2.0 WHAT IS MYOFASCIAL PAIN SYNDROME?The precise features that define MPS vary in the literature. The condition is defined by the presence of TrPs, although certain criteria must also be met before a diagnosis of MPS can be made. Travell and Simons (1983), authors of the definitive text on the subject, believe the syndrome to be comprised of sensory, motor and autonomic phenomena.
2.1 TRIGGER POINTS
The most widely accepted definition of a TrP is "a hyperirritable spot, usually within a taut band of skeletal muscle or in a muscle fascia. The spot is painful on compression and can give rise to characteristic referred pain, tenderness and autonomic phenomena" (Travell & Simons, 1983).TrPs can be categorised as active, latent or satellite. In brief, an active TrP is a source of ongoing pain, a latent TrP is only painful when compressed and a satellite TrP develops within the area of referred pain of an another active TrP (Starlanyl & Copeland, 1996).
There is considerable debate surrounding the pathophysiological mechanism behind the formation of TrPs. The most generally accepted theory implicates the interaction of calcium with adenosine triphosphate (ATP). Following either acute or chronic trauma, the sarcoplasmic reticulum in the muscle cell is damaged, leading to a release of calcium which binds to troponin and results in contraction of the muscle fibre. Because the sarcoplasmic reticulum is damaged, it is suggested that the re-uptake of calcium cannot be facilitated and the muscle fibre remains contracted. High levels of calcium increase the energy demands for ATP, and this may lead to localised hypoxia. The disabled calcium pumps in the sarcoplasmic reticulum are thought to perpetuate this cycle. The hypoxia may result in a local inflammatory response and the release of serotonin, histamine, kinins and prostoglandins. These substances are believed to sensitise muscle nociceptors which converge with other visceral and somatic inputs and are thought to lead to the perception of local and referred pain (Rachlin, 1994, Schneider, 1995).
Theory states that the perception of pain stimulates motor units via the central nervous system, thereby inducing muscle spasm, which, if left untreated will initiate a muscle pain-muscle spasm cycle. There is an associated decrease in local blood flow and an overall reduction in ATP, and the action of the calcium pumps. Over time, noxious metabolites and inflammatory mediators build up in the area, leading to fibrosis and a worsening of symptomology (Rachlin, 1994).
2.2 SENSORY PHENOMENA
Pain due to MPS can vary from an intermittent mild ache to being ever present and excruciating. It may be localised to an area around the TrP or referred to another area of the body. The sensation of localised pain can be attributed to damaged muscle membranes. As previously mentioned, the release of seratonin, histamine, kinins and prostoglandins are believed to sensitise nociceptors and lead to the sensation of pain (Schneider, 1995).The sensation of referred pain however is not as easily explained. TrPs result in specific and predictable patterns of referred pain, yet follow no dermatome, myotome or sclerotomal pattern (Fomby, 1997). There are many mechanisms that have been postulated to explain this phenomenon and implicate anatomical changes related to neural plasticity and modulations of afferent or sympathetic nervous system activity (Simons, 1993).
2.3 MOTOR PHENOMENA
The presence of taut bands and TrPs can result in a decreased range of motion at the joint/s which the muscle crosses, muscle weakness and muscular imbalances (Rachlin, 1994).
2.4 AUTONOMIC PHENOMENA
Travell and Simons (1992), report that autonomic changes found in the lower extremities include localised vasoconstriction, increased sweating and pilomotor activity. Many studies looking at thermographic imaging of TrPs have found evidence of sympathetic autonomic changes (Diakow, 1988, Fisher, 1983, Kruse & Christiansen, 1992). There tends to be an increase in thermal emissions in the vicinity of a TrP and more diffuse areas of hyperaemia along the zones of referred pain (Diakow, 1988), indicating a greater degree of autonomic change at the site of the TrP.
