American Society of Regional Anesthesia and Pain Medicine February 2018 - 43

What Is Myofascial Pain?

G

uillaume de Baillou, a
French clinician and
epidemiologist during the
16th century, prepared one of the
first manuscripts on arthritis1
and muscle pain disorders. 2
Kellgren, a British rheumatologist,
studied patterns of referred pain
in different muscle groups and
ligaments of the spine by injecting
intramuscular hypertonic saline.3
Balfour described painful inflamed
Floria E. Chae, MD
nodules in 1816. Since then,
Fellow in Critical Care Medicine
many terms have been used to
The Ohio State University,
describe trigger points (TrPs):
Wexner Medical Center
fibrosis myofasciitis, muscular
Columbus, Ohio
rheumatism, rheumatic myositis,
myogelosis, myalgia, myofascial
Section Editor: Dalia Elmofty, MD
pain, and fibromyalgia. 4 Travell
and Rinzler published the first
summary of specific referral patterns and tenderness from
referred trigger points in 1952.5 Travell and Simons furthered the
knowledge regarding myofascial pain in the two-volume work
titled Myofascial Pain and Dysfunction, published in 1983. Travell
introduced the term myofascial pain syndrome (MPS) to describe
pain generated from TrPs in muscles, tendons, skin, fascia, and
ligaments.

CINDERELLA HYPOTHESIS
Several hypotheses imply that muscle overload and overuse are
required for developing MTrP. The Cinderella hypothesis describes
how muscle recruitment patterns during low-level, static exertions
may lead to musculoskeletal disorder symptoms. Because smaller,
type I muscle fibers are continuously activated and metabolically
overloaded, whereas larger motor fibers spend more time
inactivated, type I or Cinderella fibers are more susceptible to
muscle damage and calcium dysregulation, which are key factors
in the formation of TrPs.9 Research has demonstrated that upper
trapezius MTrPs developed after continued typing for as little as
30 minutes, which supports the theory that even low-level static
exertions can cause MTrPs.10
ELECTROPHYSIOLOGY
Electromyographic studies show spontaneous electrical activity
(SEA) generated at MTrP loci, which are not seen in surrounding
tissue. SEA results from increases in miniature endplate potentials
and excessive acetylcholine release.11 These dysfunctional motor
endplates may explain the taut band phenomenon. Others have
hypothesized that excessive acetylcholine release sustains a
contracture of the muscle fibers and thus increases metabolic
demands.8

The term myofascial pain
syndrome today indicates
a specific condition that is
different from other softtissue pain disorders such
as fibromyalgia, tendonitis,
or bursitis. MPS can be
regional or widespread,
where pain often crosses
multiple dermatomes, and is frequently accompanied by
increased tension and decreased flexibility. It can coexist with
other pain conditions such as fibromyalgia, radiculopathies,
joint dysfunction, migraines, pelvic pain and other urologic
syndromes, postherpetic neuralgia, and complex regional pain
syndromes. 6

INTEGRATED TRIGGER POINT HYPOTHESIS
Simons introduced the integrated trigger point hypothesis, which
ties together several findings to describe a possible sequence of
events in the development
of MTrPs. An energy crisis
perpetuates sustained
contracture of the muscle
fibers near an abnormal
endplate. The excessive
acetylcholine release and
the sustained sarcomere
contracture lead to
increased local metabolic
demands and compressed capillary circulation. With the decreased
blood flow and sources of adenosine triphosphate, muscle fibers
remain in a contracted state and are unable to return calcium to the
sarcoplasmic reticulum for muscle relaxation.7 The local hypoxic
condition leads to release of ischemic mediators that can sensitize
peripheral nociceptors and generate pain.12

MPS affects every age group and is characterized by myofascial TrP
(MTrP) and pain. An MTrP is classically defined as "a hyperirritable
spot in skeletal muscle that is associated with a hypersensitive
palpable nodule in a taut band."7 Palpation of MTrP produces local
pain as well as referred pain in a known pattern. MTrP can be
classified as active or latent: active MTrP causes spontaneous pain
and pain on palpation, whereas latent MTrP causes pain only on
palpation.8

NOCICEPTORS
Muscle nociceptors can comprise up to 50% of muscle nerves.
This may explain the severity of pain and tenderness in muscles
on palpation. Nociceptors also innervate the connective tissue of
muscle fibers. They can be activated by several stimuli, depending
on whether they contain chemoreceptors, mechanoreceptors,
or thermoreceptors.13 Active and latent MTrPs have biochemical
differences, as well as healthy muscle tissue by microdialysis.

"It is important to understand the
pathophysiology of myofascial pain
because it is common and distinct entity
from other musculoskeletal disorders."

American Society of Regional Anesthesia and Pain Medicine
2018

43



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