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
Generalized STPs involve
(FMS), chronic fatigue syndrome (FMS-like when widespread
body pain present), and hypermobility syndrome.
Regional STPs such as MP are limited in
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
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
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
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
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
Diagnostic Characteristics of Myofascial Trigger Points
OTHER CLINICAL CHARACTERISTICS
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
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
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.
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
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
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
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.