Hubscher manoeuvre

If we see a physical impingement, is this functional hallux limitus? I think not, since it is a structural limitation.

See Roukis et al. 1996 http://www.japmaonline.org/cgi/content/abstract/86/11/538

"First metatarsophalangeal joint dorsiflexion decreased 19% as the first ray was moved from the weightbearing resting position to 4 mm dorsiflexed, 19.3% as the first ray was moved from 4 mm dorsiflexed to 8 mm dorsiflexed, and 34.7% as the first ray was moved from the weightbearing resting position to 8 mm dorsiflexed."

Then see: Michaud & Nawoczenski 2006 http://www.ncbi.nlm.nih.gov/pubmed/16396732

"A custom-made semirigid orthosis posted medially and made from a neutral position off-weight-bearing plaster cast can alter motion in the forefoot during the propulsive period by increasing first metatarsal plantar flexion and decreasing excessive first MTP joint dorsiflexion."

Y'all see the problem now? Somebody wrong somewhere. OR, both plantarflexion and dorsiflexion of the metatarsal reduces 1st MTPJ dorsiflexion, or what happens in static stance isn't the same as what happens during gait...

 

So would it be safe to assume thet either we have a very inacurate ay of measuring the range of motion (likely), and/or the relationship of the hallux to the first ray and the rest of the foot affects what me measure due to osseous positiona nd tensions form soft tissues?

 

Just spotted this typo.

 

Things like that seem to happen when the Arena'ettes are chomping at the ankle and at the keyboard :dizzy:

 

We will have one in press soon that shows what design parameters reduce the force needed to dorsiflex the hallux (assuming that making it easier for the windlass to be established during gait is a good thing and assuming that a static measure of this is related to the dynamic function).

 

IF....

... an orthotic device corecting the midfoot lifts the MLA at the talonavicular region, elevates the base of the first metatarsal, thus allowing plantarflexion of the metatarsal head and subsequently allows dorsiflexion of the hallux and activation of the windless mechanism... (traditional idea)....

Theroetically the length over which the plantar fascia has to work point to point is reduced in a straight(ish) line. BUT.... when an orthotic is introduced.. doesn't the plantar fascia have to also work around the orthotic device, i.e. in a more curved line, thus really not work over a shorter distance at all?

...and perhaps this lends to an idea whereby plantar fascia pathologies get better with orthotic therapy due to correction of other abnormal forces on the foot and other pathological alignmnets in the foot which subsequently reduces pathological forces on the plantar fascia?

 

I dont do this test.Anyone tell me why I should?

Is the result ever a surprise? Low arch = hallux wont go up, high arch = hallux goes up easy. I over simplify but you get my drift. The test kind of helps students understand the mechanics of the human arch but its hardly predictive of pathology.

If an orthotic didnt improve this measure, would it not work?????

 

Actually, it is predictive of pathology. How many clinical tests that we do can we say that for. We have a paper in preparation that shows that the amount of force needed to do this test is correlated to plantar fasciitis - I will dig out the abstract on another computer later.

 

Sorry no find abstract at moment, but here is pdf of powerpoint.

 

Good work Craig. How does this relate to the results obtained in the Landorf trial of foot orthoses effectiveness in the treatment of plantar fasciitis?

 

What we showed was the force to dorsiflex the hallux (1st MPJ dorsiflexion stiffness) is higher on the side with plantar fasciitis in those with unilateral symptoms ... next time you see a unilateral plantar fasciitis, do the test and see for yourself (more often that not it is higher on the symptomatic side).

We do not want to jump to any conclusion if this was the cause of the plantar fasciitis (could make intuitive sense that the forces through the tissue are higher resulting in damage) or if the higher forces came after the plantar fasciitis developed (ie due the degenerative tissue changes).

Whichever it is, then the tissue stress model says that the forces in that tissue have to be reduced to get some symptomatic improvement....(do this test before and after you next apply low dye strapping .... the force goes down to almost zero! - ever wondered how/why low dye works?)

As to relating this to Karl's study we can only speculate, but the assumption is that if anyone with plantar fasciitis gets better, then its probably because the stress in the tissue is reduced to allow healing to happen....so maybe thats what happens with orthotics (we have documented the design parameters in a foot orthoses that lead to a lowering of this force, but not yet started to write it up) .... the next step is to see if that can be related to outcomes ... god put me on this earth....

 

Plantar faciitis = no windlass because of pain avoidence????????? Association is not causation.

 

Thats not what we tested.

 

Is it not still a possibility these subjects on a unconscious level did not want their windlass engaged?

 

If that was the case, then I would expect to see some sort of muscle activity for 'splintling' due to pain ... never seen it in the 1000's we have tested.

 

Craig

You make an interesting point here; however my thoughts are that in cases of degeneration (not purely inflammation) the anticipated microscopic changes (replacement of coherent collagen fibres with disorganised cellular matrix) would likely result in a more compliant aponeurosis but with greater stress transferred to the none degenerated adjacent segment and other tensile supporting structures.

This would be consistent with the observation that pain attributed to chronic plantar fasciosis is self limiting given time and may be more to do with adaptation of parallel structures than repair of the plantar fascia. This makes an interesting comparison with similar tensile overload injury of tendo-achilles which has no loadbearing parallel support and seems to have similar microscopic degenerative issues.

I think it possible that some cases of plantar heel pain attributable to tensile overload the symptoms may occur because of transfer of load bearing stress to parallel structures (which then are pain generators). This is based on my observation of little or no reduction in abnormally thickened plantar fascia insertion thickness in those with resolved symptomatic chronic (not acute) plantar heel pain.

I think that a problem in evaluating this idea is being able to separate out the contribution of FDB and Ab Hal in sharing the load bearing and not being able to differentiate insertional pain in the 3 structures. I have tried to evaluate this with US. Observing the motion of the plantar fascia with the naked eye or palpation it is tempting to interpret “that tight central band” as purely the reaction of tightening of the anoneurosis. However if you look at the same event on US it is impossible to tell if the FDB is pushing the plantar fascia or the plantar fascia is pulling the FDB because they appear so intimately coupled.

Even if what I suggest is true then I still see value in your approach given that the premise remains that tensile stress results in tissue breakdown, however I think it unlikely that chronic plantar fasciosis would increase tensile forces given my understanding of the physiologic changes most likely to have occurred.

Regards

Martin

 

Totally agree and its probably right. Its just the nature of the study design we used (a cross-sectional design) can not be used to imply causation (a prospective design needed for that) - we just have to be cautious in the interpretation of the results.

 

Another thought I was having concerns not just adaptation of parallel structures but also the plantar fascia; the microscopic response of plantar fascia to load and a dynamic equilibrium of the ratio of elastin to collagen within the proximity of the enthesis.

Assuming that the plantar fascia, exhibits adaptation in response to mechanical demand it seems reasonable to anticipate within “normal limits” that there exists the possibility of a response specific range of modulus of the plantar fascia for an individual throughout a lifetime. The most likely candidates to influence this I would expect to be this ratio, increasing collagen % increasing stiffness, increasing elastin % increasing compliance and perhaps reducing threshold of mechanical failure.

I did a pubmed search on this topic but was unable to find any evidence on this. I did however come across a great paper which hints (see below). Not sure if this has been cited before on the forum but for anyone interested; it is the most comprehensive single doc I have found on its subject.

The paper suggests this;

Present in both tendon and ligament, fascia may have a greater sensory capacity since it contains more fibroblasts than tendon.[48] Thus, in addition to passively transmitting force, the plantar fascia may also act as an active sensory structure that is capable of modulating its composition in response to external demands.

Dave (Smith), if you are still following this thread I wonder if you can throw any light on this given your recent thesis?

This may be important because protectively reducing tensile strain (foot orthosis??) may cause dependence and conversely therapeutically induced organization of collagen (autologous blood or glucose??) may avoid this in some individuals.

Also a (lazy) question; why did finite element analysis accurately predict the site of plantar fascia injury? Was it related to site of minimal Xsectional area of plantar fascia or something else?

Regards

Martin








1: Sports Med. 2006;36(7):585-611. Links
The pathomechanics of plantar fasciitis.
Wearing SC, Smeathers JE, Urry SR, Hennig EM, Hills AP.
Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland, Australia. s.wearing@qut.edu.au
Plantar fasciitis is a musculoskeletal disorder primarily affecting the fascial enthesis. Although poorly understood, the development of plantar fasciitis is thought to have a mechanical origin. In particular, pes planus foot types and lower-limb biomechanics that result in a lowered medial longitudinal arch are thought to create excessive tensile strain within the fascia, producing microscopic tears and chronic inflammation. However, contrary to clinical doctrine, histological evidence does not support this concept, with inflammation rarely observed in chronic plantar fasciitis. Similarly, scientific support for the role of arch mechanics in the development of plantar fasciitis is equivocal, despite an abundance of anecdotal evidence indicating a causal link between arch function and heel pain. This may, in part, reflect the difficulty in measuring arch mechanics in vivo. However, it may also indicate that tensile failure is not a predominant feature in the pathomechanics of plantar fasciitis. Alternative mechanisms including 'stress-shielding', vascular and metabolic disturbances, the formation of free radicals, hyperthermia and genetic factors have also been linked to degenerative change in connective tissues. Further research is needed to ascertain the importance of such factors in the development of plantar fasciitis.


Regards

 

Craig

Interesting that you used SRF in this presentation. I am still attempting to refine my own contraption (and will post some info when a bit further down the road). I am curious if you have attempted to collect any normative data? I am thinking that it would be appropriate to normalise the data according to weight, any comments?

regards


Martin

 

Mart - lets hold off discussion of SRF for another thread and keep this thread on topic ... I am putting together a You Tube video of the concept and will start a new thread on it with that video soon. However, in this case we did not control for bodyweight as it was an intra-subject comparison. When we do inter-subject comparisons, we control for bodyweight. Normative data is always going to be difficult as it will depend on velocity that strap is pulled at....another thread.

 

Simon

Thanks for that . . . . . . . . . . . well directed. :drinks

I read the paper, which is clearly not intended as a definitive research paper but non the less interesting and the only one with this approach I have seen.

The results as you suggest do not support the idea of a compensatory response to FuHL, unless, as the paper suggests more than 30 minutes is required to create significant change in gait (this being time measurements were made after foot orthosis fitting to compare 2 conditions).

My first response was to probe the methodology which given the lack of detail was impossible.

My main concern was using peak pressure as an index of function given that it doesn’t account for possible changes in measured weight-bearing area.

One example might be that with offloading the 1st metatarsal head there might be a modification in the area exposed to GRF under the hallux (increased valgus position) which may give the impression of increased force when actually surface area of contact was reduced. Likewise the 5th MTH may have reduced surface area of contact with increased momentary load (altered 5th ray angulation to ground changing stiffness to GRF vector) which may increase peak pressures without increasing force/time integral.

So I did a little, albeit loosy goosey, case study;

I have pronounced structural hallux limitus plus that rarely seen true forefoot varus alignment. I experience painful plantar 1st digit blisters with increased weight-bearing activity but symptom free with rearfoot posted foot orthosis. I believe this is due to reduced 1st metatarsal head GRF with foot orthosis, and I suspect that I tend to actively supinate my foot when barefoot as protective compensation.

I did 3 trials (yes I know but . . .) capturing FMat data for my right foot for each of the following conditions;

1 Barefoot,

2 Barefoot with 5mm semi-compressed surgical felt met bar 2-5,

3 Barefoot with 5mm semi-compressed surgical felt met bar 2-5 + 5mm semi-compressed surgical felt pad plantar digital area 1st toe.

4 Barefoot with slightly exaggerated active supination at heel strike through stance.

data added below and in subsequent post.

BEWARE; one thing that bugs me about the tekscan software is that it assigns colour to the graph plots which cannot be changed, consequently with differing analysis the colour of a plot may not represent the equivalent data in another graph USUALLY this happens which is a PITA.

What I was primarily looking for was significant changes in area of contact plantar digital area 1st toe. In fact what I saw was overwhelming consistency in contact area which pretty much negated my concerns about using peak pressures.

What surprised me somewhat was noticing a trend in conditions 2.3 and 4 for earlier heel lift BUT decreased forefoot loading. I want to repeat this experiment a little more rigorously later, the only explaination I could arrive at was misinterpretation of what I was seeing.

Can anyone please help me out with some reasoning here?

My assumptions with weight-bearing foot during late midstance for same foot, subject and speed ;

1 If mid tarsal joint(MTJ) range of motion is reduced with supination of sub-talar joint then heel rise will occur earlier all other things being equal.

2 If MTJ or ankle motion is restricted then forefoot force will increase earlier and GRF will be greater because of more rapid anterior progression of COM causing increased lever arm acting throught COP. COM will be accelerated upward more rapidly until end of single limb support when free fall of body is stopped. This seems well documented for cavus type foot and DM related limited joint mobility in foot.

By artificially creating a slight equinus postion and advancing the "3rd Rocker" timing with my test condtions, my F/T shapes should have seen an increase in 2nd hump not as I found, a decrease. One explaination might be that by reducing windlass force at crutial time of simultaneous ankle and 1st mtp dflexion moments, ankle ROM may be increased. If this is true then it would be possible to see an overal reduction in peak forefoot force during 3rd rocker.


Help appreciated considering this line of thought

Cheers

Martin

 

Rest of data from last post

 

Yeah, I have- once or twice this week They also commonly pronate more during dynamic function on this side in my experience, yet this was not evident in your study perhaps because you employed the static foot posture index. Do you think the lack in statistical difference between symptomatic feet and asymptomatic feet in terms of foot pronation observed in your study may be a result of this static evaluation and/ or related to the validity/ sensitivity of the foot posture index itself? Moreover, what we do not know from this study is whether the force required to dorsiflex the hallux is greater in symptomatic feet during dynamic function- right?

Indeed, ultrasonographic studies show a significant thickening of the plantar fascia in symptomatic feet: http://radiology.rsnajnls.org/cgi/content/abstract/201/1/257
This alone should result in increased stiffness. Martin's point re: collagen and elastin proportions is also well made.

http://www.ncbi.nlm.nih.gov/pubmed/18317390
And probably a good bit of placebo thrown in for good measure too. However, at least some of the effects appear somewhat transitory: http://linkinghub.elsevier.com/retrieve/pii/S0958259200906564

So how did the sham orthoses "work"? ;-)

 

Here's a thought: what effect would too little dorsiflexion stiffness of the hallux have on foot function? What compensatory effects might this induce?

 

Simon

I think you may have this assumption back to front.

In most cases I have seen, the plantar fascia although thickened is also hypo-echoic at the involved site and this is a well documented characteristic of chronic plantar fasciosis.


Since parallel arranged dense collagen fibres will reflect energy efficiently, with high res probe they appear bright and as you might expect fibrilar. Hypoechoicity suggests loss of collagen architecture. I would speculate that this will REDUCE stiffness.

This is why I believe the pain generator in these cases is more likely in the non injured portion of the plantar fascia or parallel structures which will likely suffer functional overload until adapted.

Care needs to be taken in examining the plantar fascia when enlarged because it also becomes fusiform, this can cause hypoechoicity if the incidence of the beam is not perpendicular to the orientation of the fibres.

This is a basic and early learnt pitfall (and diagnostic tool differentiating tissues) which is appreciated using high res US by simple rocking the probe to alter beam incidence whilst looking for the reflected changes in appearance.

Supporting reference below.

Regards

Martin

1: Ultrasound Med Biol. 2003 Dec;29(12):1787-97. Links
On the ultrasonic properties of tendon.
Garcia T, Hornof WJ, Insana MF.
Department of Surgical and Radiological Sciences; University of California, Davis, CA 95616, USA.
The strong dependence of tendon echogenicity on insonation angle is explored by analyzing echo spectra. Combining echo spectra with high-resolution images from several modalities reveals that fluid spaces surrounding fascicles and bundles are likely sources of ultrasonic scatter. Mathematical models of tendon structure are proposed to explain how the anisotropic microstructure of tendon gives rise to angle-dependent echogenicity. Echo spectra from spontaneously damaged equine tendon samples were compared with normal equine tendon and found to exhibit a dramatic decrease in anisotropic properties that appears to be related to the spatial organization and type of collagen generated during repair. Variation in echo spectra with insonation angle is a robust indicator of mechanical damage.

 

I would estimate a fair degree of redundancy in structures which influence 1st metatarso-phalangeal joint dorsiflexion stiffness given how many contractile and passive structures contribute.

Effect would be increased velocity of tibial advancement after heel off and consequently if uncompensated; instability as body falls forward with less control.

Gait adaptation might include:

Recruit more control of tibial advancement from lesser toes by increasing their contribution ie forefoot invertion slightly prior to heel off.

Alter COM vector after heel off and before end of single limb support by ; Knee flexion, backward trunk lean.

Alter basic gait parameters by slowing velocity (reduce tibial anterior velocity), increasing cadence and decreasing step length. (catch yourself faster),


That’s my penneth


Regards
Martin

 

Craig

I see in your powerpoint presentation, the results slide that covers the mean newtons of force to supinate the feet shows only 14N difference between symptomatic and asymptomatic feet.

Is this enough to be percieved clinically?? Hopefully I will find out through the course of today...

 

The difference in SRF between the symptomatic and asymptomatic side was not statistically significant (unfortunatley the results slide did not state that). Using the machine, there is always between left and right foot, but have not considered at what N the differences is clinically perceptable ... maybe there is a project in that!

 

I have been thinking about this a bit more this week and figured that since I have ever seen anything like the gait effects I speculated about in my last post they were unlikely.

To shine a bit of light on this I looked for an extreme example of loss of 1st mpj stiffness; harvest of entire hallux for thumb transplant. I found the attatched study of effects on gait, although the study was older (1988) its methodolgy was sound at looking at many vairiables despite using older technology and the results were suprising to me.

Only significant recorded gait effect in study of 10 subjects was shifting of COP laterally during late midstance, this was, as might be expected, attributed to increased demands on lesser digits for stability.

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

 

Mart, a question

What parameter are you using for decreased forefoot load? With an eariler heel off and the same duration of stance there would have to be an increased force time integral. If the parameter was peak pressure, did the location of peak pressure change?

Heel rise does not always occur at the end of range of motion of the ankle joint. If the gastroc and soleus create sufficient plantar flexion moment at a point in gait before the measured end of range of motion is reached, then you will see an earlier heel off. I vaguely remember a study that looked at measured range of motion versus ankle angle at heel off in gait. They found that the measured range of motion was usually not attained.

Perhaps the earlier heel off is earlier plantar flexion moment from Achilles tendon.

Did you mean center of pressure when you said "and GRF will be greater because of more rapid anterior progression of COM " ? I can see how an early heel off will cause a more rapid progression of the the CoP, but not necessarily of the CoM.

Vertical ground reaction force will increase more with a vertical acceleration of the center of mass. The acceleration of the center of mass, both vertical and horizontal will depend on the timing of the heel lift. If the heel lift comes before the center of mass is anterior to the center of pressure there will be more vertical force, but a slowing of the horizontal velocity of the center of mass.


Just some thoughts,

Eric

 

Eric

thanks for your thoughts.

The parameters were total force and FTI. if you look at the graph data in post # 61 and 62 you will see what I am looking at; FTCs for entire foot, these showed reduction in both max force with similar duraion ie reduced FTI.

I agree; what I meant by ankle ROM was functional ROM and this was meant to include PF moments created by triceps surae.

I did mean GRF, and I agree that it would need to be resolved in to different components of vertical and horisontal and that the horisontal component will increase as the bodies COM advanced behond the base of support as it should at normal walking speed. Assuming that the knee remains extended and hip continues to extend do you agree that this would neccessarily accelerate both COM and COP during this period of "free fall" or do think that the COM is at this point is rising?

cheers

Martin

 

Simon

I had the opportunity to examine a few patients with this in mind this past week. Using the zoom feature to magnify the degenerated portion of the plantar fascia I have revised my speculation. In some patients it is difficult to know if the hypo-echoic appearance simply represents decreased density of reflective elements due to increased volume of ground substance or actual reduction of reflective elements. In some cases there are actual anechoic areas visible, typically I have tended to make the inference of fibre rupture at this site but I am unaware that this has been validated histologically. I feel less strident in my suggestion, it would make an interesting study though.


regards

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

 

Eric

Thinking about this some more; I feel pretty certain that in normal walking gait we can assume that the COM must be accelerating towards the ground until contralateral heel stike. Logically then I cant see any reasonable explaination for the decrease in vertical GRF measured other than shifting of vector from vertical to horisontal and that seems coherent with an accelerated anterior COM position given the change in spatial relationship of COM to COP vector.

does that seem a reasonable rational ?

thanks

Martin