Does the STJ have the same action in extreme inversion and pronation?

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Hello all,

I was dabbling in the lab today with a cut down foot. All tendons and muscle were removed. Other ligaments remained intact. When I placed the foot in the position of an inversion sprain, the lateral side of the STJ tried to open….. no issue here. It did not merely open like a hinge, but rotated as well. That is, the talus externally rotated on the calcaneus during extreme inversion. The truly interesting observation was seeing this same mechanism occurring when I severely pronated the foot. That is, I freed ligaments enough to allow “extreme” motion and then created a simulated ground force reaction through the forefoot until the talonavicular joint reached its endpoint. At this point, the talus was driven posterior lateral into the same position as with supination. As a thought experiment, this seems quite logical, but I expected the joint surfaces to exceed their limits. The joints remained in contact – articular cartilage to articular cartilage – throughout the entire range. More interesting was the action of the lateral cuneiform. When the calcaneus plantarflexed it appeared that the joint angle between the lat. cuneiform and navicular increased such that the joint lost stability. This seemed to allow the lateral and medial columns to separate slightly. That is, the medial column continued to dorsiflex while the lateral column remained motionless. In other words, as soon as the STJ lost stability (in the posterior lateral direction) the midfoot created a new axis of motion for itself.

Any thoughts???

Kevin M

 

Hi Kevin

Fascinating stuff and still trying to picture it in my head. your pts must trust you as none of my pts seem willing to let me debride their foot to the same extent

My queries are 2 fold:

1. Do you think the abscence of connective tissue, muscles and tendons
(by lack of their inhibiting affects) allows for this kind of
movement?

2. Although you applied a ground reaction type force, would the same affect
occur if the force were applied during amubulation?

Other than that it is beyond my limited knowlege.

Of course you could be actually be mimicking what may occur in a foot as it turns a corner on a slight incline which is when some muscles and tendons will not be exerting a force.

Looking forward to the knowlegeable replies.

Ian

 

Cheers Ian,

Let me answer you in a round about way. I have been developing a new hypothesis for why Chiropractic works. I have been borrowing quite a bit from Gracovetsky's work on the spinal engine. He state that the spine ocillates in the gravitational field and that impulsed feed the spine during gait supply its potential energy. This implies that the lower extremities are "amplifiers" of impulses to the spine. Which, in turn, implies that the feet must efficiently transfer this impulse as well. I won't bore you with an explaination of segmental vs summary force transfer and the role of the neuromuscular component, suffice to say that If I can nail down pathomechanics, normal is not as big an issue.

So, the short version is that there is an increase in stability of these feet because they are fixed, at the same time instability because musculature is missing. BUT..... during the entire obsevation, the joint surfaces remained congruent. That is, nothing I did dislocated a joint, (subluxed, yes) suggesting all positions were in the realm of posibility for a living individual. In fact, I did not even stress this foot enough to produce a Charot type positioning.

As for the ground reaction force. I did exactly as you suggest. It occured to me that dorsiflexing the foot passively could not possibly produce the same effect as a true ground reaction. The motion used was similar to gait at initial FF loading.

One last note on inhibiting effects of musculature..... I haven't published this yet, but I have seen in the lab myotonia of muscles affecting joints that are dysfunctional. Initial EMG studies bear this out as well. The implication is interesting. If I have a mild joint injury and develope secondary myotonia, does this predispose me for further injury and increased myotonia? How much myotonia is enough to be of issue? Do I merely have to void the normal muscular balance, or develope obvious weakness? I have some suspicions, but I would like to hear what others have to say.

Kevin M