Myofascial Pain

Article Author:
Bruno Bordoni
Article Author (Archived):
Kavin Sugumar
Article Editor:
Matthew Varacallo
4/25/2019 11:26:05 AM
PubMed Link:
Myofascial Pain


The fascia is made up of a solid (muscles) and liquid (blood, lymph) elements and components.[1][2]

The myofascial system comprises contractile muscle tissue and connective tissue. The latter creates the shape of the muscle, penetrates the muscle and orients the nerve and vascular endings; it's thickening at the end of the contractile district forms the insertions and origins of the muscle on the bone tissue, transmitting the movement from the muscles to the bones to which they are attached. Within the myofascial system, there are other fascial organizations, such as the nervous and vascular tissue and the lymphatic system. Nervous tissue (axon and various afferents) and the resulting terminations are fasciae.[3]

Different tissues work in harmony to make up the myofascial continuum. Thanks to the fascial tissue, all the muscles make up a network in constant connection, and it becomes an error to consider a muscular district as a separate entity.[4][5] It is impossible to intervene or come in contact with a muscle excluding the associated connective or fascia tissues.

The myofascial system can be a source of pain and functional limitations by creating symptomatic pictures that are not always clear and not always easy to frame. The article reviews myofascial pain or myofascial syndrome, highlighting the latest news and current scientific information.

The pain of the myofascial system derives from the presence of muscular trigger points, of the well-localized areas of taut band, which at the palpation or to the active movement generate local pain or referred pain. There are active trigger points, painful areas to movement or painful even in the absence of movement, and silent trigger points, which become painful only at palpation.[6]


When considering the reasons for myofascial pain, it should be remembered that myofascia is also constituted by the fascial organization that transports fluids (blood and lymph), the nerve pathways (axon and different afferents). Vessels and nerve pathways can be a source of pain because they are innervated. The liquid fascia can be a source of pain, because according to their speed, direction and type of flow specifically stimulate the fascias in which they pass.

The causes that lead to pain are not fully understood.

  • Constants microtrauma to muscle system can increase the oxidative metabolism and quickly deplete cellular energy reserves (ATP), with abnormal area oxygenation. This altered mechano-metabolic environment creates the conditions for more sensitive nociception, particularly if the musculature has a majority of red fibers (postural muscle).[6] Type III and IV afferents send nociceptive messages from muscles, which can be activated by various substances such as potassium, prostaglandins, histamine, kinins, leading to increased stiffness. This constant peripheral stimulation could alter the response of the medullary interneurons, generating a peripheral sensitization to the pain in a first phase, and central sensitization in a second temporal phase.[6]
  • The presence of trigger points (TPs) may result from the alteration of the synaptic plaque of muscle fibers. An increase in acetylcholine with consequent uncontrolled release causes a constant local contraction of the muscle fibers, with spontaneous contractions not deriving from the central nervous system. This constant depolarization and energetic depletion would cause the release of inflammatory substances with pain and the creation of TPs.[6]
  • In the presence of a constantly altered mechano-metabolic environment, the connective tissue system that makes up the myofascial system changes its properties. The fibroblasts are transformed into myofibroblasts, contributing to the shortening of different tissues and the increase in muscle tone. The receptors present in the fascia can be transformed into nociceptors and send painful afferents for mechanical stimuli (allodynia or mechanical hyperalgesia). We know that the fascia can carry electrical information and we can suppose that an altered network of connective tissue can interact negatively with the polarization of myofibre, contributing to the spontaneous presence of local muscle contraction.[7][8]
  • Hyaluronan (HA) is a molecule of glycosaminoglycan polymer found in the extracellular matrix. If the mechano-metabolic environment alters its physiological status, HA changes its properties creating a more viscous extracellular matrix; the various myofascial layers will have difficulty slipping one on the other, making the muscle contraction harder.[9] The nerve endings of the fascia in the most viscous area will be more easily stretched, becoming constantly activated if trigger points are created, generating a pain message.[10]
  • A muscular condition where there is an alteration of blood pressure (arterial and venous), increases in systolic wave velocity and a decrease in diastolic velocity due to increased outflow resistance can be observed. This will induce an alteration of the morphology and function of the muscular capillaries with ischemia during small active movements, activating the muscular type IV terminations, contributing to myofascial pain.[11]


Myofascial pain syndrome involves about 9 million people in the United States; it is estimated that the same percentage of patients is found in Canada. The distribution of the presence of TPs is similar between men and women, while it is more prevalent in people aged 60 and over. There is no convincing data on the distribution of TPs based on ethnicity or geographical location.[12]


In the presence of a TP, one can find latent ischemia. This ischemia lowers the pH, creating an acidic environment. The latter will decrease the amount of acetylcholinesterase (AChE), while it will increase the effectiveness of action of acetylcholine (ACh), allowing prolonged muscle contraction.[11] In such an altered environment, the release of nociceptive substances such as calcitonin gene-related peptide (CGRP) is stimulated; the latter will create a loop, further stimulating the release of ACh and decreasing the effectiveness of AChE. Not only. CGRP can increase the number of receptors for ACh, implementing muscle contraction and the formation of TPs.[11]

The amount of ATP within a TP is decreased. The lack of muscle relaxation does not allow the calcium pump (Calcium ATPase) to withdraw the calcium present in the muscle fibers, with calcium (Ca2 +) accumulation. If calcium is not withdrawn completely from the cytoplasm, it becomes cytotoxic to the contractile cell, stimulating an inflammatory environment with bradykinin, CGRP, tumor necrosis factor alpha, substance P, inflammatory interleukins (IL-6, IL-8, IL-1beta), norepinephrine and serotonin, urging the sending of painful information to the nervous system.[11][13]

According to a recent theory, TPs may derive nociceptive afferents or subcutaneous accessory pain system (SAPS), which would reach the spinal cord through the dorsal branches.[14] This theory could be confirmed by the fact that cutaneous silent period (CSP), which evaluates the cutaneous sensory system of a cutaneous nerve, presents abnormal values over the musculature where TPs reside.[15] This suggests a dysfunction of the spinal and supraspinal pathways. The concept of altered electrical activity of the skin and the afferents coming from the TPs could explain the altered emotional state in patients with the myofascial syndrome (anxiety and depression).[16] There is a close relationship between the epidermis (ectodermal embryological derivation) and the limbic areas of the brain in a bi-directional way.[17] A human model study showed a reduction in the gray matter of the limbic area (thalamus, cingulate gyrus, insula, and parahippocampal gyrus), in patients with myofascial pain syndrome.[18] This means that in the light of the data, in the presence of a patient with TPs, one must also consider the skin in the treatment of myofascial pain.

Continuous nociceptive afferents from the myofascial system could cause structural and functional changes of the central nervous system (CNS), starting from the spinal cord due to inflammatory substances, leading to changes in medullary neurons (an increase of neuronal excitability) and then changes centrally.[12] This mechanism would provoke a central sensitization, with a lack of inhibition of the descending pathways for pain control, perpetuating inflammation and the formation of TPs.[12]


Muscle cells in TPs appear rounded and not uniform, curved in the middle and thinner at the periphery; infiltrations of inflammatory cells are shown.[19] There are fibers consumed and disorganized, with a reduced number of mitochondria. The thickness of the Z line of sarcomeres is thinner, with a wider band A and with the absence of band I. The muscle cell is less elastic, with damage to proteins such as desmin, titin, and nebulin; the volume of capillaries is reduced.[19]

Blood erythrocytes in patients with TPs show a lack of antioxidant substances, such as selenium and zinc. This could mean a more constant oxidative status that would stimulate a systemic inflammatory environment, but further studies are necessary to draw definitive conclusions.[20]

History and Physical

Myofascial pain is a clinical problem in which there is no standard approach for evaluation or treatment. The previous term to show TPs was "fibrositis," a term sought to describe an inflammation of the connective tissue that covered the muscle tissue. For many clinicians, the confirmation that these are trigger points is multiple painful areas in multiple muscle areas. TPs cause a general weakness of the muscle, as well as a limitation of the range of motion; a further confirmation of myofascial pain is muscular nodules for not less than 1 year.[21]

The first who described tissue myofascial pain was Guillaume de Baillou in 1600. In 1816, Balfour added some annotations, such as "thickenings" and "nodular tumors."[21] In 1843, Froriep described the TPs as an accumulation of painful connective tissue. In 1904, Gowers wrote that the TPs were accumulations of inflamed connective tissue responsible for creating these painful nodules. In 1919, Schade proposed the term "myogeloses" to show a high viscosity nodular muscle structure.

In the mid-1900s, some scientists identified painful local areas which, if stimulated (hypertonic saline), produced reported pain.[21] Janet Travell was inspired by these studies, and together with Rinzler coined the term "myofascial trigger points." Later, David Simons and Travell wrote books that after more than 40 years ago and their beliefs about TPs is still clinically applicable.

Currently, the causes of the presence of TPs are only speculative, as well as the correct evaluative and therapeutic approach.


Several diagnostic tools are available to assess the presence of trigger points, but there is no agreement on the results.[9]

  • Ultrasound imaging: Ultrasound is often used to analyze the thickness of the muscle nodule and the sliding of the various tissue layers as well as the stiffness of the TP. Some studies analyzed the TPs with ultrasound elastography by Doppler variance, inducing with an external vibration instrument. The vibrations brought to light the less elastic area, with focal and hypoechoic images, and specific patterns of blood waves to the muscle; they also highlighted latent and active triggers.[22]
  • Micro-dialysis: This method is used to measure inflammatory molecules in active TPs, such as bradykinin, substance P, tumor necrosis factor alpha, CGRP, interleukin 1 beta, serotonin, interleukin 6 and 8, norepinephrine.[22]
  • Electromyography: To evaluate the electrical activity of active and latent TPs, with an immobile patient or with the patient actively moving the muscles, respectively. Generally, the latent TPs have a wider electromyographic spectrum with active movement, compared to the musculature in the absence of latent TPs. The active TPs show a more active electric spectrum than the musculature in the absence of active TPs and with higher contracted fatigue indices.[22]
  • Infrared thermography: This tool is used to assess skin temperature and TPs areas, but there seems to be no consensus on results.[22]
  • Magnetic resonance imaging: Even with this diagnostic mode, there is no consensus on the validity of the results obtained.[22]

Treatment / Management



  • Non-steroidal anti-inflammatory drugs are often utilized by clinicians to manage patients with myofascial pain.  These medications are available in both oral and topical formulations although there is no scientific evidence to validate their use.[23]

Muscle relaxants

  • Muscle relaxants (cyclobenzaprine, tizanidine) act on the central nervous system to reduce the sensation of pain; they are prescribed when the patient needs to sleep, relieving muscular pain. However, there is no scientific evidence in the literature for their use as a treatment for TPs.[23]


  • Benzodiazepines such as clonazepam and diazepam have several side effects (ataxia, cognitive decline, depression), and although a study showed good results to treat TPs, it is not feasible to follow such a long-term therapeutic approach.[23]


  • Antidepressant drugs (tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, selective serotonin reuptake inhibitors) are used in the presence of a combination of mood disorders and active TPs; no significant studies show their effectiveness as a singular treatment.[23]

Lidocaine patches

  • A transdermal local application of lidocaine has fewer adverse effects than a needle infiltration, and in one study, its local application showed improvements in the pain sensation of TPs. Larger studies are lacking.[23]


  • Using botulinum toxin to improve the contracted and painful areas does not yet have a uniform consensus in the literature.[23]

Non-pharmacological modalities

Exercise/Physical therapy/Postural regiments

  • Active and constant physical exercise is a winning weapon on many aspects of myofascial pain; improves the range of motion, mood and raises the pain threshold. One of the exercises to be prescribed is stretching, lengthening the contracted muscular components of the TPs and may prevent the appearance of other painful areas.[23]
  • Postural rehabilitation is another strategy to use because, with myofascial syndrome, motor patterns are altered, perpetrating TPs. Controlling the body posture means restoring adequate motor coordination.[23]
  • All non-pharmacological treatments to reduce a stressful lifestyle (yoga, meditation, behavioral therapy, acupuncture) help to reduce muscle tone, promoting an increase in the pain threshold.


  • The use of ultrasound seems to favor the decline of pain of active TPs, even if the benefits are temporally limited.[23]

Dry Needling

  • The use of dry needling would seem, in some studies, to show positive results to reduce myofascial pain, probably acting on the cutaneous type A-delta fibers.[23] We await further studies.

Osteopathic Manipulative Therapy (OMT)

  • The osteopathic approach to the treatment of TPs seems to be positive, but there are no large-scale studies and with standardized techniques for objective comparison.[24][25]

Differential Diagnosis

The painful myofascial syndrome is difficult to identify as a primary cause in a symptomatic picture where local and reported pain exists. According to a recent study, there are no specific muscle areas where TPs always appear.[26] Confirmation of the diagnosis of the presence of TPs should include three signs simultaneously: muscle stiffness or spasms; a limited range of motion; painful symptoms accentuated by stress and / or palpable taut band areas. The symptoms must have been present for at least 3 months.[6][12] It is better if, in addition to the palpation, some instrumental investigation is combined, with ultrasound. Once the TPs are localized, they should be palpated again, because the contracted muscular areas do not move, to confirm the stable presence of these nodules.


Generally, if the patient is diagnosed appropriately and follows the indications of specialized personnel, the correlated symptoms decrease considerably, and pain diminishes.[27]


Undesirable effects of drug therapies may occur if the patient does not follow the doctor's instructions carefully. Similarly, if the approach to physical activity does not follow certain rules set by competent personnel, muscle trauma may occur.

Deterrence and Patient Education

If the causes are identified, it is necessary to explain to the patient that the motivations that led to myofascial syndrome must be changed. For example, if the patient is anxious at work or during daily activities, they require strategies to relax, perhaps with deep breathing or the learning other relaxation techniques with the help of a psychologist. If the pain is from a poor diet, it is necessary to teach the patient to consume a more balanced diet. If repetitive movements cause the presence of TPs, encourage the patient to perform physical activity, including stretching. A sleep disorder may lead to increased muscle tension, resulting in the formation of TPs. In this case, it is necessary to adopt strategies to improve the quality of sleep.

Enhancing Healthcare Team Outcomes

In diagnosing and treating myofascial syndrome, many professionals should interact for the patient's health. The doctor or nurse practitioner make the diagnosis, and based on the etiology, the patient will be directed to specialists, for example, the physiotherapist, the osteopath, the psychologist, and the nutritionist. It will be an interprofessional team that treats the patient because the patient needs physical, psychological, and nutritional support. Pharmacists should be included as part of the team to assure that no drug-drug interactions occur involving pain management. The clinician should not only examine painful areas but all aspects of the patient's health.


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