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 occur in the spinal cord,
thalamic nuclei, cortical and limbic areas and may alter the threshold, intensity and affect
of ones pain experience. Moreover, the dynamic changes that occur during the
initiation, amplification and perpetuation of chronic pain syndromes may provide
explanations for some of the effects observed following dry needling and other physical
medicine modalities.

Musculoskeletal pain is the most common manifestation of chronic pain. The term neuro-
musculoskeletal pain is preferable when describing a chronic musculoskeletal pain state
because it accurately implies fundamental alterations in the nervous system sometimes
irreversibly so.

Spinal Segmental Sensitization (SSS) is a hyperactive state of the dorsal horn caused by
bombardment of nociceptive impulses from sensitized and/or damaged tissue (somatic,
visceral, etc.). Active (i.e., spontaneously painful) myofascial trigger points (MTrPs) are
the most common source of sensitization. Emphasis will 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 objective physical findings of SSS. These easy-to-learn
examination skills are fundamental to the evaluation and management of chronic neuro-
musculoskeletal pain. Participants will also practice specific needling techniques and
physical medicine modalities to deactivate painful MTrPs, 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 pain 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 active MTrPs have elevated levels of a variety of
biochemicals, including inflammatory mediators, 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 upper
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 controlled by inhibitory
interneuronsstructures in the dorsal horn critically involved in preventing the transition
from acute to chronic pain. However, 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 amygdala),
which plays a critical role in modulating muscle pain and 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 the 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 physical 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:

Analyze the dynamic relationship between primary afferent nociceptors and

surrounding tissues and the concept of peripheral 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 compared 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 of
allodynia, hyperalgesia and amplification of chronic musculoskeletal pain
Analyze a mechanism for the loss of spinal inhibitory neurons 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 fiber stimulation can perpetuate spinal
facilitation and maintain chronic pain states
Understand the roles of sensitization and neuroplasticity in generating, amplifying
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.
 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 by their high-
resistance blood flow
Determine the reproducible physical manifestations of sensitization in chronic
myofascial pain
How to integrate palpation techniques in your clinical practice in order to
determine the affected dermatomes, myotomes and sclerotomes in chronic neuro-
musculoskeletal 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 neuro-
musculoskeletal 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, 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. 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.