Tendon Neuroplasticty
Background[edit | edit source]
Tendinopathy is an umbrella term used to classify the clinical presentation of pain or dysfunction occurring within a tendon which can be in the presence or absence of structural pathology.[1] Clinically tendinopathy presents with localised pain that is dependent on loading as well as impaired function[1] .
Tendon Adaptations[edit | edit source]
Tendons have the ability to change depending on which loads they are subjected to. Changes can occur not only at a structural level but also occur at a cortical level. Research in tendons and tendinopathy has mainly focused on the tendons and not as much at what is happening at a spinal cord and brain level. Similarly, muscle strength in relation to tendinopathy has been more widely researched as compared to changes in motor control.
Adaptations at the tendon level[edit | edit source]
The pathophysiology of tendinopathy is not well understood. There are various hypothesis and models that attempt to describe the pathogenesis of tendinopathy and researchers and clinicians are still unsure as to precisely what is going on.[2] Tendons were designed to adapt to load changes. Load and capacity in tendons (link to PPP) is a concept where a tendons capacity only ever exceeds its load. When an excessive load is placed on a tendon, it has the capability of becoming dysfunctional.
In 2009, Cook and Purdam described the tendon continuum model, which stages tendinopathy according to changes in the tendons structure. [3]The continuum model has three stages; the reactive tendon; tendon disrepair and degenerative tendinopathy. A tendon can be in multiple stages at the same time and depending on the intervention the tendon can move up and down the continuum.
“Treat the doughnut not the hole”[2]
Pathological tendons are often thickened. This increase in AP diameter is possibly due to the tendon trying to maintain its loading ability.[4] Docking and Cook, 2016, conducted a study that investigated patella and Achilles tendons. They found that pathological tendons, while having large areas of disorganisation, had and increased amount of aligned fibrillar structure (the “normal” part of a tendon) as compared with non-pathological tendons.[4] This fits with the rehabilitation principle in tendons “treat the doughnut, not the hole” where the goal in rehabilitation is to increase the loading capacity of the aligned fibrillar structure (doughnut) rather than to try and regenerate the disorganised tissue (the hole).[2]
Adaptations at the Brain[edit | edit source]
In tendinopathy, changes do not only occur in the periphery but also the central nervous system. Every movement the body can make is represented within the primary motor cortex of the brain and movements are a balance between excitatory and inhibitory stimuli. Rio et al 2015,[5] showed that corticospinal excitability was elevated in people with patella tendinopathy. At the same time, it has been shown that there is cortical inhibition in tendinopathy[6] . In layman’s terms, this is likened to a learner driver who would have their foot on both the accelerator and brake at the same time. For a motor unit to have both excess excitation and excess inhibition, is an unhelpful movement strategy, and this can alter the motor control of the entire kinetic chain.
These neuroplastic changes as part of a tendinopathy picture is an emerging concept. A new model of tendon rehabilitation called, tendon neuroplastic training, has been proposed as a more effective rehabilitation tool.[6] This focuses on motor control rather than muscle strength on its own as a loading strategy to treat the tendinopathy.
Pain and Tendinopathy[edit | edit source]
Tendon pain continues to puzzle the medical profession. Tendons presenting with pathological changes on imaging may not be painful.[1] The warm-up phenomenon where tendons become less painful during activity also does not fit into a typical pain presentation either[1] .
Potential contributors to nociception in tendons may be:[1]
- Changes within the extracellular matrix, particularly increased prostaglandin production
- Increased vascularity
- Change in tenocyte structure and function
- Biochemical changes (cytokines, neuropeptides, neurotransmitters and metabolites
- Changes in the ion channels within the cell membranes in tenocytes
None of these, however, fully explain the pain processes and it is likely that a combination of these and other cortical factors that result in tendon pain [1]
Pain related to tendinopathy pain is multifaceted and requires a comprehensive multimodal evaluation and management plan
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Rio E, Moseley L, Purdam C, Samiric T, Kidgell D, Pearce AJ, Jaberzadeh S, Cook J. The pain of tendinopathy: physiological or pathophysiological?. Sports medicine. 2014 Jan 1;44(1):9-23.
- ↑ 2.0 2.1 2.2 Cook JL, Rio E, Purdam CR, Docking SI. Revisiting the continuum model of tendon pathology: what is its merit in clinical practice and research?. Br J Sports Med. 2016 Oct 1;50(19):1187-91.
- ↑ Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British journal of sports medicine. 2009 Jun 1;43(6):409-16.
- ↑ 4.0 4.1 Docking SI, Cook J. Pathological tendons maintain sufficient aligned fibrillar structure on ultrasound tissue characterization (UTC). Scandinavian journal of medicine & science in sports. 2016 Jun;26(6):675-83.
- ↑ Rio E, Kidgell D, Moseley GL, Cook J. Elevated corticospinal excitability in patellar tendinopathy compared with other anterior knee pain or no pain. Scandinavian journal of medicine & science in sports. 2016 Sep;26(9):1072-9.
- ↑ 6.0 6.1 Rio E, Kidgell D, Moseley GL, Gaida J, Docking S, Purdam C, Cook J. Tendon neuroplastic training: changing the way we think about tendon rehabilitation: a narrative review. British journal of sports medicine. 2016 Feb 1;50(4):209-15.
