Chapter 18 Myofascial Pain

Question 1

Myofascial pain disorders

Answer 1

heterogeneous group of
clinical entities that share features that originate from
soft tissue pain with resultant regional symptomatology

Question 2

Examples of Myofascial Pain Disorders

Answer 2

episodic tension-type headache, myofascial pain syndrome, temporomandibular disorder, muscle cramps, and low back pain

Question 3

Muscle pain is thought to occur by two main mechanisms:

Answer 3

peripheral and central

Question 4

Peripheral factors of muscle pain

Answer 4

trauma, dysregulated deep-tissue microcirculation, and altered muscular metabolism and mitochondrial function. Mechanical, thermal, or chemical stimulation can lead to activation of intramuscular group III and group IV nociceptors, which in turn give rise to an inflammatory cascade mediated by immune cells, leading to further recruitment
of inflammatory cells and propagation of local inflammation and sensitization

Question 5

Central factors of muscle pain

Answer 5

Pain transmission occurs along
Ad and C-fibers into the inner lamina of the spinal cord, where complex changes occur, leading to sensitization and
chronic pain. Continuous nociceptive input via these pathways can lead to central sensitization of higher-order neurons, –> enhanced sensitivity to painful stimuli via
excitatory glutamate and aspartate-related neurotransmitter release (hyperalgesia),reduced thresholds to nonpainful stimuli (allodynia), and increased receptive fields, causing referred pain

Question 6

Supraspinal mechanisms contribute to chronic muscular pain states include

Answer 6

decreased cerebral activity, hippocampal suppression, and possibly impaired stress responses. Once central sensitization occurs, pain becomes autonomous from sensory input from the affected
muscle(s)

Question 7

The International Headache Society classifies tension-type

headaches (TTHs) as

Answer 7

infrequent episodic (,12 days/yr), frequent episodic (12 to fewer than 180 days/yr), and chronic (180 days/yr).

Question 8

Pathophysiologic mechanisms responsible for TTH can be divided into

Answer 8

peripheral and central causes

Question 9

Peripheral factors of tension-type headaches

Answer 9

Peripheral mechanisms are demonstrated by increased tenderness of pericranial myofascial tissue and increased electromyographic
and algometric pressure recordings

Question 10

Central factors of tension-type headaches

Answer 10

Continuous nociceptive

input can lead to central sensitization, thereby converting episodic TTH into chronic headaches

Question 11

Temporomandibular disorder (TMD)

Answer 11

is a broad term used to describe conditions arising in the jaw joint, muscles of mastication, and associated craniofacial structures. These conditions most commonly include pain, dysfunction, arthritis, and internal derangement

Question 12

In patients with TMD Electromyographic recordings have demonstrated

Answer 12

altered muscular contraction,

as well as increased muscular tone

Question 13

myofascial pain syndrome (MPS) characterizes by the

Answer 13

presence of loci of hypersensitivity within a tender, taut, palpable band of
muscle called a trigger point (TP)

Question 14

trigger point

Answer 14

TPs are characterized by
referred pain on palpation and elicitation of a local twitch
response (LTR) with application of mechanical pressure

Question 15

Trigger points can be classified into

Answer 15

active TPs or latent TPs.
Active TPs are described as pain in a motor locus
associated with spontaneous electrical activity, whereas
the more common latent TPs do not cause spontaneous
pain, but can be triggered by factors such as mechanical
stressors, dysfunctional postures, changes in weather, and either excessive immobility or the exaggerated use of muscles

Question 16

What leads to the formation of a TP circuit?

Answer 16

It has been suggested that a positive feedback
cycle involving disproportionate acetylcholine release, sarcomere shortening, and increased concentrations of sensitizing substances leads to the formation of a TP circuit,
which upon connection with other spinal dorsal horn
neuronal pathways, activates latent TPs to become an
active TP

Question 17

Spine structures functions,

Answer 17

protecting the spinal cord, maintaining posture and truncal stability, and acting as a steadying force for movement of the extremities.

Question 18

Skeletal and ligamentous

structures serve as a

Answer 18

protective foundation from which attached muscles provide functional motor control, flexibility, and movement coordination

Question 19

Weakness in the core muscles
(lumbo-pelvic-hip complex), unbalanced gait mechanics,
or dysfunctional muscular proprioception can
lead to

Answer 19

tears, strains, sprains, or spasm within the paraspinal musculature

Question 20

True muscle cramps

Answer 20

painful involuntary skeletal
muscle contractions associated with electrical activity. EMG studies show fast rates of repetitive firing of motor units in affected muscles. True muscle cramps occur in the absence of fluid or electrolyte imbalance,

Question 21

True muscle cramps are

more commonly found in patients with

Answer 21

well-developed muscles, in the third trimester of pregnancy, and in metabolic disorders such as cirrhosis and renal disease

Question 22

causes of muscle cramps include

Answer 22

medications, lower motor neuron disease, hypothyroidism, and hereditary
disorders

Question 23

Painful cramps can often be terminated by

Answer 23

stretching the cramped muscle.

Question 24

Tricyclic antidepressants (TCAs)

Answer 24

amitriptyline, nortriptyline,

desipramine, and imipramine

Question 25

Tricyclic antidepressants (TCAs) Mechanism of Action

Answer 25

provide analgesia
independent of their antidepressive effects by multiple mechanisms, which include norepinephrine and serotonin reuptake inhibition in inhibitory descending pathways. Other active mechanisms include blockade of peripheral neural sodium channels, muscarinic and nicotinic acetylcholine receptors, alpha adrenergic
receptors, NMDA receptors, substance P release, and to a
lesser extent, dopamine receptors

Question 26

TCAs to be effective in

reducing the frequency and intensity of

Answer 26

tension-type headaches (TTHs) and facial pain/TMD.

Question 27

Tricyclic antidepressants (TCAs) 
use is limited secondary to

Answer 27

myriad side effects, which include dry mouth, constipation, fluid retention, weight gain, difficulty concentrating, and cardiotoxicity

Question 28

TABLE 18–2

Answer 28

Tricyclic Antidepressants

Question 29

Calcium Channel Antagonists

Pregabalin and gabapentin

Answer 29

an analog of GABA, exert their
analgesic effects by acting on the a2-d1 subunit of cellular
calcium channels and blocking neurotransmitter release.
Their binding to calcium channels results in suppression of abnormal neuronal discharges and an increased threshold for nerve activation

Question 30

most common side effects of gabapentin and pregabalin

Answer 30

include dizziness, sedation, lightheadedness, somnolence,

and weight gain

Question 31

first-line treatment for headache prophylaxis.

Answer 31

gabapentin

Question 32

TABLE 18–3

Answer 32

Calcium Channel Antagonists

Question 33

Gabapentin beneficial

Answer 33

in reducing spasticity in npatients with multiple sclerosis and spinal cord injury and for chronic
masticatory myalgia.

Question 34

Usefullness of sodium valproate in Myofascial Pain

Answer 34

an anticonvulsant that acts via
a variety of mechanisms including the blockade of
T-type calcium and sodium channels, and facilitation of
GABA, have shown benefit in TTH and chronic daily
headaches

Question 35

Skeletal muscle relaxants

Answer 35

cyclobenzaprine (Flexeril),
chlorzoxazone (Paraflex), carisoprodol (Soma), methocarbamol
(Robaxin, Robaxisal), tizanidine (Zanaflex), and
baclofen (Lioresal)

Question 36

Skeletal muscle relaxants believed to exert their mechanism of action

Answer 36

primarily within the brain and in some cases spinal motor neurons

Question 37

cyclobenzaprine (Flexeril)

Answer 37

Cyclobenzaprine, structurally related to first-generation tricyclic antidepressants, inhibits the reuptake of norepinephrine in the locus coeruleus and inhibits descending serotonergic pathways in the spinal cord. The latter effect may have an inhibitory effect on alpha motor neurons in the spinal cord, resulting in decreased firing and a reduction in mono- and polysynaptic spinal reflexes

Question 38

tizanidine (Zanaflex)

Answer 38

Tizanidine acts as a weak agonist at alpha-2 adrenergic
receptors, and enhances presynaptic inhibition at spinal
motor neurons

Question 39

Carisoprodol

Answer 39

a precursor of the sedative hypnotic meprobamate, is believed to produce muscle relaxation by blocking interneuronal activity in the descending reticular formation and spinal cord.

Question 40

Baclofen

Answer 40

activates GABA-B receptors in the brain and reduces the release of excitatory neurotransmitters in both the brain and spinal cord. Baclofen also acts by inhibiting the release of substance
P in the spinal cord

Question 41

Baclofen Indications

Answer 41

Strong—spasticity of spinal cord origin Moderate—cervical
dystonia, upper motor neuron
disease, stiff-person syndrome, acute back pain

Question 42

Tizanidine indications

Answer 42

Moderate— spasticity, paravetebral muscle spasm

Weak—TTH

Question 43

Carisoprodol Indications

Answer 43

Moderate—acute musculoskeletal pain, not for spasticity

Weak—TMD

Question 44

Chlorzoxazone (Paraflex,

Parafon, Forte)

Answer 44

Exact mechanism unknown, likely inhibits polysynaptic

reflex pathways in spinal cord (central-acting)

Question 45

Chlorzoxazone (Paraflex,

Parafon, Forte) indications

Answer 45

Moderate—acute musculoskeletal pain, back pain, acute lumbosacral muscle strain

Question 46

Cyclobenzaprine( Flexeril) indications

Answer 46

Strong—cervical and lumbar spinal pain, muscle spasm

Moderate—TMD with myofascial pain

Question 47

Skeletal Muscle Relaxants metabolism and excretion

Answer 47

Liver metabolism

and urine excretion;

Question 48

Skeletal Muscle Relaxants

Adverse Side Effects

Answer 48

Dry mouth, drowsiness,
headache, diarrhea, constipation, dizziness, nausea,
confusion, lightheadedness,

Question 49

Benzodiazepines Mechanism of Action

Answer 49

enhance presynaptic inhibition in the spinal cord by targeting inhibitory neurotransmitter receptors that are directly activated by GABA. Benzodiazepine receptor
binding facilitates GABA A receptor binding, increasing
the influx of negatively charged chloride ions across the cell membrane.

Question 50

The increased membrane conductance leads to

Answer 50

hyperpolarization of Ia afferent terminals at neuronal These changes in membrane polarization lead to inhibition of normal neuronal transmission and reduced motor neuron output.synapse

Question 51

Benzodiazepines Common side Effects

Answer 51

include dizziness, somnolence, confusion, memory loss, ataxia, sedation, and physical dependence with sustained use. Psychological effects include paradoxical anxiety, depression, paranoia,
and irritability

Question 52

Benzodiazepines

Answer 52

Diazepam (Valium),

Clonazepam (Klonopin), Alprazolam (Xanax), Midazolam (Versed)

Question 53

Benzodiazepines Common

Adverse Side Effects

Answer 53

Drowsiness, dizziness, ataxia,
headache, nausea, somnolence, diarrhea, constipation, dry mouth,
fatigue, headache, tremor, dysuria, hypotension, tremor, sedation

Question 54

Diazepam Indications

Answer 54

Strong—spasticity of spinal cord origin Moderate—chronic

orofacial muscle pain, tension-type headache Weak—TMD

Question 55

Clonazepam Indications

Answer 55

Moderate—TMD with myofascial

pain, nocturnal muscle spasms

Question 56

Alprazolam Indications

Answer 56

Moderate—TTH