Clinical Guide to Positional Release Therapy PDF

Clinical Guide to Positional Release Therapy Muscle contraction submaximal concentric, eccentric Hypoperfusion Sympathetic nervous system activity Ischemia Hypoxia Muscle injury CGRP release from motor nerve terminal Acidic pH K+, BK, cytokines, ATP, SP H+ Muscle nociceptor activation Ach...

Clinical Guide to Positional Release Therapy Muscle contraction submaximal concentric, eccentric Hypoperfusion Sympathetic nervous system activity Ischemia Hypoxia Muscle injury CGRP release from motor nerve terminal Acidic pH K+, BK, cytokines, ATP, SP H+ Muscle nociceptor activation AchE inhibition CGRP release Increased ACh concentration in the synaptic cleft AChR up-regulation Tenderness, pain ACh release from motor nerve terminal Increased frequency of MEPPS, sarcomere hypercontraction, taut band Figure 2.4 Gerwin and colleagues’ (2004) schematic of the expanded integrated hypothesis of trigger point formation. Ach: acetylcholine; AChE: acetylcholinesterase; AChR: acetylcholine receptors; ATP: adenosine triphosphate; BK: bradykinin; CGRP: calcitonin gene-related peptide; H+: protons; K+: potassium; MEPP: miniature endplate potentials; SP: substance P. E6296/Speicher/Fig. 02.04/531996/JG/R2 Springer and Current Pain and Headache Reports, volume 8(6), 2004 of publication, 468-475, “An expansion of Simons’ integrated hypothesis of trigger point formation,” R.D. Gerwin, figure 1, ©2004. With kind permission from Springer Science and Business Media. al. 2004; Kovyazina et al. 2003). Therefore, ACh continues to rise at the neuromuscular junction because it cannot be removed effectively from its postsynaptic receptors by the limited amount of AChE. Also, its release is inhibited as a result of low levels of ATP and oxygen. To compound the rise in ACh at the synaptic cleft, CGRP also downregulates AChE to limit ACh, but CGRP release increases when pH is lowered, further limiting the breakdown and inhibition of ACh. In sum, Gerwin and colleagues (2004) contended that, in part, an elevated level of CGRP drives trigger point chronicity by producing and enhancing the presence of ACh. This results in a flood of nociceptor signals at the dorsal horn, which over time leads to neuroplastic changes that continually activate nociceptor fields within the spinal segment, but also above and below the facilitated segment. This is due to the cortical tract arrangement of the spinal segments. 22 Preceding theories have highlighted muscle contraction, hypoperfusion, neuroactive peptides, pain, and proprioceptive dysfunction as some of the primary causes of the production and maintenance of somatic dysfunction at multiple spinal segmental levels. Speicher and Draper, however, posited in 2006 that metabolic, neurochemical, and proprioceptive influences propagate structural dysfunction at the actin–myosin filaments, augmenting the development and maintenance of somatic dysfunction. Mechanical Coupling Theory The mechanical coupling theory (MCT) proposed by Speicher in 2006 posits that somatic dysfunction is produced and maintained through metabolic, neurochemical, and proprioceptive influences that produce a structural dysfunction of the fusimotor complex (figure 2.5). The MCT adds to previous T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Positional Release Therapy Research and Theory models of somatic dysfunction through its attention on the influence of the ATP energy crisis on ATP hydrolysis and filament coupling. Under homeostatic conditions, thick myosin protein filaments mechanically couple and uncouple with thin actin protein filaments to produce muscular contraction (Matthews 1981). As described by Vandenboom (2004), the regulation of the mechanical coupling process is driven by the conversion of chemical energy to mechanical energy from the following process: During the excitation/contraction coupling (ECC) process, calcium (Ca2+) ions released from the sarcoplasmic reticulum (SR) bind to troponin C (TnC) to activate the thin filament and allow myosin to interact with actin. Formation of this myofibrillar complex allows myosin to transduce the free energy liberated by the hydrolysis of adenosine triphosphate (ATP) into mechanical work against the thin filament. (p. 331) A further understanding of how a disturbance in the mechanical coupling process may result in and sustain somatic dysfunction can be gleaned Alpha efferents and muscle spindle Stimulates Injury Stimulate Releases Inflammatory metabolites Ca 2+ To cause Sensitizes Nociceptors Muscle contraction If sustained Maintains or increases Gamma gain Sensitizes Increase Facilitates Hypoxia from Vandenboom’s (2004) foundational work on myofibrillar fatigue. Whereas increased calcium ion (Ca2+) concentrations at the sarcoplasmic reticulum (SR) increase myofibril contractility (McPartland and Simons 2007; Proske and Morgan 2001), Ca2 + concentration is reduced in the presence of fatigue (Vandenboom 2004), which has been linked to a reduction in muscular function and force production (Proske and Morgan 2001). Regardless of an increase or decrease of Ca2+ at the SR, an increased or decreased amount can produce SR dysfunction and, in turn, impair myofibrillar protein function (Proske and Morgan 2001). Thick myosin proteins hydrolyze (break apart) ATP to liberate its free energy to power the myosin–actin crossbridge power stroke to produce muscle contraction (Vandenboom 2004). The myosin heads contain nucleotide sites that regulate the binding ability of the actin filaments (Matthews 1981). Coursing along the thin actin filaments is a chain of regulatory proteins ensconced in the tropomyosin protein that forms the tropomyosin–troponin complex (figure 2.6) The complex contains the subunit protein TnC, which regulates the nucleotide-binding Fires Results in ATP decrease Which increases Reciprocates with ACh Somatic dysfunction Inhibits reuptake May cause Results in Binds to TnC Figure 2.5 Results in Impaired hydrolysis Produces Inefficient uncoupling of myosin and actin The mechanical coupling theory. © Timothy E. Speicher T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. E6296/Speicher/Fig. 02.05/531997/JG/R1 23 Clinical Guide to Positional Release Therapy Sarcomere Troponin Tropomyosin Actin Myosin with heads of cross-bridges Figure 2.6 The tropomyosin–troponin complex. sites for the actin protein on the myosin filament, E6296/Speicher/Fig. 02.06/531998/JG/R2 covering and uncovering them through a cascade of neurochemical reactions (Matthews 1981). The interaction of calcium and TnC plays an integral role in the exposure of these binding sites and hence in the regulation of muscular contraction. As previously discussed, when Ca2+ levels at the SR are high and ATP levels are low, an energy crisis, or what Vandenboom (2004) termed a chemical crisis, ensues. McKillop and Geeves (1993) proposed a model that elucidates how the binding of Ca2+ with TnC influences both myosin and actin filament interactions. When calcium levels are low, actin filament binding to the myosin head is blocked, impairing the ability of the actin–myosin proteins to produce a strong crossbridge connection. However, “a strongly bound cross-bridge [in the presence of high Ca2+ levels] has a high affinity for actin and can generate force and perform work against the thin filament” (Vandenboom 2004, 333). Houdusse and colleagues (1997) highlighted that when TnC is in the presence of calcium, it serves as a switch to power ATP hydrolysis. When 24 ATP is hydrolyzed during the crossbridge power stroke, Pi (inorganic phosphate) and ADP (adenosine diphosphate) are released as by-products to work in concert with ATP to regulate the coupling and uncoupling of myosin and actin filaments (Vandenboom 2004). However, Vandenboom pointed out that if ADP release is inhibited, which occurs in the presence of lowered pH, then ATP will fail to uncouple the filaments, creating a “rigor cross-bridge . . . not capable of generating further force” (p. 335). The inefficiency of the coupling and uncoupling process produces a structural dysfunction and deformation of the filament complex, assisting in the maintenance of its coupled position, which may result in the recalcitrant taut band or knot observed with osteopathic lesions. ATP helps to prime the myosin–actin complex for recoupling or attachment, much like how gamma motor neurons help to prime, or ready, the muscle spindle for stimulation. The inefficiency of the uncoupling of the myosin–actin filaments as a result of low ATP and TnC and calcium binding may explain why increased strength has been observed when hip trigger and tender points have been released with SCS (Wong and Schauer-Alvarez 2004). Not only are the actin–myosin filaments in a structural position to produce work because they have been uncoupled, but the ATP, Pi, and ADP balance has also been restored to assist in the coupling process. However, if calcium and ACh levels remain high in the presence of TnC, myofibrillar binding may be sustained, resulting in myofibrillar fatigue that produces an inefficient coupling of the actin–myosin filaments (Vandenboom 2004). The mechanical coupling theory builds on existing models of somatic dysfunction by affirming the cascade of neurometabolic events that occurs when tissue is damaged. The discovery of the impairment to ATP hydrolysis and its impact on the coupling of actin—myosin crossbridges may further research into this mechanism and others that produce and sustain somatic dysfunction. Even though the theoretical foundation for somatic dysfunction and its associated trigger and tender points is solidifying, further research is needed to test the propositions and explore how they may translate to the clinical application of PRT for the treatment of somatic dysfunction. Based on my clinical experience with PRT as well as its instruction, I have chosen not to include in this text the traditional tender point locations originally outlined by Jones, in order to encourage T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Positional Release Therapy Research and Theory practitioners to explore the entire tissue during palpation. Even though common tender and trigger point locations have been identified across patient conditions and populations, most practitioners are often surprised to find undocumented points during examination. In the absence of a thorough palpation examination and exploration, critical dominant tender and trigger points may be missed. In part, this is why this text has moved away from the traditional point-by-point approach and toward a more exploratory approach when investigating somatic lesions and, hence, why the palpation of specific tissue structures is emphasized. Although not all tissues that can be treated with PRT have been presented in this chapter or text, those readily palpable and frequently affected by somatic lesions are presented. However, the clinical training and experience of the practitioner should be paramount when ascertaining the origin and cause of the patient’s somatic dysfunction. Clinical Implications Although it may be tempting to treat PRT as a panacea for somatic dysfunction, it is just one tool for facilitating the resolution of somatic dysfunction, albeit a versatile and powerful one. During the acute inflammatory process, PRT can be used to limit muscle spasm, improve blood flow, and limit the neurochemical cascade that results in the formation of osteopathic lesions. Controlling the formation of these lesions early may reduce the propensity for central sensitization, ischemia, and tissue atrophy. One of the major concerns during the acute stage of healing is protecting the tissue from further damage by controlling the inflammatory response (Knight and Draper 2012). By mitigating the unbridled release of proinflammatory mediators and ACh and limiting capillary restriction, practitioners can avoid a dive into the abyss of chronic inflammation, thereby facilitating an optimal environment in which the patient can move into the repair phase of the healing process. To heal adequately in the repair phase, tissues need adequate blood flow to receive nourishment. Most important, pain must be controlled to permit the range of motion needed for encouraging phagocytosis and fibroplasia (Knight and Draper 2012). However, when lesions do develop, range of motion is often restricted (Jones 1973), resulting in irregular scar formation and potentially weakening the tissue and making it more susceptible to further injury when stressed. If pain is not controlled, then the patient will likely regress into the inflammatory phase, delaying healing and producing unwanted scar tissue. Also, uncontrolled or intentionally delivered pain from direct therapeutic interventions may entrench and spread somatic dysfunction to other areas of the body, affecting strength, range of motion, and functional movement patterns. If PRT is applied to tissue lesions during this phase of healing, perfusion should improve to deliver critical blood flow to facilitate fibroplasia and tissue nourishment. Moreover, if blood flow is adequate, the primary culprit of somatic dysfunction, ACh, will be marginalized. For patients who do not progress through the repair phase and fall into a state of chronic inflammation, PRT can assist in freeing them from its grip. It does so by decreasing the gamma gain that may be driving a sustained myotatic reflex, interrupting the myotatic reflex by silencing the muscle spindles’ aberrant neural discharge and increasing perfusion to blood-thirsty tissues, resetting the neural firing patterns of type II spindle afferents, decreasing GTO inhibition from a reduction in musculotendinous tension produced by a lesion, and potentially recalibrating nociceptive fields and alpha motor neurons at the dorsal horn to eradicate central sensitization. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 25 Clinical Guide to Positional Release Therapy Summary With an understanding of the foundational neurophysiological underpinnings of how sensation and pain affect the somatic system, the theories that may explain the development and persistence of somatic dysfunction, as well as their implications for the clinical practice of PRT, aspiring positional release therapists will be poised to understand, learn, and apply PRT to a multitude of conditions arising from somatic dysfunction. The age-old concept of no pain, no gain is not easily set aside in the current therapeutic culture and training environment. Although there is a place for direct painful therapies, the option of accomplishing the same or a more optimal therapeutic outcome with an indirect technique such as PRT may be more appealing once we understand how pain travels throughout the somatic system. Pain does not reside only where it is caused or felt, but permeates the entire somatic system, crossing the spinal column and facilitating multiple segmental levels and the tissues they innervate, both somatic and visceral. Additionally, pain, either felt or caused, also activates other spinal reflexes such as the cross-spinal reflex that could produce tender and trigger points in antagonist musculature or in unintended areas of the body. Although acute pain or that induced by a therapist may be a trigger for the development of osteopathic lesions, multiple metabolic, neurochemical, and proprioceptive influences may work together to produce and sustain somatic dysfunction and a resultant structural dysfunction of the fusimotor complex. Korr’s proprioceptive theory (1975) laid the foundation for other theories of somatic dysfunction to follow. Simons and colleagues’ (1999) integrated hypothesis of trigger point formation encapsulated Korr’s idea that the muscle spindle was dysfunctional. However, Simons et al. (1999) postulated that the primary culprit in spindle dysfunction is motor end plate dysfunction and central sensitization, which has been supported since the theory’s introduction. The theory has been bolstered and expanded on further. Gerwin and his colleagues (2004) provided additional evidence to support the integrated hypothesis through their expanded model and proposed additional mechanisms that may lead to the development and maintenance of trigger points such as unaccustomed muscle contraction, tissue acidity, calcitonin gene–related peptide (CGRP), and hypoperfusion. Speicher affirmed and incorporated these somatic dysfunction theories into his mechanical coupling theory (2006). This theory places a spotlight on how metabolic, neurochemical, and proprioceptive influences may work together to develop and sustain a dysfunctional fusimotor complex, leading to the inefficient coupling and uncoupling of myosin–actin filaments. Although not all theories of somatic dysfunction have been presented in this text, the ones that have provide a guide for how to integrate PRT into the overall treatment plan for both acute and chronic maladies. Regardless of where it is used in the healing process, PRT is a nonpainful therapeutic intervention that limits pain and spasm and restores range of motion. Compelling evidence is mounting that supports the use of this therapy for the treatment and prevention of somatic dysfunction in all populations and clinical settings (see table 2.1). As evidence builds to support the efficacy of this therapy, I suspect that we will look back and wonder what took so long for PRT to become a cornerstone of our therapeutic foundation and treatment philosophy. 26 T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics.