Abstract
Myofascial pain syndrome (MPS) is a painful disorder characterized by the presence of myofascial trigger points (MTrPs), distinct sensitive spots in a palpable taut band of skeletal muscle fibers that produce local and referred pain. The patient with MPS generally complains about dull or achy pain, sometimes poorly localized, particularly occurring during repetitive activities or during activities requiring sustained postures. Symptoms are exacerbated with digital pressure over tender areas of muscle with reproduction of the patient’s usual pain. To clinically identify MTrPs, the clinician palpates a localized tender spot in a nodular portion of a taut, rope-like band of muscle fibers. Manual pressure over a trigger point should elicit pain at that area and may also elicit pain at a distant site (referred pain) from the point under the fingertip. The diagnosis is made primarily by history and physical examination. Initial treatment includes therapeutic modalities. Nonsteroidal anti-inflammatory drugs and other pharmacotherapy should be used in conjunction with an active treatment program. Physical therapy techniques that focus on correction of muscle shortening by targeted stretching, strengthening of affected muscles, and correction of aggravating postural and biomechanical factors are generally considered to be the most effective treatment of MPS. Other treatment options include trigger point injections, dry needling, acupuncture, and the use of botulinum toxin therapy.
Definition
Myofascial pain syndrome (MPS) is a painful disorder characterized by the presence of myofascial trigger points (MTrPs), distinct sensitive spots in a palpable taut band of skeletal muscle fibers that produce local and referred pain. Thus, MPS is characterized by both a motor abnormality (a taut or hard band within the muscle) and a sensory abnormality (tenderness and referred pain) ( Fig. 105.1 ). In addition to pain, the disorder is accompanied by referred autonomic phenomena as well as by anxiety and depression. The pathophysiologic mechanism of MPS is not clearly understood, in part because of the scarcity of reliable valid studies. Moreover, concomitant disorders and frequent behavioral and psychosocial contributing factors in patients with MPS contribute to the complexity of human studies. Symptoms of MPS are generally associated with physical activities that are thought to contribute to “muscle overload,” either acutely by sudden overload or gradually with prolonged repetitive activity. MPS is reported to have a prevalence ranging from 30% to 93% and to be common in regional musculoskeletal pain syndromes; however, MPS can be classified as regional or generalized. Some authors broaden the definition of myofascial pain to include a regional pain syndrome of any soft tissue origin. Thus, MPS may be considered either a primary disorder causing local or regional pain syndromes or a secondary disorder that occurs as a consequence of some other condition, such as a radiculopathy or spondylosis.
The MTrP is generally considered the hallmark of MPS; therefore, much attention has been given to characteristic features of MTrPs in skeletal muscle. One such feature of the MTrP is the so-called twitch response. This local response is considered a characteristic finding of the MTrP. Mechanical stimulation (“snapping” palpation, pressure, or needle insertion) can elicit a local twitch response that frequently is followed by non-dermatomal, non-myotomal referred pain. The twitch response is accompanied by a burst of electrical activity (“end-plate noise”) within the muscle band that contains the activated trigger point, whereas no activity is seen at other muscle bands. End-plate noise is significantly more prevalent in MTrPs than in sites that lie outside of the MTrP but still within the end-plate zone. This observation has been attributed to a spinal reflex, as the response is abolished by motor nerve ablation or infusion of local anesthetic. Moreover, spinal cord transection above the neurologic level of the MTrP fails to permanently alter the characteristic response.
A number of hypotheses have been put forward to explain the findings observed in MTrPs. One theory proposes that MTrPs are found only at the muscle spindle; however, this idea does not fully explain the electromyographic (EMG) findings recorded at the MTrP. Another theory is related to excessive release of acetylcholine in abnormal end plates, as the EMG activity recorded at the trigger points resembles findings described at the end-plate region. Abnormal and excessive release of acetylcholine shortens sarcomeres and produces a “contraction knot,” which is thought to be the mechanism of MTrP development. Botulinum toxin, an inhibitor of the release of acetylcholine resulting in decreased local muscle contraction, has therefore been studied in the setting of MPS.
Myofascial pain may become persistent, resulting in chronic pain, due to central sensitization processes. Central neurologic processes are increasingly viewed as essential factors in chronic pain syndromes. The medial thalamus is the principal relay of nociceptive input to the anterior cingulate cortex, and persistent stimulation of this pathway by pain in peripheral tissues, such as in chronic myofascial pain, has been demonstrated to change neurons in the cingulate cortex. Thus, persistent pain is associated with long-term changes in the morphology, neurochemistry, and gene expression of the anterior cingulate cortex, which has the most direct connection with autonomic arousal, thereby contributing to the maintenance and exacerbation of pain. In MPS, evidence also suggests that trigger points can sensitize dorsal horn neurons through sustained nociceptive input, resulting in neuronal microstructural alterations. Diffusion kurtosis imaging technique, which is particularly sensitive to neuronal microstructural perturbation, has been studied to monitor the MTrPs-related microstructural alterations induced in neurons due to MPS-related chronic noxious stimuli. When compared to healthy controls, patients with chronic myofascial pain develop abnormalities in the cerebral gray matter and throughout the limbic system (i.e., cingulate gyrus, parahippocampal gyrus, insula, and thalamus). Activation of the limbic system and thalamus contributes to the regulation of skeletal muscle pain and the resulting emotion, mood, and stress response. Therefore, in addition to being a cause of central sensitization, the referred pain phenomenon seen in MPS patients has been thought to be an effect of central sensitization processes. Newer studies further extend this knowledge about the supraspinal effects of MPS. Patients with chronic MPS have been shown to exhibit gray-matter atrophy in the dorsal and ventral prefrontal cortex with the level of atrophy correlating with pain thresholds in patients (the more atrophy, the lower the pain threshold), suggesting the presence of pain disinhibition. Gray-matter atrophy is also noted in the anterior hippocampus, but no evidence was found associating the atrophy with stress. Further research should determine whether the observed atrophy contributes to the chronic pain state or is caused by the ongoing nociceptive input.
Fibromyalgia, a chronic musculoskeletal pain condition that predominantly affects women, is characterized by diffuse muscle pain, fatigue, sleep disturbance, depression, and skin sensitivity (see Chapter 102 ). The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia include three conditions. A widespread pain index (WPI) ≥7 and symptom severity (SS) scale score ≥5 or WPI 3 to 6 and SS scale score ≥9. Secondly, symptoms need to be present at a similar level for at least 3 months. Thirdly, the patient does not have a disorder that would otherwise explain the pain. Treatment of MPS and fibromyalgia is similar, as evidence supports the role of exercise, cognitive-behavioral therapy, education, and social support in the management of both fibromyalgia and chronic MPS. However, there is controversy as to whether fibromyalgia and MPS represent distinct pathologic processes or are descriptive terms of clinical conditions with overlapping pathology. Objective evidence of muscle abnormalities in fibromyalgia has been demonstrated by histologic studies showing disorganization of Z bands and abnormalities in the number and shape of muscle mitochondria. Biochemical studies and magnetic resonance spectroscopy have also shown inconstant abnormalities of adenosine triphosphate and phosphocreatine levels. It is unclear whether these abnormalities are a result of physical deconditioning, which could be relevant to both conditions, or if abnormalities are due to problems in energy metabolism. There are no clear biochemical markers that distinguish patients with fibromyalgia. Thus, whereas the pathogenesis is still unknown, there has been evidence of increased corticotropin-releasing hormone and substance P in the cerebrospinal fluid of fibromyalgia patients as well as increased substance P and interleukins 6 and 8 in their serum. One hypothesis supports the idea that fibromyalgia is an immunoendocrine disorder in which increased release of corticotropin-releasing hormone and substance P from neurons triggers local mast cells to release proinflammatory and neurosensitizing molecules. If there is a pathologic link between fibromyalgia and MPS, this hypothesis fits well with discoveries of neuropeptides found in the muscles of patients with active MTrPs.
Symptoms
The patient with MPS generally complains about dull or achy pain, sometimes poorly localized, particularly occurring during repetitive activities or during activities requiring sustained postures. Symptoms are exacerbated with digital pressure over tender areas of muscle with reproduction of the patient’s usual pain. Symptoms are relieved with rest or cessation of repetitive activities. In contrast, the patient with fibromyalgia typically presents with sleep disturbances, depressed mood, and fatigue.
Physical Examination
The most important part of the physical examination is generally considered to be finding and localizing MTrPs to provide an accurate diagnosis of MPS. Travell & Simons ’ Myofascial Pain and Dysfunction: The Trigger Point Manual is considered the criterion standard reference on locating and treating MTrPs. Active MTrPs, attributed to cause pain, exhibit marked localized tenderness and may refer pain to distant sites, disturb motor function, or produce autonomic changes. Specific clinical training is required to become adept at identifying MTrPs, as evidence suggests that “non-trained” clinicians do not reliably detect the taut band and local twitch response. To clinically identify MTrPs, the clinician palpates a localized tender spot in a nodular portion of a taut, rope-like band of muscle fibers. Manual pressure over a trigger point should elicit pain at that area and may also elicit pain at a distant site (referred pain) from the point under the fingertip ( Fig. 105.2 ). MTrPs, when palpated, should also elicit pain that mirrors the patient’s experience. Applied pressure often reproduces the pain. Insertion of a needle, abrupt palpation, or even a brisk tap with the fingertip directly over the trigger point may induce a brief muscle contraction detectable by the examiner. This rapid contraction of muscle fibers of the ropy taut band is termed a local twitch response. In muscles that move a relatively small mass or are large and superficial (such as the finger extensors or the gluteus maximus), the response is easily seen and may cause the limb to visibly move when the examiner introduces a needle into the trigger point. Localized abnormal response from the autonomic nervous system may cause piloerection, localized sweating, or even regional temperature changes in the skin attributed to altered blood flow. Active and latent MTrP detection by palpation, in hip and thigh areas, has been shown to have moderate to substantial inter- and intra-tester reliability.
Functional Limitations
Similar to fibromyalgia, patients may be limited in their daily activities and exercise tolerance by both pain and fatigue. Unlike fibromyalgia, however, cognitive dysfunction is not a hallmark of MPS. Individuals may have more pain related disability if they report higher pain scores, work at a job that requires heavy physical labor, have poor coping strategies and feel helpless, or are involved in litigation.
Diagnostic Studies
No definitive laboratory test or imaging method is diagnostic of MPS. Thus, diagnosis is made primarily by history and physical examination. Whereas no specific laboratory tests confirm (or refute) a diagnosis of MPS, some tests can be helpful in looking for predisposing conditions, such as hypothyroidism, hypoglycemia, and vitamin deficiencies. Specific tests that may be helpful in this regard include complete blood count, chemistry profile, erythrocyte sedimentation rate, and levels of vitamins C, B 1 , B 6 , B 12 , and folic acid. If clinical features of thyroid disease are present, an assay for thyrotropin may be indicated.
Fibromyalgia
Trochanteric bursitis
Neuropathic pain
Post-exercise muscle soreness
Articular dysfunction
Referred pain
Myopathy
Radiculopathy
Treatment
Initial
Providers should counsel patients on the importance of self-care in the setting of MPS, as relatively simple measures, to include active patient engagement in physical activity and stretching, and more passive therapies such as superficial heat, massage, and non-opioid analgesic use, if warranted, can empower patients to be active participants in treatment. After the consideration for medications that cause muscle pain, such as statins, and systemic illnesses that can cause muscle dysfunction and exacerbate myofascial pain, such as Parkinson disease, patients should be reassured that there are numerous treatment options. Therapeutic modalities such as biofeedback, ultrasound, and massage may be useful in relieving initial pain to allow participation in an active exercise program. Data suggest that the addition of therapeutic physical modalities, such as heat, and various forms of muscle and nerve stimulation, are beneficial in the initial treatment of MPS. Biofeedback, therapeutic ultrasound, transcutaneous electrical nerve stimulation (TENS), and laser therapy are examples of electromedical treatments for MPS. If these are insufficient, MTrP deactivation therapy, which can be accomplished by manual techniques, trigger point injections (TPIs), and/or dry needling (DN), is used to “neutralize” the chronically hyperactive/hypersensitive muscle tissue. Ongoing active patient engagement and participation in a home exercise program, especially to build and maintain muscular resilience, which is particularly relevant in older adults, is an important but often overlooked component of treating MPS.
Acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) may be useful adjuncts to active exercise-based treatment of MPS but are generally considered beneficial when they are used in conjunction with an active treatment program. However, no randomized placebo-controlled clinical trials exist to support efficacy of these medications in this condition. Interestingly, the NSAID diclofenac, when it is injected into the MTrP, was shown to be superior to lidocaine in one small clinical trial. Gabapentin, an anticonvulsant considered to be a neuropathic analgesic, has been shown to be effective in the treatment of MPS. Low-dose amitriptyline is widely used in patients with fibromyalgia and is thought to help improve the patient’s sleep cycle. In MPS, an open trial showed good pharmacotherapeutic response with tricyclic antidepressants (amitriptyline and nortriptyline) and gabapentin, with 54.8% of patients reporting a greater than 50% pain improvement measured via the verbal pain scale. Muscle relaxants may also provide benefit to patients with MPS. For example, cyclobenzaprine hydrochloride, a commonly prescribed muscle relaxant, is indicated as an adjunct to rest and physical therapy for the relief of muscle spasm associated with acute, painful musculoskeletal conditions. In contrast to low-dose (5 mg three times daily) cyclobenzaprine, a higher dose (10 mg three times daily) is associated with more somnolence and dry mouth. Importantly, there does not appear to be a relationship between somnolence and pain relief. A large, multicenter, community-based trial of patients with acute pain and muscle spasm evaluated low-dose cyclobenzaprine (5 mg three times daily) alone compared with combination therapy with two doses of ibuprofen. It is possible that low-dose cyclobenzaprine or high-dose ibuprofen alone may be sufficient to relieve acute musculoskeletal pain. For oral agents, providers should reflect that there is a potential for adverse effects, especially in older adults, and should prescribe these with caution. For a topical medication choice, five percent lidocaine patch compared to placebo has been shown to reduce pain intensity and EMG activity on MTrP in the upper trapezius muscle. Baseline spontaneous pain levels prior to treatment were similar, but after treatment the lidocaine group had significantly lower pain levels. On EMG, those in the lidocaine group had higher maximum muscle contraction. Various other topical medications, such as topical methylsalicylate, menthol, diclofenac, and thiocolchicoside, have favorable safety profiles and can be trialed if warranted.
Rehabilitation
Physical therapy techniques that focus on correction of muscle shortening by targeted stretching, strengthening of affected muscles, and correction of aggravating postural and biomechanical factors are generally considered to be the most effective treatment of MPS. The correction of biomechanical factors may include ergonomic evaluation. Manual therapies include stretching (such as post-isometric relaxation and spray and stretch) and/or massaging therapies (such as ischemic compression and myofascial release). Combined with the correction of postural and biomechanical factors, this rehabilitation approach is supported by a line of evidence examining the relationship between muscle overload and MTrPs, suggesting a direct relationship between exercise and MPS.
A systematic review of a limited number of trials indicates that combined stretching and strengthening exercise has positive small to moderate effects on pain intensity in MPS. The goal for the treatment of MPS is to engage patients in active therapy to prevent the development of chronic pain syndrome and/or to rehabilitate patients from its disabling interacting symptoms if it has developed. Chronic MPS is not a diagnosis but a descriptive term for individuals who not only report persistent pain but also evidence poor coping, self-limitations in functional activities, significant life disruption, and dysfunctional pain behavior. Other common symptoms of chronic pain syndrome related to an accompanying disuse syndrome include the multiple physical systems effects of deconditioning as well as insomnia, fatigue, anxiety, and depression. A central feature of chronic MPS is a disability conviction and resulting avoidance of activity based on the fear that engaging in functional activity will increase pain (fear-avoidance). The critical importance of addressing such a belief is underlined by prior studies indicating that patients’ beliefs about their pain are the best predictors of task performance, medical utilization, and long-term rehabilitation. Preventing the development of such a disability conviction begins by assisting patients to shift from a biomedical perspective, in which there is an ongoing search for the cause of an illness to be “cured” or “fixed,” to a biopsychosocial rehabilitation perspective. This perspective views MPS as a multifactorial condition that need not be disabling if it is actively managed by the patient. Cognitive-behavioral therapy is the psychological approach that focuses on changing dysfunctional beliefs or “schemas” by which individuals process, store, and act on information. For individuals with chronic pain to successfully participate in a functionally oriented rehabilitation approach, they need to understand or to believe the following:
- 1.
The nature of the pain has been thoroughly evaluated, and there is no cure (i.e., surgery or another procedure) for the pain.
- 2.
The rehabilitation approach involving physical activity and conditioning will increase functional capabilities and eventually reduce suffering.
- 3.
The hurt engendered through physical conditioning will not cause harm.
- 4.
Reinjury or worsening of the painful condition is unlikely, and it is in the individual’s best interest to become more functional.
The first point most often can be addressed by the physician in the office, but the critical shift in belief that hurt will not cause harm generally requires the patient to have repeated experiences that contradict the prior life experience that if something hurts, one should stop doing it. For a patient with MPS to exercise consistently and sufficiently to contradict the common sense to avoid pain, an interdisciplinary team approach is often required. In such an approach, the physical therapist educates and guides the patient through a progressive physical reconditioning regimen. The physician periodically reevaluates the patient, reassuring and encouraging the patient that there is no problematic change in condition while adjusting medications to facilitate involvement in the program. Concurrently the psychologist provides training in stress management, pacing, and pain coping strategies. This is often best done in a group setting that normalizes the reactions and experience of the patient and where the social support and encouragement of the patient’s peers is of significant benefit. Ultimately, though, it is the patient’s repeated mild increases in pain without harm, as functioning improves, that change beliefs about pain and fear-avoidance of activity. It is largely for this reason that multidisciplinary pain programs that include a cognitive-behavioral approach have been found to be most effective for individuals with chronic pain on a range of key outcomes. A cognitive-behavioral, functional restoration approach is particularly effective for chronic MPS because, unlike in many other chronic pain conditions, one can be certain that the hurt experienced through increased activity will not only not cause harm but will lead to long-term benefit.
In addition to the cognitive changes noted, patients should be educated on the interacting effects of pain leading to increased sympathetic arousal (“stress response”) further leading to increased muscle tension and increased pain. Patients therefore can reduce pain by reducing their reactivity to pain as well as other stressors in their life. Techniques for doing so include relaxation training, progressive muscle relaxation, mindfulness meditation, and hypnosis. Hypnosis is increasingly being integrated into multidisciplinary treatment approaches: While patients are trained to develop a relaxation response, the provider can also intersperse suggestions to encourage changes in thinking regarding stress and arousal. In other words, hypnosis is a tool that can be used not only to assist patients in reducing their attention to the sensation of pain but, more important, to reduce their affective distress and autonomic reactivity.
Another approach to reducing affective distress and autonomic reactivity in response to pain that has received increasing attention is mindfulness meditation. Mindfulness has been defined as “paying attention in a particular way: on purpose, in the present moment, and nonjudgmentally.” Zeidan and colleagues expanded on this description to operationally define mindfulness as involving “(a) regulated, sustained attention to the moment-to-moment quality and character of sensory, emotional, and cognitive events, (b) the recognition of such events as momentary, fleeting, and changeable (past and future representations of those events being considered cognitive abstractions), and (c) a consequent lack of emotional or cognitive appraisal and/or reactions to these events.” Pragmatically, this tends to involve training in focused attention (Samatha meditation) and open awareness (Vipassana meditation). The patient is taught that such thoughts are momentary and fleeting and that one need not react to them. Whereas mindfulness-based stress reduction has been viewed as the “gold standard,” there have been other variations including mindfulness-based cognitive therapy. For example, brief mindfulness training can have a significant impact on experimentally induced pain and cognition. Although the specific mechanisms remain unclear, accruing evidence indicates that through processes of neuroplasticity, significant changes can occur in brain structures associated with the processing of pain, especially the prefrontal and anterior cingulate cortices. In this way, one can therapeutically use the neuroplasticity of the brain to enhance pain control, in a manner that is the reverse of the central sensitization described earlier.
Procedures
In combination with other therapies, most commonly targeted stretching, interventional techniques aimed at trigger point deactivation can be an effective adjunct in the multidisciplinary management of patients with MPS. MTrP injections, also called TPIs, should be individualized for both the patient and the clinician. Alcohol, if it is used to clean the skin, should be allowed to dry completely to prevent additional pain. Use of operating rooms or special procedure (sterile) rooms equipped with monitoring devices for the purpose of intramuscular injections with small-caliber needles is not necessary. Most patients can be treated safely in an office setting by experienced clinicians. The diagnostic skill required to find active MTrPs depends on considerable innate palpation ability, authoritative training, and extensive clinical experience. Application of TPI begins by determining the equipment needs according to the needs of the patient, the clinician’s training, and the anatomic target for injection. Typically, a 1.0-mL tuberculin-type syringe with ⅝-inch 25-gauge needle is adequate for superficial muscles. For small muscles (e.g., facial muscles), a 1-inch 30-gauge needle is sufficient. For larger muscles, a 1-inch or 11⁄2-inch 25-gauge needle is adequate. After the patient is placed in a position in which the desired muscle can be relaxed, the MTrP is located. The MTrP is generally ascertained by gentle pressure from the end of a fingertip or a ballpoint pen applied at regular 1-cm intervals. The patient is observed closely during the palpation because pressure on the markedly tender MTrP usually causes the patient to jump, to wince, or to cry out. Each muscle has a characteristic elicited referred pain pattern that, for active MTrPs, is familiar to the patient. Thus, the patient will respond that this pressure reproduces the usual pain and, when questioned, will describe painful sensations at a site slightly distant to the point under the examiner’s finger. Once the MTrP has been located, the skin is marked and prepared. The site is injected with no more than 1 mL injectate (usually local anesthetic) per site after negative aspiration for blood. The advancement of the needle to the MTrP may elicit a local twitch response, although a local twitch response is not observed all of the time despite significant improvement of myofascial pain with TPI. Other findings that may help determine the needle entrance to the MTrP are the patient’s confirmation of reproduction of the usual pain pattern and the clinician’s sensation of increased resistance as the needle is advanced from normal muscle tissue to the taut band. The importance of needling during the procedure, in that it appears to reduce hyperactivity of the sympathetic nervous system and irritability of the motor endplate, has also been studied.
DN, usually with a filament needle, is a non-acupuncture Western-based medicine technique used for treating MPS; it was initially recommended by Dr. Travell and remains popular. DN has been evaluated for myofascial pain and has been shown in some studies to be equally as effective as local anesthetic. One meta-analysis of DN shows DN was more effective at increasing range of motion, but was not as effective at reducing pain after 3 to 4 weeks post-procedure. Another study looked at the beneficial effects of DN for the treatment of chronic myofascial pain 6 weeks after treatment. Patients had sustained reduction of pain scores after DN and it appears that early intervention can contribute to sustained clinical response. A systemic review of randomized clinical trials concerning DN found some evidence that DN has demonstrated some positive effect even in the short term. Another systematic review and meta-analysis looked at DN for MTrPs in the neck and shoulder and found that DN can be recommended; it has a positive effect for both short- and medium-term durations post-procedure. There is also evidence that DN can be helpful for trigger points in multiple body regions.
Acupuncture, an Eastern medicine technique using a filament needle to stimulate points on the body, typically along meridian lines, is also popular for the treatment of myofascial pain, as it is thought to inactivate the neural loop of the trigger point, reducing pain and muscular hypertonicity. In single studies, manual acupuncture (MA) and electro-acupuncture, which passes an electric current through the needle, have been shown to decrease the pain and intensity of MPS. A systematic review and meta-analysis of MA for MPS found that with stimulation of MTrPs, MA can help with pain relief and muscle irritability, though further studies will need to determine the optimal number of treatments. A systematic review revealed that despite weak scientific evidence, acupuncture appears to help reduce pain in myofascial temporomandibular disorder.
Botulinum toxin should be considered for MPS if other traditional therapies fail. Khalifeh et al. conducted a systematic review of the efficacy of botulinum toxin A (BoTN-A) in the treatment of MPS. They found that pain was reduced significantly in the group that received BoTN-A at 2 to 6 months post-procedure. Botulinum toxin has also been shown to be helpful for pericranial myofascial pain. Those who responded had a greater than 70% reduction in headache days, greater than 50% reduction in cervical pain and muscle tenderness, and an 81% decrease in triptan use. Botulinum toxin injection can also be combined with physical therapy, as is typically employed in the setting of myofascial pelvic pain. Patients with trigger points in the iliococcygeus, puborectalis, obturator internus, and rectus muscles were injected with onabotulinumtoxinA and underwent soft tissue myofascial release under anesthesia. After treatment, these patients responded with 58% lower pain scores and less trigger points.
In the treatment of MPS, other than TPIs, interventional procedures (e.g., epidural steroid injections, sacroiliac joint injections, and medial branch blocks) are usually not employed. However, at times, myofascial pain is associated with or caused by other underlying conditions. For instance, lumbar myofascial pain may also have some component of lumbar facet arthropathy. Lumbar medial branch blocks and radiofrequency denervation, alone or in combination with the other therapies (e.g., muscle relaxants), may work together to relieve myofascial pain. Therefore, underlying disease may respond to more aggressive interventional methods and in turn synergistically provide pain relief to select patients with MPS.
Technology
The diagnosis of MPS relies on a thorough history and examination. However, there are new technologies that are being studied to help in the diagnosis. Ultrasound imaging has been used to assess MTrPs. In a study, the sternocleidomastoid muscle was assessed and a force gauge was attached to a transducer to monitor muscle stress levels. Ultrasound images were taken of the muscle with and without stress. Measured strain and the elastic (Young’s) modulus were then determined. In this manner, it has been found that MTrPs were stiffer than normal parts of the muscle. For treatment, therapeutic ultrasound is argued to stimulate the subdermal tissue using high frequency waves; these would potentially shorten the healing process by improved vascular flow followed by a secondary reduction in inflammation and pain. Ultrasound has therefore been looked at as a potential treatment for MPS. However, a systematic review and meta-analysis revealed that the current data do not support ultrasound as an effective method to treat MPS. Therapeutic ultrasound, with and without stretching, however, has been found to be superior to muscle stretching alone and continuous ultrasound has been shown to be superior to pulsed ultrasound in reducing pain at rest in MPS. Other electromedical technologies, such as surface electromyographic (SEMG) biofeedback, TENS use, and low-level laser therapy (LLLT) have some evidence of positive beneficial effects. Although SEMG has not been specifically studied for the treatment of MPS, SEMG biofeedback utilizes EMG to measure muscle activity, providing patients with feedback to self-reduce muscle tension. TENS has been widely employed to treatment of pain, making use of stimulating the release of endogenous opioids and exciting non-nociceptive afferent fibers to inhibit nociceptive input via the gate control theory. In a study, high frequency, high intensity TENS was found to be effective for reducing myofascial pain but not by altering local trigger point sensitivity. Ultrasound has been shown to be more effective than TENS in improving analgesic response and cervical range of motion in patients with upper trapezius trigger points. LLLT utilizes a low-powered laser, typically limited to a wavelength between 600 and 1000 nm, applied to the body surface with the aim of cellular regeneration and pain relief. LLLT therapy and intramuscular electrical stimulation (IMS) have yet to be validated, and the literature is often conflicting, but some studies show efficacy in treating MPS: A randomized controlled study evaluated use of LLLT with stretching versus IMS with stretching and found statistically significant improvements in pain for the groups that combined stretching with either LLLT or IMS when compared to either the control or stretching alone groups. Although more studies are needed, these are low cost and safe modalities that seem to be reasonable approaches to MPS.
Biomarkers (such as bradykinin, substance P, calcitonin gene-related peptide, tumor necrosis factor-alpha, interleukin 1beta [IL-1beta], IL-8, IL-6, serotonin, and norepinpherine) may provide an objective test for MTrP identification; however, sample testing and technology for biomarkers is not yet developed in the setting of MPS and may not be efficient given that MTrPs can be diagnosed by manual palpation.
Other newer technology treatment options for MPS include extracorporeal shockwave treatment (ESWT). ESWT may benefit MPS by increased perfusion, enhanced angiogenesis, and by altering the pain signaling in ischemic MPS tissues. Furthermore, free nerve endings degenerate after the application of ESWT, which produces a transient dysfunction in nerve excitability at the neuromuscular junction, which reduces pain; an additional possible explanation for pain improvement in MPS with ESWT could be that the shockwaves break up actin-myosin links at the trigger points.
A randomized, double blind, factorial design and controlled placebo-sham clinical trial has looked at the effect of deep intramuscular stimulation and repetitive transcranial magnetic stimulation to treat chronic MPS. The results revealed that both treatments provide some pain relief, there was no evidence of synergy. Other newer analgesic technologies, such as virtual reality technology, have not yet been studied in MPS but may benefit MPS patients through immersive distraction.
Surgery
Surgery is not indicated in the treatment of patients with MPS.
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