Myofascial Pain Syndrome: Uncovering the Root Causes
Myofascial pain is an increasingly recognized etiology of non-acute musculoskeletal pain. Although not often considered in the differential diagnosis of musculoskeletal pain until the past 10 to 15 years, myofascial pain is now estimated to affect approximately 44 million Americans.1 Recent studies have identified a myofascial component of pain in 30% of patients in an internal medicine practice, 55% of those in a head and neck pain clinic, and up to 85% to 95% of cases in a pain center.2-5 Although the exact mechanism is not fully understood, myofascial pain syndrome (MPS) is characterized primarily by the development of trigger points. These trigger points are found within the muscle, fascia, or tendinous insertions and are diagnosed routinely by palpation.6
Trigger points are most commonly characterized by the following two primary features as well as two secondary features.
- Palpable taut muscle fibers
- Consistent localized or referred pain generation by palpation
- Restricted range of motion of involved muscle
- Local twitch response with needle insertion7,8
Although trigger points are usually differentiated from tender points, there are some suggestions that both are part of one clinical spectrum. The major reported difference is that trigger points produce pain in a referred pattern, whereas tender points generate pain at the site of palpation.9 Trigger points are further classified as active versus latent. Latent trigger points elicit painful sensation only with the application of direct compression. Active trigger points elicit pain spontaneously as well as with compression.10 For the purposes of this discussion, MPS will encompass both tender and trigger points.
Clinical Presentation And Pathophysiology
Clinically, myofascial pain often presents as a deep aching sensation, described as an area of “tightness” or “stiffness” by the patient. Myofascial pain is aggravated by use of the affected muscle and frequently responds to mechanical stressors such as stretching, pressure, anxiety, cold, or heat. It is occasionally associated with paresthesias. In many cases, it is preceded by acute or repetitive muscle trauma.
Multiple contributing factors are identified in the development of MPS including trauma, postural imbalances, psychological stressors, sleep deprivation, chronic disease states, vitamin insufficiencies, and spinal degenerative conditions (Table 1).8 Theoretically, these states of medical or structural aberrance induce motor endplate dysfunction of the affected neuromuscular junctions. Prolonged motor endplate malfunction results in a cascade of myoneural changes including muscle fiber degeneration, regional fibrosis, and formation of the characteristic taut bands of MPS. Likely due to frequent overloading, the trapezius is often the most commonly affected muscle. A review of more recent medical literature suggests that the etiology may be linked to structural conditions such as cervical radiculopathy, muscular trauma such as whiplash, and postural-related stressors. MPS may serve as a “red herring,” distracting health care providers from other underlying issues. We suggest a deeper investigation in the setting of MPS with prior history of trauma or other regional complaints before treating MPS in isolation.
Cervical radiculopathy (CR) is a condition characterized by pain in the neck, shoulder, and usually one or both upper extremities due to compression or irritation of one or more of the cervical spinal nerve roots.11 It can be associated with paresthesias, sensory and/or motor dysfunction, as well as reflex changes typically within the distribution of the affected nerve root.11 The C7 nerve root is the most commonly involved level.11
Although CR typically results from cervical disc herniation (posterolateral is most common) or cervical spondylosis, several recent studies suggest myofascial pain may play a role in its clinical presentation. In one cross-sectional study of 16 subjects diagnosed with unilateral cervical radiculopathy by history and physical exam findings, a greater number of tender points were found on the affected side (75 vs 34, P<0.01) compared to the asymptomatic side.12 A myotomal subgroup analysis of those subjects with C7 radiculopathy demonstrated a significantly higher number of trigger points among those muscles innervated by C7 on the affected (23 vs 7, P<0.02).12
A larger study evaluated 244 patients diagnosed with CR by both clinical presentation as well as concordant magnetic resonance imaging (MRI) findings to compare the prevalence of latent and active trigger points to those of asymptomatic controls.13 Data analysis revealed that active trigger points were found only in those patients with CR. Interestingly, there was no difference in the number of latent trigger points between groups. Additionally, the number of active myofascial trigger points was significantly greater in those patients with a medial disc herniation compared to a posterolateral herniation (P=0.041). The results of this study demonstrate an association between myofascial pain and CR.13 Other studies (mostly retrospective in nature) have more closely delineated this association by correlating a cluster of trigger points within a specific muscle group with lesions of its corresponding nerve root.14 Some research has even shown a higher pain intensity level of those trigger points found in patients with cervical disc lesions compared to those of patients without cervical pathology.14