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1,2,7,10,11 Available evidence supports the hypothesis that TrPs are a persistent peripheral source of nociception, contributing to pain propagation and widespread, referred pain elsewhere. 7,8 The biochemicals released account for the peripheral sensitization of nociceptors, which contribute to the pain associated with active trigger points, allodynia, and hyperalgesia. Together, the sustained sarcomere contraction and increased EPPs promote formation of a taut band of muscle tissue. The acidic environment inhibits the breakdown of acetylcholine, resulting in increased acetylcholine within the synaptic cleft and increased frequency of miniature end plate potentials (EPPs).
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In addition, a reduction of locally available adenosine triphosphate (ATP) to muscle tissue results in inhibition of return of calcium to the sarcoplasmic reticulum, causing a sustained contraction of the sarcomere. This leads to local capillary constriction and ischemia, an increase in sympathetic nervous system adrenergic activity, formation of an acidic hydrogen ion concentration within the muscle tissue, and the release of sensitizing substances (substance P, calcitonin gene-related peptide, protons, serotonin, norepinephrine, prostaglandins, bradykinins, tumor necrosis factor α, interleukin (IL)-6, IL-8 and IL-1β). 1,7-9,10 According to this hypothesis, the initiating event is muscle overload and/or injury. The most accepted theory of trigger point formation is Travell and Simons’ integrated hypothesis. MPS affects up to 95% of patients with chronic pain, and in one study, MPS was found to be the primary cause of pain in 85% of patients attending a large pain center. Approximately 9 million people in the United States are thought to suffer from myofascial pain. This lack of consensus-driven, reliable diagnostic criteria makes it difficult to establish accurate statistics about incidence and prevalence. Myofascial pain is a purely clinical diagnosis, and lacks objective and systematic diagnostic criteria. 2-5, 20 Epidemiology including risk factors and primary prevention
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Nonstructural factors including anxiety, depression, sleep deprivation, fatigue, chronic infection, and iron, vitamin, mineral, and endocrine deficiency states may contribute to the development and persistence of TrPs. Mechanical causes of chronic stretch and overload include unaccustomed or intense exercise, sustained sub-optimal postures, anatomic abnormalities, abnormal muscle firing patterns, joint dysfunction, chronic repetitive overuse, and poor work-related ergonomics. EtiologyĬhronic muscle stretch and overload are thought to play a key role in the development of TrPs, with direct and indirect trauma as possible but less likely causes. 1,2 MPS is characterized by pain, both local and referred, muscle stiffness, and sensory changes. A TrP is defined as a hyperirritable spot in a palpable taut band of skeletal muscle. Myofascial pain syndrome (MPS) is a regional muscle pain syndrome caused by myofascial trigger points (TrPs).