Tendon Neuroplasticty: Difference between revisions

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== Tendon Adaptations ==
== Tendon Adaptations ==
Tendons have the ability to change depending on which loads they are subjected to. The capacity of a tendon just exceeds the loads placed on it. When an excessive load is placed on a tendon, it may become dysfunctional. For more information, please see: [[Tendon Load and Capacity]].
Tendons have the ability to change depending on which loads they are subjected to. The capacity of a tendon just exceeds the loads placed on it. When an excessive load is placed on a tendon, it may become dysfunctional. Tendon pathology and pain are thought to a result of repetitive application of excess loads beyond the capacity of the tendon.<ref>Cardoso TB, Pizzari T, Kinsella R, Hope D, Cook JL. [https://www.sciencedirect.com/science/article/pii/S1521694219300233?casa_token=y5irK5QLRAgAAAAA:C8IDouQjejbc5zvP6jr-kYoujaeP67pMoiZXI0tlp7B_TFfILZ0e2Vx_EgCfNfQFPjqRcoc Current trends in tendinopathy management. Best practice & research] Clinical rheumatology. 2019 Feb 1;33(1):122-40.</ref> For more information, please see: [[Tendon Load and Capacity]].


Most research on tendons and tendinopathy has tended to focus on the tendons themselves and not at what is happening at a spinal cord and brain level. However, changes can occur both at a structural level, and at a cortical level.<ref name=":3" /> Similarly, tendon research has focused more on muscle strength than changes in [[Motor Control and Learning|motor control]].<ref name=":3" /> Emerging literature is now investigating the cortical adaptations that occur in tendinopathy.  
Most research on tendons and tendinopathy has tended to focus on the tendons themselves and not at what is happening at a spinal cord and brain level. However, changes can occur both at a structural level and at a cortical level.<ref name=":3" /> Similarly, tendon research has focused more on muscle strength than changes in [[Motor Control and Learning|motor control]].<ref name=":3" /> Emerging literature is now investigating the cortical adaptations that occur in tendinopathy.  


=== Adaptations at the Tendon Level ===
=== Adaptations at the Tendon Level ===
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** degenerative tendinopathy
** 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.<ref name=":1" />
* 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.<ref name=":1" />
Pathological tendons are often thicker than their unaffected counterpart. This increase in AP diameter is possibly due to the tendon trying to maintain its loading ability.<ref name=":2">Docking SI, Cook J. [https://onlinelibrary.wiley.com/doi/abs/10.1111/sms.12491 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.</ref> Docking and Cook<ref name=":2" /> conducted a study that investigated patella and Achilles tendons. They found that while pathological tendons have areas of disorganisation, their mean cross-sectional area of aligned fibrillar structure (the “healthy” part of a tendon) was greater than in non-pathological tendons.<ref name=":2" /> This could potentially show that tendons with pathology, increase the amount of healthy tendon as an attempt to maintain its homeostasis and loading ability. <blockquote>“Treat the doughnut not the hole”<ref name=":1" /></blockquote>Considering that pathological tendons still have portions of the healthy tendon the rehabilitation principle in tendons “treat the doughnut, not the hole” has been suggested. This is where the goal in rehabilitation is to increase the loading capacity of the aligned fibrillar structure, the healthy part or "doughnut" rather than to try and regenerate the disorganised tissue, the hole.<ref name=":1" />{{#ev:youtube|NFJeC2FjNmU}}
Pathological tendons are often thicker than their unaffected counterpart. This increase in anteroposterior (AP) diameter may be an attempt by the tendon to maintain its loading ability.<ref name=":2">Docking SI, Cook J. [https://onlinelibrary.wiley.com/doi/abs/10.1111/sms.12491 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.</ref> A 2016 study by Docking and Cook<ref name=":2" /> investigated the patella and Achilles tendons. They found that while pathological tendons have areas of disorganisation, their mean cross-sectional area of aligned fibrillar structure (i.e. the “healthy” part of a tendon) was greater than in non-pathological tendons.<ref name=":2" /> This could indicate that tendons with pathology, increase the amount of healthy tendon in order to try and maintain homeostasis and loading ability.  
 
Because pathological tendons still have portions of the healthy tendon, it has been suggested that we should “treat the doughnut, not the hole”.<ref name=":1" /> Thus, the goal of rehabilitation is to increase the loading capacity of the aligned fibrillar structure, the healthy part of the tendon (or the "doughnut") rather than to try and regenerate the disorganised tissue (the hole).<ref name=":1" /><blockquote>" We want to load the healthy doughnut and not worry about the whole of the jam bit in the middle."<ref name=":7">Rio E. [https://members.physio-pedia.com/tendon-plasticity-course/ Tendon Plasticity Course]. Plus, 2019.</ref> -- Ebonie Rio</blockquote>The following optional video provides an overview of Cook and Purdum's continuum model.{{#ev:youtube|NFJeC2FjNmU}}


=== Adaptations at the Brain ===
=== Adaptations at the Brain ===
In tendinopathy, changes do not only occur in the periphery but also in the central nervous system. Every movement the body can make is represented within the primary motor cortex of the brain. Movements are a balance between excitatory and inhibitory stimuli. Rio et al 2015, showed that corticospinal excitability was elevated in people with patella tendinopathy.<ref>Rio E, Kidgell D, Moseley GL, Cook J. [https://www.bodyinmind.org/wp-content/uploads/Rio_et_al-2015-Scandinavian_Journal_of_Medicine__Science_in_Sports.pdf 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.</ref> At the same time, it has been shown that there is cortical inhibition in tendinopathy.<ref name=":3">Rio E, Kidgell D, Moseley GL, Gaida J, Docking S, Purdam C, Cook J. [https://bjsm.bmj.com/content/50/4/209?hootPostID=abb512edf89cceb93b26573b726c25fc&utm_source=trendmd&utm_medium=cpc&utm_campaign=bjsm&utm_content=consumer&utm_term=0-A 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.</ref> In layman’s terms, this is likened to a learner driver who would have a foot on both the accelerator and brake and press them 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.  
As mentioned above, in tendinopathy, changes not only occur in the periphery but also in the central nervous system.  


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.<ref name=":3" /> This focuses on motor control rather than muscle strength on its own as a loading strategy to treat tendinopathy. {{#ev:youtube|2iZ5x4QXNNI}}
Every movement the body can make is represented within the primary motor cortex of the brain. Movements are a balance between excitatory and inhibitory stimuli. In 2016, Rio et al.<ref>Rio E, Kidgell D, Moseley GL, Cook J. [https://www.bodyinmind.org/wp-content/uploads/Rio_et_al-2015-Scandinavian_Journal_of_Medicine__Science_in_Sports.pdf 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.</ref> showed that corticospinal excitability was elevated in people with patella tendinopathy. In another study from the same year, Rio et al.<ref name=":3" /> found that there is cortical inhibition in tendinopathy.<ref name=":3">Rio E, Kidgell D, Moseley GL, Gaida J, Docking S, Purdam C, Cook J. [https://bjsm.bmj.com/content/50/4/209?hootPostID=abb512edf89cceb93b26573b726c25fc&utm_source=trendmd&utm_medium=cpc&utm_campaign=bjsm&utm_content=consumer&utm_term=0-A 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.</ref> <blockquote>Ebonie Rio explains this concept with the following analogy: "everything that you do, all of your movements as a balance between the amount of excitability and inhibition. And you can think of excitability inhibition, like the accelerator and the brake of a car. Excitability is the accelerator obviously, and inhibition is the brake."<ref name=":7" /> In tendinopathy, changes in corticospinal excitability and inhibition have the following effect: "So they had changes to both their accelerator and their brake [...] they had an increase in their accelerator. It's like they had their foot stuck on and they had an increase in their inhibition. So it's like they had their foot stuck on the brake as well. So they had one foot on the accelerator and one from the brake." </blockquote>These neuroplastic changes are an emerging concept in tendinopathy research. Based on this information, a new model of tendon rehabilitation, called ''tendon neuroplastic training'', has been proposed as a more effective rehabilitation tool.<ref name=":3" /> As explained in the following video, this type of training focuses on motor control rather than just muscle strength training as a loading strategy to treat tendinopathy. {{#ev:youtube|2iZ5x4QXNNI}}


== Pain and Tendinopathy ==
== Pain and Tendinopathy ==
Tendon pain continues to puzzle the medical profession. Tendons presenting with pathological changes on imaging may not be painful.<ref name=":0" />  The warm-up phenomenon where tendons become less painful during activity also does not fit into a typical pain presentation either.<ref name=":0" /> 
Tendon pain continues to puzzle the medical profession:
 
<nowiki>**</nowiki> Tendon pathology and pain are thought to a result of repetitive application of excess loads beyond the capacity of the tendon<ref>Cardoso TB, Pizzari T, Kinsella R, Hope D, Cook JL. [https://www.sciencedirect.com/science/article/pii/S1521694219300233?casa_token=y5irK5QLRAgAAAAA:C8IDouQjejbc5zvP6jr-kYoujaeP67pMoiZXI0tlp7B_TFfILZ0e2Vx_EgCfNfQFPjqRcoc Current trends in tendinopathy management. Best practice & research] Clinical rheumatology. 2019 Feb 1;33(1):122-40.</ref>


Potential contributors to nociception in tendons may be:<ref name=":0" />  
* tendons that have pathological changes on imaging may not be painful<ref name=":0" />
* Changes within the extracellular matrix, particularly increased prostaglandin production
* the warm-up phenomenon, where tendons become less painful during activity, also does not fit into a typical pain presentation<ref name=":0" /> 
* 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 <ref name=":0" />


Pain related to tendinopathy pain is multifaceted and requires a comprehensive multimodal evaluation and management plan
Potential contributors to nociception in tendons may include:<ref name=":0" />
* changes within the extracellular matrix, particularly increased prostaglandin production
* increased vascularity
* change in the tenocyte structure and function
* biochemical changes (cytokines, neuropeptides, neurotransmitters and metabolites)
* changes in the ion channels within the cell membranes in tenocytes
However, none of these theories fully explain the pain processes, and it is likely that tendon pain is caused by a combination of these and other cortical factors.<ref name=":0" /> Because of its multifaceted nature, pain in tendinopathy requires a comprehensive multimodal evaluation and management plan.


== Additional Resources ==
== Additional Resources ==
[https://www.physiospot.com/physiopedia/an-interview-with-professor-jill-cook-on-tendinopathy/ An Interview With Professor Jill Cook on Tendinopathy]


[https://soundcloud.com/bmjpodcasts/treat-the-donut-not-the-hole-what-utc-imaging-teaches-us-about-tendon-pathology-dr-sean-docking Treat the donut, not the hole: What UTC imaging teaches us about tendon pathology.] Dr Sean Docking
* [https://www.physiospot.com/physiopedia/an-interview-with-professor-jill-cook-on-tendinopathy/ An Interview With Professor Jill Cook on Tendinopathy]
* [https://soundcloud.com/bmjpodcasts/treat-the-donut-not-the-hole-what-utc-imaging-teaches-us-about-tendon-pathology-dr-sean-docking Treat the donut, not the hole: What UTC imaging teaches us about tendon pathology.] Dr Sean Docking


== References ==
== References ==

Revision as of 22:50, 24 October 2023

Original Editor - Mandy Roscher Top Contributors - Mandy Roscher, Kim Jackson, Jess Bell, Tarina van der Stockt, Lucinda hampton and Robin Tacchetti

Background[edit | edit source]

Tendinopathy is an umbrella term used to classify the clinical presentation of pain or dysfunction occurring within a tendon. This pain or dysfunction can occur with or without structural pathology.[1] [2] Clinically, tendinopathy presents with localised, load-dependent pain, reduced exercise tolerance and impaired function.[1][3] Overuse (e.g. at work or during sport) is the most common cause for tendon pathology.[2]

While there is significant interest in tendinopathy, the exact definition for this term remains unclear.[4]

According to Leikin, "Tendinopathy is currently diagnosed as a clinical hypothesis based on the patient symptoms and physical context."[4]

Silbernagel et al. define tendinopathy as: "either degeneration or failed healing due to continuous overload without appropriate recovery. [...] At the tissue level, tendinopathy is characterized by localized or diffuse increases in thickness (tendinosis), loss of normal collagen architecture, an increased amount of proteoglycans, and general breakdown of tissue organization."[5]

Tendon Adaptations[edit | edit source]

Tendons have the ability to change depending on which loads they are subjected to. The capacity of a tendon just exceeds the loads placed on it. When an excessive load is placed on a tendon, it may become dysfunctional. Tendon pathology and pain are thought to a result of repetitive application of excess loads beyond the capacity of the tendon.[6] For more information, please see: Tendon Load and Capacity.

Most research on tendons and tendinopathy has tended to focus on the tendons themselves and not at what is happening at a spinal cord and brain level. However, changes can occur both at a structural level and at a cortical level.[7] Similarly, tendon research has focused more on muscle strength than changes in motor control.[7] Emerging literature is now investigating the cortical adaptations that occur in tendinopathy.  

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. However, researchers and clinicians are still unsure exactly what is going on.[8]

"The complexity of normal tendon structure, the multifaceted nature and magnitude of the tendon’s response to injury, and the difficulty in creating an experimental model that mimics load-related tendon pathology in humans make it difficult to construct a simple and robust model that accommodates all aspects and phases of the condition."[8]

In 2009, Cook and Purdam[9] described the tendon continuum model, which stages tendinopathy according to changes in the tendons structure.

  • the continuum model has three stages:[9]
    • reactive tendon
    • tendon disrepair
    • 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.[8]

Pathological tendons are often thicker than their unaffected counterpart. This increase in anteroposterior (AP) diameter may be an attempt by the tendon to maintain its loading ability.[10] A 2016 study by Docking and Cook[10] investigated the patella and Achilles tendons. They found that while pathological tendons have areas of disorganisation, their mean cross-sectional area of aligned fibrillar structure (i.e. the “healthy” part of a tendon) was greater than in non-pathological tendons.[10] This could indicate that tendons with pathology, increase the amount of healthy tendon in order to try and maintain homeostasis and loading ability.

Because pathological tendons still have portions of the healthy tendon, it has been suggested that we should “treat the doughnut, not the hole”.[8] Thus, the goal of rehabilitation is to increase the loading capacity of the aligned fibrillar structure, the healthy part of the tendon (or the "doughnut") rather than to try and regenerate the disorganised tissue (the hole).[8]

" We want to load the healthy doughnut and not worry about the whole of the jam bit in the middle."[11] -- Ebonie Rio

The following optional video provides an overview of Cook and Purdum's continuum model.

Adaptations at the Brain[edit | edit source]

As mentioned above, in tendinopathy, changes not only occur in the periphery but also in the central nervous system.

Every movement the body can make is represented within the primary motor cortex of the brain. Movements are a balance between excitatory and inhibitory stimuli. In 2016, Rio et al.[12] showed that corticospinal excitability was elevated in people with patella tendinopathy. In another study from the same year, Rio et al.[7] found that there is cortical inhibition in tendinopathy.[7]

Ebonie Rio explains this concept with the following analogy: "everything that you do, all of your movements as a balance between the amount of excitability and inhibition. And you can think of excitability inhibition, like the accelerator and the brake of a car. Excitability is the accelerator obviously, and inhibition is the brake."[11] In tendinopathy, changes in corticospinal excitability and inhibition have the following effect: "So they had changes to both their accelerator and their brake [...] they had an increase in their accelerator. It's like they had their foot stuck on and they had an increase in their inhibition. So it's like they had their foot stuck on the brake as well. So they had one foot on the accelerator and one from the brake."

These neuroplastic changes are an emerging concept in tendinopathy research. Based on this information, a new model of tendon rehabilitation, called tendon neuroplastic training, has been proposed as a more effective rehabilitation tool.[7] As explained in the following video, this type of training focuses on motor control rather than just muscle strength training as a loading strategy to treat tendinopathy.

Pain and Tendinopathy[edit | edit source]

Tendon pain continues to puzzle the medical profession:

  • tendons that have 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[1] 

Potential contributors to nociception in tendons may include:[1]

  • changes within the extracellular matrix, particularly increased prostaglandin production
  • increased vascularity
  • change in the tenocyte structure and function
  • biochemical changes (cytokines, neuropeptides, neurotransmitters and metabolites)
  • changes in the ion channels within the cell membranes in tenocytes

However, none of these theories fully explain the pain processes, and it is likely that tendon pain is caused by a combination of these and other cortical factors.[1] Because of its multifaceted nature, pain in tendinopathy requires a comprehensive multimodal evaluation and management plan.

Additional Resources[edit | edit source]

References[edit | edit source]

  1. ↑ 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. ↑ 2.0 2.1 Loiacono C, Palermi S, Massa B, Belviso I, Romano V, Di Gregorio A, Sirico F, Sacco AM. Tendinopathy: pathophysiology, therapeutic options, and role of nutraceutics. A narrative literature review. Medicina. 2019 Aug 7;55(8):447.
  3. ↑ Millar NL, Silbernagel KG, Thorborg K, Kirwan PD, Galatz LM, Abrams GD. Tendinopathy. Nat Rev Dis Primers. 2021;7(1):1.
  4. ↑ 4.0 4.1 Leikin JB. Foreword for: Current understanding of the diagnosis and management of the tendinopathy: An update from the lab to the clinical practice. Disease-a-month: DM. 2022 Jan 3:101313-.
  5. ↑ Silbernagel KG, Hanlon S, Sprague A. Current clinical concepts: conservative management of Achilles tendinopathy. Journal of athletic training. 2020 May;55(5):438-47.
  6. ↑ Cardoso TB, Pizzari T, Kinsella R, Hope D, Cook JL. Current trends in tendinopathy management. Best practice & research Clinical rheumatology. 2019 Feb 1;33(1):122-40.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 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.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 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.
  9. ↑ 9.0 9.1 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.
  10. ↑ 10.0 10.1 10.2 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.
  11. ↑ 11.0 11.1 Rio E. Tendon Plasticity Course. Plus, 2019.
  12. ↑ 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.
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