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 two decades, has muscular dysfynction 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/chapter 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 (TP's) 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 phenomenon. This muscle dysfunction ("myo") can by itself cause pain and can even lead to connective tissue ("fascial") breakdown i.e. tendinosis, periostosis due to failure/malfunction of a specific muscle. MD of a particular muscle can even present as several different musculoskeletal (MS) disorders i.e. MD of the supinator can lead to either 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 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 dysfunction ("chicken-or-egg" conundrum). Therefore, a joint problem i.e. sacro-iliac joint dysfunction (SIJD) with secondary muscle pain and MD with secondary joint dysfunction can be considered as separate clinical entities. Confusion arises when satellite TP's which develop in muscles within the referral zone or in synergistic muscles of the original primary TP (T&S I) are found on physical examination (PE). The end result being that patients often receive multiple TP injections administered over a long course of treatment and still fail to respond. Since muscles work as agonist/antagonist and/or myotatic units, the primary TP if left untreated can lead to the development of other secondary TP's and the TP's treated may be reactive or secondary to another muscle in that articular unit. This leads to the concept described by Campbell as regional MD, that is best described as multiple TP's in multiple muscles surrounding a dysfunctional joint (Campbell). Confusion as to which muscle TP's to treat was partially clarified by Rosen, who developed the concept of gateway muscles, where treatment of a key muscle in a MS dysfunction unlocks satellite TP's 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 they also tend to be the deepest muscles sorrounding the joint (Ingber).

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

Criticism has been made that TP's and MD exists 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 TP's can be unequivocally demonstrated by electromyographic (EMG) recordings. Friction et al. compared the local twitch response (LTR) in 16 subjects with unilateral neck/shoulder pain and TP tenderness of the upper trapezius muscle. The diagnosis of MD was based on clinical complaints, examination findings and ruling out 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 motorunit 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 500-1000µV amplitude activity, in the nidus of all TP's of the trapezius muscle. This EMG activity was not found in non-TP's in 2 patient groups of tension headaches and fibromyalgia. So the existence of TP's 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 questions that need to be answered are 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 our clinical treatment until the scientific data have been made available. Muscles are the main controllers of the forces on the musculoskeletal (MS) system. When forces overload the MS system, connective tissue injury i.e. tendinosis, periostitis occurs. Animal models have shown that muscle malfunction can result from acute strains i.e. falls, trauma or rapid decelerations and chronic repetitive stress/overload. Hasselman et al., by performing progressively increasing controlled stretch/strain of rabbit tibialis anterior and extensor digitorum longus, demonstrated that a threshold and a continuum of muscle injury exists. Muscle fiber disruption at the myotendinous junction is observed initially at forces 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 (Reddy) showed shortening and hypercontraction of the sarcomeres closest to the site of rupture at the MTJ, normalizing by 300-500 µm from the site of the rupture. An animal model for chronic repetive 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 with ultrastructural abnormalities on electron microscopy observed only with eccentric contraction (Lieber 1991). The consequence of eccentric contraction is muscle weakness, loss of ROM and tenderness (Evans) 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 possibly explaining the weakness. Another possible explanation for the loss of strength is the observed shortening of the muscle fibers, decreasing its ability to cause tension since shortening moves the contraction down and to the left on the L-T curve. Garrett et al. (1987), 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 (Melvil, Greenwood 76), both of which are absent in labyrinthectomized cats (Watt 75) and humans with loss of labyrinthine function (Greenwood 76). Therefore, during rapid deceleration as in a motor vehicle accident, labyrinthine-dependent reflexes are used to recruit specific muscles to increase the bodies ability to absorb energy and force through eccentrically loaded muscles. In cervical radiculopathy patients treated with dry needling of TP's, Chu (II) 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/recruited preferentially?

Which tissue is injured in whiplash injuries and falls is not exactly clear but the orthopedic model fails to include muscles in the equation. If one considers a hypothetical equation (Eq. 1)

Then at high speed and rapid impact, i.e. 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 and synovium and possibly bone while the other factors approximate zero and drop out of equation 1. Moderate speeds and impact, i.e. falls and whiplash inuries 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 seem to drop out of Eq. 1.

The amount of damage can be easily conceptualized when considering the relationship of momentum, velocity and rate of impact or deceleration in Eq. 2

When momentum is rapidly dissipated with a shortened _t , since momentum is conserved the peak force is very high and damage is more substantial to the "harder" tissues of the MS system. A good example would be a skier falling and hitting an immovable tree and sustaining bone fractures and 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 avoided e.g. a falling footbal player who tumbles and rolls instead of falling on an outstretched hand. Whiplash injuries, caused by a rapid change in momentum, lead to a considerable amount of impulse loading to the MS system which, although cushioned by padding and seat belts which lengthens the _t sufficiently to avoid significant "structural" damage, still leaves behind a significant strain in a muscle(s). The magnitude of strain, not force, determines the degree of muscle damage (Lieber 1993). Studies with MRI scans using 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 which rapidly eccentrically contracts in an effort to protect the body from more substantial damage by controlling the load to absorb some of the energy/force.

The hypothesis that specific muscle strain may be the cause involved in MS 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 as compared to a group of mixed chronic pain patients. Hasselman et al. demostrated 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 utilized 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 due to inefficient muscle contraction with a leftward shift on the L-T curve due to muscle shortening. The muscles then are overused when stressed such as by lack of sleep, long hours working or repeated bouts of excessive exercising leading to overuse. Latent TP's are then activated causing pain with prolonged muscle activation and active TP's can be aggravated causing pain at rest, with change in posture i.e. 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 (Taylor) and shortening of the sarcomeres (Reddy) immediately after the injury. After a relatively minor injury, if muscles are incompletely rehabilitated, the muscles function suboptimally with latent weakness due to the left shift on the L-T curve increasing susceptibility to further injury. The residual shortening of these muscles is the hallmark of Myofascial dysfunction (MD).

Which muscles to treat for a specific problem has not been definitively determined due to the desperate lack of controlled clinical trials, leaving the choice to the individual practitioner. If satellite trigger points are being treated and the primary trigger points are not being treated, this may result in recurrences and too frequently repeated trigger point injections. There surely must be some clinical importance to TP's, since Melzack et al. found a very high degree of correlation (71%) between TP's 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 TP's.