Jay P. Shah, MD is a physiatrist and clinical investigator in the Rehabilitation Medicine Department at the National Institutes of Health in Bethesda, Maryland. His interests include the pathophysiology of myofascial pain and the integration of physical medicine techniques with promising integrative approaches in the management of neuro-musculoskeletal pain and dysfunction. He also completed the 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, 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 (MTrPs) 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. 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.

This lecture will explore the dynamic and pivotal roles that MTrPs, sensitization, wide dynamic range neurons, and limbic system dysfunction play in the evaluation and management of chronic myofascial pain. Muscle pain’s unique neurobiology is due, in part, to the dynamic interplay of muscle nociceptors and endogenous biochemicals that contribute to the initiation, amplification and perpetuation of central sensitization. Active (i.e., spontaneously painful) MTrPs have elevated levels of inflammatory mediators, neuropeptides, catecholamines, protons and pro-inflammatory cytokines. These substances are known to be associated with neurogenic inflammation, central sensitization, inter-cellular communication, persistent pain states, and somato-visceral interactions. They actions may also underlie the objective, reproducible physical findings of allodynia and hyperalgesia commonly found in patient with chronic myofascial pain. Learning Objectives Upon completion of this course, participants will be able to: 1) Examine 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 2) Demonstrate that active MTrPs have elevated levels of inflammatory mediators, neuropeptides, catecholamines and cytokines – substances known to be associated with inflammation, sensitization, inter-cellular communication and persistent pain states 3) Understand that persistent nociceptive bombardment, neurogenic inflammation, wide dynamic range neurons, subcortical structures (e.g., the limbic system) and dysfunctional descending inhibition all play a pivotal role in muscle sensitization, pain chronification, somato-visceral interactions and the objective, reproducible physical findings of allodynia, hyperalgesia and referred pain patterns