Chapter 18 Myofascial Pain Flashcards Preview

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Flashcards in Chapter 18 Myofascial Pain Deck (56):
1

Myofascial pain disorders

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

2

Examples of Myofascial Pain Disorders

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

3

Muscle pain is thought to occur by two main mechanisms:

peripheral and central

4

Peripheral factors of muscle pain

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

5

Central factors of muscle pain

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

6

Supraspinal mechanisms contribute to chronic muscular pain states include

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)

7

The International Headache Society classifies tension-type
headaches (TTHs) as

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

8

Pathophysiologic mechanisms responsible for TTH can be divided into

peripheral and central causes

9

Peripheral factors of tension-type headaches

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

10

Central factors of tension-type headaches

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

11

Temporomandibular disorder (TMD)

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

12

In patients with TMD Electromyographic recordings have demonstrated

altered muscular contraction,
as well as increased muscular tone

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myofascial pain syndrome (MPS) characterizes by the

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

14

trigger point

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

15

Trigger points can be classified into

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

16

What leads to the formation of a TP circuit?

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

17

Spine structures functions,

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

18

Skeletal and ligamentous
structures serve as a

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

19

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

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

20

True muscle cramps

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,

21

True muscle cramps are
more commonly found in patients with

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

22

causes of muscle cramps include

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

23

Painful cramps can often be terminated by

stretching the cramped muscle.

24

Tricyclic antidepressants (TCAs)

amitriptyline, nortriptyline,
desipramine, and imipramine

25

Tricyclic antidepressants (TCAs) Mechanism of Action

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

26

TCAs to be effective in
reducing the frequency and intensity of

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

27

Tricyclic antidepressants (TCAs)
use is limited secondary to

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

28

TABLE 18–2

Tricyclic Antidepressants

29

Calcium Channel Antagonists
(Pregabalin and gabapentin)

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

30

most common side effects of gabapentin and pregabalin

include dizziness, sedation, lightheadedness, somnolence,
and weight gain

31

first-line treatment for headache prophylaxis.

gabapentin

32

TABLE 18–3

Calcium Channel Antagonists

33

Gabapentin beneficial

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

34

Usefullness of sodium valproate in Myofascial Pain

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

35

Skeletal muscle relaxants

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

36

Skeletal muscle relaxants believed to exert their mechanism of action

primarily within the brain and in some cases spinal motor neurons

37

cyclobenzaprine (Flexeril)

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

38

tizanidine (Zanaflex)

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

39

Carisoprodol

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.

40

Baclofen

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

41

Baclofen Indications

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

42

Tizanidine indications

Moderate— spasticity, paravetebral muscle spasm
Weak—TTH

43

Carisoprodol Indications

Moderate—acute musculoskeletal pain, not for spasticity
Weak—TMD

44

Chlorzoxazone (Paraflex,
Parafon, Forte)

Exact mechanism unknown, likely inhibits polysynaptic
reflex pathways in spinal cord (central-acting)

45

Chlorzoxazone (Paraflex,
Parafon, Forte) indications

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

46

Cyclobenzaprine( Flexeril) indications

Strong—cervical and lumbar spinal pain, muscle spasm
Moderate—TMD with myofascial pain

47

Skeletal Muscle Relaxants metabolism and excretion

Liver metabolism
and urine excretion;

48

Skeletal Muscle Relaxants
Adverse Side Effects

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

49

Benzodiazepines Mechanism of Action

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.

50

The increased membrane conductance leads to

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

51

Benzodiazepines Common side Effects

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

52

Benzodiazepines

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

53

Benzodiazepines Common
Adverse Side Effects

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

54

Diazepam Indications

Strong—spasticity of spinal cord origin Moderate—chronic
orofacial muscle pain, tension-type headache Weak—TMD

55

Clonazepam Indications

Moderate—TMD with myofascial
pain, nocturnal muscle spasms

56

Alprazolam Indications

Moderate—TTH

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