• LecturehallBiomechanics of the Normal Gait Cycle
  • Lecture Transcript
  • Male Speaker: I am going to dive into a topic, Biomechanics of the Normal Gait Cycle. You’ve heard me speak many times. You’ve heard my passion for foot function, biomechanics, the role it plays relative to surgical procedures, conservative control. Now we are going to look a little bit closer into what I teach for the last 45 years at the Temple School of Podiatric Medicine in Biomechanics. We’re going to understand little different in the phases, the role of the foot in the lower extremity, identify the functions of the foot and gait, and understand the difference between swing phase and stance phase. I’m sure they’re not going to bore you with slides showing you planes, sagittal, frontal, transverse, which is basic understanding of how the extremity and/or the foot may be moving. We recognize quickly that when we look at the foot, it has a component of triplanar motion. We refer to that as pronation and supination. We will also know that there is open chain and closed chain. Open chain pronation and supination occurs in the swing phase of gait. It occurs if you lift your foot off the ground and pronate and supinate the foot, all of the motion in open chain is actually below the level of the talus. The talus stays locked in the mortise and the dorsiflexion knee version abduction that we talked about is occurring below that level. When we talk about closed chain motion, this happens as soon as we begin to hit the ground and we have a reactive force of gravity pushing back against the foot. This in my opinion is the most critical portion of the gait cycle that we have to utilize. In closed chain motion, the talus accurately moves with the foot and relative to the foot. As we pronate, the talus plantar flexes and abducts. The arch is dropping down. A lot of that motion takes place at the subtalar complex and the midtarsal complex. I’ve referred to talonavicular joint of the midtarsal complex as a ball and socket joint of the foot. There are two joints I consider ball and socket in the foot. One is the talonavicular. The other is the first metatarsophalangeal joint. You rarely hear people refer to that as a ball and socket joint. When closed chain motion occurs, the calcaneus either everts as the foot pronates or inverts as the foot supinates. Interestingly, in closed chain motion, the leg becomes a critical component. During the gait cycle, we are going to evaluate the fact that the leg may be internally rotating or externally rotating. With the foot planted on the ground, the talus locked in the mortise has to follow what the leg does. It is in essence a driving force. You can just look at this when you look at the axes of motion, which are an important component to evaluate. When we look at an axis of a subtalar joint, it only deviates 16 degrees from the sagittal plane. The least component of motion at the subtalar level, therefore, is sagittal plane. When we look at compensatory mechanisms of the foot, we talk about equinus. We relate to the fact that the foot pronates to give us additional dorsiflexion. To understand why it can’t only happen at the subtalar complex is because of that axis. What the subtalar joint can do to compensate is pronate to its maximum. That unlocks the midtarsal joint. The subtalar complex is a locking mechanism of midtarsal function. If we go to the midtarsal joint, we recognize two axes, a longitudinal and an oblique. The oblique axis, dominant motion in transverse and sagittal plane. That’s the guy I need to compensate for equinus. Unfortunately, when you open that midtarsal complex at the oblique axis, you’re going to see a significant amount of arch depression, which we relate to as a flat foot or a hyperpronated foot, and the transverse plane dominance, which I relate to yesterday as an etiologic component of hallux abducto valgus.


    Interesting simultaneous, the longitudinal axis of the midtarsal joint gives us inversion as a primary motion. Therefore, we develop forefoot supinatus in the severely pronated foot. The severely pronated foot is pronating the subtalar to its maximum, midtarsal oblique axis to its maximum, and longitudinal axis. Lo and behold you look at significant amounts of inversion of the forefoot to the rearfoot, and you say, “My God, am I going to post that with an orthotic?” You’d be looking at 10 to 15 degrees. We know that that inversion component is part of supination. We refer to it as forefoot supinatus. A dry plain soft tissue deformity, that’s actually reversible. The peroneus longus, if it can function properly with stability of the rearfoot, will pull down the medial collum. Too often in the operating theater, we treat a flat foot, we relocate a calcaneal position. We may elongate the lateral column with an Evans and then let’s do Cotton to plantar flex the first ray. We’re trying to do too much at one time. Once you’ve restored and realigned the rearfoot, allow the mechanical function of the peroneus longus to derotate the medial collum, reduce the supinatus. Forefoot varus as a single plane osseous deformity is just that it’s osseous. That patient lives with forefoot varus. That’s the patient we do post with an orthotic in the forefoot. Supinatus reduces if you control rearfoot pronation. The ideal of subtalar joint has a neutral position. We talked about it. We tried to place the foot in it. How do you define it? Neutral position is a point from which? The subtalar joint can supinate twice as much as it can pronate. The neutral normal foot, when you’re standing in position, the subtalar joint is pretty neutral. Congruous joint, neither pronated nor supinated, from around which all type of function is going to take place. When you look at a transection through the midtarsal complex, look at the relationship of the talus to the calcaneus. In the neutral position, you have obliquity to the axis of the talonavicular and calcaneocuboid joints. As you supinate, you realize the talus comes up on top of the calcaneus. Then as you pronate, the talus plantar flexes and adducts. Within a normal range during the walking cycle, we’re looking at 4 to 6 degrees of motion going from an inverted slightly position and heel strike to a pronating position. It’s only about 4 to 6 degrees of excursion and motion until you get into the pathologic foot type. Transverse plane domination, it’s a component that we see at heel strike. It’s going to create talar response, midtarsal transposition, and propulsive dominance. Interestingly, the youngster who toes in has posterior medial heel wear and it has one of the most extensive hyperpronated feet that you will see. Internal torques are severe hyperpronators. I put them in the same category as primary equinus or compensatory equinus or compensated flexible forefoot valgus. That’s how bad that foot will respond as a severe pronator. Take a look at the ankle mortise. Almost looks like a box shape and you recognize nicely how the talus is locked in that mortise. As the leg internally and externally rotates, something has to happen to allow it to occur. Non-weight bearing, as you’re sitting in your chair, you can internally and externally rotate your leg, the foot doesn’t do a thing. As soon as you begin to hit the ground, there is internal rotation of the lower extremely. There’s ground reactive force, now something has to allow that transverse plane motion to continue. One of the functions of the foot and gait, one of the most important ones is as a torque converter.


    It actually allows transverse plane motion of the leg to occur through subtalar pronation. How important is that concept? You wonder why with ankle joint replacements, we have significant problems with changes in the bone dislodging where of the materials, pain, swelling because the majority of implants of the ankle have no mechanism built in to allow for rotation to take place once the foot hits the ground. You have arthritic change in the subtalar complex just as well as the ankle in the majority of these patients. If you take away the torque conversion, all of that force in the transverse plane is transmitted into the components of the replaced ankle joint. There’s only one joint at the present time that allows for mobility supposedly in the transverse plane and as been recognized to do so. One of the reasons majority of these implants are critically failing. Take a look at this. This is an eye opener. I just talked about ball and socket joints of the TM and the first MPJ. Here is a ball and socket ankle joint. How does that happen? That happens in youngsters who might be born with a tarsal coalition, who have no ability to allow for transverse plane motion of the [indecipherable] [11:40]. So what happens? The continued internal and external rotation with every step that we take implies a force onto the talus and takes that nice rhomboid shape bone. It is soft, it’s somewhat malleable in the youngster and actually begins to turn it into a ball and socket joint, very effective in functional joint by the way. This is one of the reasons we began to realize the importance of internal and external rotation of the leg and subtalar function. The other was in post-amputees where a beautiful prosthetic limb would be place on a BK amputation. The biggest concern over time was stump burns. Nobody truly understood why. The stump burn occurred because of internal and external rotation that begins at the thigh, is down into the leg and down into the foot. Well, at the interface of this stump from the amputation and the prosthetic, you have friction, stump burns. It could be a disaster for a patient who has continued irritation and ulceration and infection. So what happens? The educational process says we better have a mechanism at the lower end of that prosthetic limb to allow for the internal and external rotation of the leg to take place. We’re going to find that as we go from heel strike to midstance to toe off, many things happen that the foot must undergo. We hit the ground. There’s a shock component, there’s a mechanism within the foot that absorb shock. It’s the fat pad, it’s the cancellous bone of the calcaneus, its’ motion at the ankle, it’s the muscular, it the soft tissue. We are allowing internal and external rotation to occur, we are pronating. The subtalar joint is considered a pronating mobile adaptor. Why? We walk on irregular terrain. The subtalar joint is going to unlock the midtarsal complex, the foot is going to loosen somewhat and the internal rotation of the leg is going to be allowed to take place. There is three functions of the foot and gate. And then when we finally get to the propulsive phase, we need to tighten that structure up again. Because when you push off, if you try to push off a loose bed of rocks, you’re not going to have much stability or propulsive capability. If you put it all together, you create cement. We now convert to foot from a pronating mobile adaptor to a supinatory rigid lever. The first ray is going to be pulled down. Very interesting, we have heard many talks about first ray function, hallux limitus, rigidus and bunion deformities look in the propulsive phase what happens to the first metatarsal. It actually is rotating up on top of the sesamoid apparatus.


    In order to get 65 degrees of dorsiflexion that we talked about in the propulsive phase at the great toe joint, the metatarsal has to be pushed down and back. That’s going to require a change in the motion within the foot and intrinsic musculature as we go into the propulsive phase. This is why the first ray has to be shorter than the second. If you have a long first ray, you cannot go up onto a sesamoid apparatus, you jam the great toe joint and either start to develop an HAV deformity or hallux limitus rigidus. That’s why we talk about one to two millimeter difference in length. It’s necessary for normal function as that foot supinates. Yesterday, I showed slides and pictures of hypermobility of the first ray, motion occurring at a time when it shouldn’t, causing an elevated position in propulsion. There’s no way you can rotate up onto the sesamoid apparatus. When I look at the failure rate that was presented this morning doing different type of procedures for hallux limitus rigidus, I heard one thing that missed or was missing completely. It was probably the lack of the word that I heard. Back to controlling that foot. If you allow that foot to continue to hyperpronate which is part of the etiology of hallux limitus rigidus, how do you expect that joint to ever function? How do you expect the range of motion to improve? Certainly, if you have post traumatic syndrome with the great toe joint, that somebody drops an object down the great toe joint and develops degenerative change as post traumatic arthritis, that’s a different animal. From a biomechanical standpoint, we talk about a foot type called subtalar varus. Fully compensated subtalar varus causes pronation to occur to a point where the heel is vertical. These foot types don’t necessarily even look hyperpronated. The fully compensated subtalar varus foot leads to elevation of the first ray, hypermobility and propulsion. Without the transverse domination, you get hallux limitus rigidus. If it’s severely pronated with oblique midtarsal function, you go on to transverse plane effect, hallux adbucto valgus. It all comes back to the fact that if we don’t control our patients postoperatively, how in the heck do we expect to get a beautiful end result other than the operating table. In my practice, I watched everybody walk. Now, visual gait analysis, I think it’s an important thing. You want to watch somebody who toes in, you want watch hypermobility, you want to see varum or valgum deformities from the knee that are influencing or affecting the foot. I want to listen to the patient walk. There’s a sound to somebody who has no shock absorption. How much hyperpronation occurs as the heel comes off the ground? Is that foot resupinating or has it remained hyperpronated right through the stance phase of gait? Do they have an abductory twist? Because the great toe joint is jamming, the abductom be able to move forward. These become important factors in the determination of a bunion procedure I’d like to. A lapidus, this is a critically important and powerful procedure if I can’t control a hyperpronation postoperatively. Now I tried to, whether I used arthroereisis or other types of surgical procedure for the hyperpronation syndrome with TALs or whatever else. This is a science of evaluation of a patient, differentiating us from any other profession. Mike Trippel [Phonetic] repeated that this morning. Nobody does what we do in the evaluation process. If we can apply the principles that we know are effective, we’re happy campers. During the walking cycle which we call gait, there are really two components to it, a swing phase and a stance phase. It really begins that heel strike at one point and then heel strike again. The stance phase of gait is about 60 to 65% of the entire gait cycle and is the most important part of gait. So we looked at contact period.


    During contact phase, the normal foot pronates. The normal foot is going to allow for adaptation to the supporting surface. It’s going to absorb shock. It’s allowing internal rotation of the leg to occur. Visibly, you can actually see the arch come down somewhat during contact phase. The leg is internally rotating. What stops, what reverses the process, how does the foot know to stop pronating and then begin resupenating? As we are pronating, we’re having internal rotation of the weight bearing side. The swinging limb is behind it. As soon as we begin to initiate the next step is the swinging limb comes forward, we get a counter torque on the weight bearing side. That initiates, that stops the hyperpronation as long as there’s no reason for the foot to continue to compensate by pronating. So it’s actually toe off of the opposite limb that initiates resupination of the weight bearing limb. It’s not muscle activity, it’s not the strongest supinator of the foot, the tibialis posterior that’s doing it. It’s not the gastroc-soleus complex. These certainly are structures that are firing. We can look at basic activity and realize when they fire, these are stance phase muscles. But the majority of the time, the guidance and repositioning and posturing of the foot is coming from the rotation of the leg. The musculature, the strongest supinator, tibialis posterior, the strongest pronator, the peroneus brevis are firing at the exact same time. The reason for it is provide stability to the subtalar and midtarsal complex. You look at this two big anchors, one is inserting into the base of the fifth metatarsal at a strong insertional point. The other, to the tuberosity of the navicular, they’re anchors on both sides of the foot. And then of course your other muscles, flexors, peroneals, et cetera are firing as this foot is now moving into what we call midstance. Interestingly at about 10% of the stance phase of gait, the forefoot comes down to the ground. It’s not bearing much weight however until the body starts to come over, now we reach a point where forefoot and rearfoot are bearing significant weight pretty evenly. As we continue to move forward, the heel comes off the ground. That’s where we see a significant amount of inversion of the calcaneus. That’ that resupenation that we see. With patients with posterior tibial dysfunction or inefficient function of the posterior tibial tendon or tear, you ask them to get up on their toes and it’s pathognomonic when you see the calcaneus stays in an everted position. They cannot go into this significant supinatory phase which is the propulsive phase. They are blocked and there’s nothing that’s going to return that foot back into a supinative position other than surgical intervention or a bracing if you can accomplish that. So we’re looking at the complete environment of function. As this foot is going through his phase, we take this for granted. You just go up, get up and take a step. When you go to the end of the room, gets a cup of coffee not thinking in terms of this mechanism of action bringing me to this final phase so you look at what’s going on in this stance phase. The internal rotation of the leg, the contact phase component, the pronation. We actually will pass through this subtalar neutral position during this contact phase. Then the midstance and look at the amount of time. External rotation of the leg is taking place during the stance phase of gate. The resupination component that we will now again pass through neutral and continue into the supinatory phase. As that foot resupenates in the rearfoot and gain stability, now the peroneus longus can function very nicely around a lateral column which is stable. There’s two columns of the foot, a lateral column stable, medial column which is dynamic. I need that lateral column completely stable to allow for the peroneus longus to derotate the first ray. Normal function, the first ray moves up and moves down as we walk. That’s not hyper mobility. That’s normal function.


    Hypermobility is motion occurring at a time when it shouldn’t and that begins as forefoot loads and we continue to hyperpronate. There’s nothing that’s going to bring that first ray back down to the ground. And then we go into that final propulsive. You can look at what’s going on, by the way, of forefoot or rearfoot. As you strike the ground with metatarsals pretty much perpendicular to the rearfoot, forefoot comes down, first ray allows the rest of the foot to evert somewhat and the ray sits on the ground. You bring it back to neutral, the heel comes off the ground, first ray comes down into a more plantar position relative to the second and lesser metatarsals. It’s interesting when you talk about what brings the heel off the ground as you walk? The first things you’re going to say is well, the gastroc-soleus complex. That’s not the thing that raises the heel off the ground. It’s the fact that you are walking forward. You’re not going anywhere if you don’t raise the heel off the ground. So it’s actually your movement and body movement coming forward, knee flexion extension, all these things as taking place as well as you move forward. The heel comes off and the gastroc-soleus complex is a beautiful supinator. It’s probably our strongest supinator functioning along with the tibialis posterior and the flexors. So we are now converting from pronation to supination and you look at the activity that it takes. External rotation of the leg, muscle activity, intrinsics, critically important, windlass effect which is the plantar fashion functioning from a point of insertion to origin. So as they toe are on the ground, the foot is actually coming up over the toes. We increase the tightness on the fascia. It helps in inverting the calcaneus. Toe break, not that somebody broke your toes. It’s just the angulation. When you come off the ground, you are encouraging a supinatory direction. Certainly, that finally, the allowance of hallux dorsiflexion. Interestingly, the intrinsics have an adductor hallucis and flexor hallucis brevis push back on the first ray. Because of their functional activity, the first ray coming up on a sesamoid apparatus, their muscle activity helps pull in the first metatarsal back as it rotates on to the sesamoid apparatus. This is Hubscher maneuver to show the effect of the hallux with raising of the arch for some flexibility. This is a normal force curve. This was shown many, many years ago by [indecipherable] [28:01], how arch pressure goes from the lateral side of the foot to the medial. I consider the propulsive organ as we push forward the great toe. This is why I’ve always been a believer that if I can retain and maintain the function of the first toe, we are duplicating as close as possible the normal function of the foot and gait. I apologize for going over a little bit in time. I do want to thank my faculty. They did an outstanding job. You do an outstanding job of sitting here all this time and listening to us. Blow off a lot of hot air, maybe. But at the end of the day, I think we accomplished something. We may be just a little better as we leave this room and be able to convey maybe just a little bit more information with patient care. I thank you for your time.