This first offering is a very short and introductory video discussing the way this information will be delivered, and some of the potential topics for future discussion.  I am of course very open to comments , and if I get enough requests for one subject then I will try to provide something if I can.

The videos will all be quite short (10-15 mins at most) and I aim to keep them quite simple, so they may be more appropriate for the undergraduate student or newly qualified Podiatrist.

More to come soon…

Following a media frenzy in 2010, the concept of running barefoot came under rather close scrutiny.  With respect to its potential long term risks/benefits the research is not yet available, so for many professionals the jury is still out and they remain healthily sceptical.  However these same professionals generally recommend road running shoes based on a model which has been used for decades.  At this point in time it seems only fair that this is re-visited and also put under the same scrutiny, with some of the available research relevant to running shoes looked at in closer detail.  This blog aims to do just this; to discuss how road running shoes are currently ‘prescribed’, and to see if there is any rationale for this current practice.

History

Road running shoes can be generally split into 3 groups – motion control shoes, stability shoes, and neutral/cushioned shoes.  Historically we have all been told that there are 3 main foot types (what a fantastic coincidence I hear you cry…) – the ‘flat’ or ‘pronated’ foot, the ‘normal’ or ‘neutral’ foot, and the ‘high arched’ or ‘supinated’ foot.

1. Flat/Pronated foot = Motion Control shoe 2. Normal/Neutral foot = Stability shoe 3. High/Supinated foot = Neutral/Cushioned shoe

It is not entirely clear where this model of shoe selection came from.  It’s conception may have been based upon the work of Colonel Harris and Major Beath, who performed an Army foot survey back in 1947, and whilst doing so invented an ingenious new method of assessing footprints.¹ It was in 1980 that ‘The Running Shoe book’ showed the first picture (as far as I’m aware) of the three arch types and how these may relate to running shoe selection.² Despite the lack of certainty regarding its origins, pretty much every edition of Runners World magazine printed since has regurgitated this information, as have most running shoe shop assistants, not to mention numerous websites (including those of many major shoe companies and sports injury professionals).  For several decades runners have therefore been advised to check their footprints (often easily assessed by observing the mark a wet foot leaves behind) and pick the corresponding shoe.  They are told this ensures ideal alignment and minimises injury risk.  Simples.  Or is it?

Before we continue take a look at the following foot (a freeze frame during running):

Have a think about what running shoe you would recommend for this individual based on the visual information you have.

To identify whether the well known model of shoe selection is appropriate we need to break it down and analyse the preconceptions it is based upon.  These are:

(A)   Pronation is consistently predictive of injury.

(B)   All individuals should be aligned identically (i.e. ‘normal’ or ‘neutral’).

(C)   The wet foot test (i.e. foot shape) is predictive of dynamic function.

(D)   Running shoe technology will actually achieve what it claims to.

If these points are not true, or not backed up by research, then the entire model falls apart.  So, let’s take a look at these preconceptions one at a time.

(A) Pronation is consistently predictive of injury.

Running stores and magazines seem to be fixated on pronation.  Most shoes are marketed with respect to how much ‘pronation control’ they offer.  Why is this?  Well, it has generally been thought that a more pronated foot type is a significant risk factor for injury.  However the fact is that there are very few prospective studies which have actually shown this, with numerous studies actually concluding that there is no association between foot type and injury.^3-9Two studies have even shown that a pronated foot is actually a protective factor against injury.^10,11

The point I’m trying to make is that the relationship between foot mechanics and lower limb injury is still not as well understood as we think (or as we would like).  But what we do know is that functioning in a pronated position does not mean that you will necessarily get injured.  In fact the experimental evidence suggests you are much more likely to get injured from training errors¹² or from dysfunctional hip musculature.¹³

Verdict = Pronation is not consistently predictive of injury

(B) All individuals should be aligned identically (i.e. ‘normal’ or ‘neutral’).

When referring to ‘ideal’ alignment what is actually meant?  What exactly is ‘normal’ when it comes to the alignment of the lower extremity?  Answer: We don’t know.  The word ‘normal’ is probably an inappropriate word to apply to the human body.  As far as normal foot alignment or mechanics is concerned, the normal (average) foot type reported in sampled populations is actually mildly to moderately pronated.^14-17 So why then is the main aim of the current running shoe selection model to align runners to ‘neutral’ (i.e. the foot sitting perpendicular to the horizontal ground)?

When we consider that the subtalar joint (the joint where pronation and supination occurs) has variable anatomy ^18,19it seems obvious that function will not be the same for everyone, and therefore that the ‘optimum’ position to be in would differ from person to person.  Unsurprisingly, differences in foot alignment between individuals is reported to be high.²⁰

It still amazes me that in a world where human variation is so vast in almost every aspect of our being, that when it comes to running there is a suggestion that we should all be in one particular alignment or position.  The reality is that each of us most likely has own preferred alignment – a subject specific ‘normal’.

Verdict = Individuals should not all be aligned similarly. ‘Normal’ alignment is subject specific.

(C) The wet foot test (i.e. foot shape) is predictive of dynamic function.

The association between static foot measures and dynamic function has been well researched in the literature.  Several different methods of assessing foot shape, arch height and foot posture in static standing have been investigated, with the conclusions generally being that there is no association between these measures and dynamic function (what the foot does when we actually run).^21-25

The work which really puts the wet foot test out of business was completed by a team of researchers from the US army over the last year or so.  Their prospective studies assigned running shoes based on plantar foot shape prior to basic military training, and investigated if this influenced injury risk at all.  They showed that assigning running shoes based on the footprint shape had little influence on injury risk in Air Force Basic Training,²⁶ Marine Corps Basic Training,²⁷and Army Basic Combat Training.²⁸

Verdict = Foot shape is NOT predictive of dynamic function.  The wet foot test is nonsense.

(D) Running shoe technology will actually achieve what it claims to.

The technology that shoes provide can be generalised into 2 main areas.  They offer cushioning, and market this as essential for the dampening of the high impacts associated with running, and they offer increased durometer (stiffer/harder) midsoles which are aimed at controlling or reducing pronation.  These technologies have been called into question before, with some researchers suggesting that the protected environment a modern running shoe provides will diminish sensory feedback, resulting in inadequate impact moderating behaviour and actually serve to increase injury risk.^29,30

A 2010 study concluded that the prescription of shoes with elevated cushioned heels and pronation control systems tailored to an individuals foot type was not evidence based³¹ and another very recent piece of research suggested this approach was overly simplistic and potentially injurious.³² How did the latter study come to this conclusion? Well to very briefly summarise: every single runner in their study who had been classified as having a ‘highly pronated’ foot type and was subsequently put into a motion control shoe reported an injury during a 13 week half marathon training programme.  Let me repeat that – highly pronated feet that were put into motion control shoes resulted in injury.  Yet that is exactly what the current shoe selection model suggests.  So, let’s go back to the video gait analysis snapshot:

Given what you have read so far, what shoe would you recommend this person now? Has it changed from earlier?

Back to the running shoe research:  Numerous studies agree that shoes with softer midsoles (cushioned/neutral shoes) result in greater pronation values, and shorter times to reach maximum pronation i.e. they make individuals pronate more, and pronate quicker.^33-36 Does this sound bad to you? [If so go back and read the research which refutes preconception (A)].  Most of these studies also concluded that harder/stiffer midsoles (such as those found in stability and motion control shoes) significantly decrease the speed and magnitude of pronation.  Some of these shoes now also have a slight varus tilt (they are higher on the inside of the heel than they are on the outside).  Research has also shown that this decreases foot level pronation.^37,38 (Remember these studies are just investigating kinematics/alignment and not injury).

So ‘anti-pronatory’ shoes with stiffer midsoles are actually doing what they promise to.  The problem is we don’t know whether we need them to do it for us or not.  And as an aside, varus posting/tilting was shown in one study to increase tibial shock and vertical loading rates.³⁹ (Is this perhaps why all those injuries occurred in the motion control shoes in the aforementioned study?)

Finally, let’s not forget cushioning.  That must reduce the amount of force we are subjected to when running – right?  Wrong.  As shoe cushioning decreases runners modify their patterns to maintain constant external loads.⁴⁰ However, it is thought to contribute to comfort, and this seems to be the most important variable on which to select sports shoes, which we will talk about shortly.

Verdict = There is very little research investigating the relationship between running shoes and injury prevention.  Stiffer midsoles do reduce pronation speed and magnitude, but in doing so may increase vertical loading rates.  Running shoe ‘cushioning’ may be a myth.

Summary

It seems that the current model upon which running shoes are recommended/chosen is erroneous.  Its foundations are based upon preconceptions which have been shown to be false.  Due to significant within-species variation it is ridiculous to try and align people identically, (and to aim to do so in a pre-selected ‘normal’ position which is highly unlikely to be ‘normal’ for most individuals is potentially injurious).  Shoes do seem to generally achieve what they claim to.  However, our understanding of whether they actually need to achieve these variables (and who would benefit from each variable) is poor at present.

And so, the current method of being recommended a shoe still continues (and I imagine it will for some time).  Why?

1. Very few people realise it is erroneous.
2. At the moment we do not have anything to replace it with.
3. It is fantastically simple.
4. People don’t generally like change.

The future

Moving forward, a much better model would be to focus on identifying an optimum midsole stiffness (which may be variable) for an individual, combined with their optimum alignment/movement patterns for a given activity (i.e. the position in which their injury risk is minimised and their performance is maximised, irrespective of its visual alignment). However, much more research is required before we fully understand how to clinically achieve this.

The concept of intelligent shoes which modify their midsole characteristics depending on the step by step requirements and effectively ‘tune’ themselves to the wearer and the surface they are on may sound like something from Back to the Future, but it is probably only a matter of time before we start seeing this sort of advancement in our running shoe technology.  However, it doesn’t change the fact that we need a greater understanding of injury risk factors, and that these are still likely to be subject (and activity) specific.

Conclusions

So where does this leave the runner choosing a pair of shoes in 2011? There are many choices. Neutral? Stability? Motion Control? Vibram Five Fingers? Barefoot? Hopefully by now you realise that there is no simple answer.

All decisions could and should be based on one main factor in my opinion: comfort. Believe it or not comfort has been linked to injury frequency reduction⁴¹ and is thought to be the most important variable for sports shoes, and a focal point for any future sports shoe development.⁴² We all know that comfort is subjective and subject specific⁴³ so with that in mind only the wearer can confidently choose the most appropriate shoe for themselves.  [Be wary of the shop assistant/Podiatrist who tells you the exact make and model shoe which is best for you]. What one person finds comfortable will differ greatly from another; perhaps this is why some people find that stiff supportive shoes work best for them, and others discovered that barefoot running was the answer to their long history of injury woes.

As most runners know, it can often be a little bit of trial and error with regard to finding the ‘right’ shoe.  Once you’ve found what works for you (or if you have found it already) then don’t change it.

Irrespective of the advice given in the shoe shop/magazines about your ‘pronation’; on current evidence you may be just as well off picking a shoe based on comfort alone, and subscribing to a course of Pilates and adopting sensible training habits.

P.S. How are you getting on with your decision on what shoes to recommend for this chap?

References

1. Harris RI, & Beath T: (1947). Referenced from a secondary source: The Journal of Bone & Joint Surgery (1950), Vol 32B, No 1, p143-144.
2. Cavanagh PR: The Running Shoe Book, Anderson World, Inc., Mountain View, California, 1980.
3. Barrett JR, Tanji JL, Drake C, et al: High versus low-top shoes for the prevention of ankle sprains in basketball players. A prospective randomized study. The American Journal of Sports Medicine 21: 582, 1993.
4. Twellaar M, Verstappen FT, Huson A, et al: Physical characteristics as risk factors for sports injuries: a four year prospective study. International Journal of Sports Medicine 18: 66, 1997.
5. Wen DY, Puffer JC, Schmalzried TP, et al: Injuries in runners: a prospective study of alignment. Clinical Journal of Sport Medicine 8: 187, 1998.
6. Beynnon BD, Renstrom PA, Alosa DM, et al: Ankle ligament injury risk factors: a prospective study of college athletes. Journal of Orthopaedic Research 19: 213, 2001.
7. Hetsroni I, Finestone A, Milgrom C, et al: A prospective biomechanical study of the association between foot pronation and the incidence of anterior knee pain among military recruits. Journal of Bone and Joint Surgery Br88: 905, 2006.
8. Reinking MF, Austin TM, Hayes AM: Risk factors for self-reported exercise-related leg pain in high school cross-country athletes. Journal of Athletic Training 45: 51, 2010.
9. Franettovich M, Chapman AR, Blanch P, et al: Altered neuromuscular control in individuals with exercise-related leg pain. Medicine and Science in Sport and Exercise 42: 546, 2010.
10. Giladi M, Milgrom C, Stein M, et al: The low arch, a protective factor in stress fractures. Orthopaedic Review 14: 81, 1985.
11. Cowan D, Jones B, Robinson J: Foot morphologic characteristics and risk of exercise related injury. Archives of Family Medicine 2: 773, 1993
12. James SL, Bates BT, Osternig LR: Injuries to runners. American Journal of Sports Medicine 6: 40, 1978.
13. Ferber R, Hreljac A, Kendall KD: Suspected mechanisms in the cause of overuse running injuries: a clinical review. Sports Health: A Multidisciplinary Approach 1: 242, 2009.
14. Sobel E, Levitz SJ, Caselli MA, et al: Re-evaluation of the relaxed calcaneal stance position. Journal of the American Podiatric Medical Association 89: 258, 1999.
15. Scharfbillig R, Evans A, Copper A, et al: Criterion validation of four criteria of the foot posture index. Journal of the American Podiatric Medical Association 94: 31, 2004.
16. Redmond A, Crosbie J, Ouvrier R: Development and validation of a novel rating system for scoring standing foot posture: the foot posture index. Clinical Biomechanics 21: 89, 2006.
17. Redmond AC, Crane YZ, Menz HB: Normative values for the foot posture index. Journal of Foot and Ankle Research 1: 6, 2008.
18. Bruckner J: Variations in the human subtalar joint. Journal of Orthopaedic and Sports Physical Therapy 8: 481, 1987.
19. Forriol Campos F, Gomez Pellico L: Talar articular facets. Acta Anatomica 134: 124, 1989.
20. Nester CJ: Lessons from dynamic cadaver and invasive bone pin studies: do we know how the foot really moves during gait? Journal of Foot and Ankle Research 2: 18, 2009.
21. Razeghi M, Batt ME: Foot type classification: a critical review of current methods. Gait and Posture 15: 282, 2002.
22. Hamill J, Bates BT, Knutzen KM, et al: Relationship between selected static and dynamic lower extremity measures. Clinical Biomechanics 4: 217, 1989.
23. McPoil TG, Cornwall MW: The relationship between static lower extremity measures and rearfoot motion in gait. The Journal of Orthopaedic and Sports Physical Therapy 24: 309, 1996.
24. Cashmere T, Smith R, Hunt A: Medial longitudinal arch of the foot: Stationary versus walking measures. Foot and Ankle International 20: 112, 1999.
25. Trimble MH, Bishop MD, Buckley BD, et al: The relationship between clinical measurements of lower extremity posture and tibial translation. Clinical Biomechanics 17: 286, 2002.
26. Knapik JJ, Brosch LC, Venuto M, et al: Effect on injuries of assigning shoes based on foot shape in air force basic training. American Journal of Preventative Medicine 38: S197, 2010.
27. Knapik JJ, Trone DW, Swedler DI, et al: Injury reduction effectiveness of assigning running shoes based on plantar shape in marine corps basic training. American Journal of Sports Medicine 38: 1759, 2010.
28. Knapik JJ, Swedler DI, Grier TL, et al: Injury reduction effectiveness of selecting running shoes based on plantar shape. Journal of Strength and Conditioning Research 23: 685, 2009.
29. Robbins SE, Hanna AM: Running-related injury prevention through barefoot adaptations. Medicine and Science in Sports and Exercise 19: 148, 1987.
30. Robbins SE, Gouw GJ: Athletic footwear: Unsafe due to perceptual illusions. Medicine and Science in Sports and Exercise 23: 217, 1991.
31. Richards CE, Magin PJ, Callister R: Is your prescription of distance running shoes evidence-based? British Journal of Sports Medicine 43: 159, 2010.
32. Ryan MB, Valiant GA, McDonald K, et al: The effect of three different levels of footwear stability on pain outcomes in women runners: a randomised control trial. British Journal of Sports Medicine (2010). doi: 10.1136/bjsm.2009.069849.
33. Clarke TE, Frederick EC, Hamill CL: The effects of shoe design parameters on rearfoot control in running. Medicine and Science in Sports and Exercise 15: 376, 1983.
34. Hamill J, Bates BT, Cole KG: Timing of lower extremity joint actions during treadmill running. Medicine and Science in Sports and Exercise 24: 807, 1992.
35. Wit BD, Lenoir M: The effect of varying midsole hardness on impact forces and foot motion during foot contact in running. Journal of Applied Biomechanics 11: 395, 1995.
36. Kersting UG, Bruggermann GP: Midsole material-related force control during heel-toe running. Research in Sports Medicine 14: 1, 2006.
37. Van Woensel W, Cavanagh PR: A perturbation study of lower extremity motion during running. International Journal of Sports Medicine 34: 1844, 1992.
38. O’Connor K, Hamill J: The role of selected extrinsic foot muscles during running. Clinical Biomechanics 19: 71, 2004.
39. Perry SD, Lafortune MA: Influences of inversion/eversion of the foot upon impact loading during locomotion. Clinical Biomechanics 10: 253, 1995.
40. Kong PW, Candelaria NG, Smith DR: Running in new and worn shoes: a comparison of three types of cushioning footwear. British Journal of Sports Medicine 43: 745, 2009.
41. Mundermann A, Stefanyshyn DJ, Nigg BM: Relationship between footwear comfort of shoe inserts and anthropometric and sensory factors. Medicine and Science in Sports and Exercise 33: 1939, 2001.
42. Nigg BM: Biomechanics of Sports Shoes, Topline Printing Inc, Calagary, Alberta, Canada, 2010.
43. Miller JE, Nigg BM, Liu W, et al: Influence of foot, leg and shoe characteristics n subjective comfort. Foot and Ankle international 21: 759, 2000.

Historically, it has been commonly accepted that heel spur formation is an abnormal finding and very closely correlated with the symptoms of heel pain.  It was reported that excessive traction (pulling) of the plantar fascia on its attachment at the heel resulted in chronic inflammation, which in turn resulted in a reactive ossification and subsequent extra bone forming in the shape of a ‘spur’. ^1-3 This is perhaps why heel spurs and ‘plantar fasciitis’ are still to this day thought by many to be one entity.  Causation has been a point of confusion; does the traction and inflammation cause a heel spur, or does a heel spur cause tissue inflammation?  A chicken and egg scenario.  It is not uncommon to see statements that ‘plantar fasciitis’ is caused by heel spurs (admittedly this is on websites rather than academic journals), but is this factually correct?

The plantar calcaneal spur has been classically described as a bone outgrowth localised just anterior to the medial tuberosity of the calcaneus.⁴ This can not often be palpated clinically, but only seen radiologically as shown in the x-ray on the right above.

Another long term belief has been that individuals with heel pain are more likely to have pronated (flat) feet.^5,6 As research has shown that lowering of the medial longitudinal arch of the foot increases plantar fascial tension⁷ it is easy to see how the connection between foot pronation, heel pain and heel spurs has been made.  However the concern is that any individual who presents to a specialist with heel pain and ‘flat feet’ could be hastily assigned a diagnosis of “plantar fasciitis caused by a heel spur”.  This is clearly unacceptable, and a specialist should have a much more thorough understanding of the research behind the pathological process.  So, how common are heel spurs?  Are they always problematic? Are they actually caused by traction? And what is their relationship with the plantar fascia?

How common are heel spurs?

Studies have shown that heel spurs are more common in pain free individuals than first thought, and it has been reported that anywhere between 11 and 27% of the population have radiographic evidence of a spur.^5,8-13 Clearly this suggests they are not always associated with symptoms, and are not necessarily considered as ‘abnormal’ as once thought.  Interestingly, even a study performed over 45 years ago on 323 patients concluded that the plantar calcaneal spur was never the cause of pain and probably a normal manifestation of the aging process.¹⁴

However, the research does suggest that calcaneal spurs do seem to be over-represented in certain groups, such as females,^10,11,13 individuals with osteoarthritis^15,16 and older people.^11,13,15,16 Calcaneal spurs have also found to be more common in those who are overweight.¹⁷

Where are heel spurs?

MRI of heel spur (arrow). PF=plantar fascia. M=1st layer of foot muscles

As I have already mentioned, it has long been thought that heel spurs and plantar fascia problems were undeniably linked.  Google ‘heel spurs’ and the term ‘plantar fasciitis’ is never far behind.  However, it is interesting to hear how the anatomic studies report the actual location of the bony protrusion.  Far from agreeing it resides solely within the plantar fascia as once thought, many studies found it can also be found above the plantar fascia.^4,12,18 Some found it was much more commonly located in the other intrinsic musculature, (namely Flexor Digitorum Brevis and Abductor Digiti Minimi)^4,18,19 and one study was as bold to firmly conclude that spurs do not develop within the plantar fascia.²⁰

What is clear is that there is huge variability in the location of heel spur formation, and if we cannot unequivocally state that the spur is within the fascia (which we cannot) then the validity of its link with ‘plantar fasciitis’ is questionable.

What causes heel spurs?

As previously mentioned, the traditional theory for formation of plantar calcaneal spurs is what Menz and colleagues¹⁶ refer to as the longitudinal traction hypothesis, i.e. the plantar fascia pulling on the heel bone and causing the formation of a spur.  Despite the anatomical studies showed that the spur is far from consistently found in the fascia, it has been suggested that there could be an element of tensile force exerted on the calcaneus from a variety of the other structures which attach to it.^4,19

An alternative theory, termed the vertical compression hypothesis¹⁶ and was proposed by Kumai and Benjamin in 2002.²⁰ This theory suggests that calcaneal spurs are outgrowths which form in response to repetitive vertical stress in an attempt to protect against microfractures.  This idea is supported by histological studies which show that the bony trabeculae are NOT aligned in the direction of soft tissue traction.^16,18 Li and Muehleman¹⁸ found that the direction of the trabeculae suggested that the force causing the pathological response was consistent with the external ground reaction force vector.

Conclusions

So what does all this mean in plain English?  It means that we used to think a spur was caused by the plantar fascia pulling on the bone.  This is highly unlikely as the spur is seldom found in the plantar fascia.  If traction is the cause it is more likely to be caused by other musculature such as Flexor Digitorum Brevis or Abductor Digiti Minimi.  However these bony protrusions could instead be caused by the repetitive vertical loading (the heel continuously hitting the floor, and the floor of course hitting it back) with the spur forming as a protective mechanism.  Of course we cannot overlook the fact that there may be a combination of both traction and compression present in the aetiology of spur development.  We also know that anywhere up to a quarter of the population may have a heel spur, but this will not always be problematic.

So, in summary:

The pathophysiology of plantar calcaneal heel spurs is poorly understood.

The presence of a plantar calcaneal spur does not always lead to the development of heel pain.

Plantar calcaneal spurs do appear to be associated with obesity, osteoarthritis and the aging process.

It is unclear whether spur formation is due to longitudinal traction of the plantar tissues or an adaptive response to vertical loading/compression (or both).

It is erroneous to assume there is a causal relationship between plantar calcaneal spurs and ‘plantar fasciitis’.

References

1. DuVries, H.L. (1957). Heel spur (calcaneal spur). Archives of Surgery, 74: 536-542.
2. Furey, J.G. (1975). Plantar fasciitis: the painful heel syndrome. Journal of Bone and Joint Surgery Am, 57: 672-673.
3. Bergmann, J.N. (1990). History and mechanical control of heel spur pain. Clinics in Podiatric Medicine and Surgery, 7: 243-259.
4. Abreu, M.R., Chung, C.B., Mendes, L. et al. (2003). Plantar calcaneal enthesophytes: new observations regarding sites of origin based on radiographic, MR imaging, anatomic, and paleopathologic analysis. Skeletal Radiology, 32: 13-21.
5. Prichasuk, S., Subhadrabandhu, T. (1994). The relationship of pes planus and calcaneal spur to plantar heel pain. Clinical Orthopaedics and Related Research, 306: 192-196.
6. Irving, D.B., Cook, J.L., Young, M.A. et el. (2007). Obesity and pronated foot type may increase the risk of chronic plantar heel pain: a matched case-control study. BMC Musculoskeletal Disorders, 8: 41.
7. Kogler, G.F., Solomonidis, S.E., Paul, J.P. (1996). Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clinical Biomechanics, 11: 243-252.
8. Rubin, G., Witten, M. (1963). Plantar calcaneal spurs. American Journal of Orthopaedics, 5: 38-41.
9. McCarthy, D.J., Gorecki, G.E. (1979). Anatomical basis of inferior calcaneal lesions: a cryomicrotomy study. Journal of the American Podiatric Medical Association, 69: 527-536.
10. Shama, S.S., Kominsky, S.J., Lemont, H. (1983). Prevalence of non-painful heel spur and its relation to postural foot position. Journal of the American Podiatric Medical Association, 73: 122-123.
11. Banadda, B.M., Gona, O., Vas, R., et al. (1992). Calcaneal spurs in a black African population. Foot & Ankle, 13: 352-354.
12. Barrett, S.L., Day, S.V., Pignetti, T.T. et al. (1995). Endoscopic heel anatomy: analysis of 200 fresh frozen specimens. Journal of Foot & Ankle Surgery, 34: 51-56.
13. Riepert, T., Drechsler, T., Schild, H. et al. (1996). Estimation of sex on the basis of radiographs of the calcaneus. Forensic Science International, 77: 133-140.
14. Lapidus, P.W., Guidotti, F.P. (1965). Painful heel: report of 323 patients with 364 painful heels. Clinical Orthopaedics and related Research, 39: 178-186.
15. Gerster, J.C., Vischer, T.L., Bennani, A. et al. (1977). The painful heel. Comparative study in rheumatoid arthritis, ankylosing spondylitis, Reiter’s syndrome, and generalised osteoarthritis. Annals of the Rheumatic Diseases, 36: 343-348.
16. Menz, H.B., Zammit, G.V., Landorf, K.B. et al. (2008). Plantar calcaneal spurs in older people: longitudinal traction or vertical compression? Journal of Foot & Ankle Research, 1:7.
17. Sadat-Ali, M. (1998). Plantar fasciitis/calcaneal spur among security forces personnel. Military Medicine, 163: 56-57.
18. Li, J., Muehleman, C. (2007). Anatomic Relationship of Heel Spur to Surrounding Soft Tissues: Greater variability than previously reported. Clinical Anatomy, 20: 950-955.
19. Smith, S., Tinley, P., Gilheany, M. et al. (2007). The inferior calcaneal spur – Anatomical and histological considerations. The Foot, 17: 25-31.
20. Kumai, T., Benjamin, M. (2002). Heel spur formation and the subcalcaneal enthesis of the plantar fascia. The Journal of Rheumatology, 29: 1957-1964.

The existence of a transverse arch at the metatarsal region would require the pressure to be greatest at the areas beneath the 1^st and 5^th metatarsal heads, and the area of the 2^nd, 3^rd and 4^th metatarsal heads to be elevated relative to this.  This gives us the ‘tripod’ like weight distribution of the foot which was first described by Kapandji in 1970.² However, the first descriptions of the transverse metatarsal arch date back as far as 100 years prior to Kapandji’s work³ and several papers published in Germany between 1882 and 1927 actually concluded that no transverse arch of the foot was usually present.^4-7 Much of the research produced following Kapandji’s work concurs with these conclusions regarding the transverse metatarsal arch being a misnomer.

So if the presence of a transverse metatarsal arch has long been questioned, why have so many authors, and indeed medical professionals, subscribed to this theory for so long (and continue to do so) in spite of growing evidence against it?

The conception of the foot bearing its weight on three points must be quite attractive in order to persist (Jones, 1941)⁸

When a patient presents with diffuse pain across the forefoot, what should be performed is thorough examination of the region, identification of the anatomical structure which is involved, and then a management plan directed towards reducing the symptoms with the most appropriate treatment available.  However, all too often a clinician will diagnose ‘metatarsalgia’ (NOT a diagnosis, but we’ll save that for another blog) caused by ‘dropped metatarsals’ or ‘a fallen metatarsal arch’.  It’s very quick and very easy, and you can see how it doesn’t require too much thinking.  For these clinicians to accept that a transverse metatarsal arch does not exist would require them to change their entire clinical practice, and for many this sort of paradigm shift in thinking is too uncomfortable to accept, so instead they continue as they are.

So, 100 year old journal articles written in German aside, lets look at some of the more current research which has looked at the mythical transverse metatarsal arch.

In 1997, Daentzer et al.⁹ performed a study on 100 feet.  The age range of the participants in the study was between 10-72 years old.  None of the participants had any foot deformity or symptoms.  Ultrasonography was performed at the level of the metatarsal heads in both non weight bearing and weightbearing.  Barefoot plantar pressure measurements were recorded using a force plate.  Their findings/conclusions: Pressures are usually highest underneath the 2^nd, 3^rd and 4^th metatarsal heads, there is no transverse metatarsal arch, and the forefoot is normally flat at the level of the metatarsal heads.

In 1999, Luger et al.¹⁰ performed a study on 720 feet (the largest study to my knowledge).  The age range of the participants in the study was 18-83 years old.  Interestingly they included individuals with a variety of foot symptoms and abnormalities as well as pain free individuals.  The all had static and dynamic barefoot pressure measurements taken.  Their findings/conclusions: Only 22 feet out of 720 (3%) had a dynamic metatarsal arch whilst walking, and this was only found in the feet classified as having deformity or pain.  Not only was a transverse metatarsal arch rarely seen, but they concluded that it actually indicated a possible pathological deformity (i.e it is an abnormality which may cause problems)

In 2003, Kanatli et al.¹¹ performed a study on 32 feet.  The age range of the participants in the study was 20-30 years old.  All participants were pain free and had no foot deformities.  Barefoot plantar pressure measurements were taken whilst walking.  Their findings/conclusions: Significantly higher pressures were recorded beneath the 2nd and 3^rd metatarsal heads, and the transverse metatarsal arch did not exist in normal subjects.

As you can see one of the common findings seen in the research discussed has been that higher pressures are not seen beneath the 1^st and 5^th metatarsal heads during gait.  Other authors have investigated this employing pressure measurement equipment and found that the pressures in the middle metatarsals are consistently greater than the 1^st and 5^th metatarsals.^12,13 All of the research suggests that the tripod configuration of the foot is completely erroneous, and without this, it is obvious that it is not possible for there to be a transverse metatarsal arch.  Clinicians who continue to talk about the transverse arch, and offer treatments for its ‘collapse’ are either uninformed, bogged down in old habits or in denial.

References

1. Williams, P.L. et al. (1995) Gray’s Anatomy. 38^th Edition, Churchill Livingstone, New York.
2. Kapandji, L.A. (1970) The Physiology of the Joints. E & S Livingstone, Edinburgh.
3. Henle, J. (1871) Handbuch der Knochenlehre des Menschen. Vieweg, Braunschweig.
4. Beely, F. (1882) Zur Mechanik des Stehens. Uber die Bedeutung des Fussgewolbes im Stehen. Arch klin Chir, 27: 457-471.
5. Momburg, F.A. (1909) Die Stutzpunkte des Fusses beim Gehen und Stehen. Dtsch med Wschr, 4: 148-152.
6. Frostell, G. (1925) Beitrag zur Kenntnis der vorderen Stutzpunkte des Fusses, sowie des Fusswinkels beim Stehen und Gehen. Z  Orthop Chir, 47: 3-54.
7. Abramson, E. (1927) Zur Kenntnis der Mechanik des Mittelfusses. Skand Arch Physiol, 51: 175-234.
8. Jones, R.L. (1941) The Human Foot. An experimental study of its mechanics, and the role of its muscles and ligaments in support of the arch. American Journal of Anatomy, 68: 1-39.
9. Daentzer, D., Wulker, N., & Zimmermann, U. (1997) Observations concerning the transverse metatarsal arch. Foot and Ankle Surgery, 3: 15-20.
10. Luger, E.J., Nissan, M., Karpf, A., Steinberg, E.L., & Dekel, S. (1999) Patterns of weight distribution under the metatarsal heads. The Journal of Bone & Joint Surgery (Br), 81: 199-202.
11. Kanatli, U., Yetkin, H., & Bolukbasi, S. (2003) Evaluation of the transverse metatarsal arch of the foot with gait analysis. Arch Orthop Trauma Surg, 123: 148-150.
12. Cavanagh, P.R., Rodgers, M.M., & Iiboshi, A. (1987) Pressure distribution under symptom-free feet during barefoot standing. Foot and Ankle, 7: 262-276.
13. Hennig, E.M., & Milani, T.L. (1993) Die Dreipunktuntersttzung des Fusses. Eine Druckverteilungsanalyse bei statischer und dynamischer Belastung. Z Orthop, 131: 279-284.

Understandably the FA have been getting a bit of a hard time in the press regarding the playing surface (and not just from disgruntled Spurs fans).  It is well documented that the schedule at Wembley is very heavy, and includes many other events such as rugby, motor racing and music concerts, and the pitch seems to have been in trouble since day one – having been re-laid 10 times already since July 2006.  The FA released this statement today:

A Wembley Stadium spokesperson said: “We accept and understand the frustrations around the standard of the pitch at Wembley for last weekend’s FA Cup Semi-Finals.

“The problems faced on Saturday were due to the way the surface was prepared and the measures used overnight were unable to resolve the situation sufficiently for the match on Sunday.

“There is a unique challenge with the surface at Wembley and we are working with expert pitch consultants to get it right. Wembley Stadium is a multi-purpose venue and we have to hold other events as part of the business plan, which means regular pitch replacements each year.

“Football is the number one priority and we understand we have to find a way to deliver and sustain a consistent quality pitch and replicate the successful formula that we developed in the second half of last year.

“We are currently reviewing all options to provide the best surface for the busy period going forward, including a probable pitch replacement. We will make this decision after the weekend.”

However in the two weeks running up to the England Vs Mexico friendly on May 24^th the Wembley surface is still to be used a further 5 times:

1. FA Trophy Final on May 8^th
2. FA Vase Final on May 9^th
3. FA Cup Final on May 15^th
4. Football Conference Final on May 16^th
5. Championship play-off Final on May 22^nd

I for one will be watching our last international friendly before the squad leaves for South Africa very nervously, as I feel the pitch in its current condition is nothing less than a major risk to the safety of our players.

Playing surfaces and the relationship with shoes (and injury)

Football is characterised by sprinting, stopping, cutting and pivoting – situations where shoe-surface interactions are essential and frictional resistance must be within an optimal range.¹ Not to mention of course that when playing football you are also required to spend a lot of time on only one leg, so a stable base of support is crucial.  Research has suggested that the footing or ‘grip’ a playing surface provides (its traction) may relate to injury in football.^1,2

The BBC commented that one word used to describe the pitch at Wembley by Premier League managers was ‘spongy’.  The most common compensation for a very soft and slippery pitch that players will make is to wear boots with longer cleats/studs as this will increase traction and therefore decrease slippage.³ This was illustrated clearly in the first half of the Aston Villa and Chelsea game on Saturday with many players running to the side lines to change their boots.  My main concern here being that longer studs have been shown by many studies to increase in shoe-surface traction (torque) possibly outside of the optimal range, and with it increase the risk of knee injuries.^4,5

The majority of the literature on surface traction suggests that increased shoe-surface traction may be a risk factor for non contact lower limb injury in football.⁶ A pitch such as Wembley encourages players to take measures to increase this shoe-surface traction as we have discussed above; as performance considerations (i.e. not falling over) will trump this relative increase in injury risk (in their minds anyway).

The sort of injuries most of the aforementioned studies refer to are the non contact kind where the shoe-surface relationship is the primary cause, the key injury generally considered to be knee injury.  However as those with a knowledge of the game know, different playing surfaces do tend to result in the timing of tackles or challenges varying greatly which can often lead to knocks being picked up which ordinarily may not have been.

My closing comment on this is simple.  I think the FA would find itself in a very uncomfortable situation if one of our key players was to get injured (due to the playing surface) just a few weeks before the start of the World Cup Finals.  To see Rooney, Gerrard or Terry damage their anterior cruciate ligament just because it’s part of the FA’s business plan to keep Wembley as a multi-purpose venue would be very difficult to swallow.

References

1. Nigg, B. M. & Ekstrand, J. (1989). Surface-related injuries in soccer. Sports Medicine. 8(1), 56-62.
2. Milburn, P. D. & Barry, E. B. (1998). Shoe-surface interaction and the reduction of injury in rugby union. Sports Medicine. 25(5), 319-327.
3. Yu, B., Kirkendall, D. & Garrett, W. (2002). Anterior cruciate ligament injuries in female athletes: anatomy, physiology and motor control. Sports Medicine & Arthroscopy Review. 10, 58-68.
4. Lambson, R., Barnhill, B. & Higgins, R. Football cleat design and its effect on anterior cruciate ligament injuries: a three-year prospective study. American Journal of Sports Medicine. 24(2), 155-159.
5. Torg, J. S. & Quedenfeld, T. (1971). Effect of shoe type and cleat length on incidence and severity of knee injuries among high school football players. Research Quarterly. 42(2), 203-211.
6. Orchard, J. (2002). Is there a relationship between ground and climatic conditions and injuries in football? Sports Medicine. 32(7), 419-432.

The golf swing is a highly co-ordinated and individual motion with significant subject to subject variation.² This blog certainly does not intend to be an all encompassing discussion on swing biomechanics.  Instead we will look at a brief summary of the injury statistics, and then some of the lower limb considerations.  A right handed golfer is used for all descriptive purposes.

Golfing Injury

The most common locations for injury are generally reported as being the lower back, and the upper limb (shoulder, elbow and wrist).^3,4 Pietrocarlo reported that foot issues can include blistering, Mortons Neuroma, ankle ligament damage and Achilles tendon problems.⁵ Due to golf being a non-contact sport at least 80% of injuries reported are overuse injuries⁶ and direct impact trauma is fortunately quite rare.  A study in 2003 by Gosheger and colleagues⁶ found that there was an increase in injury risk for individuals who played 4 rounds or more or hit 200 range balls or more per week.  This is likely to be the reason that the incidence of injury is much higher in professional golfers than in amateurs.  They also discovered that carrying a golf bag increased the chances of back, shoulder and ankle problems.

And then of course there are what we tend to refer to as ‘aches and pains’.  Not specific injuries as such, but musculoskeletal niggles which come on at some point (usually on the back 9).  The sore feet I experienced by hole 14 during a recent round of golf I played over Easter got me thinking about how much walking was actually involved.  The course was just over 6000 yards in total (about 3.5 miles) and my score of 111 suggests I walked a bit further than that.  On average a round of golf takes 3-4 hours and is realistically likely to involve up to 5 miles of walking.

Lower Limb Considerations

The golf swing is considered one of the most difficult biomechanical sporting motions to execute² and is ideally made up of a good stance, posture and grip.  A portion of the swing power is derived from the lower body⁷ and greater club head velocity (the speed of the club face at time of impact with the ball and the consequent distance the ball will then travel) can be achieved with optimum weight transfer from the back (right) to the front (left) foot during the downswing.⁸ Therefore it is easy to see that the shoe/ground interface is a vital link that allows a golfer to perform the specialised movements during their swing.⁹ For those who are not familiar with the golf swing it can be seen below

During the back swing (phase 2) weight shifts to the back foot, and then during the down/forward swing (phase 3) and onwards the weight transfers to the front foot.^10,11 In order to maximise the club head velocity at impact (phase 4) considerable ground reaction force must be produced.⁹ Ground reaction force is essentially how hard the ground pushes up on the foot, which in accordance with Newtons 3^rd Law is exactly the same amount of force as the foot pushes down into the ground with. It is well documented that low handicap/professional golfers have significantly higher ground reaction forces and a faster weight transfer to the front foot than high handicap/amateur golfers.^12,13

Due to the centrifugal force of the club, the magnitude of these forces is often greater than the golfers body weight.¹⁰ Cooper¹¹ found that it was 150% of body weight with a driver, and 133% body weight with a 3-iron.  Williams & Cavanagh⁹ report maximum vertical ground reaction forces of 1.6 times body weight when using a driver.  Believe it or not the magnitudes of ground reaction force during a golf swing have been said to be comparable to running at a velocity of 4m/sec.^8,14

Finally, we also need to consider torque.  This is the tendency of a force to rotate an object – if force is a push or a pull then image torque like a twist.  Maximal torque is doubled at the front foot (left) when compared to the back (right) foot.¹⁵ Generally there does not appear to be a difference in this torque between clubs, although low handicap golfers do seem to generate increased torque when using the driver.

This should give some indication of the sort of forces at foot level for each golf swing (remember this is on top of that 5 mile walk we mentioned).  What should be clear by now is the very different function of the left (front) and right (back) feet during the golf swing.  This was highlighted by Williams and Cavanagh⁹ who discussed the implications this could have on golf shoe design.

Golf and Foot Orthoses

There is not an incredible amount of literature regarding the use of orthoses but what there is seems favourable.  Prefabricated (off the shelf) orthoses have been shown to improve the posture of the back (right) foot, and also improve lower limb pain levels.¹⁶ However it should be noted that the placebo in this randomised control trial did just as well as the orthoses in improving comfort.  Considering the asymmetrical function of the feet which we have just discussed it intuitively seems that orthoses which are symmetrical (such as prefabricated devices) may not be the most beneficial for a golfer.

A study by Stude and Gullickson in 2000 investigated custom made orthoses.¹⁷ These had the advantage of the device for the left foot and the right foot being designed independently of each other and bespoke to each golfer.   Following 6 weeks of wearing custom made orthoses it was found that club head velocity increased by 7%.  In real terms this was equivalent to the golf ball travelling a further 15 yards per shot.  It was also found that the orthoses reduced the effects of fatigue associated with 9 holes of golf; and therefore may also improve consistency of performance.

Summary

(1) Low handicap and professional golfers tend to suffer with more overuse musculoskeletal injuries than high handicap/amateur golfers despite their superior swing technique.  (This is likely due to the increased volume of golf they play and possibly the greater ground reaction forces and torques generated).

(2) Injury risk can be reduced by playing less than 4 rounds a week, and always using a trolley or cart rather than carrying your bag.

(3) Foot orthoses can reduce lower limb fatigue whilst playing, and in some instances may improve club head velocity and therefore increase the distance the ball is hit.

(4) The demands on the left and right feet when performing a golf swing are very different, and this has implications for custom made orthoses prescription.

References

1. Theriault, G. & Lachance, P. (2005). Golf injuries: an overview. Sports Medicine, 26(1), 43-57.
2. Nesbit, S.M. (2005). A three dimensional kinematic and kinetic study of the golf swing. Journal of Sports Science & Medicine, 4, 499-519.
3. McHardy, A., Pollard, H., & Luo, K. (2006). Golf Injuries: A review of the literature. Sports Medicine, 36(2), 171-187.
4. Batt, M.E. (1992). A survey of golf injuries in amateur golfers. British Journal of Sports Medicine, 26(1), 63-65.
5. Pietrocarlo, T.A. (1996). Foot & Ankle Considerations in Golf. Clinics in Sports Medicine, 15(1), 129-146.
6. Gosheger, G., Liem, D., Ludwig, K., Greshake, O. et al. (2003). Injuries and Overuse syndromes in Golf. American Journal of Sports Medicine, 31(3), 438-443.
7. Gatt, C.J., Pavol, M.J., Parker, R.D. et al. (1998). Three dimensional knee joint kinematics during a golf swing: Influences of skill level and footwear. American Journal of Sports Medicine, 26(2), 285-294.
8. Hume, P.A., Keogh, J., & Reid, D. (2005). The Role of Biomechanics in maximising distance and accuracy of golf shots. Sports Medicine, 35(5), 429-449.
9. Williams, K.R. & Cavanagh, P.R. (1983). The mechanics of foot action during the golf swing and implications for shoe design. Medicine & Science in Sports & Exercise, 15(3), 247-255.
10. Carlsoo, S. (1967). A kinetic analysis of the golf swing. Journal of Sports Medicine & Physical Fitness, 7, 80-81.
11. Cooper, J.M., Bates, B.T., Bedi, J., & Scheuchenzuber, J. (1974). Kinematic and kinetic analysis of the golf swing. In: Biomechanics IV; Proceedings of the 4^th International Seminar. Baltimore: Unoversity Park Press.
12. Wallace, E.S., Graham, D. & Bleakley, E.W. (1990). Foot to ground pressure patterns during golf drive: A case study involving a low handicap player and a high handicap player. Science & Golf I; Proceedings of the 1^st World Scientific Congress of Golf. London: E+FN Spon, 25-29.
13. Koenig, G., Tamres, M., & Mann, R.W. (1994). The biomechanics of the shoe-ground interaction in golf. Science & Golf II; Proceedings of the 1^st World Scientific Congress of Golf. London: E+FN Spon, 40-45.
14. Nachbauer, W. & Nigg, B.M. (1992). Effects of arch height of the foot on ground reaction force in running. Medicine & Science in Sports & Exercise, 24(11), 1264-1269.
15. Worsfold, P., Smith, N.A., & Dyson, R.J. (2008). Low handicap golfers generate more torque at the shoe-natural grass interface when using a driver. Journal of Sports Science & Medicine, 7, 408-414.
16. McRitchie, M. & Curran, M.J. (2007). A Randomised Controlled Trial for evaluating over-the-counter orthoses in alleviating pain in amateur golfers. The Foot, 17, 57-64.
17. Stude, D.E. & Gullickson, J. (2000). Effects of orthotic intervention and nine holes of simulated golf on club head velocity in experienced golfers. Journal of Manipulative and Physiological Therapeutics, 23(3), 168-174.

Personally, I cried into my cornflakes on the morning of Monday 15^th March as I read he had a suspected (at that time) Achilles tendon rupture.  If a similar heel injury was responsible for the death of Achilles during the Trojan war perhaps it didn’t bode well for David making a record breaking trip to South Africa in under 3 months time.

So what actually happened?

Sunday 14^th March.  AC Milan are hosting Chievo in a Serie A game.  It’s the 87^th minute.  David Beckham receives the ball in the centre of the pitch with plenty of space.  He takes a touch with his left foot, opens up his body and looks up to see where his team mates are as he is stepping back on his left foot…

If you look closely as his left heel nears the floor you can almost see it ‘pop’.  Watch David’s immediate reaction – he turns to see who is there.  I guarantee if he ever speaks of this experience he will explain the way he thought someone had kicked him.  After trying to take one step on it he knew he was in trouble.  He then feels the back of his ankle, and would not have felt the prominent firm tendon which he has probably felt every single day for the last 20 years.  At this point he would immediately have realised how serious his injury was.  Some newspapers report he looked over to the bench and made a ‘breaking twig’ gesture with his hands.  Within 48 hours he has been operated on by Professor Sakari Orava in Finland and knows his World Cup dream is over.

The Achilles tendon

The Achilles tendon is one of the most commonly ruptured tendons.¹ It is well documented that it has a zone of hypovascularity, ^2,3,4 which is an area of reduced blood supply and is located approximately 2-6cm up from the heel bone.  This zone of hypovascularity is the site of around 80% of all Achilles tendon ruptures.⁵ Despite the Achilles tendon generally being referred to as the strongest tendon in the human body, there is good research which actually disproves this and found that its material properties are instead similar to most other tendons.⁶ However we do know it has to cope with far more mechanical loading than most other tendons which may explain the relatively high incidence of Achilles injury.

The Achilles tendon can cope with loads of approximately 100N/mm² and can be stretched approximately 8% of its length before rupturing.⁷ To put this into perspective, an Achilles Tendon with a cross sectional area of 90mm² (which is about normal for an adult male) could theoretically cope with a force of approximately 1 tonne.  In a 75kg man (David’s current weight according to Google) this equates to twelve times his body weight.  So considering this tensile strength, how and why do they suddenly rupture?

All human tissues are what we term viscoelastic.  This basically means they will change shape (or deform) when a force is applied to them, but then return back to normal once the force is removed – a bit like an elastic band.  If they are deformed or stressed outside of the limits of their tolerance they will fail (in our elastic band example it snaps, in our Achilles tendon example it ruptures).  I explain this in a bit more detail on my website here.  When reviewing David’s mechanism of injury it is difficult to imagine the tendon being loaded with a force it couldn’t cope with (or equivalent to twelve times his body weight).  He was simply moving in a way he has done hundreds of times a day for almost two decades ; and therein may lay the key.

David has been playing the highest level of football for 18 years, ever since he made his professional debut for Manchester United back in 1992.  He has played for three of the biggest clubs in the World (four if you are a Preston North End fan).  He is the most capped outfield England player in history and has played in three FIFA World Cups.  This is undoubtedly a huge demand on the human body (and testament to what a conditioned athlete he is that he hasn’t been injured more in my opinion).  He is world renowned as being one of the best dead ball specialists in the modern game.  It is no secret that he often stays behind after training and practises his free kicks again and again.  And he is right footed.  So it would be reasonable to assume he has spent a lot more of his life balanced only on his left leg (just take a look at his left foot in the picture and imagine the strain on the Achilles tendon).  He certainly has the repetitive load history which could have led to some tendon/collagen deterioration, and it is my belief that the seemingly innocuous movement he made in the San Siro stadium less than a week ago was simply the ‘straw that broke the camels back’.

Unfortunately for David (and every English football fan) he was also in the right demographic for an Achilles tendon rupture.  It is more common in males ⁸, and more common between 30-50 years old.⁹ I don’t know David’s blood group (even Google can’t tell us that) but individuals with blood group O have been shown to be at higher risk of tendon rupture ^10,11 so it would be interesting information to know.

Recovery

Professor Orava tells us the operation was successful and David will make a full recovery.  I am no surgeon, and do not profess to know what procedure was performed, but in simple non surgeon speak the tendon would have been sewn back together (possibly requiring a graft of tissue from another part of his body).  A task which no doubt requires serious skill and expertise on the Surgeons part.

For David the worst is probably yet to come.  Long rehabilitation is a certainty, and from the sportsmen I have spoken to regarding their ruptures, the first two months are miserable and they wouldn’t wish the injury on their worst enemy.  Assuming there are no post-operative complications (incidence of deep vein thrombosis following Achilles tendon rupture is high¹²) many months of Physiotherapy await.  It pains me to say it, but David may have played his last game for England (I hope he proves me wrong).  He has almost certainly played his last game in a World Cup.  So, is his career over, or will he return to elite sport and be back to his best?  I wouldn’t like to say.  Recent research on recreational athletes suggested significant reductions in playing sports following a rupture.¹³ However, that was recreational athletes – what about the professionals?  A study showed that 32% of professional American Football players who sustained Achilles tendon ruptures between 1997-2002 never returned to play in the NFL and on average players experienced a greater than 50% reduction in power ratings following the injury.¹⁴

Get well soon Becks.  I genuinely hope to see you play again.

References

1. Kannus, P., & Jozsa, L. (1991). Histopathological changes preceding spontaneous rupture of tendon. Journal of Bone & Joint Surgery, 73, 1507-1525.
2. Carr, A. J. & Norris, S. H. (1989). The blood supply of the calcaneal tendon. Journal of Bone & Joint Surgery Br, 71, 100-101.
3. Schmidt-Rohlfing, B., Graf, J., Schneider, U. & Niethard, F. U. (1992). The blood supply of the Achilles tendon. International Orthopaedics, 16, 29-31.
4. Theobald, P., Benjamin, M., Nokes, L. & Pugh, N. (2005). Review of the vascularisation of the human Achilles tendon. Injury International Journal of the Care of the Injured, 36, 1267-1272.
5. Lesic, A. & Bumbarsirevic, M. (2004). Disorders of the Achilles tendon. Current Orthopaedics, 18. 63-75.
6. Wren, T. A. L., Yerby, S. A., Beaupre, G. S. & Carter, D. R. (2001). Mechanical properties of the human Achilles tendon. Clinical Biomechanics, 16, 245-251.
7. McNeill Alexander, R. (1994). Human elasticity. Physics Education, 29, 358-362.
8. Leppilahti, J., Puranen, J. & Orava, S. (1996). Incidence of Achilles tendon rupture. Acta Orthopaedica Scandanavia, 67(3), 277-279.
9. Wapner, L. K. (1999). Achilles tendon ruptures and posterior heel pain. In: Kelikian AS (Ed). Operative treatment of the foot and ankle. Stanford, Connecticut; Appleton & Lange. P369-387.
10. Jozsa, L., Balint, J. B., Kannus, P., et al. (1989). Distribution of blood groups in patients with tendon rupture. An analysis of 832 cases. The Journal of Bone & Joint Surgery Br, 71(2), 272-274.
11. Kujala, U. M., Jarvinen, M., Natri, A., Lehto, M., et al. (1992). ABO blood groups and musculoskeletal injuries. Injury, 23(2), 131-133.
12. Nilsson-Helander, K., Thurin, A., Karlsson, J. & Eriksson, B. I. (2009). High incidence of deep vein thrombosis after Achilles tendon rupture: a prospective study. Knee Surgery, Sports Traumatology, Arthroscopy, 17(10), 1234-1238.
13. Kinner, B., Seemann, M., Roll, C., Schlumberger, A. et al. (2009). Sports and activities after Achilles tendon injury of the recreational athlete. Sportverletz Sportschaden, 23(4), 210-216.
14. Parekh, S. G., Wray III, W. H., Brimmo, O., Sennett, B. J. et al. (2009). Epidemiology and outcomes of Achilles tendon ruptures in the National Football League. Foot & Ankle Specialist, 2(6), 267-270.

This first entry is going to be quite short but it was the first thing I was ever taught regarding orthoses so seems as good a place as any to start; and it is simply regarding correct and incorrect terminology.  This was drilled into me so religiously that unfortunately it made me a little bit pernickety about it.  So what should we call the things we issue people to wear in their shoes? Insoles?… Inserts?… Orthotics?… Prosthetics?  Certainly I’ve heard them called all these things.  The general rule for their naming is perfectly summed up by Ray Anthony at the start of his 1991 book:

It is an Orthosis

They are Orthoses

They are Orthotic Devices

They are not Orthotics

Funny really, as ‘orthotics’ are probably what I hear them called (by patients and healthcare professionals alike) with the most frequency, despite this being considered poor terminology.  Does this really matter?  I suppose not in the big scheme of things.  But I can’t help but cringe a little when I read or hear them referred to incorrectly – the legacy of a pedantic (but brilliant) university lecturer almost 10 years ago.

References

Anthony, R. J. (1991). The manufacture and use of the functional foot orthosis. Karger; Basel, Switzerland.

Historically when examining the weightbearing foot all of our attention has been on its visual appearance (or posture).   Indeed these visual observations and measurements still form the main portion of an objective clinical assessment, and for many will also dictate the prescription variables for foot orthoses.  The potential problem with solely relying on visual alignment (or kinematics as they are referred to in biomechanics terminology) is that there is surprisingly little literature which shows that foot posture is actually predictive of injury.  What this means is that the pronated foot type is not necessarily as evil as we had previously thought.  Dr Christopher Nester of Salford University sums things up perfectly in his recent paper from the Journal of Foot & Ankle Research:

Rather than continue to apply a poorly founded model of foot type where the focus is to make all feet mechanically ‘normal’ we must embrace variation between feet and develop patient specific models of foot function.

In addition to this when we look at the research of how orthoses exert their effects (or ‘work’) it is clear that kinematic responses to orthoses are also variable and subject specific (Nigg et al, 2003; Huerta et al, 2009).  This means that not all feet will respond the same if given the same orthotic prescription.  And even if they did respond in a predictable way would this mean they would all get better?  Sadly not, as Zammit and Payne discovered in 2007, when they investigated the relationship between kinematic response to an orthotic device (how much it ‘realigned’ the rearfoot) and the reduction in the individuals symptoms; and found that there was no correlation between the two.

Confused? So was I.  I was taught that a pronated foot was a huge risk factor for injury.  I was then taught to measure how much it was pronated, write a prescription based on this number and the orthotic device I issued would duly realign the foot into ‘neutral’ and the patients symptoms would of course disappear.  It was a simpler time as you can imagine.

Not until I read an excellent research paper by Williams et al (2003) in the Medicine and Science in Sports and Exercise Journal did it start to make sense to me.  This research took a group of individuals and made them run in 3 conditions: no orthoses, ‘standard’ orthoses and inverted orthoses (between 15-25 degrees inverted).  It measured the kinematics (alignment) and the kinetics (the forces we can’t see).  The results were astounding – there was no statistically significant difference in rearfoot alignment between the 3 conditions.  However, when looking at the forces involved (particularly how hard Tibialis Posterior had to work) the more inverted an orthotic device was significantly reduced the demand on the soft tissues.  The inverted orthoses reduced this demand almost 4-fold when compared to the no orthoses condition.  Immediately we realised that our orthoses made people pain free by reducing damaging force, and not by ‘re-aligning’ them.

So what does all of this have to do with the supination resistance test? Well it is one of very few tests which give us insight into these forces (which may well be more predictive of injury risk and may better determine orthoses prescriptions than our visual assessment techniques do).  If a foot requires a large force to supinate it then it is assumed that a greater contractile force from extrinsic supinators, such as Tibialis Posterior, may be required functionally (does this increase injury risk?)  It may also dictate the sort of orthotic device which would be most appropriate.  The harder it is to supinate a foot then the greater force an orthotic device would need to cause a supination moment, and conversely the easier it is to supinate a foot then the lower the force required from an orthotic device.

So how is the test performed?

1. The patient is asked to stand in a relaxed position on two feet
2. They are instructed to relax their feet during the test, and not help in any way
3. The clinician places the tips of the index and middle fingers just beneath the navicular
4. The clinician pulls directly upward (parallel to the tibia)
5. The clinician notes the magnitude of force that is required to supinate the foot from its resting position
6. The test is performed on the other foot

When done in this clinical setting the test is a little subjective, but with repetition gives the clinician a good idea of the forces involved (and despite its subjectivity may still offer more important information that visual assessment).

The research team at La Trobe University in Melbourne took this one step further and built a machine which quantitatively measured this supination force in Newtons.  They found some fascinating results:

1. The manual version of the test (as described above) is reliable for experienced users
2. The amount of force required to supinate a foot is only weakly related to how pronated it is
3. The amount of force required to supinate a foot is highly correlated to the subtalar joint axis position (I won’t go into this now – it is worthy of its own blog entry and will get one in due course)
4. Body weight explains about a third of the force required to supinate the foot

These findings are what we see clinically when performing the test – the force to supinate feet is variable, and does not seem to be hugely influenced by body weight (I have experienced a 13 year old girl who weighed 7 stone have a higher supination resistance than a 19 stone rugby prop forward).

The team at La Trobe have also done much research which has not been published yet (personal communication with Craig Payne) and one which interests me particularly.  They took 28 individuals all who had problems with only one limb and all of which had been previously considered to be due to ‘excessive pronation’.  They recorded the Foot Posture Index (a protocol which classifies feet into categories based on visual observations) on the injured side versus the uninjured side, and then measured the supination resistance on the injured side versus the uninjured side.  They found that when looking at foot posture the injured side was more pronated in 15 out of the 28 subjects.  However when looking at supination resistance it was higher on the injured side in 25 out of the 28 subjects.  Does this tell us that supination resistance is more predictive of injury that foot posture? Well not quite as it was a cross-sectional design, but it certainly suggests this is worth investigating further in a prospective study.

The supination resistance test is probably now one of the key things from my assessment of patients which dictates my orthoses choices.  I pay more attention to it than I do the foot posture.  However further work is required to fully understand supination resistance and whether it is prospectively predictive of injury risk (or can validly be used to determine dynamic kinematic responses to different levels of force from foot orthoses).

References

Picture from: Kirby, K. A. (2002). Supination Resistance Test. Foot and Lower Extremity Biomechanics II: Precision Intricast Newsletters, 1997-2002 (pp. 155). Payson, Arizona: Precision Intricast, Inc.

Huerta, J. P., Moreno, J. M. R., & Kirby, K. A. (2009). Static response of maximally pronated and nonmaximally pronated feet to frontal plane wedging of foot orthoses. Journal of the American Podiatric Medical Association, 99(1), 13-19.

Kirby, K. A., & Green, D. R. (1992). Evaluation and nonoperative management of pes valgus. In S. DeValentine (Ed.), Foot and Ankle Disorders in Children (pp. 295).  New York: Churchill Livingstone.

Nester, C. J. (2009). Lessons from dynamic cadaver and invasive bone pin studies: do we know how the foot really moves during gait? Journal of Foot & Ankle Research, 2 (18)

Nigg, B. M., Stergiou, P., Cole, G., Stephanyshyn, D., Mundermann, A., & Humble, N. (2003). Effect of shoe inserts on kinematics, centre of pressure, and leg joint moments during running. Medicine & Science in Sports & Exercise,35, 314-319.

Noakes, H., & Payne, C. B. (2003). The reliability of the manual supination resistance test. Journal of the American Podiatric Medical Association, 93 (3), 185-189.

Payne, C. B., Munteanu, S., & Miller, K. (2003). Position of the subtalar joint axis and resistance of the rearfoot to supination. Journal of the American Podiatric Medical Association, 93 (2), 131-135.

Payne, C. B., Oates, M., & Noakes, H. (2003). Static stance response to different types of foot orthoses. Journal of the American Podiatric Medical Association, 93 (6), 492-498.

Williams, D. S., McClay Davis, I., & Baitch, S. P. (2003). Effect of inverted orthoses on lower-extremity mechanics in runners. Medicine & Science in Sports & Exercise, 35, 2060-2068.

Zammit, G. V., & Payne, C. B. (2007). Relationship between positive clinical outcomes of foot orthotic treatment and changes in rearfoot kinematics. Journal of the American Podiatric Medical Association, 97, 207-212.



The more I read the more I discovered that 10 degrees as a normal value was erroneous (infact it was not possible to even find the reference that this figure originated from).  What happens if you walk slower, or faster? What happens if you run? Was 10 degrees still valid?  The truth was that ankle range seemed to be hugely variable, and both subject and activity specific.

Then there was the actual method of assessing the ankle range – how hard should we push the foot when measuring dorsiflexion? Common sense would suggest we should apply as much force to the foot as is applied during gait.  Could we physically apply this much force?  Probably not.

At the same time I was trying to take in the bombshell that 10 degrees of ankle dorsiflexion was no longer something I needed to worry about I was reading a lot of work by Dr Kevin Kirby; a Sacramento based Podiatrist and Professor of Biomechanics who was pivotal in highlighting to me (amongst many others I’m sure) the importance of thinking more like an engineer.  In the discipline of engineering terms such as flexibility, mobility and rigidity are not used as they lack the precision to be mathematically quantified.  Instead the term ‘stiffness’ is used, and this describes motion or deformation in response to an externally applied force.  So when applying this concept to the ankle joint instead of reporting simply how much it moves (its range), we should instead consider how much it moves when various forces are applied to it (its stiffness).  Given that the foot and ankle are predominantly asked to perform their daily functions during weightbearing activity ‘stiffness’ seems much more relevant than non weight bearing range of motion.

So after abandoning non weightbearing ankle range and the mythical 10 degrees of dorsiflexion from my thought processes, and getting my head around the concept of stiffness Vs range of motion I stumbled across the Lunge Test – a weightbearing assessment of the ankle joint range which factored in the individuals body weight.  This is a test which has been shown to have very good reliability / repeatability (Bennell et al, 1998) and prospective studies have also shown it to be predictive of injury (Pope et al, 1998; Gabbe et al, 2004).  There are actually very few clinical tests we perform which have been shown to be prospectively predictive of injury so this is a test which should certainly not be left out (especially when screening uninjured sportsmen and women).

So how is the test performed?

1. Patient stands against wall with about 10cm between feet and wall.
2. They move one foot back a foot’s distance behind the other.
3. They bend the front knee until it touches the wall (keeping the heel on ground).
4. If knee can not touch wall without heel coming off ground, move foot closer to wall then repeat.
5. If knee can touch wall without heel coming off ground, move foot further away from wall then repeat.
6. Keep repeating step 5 until can just touch knee to wall and heel stays on ground.
7. Measure either: a) Distance between wall and big toe (<9-10cm is considered restricted) or b) The angle made by anterior tibia/shin to vertical (<35-38 degrees is considered restricted)
8. Change the front foot and test the other side (symmetry is ideal)

It is worth remembering that there are some validity issues with the wall to big toe measurement with respect to the proportions/ratios between an individual’s leg length and foot length.  Anyone who is very tall is likely to have the minimum distance required and anyone who is very short will probably not have the minimum distance; therefore it is generally considered better practice to use the tibial angle when interpreting the results.

So what does this test mean?

A restricted Lunge test essentially suggests there in an increased ankle joint dorsiflexion stiffness.  Research tells us this may increase an individuals risk for lower extremity injury.  It is also something which will often be considered by a Podiatrist when recommending footwear or foot orthoses for someone who is already injured.  The test is generally performed when shod (to allow for the heel height differential of the shoe) and whilst wearing orthoses; modifications are made as required in order to achieve an appropriate tibial angle.  It may also dictate the appropriateness of concurrent joint mobilisations or a soft tissue stretching programme.

References (please contact me if you would like a copy of any article)

Bennell, K. L., Talbot, R., Wajswelner, H., Techovanich, W., & Kelly, D. (1998). Intra-rater and Inter-tester reliability of a weightbearing lunge measure of ankle dorsiflexion. Australian Physiotherapy, 24(2), 211-217.

Gabbe, B. J., Finch, C. F., Wajswelner, H., & Bennell, K. L. (2004). Predictors of lower extremity injuries at the community level of Australian football. Clin J Sport Med, 14(2), 56-63.

Kirby, K. A. Foot and Lower Extremity Biomechanics Volume 3: Precision Intricast Newsletters, 2002-2008. Precision Intricast: Payson, Arizona, 2009, p50.

Pope, R., Herbert, R., & and Kirwan, J. (1998). Effect of ankle dorsiflexion range and pre-exercise calf muscle stretching on injury risk in Army recruits. Australian Physiotherapy, 44(3), 165-172.