New Frontiers in the Matrix of Myofascial Pain: Integrating Objective Physical Findings with Pain Mechanisms and Treatment Strategies Jay P. Shah, MD Oslo 17-18 oktober 2014 Course Background and Purpose:
Chronic pain states are characterized by profound changes in neuronal excitability and architecture in the pain matrix. These neuroplastic changes o ccur in the spinal cord, thalamic nuclei, cortical and limbic areas and may a lter the threshold, intensity and affect a ffect of one’s pain experience . Moreover, the dynamic dynamic changes that occur during during the initiation, amplification and perpetuation of chronic pain syndromes may provide explanations for some of the effects observed following dr y needling and other p hysical medicine modalities. Musculoskeletal pain is the most common manifestation of chronic pain. The t erm neuromusculoskeletal pain is preferable when describing a chronic musculoskeletal pain state because it accurately implies fundamental alterations alterations in the nervous system – system – sometimes sometimes irreversibly so. Spinal Segmental Sensitization (SSS) is a hyperactive state of the dorsal horn caused by bombardment of nociceptive impulses from sensitized sensitized and/or damaged tissue (somatic, visceral, etc.). Act A ctii ve (i.e., spontaneously painful) myofascial trigger po ints (MTrPs) are the most common source of sensitization. Emphasis w ill be placed on their identification and treatment. Objective, reproducible manifestations of SSS include dermatomal allodynia and hyperalgesia, sclerotomal tenderness and MTrPs within the involved myotomes. In this workshop, participants will learn important palpation skills and how to identify clinically relevant MTrPs and and objective physical findings of SSS. These easy-to-learn examination skills are fundamental to the evaluation and management of chronic neuroneuromusculoskeletal pain. Participants will also practice specific needling techniques and physical medicine modalities to deactivate painful MTrPs, desensitize desensitize the involved spinal segment and learn how to objectively determine whether the MTrP and physical manifestations of SSS were resolved following their treatment selection.
This workshop will integrate emerging knowledge from the pa in sciences in a clinically accessible way. For example, participants will learn how microanalytical techniques provide unique insight into the local biochemical milieu of human muscle. These techniques have confirmed that acti var iety of acti ve MTrPs have elevated levels of a variety biochemicals, including inflammatory mediators, neuropeptides, neuropeptides, cytokines and
catecholamines. Not only are these substances are known to be associated with persistent pain states and inflammation, but they are also very effective at sensitizing peripheral nociceptors, leading to peripheral sensitization. Furthermore, persistent noxious input from peripheral nociceptors can then lead to central sensitization. The results of these processes are local pain and muscle tenderness, allodynia, hyperalgesia and referred pain, among other symptoms. Course participants will also learn how innovative applications of ultrasound techniques are being used to visualize MTrPs and measure their stiffness properties and local blood flow. These quantitative, office-based techniques demonstrate that MTrPs in the up per trapezius are stiffer than the surrounding tissue and that active MTrPs can be distinguished from latent MTrPs by their high resistance blood flow. There has been a fundamental change in our understanding of the factors involved in the initiation, amplification and perpetuation of persistent musculoskeletal pain states. For example, prolonged noxious input, especially from muscle (i.e., from an active MTrP), may lead to long-term changes in gene expression, somatosensory processing and synaptic structure in dorsal horn neurons and other CNS structures. Under normal circumstances, neurons carrying nociceptive information are co ntrolled by inhibitory interneurons — structures in the dorsal horn critically involved in preventing the t ransition from acute to chronic pain. Ho wever, continuous noxious input, particularly that coming from muscle nociceptors, results in the co-release of glutamate and substance P (SP). Together, these two biochemicals bind to their respective receptors on post-synaptic neurons, and induce sensitization of wide dynamic range (WDR) dorsal horn neurons (i.e., central sensitization). Furthermore, sustained release of SP and glutamate will cause inhibitory neurons to undergo apoptosis (i.e., programmed cell death), leading to a persistent sensitized state. This lowers the neurons’ activation threshold and opens previously ineffective synapses, causing an expansion of the receptive field of pain, referral of pain, allodynia and hyperalgesia. Central sensitization may also facilitate additional responses from other receptive fields as a result of convergent somatic and visceral input at the dorsal horn via WDR neurons . The resulting somato-visceral and viscero-somatic reflexes provide important clues about underlying pain mechanisms. Upon reaching the dorsal horn, the stimuli ascend the spinothalamic tract to reach higher brain centers. In addition to activating the thalamus, muscle afferent input preferentially activates the limbic system (i.e., the anterior cingulate gyrus, insula and a mygdala), which plays a critical role in modulating muscle pain a nd the emotional or affective component to persistent pain. Increased activity in the limbic system leads to greater fear, anxiety and stress. There is a dynamic balance between supraspinal descending facilitation and inhibition. For example, the rostral ventral medulla (RVM) is a relay area between the periaqueductal gray (a structure located in the midbrain) and the spinal cord. The RVM
contains a population of “on” cells and “off” cells which can either increase or decrease the level of pain, respectively. It does so though projections that modulate activity in the dorsal horn. The purpose of this workshop is for participants to learn about t he exciting and impactful advances in the pain sciences and immediately integrate this information in their clinical practice. Participants will learn how to identify active MTrPs and determine the objective, reproducible manifestations of spinal segmental sensitization. Demonstrations will include needling techniques and p hysical medicine modalities that are essential for effective pain management of neuro-musculoskeletal pain, targeting both the peripheral pain generators and the central paraspinal manifestations of SSS. Learning objectives: •
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Analyze the dynamic relationship between primary afferent nociceptors and surrounding tissues and the concept of per ipheral sensitization Integrate the concept of polysensory synaptic convergence, activity-dependent neuroplasticity and central sensitization of dorsal horn neurons Understand the concept of “afferent drive” Discuss the unique characteristics of muscle pain co mpared to cutaneous pain Understand the mechanisms of muscle pain underlying pain referral patterns, development of hyperalgesia and expansion of the receptive field of pain Discuss the critical role of dorsal horn synaptic connections in the development o f allodynia, hyperalgesia and amplification of chronic musculoskeletal pain Analyze a mechanism for the loss of spinal inhibitory neuro ns and the creation of an uninhibited segment Understand the components of spinal facilitation and how it is generated and amplified Discuss the mechanisms by which even A ß fiber stimulation can perpetuate spinal facilitation and maintain chronic pain states Understand the roles of sensitization and neuroplasticity in generating, a mplifying and perpetuating chronic musculoskeletal pain Discuss the interplay of somato-visceral/viscero-somatic integration and spinal facilitation Discuss how muscle pain preferentially activates limbic system structures, providing a neuro-physiological basis for increased anxiety, stress and fear Review the pathophysiology, diagnosis and referral patterns for common myofascial trigger points Learn palpation techniques to identify common myofascial trigger points (MTrPs) Discuss treatment techniques for myofascial pain Demonstrate that active myofascial trigger points in the upper trapezius have a unique biochemical milieu of substances known to be associated with persistent pain states, sensitization and inflammation Discuss how subjects with an active MTrP in the upper trapezius have elevated levels of inflammatory mediators, neuropeptides, and cytokines, etc. in a remote, uninvolved muscle compared to latent and normal subjects.
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Demonstrate how the concentration of specific analytes dramatically changes in response to initial acupuncture needle insertion and also following a local twitch response with dry needling, particularly in active MTrPs Introduce novel applications of ultrasound techniques to visualize MTrPs, measure their stiffness properties and local blood flow Demonstrate that MTrPs in the upper trapezius are stiffer than surrounding tissue and that active MTrPs can be distinguished from latent MTrPs b y their highresistance blood flow Determine the reproducible physical manifestations o f sensitization in chronic myofascial pain How to integrate palpation techniques in your clinical practice in order to determine the affected dermatomes, myotomes and sc lerotomes in chronic neuromusculoskeletal pain Demonstrate needling techniques and physical medicine modalities used to desensitize the involved segments, eliminate active MTrPs and alleviate chronic neuro-musculoskeletal pain Understand the critical role of sensitization and neuroplasticity in generating and perpetuating neuro-musculoskeletal pain Determine objectively whether the physical manifestations of segmental sensitization were eliminated following your treatment selection
Speaker Bio:
Jay P. Shah, MD is a physiatrist and clinical investigator in the Rehabilitation Medicine Department at the National Institutes of Health in Bethesda, Maryland USA. His interests include the pathophysiology of myofascial pain and the integration of physical medicine techniques with promising complementary approaches in the management of neuromusculoskeletal pain and dysfunction. He also completed a two-year Bravewell Fellowship at the Arizona Center for Integrative Medicine. Jay is a well-known lecturer on mechanisms of chronic pain, myofascial pain, a cupuncture techniques and other related topics. He and his co- investigators have utilized novel microanalytical and ultrasound imaging techniques that have uncovered the unique biochemical milieu and viscoelastic properties of myofascial trigger points and surrounding soft tissue. Jay has taught invited hands-on workshops for physicians, dentists, manual and physical therapists, naprapaths, acupuncturists, chiropractors, massage therapists, among other professional groups. His workshops integrate emerging knowledge from the clinical pain sciences in order to improve evaluation and management approaches to musculoskeletal pain and dysfunction. He was selected by the American Academy of Pain Management as the 2010 recipient of the Janet Travell Clinical Pain Management Award and by the National Association of Myofascial Trigger Point Therapists as the 2012 recipient of the David G. Simons Award.
