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 dysfunc-tion, 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 proinflam-matory 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 interven-tions 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 crit-ical 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 inflam-mation, 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, inter-rupting 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.
Summary
With an understanding of the foundational neurophysiological underpinnings of how sensa-tion 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 dysfunc-tion to follow. Simons and colleagues’ (1999) integrated hypothesis of trigger point formadysfunc-tion 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 dysfunc-tion and central sensitizadysfunc-tion, which has been supported since the theory’s introducdysfunc-tion. 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 pre-sented 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.
Neurometabolic event Increased ↑ Decreased ↓ Supporting literature Potential PRT impact
Inflammatory metabolites X McPartland 2004; Proske
and Morgan 2001;
Reinöhl et al. 2003
Decrease
Tissue pH X Gerwin et al. 2004; Sluka
et al. 2001; Sluka et al.
2003
Increase
Stretch reflex arc activity X Howell et al. 2006; Wynne
et al. 2006 Decrease
Gamma activity X Appelberg et al. 1983;
Capra et al. 2007;
Thunberg et al. 2002
Decrease
ACh X Dolezal et al. 1992;
Dommerholt et al. 2006;
Maekawa et al. 2002;
Simons et al. 1999;
Wessler 1996
Decrease
AChR X Dolezal et al. 1992; Gerwin
et al. 2004; McPartland and Simons 2006
Decrease
AChE X Gerwin et al. 2004;
Kovyazina et al. 2003;
McPartland and Simons 2006
Increase
ATP X Dommerholt et al. 2006;
McPartland and Simons 2007; Reinöhl et al. 2003;
Wessler 1996
Increase
Calcium release X McPartland and Simons
2007; Proske and Morgan 2001; Vandenboom 2004
Decrease
TnC calcium binding X Houdusse et al. 1997;
McKillop and Greeves 1993; Vandenboom 2004
Decrease
Nociception X McPartland 2004;
Reinöhl et al. 2003 Decrease
Motor end plate activity X Hong and Yu 1998;
Hubbard and Berkoff 1993;
Kostopoulos et al. 2008
Decrease
Tissue perfusion X Gerwin et al. 2004;
Larsson et al. 1999;
Maekawa et al. 2002;
Rosas-Ballina et al. 2011
Increase
CGRP release X Domhnall and Bloom
1991; Gerwin et al. 2004;
Shah et al. 2003
Decrease
CHAPTER
CHAPTER OBJECTIVES
After reading this chapter, you should be able to do the following:
Understand important considerations when working with special populations.
Articulate special considerations and therapeutic interventions to be taken when working with youth and elderly patients.
Treat unique injury conditions such as mastectomy pain based on somatic lesion patterns.
Apply special therapeutic considerations and precautions when treating
competitive athletes and pregnant clients with positional release therapy (PRT).
Clinically approach the evaluation and treatment process for patients with diseases and disabilities such as obesity, diabetes, and fibromyalgia through the lens of PRT.