicondylitis, is described as pain over the lateral epicondyle of the humerus. It is a common presentation between 35-45 years of age. Smoking, obesity, manual work requiring repetitive loading of wrist extensors and tennis players are considered to be risk factors of Tennis Elbow[1]. Most seen in dominant arm[2].

Tennis Elbow has great effects on the quality of life as well as the participation in work, sports and leisure activities.

Despite the fact that tennis players represent 5-10% of the represented cases, the term Tennis Elbow is widely recognized among physiotherapists, general practitioners and patients more than Lateral Epicondylitis. [3]

Annually, 4-7 out of 1000 cases are Tennis Elbow[2] Lateral Tendinopathy is seen in 1-3% of the general population.

Although up to 90% of the presentations are self-limiting,, not all of them experience full recovery and the pain and discomfort last up to a year. Recurrence is also common in Tennis Elbow and around 5% need surgery.

Work absenteeism is documented in 5% of affected working adults, with a median duration of 29 days in the previous 12-month time period[4].

In a recent randomized controlled trial, 72% of patients reported a recurrence in their condition within 12 months of receiving a corticosteroid injection in comparison to 9% with a ‘‘wait and see’’ policy[5].


The structural pathology is not always evident in various clinical presentation. In fact, some studies reported discordance between clinical severity and tendon pathology in patients with tendinopathy. This drives our attention to the multi-factorial nature of many MSK conditions. Psychological factors, central sensitization and/or other CNS-mediated factors may play roles in the onset and prognosis of the condition[1].

From a histological point of view, Lateral Teninopathy seems to be progressing as any other tendinopathy, increased cellularity, an accumulation of ground substance, collagen disorganization, and neurovascular ingrowth. In the case of Tennis Elbow this process is observed in the deep and anterior fibers of the extensor carpi radialis brevis (ECRB). In sever presentations, the ECRB is often merged with the lateral collateral ligament (LCL), which fuses with the annular ligament of the proximal radioulnar joint.

Understanding tendon changes associated with Tennis Elbow affects the rehabilitation decisions.

Baseline sever pain is predictable of poorer outcomes

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

Coombes et al [2]proposed a pathophysiological integrative model of Tennis Elbow based on previous studies. The pathophysiology is multifactorial and not all individuals are present with the same clinical presentation. An integration of the local tendon pathology, changes in the pain system and impairment in the motor system are hypothesized to be the etiology of TE. This model is great to understand TE and also to facilitate patients' sub-grouping.

Similar to other tendons, the ECRB is subjected to the same structural changes (angiofibroblastic hyperplasia) describing this process as mainly degenerative rather than inflammatory. as a result of overuse, underuse or a cobmbination of different forces across the tendon insertion. Both very high strain and low strain levels predispose the tendon to structural changes.

The presence of neurochemical pain mediators is evident in TE which is believed to be one of the contributing factors to the reduced pain threshold in TE.

Pain free gripping strength is reduced by about 60% in affected side TE compared to the opposite side[9], often biliaterally[6]. Muscle weakness of upper limb was studied in individuals with TE and found to be reduced except in the metacarpophalangeal joint associated with morphological changes in the muscle finbers[10]. .72 It was suggested that LE sufferers may maintain or increase strength of the finger extensors to compensate for weakness in the wrist extensors. This weakness last even after resolution of symptoms indicating incomplete recovery[9]. Electromygraphic studies on tennis players with TE found activity within ECRB muscle in LE-affected players was significantly lower during the early acceleration phase, while greater at ball impact compared with uninjured players. Also ECRB was found to produce 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. poor proprioception, deficits in wrist position during extension and reaction time during reaching activities suggesting motor impairments[9].

Lateral Elbow Teninopathy

Simply, a normal tendon composes of type I collagen arranged in parallel fibers. Tensocytes are present between the rows of collagen, they respond to mechanical loading by structural changes. Chnages in cellularity, vascularity and collagen abnormailites are observed in tendinopathies. Cellular changes associated with tendinosis are hyperplasia, hypertrophy, rounding of the tenocytes, and a decreased nucleus-to-cytoplasm ratio, increased metabolic activity and production of type 3 rather than type 1 collagen.

In grade 1 disease, the collagen fiber pattern becomes increasingly wavy. Although cellular and vascular changes are minimal, there is an increase in the proportion of type 3 collagen. In grade 2, there is tendinosis and angiofibroblastic hyperplasia as first described by Nirschl and Pettrone,66 with further disorganization and fragmentation of the collagen fibers, cellular hyperplasia, rounding of tenocytes, and neovascular hyperplasia. In grade 3 tendinopathy, programmed cell death leads to the depletion of functional tendon cells and breakdown of collagen and extracellular matrix. Finally, grade 4 presents with gross structural disruption and mechanical failure. These changes may cause malfunction of tendon and joint biomechanics. As a major contributor to tissue tensile strength, it was suggested that collagen turnover dynamics may be altered under conditions of stress and immobilization. These authors concluded that synthesized collagen fibers in such immobilized ligaments must be laid down in a haphazard manner due to the absence of the usual controls of matrix orientation as imposed by physical forces.

Wang et al102 designed a bioreactor system allowing the application of mechanical stimulation on ex vivo rabbit Achilles tendons. They showed that in the absence of any load, tendons bathed in growth medium displayed typical histological features of tendinosis after only 6 days. By 2 weeks, 95% of the cells in these unloaded tendons had undergone apoptosis. Tendons subject to 3% cyclical tensile strain displayed similar but milder features, without the high rates of apoptosis. In contrast, tendons subject to 6% cyclical strain were histologically normal. At the other end of the spectrum, tendons subject to 9% strain had partially torn and again showed histological features of severe tendinosis. These findings complement the results from previous studies37,44 and begin to identify the ideal strain conditions for tendon homeostasis[11].

Tennis Elbow and Central Sensitization

Hightened Withdrawl reflex is evident in Tennis Elbow in addition to mechanical hyperalgesia and cold hyperalgesia. Clinical ice pain test, a simple test allows clinicians to examine pain senstivity. Pain intensity of more than 5/10, after 10 seconds of ice application indicated 90% likelihood of cold hyperalgesia.

Clinical assessment that identifies increased responsiveness to a variety of physical and emotional stimuli, heightened response to neurodynamic testing, or expansion of symptoms to sites outside the injured area may provide the clinician with important clues for central sensitization.

A study focused on detecting central senstization signs in MSK pain in clincial setting, a thorough history taking is essential to determine sentral senstization symptoms such as stimuli including mechanical pressure (Desmeules et al., 2004), chemical substances (Morris et al., 1997), cold temperature (Kasch et al., 2005), heat temperature (Meeus et al., 2008), electrical stimuli (Banic et al., 2004; Desmeules et al., 2004), stress, emotions, and mental load. hypersenstivitiy in general

Although there is currently no convincing evidence in support of their association with central sensitization, ‘central’ symptoms such as fatigue, concentration difficulties, sleep disturbances, and non-refreshing sleep are all frequently experienced by patients with central sensitization (Wolfe et al., 1990, Yunus, 2007b). Thus, questioning the patient with musculoskeletal pain about the presence of these symptoms might be warranted when searching for central sensitization.Firstly, the presence of a local pain condition prior to the onset of a trauma or injury increases the probability for developing peripheral and central sensitization.

Some MSK consitions are not purely central senstization in nature, but rather associated with signs of central senstization

Firstly, it starts with the medical diagnosis, some medical consitions are characterized as being a central sensitization in nature, otherwise central senstization is charactrized in some subgroups. The presence of central senstization in Tennis elbow has not been investigated enough and the results remain inconclusive. However, the search for central senstization continues through history taking. There are some information obtained in history relates to the presence of CS such as: hypersenstivity to : bright light, touch, noise, mechanical pressure, medication, temprature. 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 clue for CS, if non present CS is excluded. If any of these symptoms are present, the clinicians may take it further to examining pain thresholds, sensitivity to touch during manual palpation, sensitivity to vibration, sensitivity to heat and sensitivity to cold at sites remote from the synptomatic area. Also, assessment of pressure pain thresholds during and following exercise, assessment of joint end feel and Brachial plexus provocation test[12].


Pain provoking tests are the most utilized method of dianosing 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[1].

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:

  • clicking
  • loss of control
  • difficulty with pushing up with the forearm supinated

The posterolateral rotary drawer test can be used if instability was suspected which may need to be further examined by imaging[1].

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

Postural analysis and correction to influence the whole kinematic chain.

Individuals with Tennis Elbow commonly grip with the elbow in a more flexed position and display reduced pain-free grip force and weakness of the short wrist extensors (ECRB) but not the finger extensors. the weakness is widespread in the muscles of the affected upper limb. Also, bilateral deficits in reaction time and speed of movement were found in individuals with TE. This may refer to maladaptive cortical organization changes. therefore motor control training, strength and enduarance training should be put into consideration in the rehabilitaiton plan.

Outcome Measures

The pain-free grip test and the Patient Rated Tennis Elbow Evaluation (PRTEE). Although the pain free grip test is a reliable and sensitive measure, the grip strength is not always impaired in Tennis Elbow and it may exacerbate the symptoms. A study supported the use of PFG with thte elbow in extension as the most indicated monitoring of recovery in TE

PRTEE is a good measure for categorizing pain and disability and also to track improvement.Furthermore, patients with severe symptoms (PRTEE scores greater than 54) have been found to display more pronounced sensory disturbances that may be targeted by different pharmacological therapies

The Patient-Specific Functional Scale (PSFS) is another validated and reliable measure that could measure disability in functional activities as a general[1].


A literature review summed the following[1]:

  • MRI is sensitive but not specific
  • Ultrasonography detected tendopathic changes on 90% affected and 50% unaffected tendons
  • The severity of tendon changes is not always reflected by the degree of symptoms. This is general to all tendinopathies and not exclusive to Tennis elbow.
  • 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
  • Ultrasound can detect tendon changes, tendon tears, calcification or bony irregularity
  • Tendon neovascularisation in LE has been detected with Doppler ultrasound and correlated with degenerative tissue on biopsy.41 47 Comparison of these two imaging modalities by du Toit et al (2008) found neovascularity detected by power-Doppler to be diagnostically superior in identifying. chronic LE compared with grey-scale changes.The absence of both tendon neovascularity and grey-scale changes was shown to conclusively rule out LE as a diagnosis and should prompt further investigation. Neovascualrity wasn't associated with pain severity or function.

Differential Diagnosis

A research paper suggested a table to differentiate Tennis Elbow from other similar pathologies. This could be challenging for clinicians as the symptoms are often similar.


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  2. 2.0 2.1 2.2 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.
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