MPS treatment is directed at two primary targets: (1) treatment of the associated TrPs and (2) removal of the causative/perpetuating factors.

A number of treatments for the deactivation of TrPs have been described. The results of different studies and reviews demonstrate various modalities and techniques as being effective or ineffective. The principal methodologies are reported here.

Stretch is important in isolated TrPs of early onset, though appears to be somewhat less effective in long-standing, diffuse TrPs. The muscle containing the TrP should be stretched slowly to the point of discomfort. The theory behind the effectiveness of stretch in TrP inactivation is the belief that lengthening the sarcomeres reduces the local consumption of energy and interrupts the “energy crisis,” leading to muscle pain and TrP formation. On the other hand, stretching a painful muscle can stimulate sympathetic activity, inducing the TrP mechanism. In order to reduce this rebound phenomenon, it is preferable to first apply a vapocoolant spray to the overlying skin surface, which will inhibit pain as well as the reflex motor and autonomic responses in the CNS; the analgesic effect of cooling also permits more effective relaxation and stretching of the involved muscle groups (Mense, Simons, & Russell, 2001; Simons & Travell, 1999).

“Pressure release” replaces the old terminology “ischemic compression.” The provider applies gentle pressure, gradually increasing pressure on the TrP until an increase in resistance is encountered, correlating with the onset of patient discomfort. Pressure should be maintained, until palpable tension is released, then the finger is advanced further until further resistance is encountered. Again, the pressure is maintained until release of the tension; this process is repeated until tension is released throughout the involved area (Mense et al., 2001).

TrP injection is the gold standard for treatment of MPS. It is superior to stretching alone and has been shown to be one of the most effective modalities for inactivating TrPs and providing prompt relief of symptoms. Scott, Guo, Barton, and Gerwin (2009) reviewed published reviews and randomized controlled trials on TrP injections and confirmed TrP injections to be an efficacious treatment, safe in the hands of trained clinicians, and that the addition of TrP injections to stretching maneuvers augments clinical outcomes.

In terms of the substances injected, many studies indicate that “dry needling” may be as effective as injection of local anesthetics. Ay, Evcik, and Tur (2010), who used randomized controlled trial, illustrated that both dry needling and lidocaine injection have significant, but comparable, effects in MPS symptomatology. Injections were coupled with home stretching exercises to maximize benefit. The efficacy of dry needling is most likely based on mechanical disruption of the integrity of dysfunctional end plates. Many practitioners still prefer to use local anesthetic for patient comfort, both during the procedure and afterwards, to promote the patient’s tolerance of post-procedure stretching exercises. In general, injection of any solution (including saline) may relieve symptoms by dissipating local sensitizing agents in the region of pain (Ay et al., 2010; Kalichman & Vulfsons, 2010; Mense et al., 2001).

Injection of botulinum toxin has also been anecdotally reported to reduce symptoms in myofascial pain disorders (Ho & Tan, 2007; Lang, 2002). However, a systemic review by Peloso et al. (2007) concluded that there is no supporting evidence for its use in the treatment of MPSs, as injection of botulinum toxin A was not superior to injection of local anesthetic.

One recommended technique for injection of TrPs has been described by Hong (1994). The operator should rest the wrist on the patient’s body, then grasp the syringe between the thumb and the last two fingers, using the index finger to depress the plunger. This technique allows the operator improved control of the needle in the event that the patient moves unexpectedly during the procedure. The elicitation of a local twitch response during needle penetration would suggest greater efficacy of the injection.

Therapy for MPS should include identification and correction of factors that have promoted TrP formation. Therefore, postural abnormalities should be evaluated and treated, including ergonomic evaluations. Practitioners should address any anatomical defect contributing to muscle imbalance and repetitive strain/trauma (i.e., leg length discrepancy). Other perpetuating factors such as stress/mood disorders and sleep disorders should also be identified and corrected when possible (Edwards, 1988).

Intramuscular injection of diclofenac has shown significant pain relief in the treatment of MPS. However, this agent is of limited utility in the treatment of chronic MPS due to the multiple adverse risks associated with chronic nonsteroidal anti-inflammatory drug (NSAID) usage (Frost, 1986). In general, nonsteroidal anti-inflammatory drugs have shown limited benefit in the treatment of MPS. Amitriptyline was shown to be somewhat effective in reducing pain (Bendtsen & Jensen, 2000). As a drug class, muscle relaxers have shown little utility in treating MPS, possibly because the underlying pathophysiology in MPS is endplate dysfunction and not true “spasm” (Mense et al., 2001; Simons & Travell, 1999).

One recent open label study showed statistically significant reduction in pain scores among participants with trapezius MPS treated with tizanidine, a presynaptic alpha 2 agonist utilized as a muscle relaxant. In the study, anywhere from 2 mg daily to 4 mg three times daily was utilized, at the researcher’s discretion (Malanga, Gwynn, Smith, & Miller, 2002).

There is considerable overlap between MPSs and fibromyalgia. Thus, medications useful in the treatment of fibromyalgia are often utilized in myofascial pain disorders. Pregabalin, serotonin-norepinephrine reuptake inhibitors, and tramadol have all shown efficacy in the treatment of fibromyalgia. Unfortunately, there are no randomized controlled trials evaluating these agents in the treatment of MPSs. The management of fibromyalgia, a central sensitivity pain disorder, is beyond the scope of this chapter.

Overuse disorders of tendons or “tendinopathies” typically affect young people (20–30 years old) and middle-aged people (40–60 years old) and are often difficult to manage. Histologically, these disorders are characterized by angiofibroblastic hyperplasia, including hypercellularity, neovascularization, increased protein synthesis, and disorganization of matrix, but not inflammation (Khan, Cook, Kannus, Maffulli, & Bonar, 2002; Kraushaar & Nirschl, 1999; Maffulli, Testa, Capasso et al., 2004; Rees, Maffulli, & Cook, 2009). The lack of inflammation, as well as poor clinical outcomes and adverse risk associated with repeated corticosteroid injections, has led many practitioners to utilize other injectates for ligament pain (such as platelet-rich plasma (PRP), botulinum toxin, proteinases, and polidocanol). A systematic review of injections used in the treatment of various tendinopathies supports the use of corticosteroid injections for acute tendinopathies but conversely shows that corticosteroid injections are actually worse than other treatments for intermediate- and long-term management of chronic tendinopathies (Coombes, Bisset, & Vicenzino, 2010).

Tendinopathies can often become chronically painful conditions. Rotator cuff tendinopathies, lateral elbow epicondylosis, and Achilles tendinopathy are commonly seen in the chronic pain population. Unfortunately, there is a wide range of treatments but lack of consensus among physicians when treating these disorders. Such incongruency may be attributed to lack of understanding of the etiology of these conditions, including lack of understanding of the nociceptive properties of tendon tissues. Experimental studies have illustrated nociceptive characteristics of tendinous tissues. Gibson, Arendt-Nielson, and Graven-Nielson (2006) illustrated pain provocation in study subjects when hypertonic saline was injected into tendon tissue. Other studies have shown N-methyl-d-aspartate and transient receptor potential vanilloid 1 (TRPV1) receptors to be functionally relevant in the pathophysiology of tendon pain, as peritendinous injections of glutamate and capsaicin, respectively, induced tendon nociception (Gibson, Arendt-Nielson, Sessle, & Graven-Nielson, 2009). With little understanding of the pathophysiology of tendon pain, there is little consensus in the treatment of chronic ligament and tendinous pain disorders. For chronic ligament pain, practitioners have injected various compounds around ligaments for years in attempts to produce a sclerosing effect (Dagenais, Haldeman, & Wooley, 2005). Despite the popularity of new injection therapies for tendinopathies, many questions still remain regarding their therapeutic effect as well as their mechanism of action.

Osteoarthritis has a high prevalence and is a significant cause of disability among the elderly. The most common joint involved in chronic osteoarthritis pain is the knee. Among other mechanisms, peripheral and central sensitization may contribute to pain perception in osteoarthritis (Imamura et al., 2008). Therefore, eliminating the inflammatory component of the pain generator may still not completely resolve the pain syndrome. Central sensitization may explain why some patients may still complain of knee pain after a total knee arthroplasty. The management of arthritis differs significantly between rheumatoid arthritis (or other inflammatory arthropathies) and osteoarthritis. Early referral to a specialist is recommended for any patient with rheumatoid arthritis or possible synovitis. Treatment of RA favors the use of a combination of disease-modifying antirheumatic drugs (DMARDs) and analgesic treatment. Some patients respond rapidly and completely to disease-modifying treatments, further supporting the practice of early referral to appropriate specialists. Some of the analgesics often used are presented in Table 18.2.