Myofascial Pain

Definition

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 sensory changes.

Etiology

Chronic muscle stretch and overload are thought to play a key role in the development of TrPs, with direct and indirect trauma as possible but less likely causes. Mechanical causes of chronic stretch and overload include unaccustomed or intense exercise, sustained sub-optimal postures, anatomic abnormalities, abnormal muscle firing patterns, joint dysfunction, chronic repetitive overuse, and poor work-related ergonomics. Nonstructural factors including anxiety, depression, sleep deprivation, fatigue, chronic infection, and iron, vitamin, mineral, and endocrine deficiency states may contribute to the development and persistence of TrPs.^{2-5, 20}

Epidemiology including risk factors and primary prevention

Myofascial pain is a purely clinical diagnosis, and lacks objective and systematic diagnostic criteria. This lack of consensus-driven, reliable diagnostic criteria makes 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

Patho-anatomy/physiology

The most accepted theory of trigger point formation is Travell and Simons’ integrated hypothesis.^1,7-9,10 According to this hypothesis, the initiating event is muscle overload and/or injury. This leads to local capillary constriction and ischemia, an increase in sympathetic nervous system adrenergic activity, formation of an acidic hydrogen ion concentration within the muscle tissue, and the release of sensitizing substances (substance P, calcitonin gene-related peptide [CGRP], protons, serotonin, norepinephrine, prostaglandins, bradykinins, tumor necrosis factor α, interleukin (IL)-6, IL-8 and IL-1β). In addition, a reduction of locally available adenosine triphosphate (ATP) to muscle tissue results in inhibition of return of calcium to the sarcoplasmic reticulum, causing a sustained contraction of the sarcomere. The acidic environment inhibits the breakdown of acetylcholine, resulting in increased acetylcholine within the synaptic cleft and increased frequency of miniature end plate potentials (EPPs). Together, the sustained sarcomere contraction and increased EPPs promote formation of a taut band of muscle tissue.^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, referred pain elsewhere.¹²

Quintner and Cohen have proposed a plausible alternative to Travell and Simons’ 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 (spontaneously painful and tender) or latent (not spontaneously painful but tender to touch). Latent TrPs can be regarded as a preclinical or subclinical phase of MPS.^1,2,15,21 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, periarticular muscle pain in a patient with underlying tendinosis, 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

Essentials Of Assessment

History

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, varying in intensity, may sudden or gradual in onset, and typically exacerbated by certain prolonged postures that place the affected muscle groups on chronic tension or stretch. 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, such as repetitive movement patterns or sustained positions. Response to prior treatments should also be assessed.

Physical examination

A distinct, taut band of muscle tissue is the primary identifiable abnormality on physical exam. Tenderness and reproduction of usual or spontaneous pain with palpation of this taut band are essential features of MPS.² It is important to identify whether palpation of TrPs produces referred pain patterns or just local tenderness, as referred pain may assist the diagnostician in understanding symptoms at distant sites. For example, palpation of trigger points in the cervical musculature that results in pain referral in a more cephalad direction may assist with understanding headache etiology. 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. Pincer palpation often produces a local twitch response.¹⁵ Furthermore, pressure on a TrP may elicit a reflexive withdrawal in response to the painful stimulus. Muscle weakness and painful limitation of range of motion from the TrP should be evaluated to assist with identifying possible contributing underlying joint dysfunction or neurologic comorbidities.

The clinician should also examine for biomechanical discrepancies, postural imbalance, pelvic and shoulder symmetry, evidence of hypermobility, 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, 22}

Functional assessment

Inquiries into work status, leisure status, level of daily activity, mood, and sleep status allow the clinician to evaluate extent to which myofascial pain is contributing to functional impairment.

Laboratory studies

Routine laboratory screening is not indicated or recommended for most cases of MPS. However, in complex or refractory cases, such as in the presence of other comorbidities or if concern for an inflammatory myopathy, laboratory screening may be warranted. Laboratory testing may include rheumatologic markers (ESR, CRP, ANA, RF, anti-CCP antibodies), chronic infections like hepatitis C and Lyme disease, iron, liver function, thyroid, estrogen, growth hormones, and levels of vitamins B1, B6, B12, and D.²

Imaging

MPS is a clinical diagnosis, and there are no established imaging studies routinely used in its diagnosis. There is no standard imaging criteria for TrP identification. However, if there is high suspicion for an underlying joint or connective tissue disorder, spine radiographs, diagnostic musculoskeletal ultrasound, and/or magnetic resonance imaging may be useful to identify other potential contributors such as tendinopathies, osteoarthritis, disc herniations, facet disease, or radiculopathy.

Diagnostic musculoskeletal 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 comparing their relative stiffness.¹⁶ This feature is available only on high-end ultrasound 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 (EMG) 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 diagnostic 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-1β in active TrPs compared with normal muscle and latent TrPs.¹¹ However, this is currently only used as a research tool.

Environmental

Occupational risk factors for development of MPS include repetitive work activities, sub-optimal ergonomics, and work environments that result in both visual and postural stress.¹⁸

Rehabilitation Management And Treatments

At different disease stages

MPS therapies are directed toward inactivation of both 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 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, however myofascial release, active release technique, and muscle energy technique are commonly used. The modalities are beneficial only for short-term relief and are best used as adjunctive therapies.

Dry needling (DN) and trigger point injections (TPI) have been shown in numerous studies to be effective, though neither is clearly superior to each other or to placebo.¹⁹ DN is minimally invasive, inexpensive, easy to learn with appropriate training, and low risk when performed safely and correctly. It can be performed by physical therapists in many states. TPI are usually performed with a local anesthetic injectate. Lidocaine diluted to a concentration of 0.25% has been demonstrated to be less painful to inject than a 1% solution, with comparable or better efficacy. Botulinum toxin has been used in resistant TrPs, although downsides include high cost and relative lack of evidence for its use in MPS. It is advised against using corticosteroid because of potential side effects including muscle necrosis and skin depigmentation. The effectiveness of DN and TPI is dependent upon the ability of the examiner to accurately palpate, identify, and needle TrPs. 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 (a 5-HT3 antagonist 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 significant literature support. Opioids are generally to be avoided in MPS due to concern for opioid-induced hyperalgesia with chronic use.

Removal of underlying pathology
Any direct intervention for TrPs, such as dry needling or trigger point injection, will only lead to short-term improvement if correction of perpetuating factors is not achieved. Any abnormal posture or muscle imbalance should be identified and addressed.¹⁵Depression, anxiety, sleep disturbance, and metabolic abnormalities should be treated if present. Psychosocial stressors, fear avoidance behaviors, and kinesiophobia should be identified and an individualized treatment strategy developed. The patient should be encouraged to take an active role in recovery.

Patient & family education

Patient education is critical for long-term treatment success. Postural training, corrective exercise, avoidance of muscle overload positions, progressive relaxation, and diaphragmatic breathing techniques should be taught to the patient. Recent evidence suggests that simple awareness of and education about the neurobiology of pain can be effective in reducing pain perception 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 diagnosis. Training is required to become proficient at both identifying and treating TrPs, and perhaps more importantly, to understand how and when to rule out underlying systemic, joint, or connective tissue conditions. Physiatrists are perhaps the best equipped to diagnose and treat this very common musculoskeletal disorder.

Cutting Edge/ Emerging And Unique Concepts And Practice

NA

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.

References

1. 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.
2. Malanga GA, Cruz EJ. Myofascial low back pain: a review. Phys Med Rehabil Clin N Am. 2010;21:711-724.
3. Yap EC. Myofascial pain: an overview. Ann Acad Med Singapore. 2007;36:43-48.
4. Gerwin RD. A review of myofascial pain and fibromyalgia , factors that promote their persistence. Acupunct Med. 2005;23:121-134.
5. Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003;78:1463-1470.
6. 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.
7. 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.
8. McPartland JM. Travell trigger points, molecular and osteopathic perspectives. J Am Osteopath Assoc. 2004;104:244-249.
9. Simons DG. New views of myofascial trigger points: etiology and diagnosis. Arch Phys Med Rehabil. 2008;89:157-159.
10. Gerwin RD, Dommerholt J, Shah JP. An expansion of Simons integrated hypothesis of trigger point formation. Curr Pain Headache Rep. 2004;8:468-479.
11. 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.
12. Fernandez-de-las Penas C, Dommerholt J. Myofascial Trigger Points: Peripheral or Central Phenomenon? Current Rheumology Reports. 2014:16:395-401.
13. Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the “myofascial pain” construct. Clin J Pain. 1994;10:243-251.
14. Quintner JL, Bove GM, Cohen ML. A Critical Evaluation of the Trigger Point Phenomenon. Rheumatology(oxford).2015. Mar;54(3) 392-9.
15. Giamberardino MA, Affaitati G, Fabrizio A, Costantini R. Myofascial pain syndrome and their evaluation. Best Pract Res Clin Rheumatol. 2011;25:185-198.
16. 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.
17. Chen Q, Basford J, An KN. Ability of magnetic resonance elastography to asses taut bands. Clin Biomech. 2008;23:623-629.