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Special Populations Pennick and Liddle (2013) noted a greater reduction in pregnancy-related low back and pelvic pain when aquatic exercise or acupuncture was used over traditional physical therapy; however, Ee and colleagues (2008) reported only a limited level of evidence for the use of acupunctu...

Special Populations Pennick and Liddle (2013) noted a greater reduction in pregnancy-related low back and pelvic pain when aquatic exercise or acupuncture was used over traditional physical therapy; however, Ee and colleagues (2008) reported only a limited level of evidence for the use of acupuncture. Likewise, the use of spinal manipulative therapy (SMT) or OMT for the treatment of pregnancy-related low back and pelvic pain has also yielded only limited support (Khorsan et al. 2009; Licciardone et al. 2010; Pennick and Liddle 2013). Based on the evidence to date, Clemente-Fuentes, Pickett, and Carney (2013) suggested that both physical therapy and aquatic therapy and acupuncture (including auricular acupuncture) will help to relieve low back pain and improve function and that OMT may improve disability slightly. Even though the use of acetaminophen and corticosteroid injections have been found to be safe for use during pregnancy for reducing lumbopelvic pain (Clemente-Fuentes et al. 2013), nonprescription pain-relieving alternatives are advocated and sought after by pregnant women (Ritchie 2003) because of the unknown consequences of pain medications on fetal development. Remaining active during pregnancy may also mitigate pregnancy-related pain (Ritchie 2003). Women who have been exercising previously and are not expected to have a complicated pregnancy are encouraged to continue exercising. Competitive athletes engaging in strenuous exercise while pregnant should receive close medical attention (Pivarnik, Perkins, and Moyerbrailean 2003) because eccentric exercise may result in the development of somatic dysfunction (Fridén and Lieber 1998). Although there have not been any studies to date examining the use of PRT for the treatment of pregnancy-related back and pelvic pain, PRT is an excellent therapeutic alternative to mitigate a pregnant patient’s low back and pelvic girdle pain (see figure 3.3) because of its exceptional ability to treat somatic dysfunction with a passive, gentle approach. When working with pregnant women, therapists should take the following considerations into account: • Because joints will be more lax as the patient progresses through pregnancy, the amount of joint compression and distraction applied during PRT should be decreased accordingly. • With slight modification, almost all PRT treatment positions can be done safely in a side-lying position. • The placement of a pillow or bolster between the thighs and knees during treatment often reduces strain to the lumbopelvic area. Populations With Disabilities and Disease Although PRT has not been widely reported in the literature to cure physical or emotional disability or disease, the therapy can dramatically improve quality of life by reducing pain and spasm, improving function and enhancing overall well-being, and reducing hospital length of stay. Schwartz (1986) advocated the use of counterstrain, or PRT, for hospital patients suffering from acute illness. Schwartz commented that the therapy is an excellent prescription for nearly all bedridden patients, particularly those suffering from pain and somatic dysfunction as a result of acute CLINICIAN THERAPEUTIC INTERVENTIONS Pregnancy-Related Pain • The patient should be positioned for treatment in the most comfortable position (e.g., side-lying). Figure 3.3 A piriformis PRT procedure performed on a pregnant woman. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 37 Clinical Guide to Positional Release Therapy fracture, postsurgical pain, and osseous metastatic disease, provided they can be moved without complication. Radjieski, Lumley, and Cantieri (1998) reported a significant decrease in length of hospital stay by 3.5 days in pancreatitis patients treated with both OMT and traditional care versus patients treated with traditional care alone. In their randomized and blinded pilot study (N = 14), some patients were treated with primarily counterstrain and myofascial release and rib manipulation (n = 6), whereas those in the control group (n = 8) received standard care. The researchers hypothesized that the use of OMT for this population helped to improve intracellular function “through improved circulation and respiration, and by decreasing or intercepting prolonged sympathetic activity” (p. 265). As previously discussed, pain and the somatic dysfunction that ensues can heighten sympathetic activity, disturbing the homeostasis of the entire human organism. Although we must exercise caution when interpreting pilot study findings, further rigorous investigations of the use of PRT for the treatment of patients with disease or disability both in and outside a hospital setting are warranted based on the therapy’s potential clinical implications for this population. I am regularly surprised at how PRT helps those with disabilities and disease reestablish homeostasis. Patients often report treatment effects such as improvements in energy, mood, mental concentration, sleep, eating habits, and function with activities of daily living and recreation, as well as decreased depression. Although it is not within the scope of this text to discuss all of the diseases and disabilities that can be treated with PRT, the ones highlighted have shown promise and often require special considerations during the evaluation and treatment process. Patients With Obesity and Diabetes A person can be born with a disability, but disablement can also manifest over a lifetime from conditions such as obesity and diabetes. According to the World Health Organization (World Health Organization [WHO] 2014), obesity is a global burden both from a health care and a financial standpoint. The WHO reported in 2008 that 1.4 billion adults worldwide suffered from obesity, and women outpaced men. In 2013 the organization estimated that 42 million children worldwide were classified as either overweight or obese. Obesity is 38 now identified as one of the top five reasons for death worldwide and often presents with associated comorbidities (Ellulu et al. 2014; Horne et al. 2014) such as diabetes, cardiovascular disease, metabolic syndrome, osteoarthritis, headache, and migraine. Chai and colleagues (2014) found a 40 to 80% increased risk for migraine in those with progressive obesity, and the increase peaks during the childbearing years. However, the authors did not find a tenable connection between tension-type headache and obesity in adults. Oakley and colleagues (2014) reported that the current evidence suggests a possible connection between obesity and headache disorders in the pediatric population, including tension-type headaches. In light of rising childhood overweight and obesity figures (Ellulu et al. 2014) and the reported negative impact on quality of life and risk for developing illness and musculoskeletal impairments such as osteoarthritis (Blagojevic et al. 2009), experts contend that the disease must be curbed. In addition, clinicians will likely be faced with treating obese patients of various ages, including the young, who possess not only one or more of the health problems associated with the disease, but also the pain they produce (Vincent et al. 2012). Obese patients often present with persistent musculoskeletal and joint pain (Ellulu et al. 2014; Vincent et al. 2012) and resultant somatic dysfunction caused by the abnormal and excessive loading of joints, particularly at the knee and hip (Blagojevic et al. 2009; Toivanen et al. 2010). Based on a literature review, Finckh and Turesson (2014) proposed that obesity may be a risk factor for rheumatoid arthritis (RA), particularly in young women. The researchers suggested that adipocytes may be one of the causes because those found in adipose tissue release adipokines. Adipokines are cell-signaling proteins that have varied metabolic functions, but they are both pro-inflammatory and anti-inflammatory (Kwon and Pessin 2013). However, in both obese humans and rodents, pro-inflammatory adipokines are more prevalent than anti-inflammatory adipokines (Kwon and Pessin 2013), which may cause increased and sustained pain in the obese because of a heightened inflammatory response (Finckh and Turesson 2014). Moreover, obese patients also present with comorbidities the longer they are obese (Ellulu et al. 2014), especially type 2 diabetes (T2D), which is the most widely recognized (Toivanen et al. 2010). Therefore, clinicians should T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Special Populations take the following into account when working with obese patients: CLINICIAN THERAPEUTIC INTERVENTIONS Obese Patients • Obese patients should be placed on a lifestyle and behavioral modification program if they are not formally engaged in one. • The somatic dysfunction and pain obese patients exhibit typically respond more slowly to treatment until a healthy weight or body composition is attained. • Investigate whether obese patients have comorbidities and how they are currently managing them, as well as the association of those conditions with the patients’ pain and somatic dysfunction. • Older obese patients are more likely to have comorbidities such as T2D or OA. Therefore, consider decreasing the amount of compression, distraction, mobilization force, and palpatory pressure used during treatment. • When assessing obese patients for osteopathic tissue lesions, place them on their side or in a position that uses gravity to move the adipose tissue away from underlying structures to be palpated. • Use a high-low table, bolsters, and an exercise ball to alleviate the strain of performing PRT on obese and overweight patients. • Perform a biomechanical and functional assessment for obese patients to ascertain whether an underlying biomechanical or functional impairment is causing or complicating their condition. According to the American Diabetes Association (ADA), 29.1 million Americans, or 9.3% of the population, were afflicted with diabetes in 2014, resulting in direct medical and reduced productivity costs of $245 billion that year. Diabetes is also known to result in multiple complications and a myriad of comorbid conditions such as peripheral neuropathy (Martin et al. 2014), hypertension, and cardiovascular disease (ADA 2014). Diabetic patients may also present with joint pain (Schett et al. 2013) and somatic dysfunction, which typically moves upward from the feet. Symptoms tend to worsen as the disease progresses (Martin et al. 2014). Although type 1 diabetes is found in obese patients and among 5% of the general U.S. population, type 2 diabetes (T2D) is more prevalent among the obese (ADA 2014). Obesity is known to be associated with underlying medical and psychological conditions that inhibit weight loss, although such conditions are less frequent causative factors than poor health style and behavioral choices (Toivanen et al. 2010). Even though PRT may improve somatic dysfunction among patients with both obesity and diabetes, the foremost therapeutic intervention should be to help patients attain a healthy lifestyle that not only moves them out of obesity, but also helps them control and manage their diabetes. Both cardiorespiratory exercise and resistance training are advocated for the T2D obese patient regardless of the stage of the disease to help them regain a healthy weight and control of the disease (Schett et al. 2013). Regular physical activity may also help the type 2 obese diabetic patient avoid the development of knee and hip osteoarthritis. Schett and colleagues (2013) examined 927 men and women between 40 and 80 years of age with T2D over a period of 20 years and found that T2D was an independent risk factor for the development of osteoarthritis (OA) based on the incidence of hip or knee arthroplasty, which was found to be independent of age and BMI. An increased probability for arthroplasty was observed among patients with a high BMI and also as patients aged. The findings of this study point to a metabolic influence on the development of OA among type 2 diabetics, bridging several of the disease and disability conditions discussed thus far. Diabetes, obesity, arthritis, and headache often appear in combination among chronic patient populations regardless of age or physical activity level. Therefore, clinicians should consider the therapeutic interventions discussed thus far in this chapter in addition to the following when treating the diabetic patient: CLINICIAN THERAPEUTIC INTERVENTIONS Diabetes • Evaluate the lifestyle or physical activity behaviors of type 2 diabetic (T2D) patients for potential modification. • Progressive T2D patients may present with cardiovascular disease, diabetic peripheral neuropathy (DPN), or autonomic cardiovascular neuropathy. Consult with the patient’s > continued T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 39 Clinical Guide to Positional Release Therapy Clinician Therapeutic Interventions: Diabetes > continued attending physician prior to initiating a physical activity modification program (Colberg et al. 2010). • Because patients with DPN have increased pain, altered sensation, and decreased perfusion in their extremities (Martin et al. 2014), exercise caution when attempting to locate and demarcate osteopathic tissue lesions. Currently, no studies have examined the impact of PRT on DPN patients or those with any diabetic condition; however, the diabetic patient often reports pain reduction, improved sensation, and increased tolerance to ambulatory pressure after the application of PRT. • Post-PRT massage and the exercise of distal extremities are advocated to facilitate further tissue perfusion. • The resolution of somatic dysfunction among T2D patients is often predicated on their ability to maintain a healthy weight. Patients With Fibromyalgia First described as rheumatic thickenings of tissue in 1816 by Balfour in Stockman (1920), widespread painful somatic lesions have been a topic of debate and speculation since (Smith, Harris, and Clauw 2011). The tissue thickenings observed by Stockman (1920) were painful to palpation, widely distributed throughout the body, and often in an irregular pattern. Because the lesions were initially thought to be associated with inflammation as the result of trauma, the term fibrositis was adopted to describe the condition (Gowers 1904). In 1945 Kelly commented that the condition was often thought to be “psychogenic” because of its mysterious nature and recalcitrant response to treatment. Kelly (1945), however, was convinced that fibrositis was not psychogenic, but a result of a reflex phenomenon that produced tender myalgic spots that referred pain to deeper tissues that could manifest anywhere in the body but appeared to have an affinity for musculotendinous junctions. In 1948 Korr also identified these myalgic spots, which he described as osteopathic lesions that resulted in widespread somatic dysfunction and pain. Until the early 1990s, the term fibrositis was used by the rheumatic community to describe the presence of widespread painful tissue lesions. However, Smythe and Moldofsky (1977) and others 40 who followed them determined that patients with fibrositis often demonstrated symptoms other than just painful tissue lesions, such as sleep disturbance, which could also be produced in healthy people when deprived of sleep. Moreover, the presence of widespread somatic lesions and their resultant pain was observed among those with other somatic disorders such as irritable bowel syndrome and headache, suggesting that fibrositis was associated with a much larger spectrum of disorders than first thought (Smith et al. 2011). When it became apparent that somatic tissue lesions resulted from factors and conditions other than inflammation, the term fibrositis was abandoned and fibromyalgia was adopted (Wolfe et al. 1990). The American College of Rheumatology (ACR) in 1990 was the first to provide criteria for the classification of fibromyalgia, which provided the initial framework for a standard of diagnosis and research of this condition (Wolfe et al. 1990). In their attempt to provide a framework, Wolfe and colleagues (1990) examined 293 patients with fibromyalgia and 265 controls who were not deemed to have fibromyalgia, but who had other painful conditions such as lumbago. The researchers investigated primarily the presence of painful tender points in 30 anatomical sites throughout the body through dolorimetry and manual palpation and previously identified global indicators such as sleep disturbance, fatigue, morning stiffness, anxiety, and sensitivity to auditory stimuli. Among fibromyalgia subjects, the primary findings were axial and extremity tender points of moderate sensitivity at 18 of the 30 anatomical sites investigated and secondary complaints of generalized whole body pain, sleep disturbance, fatigue, and morning stiffness. These findings led investigators to classify fibromyalgia as a condition requiring a prolonged history of widespread pain and the presence of moderately sensitive tender points in multiple regions of the body, including the axial skeleton and extremities. (See Wolfe and colleagues [1990] for a full review of the ACR classification of fibromyalgia.) The 1990 ACR classification of fibromyalgia has served as an excellent guide for numerous studies that have followed, but the identification of tender points in the clinical setting based on the ACR criteria, although useful for research purposes, has been deemed unrealistic and unnecessary for diagnosis (Smith et al. 2011). Instead, it is advocated that global complaints of pain, fatigue, and sleep disturbance be considered the primary T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Special Populations criteria for diagnosis (Smith et al. 2011). Smith and colleagues provided an excellent in-depth review of the research supporting the rationale for the shift away from the use of tender points and toward the use of the revised criterion. They suggested various survey tools to assess them such as the fibromyalgia assessment status (FAS) index. The new evaluative criteria expand the definition of fibromyalgia beyond the symptoms of pain and its resultant somatic dysfunction. However, reports of pain and findings of tissue tenderness, although no longer considered central to a diagnosis, should not be abandoned (Smith et al. 2011). Although more clarity is developing on how to define or diagnose fibromyalgia, widespread pain, fatigue, and sleep disturbance remain central to its diagnosis. However, “the pathophysiology of fibromyalgia remains uncertain but is believed to be largely central in nature” (Smith et al. 2011, 217). Fibromyalgia has been proposed to have both direct and indirect costs that are comparable to those of osteoarthritis (Smith et al. 2011). Thus, it is critical that we understand why the condition develops and explore how best to address its etiology. Smith and colleagues (2011) reported the primary symptoms of fibromyalgia as “multi-focal pain, fatigue, sleep disturbances, and cognitive or memory problems” with secondary symptoms of “psychological distress, impaired functioning, and sexual dysfunction” (p. 217). These symptoms are also often present in many other somatic conditions (Gerwin 2005; Smith et al. 2011; Wolfe et al. 1992), raising the question of whether fibromyalgia is a unique condition or simply a manifestation of multiple injury and disease mechanisms (Gerwin 2005). Wolfe and colleagues (1992) examined the presence of localized tenderness (tender points) and taut, painful muscle bands (myofascial trigger points) in patients diagnosed with both fibromyalgia and myofascial pain syndrome and also among healthy subjects. The researchers found that both disease groups possessed tender points, but those with myofascial pain syndrome possessed them in greater proportions. Even though the study had significant methodological limitations, its preliminary finding that myofascial pain syndrome patients possess more trigger points than tender points has continued to be the differentiating factor between the two conditions (Gerwin 2005), although both appear to be triggered by and persist for similar reasons. Fibromyalgia and many somatic conditions are often precipitated by underlying conditions such as infection, psychological stress, a disease state, or trauma. However, “there is no objective tissue pathology or standard to which “[the] disease” can be anchored” (Smith et al. 2011, 274), which makes diagnosis and treatment challenging. Gerwin (2005) also suggested that fibromyalgia may ensue from a metabolic insufficiency caused by a deficiency in vitamin D, iron, and vitamin B12 and from hormonal imbalances caused by hypothyroidism. Rather than being a single entity, fibromyalgia appears to be part of a larger continuum of somatic conditions such as irritable bowel syndrome, myofascial pain syndrome, tension-type headaches, and migraines, leading some researchers to group them because of their overlapping clinical symptoms. Yunus (2008) proposed a collective term for these somatic conditions, central sensitivity syndrome (CSS), because it is now believed that patients along the somatic spectrum have a “fundamental problem with pain or sensory amplification rather than a structural or inflammatory condition in the specific region where the pain is being experienced” (Smith et al. 2011, 219). Additional mechanisms that may also be at play are neurogenic inflammation, dysfunction of the autonomic nervous system, and hypothalamic pituitary dysfunction (Smith et al. 2011). Smith and colleagues (2011) provided an in-depth review of the evidence supporting the pathophysiology of fibromyalgia, which is worth reviewing. They discussed evidence pointing to why there may be an amplification of pain and sensoryprocessing centers in CSS patients. They posited that an imbalance exists between the release and reuptake of neurotransmitters in the central nervous system, which is responsible for increasing the sensitivity, or “gain,” of the pain and sensoryprocessing centers, thereby facilitating central sensitization to occur. The hyperactivity or increased volume of the pain and sensory-processing centers may in part explain why fibromyalgia patients experience widespread chronic pain and subsequently a poorer quality of life than those who do not have the condition. Historically, the predominant therapy for treating fibromyalgia, or CSS, has been pharmacological. Pharmacological therapies showing promise include: tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, and alpha-2-delta ligands such as gabapentin and pregabalin, gammahydroxybutyrate, and tizanidine (Smith et al. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 41 Clinical Guide to Positional Release Therapy 2011). The central purpose of these pharmacological compounds is to regulate and reestablish the balance between neurotransmitter release and reuptake. However, many patients seek a nonpharmacological approach to treating CSS. PRT may be an excellent one because of its ability to decrease afferent sensory reflexes, pain, and sensory amplification by reducing gamma gain at the third-order neuronal level. How PRT affects neurotransmitter release and reuptake has not yet been established, and to date, no studies have examined its use as a primary therapy intervention for the treatment of fibromyalgia. Salient PRT and Fibromyalgia Research Findings • Imaging studies reveal that fibromyalgia patients are hypersensitive to all sensory stimuli, including sensory pressure and auditory, heat, cold, and electrical stimuli. • Fibromyalgia patients demonstrate an increased sensitivity, or gain, to painful pressure. • Those with fibromyalgia show elevated cerebrospinal fluid levels of pronociceptive neurotransmitters such as substance P, glutamate, nerve growth factor, and brain-derived neurotrophic factor and decreased levels of serotonin, norepinephrine, and dopamine. • CSS patients show a strong genetic and familial predisposition. • CSS patients do not experience significant pain relief with endogenous opioids. • CSS patients may possess a metabolic or nutritional deficiency. • A multifaceted approach to treatment should be pursued, consisting of pharmacological therapy, education, mild to moderate exercise, cognitive behavioral therapy, and PRT. My clinical experience with fibromyalgia patients suggests that many of them fall somewhere on the somatic dysfunction spectrum with varying degrees of symptomology and impairment. Moreover, many CSS patients report an early trauma in life that caused what they believe is a spreading of pain throughout the body. However, 42 some patients also report an underlying disease condition that they believe may have caused the condition, such as Lyme disease or irritable bowel syndrome. Typically, CSS patients fall into one of two prognostic categories: those whose somatic dysfunction resolves with treatment and those whose condition does not resolve but their quality of life does with treatment. The disease or somatic condition of people in the latter category often does not resolve because of an underlying trigger or disease condition that cannot be treated, such as an autoimmune dysfunction. Therefore, when working with CSS patients or those diagnosed as having fibromyalgia, clinicians should perform a thorough investigation into the factors that may have precipitated the condition as well as its maintenance. CLINICIAN THERAPEUTIC INTERVENTIONS Fibromyalgia • Perform a thorough history and diagnostic workup to identify causative or perpetuating factors for the patient’s condition. • Consider requesting a blood chemical profile to identify any nutritional deficiencies. • Assess and document the patient’s quality of sleep and pain and fatigue levels throughout the assessment and treatment process. • Use a multimodal treatment approach consisting of manual, behavioral, nutritional, and pharmacological therapy coupled with progressive therapeutic exercise and stress management interventions. • Assess and treat the patient’s somatic dysfunction according to the area of concentration and the level of intensity. However, also consider the 18 designated fibromyalgia tender point locations identified in the 1990 ACR criteria as key areas for treatment. • Palliative modalities such as heat, cold, and light massage may be helpful for those who cannot tolerate deep manipulative stimuli. For patients who cannot tolerate these palliative modalities, focus on the application of PRT until pain and sensory amplification has diminished; then implement these complementary modalities for further pain control and healing. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Special Populations Summary Although PRT is a safe, nonpainful, and passive modality for the treatment of somatic dysfunction, each patient and special population requires modifications to the application of the therapy. More important, internal and external factors must be taken into account such as age, level of physical activity, surgical history, body composition, disability, and underlying disease or comorbidities because they may affect the assessment and treatment of the condition. Some underlying disease states may not be remedied through therapeutic, surgical, or pharmacological interventions, but many of the somatic conditions discussed in this chapter possess underlying triggers or mechanisms that, if addressed, will help to resolve the patient’s condition. A prime example is obesity. It is accepted that being overweight or obese perpetuates a host of injury and disease conditions (Ellulu et al. 2014). For example, the obese are at greater risk for the development of knee osteoarthritis (Blagojevic et al. 2010), type 2 diabetes (Toivanen et al. 2010), headache (Chai et al. 2014), breast cancer (Jemal et al. 2011), rheumatoid arthritis (Finckh and Turesson 2014), and chronic pain (Vincent et al. 2012). If the therapist can help the patient address his obesity, then many of the associated conditions will also be addressed. However, by the time chronic pain patients seek treatment, they often possess widespread pain and a poor quality of life, typical of the ACR 1990 definition of fibromyalgia. These patients are often in too much pain to engage in exercise, even of light intensity, as a result of worn-out joints, pain, weakness, or fatigue. The balancing act the clinician must perform is to reduce the patient’s somatic dysfunction with PRT and complementary therapies while addressing underlying disease(s) and trigger(s) without further aggravating the condition. The list of special populations that may benefit from PRT presented in this chapter is not exhaustive. However, all typically show signs of pain and sensory amplification resulting from central sensitization that negatively affects their quality of life. What may first be a simple ankle sprain may over time develop into fibromyalgia, resulting in widespread pain, fatigue, and sleep disturbance. The clinical presentation of fibromyalgia may be one of many somatic dysfunctions on a spectrum of chronic pain disorders that share a similar pathogenesis among all populations and age groups irrespective of diagnosis. With this in mind, clinicians must address somatic dysfunction early and correct structural and mechanical abnormalities as well as precipitating factors such as nutritional, hormonal, and physical activity issues to prevent somatic dysfunction from becoming widespread. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 43

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