Symptoms


Informational
Handouts


Information
in Spanish


Information
in German


Information
in Dutch

  

Chronic
Myofascial Pain


Fibromyalgia Subsets


Health Care
Providers Bibliography


References for
Research
Purposes


Resources


Home


 

FIBROMYALGIA AND TRIGGER POINTS for CARE PROVIDERS
© copyright, Devin J. Starlanyl 2012. All rights reserved. http://www.sover.net/~devstar

Fibromyalgia

If you have been a medical, dental care, or an allied health care provider for six months or more, you have most likely seen patients with myofascial trigger points (TrPs) and fibromyalgia (FM) central sensitization. You may not have been aware of it at the time. These conditions impact every medical practice, and the impact is becoming more apparent. Research hasn't been filtering down to the people in the trenches as quickly as is needed.

The FM construct is confusing at best, and research on the subject has been contradictory. You may be used to the FM "tender point" diagram. Tender points and their related criteria have generated a lot of controversy. Have we been trying to fit a bicycle into a shoe box?

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.

This diagram may better illustrate the form of central sensitization that we call fibromyalgia. ( I promise to explain central sensitization later.) I'll try to clear away some of the clouds (and misinformation), and document what you need to be more effective in your practice. I'll attempt to accomplish this without putting you to sleep from sheer boredom or having your eyes and synapses cross as you try to make sense of obtuse language. I could dazzle you with erudition, but the object of my writing is to communicate information.. These conditions are complex, but not so much as some would have you believe. Space constraints will not enable us to dive into minutiae concerning the variety of biochemical abnormalities that can be present in FM, the possible activation of glial cells through fractalkine, or the epsilon isoform of protein kinase C. Medline, PubMed, (or the annotated References for Research Purposes found on this website) are resources to be utilized for those.

The idea that FM is a psychiatric disorder is not only unfounded, it has the potential to cause harm to patients. (Nielson WR, Merskey H.. 2001) Maladaptive emotional coping mechanisms and psychological dysfunctions that might be associated with one subset of FM patients do not apply to the whole FM community. (Salgueiro M, Aira Z, Buesa I et al. 201) The central sensitization state called FM is most closely defined by bodywide diffuse and centrally augmented pain that's been documented by tests such as functional neuroimaging and measurement of evoked electrical potentials, with multiple abnormalities. (McLean SA, Clauw DJ. 2005) Although the patient feels diffuse muscle pain, FM can cause amplified sensitivity to multiple sensory stimuli. (Geisser ME, Glass JM, Rajcevska LD et al. 2008) The "hallmark" of FM is allodynia; pain from normally non-painful stimuli. (Russell IJ, Larson AA. 2009.) Bright or flashing lights; sudden, loud or staccato noises; touch, and even smells may cause irritation, confusion, or pain, leading to what I call sensory overload as the brain struggles to process stimuli that are coming in way too fast.

One of the most important, though little remarked, aspects of the FM central sensitization state is called wind-up, or temporal summation of second pain (TSSP). After a response to nociceptive stimuli (first pain), a second nociceptive stimulus provokes greater pain of longer duration. The base pain may not return to its initial level, or it may return ever-so-slowly, due to neural plasticity. The central nervous system (CNS) has changed, becoming more sensitive to pain (hyperalgesia.) Dr. Staud was aware of my work stressing the importance of peripheral nociceptive generators such as trigger points (TrPs) in FM, (Starlanyl DJ, Copeland ME. 2001) and when I thanked him for his articles, he took my hands in both of his and told me that I'd be pleased with his recent findings. His research indicated that TSSP and central pain in FM resulted primarily from peripheral stimuli, and that in FM patients, CNS sensitization can be caused by less pain, and the after-effects of pain are greater and more prolonged. (Staud R, Cannon RC, Mauderli AP et al. 2003)

Augmented TSSP in FM occurs in all pain-related brain areas, and is not due to emotional stress. (Staud R, Craggs JG, Peristein WM et al. 2008) The process of TSSP can lead to central sensitization. (Li J, Simone DA, Larson AA. 1999) The best predictor of FM pain intensity was the magnitude of TSSP. (Staud R. 2004) Furthermore, once augmented TSSP occurred in FM patients, it took less pain to maintain enhanced wind-up (central sensitization) than for control subjects. (Staud R, Price DD, Robinson ME et al. 2004) Researchers found that "...decreasing pain in some muscle areas by local anesthetics or other means may improve overall clinical pain of FM patients." (Staud R, Koo E, Robinson ME et al. 2007) Another of Dr. Staud's teams found that counting the number of localized pain areas on body diagrams predicted pain intensity more accurately than counting tender points. (Staud R, Price DD, Robinson ME et al. 2004) Mean-while, more FM documentation was piling up, including studies that indicated FM patients were losing grey matter in the brain at 9.5 times the normal loss, and that "...fibromyalgia appears to be associated with an acceleration of age-related changes in the very substance of the brain." (Kuchinad A, Schweinhardt P, Seminowicz DA et al. 2007)

Cognitive dysfunctions may be the most disruptive aspect of fibromyalgia, although some of those disruptions are due to chronic pain.(Dick BD, Verrier MJ, Harker KT et al. 2008) Some patients have difficulty reading a book or watching a television show because they can't remember the characters. (Russell IJ, Larson AA. 2009) Patients call this symptom "fibrofog." The working, episodic and semantic memory impairments of FM patients equals adding about 20 extra years of aging. (Glass JM. 2008) "The existence of these symptoms has been confirmed...by the results of objective tests of metamemory, working memory, semantic memory, everyday attention, task switching, and selective attention. More complex tasks cause greater difficulty, as does distraction. Short-term memory can be especially affected by distraction." (Leavitt F, Katz RS. 2006) Cognitive impairments can vary with fatigue and mood. Pain had the greatest effect on perceived language deficits, not concentration or attention, and lack of restorative sleep most affected perceived memory deficits. (Williams DA, Clauw DJ, Glass JM. 2011) Fibromyalgia cognitive deficits can be profound, and yet be undetected by conventional cognitive assessment techniques. (Leavitt F, Katz RS. 2009) Research has "...revealed a pattern of impairment in working memory and attention/executive control as well as memory impairment. " (Glass JM. 2010) Even when global processing is unimpaired, there is frequently a significant impairment in selective deficits such as specific naming speed skills. (Leavitt F, Katz RS. 2008) There are new simple tests that may prove useful. (Leavitt F, Katz RS. 2011)

Spatial memory may be more impaired in FM patients than verbal memory. (Kim SH, Kim SH, Kim SK et al. 2011) It is logical to suspect that this may be caused by biochemical brain trauma from the sidetracking of tryptophan to the kynurenine pathway. On this metabolic path, instead of needed serotonin, the result is quinolinic acid. We know that this metabolic pathway is utilized in at least a subgroup of FM patients. (Schwartz MJ, Offenbacecher M, Neumeister A et al. 2003) We know that quinolinic acid is a neurotoxin that causes spatial memory impairment in rats. They can no longer run their mazes. Is quinolinic acid causing the same chemical brain trauma in FM patients? The experiment may be on-going without our knowledge, (perhaps as FM patients attempt to traverse the maze of medical insurance?) We don't yet know, and certainly haven't given consent. (Neither did the rats.) We do know that FM patients can have significant cognitive deficits that tend to increase in times of stress, or if hormones are unbalanced. This is important for care providers to remember, especially as this may make communication difficult in emergency situations, or during stressful office visits or medical procedures. These cognitive deficits could also be mistaken for dementia in the elderly.

Fibromyalgia is not heterogeneous, but consists of many subgroups. (Walen HR, Cronan TA, Server ER. et al. 2002) I was part of one team that proposed a protocol for FM subgroups. (Eisinger J, Starlanyl D, Blotman F et al. 2000) Fibromyalgia is a systemic condition. It does not cause local pain. "Tender points" of FM are localized, and not the best predictors of FM pain. (Staud R. 004) In FM, a variety of neurotransmitters, hormones, peptides and other biochemicals may be out of balance, and each patient may be a little bit different in this aspect. In FM, a variety of factors may initiate CNS neural plasticity, resulting in a changed perception of pain. Even chronic pain itself may initiate or intensify central sensitization. (Bruehl S, Chung OY, Ward P et al. 2004) Control of pain is of vital importance.

Fibromyalgia is not exclusionary. One may have FM and many other conditions. Impaired balance, falls, dizziness, irritable bowel, sexual dysfunctions, sleep impairment, numbness, dyspnea, burning, etc. often ascribed to FM may be from co-existing conditions such as insulin resistance, thyroid resistance, vestibular dysfunction. One of the first steps in managing FM is to discover what condition is causing or contributing to the most significant symptoms. It is important to know that when the CNS is hypersensitized, pain is not the only symptom that is enhanced. (Geisser ME, Glass JM, Rajcevska LD et al. 2008.) Fibromyalgia is invisible. You can't see pain. Along with the pain and cognitive deficits come sleep deprivation and fatigue. Patients may feel anxious or depressed because no one can tell them why they hurt or what they can do about it. Quality of life can spiral downhill as financial and other resources are depleted. Friends don't know what to do or say, and patients and their care givers may become isolated. For the longest time, many people didn't believe that FM existed. Some still don't.

Fibromyalgia is a central sensitization state. When pain and other stimuli bombard the CNS, it gets annoyed. Very annoyed. Eventually, TSSP causes the CNS to become exceedingly hypersensitive, and hyperalgesia and allodynia result. Central sensitization isn't specific to FM. It can occur in osteoarthritis. (Arendt-Nielsen L, Nie H, Laursen MB et al. 2010) Headaches, (Filatova E, Latysheva N, Kurenkov A. 2008) irritable bowel syndrome (IBS) and migraine are other examples of central sensitization states. "Pathogenetic research is focused increasingly on a central dysregulation in pain perception and pain processing, leading to the concept of 'central sensitization' as a final common pathway for fibromyalgia and similar syndromes." (Spaeth M. 2011) Low local pH, common in areas of localized hypoxia, can sensitize receptors in the muscle, cause central sensitization, hyperalgesia and allodynia. (Mense S. 2003) Evidence is accumulating that peripheral pain generators "... might either initiate or maintain central sensitization, or both.... Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state."(Staud R. 2006)

Fibromyalgia is a pain (and other symptom) amplifier. Trigger points and articular conditions such as arthritis, are pain generators. Trigger points are commonly associated with arthritic and other conditions, are often mistaken for them, and are common in central sensitization states. Trigger points are common in migraines, (Calandre EP, Hidalgo J, Garcia-Leiva JM et al. 2006) IBS, (Doggweiler-Wiygul R. 2004) and other central sensitization states, tension headaches (Fernandez-de-las-Penas C. 2010) and chronic pain after whiplash. (Dommerholt J. 2005) Unfortunately, for a long time with few notable exceptions, most "fibrodocs" and TrP care providers didn't spend a lot of time looking at each others' research. Yet it was noted that control of peripheral pain generators is imperative in the management of FM. (Borg-Stein J. 2002) Many of us with our feet predominantly in the TrP world were concerned by each new attempt to clarify FM criteria for diagnosis. These attempts ignored TrPs, or mixed FM and TrP symptoms, and continued the danger that research based on each FM criterial iteration would lead to misidentification of TrP symptoms for FM symptoms. This occurs indeed, with alarming frequency. There have been attempts to explain this concern, in person and in print, (Starlanyl DJ. 2006) but they have not been received with either open arms or open minds by those of the "fibro mindset," even though FM "tender points" are usually TrPs. (Gerwin RD. 2010b)

This misunderstanding can lead to research confusion and often misleading results. For example, electromicrographic studies of FM patients' skin show unusual patterns in nerve fibers and associated Schwann cells, (Kim SH, Kim DH, Oh DH et al. 2008) as well as skin protein amino acid composition. (Ribel-Madsen S, Gronemann ST, Bartels EM et al. 2005) Are these results due to FM, to co-existing TrPs, or even other co-existing conditions? We can't be sure until patients are assessed for both TrPs and FM, and there are only a few articles that do that. Local and referred pain from TrPs in women can completely reproduce the diffuse spontaneous pain of FM. (Alonso-Blanco C, Fernandez-de-las-Penas C, Morales-Cabezas M et al. 2011) Multiple active TrP pain can mimic FM pain, and those TrPs may be the main pain generator that the FM (central sensitization) amplifies. (Ge HY, Wang Y, Danneskiold-Samsoe B et al. 2009) "Active MtrPs as tonic peripheral nociceptive input contribute tremendously to the initiation and maintenance of central sensitization, to the impairment of descending inhibition, to the increased excitability of motor units, and to the induction of sympathetic hyperactivity observed in FM. The considerable overlap of MTrPs and FM in pain characteristics and pathophysiology suggests that FM pain is largely due to MTrPs." (Ge HY. 2010) As myofascia twists and sticks to other tissues, it can entrap nerves, blood and lymph vessels, and perhaps even ducts. This can lead to symptoms such as swelling, numbness and tingling, and all sorts of other diagnostic nightmares for care providers and real horror for patients living with them.

Too many have lumped FM and TrPs together into one entity. Some even stated that TrPs are a form of FM. This can do considerable harm to patients in several ways. We can treat the specific TrPs, and we can eliminate or manage their perpetuating factors. We need to separate, and not lump, to avoid churning out FM research with suspect conclusions. So many TrP symptoms are commonly misdiagnosed as FM, or considered of unknown origin. 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. Cookbook medicine does not work well in chronic pain, as many patients have multiple conditions. Differential diagnosis has its place, but these conditions require the ability to manage interactive diagnoses, because many patients with chronic pain have multiple diagnoses.

For example, 30% to 70% of FMS patients have IBS. (Wallace DJ, Hallegua DA. 2004) "Women with chronic pain from fibromyalgia are at an increased risk for metabolic syndrome..."(Loevinger BL, Muller D, Alonso C et al. 2007) and this cannot be taken lightly. "Up to 80% of patients with the metabolic syndrome die as a result of cardiovascular complications. (Lombard L, Augustyn MN., Ascott-Evans BH. 2002) Trigger points contribute to many chronic regional and widespread pain conditions. One of the first quests my mentor, David G. Simons, proposed for me was the separation of FM and TrP symptoms. At the time, neither of us had any how difficult that task might be, nor where the answers would lead us. It's time to look closer at those pesky but ubiquitous critters: the trigger points.

Trigger Points

Trigger points can form in skin, scars, bone linings, tendons, ligaments and other tissues. 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. The definitive texts on trigger point have been available, but greatly underutilized, for some time.(Simons DG, Travell JG, Simons L S 1999; Travell JG, Simons DG 1992) In those texts, Janet G. Travell and David G. Simons provided a great foundation on which to build, but further construction was sporadic and isolated for some time. Fortunately for patients and the world at large, Robert D. Gerwin kept the knowledge alive with the "Focus on Pain" seminars while the some of rest of us caught up to the pioneers. Most of the medical world, with the exception of some osteopathic, chiropractic and bodywork schools, refused to believe that TrPs existed or hadn't heard of them.

Myofascial TrPs are hyperirritable nodules found in taut bands within skeletal muscle sarcomeres. The deformation of sarcomeres created the characteristic contraction nodule. Sarcomeres on either side of the contraction knot are lengthened, creating the taut band. The taut band is the one consistent finding in both active and latent TrPs. The ropy bands may not always be palpable, but they are there. Within the dysfunctional endplate area, there is a situation of increased energy demand and lower energy supply that is self-perpetuating. Active TrPs can cause spontaneous characteristic referred and/or local pain and/or other symptoms. Sometimes those patterns are in the area of the TrP, but they may also cover several muscles. The pattern may not even include the muscle that holds the TrP at all. Latent TrPs cause pain only when pressed. Although one may automatically think of pain when considering TrPs, they also cause dysfunction, including muscle weakness. A knee may buckle, or grip may fail. Myofascial TrPs also have autonomic and proprioceptive concomitants. One needs to think of TrPs not just in terms of pain, but for symptoms such as nausea, vomiting, illegible handwriting, eyelid twitching, runny nose, incontinence, or erectile dysfunction. It was one of Dr. Simons' concerns that the "other symptoms" associated with TrPs might get lost in the pain. He was delighted that a book written for care providers and patients and focusing on both aspects was in progress. (Starlanyl, Sharkey. 2012)

Myofascial TrPs form with excess acetylcholine release at the motor end plate. This results in physiological contracture of muscles. Inside the TrP zone, there is a region of extreme hypoxia consistent with capillary compression. Tissue outside the TrP zone is normal. Spontaneous endplate activity (SEA) is associated with TrPs, as is the local twitch response (LTR). Simons' Integrated Trigger Point Hypothesis fits with the facts we know. The missing piece of the hypothesis may well be the source of excess calcium and the cause of the endplate noise: a leaky ryanidine receptor calcium channel on the sarcoplasmic reticulum.(Gerwin R. 2010a) This would place the myofascial TrP firmly in the category of calcium channelopathy.

"Spontaneous pain is mainly due to ongoing activity in nociceptive neurons in the spinal cord. Allodynia and hyperalgesia can be explained by a sensitization of central nociceptive neurons (central sensitization). One mechanism of central sensitization is the release of substance P together with glutamate from presynaptic terminals of nociceptive fibers from muscle. Other steps of sensitization are the opening of N-methyl-d-aspartate channels on postsynaptic neurons and the de novo synthesis of ion channels. The current concept of pain referral assumes that the efficacy of synaptic connections of central dorsal horn neurons can change under the influence of a nociceptive input. Thus, ineffective synaptic connections can become effective. Pain referral appears to reflect the formation of new effective central nervous connections....Myofascial TrPs are not merely a peripheral phenomenon, the input from TrPs leads to hyperexcitability of central neurons that manifests itself in allodynia, hyperalgesia, and pain referral. These central changes are mainly based on an increase in the synaptic efficacy of central connections induced by nociceptive input." (Mense S. 2010) Simple TrPs, if diagnosed and treated promptly, can be very easy to treat successfully. If they remain untreated, the body compensates. Movement patterns change to ease the stress on the TrP-laden muscles. Habits are set in motion that will further perpetuate TrPs, stress other muscles, and take time to unlearn. As muscles weaken with TrPs, other muscles are recruited to take up the work of the weaker ones. They develop satellite TrPs. Muscles that are in the referral pain pattern of a TrP are also subject to stress. These muscles can develop satellite TrPs too. This expansion of TrPs may give the perception of a progressive disease, although it is not. It is very important to understand that TrPs are not part of FM, and there are no "fibromyalgia TrPs."

Palpation gives some of us sufficient evidence of TrPs. Placing the muscle in a lengthened position will exaggerate the ropy bands and should make them more noticeable to listening fingers. Contraction knots can be small or large, depending on a number of variables, such as how many TrPs make up the contraction knots, the tissue consistencies, and the amount of fluid infiltration involved. The lack of palpation skills and training is one of the reasons myofascial pain due to TrPs so often goes undiagnosed. (Lewit K, Liebenson C. 1993) We now have objective evidence of the existence of TrPs for those who remain skeptics. When I first saw the video of a TrP twitch, I was as excited as an irritated nerve, only in a good way. (Gerwin RD, Duranleau D.1997) Unfortunately, as this video is not available on Netflix, unbelievers remained. Then, a brilliant young researcher invented a new microdialysis technique to find out what occurs to the environment of a TrP when it twitches. Using hollow acupuncture needles, the milieu of the TrP was sampled during the local twitch response. (Shah JP, Gilliams EA. 2008)

A TrP can twitch even from the stimulation of a breeze, draft, the weight of a feather, or even spontaneously. The twitch can be mild enough to be unnoticed by the patient while visible to a care provider, but I've had LTRs in the rectus femoris strong enough to startle a cat from my lap. Dr. Shah and his team found that when a TrP twitches, it releases irritating chemicals into the interstitial fluid around the TrP. An LTR from an active TrP sends forth a "sensitizing soup" of over 30 biochemicals, including significantly higher amounts of bradykinins, calcitonin gene-related peptide, IL- α, serotonin, tumor necrosis factor and norepinephrine than from a latent TrP, and the pH of the area dropped to about 5. Substance P and CGRP dropped significantly after the LTR. (Shah JP, Phillips TM, Danoff JV et al. 2005) The pH drop and release of irritating biochemicals are sufficient to change the pain sensitivity in the TrP area. "The continual pain barrage can affect central nervous system plasticity, resulting in hyperalgesia and allodynia as well as referred pain." (Gerwin RD, Dommerholt J, Shah JP. 2004) Another exciting article included 2 dimensional greyscale and vibration sonoelastography imaging of a myofascial trigger point in the upper trapezius. (Sikdar S, Shah JP, Gilliams E et al. 2008) The article notes that almost 10% of the population of the USA have myofascial TrPs and as many as 85-93% of chronic pain patients in specialty pain management centers have MTrPs.

Using functional MRI to image regions that are dysfunctional in FM patients, other researchers used a needle electrode or pressure to stimulate MTPs. Both stimulations produced a higher pain response than in normal controls, with "significantly enhanced somatosensory activity (SI, SII, inferior parietal, mid insula) and limbic (anterior insula) activity and suppressed right dorsal hippocampal activity in patients compared with controls," (Niddim DM, Chan RC, Lee SH et al. 2008) showing that the hyperalgesic state in TrP patients is associated with abnormal brain activity in the areas that process stimulus activity and negative affect. Another study proclaimed "...myofascial trigger points may be classified by area using sonoelastography." (Ballyns J, Shah JP, Hammond J et al. 2011) Myofascial TrPs have been imaged at the Mayo Clinic. These imaging systems are available only in research facilities, but they do prove that TrPs are real.

Latent TrPs are common, even in the general population. (Lucas KR, Rich PA, Polus BI. 2008) Latent TrPs hurt if you or someone else puts pressure on them, but when left alone, they don't cause pain. This often causes people to avoid bodywork or any exercise, because they activate TrPs, and this can be difficult if pain control is inadequate. This is not a sign of mental illness and "pain avoidance behavior," it is simply logical. Sane people avoid doing things that hurt them, and TrPs cause pain at the end of range of motion. Latent TrPs are actually very insidious, because they do provoke restriction of motion and contribute to non-pain symptoms, and any sudden stressor could cause them to activate. Latent TrPs in one muscle can increase the activity of TrPs in another muscle. (Fernandez-Carnero J, Ge HY, Kimura Y. 2010) This is one of the many ways TrPs can "spread." Latent TrPs are more common in the elderly population, because they tend to move less. Especially when it hurts to move. This can enhance a debilitated state as the patient becomes less and less able to perform self care and microcirculation problems increase. Then a stressor such as a fall, infection, or other TrP activator causes a rapidly deteriorating condition as the patient becomes unable or less able to care for himself or herself as care providers struggle to figure out where all this pain is coming from. We don't know how often this occurs, or how often death results.

When one major joint is restricted in its range of motion, the energy expenditure can increase up to 40%, and when another joint in the same extremity is restricted, it can increase by up to 300% (Greenman, 1996) Imagine the fatigue that can be produced by energy expenditure of TrPs restricting the hip and knee. If latent TrPs are diagnosed and treated early enough, the development of chronic myofascial pain may be prevented. (Ge HY, Arendt-Nielsen L. 2011) The transition between active and latent TrPs is not always a clean one. In medicine, especially in anatomy, demarcations tend to be artificial and in flux. In this transition state, a temporalis TrP may cause spontaneous pain, for example, but not refer in the characteristic pattern. I have never seen this documented, but have conducted an unofficial poll of some TrP experts and they all have seen this. Fascinating.

There are some concerns with TrPs and research. Some researchers use the term "myofascial pain syndrome (MPS)" as synonymous with temporomandibular dysfunction (TMJD), without explaining the definition...." (Simons DG. 1995) These papers are mostly by dental and mental health care professionals. Others may be unaware of this, glance at these abstracts, and then use them in forming erroneous conclusions concerning myofascial pain due to TrPs. It is also important to avoid the use of descriptions as diagnoses. Terms such as trapezius myalgia, plantar fasciitis, chronic low back pain, chronic abdominal wall pain, chronic pelvic pain, tennis elbow, and muscle tension headache are descriptions, not diagnoses. Terms such as levator ani syndrome, pelvic floor tension myalgia, pudendal neuralgia and cramps are descriptions, not diagnoses. Trigger points are one of the most common sources of chronic pelvic pain. (Samraj GP, Kuritzky L, Curry RW. 2005) We can't describe a set of symptoms and call that a diagnosis. We must find the cause and treat it. Once you become adept at palpating TrPs, you will be surprised at how common they are. David Simons told me once that was what had amazed him the most: the ubiquity of TrPs.

Myofascial trigger points can mimic almost any condition, depending on where they are and in what combination. (Flax B J. 1995) They can also occur in combination with what they mimic. For example, there may be radicular pain and TrPs, toothache and TrPs, visceral pathology and TrPs. When there are active TrPs, something has activated them. If they continue in spite of treatment, there are one or more perpetuating factors. (See "Perpetuating Factors" on this website.) The ability to diagnose and treat TrPs can avoid some surgery. For example, a myofascial component is part of most failed back surgeries. (Teixeira MJ, Yeng LT, Garcia OG et al. 2011) Clinicians may forget that myofascial TrPs can cause blood vessel, lymph and nerve entrapment, and that "...by releasing restricted fascia, myofascial techniques may influence the duration and severity of the vasospastic episodes experienced in primary Raynaud's phenomenon." (Walton A. 2008) When there are multiple TrPs and they have become chronic, the situation becomes more difficult for the care provider. (It's even worse for the patient.) When there is central sensitization (FM) amplifying pain and other symptoms, life for both of you can be increasingly complex. Help to guide you through chronic myofascial pain (CMP) history, exam, diagnosis and treatment is in "Chronic Myofascial Pain" on this website.

There are some issues that must be stressed. When there are cognitive deficits, ensure important instructions are written down. Even exercises must be performed once in front of the care provider and be accompanied by written instructions. Patients frequently need to make substantial lifestyle changes, and changes are stressful of themselves. Patients who have been dealing with invisible illness may be drained of resources, and lack resilience. They often look fine, so people expect them to act accordingly, invalidating the patient's needs and situation. "Invalidation as perceived by patients with fibromyalgia includes active negative social responses (denying, lecturing, and overprotecting) as well as a lack of positive social responses (supporting and acknowledging) with respect to the patient and the condition of the patient." (Kool MB, van Middendorp H, Boeije HR et al. 2009) One of the key perpetuating factors of FM is the lack of support of spouse, other family members, co-workers or classmates and friends. This can come in the form of patronizing, dismissing, and other types of abuse, and more research is needed on how this negative attitude affects people with invisible illnesses.

Assess the patients for toxic relationships, and guide the patients to positive resources for them and their families and companions. Patients with chronic pain need to avoid negativity and negativity-generating events and people as much as possible, or they will suffer the consequences. The stress from having untreated or undertreated chronic pain that is not understood and often met with disbelief rather than support would cause anyone to feel depressed. It's very difficult to be carefree when you are living with a bewildering number of symptoms, often caused by a multitude of co-existing conditions, many of which are unrecognized by care providers. Negative events can profoundly affect the pain, mood and fatigue levels the next day. Use available resources to see that your patient gets instruction in pacing techniques. Do your best to ensure that your time with the patient is not one of these negative events. Give them the support they need. If they are to diet, exercise, change sleep patterns, etc., give them written instructions and see that they get the needed support. Utilize both medicinal and nonmedicinal pain control, and, as soon as the patient is able, develop self-treatment strategies when possible. This all requires adequate pain control. Imagine trying to concentrate on proper stretch technique while a bear is chewing on your leg. Be patient. These Gordian knots take time to unravel.

Exercises must be prescribed as carefully as medicine. The muscles are physiologically weakened. "Work-hardening" and repetitious "strengthening" exercises will further weaken the muscles and cause more pain. These muscles are already crying out for more energy. Don't increase their energy crisis. When planning a treatment strategy, it is vital that the treatment goals and expectations of the patient and the care provider are the same, or at least congruent. Work together for the optimum quality of life for the patient, with minimum outside intervention. Central sensitization states, such as FM, are pain amplifiers. CMP and FM are high maintenance illnesses that may hold many causes for frustration. Much will depend on patient education and ability to manage symptoms and co-existing conditions. Your patient must be your partner. It's all about patient empowerment and acceptance of needs for pacing and respect of body and mind limits. Patients often need to recover not only from the illnesses, but from a feeling of helplessness and hopelessness. It's not failure if you can't accomplish a cure. Both patient and care provider need to understand this. Chronic pain and dysfunction is just that-chronic. You do the best you can with what you've got, and try to continually improve what you've got. Some of your "problem" patients can metamorphose into your greatest success stories. Once you learn how to diagnose and treat TrPs and central sensitization, some of these cases can literally be a "take up your bed and walk" kind of event. There's nothing like taking a patient who is bedridden on a morphine pump and having her or him out walking and managing self-care. It happens. The lame, at least some of them, can, eventually, leap like a deer. Glorious.

In the article "Chronic Myofascial Pain" you will learn more about the concept of interactive diagnoses in chronic pain. Most patients with FM have at least one other condition. (Silver DS, Wallace DJ. 2002) That is, in addition to the CMP. Such complexity should not dismay care provider and patient Look on the discovery of every perpetuating factor as one more avenue to control symptoms. Taking the medical history is a crucial part of this discovery, and is explored in depth in that article. Observations can be tricky. For example, when you see a patient without a cane who occasionally uses one, it doesn't necessarily signify improvement. For example, canes are hard to manage if TrPs and/or arthritis in the hands and wrists are active. Mobility can be affected as much by upper body TrPs as by lower. This is especially important to remember for patients who use walkers and live alone. Ask. Keep the dialogue going, through exam and treatment. The development of a trusting relationship is crucial. Fibromyalgia patients often have boundary problems, so be attentive to this as well, and ensure that the patient has a good network of supporters.

It's impossible to become an expert in TrP diagnosis and treatment by looking at referral patterns. It takes understanding of functional anatomy, training and experience in palpation to find TrPs. The Trigger Point Manual diagrams had "X" marks as guidelines, indicating possible placement of some common TrPs. Trigger points can be found in any location in many types of tissues. You must understand the nature of the TrP, as well as the proper performance of the therapy involved. For example, TrP injections are not given like flu shots. The TrP must be located by (the care provider's) palpation, the injection must be according to procedure and into the TrP itself, and stretch must be an integral part of the injection process. "Stretching after the trigger point injection is the most integral part of the treatment. Not stretching after injection or needling is the same as receiving no treatment at all. Relief is usually long-lasting, but only when mechanical and systemic perpetuating factors are corrected." (Doggweiler-Wiygul R. 2004.) It is not sufficient to inject and then tell the patient to stretch when they get home. Stretch is part of the process. Perpetuating factors must be identified and brought under control to obtain lasting and maximum effect per treatment.

Anatomy is your friend. Know it. Know the ligaments, tendons and all tissues and how they interact. Most patients have similar referral patterns from TrPs in specific areas. Referral areas may enlarge in the presence of central sensitization and be complicated by multiple area TrPs, resulting in large and complicated overlapping referral patterns. History is the key to finding many TrPs. It gives you the clues you need to tell you where to look for TrPs. You need to take time to take a good history, and a good history will save time later on. There is a need to educate insurance companies about the patient time required, and also the money to be saved preventing further injuries. Be gentle with the examination. It will probably activate multiple TrPs, and your patient may take weeks to recover. Once central sensitization has taken place, it takes time to normalize the body. This doesn't mean it's impossible to do so, only that the patient and the clinicians must try to restore body harmony carefully. Each change in biochemical imbalance affects other biochemicals. Each myofascial release affects other tissues. Give it time. All perpetuating factors must be addressed and the body given a chance to reestablish balance. There is no quick fix. It takes time.

In complex cases, find the cause of the most life-altering symptoms and deal with them as thoroughly as possible. With co-existing conditions, easing one symptom may often help others. The relief of one TrP may give the patient the hope to continue with therapy. The "...assessment and treatment of concurrent TrPs in FMS should be systematically performed before any specific fibromyalgia therapy is undertaken." (Giamberardino MA, Affaitati G, Fabrizio A et al. 2011) If the patient has disc disease, check for TrPs. "...there is a possibility of a myofascial pain syndrome component when there is lumbar disc disease, and it also corresponds to the same myotome level of the lesion." (Samuel AS, Peter AA, Ramanathan K. 2007) If there are resistant TrPs, check discs and facets. Bones follow muscles. When muscles are contractured, that may result in uneven tension on joints, causing osteoarthritis and other articular problems.

Fatigue may be due to non-restorative sleep. Sleep assessment must be part of pain control. (Edwards RR., Almeida DM., Klick B et al. 2008) Investigating sleep quality and quantity is an important part of addressing chronic pain. (O'Brien EM, Waxenberg LB, Atchison JW et al. 2011) After sufficient sleep, a healthy person awakes refreshed. Unrestorative sleep is misery, and the patient may not be aware how bad it is because they may know nothing else. Insomnia in chronic pain patients may not be due to the pain. (Schneider-Helmert D, Whitehouse I, Kumar A et al. 2001) "Special problems arise in chronic non-organic pain. It is clear from all these aspects that PSG (polysomnography–sleep study) is indispensable in insomnia." (Schneider-Helmert D. 2003.) Polysomnography can reveal treatable co-existing conditions such as sleep apnea or restless leg syndrome. Successfully treating the sleep dysfunctions in FM patients may also address some of the cognitive problems. (Miro E, Lupianez J, Hita E et al. 2011) Controlling co-existing conditions such as sleep apnea, providing adequate pain control, and ensuring good sleep hygiene may be all that is needed to provide refreshing sleep. Although multiple studies have shown that sodium oxybate is safe and effective to restore deep sleep and improve multiple symptoms for FM patients,(Moldofsky H, Inhaber NH, Guinta DR et al. 2010; Russell IJ, Holman AJ, Swick TJ et al. 2011; Spaeth M, Bennett RM, Benson BA et al. 2012), it remains unapproved by the Food and Drug Administration except for narcolepsy, mostly due to concern over its potential diversion. (Staud R. 2011) Most neurotransmitters and other biochemicals are balanced during the deep sleep phase. If polysomnography proves that the patient does not experience deep sleep in spite of other available aids such as medications and CPAP, most insurance companies will reimburse for sodium oxybate on the basis of deep sleep restoration.

Treatment: Now What?

By now, you should know that the central sensitization called FM exists, that it's more than pain, and that it can be initiated by TrPs. No matter what the initiating factor, FM (central sensitization) can be maintained by TrPs. Trigger points are real, and they are everywhere. You can't take money for treating chronic pain patients unless you know how to treat chronic pain patients, and that means knowing TrPs. If you didn't know that before, and maybe even if you did, you may be feeling a bit apprehensive by now. Nobody can learn myofascial TrPs overnight. Fear not. Resources are available for you. There are those lovely red texts, Travell and Simons' Trigger Point Manuals. There is magnificent hands-on TrP training available. Check out information at www.myopainseminars.com (In the spirit of disclosure, I have no connection to that organization except as a member of Myopain International and a deep and sincere respect and abiding appreciation for Dr. Robert Gerwin.) There is a cadre of nationally certified specialists called myofascial trigger point therapists who have been trained to assess and treat TrPs and assess and control some perpetuating factors. They can be located on the National Association of Myofascial Trigger Point Therapists website. If there is a TrP therapist near you, you are blessed. If not, my advice is to lure away one of the students as soon as they graduate.

Educate your patients. There are resources for them to use, including newsletters, books, and websites, although there is a lot of misinformation out there. Fibromyalgia patients need to realize that their understanding of TrPs and other pain generators are essential to their quality of life. It may be coincidence that FM gained validation (and advertizing) once their were expensive pills for it; perhaps not. There aren't expensive pills for TrPs, so we need to educate patients without pharmaceutical money. Soon there will be a book showing all known TrPs, with patient and care provider treatment guides, to be a tool for patients so they can point out specific TrP patterns that they have. (Starlanyl, Sharkey) It will provide education for care providers and patients concerning issues dealing with the combination of central sensitization and TrPs, as well as for single muscle TrPs. Patients are not passive recipients of care. Educated, motivated patients are one of your best resources. Patients want to know why they have these symptoms and this pain. Pain is often what drives the patient to seek care, but if other symptoms are recognized promptly, perhaps pain and chronicity can be prevented. A hand or arm may not hurt, but the handwriting may be increasingly illegible (even if they are not doctors) and the grip may fail due to latent TrPs. There may have been pain initially due to an injury. Then movement became more restricted to avoid pain, and the initial pain was forgotten. Your patients may have multiple latent TrPs. They are like land mines, waiting to go off. All it takes is some initiating factor such as an infection or a fall to initiate what is often called an "FM flare." but is actually multiple TrP activations enhancing the level of central sensitization. During flare, current symptoms are intensified and new ones can appear. Once patients realize that flares don't just happen, but something activates multiple TrPs, they can gain some control over their lives.

Treat the patient and not the test, whether X-ray, blood work or other imagery. Those are useful tools, especially for finding perpetuating factors, but don't show the whole picture. Soft tissue problems such as TrPs may not show on imagery, but may contribute significant pain and other symptoms. The TrPs may even be causing or contributing to radiological deformities. The key to successful treatment of central sensitization, TrPs, (and all other conditions) is identifying and controlling or eliminating perpetuating factors.

Chronicity may often be prevented by prompt and thorough acute care. 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. (See Perpetuating Factors) In other patients, it may require more complex intervention. Treatment for central sensitization and TrPs differ. Doctors who don't know TrPs are not going to be looking for ill-fitting furniture or a proportionally long torso as perpetuating factors. TrPs can physiologically weaken muscles. Most physical 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 good TrP injections can in an instant, even if the patient has been hurting for years. (Nelson J, Fernandez-de-las-Penas C, Simons DG. 2008; Travell J.1981) Proper TrP therapy may be able to relieve the pain and other symptoms in some cases, although it may take emotional support if, for example, a patient who has been incontinent or impotent for decades responds to a few manual TrP treatments. They may need help to cope with the needless loss of function for those years.

Use the least invasive option for therapy, with the understanding that most treatment options may activate more TrPs and cause temporary increase in pain. Toxins and waste materials trapped in the myofascia must be processed by the body and be eliminated, and that can only proceed so fast. It takes a while for the Gordian knot to unravel, and the process is not fun for the patient. A combination of therapies such as myofascial release, craniosacral therapy, chiropractic Activator release, ultrasound, specific frequency microcurrent, massage and galvanic stimulation may be useful. There are a lot of choices, and it may take time to find what is most beneficial to the patient. A good treatment team that works together, communicates, and is not easily frustrated is to be desired.

For chronic pain patients, "multidimensional rehabilitation is an effective intervention for patients with widespread chronic pain."(Wigers SH, Finset A. 2007) This study included patients with fibromyalgia and patients with myofascial pain. Some patients who went through the program no longer met the criteria for FM. More patients returned to work or had fewer sick days, but more received disability pensions. Multidimensional rehab of this type seems to help patients find the best quality of life and return to the highest function possible. For some patients, this still means disability. When geloid masses have formed over areas of resistant TrPs, manual therapy may be nearly unendurable and special care must be taken. (Starlanyl DJ, Jeffrey JL, Roentsch G, Taylor-Olson C. 2201-2202) The geloid mass must be treated with hyaluronidase or T3 cream, and microcirculation must be addressed by treating the surrounding area first.

Myofascia is piezoelectric, so it responds well to manual therapy and forms of electrotherapy. High voltage galvanic stimulation can be useful for myofascial pain; softening tight, contractured tissues and improving microcirculation. (Tanrikut A, Nadire O, Huseyin AK et al. 2001) Patients with central sensitization are prone to be hyperreactive to electrotherapy and require treatment that takes into consideration their amplification of stimuli. For those who treat patients manually, refer to "What Your Bodyworker Should Know" on this site. Frequency specific microcurrent is useful for treating FM (McMakin CR, Gregory WM, Phillips TM. 2005) TrPs (McMakin C. 1998), and some co-existing conditions, and improves microcirculation and the cellular condition at the biochemical level.

"TPI (trigger point injection) is a safe procedure when used by clinicians with appropriate expertise and training. It relieved symptoms when used as a sole treatment for patients with chronic head, neck, shoulder, and back pain or whiplash syndrome, regardless of the injectant used, and may be a useful adjunct to intra-articular injection in the treatment of osteoarthritis pain. (Scott NA, Guo B, Barton PM et al. 2009) The least myotoxic local anesthetic should be used, (Zink W, Sinner B, Zausig Y et al. 2007), and lower strength anesthetic can be effective and allow for more injections to be given.(Iwama H, Akama Y. 2000) Dry needling is useful when there are few TrPs, but in cases of central sensitization, local anesthetic helps reduce the pain of injection (which may be considerable) and the chance of further aggravating the CNS. "Patients with FMS are likely to experience significant but delayed and attenuated pain relief following injection of their active TrPs compared to myofascial pain patients with similar TrPs but without FMS. Also, FMS patients are likely to experience significantly more post-injection soreness for a longer period of time."(Hong CZ. 1996. Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil. 77(11):1161-1166.)

Patients who have FMS may not have the pain-reducing effects of some exercise that other people experience. (Staud R, Robinson ME, Price DD. 2005) Exercise must be as carefully tailored to patients as medications. Stretching is important, but the patient must be taught the correct technique. Repetitions can cause worsening contracture. A set of stretches, each performed once, can be done often during the day. Work must be planned to avoid repetitious motions. One of the most helpful exercise tools for TrPs is the tennis ball, but again, the patient must be taught how to use it properly. Empower and educate your patients to manage their conditions. A specific self-management program tailored to a chronic pain patient's needs can significantly reduce health care costs while raising the quality of life, even when there are multiple conditions. (Lorig KR, Sobel DS, Stewart AL et al. 1999)

Chronic Myofascial Pain (CMP)

So much can be done to prevent the formation and spread of TrPs, but there is presently a cadre of patients with too many TrPs to count, in multiple levels in multiple muscles. If TrPs aren't treated promptly and perpetuating factors aren't identified and brought under control, CMP can develop. A patient may have multiple articular dysfunctions; heightened central sensitization; sensitivity to touch, heat, light, cold and pressure; dysfunctional muscle use patterns; torqued muscles; multiple co-existing conditions; muscle calcification and fibrosis. The muscles may be so tight and swollen that you can't see them move beneath the skin, and the pain levels escalate. These patients may have had multiple surgeries and procedures; many perhaps unnecessary. There may have been multiple traumas. There may be a wide variety of perpetuating factors. Some patients were once very high functioning, often with an extreme level of physical activity. There is the false impression of progressive disease as the TrPs spread. It is of vital importance that you convince your patient that you know that what they feel is real, and that you will work together to find out what is perpetuating the symptoms, and also that much of the symptom burden can be relieved. Show them the pain patterns, and explain that the TrPs are largely reversible, and the symptoms are controllable. Give them validation. Many of these patients have been treated as pariahs because their care providers haven't had the education to provide the treatment they needed. I lectured all morning in France one day; care providers in the morning and patients in the afternoon. During the lunch break, one physician told me he would have stayed but had patients all afternoon, and he needed to go and apologize to them. God bless him; he "got it."

Remind your patient-and yourself-that the patient didn't get like this overnight. Getting as well as possible - optimizing quality of life - takes commitment and patience, and there are no quick fixes. Control of pain is crucial. Physical therapy and all 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. It's important to stress that treatment can be painful to the point where the patient can go into shock. When one TrP may be excruciating, hundreds amplified by central sensitization may be intolerable. Suicide is not a valid pain management option, but it still occurs because patients don't know what is causing their pain, can't find care providers who know what they have. They feel helpless and hopeless, and the symptoms have become too much to endure. One of the best things you can give to your patient is hope through education and empowerment. A lot can be done to relieve FM and CMP, lighten the symptom load and return at least some function. It's important for the patients to take on the responsibility of managing their own treatment, and it takes concentrated focus and commitment to change the habits of a lifetime. It isn't easy, but it's possible. Now go to Chronic Myofascial Pain (on this website) next.

-- With thanks to Nye Ffarrabas for proofreading and support.

References:

Alonso-Blanco C, Fernandez-de-las-Penas C, Morales-Cabezas M et al. 2011.Multiple active myofascial trigger points reproduce the overall spontaneous pain pattern in women with fibromyalgia and are related to widespread mechanical hypersensitivity. Clin J Pain 27(5):405- 413.

Arendt-Nielsen L, Nie H, Laursen MB et al. 2010. Sensitization in patients with painful knee osteoarthritis. Pain 149(3):575-581.

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

Borg-Stein J. 2002. Management of peripheral pain generators in fibromyalgia. Rheum Dis Clin North Am 28(2):305-17.

Bruehl S, Chung OY, Ward P et al. 2004. Endogenous opioids and chronic pain intensity: interactions with level of disability. Clin J Pain 20(5):283-292.

Calandre EP, Hidalgo J, Garcia-Leiva JM et al. 2006. Trigger point evaluation in migraine patients: an indication of peripheral sensitization linked to migraine predisposition? Eur J Neurol 13(3):244-249.

Dick BD, Verrier MJ, Harker KT et al. 2008. Disruption of cognitive function in fibromyalgia syndrome. Pain 139(3):610-616.

Doggweiler-Wiygul R. 2004. Urologic myofascial pain syndromes. Curr Pain Headache Rep 8:445-451.

Dommerholt J. 2005. Persistent myalgia following whiplash. Curr Pain Headache Rep 9(5):326-330.

Edwards R.R., Almeida D.M., Klick B et al. 2008. Duration of sleep contributes to next-day pain report in the general population. Pain 137(1):202-207.

Eisinger J, Starlanyl D, Blotman F et al. 2000. Protocole d'informations anonyme sur les fibromyalgiques. Med du Sud-Est 1:9-13.

Fernandez-Carnero J, Ge HY, Kimura Y. 2010. Increased spontaneous electrical activity at a latent myofascial trigger point after nociceptive stimulation of another latent trigger point. Clin J. Pain 26(2):138-143.

Fernandez-de-las-Penas C. 2010. New evidence for trigger point involvement in tension-type headaches. J Musculoskel Pain 18(4):354-360.

Filatova E, Latysheva N, Kurenkov A. 2008. Evidence of persistent central sensitization in chronic headaches: a multi-method study. J Headache Pain 9(5):295-300.

Ge HY, Arendt-Nielsen L. 2011. Latent myofascial trigger points. Curr Pain Headache Rep 15(5):386-392.

Ge HY. 2010. Prevalence of myofascial trigger points in fibromyalgia: the overlap of two common problems. Curr Pain Headache Rep 14(5):339-345.

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

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 R. 2010a. Myofascial pain syndrome: here we are; where must we go? J Musculoskel Pain 18(4):329-347.

Gerwin RD. 2010b. Fibromyalgia Tender Points at Examination Sites Specified by the American College of Rheumatology Criteria Are Almost Universally Myofascial Trigger Points. Curr Pain Headache Rep 15(1):1-3.

Gerwin RD, Dommerholt J, Shah JP. 2004. An Expansion of Simons' integrated hypothesis of trigger point formation. Curr Pain Headache Rep 8:468-475.

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

Glass JM. 2010. Cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain 18(4):367-372.

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

Greenman, PE. 1996. "Principles of Manual Medicine." Baltimore MD: Williams and Wilkins.

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):393-395.

Hong CZ. 1996. Difference in pain relief after trigger point injections in myofascial pain patients with and without fibromyalgia. Arch Phys Med Rehabil 77(11):1161-1166.

Iwama H, Akama Y. 2000. The superiority of water-diluted 0.25% to neat 1% lidocaine for trigger-point injections in myofascial pain syndrome: a prospective, randomized, double-blinded trial. Anesth Analg 91(2):408-409.

Kim SH, Kim DH, Oh DH et al. 2008. Characteristic electron microscopic findings in the skin of patients with fibromyalgia-preliminary study. Clin Rheumatol 27(3):407-411.

Kim SH, Kim SH, Kim SK et al. 2011. Spatial versus verbal memory impairments in patients with fibromyalgia. Rheumatol Int [Jan 19 Epub ahead of print].

Kool MB, van Middendorp H, Boeije HR et al. 2009. Understanding the lack of understanding: invalidation from the perspective of the patient with fibromyalgia. Arthritis Rheum 61(12):1650-1656.

Kuchinad A, Schweinhardt P, Seminowicz DA et al. 2007. Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain? J Neurosci 27(15):4004-4007.

Leavitt F, Katz RS. 2006. Distraction as a key determinant of impaired memory in patients with fibromyalgia. J Rheumatol 33(1):127-132.

Leavitt F, Katz RS. 2008. Speed of mental operations in fibromyalgia: a selective naming speed deficit. J Clin Rheumatol 61(6):740-744.

Leavitt F, Katz RS. 2009. Normalizing memory recall in fibromyalgia with rehearsal: a distraction-counteracting effect. Arthritis Rheum 61(6):740-744.

Leavitt F, Katz RS. 2011. Development of the Mental Clutter Scale. Psychol Rep 109(2):445-52.

Lewit K, Liebenson C. 1993. Palpation—problems and implications. J Manipulative Physiol Ther 16(9):586-590.

Li J, Simone DA, Larson AA. 1999. Windup leads to characteristics of central sensitization. Pain79(1):75-82.

Loevinger BL, Muller D, Alonso C et al. 2007. Metabolic syndrome in women with chronic pain. Metabolism 56(1):87-93.

Lombard L, Augustyn MN., Ascott-Evans BH. 2002. The metabolic syndrome--pathogenesis, clinical features and management. Cardiovasc J S Afr 13(4):181-6.

Lorig KR, Sobel DS, Stewart AL et al. 1999. Evidence suggesting that a chronic disease self-management program can improve health status while reducing hospitalization: a randomized trial. Med Care 37(1):5-14.

Lucas KR, Rich PA, Polus BI. 2008. How common are latent myofascial trigger points in the scapular positioning muscles? J Musculoskel Pain 16(4):279-286.

McLean SA, Clauw DJ. 2005. Biomedical models of fibromyalgia. Disabil Rehabil 27(12):659-665.

McMakin C. 1998. Microcurrent treatment of myofascial pain in the head, neck and face. Top Clin Chiro 5(1):29-35.

McMakin CR, Gregory WM, Phillips TM. 2005. Cytokine changes with microcurrent treatment of fibromyalgia associated with cervical spine trauma. J Bodywork Move Ther 9:169-176.

Mense S. 2010. How do muscle lesions such as latent and active trigger points influence central nociceptive neurons? J Musculoskel Pain 18(4):348-353.

Mense S. 2003. The pathogenesis of muscle pain. Curr Pain Headache Rep 7(6):419-415.

Miro E, Lupianez J, Hita E et al. 2011. Attentional deficits in fibromyalgia and its relationships with pain, emotional distress and sleep dysfunction complaints. Psychol Health 26(6):765-780.

Moldofsky H, Inhaber NH, Guinta DR et al. 2010. Effects of Sodium Oxybate on Sleep Physiology and Sleep/Wake-related Symptoms in Patients with Fibromyalgia Syndrome: A Double-blind, Randomized, Placebo-controlled Study. J Rheumatol 37(10):2156-2166.

Niddim DM, Chan RC, Lee SH et al. 2008. Central representation of hyperalgesia from myofascial trigger point. Neuroimage 39:1299-1306.

Nelson J, Fernandez-de-las-Penas C, Simons DG. 2008. Cervical myofascial trigger points in headache disorders. Prac Pain Manage 8(7):59-60.

Nielson WR, Merskey H.2001. Psychosocial aspects of fibromyalgia. Curr Pain Headache Rep 5(4):330-7.

O'Brien EM, Waxenberg LB, Atchison JW et al. 2011. Intraindividual Variability in Daily Sleep and Pain Ratings among Chronic Pain Patients: Bidirectional Association and the Role of Negative Mood. Clin J Pain 27(5):425-433.

Russell IJ, Holman AJ, Swick TJ et al. 2011. Sodium oxybate reduces pain, fatigue and sleep disturbance and improves functionality in fibromyalgia: results from a 14-week, randomized, double-blind, placebo-controlled study. Pain 152(5):1007-1017.

Russell IJ, Larson AA. 2009. Neurophysiopathogenesis of fibromyalgia syndrome: A unified hypothesis. Rheum Dis Clin N Am 35:421-435.

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]

Samraj GP, Kuritzky L, Curry RW. 2005. Chronic pelvic pain in women: evaluation and management in primary care. Compr Ther 31(1):28-39.

Samuel AS, Peter AA, Ramanathan K. 2007. The association of active trigger points with lumbar disc lesions. J Musculoskel Pain 15(2):11-18.

Schneider-Helmert D. 2003. Do we need polysomnography in insomnia? Schweiz Rundsch Med Prax. 92(48):2061-2066.

Schneider-Helmert D, Whitehouse I, Kumar A et al. 2001. Insomnia and alpha sleep in chronic non-organic pain as compared to primary insomnia. Neuropsychobiology 43(1):54-58.

Schwartz MJ, Offenbacecher M, Neumeister A et al. 2003. Experimental evaluation of an altered tryptophan metabolism in fibromyalgia. Adv Exp Med Biol 527:265-275.

Scott NA, Guo B, Barton PM et al. 2009. Trigger point injections for chronic non-malignant musculoskeletal pain: a systematic review. Pain Med 10(1):54-69.

Shah JP, Gilliams EA. 2008. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. J Bodywork Move Ther 12 (4):371-384.

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.

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.

Silver DS, Wallace DJ. 2002. The management of fibromyalgia-associated syndromes. Rheum Dis Clin North Am 28(2):405-17.

Simons DG. 1995. Myofascial pain syndrome: One term but two concepts; a new understanding. J Musculoskel Pain 3(1):7-14.

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.

Spaeth M. 2011. Fibromyalgia. Z Rheumatol 70(7):573-587.

Spaeth M, Bennett RM, Benson BA et al. 2012. Sodium oxybate therapy provides multidimensional improvement in fibromyalgia: results of an international phase 3 trial. Ann Rheum Dis 2012 [Jan 31 Epub ahead of print]

Starlanyl DJ. 2006. Comment on Canadian consensus document on fibromyalgia syndrome. J Musculoskel Pain 14(4):75-81.

Starlanyl D J, Copeland ME. 2001. "Fibromyalgia and Chronic Myofascial Pain: A Survival Manual," ed. 2. Oakland: New Harbinger Publications.

Starlanyl DJ, Jeffrey JL, Roentsch G, Taylor-Olson C. 2201-2202. The effect of transdermal T3 (3,3',5-triiodothyronine) on geloid masses found in patients with both fibromyalgia and myofascial pain: double-blinded, N of 1 clinical study. Myalgies 2(2):8-18.

Starlanyl DJ, Sharkey J. 2012. "A Practical Guide to Trigger Points": Chichester: Lotus Publishing. [In progress.]

Staud R. 2011. Sodium oxybate for the treatment of fibromyalgia. Expert Opin Pharmacother. 12(11):1789-1798.

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.

Staud R, Craggs JG, Peristein WM et al. 2008. Brain activity associated with slow temporal summation of C-fiber evoked pain in fibromyalgia patients and healthy controls. J Pain 12(8):1078-1089.

Staud R, Koo E, Robinson ME et al. 2007. Spatial summation of mechanically evoked muscle pain and painful aftersensations in normal subjects and fibromyalgia patients. Pain 130(1-2):177-187.

Staud R, Price DD, Robinson ME et al. 2004. Body pain area and pain-related negative affect predict clinical pain intensity in patients with fibromyalgia. J Pain 5(6):338-343.

Staud R, Robinson ME, Price DD. 2005. Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 118(1-2):176-184.

Tanrikut A, Nadire O, Huseyin AK et al. 2001. High voltage galvanic stimulation in myofascial pain syndrome. J Muscoloskel Pain 11(2):11-15.

Teixeira MJ, Yeng LT, Garcia OG et al. 2011. Failed back surgery pain syndrome: therapeutic approach descriptive study in 56 patients. Rev Assoc Med Bras 57(3):286-291

Travell J. 1981. Identification of myofascial trigger point syndromes: a case of atypical facial neuralgia. Arch Phys Med Rehabil 62(3):100-106.

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

Walen HR, Cronan TA, Server ER. et al. 2002. Subgroups of fibromyalgia patients: evidence for heterogeneity and an examination of differential effects following a community-based intervention. J Musculoskel Pain 10(3):9-32.

Wallace DJ, Hallegua DA. 2004. Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep 8(5):364-368.

Walton A. 2008. Efficacy of myofascial release techniques in the treatment of primary Raynaud's phenomenon. J Bodywork Move Ther 12(3):246-256.

Wigers SH, Finset A. 2007. Rehabilitation of chronic myofascial pain disorders. Tidsskr Nor Laegeforen 127(5):604-608.

Williams DA, Clauw DJ, Glass JM. 2011. Perceived cognitive dysfunction in fibromyalgia syndrome. J Musculoskel Pain 19(2):66-75.

Zink W, Sinner B, Zausig Y et al. 2007. Myotoxicity of local anaesthetics: experimental myth or clinical truth? Anaesthesist. 56(2):118-127.


Back to Top

 


Most Books on our site are available from:

In Association with Amazon.com

and

In Association with Amazon.ca

Why buy at Amazon?

 

This site is a


Editor's Choice Site

 

 

Except as noted, all content and copy is copyright 1995-2012
Devin J. Starlanyl


Site Maintained by
EnigamI, Inc.
Most recent revision 04/16/2012

For questions regarding this site contact the Webmaster