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© copyright, Devin J. Starlanyl 2012. Revised 2014. All rights reserved.


FM: fibromyalgia
CMP: chronic myofascial pain
CNS: central nervous system
TrP: trigger point



Fibromyalgia is a central sensitization condition. In FM, the central nervous system (CNS) is hypersensitized. Patients with FM have enhanced sensitivity to a number of stimuli; not just pressure and pain. (Geisser ME, Glass JM, Rajcevska LD et al. 2008.) FM has been called the irritable everything syndrome. Central sensitization is not specific to FM. We are finding that it also can occur in osteoarthritis (Arendt-Nielsen L, Nie H, Laursen MB et al. 2010) Irritable bowel and migraine are other examples of central sensitization states.

The nervous system is divided into central (brain and spinal cord) and peripheral (everything else) nervous systems. When the central nervous system is sensitized, hormones and other informational substances lose their balanced states. In the brain and spinal cord there are neurons. Those nerve cells have been studied longest and received the most attention, and many medications available act on them. There are also glial cells. Once considered only scaffolding for neurons, we now know those glial cells are what affect the spinal neuron sensitivity. (Wieseler-Frank J, Maier SF, Watkins LR. 2005.) Central sensitization results when the glial cells become irritated. When the CNS is hypersensitized, any pain sensation is amplified (hypersensitivity), and normally non-painful sensations such as touch, sound, light, and even smell can be translated by the CNS as pain (allodynia). Too much stimulation creates what I call "sensory overload." The CNS is "pre-occupied" with processing stimuli and can't handle anything else.

This all has to do with something that everyone who has FM or knows someone who has it needs to understand. This concept is called wind-up, or temporal summation of second pain (TSSP). TSSP is the best predictor of FM pain intensity. (Staud R. 2004.) When the CNS is bombarded with a significant amount pain or by some other stressor for the first time, that is considered "first pain." If the CNS is irritated again, its response can change. It begins tensing the shoulders of the brain, quivering those little nerves, and waiting for the next blow to fall. It can get wound up like a spring. If the stimulation continues or recurs, the "second pain" level climbs even higher, and doesn't return to the previous level as quickly as it did with first pain. It may not ever come all the way back down. Additional stimuli can further increase the pain level, further sensitizing the CNS. In FM patients, central sensitization takes less stimulation to occur, and after-effects are greater and more prolonged. (Staud R, Cannon RC, Mauderli AP et al. 2003.) Some days, everything can hurt. Even the pounding of rain can feel as if sharp crystals are whipping at your cells. That's just part of the world of central sensitization, and FM, but people with FM look fine and are expected to act accordingly. You can't see the pain.

There are cognitive deficits, brain dysfunctions, associated with FM. Some of these, such as memory problems, are common in chronic pain conditions. Brain dysfunction specific to FM, including "fibro fog" has been documented. (Glass JM. 2008) Cognitive deficits can cause difficulties with even the simplest of tasks, such as recognizing familiar objects when they are in an unfamiliar place. Dr. Glass and her team have shown that for patients with FM, working tasks, executive memory, and semantic memory deficits equal about 20 years of extra aging. Research indicates that psychological maladaptation once supposed to be part of FM is only found in a subset of people with FM. (Salgueiro M, Aira Z, Buesa I et al. 2011) FM is not psychological; it is physiological.

Many if not most symptoms called FM are part of co-existing conditions that have been unrecognized. Hormones and other biochemicals can get out of balance in response to chronic pain and resultant lack of restorative sleep, and these can vary from person to person. The initiating factors for central sensitization can be many and varied. Infections, sustained or overwhelming grief, trauma of many varieties, toxic exposure–whatever aggravates those glial cells. Many cases of FM are multiufactorial. People are born with genetic tendencies towards developing FM, and then something happens to cause it to develop. Once central sensitization is established, no matter what they initiating event or events, only minimal peripheral pain stimulation is required to maintain central sensitization. (Staud R. 2006.) Fibromyalgia is a dysfunction of CNS. It causes systemic symptoms; not local ones. FM central sensitization is a pain amplifier. What is the source of the peripheral pain causing and maintaining CNS stimulation?

Trigger Points and Fibromyalgia: the Connection

Active trigger points (TrPs) cause pain or other symptoms in a specific, recognizable pattern. Latent TrPs hurt if you or someone else puts pressure on them, but when left alone, they don't cause pain. They still cause restriction of motion and contribute to dysfunctions. For example, the hand or arm may not hurt, but your handwriting may be illegible, and if you keep writing, the hand or arm will hurt, because the latent trigger points become active with the repetitive trauma of writing. Since TrPs, even latent ones, cause pain at the end of the range of motion, your movements become more restricted to avoid the pain, and you often forget the initial pain. You don't move, exercise, or get bodywork because it hurts. It hurts because it activates the TrPs. Those latent TrPs are just there, like land mines, waiting to go off. All it takes is some initiating factor such as an infection or a fall. That may be what initiates an "FM" flare, but could be multiple TrP activations enhancing the level of central sensitization. "Flares" don't just "happen." Something activates multiple TrPs. Understand this, and you gain some control over your life and your symptoms.

Pain from active TrPs mimics FM pain. (Ge HY, Wang Y, Danneskiold-Samsoe B et al. 2009.) Many of the symptoms that are blamed on FM are actually due to TrPs. For example, tingling and/or numbness may have many causes, including nerve entrapment by myofascial TrPs (the most common cause), but FM is not one of them. The central sensitization state of FM causes diffuse, bodywide pain. Local pain, and other localized symptoms, are not FM. Headache, backache, burning skin, vulvodynia, dizziness, toothaches, irritable bowel, shortness of breath, and other symptoms may be due, at least partly, to myofascial TrPs. Myofascial TrPs often co-exist with FM, but have been ignored by the majority of researchers and clinicians. We can't be sure what symptoms attributed to FM are actually due to the central sensitization state, because studies on FM patients have mostly ignored co-existing TrPs and other conditions such as insulin/thyroid resistance (same gene), or Ehlers-Danlos Syndrome Hypermobility Type. At the 2013 Myopain Congress, Dr. H.Y. Ge presented the results of 11 studies indicating that myofascial TrPs can cause and often maintain FM central sensitization, and that inactivating the TrPs can significantly reduce pain and dysfunction in FM patients. (Ge HY, 2013)

One Lump or Two?

Anyone who has ever had a lumpy, tight muscle may have experienced a myofascia TrP or two. Athletes get them, and they can be treated and resolve, and the muscle is lengthened. These respond to sports medicine therapies. But chronic myofascial pain is different. In pain management centers, as many as 93% of chronic pain patients have myofascial TrPs. (Sikdar S, Shah JP, Gilliams E et al. 2008.) TrPs can form anyplace in the 3-dimensional web of connective tissue called myofascia that permeates the skeletal muscles, but they can also occur in many other tissues. The myofascial TrPs specific referral patterns have been mapped and documented in medical texts. (Simons DG, Travell JG, Simons L S; Travell JG, Simons DG) Myofascial TrPs are a preventable cause of musculoskeletal pain, they cause dysfunctions, such as blurry vision, erectile dysfunction, balance disturbance and dizziness, irritable bowel, diarrhea, vomiting, volce disturbances, and loss of fine motor control. They can cause colic in babies or contribute to falls in the elderly--and in the rest of us. Yet they are largely ignored by health practitioners due to lack of understanding and training. Unfortunately, many "fibrodocs," (and fibro patients) skip information about myofascial TrPs. I get letters from readers telling me how my books have saved their life, and how their "fibro" pain is just like in the pain diagrams, or that the FM in their hands, or feet, etc. has gotten better. This kind of "fibro mind set" is partly why there are so many chronic pain patients in the first place.

Imaging has been done of an actual TrP twitch inside a muscle, (Gerwin RD, Duranleau.D 1997) and photos have been taken of TrPs, using special technology (Ballyns J, Shah JP, Hammond J et al. 2011) at the Mayo Clinic. Trigger points can twitch when they're irritated. When TrPs twitch, they release neurotoxic biochemicals that have been analyzed and documented. (Shah JP, Phillips TM, Danoff JV et al. 2005) Trigger points are unequivocally real, and so are the symptoms they cause. There are no inexpensive, easy, available tests for TrPs, and it takes a lot of time and effort to learn skillful palpation (the art of touching for diagnostic purposes) and to know all possible TrPs and their related symptom patterns. We're still discovering new TrPs. Research is mounting showing that peripheral stimuli and increased pain can be the true cause of widespread chronic pain conditions such as FM. (Staud R.2011) By stimulating active TrPs in many muscles, you can reproduce the widespread pain of FM (Ge HY, Wang Y, Fernandez-de-Las-Penas C et al. Research indicates that fibromyalgia "... is mainly rooted in the central nervous system, while trigger points have a peripheral origin….Several attempts have been made to assess the effects of treatment of co-occurring trigger points in fibromyalgia syndrome. We report the outcomes of these studies showing that local extinction of trigger points in patients with fibromyalgia produces significant relief of fibromyalgia pain. Though further studies are needed, these findings suggest that assessment and treatment of concurrent trigger points in fibromyalgia syndrome should be systematically performed before any specific fibromyalgia therapy is undertaken." (Giamberardino MA, Affaitati G, Fabrizio A et al. 2011) That means that any care provider who treats FM patients must know how to diagnose and treat patients with myofascial TrPs. They must understand that there are no fibromyalgia trigger points. We know that TrPs play a significant role as pain and symptom generators in multiple pain conditions, including FM, headache and visceral disease. (Giamberardino MA, Affaitati G, Fabrizio A, et al. 2011)

Most therapists are taught to strengthen muscles, but repetitive exercises with "strengthening bands" or exercise machines worsen TrPs because muscles with TrPs are already physiologically contractured. That is different than being contracted. The biochemicals released during a TrP twitch can create this contractured state. All the relaxation and behavioral techniques in the world won't change calcium contracture, but a good TrP injection can do it in an instant. (The problem is finding a physician who can do a good TrP injection.) If there are only a few TrPs, this technique is logical. Manual therapy that is specific to TrPs, and techniques such as "stretch and spray," can work very well. The perpetuating factors (see handout) must be brought under control to maintain muscle release. If the perpetuating factors are not brought under control, satellite TrPs can develop in muscles that overwork trying to compensate for the TrP-weakened ones, or in muscles in the referral zone. Once primary TrPs develop satellite TrPs in other body areas, life, and treatment, becomes more complex. The satellites themselves can develop more satellites involving more of the body. Trigger points can cause body-wide pain.

Chronic Myofascial Pain (CMP)

Unless doctors have a thorough knowledge of and familiarity with individual TrPs, they can't sort out CMP symptoms easily. You can't identify individual TrPs easily without familiarity with their referral patterns. When the whole body, or a large portion of it, is riddled with TrPs, identification and treatment becomes a matter of patience and unraveling the Gordian knot of overlapping referral patterns and co-existing conditions. The goal becomes finding the best attainable level of health with the minimal outside intervention. Chronic means chronic, and unless all perpetuating factors are brought under complete control, including pain itself, we look for management of CMP at this stage. The least invasive treatments are preferable. Surgery is not a viable option for TrPs. There is no quick fix, and some treatments, such as myofascial trigger point therapy, dry needling, or TrP injections are not yet available in some locations.

Physical therapy and all other forms of treatment must proceed carefully when both central sensitization of FM and TrPs are present, because any excess pain caused by the therapy can further sensitize the CNS, and that will worsen the TrPs, further sensitizing the CNS. Any treatment regimen will be both more complicated and less successful than if the patient has only one of the two conditions. A lot can be done to relieve FM and CMP, lighten the symptom load and return at least some of your function. Much of this is under patient control. It's important for the patients to take on the responsibility of managing their own treatment. It isn't easy, and it takes concentrated focus to change the habits of a lifetime. Getting as well as possible — optimizing your quality of life — takes commitment and patience. You didn't get where you are overnight, and there are no quick fixes. One of your best hopes in the challenge to regain function and well-being is education, both yours and that of your medical care team. This website is dedicated to providing both.


Arendt-Nielsen L, Nie H, Laursen MB et al. 2010. Sensitization in patients with painful knee osteoarthritis. Pain. 149(3):573-581.

Ballyns J, Shah JP, Hammond J et al. 2011. Objective sonographic measures for characterizing myofascial trigger points. J Ultrasound Med 30(10):1331-1340.

Ge HY. 2013. Overlapping Features and Mechanisms of Myofascial Pain and Fibromyalgia. Presented at the Ninth World Congress of the International Myopain Society, August 15-18. Seattle.

Ge HY, Wang Y, Danneskiold-Samsoe B et al. 2009. The predetermined sites of examination for tender points in FM syndrome are frequently associated with myofascial TrPs. J Pain. 11(7):644-651.

Ge HY, Wang Y, Fernandez-de-Las-Penas C et al. 2011. Reproduction of overall spontaneous pain pattern by manual stimulation of active myofascial TrPs in FM patients. Arthritis Res Ther. 13(2):R48.

Geisser ME, Glass JM, Rajcevska LD et al. 2008. A psychophysical study of auditory and pressure sensitivity in patients with fibromyalgia and healthy controls. J Pain 9(5):417-422.

Gerwin RD, Duranleau.D 1997. Ultrasound identification of the myofascial trigger point. Muscle Nerve 20:767-768.

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Giamberardino MA, Affaitati G, Fabrizio A et al. 2011. Effects of treatment of myofascial trigger points on the pain of fibromyalgia. Curr Pain Headache Rep.15(5):393-399.

Glass JM. 2008. Fibromyalgia and cognition. J Clin Psychiatry. 69 Suppl 2:20-24.

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Sikdar S, Shah JP, Gilliams E et al. 2008. Assessment of myofascial trigger points (MTrPs): A new application of ultrasound imaging and vibration soloelastography. Arch Phys Med Rehab 89(11): 2041-2226.

Shah JP, Phillips TM, Danoff JV et al. 2005. An in-vivo microanalytical technique for measuring the local biochemical milieu of human skeletal muscle. J Appl Physiol. 99(5):1977-1984.

Simons DG, Travell JG, Simons L S. "Travell and Simons' Myofascial Pain and Dysfunction: The Trigger Point Manual," vol I. 2nd ed. Baltimore: Williams and Wilkins;1999.

Staud R.2011. Peripheral pain mechanisms in chronic widespread pain. Best Pract Res Clin Rheumatol. 2011 Apr;25(2):155-64.

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Staud R. 2004. Predictors of clinical pain intensity in patients with fibromyalgia syndrome. Curr Rheumatol Rep. 6(4):281-286.

Staud R, Cannon RC, Mauderli AP et al. 2003. Temporal summation of pain from mechanical stimulation of muscle tissue in normal controls and subjects with fibromyalgia syndrome. Pain 102(1-2):87-95.

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Wieseler-Frank J, Maier SF, Watkins LR. 2005. Immune-to-brain communication dynamically modulates pain: physiological and pathological consequences. Brain Behav Immun. 19(2):104-111.

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