That Low Back Pain May Be Fascia, Not Muscle──Fascia as a Source of Pain

Introduction

When the lower back hurts, most of us picture muscle: muscle that is knotted, tight, or strained.

In recent years another perspective has been added to that view. Fascia itself is a tissue that senses pain and at times produces it — and, moreover, senses it more acutely than the muscle beneath it.

In another post I described fascia from the perspective of a site where inflammation occurs. This post is its sequel. I want to consider another aspect of that same living face — the phenomenon of pain — from the perspectives of immunity and the nervous system, taking as a starting point one of the most familiar of complaints: low back pain (LBP). At the same time, it should be noted that much of this remains a work in progress.

Fascia Senses Pain — the Nociceptor as an Instrument

First, what it means to sense pain.

The nerve endings that signal danger to tissue are called nociceptors. They are fine free nerve endings that respond to strong mechanical stimulus, to heat, or to chemical stimulus, sending a signal — this place is at risk — to the spinal cord and on to the brain.

The question is whether these receptors are present in fascia as well. The answer is that they are. Research examining the fascia of the lower back — the thoracolumbar fascia (TLF) — showed that this tissue is innervated by sensory fibers that convey pain (nociceptive fibers containing substance P and CGRP). These fibers are more numerous in the outer layers of the fascia. Fascia can be seen not as a mere wrapping but as a sensing tissue with pain sensors woven into it.

Fascia Hurts More Than Muscle — the Hypertonic Saline Experiment

How, then, does that pain differ from pain in the muscle beneath? There is a clinical report confirming this in humans.

In twelve healthy participants, hypertonic saline (a pain-inducing stimulus) was injected under ultrasound guidance into three layers of the back — the erector spinae, the thoracolumbar fascia (posterior layer), and the subcutaneous tissue — and the intensity, duration, and quality of the pain were compared. Injection into fascia produced stronger and longer-lasting pain than injection into muscle or subcutaneous tissue. The spread of pain and the degree of unpleasantness were also greater for fascia.

Notably, participants described the fascial pain as burning, throbbing, and stabbing. This suggests the involvement of nociceptors in both the fast-conducting A fibers and the slow, aching C fibers. In the lower back, fascia was a tissue more sensitive to chemical stimulus than the muscle beneath it — which points toward the view of fascia as a source of pain.

Chronic Low Back Pain and Fascia That Does Not Glide — Findings in Humans

There is another clinical study in humans connecting chronic low back pain with fascia.

The thoracolumbar fascia is structured as layers of dense connective tissue stacked with layers of loose connective tissue between them. The loose layers are what allow the dense layers to glide against one another as the trunk moves. In a study examining 121 people by ultrasound — 71 with chronic low back pain lasting more than twelve months, and 50 without pain — the fascia of those with chronic low back pain showed roughly 20% less glide between these layers (shear strain).

Why is that glide lost? Is it due to altered patterns of trunk movement, or to changes in the tissue itself — fibrosis, or disordered alignment? Probably both are involved. Here the account of fibrosis from the inflammation post returns. Inflammation that fails to resolve prepares the ground for fibrosis and tips fascia, which ought to glide smoothly, toward an adhered and stiffened state. “Fascia that does not glide” may be one consequence of that.

Pain Calls Forth Pain — Sensitization and Central Sensitization

Fascial pain has one further, deeper layer: pain is not always proportional to the strength of the stimulus.

First, something can happen in the periphery. Inflammatory mediators and substances such as nerve growth factor (NGF) sensitize the nociceptors of fascia. A sensitized receptor has a lowered threshold and responds even to light stimulus that would not ordinarily hurt. Administering NGF to human fascia has in fact been shown to make that area more sensitive to pain. The embers of inflammation render the pain sensors hypersensitive.

Second, something can happen centrally. When human thoracolumbar fascia is stimulated electrically at high frequency, pain is subsequently amplified — a phenomenon resembling long-term potentiation (LTP) in neural circuits was observed. This indicates that pain signals can be amplified not only peripherally but at the level of the spinal cord and brain. In chronic pain, the circuits that convey and process pain can themselves be altered. This is known as central sensitization.

This is why chronic low back pain cannot be fully accounted for by the extent of tissue damage alone. Pain is a joint product of tissue, of the nervous system, and of the brain.

Is Muscle Soreness Actually Fascial Pain?

One more familiar example is worth raising: delayed onset muscle soreness (DOMS), which arrives the day after exercise.

It is called muscle soreness, but is the source of that pain really muscle? A study examining DOMS in the lower back in detail found that the pattern in the quality of the pain suggested sensitization of fascial afferents rather than muscle afferents. At least part of the “muscle soreness” felt after unaccustomed exercise may in fact be pain from fascia. Increased fascia-derived pain after eccentric exercise has also been reported in both animals and humans.

Moving and Being Touched — How Far Can This Be Taken?

What, then, does this knowledge suggest about living with pain? Here I want to be careful and measured.

Beginning with what is most certain: for non-specific low back pain, keeping in motion and continuing moderate exercise is a relatively well-established finding. As seen in the inflammation post, gently lengthening tissue may support the resolution of connective-tissue inflammation, and fascial glide is reduced in chronic low back pain. Laid over one another, these make an approach aimed at restoring glide and movement look like a reasonable direction.

Hands-on bodywork is likewise a stimulus that deforms tissue and engages glide.

That Rolfing values fascial continuity, gliding, and the re-education of movement makes sense on this map. But — and this is the crucial part — direct evidence that hands-on work cures low back pain has not been established. Even where pain eases, the reason need not be that tissue has physically changed; there is a substantial possibility that the workings of the nervous system have changed instead — its hypersensitivity, or fear of movement. What can be said extends only as far as this: these views resonate with one another.

Being Honest About the Limits

Precisely because the subject is appealing, a line is worth drawing.

First, that fascia may be involved in pain and that fascia is the principal cause of pain are entirely different claims. Much low back pain is non-specific, with no single identifiable cause, and is a multifactorial phenomenon involving discs, joints, muscle, nerves, lifestyle, and more. Fascia is only one of the characters in it.

Second, chronic pain is not a problem of peripheral tissue alone. Central sensitization, and psychosocial factors such as anxiety, stress, sleep, and belief, are substantially involved (the biopsychosocial model). This is not a simple matter in which pain disappears once fascia is put in order.

Third, even where hands-on work or exercise eases pain, the mechanism need not be tissue change; it is more likely mediated by the nervous system. Positioning Rolfing as a treatment for low back pain is not justified at present.

Fourth, the human studies described here are still limited in number. Methods for measuring the thoracolumbar fascia by ultrasound are also still being standardized.

And when pain is severe or persistent, or is accompanied by numbness in the leg, weakness, or fever, being examined at a medical facility comes first. An account of fascia is no substitute for that consultation.

Even so, the fact that fascia is a living tissue that senses pain and at times produces it — and the possibility that moving and being touched may engage the circuits of that pain — offers one suggestion for living with pain.

Conclusion

Fascia senses. And at times, it hurts.

Pain is not an enemy. It is also a signal from the body, attempting to make something known. Moving, and being touched, engage that signal woven from tissue, nerve, and brain. To look at pain again not as something to be forced into submission but as a partner in dialogue — as one handhold for that, the view of fascia as a source of pain may be of use.

References

  • Tesarz J, Hoheisel U, Wiedenhöfer B, Mense S. Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience. 2011;194:302–308. doi:10.1016/j.neuroscience.2011.07.066
  • Schilder A, Hoheisel U, Magerl W, Benrath J, Klein T, Treede RD. Sensory findings after stimulation of the thoracolumbar fascia with hypertonic saline suggest its contribution to low back pain. Pain. 2014;155(2):222–231. doi:10.1016/j.pain.2013.09.025
  • Langevin HM, Fox JR, Koptiuch C, Badger GJ, Greenan-Naumann AC, Bouffard NA, Konofagou EE, Lee WN, Triano JJ, Henry SM. Reduced thoracolumbar fascia shear strain in human chronic low back pain. BMC Musculoskelet Disord. 2011;12:203. doi:10.1186/1471-2474-12-203
  • Deising S, Weinkauf B, Blunk J, Obreja O, Schmelz M, Rukwied R. NGF-evoked sensitization of muscle fascia nociceptors in humans. Pain. 2012;153(8):1673–1679. doi:10.1016/j.pain.2012.04.033
  • Schilder A, Magerl W, Hoheisel U, Klein T, Treede RD. Electrical high-frequency stimulation of the human thoracolumbar fascia evokes long-term potentiation-like pain amplification. Pain. 2016;157(10):2309–2317. doi:10.1097/j.pain.0000000000000649
  • Gibson W, Arendt-Nielsen L, Taguchi T, Mizumura K, Graven-Nielsen T. Increased pain from muscle fascia following eccentric exercise: animal and human findings. Exp Brain Res. 2009;194(2):299–308. doi:10.1007/s00221-008-1699-8
  • Brandl A, Egner C, Schleip R, et al. Pain quality patterns in delayed onset muscle soreness of the lower back suggest sensitization of fascia rather than muscle afferents. Pflugers Arch Eur J Physiol. 2023. doi:10.1007/s00424-023-02896-8
  • Wilke J, Schleip R, Klingler W, Stecco C. The lumbodorsal fascia as a potential source of low back pain: A narrative review. Biomed Res Int. 2017;2017:5349620. doi:10.1155/2017/5349620

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Hidefumi Otsuka, Ph.D. | Certified Advanced Rolfer™ / Rolf Movement Practitioner

Completed his doctorate at the University of Tokyo Graduate School of Medicine. After working in medical marketing at an international pharmaceutical company, he has offered Rolfing® sessions in Shibuya since 2015. His work centers on the integration of science and practice.

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Hidefumi Otsuka

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