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How Watching An Evidence Based Doctor Helped Me Learn About FAI

An athlete came in experiencing some groin/adductor pain after the game.

I chatted with them a little bit and got them on the table. I did FABER’s test which resulted in a negative, but figured I would do a bit of massage to calm things down.

Then from behind me the doctor (who is much smarter, and more experienced than I am) came up and asked what was going on, so I explained what I had found.

She then asked, “oh did you try FADIR’s test?”.

I stood there looking like a deer in the headlights because I couldn’t for the life of me remember that test, I felt like an idiot.

So she grabbed the athlete, did FADIR’s (flexion, adduction, internal rotation of the hip), got a positive and then looked at the joint with a portable ultrasound machine and determined there was a possible FAI.

FAI stands for Femoroacetabular Impingement and to this point in my career had never encountered it (that I know of), so I just sat back, watched, and learned.

Femoroacetabular Impingement What Is It?

So what exactly is this anyway?

It can be defined as an abnormal bony feature of the acetabulum or femoral head or both, that leads to abnormal joint contact and stresses with deep flexion and rotation movements.  This can also lead to labral injuries, and has been related to osteoarthritis of the hip.

This can be further broken down into three different classifications:

  1. CAM type impingement – anterolateral or lateral femoral head-neck junction or the entire femoral head is prominent (the femoral head isn’t perfectly round).
  2. Pincer type impingement – acetabulum presents general or focal coverage (there is excessive coverage of the femoral head)
  3. A combination of both of the above.

This usually effects young and middle-aged active people and presents with groin pain and no history of trauma to the area. It is quite commonly seen in young athletes and has been proposed there is a possibility of gender differences which contribute to the issue. One study showed that males had less ROM with internal and external rotation when the hip was flexed at 90° as well as internal rotation with the hip at 0° of extension. But the presence of a positive FADIR test was pretty much the same for both genders. 

However, athletes who had a positive test did have greater external rotation with the hip at 0° extension than those who tested negatively. Athletes also had a higher prevalence of positive tests in asymptomatic people compared to our general population. 

There is also some discussion around physical or activity impairments and one systematic review set out to see which impairments are prevalent. They found the main issues were with range of motion (particularly with movement toward impingement, basically the FADIR test) and showed that pain likely played a role in this compared to the asymptomatic group.

When looking at the asymptomatic group, they had reduced ROM as well,  but this is likely due to bony impingement, or damage to the surrounding soft tissue and even suggests that 35% of young adults have asymptomatic FAI. 

Hip ROM when walking was also called into question but the review pointed out the amount of reduction is of little clinical relevance. The only other significant issue with movement was with squatting which could be due to the shape of the hip and pain avoidance strategies.

FADIR  is quite often used to detect pain in the hip however it’s a good test for detecting sensitivity but is not very good for specificity (60% and 52% in youth hockey players), which results in a lot of false positive outcomes. It usually elicits groin pain when being performed, some studies have shown there to be lateral hip and buttock pain as well. 

So, part of the issue with this test is the prevalence of a positive test in asymptomatic people. For this reason it can only be used as a screening tool and has to be coupled with some medical imaging to get a proper diagnosis. One study also shows that in addition to imaging, symptoms, and reduced function have to be key aspects of a diagnosis. Fortunately, the doctor in this story had imaging done, the athlete presented with symptoms and reduced function, so the doctor checked all the boxes to get a proper diagnosis (which is great to see an evidence based practitioner at work especially since diagnosing is out of my scope). 

Surgery Or Treatment?

The indication for this is usually surgery, but there are some things to take into account.

One study set out to determine if conservative treatment could be effective (although it was based on “mild” impingement). To do so, they put patients through four phases of conservative treatment:

  1. Avoidance of excessive physical activity and use of NSAID’s during an acute attack.
  2. Physiotherapy and stretching for hip external rotation, abduction, extension, and flexion.
  3. Performing ADL’s with reduced ranges of motion in internal and external rotation.
  4. Modifications of ADL’s with running and cycling (some avoidance or altered movements when not avoidable).

With the study the authors had some reasonable success with the goal of conservative treatment to be a reduction in hip pain, and avoiding further cartilage damage without reducing ADL’s. However, the results were only good if the patients could modify ADL’s so the hip could adapt. 

Another interesting point is while it was commonly believed that FAI would lead to Osteoarthritis of the hip, one analysis showed that 82% remained free of OA for 18.5 years, some up to 19 years and to date there are no studies that actually show this progresses to OA of the hip. Some surgeons even suggesting surgery is happening unnecessarily.

One systematic review showed that surgery had been the most successful, but it was also necessary to look at the reasons why people were electing for surgery. The main reasons were:

  • 33% was to alleviate pain.
  • 20% feared the condition was getting worse.
  • 16% hoped to improve ADL’s.
  • 11% due to failed non-operative treatments.
  • 10% hoped to improve for sport.
  • 10% other reasons.

So the review showed many asymptomatic people have abnormal imaging, so it is important to “treat the person not the x-ray.”

It also showed that 50% of people are overly optimistic about the surgical results and improvement, but since this does not necessarily equate to “feeling good,” it is necessary to take psychometric properties into account.

With all we know nowadays around the biopsychosocial aspects of pain, when we look at this list above, how can this change the way we’re helping people with this condition? Well, first we want to make sure every aspect of a diagnosis is done. Next we can look at ways help alleviate pain, but also build up the patients resilience and provide reassurance that the condition is probably not going to get worse (well at least for 18-19 years). Can we change up their ADL’s enough that they’re still doing the things they enjoy, but maybe just in a different manner, frequency, or intensity? In the case of the athlete, is there a guarantee that surgery will improve them for their sport? For the athlete, this may be the one area where a surgery might be necessary, but let’s take into account every option first. And as suggested, let’s make sure we treat the person, not the X-ray.

I will admit, that while I felt like a bit of an idiot when this happened (because I wasn’t familiar with the test and FAI in general), it was a GREAT learning opportunity to watch someone with more education, more experience, and let’s face it smarter than me do their work. Fortunately the doctor was pretty gracious in sharing her knowledge with me, and it made me look at the research on this and write this blog…so I learned a lot. 

Articles Of The Week March 1, 2020

I’ve never really given any consideration to the history of cupping but this is a really interesting history on the history of cupping. While it is still an ancient remedy, it did not come from where many blogs and articles have cited it’s history.

“Did Ancient Egyptians Invent Cupping?” – Rachel Scott

Pain is a real part of everyday life for each of us. While some deal with it less than others, we will all experience pain at some point of our lives. So, how do we help our patients who are coming in and dealing with this? By helping them move from being patients, to being people.

“Did You Miss Me?” – Bronnie Thompson

We have long been proponents of involving the reading of research in your practice. This is a great article that will help you determine what’s good research and what’s bad research.

“Six Details To Ask When Reading Massage Therapy Research” – Nick Ng

You know if I see an interview with an athlete praising the use of massage therapy in their recovery, I just have to share it.

“A Conversation With Michael Phelps” – AMTA

This one stirred up some controversy this week, but I still like it. As Massage Therapists, we are involved in healthcare and the way we speak, conduct ourselves, and treat our patients should all be reflective of an evidence based practice.

“Massage Therapy Is Healthcare, So Start Acting Like It” – Lauren Cates

 

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.

IT’S VARIABLE

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).

MOVEMENT DOES NOT EQUAL FORCE

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.

A DIFFERENT PERSPECTIVE?

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.

LOOK AT THE INDIVIDUAL

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.

SOME EXAMPLES OF UNHELPFUL

 

IT COULD BE THAT A MOVEMENT LOADS A SPECIFIC BODY PART THAT IS CURRENTLY SENSITIVE

Example

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.

PRE MOVEMENT BEHAVIOURS

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.

Example

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.

IT COULD BE THEY ONLY HAVE ONE MOVEMENT STRATEGY

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.

Example

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.

TAKE AWAYS

  • 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

Articles Of The Week February 9, 2020

 

While this article is pointed toward physiotherapists, its equally as applicable to anyone in the manual therapy professions. It’s time for our professions to start a philosophical change in how we are helping and educating our patients dealing with pain.

“Philosophical Hurdles For Musculoskeletal Pain” – John Quinter

I was told repeatedly in college that people with a rotated sacrum could be dealing with pain from a resulted leg-length discrepancy. But, is this something we should really be worried about, or defining as the source of someone’s pain? Probably not like we used to believe.

“Should You Fix Leg-Length Discrepancy” – Nick Ng

Have any patients that are considering, or already scheduled for surgery? Here’s a real-time example of someone dealing with the struggles of post-surgery and what patients should probably know.

“Things They Don’t Tell You About Going Under The Knife” – Sarah Black

It’s not uncommon for one of our patients to come in with a hamstring strain and one of the best things we can do for this is to start loading the tissues. Here are some great variations on how you can do this to help with hamstring injuries.

“4 Reasons ‘Tight’ Hamstrings Lead To Hamstring Strains” – The Prehab Guys

When is the last time you took a holiday? It can be a struggle to fit them in sometimes when you’re self-employed, but if we just make a few changes in our schedule, maybe we can fit one in.

“RMT Burnout: Changing Your Schedule Can Free Up Much-Needed Vacation Time” – Ken Ansell

 

Getting To Yes. Using Negotiation In The Therapeutic Process

 

 

In this article, I want to dive deeply into options available to the therapist, explicitly using a patient-centered, negotiation-driven model of care. A model such as this becomes a therapeutic partnership, an alliance set up for a common goal. Contrast this model to a therapist-centered model. While therapists immersed in their expertise may take umbrage to my characterizations, I ask a bit of patience to allow this explanation to play out. While we may be making changes in the tissues, our in the periphery, we know that the central nervous system is picking up our manual care and shuttling it to the brain.

I believe in using negotiation throughout the process of patient evaluation and negotiation.

Without negotiation, the application of intervention becomes one-sided. Without negotiation, intervention derives from the beliefs and experience (ego) of the therapist, possibly missing out on an outcome that has better meaning to the patient. Negotiation is the core principle I use in my process of manual therapy. While learning manual therapy, or more specifically myofascial release (MFR), may seem like an entirely new intervention, I see it as quite parallel to your current skillset. We are all working toward improving function. MFR is simply another road to explore. Please note that I consider myofascial release a subset of manual therapy, as are the many styles of intervention available to therapists. One might include manual circumlaryngeal treatment as a separate subset, though all are not so dramatically different to warrant their classification. Manual therapy is a common denominator in all of these approaches. 

Getting to Yes,” by Roger Fisher, was a best-selling business book published in 1991. The Amazon.com summary states, “­­­­­­­­­it is based on the work of the Harvard Negotiation Project, a group that deals with all levels of negotiation and conflict resolution. Getting to Yes offers a proven, step-by-step strategy for coming to mutually acceptable agreements in every sort of conflict.” I remember hearing of it earlier in my career, and the memory surfaced recently as a potential frame of reference with regards to the work I teach. While the phrase, getting to yes, might be somewhat narrowly focused, with regards to the outcome of manual therapy, I do see it as a productive and necessary step to fulfill before determining treatment. The concepts presented in “Getting to Yes” have meaning today.

The timeline of a therapist’s inclusion of manual therapy/MFR has a typical pattern, one that I’ve witnessed since beginning my MFR training in 1992. The applications matter little, whether the commonly seen problems of and movement disorders faced by the PTs well as trying to reduce the severity of the impact of dysphagia, dysphonia, trismus, or the full range of other diagnoses facing the SLP.

The timeline often proceeds as follows: when first exposed to a new type of intervention strategy, typically through continuing education, the clinician conservatively doses the therapy, not quite sure of its value or their level of skill. As they gain experience and pursue additional training, therapists use the modality with greater comfort. An illusion is formed, thinking that their expertise and knowledge improve the ability to determine the cause of a problem better.

With that confidence often comes the belief that they have a better ability to determine both what is wrong with the patient and that they know what to do to remediate the issue.

These seem logical conclusions based on principles of advanced learning, but might moving into such certainty begin to minimize the patient’s perspective and preferences? No matter our profession, we are seen as experts in our respective fields, well-prepared to understand the deeper issues underlying a disorder and knowing which intervention to choose to apply. This line of reasoning seems standard practice in most of healthcare and typically meets with success; however, are there ways to improve outcomes? Are there ways to enhance patient by-in? Are there ways to better honor the three aspects of the evidence-based model (EBM)? I ask readers to keep in mind the three equal elements of EBM: 1. The published evidence, 2. Clinician’s experience applying the evidence, and 3. Patient perspectives and preferences with regards to the evidence and the clinician’s perspectives.

I believe that patient perspectives and preferences are given far too little emphasis and respect across the broad spectrum of healthcare, though recent trends in narrative medicine and other more-patient-centric approaches are beginning to create changes. I propose a method that elevates patient perspectives and preferences to carry equal weight with both the evidence as well as clinician experience applying said evidence.

In my years learning and applying MFR, I’ve been exposed to many models of learning. Being encouraged to pursue additional MFR course work was a given and actively encouraged and, at-times required. Working from an intuitive approach was highly stressed, though ill-defined. I was invited to develop my intuition; to work toward having a deeper understanding of processes that, in essence, allowed me to see inside; to be able to determine what was wrong with my patient by merely looking at them. These skills involved conventional evaluator methods, such as postural assessment and movement observance. Still, I was also encouraged to “read” the body, seeing patterns, colors, and holding patterns that would lead me into knowing what treatment needed to be done.

If all of this sounds far-fetched, welcome to the world of pseudoscience. To many, these concepts are logical but are often merely logical fallacies. Using the approach as taught did seem to result in positive outcomes and armed with such power, why would I have stopped believing in the basic tenants of the MFR approach?

In the typical manual therapy intervention, the clinician is tasked with determining if their preferred style of treatment might be useful. That task alone is biased, especially if, in the eyes of the therapist, manual therapy is one of their go-to tools. I recognize this bias as my own, though I try to see through it. For nearly thirty years, myofascial release has been my bias, my tool, my belief. People come to me daily in pain or living with dysfunction, and I apply my biases toward their issues. Over the years of using MFR, I saw the trend I sank into, objectifying their condition as a simple set of fascial restrictions set in place from injury, trauma, surgery, or other conditions; conditions that my skillset was especially good at remediating. Every patient became the nail, well-suited for my hammer. My biases were reinforced by success with many of the patients who sought me out. If the theories behind my fascial training were correct, then my interventions should be helpful, which they were. No dilemma existed, even though many outside my MFR family saw significant problems with the explanatory narrative utilized in MFR, as well as many other modalities targeting tissues and pathologies. 

To the uninitiated, those new to manual therapy, this dilemma seems pointless. But to those who’ve spent time exploring the various modality rabbit holes, the dilemma is real. How can so many modalities have the answer? Can each tissue/pathology-based manual therapy model truly singularly and selectively access and intervene in that dysfunction? Can there be so many unique tissue-based problems in the body that lies in wait for the therapist specially trained in a model devoted solely to that problem?

These questions are often seen as heretical by devotees of tissue and pathology-based manual therapy modality families as they question the fundamental underpinnings that are taught. Such talk is often squelched. However, these are conversations that are needed. 

Manual therapy is often helpful for a wide range of disorders, whether in the niche of voice and swallowing, or the larger body of conditions impacting human existence. But does it work in the manner described by its champions? Diving deeply into the evidence pulls out a relative lack of irrefutable proof of both the tissue-based dysfunctions said to be responsible for the disorders which we treat as well as our ability to selectively impact those tissues for intervention. Such omissions are lacking in nearly all of the published scientific literature that studies the efficacy of manual therapy, though many readers of the evidence fail to see the problem. In most manual therapy papers, there is a conflation of the mechanism of action and efficacy. Proving efficacy is often allowed to be sufficient proof of the stated mechanism of action. In a recent article I wrote, Anatomy matters…but which anatomy?, I speak to this problem and how time and research have moved the bar from tissue-based explanations of causation and therapeutic impact to brain-based models. The complexity of the human condition is seldom reducible to problems in one tissue, be it muscle (tension or spasm) or fascia (restrictions), especially within the context of a biopsychosocial model of dysfunction. 

Despite enormous progress in scientific understanding of pathologies and models of care, we are still not at a place of full understanding. Instead of choosing a tissue or pathology-based model of manual therapy, I’ve modified my process toward one of allowing the patient to be the focus of care rather than my skill and beliefs.

While I fully admit I am unable to completely abandon my knowledge, training, and experience (ego/bias), I attempt to temper it and foster a relationship where my patient plays a more active role in determining treatment. In my seminars, I speak to this as a point of demarcation between many other modalities. In many trainings, whether it is a model teaching manual circumlaryngeal treatment (MCT) or more broadly applied myofascial release and manual therapy training, the clinician is tasked with locating the problem, which is often based on palpation. The clinician’s training strongly biases this palpation. While one therapist, trained in MCT, for instance, may feel excessive muscle tension, another clinician, trained in myofascial release, may feel fascial restrictions. It is quite possible that what they are feeling as a result of their palpatory expertise is indeed the same “thing,” though the therapeutic diagnosis/assessment will differ significantly.

These palpatory findings are typically the determinant for intervention; in essence, “I’ve found the problem that needs to be addressed.” Patients seek us out for this skill and is simply a derivative of the standard model of medical care. They give over trust to us, hoping that we can help. The evaluative findings are turned into treatment dosing. 

In my view, this common model lacks one major component; no matter how much I know, how much training I’ve had, I am unable to determine what a patient is feeling. I am unable to palpate when a patient feels might be helpful or harmful. I am unable to palpate or evaluate a patient’s expectations, preferences, and perspectives. None of these are possible when evaluation evolves into an intervention without including the patient in this process. So, with all of this uncertainty, why do I strive to get to yes? How does using a patient-centered model, one that instills ownership to the patient’s perspective and preferences, a matter within the uncertainty mentioned above? I believe that it matters because of the uncertainty. In the future, more will be understood about how manual therapy impacts the local tissues, though I would predict it will be an indirect effect, that is, one mediated by and through the brain and central nervous system. Those who inform my views are researchers such as Roy (1) and Holzman (2), who point to higher levels of control in terms of why changes might be elicited in the periphery.  

I continue to use palpation in my intervention and teach it during each of my seminars. But instead of palpating to locate the cause or even the actual location of a condition, like most other manual therapy models, I use palpation to begin a process of communication with my patient.

In older models, palpation leads to the conclusion; “I’ve found your (muscle tension, fascial restriction, etc.); let’s see what we can do about this.” Treatment typically follows the findings of palpation. I propose a model that uses that same palpation, though not to conclude, instead I use it to begin a conversation with my patient. I cannot discard all of my experience, as I’ve been through these steps thousands of times in the past, most probably in cases nearly identical to the one facing me at that moment. But I’ve also seen sufficient numbers of patients to know that many times I get it wrong. I do believe that our ego tends to dismiss those memories quite easily and hold on to the times that we were correct. But I try to temper my successes with the knowledge that I do not know what my patient is feeling, what they hope for, and what they might fear unless I ask. I have no way of truly knowing if they will ask me to move into pain, which could mean more aggressive work because they feel it must be helpful or because they’ve been told to expect it unless I ask.

I have no way of knowing what sort of threshold to pressures that they might have, whether it is wide or narrow unless I ask. I have no way of knowing if the things that I’ve located through palpation, or other evaluation means, feels like it could be significant, could feel useful, or could feel harmful unless I ask. Despite all of my training and experience, I can never know the answers to these and countless other questions, unless I ask. But most manual therapy training is built on a process that doesn’t ask; the input of the patient is often minimized or at least deferred to the clinical expertise of the therapist. Many times, this all works out well in the end, but are they ways to improve upon this process? 

Coupling our expertise and training with the expectations and perspectives of the patient is the crux of my approach. It is what gets us to yes. It brings the therapeutic process into a partnership, an alliance.

Of course, we can’t just ask our patients what they think is wrong with them, ask them what we should do, and then do it…or can’t we? The way I teach my work is to use palpation only as a place to start a meaningful conversation about what brought them (the patient) into my clinic. As soon as I feel something that, form my past, feels interesting, I see if I am getting the attention of my patient. I immediately try to ascertain if they are feeling something familiar, something they’ve felt before or associated with the condition or issues that brought them to see me. I put them to work in ways many have never experienced. I, in essence, force them to help me help them. I work toward finding a tactile cue that connects with a feeling that they’ve felt before, good or bad, and is somehow relevant to them. I do very little selling of an approach or beliefs. If what I’m palpating does not replicate one of these conditions, then I move on. If it does connect with their experience, I ask them if the stretch that I am performing feels like it might be helpful? If so, I ask them if they would like me to hold the stretch for a while to see if we can change the outcome? If there is anything about my palpation-found stretch that feels like it may not be helpful, I will ask them if it feels like it might be harmful? If so, I immediately stop. I am attempting to get to yes with them; to find a pressure, stretch, or engagement that they feel will be useful; helpful. I let them decide what constitutes a yes, not me. I allow them to decide what level of pressure or engagement is too much or ineffectual, not me. I require them to be a full participant in the therapeutic process and put them in a position of responsibility for helping me help them. Getting to yes, to me, forms a crucial tipping point in the process that moves us from evaluation into treatment. 

Have you ever heard of a patient/client leaving a massage session, for instance, saying something like, “that therapist was so good that they were able to find things I didn’t even know that I had!” I have, and I detest such statements, only because the therapist did a somewhat unethical job of selling pathologies onto a vulnerable public. Nothing I find is meaningful unless confirmed by my patient. All of this is hard work, though I think it to be good work.

Getting to yes. That is my mandate.

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.

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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.

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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.

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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!

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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.)

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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.

Learning

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.

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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.

Conclusion

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.

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*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.