The Internet and social media have changed things. One of those is how easy it is for a concept to “go viral,” meaning to expand quickly through social media. One of those concepts in pain medicine that is also cashing in on the lucrative physical therapy education market is called pain neuroscience education, or PNE. It’s mostly the same pseudoscientific hocus-pocus that was spouted back in the day by chronic pain programs, updated for what we know about pain in the 21st century, with heavy helpings of quasi science. This morning I’d like to scientifically review one of the three pillars on which the movement is built and show that instead of being made of solid and reliable stone, it’s in fact made of the same straw of which the first little pig built his house.
Why take my very limited time to review the research that supports PNE? Because I see legitimately hurt patients every day who are about to be swallowed whole by this viral movement. Meaning that the quality of physical therapy care in the U.S. is about to fall off a cliff as armies of newly trained PNE chronic pain deniers are about to tell these poor, unfortunate people that the pain they experience isn’t related to any problems they may have, but instead is a fiction of their overactive nerves.
What Is PNE?
Pain neuroscience education is a reboot of a failed idea from the ’80s and ’90s, and since most physical therapists being taught this stuff were in grade school at that time, they think it’s a new concept. Basically, the old “biopsychosocial” model that tells patients with chronic pain that it’s really just all in their head. Given that multiple research studies using advanced imaging techniques have shown that pain can now be measured in hyperactive nerves, the reboot of this idea called PNE just substitutes the word “head” for “nerves” and calls it good. So PNE therapists are taught that since chronic pain doesn’t come from real tissue damage, they need to focus instead on educating patients to ignore pain signals. In fact, this concept that spinal tissue damage isn’t really causing pain is critical, as if it is, the physical therapist could be committing malpractice by ignoring that damage.
The Three Pillars of PNE
In the graphic above, taken from the British Journal of Sports Medicine (citation on the image), the three pillars of the PNE religion are elucidated:
- Back pain is not caused by tissue damage.
- The back is not vulnerable to injury and doesn’t need protection, even when symptomatic.
- It makes no sense to direct treatment at specific damaged tissues.
Given that these are the main concepts on which the whole PNE movement is based, what if these statements turned out to be demonstrably false? Let’s take the first one today.
Back Pain Is Not Caused by Tissue Damage
Based on my review of multiple publications by Pete O’Sullivan (one of the big PNE lecturers on the lucrative PT circuit), the argument that supports this statement is firmly rooted in the failures of modern imaging, such as MRI. On one level, Dr. O’Sullivan is right: modern imaging of back pain is an undeniable mess, rife with false positive and negatives. However, we have ample evidence that back pain is in fact caused by tissue damage.
I have blogged extensively on the idea that the imaging of the spine and predicting pain is a dicey endeavor. However, there are limitations to that argument, and Dr. O’Sullivan exploits those limitations. For example, while traditional old-school MRI imaging by itself as a predictor of pain fares poorly, the purpose of imaging should never be to diagnose a condition without the correlation of history and exam. Let me explain.
If we try to use MRI images of 100 patients with chronic low-back pain and 100 patients without chronic low-back pain to identify which patients should be in which group (pain or no pain), we’ll likely fare poorly in our prediction. However, that’s not how images should be used in best clinical practice. If, on the other hand, we use an MRI showing foraminal stenosis on the right at L5–S1 (not enough room for the L5 spinal nerve due to arthritis) and the patient has pain in his right leg consistent with that finding and a physical exam that matches, the MRI is useful in confirming a clinical diagnosis. Again, the purpose of MRI is to confirm a diagnosis suspected based on history and exam. That’s not to say that there may not be many others things on that MRI that aren’t causing symptoms.
To put it more simply, if an expert mechanic examines your older car right now that seems to be running just fine, he will likely find many different problems, any of which, in some cars, could cause failure. That, of course, doesn’t mean that in a car that has failed and won’t start, that examining the car for broken parts and systems is worthless. In fact, it’s a critical way to figure out what’s wrong, and due to the complexity of the system, sometimes that’s through trial and error.
Hence, the PNE movement uses research showing that old-school MRI by itself is poorly predictive of pain and draws an erroneous conclusion that damaged or abnormal structure in the low back is not painful. They do this just like our study of an older car, which will have many failing systems but runs fine.
Let’s explore this further by now delving more deeply into the idea that tissue damage doesn’t cause pain. This review is on top of many others I have done that revealed different studies showing that spine pain is quite real, related to tissue damage, and can have dramatic impacts on the brain. For example, in several studies, the pain signals from the low back cause atrophy of parts of the brain.
What evidence, just from the last two years, do we have that tissue damage causes pain?
- We can use MRI to predict a lumbar-stenosis patient’s ability to walk by looking at the shape of the spinal canal. One type of triangular shape doesn’t impact walking, while a different shape does.
- In another study using usual MRI techniques, the authors were able to determine the rate of return to play for athletes by looking solely at atrophy of the main stabilizing muscle (multifidus). Those with more atrophy didn’t return to play as often than those with less.
- In another recent research article, patients followed forward who developed disc herniations, annular tears, and nerve-root compression were more likely to have back pain.
- In this study, the authors used a new imaging sequence that measures the disc content of proteoglycans (UTE) and found that while normal MRI metrics associated with degenerated discs (T2 weighted images) didn’t correlate with pain, the UTE measure did correlate.
I could go on, but suffice it to say that we have more and more evidence that certain structural changes on MRI do equate with pain. These are newer concepts than the studies quoted by PNE fanatics. In addition, better MRI techniques beyond the original old-school methods are also showing more detail of what’s going on. The same holds true for advancements in imaging the nerve alterations and chemical changes that occur due to tissue damage.
For example, we can measure the neurological effects of pain using functional MRI (fMRI) in patients with failed low-back surgery. These changes can be seen in the brain networks that control pain processing, sensation, and movement. In another new study, the authors used PET/CT to measure the altered metabolic activity of the spinal cord in patients with chronic low-back pain. The ability to measure changes in the brain and spinal cord due to chronic pain on advanced imaging is only the beginning as new biomarker studies are showing why traditional MRI was so poor at diagnosing pain.
The idea that biomarkers would correlate better with pain was actually born out of the frustration with simple interpretations of old-school MRI not being great at diagnosing painful conditions. The concept is that while the MRI may look normal, that image is only giving us one small part of a much bigger story. For example, it’s not showing us critically important chemical changes that are happening in tissue and that are more directly related to damage and pain.
As an example, research this year found higher inflammatory cytokine levels (TNF-alpha) in patients with low-back pain due to disc disease than in those patients with abnormal discs on MRI but no pain. Other biomarkers, like FAC (fibronectin-aggrecan complex), are also specific for painful discs, independent of older imaging findings. It should be noted that FAC is a product of tissue damage. In fact, the FAC data has taken the other direction, and when the biomarker is found, treatment with epidural steroids causes relief, but this relief is less likely in those patients who are FAC negative. Finally, patients with spinal stenosis and degenerative disc disease have higher levels of IL-6 (an inflammatory cytokine) than patients with a herniated disc. While that’s interesting, more fascinating is that patients with a herniated disc who had higher IL-6 levels were 3.5X less likely to recover over the first year. Obviously, none of this had anything to do with their perception of their pain.
In conclusion, the PNE pillar that states that tissue damage in the back doesn’t cause pain is based on drawing erroneous conclusions from studies of older MRI techniques that tried to use the modality in isolation to diagnose back pain. Newer reading techniques that focus on specific structures are able to diagnose a higher likelihood of pain via imaging. Finally, newer imaging technologies and biomarker concepts (like measuring inflammatory cytokine levels) also show a good correlation between tissue damage and pain. Hence, this pillar of PNE is currently resting on rapidly eroding quicksand.
The upshot? One of the main pillars of PNE is not solid. It was built of straw by focusing on a misuse of older imaging studies to create the false appearance that tissue injury and pain in the low back were unrelated. I will also tell you that the other two pillars are similarly weak. Hence, PNE and its chronic pain deniers suffer from the same issues that the chronic pain programs of the ’80s and ’90s created, self-fulfilling prophecies based on limited data and knowledge of the anatomy and physiology of structural low-back damage that leads to pain.