Hip Biomechanics: Part 4 of 6

This diagram (Figure 4) also shows a balanced equation; HAM x D1 = D2 x BW.  (where HAM=hip abductor/g.medius, D1 and D1 are lever arms, BW= body weight). This is not exactly a desirable scenario or strategy to obtain when it comes to joint compression mechanics however it is close to representing what is accurate in the human hip.  Since the gluteus medius muscle is the primary joint compressor in the frontal plane (it applies two thirds of the compressive forces across the joint) we would ideally never want such a large HAM force.  Typically the internal to external moment arm ration is 2:1 thus this model would require a HAM force twice the body weight to maintain a balanced system.  None the less, we would want to offset these forces somehow.  The only way to offset the large HAM would be to move the pivot point closer to the BW thereby increasing the D1 (increase D1 and you can reduce HAM and thus joint compression load).  In a physical person the pivot point, the joint axis of movement, is fixed so there is no real strategy to improve the situation without surgery.  These patients are unlucky and have no strategies to improve their high compression forces unless they loose weight; due to the fact of the 2:1 ratio, for every pound of body weight loss there is a 2 pound force decrease in the HAM.  Obesity is going to wreak havoc on our populations hips.

As mentioned previously, the model presented is very much incomplete.  Muscular forces surround the joint, movement occurs in every cardinal plane and there is acceleration of body segments which requires even greater muscular contraction isometrically, concentrically and eccentrically.  These factors all considered, it has been calculated that the total hip force crossing the joint can reach 3 times the body weight during walking.   This force is welcomed for maintaining joint stability but it can be an unwelcome force in a degenerative arthritic joint where the cartilage is less pliable and flexible.  The loading forces in an arthritic joint rhythmically pass into the acetabulum and femoral head as a result of the compromised cartilage necessitating increased bone mass and sclerosis within them.  This compromised arthritic joint will have some minor laxity due to the loss of the cartilage bulk and thinning of the acetabular labrum.  Thus the joint will have a slight increase in translatory/accessory movement and require greater muscular contraction to minimize/stabilize these movements.  These increased forces will be unwelcomed as they will generate more pain.  Additionally, the increased movements and degenerative debris within the joint will cause irritation and inflammation of the joint capsule and synovial lining causing further pain.  This entire scenario will cause the patient to investigate conscious and subconscious gait strategies to reduce the compression across the joint, in other words, they will essentially seek gait strategies that will reduce HAM (gluteus medius contraction) and increase the D1 internal moment arm.  These strategies will reduce the perpendicular joint compression forces that likely will be causing pain but if performed well they will be devastating to the normal frontal plane equilibrium since the gluteus medius muscle will be essentially shut down and inhibited.  Thus, the patient’s gait strategy will give us the compensated Trendelenburg gait pattern.  The uncompensated Trendelenburg gait will show a dropping of the contralateral hemipelvis on the swing side during gait, this is the pathologic gait pattern we see when the patient has not implemented strategies to reduce their pain but it is more likely seen when the patient is not yet at the painful stage in which they need to implore strategies to avoid the movement.  Comparatively, compensated Trendelenburg gait pattern will display a lifting of the contralateral hemipelvis.  This strategy is not implemented by activation of the gluteus medius on the side in question, rather it is a compensation move performed by shifting the patient’s body weight over the pathologic hip thus causing the hip that is dropping to be passively raised into a more normal range in the frontal plane.  This passive frontal plane move by the patient over the painful hip is at first difficult to embrace logically as one does not expect to want to load their body weight further over top of the painful hip.  However, upon investigation of the mathematical equation one will see that the shift of body weight (BW) over the affected hip will significantly reduce the D2 external moment arm, significantly increase the D1 internal moment arm and thus deliver us the desirable significant reduction in the HAM gluteus medius compressive contraction across the painful hip.  Thus, the pathologic compensation gait pattern in the frontal plane will markedly reduce the patient’s hip pain.  From a kinetic chain perspective however, there is always a price to pay.  This implemented strategy of ipsilateral trunk lateral flexion is performed by utilization of the thoracolumbar paraspinals and quadratus lumborum on the painful hip side. The resulting abnormal muscular and joint strategies now imparted on the lumbar spine and pelvis interface frequently begins a cascade of muscular and joint pain in the low back and abnormal loading of the lumbar discs.  The strategy also begins an unwelcome increased loading of the non-painful hip as the patient is loading the hip greater than normal due to the height from which the hip and pelvis drop from the compensated Trendelenburg position.  In other words, by protecting the painful arthritic hip from increased loads we sacrifice the healthy hip for a period of years until the forced finally amount to enough damage that pain begins here as well.  Fortunately, we have the ability to mediate some of these dramatic movements and forces by using logic and a cane.  By placing a walking cane in the hand opposite to the painful hip and by asking the patient to contact the cane with the ground when they initiate contact with the painful limb we can offset some of the excessive compensations and forces.  When the cane contacts the ground the patient is to apply a mild to moderate downward force through the cane via arm contraction.  This downward force will afford us a resultant upward ground reactive force through the cane delivering us a lifting effect on the dropped hemipelvis side (dipping hip side/non-painful side).  This strategy will allow us a more passive shifting of the body weight (BW) over the painful hip side without having to lift or pull the body weight (BW) over the painful hip with the hip abductor muscles (HAM).  These passive forces (which can be more than  half of those normally needed to be generated by the HAM) will help to markedly reduce the muscular forces needed by the spinal and quadratus muscles while also rendering the desired marked reduction in HAM compressive forces across the painful joint.  It is interesting to note that the further the cane is placed from the body, the longer its moment arm and thus the less downward force necessary by the patient’s arm.  It is quite possible, that if used correctly, a cane can almost completely offset the required contralateral HAM force.  Another passive strategy would be to carry objects (purses, books, grocery bags, etc) on the affected hip side.  This action will also balance the teeter-totter  in favor and thus reduce the muscular forced necessary to perform the same task.  It must be noted however that increasing any body load is undesirable and should be avoided not so much because of issues pertaining to the painful degenerative hip but because of the increased load on the healthier hip.

Shawn and Ivo, The Gait Guys

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Dr. Shawn Allen discusses Gait Biomechanics again, this time pure hip biomechanics and how it applies to gait and running and compensation patterns. This is Part 1 of 2 of the Hip Biomechanics. This is essentially applied biomechanics.

Yesterday’s Video Case: The Gaits of Hell

We have received many emails on this case already. Overwhelmingly people are saying……. “Hey, this isn’t easy….. It’s easy when you guys tell us right away because we can see it."  
Yes, when we are all alone to solve these gait problems our heads can start to swim with all the variables. Gait analysis is not easy.  Even the video assessment computer programs do not give you the answers and diagnosis, they just give you variables and data.  The thinking still has to be  done at the end of the day.

I remember how much I struggled with this case back during my orthopedics residency. I remember even pulling out my undergrad notes from Univ. of Waterloo as a student of the famous Dr Stewart McGill and mapping out FBD’s (Force-Body Diagrams) on this case. Oh, the horror !!!  I still have occasional FBD nightmares, being asked to solve an equation in front of the whole class. Pure anxiety ! Holy night terrors ! But, it is amazing what a few decades of study will do for you, we can now look at this case and see things for what they are, see them quickly and know what is going on almost immediately.  It takes some time, so if you are new to this stuff, be patient…… it will come.

CASE REVIEW:

in this video we see the following:

1. large step length off of the left foot abruptly onto the right, this step is sudden and he crashes down on to the right foot sooner than he normally would to catch his forward moving body mass. ( this will make more sense after reading #5).
2. there is a delayed left heel rise and delayed left calf recruitment , actually, it’s not delayed, it’s absent. )
3. the left foot remains supinated through the entire gait cycle. 
4. the left foot shows extraordinary long toe flexor recruitment (seen on the end of the video during the foot close up)…….this point is important
5. pelvic unleveling is apparent but a mirage for the most part. We really do not see a true Trendelenberg style gait (although it sort of looks like the left hip drops) rather, what you see is the result of the manufactured delayed left limb departure and subsequent impact at right limb load … but this is not a Trendelenberg gait, he had no Gluteus medius weakness.  Explained another way, he is having troubles departing off of the left foot (this diagnosis is the reason, he has compensated from a neurologic lesion affecting the strength of the calf) and so he extends ( behind him) the left leg longer and further than normal because he cannot push off, plus he hyperextends the left knee because of these factors. Normally, the calf fires after passive heel lift occurs. But with a lesion affecting the calf it has arrested the push off. So, in his case, the heel stays on the ground until it is dragged off from enough  forward body carriage. So, when you see this from a sagittal view the left hip will look like it is dipping as it does here, but it is not truly, he is just taking a long lurching step off of the left and onto the right, the longer left hip extension behind him sets up the illusion of a left hip drop.  Try this at home to feel this gait, walk down your hallway and try to delay the left heel rise for as long as you can.  You will find that you get into your left gluteals more, take a longer step on the left, and take a sudden lurching load onto the right limb to catch your forward progressing body mass. This is exactly what this chap is doing.  But why ? The left calf lesion. 
6. continuing on #5, there is abrupt right frontal plane loading (because of the sudden transition from left foot to right the frontal plane is engaged longer than normal) and thus the pelvis is carried further to the right in the frontal plane.  He makes a  noble attempt to protect this range by turning out the right foot into the frontal plane (aka. increased right foot progression angle) to allow the quadricep muscles to assist the gluteus medius, abdominal obliques and lateral limb stabiliers in decelerating this frontal plane challenge.

Diagnosis:This doctor came to see me while I was completing my orthopedics residency and mid way through my course work in the neurology post doctoral program. He had been treated for mechanical low back pain with failed results ( well, to be accurate. his low back pain had resolved but pain had peripheralized into the left leg. To review, peripheralizing pain is rarely a good neurologic sign.)  After an examination showing an absent left S1 Achilles reflex it was highly suspicious we were dealing with a radiculopathy. An MRI confirmed a substantial left foraminal disc herniation obliterating the left S1 nerve root foraminally. The S1 nerve root expands into branches feeding input into the lower limb muscles.  In this case, the unfortunate group affected was the gastrocnemius almost exclusively. So in this case this makes sense to what is presented clinically and on gait evaluation. He is overutilizing his long toe flexors (fortunately untouched) as seen in the video because they are basically all that is available to him to plantarflex the foot ( create heel rise and push off).  They are certainly not well suited for this task but subconsciously the brain will use what is available to it, worthy or not. In this case they are a feeble attempt at best. There is no way the long toe flexors can lift his body mass into heel rise and propulse it forward, they are synergists of this task and not agonists / prime movers.
Sequencing Summary:So, this is a case of an aberrant or pathological gait pattern that will be permanent because the nerve damage was fixed by the time i had seen him.  Muscular wasting of the gastroc complex had already occurred.  The culprit was the space occupying lesion (disc in this case) in the left spinal vertebral foramina effacing and deforming the nerve root sufficient enough to create dennervation.  A surgical consult and EMG/NCV (as best as i can recall) confirmed this case was non-surgical at that time (no one wanted to touch the case).  The nerve damage disabled the calf so that push off was impaired.  He thus delays his ability to create adequate heel rise and propulsion so the long toe flexors are called to attempt the feat.  The foot supinates to maintain its rigidity ( it is also hard to pronate through the foot when the toe flexors are in an all out contraction). And because the heel does not rise on its own from muscular strategies, the foot waits to be lifted off of the ground by simple forward progression of the body.  This creates an increased left hip extension range and gives the appearance of a left hip drop which is a false appearance pseudo-Trendelenberg sign.  Due to the fact that he is on the left limb longer, he will be on the right limb for a shorter period.  This right stance phase is initiated abruptly as he falls from the delayed left stance phase. The abruptness of the load on the right challenges the right frontal plane as evidenced by the right foot turn out and right pelvis sway (subtle).  He then departs off the right to  begin the cycle once again.
PS: It is coming a little late, but thank you Dr McGill. Your teachings to a young undergrad set my biomechanical thinking on the right path very early in my studies of human kinetics. Thank you, Sincerely. 
Dr Shawn Allen…… The other half of The Gait Guys