Abstract
Myofascial pain (MP) is a soft tissue pain syndrome (STP) with local and referred pain arising from trigger points (TrPs). Local STPs include bursitis, tenosynovitis, and enthesopathies. Regional STPs include myofascial pain syndrome (MPS) and complex regional pain syndrome (types I and II). Generalized STPs involve fibromyalgia syndrome (FMS), chronic fatigue syndrome, and hypermobility syndromes. Regional STPs such as MPS are limited in anatomic distribution over a specific region or quadrant of the body. Myofascial pain can occur independent of other pain generators (primary myofascial pain). Alternatively, MP often coexists with or is secondary to other acute and chronic painful musculoskeletal conditions. MP is most effectively treated with a multimodal therapeutic regimen including injection, physical therapy, postural or ergonomic correction, and treatment of underlying musculoskeletal pain generators. MPS can often be refractory to treatment. If the patient is unable to participate in an active functional rehabilitation program due to the limitations of pain, then a comprehensive approach should be considered. A multidisciplinary approach may include psychological counseling for coping strategies, relaxation techniques and biofeedback, cognitive behavioral therapy, and complementary and alternative medicine in addition to standard medical evaluation and management. Despite an abundance of clinical experience and successful outcomes, we need better-designed, short- and long-term outcome studies on myofascial pain to assess the efficacy and efficiency of traditional and emerging therapies.
Keywords
injection therapy, myofascial pain syndrome, pharmacotherapy, physical modalities, trigger points
Myofascial pain (MP) is a soft tissue pain syndrome (STP) with local and referred pain arising from trigger points (TrPs). The term muscular rheumatism of Sir William Osler’s time gradually gave way to the term nonarticular rheumatism, and more recently, to the newer term soft tissue pain syndromes, which can be abbreviated as STP. Local STPs include bursitis (subacromial, olecranon, trochanteric, prepatellar, and pes anserine), tenosynovitis (biceps, supraspinatus, infrapatellar, and achilles), and enthesopathies (lateral epicondylitis and medial epicondylitis). Regional STPs include myofascial pain syndrome (MPS) (MPS involving muscles of the trunk and extremities), myofascial pain dysfunction syndrome (MPS involving facial muscles), and complex regional pain syndrome (types I and II). Generalized STPs involve fibromyalgia syndrome (FMS), chronic fatigue syndrome (FMS-like when widespread body pain present), and hypermobility syndromes. Regional STPs such as MP are limited in anatomic distribution over a specific region or quadrant of the body.
TrPs generating MP are localized painful areas of skeletal muscle containing taut bands that can be exquisitely sensitive to digital pressure. TrPs may be active or latent. Active TrPs are present in patients with painful regional conditions. Latent TrPs are asymptomatic but may be revealed by deep palpation on physical examination. Latent TrPs have been found in the shoulder girdle muscles of 45% to 55% of healthy young adults.
MP can occur independent of other pain generators (primary MP). Alternatively, MP often coexists with or is secondary to other acute and chronic painful musculoskeletal conditions including (1) head and neck pain (temporomandibular disorders, cervical degenerative disc disease, cervical facet arthropathy, neck pain after whiplash injury, cervicobrachial syndrome, cervicogenic and chronic tension-type headache), (2) thoracolumbar back pain (degenerative disc disease, kyphosis, scoliosis, lumbar facet arthropathy), (3) pelvic pain, and (4) upper and lower extremity pain. MP is most effectively treated with a multimodal therapeutic regimen including injection, physical therapy, postural or ergonomic correction, and treatment of underlying musculoskeletal pain generators.
Prevalence
Reliably establishing the prevalence of MPS proves to be challenging, as there are no widely accepted diagnostic criteria. Few epidemiologic studies have been published, however, and the reported prevalence of MPS ranges from 20% to 95% of patients presenting with musculoskeletal pain at general medical clinics and pain management centers. One study designed to evaluate the prevalence of MPS in an academic internal medicine practice was performed by Skootsky and colleagues. Of 201 patients initially screened, 54 patients had initial complaints of musculoskeletal pain and were studied further. Those that had pain conditions potentially related to MPS had a careful TrP examination performed. MPS was diagnosed when digital pressure on the TrPs for a standardized time period intensified regional pain, and the pain referral pattern corresponded with established referral maps. Ultimately, 16 patients were diagnosed with MPS, representing 30% of patients with musculoskeletal pain and 8% of the 201 originally screened patients. More recently, a study by Chen and Nizar reported an MPS prevalence of 63.5% ( n = 80/126) among chronic back pain patients, wherein MPS was diagnosed using the following criteria: the presence of a trigger point, reproducible pain, taut band, referred pain, and jump sign. Interestingly, they report that the majority of MPS (81.2%) in their population was secondary to other musculoskeletal or medical causes as opposed to primary MPS.
MPS can be commonly found in select patient populations. MPS is more commonly seen in patients with chronic tension-type headache, temporomandibular disorders, pain in the face–jaw region, and in postwhiplash syndrome than in the general patient population. One cross-sectional study surveyed 111 older adults with chronic low back pain versus twenty who were pain free. They were assessed by clinical history and physical examination. Biomechanical and soft tissue pathologies were significantly more common in older adults with chronic low back pain (90%) than in pain-free patients with MPS (10%). Limited data are available regarding risk factors for MPS; however, MPS has been reported to be more prevalent in female patients than male patients.
Pathophysiology
While much remains to be discovered about the etiology of MPS, several theories regarding its pathophysiology have been advanced in recent years. Underlying biomechanical and postural factors may interact with neurologic factors (e.g., radiculopathy), psychological elements including depression and anxiety, and hormonal and nutritional imbalances. These factors (in sum or in part) may create an autonomic dysregulation and, ultimately, central spinal cord sensitization which can amplify the experience of MPS. Vasoactive mediators, algogenic neurotransmitters and inflammatory mediators including bradykinin, norepinephrine, serotonin, calcitonin gene–related peptide, substance P, tumor necrosis factor alpha, and interleukin 1-B have been identified in the hyperirritable loci of TrPs. These substances sensitize nociceptors and are responsible for the sensory experience of MP, including referred pain and the local twitch response (LTR).
The motor phenomena of MP have been hypothesized to be caused by excessive acetylcholine (ACh) leakage, which creates dysfunctional endplates that are responsible for taut muscle band formation. Excessive ACh release causes sustained muscle contraction by increased depolarization of the postjunctional endplate. Evidence of maximal sarcomere shortening in TrPs has been found in canine and human subjects. A positive feedback cycle may be created by the interplay of increased ACh release, sarcomere shortening, and the release of sensitizing substances. In a study investigating the hypothalamus-pituitary-adrenocortical and sympathetic-adrenal-medullary system responses to experimentally induced stress in patients with MP, plasma concentrations of cortisol, epinephrine, and norepinephrine were found to be significantly higher in MP patients than in healthy controls.
The taut muscle band present in MPS has a higher resting tension and contains hypercontracted muscle fibers. Chronicity may increase local energy consumption and cause areas of tissue hypoperfusion and ischemia. Vasoactive mediators are released in the setting of muscle ischemia, causing increased ACh release, exacerbation of local ischemia, and sensitization of peripheral nociceptors, thereby causing pain. Abnormal spontaneous electrical activity is present at the site of TrPs, with excessive ACh release creating endplate noise seen on electrophysiological studies at the neuromuscular junction. Spontaneous electrical activity is observed as having two components: a constant, low amplitude background activity of approximately 50 μV and intermittent higher amplitude spikes of 100–700 μV. Spontaneous electrical activity occurs more often in TrPs than in normal tissue and displays aberrant patterns in TrPs. Therefore, this spontaneous electrical activity is distinct from normal miniature endplate potentials. The abnormal electrical activity observed in TrPs is thought to be directly related to excessive ACh release.
The clinical manifestation of abnormal electrical activity in the TrP is an LTR and thought to be mediated by a segmental spinal reflex. Snapping palpation or needling the TrP causes a brisk muscle contraction in the taut band. The location of the LTR is called the “sensory locus,” which has been correlated histologically with sensory receptors. The “active locus” is the site where spontaneous electrical activity is recorded, the waveforms of which correspond to published reports of motor endplate noise. According to this model, the sensory locus and the active locus act as the nociceptor and the motor endplate and are distributed throughout muscle. Where these align and are highly concentrated, we observe myofascial TrPs ( Box 25.1 ).
Diagnostic History
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Regional pain
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Onset with sudden muscle overload
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Onset with sustained muscular contraction in shortened position
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Onset with repetitive activity (symptoms increase with increasing stressfulness)
Diagnostic Physical Examination
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Taut band
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Focal spot muscle tenderness
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Pressure-elicited referred pain pattern
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If active, pressure elicits pain recognized as familiar
Other Clinical Characteristics
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Local twitch response—confirmatory, difficult to elicit
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Prompt release of taut-band tension by specific myofascial trigger-point therapy
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Central/attachment myofascial trigger points
Vasoactive mediators such as those released in the taut bands of MP have been known to sensitize peripheral nociceptive nerve fibers such as those found in skeletal muscle. In a sensitized state, nociceptors spontaneously discharge with a lower threshold to painful stimulation and also exhibit discharge to nonpainful stimuli. Over time, this heightened abnormal peripheral sensory input creates a state of central neuronal sensitization.
Diagnosis
In a survey of 403 responding clinician members of the American Pain Society, 88.5% considered MPS to be a valid clinical disorder and 81% believed it was distinct from FMS. A careful history and physical exam remain the cornerstone of effective diagnosis. The most common presentation of MPS includes the following diagnostic criteria: regional body pain and stiffness, limited range of motion of the affected muscle, twitch response produced from a taut band, referred pain from a TrP to a zone of reference, and resolution of the symptoms with local anesthesia applied to the TrP. MPS may occur after injury, chronic strain with repetitive microtrauma, or without clear precipitating event. Aberrant body mechanics or postural abnormality may initiate or perpetuate the problem. The quality of pain tends to be a deep “aching” of variable intensity, and the pain is confined to a specific anatomic region. Characteristic referred pain patterns are associated with specific muscles, although these referral patterns are often unreliable.
It is essential to have hands-on formal training in the physical examination of MP and TrPs to achieve a reliable result. Musculoskeletal examination should be performed with the objective of identifying orthopedic or neurologic dysfunction that may play a role in generating secondary MPS. Although there are no universally accepted diagnostic criteria for MP, physical findings may be helpful in establishing a diagnosis. A distinct pattern of TrP findings may reveal itself in MPS after a given insult. Active TrPs may be identified by palpation with gentle digital pressure oriented across and perpendicular to the muscle fibers. TrPs are present as a taut muscle bands within skeletal muscle, and palpation of these points may elicit involuntary muscle contraction, the twitch response or “jump” sign. These painful TrPs limit full range of passive motion in the afflicted muscle group. Although these findings have been suggested as diagnostic criteria, investigators have found it problematic to demonstrate consistent agreement in the presence or absence of TrPs among examiners in blinded studies with control groups. Inconsistencies may be attributed in part to a lack of standardized examination technique and variability in the interpretation of examination findings. Variability in muscle anatomy, physical conditioning, and deconditioning pose obstacles as well. The most reproducible diagnostic findings on physical examination include observation of a TrP in an affected muscle, referral of pain to a zone of reference, and reproduction of the patient’s usual pain on physical exam.
Differential diagnosis of MP should include (1) musculoskeletal and neuropathic disorders such as arthritis, degenerative disc disease, radiculopathy, bursitis, and tendonitis; (2) autoimmune or infectious etiologies; (3) metabolic and endocrine dysfunction including hypothyroidism; (4) psychiatric disorders including depression and anxiety; and (5) fibromyalgia. It has been postulated that MPS may be an evolving component of FMS. While on the surface there are similarities, several well-documented findings argue against the connection between MPS and FMS ( Table 25.1 ). Patients with MPS do not exhibit widespread tender point hypersensitivity as in those with FMS. Additionally, FMS tender points do not refer pain to a zone of reference as do the TrPs in MPS. The common TrPs in MPS can coexist with the widespread tender points of FMS.
| Clinical Feature | Myofascial Pain | Fibromyalgia |
|---|---|---|
| Pain pattern | Local or regional | Generalized |
| Least distribution | A single muscle | 11 tender points |
| Muscle spasm | +++ | ++ |
| Trigger points | Local, regional | Not a feature |
| Tender points | Not a feature | Common, widespread |
| Taut band | ++ | — |
| Twitch response | ++ | — |
| Referred pain | +++ | — |
| Fatigue | + | ++++ |
| Sleep disturbance | +++ | ++++ |
| Paresthesias | Regional | Distal |
| Headaches | Referred head pain | Occipital origin |
| Irritable bowel | Not a feature | +++ |
| Swelling sensation | + | ++ |
Common muscle groups associated with MPS can be categorized by the regions in which the muscles anatomically exist or where the muscles can refer pain to. The common regions for MPS include head and neck, shoulder, chest, abdomen, low back, pelvis/hip, knee, and ankle/foot. Box 25.2 describes the muscles that can contribute to pain in each of these regions.
Head and Neck
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Posterior cervical
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Splenius capitus and cervicis, semispinalis capitus and cervicis
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Sternocleidomastoid
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Upper trapezius
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Levator scapulae
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Facial muscles
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Temporalis
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Masseter
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Shoulder
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Trapezius
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Supraspinatus
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Infraspinatus
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Subscapularis
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Teres major and minor
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Latissimus dorsi
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Levator scapulae
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Posterior serratus
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Deltoid
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Pectoralis major and minor
Chest
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Pectoralis major and minor
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Abdominal obliques
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Intercostal muscles
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Serratus anterior
Abdomen
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Serratus anterior
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Abdominal obliques
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Rectus abdominus
Low Back
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Psoas
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Quadratus lumborum
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Paraspinal muscles
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Iliocostalis
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Longimus thoracis
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Multifidi
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Abdominal obliques
Pelvis/HIP
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Abdominal muscles
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Psoas
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Quadratus lumborum
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Gluteal muscles
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Piriformis
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Pectineus
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Semitendinosis
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Obturators
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Gemellae
Knee
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Vastus medius and lateralis
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Hamstrings
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Gastrocnemius
Ankle/Foot
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Gastrocnemius
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Soleus
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Tibialis anterior
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Fibularis longus and brevis
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Long flexor and extensor muscles of the leg
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Intrinsic foot muscles
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