Phys. Med. Rehabil. State of the Art Reviews     13(3): 473-493, 1999.

Few conditions in clinical practice have generated as many methods of treatment and debate as musculoskeletal pain and, in particular, low back pain (LBP). Only recently, in the past 2 decades, has muscular dysfunction been considered a factor in musculoskeletal pain. Since then, many misconceptions have arisen regarding myofascial dysfunction (MD), and, therefore, clinical treatment has not yet been standardized among practitioners. This discussion will specifically address focal MD and not fibromyalgia, a separate clinical entity. The concept of MD as envisioned by Travell and Simons was that trigger points (TPs) were defined as a hyperirritable focus in a palpable taut band of a skeletal muscle giving rise to characteristic referred pain, local tenderness and autonomic phenomena. This muscle dysfunction (“myo”) can by itself cause pain and can even lead to connective tissue (“fascial”) breakdown, such as tendinosis and periostosis due to failure or malfunction of a specific muscle. MD of a particular muscle can even present as several different MS disorders. For example, MD of the supinator can lead to lateral epicondylar periostitis, wrist tenosynovitis or radial nerve entrapment. This concept differs significantly from the osteopathic concept of MD, as described by Greenman. The osteopathic model conjectures that the fascial component is causing the muscle dysfunction, and therefore the fascia is the primary focus in treatment while the muscle is of secondary importance. The model of Travell and Simons posits that the muscle dysfunction is often primary and leads to the fascial breakdown.

Another method of description more familiar to rheumatologists and orthopedic surgeons is that a primary joint dysfunction can often lead to a muscular dysfunction subsequently developing secondary TP phenomenon or that a primary MD of a muscle can lead to imbalances among the muscles controlling joint forces, leading to abnormal stresses (“stress risers”) that predispose them to secondary joint (“chicken-or-egg” conundrum). Therefore, a joint problem, such as sacroiliac joint dysfunction (SIJD), with secondary muscle pain and MD with secondary joint dysfunction can be considered as separate clinical entities. Confusion arise when satellite TPs, which develop in muscles within the referral zone or in synergistic muscles of the original primary TP, are found on physical examination. This often results in patients receiving multiple TP injections administered over a long course of treatment and still failing to respond. Because muscles work as agonist-antagonist or myotatic units, the primary TP if left untreated can lead to the development of other secondary TPs, and the treated TPs may be reactive or secondary to another muscle in that articular unit. This leads to the concept of regional MD described by Campbell, which is best described as multiple TPs in multiple muscles surrounding a dysfunctional joint. The confusion over which muscle TPs to treat was partially clarified by Rosen, who developed the concept of gateway muscles, where treatment of a key muscle in an MS dysfunction unlocks satellite TPs in antagonistic, synergistic, or referral zone muscles. He postulated that “these muscles tend to be flexors and internal rotators.” The clinical experience of this author is that the gateway muscles also tend to be the deepest muscles surrounding the joint.

Problems have arisen with the use and abuse of TP treatment because asymptomatic individuals can harbor latent TPs, subtle loss of range of motion (ROM) or weakness. An asymptomatic individual’s latent TPs may be due to a previously in completely resolved injury or injuries. An episode of LBP can then occur in the future when these latent TPs are stressed or overloaded by another trauma, such as a fall or slip or overload from resuming unaccustomed exercise or long work hours. However, a precise definition with clinical criteria is lacking because there is no specific blood test or radiologic study available that can diagnose MD.

Criticism has been made that TPs and MD exist only in the mind, fingers and pockets of the clinical practitioner since MD is often diagnosed by the response to the myofascial treatment. The existence of TPs can be unequivocally demonstrated by electromyographic (EMG) recordings. Friction et al. compared the local twitch response (LTR) in 16 subjects with unilateral neck or shoulder pain and TP tenderness of the upper trapezius muscle. The diagnosis of MD was based on clinical complaints, examination findings and the ruling-out of other diagnoses. Snapping palpation of the symptomatic upper trapezius TP produced 3.81 EMG recordings by visual scoring and 31.81 by spike counting as compared to the asymptomatic side where values were 0.81 and 8.75, respectively (p 0.001). This increase in motor unit electrical activity can then be observed clinically as the hyperirritability and reactivity of the TP. Hubbard and Berkoff found spontaneous EMG activity, in the form of constant, low- level, 50 µV amplitude and a superimposed irregular 500—1000 µV amplitude activity, in the nidus of all TPs of the trapezius muscle. This EMG activity was not found in non-TPs in 2 patient groups of tension headaches and fibromyalgia. So the existence of TPs as a hyperirritable muscle focus cannot be questioned. What is still in doubt, for lack of clinical trials, is whether TP injections in clinical practice are effective in pain relief, functional improvement and cost savings. Other issues that need to be addressed include which muscle or muscles are more important in treatment.

Research is clearly needed to understand what causes MD in the first place, but understanding muscle function and pathophysiology can be helpful in directing clinical treatment until the scientific data have been main controllers of the forces on the musculoskeletal system system. When forces overload the musculoskeletal system, connective tissue injury (tendinosis, periostitis) occurs. Animal models have shown that muscle malfunction can result from acute strains, e.g., from falls, trauma, or rapid decelerations, and from chronic repetitive stress or overload. Hasselman et al., by performing progressively increasing controlled stretch/strain of rabbit tibialis anterior (TA) and extensor digitorum longus (EDL), demonstrated that a threshold and a continuum of muscle injury exists. Muscle fiber disruption at the myotendinous junction is observed initially at 70% of the force to passive failure, and muscle belly and connective tissue disruption occurs only at larger displacements of 80% and 90%. Acute muscle strains of rabbit EDL muscles beyond the physiologic ROM showed shortening and hypercontraction of the sarcomeres closest to the site of rupture at the musculotendinous junction, normalizing by 300—500 µm from the site of the rupture. An animal model for chronic repetitive stress was developed by Lieber et al. using rabbit TA. Maximal tetanic contraction was more significantly reduced when a 25% strain was performed during eccentric contractions as compared to isometric contractions; ultrastructural abnormalities on electron microscopy were observed only with eccentric contraction. The consequences of eccentric contraction are muscle weakness, loss of ROM and tenderness due to the newly injured muscle fibers. The site of injury has been shown electromicroscopically to be in the sarcoplasmic reticulum, disrupting the muscle’s ability to store calcium, which is required for muscle contraction. This possibly explains the weakness. Another possible explanation for the loss of strength is the observed shortening of the muscle fibers, decreasing their ability to cause tension because shortening moves the contraction down and to the left of the length-tension (L-T) curve (Fig. 1). Garrett et al., using rabbit EDL muscles, demonstrated that active muscle contraction during rapid lengthening to the point of failure increased the energy absorbed and force to tear. Studies of humans landing from an unexpected fall showed two bursts of EMG activity: the first a response to release and the second in relation to landing, both of which are absent in labyrinthectomized cats and humans with loss of labyrinthine function. Therefore, during rapid deceleration as in a motor vehicle accident, labyrinthine-dependent reflexes are used to recruit specific muscles to increase the body’s ability to absorb energy and force through eccentrically loaded muscles. In cervical radiculopathy patients who were treated with dry needling of TPs, Chu observed considerably more improvement in patients whose injury resulted from a motor vehicle accident.’ This leads one to suspect cervical muscle strain as etiologic in whiplash injury, but which muscle(s) are injured or recruited preferentially?

Which tissue is injured in whiplash injuries and falls is not exactly clear, but the orthopaedic model fails to include muscles in the equation. Consider the following hypothetical equation (Equation 1):

(I) Injury =   I skin + I subcu +I ligament +I cartilage +I cartilage +I meniscus +I synovium +I muscle                                                                                                                        +I tendon + I bone + I nerve

High speed and rapid impact, such as a football player getting tackled with a helmet to the lateral aspect of the knee while the limb is weight bearing, will likely cause damage in the ligament(s), meniscus, synovium, and possibly bone, while the other factors approximate zero and drop out of the equation. Moderate speeds and impact such as falls and whiplash injuries would have a mixed injury in the ligament (sprain), meniscus and musculotendinous junction (strain). Low levels of trauma such as chronic repetitive stress or tendinosis would likely have more injury in the soft tissues such as muscles, tendons, bursae, or nerve roots, while the other factors would approximate zero and drop out of the equation.

The amount of damage can be easily conceptualized when considering the relationship of momentum (m), velocity (V) and rate of impact or deceleration (t) in equation

(2) Momentum mV = F  t = Impulse

When momentum is rapidly dissipated with a shortened t and because momentum is conserved, the peak force is very high and damage is more substantial to the “harder” tissues of the musculoskeletal system. A good example would be a skier falling and hitting a tree and sustaining bone fractures, ligamentous injury, and possibly spinal cord injury if the vertebral bones and ligaments are disrupted. On the other hand, when the t can be made more prolonged, the peak force can be diminished and injury can be avoided. An example is a falling football player who tumbles and rolls instead of falling on an outstretched hand (Fig. 2). Whiplash injuries, caused by a rapid change in momentum, lead to a considerable amount of impulse loading to the MS system. Although cushioning, padding and seat belts provide some protection by lengthening the t sufficiently to avoid significant “structural” damage, enough force remains to cause a muscle strain. The magnitude of strain, not force, determines the degree of muscle damage. Studies with magnetic resonance imaging (MRI) scans using short tau inversion recovery (STIR) sequence with contrast to look at muscle damage 3 days, 3-6 weeks and 6-12 months after an acute whiplash injury may yield a possible site of injury as no definitive etiology has ever been established. The same holds true for a slip on the ice or a rapid twisting injury where ligamentous tears in the annulus are often postulated but not proven. Perhaps there is a specific muscle strain that rapidly eccentrically contracts in an effort to protect the body from more substantial damage by controlling the load to absorb some of the energy and force.
The hypothesis that specific muscle strain may be the cause of musculoskeletal dysfunction is borne out by both clinical and animal studies. Roth et al. found that a trauma-induced complaint was more likely in MD pain patients than in a group of mixed chronic pain patients. Hasselman et al. demonstrated that it is the contractile elements of the muscle that are injured first and commented that rehabilitation and prevention should be focused more on the muscle structure.
This same model can be used to analyze which exercise to perform and for which muscle so as to design the optimal rehabilitation program. After the initial trauma, further muscle dysfunction can then ensue because of inefficient muscle contraction with a leftward shift on the L curve (see Figure 1) caused by muscle shortening. The muscles then are overused when stressed, such as by lack of sleep, long hours of working or repeated bouts of excessive exercising, leading to overuse. Latent TPs are then activated, causing pain with prolonged muscle activation. Active TPs can be aggravated, causing pain at rest, with change in posture (e.g. sit-to-stand), or during sleep. Optimal muscle function must be achieved for optimal MS function so the treatment should include specific deep muscle stretching to maximize the L-T curve for the injured muscle.
Whether acute or chronic, the result of muscle injury is shortening of muscles, making the muscles less efficient mechanically (moves to left on L-T curve). Experimental strain injuries of rabbit leg muscles demonstrate decreased peak load to failure and shortening of the sarcomeres immediately after the injury. After a relatively minor injury, if muscles are incompletely rehabilitated, the muscles function suboptimally with latent weakness due to the leftward shift on the L-T curve, increasing muscle fatigability and susceptibility to further injury. The residual shortening of these muscles is the hallmark of MD.

The issue of which muscles to treat for a specific problem has not been definitively determined because of the desperate lack of controlled clinical trials, leaving the choice of muscles to the individual practitioner. If satellite TPs are being treated and the primary TPs are not being treated, recurrences and too frequently repeated TP injections may result. There surely must be some clinical importance to TPs, because Melzack et al. found a very high degree of correlation (71%) between TPs and acupuncture points. Acupuncture has been recognized by the medical community as a beneficial adjunct in the treatment of MS pain, and its clinical basis may eventually prove to be motor TPs.