Welcome to tendinopathy blog 20.
Pleased to say the Portland, Oregon course June 17/18 is full - looking forward to it! I must apologise for spelling it Oregan on multiple prior blogs (and no one picked me up on it!).
Ripper blog this week by Ben Cormack, from Cor-Kinetic (Twitter: @CorKinetic). He loves his movement variability and pain science and does a fabulous job of combining them on his courses.
He explores a recent study by Chang et al. 2015 that investigates the local, spinal and supraspinal neuromotor changes in Achilles tendinopathy – with a focus on how they may be interpreted and clinical implications. A very worthwhile read.
Until next time, keep joining the dots
The neuromechanical adaptations to Achilles tendinosis
Yu-Jen Chang and Kornelia Kulig
Movement relies on hierarchical control system including muscle, tendon & CNS. Chang et al. 2015 were interested in the mechanical properties of a tendinopathic tendon, the CNS modulation accompanying this and also the mechanical behavior of the local muscles.
Their hypothesis was that the Achilles tendon would be more compliant (as per previous research) and motor neuron excitability and muscular behavior would be increased. This muscular behavior would be due to increased descending neural drive supraspinally and during functional activity this would serve as a protective mechanism from further injury or rupture and compensate for mechanical deficiencies of compliant tendon.
What they did: They recruited nineteen men, 9 with Achilles tendinopathy and 10 controls. They had a mean age of 48 years. Midportion Achilles group had a history (>2 weeks duration) of unilateral discomfort and sonographically confirmed focal thickening in the midportion. The tendinopathy group (AT) had an ABSENCE of pain with walking and running at time of the study.
They measured tendon stiffness during maximal calf isometric contraction with dynamometry, ultrasound and EMG. Measures of electromechanical delay (EMD) were also collected as well as spinal and supra spinal responses via H reflex and V wave. A rhythmic hopping task was performed on a force platform with video analysis and EMG measures to calculate muscle activation.
H reflex – Measures motor neuron excitability at a spinal cord level.
V wave – Measures supraspinal cortical contribution.
What they found: Firstly tendon stiffness was calculated to be significantly lower in the AT group compared to the control group. During the hopping task the AT group displayed earlier preactivation (90ms compared to 67ms for control group) of the medial gastrocnemius on the involved side. This is hypothesized to increase muscular stiffness in the presence of the increased Achilles tendon compliance in the AT group. This predictive feedforward increase in stiffness maybe a learned adaptive response over time and fits with a forward model of motor control as suggested by Wolpert & Miall 1996.
The AT group also showed an alteration in the muscular behavior, measured via EMG, during the hopping task with a lower contribution from the triceps surae and tibialis anterior and an increased contribution from the peroneal longus.
Measures of both the H reflex (spinal) and V wave (cortical) were found to be increased in the AT group, the authors felt this may be due to decreased Ia (golgi tendon) afferent input from the compliant tendon, to compensate for the decreased feedback the CNS may up regulate the feedforward control in the form of the increases in H reflex and V wave.
We see an earlier pre activation but a decrease in EMG output of the muscles directly associated with the Achilles tendon with the AT group. With earlier preactivation but less actual force output the net result of this could reduce the load to the Achilles tendon as a protective mechanism whilst still being able to achieve the functional task of hopping.
Neuromotor and tissue changes are summarised nicely in this figure from the paper.
So what does this mean?
There appears to be a clear alteration in the CNS strategy, at local, spinal and supraspinal levels, during a hopping task on the involved side with a tendinopathic tendon. This is in the absence of pain but maybe an adaptive, or potentially maladaptive, response to previous pain and/or physical state of the tendon.
Maqarriain & Kokalj 2014 found that only 1 week of NSAIDs had the effect of normalizing leg stiffness during hopping in Achilles tendinopathy. That was not the case however in the Chang paper which suggests movement adaptations persist beyond the cessation of pain.
What I would have like to have seen!
Kinematic measures for actual task outcome of the hop.
Did the alternative muscular strategy that the AT group displayed result in a different kinematics such as less joint excursion at the ankle and increased excursion elsewhere in the kinetic change?
My personal bias would also be to look at rep to rep differences to see if the muscular strategy was more or less variable compared to the control group with the kinematics or even the EMG measures in the existing data.
The actual performance of the hop in terms of vertical height or leg stiffness.
This may tell us if the task is compromised in terms of power output with the reduction of EMG of the triceps surae or if the adaptation provided an equally good strategy.
Does this potentially protective strategy reduce load to the tendon and provide a form of stress shielding? If we had kinematic measures we could see if this results in decreased joint excursion. If so this motor strategy may reduce load to the tendon during therapeutic exercise. To truly understand this we would need kinematic and kinetic measures along with the information in this study. This would allow the descending motor output to be matched with the movement at the joint and also the load that this applies to the tendon. Does this adaptive strategy increase risk of reoccurrence or in another group chronicity? It could also be tied into pain responses for those displaying painful tendinopthies. Could this lead to risk of overload and pain elsewhere?
Simply ‘loading’ may not alter these CNS responses. This could have longer term implications for tendon pathology/pain if protective movement/activation patterns are maintained.
Going beyond simply loading the tendon with tasks such as hopping, that provide different stimulus for the CNS may be useful. This could be done through introducing variability into the hop in terms of height, amplitude and joint position. A hop with increased amplitude would require a change in joint excursion and muscular stiffness. Hopping side to side may increase the relative contribution from different muscles around the ankle to decelerate and accelerate through different joint positions. Movement variability is a personal bias of mine and has certainly been discussed with regards to tendinopathy in a couple of recent paper e.g. Rio et al 2016 & Michener & Kulig 2015. In fact I can feel another blog coming on!
The goal maybe to alter the feedforward CNS ‘default’ through learning so providing alternative stimulus and feedback may require the CNS to update its feedforward activation levels.
There is no reason, symptoms allowing, that two rehab strategies cannot be employed during the rehab process. One designed to increase load tolerance through extrinsic factors and also in parallel inputs designed to affect how the CNS processes load intrinsically and potential maladaptive movement/activation strategies.
Clinical gems and awesome management models. Your patients will love you for it!