Chapter 48 Myofascial Pain Syndrome Flashcards

KEY POINTS 1. Myofascial pain syndrome is a type of regional soft tissue pain syndrome involving muscles of the trunk and extremities. 2. Although myofascial pain may generalize, it remains distinct from fibromyalgia. 3. Hyperirritable loci of trigger points have been found to contain vasoactive mediators, algogenic neurotransmitters, and inflammatory mediators. 4. Excessive acetylcholine leakage has been hypothesized to contribute to dysfunctional motor end plates, creating the sustained

1
Q

Myofascial pain (MP)

A

soft tissue pain syndrome with

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

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2
Q

Local soft tissue pain syndromes STPs include

A

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

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3
Q

Regional STPs include

A

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).

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4
Q

Generalized STPs involve

A

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

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5
Q

Regional STPs such as MP are limited in

A

anatomic distribution

over a specific region or quadrant of the body

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6
Q

Trigger points generating MP

A

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

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7
Q

TPs may be active or

latent.

A

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

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8
Q

Myofascial pain often coexists with other acute and chronic

painful musculoskeletal conditions including

A

(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

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9
Q

MP is distinct from

A

fibromyalgia

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10
Q

MP is most effectively

treated with a

A

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

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11
Q

MPS is more commonly seen in patients with

A

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

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12
Q

Pathophysiology of MPS

biomechanical

A

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.

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13
Q

Vasoactive mediators leading to spinal cord sensitization.

A

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).

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14
Q

The motor phenomena of MP have been hypothesized

to be caused by

A

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

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15
Q

The taut muscle band present in MPS has a higher

A

resting

tension and contains hypercontracted muscle fibers.

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16
Q

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

A

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

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17
Q

Abnormal spontaneous electrical activity is present at

A

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

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18
Q

Spontaneous

electrical activity is observed as having two components:

A

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

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19
Q

Spontaneous electrical activity occurs more

often in

A

TPs than in normal tissue and displays aberrant

patterns in TPs.

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20
Q

The abnormal electrical activity observed in TPs is

thought to be directly related to

A

excessive ACh release

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21
Q

The clinical manifestation of abnormal electrical activity

in the TP is a

A

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

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22
Q

Snapping palpation

or needling the TP causes a

A

brisk muscle contraction

in the taut band

23
Q

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

A

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

24
Q

The “active locus” is the site

where

A

spontaneous electrical activity is recorded, the

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

25
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.
26
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
27
Diagnostic Characteristics of Myofascial Trigger Points
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
28
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 therapy l Central/attachment myofascial trigger points
29
the cornerstone of effective diagnosis of MPS
A careful history and | physical exam
30
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
31
MP may occur after
injury, and chronic strain with repetitive | microtrauma or without clear precipitating event.
32
Musculoskeletal examination should be performed | with the objective of
identifying orthopedic or neurologic dysfunction that may play a role in generating MP.
33
Active TPs may be identified | by
palpation with gentle digital pressure oriented | across and perpendicular to the muscle fibers.
34
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.
35
painful TPs limit full range of passive motion in the
afflicted muscle group.
36
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.
37
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.
38
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.
39
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.
40
Guided stretching
has been well documented as successful in reducing MP. This fits mechanistically with the model of shortened sarcomeres in MPS
41
may be of benefit as part of a comprehensive strategy in refractory cases
Acupuncture, transcutaneous electrical nerve stimulation (TENS), and laser therapy
42
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.
43
long-term side effects of NSAIDs include
cardiovascular morbidity and | mortality, gastritis, and renal dysfunction
44
Muscle relaxants are widely used in MP to
reduce muscle spasm, to relieve pain, and to improve sleep disturbance related to MPS pain.
45
when the patient has failed more conservative medications.
``` Systemic opioids (including mixed opioid analgesics such as tramadol) ```
46
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
47
With long-term use and dose escalation comes the risk | of
``` 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 ```
48
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
49
Lidocaine patches
may be an effective noninvasive therapy | for MP in an appropriately selected patient population
50
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.
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
TPI is initially employed to reduce pain in patients otherwise intolerant of physical therapy or stretching, allowing the physical modalities to be more effective.
52
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
53
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.
54
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