Archive for category: Uncategorized

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.

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.

Movement variability has definitely been receiving a bit more attention over the past year or so and coming into more and more discussions about movement. Anyone who has kept an eye on this blog will see it has been mentioned regularly over the past few years. If we explore the research into this area we see it has been a focus in academic circles for a great deal longer although it is filtering down at a glacial rate to training and rehab programs.

Hopefully we are starting to shift our understanding of the human body away from the mechanical and towards more of a biological perspective. This may help us to understand why changes in someone’s posture and ‘imbalances’ in general within the body don’t actually matter quite as much as they would in a purely mechanical system. The tolerances of the human biological system are probably much greater than we give them credit for.

Rage against the machine

Within the paradigm of a mechanical system, seemingly the predominant model taught today, the operation of the body is viewed as a precision machine. If one part of a machine breaks or operates outside of the precise narrow parameters set for it then it spells disaster for the machine as a whole. We often blame deviation from poorly defined ideals and ideal relationships within the body for various injuries and diseases when often they do not have clear correlations.

Pain and its relation to posture would be a perfect example of this, as would concepts such as ‘overpronation’ and muscle firing patterns and timings. Movement is just the same, there are not many ‘right’ ways to move that have been objectively defined and can therefore be blamed, instead we have wide parameters of what we can consider ‘normal’.

Humans are simply not like machines, they have a wide variety of ways in which they operate as well as different tolerances, adaptation and rates of adaptation. Metal will have a finite point at which it breaks whereas the body as a biological organism can adapt and increase its tolerances. Wolff’s law is a perfect example of this, as is going to the gym! Sometimes we can exceed these tolerances though as well as asking too much of our adaptive mechanisms.

Variations within movement have been traditionally viewed as ‘error’. These ‘errors’ are seen as redundant, no longer needed, and in the traditional model of motor control through practice this error is hopefully eliminated. A quite different view is now being put forward with the concept of motor ‘abundance’, the redundant elements now being seen instead as positive aspects of physical capacity to be utilised and indeed vital for movement.  This paper “The bliss (not the problem) of motor abundance (not redundancy)” from Latash *Click Here* outlines this new view superbly.

When we are taught exercises we are shown the ‘right’ technique that has been designed to target a muscle based on the fixed ‘correct’ way a muscle contracts based on its static anatomy. The exercise is designed to be repeated, rigid and invariant for a specific outcome. A specific unvarying overload is the aim with the outcome of making something bigger and/or stronger. If movement is variable then so must muscle function be to! This basic reality is left out when we are taught about anatomy and movement, perhaps it is too complex for the mechanical model!

Bernstein’s original studies in the 1930’s into Blacksmiths striking a chisel with a hammer found experienced task-based workers to display “repetition without repetition”, the striking and hammer trajectory displayed low variability vital to a stable repeatable performance. The end point of the skill was the same but the joint angles and segmental variability was high.

This segmental variability is called the coordinative variability *Click Here* This is vital to an ability to maintain performance and not break down due to the specific overload a repeated performance of a skill may incur. This would be very relevant to running for example and decreased variability and patellofemoral pain is discussed *Click Here*
The runners in the PFP group displayed tighter coupling (less variability) between segments whereas a looser coupling was the norm in the healthy group.

Seay et al *Click Here* found differences in variability between groups who had suffered on going LBP, single bouts of LBP and those who had never suffered LBP. The differences in variability between those injured, recovered from an injury versus those never injured may gives us valuable insights into elements that may need to be focused on in rehabilitation.

We will discuss this in greater detail later.

Their conclusion was:

“Taken together, 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”

Movement variability is inherent within a biological system. Not only is it inherent it is also beneficial for reducing risk of overload and enabling the ability to adapt to events that occur within our ever-changing environment. Elite athletes cannot reproduce exact and invariant movement patterns repetitively even through hours of devoted practice. The best movers are those that can execute the same stable end point skill but in many variable ways dependant on the constraints and context of performance. It could be that part of being resilient and robust lies in variability. The ability to tolerate load may come in part in the way in which it is internally processed through our coordinative variability.

Movement is often studied and the data homogenised to reflect a measure of the group being studied. We should also look at the inter (between) people and intra (task to task variation) information as well to better understand the wide ranges of movement variability that exists and what this may tell us rather than this vital data being swallowed up *Click Here*

Here is an example of 5 single leg squats collected by me from the same person using wearable motion sensor tech. Each one is subtly different for the measures taken.

As a little self driven experiment try signing your name repetitively 10 times in the same place. How many of them are exactly the same? They will be similar around the same general outline but never exact and this will be a movement you have practised thousands of times.

Vital for rehab

So why does all this matter to rehab?

Simply put pain changes movement.

Lets start by looking at pains affect on movement variability where we find a significant relationship. Any rehabilitation program should look at the effect of pain on the subsequent function of the individual. Targeting deficits in functionality that are highlighted by research should be regarded as ‘best practice’ during rehabilitation.

Adaptations to movement during a pain state can often be beneficial; a limp is a great example of that decreasing the load to the injured tissue through changing movement patterns. These changes may not be only in a specific pattern of avoidance but also the speed, range and variability of movement. The system can create ‘protection’ through increasing mechanical stiffness and decreasing the variability of movement the injured area and associated areas go through.

Here is a new paper from Hodges outlining some of these changes in more detail *Click Here*

Here is one of my favourite quotes

"Adaptation to pain has many short term benefits but with potential long term consequences" P Hodges - Moving differently in pain 2011

The problems come when the short-term benefit is no longer beneficial. This can be described as maladaptive. The goal of protection is no longer necessary but no one has come along and told the system that quite yet!
Long term consequence of movement maladaptation at a tissue level can be increased load to certain tissues and deconditioning in tissues being used less thus increasing risk of overload, especially if this strategy now becomes invariant.

On a cognitive level we may start to see factors such as fear avoidance behaviors reduce the variability of someone’s movement. A top down (cognitive) based approach may also be useful for helping people to become more variable again. A combined top down and bottom up (physical movement) is a promising way to address two elements that are implicated in a successful rehabilitation.

Zusman here outlines an excellent process *Click Here*. Creating new, different, and novel memories to be used would be an aim of rehab using this combined process. Nijs et al also outline a similar process here *Click Here*

An invariant strategy may also lead to repetitive proprioceptive information that has become coupled with pain and specific movements at a neural (neurotag) level reinforcing the pain experienced and maintenance of that pain. I discuss the concept of ‘pain memories’ here. *Click Here*

Moseley and Hodges discovered that movement variability was linked to cognitive factors. They found that for those that experienced a decrease in postural variability after experimental pain that normal resolution of their original postural strategy did not occur and was also linked to their cognitive beliefs about back pain.

This may affect both continuation and reoccurrence of back pain and was discussed in the article as a potential risk factor for the development of chronic LBP. *Click Here* We also see this from Jacobs et al *Click Here*

Decreases in movement variability are associated with chronic pain consistently in the literature and I will explore some more of it below. Acute pain is associated with an increase in movement variability. This is theorized to be due to the motor system trying to find non-painful movement variations. If someone does not have a system capable of varying its movement then finding alternative strategies may be problematic and thus possibly lead to chronicity.

As a potential predisposing factor for chronicity of an injury we must both see it as a key rehabilitation component for chronic injury and also a prophylactic measure to help prevent the transition to chronicity. Certainly it may give us some insight into why previous injury has an effect on future analogous injury.

Debra Falla’s group *Click Here* took nineteen CLBP sufferers and matched them against age and gender controls during a repetitive box lifting task. The CLBP group displayed altered movement including reduced movement from the spine hypothesized to be due to increased stiffening of the spinal region. Another measure they took was EMG activity of different portions of the lumbar erector spinae. They found that the CLBP group performed the task using the same portion of the muscle. In contrast the control group activated different regions of the muscle at different times during the task. The non-varying strategy of the CLBP group was associated with increased pressure pain sensitivity of the lumbar area. They theorized that

“Reduced variability of muscle activity may have important implications for the provocation and recurrence of LBP”

This paper *Click Here* looked at the running kinematics of twelve individuals with a chronic Achilles tendon injury vs twelve matched uninjured control subjects. They found the entire Achilles injury group displayed a “distinctive and consistent pattern of loading” whereas the control displayed a markedly different pattern of variation with increased levels, in essence a higher degree of variability.

This study *Click Here* looked at female runners who had had a previous tibial stress fracture and they were compared with mileage matched uninjured female runners. They then looked at their inter limb variability (coordinative variability). The previously injured runners displayed decreased hip-knee and knee-ankle (the largest effect) variability in the injured limb compared to the uninjured limb. The controls displayed no difference between limbs.

Decreased variability could be potentially be both a cause and effect of pain. Stergiou in his paper "Human movement variability, nonlinear dynamics, and pathology: Is there a connection?" explores this question.
Decreased variability as a causative factor in the absence of a previous event certainly needs exploration through future prospective studies. This paper *Click Here* looks at movement variability in stereotypical occupational activities and the risk that reduced variation may pose.

To be variable we probably need well functioning and reasonably accurate basic movement hardware such as the proprioceptive system and cortical areas associated with movement. It is well documented that these are both affected by pain. We then need to couple this with a memory bank of movement experiences and skills that form what I term a basic ‘movement vocabulary’ that allow us to be variable and adaptable to different situations and variable stimulus. These basic movement skills are also often missing after injury especially in those with a chronic injury or pain.

As I have gone on for quite a while here I will expand on a few of the aspects discussed here in a second part to this. I would like to go into more detail on the neural aspects involved in variable movement as well as expanding on end point and coordinative variability. I will also address some basic ways of increasing variability in a simple, easily applicable and practical way.

For some reason I keep receiving emails extoling the virtues of ‘corrective exercise’. Whenever I hear the term ‘corrective exercise’ the question that always pops into my head is “what the hell are we correcting?” especially as ‘corrective’ exercise is often touted as alleviating or eliminating pain and preventing injury.

Over the past few years delving into the research on movement, posture, pain, muscle firing etc. one thing that is consistent is that there are not too many well defined ‘corrects’ that we can use to ‘correct’ to.

Surely to confidently embark on what you feel is a ‘corrective’ strategy you would have to have objective evidence of a ‘correct’ and evidence that deviation from this ‘correct’ is the cause of whatever you are trying to cure or prevent? Perhaps I am being over analytical here!?

One of the underpinning concepts it would seem in the field of ‘corrective exercise’ is that we need to have ‘good’ posture and ‘balanced’ muscles. One thing I rarely see adequately explained is how these postures or imbalances actually lead to acute or chronic pain and the mechanisms involved. This fear mongering is heavy on the melodrama and light on evidence.

Where does this magical blueprint come from? I am unaware of an agreed upon definition of ‘good posture’ that we can objectively use to then define ‘bad’ and then ‘correct’ to. We seem easily seduced by complex anatomical theories about ‘correcting’ and ‘neutral’ that often are not really supported by the available evidence. perhaps we should apply this scrutiny to many of the ideas that propose deviation from a 'correct' as the cause of pain?

Even before we look at any of the evidence we should really have a look at the basic scientific plausibility of the idea.

Basic science

Part of the process of pain originating from a specific tissue, such as a muscle, occurs by the stimulation of nociceptors contained within the tissue. Nociceptors are receptors that sense noxious stimulus or more plainly put danger! They encode this stimulus and then relay this message to the brain via the spinal cord. The brain then decides if this information it is receiving is sufficient to then become the experience or output of pain. We have to appreciate that this information from the tissue may not be enough on its own to be translated into the perception of pain.

Some nociceptors can be polymodal meaning they sense mechanical, chemical and thermal stimulus that could cause a threat to the tissue, others just sense a single stimulus and some are quick at sending information and others slow.

Now nociceptors are set to have a high threshold meaning that the stimulus required to make them send a signal back to the brain needs to be pretty high. This makes perfect sense because if the nociceptors had a low threshold to a stimulus then they would be popping off all the time and life would become a pretty painful experience.

These sensitivity levels can alter and we may see this with people in persistent pain and also when the state of the tissue changes such as during periods of inflammation and the resultant chemical cascade that occurs.

If we think about people with a normal tissue state then ‘poor’ postural ‘deviations’ will provide a mechanical stimulus to the tissue that is actually very low, much more of a position rather than a motion. The likelihood is that the mechanical stimulus would not reach the level required to activate the receptors designed to sense a high stimulus and then transduce this back to the brain.

Now it could be hypothesised that a prolonged low-level mechanical stimulus could create pain, the question is do we have the required research to suggest that a persistent low-level mechanical stimulus will activate a high threshold receptor?

Another theory is that poor posture over the long term leads to tissue damage that then causes nociception. Unfortunately this does not seem to hold water either. If wear and tear to our tissues was simply to blame for pain then we would not see many asymptomatic people with tissue damage…...but we do!

This study of spine imaging *Click Here* estimated the prevalence of disc degeneration was 52% for ASYMPTOMATIC 30 year olds rising to 80% for the 50 year olds. Wear and tear to our tissues is the same as getting grey hair, going bald or getting wrinkles it’s just less apparent as it’s not external. Your brain may not recognize this as a threat as it may not your grey hair.

How many people have what could be considered as ‘poor’ postures and never develop any pain? I bet you can think of quite a few people you know. Going back to the beginning of the piece you will remember that nociception from the tissue on its own is not enough for the perception of pain.

We are adaptable

Tissues are amazing at adapting to increased loads. In fact if you go to the gym that is exactly what you are asking your tissues to do, adapt to an increased load. These loads will be much higher and in more extreme joint ranges than your average bad posture.

The same maybe true of a muscle being ‘overworked’ and fatigued via a faulty posture as a source of pain. Surely over time a muscle would adapt to the level of endurance required to meet the demands of a task? A bit like training for a marathon! It has also been discussed that we have alternating recruitment of muscle fibres within muscles to avoid becoming so fatigued.

The human biological system has the ability to adapt and to self-repair. We have large tolerances and variations in both anatomy and function. The ‘corrective’ paradigm seems to assume an inherent fragility with the most minor deviations causing major problems.

We certainly seem to have a body of evidence that suggests people in persistent pain do not have very different postures from those that are not in pain.

Here we see cervical spine postures no different between people with and without neck pain *Click Here*

There was no difference here in this study of lumbar lordosis of those that had back pain and those that didn’t *Click Here*

I pulled together some of the evidence on posture and pain in this blog *Click Here*

Surely if posture, pain and tissue damage were closely correlated we would see this clearly and consistently reflected in the evidence base? We could then make a good case for a ‘corrective exercise’ program but unfortunately we don’t.

Another proposed cause of pain from poor posture is ongoing tissue stress and subsequent inflammation. Have we solid evidence that ‘poor’ posture leads to an inflammatory state of the tissue that could lead to pain? If you are reading this and have some then please send it to me.

Again surely if postural deviations created inflammation and a change in the chemical state of the tissue then we would see a more consistent correlation between people with ‘poor’ posture and pain?

Is the proposed prolonged low-level mechanical stimulus enough to trigger an inflammatory response? If we look at Dye’s excellent model of ‘tissue homeostasis’ *Click Here* then the stimulus would have to be large enough to exceed the zone of normal tolerable loading and enter the zone of supra-physiological loading disrupting the bodies normal physiological processes, I am unconvinced it would.

Postural positions adopted for extended periods certainly could negatively influence nerves through tension and compression of both the nerve itself and via forces applied to the nerve from prolonged muscular contraction.

This may affect the intra neural blood flow and nerves are especially sensitive to decreases in oxygen and resultant ischemia with associated low tissue PH (acidosis) that can occur from the reduced flow of blood. The sensitised nerve may then be triggered into sending danger signals by much more normal forces applied to the nerve rather than the usually higher forces required to trigger danger signals.

This could actually happen to ANY posture that we adopt for an extended period of time. That could be a hunched posture or what we maybe described as a ‘good’ posture. The major factor would be that the posture is unchanging not the actual position that we adopt. Rather than the postural position it would be a lack of MOVEMENT that is problematic.

This is why after we sit for a long time we often need to get up and move around. We feel stiff and irritable and in need of some basic pump and flow to our tissues to drive more of the good stuff and flush out the bad! Often we will get up move about for a bit and feel much better, it is just a basic warning system to move!

In this situation ANY movement might help without the need for it to be ‘correct’ or ‘correcting’

Muscle imbalances

One of the reasons I often hear blamed for poor posture is a ‘muscle imbalance’, one muscle being stronger than another around a joint pulling it out of the ‘correct’ position.

I imagine this like a bit of a tug of war!

A question that pops into my mind, which I warn you can be a strange place, is that in a situation that requires a small percentage of contractile force would this difference in strength become apparent?

During the low-level isometric contractions employed in maintaining a posture it is estimated we use between 4-7% of MVC (maximal voluntary contraction). (The Ergonomics of working postures P142, Corlett E et al 1985)

Perhaps only above the threshold of the difference in strength would one muscle actually “win” the battle. At a lower level demand perhaps they simply balance each other out if it were in fact a tug of war. So would we be likely to see strength imbalance lead to postural changes when such low levels of MVC are required to maintain a posture?

Our posture is also influenced by a number of different systems such as the visual and vestibular systems not solely the strength or length of two opposing muscles (amongst many) around a joint. Perhaps just looking at two muscles is an overly simplistic view of posture.

We often look to ‘correct’ muscle firing patterns, especially with back pain, with no real evidence of how they should fire in the first place. Here we see two pieces of research that show abdominal muscle firing and function have little to do with getting better from back pain *Click Here* & *Click Here*. Perhaps altered muscle firing is a result of rather than a cause of back pain and therefore is not implicated in resolving the pain.

This paper challenges the idea that we have a ‘correct firing’ of the core muscles independent of functional activity *Click Here*

Here is a bit more on the core stability debate and a look at some of the evidence *Click Here*

Psychological impact

We must also think about the psychological impact here as well. How does telling someone they are ‘imbalanced’ and in need ‘correcting’ affect their sense of fragility? Could this translate into an interpretation of being ‘broken’?

Could we see the term as a nocebo? The nocebo is the opposite of a placebo, essentially it has the potential to make things worse not better especially if there is no problem to begin with and one is created.

The awareness of the importance of this side of our interaction with people is growing *Click Here* and even if we had credible evidence that people are in need of ‘correction’ it would probably be better to not dress it up as such.

It may also reinforce the role of the therapist or trainer as the person required to ‘fix’ their ‘posture’ or ‘muscle firing’. Both of which are quite possibly based more in the imagination rather than reality.