Your cranky nerves: A primer for patients to understand pain

Audience: Patients with any type of pain or injuryPurpose: to learn a little about pain and convince you that pain is not in your head even though your brain plays a big role

Why? Understanding pain helps decrease pain and helps us make better choices in the treatment of injury

Some brief pain information tidbits

  • you don't need a leg to feel pain in that leg (e.g. phantom limb pain)
  • you always need a Brain to feel pain
  • pain can become a habit - and like all habits lots of factors help keep it going
  • Changes in how we feel pain can also come from changes in the brain and the nervous system
  • tissue damage or degeneration does not have to lead to pain - but it certainly can

Damage does not always equal pain


The idea that lots of pain equals lots of damage is a very difficult concept to shake.  It is entrenched in how we think about pain, arthritis, surgery and injuries.  When we have pain we want to know what is causing it. We assume there must be something damaged and that causes our pain.  The problem with this is that the majority of us are walking around with some degenerative joint disease, disc protrusions, tears in our shoulder rotator cuff and all kinds of things that look like damage YET we have no pain.  Conversely, you can have a lot of pain and all the imaging shows that there is no damage.  This can be extremely frustrating for someone in pain. Take a look at this rather dry post that details a number of research studies showing the poor relationship between joint damage and pain.

However, sometimes damage certainly does lead to pain.  If you break your arm it will hurt.  But in a week, that arm will still be broken but you can be out of pain.  I also know, that many people with hip degeneration are in a lot of pain, they then get a hip replacement and they are out of pain.  This is wonderful.

So why does some damage end up leading to pain and other damage doesn't?

Several factors can contribute to our experiencing pain.  The leading theory on pain is the Neuromatrix Theory.  In a crude nutshell, it suggests that the brain ultimately decides how much pain you will feel.  The brain takes in all kinds of information and then makes a decision.  With a recent injury we think that you feel pain, swelling, weakness, tightness, guarding all because the brain is trying to protect you.  The area of the injury will get more sensitive and your brain can get better at producing pain.  The brain thinks that pain is a good thing.  Unfortunately, pain can persist for a long time after the pain is useful.  For whatever reason the brain, your nerves, your muscles, your immune system, your endocrine system all stay sensitized.  Its now easier for you to feel pain.

But none of this is all in your head.  In fact, this is how athletic excellence works

The brain learns and you become a better athlete/guitar player/knitter


In some ways we can think of pain as habit.  Our nerves and brain get better at making pain.  Now, I know this sounds like I am saying this is psychological because I'm talking about the brain.  But would you ever say its psychological when you get stronger after working out for 6 weeks? Of course not, but after exercise training much of the reason we get stronger or perform better is because the brain and nervous system become better at the task.  This is similar to what happens with pain.  We get sensitized and better at producing pain.

Pain is neither a barometer or a GPS

The pain we feel gets out of whack with any damage we have.  The pain becomes the bigger problem than any wear and tear.  Pain is now a poor guage of how much injury there is.  Pain is also horrible for telling us where the problem is.  Where do people feel pain when they have a heart attack?  Their arm, neck, chest and back.  There is nothing wrong with their arm.  This is how we need to think about pain.  It is just an alarm that goes off.

The overly sensitive alarm

NO! Don't make me do crunches!
NO! Don't make me do crunches!

If a fire alarm goes off in a building we have no idea if the alarm is due to a large fire, lighter held underneath a sensor, a little bit of smoke or even some problems with the wiring.  We can even put of the fire and the fire alarm will still go off.  This is how we can think about the pain alarm that goes off in our body.  It can stay on long after any damage has healed. You can even think of pain as a cranky toddler.  The pain or response of the toddler is often out of proportion to their injury.  At an unconscious level this is what can happen with our body.  A disconnect between damage and pain and we are left with screaming joints or muscles.

Again, the pain is not in your head

You might ask why I keep talking about cranky nerves and a cranky brain when you know that there are problems with your muscles and your joints.  I would probably agree with you.  When we have pain for awhile we move differently.  We can get weaker, we can get stiffer, muscles can compensate, you might slouch or limp or move poorly.  All of these things can either be caused by your pain or can be contributing to it.  Addressing them can be helpful but surprisingly it is not often necessary.  Often, we can change your pain immediately and you will have immediate change in strength or range of motion.

Treatment is about decreasing the sensitivity of the system

You have threshold to where you feel pain.  Treatment is about increasing this threshold.  This can be done a number of ways.  Good treatment should try to address as many different factors that influence pain.

The significance of everything above means that you can have damage. You can have joint degeneration and certainly can have the normal wear and tear associated with arthritis.  Whats great is you can change the amount of pain that you feel without ever changing the amount of arthritis, wear and tear or even damage in different body parts.

Treatment helps turn down the sensitivity of our nervous system.

See here for a description of my treatment approach.  But what we need to remember is that since pain is influenced by many factors many things can influence the pain we feel.

Related Pain Links

1. Pain videos


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.

The relationship between functional tests and athletic performance: Part I - The single leg balance test.

Background: Testing and assessing an individual is popular.  There is an old saying that if you aren't assessing than you are guessing.  The assumption here is that the tests and assessments you do are somehow relevant and meaningful yet I would suggest that the majority of tests and the information gleaned from them hardly change (10% ish) a therapeutic approach once you have heard your patients history. I can have a patient with knee pain and run them through 30 different tests and the results of those tests may hardly change my treatment.  Tests have to provide us meaningful information that we can do something with.What the hell am I talking about?

This blog post is the first of what I hope to be many posts that review the research on our physical tests of purported function.  We make a lot of assumptions about the tests that we commonly use in the clinic.  For example, someone might tell you that your hamstrings or psoas muscles is tight and this will cause you to be hyperlordotic (pelvic anterior tilt) during running.  Or you might hear that you suck at doing a squat and without being able to squat your form during other activities will suffer.  Ultimately, "failing" these tests can lead to you spending time doing lots of "corrective exercise" to fix a test.  This fix is assumed to help with function in other realms of activity.  I want to explore the assumptions behind the tests we use and then the purported fixes that follow.   Some of the topics I might explore:

- assessing tightness in a runner and whether or interventions influence running form

-  how strength training influences joint biomechanics/dynamic form

- how tests of static function relate to dynamic form (e.g. running)

- how simple dynamic tests (e.g. a squat) relate to dynamic form/joint biomechanics

- how measures of joint strength or ROM relate to dynamic form/joint biomechanics

- whether dynamic tests (e.g. a single leg squat) actually give insight into what they are supposed to be giving insight into (e.g. pelvic stability, hip abductor strength and a surrogate for hip control when running etc).

I have touched on these ideas in a number of other posts below:

- specificity of movement training (looks at our ability to change posture) (link here)

- the inability of tests to identify functional hallus limitis  (link here)

- weakness of the prone hip extension (Janda) test. (link here)

So here goes with a look at a common test for runners...

The Standing on one leg balance test is not a relevant test for Runners

Whoa, quick disclaimer.  This first post is an opinion as there is no evidence that specifically looks at this.  However, there is plausibility and I want to make the argument that being able to balance on one leg has nothing to do with the act of running.  This is a common test advocated by rehab professionals (many of whom I greatly respect and one has good book out on running biomechanics and injury here) looking to screen for deficits in function that are assumed to affect ideal running.  But I just don't see it.  It makes no sense to me so if you are reading this and think I am wrong please let me know.

The one leg balance test has you simply balancing on one leg with your eyes open or closed.   If you can't do it the assumption holds that you will be prone to injuries during running or you  may end up with some sort of issues with your running form.  The test is based on the idea that running is merely a succession of leaps through the air interspersed with balancing on one leg until the next leap.  I would respectfully suggest not.  Here is my reasoning:

1. The skill of running is completely different from the skill of one legged balancing. Running is not balancing on one leg as you are not static like you are during the balance test.  These two tasks are completely different. And we should not expect that one can be a surrogate for the other and reflects the same demands.  Our ability to balance is activity and context dependent.  I don't think we can assume that balancing skill in one task will carryover to another completely different task.  The same holds true for that crazy dead fad of doing squats on BOSUs or balance balls with the assumption that training this form of balance will carryover to the balance needs of a golfer or hockey player.  The latter is from Mars and the former is from Uranus.

                                                                   2. Static versus Dynamic Analogy

Running is dynamic.  You do not pause and balance on one leg.  Comparing one leg balance to running is like comparing the ability of a stationary top to balance on its point with the ability of a SPINNING top to balance on its point.  Suggesting that we need to be able to balance on one leg in order to run safely is like arguing that in order to ride a bike properly you have to be able to hop on the bike, clip in and then balance in place without moving.  I have been having my five year old do this for months before I will let her ride her bike and surprisingly she still can't ride a bike...and that bruised little monkey hates me for it.  (Obvious disclaimer: I am kidding).  But this example illustrates my point.  If it seems absurd on a bike then it is just as absurd on your feet.

Caveat of Ignorance

I reserve the right to change my opinion with new research or with fresh ideas.  I can also be convinced to think otherwise.  My mind is not as closed as my writing might indicate.  As a further hedge I also recognize that it is possible that some cross sectional study might come out and suggest that one leg balance is compromised in runners with knee/ankle/back/hip pain.  I don't doubt a correlation might exist BUT this does not imply that the decrease in balance ability is the cause of the pain.  This can merely be correlation.

Last, this does not mean that one leg balance training can not be beneficial for runners in preventing injuries or improving performance.  The act of doing one leg squats, one leg hops, hip airplanes, front scales and other great exercises could certainly improve your balance and would also change other aspects of muscle function.  In this case the improvements in balance could be secondary to other aspects of improved function that are the true drivers of improvement in performance and injury resilience.

Last point, honest- perhaps we over assess and our assessments change nothing in practice

What I think can be argued with this assessment test (along with many other tests) is that it just isn't necessary and is plausibly not valid.  If I am working with a runner or an athlete their conditioning program would be all encompassing and comprehensive.  This would include exercises that ultimately improve their balance along with other variables.  I don't need a rudimentary test to tell me to add these exercises.  I just need that human in front of me that tells me that they want to run and be an athlete.  I don't want to freak them out because of their shitty balance or advise against doing these wonderful exercises because they have great balance during a static, albeit not relevant to running test.

Postural correction and changing posture. Can we treat our patients like puppets?

Audience: Therapists and Strength CoachesPurpose: To justify the use of a variety of exercises (even general exercises) for training, rehabilitation and injury prevention and question the application of movement specificity principles.

The Gist of this Post: Specificity of training is an important component of rehabilitation and strength and conditioning but I think the application of specificity can be taken too far when we attempt to mold our posture.

A related post by Tony Ingram touches on many of these ideas in relation to pain and posture.


The godfather of specificity was a former professor of mine, Digby Sale.  For a brief review see here.  Very briefly the research suggests:

"Evidence supports exercise-type specificity; the greatest training effects occur when the same exercise type is used for both testing and training. Range-of-motion (ROM) specificity is supported; strength improvements are greatest at the exercised joint angles, with enough carryover to strengthen ROMs precluded from direct training due to injury. Velocity specificity is supported; strength gains are consistently greatest at the training velocity, with some carryover. Some studies have produced a training effect only for velocities at and below the training velocity while others have produced effects around the training velocity"

Another great review article is by Cronin et al (2002) link here:  A quick quote from the abstract:

"It has been suggested that training at a specific velocity improves strength mainly at that velocity and as velocity deviates from the trained velocity, the less effective training will be. However, the research describing velocity-specific adaptation and the transference of these adaptations to other movement velocities is by no means clear".

My thesis: The applications of specificity can be taken too far in three ways

1. The repeated performance of an exercise leads to plastic deformation of tissues or changes in motor control that cause significant changes in posture and movement capabilities (aka form).

I question if the body is really this malleable and ahem, stupid.  It assumes that consistently training certain movements makes you move in that specific way and you lose the ability to move in other ways (i.e. your posture and form become changed).   I believe it is an inappropriate extension of you become what you train.  It is a training belief related to the idea that hip flexors become shortened because we sit all day (see a previous post here).  I don't doubt that you can train habits of movement that might carryover into other tasks.  What I question is whether are tissues are so readily plastic and they can't control their destiny because of some passive changes in the make up of the tissue. 

An example...

I was listening to a podcast where the speakers objected to what they felt was the rampant, unjustified, often silly and apparently detrimental usage of the front and side plank (bridge) by physiotherapists and trainers the world over.   What the speakers argued was that performing these repetitive planks with no motion between the hips and the thorax would somehow create runners that will run like robots and lose the ability to dissociate the hips from the thorax.  As if twenty minutes of planking a week will somehow carryover to the automatic movements that occur during running.

I just don't buy this and consider it such a pessimistic and wholly unfounded structural view of the body.  It assumes that the body is stupid and a few minutes of planking will somehow override what ever neural control mechanisms, not to mention physical forces, that create subtle movement in the spine when we run. 

A brief review of 3D spine kinematics during running can be found here (Schache et al 2002 ) and here (Saunders et al 2005).

We don't change form through simple exercises...or do we?

The belief that planking makes you rigid and run like a robot has not been tested but assumes that planking will somehow stiffen up all the muscles of the trunk within the neutral zone and also cause our brain to change the automatic way in which it recruits muscles during locomotion.  That is some powerful planking to override our nervous system like that.  It is very difficult to change running kinematics even when we try to change running kinematics by volitionally changing our posture.  But somehow, a little bit of planking can do this despite us trying to run normally. 

Same holds true for the knock on the curl ups.  I think it is a fair to critique curl ups  for other reasons (e.g. there are better exercises, you may not think they are functional, you don't like the idea of compressing a disc with some flexion) but I don't think we can turn people into kyphotic zombies.  Unless you've been bit by a Kyphotic zombie and those are biochemical changes not biomechanical. Curl ups get critiqued because it is assumed that doing a lot of curl ups will end of shortening the rectus abdominis and will therefore be constantly flexed.  I just don't see any research suggesting that this happens.  While we might increase the stiffness of the rectus abdominis this is different than making that muscle shorter at its resting length.  The muscle has a stress strain curve where there is hardly any resistance to movement around its resting length (i.e. the neutral zone) while strength training might shift that curve if stiffness increases it still has a "toe region" of the neutral zone where hardly any passive force is created.  Certainly not enough to crank down the thoracic spine and all of the other opposing muscle groups

Some Research on changing posture and form through exercise

Here is a sampling of studies looking at both strengthening and stretching programs designed to change Scapular position or posture in general .  This is ridiculously difficult to do.  None of the following studies were able to do it:

- a review here by Con Hrysomallis looking at Shoulder position

- a review by Hrysomallis looking in general at the ability to change posture:

-Wang et al (1999) Stretching and strengthening exercises: their effect on three-dimensional scapular kinematics.:

- McClure et al (2004) Shoulder function and 3-dimensional kinematics in people with shoulder impingement syndrome before and after a 6-week exercise program:

-Hibbard et al (2012) Effect of a 6-Week Strengthening Program on Shoulder and Scapular Stabilizer Strength and Scapular Kinematics in Division I Collegiate Swimmers:

Serendipity of the internets

I have been writing and thinking about this post for months and along comes a post from Bret Contreras arguing that strength training alone does not change form. He argues that motor control training changes form.  This is a component of what I am trying to say.  Here is a link to Bret's piece

MY ARGUMENT DOES HAVE SOME RESEARCH AGAINST IT...Sort of weaken my arguement (and engender some healthy doubt or hope :) ) there are some papers that do show a change in posture albeit inconsistent. 

 1. Here is a great paper by Scannell and McGill(2003) - Stu does all the great stuff!

But, there was not a change in the stiffness of the spine nor did this lordotic static change carryover to a functional task

There were no changes in the size and location of the NZ of each group recorded during the mid-training and posttraining tests.

Relative to the pretraining test, all 3 groups sat in more lumbar flexion during the mid-training test (P=.005) (lumbar flexion increased by 4° in subjects with hypolordosis, by 5° in subjects with hyperlordosis, and by 5° in control subjects) and the posttraining test (P>.5) (flexion increased by only 1° more in all 3 groups relative to the mid-training test results). The changes in the sitting position between the pretraining and mid-training tests were seen in all 3 groups and therefore cannot be considered a treatment effect

Above Figure Description: The changes in the neutral zone (depicted by the black bars) and the lumbar position during sitting, standing, and walking (50% level of the amplitude probability distribution function) across the pretraining test (1), mid-training test (2), and posttraining test (3) are shown. The subjects with hyperlordosis stood in less lumbar extension during the mid-training and posttraining tests. Subjects in all 3 groups sat in more lumbar flexion during the mid-training test. No changes in the lumbar spine position during walking were found during the mid-training and posttraining tests. Positive values greater than the neutral zone represent extension.

An interpretation of the Scannell Paper

The Scanell paper certainly shows a change in resting posture (e.g. lordosis) but we see no change in lordosis during functional activities nor is their change in the stiffness of the spine.  This suggests that we aren't changing passive properties of the spinal tissues with these exercises but we are doing something else to change resting posture.  Did the participants change habits while doing the exercises and became more comfortable standing in a more neutral posture?  Was their standing posture a choice?

What I take from the conflicting research is that if there is a change in form with basic exercise it is not robust nor is it consistent.  And there is not sufficient information or even biological plausibility to assume that doing the plank daily for 3-5 minutes will somehow result in all of us moving like robots during an activity like running which appears governed by more central patterns.  I can't even imagine trying to run with a non-moving spine.  

A few more papers showing changes in posture with exercise:

2.  Misconception #2: Exercises must be specific in terms of every variable to be considered "specific"

This happened to me when I was trying to publish a paper on strength and conditioning for golf and I had the pickiest reviewer who kept saying that none of the exercises I was advocating as being specific to golf (e.g cable chops, one arm cable punches/pulls, weighted swings, med ball rotational tosses, Swing fan swinging) were specific to the golf swing as they all either had slightly different mechanics or different speeds.  I believe that I asked if a weighted sled exercise was specific to running and I was told that no it was not. I just think it is realistic to assume that a definition of specificity recognizes that some differences in terms of velocity or kinematics is acceptable and that we will still get benefits in the task we want to improve.  The early papers mentioned by Behm and Sale and by Cronin et al certainly support this.

3. Misconception #3: Non-specific or general strength exercises can't carry over to performance/injury reduction for specific tasks.

This is essentially the opposite of number two.  It is a pretty big debate and would rear its head with those arguing for functional exercises versus non specific exercises.  You could also ask "Are specific or functional tasks always better than general exercise?".  MOst of the time people assume (myself included) that specific tasks are better but I think we would ignoring a lot of research that suggests otherwise.

 A specific example can be seen in respect to doing a plank exercise for a runner.  Obviously, no runner gets into this position.  It is not specific in terms of body position with respect to gravity, the movements of running and certainly not velocity.   So the knock against this exercise is that it is not specific to running and therefore can't help the runner.  And I say, who cares? Why does it have to be specific to running? Can't an exercise give us benefits that carryover to other tasks?  Of course they can.  The plank obviously trains the trunk muscles and the lateral hip muscles.  We know that many runners with pain have weak abductors (whether this is a cause or correlation is hotly contested) and at the same time we have some evidence to suggest that training the hip musculature (with exercises that are nothing like the running movement) can be effective in returning people to running and decreasing pain in those with knee injuries. 

What is the mechanism for non-specific exercise benefits

Interestingly, the reason why these exercises are effective often has nothing to do with the purported biomechanical rationale for training the hip musculature in runners.  Specifically, we can advocate training the hip musculature under the assumption that this might change hip valgus and femoral internal rotation during the stride as there is some evidence to suggest that these mechanics are occasionally linked with knee dysfunction.  However, when we implement these hip exercise programs (again with exercises that are basic and totally not specific to running) we will see decreases in pain and return to running WITHOUT changes in the assumed dysfunctional mechanics (check out these papers here, here, here,  here  and here). Of course there are some studies showing that form does change (here and here - albeit no change in kinematics, just moment)  To me, this suggests that there is something generally beneficial about these exercises and that specificity does not have to occur.  But, if you want to change running form than the intervention should probably specifically try to change running form through feedback and training. (see here, here and here)

In terms of performance, I am biased, I do like creating exercises or stealing them that are somehow specific to the task at hand.  However, I recognize that there is a great deal of research that shows that exercises that are not specific to the sporting task can still improve performance (e.g. squats for sprinters).  Again, arguing that specificity is not always necessary.   My main point is the body craves variety and our programming and rehabilitation should reflect this desire.  We don't  have to be so rigid in our prescriptions or believe that there is only one way to get benefits.  The body adapts, lets exult in this.

Future Posts Related to this Topic

This post is a bit of a jumble with a lot different ideas.  I have few posts written half-assed in my head that are related. If anyone wants to write any of the following with me please let me know.  Or stay tuned for these upcoming posts.

These posts will ideally be a gathering of information that generates questions.

1. A catalogue of exceptions to the Joint-by-Joint Approach.

This post will use the framework of the joint by joint theory to consider the research that looks at injury risk factors.  It is not so much a critique of the approach but more a means to understand it limits and explore how it can still be useful.

2. A catalogue of examples that support the Joint-by-Joint Approach

3. Is there an optimal way to move? A catalogue of theories and evidence for ideal movement 

4. Can form be changed with via mechanical changes in tissue?

5. Changing running form through feedback and training.

Critique and update of Janda's Prone Hip Extension - making it useful

Audience: Therapists and patients with too much time on their hands Purpose:  Provide a mild critique of the utility of the prone hip extension test



The prone hip extension test (or prone leg extension - PLE) is a very common clinical test in use for more than 20 years.  Two influential clinicians have advocated its use although for slightly different reasons.  Both Vladmir Janda and Shirley Sahrmann have described its use for decades.  This blog will focus more on the clinical rationale that Janda proposed.

Briefly, the test asks the patient to lie prone on a plinth, hands palm up at the side of the patient.  The patient is then asked to lift a leg off of the table approximately 6 inches.

It has been suggested that there exists an ideal movement pattern when lifting the leg off of the table.  It is proposed (Rehabilitation of the Spine,  by Craig Liebenson pg 214 -great book by the way) that his hip hyperextension movement is performed to analyse the hip extension that occurs during the terminal stance phase of gait.

Deviations from the ideal pattern while prone are indicators of the dysfunction that could be occurring during gait or possible other tasks (e.g. an individual might hinge at the spine during a squat rather than the hinge because of a weak/inhibited gluteus maximus aka. gluteal amnesia).

The crux of this test is that there is an ideal or optimal way to lift the leg off of the bed.  Deviations from this pattern would therefore indicate dysfunction and dysfunction would then be the cause of all manner of nasty stuff.

Janda proposed that a normal pattern of muscle activation timing occurs during the PLE.  The ideal order of muscle firing being:

1. Gluteus Maximus

2. Hamstrings

3. Contralateral erector spinae

4. Ipsilateral erector spine


Deviations from this pattern or alterations from abnormal recruitment patterns (both amplitude of muscle activation and timing) may result in the observations of the following assumed dysfunctions:

1.  Hinging does not occur at the hip joint rather it occurs in the lower spine.  This is assumed to occur because of weakness or inhibition in the Gluteus Maximus.  The patient therefore gets thigh extension from an anterior pelvic tilt rather than the hip actually extending.

2. Flexion of the knees occurs suggesting hamstring dominance

3. An observable (or palpable) delay or absence of Gluteus Maximus firing.  (aka, hey where is your butt?)

4. rotation in the lumbar spine

5.  initiation of hip movement by periscapular muscle activation


The research, tinged by opinion, on this test

Full disclosure, I use this test with my patients yet I have also published research questioning its validity.  My initial research in 2004 suggested that a delay in the firing of the gluteus maximus was common in all subjects and the range of timing across muscles is probably something that can not be seen by the human eye.  In other words, the timing is so close together between 20 and 500 milliseconds that I doubt you can see what muscle turns on first.  Especially, with fat being distributed differently over the different regions.


My research was nothing brilliant or new. Researchers before me had this found this as well (Pierce and Lee , Vogt et al 1997) and many researchers after me (Oh et al 2007, Sakamoto et al 2009)

Some interesting work has even looked at changing the timing and the amplitude of muscle activity (Chance-Larson et al 2010, Lewis et al 2009) but they still showed that the Gluteus Maximus fires last BUT it can be taught to fire sooner BUT without actually changing the order of activation.  NEAT...and I don't know if it is relevant.


So, the research suggests that the originally suggested firing order may not accurate.

The question now is "Should we then conclude that the test is invalid?".

My personal opinion is that we can't make this conclusion yet.    I even argued this in a paper I published in 2006 which is often cited to discredit the PLE test (kind of the opposite of what I was going for in my discussion but stuff happens).  In this study, my girlfriend at the time (now wife) sprained her ankle.  She had previously been a subject of mine in the 2004 study.  I therefore, had data on her in an uninjured state.  I immediately rushed her to my lab, through electrodes on her butt (something we already did for fun, just kidding), hamstrings and back and tried to see if this ankle injury influence muscle activation timing over the course of 8 weeks (click here for the study).  We found nothing, the variability was huge and it was a mess.

But I was not ready to throw out the test.  Here is why...

Most research to date only looks at EMG timing.  It does not really look at amplitude of muscle activation and certainly does not look at the force contributions from the various muscles to the movement.  Nor does any of the research look at Kinematics (e.g. what the movement looks like).  And it is with this information that I think  people use this test.  I don't think it is valid to look at a the posterior chain and conclude that the glutes are slightly delayed after the hamstrings.  But I do think you might be able to say that the Gluteus Maximus is not turning on at all. For example, the GMax might be remaining completely flaccid on one side and be hard as rock on the other.  This type of obvious difference might be something that is relevant.

What about alterations in form?

We can't discount the idea that a movement pattern that sees the patient spinal hinge or anteriorly tilt their pelvis a great deal rather than merely extending at the hip is not dysfunctional.  I am not saying that it is dysfunctional, just that no one has proven that it is not (they haven't proven that it is but I am sure a biomechanical - tissue overload argument could be made and is made).  This research needs to be done, but it is much a larger question.  This is the question of whether there is an optimal way to move and if you don't move in a certain pattern then you are dysfunctional and therefore more prone to injuries.  This a huge and difficult question.

How might the test be Useful?

I am very hesitant to look at how someone moves and say that it is a dysfunctional pattern - especially if there is no pain.  But a painful PLE might be relevant and useful clinically under certain circumstances.  We just need to Reconceptualize the test.  Here is an example:

A runner complains of low back pain while running.  When running it looks like they are very upright and leaning backwards.  They also have a long stride and therefore a low stride rate.  When they arch backwards it hurts. Passively and actively they don't have much hip extension.  When the do the prone leg extension test it hurts and it seems like they arch their back a great deal.  This is easily observed and doesn't require some magical EMG sensors to built into your eyes to see a muscle activation.  These are BIG ROCKS hitting you in the face.  This might be a case where the pattern is relevant.

Why and how is the pattern relevant clinically?

The painful pattern is relevant because:

1. The movement is kinematically and symptomatically similar to the painful functional task (running).

2. The painful PLE might give us insight into a HABIT of movement that is painful.  Its odd, but people often keep doing the same movement/posture adoption even when it hurts

3.  The lack of hip extension might decrease their movement options so they have to move in a pattern that is already sensitized...they can't/don't move differently to give themselves a break.

Clinical Decision Making & Treatment

We can try to do things to desensitize the pattern. Lets not view the PLE as faulty but just sensitive.  The movement has become coupled with pain.   Desensitizing the painful PLE and doing things to desensitize the painful running gait would go hand in hand.  What is possible as well is that you just desensitize this for the short term and perhaps they can go back to running the same way in the future.  So, how do you desensitize it?

Desensitizing the pattern

1. Running Changes: EASY-PEASY- 1. shorten their stride and maybe try leaning forward and if all else fails very temporarily have them posteriorly tilt their pelvis (they will hate this but frame it only as temporary).  Shortening the stride might be enough.  Do FORM FARTLEKS of 30 seconds of the knee running style and 3 minutes of the old.  Keep them running because this is meaningful.  As long as they don't flare up keep them active.

2. Load locally - my guess is that spine stability exercise "work" because you load locally and this has an analgesic and cognitive influence.  You confront with strength.  Load is good.

3. Sensitivity/Symptom Modification: Modify the prone leg extension in a billion ways (it doesn't matter how) and have them extend that hip with decreased pain.  Learn a new habit.  Maybe we are uncoupling pain from that movement.  Then go back and try to do the movement again and see if it hurts less.  Sometimes it carries over.  If it doesn't no worries.  Keep doing the symptom modifying exercise hourly for a few days.

4. Maybe stretch the hip flexors - can't believe I'm saying it.  It won't hurt and this is a case where the impairment may be relevant.

5. Load Globally: General hip, spine and leg exercises help sometimes.  We don't need a fancy kinematic explanation.

I think there are a few take home points

1.  The research against the test suggests that for the majority of people a delay in Gluteus Maximus is the norm.

2.  There is no research* investigating whether alterations in form (i.e. kinematics) that are different than the ideal (e.g. the spine hinges or twists) are normal and harmless variations on how to move or are indeed painless dysfunctions that are related to current or future injuries.  *When I say research, I mean a direct link.  I recognize that many esteemed biomechanists and clinicians can provide a very plausible biomechanical or clinical rationale (hence, I admit I use this test occasionally)

3. Activation patterns and even amplitude can be changed. One biomechanical model suggests that changing the activation patterns and amplitudes can influence anterior hip joint health.  See my post here on the great research of Dr. Cara Lewis.

4. "Dysfunctional" patterns may not be absolute.  They are probably more relevant in specific cases.


Some relevant points that I did not even touch on

1. You can criticize the test and say that an open chain hip extension test is not at all relevant to what occurs the hip extension during walking.  I have lab EMG research showing that the Glut Max barely fires during walking and this is supported by Dr Lieberman's (of barefoot running fame) EMG work on the role of the Gluteus Maximus during running (see the paper here). Hip extension during terminal stance may even be mostly passive in that the hip extensors work more to slow the hip down and then accelerate during terminal swing and early stance rather than provide any extensor thrust backwards. I believe this is why Dr. Sahrman advocates testing hip extension with the starting point of having the hip in 30 degrees of flexion.  However, even if the criticism is watertight it does not mean that the test is useless.  Just that the rationale behind its use may need to evolve.

2.  We should question rather the PLE is related to the movement that occurs during our functional tasks.  While it is true that a lack of hip extension during running is compensated for by an increase in anterior pelvic tilt it has also been shown that our static tests for decreased hip extension (e.g. the Thomas test) do not correlate with the amount of hip extension that occur during running.  This area would really be a great PhD and another post.  It is the idea that many of our clinical tests of function might not even be appropriate surrogates for tests of dynamic function. For example, dysfunctions during a single leg squat (e.g. knee valgus, femoral internal rotation) may not consistently correlated with the same dysfunction during running or even be related to Gluteus Medius strength (reference to follow)

3. We can't conclude that the gluteus maximus does not become weak or inhibited.  Maybe we just don't have the best test.  Other researchers (Stu McGill) have advocated testing its function with the supine bridge.


As always, more research is needed but no one wants to do it and no one will pay for it. Hence, I am no longer a researcher.


All the best,


Greg Lehman

Physiotherapist, Chiropractor and reformed biomechanist


What is injury treatment? The judicious use of stress.

Audience: Patients

What is this about:  Injury Treatment

Injuries can be treated a number of ways and many different ways are often successful. But if I am asked to be very simple about what treatment is I start with one basic assumption.  THE BODY ADAPTS TO STRESS. 

Often the body adapts positively to stress.  This is why exercise is important.  We stress the body with running, strength training or yoga and the body says "what are you doing this to me? I can only handle this for so long, I had best ADAPT".  This is also said in an australian accent.

Unfortunately, the body is sometimes overloaded with stress and its adaptability is overcome with too much stress.  Hence, an injury and sometimes pain.  An injury is merely the body's lack of ability to adapt.

What treatment is, is the judicious modification of stress.  We can stress a tissue or system of the body with some form of modality (active release technique, massage, exercise, ultrasound, LASER, needles etc, although I don't really do the latter three) and this will in turn challenge the body to be the unbelievable adaptive system that it is...and get better.  We can also modify the stress on tissues.  We might do this physically (e.g. teaching spinal sparing postures, taping a foot, perhaps joint manipulation or tissue manipulation) or even through a cognitive-behavioral approach (e.g teaching a patient that hurt does not equal harm may change movement patterns that overload cranky or injured tissue).

That in a large nutshell is how I view treatment and injury.  The body adapts and we can facilitate this.


Greg Lehman

Your Toronto Physiotherapist

Chronic Pain - Do therapists contribute? An unsolicted rant

Become invisible and walk into a Chiropractic, Physiotherapy or Massage Therapy office one day. Watch them speak with a patient who has back pain or maybe a little bit of knee pain. You may hear the following: -you need stability exercises -these muscles are very tight -you need therapy as you don't want this degeneration to progress -no more running or arthritis will certainly flare up and you will have real problems down the road -you have dysfunctional movement patterns -your glut muscles don't turn on -oh, it hurts here (pressing on upper traps). There some adhesions in the muscle -I need to see you 2-3 times a week for the next 4-6 weeks.

All of the above statements are from good, well meaning people. And some of these statements might even be appropriate under certain conditions. These statements typically are not from the quacks and crooks that look to exploit anyone who has been in a car accident or might have fallen off their bike when they were six (and therefore their spine is permanently in trouble because of this "trauma').

My concern is how all of these things sound to our patients - which is different from what we hear. If you tell someone they need stability exercises they probable assume their spine is unstable. That probably does not sound good to a patient with an incredible amount of pain. When we poke on areas that are "tight" or "sore" in everyone (e.g. the upper traps, you can't find someone who is not tender there) we catastrophize, comment on how tight it is and reinforce a pain belief with our poking and create beliefs in people that there is something wrong with their muscles.

Not encouraging patients to resume their normal activities and to keep active contributes to fear and movement avoidance.

Telling patients that the way they move is dysfunctional based on an arbitrary standard of how someone should move again creates the belief in people that something is seriously wrong when there is usually no serious dysfunction.

Seeing someone 3x/week for 6 weeks for whiplash or a simple backache. Come on. Common sense says this is bad practice even though it is somehow in many guidelines.

The bottom line is we  need to watch our words.  I am no exception,  I catch myself doing this too often.  An unstable spine means something completely different to a therapist than it does to a patient. The phrase degenerative joint disease should be banned - they have a joint that is changing like everyone's joints  and most minor symptoms have nothing to do with those normal changes.

Just some thoughts,

Greg Lehman