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Dryneedling.nlCurr Pain Headache RepDOI 10.1007/s11916-011-0205-3 Effects of Treatment of Myofascial Trigger Pointson the Pain of Fibromyalgia Maria Adele Giamberardino & Giannapia Affaitati &Alessandra Fabrizio & Raffaele Costantini # Springer Science+Business Media, LLC 2011 Abstract Myofascial pain syndromes (MPSs) from trigger points (TrPs) and fibromyalgia syndrome (FMS) are commonmusculoskeletal pain conditions that frequently coexist in the Myofascial pain syndromes (MPSs) from trigger points same patients. In recent decades, it has become evident that (TrPs) and fibromyalgia syndrome (FMS) are common these entities greatly influence each other’s clinical expres- forms of musculoskeletal pain. Though distinct in diagnos- sion. FMS is mainly rooted in the central nervous system, tic criteria and clinical features in typical cases (with while TrPs have a peripheral origin. However, the nociceptive regional pain in MPSs and generalized pain in FMS), these impulses from TrPs may have significant impact on symp- two entities very often can be confused with each other in toms of FMS, probably by enhancing the level of central clinical practice, mostly because of their frequent coexis- sensitization typical of this condition. Several attempts have tence in the same patient. This can pose problems of been made to assess the effects of treatment of co-occurring differential diagnosis and treatment ].
TrPs in FMS. We report the outcomes of these studies In recent decades, it has become increasingly evident showing that local extinction of TrPs in patients with that this coexistence is not a merely by-chance association, fibromyalgia produces significant relief of FMS pain. Though but rather reflects a cause–effect relationship. On one hand, further studies are needed, these findings suggest that in fact, TrPs are more frequent in FMS due to a higher assessment and treatment of concurrent TrPs in FMS should susceptibility in FMS to microtraumatic events that are be systematically performed before any specific fibromyalgia recognized causative factors for TrP formation On the other hand, muscle TrPs in any individual represent apowerful peripheral source of nociceptive impulses; in time, Keywords Myofascial trigger points . Local injection .
these are likely to favor the development of central Fibromyalgia . Fibromyalgia syndrome . Pain syndrome .
sensitization phenomena that can promote the clinical Peripheral pain generators . Myofascial pain . Pressure pain manifestation of FMS in predisposed individuals .
threshold . Musculoskeletal pain . Central sensitization .
These findings have raised the question as to whether Comorbidity . Taut band . Anesthetic . Management .
treatment of TrPs in patients with the two conditions may have Pathophysiology . Tender point . Antidepressants . Local a significant impact on the pain of the more severe of the two: fibromyalgia. Though not yet very numerous, recent clinicalstudies have addressed this issue and found a significantbenefit of local TrP extinction for the generalized FMS pain.
M. A. Giamberardino (*) : G. Affaitati : A. Fabrizio This article provides updated information on this complex Pathophysiology of Pain Laboratory, Ce.S.I., “G. D’Annunzio” issue, summarizing the current knowledge about clinical Foundation, University of Chieti,Chieti 66100, Italy features, pathophysiology, and classic treatment of MPSs/ TrPs and FMS separately; discussing the critical elements indifferentiating the two in routine medical practice; and reporting the results of the studies showing the impact of Institute of Surgical Pathology, University of Chieti,Chieti 66100, Italy MPS treatment on FMS symptomatology.
Myofascial Pain Syndromes from Trigger Points snapping or pincer techniques (muscle accessible from oneor two directions, respectively) [Both potentially elicit the “local twitch response” (LTR), a brief local contraction ofmuscle fibers. The TrP is identified as the point within the MPSs are acute, recurrent, or chronic forms of regional band of maximal tenderness upon firm digital pressure; this musculoskeletal pain whose mean prevalences among elicits pain locally and in the target if the TrP is sufficiently middle-aged (30–60 years) men and women are 37% and hyperirritable, and provokes a painful reaction by the patient, 65%, respectively, and 85% in elderly (> 65 years) adults An MPS is a “complex of sensory, motor and autonomic symptoms caused by myofascial trigger points”, where TrPsare “spots of exquisite tenderness and hyperirritability in Hyperalgesia has been shown by decreased pain thresholds muscles or their fascia, localised in taut, palpable bands, (pressure, electrical stimuli) at TrP level (in muscle, subcutis, which mediate a local twitch response (LTR) of muscle and skin) and at target level (always in muscle, with extension fibres under snapping palpation and, if sufficiently hyper- to subcutis and/or skin only in high TrP hyperirritability) irritable, give rise to pain, tenderness and autonomic TrP treatment by injection (see below) produces desen- phenomena as well as dysfunction in areas usually remote sitization not only locally but also in the target (thresholds from their site, called targets” . Active TrPs provoke significantly increased in skin, subcutis, and muscle), spontaneous pain, and thus, an MPS; latent TrPs are confirming the interdependence of the sensory changes at clinically silent but frequently evolve into active TrPs in target level and the trigger activity [, ]. Areas outside time. A primary TrP is located in a muscle directly the TrPs and targets show sensory normality in patients subjected to overload/repetitive overuse; a secondary TrP with MPS who have no concurrent pain conditions is induced in a muscle, neurogenically or mechanically, by potentially affecting general pain sensitivity ].
the activity of a nociceptive focus in a different structure(deep somatic or visceral) ].
Routine Laboratory and Instrumental Tests Diagnostic criteria for MPS derived from international multicentric studies or expert consensus meetings still are Specific tests for MPS identification still are needed, lacking. At present, the most clinically relevant features for though some findings can be confirmatory of the clinical diagnosing an MPS in current practice include identifica- diagnosis (eg, spontaneous electromyography (EMG) ac- tion of the taut band and reproduction of the spontaneous tivity at TrP, visualization of an LTR at ultrasounds) pain complaint by exquisite pressure on a point of Microdialysis provides very interesting results (ie, high levels of pronociceptive substances in active TrPs), but the Essential steps in the approach to patients with suspected technique is not suitable for routine application in medical MPSs are clinical history collection and physical examina- tion TrPs most often result from muscle traumas/microtraumas; thus, patients should be questioned about any event, activity, or habit potentially causing muscleoverload, overuse, or disuse. Possible secondary TrPs also A TrP would be a dysfunctional site where an abnormal should be explored by asking questions about any previous increase is present in the production and release of acetylcho- painful visceral disease or other deep somatic pain sources line packets from the motor nerve terminal under resting within the neuromeric field of the involved muscles [, ].
conditions (dysfunctional endplate). This mechanism would MPS pain, at rest and/or on movement, is tensive, be enhanced by an initiating traumatic/microtraumatic event constrictive, or cramplike and of variable intensity and (primary TrPs) or referral process (secondary TrPs), with duration, with sudden or gradual onset. It rarely is located in increased motor endplate activity, persistent release of the TrP zone, but most often occurs in a distant area (target), acetylcholine, and sustained depolarization of the postjunc- typical of each muscle/TrP. Accompanying symptoms are tional membrane of the muscle fiber. This could, in turn, cause altered muscle motor function, cooling, sweating, and a continuous release and inadequate uptake of calcium ions pilomotor activation, or even lacrimation, imbalance, dizzi- from the local sarcoplasmic reticulum (SR), producing ness, and tinnitus for MPSs in the head/neck region [ sustained shortening of sarcomeres. A vicious circle of At inspection during physical examination, the physician hypoxia (with release of vasoactive/algogenic substances, should look for any biomechanical discrepancy and asymme- responsible for local nociceptor sensitization, and thus, try that may have caused muscle overload ]. Palpation of hyperalgesia), failed Ca++ reuptake from the SR (due to muscles is first aimed at identifying the taut band through energy impairment), and perpetuation of the contracture (“integrated hypothesis” of the original “energy crisis” symptoms. Should they became unanimously recognized, we probably would witness a change in the profile of thetypical fibromyalgia patient, with an expansion of the population receiving this diagnosis in the future [ The onset of FMS symptoms can be either gradual or Deactivation of TrPs must be combined with removal of post-traumatic (physical injury/psychological stress). The perpetuating factors (eg, microtraumas, chronic infection, typical spontaneous pain is a persistent, diffuse, deep, and stress/mood disorders, poor sleep, and nutritional/metabolic aching sensation in muscles, most often continuous with periodic exacerbations of high intensity (flares). Associated The most frequently applied techniques for TrP deacti- symptoms (eg, affective dysfunction, cognitive deficits, vation are spray and stretch, TrP pressure release, and local short-term memory loss, dizziness, syncope, nonrestorative injection (see [, ] for a more detailed description of sleep, daytime fatigue, prolonged morning stiffness, numb- these and other techniques). The latter represents the gold ness, tingling, and dysesthesias) are present in various standard; it can consist of “dry needling” or injection of combinations. Comorbidity frequently occurs with depres- active substances, particularly local anesthetics. The effec- sion, anxiety, irritable bowel syndrome, dysmenorrhea, tiveness of dry needling probably lies in the mechanical interstitial cystitis, other rheumatic conditions, chronic disruption of the integrity of dysfunctional endplates.
fatigue syndrome, myofascial pain syndrome, low back However, injection of an analgesic markedly reduces the pain, temporomandibular joint disorder, and headache.
patient’s discomfort during and after the procedure, and Patients with FMS report even light stimuli applied to their thus, enhances the global outcome of the therapy. Injection somatic structures as painful. As documented by many of any solution in general, including saline, may relieve experimental studies, this is due to a generalized increased symptoms temporarily by diluting and dissipating sensitiz- sensitivity to pain in terms of lowered pain thresholds of ing substances in the region of the energy crisis ].
skin, subcutis, and muscle to a variety of stimuli (eg, Injection of botulinum toxin also is effective, but its mechanical, thermal, electrical, chemical) in both painful efficacy is no greater than that of the local anesthetic; the latter, being much less expensive, is thus preferred ].
Though the origin of the syndrome has not been completelyclarified yet, there is a general consensus that the main disturbance behind FMS is an altered processing of the painsignal. On the whole, a number of neuroendocrine (ie, FMS is a chronic condition of widespread musculoskeletal dysfunction of the hypothalamic-pituitary-adrenal axis), pain and tenderness accompanied by numerous aspecific neurotransmitter (ie, altered metabolism of serotonin, symptoms, among which sleep disturbance and affective norepinephrine, and dopamine, as well as substance P, and dysfunction are particularly frequent. It affects about 4% of nerve growth factor) and neurosensory (ie, central sensiti- the general population; its sex distribution, nearly equal in zation, abnormalities of descending inhibitory pain path- childhood, is up to sevenfold more common in women than ways) disturbances have been implicated in the generation of the syndrome. Patients with FMS have aberrant Criteria for FMS diagnosis still remain those established responses to pain on functional brain neuroimaging and by the American College of Rheumatology Committee in also show an accelerated loss of brain grey matter, 1990 [1) a history of widespread pain (involving all interpreted by some as a sign of premature aging of the limbs and the trunk) of at least 3-months duration; and, 2) brain ]. A genetic predisposition would be essential for a tenderness to digital palpation (with a pressure of 4 kg) in at variety of environmental stressors to lead to the clinical least 11 of 18 (9 symmetrical) predetermined body sites called tender points (TePs). A TeP is a site of exquisitetenderness in soft tissues that, in contrast to the TrP of MPS, is not included in a taut band of muscle fibers, doesnot evoke LTR under snapping palpation, and, especially, Though not threatening the patients’ life, FMS severely does not refer pain at a distance when stimulated [••].
impacts on the quality of life and physical function [ A critical revision of the above criteria is currently Complete resolution of symptoms is rarely achieved, but a underway. The newly proposed criteria no longer consider significant improvement is obtained with an adequate the presence of TePs, but only assess clusters of clinical After a comprehensive evaluation of pain, function, and activating/precipitating factors of conditions other than psychosocial context of the patient, a multidisciplinary treatment approach should systematically be taken, includ- As stated above, the coexistence of TrPs and FMS is ing a combination of pharmacologic and nonpharmacologic very common epidemiologically, TrPs being significantly interventions. Options for pain treatment include para- more frequent in patients with FMS than in the general cetamol or weak opioids, such as tramadol, while NSAIDs population . This probably happens because FMS or corticosteroids are not recommended unless a coexisting patients, due to their chronic pain and disability and inflammatory/autoimmune disorder is present.
consequent poor posture/antalgic attitudes, are more prone Antidepressants are recommended for long-term treat- to muscle microtraumas, well-known promoting factors for ment (cycles of several months) because they decrease pain TrP formation. Once developed, TrPs can, in turn, enhance and often improve function. Particularly employed are FMS symptoms through their input to the central nervous tricyclics (especially amitriptyline), but also selective system [Several authors have thus evaluated the serotonin reuptake inhibitors (eg, fluoxetine) or dual possible contribution of TrPs to fibromyalgia symptoms, (serotonin and noradrenalin)-reuptake inhibitors (eg, ven- though with some methodological differences among lafaxine, duloxetine, and milnacipran). Antiepileptics, es- pecially pregabalin, also are recommended for pain Alonso-Blanco et al.  systematically explored the treatment in FMS [While the U. S. Food and Drug presence of TrPs in multiple muscles in 44 patients with Administration has officially approved the use of three FMS versus 50 control subjects and determined whether the compounds, duloxetine, milnacipran, and pregabalin, for local and referred pain from active TrPs reproduced the FMS, no official drug specific for the syndrome has been overall spontaneous fibromyalgia pain pattern and whether approved in Europe, where these compounds are currently widespread hypersensitivity (pressure pain thresholds used off-label for the syndrome, by the European Medicines [PPTs] at TePs sites) was related to the presence of widespread active TrPs. FMS patients had a mean of 11 Nonpharmacologic management includes heated-pool TrPs (10 active, 1 latent) in contrast to control subjects only treatment, individually tailored exercise programs (eg, showing latent TrPs (mean: 2). The combination of the aerobic exercise, strength training), and cognitive- referred pain patterns from active TrPs fully reproduced the behavioral therapy. Relaxation, rehabilitation, physiothera- overall spontaneous pain area of FMS. Patients with FMS py, and psychological support also can be of help in many had significantly lower PPTs than control subjects and a significant positive correlation between the number of One approach gaining progressively more importance active TrPs and spontaneous pain intensity. The authors in FMS management is treatment of the so-called interpreted these results as an indication of the contribution “peripheral pain generators.” It had been noted for quite of nociceptive inputs from active TrPs to central sensitiza- some time in clinics that FMS patients with concurrent sources of nociceptive pain in their somatic periphery, According to several authors, in addition to having such as an MPS from TrPs or a painful joint (a very more frequent TrPs than the normal population at all frequent situation, given the high comorbidity level in muscle levels, patients with FMS would commonly FMS) , have exacerbation of their typical fibromyalgia harbor TrPs at the very site of their TePs, with a pain [This has suggested that, after appropriate significant overlap between TePs and TrPs [, ]. In identification, local suppression of these peripheral sour- 2010, Ge et al. ] indeed tested the hypothesis that the ces of nociceptive inputs may be beneficial not only for 18 predetermined sites of TePs in fibromyalgia frequently the local pain but also for the widespread symptoms of are associated with myofascial TrPs and that the induced FMS . An account of the recent studies specifically pain from active TrPs at TeP sites may mimic fibromyalgia addressing this issue in the case of myofascial TrPs in pain. In their study of 30 patients with FMS, the TeP sites were specifically tested for trigger characteristics, bothmanually and at EMG recording of spontaneous activity,and the features of the spontaneous FMS pain were Effects of Treatment of Myofascial Trigger Points compared with those of the pain evoked by TrP stimula- tion. The authors found that most of the TeP sites wereTrPs, with local and referred pain from active triggers TrPs in muscles are recognized powerful sources of partly reproducing the overall spontaneous pain pattern.
peripheral nociceptive impulses that can have profound The total number of active TrPs was positively correlated influences on the sensory processing of painful messages at with the spontaneous FMS pain intensity. This study central level [In this view, they can be potential provided evidence in FMS patients of the importance of active TrPs, which may serve as peripheral generators of The study protocol was double-blind, with neither fibromyalgia pain, and the authors suggested that inacti- patients nor clinicians collecting data and sensory evalua- vation of active TrPs may be an alternative for the tion being aware of the patients’ group. Only the clinician treatment of FMS. Indeed, the year before (2009), a paper performing therapy was unblinded. After treatment, in the by Staud et al. [•], in which the role of peripheral active-treatment group but not placebo-treated group, muscle input was explored in the initiation and mainte- number and intensity of myofascial episodes and para- nance of FMS, was published. In a randomized, double- cetamol consumption decreased while PPTs at TrP site blind, placebo-controlled trial of 22 female control sub- increased, with all changes being significant. In parallel, jects and 28 female patients with FMS, the authors tested FMS symptoms also significantly improved; pain intensity the effects of trapezius muscle TeP injections with 1% decreased and all thresholds increased progressively in the lidocaine on local pain thresholds and remote heat hyper- TePs and nonpainful site. At day 8, all placebo-treated algesia in the forearm. Before muscle injections, shoulder patients requested active local therapy, which was delivered pain was standardized by tonic mechanical muscle stimu- on days 8 and 11, while none of the patients under active lation, resulting in local pain ratings of 4.0 ± 0.5 visual treatment requested additional therapy. At a 3-week follow- analogue scale (VAS) units. This stimulation was interrupted up (days 30 or 37), FMS pain still was lower than the for the injections but continued afterwards at the same initial, pre-study pain in patients not undergoing further level. Both control subjects and patients showed signif- therapy and had decreased in those receiving active therapy icantly increased PPTs at the trapezius after lidocaine injections, but not placebo. Heat hyperalgesia in the The results of this study thus showed that in fibromy- remote site also was significantly reduced by lidocaine, algia patients with concurrent MPSs due to TrPs not but not placebo, in patients with FMS. Neither lidocaine coincident with TePs sites, local treatment of the peripheral nor saline injections significantly affected clinical FMS muscle sources not only relieves regional symptoms but pain ratings, probably due to the very low dose of lidocaine also produces a significant improvement of the widespread employed (50 mg). These results confirm the important role of FMS symptoms (ie, lesser spontaneous pain and TePs peripheral inputs in maintaining central sensitization in hypersensitivity as well as reduced generalized hyper- fibromyalgia. In this study, the injection site was apparently algesia). The authors claimed that the diffuse tissue not specifically tested for TrP characteristics. However, given desensitization observed is not attributable to a systemic the high frequency of coincidence of the trapezius TeP action of the drugs delivered locally to TrPs because TrP with a TrP area, it is highly probable that the beneficial anesthetic infiltration previously had been shown to not effects of treatment in these patients were indeed due to produce any significant change in pain thresholds in a nonpainful area in patients without fibromyalgia ]. The A recent paper by Affaitati et al. ••] specifically decreased level of generalized hyperalgesia, as well as of evaluated the effects on fibromyalgia pain of treatment of spontaneous diffuse pain, must thus reflect other mecha- concomitant TrPs that were not coincident with the TeP nisms related to the hypothesized pathophysiology of FMS sites. They studied 68 female FMS patients with coexisting (ie, a reduction of the degree of central sensitization). The unilateral MPSs of the upper body, manifesting as accesses extent of symptom decrease obtained in this study is not of regional pain from active TrPs in the trapezius (1 trigger such to allow suspension of specific FMS treatments, but is in the medial third of the upper border, clearly distinct from sufficiently marked (22%–30%) to hypothesize either a the fibromyalgia TeP in the same muscle; n = 20) or possible dose reduction of chronically administered drugs infraspinatus muscle (1 or 2 triggers; n = 48).
for FMS or a better symptom control at the same doses, In basal conditions, patients were assessed for their with obvious advantages for the patients. The authors thus myofascial pain symptoms, (ie, number/intensity of pain proposed that identification and treatment of peripheral pain episodes, PPTs at trigger site, paracetamol consumption), generators represent the first approach to FMS before any and FMS symptoms (ie, spontaneous diffuse pain [VAS] other therapy is initiated. In this research, only FMS pain and hypersensitivity [PPTs at TePs sites, PPTs and electrical symptoms were tested; it will be important in future studies pain thresholds in skin, subcutis, and muscle in a distant, using a similar protocol to verify if other typical FMS nonpainful area at quadriceps level]). They then were complaints, such as sleep disturbance, fatigue, physical randomly assigned to two groups of 34 patients each to impairment, or affective dysfunction, also can actually receive either active or placebo-like local TrP treatment benefit from extinction of peripheral nociceptive sources.
(TrP injection with anaesthetic [1 mL of 0.5% bupivacaine No other controlled study to date appears to have hydrochloride] or needle penetration in an area near the addressed the impact of treatment of clearly identified TrPs trigger) on days 1 and 4. Evaluations were repeated on days on FMS symptoms. However, a recent study by Castro- Sánchez et al. ] has shown how local treatment of muscles, through massage able to release the TeP areas, has ably forecast a dose reduction of specific drugs for FMS, a positive impact on FMS symptoms. In view of the and/or a better symptom control at the same doses. Thus, a elevated number of TrPs in patients with fibromyalgia, it is systematic search for TrPs in FMS, at the TePs sites as well probable that the observed beneficial effects of this as in other locations, and their extinction is an approach that treatment are secondary to TrP extinction. In this random- should systematically be adopted before any other therapy ized controlled trial, 74 patients with FMS were randomly is initiated when faced with a patient with fibromyalgia.
assigned to experimental (massage–myofascial releasetherapy) and placebo (sham treatment with disconnectedmagnotherapy device) groups for an intervention period of No potential conflicts of interest relevant to this article 20 weeks. Pain, anxiety, quality of sleep, depression, and quality of life were determined at baseline, after the lasttreatment session, and at 1 and 6 months. Immediately aftertreatment and at 1 month, anxiety levels, quality of sleep, pain, and quality of life were improved in the experimentalgroup over the placebo group. Significant differences Papers of particular interest, published recently, have been persisted at 6 months in the quality-of-sleep index.
Myofascial-release techniques thus improved pain and On the whole, the results of the reported studies indicate that nociceptive muscle input in FMS, most often originat- 1. •• Mense S, Gerwin RD (Eds): Muscle Pain. Diagnosis and ing from TrPs, exacerbates FMS symptoms, and that Treatment. Heidelberg, Dordrecht, London, New York: Springer; reduction/extinction of this input substantially contributes 2010: 365 pp. This book provides a comprehensive description ofmusculoskeletal pain conditions, particularly myofascial pain to improving the fibromyalgia condition ].
syndromes from trigger points and fibromyalgia, and criticallydiscusses their overlap, interaction, and implications for therapy.
2. Cummings M. Regional myofascial pain: diagnosis and manage- ment. Best Pract Res Clin Rheumatol. 2007;21:367–87.
3. Borg-Stein J. Management of peripheral pain generators in fibromyalgia. Rheum Dis Clin North Am. 2002;28:305–17.
In synthesis, several recent studies have proven the 4. Gerwin RD. Classification, epidemiology, and natural history important role of peripheral nociceptive muscle inputs in of myofascial pain syndrome. Curr Pain Headache Rep.
maintaining the diffuse level of sensitization in fibromyal- 5. Podichetty VK, Mazanec DJ, Biscup RS. Chronic non-malignant gia, showing how local treatment of these sources is able, at musculoskeletal pain in older adults: clinical issues and opioid least to some extent, to improve the diffuse symptoms of intervention. Postgrad Med J. 2003;79:627–33.
FMS. Not all of these studies involve a specific distinction 6. Mense S, Simons DG, Russell IJ, editors. Muscle pain. Under- between TrPs and TePs. Some research has provided standing its nature, diagnosis, and treatment. Philadelphia:Lippincott Williams & Wilkins; 2001. p. 385.
evidence that local anesthetic infiltration of TePs is 7. Giamberardino MA, Affaitati G, Fabrizio A, Costantini R: beneficial. However, because several well-controlled stud- Myofascial pain syndromes and their evaluation. Int J Clin ies have shown that most TePs sites indeed coincide with areas of active TrPs, it is highly probable that the beneficial 8. Simons DG, Travell JG, Simons LS (Eds): Travell & Simons' Myofascial Pain and Dysfunction. The Trigger Point Manual, Vol effects obtained on FMS are due to suppression of the input 1. Upper Half of Body, 2nd edn. Baltimore: Williams & Wilkins; from TrPs. Other research in which a clear distinction was made between TePs and TrPs, with injections performed in 9. Alvarez DJ, Rockwell PG. Trigger Points: diagnosis and manage- TrPs not coinciding with TePs sites, also showed a ment. Am Fam Physician. 2002;65:653–60.
10. Majlesi J, Unalan H. Effect of treatment on trigger points. Curr significant improvement of the widespread pain and Pain Headache Rep. 2010;14:353–60.
hypersensitivity of fibromyalgia. On the whole, the data 11. Graff-Radford SB. Myofascial pain: diagnosis and management.
so far available would indicate an important therapeutic Curr Pain Headache Rep. 2004;8:463–7.
effect of local treatment of TrPs in FMS, whether or not 12. Vecchiet L, Giamberardino MA, Saggini R. Myofascial pain syndromes: clinical and pathophysiological aspects. Clin J Pain.
these sites coincide with those of TePs. If this local treatment provides a clear relief of FMS pain, its possible 13. Affaitati G, Fabrizio A, Savini A, et al. A randomized, controlled effects on other FMS symptoms, such as poor sleep, study comparing a lidocaine patch, a placebo patch, and anesthetic fatigue, or affective disturbances, still need to be investi- injection for treatment of trigger points in patients with myofascialpain syndrome: evaluation of pain and somatic pain thresholds.
gated. In the examined studies, the improvement of FMS pain by TrP treatment is always partial, but of sufficient 14. Vecchiet L, Giamberardino MA, de Bigontina P, Dragani L: clinical relevance, both in extent and duration, to reason- Comparative sensory evaluation of parietal tissues in painful and nonpainful areas in fibromyalgia and myofascial pain syndrome. In 29. Cakit BD, Taskin S, Nacir B, et al. Comorbidity of fibromyalgia Proceedings of the 7th World Congress on Pain, Progress in Pain and cervical myofascial pain. Clin Rheumatol. 2010;29:405–11.
Research and Management. Edited by Gebhart GF, Hansmond DL, 30. Ge HY, Nie H, Madeleine P, et al. Contribution of the local and Jensen TS. Vol 2. Seattle: IASP Press; 1994: 177-185.
referred pain from active myofascial trigger points in fibromyalgia 15. Shah JP, Phillips TM, Danoff JV, Gerber LH. A in vivo microana- lytical technique for measuring the local biochemical mileu of human 31. •• Alonso-Blanco C, Fernández-de-Las-Peñas C, Morales-Cabezas skeletal muscle. J Appl Physiol. 2005;99:1977–84.
M, et al.: Multiple Active Myofascial Trigger Points Reproduce The 16. Kuan TS. Current studies on myofascial pain syndrome. Curr Pain Overall Spontaneous Pain Pattern in Women With Fibromyalgia and are Related to Widespread Mechanical Hypersensitivity. Clin J Pain.
17. Srbely JZ. New trends in the treatment and management of 2011 Feb 28. Epub ahead of print. This article demonstrates the high myofascial pain syndrome. Curr Pain Headache Rep.
prevalence of active TrPs in multiple muscles of FMS patients, as compared to control patients, and the correlation between TrP 18. Scott NA, Guo B, Barton PM, Gerwin RD. Trigger point activity and FMS pain and hypersensitivity.
injections for chronic non-malignant musculoskeletal pain: a 32. Ge HY. Prevalence of myofascial trigger points in fibromyalgia: systematic review. Pain Med. 2009;10:54–69.
the overlap of two common problems. Curr Pain Headache Rep.
19. Ho KY, Tan KH. Botulinum toxin A for myofascial trigger point injection: a qualitative systematic reviews. Eur J Pain.
33. • Ge HY, Wang Y, Danneskiold-Samsøe B, et al.: The predeter- mined sites of examination for tender points in fibromyalgia 20. Wolfe F, Smythe HA, Yunus MB, et al. The American College of syndrome are frequently associated with myofascial trigger points.
Rheumatology 1990 criteria for the classification of fibromyalgia.
J Pain. 2010;11:644-651. This article shows that most of the TePs Report of the multicenter criteria committee. Arthritis Rheum.
sites in FMS are TrPs. It underlines the role of TrPs as peripheral generators of fibromyalgia pain and suggests that their inactiva- 21. Wolfe F, Clauw DJ, Fitzcharles MA, et al.: Fibromyalgia Criteria tion may be an important option for the treatment of FMS.
and Severity Scales for Clinical and Epidemiological Studies: A 34. • Staud R, Nagel S, Robinson ME, Price DD: Enhanced central Modification of the ACR Preliminary Diagnostic Criteria for pain processing of fibromyalgia patients is maintained by muscle Fibromyalgia. J Rheumatol. 2011 Feb 1. Epub ahead of print.
afferent input: a randomized, double-blind, placebo-controlled 22. Abeles AM, Pillinger MH, Solitar BM, Abeles M. Narrative study. Pain 2009;145:96-104. This article emphasizes the impor- review: the pathophysiology of fibromyalgia. Ann Int Med.
tant role of peripheral impulse input in maintaining central sensitization in FMS by showing a reduction of local and distant 23. Bennett RM. Clinical manifestations and diagnosis of fibromyal- hyperalgesia upon anesthetic injection of the trapezius tender gia. Rheum Dis Clin North Am. 2009;35:215–32.
24. Robinson ME, Craggs JG, Price DD, et al.: Gray Matter Volumes 35. •• Affaitati G, Costantini R, Fabrizio A, et al.: Effects of treatment of Pain-Related Brain Areas are Decreased in Fibromyalgia of peripheral pain generators in fibromyalgia patients. Eur J Pain Syndrome. J Pain 2010 Dec 9. Epub ahead of print.
2011; 15:61-9. This article provides clear evidence of the effects of 25. Giamberardino MA: Update on Fibromyalgia Syndrome. PCU local treatment of TrPs (not coinciding with the sites of TePs) on pain symptoms of fibromyalgia using a standardized experimental 26. Carville SF, Arendt-Nielsen S, Bliddal H, et al. EULAR evidence based recommendations for the management of fibromyalgia 36. Castro-Sánchez AM, Matarán-Peñarrocha GA, Granero-Molina J, syndrome. Ann Rheum Dis. 2008;67:536–41.
et al. Benefits of massage-myofascial release therapy on pain, 27. Sommer C: Fibromyalgia: a clinical update. PCU 2010; XVIII anxiety, quality of sleep, depression, and quality of life in patients with fibromyalgia. Evid Based Complement Alternat Med.
28. Xu YM, Ge HY, Arendt-Nielsen L: Sustained nociceptive mechanical stimulation of latent myofascial trigger points induces 37. Staud R. Is it all central sensitization? Role of peripheral tissue central sensitization in healthy subjects. J Pain nociception in chronic musculoskeletal pain. Curr Rheumatol Rep.
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