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Our early research identified imbalance in vasti activation in people with patellofemoral pain (PFP) and that vasti retraining programmes could restore motor control and improve outcomes.1 2 For around a decade, many patients benefitted from this research and its translation into practice. However, it might be time to revisit this paradigm.
Rethinking the current evidence
Consistent evidence from cadaver and modelling studies confirm that imbalance in medial (vastus medialis obliquus (VMO)) and lateral (vastus lateralis (VL)) quadriceps’ forces affect patellofemoral stress (ie, if the medial vasti force is relatively lower, there will be greater lateral patellofemoral stress).3 The evidence supporting an imbalance in vasti motor control is less clear. Although VMO onset delay is evident in many people with PFP, it is not present in everyone with this condition.4 5 Additionally, we have no evidence that altered vasti onset timing changes the muscle forces, and we cannot measure patellofemoral force in vivo. While the clinical relevance of subtle medial vasti onset delays (<20 ms) remain unclear, in healthy individuals (military population), a delay in VMO onset (<5 ms) is a risk factor for PFP development.6
The most compelling evidence forcing a rethink of underlying paradigms is the strong evidence supporting exercise therapy without specific focus on a vasti retraining component.7 There is consistent evidence that an exercise therapy programme can reduce pain and improve function in people with PFP. A programme with a hip muscle focus in isolation (or combined with a quadriceps muscle focus) is superior to an isolated quadriceps focused programme.7 8 Furthermore, a generalised exercise therapy programme can also change vasti timing.9 More robust clinical trials are required to identify optimal exercise therapy regimes and methods to tailor these to individuals. However, there is convincing evidence that exercise therapy (regardless of vasti retraining) works.
Rethinking the previous models
Using motor retraining principals, our original research focused on: (1) using biofeedback (mostly surface electromyography or palpation) to ascertain activation in the VMO, ideally with greater VMO than VL activation; (2) obtaining activation of the VMO in minimal weight-bearing positions, usually isometric, and low load contractions; (3) progressing to obtaining VMO activation during gradually more complex tasks (step ups, then step downs, double leg squats and then single leg squats); and finally (4) VMO activations in more loaded activities, including sports-specific activities. Due to a potential pain inhibition, we used a pain monitoring model (adapted from Thomeé10 to keep pain <3/10 during and after exercises.
While this approach was superior to placebo physiotherapy, and effective in clinical practice, we think that our positive effects could also be attributed to our graduated increase in patellofemoral joint and lower extremity loading.
A new approach aims to provide a progressive increase in patellofemoral joint load. We explain that some pain will accompany this increasing joint load but keep pain <3/10 during and after exercise. This provides feedback on patient response to the level of load, may address some fear of pain and gives patients confidence to take control over their rehabilitation. By commencing exercise at the highest patellofemoral load possible, while maintaining pain at a ‘discomfort’ level, we can address the perception that pain indicates joint damage and reduce the likelihood of pain inhibition. Depending on patient presentation and needs, this might mean starting with isometrics (but not necessarily low load), or with more dynamic task (stepping, squatting and so on). Progression of exercises ensures that patients exercise with the highest applied load possible while maintaining control of their pain (<3/10). The final stage is high loading rate activities, incorporating a sports-specific component.
Does rethinking the previous models change what we do or how we do it?
For many patients, engaging in an exercise therapy programme is paramount, and how we explain exercises and obtain adherence is less important than getting adherence. Recognising that there are many different approaches to reach the same endpoint gives us more flexibility to tailor our approach to the individual (patient). For example, spending a number of sessions, trying to get an ‘isolated’ VMO contraction, may not be the best approach for your patient. Physiotherapist’s time might be better spent explaining PFP, quashing beliefs about joint damage, imaging results and how exercise might damage their knee and emphasising the role of exercise in rehabilitation. Getting people to be able to move, walk, run, lift, get out of a chair with the least amount of pain and best function is our goal. Rethinking how we get there might give us more freedom and creativity with treatment options and change the way that we assess treatment success.
Correction notice This article has been corrected since it published Online First. The title has been corrected.
Contributors Both authors contributed equally to this editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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