Are The Days Of Assessing Movement Over

In all honesty in its current format the answer here has to be an unreserved YES, we should STOP assessing movement.

This opinion is based on the two predominant concepts we appear to have currently when assessing movement.

Firstly the concept that a deviation from a movement or muscle firing ‘ideal’ is the cause of someone’s pain such as seen with the pathokinesiology model.

Secondly that we can also ‘screen’ movement to identify faulty movement that might lead to injury, this is FAR too big a subject to get into but it seems we weekly have new data suggesting screening does not fulfil the role it was designed for.

Both of these concepts have so far proved to be elusive in providing concrete evidence that they do exactly what they say they do.

A modern understanding of all the contributors to pain means the likelihood of pain being consistently caused by one single factor across ALL people is pretty absurd really.


The more we study movement the more we find that it is in essence highly variable. This variability is not only between people but even the same person seems to move differently when they repeat a movement. It has been suggested, and with a fair amount of evidence, that healthy movement is variable and losing variability may be a problem within itself. It is important to realise this about movement because it allows us to appraise the idea of movement assessment more critically.

I have previously discussed this *Here* and *Here* along with the concept of corrective exercise.

Now this means that being able to identify a ‘faulty’ movement pattern will be highly likely if you are measuring it against a singular ‘ideal’ version. The problem is the singular ideal version does not really exist and also does not seem to be linked to very much, rendering the whole process a bit of a waste of time.Slide1

It makes little sense not to be variable:

  • Multiple options affords us redundancy
  • Ability to respond to varying stimulus
  • Spreading load over a joint in repetitive tasks
  • Avoiding fatigue through variable motor unit recruitment
  • Unavoidable at a biological level

We also may go further down the rabbit hole in that some now ASSUME that pain is simply the RESULT of a faulty movement pattern without any kind of critical analysis at all. Think how some people approach back pain, “Its your TvA not be firing” rather than lets find out if it is or not (obviously no clinical test tells us this, just an example).


Now I am no biomechanist but we also must realise that just because a movement goes into a potentially ‘faulty’ position does not tell us the whole picture of how much damage that poses to a tissue. Sure it might increase the risk in some contexts but alone it does not give you the ACTUAL force applied and we would also need to know the acceleration as well. A fast movement within proposed ‘safe’ parameters that generates a large force (F=MA) could provide a much greater load to a tissue than one that was proposed as ‘faulty’ that moved much slower.

In fact under greater loads our movement seems to change, so assessing in a low load environment may not give you an indication of how movement is in another situation. This was an interesting piece from Frost et al *Here* showing exactly that!

Some seem to have developed the idea that if you get a movement right you can put it under ANY load. The way the body manages loads internally through the way it moves may be far LESS important the overall volume of load that the body may go through overall and this could be in volume, frequency or intensity.


So can we STILL look at movement in practice?, I believe so. Everything has it uses and limitations and its working out WHEN thats the tough bit.

Pain DOES have an effect on the way we move, this is pretty well researched showing alterations in what happens with both kinematics AND kinetics at a joint, to adjacent joints and right up to avoiding movement completely for fear of pain. This is a great paper by Hodges & Smeets discussing this *HERE*

Like any other thing that we can measure, it may or may not be related to the problem and may or may not have to change to get a successful result.

Certainly it very difficult to suggest that the way someone moves is a cause of their problems. Do you know what it looked like before? Could it be the RESULT not the cause or pain? BUT is there also a possibility that a change in movement strategy COULD also have an effect on reoccurrence or another injury. We know that the best predictor of future injury is previous injury *Here* and this could be a factor. This has also been mooted with back pain *Here*.

It is a good place to use your reasoning skills. Is this the first time it has happened? Is it acute? Both of these simple questions might help to determine if it is currently an adaptive strategy (helpful) because of pain or is it a maladaptive behaviour (unhelpful) that maybe contributing to the maintenance or reoccurrence of a problem.


A potentially more individualised concept for how we view movement is that rather than a binary right and wrong view that we have currently, we could say your current strategy is unhelpful and swapping that for another might be more helpful, there are often a whole bunch of other ways that could be beneficial rather than the ‘right’ way.

This might only be for the short term, such as a symptom modification, or for the longer term if you believe a movement behaviour maybe coupled with a pain response.

Gait re-eduction for runners seems to follow this rationale, see whats going on, does that potentially relate to the issue and can we subtly alter it.

Now there maybe certain scenarios that do carry more risk such as loaded lumbar flexion or extreme knee valgus but they seem to be pretty load related. Unless someone is regularly under these loads perhaps it matters less. But ask yourself how many people in the gym have popped an ACL doing a single leg squat? Perhaps the caution can cause more problems than it solves here? Especially with the unhelpful beliefs people seem to be prone to forming.





If some one has a very hip driven strategy whilst currently suffering from a proximal hamstring tendinopathy altering this could reduce further load/compression to the tendon to allow it to desensitise.


It could be that be that someone is bracing BEFORE they move and this is an unhelpful component. This maybe seen with lower back pain sufferers.


Before bending over to do their shoelaces someone specifically braces and this has become coupled with the pain they are experiencing. Attempting to change this part of the motor strategy MAY affect the outcome.


We see decreased variation linked with chronic pain at a number of areas of the body. This could cause repetitive loading or consistent patterns ASSOCIATED with pain.


A specific task maybe is performed in a repetitive way. This might be the way someone lifts, reaches or even runs. A way to assess this could be to provide variable challenges and see how well someone can adapt.

What we do have to remember that this is all TRIAL & ERROR.

It may or MAY NOT have an effect and essentially this is everything we do. We should try to be informed by current best evidence but also  remember is just a probability generated in a controlled environment and may not directly translate to this person you are dealing with.


  • Specific movement ideals are pretty unsupported, especially linking them to pain
  • Movement screening is literally a can of worms
  • Movement is variable, EMBRACE it! This means it is tough to assume causative link with pain
  • Low load assessment tells little about high load behaviour
  • A movement does not simple equal the force applied to the tissue
  • Look at the individual
  • Be prepared that altering movement may have NO EFFECT or a very positive one

The Science Of Placebo


What does the word placebo mean?

Does the placebo effect involve actual health benefits or just imagined benefits?

Is placebo “mind over body” or “all in your head”? Is it unethical to provide a client with placebo treatments? And what about nocebos?

In this article, I’ll answer these questions and discuss some fascinating research by Fabrizio Benedetti and colleagues.

After reading this you will have a better understanding of placebo, and you might even stop using the word, because it’s fairly ambiguous, and often a poor explanation for why a treatment helps someone to move better or feel better.

What Exactly Is The Placebo Effect?

Placebo is a confusing term because it means different things when used in different contexts.*

For purposes of this article, it has the following meaning: A placebo is a treatment that reduces symptoms only because the patient expects a benefit, not because the treatment itself has any effect.

For example, a sugar pill can be a placebo that will improve a headache only if the person taking the pill expects that it will provide benefits. But if the person does not expect benefit, it’s no longer a placebo, and does nothing.

The placebo effect is the physiological process by which expectations about a treatment cause changes in the brain that initiate an improvement in symptoms. These changes are real, not imagined.

In other words, if someone experiences a real placebo effect, they are not just imagining some improvement – there are objective and measurable changes in their physiology to prove it.

The nocebo effect is basically the opposite: It causes negative changes in symptoms (e.g. more pain and reduced function) when there is an expectation that an otherwise harmless stimulus will cause harm.

Clearing Up Mind-Body Confusions

Placebo is often described in terms of a “mind-body connection.”

This suggests it involves some sort of mysterious process, or that we need to radically change our way of thinking to understand it.

But in fact, the connection between abstract thought and events in the body should be intuitive and trivially obvious. If I form an intention to reach for a cup, my hand actually reaches for the cup! If I think there is an intruder in my house, my heart will beat faster and I may begin to sweat. If I spend my life worrying, I increase my risk of headaches and heart attacks.

So we already know that thoughts affect the body.



In other words, the placebo effect does not involve anything magical. It is one of many ways that our cognition affects our physiology. But it is a very interesting and clinically relevant phenomenon because it reveals the mechanisms by which our thoughts and expectations affect the way we move and feel.

What Can The Placebo Effect Do?

Placebos can cause changes in pain level, motor control, muscle tension, strength, endurance, energy level, depression, immune response, heart rate, and glucose level.

They can even make you drunk!

But placebos don’t help with everything. They won’t cure cancer, make you taller, and they probably don’t help with asthma. Placebo effects are often significant. In the case of pain, they can change self-reported pain scores two points on a ten-point scale.



The rest of the article will focus on placebo effects as they relate to pain.

How Does The Placebo Effect Work To Reduce Pain?

The easiest way to understand how a placebo can affect pain is by considering the purpose that pain serves.

Pain is an unpleasant feeling designed to protect you from perceived threat to the body.

Placebos alter the perception of threat and therefore the pain. And that works as follows. The brain is always in the process of unconsciously analyzing threats to the body, based on all the information it can gather. This information comes from a wide variety of sources, including sensory data from the body, visual data from the eyes, memories, opinions, and, importantly, information that is provided by medical authorities.

Thus, when a doctor tells you something about some condition in your body, or the medicine intended to treat it, this becomes part of the evidence base from which your brain unconsciously determines whether pain is needed to protect you from that condition. Put another way, your opinions about the effects of a placebo treatment become one of many cognitive inputs that modify the output of pain.



The research of Benedetti and others has identified three different patterns of mental processes that create the placebo effect: (1) expectations of benefit; (2) reduction of anxiety; and (3) learning through association. Let’s look at each in turn and the associated physiological processes.

Expectation Of Reward

One way placebos work is by creating an expectation of benefit, which activates the reward system of the brain.

The reward system motivates us to engage in behaviors that maximize the spread of our genes, such as eating food, having sex, getting money, and basically doing all the things that humans are generally very motivated to do. The reward system involves release of dopamine. For example, when you experience the reward of getting social approval, you get a little hit of dopamine, which makes you want to do it again.

It’s like a built-in dog trainer. Facebook likes, good boy!



Here’s how we know the reward system is involved in placebos that reduce pain.

The placebo effect is greater in people who get more dopamine release when rewarded. It’s also stronger in people who experience more rewards from receiving money. Further, nocebo effects are associated with dopamine reduction. Also, the improvement in motor control that a Parkinson’s patient experiences after a placebo is correlated with release of dopamine in parts of the brain related to motor control.

So how exactly does activation of the reward system reduce pain?

One mechanism for reward-based analgesia is descending inhibition of nociception. This involves the brain sending opioids or other drug-like substances down the spinal cord to block nociceptive signals (danger signals that often result in pain) from getting to the brain. David Butler calls this system the “drug cabinet in the brain.

How do we know this system is involved in the painkilling effects of placebo? Because when you give people drugs that block the operation of this system, they don’t get any placebo effect from expecting a reward. Here’s a cool example to illustrate.

Researchers put tourniquets on the arms of subjects and asked them to squeeze a ball for as long as possible, to the limits of their pain tolerance. One group was told the procedure would benefit their muscles, and the other was told nothing. Not surprisingly, the group expecting benefit was able to tolerate the pain longer. Here’s the cool part: increased pain tolerance from an expectation of benefit was completely eliminated by drugs which prevented activation of the descending inhibition system.

So we know that descending modulation is involved in placebo effects related to expectation of reward. I think it probably plays a role in the pain relief we often see from exercise, foam rolling or trigger point work. Interestingly, many common chronic pain conditions such as fibromyalgia, chronic fatigue, and IBS are characterized by the relative inefficiency of the descending inhibitory systems. We should expect that these groups are less likely to experience placebo effects based on the expectation of reward.

Anxiety Reduction

Another mechanism by which placebos work is reduction of anxiety. Anxiety basically means the state of expecting a future threat. (It can be distinguished from fear, which is the perception of a current threat.)



Research shows that placebos can reduce anxiety, which tends to decrease pain.

Nocebos do the opposite – they increase anxiety and pain. For example, in one study, researchers told volunteers that a very low-intensity electrical stimulus would be painful. And so it was, even though it shouldn’t have hurt much at all.

Again, the effects are real not imagined – researchers measured the increase in anxiety and pain not just by subjective report, but objective measures of activity in relevant brain areas. Further evidence that nocebos have real physiological effects comes from research showing that it can be eliminated by drugs that reduce anxiety, such as benzodiazepine and diazepam.

In other words, if you can’t be made anxious by false suggestions that something will hurt you, it won’t hurt any more than it should. Anxiety also works to antagonize the dopamine and opioid networks that cause placebo pain relief.


If you consistently experience pain relief right after a certain stimulus, you will learn to associate the stimulus with reduced pain.

For example, if you regularly take aspirin to help with a headache, you will begin to associate the appearance of the pill with feeling better. If someone then gives you a fake aspirin that looks like the real one, you will get a much better placebo effect than without the prior conditioning.

Thus, past experience can make you “expect” benefit from a particular stimulus, even if that expectation is purely unconscious and based on past associations.



These associations can be “unlearned” as well.

If you ring a bell for a Pavlovian dog, he will salivate – but if you keep ringing and never bring dinner, at some point he will figure it out and stop drooling.

And if you keep taking that same placebo aspirin without its active ingredient, it will eventually lose any learned placebo effect.

Here are some interesting experiments that demonstrate how learning through association can create placebo effects.

Rats who learn to associate a favored liquid with receiving an immunosuppressive drug will experience immune suppression after drinking the liquid, even if the drug is removed. Similar results have been obtained in humans. A tasty beverage will improve runny noses in people with allergies if it is first consistently paired with an antihistamine.

Unconscious learning can also create placebo effects in the endocrine system. A fake insulin injection can lower blood sugar after a conditioning process with actual insulin.

This is all very interesting to be sure, but why should a manual or movement therapist care? 

We are (hopefully) not in the business of giving our clients drugs during treatment to cause them to associate our care with pain relief.

Here’s why we should care: This research gives insight into what is probably a major player in pain relief related to movement therapy – “unlearning” negative associations between movement and pain. These associations can arise after an injury, and remain to cause a big fat nocebo effect even after the injury heals. Imagine you injure your back, and then experience nociception and pain whenever you forward bend into full lumbar flexion. You will start to consciously or unconsciously associate this movement with pain, and you will gradually learn to expect pain when you do the movement.

After a while, the back injury heals but the association remains. 

Forward bends are now a nocebo that can create pain even without the “active ingredient” of nociception. How do we stop this nocebo effect? By breaking the learned association between forward bending and pain.

If you repeat the forward bend enough, especially in ways that are slow, novel and non-threatening, your brain will eventually realize that the “active ingredient” of nociception is no longer present. You will start to unlearn the association between movement and pain, and eventually recover full pain free flexion.

But what if you don’t fully go through this unlearning process?

Maybe the injury heals and nociception is gone, but you avoid the movement completely because you’re too scared to revisit it. The nocebo effect remains because you never break the association between pain and movement. This is perhaps one of the reasons why fear of movement (kinesophobia) is a good predictor of when acute injuries will develop into chronic pain. I think the one of the main ways that movement therapy can help us get rid of chronic pain is to progress slowly and carefully into movements which we expect either consciously or unconsciously to cause pain.

For an amazing and dramatic example of this process, check out this video by Peter O’Sullivan.


The science of placebo is very interesting and informative.

It is not unreasonable to suppose that a good degree of the success seen in movement-based therapies is through placebo-like effects, or through getting rid of nocebos.

But I think the word placebo can be confusing. It refers to a wide variety of different phenomena that have different effects through different mechanisms. Some placebo effects work through anxiety reduction, others through activation of the reward system, and others through descending inhibition of nociception. The common thread is they are all created by cognitive inputs – information that changes what the patient expects or believes about their health.

And this relates to another problem with the word placebo – it suggests that treatments which work through changes in client expectation are somehow inert, or ineffective, or not meaningful, or unethical, or even a scam. Of course this may very well be the case when the treatment is a sugar pill, or based on pseudoscience or quackery. In these instances, the clients’ expectations and beliefs are changed because they are deceived, and this is in most cases unethical.

But what if a treatment works primarily through changes in belief and expectation, but in a way that changes those beliefs to be more accurate? Consider the following scenarios, all of which might be described as involving placebo effects, but none of which involve deception:

  • a client is given accurate information about the poor correlation between back pain and objective MRI findings. This lowers his anxiety and pain.
  • a client is shown through passive and active movement that it is possible for her to bend forward without pain if she does so in a different manner. This reduces her anxiety, makes her expect benefit from therapy, and this reduces her pain.
  • a client receives compassionate and empathetic treatment from a caring therapist. This lowers his anxiety, makes him expect benefit, and thereby reduces his pain.
  • a client has had many past experiences with massage causing pain relief, and this learned association contributes to further pain relief from massage.

Are these all placebo effects?

It is true that they all work in large part by changing the client’s beliefs. But that was the whole point of the treatment in the first place! So there should be no suggestion that the treatments are inert, ineffective or deceptive. Using the word placebo in these cases can be stigmatizing and confusing.

I prefer to look at it this way: pain results from perception of threat, and it can be treated by providing the client as much good news as possible about the threat in question. Does this present an ethical issue? Only when that good news is built from lies and not the truth. Fortunately, I think there are many optimistic truths that clients can learn from therapists through touch, movement, and conversation.



*Another meaning for placebo is used in the context of research trying to determine whether some treatment is effective. This meaning includes various reasons the data reflects that a subject feels better after a treatment, such as spontaneous remission of the disease, data error, or regression to the mean. In this context, if my headache was about to get better in the next hour, and I took a pill right before that, my improvement would be attributed to “placebo.” Yet another meaning for placebo is something that causes a subject to think that they feel better, or to report that they feel better, even when there haven’t been any real objective changes in their symptoms.

Pain Education – What Might Make It More Effective


Pain education is a valuable tool for some, but certainly not all, patients. It can help to provide a narrative or explanation for problems that may remain unexplained by ‘traditional’ medicine or therapy.

This paper HERE regarding chronic lower back pain explores what people are looking for from a visit to a therapist.

more than 90% of patients expected a physical examination, tests or investigations, a diagnosis, reassurance and advice, and clear explanations of causation, symptom management”

How tough is this in many instances with no clear diagnosis or causation available?

Up to 90% of back pain is described as ‘non-specific’ for this very reason. We know that uncertainty is a big deal for many patients. Mishel first proposed this in the “theory of uncertainty of illness” HERE.

Carroll’s paper HERE How Well Do You Expect to Recover, and What Does Recovery Mean, Anyway? Qualitative Study of Expectations After a Musculoskeletal Injury” also discusses the process of diagnosis, uncertainty and the subsequent effect on expectations of recovery.

But although data suggests pain education can help it can also be very tough to deliver.

This quote from Louis Gifford sums it up nicely.

“The patient that learned from their pain explaining therapist that their pain didn’t really mean anything, who suddenly got out of the chair, went home and went riding their bike for the first time in 5 years…just doesn’t really exist!”


A question I often ponder is have we replaced anatomy with neurobiology? Do we now bombard people with complex processes involving brains, nerves, and receptors rather than complex biomechanical stories? How much neurobiology or neuroscience is actually required?

In some cases certainly it will be useful, but in many cases maybe it could actually hinder. This does not mean that some of the key concepts such as plasticity, sensitization and the brain’s role in pain are not important but maybe the minutia of information that can be focused on is unnecessary.

Perhaps we can apply some of the information in this paper HERE. Simplifying MRI reports appears to have a positive effect on how they are received. This may also apply to the delivery of pain education. What does nociception or Ion channel mean to a patient? It could end up very similar to VOMIT (Victims of Medical Imaging Technology) HERE if poorly delivered.

Should the focus now be on the delivery and context of information rather than the information itself?


I thought it might be nice to get some other opinions on some of the key elements that go into making successful pain education and reached out to colleagues from around the world, using social media, to pitch in.

Some of the key components I already advocate, but I must admit some others I had not considered and provide valuable food for thought for myself and perhaps also the wider therapeutic community.

I was pleasantly surprised by the elements discussed, almost none related to the actual information itself but instead on the delivery and thought process involved.

Here they are



The most consistent point made by the contributors as a whole was listening.

Listening is a key clinical tool. Although pain education is often thought of as the delivery of information, it should start with listening. I think this is advocated on many fronts but as we know patients can often be interrupted pretty quickly HERE and this is always worth keeping in mind.

The desire to be listened to also appears to be valued from a patient perspective and helps to build therapeutic alliance HERE. This is probably vital for those receiving and processing the information. delivered.

This is a good paper on ‘listening as therapy’ HERE


A couple of patients also contributed to the discussion and they felt that someone listening to and validating their experiences was a big part of their recovery. This also ties into the paper above regarding a patient’s perspective. If symptoms cannot be ‘medically’ explained or solved by traditional interventions, then patients may feel that they are being seen to ‘make it up’ or exaggerate their painful experience. All pain is real and although it can often be hard to describe it is also exactly the way that someone says it is. It cannot be anything else!


Another of the key points consistently put forward was about individualizing the delivery and placing into a relevant context. Now I personally have a bias for placing pain education in context with someone’s current situation. By weaving it into their story and using their painful examples to tie in some of the key concepts I think we are more likely to get some elements of comprehension.

This fits well with the key component of listening. Without listening we cannot place the information in the context of the patient’s narrative.

The question is, is this more effective than information generically delivered? I just don’t know. I think this would be an interesting comparison to study.


One thing I must admit to NOT asking was simply “do you want to know more about pain?” This was brought up by a number of people. This may avoid the very real problem of ramming pain science where it is not wanted. Pain science should be judiciously applied where it is needed AND wanted rather than a therapist dropping knowledge bombs expecting an instant epiphany.


Remember there are two equal people involved in this. It is not simply a teacher-pupil relationship. Patients lived experiences are also important. The therapist can also learn from the patient, especially when it comes to the patient experiences. Perhaps it should be seen as a journey by two people to find mutual meaning in a negative situation rather than simply an educational experience.


One of the criticisms that I have seen recently of the application of pain education is that it is seen as a standalone intervention. So rather than bombarding people with statements or analogies that have been previously heard for explaining pain, the concepts and ideas should affect the way we reason, interact, explain and apply the treatment provided.


It’s not just about talking; doing is also a powerful educator. Perhaps sometimes talking is needed before and after the doing, but without the actual doing, we cannot ‘prove’ the point. Beliefs about the body are a good example of this. Without SEEING or FEELING a different, positive outcome to that expected, potentially a number of times, a belief may remain in place.

Again listening is key. What are the key experiences that need to be reconceptualized in a physical sense as well as a cognitive sense?


As with any part of the therapy process, pain education has the potential to have a NEGATIVE outcome as well as a positive one. We may well baffle people with talk of brains and outputs etc and HOW they interpret this information is the arbiter of success, however well meaning or comprehensive the input by the therapist.

This may boil down to wording, health literacy, and therapeutic alliance. The list of potential influencers is endless, but essentially the ability to mitigate any negative effects could be dependent on simply asking!

We may be able to influence this interpretation by being clear and concise, using bite-sized chunks of information, avoiding confrontation regarding beliefs and also avoiding negative or long-winded medical or anatomical jargon and terms.


Don’t just provide statements, also use reflective questioning. This may help to facilitate understanding and apply this new information to their own personal experiences and think critically about some of the beliefs they may hold.

Let’s say someone has a negative belief regarding their back because of a slipped disk a number of years ago. We could suggest that structure and symptoms don’t always display a consistent relationship. We could follow this up by asking if their symptoms come and go (as long term back pain generally does) and would this be a sole cause if the ‘slipped’ disc remained a constant.

Of course, this is just some opinion/s but collectively they could be valuable!


  • People are looking for answers
  • Uncertainty makes things worse
  • Pain education may provide some explanation
  • It is tough and often fails


  • Listening
  • Validation
  • Individualisation
  • Asking if it is wanted/needed
  • It is not a passive exchange
  • Pain science is a way of thinking not an intervention
  • Experience is as powerful as talking
  • Find out HOW your education has been interpreted
  • Reflective questioning

Why Your Body Is A Hypocrite

What you see is affected by what you know, and what you hear, and what you touch, and vice versa. This is an example of multi-modal perception. The brain is very complex, and all its different parts integrate and share information acquired from any source – eyes, ears, touch, memories, predictions, expectations, Facebook, etc. We often think pain relates only to “issues in the tissues” but in fact other sources of information about the state of the body matter as well. It’s all connected.

Or is it?

I am currently reading a great book by Robert Kurzban called Why Everyone (Else) Is a Hypocrite. The title is a little bit misleading because the book is not so much about explaining why people lie, but more about working through implications of the modular theory of mind. Kurzban is an evolutionary psychologist, and one of EP’s main theoretical claims is that the mind is modular, meaning that it evolved to have certain specific competencies, as opposed to a general all-purpose problem-solving intelligence.

This idea is best understood in reference to creatures that are far less intelligent than humans, such as spiders. Spiders are architectural geniuses when it comes to building webs, and are also very good at solving problems related to getting food, avoiding predation, and finding mates. But outside these specific contexts, they are idiots.

Natural selection provides living things with specific cognitive competencies, not general all-purpose intelligence. We can look at the mind as a smartphone with various apps, or a swiss army knife with separate tools. Humans have far more computing power and apps than spiders, but it is the same basic modular operating system, which is why we are amazing geniuses in certain areas, such as motor control and language (where we outperform any computer), and not so strong in others, such as math computation (where we are put to shame by simple calculators.)

Kurzban’s interesting twist on this idea is that the different modules don’t necessarily share information with each other. They often work independently, and mistakes in one area can’t necessarily be corrected by more accurate information in another. He uses two common visual illusions to illustrate.

What do the dots in this picture show?


If you don’t already know the answer, you might struggle for a few minutes before you “see” the dalmatian. As soon as you know what’s in the picture, you can see it almost immediately, and in fact, it becomes hard to “unsee” as well. According to Kurzban, this means that a conscious module in the brain shared information about the picture with a visual processing module, and this affected its computations and therefore your perception of the picture. For similar reasons, this is why wine tastes better when we think it is expensive, and pain hurts more when we think it is caused by major damage in the body, as opposed to some innocuous healing process. But “top-down” information sharing won’t always change your perception.

Consider the checkerboard illusion. Squares A and B are actually the same color!


There is a visual processing module that processes a ton of information to provide you with this (incorrect) perception. It considers the location of the cylinder, the shadow that it casts, the regularity of the squares on the checkerboard. Based on all of this computation, it “decides” that the squares are different colors, and therefore you see them that way. You are never provided with the “raw data”, the set of assumptions, or the thinking process that led to this conclusion. You just get the final product – a mental picture showing the squares as the same color.

And, interestingly, your conscious knowledge that the squares are in fact NOT the same color does nothing to change your perception. Unlike the dalmatian photo, conscious knowledge is not used by the visual processing module to make your perception more accurate. So the illusion remains. According to Kurzban, this is evidence that the work done by the modules is often fairly independent, immune to correction or maybe even input from other modules that know better.

(This is part of why Kurzban thinks we can be hypocrites – there is a social relations module in the brain – a public speaker – whose priority and function is giving you high social status. It doesn’t really care or maybe even know about information located in other modules of the mind, which proves that you aren’t as smart or moral or innocent as you claim in public. The separation of the modules creates “strategic ignorance.”)

Now consider this idea in the context of pain. Sometimes our knowledge and conscious thought processes about the body will affect how a body part feels. If we think that a body part is broken, degenerated, falling apart, unstable, this can make pain worse. And if we think that our body is robust, strong, and capable, this can make us feel better. This is multi-modal perception – sharing of information between the different modules. It explains why in the Dalmatian picture, conscious knowledge about the meaning of the picture affected our perception.

But pain is unfortunately sometimes more like the checkerboard illusion – immune to logic. People often have pain in areas where there is no damage, and sometimes in areas where there aren’t even body parts! Having conscious knowledge about these facts sometimes cannot affect perception. In terms of modules, we could say that the pain module is just not very interested in hearing corrective information from the cognitive modules. It was designed to be strategically ignorant about their conclusions. This is frustrating, but I think an interesting theoretical way to look at the problem of pain having “a mind of its own.” If the pain module won’t “listen” to the more cognitive modules, which modules might be better at speaking its “language?” The movement modules would be first on my list. If you move in a way that demonstrates strength, endurance, or skill, you will get a visceral “bottom-up” feeling of safety that speaks a different and more powerful language than Stuart Smally-style top-down daily affirmations.

Learn How Education And Movement Can Help Frozen Shoulder

If I’ve heard it once, I’ve heard it 1000 times in my career (okay this is an exaggeration, it’s probably only a few dozen times), “I think my frozen shoulder is acting up!”

Meanwhile, the patient is moving their arm all over and wincing with a bit of pain.

The very name is enough to strike long term fear into a patient.

“Frozen Shoulder” it just sounds like something utterly debilitating, no wonder patients catastrophize over the diagnosis.

Part of the problem with this diagnosis is that all too often as soon as someone has an issue with their shoulder, it gets labeled, labeled with a damning diagnosis, and usually an improper one.

So, how do we convince someone their shoulder is probably okay and just needs to be de-sensitized, or actually realize frozen shoulder is the issue? Well, there are several ways, and while we can’t “diagnose” there are certainly some signs and symptoms we can look at which will help us recognize the difference and refer out when necessary.

Getting To Know Frozen Shoulder

Most of the time a detailed intake form, case history, and clinical examination should be enough to manage those who are coming in with shoulder pain, however, there are things we need to look for during this to determine the severity of a shoulder issue.

Frozen shoulder’s clinical name is “adhesive capsulitis” and is characterized by patients experiencing pain along with limited range of motion and disability of the glenohumeral joint which lasts anywhere from 1-24 months. There are two types of adhesive capsulitis:

  1. Idiopathic (primary): occurs spontaneously from a chronic inflammatory response (possibly an abnormal immune system response).
  2. Secondary adhesive capsulitis: happens after a shoulder injury or surgery and can be associated with conditions like diabetes, rotator cuff injury, cerebrovascular accident, or cardiovascular disease.

It seems those with diabetes (10-36% of diabetic patients) are quite prone to dealing with frozen shoulder as both types I and type II diabetics are susceptible and have worse outcomes compared to non-diabetics. They also experience more severe symptoms and are more resistant to treatment. Those who have had a stroke are also quite susceptible as it happens to 25% of stroke patients within 6 months, which is likely due to some muscle spasticity on the affected side. Some studies have also shown an association with Dupuytren’s disease, hypothyroidism, and Parkinson’s disease (however these last few are much rarer).

Mostly this affects people in their 50’s with the peak age being 56, but rarely happening to people under 40, and more commonly affects women than men (sorry ladies). However, some research suggests a high prevalence of shoulder issues among the elderly, who aren’t seeking medical attention for the issue.

One study tried to develop a new clinical sign to help diagnose a frozen shoulder with something called the “Coracoid Pain Test”. This is essentially putting digital pressure on the coracoid process, which creates more intense pain compared to the unaffected shoulder. In the study, 96.4% of patients with this condition complained of pain when the test was done, which they argue shows a high specificity rating, but I don’t know if this is widely accepted yet.

If we have a patient come in who is experiencing shoulder pain, trying to get a differential diagnosis is important (even though we can’t diagnose), but if we look at the above instances, these are all things which could be on our intake form that could help us narrow down and understand that maybe our patient is dealing with frozen shoulder as opposed to just some simple shoulder pain. One other thing that stands out as being consistent with a frozen shoulder is the complete loss of external rotation.

Once we understand this, it is also important to understand the “phases” this condition goes through.

There are 3 phases with varying degrees of length:

  1. The painful phase:
    • Pain with AROM & PROM.
    • Reduced flexion, abduction, and rotation.
    • Pain worse at night.
    • Duration lasting 10-36 weeks.
  2. Adhesive “frozen” phase:
    • Pain starts to subside (still bad at full range) but still stiff.
    • Almost no external rotation.
    • Rigid “end feel”.
    • Duration 9-15 months.
  3. Resolution “thawing” phase:
    • Spontaneous improvement in ROM.
    • Minimal pain.
    • Happens during 15-24 months since issues started.

While it is quite common for the symptoms to resolve themselves, it does take a considerable amount of time for that to happen and of course, this depends on whether things like diabetes are influencing the healing process. There are studies showing that 39% of people had a full recovery, the remaining 61% had some issues with pain and or range of motion.

However, there are things we can do to help move this along and education with movement looks like the primary treatment.

Of course, the treatment we are giving must be tailored not only to the patient but also the phase of the condition.

During the painful phase, the main thing we are looking for is pain relief and movement within pain-free tolerances and using graded exposure to get to the edges of painful movement. We did an article a couple of weeks ago where you can see how to do this by clicking HERE. While much of the literature points to the use of NSAIDs, there isn’t a lot to confirm its effectiveness for frozen shoulder.

One study on Idiopathic Adhesive Capsulitis showed good success with an exercise program that involved a four-direction shoulder stretching program that included passive forward flexion, passive external rotation, passive horizontal adduction, and passive internal rotation. With this program they had 64% of patients report a satisfactory outcome, 7% not satisfied, and 5% who went for surgery.

Treatments during the adhesive phase should be more aggressive toward longer stretches and a low load to push toward an increase in range of motion.

When these exercise interventions don’t work, the patient is often referred for surgery or for manipulation under anesthesia and have relatively good outcomes. There is also well-documented use of injected steroids, which when combined with manual therapy have some good outcomes as well. Although, in reading over Paul Ingraham’s post on frozen shoulder, there is also a risk of causing shoulder issues with various types of injections, so this should be considered as well.

Much of this is going to be left up to your clinical decision making, but having a good understanding of the timelines and what is happening, along with feedback from your patient should give you a good idea of how to manage this, should someone come in for treatment.


As mentioned in this post, education is a major part of helping someone with this condition. 

Unfortunately, this probably isn’t done as much as it should be. While most patients are probably looking for a “quick fix”, the reality is, this is just going to take some time and effort on their part and yours. 

There is a normal course the condition takes and at the 12-24 month period it falls into a resolution phase and there is a greater improvement in range of motion. While any patient would look for complete resolution one study showed at the 5-10 year follow up of 41 patients: 

  • 39% had full recovery.
  • 54% had some limitation without functional disability.
  • 7% had functional limitations. 

And still another study showed 50% of their patients had some degree of pain and stiffness seven years after the condition started. 

However, the above studies did show that the longer the person was in the stiffness stage, the longer the recovery stage, there was a direct correlation. So, perhaps proper education and movement in the painful phase could, in turn, shorten the stiffness and recovery stage?

Interestingly one of the previously mentioned studies showed that prior “physical therapy treatment and a workman’s compensation claim or pending litigation were the only variables that were associated with the eventual need for manipulation or capsular release”.

This is a fact I find really interesting. While some argue that the biopsychosocial approach to pain isn’t in our scope, how can we look at that study and say these other factors are not a contributing factor to a persons pain and disability? In my old job I was told by a compensation representative that their studies had shown if someone was off work for 18 months on an injury claim, chances are they were never going back to that job. And here we have studies showing us that a compensation claim is one of the contributing factors to needing more aggressive treatment for this condition. While we cannot counsel a patient on this, it is something we should be cognizant of when treating them (if a compensation claim is part of their issue).

While we would never want to tell a patient there is only a 50% chance that after seven years they would be pain-free, we do want to try to educate, encourage, and build resilience with them through each phase of this condition, giving them hope for the most positive outcome possible. Reassuring them that there is a bit of a longer recovery process compared to other shoulder issues, but that full recovery is possible will probably bring a better chance of shortening the stiffness, and recovery stages.

Many Orthopedic Surgeries Don’t Work Better Than Placebo

Unlike drugs, orthopedic surgeries can be sold to the public before they undergo rigorous testing to ensure they are safe and effective. Thus, millions of surgeries for knee, shoulder, and back pain have been done without studies to confirm they actually work. Recently, research has found that many popular surgeries (but not all) work no better than a placebo. And yet these surgeries are still done at the rate of hundreds of thousands per year. This is something you should know if you are considering surgery, or in the business of treating chronic pain.

Knee Surgery

Osteoarthritis of the knee is common but does not necessarily result in pain — many people have arthritis and no pain at all. But surgery to correct arthritis is popular, numbering as many as a half-million per year in the U.S. alone. (1)

About 15 years ago, two of the most common procedures were debridement (removal of damaged cartilage or bone) or lavage (irrigation with saline solution). The goal of either surgery was removal of rough fragments of cartilage that may be irritating the joint. The surgery’s benefits were known to be not so impressive, so people started to wonder whether they were caused by placebo, or could be achieved with less invasive treatment.

To answer these questions, a study was done using a “sham” surgery: one group of patients received real knee surgery, and the other a fake, which involved just an incision on the skin. At several times over the course of a couple of years, the two groups reported their levels of knee pain and function. The result? The sham group did just as well as the surgical group at all points in time. (2) This strongly suggests the surgery worked by changing psychology, not structure.

This study was slow to have an effect on the behavior of surgeons. Years later, hundreds of thousands of these surgeries were still being performed at the cost of $3 billion a year. (3) Subsequent research confirmed they provide no more benefit than common sense interventions like exercise, weight loss, and the occasional use of over-the-counter pain medicine. (4) Debridement and lavage eventually became less common but were soon replaced by arthroscopic partial meniscectomy. But the new surgery proved to be equally weak. Like its predecessors, it worked no better than a sham.

In 2015, researchers summarized the results of nine studies on arthroscopic procedures for the knee and concluded that they showed little if any benefit, and the possibility for serious harm. (5) Further studies in 2017 came to similar conclusions. (5a)

A recent editorial in the British Journal of Medicine offered the scathing opinion that arthroscopic surgery for knee pain is: “a highly questionable practice without supporting evidence of even moderate quality.” (6) A clinical guideline issued in 2017 made a “strong recommendation against the use of arthroscopy in nearly all patients with degenerative knee disease” and noted that “further research is unlikely to alter this recommendation.” (7) In spite of this advice, arthroscopic knee surgery continues to be the most common orthopedic procedure in the U.S., with close to 700,000 performed each year. (6)

Why the disconnect between research and practice? The simple answer is that many doctors trust their personal experience over-controlled research. They will say they have seen surgery provide benefit after conservative therapies failed. Surely this sometimes occurs, but we should be skeptical that the cause is structural change in the knee. Instead, successful treatment for chronic knee pain, through surgery or otherwise, may be caused by complex changes in psychological or neurological processes.

Back Surgery

As with knees, there is a wealth of evidence that backs can have major structural damage and still not hurt. Further, backs can hurt a lot even when they have no apparent damage. In fact, this is quite common — most chronic low back pain is classified as “non-specific”, meaning it cannot be explained in reference to a mechanical or structural cause. Although there is only a poor correlation between back pain and structural back damage, there are many surgeries to correct any damage that happens to appear on an MRI. Several perform no better than conservative care.

For example, vertebroplasty attempts to treat back pain by injecting bone cement into fractured vertebrae. A study published in 2003 showed it works as well as no treatment at all after six weeks. (8) In 2009, two studies showed it worked no better than a sham procedure for fractures related to osteoporosis. (9)

Low back fusion is a common procedure and is intended to enhance low back stability. In 2013, the Spine Journal published a study comparing spinal fusion to non-operative treatments like cognitive behavioral therapy and exercise. It found no difference in long term outcomes and concluded that “the use of lumbar fusion in chronic low back pain patients should not be favored” over conservative care and exercise. (10)

In 2014, an analysis of multiple studies concluded that:

There is strong evidence that lumbar fusion is not more effective than conservative treatment in reducing perceived disability because of chronic low back pain among patients with degenerative spinal diseases. It is unlikely that further research on the subject would considerably affect this conclusion.(11)

As with knee surgery, the research showing the relative ineffectiveness of surgery has been slow to affect practice. Nikolai Bogduk, an internationally renowned anatomist and back pain expert, explains that:

Surgeons and others believe that surgery is effective for back pain. They base this belief either on their own experience or on observational studies. This belief is, by and large, not vindicated by the outcomes in well-reported clinical trials. Those trials indicate that only a small proportion of patients do well from surgery.(12)

Shoulder Surgery

The research on shoulder surgery is less clear, but recent studies reveal a similar pattern. MRIs consistently show that a great many people without pain have torn rotator cuffs. Despite this fact, the most common diagnoses to explain shoulder pain is “impingement” on the rotator cuff by the acromion process.

Surgeries to correct these conditions include rotator cuff repair, or acromioplasty, where a portion of the acromion is removed. In the United States, there are almost half a million of these surgeries performed each year, most of them on shoulders where the damage is degenerative as opposed to traumatic. (13)

Although we cannot rule out the possibility that surgery will be substantially more effective than exercise for certain patients (14), several studies have found that popular shoulder surgeries, such as acromioplasty, are no better than exercise. (15) Further, it has been shown that surgeries for labral repair and biceps tendinosis cannot outperform sham surgery. (16)

There is also evidence suggesting that when surgery is effective at relieving pain, it is not because of structural repair. (17) MRIs of repaired rotator cuffs taken within a year after surgery often show that the cuff has fallen apart again, even though the patient has recovered. According to Dr. Lawrence Gullotta, “When your rotator cuff is torn, you attribute all your pain and dysfunction to your torn rotator cuff, then you have it fixed and you feel better, but sometimes when you take an ultrasound or an MRI, the rotator cuff looks exactly like it did before you had the surgery.” (18)

A 2017 study compared two kinds of shoulder arthroscopic surgery (with and without decompression), and found that neither provided a clinically significant benefit over no treatment at all. (19) An editorial said these findings “send a strong message that the burden of proof now rests on those who wish to defend the standpoint that shoulder arthroscopy is more effective than non-surgical interventions.” (20)

A blog post in the British Journal of Sports Medicine summed up the situation as follows: “in the light of the current evidence base, the benefits of surgical intervention for the treatment of [shoulder pain] seem glorified and overrated.” (21)


Let me make something clear: None of the above means we should not trust orthopedic surgeons, or that surgery should never be used to treat chronic pain. Many surgeries have been proven to work and are definitely a good idea under certain circumstances. I personally know many people who have received excellent and ethical advice from their surgeons, and dramatic benefits from surgery. By contrast, I also know people who got a surgery that had been proven to be ineffective, were never advised of the relevant research, and ultimately did not get a good result.

I think the lesson here is that the medical establishment has some biases in the way it treats chronic pain. It favors treatments based on simple structural explanations for pain and tends to ignore complex neurophysiological processes that may be more important. We need to be aware of these biases and learn as much as possible about the complexity of pain so that treatment can be improved. And chronic pain clients need to ask their surgeons some good questions before going under the knife.


The above article is an adapted excerpt from my new book, Playing With Movement: How to Explore the Many Dimensions of Physical Health and Performance


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2. Lubowitz, James H. 2002. “A Controlled Trial of Arthroscopic Surgery for Osteoarthritis of the Knee.” Arthroscopy 18 (8): 950–51.

3. Why ‘Useless’ Surgery Is Still Popular.

4. Kirkely, Birmingham, et al. 2008. “A Randomized Trial of Arthroscopic Surgery for Osteoarthritis of the Knee.” New England Journal. Vol. 359, 1097.

5. Thorlund, J. B., C. B. Juhl, E. M. Roos, and L. S. Lohmander. 2015. “Arthroscopic Surgery for Degenerative Knee: Systematic Review and Meta-Analysis of Benefits and Harms.” Bmj 350 (jun16 3): h2747–h2747. doi:10.1136/bmj.h2747.

5a. “Brignardello-Petersen et al. (2017). Knee Arthroscopy Versus Conservative Management in Patients with Degenerative Knee Disease: A Systematic Review. BMJ Open 7(5), e016114; Sihvonen et al. (2017). Arthroscopic Partial Meniscectomy Versus Placebo Surgery for a Degenerative Meniscus Tear: A 2-Year Follow-Up of the Randomised Controlled Trial. Annals of the Rheumatic Diseases. 77(2), 188–195.”

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7. Siemieniuk, Reed A C, Ian A Harris, Thomas Agoritsas, Rudolf W Poolman, Romina Brignardello-Petersen, Stijn Van de Velde, Rachelle Buchbinder, et al. 2017. “Arthroscopic Surgery for Degenerative Knee Arthritis and Meniscal Tears: A Clinical Practice Guideline.” Bmj, j1982. doi:10.1136/bmj.j1982.

8. Diamond, Terrence H, Bernard Champion, and William A Clark. 2003. “Management of Acute Osteoporotic Vertebral Fractures: A Nonrandomized Trial Comparing Percutaneous Vertebroplasty with Conservative Therapy.” The American Journal of Medicine 114 (4): 257–65. doi:10.1016/S0002–9343(02)01524–3.

9. Kallmes, David F., Bryan A. Comstock, Patrick J. Heagerty, Judith A. Turner, David J. Wilson, Terry H. Diamond, Richard Edwards, et al. 2009. “A Randomized Trial of Vertebroplasty for Osteoporotic Spinal Fractures.” New England Journal of Medicine 361 (6): 569–79. doi:10.1056/NEJMoa0900563.

10. Mannion, Anne F., Jens Ivar Brox, and Jeremy C.T. Fairbank. 2013. “Comparison of Spinal Fusion and Nonoperative Treatment in Patients with Chronic Low Back Pain: Long-Term Follow-up of Three Randomized Controlled Trials.” The Spine Journal 13 (11): 1438–48. doi:10.1016/j.spinee.2013.06.101.

11. Saltychev, Mikhail, Merja Eskola, and Katri Laimi. 2014. “Lumbar Fusion Compared with Conservative Treatment in Patients with Chronic Low Back Pain.” International Journal of Rehabilitation Research 37 (1): 2–8. doi:10.1097/MRR.0b013e328363ba4b.

12. Bogduk, Nikolai, and Gunnar Andersson. 2009. “Is Spinal Surgery Effective for Back Pain?” F1000 Medicine Reports 1 (July): 27–29. doi:10.3410/M1–60.

13. Jain, Nitin B, Laurence D Higgins, Elena Losina, Jamie Collins, Philip E Blazar, and Jeffrey N Katz. 2014. “Epidemiology of Musculoskeletal Upper Extremity Ambulatory Surgery in the United States.” BMC Musculoskeletal Disorders 15 (1): 4. doi:10.1186/1471–2474–15–4.

14. Steuri, Ruedi, Martin Sattelmayer, Simone Elsig, Chloé Kolly, Amir Tal, Jan Taeymans, and Roger Hilfiker. 2017. “Effectiveness of Conservative Interventions Including Exercise, Manual Therapy and Medical Management in Adults with Shoulder Impingement: A Systematic Review and Meta-Analysis of RCTs.” British Journal of Sports Medicine, bjsports-2016–096515. doi:10.1136/bjsports-2016–096515.

15. Ketola, S., J. Lehtinen, T. Rousi, M. Nissinen, H. Huhtala, Y. T. Konttinen, and I. Arnala. 2013. “No Evidence of Long-Term Benefits of Arthroscopicacromioplasty in the Treatment of Shoulder Impingement Syndrome: Five-Year Results of a Randomised Controlled Trial.” Bone and Joint Research 2 (7): 132–39. doi:10.1302/2046–3758.27.2000163.

16. Brox, Jens Ivar, Cecilie Piene Schrøder, Øystein Skare, Petter Mowinckel, and Olav Reikerås. 2017. “Author Response — sham Surgery versus Labral Repair or Biceps Tenodesis for Type II SLAP Lesions of the Shoulder: A Three-Armed Randomised Clinical Trial.” British Journal of Sports Medicine, bjsports-2017–098251. doi:10.1136/bjsports-2017–098251.

17. McElvany, Matthew D., Erik McGoldrick, Albert O. Gee, Moni Blazej Neradilek, and Frederick A. Matsen. 2015. “Rotator Cuff Repair.” The American Journal of Sports Medicine 43 (2). SAGE PublicationsSage CA: Los Angeles, CA: 491–500. doi:10.1177/0363546514529644.

18. Large Study of Arthroscopic Rotator Cuff Repair Reveals Some Surprises.

19. Beard et al. (2017). Arthroscopic Subacromial Decompression for Subacromial Shoulder Pain (Csaw): A Multicentre, Pragmatic, Parallel Group, Placebo-Controlled, Three-Group, Randomised Surgical Trial. The Lancet. 391, 329–38.

20. Schreurs et al. (2017). No Benefit of Arthroscopy in Subacromial Shoulder Pain. The Lancet. 6736 (17).21. “Unnecessary Shoulder Surgery on the Rise — BJSM Blog — Social Media’s Leading SEM Voice.”