Fibromyalgia and Chronic Myofascial Pain Information

The nervous system is divided into the central and the peripheral nervous systems, although the boundaries in places can be a bit fuzzy. When the central nervous system is sensitized, hormones and other informational substances lose their balanced states. The central part of this network consists of the brain and spinal cord. The peripheral nerves are the nerves outside those two areas. In the brain and spinal cord there are neurons, and those cells have been studied longest and received the most attention, and most medications we have for this 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, and they can become temperamental indeed! 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). The CNS screams to the world, “Leave me alone!” Too much stimulation creates what I call “sensory overload,” where the brain is literally “pre-occupied” with a bombardment of stimuli and can’t deal with anything else.

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Fibromyalgia and Chronic Myofascial Pain Information.
FIBROMYALGIA, TRIGGER POINTS AND CHRONIC MYOFASCIAL PAIN
© copyright, Devin J. Starlanyl 2012. All rights reserved.

Abbreviations

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

When I first started writing about fibromyalgia (FM), we were trying to fit pieces of a jigsaw puzzle together without knowing what the final picture looked like. Things have improved, but research hasn’t always been consistent, and a lot of the good stuff hasn’t filtered down to the patients, nor even to those treating them. There is a lot in the news about FM lately. Some of what you read and hear is trying to sell you something, and none of it covers everything. (Even this website cannot do that.) So what is FM, really? What do we know, what’s just a guess, and what is misinformation?

In FM, the pain mechanisms and the ways we perceive pain can be dysfunctional to varying degrees. The best picture we have of what is called FM is central sensitization. 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, with good reason, but that doesn’t begin to tell you what you need to know, nor does it explain to friends and family how someone with FM condition can look good and feel so miserable. 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 the central and the peripheral nervous systems, although the boundaries in places can be a bit fuzzy. When the central nervous system is sensitized, hormones and other informational substances lose their balanced states. The central part of this network consists of the brain and spinal cord. The peripheral nerves are the nerves outside those two areas. In the brain and spinal cord there are neurons, and those cells have been studied longest and received the most attention, and most medications we have for this 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, and they can become temperamental indeed! 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). The CNS screams to the world, “Leave me alone!” Too much stimulation creates what I call “sensory overload,” where the brain is literally “pre-occupied” with a bombardment of stimuli and can’t deal with anything else.

This all has to do with a vitally important concept that too few people mention when they talk or write about FM, yet it’s something that everyone who has FM or knows someone who has it needs to understand. It’s called wind-up, or temporal summation of second pain (TSSP). Doesn’t sound familiar? Yet TSSP is the best predictor of FM pain intensity. (Staud R. 2004.) So what is TSSP? When the CNS is bombarded with significant pain or by some other stressor for the first time, consider that “first pain.” The brain and spinal cord metaphorically cringe, and they do their best to recover from this first pain. If the CNS is frequently irritated by unpleasant stimuli, the brain can change. In cases of central sensitization, the “second pain” response is different. The CNS is wound up like a spring. It begins (metaphorically again) tensing the shoulders of the brain, quivering those little nerves, waiting for the next blow to fall. 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 even 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.) There is an old joke: What lies shivering at the bottom of the ocean? A nervous wreck. Well, that’s what the CNS is like with central sensitization, only the brain and spinal cord are shivering with pain inside a real person, and it’s no joke. 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, and others can’t see the pain.

Anne Félicité
When the standard depiction of fibromyalgia was first introduced, we lacked even basic comprehension of the condition, and had only a guide for researchers who were attempting to deepen this knowledge. Due to increasing research, our understanding has grown from counting tender points and focusing on painful muscles to an evolving concept of a heterogeneous set of subgroups who have central nervous system sensitivity and a countless variety of potential dysfunctional biochemical and metabolic interactions. With this new FM concept comes the need for a depiction that acknowledges the complexity of fibromyalgia.
We are delighted to present an innovative work of art, designed by artist Anne Félicité, wife of the famed French researcher Dr. Jean B. Eisinger. The figure depicts fibromyalgia in a new way, reflecting that those of us with fibromyalgia are not victims of fate (or of three Fates), are more than the sum of our tender points, and are complex individuals who are each unique in metabolic make up and needs.

Even harder to endure, or to understand, are the cognitive deficits that come with FM. Many of these are common to other chronic pain conditions, such as memory problems. The brain is otherwise employed, processing pain stimuli, and literally can’t be bothered to remember. In addition, brain dysfunction specific to FM has been documented. (Glass JM. 2008) The “brain fog,” or “fibrofog,” of FM is medically documented. You may feel as if your head is stuffed with cotton and nothing else. This can cause difficulties with even the simplest of tasks, and may cause the patient to appear and feel stupid, even if they belong to Mensa. 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. Yet you look fine, so people expect you to act accordingly. Although the stress from having untreated or undertreated chronic pain that is not understood and often met with disbelief would cause anyone to feel depressed. But no matter how much some psychologists would like us to believe otherwise, new research indicates that: “The present data suggest that associated psychological distress and maladaptive emotional responses that are commonly attributed to the general FMS population may be largely a distinguishing feature of one subset of patients.” (Salgueiro M, Aira Z, Buesa I et al. 2011)

The centrally sensitized brain and body are under attack by the pain, and try to compensate. 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 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. Research indicates that it is peripheral stimulation that is responsible for maintaining the central sensitization. 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.) So what is it that’s causing this peripheral 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. This is actually very insidious, because they still cause restriction of motion and contribute to non-pain symptoms. For example, even though your hand or arm may not feel painful, your handwriting may be illegible. 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 initiate what is often called an “FM” flare, but is actually 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, FM does not cause tingling and numbness, although you probably have read that it does so. 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 many other localized symptoms, are not caused by FM. They are caused by something else. Your 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 if not always 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 resistance and thyroid resistance.
One Lump or Two?

Anyone who has ever had a lumpy, tight muscle may have experienced a myofascia TrP or two. Trigger points develop throughout life, and sometimes people rub them and they go away, right? Not so. TrPs are lumpy bands found in ropy tissue, they don’t just disappear once formed, and they are vastly misunderstood. If there are no perpetuating factors, they may become latent TrPs. If there are perpetuating factors, they may stay active, becoming chronic. 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. There are TrPs in skin, scars, bone linings, tendons, ligaments and other tissues, and we hope to have all of the documented ones in the next book. We know (or should know) more about the myofascial TrPs, because their specific referral patterns have been mapped and well documented in medical articles and texts. (Simons DG, Travell JG, Simons L S; Travell JG, Simons DG) Central sensitization states, such as FM, are pain amplifiers. It is the peripheral pain generators such as TrPs that we need to bring under control. Myofascial TrPs not only are an exceedingly preventable cause of musculoskeletal pain, they cause a lot of other symptoms, such as blurry vision, erectile dysfunction, balance disturbance and dizziness, irritable bowel, diarrhea, vomiting, vocal disturbances, and loss of fine motor control. They can cause colic in babies and restrict motion 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 (Agh!), 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.

TrP research is expanding exponentially. I’ve seen a microvideo 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) They’ve done it at the Mayo Clinic. Trigger points can twitch when they’re irritated. This can occur even from a breeze, draft, or the weight of a feather over a sensitive TrP. 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. Also, there is no easy money to be made on TrPs, and outside interests have a lot invested in calling everything “FM,” even if it isn’t. 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. 2011 As Dr. Giamberardino and her team have stated, fibromyalgia “… is mainly rooted in the central nervous system, while trigger points have a peripheral origin. However, the nociceptive impulses from trigger points may have significant impact on symptoms of fibromyalgia syndrome, probably by enhancing the level of central sensitization typical of this condition. 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’s as clear as anybody can make it. To treat FM adequately, co-existing myofascial TrPs must be treated. That means that any care provider who treats FM patients must know how to diagnose and treat patients with myofascial TrPs. 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)

FM and chronic myofascial pain are different, although they often occur in the same patients. They don’t play well with each other, interacting and egging each other on, creating a worsening symptom spiral that can go out of control. Other co-existing conditions may join in the fray as the body and brain frantically try to balance the biochemicals that are being disrupted due to the symptom onslaught. In the case of the elderly and infirm, there are often more latent TrPs as the patients tend to move less and less because TrPs cause pain at the end of the range of motion. This adds to the debilitated state as the patient becomes less and less able to perform self care. Microcirculation problems increase. Then a fall, infection, or other activator may cause a rapidly deteriorating condition, as the patient becomes less able to care for him or herself and the care providers struggle to figure out where all the pain is coming from and patients can die. We have no idea how often this happens, because care providers usually have no idea about TrPs, their ubiquity or their importance.

TrPs are not part of FM, and there are no “FM TrPs.” Right now, it looks as if TrPs can be a cause of some cases of FM, although it seems that most cases have multiple causes. If the initiating factor was an infection, perhaps the infection caused microcirculation problems that caused TrPs that caused central sensitization that is diagnosed as FM. This can be true of repetitive trauma, major trauma, and all the other possible causes of FM. We do know that TrPs are one of the leading pain generators, and it is only logical to track down all the co-existing conditions, including metabolic conditions such as diabetes and insulin resistance, and TrPs and all their possible perpetuating factors. I promised to make this as clear as possible, but I couldn’t promise simple. It would be simple if the medical care system recognized and treated TrPs promptly and effectively. That could come a long way towards solving our health care crisis.

Currently, the vast majority of physicians lump these conditions together because they see so many patients who have both. Some physicians have gotten away with this because with both conditions: the key to successful treatment is identifying and controlling or eliminating perpetuating factors. This may involve changing to a healthy diet and avoiding excess carbohydrates, adding vitamin and mineral supplements, regaining restorative sleep. adding some gentle exercise and stress-moderating activities. Deleting unhealthy habits such as smoking can make a world of difference. In other patients, it may require more complex intervention. If there are sleep disturbances, a sleep study is warranted. These conditions are also treated differently, however, and the difference is important. Doctors who don’t know TrPs are not going to be looking for ill-fitting furniture or proportionally long torso as perpetuating factors. TrPs can physiologically weaken muscles. 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. It takes outside physical intervention to reverse a contractured state. All the relaxation and behavioral techniques in the world won’t change the 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 even find individual TrPs easily without familiarity with the referral patterns. They must also be identified because certain postures and body movements, or mechanical inequalities, may be the perpetuating factors. 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. 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 therapy or TrP injections, are not available in some locations.

Physical therapy and all other forms of treatment must proceed very carefully when both central sensitization and TrPs are present, because any excess pain caused by the therapy can further sensitize 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 your 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. For example, I have 15 co-existing conditions, and cannot get a good TrP injection unless an airplane flight is involved. Sitting for a long trip isn’t kind to the spine. I managed to write 4 books and another one is on the way, but there is a cost involved. In this process, my best tool is knowledge. It’s yours too. I teach what I learn, and hope you will do the same. I pace my work, negotiating with my spinal discs and facets. When my discs and facets get mad, my glial cells and TrPs get mad, and then none of us is happy. I need to write, because the word needs to get out. 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.

Author’s Note: My background is in trauma, but I’ve been studying myofascia, fibromyalgia and trigger points for decades, and have more continuing education credits than I can count. My main teachers, aside from my mentor David G. Simons MD, have been my own 15 conditions including FM and CMP, bulging and ruptured discs and obstructive sleep apnea. Other teachers include over a thousand patients. They had many and varied symptoms, and I listened to them and tried to figure out the cause. While we wrote “A Practical Guide to Trigger Points,” my co-author John Sharkey of Dublin Ireland was working on, among other things, his medical degree in Anatomy. He, if anyone, is a master of fascia.
References:

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, 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.

Giamberardino MA, Affaitati G, Fabrizio A, et al. 2011. Myofascial pain syndromes and their evaluation. Best Pract Res Clin Rheumatol. 25(2):185-98.

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.

Salgueiro M, Aira Z, Buesa I et al. 2011. Is psychological distress intrinsic to fibromyalgia syndrome? Cross-sectional analysis in two clinical presentations. Rheumatol Int. Nov 8 [Epub ahead of print]

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.

Staud R. 2006. Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome. Arthritis Res Ther. 8(3):208.

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.

Travell JG, Simons DG. “Myofascial Pain and Dysfunction: The Trigger Point Manual”, vol II.. Baltimore, MD: Williams and Wilkins: Baltimore. 1992.

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.

Author: dtbrents

I'm a Christian, wife, mom, grandma and great grandma. I love to study the Bible. I enjoy being a keeper of the home.

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