My Unstable Back and the Ridiculous Pain Neuroscience Education (PNE) Model

pain neuroscience education

As I write this blog, I’m on vacation in Venice, Italy, with my family. My low back has been getting more unstable for the last several months. I first noticed it slipping a bit to the side as I performed injections, as I’m often sideways to the procedure table. This morning, after a 25-minute intense, on-the-road workout, I bent over to get a towel and my back “went out.” In this case, my L5 vertebra slipped slightly forward and tweaked my S1 nerve and “all heck broke loose.” I was pissed, not only because today is Father’s Day but also because of a stupid new phenomenon in physical therapy known as pain neuroscience education, or PNE. You see, what happened to my back this morning isn’t possible in PNE. In fact, this type of spinal instability doesn’t really happen because the spine is “bombproof.” So either my back didn’t go out this morning or these PNE guys are some serious idiots. Let’s explore both possibilities.

What Is Spinal Instability?

The spine is made up of many individual segments called vertebrae, which stack one on top of the other like building blocks. This design requires the proper support to keep it aligned and stable, and there are additional spinal structures that provide this support and keep it from becoming sloppy or falling apart. When there is even a small amount of extra motion in one of these structures, however, this can lead to spinal instability.

These supporting spinal structures include ligaments and the multifidus muscles. The ligaments act like duct tape, making sure the surface of the spinal joints stay aligned and assuring the spine doesn’t give too much when we stress it. The multifidus muscles are finely and precisely tuned, making slight adjustments to assure the spine stays stable as we move. When the ligaments are damaged or become lax or the muscles are injured or become weak or feeble, spinal instability is sure to follow.

When there is spinal instability, particularly moderate to severe, the spine may crack or pop, there may be joint swelling, or there may be pain after activity. Even if the spine feels more stable, there could be mild instability that could progress to arthritis down the road.

My Unstable Low Back and Multifidus Atrophy

I first injured my low back while driving between hospitals as a resident when someone cut me off. Part of the fault was mine in that I had installed big and very cool tires on my Jeep Wrangler, which meant that flipping it was just a bit easier. I wasn’t wearing my seat belt, so I was like a rag doll in a giant washing machine as the Jeep flipped over and over. I distinctly remember laying there in my wrecked Jeep and thinking that my low back hurt a lot. By the time I got to the ER, I was in agony, thinking that if this what having back pain means, that when seeing low back pain patients in clinic, I was a jerk doctor who didn’t understand their pain. Turned out that I had cracked a few transverse processes and likely did other damage they couldn’t see on the X-ray. I wore a brace for a few months, and after that, my low back was never the same.

Fast-forward a few decades. My low back has been manageable with periodic fourth-generation platelet lysate injections into the area around the irritated nerves (epidural) as well as into my ligaments and facet joints. However, these past few months my low back has become more unstable. How can I tell? First, my MRI has multifidus atrophy. This is that critical muscle that’s been shown to stabilize the backbones one on the other. In addition, I have been feeling that my L5 vertebra shifts forward on my sacrum or sideways. This often happens when I’m performing injections and my body is on the side of the procedure table. I’ll literally have to adjust myself so that the vertebra shifts back into place to be able to move.

This morning, while on vacation, I had a nice CrossFit workout, but I noticed my low back was “tweaky.” After that, I bent over to get a towel off the floor and my back “went out.” What happened was that my L5 vertebra slipped slightly forward on my sacrum and tweaked my S1 nerve, which shut down the local multifidus stabilizing muscles and sent the big muscles of my low back into instant spasm to compensate. I was able to partially rescue a big blow up, but I popped a few Tylenol (which is rare for me) and went about my day. I was pissed, however, not only at myself but at the physical therapists who believe in the fairy dust being peddled first in the U.K. and now in the U.S. known as Pain Neuroscience Education, or PNE.

What Is Pain Neuroscience Education, and How Would They Conceptualize What Happened to Me Today?

PNE is a theory that pain is really mostly in our head. Or to be more exact, pain is caused by hyperexcitable nerves. We can conceptualize these pain signals as a signal of bad things to come (catastrophizing) or not. These pain signals can all combine with a bad narrative fed to us by our medical providers to make us sicker. Hence, if we educate patients that their spinal problems aren’t so bad, we can make them report that they feel better and less disabled.

So, this morning, my unstable back really wasn’t unstable; I just thought it was because a bad medical provider (myself) put that idea in my head. My S1 nerve wasn’t really tweaked (forgetting about the S1 part of my foot that was numb). Since I was able to go about my day, I was able to perform my own PNE intervention by ignoring my pain signals.

What About My Atrophied L5 Multifidus Muscles, Disc Bulge, and Numb Side of My Foot?

The physical findings that all point to my S1 nerve in my back being tweaked are either ignored or minimized in PNE. Why is this a problem? After all, I was able to go about my day. Well, the chronically irritated S1 nerve will continue to shut down the local stabilizers, and that instability will lead to more tears in the disc, facet joint arthritis, and stenosis further pinching off nerves until I can no longer stand straight for more than 20 minutes. In fact, because I have ignored all of this and haven’t been getting treated (there is always something else more important than my back), if I sit in the wrong chair, the lack of coordination in my feet when I get up is real and I have to be careful not to trip.

So in the PNE model, I should ignore all of this? Why? Because there is nothing a physical therapist in the UK-socialized-medicine model can do about it. What if the doctors at my clinic can help it with injections and likely get me back to the point of having better stability and less wear and tear by using a 21st-century biologics model? That would only make me sicker they would argue. I would argue that if you believe that, I have some deeds in my trunk for swamp land in Florida that I’d be happy to sell you.

Why PNE Research Is Self-Fulfilling Junk Science

Let’s say we took multiple sclerosis (MS) patients with the same physical characteristics and performed a PNE research study. While these patients all have lesions on their brain and very real motor weakness, some may be in a sickness role and feel more disabled than they really are, some may be at an appropriate level of disability, and some may be outperforming their physical functional level. Meaning that there would be a wide variety of functional abilities despite the same physical ability. Hence, if we educate these patients about being maximally functional, we may see some real improvements that we could measure. However, is this really more than a clinically helpful magic trick? Meaning, does this really help these patients in the long run conquer MS? Not really. Does it help advance our understanding in how to cure MS? Nope. In fact, the magic trick takes the attention off trying to find treatments that will actually restore their physical ability. Why? PNE is dirt cheap for nationalized healthcare systems, so it may well be the biggest bang for the buck from the standpoint of a spending the fewest dollars to force patients to report better function. However, curing MS is an expensive research process. Why spend the money if the clinical sleight of hand can produce cheap results?

The same magic trick happens with all PNE research. It’s likely always possible to find some improvements in some patients’ negative response to injury and real physical problems. That’s even a helpful thing, as some patients will report that they feel better. You can do that whether the patients have back pain or MS or rheumatoid arthritis. You could also cure the back pain, MS, or rheumatoid arthritis and they also feel much better. However, the PNE approach allows clinicians to focus on the magic trick rather than the hard work of curing disease.

The upshot? Pain Neuroscience Education is clinical sleight of hand. In any PNE research on any disease, it’s likely possible to show some improvements in some patients, which makes it look like PNE is effective. However, it’s really just the magician who makes something disappear when you’re not looking. Did the card really go away into the ether? No. It was a magic trick. In the same way, real clinical problems don’t disappear with PNE, they just appear to go away. They’re still there, eating away at the spine.

 

 

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Read 9 Comments
  1. So what are you doing to fix your spine? You only talk about the problem, not the solution? What is the solution for you? More Lysate?

  2. Would Dr. David Hanscom’s protocol fall under the PNE model? He seems to be saying that degenerative disc disease 99 times out of a 100 never requires surgery and that people need to just get more sleep, lower their stress and get their mind off the pain by creating different cognitive pathways.

    1. Will,
      Not sure. With a quick glance it looks like his approach is based on looking for emotional generators for pain… We do agree that most cases of DDD do not require surgery, but our approaches to treating DDD are very different.

  3. PNE is a pathway to allow skilled Physical Therapists a window to allow for other treatments. It’s not a silver bullet or something that eliminates the need to perform our other skills. It’s been proven several times that when patients understand more about pain, they hurt less, move better via improved proprioception and reduction of fear, and begin to move more which reduces disability. PNE is a process that involves building a Therapeutic Allowance and Trust to allow the patient to become more comfortable in receiving other treatments.
    Pain is a distressing experience that involves sensory, emotional, behavioral and social factors. Pain is multiple system output activated by the brain as a result of a real or perceived threat or combination of both. Pain can exist without tissue damage. The amount of tissue damage does not correlate to the amount of pain either. This is fact.
    Furthermore, Skilled PT’s are movement experts. We optimize movement by addressing joints, nerves, muscles, and fascia and through education. Education is therapy and is only one of the several skilled services we can offer. The fact of the matter is when there are psycho-social-environmental factors that exist, the evidence supports utilization of PNE. When these factors outweigh mechanical factors, there needs to be a non-mechanical resolution. The StaRT LBP research has validated this. It doesn’t mean thought that tissues are still not addressed. I think we need to stop saying that one is better. There is not one way to treat chronic LBP, there is not silver bullet. However, Pain education (knowledge), Exercise (pacing), Sleep and proper Goal Setting are paramount in the chronic pain population. Regenerative medicine is great and very promising. I hope Physical Therapy can become more involved with ongoing research in this field to create clinical protocols for post regenerative injections. Yes, we still treat tissues and not all tissues are created equal which is why we provide skilled and patient centered services.

    1. Tom,

      You’ll get no arguments here for a balanced approach, but if you blame PS factors as soon as your therapy doesn’t work, that’s a formula for a mediocre provider. More importantly, stop the PNE idiots (like Pete O’Sullivan) from saying things like the SI joint is “bombproof” and we’ll call it good.

  4. Chris,
    Thanks for sharing your thoughts. I agree with your premise that nociceptice pain has a mechanical stimulus, and this stimulus should not be overlooked or ignored simply because we can’t identify it. Furthermore, in cases like yours, the salient point is that the pain is easily reproducible via mechanical means, indicating a true mechanical lesion and nociception genesis.

    It does seem to me, however, that perhaps you and the PNE proponents are referring to different patient populations. PNE seems to be most beneficial with patients presenting with chronic lesions and little to no acute tissue damage, whereas in the personal experience you’ve shared, the lesion is chronic in nature with acute injuries interjected. Do you feel this distinction may be accurate?

    I think most reasonable clinicians utilizing PNE would not do so immediately on a patient that suffered a sprained ankle 2 days ago- but I could be wrong. And when a reasonable clinician chooses to use PNE, I’d like to think they don’t do so in the absence of concurrent mechanical interventions… otherwise, they’re a psychologist 🙂

    For what it’s worth, I think the gist of PNE is to empower patients with information, which I imagine you’d agree is a good idea (assuming the info is accurate and relevant). I’d like to also think you’d agree that the words we (clinicians/experts) communicate to our patients carry substantial clout, a point of which PNE practitioners highlight. It seems the real point of contention may be what you believe to be negligence or ignorance by PNE practitioners to seek, identify, and address mechanical lesions in a patient with an acute lesion. I’m with you if that’s your point.

    If your ultimate goal is to pursuade PNE practitioners to utilize PNE with more discretion, I believe there are better ways to articulate your point of view. If your intention is to be a polemic, then I think your article is perfect 🙂

    Thanks again for taking the time to share your views, Chris. I look forward to your response.

    1. William, chronic lesions are as real as acute ones. PNE gives providers an easy cop out. As I always say, the first time you try something in a patient with chronic pain that doesn’t help, it’s your fault as the provider for not knowing enough. When you change the treatment and the patient still fails to respond, it’s still your fault. When you change it a third time and the patient reports no improvement, it’s still your fault. Finally, if you try a fourth method and the patient still isn’t improving, there’s maybe a 5% chance it could be the patient’s fault, and a 95% chance it’s still your fault. PNE bypasses this critical step of self-criticism of provider skills and knowledge.

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