Articles Dry Needling Certification
232 / The Journal of Manual & Manipulative Therapy, 2006
The Journal of Manual & Manipulative Therapy
Vol. 14 No. 4 (2006), 232 - 239
Myofascial Trigger Points: Translating Molecular Theory into
Manual Therapy
Address all correspondence and request for reprints to:
John M. McPartland
53 Washington Street Ext
Middlebury, VT 05753
USA
mcpruitt@verizon.net
Abstract: Theories regarding the molecular pathophysiology of myofascial trigger points
(MFTrPs) have undergone fundamental revisions in recent years. New research suggests that
MFTrPs are evoked by the abnormal depolarization of motor endplates. The motor endplate
transduces electrical potential into muscle contraction. This review article expands the
proposed etiology to include presynaptic, synaptic, and postsynaptic mechanisms, such as
excessive release of acetycholine (ACh), defects of acetylcholinesterase, and upregulation of
nicotinic ACh receptors, respectively. Dysfunctional motor endplates and sustained muscular
contraction give rise to a localized “ATP energy crisis” associated with sensory and autonomic
reflex arcs that is sustained by central sensitization. This working hypothesis has given rise
to several new approaches in the treatment of MFTrPs.
K e y Wo rd s : M y o f a s c i a l Tr i g g e r P o i n t s , M o t o r E n d p l a t e , A c e t y c h o l i n e R e c e p t o r,
Acetylcholinesterase
John M. McPartland, DO, MS
David G. Simons, MD
Simons, Travell, and Simons1 defined the myofascial trigger point (MFTrP) as “…a hyperirritable spot in
skeletal muscle that is associated with a hypersensitive
palpable nodule in a taut band. The spot is tender when
pressed, and can give rise to characteristic referred
pain, motor dysfunction, and autonomic phenomena…”
Thus each MFTrP contains a sensory component, a
motor component, and an autonomic component. These
components comprise a new “integrated hypothesis”
regarding the etiology of MFTrPs1. This hypothesis
involves local myofascial tissues, the central nervous
system (CNS), and systemic biomechanical factors. The
“integrated hypothesis” has changed our approach to
treating MFTrPs. The purpose of this paper is to review
new concepts concerning MFTrPs and to describe our
evolving approach to their treatment.
Motor Endplate: Epicenter of the
Myofascial Trigger point
Simons2 implicated the motor endplate as the central
etiology of MFTrPs. The motor endplate is synonymous
with the neuromuscular junction (the first term de-
scribes structure, the latter term describes function); it
is the site where an -motor neuron synapses with its
target muscle fibers. The -motor neuron terminates
in multiple swellings termed presynaptic boutons. Each
bouton contains many acetylcholine (ACh) vesicles,
clustered around structures called dense bars (Figure
1). Voltage-sensitive calcium channels (VsCCs, specifi-
cally P/Q-type VsCCs) also cluster near dense bars. When
voltage running down an -motor neuron reaches VsCCs
in the bouton, the VsCC channels open, leading to an
influx of calcium ions (Ca2+) into the bouton from the
extracellular space. The influx of Ca2+ causes the ACh
vesicles to release their transmitter into the synaptic
cleft (Figure 1).
Across the synaptic cleft, the postsynaptic muscle
cell membrane forms junctional folds that are lined with
nicotinic ACh receptors (nAChs). The nACh is a ligand-
gated cation channel, and ACh is its ligand. Binding of
Myofascial Trigger Points: Translating Molecular
Theory into Manual Therapy / 233
ACh to nACh opens its channel, allowing sodium ions
(Na+) and potassium ions (K+) to move in and out of the
muscle cell membrane. Movement of Na+ and K+ depolar-
izes the postsynaptic cell, forming a miniature endplate
potential (MEPP). A sufficient number of MEPPs activate
VsCCs (specifically L-type VsCCs), which subsequently
trigger another Ca2+ channel, the ryanodine receptor.
The ryanodine receptor is imbedded in the membrane
of an intracellular structure called the sarcoplasmic
reticulum, which houses intracellular stores of Ca2+.
Activation of the ryanodine receptor releases Ca2+ from
the sarcoplasmic reticulum into the cytoplasm of the
muscle cell. This triggers the interaction between actin
and myosin, and the sarcomere contracts.
Electromyography (EMG) studies of MFTrPs have
reported spontaneous electrical activity (SEA) in MFTrPs,
while adjacent muscle tissues are electrically silent3.
Hubbard and Berkoff3 originally attributed the source
of SEA action potentials to sympathetically activated
intrafusal muscle spindles. These researchers were
unaware of previous work by Liley of New Zealand, who
had demonstrated that SEA was a consequence of ACh
release at motor endplates4. Simons5 “connected the
dots” by correlating SEA with “endplate noise” that had
been described by electromyographers, and he linked
SEA to excessive ACh release, which he proposed as
the primary cause of MFTrP development. This “motor
endplate” hypothesis was tested in Hong’s laboratory6,
where MFTrPs were injected with botulinum toxin type
A, which blocks ACh release at the motor endplate. This
treatment significantly decreased SEA activity. Mense et
al7 confirmed the hypothesis using a rat MFTrP model.
They injected diisopropylfluorophosphate (DFP), a drug
that increases synaptic ACh, into the proximal half of
the gastrocnemius muscle, and the motor nerve was
electrically stimulated for 30-60 min to induce muscle
contractions. The distal half of the muscle, which
performed the same contractions, served as a control.
Proximal and distal sections of the muscle were then
examined for morphological changes. The DFP-injected
proximal half exhibited significantly more contracted
and torn muscle fibers compared to the distal half of
the muscle.
Myofascial tension may play a role in excess ACh
release. Chen and Grinnell8 showed that a 1% increase
in muscle stretch at the motor endplate evoked a 10%
increase in ACh release. These researchers postulated
that tension upon integrins (cell-surface proteins that
bind connective tissues) in the presynaptic membrane
was transduced mechanically into ACh vesicle release.
Expanding the Endplate Hypothesis
Simons’ description of a presynaptic dysfunction
(excessive ACh release), however, is only one way to
interpret the “endplate hypothesis.” We can expand
the hypothesis to include presynaptic, intrasynaptic,
and postsynaptic dysfunctions9. Intrasynaptic ACh must
be deactivated; otherwise, it will continue to activate
nAChRs in the muscle cell membrane. ACh is normally
deactivated by the enzyme acetylcholinesterase (AChE),
which is held in the synaptic cleft by a structural protein
(collagen Q, ColQ) that anchors it to the plasma mem-
brane (Figure 1). AChE deficiency permits excess ACh
Fig. 1: The motor endplate – proposed site of trigger
point dysfunction. Top illustration: The junction between
the -motor neuron and the muscle fiber. Bottom il-
lustration: Presynaptic boutons are separated from the
postsynaptic muscle cell by the synaptic cleft. Within
each bouton are many vesicles containing ACh, clus-
tered around dense bars (Db). Also clustered around
the Db are calcium channels. The Db is the site of ACh
release into the synaptic cleft. Across the synaptic cleft
from the Db, the postsynaptic muscle cell membrane
forms junctional folds that are lined with nicotinic
ACh receptors (nACh). ACh released into the synaptic
cleft activates nACh receptors, then is inactivated by
the acetylcholinesterase enzyme (AChE). Illustration
courtesy of McpArtLand.
234 / The Journal of Manual & Manipulative Therapy, 2006
to accumulate in the synaptic cleft, tonically activating
nAChRs. Several genetic mutations cause AChE defi-
ciency, including mutations in ColQ. The gene for AChE
expresses several splice variants10, which are alternative
ways in which a gene’s protein-coding sections (exons)
are joined together to create a messenger RNA molecule
and its translated protein. AChE splice variants are less
effective at deactivating ACh, and the expression of these
splice variants can be induced by psychological and physi-
cal stress10. Drugs and other chemicals may cause AChE
deficiency. DFP, the drug used in the aforementioned
experiment by Mense et al6, is an AChE antagonist.
Organophosphate pesticides are AChE antagonists, and
poisoning by these pesticides causes changes in motor
endplates and MFTrP-like pathology11-13. Muscle damage
caused by AChE antagonists has been reduced by pre-
treatment with postsynaptic L-type VsCC blockers such
as quinidine12 and diltiazem13.
Postsynaptically, a “gain-of-function” defect of the
nAChR may confer muscle hyperexcitability, a hallmark of
MFTrPs. Gain of function refers to an increased response
by the nAChR, via several possible mechanisms: nAChR
overexpression, constitutively-active nAChRs14, nAChRs
that gain responsiveness to choline (an ordinary serum
metabolite)14, or nACHRs whose channels remain open
longer than normal15. The nAChR is an assembly of five
subunits; at least 16 genes encode these subunits, so
that the nAChR is particularly susceptible to mutational
defects. Motor endplate nAChRs express a unique subunit
assembly, whereas nAChRs in the central nervous system
and in autonomic nerves express a different subunit
configuration16.
The relative consequences of presynaptic, synaptic,
and postsynaptic dysfunctions are under debate. Wang
et al17 used a variety of pharmacological tools to con-
clude that presynaptic mechanisms modulate the motor
endplate rather than synaptic (AChE) or postsynaptic
(nAChR density) mechanisms. Conversely, Nakanishi et
al18 determined that postsynaptic manipulation (using
alpha-bungarotoxin, an nAChR antagonist) modulated
motor endplates to a greater degree than presynaptic
manipulation (using botulinum toxin, an inhibitor of
ACh release).
Motor Component
MFTrPs have a motor component, whereas tender
points found in patients with fibromyalgia do not. MFTrPs
have been biopsied and found to contain “…contraction
knots…” described as “…large, rounded, darkly staining
muscle fibers and a statistically significant increase in
the average diameter of muscle fibers…” 19. Thus the
structure of contraction knots differed from that of
normal muscle fibers. Functionally, excessive motor
activity initiates several perverse mechanisms that cause
MFTrPs to persist. Muscle contraction compresses local
sensory nerves, which reduces the axoplasmic transport of
molecules that normally inhibit ACh release20,21. Muscle
contraction also compresses local blood vessels, reducing
the local supply of oxygen. Reduced oxygen, combined
with the metabolic demands generated by contracted
muscles, results in a rapid depletion of local adenosine
triphosphate (ATP).
The resultant “ATP energy crisis” 1 triggers a cascade
of pre- and postsynaptic decompensations. Presynaptic
ATP directly inhibits ACh release22, so depletion of ATP
increases ACh release. Postsynaptic ATP powers the Ca2+
pump that returns Ca2+ to the sarcoplasmic reticulum.
Hence, loss of ATP impairs the reuptake of Ca2+, which
increases contractile activity, creating a vicious cycle19.
Excess Ca2+ may snowball into “Ca2+-induced Ca2+ release,”
where Ca2+ induces further Ca2+ release from intracel-
lular stores via ryanodine receptors, triggering actin and
myosin, leading to muscle spasm.
Some controversy surrounds adenosine, a breakdown
product of ATP. Adenosine normally decreases motor
endplate activity by activating presynaptic adenosine A1
receptors, which reduce P/Q VsCC currents, thus reducing
ACh release23. However, high levels of synaptic adenosine,
from excess ATP breakdown (as is hypothesized to occur
in the ATP energy crisis model), may activate postsynap-
tic adenosine A2 receptors, which recruit L-type VsCCs
currents, thus triggering muscle contraction24.
MFTrPs exert profound yet unpredictable influences
upon motor function. MFTrPs may excite or inhibit
normal motor activity in their muscle of origin or in
functionally related muscles. Latent MFTrPs can be
equally influential upon motor function. Motor inhibi-
tion is often identified clinically as muscle weakness,
but treatment often focuses on strengthening exercises
that only augment abnormal muscle substitution until
the inhibiting MFTrPs are inactivated. This inhibition
can also cause poor coordination and muscle imbalances.
These MFTrP effects have gone largely unrecognized
because of a lack of published research studies. Headly
has explored these effects using surface electromyography,
describing inhibition of the trapezius by MFTrPs in the
same muscle25, inhibition of anterior deltoid by MFTrPs
in the infraspinatus25, inhibition of gluteal muscles by
MFTrPs in the quadratus lumborum25, and excitation
(referred spasm) of the paraspinals by MFTrPs in the
tensor fascia lata26,27.
Sensory Component
MFTrPs are painful. Pain begins in peripheral tissues
as nociception, transmitted by A and C-fiber afferent
sensory neurons (nociceptors). Mechanical pressure,
thermal stimuli, and many chemicals activate nocicep-
tors; potassium ions, protons, and free O
2
radicals are
by-products of muscle metabolism and the hypothesized
“ATP energy crisis.” Histamine is released from mast cells
that migrate into injured tissues. Serotonin is released
from platelets after they are exposed to platelet activat-
Myofascial Trigger Points: Translating Molecular
Theory into Manual Therapy / 235
ing factor (released from the mast cells). Bradykinin
is cleaved from serum proteins. All of these chemical
“activators” bind to receptors in the nociceptor and initi-
ate an action potential. “Sensitizers” are also released
from damaged tissue; examples include prostaglandins,
leukotrienes, and substance P. Sensitizers decrease the
activation threshold of a neuron, so that the nociceptor
fires with less activation. This leads to peripheral sen-
sitization and hyperalgesia. Sensitizing substances may
also generate a focal demyelination of sensory nerves.
Demyelination creates abnormal impulse-generating
sites (AIGS), capable of generating ectopic nociceptive
impulses28. Shah et al29 used a microdialysis needle to
sample tissue fluids from the upper trapezius muscle
in nine subjects; elevated concentrations of protons,
bradykinin, serotonin, substance P, norepinephrine,
calcitonin gene-related peptide, tumor necrosis factor-
a, and interleukin-1b were detected in active MFTrPs,
compared to latent MFTrPs and control subjects without
MFTrPs. The difference was statistically significant
(P<0.01) despite the small sample size.
A persistent barrage of nociceptive signals from
MFTrPs may eventually cause “central sensitization,”
a form of neural plasticity involving functional and/or
structural change within the dorsal horn of the spinal
cord. The sensitized dorsal horn becomes a “neurologic
lens,” consolidating other nociceptive signals that converge
upon the same segment of the spinal cord, including
other somatic dysfunctions and visceral dysfunctions1. As
a result, post-synaptic spinal neurons exhibit decreased
activation thresholds, increased response magnitudes, and
increased recruitment of receptive field areas. They fire
with increased frequency or fire spontaneously, trans-
mitting nociceptive signals to supraspinal sites, such as
the thalamus and cerebral cortex. Central sensitization
may also modulate spinal interneurons and descending
inhibitory pathways. Central sensitization is symptomati-
cally expressed as allodynia (pain to normally non-painful
stimuli) and hyperalgesia (abnormally increased sensa-
tion of pain). Simons, Travell, and Simons1 described
the central nervous system (CNS) as an “integrator” of
MFTrPs, akin to Korr’s description30 of the CNS as an
“organizer” of somatic dysfunction.
Autonomic Component
Autonomic phenomena associated with MFTrPs include
localized sweating, vasoconstriction or vasodilation, and
pilomotor activity (“goosebumps”)1. MFTrPs located in
the head and neck may cause lacrimation, coryza (nasal
discharge), and salivation1. The autonomic nervous system
(ANS) is primarily involved in reflex arcs, exerting control
of cardiac muscle and smooth muscle in blood vessels,
glands, and visceral organs. Hubbard and Berkoff3 re-
viewed the literature that demonstrated ANS involvement
in skeletal muscles and MPTrP formation. Sympathetic
neurons innervating vessels in skeletal muscles may exit
the perivascular space and terminate among intrafusal
fibers within muscle spindles. Sympathetic neurons
release norepinephrine, a neurotransmitter involved in
the “fight-or-flight” response. Norepinephrine activates
1
-adrenergic receptors in the intrafusal muscle cell
membrane. Activation of
1
-adrenergic receptors depresses
the feedback control of muscle length, detrimentally
affecting motor performance and possibly contributing
to the “ATP energy crisis” 31. Norepinephrine has been
shown to augment the amplitude and duration of MEPPs
in frog leg motor endplates32. Pentolamine, an antagonist
of
1
-adrenergic receptors, decreases SEA in MFTrPs33.
Similar effects have been seen with local intramuscular
injections of phenoxybenzamine, another
1
-adrenergic
antagonist34.
The ANS may indirectly exacerbate MFTrP formation
via viscerosomatic reflexes. Visceral autonomic afferents
from disturbed viscera carry signals to the dorsal horn.
Chronic input eventually facilitates neurotransmission
at that spinal level35. This form of central sensitization
accelerates in the presence of nociceptor AIGS and ep-
haptic crosstalk with neighboring autonomic nerves9.
Ephaptic crosstalk (cross-excitation) is the nonsynaptic
interaction between two nerves that are parallel and
relatively close together so that their action potentials
influence each other.
Translating Theory to Therapy
The motor endplate and “ATP energy crisis” hypoth-
eses have changed our approach to treating MFTrPs.
For example, the 1999 edition of Myofascial Pain and
Dysfunction: The Trigger Point Manual1, abandoned the
application of heavy ischemic compression upon MFTrPs.
Deep digital pressure that produces additional ischemia
is not beneficial. Instead, Simons, Travell, and Simons1
recommended applying gentle digital pressure to MFTrPs
to avoid exacerbating tissue hypoxia. They named their
technique ‘”trigger point pressure release.” A single finger
pad palpates the MFTrP while the affected muscle is pas-
sively lengthened to a point of tissue resistance. Next, the
MFTrP is pressed with slowly increasing pressure until
the palpating finger encounters a barrier (local tissue
resistance). The engaged barrier is held until a release
of tension is palpated. The finger “follows” the released
tissue by taking up tissue slack, engaging a new barrier,
and repeating the sequence. This “press and stretch” is
believed to restore abnormally contracted sarcomeres
to their normal resting length. We hypothesize that
“press and stretch” mechanically uncouples myosin from
actin, a process that normally requires ATP, so that the
technique reduces ATP demand and breaks the energy
crisis cycle. Press and stretch may also help release the
“stuck” spring function of the titin connection to the
Z bands within sarcomeres.
Simons, Travell, and Simons’ new Manual1 also em-
phasized the relationship between MFTrPs and nearby
236 / The Journal of Manual & Manipulative Therapy, 2006
articular dysfunctions. They correlated suboccipital
MFTrPs with occipito-atlantal dysfunction, semispinalis
capitus MFTrPs with occipito-atlantal and atlanto-axial
dysfunctions, and splenius MFTrPs with upper thoracic
articular dysfunctions1. This close association between
MFTrPs and articular dysfunctions is the result of
a positive feedback loop. Lewit has emphasized this
close association in several publications36,37. A MFTrP
in a muscle that crosses an articulation reduces this
articulation’s full range of motion, and the MFTrP taut
band exerts continuous compression upon the articula-
tion. Soft tissues surrounding the articulation cannot
withstand chronic compression or tension, and they
respond with increased sensitivity. When sufficiently
sensitized, these structures send continuous nociceptive
messages to the central nervous system, which responds
by further activation of MFTrPs, which in turn increases
the muscle tension. This positive feedback loop aggra-
vates the articular distress. Articular dysfunctions can be
treated directly by muscle energy technique (similar to
contract-relax or post-isometric relaxation techniques),
joint mobilization, and high-velocity, low-amplitude
thrust techniques. Articular dysfunctions can be treated
indirectly with techniques that address dysfunctional
muscles or fascia that cross the articulations, such as
strain-counterstrain and myofascial release. Indications
and precautions for these techniques are the same as
with any articular dysfunctions. Methods for treating
MFTrPs and articular dysfunctions work best when
combined with patient education.
Patient Education
Postural training is paramount. Postural disorders
often contribute to the perpetuation of MFTrPs. For
example, postural strain of the suboccipital muscles
may cause MFTrPs in these muscles1, thus leading to
further deterioration in muscle structure and function,
including radiating somatic pain and atrophic changes,
such as muscle atrophy, fibrosis, and decreased tensile
strength38. Suboccipital muscles contain a high density
of proprioceptors39, so muscle atrophy leads to a loss in
proprioceptive balance and a loss of proprioceptive “gate
control” at the dorsal horn. This gives rise to chronic
pain syndromes including neck pain and headache38.
In these patients, proprioceptive exercises can be very
helpful, such as close-eyed balance training. Biomechanical
factors that stress muscles, such as repetitive activities,
must be avoided. Biomechanical stress of a cold muscle
is a key factor in the formation of MFTrPs1. Cooling the
muscle apparently upregulates nAChR activity at the
motor endplate40.
Patients with MFTrPs should avoid excess coffee41;
caffeine up-regulates the motor endplate by acting as
a ryanodine receptor agonist42. Tobacco should also be
avoided, as nicotine upregulates L-type VsCCs and nAChR
expression, which may lead to muscle hyperexcitability43.
Nicotine activates nAChRs in the CNS and autonomic
nerves. Although nAChRs in motor endplates are not
normally activated by nicotine, mutational defects may
sensitize motor endplate nAChRs. One study indicated
that ethanol also facilitates motor-end plate activity, via
a presynaptic mechanism44.
Simons, Travell, and Simons1 recommended a diet
adequate in vitamins and minerals for the prevention of
MFTrPs. Amazingly, in the 20+ years since that recom-
mendation, no well-designed study has been published
concerning the effects of vitamin supplementation
upon MFTrPs. However, a wealth of clinical experience
suggests that low-normal and subnormal levels of vita-
mins and minerals act as strong perpetuating factors
of MFTrPs. Many case histories attest to patients who
responded weakly to manual and/or injection treatment,
but adequate supplementation (the return of blood
vitamin levels to within mid-normal range) brought
about an effective response to the same treatment and
with continued supplementation, the patients had no
relapse. Interestingly, in two cases, a VA hospital physi-
cian advised discontinuation of “unnecessary” vitamin
supplements, and within a few months the patients re-
turned to the myofascial pain clinic with active MFTrPs
as before. Reinstatement of their supplement regimen
and a replication of previous treatment restored their
health (Simons, unpublished data). Similarly, anemia is
a perpetuating factor of MFTrPs that must be corrected
to achieve lasting results from treatment45. Inadequate
hemoglobin perpetuates the hypoxia present in MFTrPs46.
The importance of calcium and magnesium for normal
muscle function is well documented, and trace elements
are well known to be essential for many body functions
including muscle function. Supplementing the diet
with phosphatidyl choline has been recommended for
the treatment of fibromyalgia47, but this may actually
provoke MFTrPs in some patients. Choline is a percur-
sor to ACh, and a nAChR gain-of-function mutation may
enable choline to directly activate the mutated recep-
tors14. High doses of phosphatidyl choline are found in
supplements containing lecithin, with lower amounts
in raw egg yoke, organ meats, soybeans, peanuts, wheat
germ, and brewer’s yeast.
An estimated 50% of patients with chronic muscu-
loskeletal pain take herbal remedies, so it behooves all
health practitioners to understand the mechanisms of
herbal medicines48. Clinical experience has shown that
myofascial pain can be improved with many herbal rem-
edies and essential oils47, including lavender (Lavandula
angustifolia), lemon balm (Melissa officinalis), rosemary
(Rosmarinus officinalis), kava kava (Piper methysticum),
skullcap (Scutellaria lateriflora), passionflower (Passiflora
incarnata), rose (Rosa species), and valerian (Valeriana
officinalis). Nearly all these herbs contain linalool, a
monoterpene that inhibits ACh release (a presynaptic
mechanism) and nAChRs (a postsynaptic mechanism)49.
Myofascial Trigger Points: Translating Molecular
Theory into Manual Therapy / 237
Marijuana (Cannabis species) also produces linalool,
although the herb’s efficacy may be due to tetrahydro-
cannabinol (THC), which inhibits P/Q-, N-, and L-type
VsCCs via cannabinoid receptors found in the motor
endplate50. Sativex, a standardized extract dispensed as
an oromucosal spray, has been approved for the treat-
ment of muscle spasticity and pain in Canada51. THC
works by mimicking an endogenous neurotransmitter
named anandamide50. Anandamide and THC bind to the
same neuroreceptor, known as the cannabinoid receptor.
Enhanced release of “endocannabinoids” may be one of
the mechanisms of osteopathic manipulative treatment52,
parallel to the effects of manipulative treatment upon
serum endorphin levels53.
Getting to the Point
Needling may be necessary to inactivate MFTrPs.
The “motor endplate hypothesis” led to the injection of
MFTrPs with botulinum toxin type A (BoToxA), which
blocks ACh release54. A variety of VsCC blockers have
also been injected. Recall that P/Q-type and L-type
VsCCs are the primary pre- and post-synaptic Ca2+ chan-
nels (respectively) in normal adult motor endplates.
The P/Q-specific antagonist omega-agatoxin IVA (also
known as omega-conotoxin GVIIC) has shown promise
in rat studies55, while verapamil, a L-type VsCC blocker,
reduced MFTrP excitability in rabbits56. The drug had no
effect on MEPP (a presynaptic measure), but it decreased
post-synaptic currents57. Thus, verapamil may function
as a nAChR antagonist, rather than by way of its known
VsCC antagonism. Similarly, quinidine, another L-type
antagonist, also downregulates nAChRs and may restore
AChE activity12. Diltiazem also merits investigation. This
L-type Ca2+ channel blocker corrects myopathies caused
by defects in AChE activity13. However, nifedipine, yet
another L-type antagonist, unexpectedly increased ACh
activity at motor endplates, due to a unique effect upon
ryanodine-sensitive intracellular Ca2+ stores58. Hence,
research with VsCC blockers has generated conflicting
results, and recent clinical trials with BoToxA have
produced mixed results59. Dry needling is usually as ef-
fective as injecting anything; if the procedure elicits a
local twitch response, dry needling should be as effective
as BoTox and much less expensive.
Some nAChR antagonists and channel blockers can
directly penetrate skin, so they need not be injected.
Lidocaine patches have recently been suggested60. As
cited by Simons et al1, Simons, Travell, and Simons in
1983 recommended dimethisoquin ointment (Quotane )
for massaging MFTrPs in superficial muscles such as the
orbicularis oculi, frontalis, and occipitalis. Dimethisoquin,
a local anesthetic, inhibits voltage-gated Na+ channels
(conferring its anaesthetic effect), but it also acts as an
nAChR antagonist61. Its potency is much greater than
lidocaine and procaine, and dimethisoquin is uniquely
selective for the motor endplate nAChR subtype. Massage
with capsaicin cream (available over the counter as a
0.075% cream) is useful for treating MFTrPs located
in surgical scars62, which are particularly refractory to
treatment1. This seems contra-intuitive: Capsaicin is the
primary active ingredient in hot peppers, and it activates
the vanilloid receptor (TRPV1) in nociceptors. However,
with repeated exposure to capsaicin, TRPV1 receptors
become desensitized, which explains the seemingly
paradoxical use of capsaicin as an analgesic63. Another
“massage” treatment of MFTrPs uses frequency specific
micro-current (FSM), which delivers electromagnetic
currents through graphite-conducting gloves. In relation
to the MFTrP “energy crisis” model, studies have shown
that FSM increases ATP production in muscle tissues
as well as reducing cytokine levels64. To successfully
treat MFTrPs with FSM, a clinician must be skillful at
finding MFTrPs.
Conclusion
The MfTrP, according to our working hypothesis,
centers upon dysregulated motor endplates, sustained by
a neural loop of sensory afferents and autonomic effer-
ents. The resulting “ATP energy crisis” links with a spinal
reflex disorder known as central sensitization. Treatment
must simultaneously address the symptomatic trigger
points and their underlying causes. Appropriate treat-
ment includes dry needling (also know as acupuncture),
vapocoolant spray-and-stretch, and thermal treatment
(including ultrasound and infrared laser), some of which
are discussed in other articles presented in this JMMT
series. New approaches described in this article, includ-
ing manual techniques (“press-and-stretch” and articular
methods) patient education, and ACh- or VsCC-attenuation
techniques (e.g., medications, herbs, and nutrition), have
evolved from our new etiological concepts.
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Shah-archives2007.pdf
Biochemicals Associated With Pain and Inflammation are Elevated in Sites Near to and Remote From Active Myofascial Trigger Points
METHODS
Participants
Instrumentation
Procedures
Statistical Design and Analysis
RESULTS
DISCUSSION
Study Limitations
CONCLUSIONS
APPENDIX 1: COLLECTION SCHEDULE FOR DIALYSATE SAMPLES
References
Suppliers
katagiri sniff test 2003.pdf
Neck and abdominal muscle activity during a sniff
Introduction
Methods
Electrode insertion
Measurement techniques
EMG analysis
Statistical analysis
Results
SNIP and raw EMG of scalene and sternocieldomastoid
Relationship between increasing SNIP and neck muscle moving average EMG
Impact of posture on SNIP and neck muscle EMG
Relationship between SNIP and TA EMG activity
Discussion
Validity of SNIP values
Sniff measurement of inspiratory muscle strength
Activity of respiratory muscles during sniff
Acknowledgements
References
Gerwin et al expansion simons 2004.pdf
An Expansion of Simons’ Integrated Hypothesis of Trigger Point Formation
An Expansion of Simons’ Integrated Hypothesis of Trigger Point Formation
Robert
Robert
D.
Gerwin,
MD*,
Jan
Dommerholt,
PT, MPS, and
Jay
P.
Shah,
MD
Address
Address
*Johns Hopkins University,
*Johns Hopkins University,
Pain and Rehabilitation Medicine,
7830 Old Georgetown Road, Suite C-15,
Bethesda,
MD
20814-2432,
USA.
E-mail: gerwin@painpoints.com
Current Pain and Headache Reports
Current Pain and Headache Reports
2004,
Current Science Inc. ISSN
Copyright © 2004 by Current Science Inc.
Simons’ integrated hypothesis proposed a model of trigger point (TrP) activation to explain known...
Introduction
Introduction
Myofascial pain syndrome (MPS) is a myalgic condition characterized by local and referred pain th...
Local myofascial pain occurs because of the release of substances from damaged muscle, such as ad...
This article presents known data about the TrP and discusses in detail salient features of muscle...
Features of Myofascial Trigger Points and Muscle Nociceptors
Features of Myofascial Trigger Points and Muscle Nociceptors
Certain features of the myofascial TrP relevant to the problem of how the taut band develops and ...
A taut muscle band may contain a latent TrP, without tenderness. However, in MPS, tenderness is a...
A marked increase in the frequency of low-voltage (50– 100 microvolts) electrical activity is fou...
Areas of intense focal sarcomere contraction have been described in the muscles of animals with n...
There are a number of biochemical alterations identified by microdialysis sampling techniques at ...
Exercise under ischemic conditions [
Tendon organs (sensory receptors located at the muscle -tendon junction in skeletal muscle) are r...
Intramuscular hypoperfusion is likely to occur in myalgic syndromes such as myofascial pain [
Hypoxia (extremely low PO
Individuals with work-related trapezius myalgia have a deficit of cytochrome C oxidase [
a
a
Muscle nociceptors are dynamic structures whose receptors can undergo conformational change depen...
The nociceptor terminal contains stored substances, (
Implications
Implications
Taken together, these points suggest that a possible activating event in MPS is exercise under co...
The increase in CGRP that occurs in ischemia-induced muscle injury could result in an apparent in...
The work of Shah
Muscle Injury Related to Eccentric Muscle Contraction and Maximal Concentric Muscle Contraction
Muscle Injury Related to Eccentric Muscle Contraction and Maximal Concentric Muscle Contraction
Unaccustomed or intense exercise-induced weakness and muscle damage is well documented, particula...
Eccentric exercise is associated with muscle soreness and muscle damage. Immediate injurious effe...
Muscle fiber injury occurs rapidly in eccentric muscle contraction. Desmin is a muscle cytoskelet...
The regions of sarcomere disruption are thought to act as foci for further damage with repeated, ...
One result of muscle damage is an immediate reduction of muscle force-generating capacity [
Calcitonin Gene-related Peptide, Acetylcholine Receptors, and Acetylcholinesterase
Calcitonin Gene-related Peptide, Acetylcholine Receptors, and Acetylcholinesterase
Calcitonin gene-related peptide
Calcitonin gene-related peptide
Calcitonin gene-related peptide coexists with ACh at the synaptic endings of the motor nerve and ...
Calcitonin gene-related peptide receptors consist of protein complexes that span the membrane and...
Calcitonin gene-related peptide increases the contractile force of nerve-induced muscle contracti...
Calcitonin gene-related peptide increases or decreases ACh release from motor nerve terminals as ...
Acetylcholine receptors
Acetylcholine receptors
The AChR is a transmembrane complex that has an outer ligand-binding configuration, an intramembr...
When the AChR is activated, ionic channel currents are generated that result in miniature endplat...
Acetylcholine release
Acetylcholine release
Acetylcholine release is quantal and nonquantal. Quantal release is calcium-dependent whereas non...
Muscle contraction takes place through depolarization of the muscle fiber membrane at the motor e...
Acetylcholine also acts through a feedback mechanism to regulate its own release at the neuromusc...
Presynaptic sympathetic nerve modulation of acetylcholine release
Presynaptic sympathetic nerve modulation of acetylcholine release
The sympathetic nervous system modulated the observed endplate noise at the TrP, reducing it by a...
Acetylcholinesterase
Acetylcholinesterase
Acetylcholinesterase is present in the synaptic cleft. It breaks down ACh and thereby can inhibit...
Acidic pH and Muscle Pain
Acidic pH and Muscle Pain
The work of Sluka
Figure 1. A schematic outline of the expanded trigger point hypothesis. The activating event is ...
Figure 1. A schematic outline of the expanded trigger point hypothesis. The activating event is ...
Hypothesis
Hypothesis
It can be hypothesized that the activating event in the development of the TrP is the performance...
Conclusions
Conclusions
There normally is an equilibrium between the release of ACh, the breakdown of ACh, and its remova...
References and Recommended Reading
References and Recommended Reading
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Myofascial dysfunction pelvis Jarrell.pdf
Myofascial Dysfunction in the Pelvis
Myofascial Dysfunction in the Pelvis
John
John
Jarrell,
MD, MSc
Address
Address
Department of Obstetrics and Gynecology,
Department of Obstetrics and Gynecology,
University of Calgary,
1403 29th Street N.W.,
Calgary, AB,
Canada
T2N 2T9.
E-mail: john.jarrell@calgaryhealthregion.ca
Current Pain and Headache Reports
Current Pain and Headache Reports
2004,
Current Science Inc. ISSN
Copyright © 2004 by Current Science Inc.
Chronic pelvic pain is a potentially devastating condition that affects many women with severe co...
Introduction
Introduction
Chronic pelvic pain in women is defined as persistent pain in the pelvic region that has been pre...
The causes of the condition are poorly understood for many reasons. Initial studies of the causes...
The exact prevalence is unknown. Alberta Health and Wellness reported the presence of chronic pai...
The spectrum of diseases that have been associated with chronic pelvic pain are manifold. They in...
A further confounding problem in addition to depression and poor social interactions has been an ...
Common Visceral Conditions Associated with Chronic Pelvic Pain Observed at Laparoscopy
Common Visceral Conditions Associated with Chronic Pelvic Pain Observed at Laparoscopy
Endometriosis is a degenerative condition that commonly acts like a benign tumor because of its l...
Adhesions are areas of tissue growth that cause the union of tissues that usually are free of one...
At laparoscopy, the presence of endometriosis and adhesions make up most of the diagnoses of cond...
Myofascial Dysfunction: The Great Pretender
Myofascial Dysfunction: The Great Pretender
Myofascial dysfunction is an important consideration because it may represent a substantial porti...
The clinical presentation of the syndrome is the presence of severe tenderness and a nodule or ba...
The management of myofascial disorders is based on the principle that the vicious cycle can be br...
Approach to the Intrapelvic Muscles
Approach to the Intrapelvic Muscles
There is a significant muscular composition to the pelvis. The major muscles include the levator ...
Examination of patients with chronic pelvic pain should be modified to eliminate the possibility ...
Table 1. Clinical characteristics of subjects
Age
Gravida
Para
Number
Duration, y
Number
52
53
53
55
49
Mean
35
1
0.9
3.7
4.8
Minimum
19
0
0
1
0.2
Maximum
71
9
5
9
19
Standard deviation
11.6
1.9
1.2
2.4
4.5
The approach to the treatment of these bands is as presented by Gerwin [
As in abdominal wall problems, one must be cautious in the simple treatment of the trigger points...
Cross-sectional Study of Patients with Pelvic Pain and Myofascial Dysfunction
Cross-sectional Study of Patients with Pelvic Pain and Myofascial Dysfunction
Just as it is important not to miss muscle pain in the clinical evaluation of the abdomen and pel...
Figure 1. The relationship of age and the number of myofascial trigger points identified.
Figure 1. The relationship of age and the number of myofascial trigger points identified.
In this analysis, the number of trigger points was found to range from one to nine. The duration ...
In this limited study, the presence or absence of a trigger point in the abdominal wall was a ver...
Table 2. Presence of visceral disease among subjects with abdominal wall trigger points
Visceral disease
Positive
Negative
Tender point
Positive
Negative
Total
predictive value
predictive value
Present
37
4
11
Absent
4
7
41
0.9
41
11
52
0.64
Sensitivity
0.9
Specificity
0.64
Prevalence
79.8
Furthermore, there was an interesting observation that the actual number of trigger points that c...
Conclusions
Conclusions
This study was done to determine if the link between myofascial dysfunction and visceral disease ...
The processes of myofascial dysfunction appear somewhat dynamic on the basis that there are age-r...
The relationship of abdominal wall trigger points and visceral disease is of interest because it ...
From a clinical perspective, this study is relevant to the management of myofascial dysfunction. ...
References and Recommended Reading
References and Recommended Reading
Papers of particular interest, published recently, have been highlighted as:
Papers of particular interest, published recently, have been highlighted as:
• Of importance
•• Of major importance
1. •• Steege
1. •• Steege
1. •• Steege
JF,
Metzger
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Chronic Pelvic Pain,
edn 1.
Philadelphia:
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The current standard for a comprehensive but readable text of a complex societal and medical prob...
2. Health Surveillance Alberta Health and Wellness EA:
2. Health Surveillance Alberta Health and Wellness EA:
2. Health Surveillance Alberta Health and Wellness EA:
Chronic pain in Alberta: A Portrait from the 1996 National Population Health Survey and the 2001 ...
http://www.health.gov.ab.ca/public/diseases/pdf/ChronicPainReport.pdf
. Accessed May 1, 2004.
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2007.CNP.itoh.pdf
Randomised trial of trigger point acupuncture compared with other acupuncture for treatment of chronic neck pain
Introduction
Methods
Patients
Design
Blinding
Treatment
Standard acupuncture (SA) group
Trigger point acupuncture (TrP) or non-trigger point (non-TrP) group
Sham acupuncture (SH) group
Evaluation
Assessment of blinding technique
Statistical analysis
Results
Patient characteristics
VAS score
Functional impairment
Assessment of the blinding technique
Discussion
Effectiveness of the trigger point as a treatment site of acupuncture
Acknowledgments
References
chen-Elastography-MRI-2007.pdf
Identification and Quantification of Myofascial Taut Bands With Magnetic Resonance Elastography
METHODS
Bovine Gel Phantom
Finite Element Simulation
Participants
RESULTS
Taut Band Phantom
Finite Element Simulation
Participants
DISCUSSION
Study Limitations
CONCLUSIONS
References
chen et al elastography 2008.pdf
Ability of magnetic resonance elastography to assess taut bands
Introduction
Methods
Magnetic resonance elastography on bovine gel phantom
Finite element modeling
Magnetic resonance elastography on human subjects
Results
Magnetic resonance elastography on bovine gel phantom
Finite element simulation
Magnetic resonance elastography on human subjects
Discussion
Acknowledgments
References
shah et al review 2008 jbmt.pdf
Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: An application of muscle pain concepts to myofascial pain syndrome
Introduction
Historical terminology
Myofascial trigger point diagnostic criteria
Motor abnormalities of the myofascial trigger point
Electrophysiology
The Integrated Trigger Point Hypothesis
The Cinderella Hypothesis
Sensory abnormalities of the myofascial trigger point
Nociceptor properties
Chemical activation of afferent nerves
Peripheral and central sensitization
Uncovering the biochemical milieu of myofascial trigger points
Microdialysis sampling of the trapezius
Microdialysis sampling of the trapezius and gastrocnemius
Roles of biochemical substances associated with pain and inflammation
pH
Neuropeptides
Catecholamines
Cytokines
Conclusion
References
chang chen chang neuroaxonal degeneration.pdf
Evidence of neuroaxonal degeneration in myofascial pain syndrome: A study of neuromuscular jitter by axonal microstimulation
Introduction
Subjects and methods
Patients profile
Stimulated SFEMG study
Statistical analysis
Results
Discussion
Acknowledgements
References
ge et al topography TrP 208.pdf
Topographical mapping and mechanical pain sensitivity of myofascial trigger points in the infraspinatus muscle
Introduction
Materials and methods
Patients
Experimental protocol
Assessment of muscle mechanical pain sensitivity
Topographical PPT mapping
Dry needling procedure
Statistical analysis
Results
The number of MTrPs bilaterally in the infraspinatus muscles
PPT bilaterally in the infraspinatus
Location of MTrPs bilaterally in the infraspinatus muscles
Discussion
Multiple active MTrPs are associated with unilateral shoulder pain
Presence of latent MTrPs bilaterally in the infraspinatus
Peripheral sensitization is crucial to the development of myofascial pain syndrome
References
Ge et al induction of muscle cramps and latent MTrP exp brain res.pdf
Induction of muscle cramps by nociceptive stimulation of latent myofascial trigger points
Abstract
Introduction
Materials and methods
Subjects
Experimental protocol
EMG-guided intramuscular injection
EMG-guided injection needle recordings
Muscle cramp as deWned by EMG
Assessment of local muscle pain intensity
Statistical analysis
Results
Pain intensity
EMG activity before and after glutamate and isotonic saline injections
Occurrence of muscle cramps
Discussion
Association of muscle cramps with MTrPs
Increased nociceptive sensitivity at MTrPs mediates the occurrence of muscle cramps
References
Ge sympathetic facilitation.pdf
Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain
Introduction
Subjects and methods
Subjects
Experimental protocol
Measurement of PPT and PTRP
Statistical analysis
Results
Effect of increased sympathetic activity on PPT at the tender and trigger points
Effect of increased sympathetic activity on PPT in the tibialis anterior muscle
Effect of increased sympathetic activity on PPT, referred pain threshold (PTRP), and local and referred pain intensities at the trigger point
Discussion
Sympathetic hyperactivity at myofascial tender and trigger points
Sympathetic hyperactivity and referred muscle pain
Acknowledgements
References
Giamberardino TrP and Migraines.pdf
Contribution of Myofascial Trigger Points to Migraine Symptoms
Materials and Methods
Phase 1: Main Experiment
Patients and Subjects
Experimental Procedures
Palpation of Cervical Muscles for Trigger Point Assessment
Pain Thresholds and TrP Treatment
Migraine Parameters
Technique of Pain Threshold Measurement to Electrical Stimulation
Cutaneous Thresholds in Migraine Sites of Patients Without Active Cervical Trigger Points
TrP Infiltration Technique
Phase 2: Secondary Experiment
Statistical Analysis
Results
Phase 1: Main Experiment
Pain Thresholds
Cutaneous Thresholds in Migraine Sites of Patients Without Active Cervical Trigger Points
Migraine Parameters
Pain Thresholds Versus Migraine Parameters in Treated Patients
Phase 2: Secondary Experiment
Pain Thresholds
Migraine Parameters
Discussion
Acknowledgments
References
pathogenesis of muscle pain mense.pdf
The Pathogenesis of Muscle Pain
The Pathogenesis of Muscle Pain
Siegfried
Siegfried
Mense,
MD
Address
Address
Institut für Anatomie und Zellbiologie III, Universität Heidelberg,
Institut für Anatomie und Zellbiologie III, Universität Heidelberg,
Im Neuenheimer Feld 307,
69120
Heidelberg,
Germany.
E-mail: mense@urz.uni-heidelberg.de
Current Pain and Headache Reports
Current Pain and Headache Reports
2003,
Current Science Inc. ISSN
Copyright © 2003 by Current Science Inc.
Nociceptive nerve endings in muscles and other tissues are equipped with a multitude of receptor ...
Introduction
Introduction
In recent years, it has become more obvious that muscle pain differs in several aspects from cuta...
This article focuses on peripheral and central nervous mechanisms of muscle pain and discusses pa...
Peripheral Mechanisms
Peripheral Mechanisms
Neurobiology of muscle nociceptors
Neurobiology of muscle nociceptors
The term neurobiology includes neurophysiologic and neuroanatomic aspects. Morphologically, a no...
Recordings of the electrical activity of single muscle afferent fibers in cats and rats have show...
Well-known stimulants for muscle nociceptors are endogenous pain-producing substances such as bra...
This type of nociceptor would be well suited to mediate the pain of tonic muscle contractions, wh...
Figure 1. Schematic drawing of a nociceptive nerve ending showing membrane receptor molecules an...
Figure 1. Schematic drawing of a nociceptive nerve ending showing membrane receptor molecules an...
Data from nociceptors in joints and other tissues have shown that the previously mentioned endoge...
Receptor molecules for clinical cases of muscle pain are the so-called purinergic receptors (
Another receptor molecule of particular clinical interest is VR-1. It responds to an increase in ...
Figure 2. Proportion of rat muscle nociceptors that responded to adenosine triphosphate (ATP), ...
Figure 2. Proportion of rat muscle nociceptors that responded to adenosine triphosphate (ATP), ...
In experiments by the author’s group, ATP and acidic solutions were effective stimulants for musc...
Theoretically, the pain during tooth clenching, bruxism, and tension-type headache could be media...
Neuropeptide content of muscle nociceptors
Neuropeptide content of muscle nociceptors
There is no neuropeptide that can be regarded as specific for sensory fibers from muscle or for m...
Interactions between stimulants at the receptive nerve ending
Interactions between stimulants at the receptive nerve ending
Prostaglandin E
The concentration of PG E
Sensitization of nociceptors as the peripheral neurophysiologic basis of tenderness and hyperalgesia
Sensitization of nociceptors as the peripheral neurophysiologic basis of tenderness and hyperalgesia
Many substances released from pathologically altered tissue increase the mechanical sensitivity o...
Figure 3. Expansion of the spinal target area of the gastrocnemius-soleus (GS) muscle nerves aft...
Figure 3. Expansion of the spinal target area of the gastrocnemius-soleus (GS) muscle nerves aft...
Longer-lasting pathologic alterations of muscle tissue sensitize nociceptors and increase the inn...
Mechanisms of Muscle Pain at the Spinal Level
Mechanisms of Muscle Pain at the Spinal Level
Myositis-induced neuroplastic changes in the spinal dorsal horn
Myositis-induced neuroplastic changes in the spinal dorsal horn
Input from peripheral nociceptors to the spinal cord or brain stem is known to lead to changes in...
The cellular mechanism underlying the myositis- induced expansion of the responding neuron popula...
Neurotransmitters involved in central sensitization
Neurotransmitters involved in central sensitization
Experiments with intrathecal administration of antagonists to SP and NMDA receptors showed that t...
Patients with myositis complain of hyperalgesia, hyper aesthesia, spontaneous pain, and dysaesthe...
Mechanism of referral of muscle pain
Mechanism of referral of muscle pain
The expansion of the input region of the inflamed GS muscle nerve likely underlies the spread an...
The transition from acute to chronic muscle pain
The transition from acute to chronic muscle pain
The functional reorganization in the spinal dorsal horn is an expression of neuroplasticity becau...
Tissue sections from animals with an acute myositis (10- hour duration) showed a significant incr...
The last step in the transition from acute to chronic muscle pain is morphologic changes in the c...
In patients, the development of lesion-induced structural changes in the dorsal horn and in highe...
Conclusions
Conclusions
The data obtained in studies on nociceptive nerve endings in muscle and other tissues show that t...
The transition from acute to chronic muscle pain is considered to be a series of processes that s...
References and Recommended Reading
References and Recommended Reading
Papers of particular interest, published recently, have been highlighted as:
Papers of particular interest, published recently, have been highlighted as:
• Of importance
•• Of major importance
1. • Mense
1. • Mense
1. • Mense
S,
Simons
DG:
Muscle Pain: Understanding Its Nature, Diagnosis, and Treatment,
Baltimore and London:
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2001.
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muscle pain graven nielsen.pdf
Induction and Assessment of Muscle Pain, Referred Pain, and Muscular Hyperalgesia
Induction and Assessment of Muscle Pain, Referred Pain, and Muscular Hyperalgesia
Thomas
Thomas
Graven-Nielsen,
PhD
Address
Address
Center for Sensory-Motor Interaction, Laboratory for Experimental Pain Research,
Center for Sensory-Motor Interaction, Laboratory for Experimental Pain Research,
Aalborg University,
Fredrik Bajers Vej 7D-3,
DK-9220
Aalborg E,
Denmark.
E-mail: tgn@smi.auc.dk
Current Pain and Headache Reports
Current Pain and Headache Reports
2003,
Current Science Inc. ISSN
Copyright © 2003 by Current Science Inc.
Muscle pain can be induced and assessed experimentally by a variety of methods. Ischemic and exer...
Introduction
Introduction
The pain from deep somatic structures represents a major part of pain complaints in patients. Dee...
The neurobiologic mechanisms involved in muscle pain often are difficult to resolve from clinical...
Pain is a multidimensional perception and the reaction to a single standardized stimulus of a giv...
Table 1. Assessment methods and quantitative parameters of muscle pain
Methods
Quantitative parameter
Response-dependent
Intensity
Visual analogue scale
Verbal descriptor scale
Numerical scale
Cross-modality matching
Stimulus-response function
Quality
McGill Pain Questionnaire
Unpleasantness
Visual analogue scale
Distribution
Drawings (area, location)
Stimulus-dependent
Detection threshold (methods of limits/constant stimuli)
Pain threshold (methods of limits/constant stimuli)
Pain tolerance threshold (methods of limits/constant stimuli)
Most experimental pain research has been done on cutaneous pain, although cutaneous pain is far l...
Quantitative Assessment of Experimental Muscle Pain
Quantitative Assessment of Experimental Muscle Pain
The assessment methods of muscle pain are based on psychophysical, electrophysiologic, and imagin...
Psychophysical determinations can be divided into response-dependent and stimulus-dependent metho...
The stimulus-dependent methods are based on the adjustment of the stimulus intensity until a pred...
Stimulus-response functions are more informative than a threshold determination because suprathre...
Table 2. Stimulus modalities for induction of experimental muscle pain in humans
Type
Modality
Stimulus
Endogenous
Ischemia
Tourniquet plus contractions
Exercise
Concentric contractions
Eccentric contractions
Exogenous
Electrical
Intramuscular
Intraneural
Mechanical
Pressure
Tourniquet pressure
Focused ultrasound
Chemical
Hypertonic saline, potassium, levoascorbic acid, capsaicin, bradykinin, serotonin, calcitonin gen...
Thermal
Heated isotonic saline
(Focused ultrasound)
Verbal assessments of the experienced muscle pain intensity and other subjective characteristics ...
Experimental Muscle Pain
Experimental Muscle Pain
Various procedures can induce muscle pain and they can be divided into endogenous and exogenous t...
Ischemia
Ischemia
Lewis [
Exercise
Exercise
Exercise-induced muscle pain by concentric muscle work normally is short lasting and results from...
Electrical
Electrical
In human studies, intramuscular electrical stimulation can be used to assess the sensitivity of m...
Mechanical
Mechanical
Mechanical, painful stimulation can be achieved with pressure algometers. The most widely used te...
Tender points are anatomically determined soft-tissue body sites. Among other criteria, the patie...
An alternative to pressure algometry, with the inherent variability-related manual application, i...
Chemical
Chemical
Intramuscular injections of algogenic substances have been used to induce human muscle pain [
The sensitization of muscle nociceptors is the best established peripheral mechanism for the subj...
Glutamate receptors (ionotropic and metabotropic) are other receptor types that potentially are i...
Svensson
Referral of pain represents a common clinical sign in many musculoskeletal pain disorders and in ...
Experimentally induced referred pain is an important indicator of central sensitization in patien...
Figure 1. Assessment of the deep tissue sensitivity by automated pressure algometry. A, Pressur...
Figure 1. Assessment of the deep tissue sensitivity by automated pressure algometry.
The plasticity of the central nervous system also may alter the somatosensory sensitivity and acc...
Other modalities
Other modalities
From animal studies, afferent recordings have shown that a subgroup of muscle nociceptors respond...
Focused ultrasound has been used to induce muscle, joint, and skin pain [
Conclusions
Conclusions
Reliable methods for quantitative induction and assessment of muscle pain, referred pain, and sen...
Acknowledgment
Acknowledgment
The Danish Technical Research Council supported the time spent writing this review.
References and Recommended Reading
References and Recommended Reading
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