Assessment of Tennis Elbow: Difference between revisions

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== Introduction and Epidemiology ==
== Introduction ==
Tennis [[Elbow]], also known as [[Lateral Epicondylitis]] or Lateral Epicondylopathy, is described as pain and sensitivity over the lateral epicondyle of the [[humerus]]. <ref name=":4" /><ref>Cutts S, Gangoo S, Modi N, Pasapula C. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6926298/ Tennis elbow: A clinical review article]. Journal of orthopaedics. 2020 Jan 1;17:203-7.</ref> Tennis Elbow is the most common cause of lateral elbow pain<ref name=":4">Keijsers R, de Vos RJ, Kuijer PPF, van den Bekerom MP, van der Woude HJ, Eygendaal D. Tennis elbow. Shoulder Elbow. 2019;11(5):384-92. </ref> and it is a common musculoskeletal presentation generally (4-7 out of 1000 MSK conditions annually <ref name=":1">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.</ref>, and about 1-3% of the general population), often seen between 35-45 years of age in the dominant arm<ref name=":1" />.  
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<ref name=":0">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.</ref>. Most seen in dominant arm<ref name=":1">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.</ref>.  


Tennis Elbow has great effects on the quality of life as well as the participation in work, sports and leisure activities.  
Smoking, obesity, manual work requiring repetitive loading of wrist extensors and being a tennis player are considered to be risk factors of Tennis Elbow<ref name=":0">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.</ref>. The female gender is also associated with tennis elbow.<ref>Sayampanathan AA, Basha M, Mitra AK. Risk factors of lateral epicondylitis: A meta-analysis. Surgeon. 2020;18(2):122-8. </ref>


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. <ref>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.</ref>  
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<ref>Chesterton LS, Mallen CD, Hay EM. Management of tennis elbow. Open access journal of sports medicine. 2011;2:53.</ref>.


Annually, 4-7 out of 1000 cases are Tennis Elbow<ref name=":1" /> Lateral  Tendinopathy is seen in 1-3% of the general population.
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.<ref>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.</ref>


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.
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 <nowiki>''</nowiki>wait and see<nowiki>''</nowiki> approach<ref>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.</ref>,  and around 5% need surgery<ref name=":0" />.
 
Work absenteeism is documented in 5% of affected working adults, with a median duration of 29 days in the previous 12-month time period<ref>Walker-Bone K, Palmer KT, Reading I, Coggon D, Cooper C. Occupation and epicondylitis: a population-based study. Rheumatology. 2011 Oct 22;51(2):305-10.</ref>.
 
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<ref>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.</ref>.


== Pathophysiology ==
== Pathophysiology ==
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<ref name=":0" />.
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<ref name=":0" />.
 
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.
Coombes et al <ref name=":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.


Baseline sever pain is predictable of poorer outcomes
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|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<ref name=":1" />.


Some studies found a link between stress, anxiety<ref name=":2">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.</ref><ref>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.</ref> and TE while others reported no association<ref>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.</ref>.
Some studies found a link between stress, anxiety<ref name=":2">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.</ref><ref>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.</ref> and while others reported no association<ref>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.</ref>.


Coombes et al <ref name=":1" />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.  
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<ref name=":1" />.  


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.  
Muscle weakness is also found in Tennis Elbow. Pain free gripping was reduced by about 60% compared to non affected side<ref name=":1" />, another study found bilateral weakness<ref name=":2" /><ref>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.</ref> and another reported weakness in the whole upper limb except for the metacarpophalangeal joint muscles<ref>Ljung BO, Lieber RL, Friden J. Wrist extensor muscle pathology in lateral epicondylitis. Journal of Hand Surgery. 1999 Apr;24(2):177-83.</ref>.   The last finding suggests Tennis Elbow patients may maintain or increase strength of the finger extensors to compensate for weakness in the wrist extensors<ref name=":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<ref name=":12">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.</ref>.  


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<ref name=":12">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.</ref>, often biliaterally<ref name=":2" />. 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<ref>Ljung BO, Lieber RL, Friden J. Wrist extensor muscle pathology in lateral epicondylitis. Journal of Hand Surgery. 1999 Apr;24(2):177-83.</ref>. .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<ref name=":12" />. 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<ref name=":12" />.
=== 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<ref>Bhabra G, Wang A, Ebert JR, Edwards P, Zheng M, Zheng MH. Lateral elbow tendinopathy: development of a pathophysiology-based treatment algorithm. Orthopaedic Journal of Sports Medicine. 2016 Nov 1;4(11):2325967116670635.</ref>.
=== Tennis Elbow and Central Sensitization ===
=== 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.
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<ref name=":3" />.


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
[[Central Sensitisation|Central sensitization]] (CS) could be detected clinically starting with a thorough history taking and use of the [http://www.endoexperience.com/documents/apx4_lanss.pdf 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<ref name=":3">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.</ref>.


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.
== 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 (Maudsley's test); and having the patient grip an object<ref name=":0" />. [https://www.physio-pedia.com/Mill%E2%80%99s_Test Mill's Test] and [[Cozen’s Test|Cozen's test]] may also be included in the assessment.<ref name=":0" /><ref>Fleming J, Muller C, Lambert K. [https://ofpjournal.com/index.php/ofp/article/view/723/626 Lateral epicondylitis: A common cause of elbow pain in primary care]. Osteopathic Family Physician. 2021;13(1):34-8.</ref>


Some MSK consitions are not purely central senstization in nature, but rather associated with signs of central senstization
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 [[Postero-lateral Elbow Instability|elbow instability]] should be noted, such as clicking, loss of control and difficulty with pushing up with the forearm supinated<ref name=":0" />.  
== Examination ==
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<ref name=":0" />.


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<ref name=":0" />.
The posterolateral rotary drawer test can be used if instability was suspected which may need to be further examined by imaging<ref name=":0" />.


In the presence of arm pain or neck pain, the cervical and thoracic spines and the radial nerve should all be examined.
In the presence of arm pain or neck pain, the [[Cervical Examination|cervical]] and [[Thoracic Examination|thoracic]] spines and the [[radial nerve]] should all be examined<ref name=":0" />.  
 
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.  
Also, examination of posture and motor control should be considered to understand the kinematic influence and tackle any abnormalities in the rehabilitation<ref name=":0" />.  


== Outcome Measures ==
== 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
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.


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
[https://srs-mcmaster.ca/wp-content/uploads/2015/05/English-PRTEE.pdf 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 as a general<ref name=":0" />.
[[Patient Specific Functional Scale|The Patient-Specific Functional Scale (PSFS)]] is another validated and reliable measure that could measure disability in functional activities in general<ref name=":0" />.


== Imaging ==
{{#ev:youtube|phAC-VIWr5Q}}<ref>Measuring Grip Strength. Available from: https://www.youtube.com/watch?v=phAC-VIWr5Q</ref>
'''A literature review summed the following'''<ref name=":0" />:
{{#ev:youtube|qKSn_RNpSAE}}
* MRI is sensitive but not specific
{{#ev:youtube|2HcZbsHFkk0}}
* 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 ==
== Differential Diagnosis ==
[https://www.jospt.org/doi/pdf/10.2519/jospt.2015.5841 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.  
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<ref name=":0" />. 
 
[https://www.jospt.org/doi/pdf/10.2519/jospt.2015.5841 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'''<ref name=":0" />:
* [[MRI Scans|MRI]] is sensitive but not specific
* A recent study by Jeon and colleagues found that when MRI is combined with clinical assessment, it can help to facilitate management planning for tennis elbow<ref>Jeon JY, Lee MH, Jeon IH, Chung HW, Lee SH, Shin MJ. Lateral epicondylitis: Associations of MR imaging and clinical assessments with treatment options in patients receiving conservative and arthroscopic managements. Eur Radiol. 2018;28(3):972-81. </ref>
* [[Ultrasound Scans|Ultrasonography]] detected tendopathic changes on 90% affected and 50% unaffected tendons. It also detects tendon tears, calcification and bony irregularity. However, in 2020, Krogh and colleagues found that outcomes such as pain, disability, Patient-Rated Tennis Elbow Evaluation score, and disease duration did not correlate with ultrasound techniques, such as tendon thickness, color Doppler activity, and bone spurs<ref>Krogh TP, Fredberg U, Ammitzbøll C, Ellingsen T. Clinical Value of Ultrasonographic Assessment in Lateral Epicondylitis Versus Asymptomatic Healthy Controls. Am J Sports Med. 2020;48(8):1873-83. </ref> 
* Negative Ultrasound can be used to rule out Tennis Elbow  
* If clicking or locking are present, MRI,[[CT Scans|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|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 ==
== References ==
<references />
<references />
[[Category:Elbow]]
[[Category:Assessment]]
[[Category:Elbow - Assessment and Examination]]
[[Category:Course Pages]]
[[Category:Plus Content]]

Latest revision as of 12:11, 31 May 2023

Original Editor - Mariam Hashem

Top Contributors - Mariam Hashem, Kim Jackson, Tony Lowe, Tarina van der Stockt, Jess Bell, Nupur Smit Shah, Rachael Lowe, Simisola Ajeyalemi, Lucinda hampton, Olajumoke Ogunleye and Robin Tacchetti  

Introduction and Epidemiology[edit | edit source]

Tennis Elbow, also known as Lateral Epicondylitis or Lateral Epicondylopathy, is described as pain and sensitivity over the lateral epicondyle of the humerus. [1][2] Tennis Elbow is the most common cause of lateral elbow pain[1] and it is a common musculoskeletal presentation generally (4-7 out of 1000 MSK conditions annually [3], and about 1-3% of the general population), often seen between 35-45 years of age in the dominant arm[3].

Smoking, obesity, manual work requiring repetitive loading of wrist extensors and being a tennis player are considered to be risk factors of Tennis Elbow[4]. The female gender is also associated with tennis elbow.[5]

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[6].

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.[7]

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[8], and around 5% need surgery[4].

Pathophysiology[edit | edit source]

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[4].

Coombes et al [3] 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[3].

Some studies found a link between stress, anxiety[9][10] and while others reported no association[11].

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[3].

Muscle weakness is also found in Tennis Elbow. Pain free gripping was reduced by about 60% compared to non affected side[3], another study found bilateral weakness[9][12] and another reported weakness in the whole upper limb except for the metacarpophalangeal joint muscles[13]. The last finding suggests Tennis Elbow patients may maintain or increase strength of the finger extensors to compensate for weakness in the wrist extensors[3]. 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[14].

Tennis Elbow and Central Sensitization[edit | edit source]

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[15].

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[15].

Examination[edit | edit source]

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 (Maudsley's test); and having the patient grip an object[4]. Mill's Test and Cozen's test may also be included in the assessment.[4][16]

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[4].

The posterolateral rotary drawer test can be used if instability was suspected which may need to be further examined by imaging[4].

In the presence of arm pain or neck pain, the cervical and thoracic spines and the radial nerve should all be examined[4].

Also, examination of posture and motor control should be considered to understand the kinematic influence and tackle any abnormalities in the rehabilitation[4].

Outcome Measures[edit | edit source]

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[4].

[17]

Differential Diagnosis[edit | edit source]

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[4].

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[edit | edit source]

A literature review summarized the following[4]:

  • MRI is sensitive but not specific
  • A recent study by Jeon and colleagues found that when MRI is combined with clinical assessment, it can help to facilitate management planning for tennis elbow[18]
  • Ultrasonography detected tendopathic changes on 90% affected and 50% unaffected tendons. It also detects tendon tears, calcification and bony irregularity. However, in 2020, Krogh and colleagues found that outcomes such as pain, disability, Patient-Rated Tennis Elbow Evaluation score, and disease duration did not correlate with ultrasound techniques, such as tendon thickness, color Doppler activity, and bone spurs[19]
  • 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[edit | edit source]

  1. ↑ 1.0 1.1 Keijsers R, de Vos RJ, Kuijer PPF, van den Bekerom MP, van der Woude HJ, Eygendaal D. Tennis elbow. Shoulder Elbow. 2019;11(5):384-92.
  2. ↑ Cutts S, Gangoo S, Modi N, Pasapula C. Tennis elbow: A clinical review article. Journal of orthopaedics. 2020 Jan 1;17:203-7.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 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.
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 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.
  5. ↑ Sayampanathan AA, Basha M, Mitra AK. Risk factors of lateral epicondylitis: A meta-analysis. Surgeon. 2020;18(2):122-8.
  6. ↑ Chesterton LS, Mallen CD, Hay EM. Management of tennis elbow. Open access journal of sports medicine. 2011;2:53.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 9.0 9.1 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.
  10. ↑ 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.
  11. ↑ 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.
  12. ↑ 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.
  13. ↑ Ljung BO, Lieber RL, Friden J. Wrist extensor muscle pathology in lateral epicondylitis. Journal of Hand Surgery. 1999 Apr;24(2):177-83.
  14. ↑ 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.
  15. ↑ 15.0 15.1 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.
  16. ↑ Fleming J, Muller C, Lambert K. Lateral epicondylitis: A common cause of elbow pain in primary care. Osteopathic Family Physician. 2021;13(1):34-8.
  17. ↑ Measuring Grip Strength. Available from: https://www.youtube.com/watch?v=phAC-VIWr5Q
  18. ↑ Jeon JY, Lee MH, Jeon IH, Chung HW, Lee SH, Shin MJ. Lateral epicondylitis: Associations of MR imaging and clinical assessments with treatment options in patients receiving conservative and arthroscopic managements. Eur Radiol. 2018;28(3):972-81.
  19. ↑ Krogh TP, Fredberg U, Ammitzbøll C, Ellingsen T. Clinical Value of Ultrasonographic Assessment in Lateral Epicondylitis Versus Asymptomatic Healthy Controls. Am J Sports Med. 2020;48(8):1873-83.
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