Chapter 18 Myofascial Pain Flashcards
Myofascial pain disorders
heterogeneous group of
clinical entities that share features that originate from
soft tissue pain with resultant regional symptomatology
Examples of Myofascial Pain Disorders
episodic tension-type headache, myofascial pain syndrome, temporomandibular disorder, muscle cramps, and low back pain
Muscle pain is thought to occur by two main mechanisms:
peripheral and central
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
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
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)
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).
Pathophysiologic mechanisms responsible for TTH can be divided into
peripheral and central causes
Peripheral factors of tension-type headaches
Peripheral mechanisms are demonstrated by increased tenderness of pericranial myofascial tissue and increased electromyographic
and algometric pressure recordings
Central factors of tension-type headaches
Continuous nociceptive
input can lead to central sensitization, thereby converting episodic TTH into chronic headaches
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
In patients with TMD Electromyographic recordings have demonstrated
altered muscular contraction,
as well as increased muscular tone
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)
trigger point
TPs are characterized by
referred pain on palpation and elicitation of a local twitch
response (LTR) with application of mechanical pressure
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
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
Spine structures functions,
protecting the spinal cord, maintaining posture and truncal stability, and acting as a steadying force for movement of the extremities.
Skeletal and ligamentous
structures serve as a
protective foundation from which attached muscles provide functional motor control, flexibility, and movement coordination
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
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,
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
causes of muscle cramps include
medications, lower motor neuron disease, hypothyroidism, and hereditary
disorders
Painful cramps can often be terminated by
stretching the cramped muscle.
Tricyclic antidepressants (TCAs)
amitriptyline, nortriptyline,
desipramine, and imipramine
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
TCAs to be effective in
reducing the frequency and intensity of
tension-type headaches (TTHs) and facial pain/TMD.
Tricyclic antidepressants (TCAs) use is limited secondary to
myriad side effects, which include dry mouth, constipation, fluid retention, weight gain, difficulty concentrating, and cardiotoxicity
TABLE 18–2
Tricyclic Antidepressants
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
most common side effects of gabapentin and pregabalin
include dizziness, sedation, lightheadedness, somnolence,
and weight gain
first-line treatment for headache prophylaxis.
gabapentin
TABLE 18–3
Calcium Channel Antagonists
Gabapentin beneficial
in reducing spasticity in npatients with multiple sclerosis and spinal cord injury and for chronic
masticatory myalgia.
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
Skeletal muscle relaxants
cyclobenzaprine (Flexeril),
chlorzoxazone (Paraflex), carisoprodol (Soma), methocarbamol
(Robaxin, Robaxisal), tizanidine (Zanaflex), and
baclofen (Lioresal)
Skeletal muscle relaxants believed to exert their mechanism of action
primarily within the brain and in some cases spinal motor neurons
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
tizanidine (Zanaflex)
Tizanidine acts as a weak agonist at alpha-2 adrenergic
receptors, and enhances presynaptic inhibition at spinal
motor neurons
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.
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
Baclofen Indications
Strong—spasticity of spinal cord origin Moderate—cervical
dystonia, upper motor neuron
disease, stiff-person syndrome, acute back pain
Tizanidine indications
Moderate— spasticity, paravetebral muscle spasm
Weak—TTH
Carisoprodol Indications
Moderate—acute musculoskeletal pain, not for spasticity
Weak—TMD
Chlorzoxazone (Paraflex,
Parafon, Forte)
Exact mechanism unknown, likely inhibits polysynaptic
reflex pathways in spinal cord (central-acting)
Chlorzoxazone (Paraflex,
Parafon, Forte) indications
Moderate—acute musculoskeletal pain, back pain, acute lumbosacral muscle strain
Cyclobenzaprine( Flexeril) indications
Strong—cervical and lumbar spinal pain, muscle spasm
Moderate—TMD with myofascial pain
Skeletal Muscle Relaxants metabolism and excretion
Liver metabolism
and urine excretion;
Skeletal Muscle Relaxants
Adverse Side Effects
Dry mouth, drowsiness,
headache, diarrhea, constipation, dizziness, nausea,
confusion, lightheadedness,
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.
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
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
Benzodiazepines
Diazepam (Valium),
Clonazepam (Klonopin), Alprazolam (Xanax), Midazolam (Versed)
Benzodiazepines Common
Adverse Side Effects
Drowsiness, dizziness, ataxia,
headache, nausea, somnolence, diarrhea, constipation, dry mouth,
fatigue, headache, tremor, dysuria, hypotension, tremor, sedation
Diazepam Indications
Strong—spasticity of spinal cord origin Moderate—chronic
orofacial muscle pain, tension-type headache Weak—TMD
Clonazepam Indications
Moderate—TMD with myofascial
pain, nocturnal muscle spasms
Alprazolam Indications
Moderate—TTH
