A Special Seminar in Toronto, June 22-23, 2024

Myofascial Trigger Points and Central Sensitization in Myofascial Pain Syndrome: Exploring their Enigmatic Pathophysiology, Dynamic Clinical Manifestations and Novel Strategies for Optimizing Patient Outcomes

Presented by Jay P. Shah, MD & John Srbely, DC PhD

Participants in this state-of-the-art course will acquire an in-depth understanding of the emerging research characterizing the pathophysiology and clinical manifestations of myofascial pain syndrome (MPS). The curriculum will focus on a mechanism-based approach for the diagnosis and treatment of MPS, anchored in a neuro-segmental model that reflects the current understanding of the pathophysiology and clinical manifestation of central sensitization.

This course will also emphasize the application and interpretation of Quantitative Sensory Testing (QST) diagnostic methods, such as algometry and the windup technique. These office-based methods enable clinicians to effectively measure the degree of patient sensitization.

Such measures will be presented as objective, clinically applicable, and grounded in the known mechanisms of MPS, thus equipping clinicians with mechanism-based assessment tools that
they can seamlessly integrate “on Monday morning” into their diagnostic protocols for managing chronic myofascial pain syndrome.

Non-pharmacological approaches such as dry needling, physical modalities (electrical stimulation, therapeutic ultrasound), and manual mobilization/manipulation will be discussed, demonstrated, and practiced by attendees. These techniques aim to deactivate painful myofascial trigger points (MTrPs), desensitize affected segments, and neuro-modulate subcortical dysfunction, providing more permanent pain and symptom relief. The diagnostic and treatment techniques presented in this workshop are applicable in the management of a variety of chronic myofascial and musculoskeletal pain conditions.

Location: Courtyard Toronto Airport, 231 Carlingview Drive, Toronto, ON M9W 5E8
Schedule: Saturday June 22, 9:00 am – 6:00 pm and Sunday June 23, 9:00 am – 5:00 pm.
In-person seminar only.
Fees: Acupuncture Canada members pay $549 + tax. Non-members pay $649 + tax. Lunches included.
All clinical supplies will be provided.
Dry needling is one of several therapies that will be discussed, so participants do not need needling experience to take the course.

Learning Objectives

In this workshop 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.

(Specific topics include how to clinically employ Quantitative Sensory Testing (QST) in assessing central sensitization, temporal summation (windup) and its unique somatosensory profile (allodynia, hyperalgesia). Application and interpretation of brush allodynia, algometry, mechanical pain thresholds (MPT) and windup ratio (WUR) using a novel weighted pinprick technique will be demonstrated.)

5. How to design a mechanism-based treatment approach (e.g., dry needling [peripheral and paraspinal], trigger point release, manual mobilization/manipulation, electrical stimulation and therapeutic ultrasound) to desensitize involved segments, eliminate chronic MTrPs and alleviate chronic MPS.

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

Speaker Bios:

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 neuro-musculoskeletal pain and dysfunction. He also 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 syndromes (including chronic pelvic pain), myofascial pain, dry needling, 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. Their studies have demonstrated objective, reproducible and quantifiable muscle tissue properties associated with MTrPs and the quantitative effects of dry needling of active MTrPs on these tissue properties, in addition to showing significant improvements in pain, range of motion and patient self-report outcomes in mental health and physical function.

In addition, Jay has done novel collaborative research studies (with a gynecologist and neurologist) on chronic pelvic pain and endometriosis at the NIH. He and his team have published several landmark papers in this area. Moreover, their work has been internationally recognized and called “transformative” by the World Endometriosis Foundation. Their clinically impactful studies have helped shift the focus from studying endometriosis lesions to understanding how endometriosis and pain are related with emphasis on elucidating the underlying mechanisms of chronic pelvic pain.

Jay has given hundreds of invited lectures and hands-on courses nationally and internationally for physicians (allopathic and osteopathic), physiotherapists, physician assistants, nurse practitioners, dentists, chiropractors, manual therapists, and acupuncturists, among other professional groups. His presentations integrate the fascinating and impactful knowledge emerging from the basic and clinical pain sciences, thereby helping clinicians to optimize their 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.

John Z Srbely DC PhD holds a full-time position as Associate Professor in the Department of Human Health and Nutritional Science at the University of Guelph, Ontario, Canada. His professional journey began in 1992 as a clinician practicing chiropractic and acupuncture, specializing in the treatment of chronic myofascial pain. This early clinical experience sparked his curiosity about the physiological effects and mechanisms of chronic musculoskeletal pain and drove him to receive his PhD in neurophysiology and biomechanics in 2008, marking the commencement of his research journey.

Dr. Srbely’s research interest focuses on the pathophysiological mechanisms of myofascial pain by employing both animal and human models. His unique perspectives as a clinician and scientist enable him to effectively bridge the gap between the basic and clinical sciences. His work specifically focuses on understanding the roles of central sensitization and neurogenic inflammation in the pathophysiology of myofascial pain. In particular, he has pioneered research demonstrating the potentially important contribution of degenerative spine and/or joint disease in the pathophysiology of myofascial pain, with potentially significant implications to the clinical diagnosis and management of chronic myofascial pain.

This comprehensive research approach aims to not only deepen our understanding of these complex mechanisms but also transform this knowledge into advancing clinically feasible, mechanism-based diagnostic techniques. He is actively studying ways of standardizing quantitative sensory testing (QST) methods that specifically target the underlying mechanisms of central sensitization and windup phenomena for use in the quantitative assessment of chronic pain patients. This initiative is part of his broader efforts supported by the HEAL Initiative (NIH), reflecting his collaborations with researchers at George Mason University and the National Institutes of Health (NIH) targeting novel biomarkers for myofascial pain syndrome. His research has been internationally recognized, most notably through a prestigious Natural Sciences and Engineering Research Council of Canada (NSERC) Discovery Grant.

Full Workshop Description:
Participants in this interactive, hands-on, thought-provoking, and clinically impactful workshop 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). Participants will learn and integrate important palpation skills and psychophysical quantitative sensory testing techniques with various needling and electrical stimulation techniques to treat painful MTrPs and sensitized spinal nerve segments more effectively.

An important dichotomy in the current literature is whether the MTrP is a cause or effect (i.e., 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.

Accordingly, 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.

We will present novel clinical and animal model research from our lab demonstrating strong neuro-inflammatory responses in neuro-segmentally linked muscles and joint cartilage subsequent to both naturally occurring and experimentally induced spine osteoarthritis models. Intriguing findings greatly enhance our understanding of the underlying neuro-inflammatory, neuro-segmental mechanisms in muscle, elucidate the potential physiologic mechanisms contributing to the dynamic clinical manifestations of chronic MPS, and, most importantly, have profound implications for patient management and optimizing outcomes.

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 (e.g., endometriosis, peptic ulcer disease, cystitis, etc.) are very common sources of persistent nociception and sensitization that often results in SSS, facilitated segments, somato-visceral interactions, 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. If activated, painful MTrPs, in turn, may serve as an additional source of nociceptive input, and become a key component of a chronic visceral condition – even if the underlying visceral condition has been optimally managed – creating enormous diagnostic confusion. Apropos, the deactivation of active MTrPs through a targeted intervention may be a critical aspect to reversing central sensitization and improving pain associated with an underlying visceral disorder such as endometriosis.

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.