Pes Planovalgus and Peroneal Tendinopathy

Members do not see these Ads. Sign Up.

Hello All,

I see quite a few patients with true peroneal tendinopathy (not subfib impingement) and pes planovalgus (PPV). I understand how pes cavovarus overloads the peroneal tendons, but not PPV. Can someone give me a plausible biomechanical explanation of how excessive eversion leads to peroneal dysfunction? Is there any special way to approach this with orthoses? I typically shy away from varus posting in patients with peroneal issues. Is this correct? :bash:

Thanks,
Nick

 

Hi Nick

The way I think about it is this - in a patient with the foot posture you describe, it isn't necessarily the peroneals that are dysfunctional. If we consider that peroneals are everters of the foot, then we have to consider that a planovalgus foot posture is perhaps more related to "dysfunction" in the opposing structures medially. This may then lead to over-use (for want of a better term) of the peroneals with the consequential eversion that this would lead to and potentially the symptoms you describe. So, to try to put it simply, it's it a lack of inversion force from the medial side (ie. tib post) that results in the increased eversion.

I don't suppose I have explained that in the best way, and may not even be right, but that is my understanding of this kind of problem. Perhaps someone else can come and help out - perhaps give a more scientific explanation than I? I'd be interested in others thoughts...

 

Hi Nick, what criteria are you using to diagnose peroneal tendonopathy? When I was a student they taught us about an entity called peroneal spastic flat foot. Of the flat feet that I see, (too many toes sign) I see a whole lot more posterior tibial tendon pathology than peroneal spasm. This is flat foot and not talar coalition. I wonder if a lot of PT dysfunction was diagnosed as peroneal spastic flat foot. 'A constantly contracting peroneal muscle will create a pronation moment that could, theoretically, cause a pronated appearance. The force from the ground in a medially deviated STJ axis foot will cause a constant pronation moment in stance that could cause the appearance of a flat foot. So, what do you see when you see peroneal tendonopathy?

Eric

 

I agree with Eric. Even though I do see a small number of patients with pes plano valgus deformity develop peroneal tendinopathy, this is not common since most patients with peroneal tendinopathy have high degrees of pes cavus, metatarsus adductus and/or rearfoot varus deformities.

 

I totally agree with Eric. The foot type or condition now known as adult acquired flatfoot (AAFF) was often called or diagnosed peroneal spasm before AAFF came to be (commonly?) recognized. The differentiating factor of course, is the spasm itself. If you supinate and pronate the patient’s foot at the stj during an open chain examination of the rom of the stj, you will detect a peroneal spasm, when one is present. When you attempt to supinate the foot at the stj (during open chain exam)you will either detect a virtual absence of stj motion due to the spasm (in the most severe of cases) or you will detect a jerky motion and resistance in the direction of stj supination due to the intermittent firing of the peroneal(s). There may also be a decreased range of stj supination available, which is often unilateral and occurs on the symptomatic side. As an example, you can often detect the presence of a peroneal spasm in patients with a tarsal coalition. The peroneal spasm occurs as a protective mechanism because the spasm attempts to prohibit stj and mtj motion by holding the foot in a pronated position in an effort to prevent the pain associated with the coalition.

Jeff

 

The term "cogwheel rigidity" is often used to describe this "jerky" motion of a joint, that Jeff described. In addition to seeing this "jerky motion" or cogwheel rigidity in peroneal spams, cogwheel rigidity is also commonly found in Parkinson's disease.

Prolonged manual adduction force applied to the forefoot, generally 10-15 seconds duration or more, which applies a supination moment across the subtalar joint, will often times weaken the peroneal spasm, but will also cause increased patient pain. Relaxation of the peroneal spasm will often occur with intraarticular local anesthetic infiltration into the anterior and/or posterior subtalar joint articular compartments.

 

I agree with all but here goes my foot centering explanation.

This is a flexible rearfoot, flexible forefoot functional foot type.

At heel contact in heel contact gait, the peroneal tendons (PB and PL) are providing pronatory moments to the rearfoot that pronate the RF on the frontal plane. This is eating up a good deal of the available peroneal force capability that needs to exist later on in gait.

We are now in midstance in heel contact gait.

At this moment PL must create a pronatory moment upon the 1st ray strong enough to maintain its stiffness plantarly in closed chain so as to engage the windlass and prevent dorsiflexion to the point of fhl.

In most cases, at this time, the PL is exhausted or exhausts as the day goes on without evidence of tendonopathy as it fails to reposition the 1st ray but does not overwork.

In some cases of the double flex, however, if the PL has enough energy to continue to perform without exhausing, these patients will develop a PL tendonopathy from overuse and tissue stress along the medial malleolar-cuboid notch segment that is in effect overuse even though the foot remains problematic as a "flatfoot" with a medially deviated STJ Axis

We see this happen clinically as a side effect in treating the flex/flex FFT if we overposition the vault beyond optimal or overtrain PL in correcting the FF component of this foot type.

In these case, we simply do one or more of the following in order.

1. We reduce the ORF's that we have introduced to attack the flexible forefoot
2. We reduce the frequency and intensity of the MERF's that we have instituted to improve PL control of the forefoot vault
and if those fail,
3. We add a forefoot valgus posting temporarily to reduce the moment that PL is producing causing the tissue stress and tendonopathy. We wean it away when the tendonopathy resolves.

I would suggest these treatments in your cases

Dennis