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Biomechanical Risk Factors Associated with Neuropathic Ulceration of the Hallux in People with Diabetes Mellitus
Journal of the American Podiatric Medical Association Volume 96 Number 3 189-197 2006

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How did they measure the pronated foot?

Foot Posture Index - its was 6.6 (+4.0) in ulcer group and 4.4 (+3.6) in controls (p=0.005)

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Craig Payne
Department of Podiatry
La Trobe University
Melbourne, Australia
http://www.latrobe.edu.au/podiatry
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The views expressed above are those of the author and not that of La Trobe University
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This information is becomming more prevalent in the assessment of the Diabetic foot.

There is some excellent research now being published especially in the UK about the biomechanics of the diabetic patient. Abboud et al, Barnett, Plank, Schie etc etc have all published on the gait and biomechanics of diabetes recently.

The evidence suggests that in the flexible neuropathic foot the biomechanics are altered so that at heel strike the foot pronates and due to neuropathic changes in motor supply the foot does not resuppinate, this means that the foot is loaded for prolonged periods especially on the medial forefoot. This leads to increased plantar pressures, and loading times, which when combined are major causative factors in diabetic ulceration.

We need to begin to look at the Diabetic foot in different ways, one of which may be to look at the biomechanics and to treat accordingly with functional insoles rather than the traditional total contact insole which does not change loading times.

A good functional insole should change loading times of the forefoot by action to control the rate of pronation and the duration. Obviously the insole needs to be made of suitable materials for the neuropathic foot.

There is further work being conducted in the UK looking at this precise treatment modality for the prevention of ulceration in the forefoot in flexible neuropathic feet.

Most diabetics have poor biomechanics in general.Could be that a factor here is that there is a plantarflexed 1st ray with hallux limitus in the diabetic population,hence the hallux "cocks up" and is subsequently more prone to ulcer?

I have not seen a plantarflexed 1st ray causing hallux limitus...how does this work?
In my experience, unless there is a proximal issue causing medial column instability and dorsiflexion of the 1st ray (eg post tib dysfunction), your common, garden-variety neuropathic foot will end up with the classic "instrinsic minus" foot type, and potentially a "trigger hallux". This is more prone to ulceration of the apex, as opposed to ulceration of the plantar IP joint where hallux limitus and medially deviated STJ axis probably exist.

I think the biomechanical issues for a neuropathic foot, in no particular order, are;

* sensory neuropathy
* motor neuropathy
* non-enzymatic glycosilation of collagen causing limited joint mobility
* attenuation of the plantar fascia and plantar plates

LL

Plantar flexion of the first ray causes a FUNCTIONAL hallux limitus, due to the fact that the hallux cannot further plantarflex and therefore there is reverse windlass mechanism acting (Harradine et al 2005). This causes locking of the 1st ray and therefore prolonged loading on the 1st met head in particular this increased loading time is far more important than the high planar pressure (Barnett 2005).

The gait blocks at forefoot loading and stays loaded at the forefoot.


WRT the biomechanical issues surrounding the neuropathic foot:

As you say
1) Non-enzymatic glycosylation of soft tissues which affects joint mobilityand soft tissue movement. (a good easy test for this is the Prayer Sign).

2) Motor neuropathy which affects the Tibialis Anterior as the first muscle (Aboudd et al 2005) . This muscle is regarded as the primary muscle of decelleration of plantar flexion at heel strike. Once this muscle is affected the diabetic patient develops the classic 'slap foot' gait. The foot loads onto the forefoot almost instantly, and blocks at this point causing prolonged forefoot loading. (landsman 1995).

3) Sensory neuropathy, causes loss of proprioception which affects walking due to the lack of sensory feedback, and patients will often change the gait to a high step gait without hip roatation due to this enabling increased feedback.

4) Not sue what you mean by attenuation of PF as this structure will be affected by the glycosylation and will become much stiffer, therefore reducing the windlass mechanism.

However we need to remember that neuropathy is a PROGRESSIVE event in the diabetic and the above do not all happen at once but develop over time. Early intervention to slow down the effects is paramount, and there is VERY strong evidence that tight control of diabetes can reduce these effects,(DCCT, 1980s and UKPDS 1980s-1990s) ((both long prospective studies including 1000s of patients)).

Also once neuropathy is beginning to develop the we have a duty of care to provide protective/corrective insoles whgich off laod the forefoot inorder to reduce the risk of ulceration.

The real question is now we are developing a body of evidence to sday that the foot is (in the early stages) affected functionally can we really continue only to treat these aptients with total Contact Insoles which have no functional effects, or should we be using orthoses which act to offload the forefoot by changing the functional and thereby reducing loading times?

Robby

Rupture and tear of the plantar fascia and associated strucutres is well understood in the (diabetic) neuropathic foot. I am sure Craig Payne can give you a list of ref's on this.

My feeling is there is a chicken/egg issue associated with atrophy of the intrinsics. As progression hammertoe/clawtoe deformity occurs, and there is reverse buckling at the MTP level, I think this is the point as which the distal plantar fascia/plantar plate attenuation and rupture occurs. But it could be the other way around...

Because of this, I still don't accept that even a functional hallux limitus occurs commonly in the rectus diabetic foot (ie without significant hindfoot valgus). Plantarflexion of the 1st MT head will enable more ROM at the 1st MTP joint, particularly when the plantar fascia is so commonly compromised.

LL

I agree with you and am aware of the work which has been done on the rupture of the PF, but this tends to happen in the later stages of neuropathy development and has been associated with the development of Diabeticneuroarthropathy (Charcot Changes). Schie, Edmonds, Foster, et al.

The Diabetic neurpathic foot tends to develop the classic high arched clawed toes dropped met heads as neuropathy pregresses and the intrinsic muscularture is outbalanced by the extrinsic muscles.

FnHL has been found to be an issue in early stage neuropathy especially in young type I, in fact preadolescent children have exhibited this. Barnett et al It is also evident in the neuropathic foot which is still mobile, and pronating. This FnHL causes blocking at fore foot loading and prolonged loading times. Cavanagh et al. This reduction in progression causes abnormal loading at the fore foot Bolton & Masson

As I stated above this is associated with the change in muscle function in the anterior muscle group which leads to 'Foot Slap' Lansmann et al.

We do however need to be aware that most type II diabetic patients present after having Diabetes for a number of years before diagnosis, and they present in some cases with advanced neuropathy.

I think the issue around a plantarflexed 1st ray causing FnHL may be poorly described. As Kevin Kirby and others have re-iterated, the more relevant issue may be the stiffness or compliance of the joint. I would expect to see (due to tib ant and Extensor dig longus weakness/dysfunction) that FHL would 'pull' the 1st ray down . If the 1st ray had increased stiffness, then the foot should be 'forced' into late midstance/propulsive supination. However, if Robby has referenced the lack of re-supination research correctly in the diabetic foot (I havn't seen this work, I would be greatful for the reference), then this is not happening.
The FnHL may consequently be caused by early loading of the plantarflexed position of the 1st met taking the 1st ray prematurely to end range of motion.
This may then be a possible cause for plantar ligament rupture in the diabetic foot.As stiffness increases in the plantar ligaments (Glycolation) then stiffness in the 1st ray would increase. The tensile forces (From GRF) may then increases enough to rupture the tendon due to the Young's modulus changes reported in the nueropathic foot (The tendons become less elastic. The foot slapping may also cause increased speed of loading in the tendons, possibly changing there properties) When this is coupled with increased stiffness in the TA, secondary compensation through the midtarsal joint may again increase pronation related stress's in the plantar ligaments.
I personally think that this may be part of the severe progression of the Charcot foot, along with a few other as yet undiscovered biochemical issues.

I there fore think that although the research is very good, the use of a static measure of pronation is limited.

Phil

DaVinci:

Here is the excerpt from the paper on how the pronated foot was measured:

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Sincerely,

Kevin

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Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
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Voice: (916) 925-8111 Fax: (916) 925-8136
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Phil, Robby and Colleagues:

Certainly the idea of using stiffness to describe the load-deformation characteristics of the ankle joint, midtarsal joint and first ray (Kirby KA, Roukis TS: Precise naming aids dorsiflexion stiffness diagnosis. Biomechanics, 12 (7): 55-62, 2005) makes a lot of sense in understanding diabetic foot pathology. Using terminology that only describes "deformities" such as a "plantarflexed first ray" does not give enough mechanically relevant informaton to describe the etilogy and frequency of mechanical pathology (neuropathic plantar ulcers are also mechanical pathologies) seen in the diabetic foot.

Functional hallux limitus (FnHL) will tend to occur when the medial longitudinal arch flattens and the STJ axis is medially deviated. If the patient has a normal medial longitudinal arch (MLA) height and a relatively normal STJ axis location then FnHL is unlikely to occur. In addition, if FnHl is occuring, then the first metatarsal head will have decreased ground reaction force (GRF) and the plantar hallux will have increased GRF during the latter half of stance phase of walking. I can't understand how a "plantarflexed first ray" can cause FnHL unless the MLA flattens excessively during late midstance. In this specific case, the foot where the "plantarflexed first ray" that was noted during nonweightbearing examination would need to also possess decreased first ray dorsiflexion stiffness so that excessive first ray dorsiflexion and MLA flattening occured during late midstance which, in turn, would tend to cause FnHL to occur.

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Sincerely,

Kevin

**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
My location

Voice: (916) 925-8111 Fax: (916) 925-8136
**************************************************

Phil,
There are many papers that have been published citing the fact that there is a lack of resupination in the gait of the neuropathic patient (this also includes patients with hansen's disease).
One good COP study that was done was by Giacomozzi et al and published in Diabetes Care v25 n8 August 2002. Others include papers by Frykberg et al, van Schie, Aboudd.

etc.......

Kevin
Do you of any work done on the Stj axis location in the diabetic foot?
Also, theoretically, what effect could a tight TA and weak tib ant (possible planatar flexion of the calc?) have on the SJt axis?

Cheers
Phil

Hi, I am a 4th year podiatry student at the University of Malta currently conducting my dissertation research. My dissertation regards peripheral neuropathy and hallux plantar pressure in type 2 Maltese diabetic patients.

Can you please point out in more detail what sources did you consult in order to propose the line of thought presented hereunder, which is very interesting and relates a lot to my study...at present I am specifically researching about the effects of altered biomechanics on diabetic feet...do they exhibit more pronation as a result of neuropathy or it's only an exacerbation of a pre-existing condition...


Thanks a lot for your help!

Evan

"The evidence suggests that in the flexible neuropathic foot the biomechanics are altered so that at heel strike the foot pronates and due to neuropathic changes in motor supply the foot does not resuppinate, this means that the foot is loaded for prolonged periods especially on the medial forefoot. This leads to increased plantar pressures, and loading times, which when combined are major causative factors in diabetic ulceration."

Evan,

I would in initially suggest that you look at work done by Rammi Aboudd in Dundee also work by Sue Barnett, Mark Plank and Cath Van Shie. they have all published extensively on the biomechanics surrounding the diabetic foot and neuropathy.

you can contact me directly if you wish poddy123@hotmail.com

regards

robby

Thanks a lot for your help and interest!

Kind regards,

Evan