The biomechanical jig saw puzzle – what leads to excessive tissue stress and injury?

Welcome back to Trevor Prior for another great post on biomechanics. Trevor is a fantastic London based podiatrist, working at Premier Podiatry with more than 30 years clinical experience. Some great discussion of biomechanical principles and concept of different biomechanical factors building the puzzle for individual injury risk profile. Over to you Trevor ……………..

We have recently discussed the relevance of static measures in clinical practice and how this helps us to determine the functional capacity of an individual. However, it is clear that static assessment at best only predicts a percentage of dynamic function.

Tissue-stress model

In 1995, McPoil and Hunt1 reviewed the literature available at the time and proposed a tissue stress model for assessment and management. They noted that the evidence available indicated that the traditional approach to assessing foot function and subsequent management proposed by Root, Orien & Weed2,3 may lack validity because of the following:

  1. Poor inter tester reliability of subtalar neutral
  2. The normal foot alignment proposed by Root, Orien and Weed2,3  was not representative of the general population
  3. The subtalar joint did not function around the neutral position as defined by Root, Orien and Weed2,3

As a result, McPoil and Hunt1 proposed a tissue stress model based on concepts already established in clinical practice. Specifically, they described a load deformation curve which consisted of:

  1. An elastic region which represents the normal range of stress applied to a tissue during activity
  2. A plastic region which represents excessive load and injury to the tissues
  3. A zone of micro failure which separates the two regions rather like a transition zone

Treatment aims to maintain or return the tissue to the elastic region although clearly, if there has been permanent damage to the tissue (i.e. tendon attenuation or tear), this tissue will now be less resistant to load.

Part of the aim of this approach was to allow flexibility in the assessment and management of foot disorders.

In a roundtable discussion article, Simon Spooner4 noted how the rotational equilibrium theory described by Kirby5 provided insight into how mechanical modelling of forces acting on structures can be applied to the foot and lower limb. By combining this with the tissue stress approach, it provides the clinician with a model by which to manage patients.

Zone of Optimal Stress (ZOOS)

Spooner introduced the concept of a zone of optimal stress (ZOOS) such that, for any tissue or structure, there would be a range of loading within which that tissue could function and remain healthy. Tissue dysfunction can occur when either the load is excessive (i.e. out of the ZOOS) or the properties of the tissue have reduced in relation to normal load (or both).

The natural progression is that management should aim to alter the loading of the tissue such that the tissue is functioning within its ZOOS to allow it to heal.

However, Spooner makes a very important point;

”This should occur without inadvertently exposing other tissues to deleterious loading levels.”

It is clear that we are able to alter load through structures but this load does not just disappear, it is transferred to other structures. Thus, whenever we reduce load at one point (whether this be by orthoses, exercises, gait re-training etc.), we may increase load at another and often, we are unaware exactly how.

The question then arises, how is this predicted and managed?

Inevitably a series of questions arise in this process. Let’s use peroneal dysfunction as an example.

Let us assume a patient has peroneal longus dysfunction and our aim is to reduce the tissue stress through the tendon and return it to its ZOOS with an orthosis. Prescribing an orthosis to evert the foot or increase the pronatory moments (e.g. a lateral rearfoot or forefoot post) has the potential to reduce load through the tendon but, the foot type will determine the relative effect:

  1. A foot that demonstrates supination through gait may benefit well from a lateral post, reduce excessive load to the peroneal longus and minimise stress to other structures.
  2. By contrast a foot that demonstrates pronation will also have load to the tendon reduced by a lateral post but now, by increasing the pronation moment, has the potential to increase load on other structures. In this foot type, reducing the pronation moments (i.e. some form of medial posting / support / resistance) can also reduce load through the peroneal tendons by providing mechanical advantage (by allowing 1st ray plantarflexion), with less risk to other structures.

Pronation and supination, in themselves are not a diagnosis as we pronate or supinate for a reason. In all likelihood, the overall effect / outcome / function is a combination of all the factors that contribute towards pronation and supination summated and providing a resultant. Factors that may increase the pronation moment include an internal hip position, weak hip control, posterior muscle inflexibility, knee flexion, tibial varum, hypermobile medial column, forefoot equinus, medially deviated subtalar joint axis, hallux valgus etc.,

Simply transferring load from one foot to the other during walking moves body weight medially and thus places a pronatory force on the foot.

Our assessment allows us to gauge if we have a foot that has a tendency towards pronation / supination, the mobility of the foot and the symmetry between the feet. Do we expect this to be a foot that demonstrates more or less motion and would we expect symmetrical motion? If these factors are not observed dynamically, then it would be reasonable to consider that factors extrinsic to the foot are driving function.

This returns us to our static assessment contributing to our understanding of an individual’s structural capacity and thus helping us to determine the likelihood of our interventions increasing stress elsewhere and placing other structures out of their ZOOS.

It’s a question of scale (or range); if we can accept the principle of ZOOS, then it is clear that there is a range of load a structure can tolerate and not one finite load. This load will vary between tissues and individuals much like the variation in range and direction of midfoot function demonstrated by Nester7,8,9 and his colleagues.

This is supported statistically as we are well aware that a normally distributed population will provide a range of values and generally, it is accepted that the ‘normal’ range is defined as +/- 1 standard deviation from the average. Thus, we have a scale of one extreme to another. So, for any given variable there will be a range from low to high.

Biomechanical scale

If one then considered all of the variables assessed as a set of scales or ranges like this, a picture can be built of the degree of structural abnormality, the degree of mobility present and the relative strength / control. Thus, if dynamic analysis identifies either excessive or restricted motion, one could consider the relative contribution of the alignment, strength and flexibility and consider interventions.

Furthermore, it is quite possible to be restricted in one area and have excessive motion elsewhere. One may also identify that an area of excessive motion is being driven by dysfunction elsewhere i.e. poor hip control driving excessive foot motion or vice versa.

There is growing emphasis placed on gait retraining in biomechanical literature, but it is easy to see how these factors can be placed on this type of scale whether it be strike pattern, hip adduction, etc. For example, a heel strike runner with a knee injury may have high loads on the knee as a result of their technique. To shift this same runner left on the scale and into a normal range, we could alter their strike pattern to a forefoot strike. However, in doing so, we will shift the load profile of the foot and ankle to the right on the scale, possibly moving this runner into the high zone of the scale, increasing injury risk in this area.

It can therefore be appreciated that there are so many contributing variables, assessment and management have to be targeted to the individual and how the tissues respond in one, will be different to another.

The challenge remains for us to develop reliable assessment criteria and then a normal range of values that help identify the extent and direction of dysfunction for each individual.

The more factors an individual patient has towards one end of the scale, then the likelihood of the more rehab / intervention that is required to allow a given activity. This also helps to quantify / develop patient expectations.

If there is a lot of dysfunction for a given activity, they are likely to have to perform a higher level of rehab compared to someone else (a rehab scale so to speak). If they are not prepared to rehab to this level (or cannot due to other commitments or financial restraints) then they have to accept that they either have to adapt the level to which they perform, or if they continue to perform at that level, they will have an increased risk of injury.

Injury risk profile examples

Figure Examples of injury risk profiles. Note the differences between the two middle bars where injury threshold is crossed.

It is worth noting that, simply because any one factor sits outside of a normal range does not mean that this will result in pathology. The degree to which it is outside the normal, the number of overall factors that are outside the range and the level to which the individual is active (i.e. load repetition) will all contribute to the risk of pathology.

This scale approach can be applied to tissue stress relief. When trying to relieve stress and resolve injury, we may implement a specific tissue stress relief – this might be rehab, a walking boot, tape, orthoses etc. One should determine whether or not this intervention has moved the variable in question more towards the centre of the scale or the periphery (i.e. left or right hand side) and thus abnormal function. A boot will immobilise and rest an area but it has moved the range of motion to one end of the mobility scale and will result in reduced strength and range of motion locally, and an increased demand on proximal function to facilitate gait. Therefore, this is abnormal and clearly should be used in the short term.

Taping and orthoses have the potential to restrict motion more than might be optimal – they may relieve stress but not necessarily optimise function. They have reduced the stress on the tissue in question but may have increased stress elsewhere. For example, an orthoses restricting foot pronation in a jumping athlete will reduce tissue stress at the foot on landing, but may concurrently increase it at the knee – after all, forces don’t just disappear. In some instances, this is required in the short term to allow the injury to settle and then either the control reduced or removed. In others, they may require this level of excessive control to continue with daily activity. This may occur when tissue is pathological. In these instances, I would consider this compromised control and it can be difficult to determine the long term effect on other structures. It is therefore important to advise patients accordingly.

So, where does this leave us?

In the previous blog, I have outlined how static measures allow us to determine the functional capacity of an individual and provide part of the diagnostic jigsaw.

Unfortunately, much of the research that has investigated the relationship between static structure and dynamic function has focussed on foot and lower leg alignment. That only a percentage of foot function can be predicted by static assessment is perhaps not surprising given the many factors proximally that can contribute to dysfunction. McPoil and Cornwall1 recognised this fact when they postulated that tibial valgum and femoral torsion may cause pronation.

Determining the key variables that have the ability to affect function, developing reliable measures for assessing these variables and then producing normal ranges has the potential for us to build a more complete picture of function. Furthermore, it would help to identify which were the key areas of dysfunction. Then appropriate interventions can be developed to allow the majority of tissues to function within the zone of optimal stress.

This case history link demonstrates how assessment of structural alignment, strength, flexibility and dynamic assessment (inshoe pressure analysis and 3d kinematic assessment) can be used for diagnosis and management.

References

  1. McPoil TG, Hunt GC, Evaluation and management of foot and ankle disorders: present problems and future directions, J Orth Sp Phys Ther 1995, 21(6):381-388.
  2. Root ML, Orien WP, Weed JH, Hughes RJ, Biomechanical examination of the foot, Volume 1, Clinical Biomechanics Corporation, Los Angeles, 1971.
  3. Root ML, Orien WP, Weed JH, Biomechanical examination of the foot, Volume 1, Clinical Biomechanics Corporation, Los Angeles, 1977.
  4. Kirby KA, Spooner SK, Scherer PR, Schuberth JM, Roundtable discussion: Foot orthoses, Foot & Ankle Specialist 2012, 5(5):334-343
  5. Kirby KA, Subtalar joint axis location and rotational equilibrium theory of foot function, JAPMA 2001, 91(9):465-487
  6. Kirby KA, Prescribing orthoses: Has tissue stress theory supplanted Root theory? http://www.podiatrytoday.com/prescribing-orthoses-has-tissue-stress-theory-supplanted-root-theory
  7. Nester CJ, Findlow A, Bowker P, Scientific approach to the axis of rotation at the midtarsal joint, JAPMA 2001, 91(2):68-73
  8. Nester CJ, Bowker P, Bowden P, Kinematics of the midtarsal joint during standing leg rotation, JAPMA 2002, 92(2):77-81
  9. Nester CJ, lessons from dynamic cadaver and invasive bone pin studies: do we know how the foot really moves during gait?, JFAR 2009 2:18