Possible Physiological Mechanisms

Simons’ Integrated Trigger Point Hypothesis, introduced in 1999, may explain the role of peripheral and central sensitization. Due to abnormal endplate activity, high levels of acetylcholine (ACh) are released, which bind to receptors on the muscle membrane and initiate excessive release of calcium from the sarcoplasmic reticulum. When excessive calcium binds to troponin on the muscle fibers, the fibers enter a state of persistent contracture, leading to MTrP development. In order to release the contraction, ATP is needed to cause the conformational change of the muscle fibers and actively pump calcium back into the sarcoplasmic reticulum. Thus, the sustained contracture near an abnormal endplate leads to compressed capillary circulation w'hich reduces blood flow, forming local hypoxic conditions, and a polarized membrane potential. Consequently, this results in a lack of ATP, perpetuating an increased metabolic demand and reduced supply. The increased demand for and reduced supply of ATP form an energy crisis, w'hich may provoke the release of neuroactive substances and metabolic byproducts like BK, SP, and 5-HT that could sensitize peripheral nociceptors.30 Simons’ hypothesis explains how' sensitizing neuroactive substances may be responsible for the pain associated with active MTrPs. This hypothesis is supported by Shah et al., w'ho demonstrated that active MTrPs have elevated levels of inflammatory mediators, neuropeptides, catecholamines, and cytokines—biochemicals associated with inflammation, pain, sensitization, and intercellular signaling.142031

Remarkably, key tenets of Simons’ Integrated Trigger Point Hypothesis overlap with the role of muscle in MTrP development suggested by the Cinderella Hypothesis.32 Musculoskeletal disorder symptoms may arise from muscle recruitment patterns during sub-maximal level exertions w'ith moderate or low physical load among office workers, musicians, and dentists, in which myalgia and MTrPs have been commonly reported.29 According to Henneman’s size principle, smaller type I muscle fibers are recruited first and de-recruited last during static muscle exertions. As a result, these “Cinderella” fibers are continuously activated and metabolically overloaded, in contrast to larger motor muscle fibers that spend less time being activated and do not work as hard. This property makes these fibers more susceptible to muscle damage and calcium dysregulation, key factors in the formation of MTrPs.33 Treaster et al. demonstrated that low-level static continuous muscle contractions during 30 minutes of typing induced the formation of MTrPs, supporting the Cinderella Hypothesis.34

MTrPs can also develop with muscle overuse in cervical and postural muscles during the low- intensity activities.2934 A possible mechanism occurs during sustained low-level muscle contractions in tasks requiring precision and postural stability w'hich may then result in a decrease in intramuscular perfusion. Thus, a vicious cycle of ischemia, hypoxia, and insufficient ATP synthesis may occur in type I motor unit fibers and result in increasing acidity, Ca2+ accumulation, and subsequent sarcomere contracture. As a result, several sensitizing substances may be released, leading to local and referred pain and muscle tenderness, the clinical hallmarks of MPS.

Sikdar et al. used ultrasound imaging techniques to distinguish MTrPs from the surrounding tissue. Thirty-three sites in the upper trapezius of nine subjects were assessed and classified as active MTrP, latent MTrP, or normal by using gray-scale and color variance ultrasound imaging to distinguish palpable nodules and normal myofascial tissue based on relative stiffness and echogenicity (Figure 11.4). These findings not only confirmed the underlying morphological changes associated with MTrPs, but also suggested that the structure and characteristics of normal muscle fibers are disrupted, possibly by increased muscle contraction, injury, or ischemia. Additionally, blood flow' waveform patterns differed between active and latent MTrPs, with active MTrPs associated with retrograde flow in diastole, suggesting that pain at these active sites may result indirectly from decreased blood flow' to the region.35

Ultrasound of normal tissue versus myofascial trigger point

FIGURE 11.4 Ultrasound of normal tissue versus myofascial trigger point (MTrP). (A and B) Normal upper trapezius muscle. (C and D) Muscle with a palpable MTrP in a single hypoechoic region. (E and F) Muscle with a palpable MTrP in multiple hypoechoic regions. (Sikdar S., Shah J.P.. Gebreab T., et al. 2009. Novel applications of ultrasound technology to visualize and characterize myofascial trigger points and surrounding soft tissue. Arch Phys Med Rehabil, 90(11):1829-1838.)

Other researchers have studied the “neighborhood” of the MTrP to explain the symptom complex and physical findings. Specifically, Stecco focused on three anatomical layers: the deep fascia, the layer of loose connective tissue housing the highest concentration of hyaluronic acid, and the epimysium layer below it. Hyaluronic acid (HA), an anionic, non-sulfated glycosaminoglycan, is distributed widely throughout various tissues, and is a chief component of the extracellular matrix. Normally, HA functions as a lubricant that helps muscle fibers glide against each other without friction. However, Stecco theorized that because of muscle overuse or traumatic injury, the sliding layers start to produce immense amounts of HA, which then aggregate into supramolecular structures, changing HA’s configuration, viscoelasticity, and viscosity. Due to its increased viscosity, HA can no longer function as an effective lubricant, which increases resistance in the sliding layers and leads to densification of fascia, or abnormal sliding in muscle fibers. Interference with sliding can impact range of motion and movement including quality of movement and stiffness. In addition, the friction results in increased neural hyperstimulation (irritation), which then hypersensitizes mechanoreceptors and nociceptors embedded within this densified fascia. This hypersensitization correlates with a patient’s experience of pain, allodynia, paresthesia, abnormal proprioception, and altered movement. Very few objective studies have been conducted to validate or elucidate these concepts. Given the current limited knowledge regarding the pathophysiology of MPS, research is needed to determine not only the role of the MTrP, but also its surrounding environment.36

Clinical Evaluation of the MTrP and Sensitized Segments

A comprehensive evaluation of MPS assesses the patient not only for MTrPs, but also for sensitized spinal segments. The requisite examination skills are easy to learn and fundamentally important to the evaluation and management of the chronic pain patient. Furthermore, examination before and after treatment that is aimed at desensitizing the involved spinal segment provides the clinician and patient with meaningful, objective, and reproducible physical findings to guide future treatment.

Palpation of the skeletal muscle for the objective physical findings of active and latent MTrPs is the gold standard for the diagnosis of myofascial pain. Identifying and adequately treating active and, at times, latent MTrPs may have very important implications for the resolution of a patient’s pain. Active MTrPs can be a common source of peripheral nociceptive bombardment, which, in turn, may lead to central sensitization and perpetuation of pain. If left untreated, active MTrPs or other peripheral pain generators can re-sensitize the dorsal horn, resulting in the re-emergence of segmental findings of allodynia and hyperalgesia, and the same pain pattern even after treatment. Latent MTrPs, under certain conditions, can become active MTrPs and merit identification. To review, light-touch palpation of a latent MTrP induces pain locally and in remote areas.37 Latent MTrPs send excitatory, sub-threshold potentials to the dorsal horn. Excitatory sub-threshold potentials from latent MTrPs can summate w'ith sub-threshold potentials from active MTrPs to surpass the threshold necessary for SSS to occur. Once the myotome is sensitized, all MTrPs in that myotome may become active.

The related spinal segments may be severely sensitized, and, should be assessed at the derma- tomal, myotomal, and sclerotomal levels for MPS. Adjacent dermatomal levels are examined para- spinally by checking for allodynia and hyperalgesia. Allodynia is assessed by picking up the skin between the thumb and forefinger and rolling the tissue underneath, also known as a pinch and roll test (Figure 11.5). The patient is instructed to simultaneously report any sensation of pain, which is indicative of allodynia, a finding that is the most sensitive indicator for the diagnosis of sensitization. Hyperalgesia is assessed by scratching the skin with the sharp edge of a paper clip or Wartenberg pinwheel. The patient is instructed to simultaneously report any sharpening or dulling in the sensation of pain during the procedure. An increased painful response is indicative of hyperalgesia.

Myotomal levels are examined by palpating segmentally related musculatures for tender spots, taut bands, and MTrPs and measuring the pressure pain threshold (PPT) using a pressure algometer along the myotome. The PPT is the minimum pressure that elicits pain and is considered abnormal if it is at least 2 kg/cm2 lower than the value expected for a healthy subject.

Sclerotomal levels are examined by palpating segmentally related tendons, entheses, bursae, and ligaments, and measuring the PPT along these structures with an algometer.

These objective and quantitative findings help the clinician to identify the tissues and likely pain mechanisms involved in their patients’ chronic pain. The segmental findings are not only reproducible but are often indicative of the severity of the sensitized state and may provide important information about the underlying pain syndrome.

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