Chapter 48 Myofascial Pain Syndrome Flashcards Preview

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Flashcards in Chapter 48 Myofascial Pain Syndrome Deck (54):

Myofascial pain (MP)

soft tissue pain syndrome with
local and referred pain arising from trigger points (TPs).


Local soft tissue pain syndromes STPs include

bursitis (subacromial, olecranon, trochanteric, prepatellar, and pes anserine), tenosynovitis (biceps, supraspinatus, infrapatellar, and achilles), and enthesopathies (lateral epicondylitis and medial epicondylitis)


Regional STPs include

myofascial pain syndrome (myofascial pain syndrome involving
muscles of the trunk and extremities), myofascial pain dysfunction
syndrome (myofascial pain syndrome involving
facial muscles), and complex regional pain syndrome (types I
and II).


Generalized STPs involve

fibromyalgia syndrome
(FMS), chronic fatigue syndrome (FMS-like when widespread
body pain present), and hypermobility syndrome.


Regional STPs such as MP are limited in

anatomic distribution
over a specific region or quadrant of the body


Trigger points generating MP

localized painful areas
of skeletal muscle containing taut bands that can be exquisitely
sensitive to digital pressure.


TPs may be active or

Active TPs are present in patients with painful
regional conditions. Latent TPs are asymptomatic but
may be revealed by deep palpation on physical examination.


Myofascial pain often coexists with other acute and chronic
painful musculoskeletal conditions including

(1) head and neck pain (temporomandibular disorders, cervical degenerative disc disease, cervical facet arthropathy, neck pain after whiplash injury, cervicobrachial syndrome, cervicogenic and chronic tension-type headache), (2) thoracolumbar back
pain (degenerative disc disease, kyphosis, scoliosis, lumbar facet arthropathy), (3) pelvic pain, and (4) upper and lower extremity pain


MP is distinct from



MP is most effectively
treated with a

multimodal therapeutic regimen including
injection, physical therapy, postural or ergonomic correction,
and treatment of underlying musculoskeletal pain


MPS is more commonly seen in patients with

chronic tension-type headache, temporomandibular disorders and pain in the face–jaw region, and in post-whiplash syndrome
than in the general patient population


Pathophysiology of MPS


Underlying biomechanical and postural factors may interact with neurologic factors (e.g., radiculopathy), psychological elements including depression
and anxiety, and hormonal and nutritional imbalances. These factors (in sum or in part) may create an
autonomic dysregulation and, ultimately, central spinal cord sensitization which can amplify the experience of


Vasoactive mediators leading to spinal cord sensitization.

Vasoactive mediators, algogenic neurotransmitters
and inflammatory mediators including bradykinin, norepinephrine, serotonin, calcitonin gene–related peptide, substance P, tumor necrosis factor alpha, and interleukin 1-B have been identified in the hyperirritable loci of TPs. These substances sensitize nociceptors and are responsible for the sensory experience of MP, including referred pain and the local twitch response (LTR).


The motor phenomena of MP have been hypothesized
to be caused by

excessive acetylcholine (ACh) leakage, which creates dysfunctional endplates that are responsible for taut muscle band formation. Excessive ACh release causes sustained muscle contraction by increased depolarization of the postjunctional endplate


The taut muscle band present in MPS has a higher

tension and contains hypercontracted muscle fibers.


Vasoactive mediators are released in the setting of muscle ischemia, causing

increased ACh release, exacerbation of local
ischemia, and sensitization of peripheral nociceptors,
thereby causing pain.


Abnormal spontaneous electrical activity is present at

the site of TPs, with excessive ACh release creating endplate noise seen on electrophysiological
studies at the neuromuscular junction


electrical activity is observed as having two components:

a constant, low amplitude background activity of approximately 50 mcV, and intermittent higher amplitude spikes of 100 to 700 mcV


Spontaneous electrical activity occurs more
often in

TPs than in normal tissue and displays aberrant
patterns in TPs.


The abnormal electrical activity observed in TPs is
thought to be directly related to

excessive ACh release


The clinical manifestation of abnormal electrical activity
in the TP is a

local twitch response (LTR), thought to be mediated by a segmental spinal reflex


Snapping palpation
or needling the TP causes a

brisk muscle contraction
in the taut band


The location of the LTR (local twitch response) is called the

“sensory locus,” which has been correlated histologically with sensory receptors.


The “active locus” is the site

spontaneous electrical activity is recorded, the
waveforms of which correspond to published reports of motor endplate noise.


Vasoactive mediators such as those released in the taut
bands of MP have been known to

sensitize peripheral
nociceptive nerve fibers such as those found in skeletal muscle.


In a sensitized state, nociceptors

spontaneously discharge with a lower threshold to painful stimulation and also exhibit discharge to non-painful stimuli. Over time, this heightened abnormal peripheral sensory input creates a state of central neuronal sensitization


Diagnostic Characteristics of Myofascial Trigger Points

l Regional pain
l Onset with sudden muscle overload
l Onset with sustained muscular contraction in shortened position
l Onset with repetitive activity (symptoms increase with increasing
l Taut band
l Focal spot muscle tenderness
l Pressure-elicited referred pain pattern
l If active, pressure elicits pain recognized as familiar


Diagnostic Characteristics of Myofascial Trigger Points


l Local twitch response—confirmatory, difficult to elicit
l Prompt release of taut-band tension by specific myofascial trigger-point
l Central/attachment myofascial trigger points


the cornerstone of effective diagnosis of MPS

A careful history and
physical exam


The most common presentation of MPS includes the following diagnostic criteria

regional body pain and stiffness, limited range of motion of the affected muscle, twitch response produced from a taut band, referred pain from a TP to a zone of reference, and resolution of the symptoms with local anesthesia applied to the TP


MP may occur after

injury, and chronic strain with repetitive
microtrauma or without clear precipitating event.


Musculoskeletal examination should be performed
with the objective of

identifying orthopedic or neurologic dysfunction that may play a role in generating MP.


Active TPs may be identified

palpation with gentle digital pressure oriented
across and perpendicular to the muscle fibers.


TPs are present as a

taut muscle bands within skeletal muscle, and
palpation of these points may elicit involuntary muscle
contraction, the twitch response or “jump” sign.


painful TPs limit full range of passive motion in the

afflicted muscle group.


The most reproducible diagnostic findings on physical examination include observation of a

TP in an affected
muscle, referral of pain to a zone of reference, and reproduction of the patient’s usual pain on physical exam.


Differential diagnosis of MP should include

(1) musculoskeletal
and neuropathic disorders such as arthritis, degenerative
disk disease, radiculopathy, bursitis, and tendonitis;
(2) autoimmune or infectious etiologies; (3) metabolic and
endocrine dysfunction including hypothyroidism; (4) psychiatric disorders including depression and anxiety; and (5) fibromyalgia.


treatment of MPS

A comprehensive multimodal therapeutic approach is optimal
in the treatment of MPS, with the goal of patient
education, reduction of pain, and restoration of function.


As the pathogenesis
of MP frequently involves postural defect, repetitive
microtrauma, and muscle fiber shortening, it is logical

guided physical modalities play a significant role in treatment.


Guided stretching

has been well documented as successful
in reducing MP. This fits mechanistically with the
model of shortened sarcomeres in MPS


may be of benefit as part of a comprehensive strategy in refractory cases

transcutaneous electrical nerve stimulation
(TENS), and laser therapy


Systemic medications useful additions to a comprehensive
treatment plan.

nonsteroidal anti-inflammatory
drugs (NSAIDs) and antidepressants have been employed
to relieve pain associated with TPs. NSAIDs provide
symptomatic relief but at the price of long-term side effects.


long-term side effects of NSAIDs include

cardiovascular morbidity and
mortality, gastritis, and renal dysfunction


Muscle relaxants are widely used in MP to

reduce muscle spasm, to relieve pain, and to improve sleep disturbance related to MPS pain.


when the patient has failed more conservative medications.

Systemic opioids (including mixed opioid analgesics
such as tramadol)


the efficacy of opioids in MPS, side effects, and consequences of longer-term use

The occurrence of tolerance, with a loss of efficacy occurring over time, frequently leads to dose escalation


With long-term use and dose escalation comes the risk

opioid-induced hyperalgesia (a N-methyl-D-aspartate
[NMDA]–mediated phenomenon) that is characterized by
escalating pain (often insidiously) in response to increasing opioid analgesic dose


Side Effects of of long-term use of opioid

gastrointestinal slowing, nausea, sedation, respiratory
depression, pruritus, and dysphoria, opioids can cause hormonal changes and lead to osteopenia by influencing the hypothalamic-pituitary-adrenal axis and the hypothalamic pituitary- gonadal axis


Lidocaine patches

may be an effective noninvasive therapy
for MP in an appropriately selected patient population


Trigger point injection (TPI)

a widely used invasive
therapy wherein a needle is guided directly into a TP that
has been previously identified on physical examination.


TPI is best utilized in a series of injections and as part of a
comprehensive treatment plan that includes guided, structured, physical therapy. This strategy can be particularly beneficial when

TPI is initially employed to reduce pain in patients otherwise intolerant of physical therapy or stretching, allowing the physical modalities to be more effective.


Botulinum toxin serotype A produces

sustained and prolonged
relaxation of muscles by inhibiting release of ACh
at the motor endplate and is itself an analgesic inhibiting
central sensitization


New theories regarding the use of botulinum toxin for
the treatment of MP

de-emphasize injection into the TP
per se but focus upon selection of patients with significant
features of overlap among cervical MPS, headache syndromes,
and spasmodic torticollis. It is hypothesized that
patients with cervicobrachial MPS reminiscent of spasmodic
torticollis (with and without headache) may benefit
from institution of botulinum toxin therapy.


It is hypothesized
that botulinum toxin’s role is

to help restore aberrant
biomechanics and postural abnormalities in conjunction
with restorative and rehabilitative physical therapy

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