Myofascial Pain

Etiology

When considering the etiology of myofascial pain, one must remember that the myofascial compartment is also constituted by the soft tissue that transports fluids (blood and lymph) and action potentials (afferent and efferent nerves). Vascular and nerve pathways can be a source of pain because they are innervated. The liquid fascia (blood and lymph) can be a source of pain because changes in flow velocity, direction, and type of flow, can affect surrounding tissues, leading to myofascial pain.

The cause of myofascial pain is not fully understood. It may be due to one or more of the hypothesized causes given below:

• Constant microtrauma to the muscle system can increase oxidative metabolism and quickly depletes cellular energy reserves (ATP). This altered mechano-metabolic environment increases nociceptive sensation, 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 the first phase, and central sensitization in the second temporal phase.[6]
• The presence of trigger points (TPs) may result from altering the synaptic plate of muscle fibers. An increase in acetylcholine (Ach) concentration with consequent uncontrolled release from the motor endplate causes continued contraction of the muscle fibers in the absence of any central innervation. This constant contraction would deplete the tissue of ATP and cause the release of pro-inflammatory substances and the creation of TPs.[6]
• In the presence of a constantly altered mechano-metabolic environment, there is a change in the connective tissue that makes up the myofascial system. The fibroblasts are transformed into myofibroblasts, contributing to the shortening of surrounding tissue and an increase in tone. The receptors present within the fascia can be transformed into nociceptors and become sensitive to mechanical stimuli (allodynia or mechanical hyperalgesia). We know that the myofascial system can carry neural signals, and any alteration in the connective tissue structure can alter the polarization of muscle fibers, leading to spontaneous muscle contraction.[8][9]
• Hyaluronan (HA) is a component of glycosaminoglycan polymer found in the extracellular matrix. Any change in the mechano-metabolic environment causing HA to change its properties creates a more viscous extracellular matrix. This causes the fascia to have difficulty sliding between layers, making muscle contraction harder.[10] The nerve endings of the fascia in the most viscous area stretches, becoming constantly activated, creating a trigger point.[11]
• An alteration of blood flow (an increase in systolic wave velocity and decreased diastolic velocity due to increased outflow resistance) may cause myofascial pain. The change in flow velocity induces an alteration in the morphology and function of the muscular capillaries, leading to ischemia during small active movements. This activates type IV nerve endings, contributing to myofascial pain.[12]

Epidemiology

The prevalence of myofascial pain syndrome in the United States is about 9 million, and it is estimated that the same percentage of patients is found in Canada. Myofascial pain syndrome affects men and women equally, while it is more prevalent in people greater than 6o years of age. There is no convincing data to suggest a relationship between myofascial pain and ethnicity or geographical location.[13]

Pathophysiology

To understand and treat myofascial pain, it is important to know the pathological processes behind this syndrome. The myofascial trigger point is a site of latent ischemia, which could explain the cause of pain. This ischemia lowers the pH, creating an acidic environment in the myofascial compartment. This decreases levels of acetylcholinesterase (AChE) while it increases the effectiveness of acetylcholine (ACh), hence causing prolonged muscle contraction.[12] In this altered environment, the release of nociceptive substances such as calcitonin gene-related peptide (CGRP) results in the increased number of ACh receptors and ACh release while decreasing the effectiveness of AChE.[12]

The amount of ATP within a TP is decreased. Ischemia causes decreased ATP leading to a lack of muscle relaxation (ATP depletion prevents the calcium pump - calcium ATPase) from withdrawing the calcium present in the muscle fibers. This leads to calcium (Ca2+) accumulation within the myocytes. If calcium is not withdrawn completely from the cytoplasm, it becomes cytotoxic, stimulating inflammatory mediators like bradykinin, CGRP, tumor necrosis factor-alpha, substance P, inflammatory interleukins (IL-6, IL-8, IL-1beta), norepinephrine, and serotonin. Such inflammatory substances cause increased nociceptive sensitization that results in severe pain.[12][14]

According to a recent theory, TPs may derive nociceptive afferents via the subcutaneous accessory pain system (SAPS), which is an extra-innervation pathway to the spinal cord through the dorsal rami.[15] Another theory states that myofascial pain could be due to dysfunction of spinal and supraspinal pathways. The cutaneous silent period (CSP) is defined as a brief interruption of voluntary action after strong sensory stimulation. It is useful for evaluating features of the sensory nervous system that are poorly assessed by other electrodiagnostic studies, as well as the spinal and supraspinal pathways. Abnormal CSP parameters in patients with myofascial pain may suggest a problem with spinal or supraspinal pathways.[16] A 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.[17] 

Nociceptive afferent signals from the myofascial system could cause structural and functional changes of the central nervous system (CNS), starting from the spinal cord (due to an accumulation of inflammatory substances), causing changes in medullary neurons (increase in neuronal excitability) with centrifugal progression.[13] This mechanism would provoke central sensitization with a lack of inhibition of the descending pain inhibitory pathways, perpetuating inflammation and the formation of TPs.[13]

Histopathology

Myocytes in TPs are non-uniformly distributed, rounded in the middle, and thinner at the periphery with a reduced number of mitochondria and accumulation of inflammatory cells.[18] The thickness of the Z line of sarcomeres is smaller, with a wider band A and with the absence of band I. These muscle cells are less elastic with damage to proteins such as desmin, titin, and nebulin, and reduced volume of capillaries.[18]

Erythrocytes in patients with myofascial pain show a lack of antioxidants, such as selenium and zinc. This causes greater oxidative stress that would stimulate a systemic inflammatory response, but further studies are necessary to draw definitive conclusions.[19]

History and Physical

Myofascial pain syndrome comprises both acute and chronic pain. The pain experienced in this syndrome is usually dull aching and poorly localized, indistinguishable from other causes of somatic and visceral pain. Sensory paresthesias or dysesthesias may accompany myofascial pain occasionally. Sometimes, the pain produced by this condition can be felt at a point away from the actual disease process. It may persist many months or years after the insult was caused, even if the initiating event is resolved. Constricting myofascial taut bands may cause entrapment of the nervous component of the myofascial system, leading to further pain and disability. 

Myofascial pain syndrome is diagnosed by the presence of myofascial trigger points and associated pain. Myofascial trigger points are located by palpation of the tender or painful areas of the patient. A trigger point is defined by the presence of a tight band that is palpable within the muscle tissue, which through practice and experience can be palpated easily, usually in all types of muscles, either superficial or deep.  Such muscles that contain trigger points are non-uniform, having heterogeneous areas consisting of soft, firm, or hard consistency rather than uniform homogeneous consistency. On contraction of the trigger points during daily activity, the pain experienced by the patient is usually exquisite and localized. Sometimes taut bands are not painful to palpation but can alter the normal sequence of muscle activation. The correct method of palpation of the trigger points consists of palpating the muscle perpendicular to the direction of the muscle fibers.[20]

A Delphi study conducted in 2017 proposed that at least two of the following criteria must be positive for trigger point diagnosis: the presence of a taut band, a hypersensitive spot, and referred pain. The pain referred from a myofascial trigger point causes different sensory sensations that include pain traveling to a distant area, deep pain, dull aching, tingling, or burning pain.[20]

Evaluation

Several diagnostic tools are available to assess the presence of trigger points with individual advantages.[10]

• Ultrasound imaging: Ultrasound is often used to analyze the thickness and consistency of muscle nodules and the sliding of the various tissue layers. Some studies analyzed TPs using ultrasound elastography by doppler variance imaging while inducing vibrations with a handheld vibrator. Myofascial trigger points appear as focal and hypoechoic nodules, with decreased vibration amplitude. (indicates increased stiffness and modified blood supply compared to normal tissue)[21]
• Micro-dialysis: This method is used to measure inflammatory mediators in TPs such as bradykinin, substance P, tumor necrosis factor-alpha, CGRP, interleukin 1 beta, serotonin, interleukin 6 and 8, and norepinephrine.[21]
• Electromyography: This is used to evaluate the electrical activity of active and latent TPs (test is done both at rest and during active motion). Generally, the TPs have increased electromyographic activity with synergistic muscle contraction compared to the normal muscles.[21]
• Infrared thermography: This tool is used to assess skin temperature in TPs areas. At present, it is used as an auxiliary test due to conflicting results.[21]
• Magnetic resonance elastography: At present, there is no consensus on the validity of results obtained from MRE because of its low sensitivity.[21]

Treatment / Management

Pharmacotherapy

NSAIDs

• Non-steroidal anti-inflammatory drugs are often used by clinicians to symptomatically 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.[22]

Muscle Relaxants

• Muscle relaxants (cyclobenzaprine, tizanidine) act on the central nervous system to reduce central pain stimulation. However, there is no scientific evidence in the literature for their use as a treatment for TPs.[22]

Benzodiazepines

• Benzodiazepines such as clonazepam and diazepam have several side effects. (ataxia, cognitive decline, and depression) Although a study showed promising results of benzodiazepines in treating TPs, it was not feasible to follow such a long-term therapeutic trial because of the side effects of Benzodiazepines.[22]

Antidepressants

• Antidepressant drugs (tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and selective serotonin reuptake inhibitors) are used for relieving myofascial pain in the presence of mood disorders. Several recent studies support the use of amitriptyline in the treatment of myofascial pain. Nortryptyline has also been successful in some studies.[22]

Lidocaine Patches

• A transdermal patch of lidocaine has fewer adverse effects than a needle infiltration. One study showed that transdermal patches decreased pain at TPs. Larger studies are lacking at present.[22]

Botox

• Botulinum toxin targets central and peripheral nerve endings. It blocks the release of ACh from the nerve endings and hence decreases muscle spasm at TPs. Studies on the efficacy of botulinum toxin in reducing myofascial pain are mixed.[22]

Non-pharmacological Modalities

Exercise/Physical therapy/Postural Regiments

• Active and consistent physical exercise is an effective strategy in the treatment of myofascial pain. It improves the range of motion, mood, and pain threshold. One of the exercises prescribed for myofascial pain is stretching exercises which lengthens the myofascial compartments containing the TPs and may prevent the further appearance of other tender areas.[22]
• A repeated load in undesirable positions predispose to muscle injury and may cause microtrauma, increasing the risk of developing myofascial pain. Hence postural rehabilitation is another strategy that can be used for this syndrome. [22]
• All non-pharmacological measures that reduce stress (yoga, meditation, behavioral therapy, and acupuncture) help reduce muscle tone, promoting an increase in the pain threshold.

Ultrasound

• Ultrasound functions by applying mechanical and thermal energy to underlying connective tissue, improving circulation, elasticity, and metabolism. A few studies show the usefulness of ultrasound to decrease the pain of active TPs even though the benefits are temporary.[22]

Dry Needling

• Dry needling involves the insertion of a needle directly into the trigger points, which reduces myofascial pain. It is one of the quickest ways to inactivate TPs. The use of dry needling seems promising in some studies with patients diagnosed with myofascial pain. It is thought to act on the cutaneous type A-delta fibers.[22] 

Manipulative Therapy (OMT)

• The manipulation of joints in the treatment of TPs has been observed to be effective, but there are no randomized studies to prove its efficacy at present.[23][24]
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Differential Diagnosis

Fibromyalgia could be confused with the presence of myofascial pain; some studies highlight an alteration of the connective tissue with the stem cells that produce adipose tissue. The latter could cause an inflammatory environment and local pain.[25] Fibromyalgia is hardly localized; this is already a good indication of differential diagnosis.

Another syndrome that can be poorly framed with respect to myofascial syndrome is chronic pelvic pain. The latter is a condition that must be present from 6 months onwards and not necessarily influenced by movements or the presence of menstruation (in women). It is necessary to understand if there are organic dysfunctions or only the musculature is involved through ultrasound examinations (the easiest way to make a differential diagnosis).[26]

The temporomandibular joint could be involved in myofascial pain but could also be involved in a referred pain pattern. If trigger points do not improve after a manual or pharmacological approach, it could be a symptom of cardiac ischemia.[27]

Throat or neck pain, if unilateral, could be caused by Eagle's Syndrome. Pain should improve with tissue treatment; if this does not happen, the causes must be investigated.[28]

Inflammations of tendons or inflammations of purely connective formations (fasciitis, tendinopathies, and more) have a very specific anatomical area of interest that can be delimited with palpation and do not have more tense areas than other areas of the same tissue.[29]Different causes and pathologies can cause the presence of myofascial pain, where, in some cases, there may be perpetuating factors that have a feed-forward effect on myofascial pain.

There are perpetuating mechanical factors such as:

• Scoliosis
• Limb dysmetria
• Joint hypermobility
• Muscle hypertrophy
• Repetitive microtraumas
• Spondylotic radiculopathy

There are systemic or metabolic perpetuating factors:

• Hypothyroidism
• Iron deficiency
• Vitamin D insufficiency
• Vitamin C deficiency
• Vitamin B12 insufficiency

Psychosocial perpetuating factors:

• Stress
• Anxiety

Other possible perpetuating factors:

• Infectious diseases
• Parasitic diseases (e.g., Lyme disease)
• Rheumatic polymyalgia
• Use of drugs such as statins
• Hyperalgesia
• Allodynia

Prognosis

Myofascial pain syndrome usually resolves with consistent treatment and regular follow-up. However, a majority of patients with this condition suffer from this problem for decades. Long-term morbidity is lowest when an interprofessional team consisting of well-trained physicians, nurses, and physiotherapists treat such patients and constantly monitor the response to various therapies employed.

Complications

Myofascial pain syndrome can cause a reduction in the quality of life. Long-term pain is usually associated with mood disorders (depression and anxiety). It can decrease the mobility of the patient, decreasing daily activity, which further precipitates the condition.

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.