640

Myofascial Pain
Jason L. Weller, MD1,2 Douglas Comeau, DO, CAQSM, FAAFP3,4,5 James A.D. Otis, MD, FAAN, DABPM2

1 Department of Neurology, Boston VA Healthcare System, Boston, Address for correspondence Jason L. Weller, MD, Department of
Massachusetts Neurology, Boston VA Healthcare System, Boston, Massachusetts
2 Department of Neurology, Boston University School of Medicine, (e-mail: [email protected]).
Boston, Massachusetts
3 Division of Sports Medicine, Boston University, Boston, Massachusetts
4 Department of Family Medicine, Boston University School of
Medicine, Boston, Massachusetts
5 Division of Sports Medicine, Boston College, Boston, Massachusetts

Semin Neurol 2018;38:640–643.

Abstract Myofascial pain syndromes arise from acute and chronic musculoskeletal pain and
often have a referred neuropathic component. It affects more than three quarters of
the world’s population and is one of the most important and overlooked causes of
disability. The origins of pain are thought to reside anywhere between the motor end
plate and the fibrous outer covering of the muscle, with involvement of microvascu-
lature and neurotransmitters at the cellular level. Diagnosis is made by clinical

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examination for the presence of myofascial trigger points, though some ancillary
tests may provide supportive evidence. The mainstay of treatment is regular physical
therapy with the goal of restoration of normal muscle laxity and range of motion.
Adjunct therapies including pharmacologic and nonpharmacologic interventions
Keywords provide varying degrees of benefit in refractory cases, and onabotulinum toxin A
► myofascial injection has the most evidence of efficacy for these patients. Here, we discuss the
► trigger points epidemiology, pathophysiology, and diagnostic and therapeutic options for the
► onabotulinum toxin evaluation and treatment of myofascial pain syndrome.

Pain is an unpleasant sensory and emotional experience arising Up to 85% of people will experience myofascial pain at least
from actual or potential tissue damage, and it is described once during their lifetime.5 The prevalence varies according to
according to the perspective of the patient.1 Pain can be the reporting clinic, from 21% of general orthopaedic patients
classified in many different ways: acute versus chronic, inflam- to up to 93% of patients in specialty pain centers.6 MPS is an
matory, neuropathic, visceral, somatic, and nociceptive among important and often overlooked cause of disability in clinical
others. The musculoskeletal system is the largest human organ practice. Men and women are equally affected, though middle-
system by weight, and is the system associated with multiple aged, sedentary women seem to be the population at highest
pain types, often occurring simultaneously.2 Specifically, myo- risk. Regular, vigorous activity such as moderate-intensity
fascial pain is a clinical syndrome that begins as acute pain daily exercise or manual labor appears to be protective.3
arising within the musculoskeletal system with a referred
autonomic phenomenon.3 Myofascial pain syndromes (MPSs)
Pathophysiology
can be categorized further as primary (unrelated to other
medical conditions) or secondary (associated with a comorbid The exact mechanism underlying MPS and myofascial trigger
medical condition).4 Sustained contractile activity of the mus- points (MTrP) is not known, though contemporary theories
cle trigger point causes local ischemia, hypoxia, and neurophy- allude to the relationship between peripheral nociception
siologic changes at nociceptors, leading to pain sensitization and central sensitization.7 Increases in acetylcholine (Ach)
and referred pain deep to and distant from the initial stimulus. release at the motor endplate, with associated endplate noise

Issue Theme Headache and Pain; Guest Copyright © 2018 by Thieme Medical DOI https://doi.org/
Editors, James A.D. Otis, MD, FAAN, and Publishers, Inc., 333 Seventh Avenue, 10.1055/s-0038-1673674.
Shuhan Zhu, MD New York, NY 10001, USA. ISSN 0271-8235.
Tel: +1(212) 584-4662.
 Myofascial Pain Weller et al. 641

noted on electromyography, are associated with active 18 characteristic tender points which are associated with the
MTrPs but not diagnostic of MPS. The increased Ach is diagnosis of fibromyalgia, of which at least 11 must be
thought to result in localized sustained sarcomere short- present for at least 3 months. Although there may be overlap
ening, producing a contraction knot which subsequently in the clinical presentations of fibromyalgia and myofascial
causes vasoconstriction and relative ischemia of the muscle pain, the clinical evaluation and management differ between
segment. Vasoactive and proinflammatory substances such the two entities. Our focus will be only on myofascial pain
as prostaglandin, bradykinin, serotonin, and histamine are associated with trigger points.
released in response to this ischemia and sensitize muscular
pain afferents. These substances may also activate a local
Clinical Evaluation
autonomic response to release more Ach, creating a positive
feedback loop. Autonomic involvement is evident in the The first step in the evaluation of the patient with MPS is the
description of MTrP-associated allodynia, blood flow history and physical exam. Patients usually report persistent
changes, sweating abnormalities, reactive hyperemia, and pain, muscle tension, and limited range of motion. In addi-
altered pilomotor response in MPS. Chronically active MTrPs tion to review of comorbid medical conditions, allergies and
may develop convergent connections through nociceptors in medications, clinicians should ask about occupational factors
the dorsal horn of the spinal cord and activate central (heavy lifting, bending/twisting, repetitive motions, and
sensitization to adjacent myotomes through release of neu- prolonged sustained postures such as tilting the head to
rotransmitters such as substance P, N-methyl-D-aspartate, one side), psychosocial stressors, and lifestyle considerations
glutamate, and nitric oxide. such as smoking and exercise.3 A thorough physical exam
Another theory includes the role of the fascial layer in should include a complete neuromuscular examination that
MPS.8,9 The muscle fascia receives innervation with both focuses on the affected area(s). The diagnostic criteria (and
mechanoreceptors that detect changes in length and tension frequency of use) for MPS include palpation of at least one

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as well as free nerve endings that respond to nociceptor tender spot in a taut band (65%), limited range of motion
stimulation in the presence of pathological processes. Hya- (22%), patient pain recognition upon palpation of the tender
luronic acid is also present in abundance in the body’s point (53%), local twitch response (44%), and predicted pain
connective tissues and serves as a lubricant and reservoir referral pattern (44%).11,12 Palpation of fibrous taut bands
for electrolytes and nutrients. However, alterations in the within the soft tissue can be accompanied by the use of a
conformation of hyaluronic acid can result in adhesion rather pressure threshold meter to document the location and
than lubrication and stimulation of stretch receptors in the relative sensitivity of trigger points (TPs). Sensitivity and
absence of pathological stress, leading to myofascial pain. specificity of these criteria varies, and further objective study
is needed to further clarify the utility of these measures. At
present, the best evidence for reliability lies with firm digital
Trigger Points
pressure and patient feedback on the pain experience.
The hallmark clinical sign of MPS is the MTrP, a palpably tense Further evaluation depends on the affected location and
band of muscle fibers within a shortened or weak muscle.3,10 may include plain radiographs, computed tomography, and
Firm palpation of a MTrP produces a pathognomonic local magnetic resonance imaging, as well as electromyography
twitch response of the affected muscle and a positive “jump and ultrasonography.4,11 The differential diagnosis of MPS
sign” in the affected patient. MTrPs can develop within any includes common musculoskeletal and neurological disor-
skeletal muscle, though the most commonly affected muscles ders such as osteoarthritis, myopathies, and radiculopathies,
include the sternocleidomastoid, trapezius, levator scapulae, as well as fibromyalgia, and thorough physical examination
infraspinatus, and rhomboid of the upper back and neck. Active will help elucidate or eliminate these possibilities.11
MTrPs produce persistent, severe pain and are associated with Advanced imaging and electrodiagnostics are generally
acute strain, sudden overload, or cumulative trauma as well as employed to rule out other causes of myofascial pain, but
prolonged sustained posture. With decreased demand upon can be used to support a diagnosis of MPS. A diagnostic tool
the muscle, active MTrPs usually subside within 1 week. called the Symptom Intensity Scale is effective in discerning
However, mechanical and biological perpetuating factors MPS from fibromyalgia, though it has yet to be adopted by
may sustain the acute phase and evolve to chronic MTrPs. The the American College of Rheumatology as a standard mea-
irritation of chronic MTrPs can propagate to other muscles to sure. Currently, there is no gold standard diagnostic study for
create “satellite” MTrPs. Latent MTrPs are generally asymp- MPS outside of the physical exam.
tomatic, though symptoms can be reproduced with palpa-
tion of the affected muscle. Any mild systemic insult,
Treatment
including ambient temperature changes, minor overstretch-
ing, and emotional stimuli, may activate a latent MTrP.3 As The goal of treatment for MPS is return of functional ability
such, latent MTrPs should undergo prompt evaluation and through pain relief by addressing the active TPs causing
treatment to avoid activation.10 symptoms. Management strategies exist upon a spectrum
A related but clinically separate condition, fibromyalgia, is from most conservative to most invasive. For new-onset
a widespread chronic pain disorder that also includes muscle MPS, clinicians should utilize the most effective measure
pain, fatigue, sleep disturbance, and depression.2 There are while minimizing risks to the patient.

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642 Myofascial Pain Weller et al.

The basis for nonpharmacologic treatment of MPS is a specific to MPS have been performed. Tricyclic antidepressants
regular exercise routine that includes slow, sustained stretch- such as amitriptyline are effective for tension-type headache
ing of the muscles with gradual restoration of normal range of and intractable pain syndromes with muscle spasm. Selective
motion.3–5,10,11 Patients should be instructed to remain active serotonin reuptake inhibitors can improve overall pain, sleep,
but to use gentle, controlled movements. When the patient and neurocognitive symptoms in fibromyalgia but have not
encounters pain with a certain movement, exploration of slow been specifically studied for MPS. A small but significant
extension of the movement is encouraged to assist in releasing benefit has been reported when nonsteroidal anti-inflamma-
tension. Strength training is discouraged initially, as it may tory drugs are used as adjuncts to other therapies, but evidence
result in substitution of other muscles, poor functional is limited regarding their use as the first-line treatment of MPS.
mechanics, and muscle overload leading to exacerbation of Stretching and physical therapy are the mainstays of MPS
myofascial pain. However, after reduction of MTrP pain and management. A more invasive but effective practice when
restoration of normal range of motion, a graded strengthening conservative measures fail is injection of MTrPs.7 Some tech-
program combined with aerobic exercise would be the optimal niques using a needle to puncture the fascia and disrupt the
plan for recurrence prevention. dysfunctional motor endplate activity of the MTrP include fast-
Deep massage is safe and effective, though the clinician in–fast-out superficial injection, intramuscular stimulation,
must recognize areas of referred pain and trace this back to twitch-obtaining intramuscular stimulation, and infiltration
the source MTrP.4 Deep massage helps improve blood flow with medications. Contraindications to trigger point injection
and increase lymphatic drainage from the MTrP while acti- include coagulopathies or use of anticoagulant medications,
vating the release of endorphins, which together provide local infection, acute muscle trauma, or use of an antiplatelet
relief from MPS and aid in prevention of recurrence. Manual agent within 3 days of injection.11 Along with the introduction
therapy is one of the most commonly utilized noninvasive of the needle, trigger point injections employ a variety of
treatment options for MPS.11 This consists of an array of medications, including no medication. When the no medica-

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techniques including myofascial release, deep pressure mas- tion is injected, the procedure is called dry needling.8 This
sage, osteopathic manipulative treatment, and spray and practice involves the insertion of an acupuncture-like needle
stretch, which entails application of a cooling spray contain- into the skin and muscle in the MTrP location. After eliciting
ing fluoromethane or ethyl chloride while simultaneously the localized twitch response, the needle is allowed to remain
passively stretching the involved muscle. Similarly, ultra- within the muscle until MTrP inactivation and muscle relaxa-
sound therapy has been shown to promote breakdown of tion occurs. The mechanism by which analgesia is achieved by
scar tissue and increase blood flow to areas of localized this method is poorly understood, but one theory suggests that
spasm in MPS.4,5 Transcutaneous electrical nerve stimula- dry needling initiates stimulation of the enkephalinergic
tion provides relief in the form of electroanalgesia and inhibitory dorsal horn interneurons, resulting in endogenous
employs the gate control theory of chronic pain. Application opioid-mediated pain suppression. One recent systematic
of electrical stimulation at high frequency and high intensity review and meta-analysis found dry needling to be superior
(100 Hz, 250 ms pulses) is effective in the reduction of to sham or no treatment both immediately and for 4 weeks
myofascial pain without reduction in local trigger point postintervention, but did not demonstrate a significant differ-
sensitivity, but does have a cumulative effect when applied ence compared with alternative interventions for MTrP-
over multiple sessions. Low-level laser therapy involves the derived MPS.3
application of a red and infrared light source to the skin over Although dry needling provides equal pain relief as medica-
the affected muscle(s), and is thought to induce mitochon- tion injection, more postinjection soreness is reported with
drial repair of tissue, decrease arteriolar spasm, and increase dry needling.7 The most frequently used anesthetic agent for
tissue oxygenation. Biofeedback is the practice of teaching trigger point injection is lidocaine, although procaine is gain-
patients to manipulate certain bodily parameters such as ing more favor due to its short action, minimal systemic
heart rate, blood pressure, muscle tension, and pain percep- toxicity, and absence of local irritation.11 Procaine is also the
tion to improve quality of life and limit the psychological least myotoxic of the injectable anesthetics. Other anesthetics
manifestations of pain. The most effective method of bio- used include prilocaine, mepivacaine, bupivacaine, levobupi-
feedback in MPS utilizes electromyography to measure vacaine, and ropivacaine. There is no evidence to support the
muscle tension and enable patient control of muscle spasm. use of corticosteroids in trigger point injection, and there is the
Pharmacologic management of myofascial pain is generally added potential risk of local muscle necrosis with these
indicated as the first-line therapy for patients in whom phy- medications. Both dry needling and anesthetic injection
sical therapy and other noninvasive techniques are either showed better efficacy in pain relief than saline injection in
contraindicated or have failed. Muscle relaxants are a generally multiple studies
safe and effective class of medications, of which tizanidine has Botulinum toxin A is an effective but expensive agent now
the best evidence of efficacy for MPS. However, as a centrally available for use in chronic MPS.4,5,11 Multiple small, rando-
acting α-adrenergic agonist, common side effects include mized, controlled trials demonstrated an overall improve-
drowsiness and weakness due to its systemic application. ment in pain descriptors, muscle tension, and pressure pain
Tramadol is a weak opioid agonist and serotonin/norepinephr- thresholds compared with placebo (saline) or steroid injec-
ine reuptake inhibitor with some evidence of efficacy for tion, which held true at 30 and 60 days posttreatment. The
fibromyalgia and chronic low back pain, though no studies efficacy of botulinum toxin may help prove the combined

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 Myofascial Pain Weller et al. 643

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