The most common misconception about fibromyalgia is that it is a myofascial (muscle pain) problem. The research shows us that fibromyalgia is a problem with the way your brain processes pain signals.1,2,3 How the brain becomes dysfunctional in its ability to normally process pain, is a topic for another post, but I’ll tell you in one word, stress. To make improvements with fibromyalgia, you have to fix the problem with the abnormal processing pain signals in the brain, not just treat the muscle pain. With that said, muscle pain is often concomitant with fibromyalgia, and should also be addressed.6 Some of the latest research (to be released 2010) hypothesizes that fibromyalgia is caused by a dysfunctional healing response of fascia (connective tissue covering the muscles), characterized by inflammation, HPA dysfunction (Hypothalamus, Pituitary, Adrenal axis), leading to central sensitization (highly sensitized nerves that make every sensation painful).6 Fortunately for our patients, we already treat you for these problems, and this is one of the reasons we have such good results. Now, before we jump into discussing muscles, fascia, and connective tissue pain, let’s cover some foundational basics so we are on the same page when talking about this topic.
Fascia is a connective tissue just below the skin, which wraps organs, muscles, bones and nerves covering your entire body like a swimsuit below your skin. Muscles connect to bones via tendons. Your skeleton is able to move through the shortening and lengthening of your muscles, which are controlled by your nervous system. Fascia, tendons and ligaments hold the skeleton together and give it support even when the muscles are relaxed. Fascia, is also very complex in its structure and function, and is involved in the transfer of energy and loads through the entire musculoskeletal system.4 Now, all of these tissues can be injured, and will scar. Many times, you will hear scarring of these tissues referred to as adhesions. An adhesion of fascia, refers to a scar that causes two adjacent layers to stick together because of tissue damage. The tissue will “adhere” to adjacent layers as it heals because of the chemical and “inflammatory soup” that makes the tissue layers sticky. When these tissues scar and adhere to one another, they can become a source of movement dysfunction and pain.5, 6 Adhesions and trigger points, can cause decreased range of motion and require increased energy expenditure of up to 300 percent, as compared to someone without these problems.5 Does it make sense that if you have increased energy requirements just to move your body, that you may fatigue much faster than someone without these problems? To better understand what scarring in these tissues is like, picture gristle in a piece of meat. The healed scar tissue or adhesion, is different from the original tissue, and as a result, muscle, ligament, and fascia movement can be impaired, cause pain, and easily become reinjured.
The reason fibromyalgia is commonly thought of as a muscle problem by many practitioners, is because in most cases, patients come in complaining of muscle pain. Fibromyalgia diagnosis is also based on having at least 11 of 18 tender points at specific locations on the body. I personally think that your symptoms and history are more important in the diagnosis of fibromyalgia than testing the tender points. Unless the your muscles were injured at some point, or have been under high levels of mechanical stress, like from performing repetitive tasks at work, poor ergonomics when standing or sitting, lifting with poor form, or from poor posture, then your muscles should not hurt. There are some exceptions for muscle pain, like lactic acid build up, but in large part, your muscles shouldn’t hurt on a regular basis. With fibromyalgia patients, the fact is that the normal sensory information being sent from the nerves throughout your body to your brain, are being interpreted in an abnormal way. This loss of normal interpretation of pain signals means that fibromyalgia patients often feel full body pain, or pain that moves around to different areas. Most doctors don’t know that this is the problem, and they only focus on treating (muscle pain) with medications, and fail to address what is usually the major problem, abnormal pain processing in the brain. Currently, there are no medications to treat the brain for abnormal pain processing. Our treatment, using neurologically based therapy targets areas of the brain that have a decreased impulse or rate of firing. Neurologically based therapies works on strengthening neural networks and increasing firing of the brain’s weak areas. The treatments work because of neural plasticity, and the brain’s ability to “rewire” and strengthen weak neural networks. This type of treatment has been successful clinically, in the treatment of fibromyalgia and many chronic pain conditions. These therapies were pioneered by the country’s leading chiropractic neurologist, Frederick Robert Carrick, DC, PhD, DACAN, DABCN, DACNB, DAAPM, FRCPN, FACCN, FAAFN, FEAC (Neurology), FACFN, FABVR, FABES, FABCDD, FICC.
1 Burgmer M, Pogatzki-Zahn E, Gaubitz M, Stüber C, Wessoleck E, Heuft G, Pfleiderer B. “Fibromyalgia unique temporal brain activation during experimental pain: a controlled fMRI Study.” J Neural Transm. (2009) Jan;2(1):26-40.
2 McCabe CS, Cohen H, Hall J, Lewis J, Rodham K, Harris N. “Somatosensory conflicts in complex regional pain syndrome type 1 and fibromyalgia syndrome.” Curr Rheumatol Rep. (2009) Dec;11(6):461-5.
3. Chervin RD, Teodorescu M, Kushwaha R, Deline AM, Brucksch CB, Ribbens-Grimm C, Ruzicka DL, Stein PK, Clauw DJ, Crofford LJ. 2009. Objective measures of disordered sleep in fibromyalgia. J Rheumatol. Sep;36(9):2009-16.
4. Vleeming A, Pool-Goudzwaard AL, Stoeckart R, van Wingerden JP, Snijders CJ. (1995) The posterior layer of the thoracolumbar fascia. Its function in load transfer from spine to legs. Spine. Apr 1;20(7):753-8.
5. Greenman, P.E. 1996. Principles of Manual Medicine. Second Edition. Baltimore: Williams & Wilkins.
6. Liptan GL. 2010. Fascia: A missing link in our understanding of the pathology of fibromyalgia. J Bodyw Mov Ther. Jan;14(1):3-12.
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