Why Weak Glutes Aren’t A Reliable Predictor Of Low Back Pain

It seems we are constantly trying to find causes for low back pain with our patients.

Quite often we are caught up looking for biomechanical issues (which there often are) and avoiding other things that could influence a person’s pain.

One such instance is the possibility that weak glutes are a contributing factor.

I recall seeing one of my instructors demonstrate this (what I perceived to be) complicated movement test where my patient was lying prone and having them extend their leg. There was a specific pattern where the muscles in the low back down through the glutes and hamstrings were supposed to move.

This would be followed up with the comment: “your glutes aren’t firing”!

While I watched this all I could think was…”there’s no way I’m going to remember what order all of this goes in”!

But, when done with confidence and a really good explanation, it seemed to make sense to me, and the patient.

So, I worked through the low back, glutes, and hamstrings, and the patient felt better after the treatment.

I proceeded to pat myself on the back for a job well done!

However, the next time a patient came in for what I thought was the same issue, I couldn’t remember this specific pattern of movement and what it was supposed to tell me! Why couldn’t I get this!?

Well, in reality, I really didn’t have to and here’s why.

Limitations With Testing

There are a couple of tests used to see if the glutes are a contributing factor to low back pain, so let’s look at both of them.

The prone leg extension test1 is pretty commonly used to test for low back pain and lumbopelvic function (this is the one my instructor was demonstrating to me).

The pattern of movement you’re supposed to see is (if you were testing the right side) right glute max, right hamstring, left lumbar erector spinae, right lumbar erector spinae, left thoracolumbar erector spinae, then the right thoracolumbar erector spinae. A delay in glute max recruitment is supposed to show a dysfunctional pattern of movement.

There is a whole list of other patterns that are supposed to mean other things, but it’s a long list and more than I want to get into for the purposes of this post.

A studyshowed there was no consistent order of activation during the test and glute max was the last muscle to become activate with time ranging from 0.07 to 0.676 seconds in delay.

Now, these tests were done with proper EMG testing, so I have to wonder…how would we ever be able to properly assess this just using touch and vision!?

Another test we were taught was “Trendelenburg”, or “SLS” to assess for glute weakness possibly contributing to back pain. 

With this test, a practitioner stands behind the patient and has them raise one leg so the hip is between 60°-90° of flexion. A positive test shows lateral pelvic tilt on the stance leg, which is supposed to represent glute weakness on that side.

One study 2 compared the differences between those with chronic low back pain vs. a control group using Trendelenberg. It actually showed the number of positive tests was no different between the groups. There was also no difference in glute med strength between those who scored a positive and negative test.

Since there was an equal number of positive and negative tests between both groups it showed this test is unreliable to differentiate between those with chronic low back pain and those without, nor was it reliable for demonstrating a difference in glute med strength.

Another study 3 actually injected a superior gluteal nerve block to see if there were any alterations in different movement variables. They found after the injection there was no difference in contralateral pelvic drop, hip adduction, or hip abduction due to reduced strength of the glutes post-injection.

The researchers found this surprising as an impaired gluteal nerve has always been associated with the SLS test.

So, in other words, lateral pelvic drop is not associated with weak glute med muscles in our patients who are dealing with chronic low back pain. It was even suggested that glute med strength of less than 10% of body weight is required to actually get a positive SLS.

The suggestion was also made that in order to maintain your stance during this test it is because of all muscles attaching to the greater trochanter working together combined with the mechanical force of the iliotibial band. This shows a positive SLS is more likely a global issue rather than a specific spine and pelvis issue.

In light of their findings they showed how this test could not distinguish between who was experiencing low back pain and who wasn’t, nor could it identify those who had weak glutes, and in fact demonstrated the test was probably due to some other issue altogether.

Another study 4 showed the presence of low back pain was a combination of higher BMI, signs of hip abductor problems, significant glute med weakness, gluteal tenderness, and a positive SLS (but the strength testing was admittedly not reliable in the study). However, this study showed something else that is probably far more significant which we will look into next.

It was unclear if glute med muscle weakness was the cause of the low back pain…or just a consequence of it.

Muscle Activation, Weakness, Or Protection?

Quite often when discussing this kind of thing and it’s relation to low back pain, the discussion can revolve around not only issues with the glutes, but also hamstring length and activation patterns between the two.

Inevitably when discussing “weak glutes” it’s due to an S.I. joint “dysfunction”, or this dysfunction is causing the weak glutes. But really, what is dysfunctional with the S.I. joint in this case?

They 5 described S.I joint dysfunction as; low back pain below L5, pain over the posterior aspect of SI joint around PSIS and buttock with or without above the knee leg pain. They used a combination of three SI joint provocation tests (posterior shear, compression, distraction, and sacral thrust) that showed good sensitivity and specificity (although the sensitivity rating was much higher).

When we look at the discussion around which muscles are “activating” with certain movements it is usually centered around the context of the pain-spasm-pain model which suggests pain results in increased muscle activity, in turn creating more pain.4

Or, the pain adaptation model which suggests pain reduces activation of muscles when active as agonists and increases activation of muscles when active as antagonists.They say this will reduce movement and ROM which would, in turn, prevent mechanical pain and further damage to the tissues.

The funny thing is that while both of these models are trying to prove the same thing, they end up contradicting each other quite a bit and neither of these ideas can predict how back pain will affect muscle activation.

There is lots of discussion around both increased and decreased muscle activation due to pain which results in disrupting motor control. However, this systematic review 6 argues that increases in muscle activation is an adaptation that occurs for various reasons, and those changes are mainly to avoid harmful stress placed on already injured structures, and to increase stability around the spine.

In each case, they looked at any changes that were task-dependent, related to an individual problem, and highly variable between each patient. This also shows those changes are functional since they are trying to reduce unpleasant stress and provide stabilization to the spine.

One common thread through most of the research cited is glute weakness in relation to back pain. However, it’s a bit of a chicken or the egg, is the weakness a result of reduced use because of pain, or did the weakness cause the pain? I’d venture to say it’s due to the reduced use.

While this can all sound maybe a little complicated and like word salad, when we look at everything we know about pain, what is this actually telling us?

One thing we know for sure that pain is ALWAYS a protection mechanism. So, if something in our body has a decreased ROM for a period of time in order to prevent stress in a sensitive area, this is just simply a way to protect that area. If those altered movements are also providing extra support to stabilize something, it’s actually doing this to protect the area! With this understanding we have to ask, does it really matter what order a muscle fires in (especially because we’d never be able to accurately assess this with just the human eye)? What we should be concerned with is calming those sensitized areas down, reassuring the patient they aren’t broken, and educating them as to why they’ll be okay. Then get them moving in pain-free full ranges again and help strengthen the area, build up that resilience!

 

References

  1. Lehman GJ, Lennon D, Tresidder B, Rayfield B, Poschar M. Muscle recruitment patterns during the prone leg extension. BMC Musculoskeletal Disorders. 2004 Dec 1;5(1):3.
  2. Penney T, Ploughman M, Austin MW, Behm DG, Byrne JM. Determining the Activation of Gluteus Medius and the Validity of the Single Leg Stance Test in Chronic, Nonspecific Low Back Pain. Archives of Physical Medicine & Rehabilitation [Internet]. 2014 Oct [cited 2020 Apr 17];95(10):1969–76. Available from: https://search.ebscohost.com/login.aspx?direct=true&db=s3h&AN=98597253&site=ehost-live
  3. Pohl MB, Kendall KD, Patel C, Wiley JP, Emery C, Ferber R. Experimentally reduced hip-abductor muscle strength and frontal-plane biomechanics during walking. Journal of athletic training. 2015 Apr;50(4):385-91.
  4. Cooper NA, Scavo KM, Strickland KJ, Tipayamongkol N, Nicholson JD, Bewyer DC, Sluka KA. Prevalence of gluteus medius weakness in people with chronic low back pain compared to healthy controls. European Spine Journal. 2016 Apr 1;25(4):1258-65.
  5. MassoudArab A, RezaNourbakhsh M, Mohammadifar A. The relationship between hamstring length and gluteal muscle strength in individuals with sacroiliac joint dysfunction. Journal of Manual & Manipulative Therapy. 2011 Feb 1;19(1):5-10.
  6. van Dieën JH, Selen LP, Cholewicki J. Trunk muscle activation in low-back pain patients, an analysis of the literature. Journal of electromyography and kinesiology. 2003 Aug 1;13(4):333-51.

 

 

 

Knee Tilt Mobilizations – Improve Knee Flexion Past 90

This is one of my favorite old school manual therapy techniques I learned while in Fellowship with the University of St. Augustine.

When my current techniques of tibial IR, lateral tibial glide, or other Functional Mobilizations I do in closed chain don’t work to improve knee flexion, I try this knee tilt.

It can be enhanced or made much more comfortable with an EDGE Mobility Band. Try this mobilization and let me know what your results are!

Articles Of The Week April 19, 2020

 

How often do you have a patient come in who is dealing with pelvic pain? I haven’t seen it much in my practice but I think this is also partially because it’s not common for a Massage Therapist to treat this area. Well, perhaps it’s time we change that.

“Treatment of Pelvic and Abdominal Pain for the RMT” – Jocelyn Kirton

We all know I have mad respect for Todd Hargrove, so when he puts on a master class about pain, movement, and play (while also doing it for free), I think we should all take advantage!

“Pain, Movement, And Play: Common Sense For Complex Problems” – Todd Hargrove

I haven’t had a chance to do this course myself but it was recommended by someone I have HUGE respect for, so it must be good. Another great way to get some learning done during the pandemic.

“Exercise And Physical Activity For Knee Osteoarthritis” – Rana Hinman

Still not sure where to start learning about pain? This is a phenomenal resource put together on some of the top pain resources available.

“Pain Resources: A Deeper Dive” – Rebecca Hall

We all know how important exercise is. As this review points out, it’s actually very important to help decelerate cognitive decline. Although exercise might not enhance cognitive function, it does effectively decelerate the decline in cognitive function.

“The Effect of Physical Exercise on Cognitive Functioning in Individuals with MCI and Dementia” – Scott Buxton

 

Looking at Pain From Different “Levels”

 

Pain can be a complex phenomenon, meaning that many different factors might contribute to pain, and that these factors can be interwoven in a way that makes it very hard to separate one from the other, either for purposes of explaining pain or intervening to treat it in some way.

This is a major theme of my recent book Playing With Movement, where I argue that complexity science has many concepts that are useful in understanding movement and pain.

One of these concepts is that complex systems are often nested. That means the system as a whole is composed of smaller subsystems, which are also composed of smaller subsystems and so forth.

 

Example of pain complexity

Where is the pain?

For example, people are made up of organ systems (like the nervous system or musculoskeletal system), which are in turn composed of organs (like the brain and spinal cord, muscles, and tendons), which are composed of cells (like nerve cells and muscle cells) and so forth. Further, people are parts of larger systems like families and communities and economies. This is interesting because each nested system provides a different level from which we can attempt to explain and treat pain.
Here’s a diagram to illustrate:
Screen Shot 2018-05-11 at 7.17.42 PM.png

At the “lower” levels, you can analyze the health status of cells and organs like muscles, tendons, discs or nerves. For example, maybe your foot hurts because of a stress fracture. This is where you can find “issues in the tissues”, which is where traditional pain treatment has focused most of its attention. This is often called the “biomedical approach” or the “bio” part of the biopsychosocial model. You find the structure that is damaged and work to repair it.

At the “higher” levels of analysis, such as the person or the environment, you are looking at more complex phenomena – the role of thoughts, emotions, or social relationships. These are the “psychosocial” issues that are known to have very important effects on chronic pain.

Problems in these areas are often relatively subtle, more about dysregulation or imbalance than something being broken or injured. These issues are also invisible if you look for them at a lower level. For example, you can’t see catastrophising by assessing a foot – you need to talk to a person.

Fields Of Study

There are many different formal disciplines you could study to get a better understanding at each level. Note that they are very different from one another, and very few people will have significant knowledge at more than one level.

Screen Shot 2018-05-11 at 7.19.35 PM.png

At the lower levels, you could study biomechanics, exercise physiology or neurodynamics. Each would give you a better understanding of how physical structures in the body respond to stress – either by breaking down and getting injured or adapting to get stronger.

You could move up a level to study the behavior of a larger system like the nervous system, immune system or endocrine system. This would help you see that pain functions like an alarm. The nervous, immune and endocrine systems help set the sensitivity of the alarm, and determine the kinds of events that cause it to go off. “Pain science” is mostly education in the basic physiology of these systems as they relate to pain. 

We can move up another level to the “person”, where we are studying the role of cognitions and emotions in pain. This is the realm of psychology, the relevance of which should be obvious – pain is a psychological event.

Psychological concepts can be very useful in understanding why movement and physical activity help with pain. For example, cognitive behavioral therapy can explain how exercise might extinguish fears or expectancies that contribute to pain. In many cases, this perspective is more helpful in choosing an exercise program than one focused on “lower-level” concerns about muscle groups, reps, and sets.   

You could move yet higher to study the role of social and economic systems. Many social critics argue that the real pathologies causing a wide variety of chronic diseases – including drug addiction, anxiety, depression, and even chronic pain – live more at the level of society than the individual. For example, low socioeconomic status is a big predictor of chronic pain. Most readers of this blog are not active in trying to solve problems at this level but are quite aware that they have a big impact on clinical outcomes.

Comparing The Different Levels

The terms “high level” and “low level” don’t reflect any value judgment. They merely indicate different perspectives: one is taking a “micro” view of relatively small and simple things like tendons or muscles, and the other is taking a “macro” or big picture look at larger complex things like nervous systems and emotions.

In general, if you’re moving down levels in your effort to explain some problem, you could call that “reductionist.” And if you’re moving up, that might be called a more “holistic” or “systems thinking” approach.

Screen Shot 2018-05-11 at 7.37.06 PM.png
Again, there is not necessarily any right or wrong here – the right level depends on the context.  Some problems with pain, especially those related to acute injuries, benefit from a lower-level approach – strengthen this, stretch that, do X sets of Y reps for Z weeks and then you will be fixed. Other pain problems can never really be “fixed” and may be hard to manage even with a whole team of psychotherapists, social workers, and attorneys.
Although each end of the spectrum has its costs and benefits, there is no doubt that until very recently, manual and movement therapists have spent way too much time at the lower levels, looking for issues in the tissues with their microscopes, while ignoring some very real big picture human issues sitting right in front of them. If the “pain science revolution” means anything, it is trying to improve basic literacy at the higher levels. “Playing with movement” means exploring a problem from as many different levels and perspectives as possible. To put it simply, finding physical activities that are challenging, meaningful and variable will go along way toward engaging us on almost any level that matters.

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

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.

200px-Descartes_mind_and_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.

VAS-chart

 

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.

Neuromatrix-Simplified

 

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!

897px-Facebook_like_thumb

 

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.)

wallen1

 

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.

Pavlov's_dog_conditioning.svg

 

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.