Myofascial pain syndrome (MPS) is a regional muscle pain syndrome caused by myofascial trigger points (TrPs). A TrP is defined as a hyperirritable spot in a palpable taut band of skeletal muscle.1,2 MPS is characterized by pain, both local and referred, muscle stiffness and weakness, and sensory changes.
Direct or indirect muscle trauma and overload are thought to play a key role in the development of TrPs. Mechanical causes of overload include unaccustomed or intense exercise, sustained abnormal postures, anatomic abnormalities, joint dysfunction, chronic repetitive overuse, and poor work-related ergonomics. Nonstructural factors including anxiety, sleep deprivation, fatigue, chronic infection, and iron, vitamin, mineral, and endocrine deficiency states may contribute to the development and persistence of TrPs.2-5
Epidemiology including risk factors and primary prevention
The lack of well-established and reliable diagnostic criteria as well as appropriate physician training make it difficult to establish accurate statistics about incidence and prevalence. Approximately 9 million people in the United States are thought to suffer from myofascial pain. MPS affects up to 95% of patients with chronic pain, and in one study, MPS was found to be the primary cause of pain in 85% of patients attending a large pain center.2,6
The most accepted theory of trigger point formation is Simons’ integrated hypothesis.1,7-9,10 In it, the initiating event is muscle overload and injury. This leads to localized capillary constriction and ischemia, an increase in sympathetic nervous system adrenergic activity, formation of an acidic hydrogen ion concentration, a reduction of adenosine triphosphate (ATP), the release of sensitizing substances (substance P, calcitonin gene-related peptide [CGRP], protons, serotonin, norepinephrine, prostaglandins, bradykinins, tumor necrosis factor Î±, interleukin (IL)-6, IL-8 and IL-1Î²), and the lack of ATP inhibits return of calcium to the sarcoplasmic reticulum. The acidity inhibits the breakdown of acetylcholine. Combined, this results in increased acetylcholine in the synaptic cleft, increased frequency of miniature end plate potentials, sustained sarcomere contraction, and formation of the taut band.7,8 The biochemicals released account for the peripheral sensitization of nociceptors, which contribute to the pain associated with active trigger points, allodynia, and hyperalgesia.1,2,7,10,11 Available evidence supports the hypothesis that TrPs are a persistent peripheral source of nociception, contributing to pain propagation and widespread pain.12
Quintner and Cohen have proposed a plausible alternative to the myofascial pain construct, suggesting hyperalgesia secondary to peripheral or central sensitization of nociceptors and the spontaneous firing of nociceptive dorsal horn neurons as the etiology of the pain syndrome.13 Neurogenic inflammation has been proposed as a possible etiology of this peripheral or central sensitization.14
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
TrPs can be either active, that is, spontaneously painful and tender, or latent, that is, not spontaneously painful but tender to touch. The latent TrPs could be regarded as a preclinical phase of MPS.1,2,15 Examination often reveals tender taut bands in muscle and mild limitation in range of motion. Correction of biomechanical stressors and elimination of perpetuating factors may prevent the development of pain. Once TrPs become spontaneously painful, treatment intervention may be necessary to eliminate them. Acute myofascial pain due to TrPs caused by a clearly identifiable local muscle strain carries a favorable prognosis. As MPS spreads from local to regional and becomes more chronic, it becomes more difficult to eliminate.
Specific secondary or associated conditions and complications
MPS is a great imitator. It can present as shoulder pain in patients with impingement or capsulitis, hip or knee pain in patients with osteoarthritis, back or neck pain in patients with lumbar or cervical radiculopathy, or headache.3 The pain pattern is dependent on the muscle(s) involved. MPS can present as painful restricted range of motion, stiffness, referred pain, and autonomic dysfunction.2
2. ESSENTIALS OF ASSESSMENT
Characteristics of muscle pain including onset, location, quality, intensity, duration, aggravating, alleviating, and associated factors, as well as evolution over time should be investigated. MPS usually presents with a deep tense somatic pain, fairly well-discriminated, varying in intensity, sudden or gradual in onset, and typically exacerbated by movement. In the presence of latent TrPs, patients frequently complain of stiffness, tightness, fatigue, and muscle weakness.15
The patient’s age, occupation, job satisfaction, hobbies, sports, stressors, lifestyle, and family history of musculoskeletal pain should be investigated, because they may reveal precipitating factors. Response to prior treatments should also be assessed.
The taut band is the primary identifiable abnormality on physical exam. Tenderness in the taut band and reproduction of usual or spontaneous pain are essential features of MPS.2 It is important to identify whether palpation of TrPs produces referred pain patterns or just local tenderness. Palpation should be performed first with fingertips perpendicular to the direction of the muscle fiber in order to search for taut bands, and then with fingertips parallel along the taut band to isolate the myofascial TrP. Snapping or pincer palpation often produces a local twitch response.15 Furthermore, pressure on a TrP may elicit a jump sign, that is, a reflexive withdrawal in response to a painful stimulus. Muscle weakness and painful limitation of range of motion from the TrP should be evaluated.
The clinician should examine for biomechanical discrepancies, postural imbalance, pelvic and shoulder symmetry, restriction of active or passive range of motion, abnormal movement patterns, and acquired or congenital abnormalities, such as scoliosis and leg length discrepancies.2,3,18
Inquiries into work status, leisure status, level of daily activity, mood, and sleep status allow the clinician to evaluate functional impairment.
Routine laboratory screening is not recommended for local or regional MPS. If clinically indicated, screening for chronic infections like hepatitis C and Lyme disease, as well as laboratory testing for levels of vitamins B1, B6, and D, iron, liver function, thyroid, estrogen, and growth hormones may be useful.2
Generally, there are no established imaging studies used in the diagnosis of MPS. Spinal radiograph, computed tomography scan, and magnetic resonance imaging may be useful to identify other causes of regional pain syndromes, such as osteoarthritis, disk herniation, facet disease, or radiculopathy. There is no imaging criterion standard for TrP identification.
Traditional ultrasonography allows one to visualize the twitch response in a taut band but does not otherwise allow for identification of a TrP. Doppler flow studies can identify high resistance of arterial blood flow secondary to sustained contracture at active TrPs. Ultrasound vibration sonoelastography can be used to differentiate TrPs from normal surrounding tissues by their relative stiffness measured by vibration amplitude.16 This feature is available only on high-end machines. Magnetic resonance elastography measures wavelengths of vibration sent through tissues. It is able to distinguish differences in wave propagation in a taut band versus normal tissues. It cannot, however, identify the TrP within the taut band.17 These tools appear promising, but their clinical usefulness and practicality remain in question.
Supplemental assessment tools
Needle electromyography can be used to show spontaneous end plate activity within the TrPs, and thermography can reveal a hot spot in active TrPs.15 Neither, however, adds much to a skilled clinical examination for treatment purposes.
The muscle pain detection device is an electrical device that elicits muscle contractions in an attempt to distinguish painful from nonpainful muscles. Once identified, the muscles can be treated with TrP treatment methods.2
Microdialysis has shown significantly higher levels of pronociceptive substances like substance P, CGRP, protons, serotonin, norepinephrine, bradykinins, prostaglandins, tumor necrosis factor alpha, and IL-1Î² in active TrPs compared with normal muscle and latent TrPs.11 However, this is only a research tool.
Occupational risk factors for development of MPS include repetitive work activity, poor ergonomic work station, as well as a highly visual and posturally stressful work environments.18
3. REHABILITATION MANAGEMENT AND TREATMENTS
At different disease stages
MPS therapies are directed toward inactivation of the symptomatic and latent TrPs, as well as correction of perpetuating factors.15 Although there are many treatment options for MPS, there is no clear consensus regarding these interventions. Noninvasive techniques include various manual therapy techniques, stretching, and physical modalities including heat or ice, ultrasound, electric stimulation, microcurrent, and laser therapy. No particular manual therapy techniques have been shown to be superior. The modalities are beneficial only for short-term relief and are best used as adjunctive therapies.
Dry needling (DN) and trigger point injection (TPI) have been shown in numerous studies to be effective, though neither is clearly superior to each other or placebo.19 DN is minimally invasive, inexpensive, and easy to learn with appropriate training with low risk. It can be performed by physical therapists in many states. For TPI, lidocaine diluted to a concentration of 0.25% is less painful to inject than a 1% solution, with comparable or better efficacy. Botulinum toxin has been used in resistant TrPs, though it is very expensive and of questionable efficacy. Corticosteroid should not be used because of side effects including muscle necrosis and skin depigmentation. The effectiveness of DN and TPI is dependent on the ability of the examiner to accurately palpate and identify TrPs. Equally important is the ability to accurately needle the identified TrP. The best response to DN or TPI occurs when there is a local twitch response elicited by the needle. Research suggests that the concentration of sensitizing chemicals in the immediate vicinity of the TrP normalizes following the local twitch response.7 Risks with DN or TPI include pneumothorax, bleeding, and infection. Contraindications include bleeding disorders, anticoagulation, local infection, and acute muscle trauma.
Medications from multiple drug classes have been used to treat MPS. There is strong evidence to support the use of clonazepam, diazepam, and alprazolam in combination with ibuprofen, amitriptyline, or tropisetron (not available in the United States), but not as monotherapy.19 There is moderate evidence to support topical agents like methylsalicylate, menthol, and diclofenac patches. Antiepileptics, antidepressants, muscle relaxants, nonsteroidal anti-inflammatory drugs, and tramadol are all used widely, though without literature support. Opioids are generally to be avoided in MPS.
Removal of underlying pathology
Any MPS/TrPs therapy will only lead to short-term improvement without proper identification and correction of perpetuating factors. Any abnormal posture or muscle imbalance should be identified and addressed.15Depression, anxiety, sleep disturbance, and metabolic abnormalities should be treated. Identification of psychosocial stressors and fear avoidance behavior should be identified and an individualized treatment strategy developed. The patient should be encouraged to take an active role in their recovery.
Patient & family education
Patient education is critical for long-term treatment success. Postural training, corrective exercise, avoidance of muscle overload positions, as well as relaxation and diaphragmatic breathing techniques should be taught to the patient. Recent evidence suggests that education about the neurobiology of pain can be effective in chronic pain populations.
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
MPS should be considered in the differential diagnoses of all musculoskeletal pain syndromes. Careful clinical history and examination are essential in appropriate diagnoses. Training is required to become proficient at both identifying and treating TrPs. Physiatrists are perhaps the best equipped to diagnose and treat this very common musculoskeletal disorder.
4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE
5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE
Gaps in the evidence-based knowledge
The absence of accurate and reliable diagnostic criteria for MPS clouds the interpretation of research studies evaluating treatment efficacy. Further gaps in evidence-based knowledge stem from the lack of a validated TrP pathophysiology.
- Simons DG, Travel JG, Simons LS. Travel and Simons, Myofascial Pain and Dysfunction: The Trigger Point Manual Volume 1: Upper Half of Body. 2nd ed. Baltimore, MD: Williams & Wilkins; 1999.
- Malenga GA, Cruz EJ. Myofascial low back pain: a review. Phys Med Rehabil Clin N Am. 2010;21:711-724.
- Yap EC. Myofascial pain: an overview. Ann Acad Med Singapore. 2007;36:43-48.
- Gerwin RD. A review of myofascial pain and fibromyalgia , factors that promote their persistence. Acupunct Med. 2005;23:121-134.
- Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78:1463-1470.
- Tough EA, White AR, Richards S, Campbell J. Variability of criteria used to diagnose myofascial trigger point pain syndrome -evidence from a review of the literature. Clin J Pain. 2007;23:278-286.
- Shah JP, Gilliams EA. Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: an application of muscle pain concepts to myofascial pain syndrome. J Bodyw Mov Ther. 2008;12:371-384.
- McPartland JM. Travell trigger points, molecular and osteopathic perspectives. J Am Osteopath Assoc. 2004;104:244-249.
- Simons DG. New views of myofascial trigger points: etiology and diagnosis. Arch Phys Med Rehabil. 2008;89:157-159.
- Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons integrated hypothesis of trigger point formation. Curr Pain Headache Rep. 2004;8:468-479.
- Shah JP, Danoff JV, Desai MJ, et al. Biochemicals associated with pain and inflammation are elevated in sites near to and remote from active myofascial trigger points. Arch Phys Med Rehabil. 2008;89:16-23.
- Fernandez-de-las Penas C, Dommerholt J. Myofascial Trigger Points: Peripheral or Central Phenomenon? Current Rheumology Reports. 2014:16:395-401.
- Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the “myofascial pain” construct. Clin J Pain. 1994;10:243-251.
- Quintner JL, Bove GM, Cohen ML. A Critical Evaluation of the Trigger Point Phenomenon. Rheumatology(oxford).2015. Mar;54(3) 392-9.
- Giamberardino MA, Affaitati G, Fabrizio A, Costantini R. Myofascial pain syndrome and their evaluation. Best Pract Res Clin Rheumatol. 2011;25:185-198.
- Sikdar S, Shah JP, Gilliams E, Gebreab T, Gerber LH. Assessment of myofascial trigger Points (MTrPs): a new application of ultrasound imaging and vibration sonoelastography. Conf Proc IEEE Eng Med Biol Soc. 2008;2008:5585-5588.
- Chen Q, Basford J, An KN. Ability of magnetic resonance elastography to asses taut bands. Clin Biomech. 2008;23:623-629.
- Treaster D, Marras WS, Burr D, Sheedy JE, Hart D. Myofascial trigger point development from visual and postural stressors during computer work. J Electromyogr Kinesiol 2006;16:115-124.
- Annaswamy TM, De Luigi A, O’Neill B, Keole N, Berbrayer D. Emerging concepts in the treatment of myofascial pain: a review of medications, modalities, and needle-based interventions. PM&R. 2011;10:940-961.
Original Version of the Topic:
Bryan J. O’Neill, MD, Amir Tahaei, MD. Myofascial pain. Publication Date: 2012/11/27.
Bryan O’Neill, MD
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