Preliminary evidence of compensatory strategy for knee extension neuromuscular control in patellar tendinopathy – corticomotor neurone organisation differences between athletes with and without patellar tendinopathy

Introduction: Patellar tendinopathy (PT) is a common condition, that is highly prevalent in populations that participate in sports that require jumping activity. Functional impairments are apparent, although our understanding for the neural mechanisms underlying these is incomplete. Alterations to subcortical excitability have been reported in athletes with PT, which would reduce drive to the knee extensor motoneurone pool and, subsequently, could alter function. Alternatively, it is possible that changes to the functional organisation of corticomotor neurones within the motor cortex that project to the knee extensors could underlie these impairments. Similar organisational changes have been identified in certain other persistent musculoskeletal conditions, and linked to neuromuscular control impairments. We aimed to determine if the functional organisation of corticomotor neurones projecting to knee extensors differed between jumping athletes with PT and asymptomatic controls. Additionally, we aimed to determine if organisation was associated with knee extension neuromuscular control.
Methods:
Basketball and volleyball athletes with (n=8) and without PT (n=8) underwent functional magnetic resonance imaging, while completing a knee extension neuromuscular control task. This required participants to attempt to match their knee extension force to a target force, ranging between 0–5% of their maximum isometric torque. A blood oxygen level dependent filter was applied during this task, to enable identification of the location of peak corticomotor neurone activation in the standardised Montreal Neurologic Institute template (as X [medial-lateral], Y [anterior-posterior] and Z [superior-inferior] coordinates). Additionally, we quantified knee extension neuromuscular control task accuracy.
Results:
In jumping athletes with PT, the X coordinate for peak corticomotor neurone activation during the knee extension neuromuscular control task was located 9.63 (95%CI 4.80-14.45; p<0.001) mm medially, while the Y coordinate was located 5.19 (95%CI 0.36-10.01; p=0.036) mm posteriorly, compared to asymptomatic athletes. There was no between group difference for Z coordinate location (p=0.515). In the PT group, greater knee extension neuromuscular control was associated with a more posterior location of peak corticomotor neurone activation during the knee extension neuromuscular control task (r=0.749, p=0.034). We did not find any association between knee extension neuromuscular control accuracy and X (p=0.840) or Z (p=0.812) coordinate location.
Discussion:
Our findings indicate that the functional organisation of corticomotor neurones projecting the knee extensors differs between jumping athletes with and without PT, while an association between this organisation and neuromuscular control in the PT group suggests these differences in organisation might be relevant to the preservation of knee extension neuromuscular control. Plausibly, jumping athletes with PT might undergo functional reorganisation of the motor cortex. This could be a strategy to compensate for reduced subcortical excitability observed in athletes with PT, to maintain drive to the knee extensor motoneurone pool, to preserve neuromuscular control.
Impact/Application to the field:
We found preliminary evidence of functional reorganisation in athletes with PT, a mechanism through which these individuals might compensate for altered efferent drive, to preserve knee extension neuromuscular control. Future investigations could determine if cortical plasticity is a viable target of intervention in this population, if aiming to preserve or improve neuromuscular control.