Underlying tendon pathology and pain processing changes are important to understand before approaching the diagnosis. Coombes et al, provides a few articles with excellent overview of LE pathophysiology and why our previous thought that this is a tendonitis or inflammatory response is incorrect.1 Under surgical approaches, chronic LE is void of any inflammatory cells – making this process similar to that in achilles and patellar tedonosis.4 Thus perpetuating the transition from language of tendonitis to angiofibroblastic hyperplasia, or tendinosis.4 Commonly involved ECRB tendon inserts with fibers into the lateral collateral ligament and annular ligament. The tendon pathology can experience various stresses including overuse, underuse, tensile, compressive or shear forces which improperly loads the tendon and leaves it harmed.1 As I once thought that all tendonopathies are overuse injuries – I stand corrected as Coombes et al. discusses that tissues can experience lower strain levels but this change predisposes structural weakening and making it vulnerable to load.1 More specifically trauma to the tendon adversely affects the homeostasis as collagen decreases in its longitudinal alignment, fibroblasts increase, and then the tendon decreases its tensile strength.1 These tendon changes are only part of the picture though, LE is compiled of these motor impairments but also seems to demonstrate altered pain processing systems. Thus why the classic approach of localized care at the elbow is a narrow approach for LE.
Since these pathophysiological changes occur at the cellular level – but as inflammatory response is not prevalent – why do people hurt? Thus a quick stop at speculated pain matrix is of curiosity of mine – and this is a very simplified overview for therapist thought. Many pain theories are prevalent within LE. As tendinosis has an increased concentration of neurochemicals and immature collagen at the insertion of ECRB, neovessel ingrowth is a speculated source of pain.1 Biochemical irritants may include extravasations of glycosamines, especially chondroitin sulphate from the injured tendon.3 Although the primary noxious matrix is unknown, other neurotransmitters have been recognized as abnormal in tendonosis including: glutamate, substance P and calcitonin.1,3 These have been located within sensory nerve bundles at the origin of the ECRB muscle in rats and humans and as glutamate is a pain mediator – people hurt.4Although these are hypothesized reasons for pain and the actual cause and effect seems to be unknown. In my treatments, it is less important for me to understand pathophysiological model of pain in LE, as it is to understand that patients with LE have been identified to have altered pain processing or hyperalgesia. Patients with LE, similar to CRPS, have been reported to be hypersensitive to thermal stimuli.2 Also, pressure point thresholds (PPT) are noted to be lower by 45-54% in patients with LE.1 It can be speculated that these can be a possible reason that we see moderately poor clinical outcomes.
Due to this altered pain response, we need for multimodal treatment models to address the patient as a whole. Treatment models should have localized treatments at the elbow, but also a general theme of the proposed concept of “regional interdependence.” Cleleand et. al performed a retrospective review of treatments for LE, and patients who received manual therapy had much less visits per episode.5 Fifty six percent of patients who have LE report cervical spine involvement as well.1 Another article states 70% of patients with LE reported cervical or thoracic pain.12This should spark PT interest to assess spine with treatment of LE. if we are looking at pain modulation, thoracic spine manipulation may be considered as manipulation in general has been noted to have affect on thermal pain sensitivity and perceived pain in the cervical spine.7,8Vicenzino et. al repeatedly found in 1996 article then again in 2001, a 10% reduction in PPT, and improvement in grip comfort after manipulation.10,11Thus, in conjunction to exercises localized at the elbow, and shoulder, a regional approach to cervical and thoracic spine involvement is warranted.
If a therapist is looking for time to fit these treatments in, consider removal of modalities. A systematic review by Bisset et al, again states “insufficient evidence” to support ultrasound, laser, or electrical stimulation with use when compared to placebo interventions in treatment of LE.9 Thus pooling best evidence treatments involve manual approaches at cervical spine, neural mobilization, mobilization with movement (MWM) at the elbow, and exercises focused at tissue mobility and strength are of best use of time.13,9An excellent article by Bisset et al looked at MWM with exercise and compared it to steroid injections or wait and see methods. Therapy that combined MWM and exercise had better outcomes compared to wait and see (NNT = 3), and although corticosteroid did have superior short term outcomes, remember that these patients have a much higher re-occurrence rate to be considered.13
Overall, treatment of LE should be multimodal and adapt to each patient starting at the elbow, then regionally as well. Pain processing needs to be considered, which is best served with education and manual techniques to put positive afferent input into pain processing systems. Followed by exercise routine based at improvement of stability and strength assessing the patient as a whole. With this treatment model, maybe we can improve our treatment effect. And although literature is my primary reference point as I see very few cases of LE in clinic, hopefully new literature will add to future management of these patients.
Original post: September 23, 2013
1) Coombes, B. K., Bisset, L., & Vicenzino, B. (2009). A new integrative model of lateral epicondylalgia. British journal of sports medicine, 43(4), 252–8. doi:10.1136/
2) Coombes, B. K., Bisset, L., & Vicenzino, B. (2012). Thermal hyperalgesia distinguishes those with severe pain and disability in unilateral lateral epicondylalgia. The Clinical journal of pain, 28(7), 595–601. doi:10.1097/AJP.0b013e31823dd33
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5) Cleland, J. a, Whitman, J. M., & Fritz, J. M. (2004). Effectiveness of manual physical therapy to the cervical spine in the management of lateral epicondylalgia: a retrospective analysis. The Journal of orthopaedic and sports physical therapy, 34(11), 713–22; discussion 722–4. doi:10.2519/
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7) Steven Z George, Mark D Bishop, Joel E Bialosky, Giorgio Zeppieri,Michael E Robinson. Immediate effects of spinal manipulation on thermal pain sensitivity: an experimental study. BMC Musculoskeletal Disorders 2006, 7:68
8) Cleland, J. a, Childs, J. D., McRae, M., Palmer, J. a, & Stowell, T. (2005). Immediate effects of thoracic manipulation in patients with neck pain: a randomized clinical trial. Manual therapy, 10(2), 127–35. doi:10.1016/
9) Bisset, L., Paungmali, a, Vicenzino, B., & Beller, E. (2005). A systematic review and meta-analysis of clinical trials on physical interventions for lateral epicondylalgia. British journal of sports medicine, 39(7), 411–22; discussion 411–22. doi:10.1136/
10) Vicenzino B, Paungmali A, Buratowski S, Wright A. Specific Manipulative Therapy Treatment for Chronic Lateral Epicondyalagia Produces Uniquely Characteristic Hypoalgesia. Pain. 2001; 6: 205-212.
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12) Berglund, K. M., Persson, B. H., & Denison, E. (2008). Prevalence of pain and dysfunction in the cervical and thoracic spine in persons with and without lateral elbow pain. Manual therapy, 13(4), 295–9. doi:10.1016/
13) Bisset, L., Beller, E., Jull, G., Brooks, P., Darnell, R., & Vicenzino, B. (2006). Mobilisation with movement and exercise, corticosteroid injection, or wait and see for tennis elbow: randomised trial. BMJ (Clinical research ed.), 333(7575), 939. doi:10.1136/
14) Vicenzino B, Cleland J, Bisset J. Joint Manipulation in the Management of Lateral Epicondylalgia: A Clinical Commentary. Journal of Manual Therapy. 2007; 15: 50-56.