Welcome to the Podiatry Arena forums, for communication between foot health professionals about podiatry and related topics.
You are currently viewing our podiatry forum as a guest which gives you limited access to view all podiatry discussions and access our other features. By joining our free global community of Podiatrists and other interested foot health care professionals you will have access to post podiatry topics (answer and ask questions), communicate privately with other members (PM), upload content, view attachments, receive a weekly email update of new discussions, earn CPD points and access many other special features. Registered users do not get displayed the advertisments in posted messages. Registration is fast, simple and absolutely free so please, join our global Podiatry community today!
If you have any problems with the registration process or your account login, please contact contact us.
I am privileged with the honour of being invited to speak at many conferences. Most recently was at the Podiatric Surgeons conference. When I agreed to speak, I did not think to much about about the topic until I was back from another conference, then I had a OMG why did I agree to talk about that moment ? What the hell am I going to say?
I have been on the organising committee of a lot of conferences and been to a lot and I know what I want when I go to a conference and what I don't want. What I don't want is what is already in the textbooks, as textbooks are cheaper to buy that attending a conference, so the challenge was to come up with something on the topic that is not in the textbooks.
One reason I enjoy speaking at confernces is that it forces me to organise my thoughts and "put them on the line", so I thought I would try and take our traditional understanding of first MPJ dysfunction (ie hallux rigidus; functional and structural hallux limitus) and the windlass dysfunctions (ie no windlass; delayed windlass; high force to establish; disruption during loading) and reconceptualise them in the framework of the mechanial engineering terms of 'stiffness'.
While going through the dot points, I got struck by something: All functional hallux limitus really is, is a temprorary increase in the dorsiflexion stiffness of the first MPJ ! It got the thought processes going.
Traditionally we have considered FnHL as being present or absent, when in reality it probably exists on a continuum. If we conceptualise it as a temporary increase in first MPJ stiffness, it then opens the possibility of grading functional hallux limitus (ie a low temporary increase in first MPJ stiffness to a high temporary increase in first MPJ stiffness). Maybe we can measure this !
It also raises the possibility of an entity that may be the opposite of FnHL -- ie a first MPJ that has a temproray decrease in first MPJ stiffness. Does it exist? Does it have any adverse consequences?
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by Craig Payne
While going through the dot points, I got struck by something: All functional hallux limitus really is, is a temprorary increase in the dorsiflexion stiffness of the first MPJ ! It got the thought processes going.
Traditionally we have considered FnHL as being present or absent, when in reality it probably exists on a continuum. If we conceptualise it as a temporary increase in first MPJ stiffness, it then opens the possibility of grading functional hallux limitus (ie a low temporary increase in first MPJ stiffness to a high temporary increase in first MPJ stiffness). Maybe we can measure this !
It also raises the possibility of an entity that may be the opposite of FnHL -- ie a first MPJ that has a temproray decrease in first MPJ stiffness. Does it exist? Does it have any adverse consequences?
This is what I was talking about in the Hubscher thread and why I asked:
Quote:
Originally Posted by Simon Spooner
Here's a thought: what effect would too little dorsiflexion stiffness of the hallux have on foot function? What compensatory effects might this induce?
The problem with classification of this type is that it provides an artificial delineation. Take the hallux valgus classification as an example, traditionally 15 degrees of hallux abduction on it's metatarsal has been considered as the division between normal and pathological. So does this mean a foot with 14.9 degrees hallux abduction (HA) angle functions differently from a foot with 15.1 degrees?
As I also said previously in the Hubscher thread, a zone of optimal stiffness probably exists which will be person and task specific since hallux dorsiflexion stiffness can be modelled as a quantitative genetic trait thus:
P = (G+E) + (GxE)
Where:
P is the hallux dorsiflexion stiffness
G is the genotype
E is all non genetic factors , i.e. environment
This aside, first we need to better explore the predictors of hallux stiffness. Then we can begin to normalise the stiffness data for these variables. Again, I talked about this in the Hubscher thread with others adding to the initial list that I suggested.
As for too little stiffness, look to those who underwent Hallux valgus surgery and were left with a flail toe!
BTW I've been conceptualising FnHL as a temporary increase in first MPJ stiffness ever since I first read about it, I guess it's just the way I think ;-)
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by Simon Spooner
As for too little stiffness, look to those who underwent Hallux valgus surgery and were left with a flail toe!
The point I was trying to get at was not the 1st MPJ with too low stiffness; but the hypothetical situation that is the opposite of a FnHL; ie a temporary decrease in dorsiflexion stiffness.
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by Craig Payne
The point I was trying to get at was not the 1st MPJ with too low stiffness; but the hypothetical situation that is the opposite of a FnHL; ie a temporary decrease in dorsiflexion stiffness.
The differentiation being made is in terms of direction: dorsiflexion versus plantarflexion; adduction versus abduction; inversion versus eversion (how might we conceptualise hallux valgus, trigger 1st etc. using this terminology?) and timing.
The tension in the soft tissues that encompass the 1st MPJ will influence either the relative dorsiflexion versus plantarflexion, adduction versus abduction, inversion versus eversion, or a combination of these stiffnesses of the joint. Thus, all of these structures have the potential to influence the overall joint stiffness. The relative force exerted by each of these structures and the balance between antagonist tissues is, in part, responsible for maintaining a "healthy" non-pathological joint. Disruption of the normal "equilibrium" would appear to lead to pathology (Spooner S.K., Kilmartin, T.T., Merriman, L.M.: The Pathological Anatomy for the First Metatarsophalangeal Joint in Hallux Valgus, British Journal of Podiatric Medicine and Surgery 1995; 2: 35-40).
A decrease in the stiffness of any of the structures that oppose dorsiflexion should result in a decrease in dorsiflexion stiffness. For example: fatigue, weakness etc. in flexor hallucis brevis will result in a decrease in dorsiflexion stiffnesss at the 1st MPJ. The length/ tension relationship of this, and other muscles is obviously significant. This will vary from step to step due to environmental factors and probably with postural position. Also key is the phasic activity of the muscles. If flexor hallucis brevis were to fire too early we would see a temporary increase in dorsiflexion stiffness, it were to fire too late we would see a temporary decrease in dorsiflexion stiffness. Thus, any factor that may influence the phasic activity of the muscles acting on the 1st MPJ may also influence the joints stiffness. We should also require knowledge of "how much" stiffness and "when" in differentiating the "normal" from the "abnormal".
A decrease in the stiffness of any of the structures will also result in a decrease in that tissues ability to store and therefore return elastic energy.
Dorsiflexion stiffness of the 1st MPJ also appears to be influenced by first metatarsal position so theoretically the joint stiffness will be influenced by any factor that changes 1st metatarsal position. We should be able to manipulate hallux stiffness by varying the amount of 1st ray plantarflexion/ dorsiflexion.
Perhaps worth noting, the capsular pattern for the 1st MPJ is limitation of plantarflexion > limitation of dorsiflexion.
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
One after thought: One of the things observed in functional hallux limitus is a "slowing" in the rate of progression of the centre of pressure (CoP). What if this "slowing" is in fact the "normal rate" and the rest is actually "too fast"?
This is said with tongue in cheek, but obviously if CoP progression is predictive, we would be looking for a rapid increase in progression in the case of reduced dorsiflexion stiffness. Ever seen evidence of this Bruce?
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by Craig Payne
Should be reconceptualise FnHL as a temporary increase in first MPJ stiffness?
What say you?
Craig;
I suppose that is a fair reconceptualization. KK has reconceptualized hypermobility as Decreased Dorsiflexion Stiffness, so your idea seems to work well from that point at this time.
Simon, while I am sure the ommission was not intentional, don't forget the sesamoid apparatus, size and placement in respect to the metatarsal head of the sesamoids as well.
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by Craig Payne
While going through the dot points, I got struck by something: All functional hallux limitus really is, is a temprorary increase in the dorsiflexion stiffness of the first MPJ ! It got the thought processes going.
Traditionally we have considered FnHL as being present or absent, when in reality it probably exists on a continuum. If we conceptualise it as a temporary increase in first MPJ stiffness, it then opens the possibility of grading functional hallux limitus (ie a low temporary increase in first MPJ stiffness to a high temporary increase in first MPJ stiffness). Maybe we can measure this !
It also raises the possibility of an entity that may be the opposite of FnHL -- ie a first MPJ that has a temproray decrease in first MPJ stiffness. Does it exist? Does it have any adverse consequences?
Should be reconceptualise FnHL as a temporary increase in first MPJ stiffness?
What say you?
This temporary nature and the mechanical infulences is something implied from my paper on the windlass: Fuller, E.A. The Windlass Mechanism Of The Foot: A Mechanical Model To Explain Pathology J Am Podiatr Med Assoc 2000 Jan; 90(1) p 35-46
Activation of the windlass creates a supination moment at the STJ. Conversely, a high pronation moment at the STJ will increase tension of the fascia and increase dorsiflexion stiffness of the 1st MPJ. Also increased dorsiflexion moment on the forefoot (or plantar flexion moment on the rearfoot) will increase tension in the fascia and increase dorsiflexion stiffness of the 1st MPJ.
So, some of the mechanical variables that will affect tension in the plantar fascia are quite variable themselves. Specifically, relative amount of muscle activation will alter the pronation moment at the STJ or plantar flexion moment on the rearfoot. Therefore, functional hallux limitus can have a mechanical tendancy, related to transverse plane STJ axis position, among other things, and it can have a behavioral component in the relative activation of various muscles. For example, an increase in activation of the posterior tibial muscle will lead to increase in tension in the tendon and increase in supination moment from the muscle. This will cause a decrease in stiffness of the 1st MPJ. So, it might be fairly easy to quantify the non-behavioral part, but the behavioral part will be variable.
Simon's comment about a decrease in stiffness of 1st MPJ being like post Keller surgery is a good one. You will see increased 2nd met stress fractures and lower hallux pressures with decreased dorsiflexion stiffness of the 1st MPJ. With lower hallux pressures the force of body weight will have to go somewhere else. (Other toes, other met heads, other foot, crutches etc.)
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Hi Craig and colleagues
A very interesting thread to follow. The mechanical properties of the 1st MPJT must consider not just stiffness. A few years ago we evaluated stiffness relating to plantar heel pain and suggested that heel pad stiffness is influenced by many factors that include age, gender and any co-morbidity. Therefore, to look at the stiffness component alone may not give the whole story. Other mechanical properties of the 1st MPJT such as range of motion, passive resistive torque and muscle cross-sectional area must be taken account.
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Dear Craig
In my MSc thesis I looked at the windlass action in terms of the mechanical properties of the plantar fascia. I found that in 20 steps the mean peak dorsiflexion RoM in the stance thru propulsive stage was 57dgs. This was in a foot that I had deemed as Normal in terms of foot posture index ie not being excessivley pronated or supinated during gait and having normal GRF forces in all dimensions. Also a normal CoF progression. I tested these parameters with Kistler force plate and Vicon 3D motion analysis analysed in MS Excel. The 1st MPJ RoM, MLA RoM (change in length) and discreet plantar pressures were measured with rotary and linear potentiometers and an RS Scan 2mt pressure mat.
The RoM of 57dgs may be significant since this = 1 radian. Measuring the radius from centre of 1st MPJ to tibial sesamoid = 17mm (measured from X-rays) and this was equal to the change in length of the MLA from fully pronated stj and dorsiflexed 1st ray to fully supinated stj and plantarflexed 1st ray at early toe off. The total change in length of the PF was 4.5mm. 1.5mm of this occuring before heel off (start of hallux dorsiflexion) and after initial toe (hallux) contact (start of PF tensioning).
At first this may sound like the maths do not add up but in fact the change in hallux RoM was faster than the change in MLA length in the last third of the stance phase but the MLA catches up again at the end of stance phase. Therefore there is a time where the PF becomes longer and is at its max extension at 83% of stance.
3mm change in length of the PF occured during hallux dosiflexion during stance. The PF was 190mm in length but the interesting thing was that in relative terms most of the extension (1.5mm) occured in the last 30mm, which intuitively is obvious since this is the thinnest part of the PF in terms of its origin at the calcaneous and it insertion at the hallux phallanx.
FncHL appears to be present when the discreet force/pressure- time curve sub hallux exceeds and proceeds the pressure sub 1st MPJ in terms of both magnitude and time.
I thought that it may be concluded that if the hallux dorsiflexion during stance does not reach the equivalent displacement of 57dgs or 1 radian (of the radius from met head centre to tibial sesamoid) then there is a tendency toward FncHL. This tendency increases as the hallux RoM decreases. The process of FncHL is reduced by the ability of the thin end of the PF to extend more easily than the middle and origin and therefore allow hallux dorsiflexion.
In this way the condition of FncHL is progressive in nature rather than either present or not present.
How does this sound to you.
Cheers Dave
__________________
Descartes seems to consider here that beliefs formed by pure reasoning are less doubtful than those formed through perception.
Last edited by David Smith : 11th August 2008 at 12:45 PM.
Reason: Changed MPA to MLA
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Quote:
Originally Posted by David Smith
Dear Craig
In my MSc thesis I looked at the windlass action in terms of the mechanical properties of the plantar fascia. I found that in 20 steps the mean peak dorsiflexion RoM in the stance thru propulsive stage was 57dgs. This was in a foot that I had deemed as Normal in terms of foot posture index ie not being excessivley pronated or supinated during gait and having normal GRF forces in all dimensions. Also a normal CoF progression. I tested these parameters with Kistler force plate and Vicon 3D motion analysis analysed in MS Excel. The 1st MPJ RoM, MLA RoM (change in length) and discreet plantar pressures were measured with rotary and linear potentiometers and an RS Scan 2mt pressure mat.
The RoM of 57dgs may be significant since this = 1 radian. Measuring the radius from centre of 1st MPJ to tibial sesamoid = 17mm (measured from X-rays) and this was equal to the change in length of the MPA from fully pronated stj and dorsiflexed 1st ray to fully supinated stj and plantarflexed 1st ray at early toe off. The total change in length of the PF was 4.5mm. 1.5mm of this occuring before heel off (start of hallux dorsiflexion) and after initial toe (hallux) contact (start of PF tensioning).
At first this may sound like the maths do not add up but in fact the change in hallux RoM was faster than the change in MLA length in the last third of the stance phase but the MLA catches up again at the end of stance phase. Therefore there is a time where the PF becomes longer and is at its max extension at 83% of stance.
3mm change in length of the PF occured during hallux dosiflexion during stance. The PF was 190mm in length but the interesting thing was that in relative terms most of the extension (1.5mm) occured in the last 30mm, which intuitively is obvious since this is the thinnest part of the PF in terms of its origin at the calcaneous and it insertion at the hallux phallanx.
FncHL appears to be present when the discreet force/pressure- time curve sub hallux exceeds and proceeds the pressure sub 1st MPJ in terms of both magnitude and time.
I thought that it may be concluded that if the hallux dorsiflexion during stance does not reach the equivalent displacement of 57dgs or 1 radian (of the radius from met head centre to tibial sesamoid) then there is a tendency toward FncHL. This tendency increases as the hallux RoM decreases. The process of FncHL is reduced by the ability of the thin end of the PF to extend more easily than the middle and origin and therefore allow hallux dorsiflexion.
In this way the condition of FncHL is progressive in nature rather than either present or not present.
How does this sound to you.
Cheers Dave
Sounds great, when and where will it be published? A couple of questions what is the MPA? medial plantar aponeurosis? How many subjects did you study in total?
Re: Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
Simon
Quote:
A couple of questions what is the MPA?
- Typo now changed to MLA medial longitudinal arch?
Quote:
How many subjects did you study in total?
One, That took many weeks of preperation, design and testing for a novel experiment, several days of data collection and produced enough data to keep me processing for months, the logistics and cost of reproducing this experiment many times was prohibitive.
Dave
__________________
Descartes seems to consider here that beliefs formed by pure reasoning are less doubtful than those formed through perception.
Reconceptualising FnHL as a disorder of variable stiffness of the first MPJ
why did I agree to talk about that moment ? What the hell am I going to say?
!
Hybrid Mode
