Reviewed by Madison Hof
Introduction
Treatment for tendinopathies should be viewed as a multimodal approach, targeting not only the peripheral tissue but the neuromuscular adaptations that occur with persistent pain as well. Addressing the corticospinal control of the muscle by motor activation as a result of excitatory and inhibitory inputs ultimately affects tendon loading and motor production. It is important to consider neuromuscular control of the asymptomatic side as well, comparing side-to-side differences as well as differences in motor control in people with and without tendinopathy.
Motor control in people with and without tendinopathy
Muscle strength is often studied in tendinopathy research as compared to motor control. It has been understood that there is no consistent pattern of strength or performance change (increase or decrease) in tendons being studied such as in Achilles, patellar and RTC tendinopathies as well as in diagnosis such as lateral epicondylalgia. Strength deficits coupled with the presence of tendinopathy has not been consistently demonstrated in past research to reasonably target the peripheral tissue’s power production alone without assessing the neuromuscular component of muscle activation.
Imbalances in recruitment ability of excitatory and inhibitory influences around the painful tendon during muscle loading were found when comparing symptomatic and asymptomatic sides of athletes with patella tendinopathy (PT). It has been hypothesized that a protective adaptation occurs, reducing the mechanical demand that is placed on the tendon. Both peripheral and central contributions are associated with motor control changes and those with PT demonstrated landing mechanic patterns with less variability than to those without PT. Motor patterns that are invariable implies that control coming from the corticospinal tract is altered and may be due to protective strategies. Jumping abilities with less variability has been shown to be a risk factor for developing PT. In fact, these individuals were shown to be better jumpers than those without PT, coining this phenomenon the ‘jumper’s knee paradox’. Therefore, movement variability has been hypothesized as an important attribute in preventing injury.
Pain is commonly accompanied with changes in motor control as an adaptive mechanism that protects us from bodily threat. Motor control while having painful symptoms is altered due to the corticospinal drive to the motor neuron or muscle. Furthermore, there were no differences in muscle strength or activation between groups suggesting that the motor task can cause a potential pain response during jumping even in the absence of nocioception.
Motor control changes may be bilateral
Side-to-side strength deficits were found to be low following unilateral Achilles tendinopathy surgery which may reflect bilateral motor control deficits. These changes following tendinopathy pain may also be system wide which can be due to intrinsic and extrinsic factors, potentially increasing the risk of tendinopathy elsewhere in the body. An increase in global sympathetic drive implies the nervous systems’ involvement in tendinopathies. For example, there is increased inhibition responses on an affected limb following a stroke and an increased corticospinal excitatory response on the unaffected limb. This indicates an increased interhemispheric inhibition from the non-affected hemisphere to the lesioned hemisphere leading to further inhibition on the affected limb during activation of the unaffected limb. Changes in the unaffected side associated with tendinopathies may be the bodies way to attempt motor control homeostasis while trying to protect a region. This may also explain the high injury prevalence of the contralateral tendon following rehabilitation.
Conclusion and clinical implications
In order to address the differences in excitability and inhibition, an alteration to corticospinal control of muscles must be acknowledged as seen in different motor strategies used for protection. Movement variability should be considered following musculoskeletal pain even if nocioceptive input is absent due to the fact that altered motor control could be transmitted to a tendon causing a continuation of previous nocioceptive input. Altered invariable movement patterns that occur with pain are presumed to optimize performance subconsciously. This is demonstrated in those with tendinopathy displaying superior strength and performance despite having inflamed peripheral tissues. Strength training is often the focus for individuals with tendinopathy to stimulate the physiological adaptation of the muscle/tendon, but it is now known that it can modulate pain and corticospinal control of the muscle as well. Rehabilitation should be considered bilaterally to address the unaffected side as well to prevent contralateral motor adaptations from developing.
References
Rio E, Kidgell D, Moseley GL, et al. Tendon neuroplastic training: changing the way we think about tendon rehabilitation: a narrative review. British Journal of Sports Medicine. 2015;50(4):209-215. doi:https://doi.org/10.1136/bjsports-2015-095215