More Foot Rocker pathology Clues.
Is ankle rocker normal and adequate or is it limited ?  Is it limited in early midstance or late midstance ? How about at Toe off?  Is it even possible to distinguish this ? Well, we are splitting hairs now but we d…

More Foot Rocker pathology Clues.

Is ankle rocker normal and adequate or is it limited ?  Is it limited in early midstance or late midstance ? How about at Toe off?  Is it even possible to distinguish this ? Well, we are splitting hairs now but we do think that it is possible. It is important to understand the pathologies on either end of the foot that can impact premature ankle rocker. 

Look at the photo above. You can see the clinical hint in the toe wear that this runner may have a premature heel rise. However, this is not solid evidence that every time you see this you must assume pathologic ankle rocker. The question is obviously, what is the cause.

Considerations:

1- weak anterior compartment, which is quite often paired with the evil neuroprotective tight calf-achilles posterior complex to offer the necessary sagittal protection at the ankle mortise.  This will cause premature heel rise from a posterior foot aspect.

2- rigid acquired blocked ankle rocker from something like “Footballer’s ankle”. This will also cause premature heel rise from a relatively posterior foot aspect.

3- there are multiple reasons for late midstance ankle rocker pathology. The client could completely avoid the normal pronation/supination phase of gait because of pain anywhere in the foot. For example, they could have plantar fascial pain, sesamoiditis, a weak first ray complex from hallux vaglus, they could have a painful bunion, they could be avoiding the collapse of a forefoot varus. There are many reasons but any of them can impair the timely pronation-supination phase in attempting to gain a rigid lever foot to toe off the big toe-medial column in “high gear” fashion. And when this happens the preparatory late midstance phase of gait can be delayed or rushed causing them to move into premature heel rise for any one of several reasons.  Rolling off to the outside and off of the lesser toes creates premature heel rise.  

4- And now for one anterior aspect cause of premature heel rise. This is obviously past the midstance phase but it can also cause premature heel rise. Turf toe, Hallux rigidus/limitus or even the dreaded fake out, the often mysterious Functional Hallux limitus (FnHL) can cause the heel to come up just a little early if the client cannot get to the full big toe dorsiflexion range.  

We could go on and on and include other issues such as altered Hip Extension Patterning, loss of hip extension range of motion, weak glutes, or even loss of terminal knee extension (from things like an incompleted ACL rehab, Osteoarthritis etc) but these are things for another time. Lets stay in the foot today.

All of these causes, with their premature heel rise component, will rush the foot to the forefoot and likely create Metatarsal head plantar loading and could cause forces appropriate enough to create stress responses to the bone. This abrupt forefoot loading thrust will often cause a reactive hammer toe effect.  Quite often just looking at the resting nature of a clients toes while they are lying down will show the underlying increase in neuro-protective hammering pattern (increased long toe flexor and short toe extensor activity paired with shortness of the opposing pairs which we review here in this short video link).  The astute observer will also note the EVA foam compressing of the shoe’s foot bed, and will also note the distal displacement of the MET head fat pad rendering the MET head pressures even greater osseously. 

Premature ankle rocker and heel rise can occur for many reasons. It can occur from problems with the shoe, posterior foot, anterior foot, toe off, ankle mortise, knee, hip or even arm swing pathomechanics.  

When premature heel rise and impaired ankle rocker rushes us to the front of the foot we drive the front half of the shoe into the ground as the foot plantarflexion is imparted into the shoe.  The timing of the normal biomechanical events is off and the pressures are altered.  instead of rolling over the forefoot and front half of the shoe after our body has moved past the foot these forces are occurring more so as our body mass is still over the foot. And the shoe can show us clues as to the torture it has sustained, just like in this photo case.

You must know the normal biomechanical gait events if you are going to put together the clues of each runner’s clinical mystery.  If you do not know normal how will you know abnormal when you see it ? If all you know is what you know, how will you know when you see something you don’t know ?

Shawn and Ivo, The Gait Guys … .  stomping out the world’s pathologic gait mechanics one person at a time. 

Some honest movements across the big toe. Things you need to know as a runner or walker.

Lets see how good you are at this gait game at this point. 

In the video above you should see two things: you should see me manually dorsiflexing / extending the big toe / hallux.  I am creating extension through the 1st metatarsal joint (1st MTP). Essentially I am passively engaging the Windlass Mechanism of Hicks.  This mechanism is essentially a biomechanical event that wraps the end of the plantar fascia over the metatarsal head and 1st MTP joint.  So, when a person raises the heel in gait a moment of dorsiflexion/extension occurs across the joint.  In the video you see me lifting the toe but in the closed chain event the toe stays on the ground and foot moves up and over the toe but the resultant motion at the 1st MTP is the same.  It is still dorsiflexion / extension of the big toe about the 1st MTP joint. 
This wrapping or winding of the plantarfascia around the joint causes the distance from the heel to the ball of the foot to shorten and thus creates an elevation of the arch of the foot (smarter than using an orthotic to push it up  huh !) but this mechanism also raises the talus and supinates the foot.  This action makes the foot more rigid and stable. After all, when you are raising the heel and progressing over the ball of the foot don’t you want a rigid lever to press off of ?!  Ask any sprinter and they will concur. However, this mechanism occurs in all folks who  have a relatively competent foot and 1st MTP joint. 
What you NEED to see in the video is the additional motion up the limb. Watch the video again. When the toe is extended (dorsiflexed) the arch rises but the limb also externally rotates. You can see this by the subtle drift of the blue dots on the limb.  We want and need this external rotation to occur at the hip and through the limb because remember, the limb was internally rotated as we passed our body mass over the foot. This is a normal gait phenomenon.
Here is what we want to you to ponder.  Imagine a person with:

  •  a weak extensor hallucis mechanism (both longus and brevis: EHL, EHB)
  •  a hallux rigidus where the toe does not fully extend to that magical 45+ degree range or
  • if the arch of the foot is so far collapsed and pronated

IF any of these things go wrong, then a sufficiently rigid foot is not formed for push off propulsion, an incompetent arch results and insufficient talar motion and external limb rotation will occur. This means that several subsequent biomechanical events will/ may be compromised including but not limited to:

  • contralateral arm swing
  • sufficient engagement of the gluteals for stablization and propusion since optimal external hip rotation will not be met
  • inadequate pelvis posturing for spine neutrality 
  • etc. this is potentially a very very long list

Our take home point here is simple. You must have:

  •  sufficient and relatively symmetrical bilateral big toe extenion (hallux dorsiflexion) to optimize the Windlass Effect
  • you must have sufficient strength of the toe extensors to gain and stabilize this joint range at the 1st MTP joint
  • you must have both of the prior 2 in order to properly posture the foot and arch for rigid terminal loading response
  • and you must have all 3 to sufficiently externally rotate the limb at the hip to engage the propulsive components of the gait cycle.

There is so much more we could have added to this brief blog post, including hallux impingement, hallux valgus and bunion formation, supination insufficiency syndromes, tibialis posterior insufficiency syndrome, metatarsalgia etc.  The list is endless. 

Hallux dorsiflexion, both passive and active range of motion must be checked on every athlete and client you see. Otherwise gait is likely to be impaired locally and globally from subtle insufficiencies.

Shawn and Ivo
The Gait Guys