The fascia and back pain – What does a chemical stimulation tell us about it?

Back pain is a worldwide problem causing time lost from work, disability and economic cost. Over 75% of humans suffer from back pain at least once in their lifetime and the yearly prevalence of the working population is 8%, where the lower back represents the most mentioned region. Disorders of osseous structures, disc herniations or nerve root compressions that can be seen on imaging are traditionally assumed to be the only causes of low back pain (LBP). But recently, other sources of LBP, like muscles and fascia, are being more and more appreciated in basic as well as in clinical science. Moreover, immunohistochemical studies showed that the thoracolumbar fascia is innervated by nociceptive free nerve endings [1,4] and that the dorsal horn neurons receive input from the lumbar fascia [2]. From a clinical point of view, we asked the question: Is it possible to distinguish disorders of the fascia with pain of muscular origin by measuring different parameters, such as pain intensity, pain distribution, pressure pain threshold or pain quality?

We performed ultrasound-guided bolus injections of hypertonic saline into the posterior layer of the thoracolumbar fascia, the erector spinae muscle and the overlying subcutaneous tissue at lumbar level of twelve healthy volunteers [3].

We observed that the human thoracolumbar fascia was more sensitive to chemical stimulations by hypertonic saline than the underlying muscle and overlying subcutis, according to pain intensity. Control injections of identical volumes of isotonic saline induced only weak and short-lived pain sensation, indicating that distention induced by the bolus injections played a negligible role in pain induction in deep tissues.

Regarding pain distribution, pain was confined to the ipsilateral side regardless of tissue type. These distribution patterns were measured by marking the painful areas on a scheme showing the back, the abdominal, and leg region, of a drawn standardized body. The painful area after fascia injection exceeded those after intramuscular or subcutaneous injection by far and was in the typical locations of “lumbago”. It was also similar to that seen in pseudoradicular LBP patients, and even consistent with pain distribution patterns given by patients with lumbar facet joint syndrome.

Given that affective pain qualities are the ones most commonly mentioned by LBP patients, it was remarkable that only the hypertonic saline injections into the fascia, but not those into muscles or subcutis, yielded substantial affective pain ratings, like “agonizing”, “cruel”, “exhausting”, “heavy”, “severe” and “torturing”.

However, hyperalgesia to blunt pressure, a frequent sensory sign in both localized acute and widespread chronic LBP, was only induced by injections into the muscle, not fascia or subcutis.

A potential dysfunction of the thoracolumbar fascia thus might lead to a high pain intensity, large pain distribution patterns and substantially high affective pain qualities. Being theoretical, low back pain patients, suffering from spreading strong pain with high affective qualities might exhibit a structural change within the fascial tissue, while the muscle could be of minor interest. This could have positive impact on clinical characterization of patients and their treatment.

About Andreas Schilder

Andreas SchilderAndreas Schilder is a doctoral student in the department of neurophysiology at the Medical Faculty Mannheim of the Heidelberg University (Germany). He obtained his Master degree in “animal physiology” in 2011 and studied “Bioscience” abroad at the Southern Illinois University Carbondale back in 2008. The current interest of Andreas is the contribution of deep soft tissues to back pain and its general characteristics.


[1] Corey SM, Vizzard MA, Badger GJ, & Langevin HM (2011). Sensory innervation of the nonspecialized connective tissues in the low back of the rat. Cells, tissues, organs, 194 (6), 521-30 PMID: 21411968

[2] Hoheisel U, Taguchi T, Treede RD, & Mense S (2011). Nociceptive input from the rat thoracolumbar fascia to lumbar dorsal horn neurones. Eur J Pain, 15 (8), 810-5 PMID: 21330175

[3] Schilder A, Hoheisel U, Magerl W, Benrath J, Klein T, & Treede RD (2014). Sensory findings after stimulation of the thoracolumbar fascia with hypertonic saline suggest its contribution to low back pain. Pain, 155 (2), 222-31 PMID: 24076047

[4] Tesarz J, Hoheisel U, Wiedenhöfer B, & Mense S (2011). Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience, 194, 302-8 PMID: 21839150


  1. John Quintner says:

    Yes David, we have indeed been passengers on this roundabout in our efforts to understand the complexity of the problem faced by people presenting to us with chronic low back pain of as yet undetermined aetiology. Different treatment modalities have proliferated and far out-distanced available scientific theory and knowledge.

    There is indeed a very real danger that the “myofasciologists” will gratefully seize upon the findings of this study and use it to justify their various practices which in my opinion can be tersely and perhaps cynically summarized as “rubbing and needling muscles for money”.

    The words of the 19th century physician Oliver Wendell Holmes are relevant to this discussion: [T]hose kind friends who suggest to a person suffering from a tedious complaint, that he “had” better try (a particular treatment) are apt to enforce their suggestion by adding, that ‘at any rate it can do no harm.’ But it always does very great harm to the community to encourage ignorance, error, or deception in a profession which deals with the life and health of our fellow creatures. [Holmes OW. Medical Essays, 1842-1882 The Project Gutenberg EBook of Medical Essays, by Oliver Wendell Holmes, Sr Beverly Farms, MA: Project Gutenberg; 1891: 8. Available at:

  2. David Nolan says:

    Great study, thanks. I share John Quintners worries about well meaning therapist blaming another structure for chronic back pain and aiming well intentioned treatments at it. Have we not been on this roundabout for quite some time now?

  3. Andreas Schilder says:

    Thank you very much for your comments regarding TLF and (C)LBP. This study has no focus on CLBP. The stimulus chosen was a model for acute pain in healthy subjects. It was important for us to highlight the tissue differences in pain characteristics. In order to answer your mentioned questions, the next step would be to compare these results with CLBP patients. Is the quality or distribution of pain comparable in any sense? Are there any similarities? There are studies planned.

  4. Andreas Schilder says:

    Thank you all for the interest in my article and the comments. If the experimentally induced pain reflects the pain in LBP patients is not shown yet. This is a study that still needs to be performed. Furthermore, there are evidences of dysorganization characters of the fascia tissue in chronic LBP patients. And the TLF provides a higher afferent barrage than the muscle, at least to our knowledge. This is why I postulated that fascia dysfunction might contribute to LBP.

  5. Bernard liew says:

    Great work… However, 4 criteria must be considered when attempting to answer ‘what is the source of your CLBP’. I cite the work of Prof Nik Bogduk. First, could it be a source of Pain. To fulfill it, the outdated source must be innervated, and we know the TLF is. Second, can it be a source of pain. To fulfill it, stimulating it with a noxious injectant creates LBP, and your study fulfills it. Third, is it ever a cause of LBP. To fulfill it, it requires demonstration of a unique palhology on which the pain can be blamed. The study never answers this question. Fourth, is it ever a source of LBP. It requires that provocative or diagnostic block injections be performed in people with CLBP. And it must be performed in controlled conditions.

    As we can see, just because a structure can cause CLBP, does not mean it is EVER a source of pain in CLBP populations. At this stage, TLF as a source is at a level of hypothesizing. TLF hasn’t be shown to be a source of CLBP. To proceed, controlled diagnostic injection studies are the next stage. If not, TLF pain will wither down to the level of conjectures.

    But it is a nice little piece of work nonetheless.

    Regards, Bernard

  6. John Ware says:

    Is there any evidence that experimentally-induced pain in healthy individuals is comparable to the lived pain experience of those with persistent low back pain? Doesn’t this procedure mimic acute tissue damage by chemically stimulating nociceptors, whereas in those with ongoing LBP lack evidence of tissue damage? Therefore, since a chemically-mediated, tissue damage origin has not been a feature of ongoing, disabling LBP, how do the authors justify making the leap to a diagnosis of “thoracolumbar fascia dysfunction”.

  7. John Quintner says:

    Andreas, thanks for making a great contribution to our growing knowledge base in this vexed area of spinal pain mechanisms. The obvious question to answer is how to demonstrate structural changes within the thoraco-lumbar fascia. No doubt we will soon see well-meaning therapists targeting this structure with their needles and injectates and, in so doing, beg the questions as to the presence and relevance of presumed underlying pathology. This is already happening with prolotherapy being offered to patients presenting with chronic spinal pain.

  8. Matthew Pardini says:

    Good stuff! Thanks. A fascia find that we can put directly to use in treatment plans.