Hi all,
Blog number 40 coming at ya! (subscribe here). Before it does, please remember to book onto Erik Meira’s excellent Hip and Knee Course this August in Melbourne. Early bird registration ends in a few short weeks.
Also, check out this new exercise app (iPrescribe) which is great for busy clinicians who want relatively inactive patients to get more active.
This week blog focuses on an interesting paper from James Debenham (quality tendon researcher from Perth) and some of his crew. Worth a read as breaks some new ground in regards to potential mechanisms that explain chronic pain and movement issues in our tendinopathy patients. They scratch the surface here, and I look forward to future work exploring this avenue further.
See you next time
Peter
Background: Tendinopathy is difficult to define. People present with pain - that part is straight forward. They also present with multiple and variable structural and functional changes – eg tendon pathology, neuromuscular changes (e.g. muscle strength impairement, cortical inhibition), differences in movement patterns or control, tendon stiffness changes. The relationships between these factors is unclear. We know that pathology precedes pain, but also that pain and pathology are poorly correlated. We know little about the extent of neuromuscular and movement changes and how these relate to pain.
James Debenham and team have published an interesting study recently investigating tactile acuity in people with Achilles tendinopathy (AT). Cortical reorganization within the sensory cortex (SC) is closely linked with reduced tactile acuity in chronic pain, so the authors have used tactile acuity as a model to infer SC reorganization in people with AT. They talk about this type of SC reorganization as a disruption of the cortical map representing the surface of the body.
What they did:
They used to the two-point discrimination test to assess tactile acuity in the affected and unaffected side of people with unilateral AT (n=13), and controls (n=13). Diagnosis of AT was based on the following criteria: >6-week history of unilateral mid-portion Achilles tendon pain, concordant pain on palpation, pain with or after loading, morning stiffness and a Victorian Institute of Sports Assessment Achilles (VISA-A) score of <80/100. Two-point discrimination was measured with an aethesiometer with precision of 1mm. Patients and controls were tested as different sites so testers were not blind to group. Two Ascending (0mm-80mm) and two descending (80mm-0mm) runs were performed on each side, changing the distance between the points by 5mm each time.
What they found: Participants were reasonably split between males (n=7 AT; n=6 healthy) and females (n=6 AT; n=7 healthy). The mean VISA-A score was 62.7/100 (SD24.1). The mean threshold for detection of 2 points was 45.2mm(SD19.6) in the affected AT side, 33.4mm (SD10.7) on the unaffected side, and 32.1mm (SD3.9) for the healthy controls. The threshold was significantly higher on the affected AT side compared with the unaffected side and the control participants.
Clinical message: Two-point discrimination is impaired on the affected AT side compared to the unaffected side and the controls. They suggest this most likely suggests that disrupted cortical maps may contribute to the clinical presentation of Achilles tendinopathy. They do acknowledge that it is also possible that changes in local tissue acuity result from peripheral deficits eg reduction in cutaneous receptor field density secondary to tendon pathology. So what, I hear you asking?
Tactile acuity may be related to impaired planning and coordination of movement
Movement quality is likely to be affected by degradation in stored bodymaps. For example, reduced quality of stored body maps may contribute to impaired planning and coordination of movement in AT, potentially increasing tendon load and prolonging recovery.
Tactile acuity may contribute to the tendon pain experience
The authors put forward two hypotheses linking these findings to tendons pain. First, incongruence between predicted and actual sensory information due to disrupted cortical maps may contribute to the pain experience in AT (the sensorimotor incongruence hypothesis). Second, changes in body perception due to disrupted cortical map may reduce perception of tissue safety leading to heightened local sensitivity.
If you identify 2-point discrimination issues, what do you do next?
First, it is important to remember that the authors are inferring SC reorganization from tactile acuity measures, and it is one study. Second, if SC changes are present we need to know the mechanisms which will direct management. The authors suggest sensory discrimination training strategies may be useful. Question to answer first are; 1) will these changes resolve with improves pain? 2) will sensible, variable, challenging rehab improve them?
I guess the most interesting/useful aspect of this paper is that it raises the possibility of SC reorganization in AT. Until we know more, best thing to do is keep in mind when assessing people with AT that their movement ‘deficits’ may have multifactorial factorial mechanisms, including potentially sensorimotor changes.
Look forward to seeing how this work will be progressed!
See you next time
Peter
Blog number 40 coming at ya! (subscribe here). Before it does, please remember to book onto Erik Meira’s excellent Hip and Knee Course this August in Melbourne. Early bird registration ends in a few short weeks.
Also, check out this new exercise app (iPrescribe) which is great for busy clinicians who want relatively inactive patients to get more active.
This week blog focuses on an interesting paper from James Debenham (quality tendon researcher from Perth) and some of his crew. Worth a read as breaks some new ground in regards to potential mechanisms that explain chronic pain and movement issues in our tendinopathy patients. They scratch the surface here, and I look forward to future work exploring this avenue further.
See you next time
Peter
Background: Tendinopathy is difficult to define. People present with pain - that part is straight forward. They also present with multiple and variable structural and functional changes – eg tendon pathology, neuromuscular changes (e.g. muscle strength impairement, cortical inhibition), differences in movement patterns or control, tendon stiffness changes. The relationships between these factors is unclear. We know that pathology precedes pain, but also that pain and pathology are poorly correlated. We know little about the extent of neuromuscular and movement changes and how these relate to pain.
James Debenham and team have published an interesting study recently investigating tactile acuity in people with Achilles tendinopathy (AT). Cortical reorganization within the sensory cortex (SC) is closely linked with reduced tactile acuity in chronic pain, so the authors have used tactile acuity as a model to infer SC reorganization in people with AT. They talk about this type of SC reorganization as a disruption of the cortical map representing the surface of the body.
What they did:
They used to the two-point discrimination test to assess tactile acuity in the affected and unaffected side of people with unilateral AT (n=13), and controls (n=13). Diagnosis of AT was based on the following criteria: >6-week history of unilateral mid-portion Achilles tendon pain, concordant pain on palpation, pain with or after loading, morning stiffness and a Victorian Institute of Sports Assessment Achilles (VISA-A) score of <80/100. Two-point discrimination was measured with an aethesiometer with precision of 1mm. Patients and controls were tested as different sites so testers were not blind to group. Two Ascending (0mm-80mm) and two descending (80mm-0mm) runs were performed on each side, changing the distance between the points by 5mm each time.
What they found: Participants were reasonably split between males (n=7 AT; n=6 healthy) and females (n=6 AT; n=7 healthy). The mean VISA-A score was 62.7/100 (SD24.1). The mean threshold for detection of 2 points was 45.2mm(SD19.6) in the affected AT side, 33.4mm (SD10.7) on the unaffected side, and 32.1mm (SD3.9) for the healthy controls. The threshold was significantly higher on the affected AT side compared with the unaffected side and the control participants.
Clinical message: Two-point discrimination is impaired on the affected AT side compared to the unaffected side and the controls. They suggest this most likely suggests that disrupted cortical maps may contribute to the clinical presentation of Achilles tendinopathy. They do acknowledge that it is also possible that changes in local tissue acuity result from peripheral deficits eg reduction in cutaneous receptor field density secondary to tendon pathology. So what, I hear you asking?
Tactile acuity may be related to impaired planning and coordination of movement
Movement quality is likely to be affected by degradation in stored bodymaps. For example, reduced quality of stored body maps may contribute to impaired planning and coordination of movement in AT, potentially increasing tendon load and prolonging recovery.
Tactile acuity may contribute to the tendon pain experience
The authors put forward two hypotheses linking these findings to tendons pain. First, incongruence between predicted and actual sensory information due to disrupted cortical maps may contribute to the pain experience in AT (the sensorimotor incongruence hypothesis). Second, changes in body perception due to disrupted cortical map may reduce perception of tissue safety leading to heightened local sensitivity.
If you identify 2-point discrimination issues, what do you do next?
First, it is important to remember that the authors are inferring SC reorganization from tactile acuity measures, and it is one study. Second, if SC changes are present we need to know the mechanisms which will direct management. The authors suggest sensory discrimination training strategies may be useful. Question to answer first are; 1) will these changes resolve with improves pain? 2) will sensible, variable, challenging rehab improve them?
I guess the most interesting/useful aspect of this paper is that it raises the possibility of SC reorganization in AT. Until we know more, best thing to do is keep in mind when assessing people with AT that their movement ‘deficits’ may have multifactorial factorial mechanisms, including potentially sensorimotor changes.
Look forward to seeing how this work will be progressed!
See you next time
Peter
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