Chapter 48 Myofascial Pain Syndrome

Question 1

Myofascial pain (MP)

Answer 1

soft tissue pain syndrome with

local and referred pain arising from trigger points (TPs).

Question 2

Local soft tissue pain syndromes STPs include

Answer 2

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

Question 3

Regional STPs include

Answer 3

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).

Question 4

Generalized STPs involve

Answer 4

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

Question 5

Regional STPs such as MP are limited in

Answer 5

anatomic distribution

over a specific region or quadrant of the body

Question 6

Trigger points generating MP

Answer 6

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

Question 7

TPs may be active or

latent.

Answer 7

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

Question 8

Myofascial pain often coexists with other acute and chronic

painful musculoskeletal conditions including

Answer 8

(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

Question 9

MP is distinct from

Answer 9

fibromyalgia

Question 10

MP is most effectively

treated with a

Answer 10

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

Question 11

MPS is more commonly seen in patients with

Answer 11

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

Question 12

Pathophysiology of MPS

biomechanical

Answer 12

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
MPS.

Question 13

Vasoactive mediators leading to spinal cord sensitization.

Answer 13

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).

Question 14

The motor phenomena of MP have been hypothesized

to be caused by

Answer 14

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

Question 15

The taut muscle band present in MPS has a higher

Answer 15

resting

tension and contains hypercontracted muscle fibers.

Question 16

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

Answer 16

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

Question 17

Abnormal spontaneous electrical activity is present at

Answer 17

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

Question 18

Spontaneous

electrical activity is observed as having two components:

Answer 18

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

Question 19

Spontaneous electrical activity occurs more

often in

Answer 19

TPs than in normal tissue and displays aberrant

patterns in TPs.

Question 20

The abnormal electrical activity observed in TPs is

thought to be directly related to

Answer 20

excessive ACh release

Question 21

The clinical manifestation of abnormal electrical activity

in the TP is a

Answer 21

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

Question 22

Snapping palpation

or needling the TP causes a

Answer 22

brisk muscle contraction

in the taut band

Question 23

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

Answer 23

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

Question 24

The “active locus” is the site

where

Answer 24

spontaneous electrical activity is recorded, the

waveforms of which correspond to published reports of motor endplate noise.

Question 25

Vasoactive mediators such as those released in the taut

bands of MP have been known to

Answer 25

sensitize peripheral

nociceptive nerve fibers such as those found in skeletal muscle.

Question 26

In a sensitized state, nociceptors

Answer 26

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

Question 27

Diagnostic Characteristics of Myofascial Trigger Points

Answer 27

DIAGNOSTIC HISTORY
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
stressfulness)
DIAGNOSTIC PHYSICAL EXAMINATION
l Taut band
l Focal spot muscle tenderness
l Pressure-elicited referred pain pattern
l If active, pressure elicits pain recognized as familiar

Question 28

Diagnostic Characteristics of Myofascial Trigger Points

OTHER CLINICAL CHARACTERISTICS

Answer 28

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

Question 29

the cornerstone of effective diagnosis of MPS

Answer 29

A careful history and

physical exam

Question 30

The most common presentation of MPS includes the following diagnostic criteria

Answer 30

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

Question 31

MP may occur after

Answer 31

injury, and chronic strain with repetitive

microtrauma or without clear precipitating event.

Question 32

Musculoskeletal examination should be performed

with the objective of

Answer 32

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

Question 33

Active TPs may be identified

by

Answer 33

palpation with gentle digital pressure oriented

across and perpendicular to the muscle fibers.

Question 34

TPs are present as a

Answer 34

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

Question 35

painful TPs limit full range of passive motion in the

Answer 35

afflicted muscle group.

Question 36

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

Answer 36

TP in an affected

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

Question 37

Differential diagnosis of MP should include

Answer 37

(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.

Question 38

treatment of MPS

Answer 38

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.

Question 39

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

Answer 39

guided physical modalities play a significant role in treatment.

Question 40

Guided stretching

Answer 40

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

Question 41

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

Answer 41

Acupuncture,
transcutaneous electrical nerve stimulation
(TENS), and laser therapy

Question 42

Systemic medications useful additions to a comprehensive

treatment plan.

Answer 42

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.

Question 43

long-term side effects of NSAIDs include

Answer 43

cardiovascular morbidity and

mortality, gastritis, and renal dysfunction

Question 44

Muscle relaxants are widely used in MP to

Answer 44

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

Question 45

when the patient has failed more conservative medications.

Answer 45

Systemic opioids (including mixed opioid analgesics
such as tramadol)

Question 46

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

Answer 46

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

Question 47

With long-term use and dose escalation comes the risk

of

Answer 47

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

Question 48

Side Effects of of long-term use of opioid

Answer 48

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

Question 49

Lidocaine patches

Answer 49

may be an effective noninvasive therapy

for MP in an appropriately selected patient population

Question 50

Trigger point injection (TPI)

Answer 50

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

Question 51

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

Answer 51

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

Question 52

Botulinum toxin serotype A produces

Answer 52

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

Question 53

New theories regarding the use of botulinum toxin for

the treatment of MP

Answer 53

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.

Question 54

It is hypothesized

that botulinum toxin’s role is

Answer 54

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