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  1. B Vicenzino
  1. University of Queensland, Australia


    Most patients with tendinopathy report pain interfering with their physical capacity to perform to expectation, either at sport, recreation or work. Tendinopathy is a diagnosis associated with collagen disruption, increased tenocytes and ground substance, and neovessels. The relationship between these local tendon changes and patients' reported pain and disability is not a direct one, which necessitates the clinician to use clinical reasoning skills in interpreting the presenting signs and symptoms in light of the best available evidence. At this clinician-patient interface, a salient adage with which most would be familiar is: ‘Treat the patient not the disease (diagnostic image/diagnosis/pathology test result)’. For example, arthritic changes on x-ray do not match patient symptoms and level of disability. The mismatch between the pathology and presenting patient's pain and disability is particularly applicable for tendon, given that studies have shown that there is not a direct relationship between pathological findings on diagnostic imaging with reported pain and disability. Understanding pain and its underlying processes/mechanisms is imperative, if management approaches are to be advanced/optimised.

    Recent findings of local pathological changes in the tendon of the non-exercised/injured limb in experimental animal models of tendinopathy have further increased the imperative to better understand the pain and disability associated with tendon problems. These bilateral changes in unilateral injured tendons are paralleled by recent findings from quantitative sensory testing in human studies, which I propose serves as an impetus for better understanding tendon pain and disability. Quantitative sensory testing has shown that mechanical hyperalgesia is a characteristic of tendinopathy, not only locally at the site of the presenting condition (in unilateral cases) but also in the contralateral tendon site, as well as remotely (eg, at the tibialis anterior muscle for lateral epicondylalgia). It has been proposed that this widespread mechanical hyperalgesia is indicative of sensitisation of the central nervous system. Further work has shown that there is heightened spinal cord excitability to a noxious stimulus (that is, nociceptive flexor reflex) and a reduction in efficacy of endogenous pain modulation (inhibition) to a conditioning noxious stimulus, both of which imply abnormal endogenous pain inhibition mechanisms. These studies are cross sectional and thus it remains unknown if the central nervous system changes precede or follow the onset of tendinopathy. Nevertheless they contribute further to our understanding of tendon pain.

    Improved understanding of the mechanisms underlying tendon pain will better enable the clinician to treat the patient not the disease.

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