Posture and pain and not well linked in the research

 

This means no if's, no but's, no maybe’s or even worse…… “in my experience”, which of course is completely ludicrous as someone else may have had exactly the opposite experience.

Who is right? Who the f**k knows? That’s why we have science!!!!

Evidence based practice is a game of probabilities and the probabilities are well stacked against posture being a cause of many musculoskeletal problems.

There are far to many papers to list, so here is one each for some different areas of the body. If you think I have just cherry picked these, there really is shit loads of this stuff out there so go and have a look if you don’t believe me!

Shoulder posture

Cervical posture 

Lumbar posture

Thoracic posture

For a more detailed discussion on posture please check this out on anterior pelvic tilt and this on joint centration

We have no gold standard for what is good and bad posture. So what people base their correction or postural goal on has to be a reasonably arbitrary measure.

But just because we do not have a gold standard does not mean the research into posture is invalid because it is not studied in that way anyway!

Most papers seem to take a bunch of people in pain and then a bunch of people NOT in pain and then compare the postures between the two groups not against a gold standard of perfect posture.

Can a posture ever become a problem?

 

Yes.

Especially if it is the only one you have. But that is a movement problem not a postural problem.

The lumbar spine paper above shows this. There were no differences in the lordosis angle of people suffering with LBP but they did move slower and have less range of movement.

Even what we might consider a really good posture could be a problem if it does not have any movement!

We often swap something (bad) for something else (good – maybe) but we should be swapping it for 'something’s' (plural) in the form of movement and the ability to move into many different postural positions.

The postures you adopt for too long may cause problems as well. Take your amazing posture and sit in front of the computer for 8 hours and it may start to let you know about it. The key again maybe the lack of moving not the posture you had to start with.

We have some cool sensors called Acid Sensing Ion Channels or ASICS within our tissues that sense changes in the ph value. If we don’t move around, or put strain on our muscles and nerves that may reduce blood flow, then these little bad boys can sense the tissue becoming more acidic and transduce this into a sensation of discomfort or even pain.

Ever sat for to long in a lecture or seminar and felt the need to get up and stretch as you are feeling a bit sore? You probably just went through this process. ASICs may get even better at sensing changes if the cell body decides to pop some more ion channels down to the terminal ending so that sodium can get into the cell more easily and make you more sensitive to acidosis of the tissue.

What cause poor posture?

 

Well it could be pain.

In fact you may have looked at the problem the wrong way round. Pain may have been a driver to adopt an adaptive or potentially maladaptive position to reduce pain.

People with "poor posture" suffer from bouts of pain like us all, but if posture were the only driver for their pain they would probably be in permanent pain as, lets be honest people rarely seem to change their posture.

The habits people have will also probably outweigh the occasional stretch and strengthening that they do.This paper *here* discusses exactly that!

Their conclusion being:

"objective data to indicate that exercise will lead to postural deviations are lacking. It is likely that exercise programs are of insufficient duration and frequency to induce adaptive changes in muscle tendon length"

In some cases, other factors such as our visual and vestibular systems may affect our postures too so it is not simply "short and tight" and "long and weak" muscles and if it does not seem to cause pain, then who cares anyway?!

Are you justified in attempting to change posture?

 

We may have to realize that success in trying to change posture maybe due to the process (through exercise or movement) of trying to change posture. This maybe the most important element in helping painful body parts become less painful, and not the outcome such as an actual significant change in the posture. So you would be totally justified giving a body part that has a lack of options (stuck) some more options (varied movement).

In fact rehab programs designed to change posture can help people out of pain without changing their posture as we see *here* with resting scapular position!

As discussed before, if it is the only posture someone has - such as we may see at the lumbar spine with being hyper extended - focusing on this can often help. Whether success is contingent on getting a change in the posture is quite another matter entirely.

If your goal is to change the aesthetics of your or somebody else’s body by trying to alter your posture then its up to you….. but good luck with that!

Are you a THERAPIST wanting to know more about a NO BS & evidenced based approach to helping your patients?

Are you a TRAINER wanting to know more about a NO BS & evidenced based approach to helping your Clients?

 

 

 

 

 

 

There has always been this big divide between those that prefer a strength oriented approach to training and rehab and those that like to use a more movement (also called proprioceptive or motor control training) based approach.

For some reason human beings tend to gravitate into camps, tribes or teams, its just part of nature! Training and rehab seems to be no different.

So....which tribe do you belong to?

two tribes

I could not help but think of the Frankie goes to Hollywood classic!

https://vimeo.com/126022671

First thing we have to realise is that is very hard to completely divorce the two modalities.

Strength training does not mean that we have no proprioceptive input or motor pattern output. Any movement will create feed forward commands and feed back through the proprioceptive system up into the cortex. We may REDUCE the amount of feedback that  comes from differing joint positions and variability of movement during strength training as the movement is often constrained by the increased load. We must remember however proprioception is also about force regulation and a fair amount of proprioceptive research is based on measures involving force rather than being just joint position based.

Equally ‘movement’ training can involve strength and joint loads generated by acceleration & deceleration, end range tension and joint stabilization. Less utilised joint angles may also need less added load to achieve an overload effect that would stimulate a need to increase strength. ‘Strength’ training is essentially adding load to any movement after all, although often specific ‘strength’ exercises are preferred.

We seem to be looking for a one type of training or rehab that encompasses everything. Both types of will individually increase capacity AND interact in relevant situations so need to be looked at concurrently as well.

Strength:movement

Maybe it would be better to see strength and movement training as having mostly DIFFERING affects on humans. There will of course be crossover where strength affects movement and movement will affect strength but expecting movement training to increase strength and load tolerance in the same way strength training does maybe misguided. The same is true of strength training, why would it have a specific effect on a motor pattern in the same way practicing that motor pattern would?

The problem here is that this thought process does not fit the ‘tribe’ mentality.

I see this as being similar to the pain science debate and the criticism of the pendulum swinging to far from peripheral to central mechanisms (another tribal debate). Often the truth lies in the middle ground and being inclusive and aware of the impact of many types of rehab and training modalities.

So are strength and movement unrelated?

 

Now this does not mean that strength and movement are unrelated. This study *Here* (thanks to Nick Clark) found that quadriceps strength was significantly correlated with the function of the knee during walking gait after ACL reconstruction. This makes sense if the level of strength falls below that required for normal movement and this is likely to occur after a significant event such as an ACL injury. One caveat would be that kinematics and strength levels might both be related to pain levels and once pain subsides ‘normal’ motor behavior and strength levels may be restored rather than strength and movement being related to each other.

The relationship between strength and movement patterns after injury is less clear in running potentially because strength levels during or post injury do not fall enough to significantly impact on movement.

This paper *Here* looked at changes in knee biomechanics after a strength training program for the hip abductors in runners with Patellofemoral pain. Peak ‘genu valgum’ or increased hip add and the resulting knee valgus has been hypothesized to be associated (although still unclear!) with PFP. Although hip strengthening programs are designed to decrease peak hip add (and knee abd) this study found a strength training program DID increase strength and decrease pain but did NOT impact on the movement of the knee in terms of peak genu valgum (peak knee valgus) angle at post test compared to baseline. A caveat here is that the analysis of the knee was in 2D, looking at the hip adduction and shank abduction angles, and movement of the knee during running is 3 dimensional.

This study *Here* into the frontal plane kinematics of the knee in running, this time in healthy female subjects, looked at the relationship between hip abduction strength and hip adduction kinematics and found no relationship and this time they did use 3D analysis.

Another study *Here* found that a hip strengthening program did not alter running mechanics in a healthy female population. In fact ‘movement’ training in the form of a single leg squat did not alter running mechanics either but did have an effect on the single leg squat! So ‘movement’ training also displays a healthy relationship with the SAID principle (specific adaptation to imposed demand) and if you want to alter a specific movement you probably have to work on that specific movement.

Gait retraining, the SAID principle in action, is becoming more popular with running *Here* and seems to be effective in improving running kinematics and pain and function in the short term and we also see a crossover to less complex skills such as squatting. It seems running may have more to do with coordination and timing of muscular contraction within a motor pattern  rather than the strength of contraction that can be generated.

So another question is does the complexity of a skill, such as running gait which is very complex, seem to play a part in whether strength training has an impact on movement?

Potentially!

This paper *Here* looked at different training programs to improve knee alignment during landing that has been associated with both ACL and PFP injuries of the knee. They had two groups, a strength group and a jump landing training group and looked at the functional tasks of the single leg squat, single leg landing and bilateral landing.

They found that a strength training program DID affect frontal plane projection angle (FPPA) during a single leg squat AND single leg landing but NOT during a bilateral drop jump as well as increasing strength. Of course the jump landing training group DID improve landing but did NOT improve strength.

The caveat here would be that the strength training program included a single leg squat which more than likely (IMO) creates some motor learning carryover to the FPPA in the single leg test and this was fully acknowledged by the authors.

It might also be that a simpler movement is affected more by changes in strength.

The authors also pointed out that a change in the single leg landing task also improved in the strength group even though they did not train this movement. The conclusion being therefore strength was a factor in the improvement of the FPPA. However we may also see a motor learning carryover between the single leg squat to a single leg landing as they are a reasonably similar movements which has been previously shown. This study also utilised a 2D analysis that has been cited as a limitation in studies that failed to show a link between changes in strength and change in movement.

The authors did come to the most sensible conclusion of incorporating both strength and movement training to decrease FPPA at the knee and also utilised a comprehensive approach to their training programs!

Brain stuff

 

One argument is that strength training does not affect the movement representations in the cortex but why should we expect them to?

This study *Here*, and yes its not a human study, found that changes in the motor cortex were associated with skill rather than strength as coupled strength and skill training did not induce any more change than skill training alone.

This article *Here* finds that strength training and ‘movement’ training are associated with DIFFERING affects on the brain in terms of neuroplasticity after skill (movement) and strength training.

The strength training group, surprise surprise, increased strength but did not increase the neurophysiological parameters involved with skill training. The skill group improved their skill performance but not their strength. This fits very nicely with the principle of SAID.

Working on different biomotor components created different changes neurologically in terms of MEP (motor evoked potential) behavior at different times throughout the 4 week training program with skill training creating quicker changes than the slower changes associated with strength training.

*Here* we also see different cortical activity between control (movement) and strength tasks.

We may find that strength training is more about the creation of force through co-contraction and movement training is more about the coordination and timing of contraction in relation to a, potentially complex, specific functional skill.

All this does NOT mean increasing strength won’t affect performance or pain

 

A mistake often made by the ‘movement’ tribe is to reason that because strength does not seem to have a clear relationship with altering movement is that it is not beneficial. Strength, and its more functional relation power, are still bio-motor qualities associated with function and increasing their capacity will surely be beneficial.

This study *Here* found that maximal strength training over 8 weeks improved running economy and  time to exhaustion in distance runners. There maybe a number of mechanisms involved in resistance training affecting distance running performance as seen in this paper. *Here*.

We see a strong correlation *Here* between maximal squat strength and sprint performance in elite soccer players.

If we go back to the article earlier in the piece that looked at strength and knee biomechanics we see that although the strength training program did not affect peak knee kinematics it DID have an effect on PAIN. We would need a control group with knee pain however, instead of just healthies, to allow for the basic healing effects of time to make a really strong link.

Although a causal relationship between decreased strength levels and injury and pain is extremely unclear at the present time, reducing strength inhibition in rehab POST pain is a key variable as we see clearly in the evidence base that pain has an effect on strength output.

This paper *Here* showed that both strength and power (during hop test) were affected in the UNINJURED leg as well after an ACL injury. This may suggest a central modulation of strength and power output after injury not just damage to a joint, muscle or connective tissue.

This systematic review *Here* found that resistance training was beneficial for chronic low back pain, chronic tendinopathy, knee osteoarthritis and post knee surgery potentially strength training being more beneficial for chronic pain. It is important to note the authors felt that high intensity (above 70% 1RM) was more effective than low intensity approaches and did not increase injury risk that seems to be a fear of some when using resistance training.

This study *Here* found that a periodised strength training had a positive influence on strength, pain and disability in active middle to older aged men with chronic back pain.

This paper *Here* looked at the dose response between resistance training and upper and lower back pain in office workers. They found training volume per session more important than the number of sessions attended to be correlated with pain. Interestingly however the specific resistance training group and the more general physical exercise group showed pretty similar reductions in pain.

Strength and movement training were both found to be effective for chronic low back pain in this systematic review compared to controls or other treatments *Here*. It might just be that moving is better than NOT moving for those with chronic lower back pain!

We do have to remember that you could perform an exercise designed to increase strength without ever actually increasing strength because the load, and therefore overload, used does not require an adaptation from the body in terms of strength. A ‘strength’ or ‘strengthening’ exercise on its own is not guaranteed to increase strength. This could be a criticism of papers that look at strength training vs more general programs that the levels of load used are not sufficient to change strength and/or the actual changes in strength are not reported.

We may see that here with a comparison of walking and strength training for chronic lower back pain *Here* with a walking programme as effective as a specific lower back ‘strengthening’ exercises. There were no measures of actual strength or increases in strength in this paper so we do not know if strength is a factor or not and this may fall neatly into what is discussed in the paragraph above.

With CLBP we see an unclear relationship with changes in physical function such as strength and clinical outcome *Here* This does NOT mean that strength training is not beneficial it just means potentially that the moving component may be more important than any increases in strength or other physical factors and the moving component is in the format of strength training.

I have previously discussed this here Strengthening the most overused term in therapy

Some opinion

 

Certainly putting your body under regular load through resistance training should increase your tolerance to putting your body under load if the loads are sufficient for adaptation!

For example if I am a runner it is very difficult to recreate the loads associated with running without doing MORE running. This may be the cause of a running injury in the first place. However we can manipulate the application of force on the body to elicit cellular mechanotransduction and positive expressions of compounds that alter muscular architecture and subsequent tolerances to load.

Although the loads applied may not be identical in terms of mass X acceleration it does not mean they are not beneficial and the lack of replication and alternative load might be just ‘what the doctor ordered'.

Strength and Injury Prevention

 

This often cited systematic review *Here* on injury prevention shows very positive effects of strength training on decreasing injuries. This highlights the positive effects of putting your body regularly under load but should not be confused with how strong you are decreasing your injury risk.

You could regularly put your body under load without ever significantly increasing your strength equally you could be pretty strong in comparison to someone else naturally but not put your body under regular load. It is physical activity that is being studied in this paper.

It is also important to note that movement training (proprioceptive) was also shown to have an significant effect on injury prevention and if we think about the body of ACL prevention research we see beneficial effects there.

This all seems nice and clear until we look at this recent paper *Here*  on ACTUAL strength deficits in those that go on to injure their ACLs. Here we see predictive risk factors for isometric hip strength of external rotation being under 20.3% BW (percentage of body weight) or abduction strength under 35.4% BW.

What is unclear here is HOW this impacts on non contact ACL injuries. Although the rationale in this paper is that abnormal lower extremity movement is related to non contact ACL ruptures, lots of evidence on this, and that strength is then related to the abnormal movement. BUT the relationship between strength and movement is most certainly uncertain at the present time in my opinion (and this being my blog my opinion rules!) so as a modifiable risk factor we cannot ignore this data but the exact mechanism is still unclear.

Strength may be more important with relation to movement in those that require very high levels such as in multi planar athletic populations as it might also be important when strength levels do not meet the required level for ‘normal’ movement to occur such as post operatively.

Conclusion

 

So shock and surprise I hear you gasp, strength and movement training have different effects on human body.

If you want to move in more varied or ‘better’ ways and improve the bits of the body and brain involved with moving then movement training is perfect.

Want to increase strength and power and load tolerance then strength and resistance training is awesome.

Sometimes to be really effective we have to think about using a bit of both and adding load to a relevant movement to get the kind of crossover to ‘function’ that maybe required or desired.

Both will have an impact on different components associated with performance and both should help reduce injuries. We must remember though that performance is extremely hard to quantify as this is often subjective, research often test elements of performance which is quite different.

Probably the clever guys are doing a bit of both already in the fields of rehab and training/performance and realise that both movement and strength training have their part to play.....just on different aspects!

 

 

 

 

 

 

 

 

 

 

 

This is one of my favourite analogies to help us better, and simply I may add, understand predictive brain functioning so to answer that question lets first transport ourselves to the the betting shop.

Any self respecting 'bet layer' will diligently study the form of the team or horse they are about to put a bet on, otherwise it would simply be a wild stab in the dark.

form

You might ask yourself:

Firstly, are they historically winners so have a good track record of winning?

Secondly, you may want to find out if they have been winning or losing recently so what is their current form like.

If we look at Manchester United recently we see although they have a great history of winning over the past 20 years their performances over the last few seasons may temper the confidence in their current performances.

Basically we have two factors:

1. What has happened previously?

2. What is happening right now?

They will both influence my prediction of what is going to happen in the future. In the world of the betting shop that directly correlates with how much money I will bet!

To work out an uncertain future situation I have used the past and the current situation to create a probability or likelihood ratio that shapes my future actions.

This was concept was examined in relation to statistics by Rev Thomas Bayes in the 18th century with ‘Bayes Theorem’. ‘Bayesian inference’ has been applied to many contexts since including brain function.

This is a fantastic book that discusses the memory-prediction model of brain function by Jeff Hawkins. “On intelligence”

on

So what has that got to do with the brain, movement and pain I hear you ask?

 

Well this is exactly the way it has been hypothesised that our brains work.

It has been proposed we use a memory-prediction model that rather than computing all possible outcomes such as a computer might we instead auto associate current context with previous experiences to work out the probability of the potential outcome and then formulate an appropriate response.

We trigger these memories via matching them with sensory information or intentions such as planning actions. Matching stored neural patterns with current sensory input creates a probability of the potential outcome.

I have my own simple model, open to scrutiny by cleverer folk, in regards to predictive brain function.

• Patterns – Stored neural patterns to access in response to sensory information or intention patterns.

• Perceptions – Interpretation of stored pattern and actual sensory input.

• Prediction – Output program in response to perception.

If we think about pain as a response to perceived threat then our previous experiences will affect our current perception of potential threats and this has been previously discussed by the likes of Moseley and Melzack in relation to pain.

Why would the brain work like this?

 

One theory put forward is that the brain has a vast amount of power but is actually quite slow in its operation. A potential reason is the biological nature of humans. Once a neuron has been activated through depolerisation and generated an action potential it then has to repolerise and this process takes time to get back to its resting state.

depolerisation

This is a process that requires the balance of elements within the cell to change and  although we have a vast amount of neurons they are slow(ish) in their action especially as they have a refractory period.

This predictive operation may also reduce latency (delay) in processing times of information from the periphery that are often cited as reasons for models decentralising the control of physical actions.

Here is a paper discussing the forward model of motor control. "Forward models for physiological motor control"

Why is this important?

 

We often see our movement responses as the product of the mechanical action of muscles, tendons and bones to produce a physical action. Your muscles are tight or weak and they influence your movement responses so therefore we need to strengthen or lengthen them to allow the proper responses to occur.

Perhaps our current responses are not being simply constrained by physical parameters but are instead also being driven by previous experiences that shape our perception of current events and therefore the associated response.

As an example we have historically worked on the lengthening and strengthening of muscles to alter things such as posture and apart from anecdotal successes we see little empirical evidence that we can actually alter someone’s posture. The same maybe true of running gait, stretching and strengthening seems to have little effect on how someone runs as the joint ranges and muscular stiffness could actually be pre programmed before the foot hits the floor regardless of the strength of a muscle.

Our muscular responses maybe driven far more by habits that are neurally stored patterns retrieved in response to specific contexts rather than a more physical constraint.

So basically, if I have had previous painful experiences this may shape my future responses.

Situation requires: Raise arm

Subconscious analysis: Raising my arm has caused pain before it may do so again. What can I do to limit or achieve this task another way?

Now my motor response could be to stiffen the shoulder muscles as the arm is raised in response to previous painful experiences regardless of the baseline tightness or weakness of the shoulder muscles, they may tighten in response to a specific context that has been deemed as having a high probability of causing pain. This probability ratio may become higher the longer a pain may have persisted for.

We could also limit the arm moving by increasing actual pain or creating an increase in sensation as an output response.

Part of the point of having a sensory system is to alert the terminal point, the person and their brain, of what is occurring in the body and the threat that that may pose to that individual.

Putting this into practice

 

Lets think about a simple action such as catching a ball and how these predictions may play out. Firstly lets think about this from the perspective of someone who has previously had ‘good’ experiences of catching a ball.

For most of us, especially those that enjoy sports, as soon as we see a ball in a friend’s hand we have associations with this set of sensory information. My previous experiences of playing with a ball might make me happy and we have coupling between happy neurons and the activation of neurons by the visual stimulus of the ball. This is a stored neural pattern.

My brain might start to get together the motor program of catch as a prediction to the visual stimulus, the probability is that the ball is coming to me and I need to catch it.

How about if the ball was thrown in my face last time round?

My association with the sensory input maybe entirely different. Suddenly neurons associated with fear and apprehension are activated. Neurons associated with the sympathetic system and stress responses light up. My motor planning areas might create a step away from the ball or the action program of protecting my face. The same visual stimulus might create very different predictions in a number of interdependent sub systems based on previous experiences.

Now take my son when he was small. I picked up the ball and went to throw…..and got nothing. No motor program of preparing to catch and the ball just bounced off his chest when I threw it to him.

Why?

Simply he had no memory to draw on to create a prediction of outcome, this has to be learned. He has to learn what the visual stimulus of the ball means and what he has to do, my job is to provide happy learning experiences for him to learn from!

So even though catching has a unique pattern of muscular activation dependant on ball trajectory and force, this being current information to process, the activation and movement outcome, or prediction, may also be influenced by my previous experiences to create the perceived best (maybe?) result.

Is this process good or bad?

 

Of course it could be both. It just is!

A prediction could potentially become too ‘overprotective’. If I avoid an action because it has been predicted to be problematic then by no problem arising the prediction has become true. The probability is now that by avoiding it I will not get an adverse outcome.

In an acute injury situation the protective behaviour maybe entirely warranted to protect from further injury. However maintenance of this protective prediction maybe become a problem within itself once an injury has healed.

Can this prediction influence physical factors such as load tolerance?

Again lets put this into a context.

I get pain when I bend over, by not bending over I don’t get the pain. My prediction that bending over is a problem comes true and the probability that it will cause problems in the future becomes greater. My future predictions are thus reinforced.

If I do bend over the active movement components may act by stiffening or by going into spasm as a limiter based on the probability of harm. They may not be calibrated with normal proportional muscular response but instead a maladaptive process with disproportional physical responses. The physical genesis may be long gone but the associated behaviours may remain. The muscles may not be tight or weak in another context.

We are seeing a rise in the use of increased loading during therapy, which is superb and vital to local cellular responses and increasing the ‘zone of homeostasis’ of the tissue. Sometimes we must address the predictive behaviour to allow the physical loading and physical and physiological adaptations to occur in the relevant areas.

Perhaps for some breaking habits is the most important part of any therapeutic approach rather than the physical aspects and also to allow the physical factors to be influenced.

We see prediction used in sport all the time

 

In sport we see the need for prediction as in certain situations it maybe impossible to react. In tennis, as an example, we see the use of anticipatory cues and it has even been hypothesised that an elite tennis serve maybe beyond human reaction times.

This has been discussed as a perception-action process *Click Here*. To have a perception we must have some stored memory of what the physical cue may mean and this is in part shown by the fact the expert performers performed better in tennis scenarios than novice performers but not in non-specific reaction situations.

Interestingly reaction times of expert performers was quicker when playing against a live opponent rather than a machine, again potentially highlighting that increased physical cues that can be associated with stored memory enhanced the predictive process and reaction times

Here is a great video from Daniel Wolpert that discusses similar concepts.

Here are some scenarios were players in sport use the other player’s predictive ability against them.

• In tennis people ‘shape’ to hit the ball in a specific place to send people the wrong way.

• In boxing people feint a punch to draw a reaction so they can counter.

• In football they give the goalkeeper the ‘eyes’ to send them the wrong way in a penalty shoot out

• Many sports talk about players who can 'read the game'. This maybe a better memory-prediction model

Implications for chronic pain

 

This has been looked at with respect to chronic pain with the idea of ‘pain memories’ and I have written about this in detail previously. Meaningful movement, Pain ‘memories’ and Recalibration!

This is where pain associations become stored as neural patterns or ‘memories’ and maybe recalled in the absence of nociceptive signalling from the body perhaps becoming coupled with proprioceptive signals or even motor intentions/planning.

This pattern recognition, perception of associated threat and associated sensory and motor prediction of protection may go some way to explaining some of what we see in the behaviours with chronic pain patients in response to specific movements or movements from specific areas of the body.

Take home's

 

Here are some basic points I feel we can potentially take home from looking at memory-prediction/Bayesian inference models of brain function.

• Context is key for some. Addressing habits and behaviours, not simply muscles, nerves and joints etc, for longer-term change maybe required.

• Create new positive experiences to be stored and retreived. This may influence future predicted behaviour.

• Our Psychological beliefs can affect our movement behaviours.

• Our movement behaviours may affect local tissue tolerances.

“Pain is in the brain” is by far and away one of my least favourite phrases and in my opinion unhelpful in understanding a modern view of pain.

Why….?

Well there are a number of reasons.

  1. It implies (to me anyway) it is not IN the body. This for many people is tough to get their head around, and rightly so.

 

  1. This may also imply that it is “all in my head”. Again not a helpful message for many and could potentially create more problems than it attempts to solve.

 

  1. Has created polarisation. As pain obviously has a good part of its genesis within the body we now get the “pendulum has swung to far” fight back. This is a completely warranted stance against this argument. The problems potentially lie in the perception of those who think that anyone who believes the brain is major player in the pain experience is suggesting pain is all “in the brain”. It is easy to create a counter argument against a polarised opinion.

 

  1. That it is idiopathic and spontaneously erupts. Whilst this maybe true in some isolated cases for many it is a maladaptation of the system in response to a more physical genesis.

 

Human brain

 

 Pain is an output of the brain

‘Pain is an output of the brain’ seems a much more sensible way to explain the pain process in my opinion. This allows a model that incorporates both input from the body and a modulation of that input in the brain.

The more pain persists then the more it may be driven by top down rather than bottom up influences although we must remember that we can get changes, or plasticity, in the nociceptive (noxious stimulus) or danger processing system further down the chain in the periphery and the spinal cord as well.

Stimulus (danger!) processing within the brain can actually be used to turn the output or emergance of pain down as well as up. We have cleverly named ‘on’ and ‘off’ cells in our rostral ventromedial medulla (RVM) that do just that. ‘Off’ cells exert descending inhibition on nociceptive transmission while ‘on’ cells facilitate it.

'Pathological' pain

There does seem to be situations were pain itself becomes more of a pathological process. Phantom limb pain is an example where potentially the mechanism for pain is more about the representation of the limb in the brain than nociceptive signals from the limb and is very prevalent with amputees at between 60 & 80% HERE it is also worth reading Melzack and Katz’s opinion on this HERE

Harris has suggested incongruence between motor intention and movement as a source of pain HERE and sensorimotor incongruence exacerbates the pain of chronic whiplash sufferer’s HERE although this is not a consistent finding HERE

Moseley & Valyaen HERE and Zusman HERE have both proposed coupling between proprioceptive information, pain responses and memory within the brain that no longer requires nociceptive input from the body.

HERE we see that the visual distortion of a limb can actually affect the processing of pain!

These pieces of research and theory help us understand that pain is a complex process and a ‘pain’ signal is not just simply relayed from the body but it also does not mean that pain is only ‘in the brain’.

So if someone was to ask “is pain in the brain?” My answer would be no, it is much more likely that it is a complex interplay between bottom up and top down influences modulated by many factors and that the sensitivity of the systems involved in the experience of pain have the potential to change over time at peripheral, spinal and cortical levels.

Semantics

Some might, and have, suggested that this is simply semantics. I would agree completely with this because semantics matter. How people interpret meaning is a huge great big deal when it comes to pain and to not recognize that is a problem. This is a great paper by Darlow HERE and another by Barker HERE

‘Pain is in the brain’ seems open to being misconstrued by those in pain and also those who realize it has a great deal of its genesis within the body too.

Is the ‘issue in the tissue’?

Is the ‘issue in the tissue’? Well of course it can be, just sometimes a bit more and sometimes a bit less. This does not mean there has to be a pathological state of the tissue however or if there is that getting better is contingent on a change in the state of the tissue. HERE & HERE

Although we are realizing that pain and damage are not one and the same, local biochemical processes are likely to be very much at play. Whilst there may not be pathology we may have a pathophysiological process occurring, this being a physiological process that has gone a bit haywire!

An example might be if I go out and run a bit more than my body is used too and the normal reparative processes, such as tissue regeneration, becomes replaced by a different cellular expression such as pro inflammatory chemicals like neuropeptides. This has been documented with tenocyctes (fibroblastic like cells) as they transduce mechanical force (mechanotransduction) into cellular processes such as the expression of substance P potentially creating a peptidergically driven inflammatory state in the tissue HERE and HERE we see an elevation of substance P in vivo in response to load.

So we may have a situation where the local tissue state is chemically sensitized due to activity, perhaps previously under loaded tissue, and this could potentially be turned up by changes in sensitivity in the systems involved in pain peripherally, spinally or cortically dependent on individual previous pain experiences.

Physical changes in the experience of pain

 Changes in the systems involved in the emergance of pain don’t have to be ‘in the brain’ either. The sub cortical bits can play their role too with actual physical changes occuring to the peripheral nervous system (PNS) within the tissue. These changes to the PNS include an increase in number of ion channels in the terminal endings of nociceptors making it easier to get sodium ions into the cell, depolarise it and send a signal (action potential) to the CNS. We also see an increase in the number of receptors and previously silent receptors becoming active.

The signal processing at the dorsal horn can also be ‘turned up’ with more NMDA/AMPA channels making it easier for the peripheral signals to be sent up the chain and an increase in excitatory neurotransmitters, such as glutamate and aspartate, and a decrease in inhibitory chemicals such as GABA and endogenous opioids.

We can also get long-term potentiation of spinal neurons in response to repetitive stimulation or a sustained ‘volley’ of signals from the C-fibre’s. Basically put the more noxious stimulus we receive the more sensitive the dorsal horn becomes to it.

Has the pendulum swung to far?

That probably depends on your bias and opinion but if someone was to suggest that pain is solely ‘in the brain’ then I would suggest yes it has!

An inclusive model that allows physical, physiological, neurological and psychological processing changes probably fits with what we know about pain at this point in time. Sometimes the pendulum may have to swing big firstly to overcome the inertia of previously held beliefs and then hopefully comes to rest somewhere in the middle.

The human nervous system is a very adaptable place. It is constantly reacting to variable stimulus acting on it/us, simplistically we could describe it as input-process-output system although we have to remember processing is often based around a predictive, or more fancily put a Bayesian inference model.

What this means is that if we alter the input we may get a different output in response.

bayesian_inference

I have read recently much discussion about the CNS being easy to fool and also how we can ‘hack the nervous system’ and in all honesty I am not sure I agree, the CNS is not a computer after all and this to me feels like we imply that, instead I think we probably change the opinion of the nervous system by providing a different temporary input that potentially temporarily alters the outputs. We don’t swap one ‘program’ for another or hit ‘reset’ and go back to factory settings (whatever that may be?) instead the ‘program’ is in a constantly evolving state dependent on the inputs applied. Sure sometimes we get locked in a consistent input-output ‘loop’ but this habit is not often altered permanently instantaneously.

If my output, lets say joint stiffness, is based around the protection of a tissue and I am provided with a bunch of non threatening inputs then my CNS opinion may change to one of ‘we do not need so much protection’ and decrease the output of muscular tension that in turn decreases the joints stiffness. Like most habits the more ingrained it is then the more regularly a ‘positive’ input may have to be applied to change the opinion over the long term.

Is it just distraction?

In some cases this maybe more of a distraction rather than a change in opinion, the novelty and magnitude of an input applied may be far more interesting or noteworthy than the current situation. If I distract the CNS’s attention by providing another more interesting or attention grabbing stimulus then this change in input may alter the CNS output. A distraction may not provide a stimulus to positively change anything long term however.

We can consistently provide distractions without ever fostering an environment for change. How many ‘short-term therapies’ do just that?

distraction

This change in output can often be confused with more than just a temporal distraction and this maybe where we start to extrapolate a touch. Suddenly a new input can be the ‘fix’ to a long standing problem in a far away part of the body and any short term change mistaken for a miraculous missing piece to someone’s complex pain puzzle.

We can make up some fabulous back stories to accompany them encompassing the fascial system, biomechanics and fancy brain based mechanisms. All of these ‘fixes’ rely on short-term changes in range of movement, strength or sensation as a marker of success, things that are all also regulated via CNS output! Change does not imply the change is a good one, merely change, short-term change also does not imply a long-term change or ‘fix’.

We can confuse increases in strength of muscles and ROM at joints as a positive. In back pain sufferers an increase of contraction of the core muscles is associated with ongoing pain states, decreased stiffness and muscle length regulation could actually also be detrimental to controlling movement. Both strength and flexibility are context dependant.

An increase in muscle strength in an area of pain is an outcome variable potentially surrogated for the actual problem and more than likely completely unrelated to a cause.

Lets put this into context.

Someone has a pain in the elbow and a therapist or trainer provides a stimulus to the foot. This travels up the various spinal pathways, dependent on the stimulus, to the brain for processing. Suddenly the elbow may feel different better even, does this mean that the body needed a stimulus specifically from the foot and this is linked to the elbow somehow and THE cause of the problem or more simply the CNS has paid more attention to the information coming from the foot, perhaps more compared to other body parts moving, and has therefore changed its output towards other situations it is regulating in the body?

spinal path

Information burst!

Why would it pay attention to a specific body part more?

Well if we generally have limited movement coming from a joint then the proprioceptive burst of information is going to be new, noteworthy and interesting to the nervous system. We pay attention to stimulus that is new or outside of our predictions that we base on previous experiences. An example would be stepping off a curb that is much higher than normal, we suddenly become aware of this change in incoming information whereas if it were a normal height it would simply not be information worthy of paying attention too and we would walk merrily on unaware. While we are paying attention to this new stimulus the regulation of sensation or stiffness of other areas, especially if the new stimulus is sufficient in duration, might change as they are outputs of the CNS.

It may not be that the two areas are somehow linked and this is THE stimulus someone needs instead it is A stimulus they are paying attention to RIGHT NOW. In fact this level of distraction may change further down the line with the stimulus not creating the same distraction as it now provides less novelty and attention grabbing potential. We see this with soft tissue work, people graduate from foam rollers to harder materials such as kettle bell handles to provide the same level of stimulus that the body/CNS has become used to and no longer has the same effect.

Perhaps the issue that someone had originally has waxed and waned and regression to the mean has worked its magic at the same time and the assumption is the magic was the ‘cure’. This is a great read about why ineffective therapies may appear to work and the real mechanisms that are at play. Why do ineffective treatments seem helpful? A brief review

Proprioceptive information created by movement can also have a ‘gating’ effect on pain with large fibre information such as from A beta fibres inhibiting smaller fibre input from A delta and C fibres that carry noxious information. This is why we rub a painful area and is this theory is known as the ‘Gate control theory’ originally proposed by Melzack and Wall. One of the reason this theory has evolved from its original incarnation in 60’s is it requires a nociceptive input for pain, as does another neurophysiological mechanism ‘descending inhibition’, and why the idea of distraction and changing opinion appeals to me more in some cases. The reason I like the idea of a change of opinion or distraction is because it does not imply there is nociception occurring to be inhibited instead just one input competing with another or an input altering outputs.

gate control

For someone in pain a distraction may be just what they need, where we run into issues is when the input professes to be more than that with all manner of bizarre back stories, tenuous connections and nocibo inducing blame lumped on various body parts and systems.

Painful therapies or inputs may do something very similar. Foam rolling or a painful sports massage has temporal effects. They make you feel better, or different, but generally in the short term. So let’s say I feel stiff and tight after a hard workout the day before and decide a good foam roll is going to make me feel better. While I am rolling it really hurts, god it hurts, but suddenly I feel a hell of a lot less tight after, could that simply be that that my CNS is paying attention to the NEW painful sensation caused by the foam roller? It is a greater stimulus newly applied and simply overrides the previous sensation and in response to a different input also changes its sensation output.

This input could also alter muscle extensibility and ROM that is also regulated in part, certainly acute changes, via CNS output. One of the regulators of muscle length is how it feels, you stretch a muscle it feels tight and you stop as that sensation builds. If you have a greater sensation competing for attention or distracting the CNS then the regulatory sensation may simply feel less in comparison or the regulatory output has been altered in response to another competing input.

It could be akin to a child selfishly holding on to a ball until someone offers them the distraction of chocolate. To eat the chocolate they must let go of the ball but they may still be a selfish so and so, their behavior has not been fixed they have been merely distracted.

We do have other mechanisms occurring as well with painful stimulus such as DNIC (diffuse noxious inhibitory control). This is where a strong noxious stimulus causes nociceptive neurons to send impulses to the caudal medulla that triggers an efferent inhibition of nociceptive neurons or more simply put pain inhibiting pain! We would however need nociception to be occurring.

Perception, expectation and inhibition

If I have previously had good results from a certain therapy or input then I might expect good results again. My expectation might drive my CNS to take a positive view or opinion of what is occurring. It maybe that the environment or person I am dealing with induces a positive input and a positive output. You feel comfortable, relaxed and safe making your CNS put a positive spin on events.

It could be just the opposite with a cold horrid waiting room and a nasty doctor or a previous bad experience with a dentist, therapist or trainer that changes my CNS opinion or processing of an event with anxiety rising heightening the attention to or processing of any potentially damaging stimulus.

Pain relies in part on the balance between the amounts of endogenous (internally generated) inhibitory chemicals floating around your nervous system versus the amounts of chemicals involved in facilitating the pain experience rather than just a simple causal relationship.

The periaqueductal grey (PAG) can send inhibitory impulses from the brain stem to the dorsal horn via the ventromedial medulla (RVM) and dorsolateral feniculus. The PAG receives inputs from the hypothalamus, cortical regions and the limbic system so these impulses could potentially be triggered by any of the processes arising from these brain areas associated with actions such as sensation, movement, emotion and many more. Within the RVM there is thought to be ‘off’ cells that exert a descending inhibition and also ‘on’ cells that facilitate nociceptive transmission and this has been implicated in chronic pain states. With nociceptive facilitation and sensitization of peripheral receptors we may achieve encoding of nociceptive signals with what would normally be a non-noxious stimulus. We have chemicals such as endogenous opioids and GABA that have an inhibiting effect on pain and also aspartate, glutamate and NMDA that have a facilitating effect. It is certainly not all about nociception however and we can have inhibition and facilitation of the pain experience within the brain as well and not just during nociceptive transmission.

So the nice therapist comes into the relaxing room and gives you an (potentially bullshit) explanation for why no one has been able to help your pain and confidently reassures you that they have the answer. You feel understood and a glimmer of hope rises. Your brain starts pumping out chemicals that may dampen down your anxiety or may cause inhibition or decreased facilitation of any potential nociceptive signaling. Your chemical balance swings towards the ‘negative’ potential for pain. They apply a painful stimulus or burst of new and novel movement information for you and your brain to deal with and suddenly your painful XXX feels different, better even. It feels looser or stronger perhaps. This is awesome but please don’t confuse this change or distraction with a fix.

Whilst short term success is obviously a positive lets not forget it can often be long term changes in behavior that get the greatest successes.

Below are 4 key points in my opinion that can be overlooked when using exercise and movement therapeutically.

Relaxation/freedom

 

Tai chi

Therapy based exercises are generally about getting INCREASED activation, creating more strength and sometimes also getting an earlier onset timing of a muscle. This is can often described as increased 'firing' and if I had a pound for everytime someone said to me 'I have been told my glutes aren't firing' I would be a rich man!

The more we study the movement of people during and post pain the more we tend to see it can actually be an INABILITY to relax and turning muscles OFF, not sure we turn them off or on like a light switch but fits with the concept people seem to have, and stop them from firing so much.

A recent paper from Paul Hodges group found exactly this Gain of postural responses increases in response to real and anticipated pain

In this study when both a real and noxious noxious stimulus was introduced to the task we see an increase in muscle activation.

"Muscle activation was earlier and greater than that required for the task and is likely to create unnecessary joint loading. This could have long-term consequences if maintained"

This was also true of those experiencing back pain in Spine loading characteristics of patients with low back pain compared with asymptomatic individuals

"Patients with low back pain experienced 26% greater spine compression and 75% greater lateral shear (normalized to moment) than the asymptomatic group during the controlled exertions. The increased spine loading resulted from muscle coactivation"

What can we take from this?

Often the goal of an exercise is stiffness, precision, control, attempting to perfectly target a particular muscle but in many cases someone may need relaxation & freedom to allow the natural variation and flow that characterises healthy human movement.

Simply put, people in pain have altered movement. This will have implications for movement assessment and also how we get people to move when thinking therapeutically to restore relaxed and truley free movement.

Relevance

 

This was a piece of research that went well under the radar “Patient led goal setting in chronic low back pain-What goals are important to the patient and are they aligned to what we measure?” perhaps because it challenges current practice?

The results of the study found that NONE of the patient goals were aligned with common measures used by physiotherapists. The traditional measures were pain, strength and ROM.

A criticism of the paper would be none of the patient goals were described but perhaps these were goals related to specific activities such as picking up their kids or tying shoe laces without back pain that would be important to people and the quality and hapiness of their lives.

The more we understand about the psycological aspects of therapy the more important pieces of research like this become. If your measure of success is different to that of your patient then what you regard as a good outcome may not be seen in the same way by the person who really matters.

Even if we are thinking more about physical factors such as biomechanics, neurodynamics or muscle function all these things will have an element of specificity and relevance to them if thinking about a specific patient goal.

In fact working on individual biomotor components such as strength and flexibility seem to be unrelated to and have little effect on specific movements.

This study - Frontal plane kinematics of the hip during running: are they related to hip anatomy and strength? found that the kinematics of hip adduction during running was NOT associated with hip abduction strength.

This study - The effect of a hip-strengthening program on mechanics during running and during a single-leg squat found that a hip strengthening program did not alter running mechanics.

This does not mean that loading via a strengthening program, that may or may not alter strength, will not have an effect on load tolerance or have an effect on pain but will not alter a movement if that is the desired outcome. This is explored more in this blog Strengthening the most overused term in rehab?

Ranges of motion that are aquired through flexibility training do not automatically improve movement in general. In Improvements in hip flexibility do not transfer to mobility in functional movement patterns the authors conclude:

"This implies that training and rehabilitation programs may benefit from an additional focus on 'grooving' new motor patterns if newfound movement range is to be used"

It could be argued that a focus on just moving with larger ranges would kill two birds with one stone if the movements themselves were relevant to those looking to be improved.

Is a positive clinical outcome after exercise therapy for chronic non-specific low back pain contingent upon a corresponding improvement in the targeted aspect(s) of performance? A systematic review found that there was little supporting evidence that changes in the performance measures of mobility, strength or endurance were directly attributable to positive treatment effects for exercise in lower back pain!

Perhaps an approach that uses relevant movements and provides a stimulus through inputs such as external cueing that help the motor system to develop more movement options involving adaptability, tolerance and variability seems a pragmatic one!

Thoughtless/Fearless

 

How many peoples pain is exacerbated by a fear of reinjury that can also hinder the recovery process? It maybe that the physical area of the body has fully healed but the motor and sensory responses are still stuck in a more protective mode because of the psycological aspects that can become associated with the pain experience.

A fear of reinjury can negatively affect peoples recovery and we see a high level of kinesiophobia after ACL injurys as an example Kinesiophobia after anterior cruciate ligament rupture and reconstruction: noncopers versus potential copers

People often identify with having a 'bad' knee or 'dodgy' back and may actively seek to avoid activities that put undue perceived stress and strain on that area. Vlaeyen wrote this great paper back in 1995 on the topic of fear avoidance. The role of fear of movement/(re)injury in pain disability By avoiding certain activities, peoples beliefs about their body parts are reinforced and therefore they further avoid these activities.

On a physiological level this may mean that these areas develop low tissue capacity and deconditioning due to lower work needs. Low capacity may lead to an area becoming easier to overload and perhaps more susceptible to future pain.

Protective motor responses driven by fear behaviours, similar to previously discussed in relaxation section, can interupt natural phsyiological processes within the local area such as bringing blood to the tissue and taking away waste products. This could lead to acidosis and increased mechanical nociceptor sensitivity further driving perceptions of sensitivity and avoidance behaviours and beliefs.

Hypervigilance, an enhanced state of sensory sensitivity, may be applied to a specific area that has been identified as being 'at risk' and can be accompanied by anxiety of future reinjury and the subsequent implications for work or family life.

A key concept within a therapeutic movement approach is to use a graded exposure and progressive load based approach to both physical and psycological desensitisation. The aim being a thoughtless and fearless return to functional activities. Reaffirming positive movement outcomes is a key to reducing negative beliefs that can be held about movement.

Variability/Variation

 

Variabiltiy is inherent in a biological system. I wrote about this in detail here Movement variability & its relation to pain and rehab

This natural variability of movement is both affected by and could also be a cause of pain. This recent paper Interaction between pain, movement, and physical activity: short-term benefits, long-term consequences, and targets for treatment highlights some of the new theories emerging about the relationship between pain and movement. Approaches to exercise, in both the therapy and performance worlds, are often about decreasing variation to increase impact on a target tissue or movement. This may be good for hypertrophy and work capacity but is lacking in addressing a key aspect of a well documented motor system adaptation to pain that should form a target for exercise for rehabilitation.

Moseley and Hodges identified a decrease in variability as a risk factor for developing chronic low back pain. Reduced variability of postural strategy prevents normalization of motor changes induced by back pain: a risk factor for chronic trouble?

This paper Low back pain status affects pelvis-trunk coordination and variability during walking and running could identify from walking and running analysis of variability which participants had no back pain, one incident of back pain and long term back pain.

Their conclusion was:

"The data lend insight into increased injury risk and performance deficits associated with even one bout of low back pain, and suggest that clinicians need to look beyond the resolution of pain when prescribing rehabilitation for low back pain"

One of my favourite motor theories is that of 'The equilibrium-point' described by Feldman.

Latash elquently describes this in Motor Control Theories and Their Applications.

"This allows control levels of the CNS to specify where, in spatial coordinates, muscles are activated without being concerned about exact details on when and how they are activated"

So the CNS may set movement parameters whilst leaving the temporal coordination at a peripheral level to be self organised/optimised and thus variable. This has been hypothesised to be via the gamma motor neuron and feedforward/back mechanism invloving the muscle spindles.

If the parameters are set to tightly by the CNS then this may reduce the amount of variability available to the system and the ability to be able to adapt to changing stimulus.

One of my hunches (perhaps not a good thing for science!) is that the parameters may be set via interaction with the cortical map for a specific body part and also previous movement/pain experiences but this is certainly not proven!

How do we use this infromation in the trenches? Well a range of different movement patterns and variables should be utilised during a therapeutic exercise program to provide different stimulus for the person to deal with and adapt to. Much the same as they would have to away from a clinic or gym environment.

Find out more about a 'Funtional Therapeutic Movement' approach

I was driving my son to nursery this morning when I started to feel an intense burning pain in my lower back area.

That’s weird I thought why has that just started? I could not really pin point what or where the sensation was and it seemed to be spreading rapidly.

I went for a run yesterday did I irritate it then?

I also did a fair amount of sitting at the computer, did I hurt it doing that?

Then I thought about what that might mean.

I hope it does not last all day?

Will it stop me from running or working?

The burning seemed to actually intensify.

 

Lower back pain in woman isolated on white

When I got out of the car I felt around my back area and there was a big scratch there. I don’t recall doing it or where I could have done it. The burning of course was just an immune system response to minor tissue damage and I had a bunch of inflammatory chemicals floating around down there going to work and fixing my tissues.

Immediately I was relieved. I could put a meaning to the sensation. I could pin point the pain to exactly where the scratch was. It felt like lots of other scratches I have had before. I knew that the scratch was just an irritation not anything to be worried about.

I class myself as being reasonably well informed about the ins and outs of the pain experience. Still without reasoning, logic and experience to put a context to the pain it caused my brain to go into irrational overdrive about why it had happened and what that was going to mean for me.

It really helped me consider and empathise with what maybe happening in the brains of people that have no understanding of the mechanisms.

How about if their brain is full up of other peoples experiences with pain and the negative impact it has had on their lives?

What if it is filled up with internet logic about crumbling discs etc or they go and fill it with internet logic searching for answers to why they have got the pain and the prognosis? Perhaps even what they are told by their therapist or trainer?

This reminded me about how much all the other stuff associated with pain must affect people and the experiences that they go through when in pain. How this is probably heightened if our previous pain experiences have been disabling and the meaning and impact that has on someone’s life.

My back is still hurting as I am writing this but I am not worried.

This is another little short blog on the theme of lower back pain and is a follow up to another popular post from a couple of weeks ago that can be found below.

Exercise for back pain works but maybe not in the way we think it does!

One of the long-term theories of the cause/resolution of back pain is that of 'core stability'.
The deep core muscles such as the TvA are meant to fire or activate at a specific time to create stability for the spine and stop apparently damaging ‘micro movements’. I am unsure why micro movements would cause more damage than bigger movements but I will leave that to much smarter folk than me!

core stability

The theory is that the TvA contracts bilaterally or directionally independent to stabalise the spine locally (in conjunction with some other muscles although focus has always been more on TvA) and works differently to the other core muscles that are seen as more ‘global’ and actually create specific movement. This was based on Hodges et al original work on the TvA in the mid to late 90’s and has massively influenced training, injury prevention and rehab over the last 20 years.

In the original work of Hodges the onset of TvA activity was delayed in those with back pain compared to controls by 20ms or a 50th of a second with a rapid arm raising task. Firstly we do not know if this is a cause or an effect of pain, the inference from this data seems to have been that it is a cause. Can we make this conclusion from subjects already in pain? Secondly the original work was performed on a unilateral TvA and has been extrapolated to a bilateral theory of a muscular corset stabalising the spine and lastly is this delay even significant mechanically?

Does the TvA work bilaterally to stabalise the spine as we have been led to believe by theorists across the worlds of training & therapy or do they work specifically according to functional activity like most muscles?

That is exactly the question that the two papers I am going to look at below asked!

Firstly we have:

Feedforward Responses of Transversus Abdominis Are Directionally Specific and Act Asymmetrically: Implications for Core Stability Theories 2008

The inclusion of the conclusion in the title always ruins the suspense and as you can read these authors found that the TvA firing was both asymmetrical and directionally specific.

The paper firstly points out that earlier research data was not congruent with the 'muscular corset' theories formed from Hodges original work with regards to TvA activity.

So what did the data say?

Well when the subjects raised their right arm the ipsilateral TvA on the right side lagged behind the activation of the TvA on the contralateral side, the left. The activity was clearly asymmetrical and specific to movement being performed and the direction that the stimulus on the trunk was coming from.

Just so we don’t chalk this up to methodological errors the authors state:

 “Furthermore, because the laterality responses of the respective sides of the TrA muscle are replicated for left and right arm flexion perturbations, and repeated across time, the findings can-not be attributed to signal amplification or in vivo errors in fine-wire placements”

 Interestingly they also studied the rectus abdominis with the same arm movements. The rectus abdominis is seen as more of a ‘mover’ muscle with the ‘core stability’ theory but it displayed hardly any laterality at all, activating in a similar fashion for both left and right arm movements.

Another study in 2012 found exactly the same thing.

Corset hypothesis rebutted--transversus abdominis does not co-contract in unison prior to rapid arm movements.

Again another conclusion in the title not allowing me to build anticipation! This study found pretty much exactly the same thing. The movement of the arm created a rotational force on the spine and in response we see asymmetrical TvA activity. The contralateral (opposite side) TvA kicking in before the ipsilateral, TvA function was significantly related to which arm moved.

The authors conclude:

“the “corset hypothesis” for TrA bilateral co-contraction is refuted. The same techniques were used in this study as the original work forming the basis of the “corset hypothesis”

“It is only by studying muscles on both sides of the trunk that a true picture of reciprocal and co-contraction can be developed. The methods used in this study refute the original hypothesis that bilateral feed forward co-contraction of TrA is a normal strategy during rapid arm movements”

The authors felt that training the core to act independently and bilaterally would actually disrupt normal movement patterns and the function specific activity of the core muscles. Many of our functional activities are asymmetrical running, throwing, kicking and reaching are some examples and bilateral TvA activity could be unnatural and disruptive.

We have problems from both ends for a 'core stability' approach. The theory is not supported by the data and equally the efficacy of the approach based on the theory is far from promising.

Think about how many training and rehab methods that use these type of exercises and a corner stone to their approach. The point of having evidence is of course to use it and perhaps these two papers have been brushed under the carpet a touch!

 

 

 

 

 

 

 

 

 

 

Exercise for back pain seems to be reasonably positive for an issue that is fairly problematic across healthcare as a whole. A recent systematic review including a meta analysis found beneficial effects for pretty much all exercise types *Click Here* Some exercise types such as Pilates have been touted as superior but this does not seem to be the case according to a recent Cochrane review *Click Here*

I wanted to focus on two pieces of research into lower back pain that got me thinking about the way we focus on back pain and therapeutic exercise in general. Both seem to have flown a little under the radar but in my humble opinion have profound implications for how we view therapeutic exercise.

Firstly we have a systematic review from 2012.

“Is a positive clinical outcome after exercise therapy for chronic non-specific low back pain contingent upon a corresponding improvement in the targeted aspect(s) of performance?
A systematic review”

This paper looked at exercise therapy trials for cLBP. They wittled down 1217 studies from the initial search to 13 RCT’s (randomized controlled trials) and 5 non RCTs that met the inclusion criteria.

The aim of the review was to find out if the evidence contained within these trials supported the change in pain of the subjects with the targeted aspects of physical function after exercise therapy. The aspects of physical function were mobility, trunk extension and trunk flexion strength and back muscle endurance.

back pain

The point from the researchers perspective was that studies report if an exercise intervention for cLBP has an affect on key out come variables such as pain or disability but not if the outcome is actually tied into the targeted aspects of the exercise program.

10 studies explored the relationship of changes in pain and sagittal (flexion and extension) mobility. 7 found not correlation but did not provide supporting data and 3 found no correlation with data. The authors performed a meta analysis of this data and found total correlation was very low between changes in mobility and changes in pain.

9 studies and 5 studies respectively explored trunk extension and flexion strength. A meta analysis of the available data showed no significant correlation between changes in pain and strength.

Muscular endurance was explored in 7 studies none showing a correlation but without reporting specific correlation coefficients.
The correlations between disability and strength and mobility were also pretty underwhelming.

The authors stating:

“We conclude that the available literature does not appear to support a convincing association between changes in clinical outcome and changes in physical function after exercise therapy for cLBP”

“The findings do not support the notion that the treatment effects of exercise therapy in cLBP are directly attributable to changes in the musculoskeletal system. Future research aimed at increasing the effectiveness of exercise therapy in cLBP should explore the coincidental factors influencing symptom improvement”

So people can get better from exercise, we know that moving works but it may not mean that they are weak or inflexible and this is the cause of their back pain or working on this cause is the remedy to their problems. The authors here feel that the effects of exercise maybe more down to ‘central’ rather than ‘local’ changes such as psychological, cognitive or neurophysiological adaptations.

These would include changes in movement patterns and sensory input, alterations in cortical representations or body ‘schema’ and positive therapist/patient interactions. It could also involve decrease in fear avoidances and catastrophising behaviours.

I don’t think we can discount basic physiological processes associated with moving such as increases in blood flow and the effects of simply moving more on people’s general systemic health or increasing someones 'zone of homeostasis' to activity which could be on a local cellular level or more CNS based.

Another potential issue is how does telling people they need to ‘strengthen’ affect their perception of their capabilities? For many it could imply they are weak to begin and therefore at increased risk which may or may not be true but is often under quantified instead being assumed.

As I have discussed before many therapeutic exercises do little to strengthen but do involve moving more! *Click Here*

I think this paper questions how we view exercise and the potential mechanisms behind why exercise works.

Secondly a short paper on goal setting.

“Patient led goal setting in chronic low back pain-What goals are important to the patient and are they aligned to what we measure?”

This paper identified 27 unique goals from 20 participants with goals relating to physical activity being by far and away (49.2 %) the most common. The second common goal was work place related at 14.29%. I do feel this paper would have been strengthened significantly by the inclusion of some examples of what these goals were so we could get an idea of the functional activities that people found important. I suspect they would be related to things such as tying their shoe laces and picking their kids up. These are important relevant and meaningful goals that are perhaps under explored in relation to more clinical variables such as strength and range of motion (ROM). Although they may include aspects of physical performance they often are not resolved simply by working solely on these components in isolation without relevance.

The results of the study found that NONE of the patient goals were aligned with common measures used by physiotherapists. The traditional measures were pain, strength and ROM. The argument here would be that these traditional measures would go towards enabling patients to be able to achieve their goals but again this maybe an assumption. If you feel someone has achieved your success measures then their success measures maybe less relevant.

The authors state:

“Clinical outcome measures may not be providing accurate information about the success of treatments that are meaningful to the patient. Clinicians should consider a collaborative approach with cLBP patients to determine treatment interventions that are driven by patient preference”

It maybe simple to help someone experience less pain, an example would be telling someone to avoid bending over if they experience back pain doing so.
One perspective of success is no pain from bending over – Goal achieved. Another perspective would be being able to bend down to do my shoe laces again– Goal not achieved. A reduced measure of pain does not simply imply success in the eyes of another party. Maybe people would even be willing to put up with a larger amount of discomfort coupled with a greater functionality rather than no pain and a sense of disability?

Both of these papers I think challenge a traditional view of therapeutic exercise and the mechanisms behind positive outcomes. The more we understand about the mechanisms the better we can design the exercise parameters. The use of strength or ROM measures do not align with peoples goals nor is recovery dependent on these measures changing.

Perhaps success cannot always be quantified with traditional measures and ultimately the success of an outcome lies not in these measures but the perception of those that the therapeutic exercise is being applied to. I am going to go out on a limb and say these results could apply to other parts of our anatomy also!

In my opinion dosage, relevance (even if it is perceived) and enjoyment maybe the key factors in moving for those with cLBP. I would love to see those variables explored more.

When you delve into looking at how people move you will soon encounter the murky concept of what is ‘correct’ or ‘good’ movement. This is generally coupled with strong beliefs in these concepts that are hard to shift regardless of the evidence.

Alberto Brandolini sums this up very nicely:

"The amount of energy necessary to refute bullshit is an order of magnitude bigger than to produce it”

While I do not agree that the idea of being able to define ‘good’ movement is total bullshit it has certainly proved to be an elusive endeavor and is very unclear so far. Based on the available evidence it would seem the best we can do in terms of rehabilitation and helping people move whilst in pain is to simply get them moving…. DIFFERENTLY.

think

A recent look at the FMS *HERE*, a system that attempts to provide criteria for ‘good’ movement and associated injury risk for ‘bad’ movement, found that the average score of the 74 athletes who got injured during the course of the study was 14.3 for the screens performed. The 93 uninjured athletes scored….wait for it….14.1 a whopping 0.2 difference.

The only movement pattern associated with injury was the in line lunge. The athletes who scored a 3 (the best score) were MORE likely to get injured than those that scored a 2! That is the more rigidly you can stick to what is perceived as a ‘good’ movement the more you are likely to get injured. In fact those scoring a 0 or 1 (the worst scores) showed no association with injury.

Moving IN pain

Any movement assessment of someone IN pain may only be a reflection of their response to being in pain NOT the reason why they have gotten into pain. This basic reasoning process is often not considered and provides a great rational for a movement change to off load an irritated tissue or to decrease maladaptive responses such as muscle guarding and stiffness later in a rehabilitation process. ANY movement can be used a screen or assessment for this purpose, the more relevant to the individual the better!

Movement assessment should focus on how you are moving RIGHT NOW regardless of whether that is right or wrong, especially when in pain, to give an indication of what to change and how to change it. Decreased ability to move differently and have other movement options has been associated with the transition from an acute injury to chronicity *HERE*. Decreased variation is strongly associated with chronicity when we use non-linear methods to assess movement *HERE*

Good movement, in my opinion, could be characterized by having movement options and bad movement could therefore be defined as having a lack of options.

One of my favourite sayings is:

“All exercise is movement but not all movement is an exercise”

Simply this means that any exercise can be adapted and altered to provide a less painful movement or movement can be used that does not look like ANY traditional exercise. Simply altering foot positions in a squat or a lunge will adjust femoral orientation in the acetabulum and provide a different stimulus to both the tissues of the hip and the CNS for a different response - hopefully less pain. All of these positions should be available within our movement repertoire for a sizeable capacity and available options to deal with varying situations and stimuli. We specifically adapt to the stimulus we are exposed to and therefore are more able to deal with the same stimulus in the future.

dead

People are often uncomfortable with moving away from the exact invariant blueprint of how they have been taught or believe an exercise should be performed. Maybe it won’t target the same muscle or they believe it is less safe? If we look at less contrived movement such as in sport you will often move into these variations multiple times during a game. In fact you may not ever use the version you have practiced in the gym!

In a pain situation the aim may simply be to move with less pain rather than targeting a specific muscle to make it stronger. I would hope we are now moving away from a single muscle weakness as a cause of pain or biomechanical ‘dysfunction’

The more you move in the same way with pain the more you are likely to trigger the same response. The painful movement could look like ‘really good’ movement and ‘really bad’ movement could be pain free. We need to get MORE comfortable with being able to adapt exercises and movements to the person rather than shoehorning them into an ‘ideal’ version of an exercise.

Why does moving differently cause less pain?

Lets first think about what is going on in the tissue where it hurts although of course we cannot forget that the brain will also play a role in the modulation of any signal coming from the periphery. The science, which we will take a basic look at, is as important as evidence but less sexy it seems!

Secondly and perhaps more important when dealing with people in persistent pain states we must also consider associative learning and the coupling between non noxious proprioceptive stimulus and a pain response as well.

Nociceptors that encode high threshold noxious stimulus, or more plainly put danger signals, become MORE sensitive during bouts of prolonged firing and this decreases the amount of stimulus that is then required to activate them. They can be poly modal meaning they respond to a number of stimuli, heat, chemical and mechanical stimulus can all cause them to fire. All of these can be present during pain and inflammation.
So for a start simply moving in ways that have less impact on these afferent sensory neurons is a great place to start. Even finding joint positions that are less painful and can tolerate isometric loads can be a good way to stimulate an area to adapt without irritating it.

These first order afferent sensory neurons synapse in dorsal horn where the second order neurons are stimulated and throw the information upstairs to the brain. Prolonged stimulation via an impulse barrage from the periphery can cause increased excitation of the spinal cord neurons that may start to increase their receptive field; this activity can also start to excite neighboring synapses as well. This is often referred to as ‘wind up’.

Dorsal horn

Even in an acute pain situation these changes in the central processing of pain can alter or may have been altered by previous painful experiences. We often associate central mechanisms with more chronic pain states but central mechanisms will always be involved in any pain so the possibility of more central involvement is always present. If someone has had a history of pain refractory nociceptors that have previously been quiet or silent may subsequently become more active and add to this process. We may also have receptors that previously had a normal sensitivity state that now are more sensitive to future stimulus.

Once these receptors are turned on they may stay switched on for a while or never totally switch off. C fibre information travels slowly due to the lack of axon myelination so signals from the peripheral terminal endings may take some time to get to the CNS and then also some time for any inflammatory responses produced by the cell body or dorsal horn to get back down there. So as more C fibres wake up and start signaling then this probably goes some way to explaining why pain often hurts the next day and can carry on for a bit afterwards. This also helps us to understand why that fine line can sometimes be crossed in rehab when we do a bit too much in a session and it is not until the next day we become aware that the threshold has been crossed and triggered the alarm.

Part of making the alarm system of pain better, often a maladaptive response, is making the sensors more sensitive to better detect a stimulus. Once we understand this it makes complete sense why pain can easily be triggered in some people especially if they have a history of pain or injury.

Essentially some peoples CNS’s get very good at being in pain! So pain is very easy to trigger and because it is easy to trigger people become both aware and wary of this. We see this with hyper vigilance and fear avoidance. Being able to find pain free movements with these people becomes of huge value far outweighing if it is the ‘right’ exercise performed in the ‘right’ way. If we can also make movement relevant to the person then the psychological value is going to be significant. Fear avoidance is in part is maintained by avoiding perceived pain situations and therefore not getting pain, the relevance of movement and the dosage of how we interact is paramount. Not addressing relevant movement may sustain the problem.

The whole idea of helping people move differently and with less pain is to maintain moving while not triggering or adding to their current pain state. Getting comfortable with an idea of the biochemistry being a factor as much as the biomechanics is a step in the right direction. We can in fact use different mechanics to drive different chemical reactions.

Movement is good!

Movement also promotes basic fluid dynamics that can take away the nasty stuff and bring in good stuff so not moving is generally not the answer. Movement is also analgesic *HERE* An increase in corticomotor output promoting descending inhibition and an increase in endogenous opioid production have both been discussed as potential mechanisms. The more inhibitory chemicals we have floating around the spinal cord the less sensitive it is likely to be, this includes chemicals such as GABA and endogenous opioids. This top down inhibition can influence what’s happening physiologically within the tissues and even simply having positive associations with movement may have an inhibitory effect on pain.

Stiff tight muscles and complete off loading may only add to the problem. We have acid sensing Ion channels (ASICs) and TRVP1 channels in our receptors that both sense decreased PH caused by ischemic tissue states arising from prolonged positions or postures and this may add to increased local sensitivity. Using our bodies as normally as possibly will also reduce deconditioning and maintain movement ranges and tolerances.

Sensitisation

It is not just the CNS that can become sensitized. The peripheral neurons can also become more sensitive by manufacturing more Ion channels up in the cell body and then popping them down to the terminal ending in the tissue. This increase in Ion channels makes it easier for more positively charged stuff outside the cell to get into the cell to depolarize it and then send a signal up towards the CNS. These could be mechanically sensitive to stretch or ligand chemical receptors. Ligand receptors have chemical receptors built into the ion channels that open in the presence of specific chemicals such as are present in inflammation.

When the afferent sensory C fibres fire their orthodromic (towards CNS) message off to the dorsal horn they can also causes an antidromic (towards the periphery) impulse back towards the terminal ending and associated tissues, this called neurogenic inflammation. This stimulates the release of neuropeptides including substance P and CGRP that further irritate the local area causing things such as mast cells to degranulate releasing histamine and serotonin creating a pro inflammatory and nociceptor sensitizing soup. In between the orthodromic firing somehow the cell can also manage to send a barrage the other way as well. What a busy bunch of neurons! We can have central to peripheral activity from the dorsal horn as well through the dorsal root reflex.

This process will be certainly be influenced by people’s individual nervous systems, physiological responses and previous pain experiences that may have altered their physiological responses.

So essentially a mechanical force could create an noxious afferent signal towards the CNS also triggering a local inflammatory response further sensitizing the chemically sensitive receptors or receptors that are affected by both chemical and mechanical stimulus thus making them even more sensitive to movement. A loop hopefully broken by finding some pain free movement.

This is all getting quite complicated by hopefully should give us an idea that getting people moving and simply moving differently to the way they are right now rather than any ‘right’ way will probably help out with all the pain biochemistry going on in their tissues or the changes that can occur further up at the dorsal horn by stimulating different tissues and receptors. We can desensitise by not further sensitising through repetitive receptor stimulation as well as also stimulating the descending good stuff!

Non nociceptive mechanisms

Hypotheses are now emerging that look at the association of non-nociceptive information and pain. I have previously discussed the concept of pain memories in more detail *HERE*

With this line of thinking we have the association of two encoded stimuli, one being pain and the other specific proprioceptive information generated via a specific movement. Over time they may have become coupled in a neural pattern and the proprioceptive information can become a stimulus for a conditioned pain response. No actual noxious stimulus is now needed to elicit a pain response. This makes a lot of sense with reagrds to conditioned fear and apprehension behaviours present in lots of persistent pain sufferers that have experienced pain that far outlasts weighs tissue healing times. These ideas are certainly not new in the world of emotional research where they look at conditions such as fear conditioning.

neural pattern

Moseley and Vlaeyen *HERE* have put forward the ‘imprecision hypothesis’ that discusses how pain can be generated by a wide array of movements and activities. These neural associations between movement and pain can become pretty generalised rather than specific and precise. This means that a stimulus in a similar kind of ball park or of a similar type might start to trigger the conditioned pain response. This can be problematic as multiple loosely associated stimuli can now cause pain. This increased protective buffer probably serves a good adaptive purpose at some point in a more acute stage but less so later down the line when it transitions to being maladaptive.

So here we would hope different movement causes a different proprioceptive input to the CNS that is not coupled with pain and therefore generates a different output response namely no pain!

Although modifying how someone feels is great we cannot forget that pain alters movement as well as tissue sensitivity even after the pain subsides. Both may add to reoccurrence and possibly why the best predictor of future injury is previous injury. Protective movement behaviours should also be dealt with during any rehab process. Not rights and wrongs but instead a variety of movement options and skills should be introduced so the system can adapt by being able to have more variable resources.

Thanks to Butler, Gifford and Shacklock for providing the good science!