[REVIEW] Why We Sleep: Unlocking the Power of Sleep and Dreams


After being in PT for almost 20 years, I’ve spent the last 5 years looking at methods outside of traditional physical therapy and patient education. Everyone is searching for the elusive magic bullet that will help the non-responders. That is why I started studying mindfulness, nutrition, and sleep. I’ve touched upon sleep here before.

I’ve known that sleep is vital to recovery, for athletes with recurrent injuries, and is associated with individuals in chronic pain. So I wanted to dive into the why. I often educate my patients on the importance of sleep but did not have the background on the mechanisms of why sleep is so vital.

After reading Why We Sleep: Unlocking the Power of Sleep and Dreams, I’ve become convinced that of all the basic pillars (Sleep, Nutrition, Exercise), Sleep may be the most vital and often ignored.

How this Book Can Help Your Patients

Decreased sleep less than 8 hours on average can lead to

  • persistent flight or fight mechanisms – increased levels of cortisol
    • this was the most AHA moment I’ve had while listening to the audiobook on Audible, as poor sleep quality/quantity has been associated with persistent pain states and central sensitization
  • decreased athletic performance, increased likelihood of injury and delayed recovery times

Learning these vital points and learning about their specific mechanisms will only strengthen your patient education.

How this Book Can Help You

I purchased the audiobook and ebook in order to learn how to better educate my patients.  I also got A LOT out of it for my own health and recovery. Turns out my “I can get along with 6 hours of sleep a night” would put me in a less than 5% of the population with a rare genetic profile. I’ve been getting 8 hours a night for about 5 weeks. Similar to when I went mostly plant-based, I’ve had
  • increased energy levels
  • better recall – which honestly I just blamed on getting older and having an army of children
  • better ability to concentrate and increased productivity
Reading this text has been game-changing for me, in the same way, changing my entire nutritional profile has. The audiobook, in particular, is narrated excellently by Steve West, who has an accent on part with the Headspace app guy.
The author, Dr. Matthew Walker, breaks down sleep in a way accessible to everyone, and not just clinicians. It’s highly recommended and at the Top 5 of my Non-PT related books that everyone needs to read.
For this review, I purchased the Audiobook on Audible with my own funds, but the links to the book are Amazon affiliate links. If you purchase either with the link, you are supporting our blog. Thanks ahead of time if you do! Next step, get the author on Therapy Insiders Podcast!
Check it out on amazon!

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. 

The Science Of Placebo


What does the word placebo mean?

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

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

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

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

What Exactly Is The Placebo Effect?

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

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

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

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

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

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

Clearing Up Mind-Body Confusions

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

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

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

So we already know that thoughts affect the body.



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

What Can The Placebo Effect Do?

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

They can even make you drunk!

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



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

How Does The Placebo Effect Work To Reduce Pain?

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

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

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

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



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

Expectation Of Reward

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

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

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



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

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

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

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

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

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

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

Anxiety Reduction

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



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

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

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

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


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

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

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



These associations can be “unlearned” as well.

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

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

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

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

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

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

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

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

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

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

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

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

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

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


The science of placebo is very interesting and informative.

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

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

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

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

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

Are these all placebo effects?

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

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



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

The Truth About The SI Joint That You Shouldn’t Ignore

Early on in my career, I’d have people come in with hip pain and like it was a script, I had an explanation ready.

I had a couple of go-to orthopedic tests, (Gillet’s, Standing Flexion, and Supine To Sit) and I’d boast about how their Ilium was rotated to their Sacrum. This, of course, resulted in a leg length discrepancy and had to be the source of their pain!

I’d do a muscle energy technique that would cause a loud “pop” from their pubic symphysis and this look of relief would wash over the patient’s face as if I had just done some sort of magical repair.

But, as time goes on not only have I started to realize that most of the above concepts were wrong, I was SUPER wrong for believing I was doing some magical repair (I’d like to think my ego has shrunk since then).

So, the question begs, what’s really going on with this darn S.I joint!?

Well…here’s what I’ve found out.

Rotation Of The Ilium

Whenever we talk bout the ilium rotating we are discussing nutation and counternutation.

Nutation is when the sacrum is moving in anterior/inferior…think to nod your head. The interosseous sacroiliac ligament (which is one of the strongest in the body) connects the sacrum and the ilium and prevents this movement from happening.

Counternutation is the opposite, moving in posterior/superior…think looking up at the ceiling. The posterior sacroiliac ligament connects the PSIS and the iliac crest with the sacrum and also prevents counternutation.

This is essentially what we were told to test in college and it was all about how the ilium rotated on the sacrum. So, we have to ask the question, how much rotation can there be?

The degree of movement is typically measured through the axis of rotation occurring through the second sacral vertebrae so the sacrum is performing its nutation or counternutation in the sagittal plane (the body in half from head to toe). The amount of movement is thought to be anywhere between 15° and less than 3°.

There is even discrepancy as to the direction of movements as one study showed that when a patient is forward flexing (like we do for some of the SI special tests) the sacrum was just as likely to nutate as it was to counternutate.

However, there are extenuating circumstances that would allow more movement in the joint such as those who have S.I. Joint disorders (which we will get into later), but when we look at healthy individuals who are perhaps experiencing some pain in the area we see much different numbers. One study actually showed in healthy individuals the average total rotation was only around 2°. They even examined 25 patients with sacroiliac joint syndrome and found the movement range to only be 1-3° with no difference between the symptomatic and asymptomatic side.

When we look at a goniometer or a protractor to see what 1-3° looks like, it’s pretty minimal and I dare say REALLY difficult to see with the naked eye.

So, we have to ask the question, are the aforementioned orthopedic tests accurate or valuable for us to use?

Well, a systematic review showed the use of Gillett’s test to evaluate movement of the SIJ to have a 47% intertester reliability, which shows this test to be unreliable. Because the movements are so limited and minute it is even suggested the movement would be impossible to see. 

Even if we’re doing tests to look for some sort of dysfunction, another review showed the most typical tests used were: Faber, distraction/compression test, focal SIJ tenderness, seated and standing Gillett’s, femoral shear, and modified Gaenslen’s were not reliable to show the likelihood of SIJ tenderness unless three or more of those provocation tests were positive, the pain was unilateral, the pain is below L5 without lumbar pain, or if pain increases with rising from sitting. 

Now that’s a lot to take into account especially if there is no history to suggest any kind of a pain or dysfunction disorder.

Of course, some of our patients will be referred for imaging, but even that isn’t helpful in the evaluation of SIJ pain unless looking for tumors, infection, or fracture, but hopefully, you’ve ruled some of this out with your intake by ruling out red flags.

What Should We Be Looking For?

If we look at a broader term, pain around the SIJ can be referred to as Pelvic Girdle Pain Disorders (PGP).

Specifically, when we look at this, the cause is around pregnancy, trauma, arthritis, and/or osteoarthritis, but excludes things like gynecological and urological disorders.

Pregnancy is one of the factors that we know can influence women to experience PGP as the effect of hormones (higher serum levels of relaxin and progesterone) affects the ligaments in the pelvis to increase their laxity, and possibly influences stability of the pelvis, but more research is needed to clarify how the role of hormones may differ in various presentations. However, this decreased joint stability can be compensated for by a change in muscle function. There is also evidence to show some of the risk factors associated with developing PGP during pregnancy is a previous history of low back pain and previous trauma to the pelvis.

When it comes to specific pathological issues like inflammatory arthritis, sacroiliitis, fractures, or infections there’s really not much we can do as therapists as manual therapy can’t address the underlying pain mechanism of the disorder, so, much of what we are doing is most likely helping with symptoms as opposed to rectifying the cause. 

Beyond these specific pathological issues there is another group of issues classified as Non-specific pelvic girdle pain disorders:

  • Non-specific inflammatory pelvic girdle pain disorder
    • constant, disabling, non-remitting pain in SIJ, provoked with weight-bearing, pelvic compression, and SIJ provocation tests.
  • Peripherally mediated (mechanically induced) pelvic girdle pain
    • Localized pain to SIJ that in intermittent and provoked and relieved by specific postures and activities due to directional loads and weight-bearing.
    • Usually, they have a clear mechanism or time of onset due to repeated strain or direct trauma.
  • Reduced Force Closure
    • Associated with excessive strain to the SIJ coupled with motor control deficits of muscles that do force closure of the joints (pelvic floor, transverse abdominus, lumbar multifidus, iliopsoas, gluts).
    • Common with postpartum PGP and a positive ASLR (active straight leg raise) test.
    • Functional impairment associated with, sitting, standing, walking, or activities that induce rotational pelvic strain coupled with spine or hip loading activities like cycling, or rowing.
  • Excessive Force Closure
    • Localized pain to SIJ and surrounding tissues, along with positive pain provocation tests.
    • Result of excessive, abnormal, and sustained loading of sensitized SIJ
    • Negative ASLR
    • Compression and local muscle activation (pelvic floor, transverse abdominal wall, back muscles, glutes, iliopsoas) is provocative.
    • Commonly associated with the belief the pelvis is ‘unstable’ or ‘displaced’ but exercise, massage (although I wouldn’t recommend this for the pelvic floor as massage in this area is out of our scope), stretching helpful for pain relief.
  • Psychological influences on peripherally mediated pelvic girdle pain
    • May be associated with underlying stress and anxiety.
    • It can be associated with faulty beliefs, and passive coping strategies, so we have to promote accurate beliefs, relaxation, and active coping strategies.
    • If associated with positive beliefs, and active coping strategies, then focus can be on physical impairments and work on helping with pain control.
  • Central nervous system driven pelvic girdle pain disorders
    • Associated with widespread, severe, and constant pain that is non-mechanical.
    • High levels of physical impairment, social impact, and abnormal pain behaviours.
    • Dominant psychosocial factors (catastrophizing, fear, anxiety, depression, history of sexual abuse).
    • Requires a multidisciplinary approach with medical and psychological management.
  • Genetics
    • People with PGP are more likely to have a mother or sister affected.
    • Possibly a social influence here as well.

While this may seem like a lot to take in, it actually simplifies things for us.

If there is no history of pregnancy, trauma, or inflammatory issues (which we should be able to rule out fairly quickly in our intake process), then we can look at psychosocial factors influencing their pain. 

Now, I know where many are going with this…we can’t treat psychosocial (or many arguing it’s not in our scope).

Well, maybe we can’t treat it directly (okay for sure we can’t, refer out to a mental health professional for that) but we can recognize their influence and work on our treatment and communication from there. Many of these conditions revolve around beliefs, stress, anxiety, catastrophizing, depression, fears, and social impact. We can most certainly address these things by giving some proper education around what they are experiencing. Explaining to them, their hip isn’t ‘out’, their ilium isn’t rotated, they don’t have an inflammatory disease, and pain is normal. Giving them relaxation techniques, helping with symptom modification, and coping strategies can all have a large impact on helping our patients with SIJ pain. However, more importantly ‘promoting accurate beliefs’, might be one of the most important things we can do. All too often we have patients come in who have been told they’re rotated, out, or misaligned, which puts the responsibility on us to educate and correct those beliefs. Sadly, I used to be one of the practitioners telling them this. If I could go back and apologize to them I would, but many of those people I don’t see in my practice anymore. While I can hope this is because I helped and they’re doing better (and I probably did with some of them), I hope that whoever they are seeing now isn’t reinforcing those old narratives, but is giving them more accurate information. I know the way I treat SIJ now, is different than the way I did 10 years ago and now that you have this information, I hope it changes the way you do because updating our narrative is part of our responsibility as healthcare professionals. 

Pain Education – What Might Make It More Effective


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

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

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

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

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

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

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

This quote from Louis Gifford sums it up nicely.

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


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

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

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

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


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

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

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

Here they are



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

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

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

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


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


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

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

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


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


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


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


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

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


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

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

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


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

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

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


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


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

Why Your Body Is A Hypocrite

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

Or is it?

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

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

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

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

What do the dots in this picture show?


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

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


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

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

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

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

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