Ankle Joint Equinus vs Talar Equinus

Kevin,

looks like someone can't respond to a simple clinical finding.



Does taping a foot low-dye change dorsi-flexion lunge significantly? (Similarly, does placing a below ankle orthotic device (with sufficient heel appeture to allow ground heel contact and fat-pad compression during weightbearing lunge) under the foot change the dorsi-flexion lunge significantly?)



If the answer is no, then that means your wish for "podiatrists to realize that the dorsiflexion motion of the plantar foot relative to the tibia does not necessarily reflect only dorsiflexion of the talus on the tibia, but also reflects dorsiflexion of the rest of the joints of the foot distal to the talus" is the nth order issue I think it is.

If the answer is yes, then I'd like to see it.




Waiting for the answer Kevin, but thanks anyway for the free psychological profile of my view on my podiatry degree.




Ron
Physiotherapist (Masters) & Podiatrist

 

Ron

I believe the answer to your question on whether lunge value will be changed by restricting joint motion (other than talo-crural) with strapping or AFO would depend on the foot. My experience with lunge test certainly contradicts your assertion, but this needs proper exploration. If you have not spotted the parallel thread please check it out.

http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=17349

My intent is to find a conscencus on the forum about methodology to answer this important question, please let me know what you think about this.

Apart from Kevins prior posts on midfoot function which summarise Nestors work on mid tarsal joint, Nestor et al recent paper "Functional Units of the human foot" has definative data on rearfoot joint motion using in vivo 3D analysis of tarsal bones using cortical pin markers on a group of 8 walking / runnning subjects. My read on this suggests that, although the intent of the paper was for different issues, this "validated" view of mid tarsal joint kinematics is consistent with concerns about what we measure doing standard clinical ankle exam.


look forward to a concidered and likely contrary viewpoint from you

cheers

Martin


The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

Ron

This seems to suggets that you do not agree that forefoot stiffness or compliance greatly influences ankle (TC) RoM.

And yet you do agree that there is the need to differentiate in terms of the above.

Considering posterior stretch (as you put it) Surely the relative compliance of the midfoot joints in the saggital plane will influence achilles tension as the calcaneous pronates? Considering anterior block - If the the talus also plantarflexes, as it must, then any TC impingement caused by its (the talus) dorsiflexed position will be removed. How about if we consider the rocker foot, where the met -cuboid- calcaneous joint is hyper extended, doen't this allow significant dorsiflexion of the midfoot relaive to TC RoM?

I think the taping test that you quote would significantly alter lunge test results if, where the subject has a compliant cavus foot, the foot was taped in a high arched position.

Respectfully Dave

 

How far do we want to go Dave?

As the calcaneus pronates, the achilles influence surely can exert an effect at the knee joint as the gastrocs originate above it. I don't hear anybody stating that your knee has lost 10 degrees extension or 20 degrees of flexion, because of a talo-navicular issue...and nor should I.




Yet, when we talk about the sagittal plane movement of the talo-crural joint, we want to complicate it with a huge focus on the 'icing', rather than what actually matters.


Lets extrapolate on taping/orthotic to alter the ankle dorsi-flexion lunge test. If the podiatric focus of the mid-foot influencing lunge is significant and actual, then I should never be able to restore the bulk of ankle dorsi-flexion range to a patient (with physiological TC joint) that has had a midfoot fusion! Clinically, you can.




All I am saying is that if the profession dare look at the ankle joint in isolation it will start to understand it a hell of a lot better by removing the cloud of largely irrelevant podiatric theory.



Ron
Physiotherapy (Masters) & Podiatrist

 

Ron

I would estimate that motion of the ankle will have little effect on the moments acting across the Knee because the gatroc attatchments are proptionally very close to the knee joint axis. on the other hand motion of the knee will have large moment effects on the ankle because proportionately the tendo-achilles attatchment into the calc is distant from ankle axis.


I agree about how we should not unreasonably bias the value of the "icing" but unless I am mistaken you are looking at the icing, you got it reversed. The range of motion during gait measured at mid tarsal joints in invivo 3D bone marker analysis suggests they approach the same degree of saggital motion as the talo-crural joint during walking and slow running. Until recently I would not have thought about this.

As far as measuring lunge value on a foot with mid tarsal joint fusion, depending on the joints fused, I would estimate that this would be proportionally measure talocrural motion, exactly the point Kevin is making, you would then more accuratley be measuring the effect of rehabilitation of posterior group contractures since mid tarsal joint moment influence would be reduced.

mid tarsal joint fusions would make interesting subjects to examine the plantar pressure curves, do you have access to FMat or similar, it would be interesting to add this to the other thread if you do.

cheers

Martin

The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

Martin and Ron;

I would heartily disagree with you both when you state that AJ ROM does not effect extension or flexion ROM of the knee.

With loss of available AJ and midfoot ROM, the next joint available to move the leg forward along with the body is the knee.

if you see my example at http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=17349 post #8 you will get an idea of what I am talking about.

Bruce

 

While ankle pathomechanics (eg. heel walking) might tend to hyperextend a knee, and result in a genu recurvatum etc...., and push that extension boundary beyond a physiological limit....

my quote was
"I don't hear anybody stating that your knee has lost 10 degrees extension or 20 degrees of flexion, because of a talo-navicular issue...and nor should I."


Bruce, it is going to be an ultra rare, almost bizarre case that sees a direct connection between ankle joint pathology on one hand, and knee joint ROM restriction on the other.


Again, I am talking cake....large influences on ROM. Tell me how ankle joint pathology can rob a knee of 20 degrees flexion....or 10 degrees extension?

 

Bruce

The only effects that increased ankle stiffness will have on knee during walking gait are as Ron has already stated, knee hyper-extention if severe enough.

You mentioned compensatory knee flexion during stance as compensation for increased ankle stiffness. Please explain how that if possible, the only way I could see knee flexing during stance from ankle related problem would be opposite of this, ie calf muscle weakness or iatrogenic overlenghtenning of T/A.

Ron

I think perhaps the issue of the importance of the balance between ankle and MF stiffness is mostly to do with

1 overloading and failure of MTJ dorsiflexion restraining mechanisms which when then fail may cause soft tissue injury and lead to MTJ DJD, and

2 whether or not the forefoot gets overloaded (which will happen with elevated stiffness at ankle and increased MF stiffness).

the ability to differentiate and treat this I think is important and under valued given that they require a slightly different approach.

cheers


Martin

 

Ron

Try this, sit on the floor with your back from shoulders to sacrum tightly against a wall and legs out straight. Invert your foot and dorsiflex the foot and toes and attempt to extend your knee. Then repeat this but with your foot everted. Measure the height attained that you can lift your heel from the floor in each case.
In my case I get my heel 2cm more elevation when inverted than when everted.
Measuring the length of my leg from heel to knee I calculate and extra 2.4dgs of extension.

I make the assumption that the increased distance between heel and knee equals increased tension in the GSC and impedes the knee extension when the rearfoot is everted.

If I transpose this displacement to the displacement of my head over my feet I would achieve a 5cm forward displacement, assuming no flexion of any segments between head and knee. Using standard body parameters and assuming the tibia is perpendicular to the ankle joint ie vertical, this would result in a moment of 22.5Nm about the TC joint, an inertial force at the CoM of HAT and thigh combined of 37.5N. a linear acceleration of the total CoM of 0.44m/s^2 and an angular acceleration of 0.24rads/s^2.

I would say, and you may not agree, that even tho the small addition to angular RoM of a joint may seem insignificant it can have very significant clinical effects in terms of continuation of the gait and velocity of the CoM at the critical point of passing from midstance into propulsive phase IE just at that point where the rearfoot stops pushing and you rely on momentum or inertial force (depending on your perspective) of the CoM to carry you forward over the hump as it were.


all the best Dave

 

Dave, your understanding and practical implementation of neuro-meningeal tensioning seems quite real.

My only issue here is trying to relate this position (hip flexion 90 degrees and knee extension and inversion/eversion) to ADL (activities-of-daily-living) function.


Even 2nd year physical therapists can work out that touching your toes is a bit more difficult when your chin is on your chest. But I won't extrapolate that I should order an MRI of the neck when patient x can't touch their toes or if patient x has posterior knee symptoms. There are bigger fish to fry first. I am always getting back to the 'cake'. And the 'cake' in relation to the talo-crural joint is think about it without the complex largely irrelevant podiatric midfoot theory. Because in practice, it is an nth order issue.



Ron
Physiotherapist (Masters) & Podiatrist

 

Ron:

Are you suggesting that we should ignore the midtarsal joint and midfoot joints since, as far as you are concerned, they are insignificant when compared to the ankle joint? And what do you mean by "largely irrelelant podiatric midfoot theory"? Which of the many theories of midfoot function within podiatric biomechanics are you referring to?

I would think that a practitioner with the clinical experience that you have would agree that gaining a deeper understanding of the actual function of all of the joints of the foot and lower extremity is one of the keys to being a better clinician. Are you saying we should simply ignore the latest research that shows that very significant motions of the midtarsal and midfoot joints occur during normal weightbearing activities?

 

Kevin, if Osama Bin Laden captured me and gave me the option of a bullet in the ankle joint or midfoot, or MPJ, I would say "please, not the ankle joint". I hope that gives you an idea of where I put the importance of the ankle over its more distal structures.

I have said ignore the MTJ and midfoot, when dealing with ankle joint pathology. The understanding of the ankle, in the podiatry profession as I see it, is analogous to a funnel: it all converges quickly to STJ, midfoot +/- sagittal plane workings of the 1st MTJ and so on. And it should not converge quickly. When I see a hip joint presentation, I will assess thoroughly (cake) the hip itself first and foremost rather than quickly digress to lumbo-sacral or knee issues. Hip joint impingement/labral pathology needs to be picked up for instance. If I don't understand the hip, and settle for easy lazy theory from a chiro (it all comes from the back) or a physio (core stability issues) or a refexologist....well the icing aint going to get that labral pathology diagnosed and dealt with.

So am I suggesting that we should ignore the MTJ and midfoot joints? No. That is just your erroneous take on what I have clearly stated in this thread (and the lunge thread). I assess them, and if necessary intervene when warranted. What I try not to do is go on some tangiential ride.


What I have said is that the podiatry profession (as I see it generally), need to be able understand the ankle joint in isolation. And to get their understanding up to an adequate level, they need to be able to put podiatric biomechanics in the bottom drawer...albeit temporarily. In relation to the ankle in my own little world, there are some great podiatrists (I have had first and 2nd hand experiences with Augusta and Appleton....and Fairbairn is slowly getting there). But the podiatry profession at large is not great, when it comes to this critical joint...and it should be.

Any theory, both ancient and recent that suggests this consistent cataclismic influence of the midfoot on the TC joint, hip joint, SIJ and so on.

And that is one reason I spent over 9 years at uni.

No. But I will never let research, even the latest, dictate consistent clinical findings and common-sense; such as the scenario (given) whereby, if an ankle is clear, and a patient has a midfoot fusion, the bulk of sagittal ROM should be regained in the post-op period.


Kevin, over years of this podiatry internet blogging, the STJ and distal to it...and applied physics etc., you haven't many peers; but above the STJ it is a whole new heavier weight-division.





Ron
Physiotherapist (Masters) & Podiatrist

 

Ron:

Thanks for the more thorough reply, I now understand your thoughts much better. ........... And by the way, tell Osama that George Jr. is still looking for him.

I guess I'll need to start training harder and bulking up so I can understand the ankle, knee and hip as only physiotherapists can understand it.

 

Dave and Ron

Dave thanks for additional info, I am still a little confused regarding the implications of this manouver.

you said

.

My observation and interpretation of this manoever on my limb is;

When I am positioned before hip flexion, there is an irreducable gap between my knee and the floor and heel against ground. With hip extension I can lift my leg with knee fully extended, my assumption is this occurs primarily with aid of quads working against tension of hamstrings and gravity. I quickly fatique and heel drops gradually, with assistance from arms I can extend hip by about 100% (from initial postion) with knee remaining extended.


2 questions:


If my knee remains fully extended testing with both calc inverted or everted, I do not understand how tension of GSC will influence the the equilibrium of hip flexion.


As Ron mentioned, flexion of neck effected attainable hip motion, is this really effect of neural tension? If so I am inspired to learn more about this possibility, any suggestion where I might read Ron to get big slice of cake on this?

Ron

Please keep your comments on this issue flowing (the more detailed the better, since for me at least, I likely lack your depth on total lower limb function).

I think your last post clarified your position for me. Whilst I understand your concern regarding the heirarchical importance of the ankle on gait effects on the body generally, I am still not sure if you buy into the idea of the effect of the ankle on distal function, particularly the behaviour of the MTJ and its sequelae and why from a podiatric perspective (I mostly treat CHRONIC MSK foot pain) this is particular interest.

To spell out my feelings about ankle ROM of foot here's a summary;

Much chronic foot pain is mechanically induced or perpetuated.

Determination of aggrevating (normal or abnormal may be elusive in definition) forces and how to therapeutically influence them is a primary goal for MSK podiatrists.

Our complete understanding of the interelationships of functional units of the foot and how to measure them is lacking and is currently of neccessary research to improve our therapeutic goals.

Since in standing and walking gait, the behaviour of the entire passenger/locomotor unit transmits through the foot, proximal effects are, at minimum, of interest and in some instance may reveal significant underlying cause/effect on foot pain, and visa versa.

Historically gait analysis and the technology around it developed becasue of the large numbers of amputees during WW2 and solving problems with their rehab. This work then progressed to looking at significant neuromuscular gait disorders like CP. Both these areas dealt with large and comfortably measured deviations from normal gait and the technology and understanding of what this amounted to gave us a wonderful decontruction of the gross parameters of normal and abnormal gait.

Deconstruction of the "gait of the foot" is a relatively new endevour, frought with instrumentation issues and access to meaningful in vivo measurement compared to proximal segements because their scale.

If I understand you correctly you regard the effects of the "gait of the foot" to have a trivial effect on the passenger/locomotor unit as a whole, and other than pain avoidance gait strategies this seems reasonable to me. However it seems likely to me that understanding the "gait of the foot" will be an important key in unlocking understanding and improving interventions of much CHRONIC MSK foot
pain.

A basic example of our lack of ability in this matter is the issue of ankle flexibility.

How many of us do a quick standard exam of ankle dorsiflexion, relate that to say a presenting problem of forefoot overload, then glibly explain importance of posterior group contractures, demonstrate stretching exercise regimen for soleus and gastocnemius and make that a part of the treatment plan?

We see patient two months later for their forefoot problem, they have made limited progress. We do a quick exam of ankle dorsiflexion and ask if they have been conscientously performing exercise and check their technique which seems good. Problem for me is, has the exercise done anything useful, is it even relevent?

I believe that we need to attempt to improve our abilities in this area behond the scenario above, which although simplified and simplistic I feel is illustrative.


I'd be interested in your comments on this


cheers

Martin

The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

I JAPMA is not available by subscription to my university library, is anyone able to email a copy of;

Dananberg HJ, Shearstone J, Guillano M. Manipulation method for the treatment of ankle
equinus. J Am Podiatr Med Assoc 2000;90(8):385– 9.

thanks

Martin

 

You didn't put your email address - There you go anyway

 

All the best Dave

 

David and Ron;

Ankle DFion stiffnes can most definitely lead to knee compensations. If you have little ankle DFion ROM compensation will start with the midfoot. If you use up all the available ROM of both the AJ and Midfoot, the next joint to compensate for forward sagittal plane motion will be the Knee.

Some patients will most definitely compensate thru hyperextension, usually females. Most will instead flex the knee early in midstance leading to a decrease in hip extension and early heel loss of pressure or early heel lift.

This can come down to a chicken egg scenario, was the knee pathology first or was the problem w/ the AJ or MidFoot.

The closes example I can give you Ron on compensation patterns at the knee w/ ranges you suggest would be in patients pre or post knee replacement. Many of them cannot get to full knee extension pre or post surgery adn lose significan knee flexion post surgery. I see plenty of these patients who are moving towards that point with significant AJ and MF Dfion stiffness problems.

Cheers
Bruce

 

Dave

thanks for the paper and comments on your example. yes typo for hip which as you say, should read flexion not extension.

You are right regarding my hamstrings which I am convinced aggrevate mild intermittent radicular symptoms if I neglect stretching for more than a week (which I rarely do becasue the association is so strong).

I had not picked up on your requirement for knee to touch ground, now this makes more sense. I'm a bit long in the tooth for martial arts , so yoga it is, my daughter as a recent convert would be glad to give me some remidial help.

I am one of the biggest skeptics I have met and have regarded things like fascial plane theories and myofascial pain complaints as somewhat flaky. Recently, having looked at trigger point phenomena with a more open mind and actually explored what this might offer I have become slightly less of a bigot (I think).

cheers

Martin

 

Bruce

I mentioned earlier that I felt that I had never knowingly seen knee flexion as compensation for elevated ankle stiffness.

I should qualify that by also saying that within my interpretation of normal walking gait a "small" amount of knee flexion during 2nd rocker is normal and with parallax error limitations of my instrumentation impossible to quantify usefully when less than perhaps 5 degrees or so. Knee flexion compensation therefore I would expect to be accompanied by need for increased clearance of swing limb and this should also be visible in some form as verification. The issue of sensitivity and reliance of qualitative judgment then takes precedence and perhaps stops me seeing what you see. It must also work the other way round though, I am hugely cautious about trying to stop myself seeing what I expect without testing alternative interpretation. How do you deal with this? The impression I have is that you also look towards evidence from your force/time curves. I feel we need to demonstrate the reliability of that measure more before I am comfortable with that and I look forward to batting on with that in the other thread.

cheers

Martin

 

Bruce,

I think I understand what you are saying. In the old days, we used to use a much simpler terminology. We would say compensated equinus, and uncompensated equinus. Uncompensated equinus would have the early heel off. Compensated equinus would have the foot compensating in the midtarsal and subtalar joints.

I personally do not like the terminology as any joint in the kinetic chain can compensate for the equinus.

I hope this helps.

Stanley

 

Stanley;

Thanks for that input! I will try to remember to fit that into my lectures along w/ the newer terminology as well.

I agree w/ the limitations of the terminology, but it at least gives may a reference point from which to start.
Thanks again!
Bruce

 

Martin;

I'm not sure I got 100% of what you are saying Martin. I dont' agree that knee flexion is normal during walking gait. During running ok, but not w/ walking.

As far as 2D video goes, parallax is as important here as your viewing of teh AJ, no question.

I do have many videos that are unquestionable re: knee flexionon the long limb side as a compensation for opposite limb shortness. After treatment, the knee flexion will disappear completely or amost completely.

I will look for a paper reference when I'm on my laptop later that talks about Achilles tendonopathy and early knee flexion and post that. If you read most knee pathology studies you will see early or prolonged knee flexion cited in most. Unfortunately, the studies will also usually say that the AJ has an increase in DFion. I contend they are flawed in analysis of teh AJ and did not use proper set analysis from their 3D kinematics to seperate the Midfoot DFion compensation from the AJ Dfion assessment.

Cheers

bruce

 

Bruce

Just to clarify my post, I am ONLY talking about knee flexion during 2nd rocker.

I use Jaquelin Perry "Gait Analysis, normal and pathological function" as my "bible" for understanding gait on the "large scale" (as opposed to "foot gait" which perhaps this text, because of it's age, doesnt address much).

To quote Perry describing "normal gait" ; pages 90 to 92

....... the exact limits of each flexion or extension arc (knee) vary with the study reported. These differences are related to variations in walking speed, subject individuality, and the landmarks selected to designate limb segement movements.

As not all studies identified the velocity of walking at the time of knee motion was recorded, an exact relationship between these two factors can not be calculated.

she goes on to say

at initial contact the knee is flexed about 5 degrees. Subjects vary in their knee posture at initial contact between slight hyperextension (-2) and flexion (5)

Following the onset of stance the knee rapidly flexes throughout loading phase. The rate of flexion at this time (300 degree/sec) almost equals that occuring in swing. With the onset of single limb support (12% GC) the knee immediately completes stance phase flexion (18 degrees at 15% GC). This is the time the knee is under maximum weight-bearing load.

and later

differences in knee position at initial contact were unrelated to walking speed. There was notable influnce by walking speed , however, on the amount of flexion occuring during the loading responce. Slowing pace led to greater change than going faster.

and later

during rest of midstance, the knee gradually extends . Minimum stance phase flexion (averaging 3 degrees) is reached about midway in terminal stance (40% GC) and persists only a short time before knee slowly begins to flex again. The rate of knee extension is approximately half that of flexion during limb loading.

I hope this clarifies things better.

To summarise; I believe that up to 5 degrees of knee flexion during single limb support is normal (please indicate if you see otherwise) and that the small magnitudes of change in knee flexion which you might attribute to intervention are not meaningfully measured without very sophisticated 3D systen and concideration also of speed at measured comparisons.

I also feel that omission of this issue of speed may be important in other studies which looked at the issue of FuHL and have started some dialogue with Dave on this which I need a bit of time to prepare more on.

http://www.podiatry-arena.com/podiatry-forum/showthread.php?t=17349&page=2

#42

cheers

Martin

The St. James Foot Clinic
1749 Portage Ave.
Winnipeg
Manitoba
R3J 0E6
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

 

Bruce, what you are saying correlates to what I saw 30 years ago. Stance phase patellar tendonitis on one leg was seen to occur on the long side, and was treated by raising the short side. I use the term stance phase to distinguish it from swing phase, as tight hamstrings would aggrevate the condition if the patient ran quicker. The stance phase designation was applied to the patients whose conditioned worsed when running slower.
Clinically, this also appeared on the more inexperienced runners. My feeling was that this had to do with greater energy requirements than pronation or hip dropping etc., and the more experienced runners "learned" to be more efficient.

Regards,

Stanley

 

Martin;
thanks for the clarification. I will say that I agree that 5 degrees of flexion at contact and into early midstance would agree with what I see. A quote from Dr. Perry is missing re: the stance phase or true midstance phase where I see full knee extension in the majority of patients who have little to no knee pathology.

I know you were posting excerpts, but see if she talks about that at all. Terminal midstance should show no knee flexion until the 1st mpj extneds and you get contralateral heel contact. That is how I understnad things. I've been wrong before and will never cease to amaze myself in that department! ;-)

bruce