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Clinical Guide to Positional Release Therapy
368 Pages
Clinical Guide to Positional Release Therapy With Web Resource provides professionals in the sports medicine and therapy fields with an easy-to-read reference on the clinical application of positional release therapy (PRT). The book is an invaluable resource for those who desire to learn, practice, and perfect the art of PRT to gently treat patients of all ages who have acute and chronic somatic dysfunction, including tightness and pain.
Author Timothy E. Speicher, president of the Positional Release Therapy Institute, uses contemporary science and evidence-based practice to provide health care practitioners—including athletic trainers, physical therapists, massage therapists, and chiropractors—with a manual of PRT treatment techniques. The text is also suitable for students enrolled in upper-level courses in athletic training, physical therapy, and massage therapy programs.
The highly visual book is organized in a manner that enables the reader to acquire a foundation of the applications, procedures, and theory of PRT. Part I explores the research surrounding PRT, providing articles that support the use of PRT through evidence-based practice. Readers will consider special populations, such as elderly patients, competitive athletes, and patients with disabilities. Part II explores PRT techniques by anatomical area. Each region (lower quarter, pelvis, spine, upper quarter, and cranium) contains an overview of common injury conditions and their myofascial triggers, differential diagnoses, and instructions on palpating and treating specific anatomical structures. Each chapter in part II also contains self-treatment techniques where appropriate.
Clinical Guide to Positional Release Therapy dedicates considerable attention to palpation instruction, a core skill that enables successful diagnoses and applications of many orthopedic assessments and therapeutic techniques. Readers also will gain knowledge of anatomical and kinesiological structures to ensure success in assessment. Application of adjunctive therapies, such as ultrasound, electronic stimulation, massage, joint stabilization, and therapeutic exercise, is provided throughout the text to complement PRT and facilitate an optimal healing environment.
Clinical Guide to Positional Release Therapy includes more than 400 full-color photos and illustrations. The unique layout of the book displays the anatomy, palpation, and treatment techniques in one or two pages, making the techniques visually easy for practitioners and students to follow and put into practice. In addition, scanning charts listing structures and mapping of the anatomical areas specific to the chapter content appear at the end of each chapter.
The text is supplemented by a web resource featuring 61 videos demonstrating various PRT techniques described in the book. The most common conditions and the techniques used to treat them are detailed, and Dr. Speicher provides advice about adapting the techniques to other conditions and muscle groups. The supplemental videos can be accessed online.
Whether students are just being introduced to PRT or medical professionals are already seasoned practitioners, Clinical Guide to Positional Release Therapy will assist them in using PRT in a simplified and structured manner to improve patient outcomes.
Part I. Foundational Applications and Procedures
Chapter 1: Introduction to Positional Release Therapy
Strain Counterstrain
Tissue Assessment and Documentation
Strain Counterstrain Versus Positional Release Therapy
Positional Release Therapy Guidelines
Summary
Chapter 2: Positional Release Therapy Research and Theory
Neurophysiological Foundations
Somatic Dysfunction and the Osteopathic Lesion
Clinical Implications
Summary
Chapter 3: Special Populations
Youth and Elderly Patients
Mastectomy Patients
Competitive Athletes
Pregnant Patients
Populations With Disabilities and Disease
Summary
Part II. PRT Techniques by Anatomical Area
Chapter 4: Foot
Dorsal Structures
Plantar Structures
Common Injury Conditions
Summary
Chapter 5: Ankle and Lower Leg
Anterior Structures
Medial Structures
Posterior Structures
Lateral Structures
Common Injury Conditions
Summary
Chapter 6: Knee and Thigh
Anterior Structures
Medial Structures
Posterior Structures
Lateral Structures
Common Injury Conditions
Summary
Chapter 7: Pelvis
Anterior Structures
Posterior Structures
Common Injury Conditions
Summary
Chapter 8: Spine
Anterior Structures
Posterior Structures
Common Injury Conditions
Summary
Chapter 9: Shoulder
Anterior Structures
Posterior Structures
Common Injury Condition Summary
Summary
Chapter 10: Elbow and Forearm
Anterior Structures
Medial Structures
Posterior Structures
Lateral Structures
Common Injury Conditions
Summary
Chapter 11: Wrist and Hand
Anterior Structures
Posterior Structures
Common Injury Conditions
Summary
Chapter 12: Cranium
Regis Turocy, MSPT, DCHE, PRT-c
Osseous Structures
Muscular Structures
Common Injury Conditions
Summary
Timothy E. Speicher, PhD, ATC, LAT, CSCS, is president of the Positional Release Therapy Institute. He is considered a leading expert in positional release therapy (PRT). Speicher discovered and developed the fasciculatory response method (FRM), which has revolutionized the way PRT is applied, practiced, and taught. He established the Positional Release Therapy Institute to provide education on the FRM and PRT through the institute’s courses while allowing for its application to a patient population at the institute in Ogden, Utah.
Speicher frequently speaks on PRT to professional organizations and at conferences, and his research has been published in academic journals. In 2014 he received the first-place award for outstanding manuscript on evidence-based concept mapping by the Athletic Training Education Journal, published by the National Athletic Trainers’ Association (NATA). In 2013 he won the journal’s first-place award for outstanding manuscript on case-based analogical reasoning.
Speicher, who has held several faculty and research appointments at various academic institutions, is a member of the NATA and was on the board of directors of NATA Research & Education Foundation. Currently, Speicher holds two faculty appointments: affiliate faculty for the University of Idaho, where he teaches neuroscience for the master’s degree in athletic training program, and assistant professor at Rocky Mountain University of Health Professions, where he provides instruction in evidence-based medicine for the doctorate in health science.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
What is positional release therapy?
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975).
Positional release therapy, also known by its parent term strain counterstrain, is a therapeutic technique that uses a position of comfort of the body, its appendages, and its tissues to resolve somatic dysfunction. Somatic dysfunction is defined as a disturbance in the sensory or proprioceptive system that results in spinal segmental tissue facilitation and inhibition (Korr 1975). Jones (1973) proposed that as a result of somatic dysfunction, tissues often become kinked or knotted resulting in pain, spasm, and a loss of range of motion. Simply, PRT unkinks tissues much as one would a knotted necklace, by gently twisting and pushing the tissues together to take tension off the knot. When one link in the chain is unkinked, others nearby untangle, producing profound pain relief (Speicher and Draper 2006a).
Essentially, PRT is the opposite of stretching. For example, if a patient has a tight, tender area on the calf, the clinician would traditionally dorsiflex the foot to stretch the calf to reduce the tightness and pain. Unfortunately, this might lead to muscle guarding and increased pain. Using the same example, a clinician who employs PRT would place the tender point in the position of greatest comfort (plantar flexion), shortening the muscle or tissue in order to relax them. A gentle and passive technique, PRT has been advocated for the treatment of acute, subacute, and chronic somatic dysfunction in people of all ages (Speicher and Draper 2006b). Dr. Lawrence Jones, an osteopathic physician, is credited with the discovery of the therapy in the early 1950s; he initially called it positional release technique and later coined the term strain counterstrain (Jones 1964).
Jones described his clinical discovery as "a lucky accident and nothing more" (Jones, Kusunose, and Goering 1995, 2). After Jones failed to help a patient with severe back pain, the patient said that his greatest challenge was sleeping at night and that if he could find a comfortable position, he might get relief. Jones assisted the patient into various positions and discovered that a fetal position provided the greatest pain reduction. He left him in this position while he examined another patient. Upon his return, the patient arose without pain for the first time in four months. Jones didn't understand how placing a patient in a position of comfort for a short period of time could provide complete cessation of unrelenting pain after so many traditional therapies had failed. He then experimented with patient positioning with moderate success. Three years later he accidentally discovered that treatment of anterior pelvic tender points often relieved posterior pelvic pain. Based on this observation, Jones believed that tender points (TPs) were the result of a counterstrain mechanism: If a tissue is abruptly strained, the opposing tissue (antagonist) is counterstrained in its attempt to stabilize against the straining force, resulting in the production of antagonist TPs that prevent the agonist strained tissue from fully healing (Jones 1995).
Tender points, in contrast to myofascial trigger points (MTrPs), are not associated with hyperirritable bands of tissue, but are discrete areas of tissue tenderness that can occur anywhere in the body (Speicher and Draper 2006a). Myofascial trigger points are hyperirritable nodules of knotted muscular tissue that often entrap nerves and local vessels and cause pain, inflammation, and loss of function (Simons and Travell 1981). Myofascial trigger points, whether active or latent, are found in taut bands of muscular tissue. An active MTrP produces either local or referred pain or other sensory perception alterations with or without manual stimulation, whereas a latent trigger point requires manual stimulation to activate a potential pain or sensory response (Dommerholt, Bron, and Franssen 2006). Tender points can also be active or latent, but they are not commonly found within knotted muscle. Jones mapped TP locations based on segmental spinal levels, but TP locations have also been closely associated with the myofascial trigger point locations first described by Travell in 1949. Myofascial trigger points and possibly TPs may also be associated with ahi shi acupuncture points used for the treatment of pain (Hong 2000) as well as lymphatic reflex points (D'Ambrogio and Roth 1997). Melzack, Stillwell, and Fox (1977) asserted that not much difference existed between the locations of MTrPs and acupuncture points based on their finding of a 71% correlation. However, an investigation by Birch in 2003 of the correlation between trigger and acupuncture points reported in Melzack and colleagues' study found a correlation of only 18 to 19%. Birch (2003) and Hong (2000) contended that not all acupuncture points correlate with MTrPs, but they believe that ahi shi acupuncture points used for pain control do. Jones (1964) was the first to correlate the use of specific body positioning to reduce tender and trigger point associated tenderness and spasm (see figure 1.1). In the calf area alone there are different trigger, tender, acupuncture and reflex points related to pain in the soleus muscle, many of which overlap one another. Melzack et al. (1977) outlines these in greater detail.
Figure 1.1 A comparison of trigger, tender, and acupuncture points.
This text not only presents and honors the foundational work of Jones, but also provides a user-friendly guide for the clinical application of PRT. Since Jones' seminal work, research and clinical case reports have continued to emerge to support its use and efficacy for the treatment of a variety of painful ailments linked to somatic dysfunction (Wong 2012), including restless leg syndrome (Peters, MacDonald, and Leach 2012). Positional release practitioners have also advocated for its use as a comprehensive therapy.
Anterior and Middle Scalenes
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS.
The anterior and middle scalenes share an anatomical significance and are of critical importance when thoracic outlet syndrome (TOS) is suspected. Because the neurovascular bundle (brachial plexus and subclavian artery and vein) of the cervical spine passes between these two muscles, hypertonicity of these muscles can impinge on the bundle and lead to TOS. Therefore, they are grouped here for examination and exploration.
Origin: Anterior: C3-C6 transverse processes; Middle: C2-C7 transverse processes
Insertion: First rib
Action: Cervical flexion, elevation of the first rib during inspiration, cervical rotation to the same side, cervical lateral flexion to the same side
Innervation: C3-C8 (cervical nerves)
Palpation Procedure
- Place the patient in a supine position, and stand behind the patient's head. Position the anterior scalene under the distal lateral margin of the SCM with the middle scalene just behind the SCM.
- Ask the patient to slightly flex and rotate the head to the opposite side and while tucking under the SCM to gain access to the muscular belly of the anterior scalene.
- Gently strum over the anterior scalene following it inferiorly as it disappears under the clavicle.
- Ask the patient to inspire during palpation to feel its contraction.
- Now move laterally off the anterior scalene onto the middle scalene, which will be broader than the anterior scalene.
- Strum across the middle scalene following it as far as you can up and down its fibers.
- Avoid compressing this juncture when palpating these structures because doing so can cause sharp radiating nerve pain as a result of compression of the neurovascular bundle.
- Note the location of any tender points or fasciculatory response along the muscles and their attachment sites.
- Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
Anterior and middle scalenes palpation procedure.
Postmastectomy interventions
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation.
The classical treatment for breast cancer based on 2014 NCCN guidelines includes two options: breast conservation therapy consisting of a lumpectomy followed by radiation therapy, or a more aggressive approach such as mastectomy with or without radiation. Regardless of the option chosen, complications often result (Andrews et al. 2000) and can persist for several years or more if left unchecked (Ebaugh et al. 2011). Complications that often result from classical treatment are shoulder and chest wall pain, subcutaneous fibrosis, decreased shoulder range of motion, lymphedema, impaired scapulothoracic function, axillary web syndrome, shoulder girdle weakness and altered alignment (Fourie and Robb 2009), and shoulder girdle somatic dysfunction (Ebaugh et al. 2011). One reason a mastectomy patient may complain of shoulder pain and dysfunction is that the somatic dysfunction that ensues from surgery may cause rotator cuff disease (Ebaugh et al. 2011). Shoulder girdle somatic dysfunction, whether driven by active or latent osteopathic lesions, impairs range of motion, strength, and scapulothoracic rhythm (Lucas et al. 2004), which may inhibit the rotator cuff's ability to stabilize the humeral head in the glenoid fossa. This can result in the impingement of the supraspinatus tendon at the subacromial arch (Ebaugh et al. 2011).
Although early detection and survival rates have improved over time, no therapeutic interventions have been found to be superior in addressing the associated surgical complications of mastectomy (Ebaugh et al. 2011; Todd et al. 2008). In our clinical practice, we have found PRT to be an extremely effective tool to address postmastectomy pain, shoulder girdle weakness and range of motion deficits, and resultant shoulder and chest wall somatic dysfunction. Most patients report pain-free ADLs within six weeks.
The application of PRT to this population opens the door for effective rehabilitation to occur because it frees hypertonic tissues, thereby taking pressure off lymphatic and vascular tissues. This may improve perfusion-engendering tissue homeostasis, increase strength, and restore shoulder girdle function and range of motion. Most important, PRT dramatically reduces pain at rest and with ADLs, allowing postmastectomy patients to resume normal life and sport activities without physical impairment. Therapists should take the following into consideration when using PRT with mastectomy patients:
Clinician Therapeutic Interventions
Postmastectomy
- Perform an evaluation to determine the magnitude of shoulder girdle dysfunction.
- Examine the affected tissues for the presence of axillary web syndrome, which may need additional therapeutic and surgical interventions to resolve.
- Perform PRT first; then treat recalcitrant tissues with therapeutic ultrasound or another deep heating modality to facilitate collagen reorganization under range of motion restoration procedures.
- Use myofascial release and massage post-PRT treatment to increase blood flow, relax tissues, and further fascial unwinding.
- Educate the patient about chronic pain control methods such as meditation, visual imagery, ADLs, and palliative modalities.
- Initiate a progressive therapeutic program to address deficits found in the initial evaluation.
- Teach the patient how to self-release affected tissues.
Patient Self-Treatment Interventions
- Perform self-release daily.
- Perform a daily self-massage for five to eight minutes on affected tissues.
- Stretch affected tissues daily or after physical activity.
- Apply palliative modalities to control pain and spasm.
- Meditate or perform relaxation pain control techniques daily to reduce chronic pain.
Postconcussion Syndrome
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011).
A concussion is a traumatically induced disturbance in brain function that may or may not involve the loss of consciousness (Reddy 2011). Injury to the brain is mainly considered a neurometabolic dysfunction, which occurs as a result of imparted linear and rotational forces to the brain within the cranial vault (Herring et al. 2011). Concussion statistics are becoming alarming. It has been estimated that each year in the United States there are 1.7 to 3.8 million sport-related concussions and 275,000 hospitalizations and 52,000 deaths related to concussions (Selassie et al. 2013). Fortunately, 80% of concussion symptoms resolve within 6 to 12 weeks after injury (Reddy 2011). However, a percentage of patients, termed the "miserable minority" (Reddy 2011), have symptoms that last for months or years causing significant impairment in social and occupational functioning. These people are often classified as having postconcussion syndrome. Besides the presence of a headache, people with postconcussion syndrome typically present with clustered symptoms that typically fall into three categories (Gladstone 2009):
- Somatic: Dizziness, tinnitus, photophobia, phonophobia, blurred vision, diminished sense of smell, fatigability
- Cognitive: Impaired attention, concentration, speed of processing, and memory
- Psychological: Depression, anxiety, irritability, apathy, and insomnia
Postconcussion syndrome patients may have just a headache or a combination of all of the clustered symptoms. Treatment to date for an acute concussion has consisted of rest (physical and cognitive), pharmacological intervention, and neurocognitive rehabilitation.
Recently, studies in the literature have focused on other treatment options such as vestibular rehabilitation (Alsalaheen et al. 2010; Weightman et al. 2010), visual training (Greenwald, Kapoor, and Singh 2012; Weightman et al. 2010), cardiorespiratory training (Griesbach, Houda, and Gomez-Pinella 2009; Kozlowski et al. 2013; Willer and Leddy 2006), and treatment of the cervical spine (Weightman et al. 2010) with promising results. Of particular interest are the cervical spine structures that are closely linked to structures that cause many of the symptoms of concussion and postconcussion syndrome. Cervicogenic headache frequently coexists with complaints of dizziness, tinnitus, nausea, imbalance, hearing problems, and eye and ear pain. Baron, Cherian, and Tepper (2011) and Biondi (2005) identified the greater occipital nerve as the source of these symptoms. Referral patterns for the three occipital nerve roots (C1-C3) and their convergence on the nucleus caudalis of the trigeminal tract, along with their joint complexes, have been identified as possible sources of head pain and myofascial trigger points in the head and neck (Simons et al. 1999).The receptors in the cervical spine also have many connections to the vestibular and visual apparatus. Dysfunction of the cervical spine receptors can alter afferent input, subsequently changing the integration of timing and sensorimotor control (Stirimpakos 2011; Treleaven 2008).
Another area of interest that requires attention is the sphenobasilar synchondrosis and the important neurological structures that overlay this anatomical structure. Involvement of the sphenobasilar synchondrosis has been controversial since the publication of Dr. William Sutherland's classic work The Cranial Bowl (1939). Some anatomists and clinicians firmly believe that this synchondrosis does not move after age 25 (Chaitow 1999). Upledger and Vredevoogd (1983) and Chaitow (1999) wrote that sphenobasilar dysfunction in somatic illness may be a result of external forces from muscles, soft tissues, and dural membrane tension (Chaitow 1999).
It is not my intent to focus on the movement debate in this section; however, important neurological structures that lie over the sphenobasilar-occipital complex and the caudal side of the brain may be affected with concussion, such as the cranial nerves, especially the oculomotor and optic chiasm (Moore 1985; Warwick and Williams 1973). Practitioners who believe that the sphenobasilar complex can be involved in head trauma report treating the following symptoms: headaches; eye - motor difficulties; head, neck, and back pain; TMJ pain; endocrine disturbances; reading and focus difficulties; anxiety; and depression (Koren 2006). It is interesting to note that these symptoms are similar to those experienced by patients who are treated for acute concussion and postconcussion syndrome.
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