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.
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.
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.
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.
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.
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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About the Author
Christopher J. Centeno, M.D. is an international expert and specialist in regenerative medicine and the clinical use of mesenchymal stem cells in orthopedics. He is board certified in physical medicine as well as rehabilitation and in pain management through The American Board of Physical Medicine and Rehabilitation.…