Over the last couple years, by far the most common answer to my fascia science challenge has been: Langevin, Langevin, Langevin. Specifically Langevin et al.’s 2009 and 2011 papers presenting evidence that the thoracolumbar fascia is thicker and stiffer in people with chronic low back pain.4445
This is interesting evidence that comes as close to being a good answer to the challenge as anything I’ve seen yet. But I still
don’t think it actually achieves clinical significance.
I’m not going to question the findings at all for now (though of course one always can and probably should do that46). I’m going to take their results at face value and write only about what they mean to us as thoughtful therapists and patients, keen on biology but wishing to avoid false hope.
The thoracolumbar fascia is the shield-shaped sheet of thick fascia that more or less completely covers the low back.
Exactly what Langevin et al. found
In people with chronic low back pain:
- The thoracolumbar fascia was about 25% thicker in people with back pain, which is quite a bit, and a surprising finding with potentially major — but unknown — clinical significance. The authors suggest that it could be related to “genetic factors, abnormal movement patterns and chronic inflammation.”
- The thoracolumbar fascia had about 20% reduced “shear strain,” measurement of the deformation of a structure. In other words, it was 20% stiffer than in people without back pain. Again, that’s quite a bit.
What’s it all mean?
Chronic back pain is a notoriously inexplicable and invisible condition. Things that turn up on MRI that seem like they might explain the pain are often irrelevant. A clear, consistent, measurable biological sign of cLBP like thickened fascia would be inherently interesting — downright cool, even!
But that thickened, stiffened fascia is probably not the cause of back pain. At best, it’s probably a clue about the nature of back pain — inflammatory, perhaps?47 But it might be even less meaningful: it could be a trivial, transient consequence of pain and limited mobility, something that happens because you’re in pain for a long time, and which fades away as steadily as it came. It could be as boring as “use it or lose it” — we stiffen up a bit when you’re in pain for a long time. mind blown
Indeed that is the most likely explanation. And if that’s all there is to it, it’s really a big whoopty-doo.
But no one knows. The research didn’t explain a phenomenon, it just identified one. Maybe.
The purpose of this article is to challenge hype about fascia. The point of the fascia science challenge is that most science does not at this time inform diagnosis or treatment, and therefore there is no scientific justification at this time for “fascial therapy” to be a popular phenomenon.
Langevin et al.’s research clearing comes closer to influencing diagnosis or treatment than anything else I’ve seen, but I think it’s a case of so-close-yet-so-far.
Does knowing that the thoracolumbar fascia is thicker and stiffer inform diagnosis? Not really. Because no clinician can (a) know whether or not it’s actually the case, or (b) has any idea whether it’s a cause of back pain or a trivial consequence of it.
Does knowing this inform treatment? Not really. There’s no point in trying to treat it unless (a) you know it’s actually a significant cause, or a consequence that complicates, and (b) no one has the slightest idea (and it’s rather unlikely) that anyone can make it thinner or more flexible with their bare hands.
It’s conceivable that follow-up research could fill in some of these blanks, but, until then, this research isn’t good for much beyond raising eyebrows. It’s only clinically relevant insofar as it could lead somewhere clinically relevant. If the findings can reproduced. If they can be explained. If the explanation does in fact turn out to be clinically relevant.
That’s a lot of ifs.
A contrasting example: frozen shoulder
Frozen shoulder is one of the few common musculoskeletal problems that can be blamed on misbehaving fascia. It’s technical name (adhesive capsulitis) suggests that it is a disease of “stickyness” of the joint capsule, but in fact the best available evidence to date suggest that it is more a disease of shrinkage — connective tissue contracture. Maybe this contracture has something in common with what Langevin et al. observed in the low back.
In the case of the shoulder, joint capsule contracture is quite clearly an etiologic factor: it’s freezing shoulders and causing much woe.
In the case of the back, it’s technically conceivable but extremely unlikely that fascial contracture is the cause of low back pain. But, just for the sake of argument, let’s say it is. Let’s imagine that people get back pain because their thoracolumbar fascia seizes up for mysterious biological reasons, much like frozen shoulder. This is not a completely absurd notion, but I don’t actually believe it for a moment: it would be the biggest discovery in the history of musculoskeletal medicine. This is just a thought experiment!
No one has the foggiest notion how to “melt” a frozen shoulder. That joint capsule is exceedingly tough. When it contractures, that’s it: it yields only to intense, traumatic forces. Frozen shoulder defies manual therapists all the time (despite cocky claims to the contrary). And so, even if back pain is like frozen shoulder and caused by fascial contracture, I don’t think there’s a snowball’s chance in hell that it could be treated with any kind of hands-on manipulation. Both shoulder capsules and the thoracolumbar fascia are super tough human gristle, and are unlikely to change much or for long — if at all — in response to any non-traumatic external stimulus.
So even in the most spectacular hypothetical scenario where the thoracolumbar fascia is actually a major cause of back pain… even then it’s still not going to translate into a good treatment option. And so Lanvegin et al. cannot and should not be used as justification for a clinical obsession with fascia.