Biography

Jay P. Shah, MD is a physiatrist and clinical investigator in in Bethesda, Maryland. His interests include the pathophysiology of myofascial pain and the integration of physical medicine techniques with promising complementary approaches in the management of neuro-musculoskeletal pain and dysfunction. He completed the one-year UCLA Medical Acupuncture course and 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, neuro-anatomical acupuncture 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. 



 He has given many invited lectures and hands-on courses nationally and internationally for physicians, myofascial trigger point therapists, physiotherapists, osteopaths, chiropractors, massage therapists, acupuncturists, and dentists, among other professional groups. His presentations integrate the fascinating knowledge emerging from the basic and clinical pain sciences in order to optimize evaluation and management approaches to musculoskeletal pain and dysfunction.

 Jay was selected by the American Academy of Pain Management as the 2010 recipient of the Janet Travell Clinical Pain Management Award for excellence in clinical care and by the National Association of Myofascial Trigger Point Therapists as the 2012 recipient of the David G. Simons Award for excellence in clinical research.

Topic: Myofascial Trigger Points and Central Sensitization in the Neuro-Matrix of Chronic Pain: Exploring their Enigmatic Pathophysiology, Dynamic Clinical Manifestations and Novel Strategies for optimizing Patient Outcome

(2 NCBTMB Approved CE Hours)

Participants in this interactive, thought-provoking and clinically impactful lecture will explore the dynamic and pivotal roles that myofascial trigger points (MTrPs), sensitization, limbic system dysfunction and associated objective/quantitative physical findings play in the evaluation and management of chronic myofascial pain syndrome (MPS). 

An important dichotomy in the current literature is whether the MTrP is a cause or effect (chicken or the egg?) of chronic MPS. The emerging research in basic and clinical neurosciences informs novel directions in the clinical diagnosis and management of MPS.

The Integrated Hypothesis is the current prevailing theory characterizing the pathophysiology of MPS. According to this hypothesis, MTrPs are the primary source of nociception (cause) in MPS and are caused by a local injury to the muscle, either acute or chronic, leading to dysfunctional motor endplates and local muscle contracture.

Emerging research, however, suggests that neurogenic mechanisms play a foundational role in the formation of MTrPs and MPS without the need for direct local injury to the muscle. Accordingly, the Neurogenic Hypothesis proposes that the clinical manifestations of MPS are initiated, amplified and facilitated by central sensitization, in the absence of mechanical injury to the muscle.

MTrPs may form secondary to central sensitization (effect) evoked by persistent nociceptive input from a distinct primary pathologic source (either somatic or visceral) in the common neuromeric field and/or dysfunction of descending pain modulation.

Long considered a “local” pain syndrome, MPS actually has a broader impact beyond the active (i.e., spontaneously painful) MTrP and has significant associations with mood, health-related quality of life and function. In fact, recent findings compel us to look at the phenomena of MPS and MTrPs as a type of spectrum disorder of sensitization that manifests clinically by varying symptoms and signs.

Spinal segmental sensitization (SSS) is a hyperactive state of the dorsal, ventral and intermediate horns of the spinal cord caused by bombardment of nociceptive impulses. Active MTrPs, osteoarthritis and visceral conditions are a very common source of persistent nociception and sensitization that often results in SSS, facilitated segments, somato-visceral effects, and chronic myofascial pain. 

In addition, viscero-somatic convergence may not only provide the means for pain referral to somatic structures, but may also govern the reflex that induces muscle spasm and the eventual formation of MTrPs. Painful MTrPs, in turn, may serve as an additional source of nociceptive input, and become a key component of a chronic visceral condition. Apropos, their deactivation through a targeted intervention may be a critical aspect to reversing central sensitization and improving pain associated with an underlying visceral disorder. 

Conversely, maladaptive changes in subcortical structures and dysfunctional descending inhibition may create somatic tissue abnormalities (e.g., tissue texture changes, tenderness, etc.) in addition to adversely impacting mood, affect and sleep. Either way, typical manifestations of the sensitized spinal segment include dermatomal allodynia/hyperalgesia, sclerotomal tenderness and MTrPs within the affected myotomes. These objective, quantitative and reproducible findings allow the clinician and patient to identify the affected spinal segment(s) that should be treated.

Non-pharmacological approaches such as dry needling, and physical modalities (e.g., electrical stimulation) will be discussed. These techniques aim to deactivate painful MTrPs, desensitize affected segments and neuro-modulate subcortical dysfunction, providing more permanent pain and symptom relief. The diagnostic and treatment techniques presented in this lecture are applicable in the management of a variety of chronic musculoskeletal pain conditions.

Learning Objectives

 In this lecture participants will learn:       

1.  The unique neurobiology of muscle pain and the dynamic interplay of muscle nociceptors and endogenous biochemicals in the initiation, amplification, and perpetuation of peripheral and central sensitization and neurogenic inflammation. (Specific topics include determining whether the MTrP is the primary pathology or secondary manifestation in the clinical presentation of MPS.)

2.  The pivotal roles of persistent nociceptive bombardment, central sensitization, neurogenic inflammation, wide dynamic range neurons, limbic system structures, and dysfunctional descending inhibition in mediating muscle sensitization, pain chronification, receptive field expansion, and somato-visceral interactions.

3.  How novel applications of diagnostic ultrasound can be used as objective, quantifiable and repeatable outcome measures for dry needling and electrical stimulation techniques. Specific topics include ultrasound imaging to visualize MTrPs, measure their stiffness properties (elastography) and local blood flow to differentiate them from normal muscle tissue.

4.   How to identify the reproducible manifestations of spinal segmental sensitization (involving dermatomes, myotomes, and sclerotomes) and examine the objective, quantifiable and reproducible physical findings of allodynia, hyperalgesia and referred pain patterns in MPS.

5.  How to design a mechanism-based treatment approach (e.g., dry needling [peripheral and paraspinal], and electrical stimulation to desensitize involved segments, eliminate chronic MTrPs and alleviate chronic MPS.

6.  Insights into how therapists can immediately integrate these concepts and techniques into a contemporary neurophysiologic paradigm for management of chronic pain into clinical practice.

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