Core stability and low back pain: How stability exercises might help. Part Two


In part one of this post I very simple reviewed some of the ideas behind core stability and how I questioned their relevance to a patient's pain presentation.  In this follow up post I will briefly review how people with pain have different function than those without pain and give an opinion on how core 'stability" exercises may help with patients in pain in a manner that has nothing to do with stabilizing the spine.

What do we know and what can we do with patients with low back pain

- some patients with low back pain show delays in Tranny firing

- this delay can be correlated with the presence of low back pain

- changes in muscle timing occur with perturbations to the spine

-improvements in pain and function can occur and have nothing to do with changes in firing onset (see here )

-changes in firing onset can occur and have nothing to do with a motor control retraining plan (see Gary Alison's recent work here which he has been trumpeting this idea for more than a decade, here and here)

- some clinical prediction rules help identify who best responds to a "spine stability program"

- I published two literature reviews years ago that outline how peoples spines function differently with pain (Here and here). The research shows those with pain have differently behaving muscles, changes in proprioception, differences spine kinematics and differences in how they move

But so what if there are changes in function?  Do we need to know this to make improvements in pain?

None of the research suggests that these differences occurred before the pain nor does any research suggest that changing these dysfunctional parameters is necessary for pain resolution.  We probably don't need to specifically address these changes in function with our treatment and most of us aren't.  From the above list there are at least 8 means that the spine is "dysfunctional" as measured with some advanced biomechanical testing.  All of us do not do these testing on our patients yet we are often able to make them feel better.  What does this tell you about advanced testing? It probably isn't necessary.  Or is the test that is most important just the one that your clinic happens to have access to (I'm talking to you you people with Rehabilitative Ultrasound Imaging - I guess you have to justify the cost somehow :) )  We may just need to address the patient's pain, their beliefs, their attitudes, their activity levels and their habits and we will get changes in these functional outcome measures or we won't get changes in those outcome measures and we don't even need to.

These changes in how muscles work can definitely occur in the presence pain.  Where we are confused is correlation and causation. When did these changes begin in relation to onset of pain?  We have some suggestion that changing these motor control variables does not relate to improvements in symptoms (Mannion 2012).  So are these changes just a defense of the body rather than some defect?  They are assumed to be surrogates for stability but are they?

Maybe we should see them as secondary casualties in how our brain works.  The brain changes with pain.  Pain is an output of the brain.  So is motor control.  We can also see changes in swelling, heat, blood flow.  No one thinks that we have to address these secondary adaptations to help with back pain but we think we have to address the motor control or stability issues.  All of which can be secondary byproducts of the persistent pain experience rather than some original criminal mastermind of the patients pain.


What do I think my exercise prescription is doing

Breaking habits of motion, changing fear and building self efficacy

Directional preference, flexion intolerant, extension intolerant, activating neurotags etc. Patients have movements that hurt.  Sometimes they continually perform these movements and they keep hurting.  Maybe they were told that they were supposed to sit up straight, brace their spine, suck in their belly and always activate their lazy glutes.  And guess what, sometimes you have these patients relax, move their spine, sometimes slouch, sometimes put their feet up, stop worrying about their glutes and keep active and voila their pain feels better. Instead of "correcting" some stability problem we just gave the patient permission to move with a lot of variety.   We just broke a pain habit.

Sometimes, patients get pain with flexion and for some reason they keep doing activities that flex their spines and they keep having pain.  Sometimes, we suggest that they move the opposite direction, try to find a position of relief and every hour they arch backwards for a few weeks.  Then we slowly have them start flexing their back again (because we don't want them to be afraid of flexion, its what we are meant to do) and now they can flex their spine without pain.  Are these patient's spines any more or less stable? Did their tranny start firing earlier? Who knows, they have less pain.  They began to move differently than what they were previously doing and this helped.  We broke a habit, found positions of relief, built confidence that they could move without pain and transferred that confidence over to other activities.

In some patients you can give them a full spine stability program aimed at buttressing their entire spine. The exercises feel good when doing them.  The patient gets more confident.  They feel stronger and even their pain decreases.  Did their spine's stability become more robust? Maybe.  Is this what caused less pain?  Probably not.  You got this patient moving, maybe you caused exercise induced analgesia.  You put them in control and they felt better.  It probably helped if you didn't tell them there spine was unstable before you gave the exercises.


What is my point?

Keep it simple. Adam Meakins (A sport physiotherapists at  wrote a simple tweet


"In physio you cant go wrong if u do the simple things exceptionally well & save the fancy crap for show offs & bullshitters #ROM #power etc "

This might encapsulate my treatment philosophy in all its foul mouthed glory.  While the body is extremely complex and the pain experience difficult to fully understand our interventions can be quite simple.  We are not car mechanics where we are tightening something or loosening something.  We just provide some input into the body.  The body and brain then decide what to do with it.

I still advise bird dogs, side planks, front planks, curl ups, squats and all the exercises that are in the traditional North American stability paradigm.  Sometimes, I even check to see if you someone can suck in their belly button without other muscles turning on and if doing that decreases the pain in their back when they move their leg.  Do I think that any stability changes occur and this is causing their pain to decrease?  NO. There are other reasons that these movements help.

Do I think that all those planks are creating rigidity in the spine.  Of course not, this is much too simplistic.  So what the hell do I do and what do I think I am doing.

My approach and my rationale

All of the following assumes I have ruled out the nasty stuff.

1. Educate about pain.  Don't catastrophize.  Explain the difference between tissue injury and pain.  Explain that we are meant to move and that pain is normal and is not some indication that they are falling apart.  Explain that their scary x-rays and MRIs are poorly correlated with their pain.   Explain that pain is so much more than just the tissues in their back and reassure them that they can do something about it.

2. Touch them with your hands:  Move them, push, pull, rub, crack, traction, distraction, compression. Whatever.  Manual therapy has some neurophysiological pain modulator effect.  Skip the bullshit explanation about the complexity of the SI joint having an upslip, downslip, a shear or flare or whatever.  You can't feel this and you can't correct it.  But using your hands can modulate the perception of pain and can change muscle and joint performance.  This gets your patients confident that change is possible.

3. Move meaningfully.  What is important to your patients?  Find some movement related goal that is important.  Figure out a way to do this.  Set small goals related to this movement and achieve them.  They might have pain during this task but they know that pain does not mean damage and that they can do it.  Don't hammer them into fighting through pain so that they feel "Wind Up" the next day.  But keeping pushing that pain threshold up.  Keep empowering them.

4. Stress the body.  This is where I use exercise.  I find a movement that is painful.  I figure out someway to modify that movement so that it is not painful (think Mulligan).  Train that movement.  Start to break the habit of pain.  Pain is a habit.  If we activate a pain neurosignature with certain movements we can sometime modify that movement so that that neurosignature is not activated.  Do this.  This is where "spine stability" exercises can come in.  Get them working their achey back in ways that don't cause pain.  This is awesome they train a painful area without experiencing pain.  This decreases the threat associated with movement, decreases kinesiophobia and changes how they think about pain.

5. Train harder: pick a movement that is kind of related to their painful site but does not hurt at all.  Train the hell out of this.  This can be build confidence in their body.  For example, they might have shoulder pain but they can deadlift.  What a great shoulder exercise.  You work your entire body, train the shoulder but experience no nociception.  Hammer this.

6. Address beliefs: we need to understand what our patients think about their condition and how that impacts their psychosocial profile.  If they have some serious catastrophizing, fear avoidance, depression, perceptions of injustice etc this shit needs to be addressed.

An opinion on motor patterns

I have seen "faulty" motor patterns and I have also seen them "corrected" by doing exercises that have nothing to do with retraining the supposedly faulty muscles.  If a motor pattern is corrupted this pattern is most likely corrupted at the level of the brain.  If I train some movement, modulate pain with some education or mobilization we often see changes in these motor patterns.  But I didn't change these as a mechanic.  There was no tweaking at a local level of "muscle imbalances".  We aren't bloody puppeteers The imbalances get "corrected" via other means.  Or they don't get corrected and my patient is pain free and I know that "muscle imbalances" can certainly be normal variations of your complex system.

So just remember this mnemonic: KISDAS.  Keep it simple Dumb AsS.


Future posts and questions for research

Corrective Exercise: this approach, besides being an unethical cash grab for CE dollars by some questionable organizations by making good intentioned personal trainers and physios feel insecure, has a number of assumptions about human function that we all need to question.  I also want to investigate it because it is an approach that I kind of use daily (see my defense here of the lowly clamshell) although I try to simplify it and pain neuroscience it up a bit.  And besides, isn't "corrective exercise" what every good coach or therapist does automatically? Find a deficit and improve it?  Anyways,  corrective exercise has a number of interesting things that we can look at and I don't think it is worth completely discounting.  Here are some areas I hope to address:

1. It assumes that there is an ideal way that the body functions.  I think this is everything most physios, trainers and coaches do yet our research is so piss poor.  I would love a catalogue of articles that attempt to categorize the best way to move.  We need to settle this debate once and for all.  The catalogue might just show exceptions and the huge variety that is acceptable.  It might show that their instances when it is best to move on way over another.  I know it is more complicated than just avoiding knee valgus, keeping a neutral spine, not letting 'global movers" shut down "local movers" and assuming that all asymmetry is evil.

2. It assumes that isolated testing (e.g single leg squat, prone leg extension, single leg glut bridge) gives us some insight into altered functioning.  It then assumes that the altered functioning in some isolated test actually correlates with assumed altered functioning during some more meaningful performance task (e.g running, deadlifting, squatting).  I wrote a PhD proposal on this area and you would be surprised how poor our tests are at actually testing anything we think they are testing and also correlating with functional activities. Guess what? Did you know that the quadruped rock back test coupled with spine rotation actually does not "lock out" the lumbar spine and only result in thoracic rotation?  Crazy.  Or that the thoracic spine has just about the same amount of rotation capacity as the lumbar spine.

3. Muscle activation?  Such a neat, simple and prevalent idea.  Training some small movement (e.g squeezing your glutes during a bridge) while "turn on" some muscle during another activity.  I would love to see this idea put through a simple experiment.  Flippantly, it again views the body as something that is so stupid.  Certainly worthy of some good research.

4.   I would love to see a series of blog posts look at altered joint kinematics (what a corrective post assumes it is correcting) and how these alterations correlate with changes in pain or improvements in function. My big hesitation with the corrective exercise approach is that it complicates things and does not seem to recognize the uncertainty that exists in human function. Further, corrective exercise assumes that there is a limited way to "correct" the dysfunction.  aka. you need the "correct" corrective exercises.  I would suggest that there are a multitude of exercises or approaches that can influence pain perceived to becoming from a joint and the resultant aberrant kinematics.  Anyone want to look at this topic?

5. Of course we could also talk about foam rolling.   It is interesting that there does seem to be a shift in the rolling world to get away from the idea of digging out knots and adhesions and focusing on the possible neural aspect for the treatment mechanism.  But fascia is still king in some circles and I can't fathom why.

I would guess that if we look at the biomechanics and motor control literature we would find that our treatments can be much simpler, we would have lots of variety and many approaches would be successful.  We would not have to have incredible complicated solutions to simple problems (avoid the Rube Goldberg trap of exercise prescription).


Happy new year!  Anyone interested in collaborating on blog posts please email.


Core stability and pain: Is it time to stop using the word stability to explain pain?

sidebridge feet
sidebridge feet

Purpose: To cherry pick a few research articles to suggest that even though our knowledge of core stability is very impressive its link to pain is poor. Nutshell summary: People in pain have spines that function differently than those not in pain.  Many treatments can influence pain.  The spine stability model of low back pain does not explain how people have pain and takes an overly mechanical view of the pain experience.  No test has ever shown that a spine is unstable or how "increasing stability" would lead to a decrease in pain.  Thinking that our spines need more stability or control may be the completely wrong path in explaining how people have pain or how our exercises help them.   Our treatment "corrections" occur not via one specific "corrective" mechanism (e.g. improving stability) but rather through global non-specific mechanisms that our better explained by our understanding of pain neuroscience.  Making the shift from believing that "stability" is the issue with pain can thus free up to choose completely different exercise programs.  Exercise and treatment prescription thus become simpler.  We have preliminary evidence to support this view with the clinical studies that show benefits with the various exercise conditioning programs that train different schools of thought on stability or the just as effective programs that completely ignore any concepts of stability.

Caveat of Ignorance

The purpose of this post is to question things that we say about exercise, low back pain and of course "spine stability".  This is an informed opinion piece and everything I say can be challenged strongly...that's why I write it.  I am also going to put out some "notions" on how I think exercises can help with pain and function.  These are certainly subject to debate and will probably change with time.  I have also ended the piece with a general overview of what I do in Part Two.

A BRIEF and not complete background on spine stability across two hemispheres

Two schools of thought regarding spine stability and low back pain emerged in the 1990s.

The Australians and their inner muscles - Train the local muscles first

The first was based on Bergmark's classification of muscles into "segmental" stabilizers and others into "global" movers.  Segmental stabilizer muscles were often considered to be tonic (constantly on) while the others were phasic (on intermittently to create movement).  This idea of muscles having different roles was suggested decades earlier by Janda.

Low back pain was assumed to occur when the segmental stabilizer muscles were inhibited and the global muscles took over.  The research supporting this idea came from the great work of Paul Hodges (A nice review of Paul Hodges and Motor control can be seen a Todd Hargroves site  In early studies, Paul showed that in healthy subjects the transverse abdominis and the multifidus muscle (two local muscles) should fire in a feedforward manner when someone is asked to lift their arm.  Lifting the arm is a perturbation to the body and muscles in the trunk and legs must turn on for us to keep our balance (some call this "stability').  Dr. Hodges showed that the "Tranny" and MFD turn on before or within 50 milliseconds of the deltoid muscle.  Since the muscles become active  before the deltoid we can assume that the brain did some motor planning to prepare the body for the arm raising - muscle activation was NOT a reactive response to the movement of the arm.

With low back pain Dr. Hodges showed that this feedforward (or motor control planning) was delayed in the Tranny and the MFD.  And BINGO a whole  industry was born and the misapplication of science ran hogwild over common sense.  So that's it.  All Paul showed was that in those with pain you got a DELAY in firing.  No one showed that the tranny was weak, no one showed that the muscle was turned off and no one involved in the research said that the Tranny was the most important muscle on the planet.

But somehow physiotherapists, chiros and personal trainers started telling everyone to suck in their stomach when they did squats because the muscle was erroneously deemed to be super important for spine stability.  This was never what the research suggested and caused fits in the North American Spine researchers who really railed against this simple idea.

The other school of thought - Train general core stability (a brief simple version)


Fortunately, I was innoculated against this because of my MSc with Dr Stu McGill in the late 1990s.  Dr. McGill and Dr. Sylvain Grenier were excellent in challenging the supremacy of the Tranny.  I view their research as less a repudiation of Paul Hodges' ideas and more of an attack of the misuse of Paul Hodges' research.  What McGill and his colleagues had always advocated and also modeled with their biological fidelitous spine model was that spine stability (aka the ability of a system to return to its normal position after a perturbation) was most robust when all of the muscles worked together in the trunk - all muscles were important for stability.  This was again nothing new and we knew this from other joints.  Muscles co-activate, create joint compression and the cost of compression is assumed to be offset by the benefit of stability.   This North American model of stability assumes that all muscles of the trunk work together to balance the stability demands of the spine.  Hence rehabilitation from low back pain should train all the muscles of the trunk in a manner that creates stability but does not do so at a huge compressive cost or adverse tissue loading cost.

Dr. McGill was a leader and pioneer in this.  He was the only one actually evaluating exercises and measuring stability and measuring the compressive/shear loading on the spine to determine which exercises might be "safe".   Dr. McGill was able to classify exercises in to ones which were "safeish" (lower compressive or shear loading on the spine) and others which might have a high compressive penalty but an individual got a good workout (i.e. lots of muscle activity).

The clinical relevance of both the North American and the Australian views are founded on a number of assumptions and unknowns.

What both views assume is that exercise training will make the spine more robust in terms of stability (not more stable, as we know a system is either stable or unstable - you don't make it more stable) and this will lead to less pain and perhaps decrease your injury risk.

Faulty research extrapolations to people in pain and other random stability issues

Below are a number of points regarding the limitations of the relationship between spine stabiliy and pain

1. We do not know why people have low back pain. We do not know what tissue is actually cranky/irritated, fires off a volley of nociception that may ultimately result in the production of pain in the brain (if it even is coming from some cranky/irritated nerve embedded in tissue and is not wholly a production of pain from the brain in response to some perceived threat).  We can not say that a disc is pissed off, a muscle is cranky, a facet joint is upset or if some ligament wants a vacation.  Damage in the spine has a poor correlation to pain. So if you can't identify what tissue is the source of nociception (and we can't) what is the mechanical basis for the prescription of any stability exercise?  How would changing the stability of the spine decrease nociception? If you think spine stability exercises actually change stability parameters by what mechanical means does this change nociception? If you think spine stability exercises help your patients and clients but you can't explain it via a mechanical explanation (but you know it works) do you think there might be  something else going on besides stability issues that you are affecting to influence the perception of pain?

2. Who cares if a muscle is delayed 50 milliseconds?  Really, what relevance does this have.  The muscle turns on eventually and does its job during a task.  Why is a delay of 50 ms relevant in terms of biomechanics.  Is this delay a defense or a defect?  Is the problem in the spine (unlikely) or more a symptom of "something is up" with the brain (more likely, and this is where Dr. Hodges is doing most of his work now yet in popular clinical culture we are stuck at the level of spine). I will go into Hodges work later in another post because I think his work on motor control and the brain may be extremely relevant.  Big point here, Hodges never measured stability.  Just muscle activation in all the muscles that make up the trunk cylinder (side note: he did a wonderful job here, I think his research is excellent, he is an excellent researcher and his contributions to our understanding in the area of motor control are without par.  I would also prognosticate that his future research might bridge the gap from mechanical views of spine and pain neuroscience).  Everyone just jumped on the stability wagon and assumed that it was compromised.  Maybe there is something else going on here besides stability.

3. The argument for the motor control camp against bracing and planking - "Don't brace or do planks because your spine becomes rigid" is a wee bit weak.  This is the argument against the North American model of spine stability and is used to justify"motor control" or low level exercise. It suggests that if you do a bunch of planks you will become rigid and activate your muscles too much. I disagree with this puppetry view of the body. Doing planks will not somehow carry over to rigidity in our activities of daily living.  We aren't puppets where we can tighten and loosen the strings of our spine. This is catastrophizing against a therapy rather by the patient.  These exercises aren't that powerful both in a negative or a positive way.  However, if you actively brace and assume a rigid posture as a choice during all of your normal activities then you can make this argument.  Don't blame the exercise blame the conscious choice of movement.

4. Do you think your patients are really "unstable"? Patients are in pain.  They move differently, you might perceive them to have "tight" muscles.  But is their spine really unstable? Is there a vertebrae in there sloshing around, sliding this way and that, pinching on stuff.  Is the spine really buckling?  We can have patients with high levels of spondylolithesis and their spines are not unstable.  I think we might want to reconsider telling our patients that their backs are unstable and they need stability exercises.  How much fear do you think this creates?  No one has ever shown that a patient with persistent low back pain has funny uncontrolled movements at a segmental level in the spine.

5. But my SI joint needs force closure, I need to train my Tranny or MFD or some bloody fascial sling.

How  is your SI joint unstable?  What wonky movement do you really think is happening in there?   I believe that there is less than 2 degrees of movement and a few millimetres of slide in that SI joint but how is having a delay of 60 milliseconds in one muscle changing this movement?  If it does change that movement why does this cause pain? And so what if the joint slides too much.  Other joints slide around and they don't create nociception.  And if you have a delay in the tranny won't the big, bad global muscles be on at the same time and thus increase force closure and shut down the movement.

These global muscles certainly have the architectural requirements to create force closure.  None of this makes sense. Oh wait, those global muscles are on too much and that causes too much compression in the joint and that causes pain.  Oh, gotcha that makes perfect sense.  But guess what, no consistent research actually suggesting that this happens.   The studies showing increases show increases that are extremely subtle and again how this would cause pain is never laid out in any logical or supported manner.   Well what if that joint is fused?  That seems like a lot of compression.  Should that not be painful yet its not? And why would compression from muscles be painful? Would someone not be better lying down and not lifting weight, walking, running if compression was so nasty for the SI.  More compression on a joint is not necessarily bad and does not lead to pain.  There is something else going on here.

childs pose
childs pose

5. Is it really that bad to get away from the neutral spine? I agree that a neutral spine is generally stronger when the spine is undergoing maximal compressive and shear loading.  Maintaining a neutral spine when deadlifting, doing kettlebell swings, squats and picking up your sofa makes some sense to me.  But do I really need to never bend or twist my spine.  It has a certain amount of movement built into it.  Why would I not use it?  Motion is lotion.  We would never tell another body part to not move.  Taking away movement is how we torture in Guantanomo.  The majority of spine pain does not occur because of we have overloaded it to an extent where it reaches the limits of tissue injury capacity.  This may be one of those issues where we can confuse injury with pain.  Neutral spine bracing can probably help with injury and performance when under high loads but is it necessary to decrease pain in someone getting up from a chair with low back pain?  I will grant that sometimes when you brace and move with a neutral spine and get out of a chair you have less pain.  In other people it gets worse.  Maybe there is something else that explains this besides stability.

6. Patients get better with all types of spine exercise programs.

We have clinical efficacy trials showing that a motor control program (e.g sucking in your belly and then progressing with more global exercises) and a global exercise program helps for low back pain.  So do general exercise programs.   We know that exercise for the spine can help but perhaps it does not matter which exercises we do.  When we get similar results from two different theoretically supported exercise regimes perhaps there is something about the two different programs that is similar.  Perhaps it is that similarity that leads to improvements in pain.  A recent paper by Mannion et al (2012) championed a similar idea.  In other words, we get results but not for the reasons that we think we get results.

7. I think we scare the shit out of people when you tell their spine needs stability

This the default word that many of us tell our clients.  "You're unstable, you can't "control" your movement and that is why you are in pain".  Its so defeatist and catastrophizing and really has little support.  I say we stay away from these words...See my previous post here on this same topic (The words we use can harm)


You can rehab a patient using the two different schools of thought on spine stability.  You will probably have similar results.  Conversely you could just have patients exercise their entire body and they will also show improvements. You will also have good results if you just teach people about pain and give them the confidence to keep moving and not get worried about their "bloody lack of stability" that some therapist told them they once had.

Stability is probably the most inappropriate word we can use to describe our patient's spines that are in pain.  No one has documented that patients in pain have unstable spines nor is there any reliable clinical test for it...yet we have been using this word for twenty years.  That is crazy yet so many of us think that we have to "increase the stability of the spine" in those with low back pain.  No one has shown how any dysfunctions related to "stability" actually cause pain. Again, crazy.  Yet we tell patients they need stability exercises to correct some mysterious bogeyman.   When we get results with completely different movements or exercises that totally conflict in terms of spine stability theory this tells me that the reason our treatment is effective probably has nothing to do with stability.

In part two, I will layout how the spine function is different in people in pain and also give some theories on what treatment does to help our patients.

This physiotherapist's approach to treating Persistent Pain

Audience: Patients and other health care providers Purpose: To explain my treatment approach to Persistent Pain Problems.

Overview of the Treatment Program:

  1. Pain Physiology Education
  2. Movement (Graded exercise/activity exposure)
  3. Manual Therapy

The Simple Goals of Treatment

  1. Decrease pain and sufferring
  2. Resume or increase the activities of a patient's life that are important to them

Assumptions that inform the Treatment Program

Pain is the brain's response to a perceived threat

Pain is an output from the brain that is meant to protect us.  It is influenced by a lot of things including, but not limited to, situation/context, past history, beliefs and expectations. Pain is a threat detector and set up to motivate us to do something about that perceived threat.  It is not good at telling us how much damage there is or even where there is a problem.  Think about people who have pain in a phantom limb. They don't have a bloody thumb yet that thumb sure can hurt. There is no problem in the periphery as there is no periphery.  Or how about when someone has a heart attack and they feel pain in their back or jaw or arm.

One difficulty with pain is that we can get better at producing it.  It become a habit.  We need to break that habit.  What scientists call this habit is our pain "neurosignature".

More information about pain can be found here and here

Inappropriate beliefs about pain further the pain experience

Understanding pain science itself can help decrease the pain that patient's feel.  Learning about pain improves coping skills, decreases catastrophizing, increases activity through reductions in fear and can change how the brain creates movement.  Patients are capable of learning complicated neurophysiological facts about pain and this in turn can improve their situation.

Pain influences all facets of our physiological function and our social lives

Pain is more than just a booboo in some tissue. Pain is an output and pain can influence other outputs of the brain. Pain influences our stress response, our immune function, endocrine function and our movement (e.g. kinesiophobia).  Pain can be linked with psychosocial factors like perceptions of injustic, castrophizing, depression and anxiety.

Tissue Damage (nociception) does not equal pain

Patients are not their x-rays or MRIs.  The link between tissue damage (e.g joint degeneration or muscle tears) is very poor. Pain persists long after tissue healing occurs and pain can occur without even an initial injury.

Continuing to believe that the source of pain is purely in the body can lead to further impairment. Old biomechanical models of tissue breakdown as the source of pain contribute to false beliefs that lead to more pain.  Addressing these beliefs and learning about pain neuroscience guides an individual's treatment program.

More information here and here.

Treatment Program Details

Pain Physiology Education

Knowledge really is power.  If we know that our achey knees aren't falling apart and the pain in our elbow isn't due to some serious muscle damage then that knowledge teaches the brain and the patient to be empowered, confident and optimistic.

Pain education starts on the first visit and continues during the movement/exercise therapy and during manual therapy.  Pain education is supported with website links and written material.

Movement (Graded exercise/activity exposure)

Motion is lotion. Pain can be seen as a habit of our brain.  When in pain many of the areas of the brain are activated and we can call this a NeuroSignature.  We want to sneak under the radar of that neurosignature and teach the nervous system that we are in control.  Graded movement (e.g. slowly building) allows to choose novel, non-threatening movements/exercises that increase our capacity to move and be active.  At the same time doing movements that are different and new can downregulate our pain response.  Movement is the key to the drug cabinet in our brains. Movement is medicine. The movements that we choose are not always pain free but they shouldn't be so intense that you experience "wind-up" or a huge flare up the next day.  Choosing movements and activities like this can increase our threshold for flare ups and pain.

Movement and exercise selection is not about increasing stability, strength or range of motion.  These constructs are poorly related to pain resolution.  While we often get increases in strength and range of motion following treatment it is not because we increased strength or range of motion.  These were side benefits to the program.  Last, I believe that words like instability or stability or inappropriately used to explain why people have painful problems.  It is highly unlikely that a patient's spine or hip is unstable.  When we use these words I believe we create a sense of fragility and doom. Most patients are robust.  It is our nervous system's over-sensitivity that promotes pain not some weakness in tissue capacity.

Manual Therapy

Very simply manual therapy can modulate the nervous system's production of pain. We have more than two decades of research showing that the means that manual therapy work is through changing nervous system function.  This is not about joints being out of place, breaking down scar tissue or merely strengthening or stretching muscles.  Immediate changes in the perception of pain, production of strength or change in range of motion can be seen.  Its not logical to assume that a 30 minute treatment session healed tissue, broke down scar tissue or suddenly made a muscle stronger. The only physiological component that can change this quick is our nervous system.  Manual therapy affects the nervous system and can improve our function.  All manual therapy techniques can be effective.

Treatment can included peripheral nerve mobilizations, soft tissue massage, joint manipulation/mobilization, movement pattern corrections (e.g subtlely changing how we move to not activate the pain signature), dermoneuromodulation and mobilizations with movement.  Treatment is typically pain free. I'm of the opinion that pain begets pain and treating with aggressive painful techniques can reinforce our pain habits in some patients.  While a short term pain relief can be felt following aggressive treatment (mostly likely due to something called Diffuse Noxious Inhibitory Control) I feel that this is temporary and unlikely to effect long lasting change.




The Why's and How's of Treatment Justification

This post is more about the "Why" and "What" of treating pain and injury.  It is not a full explanation on the "how" of treatment.  The "how" of treatment is important because it explains the mechanisms of what we think we are doing.  If we can understand a mechanism of how pain persists and how it can be alleviated we can change our treatment techniques appropriately.  Future posts will look into the mechanisms of treatment.

Structure is not Destiny - please don't rush to freaking out about your x-ray, MRI or ultrasound

Audience: Patients Purpose: To highlight the poor link between the bogeymen found on imaging with pain or dysfunction.

Our current technology is amazing when it comes to viewing the insides of our body.  The problem with this fantastic technology is that we can see something (e.g. a tear in a muscle or a joint with some osteoarthritis) and assume that there is something wrong or that this is the source of our pain.  However, the link between tissue "abnormalities" on MRI, x-ray or Ultrasound is often quite poor.  Many, if not most, people have "bad stuff" on their MRIs or x-rays yet have no pain.

A quick anecdote...I was with a patient that had horrible left shoulder pain. Poor movement and worse strength.  His doctor ordered an MRI and my patient reported to me that sure enough the shoulder was a mess.  Torn rotator cuff, bursal thickening, arthritis in many joints, some fluid collecting - an absolute disaster.  BUT, there was a problem.  He wanted to know if the MRI picture could have been "flipped" or "mirrored" because these results were for his Right, painfree shoulder.  The results weren't flipped or mirrored, we got the results for the left later.  They were just as "bad".  Point being, structure is not destiny.  Damage or scary stuff on any imaging report does not equal pain.  This patient ended up pain free in a couple months.  His MRI report would not have changed despite the changes in his strength, mobility and pain.

This is not new

I am not breaking any news here.  We have known this for at least 15 years.  Joint degeneration, disc bulges (even herniations), rotator cuff tears, calcifications in ligaments or joints are all normal variations that can exist without pain.  At certain ages this changes, assumed to be abnormal, are actually normal and more common than a lack of these changes.

Below is a sampling of research highlighting the limitations of structural anomalies and pain.  I was going to provide some insight but instead I will use this post as a catalogue of the research that looks at the relationship between tissue damage/abnormalities and pain.


Bottom Line:  Pain is poorly correlated with damage.

One caveat: I hesitate to say this but sometimes these structural changes can be related to pain... it is just not a guarantee or some harbinger of pain doom. What I want to emphasize is that it is just not as cut and dry as many make it seem.  There are many factors that lead to pain but we tend to blame the simplest one (e.g. joint damage) when we actually know better but persist in this fallacy.

Some other links on this topic:

Diane Jacobs:

Bboy Science (Tony Ingram):

Spine Imaging Abnormalities are really just normalities

Maurer M, Soder RB, Baldisserotto M Spine abnormalities depicted by magnetic resonance imaging in adolescent rowers.Am J Sports Med. 2011 Feb;39(2):392-7. Epub 2010 Oct 2.

Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT, Malkasian D, Ross JS N Engl J Med.Magnetic resonance imaging of the lumbar spine in people without back pain. 1994 Jul 14;331(2):69-73. (abstract  here)

Weinreb JC, Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR. Prevalence of lumbosacral intervertebral disk abnormalities on MR images in pregnant and asymptomatic nonpregnant women. Radiology. 1989 Jan;170(1 Pt 1):125-8.  Link here

Takada E, Takahashi M, Shimada K.Natural history of lumbar disc hernia with radicular leg pain: Spontaneous MRI changes of the herniated mass and correlation with clinical outcome.J Orthop Surg (Hong Kong). 2001 Jun;9(1):1-7. Abstract here.

Stadnik TW, Lee RR, Coen HL, Neirynck EC, Buisseret TS, Osteaux MJ.Annular tears and disk herniation: prevalence and contrast enhancement on MR images in the absence of low back pain or sciatica. Radiology. 1998 Jan;206(1):49-55.

Matsumoto MFujimuraY, Suzuki N, Nishi Y, Nakamura M, Yabe Y, Shiga H.MRI of cervical intervertebral discs in asymptomatic subjects.J Bone Joint Surg Br. 1998 Jan;80(1):19-24. Abstract here.

Shoulder abnormalities not related to pain

Connor PM, Banks DM, Tyson AB, Coumas JS, D'Alessandro DF. Magnetic resonance imaging of the asymptomatic shoulder of overhead athletes: a 5-year follow-up study.Am J Sports Med. 2003 Sep-Oct;31(5):724-7. Abstract here.

Miniaci A, Mascia AT, Salonen DC, Becker EJ Magnetic resonance imaging of the shoulder in asymptomatic professional baseball pitchers. .Am J Sports Med. 2002 Jan-Feb;30(1):66-73. Abstract here

Jost B, Zumstein M, Pfirrmann CW, Zanetti M, Gerber C.MRI findings in throwing shoulders: abnormalities in professional handball players.Clin Orthop Relat Res. 2005 May;(434):130-7. Abstract here


Shellock FG, Hiller WD, Ainge GR, Brown DW, Dierenfield L.Knees of Ironman triathletes: magnetic resonance imaging assessment of older (>35 years old) competitors. J Magn Reson Imaging. 2003 Jan;17(1):122-30. Abstract here

Beattie KA, Boulos P, Pui M, O'Neill J, Inglis D, Webber CE, Adachi JD. Abnormalities identified in the knees of asymptomatic volunteers using peripheral magnetic resonance imaging.Osteoarthritis Cartilage. 2005 Mar;13(3):181-6. Abstract here

Shellock FG, Deutsch AL, Mink JH, Kerr R Do asymptomatic marathon runners have an increased prevalence of meniscal abnormalities? An MR study of the knee in 23 volunteers.

Zanetti M, Pfirrmann CW, Schmid MR, Romero J, Seifert B, Hodler J.  Clinical course of knees with asymptomatic meniscal abnormalities: findings at 2-year follow-up after MR imaging-based diagnosis. Radiology. 2005 Dec;237(3):993-7. Epub 2005 Oct 26.



More to come.

Peripheral Nerve Tensioner videos for that irritated nervous system

Below are Tensioner videos for your irritated and sensitive peripheral nerves. Warning: please only do this if your knowledgeable health care provider has taught these and specifically said that you should do these exercises.

Gentler "Slider" movements can be seen at a previous post here: Slider Videos

Median Nerve Tensioner

Radial Nerve Tensioner

Ulnar Nerve Tensioner

Sciatic nerve slump tensioner

Sciatic nerve long sitting tensioner


Persistent pain resources can be found here: Pain resources

The mechanical case against foam rolling your IT Band. It can not lengthen and it is NOT tight.

Audience: Patients and therapists Purpose: A brief argument on why attempting to lengthen your IT Band with stretching or foam rolling is a waste of time and not possible.

A note on terminology: This article talks about using a foam roller to "lengthen" the IT Band.  Occasionally, this gets referred to as stretching the ITB.  What is argued is that foam rolling can not "lengthen" or "stretch" this structure more than transiently.  Yes, it will deform a little bit like all viscoelastic biological structures (they all have stress-strain curves with varying degrees of stiffness) but it won't get "longer".

Warning: I recently changed the title on this post (formerly Stop foam rolling your IT Band. It can not lengthen and it is NOT tight.) because a few colleagues have suggested that it is a bit strong.  I agree and also think that such hyperbole will decrease a healthy discussion in the area.  I don't want that.

However, I have not changed the rest of the content and again recognize that some of it is a bit salty.  Much of it is how I talk to myself and entertain myself.  When reading this please just consider the arguments and not HOW they written.  I never expected 40,000 people to read this thing.

Please note, I have always been open to the idea that foam rolling might have an influence on our nervous system and ultimately pain.  My doubts have been around what many people say foam rolling does which I always found biological not possible.  This post explores those ideas.

Original Post -

I am in the minority when I cringe at the rampant unjustified use of the ubiquitous, seemingly harmless but actually evil foam roller for IT Bands.  I've seen their use climb in the past 5 years and I am sure that my success rate at convincing my patients to not roll the crap out of their IT Bands is less than 10%.  Those rollers are WINNING.  Perhaps this post will sway the voters.

Background Reading

My belief has been bolstered by two old anatomy papers by the Fairclough group that showed and proposed that IT Band dysfunction is not a Friction syndrome as the IT band does not "slide around" at the knee.  This perception of sliding is an illusion.  This group also performed a detailed anatomical analysis of the structure.  The papers are here and here.  A more recent study has also lent support to these papers with a biomechanical study looking at the strain placed on the ITB - click here. One of the authors of that paper is Andy Franklin-Miller, whose sports medicine blog you can see here.


Some quick points about the IT Band

- the IT Band is not really a strap that runs from the hip to the knee.  It is not a discrete entity.  Rather it is just the thickest part of the fascia lata.  The fascia lata being the sock that wraps around the entire thigh.  The IT Band is just the lateral thickening of this sock

- the IT Band is some dense connective tissue and probably can't be permanently deformed.  While it may be stretched in the short term this is due to its viscoelastic properties (i.e. adding a bit of grease or shaking out the cobwebs) rather than any means where it is actually permanently lengthened.  Actual lengthening would require you to damage your IT Band to get it into a lengthened state.  5 minutes on a foam roller or 10 minutes of daily stretching would not be able to do it.

- you might be able to stretch the muscles that attach to the IT Band.  However, muscle stretching is also very difficult.  The changes in muscle stiffness we see with stretching and warm up are again due to the viscoelastic properties of tissue.  Muscles don't become looser they just have increased tolerance to stretch. Update Nov 2015: some research has even challenged this idea! This is most likely an adaptation of the nervous system rather than any change in muscle tissue properties. See my post here on muscle stretching.

- the IT Band can't be lengthened because it is tethered to the entire length of the femur.  Got that?  It is tied to the leg bone.  It ain't going no where.

- it is supposed to be tight.  Therapist will tell you it is tight because they were told to look for it to be tight.  They don't have a proper method to determine this.  The test that  looks at ITB tightness (OBER's test) is really just an assessment of hip adduction range.  So many other factors influence this range that to blame it on the IT Band is just bullying (IT Bullying!).

-what if you could lengthen it? Then what? Could you over do it and have some jigglying IT Band that just wobbles when you run? No! This does not happen.  It does not stretch.

- the ITB may be similar to tendons.  Meaning it stores and releases elastic energy.  We definitely don't want to length it or change its properties.  There is little evidence that tendon stiffness can be changed through stretching so perhaps the ITB is similar.


Some thoughts and questions on Foam Rolling the IT Band

- I know this is popular.  I know people swear by it. But that does not make it right.  I don't doubt that after beating the crap out of your IT Band you feel something different in that IT Band.  That is your nervous system adapting to some huge painful stress you just placed on it.  It does not mean that your ITB got longer or you dug out some adhesions.

- How can a foam roller stretch an IT Band?  A roller compresses the band it does not tension it. Without tension there is no stretch. Don't tell me it bowstrings it.  This is negligible.

- How can a roller dig out adhesions?  This is a massive question because you can even question the existence of adhesions.  But assuming that adhesions exist between the sliding to two different layers of tissue how would a roller that just compresses tissue create some form of interlayer gliding.  If you think you are causing the IT Band to slide better in its interface with the biceps femoris than you are completely wrong because the IT Band does abut or interface with that hamstring.  If you think that the roller is freeing up the sliding between the IT Band and the Vastus Lateralis how would compression do this?  I can't fillet a chicken breast with a rolling pin.  I need some instrument to put between the two halves I want to separate.  Same with the theory between interlayer sliding.


- The foam roller improves tissue health.  Maybe.  You are certainly stressing the shit out of the IT Band, neural structures, skin, bone and everything.  You are probably even creating an inflammatory response.  This might have some merit.  But I would bet you could get a similar stress with some other movement or exercise that would have other performance or therapeutic benefit.  Why not take the thumper and thump away on your leg (I actually do this for kicks)


-Last, no real research on any of the beliefs about foam rolling.  I recognize that a lack of research is not proof but you would think something would come along by now. Update (November 2015: there is some research on foam rolling.  Feel free to wade through the mess of it. I would only ask "is foam rolling the best use of your time?")

-Super last, I am open to being convinced that it is worthwhile.  Perhaps, rolling your IT Band has some other benefit.

-when discussing foam rolling we also need to discuss fascia.  I have a related post here.


Updated Last, I was given some links to some posts by Paul Ingraham. I haven't read these yet but have read Paul's other work so wanted to post these here.


Caveat of Ignorance

For those that really disagree with me and really love foam rolling try to get past my obviously hyperbolic title.  I agree it is a little strongly worded.  Again, I write from a place of ignorance (as should everyone on this topic) so I am open to any information


UPDATE: Below are a few links that further discuss foam rolling

1. Mike Boyle disagrees with even my hesitant conclusion and does provides a rationale for foam rolling.  Basically, he believes that foam rolling prepares and individual to participate in activity as foam rolling a stress placed upon a tissue and we should expect tissues to respond positively to stress. I have mentioned that this might be something going for foam rolling I just am unsure how this would really work in practice.  He provides  No specific mechanism  just the advice that it works so we should do it.  Interestingly, he refers to me as a "muscular therapist".  I am flattered, I always thought I was quite skinny.

2. Mike Nelson provides an argument against foam rolling:

3. Carl Valle provides a very interesting piece that addresses what Mike Boyle said about foam rolling. I found this blog really very informative.  I've read Carl's stuff before and consistently find it interesting.

4.  An interesting case study looking at foam rolling and tensiomyography by Jose Fernandez.  I would be interested in learning more about the measurement properties of this technique.

5. An abstract that looks at the use of foam rolling as a warm up tool.  I have not read the full masters so can't fully comment.  They suggest that foam rolling decreases jump performance in the short term.

6. Here is a post by Dean Somerset providing a different rationale for why individuals might benefit from foam rolling.  This stuff is a good start.







Nerve Slider Videos: Calming down that irritated nervous system

Audience: Patients Purpose: Demonstrate simple movements to calm, move and make healthy some irritated nerves. Disclaimer: Not to be done if painful. Do 5-6 to start. Always under health professional guidance.

Radial Nerve

Median Nerve

Ulnar Nerve


Musculocutaneous nerve slider

Very similar to the radial nerve but instead of bending your wrist so that the back of your hand faces the floor and your palm faces backwards you should let your palm face upwards, keep your thumb tucked in and then tilt your wrist to the side of your pinky finger.

This slider may be helpful with those with anterior shoulder pain that are told they have bicipital tendinopathy.

Sciatic, Tibial or Peroneal Nerve (Slump Slider aka Flossing)

Sciatic, Tibial or Peroneal Nerve (Long sitting slider)