When assessing a patient who presents with lower extremity pathology, we tend to get fixated on the chief complaint. A person complains of knee pain, and we look at the knee…they have right calf pain, we look at the calf. A hip is tight/sore, we look at the hip.
The longer I practice and the more well-versed I get with movement assessments, a certain pattern of dysfunction seems to dominate over others. Now, we know that no one condition is an absolute, but this one does play in significantly, and it will throw off your entire movement.
Well, just how important is this movement? Consider Mike Boyle’s accepted assessment that the body is made up of stable segments and mobile joints. This pattern goes in an alternating pattern up the body…the foot is stable, the ankle mobile…the knee is stable, the hip is mobile….the low back is stable, the mid-back needs to be mobile…and so on….
Since closed kinetic and kinematic chain movements begin with foot placement (during normal gait, running, jumping, etc…), it becomes quite relevant to make sure that the ankle is doing its job of moving. The function of the foot is to absorb impact and distribute shock, and foot pronation is a major part of this….yes, the foot must pronate during normal gait to unlock and allow for ground accommodation. However, the foot must be stable enough to not over-compensate, or over-pronate. In effect, the foot needs to be stable with its movement…we don’t want to be pes cavus or pes planus, and we should do all we can to make sure that footwear is proper.
In regards to the ankle, simply put, it must be mobile. We commonly learn that about 12 degrees of dorsiflexion is necessary for normal gait, and 20 degrees is optimal for running, jumping, and other more aggressive activities. So, what are some of the sequella when we don’t have proper ankle dorsiflexion?
1. Sub-talar joint eversion to try to make up for the lost dorsiflexion at the mortise (ankle) joint
2. We will see gastrocnemius and soleus tightness that may be contributing to the ankle issue or might be a result of such
3. Internal rotation of the knee along with genu valgus, again, to help facilitate dorsiflexion…this destabilizing the knee (the knee needs to be stable)
4. Knee hyperflexion as the athlete squats more to try to make up for loss of ankle dorsiflexion
5. Hip dysfunction and fixation as the hip will follow the knee into internal rotation, but being most people lack proper internal rotation, the hip will lock up and simply not move. (the hips need to be mobile)
6. If the hips do not move the way they should, then the energy is thrown into the back, which is supposed to be stable, yet can’t be, if it has to do the work of the hips.
These are the main examples, but there are plenty more. What a mess! With improper ankle dorsiflexion, the entire chain, all the way up, is altered, and none of it is good.
So, whether we perform a FMS, SFMA, TPI assessment, or any other, what do we do to improve ankle dorsiflexion when it is found to be deficient? Well, let’s touch on a few more points and address this again…
The primary function of the ankle mortise is to allow for plantarflexion and dorsiflexion. When assessing end-feel (normal and not pathological), we should feel a firm end-feel, or springiness in the joint that is checked by the soleus and gastrocnemius musculature. If we have another type of end-feel at this joint, it means that the joint has a pathological process going on…for example, if it has a hard end-feel, you can assume that an arthritic process is limiting motion.
So, if we have a mortise joint that is only dorsiflexing let’s say 5 degrees, and let’s assume there is a non-pathological firm end-feel, what can we gather from this and what do we do?
The answer: address the facilitated posterior calf musculature. Now, we could trace this up the posterior chain and put blame anywhere along the way, but let’s start low and isolate the soleus and gastrocnemius. Of course, first make sure the mortise joint is moving properly with properly administered manipulations, if necessary…assuming the mortise joint is now moving properly and only the normal firm end-feel is left, we can address ways to ‘shut off’ the soleus and gastrocnemius. We can also use reciprocal inhibition to aid this process (facilitate the inhibited musculature that is antagonist to the soleus and gastrocnemius), and whatever soft tissue work/exercise that functions to release these tissues can be implemented.
Once we can release the posterior calf musculature, the mortise should regain more dorsiflexion, and by doing so, we should see better function all the way up the body.
So, any thoughts on this topic?