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Clinical Guide to Positional Release Therapy An understanding of how PRT promotes tissue healing through the manipulation of the somatic nervous system has only recently begun to emerge. The somatic nervous system provides the ability to experience and respond to pleasurable and painful stimuli. St...

Clinical Guide to Positional Release Therapy An understanding of how PRT promotes tissue healing through the manipulation of the somatic nervous system has only recently begun to emerge. The somatic nervous system provides the ability to experience and respond to pleasurable and painful stimuli. Stimuli perceived and transmitted by the somatic system are touch, temperature, pain, and body position or proprioception (Bear, Connors, and Paradiso 2007). This chapter explores how these four senses affect the somatic system based on foundational neurophysiological processes and prevailing and emerging theories of somatic dysfunction. This examination explains why somatic dysfunction may result in the development and persistence of osteopathic lesions. The clinical implications of the theory and research presented are also discussed. Neurophysiological Foundations A general overview of how stimuli travel in the nervous system is in order prior to discussing how they produce and sustain somatic dysfunction. Neurons located outside the spinal column are called first order neurons, those in the spinal cord are second order, and those in the cortex are third order (see figure 2.1). Sensory information from the periphery (first order) is transmitted toward the spinal cord (second order) segment’s dorsal, or posterior, horn. Pleasurable and painful sensory information flows into the dorsal horn and loops into the ventral, or anterior, horn of the spinal segment via interneuron connectors. A sensory stimulus of sufficient magnitude will both activate and inhibit alpha motor Cerebrum neurons located in the ventral, or anterior, aspect of the segment. Additionally, alpha motor neuron activation can elicit a motor response from both the somatic and visceral tissue associated with its segmental innervation. It is well known that when tissues are activated, inhibition also occurs (Byrne 1997). Therapy practitioners often use this principle during proprioceptive neuromuscular facilitation (PNF) stretching by manipulating the proprioceptors through a series of contractions interspersed with static stretching in diagonal patterns to gain greater tissue relaxation (Herbert and Gabriel 2002). Therefore, if tissues in a particular spinal segment are hyperactive, other tissues that the segment innervates may also be inhibited. The sensory to motor neuron pathway that directly controls the facilitation and inhibition of tissues forms a reflex arc known as the stretch, or myotatic, reflex (see figure 2.2). We have all had this reflex activated by having our deep tendon reflexes tested during a physical (e.g., the patellar tendon reflex). Simply, tissues subjected to an abrupt stretch produce an involuntary muscle contraction; however, pain can also activate this reflex. Although the myotatic reflex is localized to the first and second neuron levels, sensory information, whether from a painful or nonpainful origin, travels along two other primary neuronal pathways onward to the cortex. Touch travels via the dorsal column–medial lemniscal pathway, whereas pain and temperature primarily travel along the lateral spinothalamic tract (see figure 2.1). Special consideration is paid to how pain travels through the spinal segment because when a painful stimulus is sent to the spinal cord, it may not only activate an efferent Medulla Primary somatosensory cortex Third order neuron Spinal cord Dorsal column nuclei Medial lemniscus Dorsal horn First order neuron Mechanoreceptors Thalamus Proprioceptors Second order neuron Thermoreceptors Spinothalamic tract Nociceptors Dorsal column-medial lemniscal tract Figure 2.1 16 Somatic system neuron level organization. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. E6296/Speicher/Fig. 02.01/497364/JG/R2-alw Positional Release Therapy Research and Theory Afferent nerve Muscle spindle Quadriceps muscle Alpha motor (efferent) nerve Infrapatellar tendon of quadriceps Figure 2.2 Stretch reflex. and below a facilitated segment (Bailey and Dick motor response on the same sideE6296/Speicher/Fig. of the body 02.02/531992/JG/R1 1992), which may also explain why one facilitated where the stimulus occurred, but also produce segment may spark the facilitation and inhibition a motor and inhibition response on the opposite of tissues at multiple spinal levels. side of the body (Kandel, Schwartz, and Jessell When pain ascends from the facilitated segment 2000). For example, during the withdrawal reflex to higher-order neurons, such as the reticular for(touching a hot stove), the activation and inhibition mation in the brain stem and the somatosensory of anterior and posterior muscles on both sides of cortex, those at the brain stem play a major role the body allow the person to both pull away and in processing the pain response versus the perstep back from the harmful stimulus. The reflexive ception of the pain at the somatosensory cortex. cocontraction on the opposite side of the body is The medullary neurons of the periaqueductal gray facilitated by the cross-spinal reflex at the spinal matter (PAG) and raphe nuclei in the brain stem segment (Kandel et al. 2000). This may help to project to the dorsal horns to suppress activity explain why tender and trigger points develop of the nociceptor fibers (A delta and C fibers) at in both agonist and antagonist tissues as a result the dorsal horn where they terminate (Hocking of an unanticipated abrupt movement, or what 2013). These higher-order neurons have also been Jones (1973) termed a strain counterstrain (SCS) proposed to regulate gamma motor neuron activity mechanism. (Capra, Hisley, and Masri 2007), which regulates The segmental crossing of the pain pathway may the sensitivity of the muscle spindle to stretch and also activate contralateral alpha motor neurons, velocity change (Kandel et al. 2000). which explains why people often develop lesions Gamma motor neurons are located in the ven(trigger and tender points) on the side of the body tral, or anterior, horn of the spinal segment along opposite the involved side, in mirrorlike fashion. with alpha motor neurons. Unlike alpha motor Moreover, ascending and descending intersegmenneurons, however, gamma motor neurons do not tal neurons transmit nociceptive information above T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 17 Clinical Guide to Positional Release Therapy contract the extrafusal (striated muscle) fibers to produce joint movement. Gamma motor neurons contract the intrafusal fibers of the muscle spindle to regulate its sensitivity to stretch; however, activation of each type of fiber regulates the spindle differently (see figure 2.3). Muscle Spindle The muscle spindle is analogous to both how a bungee cord is constructed and how it responds to stretch. If a bungee cord is stretched, its sheath is elongated, but so are the internal strands, which produces the recoil. Each internal strand of the muscle spindle serves a specific function. The bag fibers respond primarily to the velocity of stretch and chain fibers, resting length, and joint position sense (Bear et al. 2007). The intrafusal and extrafusal fibers run parallel to one another. Because the intrafusal fibers are an internal component of an extrafusal fiber, changes in the length of the extrafusal fibers produce a response from the muscle spindle, and vice versa. The ability of the muscle spindle to produce a recoil, or to spring back from a stretch, is based on its afferent sensory fiber orientation. The wire coil seen on the end of a bungee cord is similar to the way the primary (Ia) afferent nerve fiber is arranged around the intrafusal fibers of the muscle spindle (see figure 1.2). The annulospiral endings of the Ia afferent fiber wraps around all of the intrafusal fibers (dynamic, static, and chain) and Extrafusal fiber transmits spindle changes the fastest to the second order. Type II afferent fibers, on the other hand, are slower to respond because they are connected not to the dynamic nuclear bag fibers, but to the static nuclear bag and chain fibers of the spindle. The type II afferent fiber and its respective intrafusal spindle fibers predominantly transmit information to the second order about body position and resting tissue length. It has been proposed that hyperactivity of the spindle afferents causes a sustained stretch reflex to occur, driven by increased gamma gain at the higher-order neurons (Korr 1975). Howell and colleagues (2006) observed a significant reduction in the human triceps surae stretch reflex when SCS was applied to the triceps surae musculature and surrounding tissue. Golgi Tendon Organ Another proprioceptor that works in concert with the muscle spindle to control muscle contraction is the Golgi tendon organ (GTO). The GTO is located at the musculotendinous junction, but unlike the spindle, it is responsive only to changes in tension within the musculotendinous tissues (see figure 2.3). The GTO acts much like a brake on the spindle’s fusimotor drive by communicating the level of tension of the overall complex to the second order on type Ib afferent fibers. The Ib afferent neural activity produced by GTO tension inhibits alpha motor neurons, thereby preventing the stretch reflex from damaging tissues when activated Gamma motor neuron from CNS Intrafusal fiber To CNS Sensory neuron Central region lacks actin and myosin (contractile proteins) Ib axon Muscle spindle Capsule Muscle spindle Golgi tendon organ 18 Sensory (afferent) neuron Collagen fiber Tendon Tendon Figure 2.3 Extrafusal muscle fibers Muscle spindle and Golgi tendon organ. T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. E6296/Speicher/Fig. 02.03/531995/JG/R1 Positional Release Therapy Research and Theory (Moore 2007). The greater the amount of tension applied to the complex is, the more alpha motor neuron inhibition is produced (Moore 2007). The spindle and GTO provide highly efficient proprioceptive feedback and regulation to changes in tissue elongation and tension, but not without the gamma motor neuron system’s influence. Gamma Motor Neuron System The gamma motor neuron system’s activity is influenced by visual, sensory, and motor activity (Bear et al. 2007). It is responsible primarily for regulating the sensitivity of the muscle spindle to changes in dynamic stretch as well as static length, but does not directly regulate the GTO. Gamma motor activity is heightened when a person anticipates a taxing motor activity, such as lifting a heavy object or jumping, priming the muscle spindles for the demand (Kandel et al. 2000). Pain also modulates the activity of gamma motor neurons. Inducing pain in the spinally innervated muscles of animals has been shown to both increase and decrease gamma activity of the spindles’ intrafusal fibers at rest (Appelberg et al. 1983; Thunberg et al. 2002). These observations led Johansson and Sojka (1991) to propose a pathophysiological nociceptive model. Their hypothesis is that increased fusimotor activity is the result of an accumulation of inflammatory metabolites from voluntary static muscular contraction, which stimulates A delta and C fibers, thereby elevating the neural discharge of the spindle afferents, which alters the spindles’ sensitivity to stretch during activity, but not at rest. However, validation of the influence of inflammatory metabolites on the stimulation of pain afferents and gamma motor neurons is lacking. Capra and colleagues (2007) did find that the algesic nociceptive chemical stimulation of jaw afferents in the rat both increased and decreased gamma motor neuron activity, but only at rest and not with jaw opening and closing. In the intervention group, a rise in the activity of static gamma–fusimotor activity was observed, but no effect was seen in dynamic gamma motor neuron activity levels during voluntary muscle activity. These findings both confound and lend support to Johansson and Sojka’s (1991) nociceptive model of fusimotor metabolite stimulation. Chemosensitive nociceptive afferents (pain fibers) have been shown to either inhibit or facilitate the static gamma–fusimotor activity of spinally innervated muscles at rest (Appelberg et al. 1983; Thunberg et al. 2002), but not during voluntary jaw muscular contraction (Capra et al. 2007). The presence of inflammatory metabolites produced from a painful mechanism may continue to affect spindle function and sensitivity via static gamma–fusimotor activity modulation at rest long after the initial insult has been removed. However, in the absence of pain, dynamic and static gamma activity increase with muscle contraction (Byrne 1997). Consider what occurs when a bungee cord is slack. Because the cord fibers are no longer stretched, there is no need for recoil. When no stretch stimulus is placed on the muscle spindle, the neural rate coding, or activity of the spindle afferent fibers, becomes silent, but gamma motor neuron activity increases to contract the spindle (reset its resting length) to prime it for another stretch stimulus (Bear et al. 2007; Byrne 1997). The interplay between spindle silencing and gamma activation is known as alpha-gamma coactivation, which maintains muscle tone (Kandel et al. 2000), or spindle readiness. The way the spindle and gamma system responds to slack may in part explain how PRT eliminates somatic dysfunction. When tissues are shortened, or placed in a position of comfort, the spindle’s afferent discharge becomes silent, interrupting the myotatic reflex and the stimulation of the alpha motor neurons to contract the extrafusal fibers. When spindles are silenced, gamma activity at the spindle increases to restore the resting length of the spindle (Matthews 1981) and possibly the sensitivity level of the spindle. It has been proposed that when gamma drive or volume is high, an increased sensitivity of the spindle to stretch results, which in turn hypersensitizes the monosynaptic stretch reflex (Korr 1975). Decreased sensitivity of the spindle’s stretch reflex has been observed with SCS in patients with plantar fasciitis (Howell et al. 2006), but the influence of this indirect therapy on the gamma system has not yet been evaluated in humans. Korr’s proprioceptive theory (1975) states that when gamma volume is high, proprioceptor (muscle spindle) dysfunction results during rest and an osteopathic lesion (tender or trigger point) may result. Korr’s theory is now bolstered by observations of altered static gamma–fusimotor activity to pain in the rat at rest (Capra et al. 2007) and a reduction of reflex arc activity when plantar foot spindles are shortened with an indirect positional release technique (Howell et al. 2006). T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 19 Clinical Guide to Positional Release Therapy Somatic Dysfunction and the Osteopathic Lesion Historically, the basis of somatic dysfunction was founded on the concept of the osteopathic lesion. Korr (1947) proposed that a lack of somatic system homeostasis manifests from joint derangement, also termed an osteopathic lesion. Korr described the osteopathic lesion as having five distinct attributes (1947, 191): 1. Hyperesthesia of the muscles and vertebrae 2. Hyperirritability, reflected in altered muscular activity and altered states of muscular contraction 3. Changes in the tissue texture of muscle, connective tissue [fascia], and skin 4. Changes in local circulation and in the exchange between blood and tissues 5. Altered visceral and other autonomic functions The lesion has been proposed to be associated with a hyperirritable spinal segment (Hocking 2013; Korr 1947) and shown to possess a low stimulus threshold (Hubbard and Berkoff 1993). Even when the body is at rest, the lesion’s associated motor neurons are easily activated to produce muscle contraction (Hong and Yu 1998; Hubbard and Berkoff 1993; Kostopoulos et al. 2008). Korr proposed that the main culprit in sensitizing the anterior horn cells, which regulate the efferent motor stimulation of extrafusal muscle tissue, was the postural, mechanical, and articular derangements resulting in alterations in the length–tension relationship between muscle and connective tissue—and that the change in length directly affects the proprioceptors (e.g., muscle spindle, mechanoreceptors, and nociceptors). Korr proposed not only that the spinal segment receiving afferent (sensory) impulses from the proprioceptors becomes hyperstimulated when an osteopathic lesion is present, but also that the segments above and below and all tissues receiving efferent innervation from the hyperstimulated segments also become facilitated. There has been considerable speculation and debate to date as to why and how lesions develop, as well as why they often persist, producing a multitude of theories and promising research to answer these questions. 20 Integrated Hypothesis Theory Positional release therapy’s ability to reduce somatic dysfunction has been thought to result primarily from the reduction of aberrant neural activity and the mediation of inflammation and circulation through manipulation of the somatic nervous system. Some of the earliest theories of somatic dysfunction, such as Korr’s proprioceptive theory (1975), focused on the muscle spindle as a primary culprit. Later theories moved toward a more integrated perspective, starting with the integrated hypothesis (Simons, Travell, and Simons 1999), which proposes that proprioceptors, the central nervous system (CNS), and biomechanical factors work together to produce and maintain somatic dysfunction, particularly the formation of trigger points. The crux of the integrated hypothesis theory is that electrical activity at the motor end plate (the neuromuscular junction where the alpha motor neuron interfaces with the muscle) becomes dysfunctional as a result of excessive acetylcholine (ACh) release into the synaptic cleft at the junction. Hocking (2013) contended that trigger point activation and maintenance is modulated at the alpha motor neurons within the dorsal horn, not at the motor end plate. Hocking’s central modulation hypothesis affirms that excessive ACh neuromuscular junction release causes increased motor end plate noise, or neural activity, but that the increased ACh release at the neuromuscular junction is elicited as a result of prolonged central sensitization at the alpha motor neurons, not at the motor end plate. Over time this causes a decrease in alpha motor neuron plateau depolarization levels, propagating the spontaneous release of ACh at the motor terminal. Hocking asserted that the decreased alpha motor neuron plateau depolarization “is the cause, not the result of the local energy crisis that perpetuates the TrP [trigger point]” (2013, 4). Impaired regulation of ACh release and uptake coupled with a hypoxic, or low, O2 tissue environment has been proposed to cause a depletion of adenosine triphosphate (ATP), causing an ATP energy crisis (McPartland 2004; Simons, Travell, and Simons 1999). ACh release activates nicotinic ACh receptors (nAChRs) on the postsynaptic membrane, sparking an action potential to cause extrafusal fiber muscle contraction (Matthews 1981). McPartland (2004) explained that excessive T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. Positional Release Therapy Research and Theory release of ACh either as a result of injury, genetic predisposition, or another insulting mechanism may produce sustained muscle contraction that compresses local sensory nerves within the muscular tissue. The increased release of ACh and resultant sustained muscular contraction compresses local vessels much like pinching off the flow of water from a garden hose, resulting in reduced tissue oxygenation and ATP levels. ATP serves a critical role in regulating muscle contraction. ATP is the fuel for the calcium pump, enabling the reuptake of calcium back into the sarcoplasmic reticulum, and powers muscle contraction by assisting the actin and myosin filaments to couple (attach) and uncouple (detach) from one another (Bear et al. 2007). Additionally, ATP inhibits the release of ACh (Dommerholt, Bron, and Franssen 2006). The increased demand for muscular contraction in the absence of a lack of fuel (ATP and O2) to power muscle contraction produces an energy demand that cannot be met, causing a release of proinflammatory metabolites (e.g., prostaglandin, leukotrienes, substance P) locally in the tissues to further sensitize nociceptors (McPartland 2004). The release of proinflammatory metabolites may also cause vascular endothelial dysfunction resulting in hypoperfusion of tissues (Larsson et al. 1999; Maekawa, Clark, and Kuboki 2002), producing mitochondrial damage, oxidative cellular distress, and tissue edema (Rosas-Ballina et al. 2011), which has been attributed to the formation of trigger points (McPartland and Simons 2006). Simons and colleagues (1999) hypothesized that once a trigger point forms, it generates nociceptive input to the CNS, producing central sensitization of the spinal segment. Central sensitization results from a constant barrage of nociception at the dorsal horn of the spinal cord, producing ectopic nociceptive impulses (McPartland 2004) from the second-order neurons. The abnormal pain impulses generated at the spinal cord can occur even when the insulting force has been removed and tissues are no longer acutely injured. Phantom limb pain, in which an amputee experiences pain in a limb that is no longer there, is a classic example of this phenomenon. Gerwin, Dommerholt, and Shah (2004) expanded on the integrated hypothesis of trigger point formation through a presentation of recent data of the well-known factors that cause the formation of trigger points, but provided additional propositions as to why trigger points persist. Expanded Integrated Hypothesis The expanded model (figure 2.4) presented by Gerwin and colleagues (2004) adds substantial evidence to support the basic tenets of Simons and colleagues’ (1999) integrated hypothesis, and builds on the model put forth by Shaw (2003). Their further discussion on the role of unaccustomed muscle contraction, tissue acidity, calcitonin gene–related peptide (CGRP), and hypoperfusion may help to clarify why somatic dysfunction sometimes persists beyond the acute stage of healing. (For a full review, see Gerwin et al. 2004.) A precipitating event that Gerwin and colleagues (2004) attributed to the onset of somatic dysfunction is unaccustomed or unexpected maximal muscle exertion of either an eccentric or concentric nature. Repeated eccentric contractions have been shown to damage sarcomeres and the vascular network within the muscular tissue environment (Stauber et al. 1990). Damage of the muscle’s fibrils and vascular supply produces a release of proinflammatory mediators that not only disturbs the excitation–contraction coupling system of the sarcomere (Proske and Morgan 2001), but also limits the supply of oxygen to the tissues, which produces capillary restriction (McPartland and Simons 2007). The capillary restriction and damage may impair cellular and tissue perfusion, resulting in greater acidity, or lower tissue pH (Sluka, Kalra, and Moore 2001; Sluka et al. 2003), thereby activating nociceptors, which sparks the release of calcitonin gene–related peptide (CGRP) from the motor terminal (Gerwin et al. 2004; Shah et al. 2003). CGRP is as an amino acid peptide that is well known for its ability to exert powerful peripheral vasodilation, but it has also been implicated in the mediation of the neural inflammatory response along with substance P (O’Halloran and Bloom 1991). CGRP exists side by side with ACh at the motor nerve synapse. When CGRP is elevated, ACh at the motor terminal increases because CGRP increases acetylcholine receptor (AChR) phosphorylation and prolongs the time ACh has to dock with its receptor channels at the postsynaptic membrane (Gerwin et al. 2004; Shah et al. 2003). Typically, acetylcholinesterase (AChE) breaks down ACh at the postsynaptic terminal (McPartland and Simons 2006), but AChE is pH dependent, and when pH is low, AChE production is decreased (Gerwin et T. Speicher, Clinical Guide to Positional Release Therapy, Champaign, IL: Human Kinetics, 2016). For use only in Positional Release Therapy Course 1–Sport Medics. 21