Patients &
trained Companions

Doctors & Other
Care Providers



© copyright, Devin J. Starlanyl 2012. Revised, 2014. All rights reserved. http://www.fmcmpd.org


The fibromyalgia (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.

When the standard depiction of FM was first introduced, the tender point chart was meant to provide a guideline for picking FM clinical study subjects. Our understanding of FM has grown from counting tender points to the concept of FM as a heterogeneous set of subgroups with central nervous system (CNS) sensitivity and a variety of potential dysfunctional biochemical and metabolic interactions. The central sensitization state called FM is most closely defined by body-wide diffuse and centrally augmented pain. That's been documented by objective tests such as functional neuroimaging and measurement of evoked electrical potentials, showing multiple abnormalities. (McLean SA, Clauw DJ. 2005) Although the presenting symptom is often diffuse muscle pain, FM can cause amplified sensitivity to multiple sensory stimuli. (Geisser ME, Glass JM, Rajcevska LD et al. 2008) FM also often causes 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 sensory overload and cognitive dysfunctions as the brain struggles to process confusing sensory stimuli.

Working, episodic and semantic memory impairments are the equivalent of adding about 20 extra years of aging. (Glass JM. 2008) "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, and lack of restorative sleep most affected perceived memory deficits. (Williams DA, Clauw DJ, Glass JM. 2011) FM cognitive deficits can be profound and yet remain undetected by conventional cognitive assessment tools. (Leavitt F, Katz RS. 2009) Spatial memory may be more impaired than verbal memory. (Kim SH, Kim SH, Kim SK et al. 2011) This may be due to biochemical brain trauma from the sidetracking of tryptophan using the kynurenine metabolic path; quinolinic acid is produced instead of serotonin. (Quinolinic acid is a neurotoxin causing spatial memory impairment in rats.) In FM patients, cognitive deficits tend to increase in times of stress or if hormonal axes are unbalanced. This may make communication difficult in emergency situations, office visits, or medical procedures. These cognitive deficits could be mistaken for dementia or psychiatric conditions. 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 to avoid increasing the central sensitization level.

One important aspect of FM is wind-up, or temporal summation of second pain (TSSP). After a response to nociceptive stimuli (first pain), a second nociceptive stimulus can provoke greater pain of longer duration. As the central nervous system, (CNS) becomes more sensitized, the base pain may not return to its initial level, or may return over the course of weeks. Research indicates TSSP and central pain in FM results primarily from peripheral stimuli, and that in FM, 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) In FM, augmented TSSP occurs in all pain-related brain areas, and is not due to emotional stress. (Staud R, Craggs JG, Peristein WM et al. 2008) This process can lead to central sensitization. (Li J, Simone DA, Larson AA. 1999) Other studies indicate 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)

FM is not heterogeneous. (Walen HR, Cronan TA, Server ER. et al. 2002) One research team proposed a protocol for distinguishing FM subgroups, (Eisinger J, Starlanyl D, Blotman F et al. 2000) In FM, a variety of neurotransmitters, hormones, peptides and other biochemicals may be out of balance, so each patient may differ. FM is associated with CNS dysfunction and causes systemic symptoms, not local ones. It is not a diagnosis of exclusion. One of the first steps in managing FM is to discover what is irritating the CNS and what is causing or contributing to the most significant symptoms. FM is a pain amplifier. Trigger points (TrPs) and articular conditions such as arthritis, are peripheral pain generators. Low local pH [associated with TrPs], can sensitize receptors in the muscle, causing central sensitization. (Mense S. 2003) TrPs are commonly associated with arthritic and other conditions, are often mistaken for them, and are common in central sensitization states, such as migraines, (Calandre EP, Hidalgo J, Garcia-Leiva JM et al. 2006) IBS, (Doggweiler-Wiygul R. 2004) tension headaches (Fernandez-de-las-Penas C. 2010) and chronic pain after whiplash. (Dommerholt J. 2005)

We've known 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 have been concerned by each new attempt to clarify FM criteria for diagnosis, as co-existing TrPs are ignored and FM and TrP symptoms re confused. Research based on FM criteria iteration can lead to misidentification of TrP symptoms as FM symptoms. There have been attempts to explain this concern, (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)

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) Trigger point "… 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. This can lead to swelling, numbness, and tingling. 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.

Trigger Points

Myofascial TrPs are hyperirritable nodules found in taut bands within skeletal muscle sarcomeres. The deformation of sarcomeres created the characteristic palpable contraction nodule. Sarcomeres on either side of the contraction knot are lengthened, creating the taut band. Active TrPs cause pain all the time, whether the muscle they are in is being used or not. Latent TrPs cause pain or other symptoms only when they are stimulated, such as with pressure. The referral patterns are fluid, as any specific TrP can vary from latent to active and back again. TrPs that do not cause the recognized pattern are transitional TrPs. (Starlanyl DJ, Sharkey J, 2013) TrPs can form in skin, scars, bone linings, tendons, ligaments and other tissues. We know most about myofascial TrPs, because their referral patterns have been mapped and documented in medical articles and texts. The definitive texts on TrPs have been available, but greatly underutilized, for some time. (Simons DG, Travell JG, Simons L S 1999; Travell JG, Simons DG 1992) The taut band is the one consistent finding in both active and latent TrPs. The ropy bands may not always be palpable, due to fluid infiltration, fibrosis, calcification, or layers of TrPs in overlying muscles, 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. In some cases, the referral pattern may not include the muscle with the TrP.

Although one may automatically think of pain, TrPs also can cause dysfunction, including muscle weakness due to reciprocal inhibition. A knee may buckle, or the grip may fail. Myofascial TrPs also may have autonomic and proprioceptive concomitants. Think of TrPs in terms of pain, but also for symptoms such as nausea, vomiting, illegible handwriting, eyelid twitching, runny nose, blurry eyes, nonotogenic toothache, cognitive dysfunction, disorientation, incontinence, or erectile dysfunction. Travell and Simons texts indicate that in TrP formation, 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, but tissue outside TrP zones are 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.

Simple TrPs, if diagnosed and treated promptly, are easy to treat. 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, but this progression is reversible. A TrP can twitch even from the stimulation of a breeze, draft, the weight of a feather, or even spontaneously. This local twitch response (LTR) 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. Taut bands and TrPs have been imaged at the Mayo Clinic and the National Institutes of Health. This required expensive specialized equipment, but training and experience in the art of TrP palpation is available to all.

Even latent TrPs cause pain at the end of range of motion. Latent TrPs are insidious, because they contribute to non-pain symptoms, and any sudden stressor can 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 way TrPs can "spread." Latent TrPs are more common in the elderly, because elders tend to move less, especially when it hurts to move. This can enhance a debilitated state as the patient becomes less able to perform self-care, and microcirculation worsens. 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 him/herself. If latent TrPs are diagnosed and treated early enough, the development of chronic myofascial pain may be prevented. (Ge HY, Arendt-Nielsen L. 2011)

Some researchers, mostly dental and mental health care professionals, use the term "myofascial pain syndrome (MPS)" as synonymous with temporomandibular dysfunction (TMJD), without explaining the definition...." (Simons DG. 1995) Others see them and use their results to form 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. We can't continue to describe a set of symptoms and call that a diagnosis. We need to find the causes and treat them.

Myofascial TrPs can mimic almost any condition, and can also occur in combination with those conditions. 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. For example, a myofascial component is part of most failed back surgeries. (Teixeira MJ, Yeng LT, Garcia OG et al. 2011) And "...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). The TrP component is treatable.

Prescribe exercises as carefully and individually as medicine. TrP-laden muscles are physiologically weakened. "Work-hardening" and repetitious "strengthening" exercises will exacerbate the energy crisis and further weaken the muscles and cause more pain. You cannot treat chronic pain patients with TrPs the way you can treat a, athlete with a few uncomplicated TrPs. These muscles are hypoxic. They start out fatigued, and so does the patient. 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. CMP and FM are high maintenance illnesses that may cause frustration, but much of the maintenance is done by the patient. It's not failure when you can't cure a chronic illness, but you can improve quality of life and function.

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. Every perpetuating factor is one more avenue to control symptoms. It's impossible to become an expert in TrP diagnosis and treatment by looking at referral pattern diagrams. It takes understanding of functional anatomy, training and experience in palpation to find TrPs. The Trigger Point Manual diagrams had "X" marks as guidelines. TrPs 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 palpation after the patient is properly positioned for that muscle, the injection must be into the TrP itself, and stretch must be an integral part of the injection process. "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.) Perpetuating factors must be identified and brought under control to obtain lasting and maximum effect for any treatment.

In complex cases, start by working on the four most life-altering symptoms, and control them as thoroughly as possible. 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. (Samuel AS, Peter AA, Ramanathan K. 2007) If there are resistant TrPs, check discs and facets. Bones follow muscles. When muscles are contractured, that results in uneven tension on joints, perhaps causing osteoarthritis and other articular problems.

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 energy expenditure of TrPs restricting the hip and knee. Fatigue may also 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) and should be one of the first symptoms addressed. 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. 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 potential diversion. (Staud R. 2011) Most neurotransmitters and other biochemicals are balanced during the deep sleep phase. If polysomnography indicates 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.

Resources are available: Travell and Simons' Trigger Point Manuals; hands-on TrP training (www.myopainseminars.com); the International Myopain Society (www.myopain.org); the cadre of nationally certified myofascial TrP therapists (www.myofascialtherapy.org). Educate your patients. There are resources for them to use, including newsletters (National Fibromyalgia Partnership's Fibromyalgia Frontiers), books (Starlanyl and Sharkey) and websites (www.fmcmpd.org).

Fibromyalgia patients need to know that their understanding of TrPs and other pain generators are essential to their quality of life. Educated and motivated patients are one of your best resources. Pain may be 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, and the grip may fail, due to latent TrPs. All it takes is some event such as an infection or a fall to initiate what is often called an "FM flare." but is actually multiple TrP activations enhancing central sensitization. During flare, current symptoms are intensified and new ones can appear. When they learn about TrPs, patients gain some control over their lives. The key to successful treatment of FM central sensitization and CMP is identifying and controlling or eliminating perpetuating factors.

Use the least invasive option for therapy, with the understanding that most treatment options may activate more TrPs and cause a 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. 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 FM and patients with TrPs. 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.

"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 of TrPs can also be very helpful.

Most physical therapists are taught to strengthen muscles, but repetitive exercises with "strengthening bands" or exercise machines worsen TrPs because muscles with TrPs are 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 contracture. 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)

Chronic Myofascial Pain

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. They have chronic myofascial pain (CMP). 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. There may have been multiple traumas. There may be a wide variety of perpetuating factors. 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. 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.


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.

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.

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.

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.

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.

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.

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

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

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

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

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

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.

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.

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.

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, 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.

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, 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 DJ, Sharkey J. 2013. "Healing through Trigger Point Therapy: A Guide to Fibromyalgia, Myofascial Pain and Dysfucntion": Chichester: Lotus Publishing.

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

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.

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.

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


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 1995-2016
Devin J. Starlanyl

Site Maintained by
EnigamI, Inc.
Most recent revision 08/24/2016

For questions regarding this site contact the Webmaster