Upload
wilbrinkfysio
View
117
Download
0
Embed Size (px)
Citation preview
1
Myofascial Pain Syndrome
in the Craniomandibular Region#
Jan Dommerholt, PT, MPS*
# Previously published as Dommerholt, J: “El sindrome de dolor miofasical en la region craneomandibular”. In: Padrós Serrat,
E. (ed) Bases diagnosticas, terapeuticas y posturales del functionalismo craniofacial. Madrid, Ripano, 2006: 564-581
* Bethesda Physiocare / Myopain Seminars, 7830 Old Georgetown Road, Suite C-15, Bethesda, MD 20814 – 2440, USA;
+301.656.5613 (phone); +301.654.0333 (fax); [email protected]
Craniomandibular disorders (CMD) are characterized
by a combination of symptoms that may include pain,
tenderness and dysfunction of the temporomandibular
joint, the mouth and the occlusal contacts, the cervical
spine, and the muscles of mastication. Patients may
present with local dentoalveolar pain; muscle pain;
head, facial and neck pain; sounds during condylar
movements; deviations and limitations of mandibular
movements; altered occlusal relations; parafunctions
and poor oral habits; and functional limitations of
mastication. Craniofacial pain conditions have special
emotional and psychological meaning. The face, the
mouth, speech, and other oral functions are essential for
nearly all human interactions; craniofacial pain
conditions interfere with such functions and with the
ability to communicate.
Approximately 10% of the general population
experience craniomandibular pain (1). The prevalence
is estimated to range from 0% to 10% for males and
from 2% to 18% for females. The prevalence in
children and adolescents is estimated to range between
2% to 6% (2). Pain complaints range from acute and
transient conditions such as toothaches to chronic
ailments, such as trigeminal neuralgia and
temporomandibular disorders. While in the majority of
pain patients, pain decreases over time with or without
treatment, for a small percentage the pain complaint
persists. Similarly to other musculoskeletal pain
problems, between 5% and 15% of all CMD patients
become chronic pain patients (3-5). Patients with
persistent craniomandibular pain without objective
clinical or radiographic findings are especially
challenging not only to the general dentist, but also to
orthodontists, oral surgeons, TMJ specialists, and other
clinicians. Some patients may be considered good
candidates for splint therapy. Others are referred to
oral surgeons when common dental procedures fail to
offer relief. Some frustrated pain patients may even
request surgical treatment in an effort to eliminate
chronic craniomandibular pain (6).
It is generally accepted that CMD have a
multifactorial etiology (7). Although many diseases,
such as dental disease, infections and tumors, can be
associated with pain, most chronic pain problems are
thought to be musculoskeletal in nature. Different
perspectives of the primary source of pain have passed
the revue. Some researchers and clinicians have
emphasized joint dysfunction (8, 9); others have
focused more on muscular problems (10-12). The
relation between occlusion and CMD has been the
subject of several investigations (13-16). Multiple
studies have considered the impact of stress on CMD
and in particular the impact of stress on pain and
tenderness of the masticatory muscles (17-19). With
the advancement of the pain sciences, more and more
emphasis is placed on peripheral and central nervous
system sensitization (20-23).
2
Functional relations with spine dysfunction
need to be considered in the management of patients
with craniomandibular pain syndromes (24, 25).
Rocabado has developed a pragmatic approach
incorporating the intricate relationships between the
cervical spine and mandible and temporomandibular
function. He has demonstrated that centric position can
only be achieved when there is a balance between the
position and movement patterns of the subcranial
region, the mid and lower cervical spine, the hyoid, and
the mandible (26, 27). A detailed biomechanical
assessment is important. Rocabado’s “pain map” is an
excellent tool to determine which joint structures cause
or may contribute to the pain complaint (see
Rocabado’s chapter in this book for a more detailed
description of his approach).
In addition to a biomechanical joint
assessment, clinicians need to include a detailed
evaluation of the muscles in the cervical and
craniomandibular region. Numerous studies of
craniomandibular muscle pain and dysfunction have
incorporated the “research diagnostic criteria for
temporomandibular disorders” by Dworkin and
LeResche, which include a section on muscle
dysfunction (28). The research criteria were developed
to classify and quantify both the physical and
psychosocial components of temporomandibular
dysfunction. Although the criteria are widely used in
dental research, they are remarkable simplistic where it
involves muscle dysfunction. The section “Axis I,
Group I, Muscle Disorders” of the criteria includes only
two options to describe muscle dysfunction: tender
muscles with or without limited mouth opening.
The inclusion of the word “diagnostic” in the
title of Dworkin and LeResche’s classification criteria
may be interpreted that the criteria can be used in
clinical practice. However, research criteria do not
necessarily provide a mechanism for clinical diagnosis.
For example, MTrPs, myositis, and other less common
conditions affecting muscles, such as myoadenylate
deaminase deficiency or fascioliasis can not be
diagnosed using the research criteria. Therefore,
Dworkin and LeResche’s criteria do not provide any
starting points to treat patients with craniomandibular
muscular dysfunction in clinical settings, even though
they have been validated for research purposes (29-32).
Myofascial Pain Syndrome
In the dental literature, muscle pain with or
without limits in mouth opening is commonly referred
to as “myofascial pain dysfunction syndrome,” a
somewhat unfortunate term, as it is often confused and
used interchangeably with the more practical and better
defined concept of “myofascial pain syndrome” (MPS)
described by Simons, Travell and Simons (33). MPS is
the main subject of this chapter and can be described as
the sensory, motor, and autonomic symptoms caused by
myofascial trigger points. A myofascial trigger point
(MTrP) is clinically defined as a hyperirritable spot in
skeletal muscle that is associated with a hypersensitive
palpable nodule in a taut band. The spot is painful on
compression and can give rise to characteristic referred
pain, referred tenderness, motor dysfunction, and
autonomic phenomena (33). Although there are many
peer-reviewed studies and reports in the international
medical literature supporting the importance of MTrPs
in clinical practice, many of these reports are not
included in major medical library indices. Fortunately,
several prominent researchers are now investigating
MTrPs and the results of many of these studies support
the theoretical foundations and clinical applications.
Nevertheless, there is a substantial lack of basic
scientific studies; in general, MTrPs are underexplored
by research investigators (34).
A better understanding and working
knowledge of MTrPs and MPS will provide dentists,
orthodontists, oral surgeons, and other clinicians with
an effective approach to relieve human suffering, and
contribute significantly to their patients’ quality of life.
If MTrPs are not considered in the differential
diagnosis, a common cause of patients’ pain complaints
will be overlooked (34, 35). MPS should be considered
with any pain syndrome in the head, neck, face, and
TMJ area (12, 33, 36). Dentists need to be aware that
apparent dental or TMJ pain does not necessarily have
a dental or joint origin (37).
Myofascial pain tends to be dull, poorly
localized, and deep, in contrast to the precise location
of dental pain and cutaneous pain. Muscles can refer
pain to other deep somatic structures, such as fascia,
joints, viscera, and other muscles (38). Clinically,
referred pain is confusing to many clinicians, as
frequently, patients complain more of pain in the
referred pain zone and not necessarily of pain in the
immediate area of a MTrP. Signs and symptoms
suggestive of non-odontogenic pain include an
inadequate local dental cause for the pain; a recurrence
of pain in spite of reasonable dental therapy of the tooth
or TMJ; poor lasting pain relief after local anesthetic
blocking; positive findings with Rocabado’s pain map;
postural abnormalities such as forward head posture;
and other pain problems, such as chronic and recurrent
headaches and widespread chronic pain conditions.
Patients with MPS usually have a history of
acute or chronic muscle overload. In dental practice,
MPS is commonly seen in patients with a history of
3
bruxism or clenching (12, 39-41). A common
iatrogenic cause of MPS occurs when patients are
required to keep their mouths open for prolonged
periods of time during dental procedures (42). Patients
with MPS in the head-neck region often are unable to
relax their muscles in between contractions, i.e., the
masseter, sternocleidomastoid and trapezius muscles.
The muscles are in continuous contracture, which can
result in muscle ischemia, fatigue and pain (23, 43, 44).
Historical Overview of Myofascial Pain Syndrome
MTrPs are the principal characteristic of MPS.
During the past nearly 200 years, numerous authors
have described MTrPs in the English, German, Dutch,
and French medical literature, illustrating that
musculoskeletal pain due to MTrPs is very common
(45, 46). Already in 1816, British physician Balfour
described MTrPs as “nodular tumours and thickenings
which were painful to the touch, and from which pains
shot to neighbouring parts.” Balfour speculated that the
nodules were due to inflammation of the fibrous
connective tissue in muscle (47). Historically, multiple
terms have been used to describe muscle pain
syndromes, many of which would have been diagnosed
as MPS using the current definition, including
fibrositis, myofasciitis, muscular rheumatism,
rheumatic myositis, muscle hardening, myogelosis,
myalgia, myofascial pain, and even fibromyalgia (45).
In 1938, British rheumatologist Kellgren
published a seminal paper describing specific referred
pain patterns of many muscles and spinal ligaments
following injections of hypertonic saline. In 1952,
Travell wrote the first of many articles introducing the
myofascial genesis of pain illustrated by specific
referred pain patterns of over 30 muscles (48). Travell
(1901 - 1997) has been referred to as the pioneer in the
treatment of musculoskeletal pain through the
recognition of MTrPs. She coined the term
“myofascial pain syndrome” to describe pain as a result
of trigger points in muscle, tendon, skin, fascia, and
ligaments (the term “trigger point” was introduced by
Steindler in 1940 (49)). Several of Travell’s
subsequent papers included referred pain patterns
relevant for head, neck, facial, and craniomandibular
pain (50-52). Travell and Simons authored the classic
two-volume text “Myofascial Pain and Dysfunction -
The Trigger Point Manual.” The first volume was
published in 1983 for the upper half of the body
followed by the second volume in 1992 for the lower
half (53, 54). The second edition of the first volume,
authored by Simons, Travell and Simons, was released
in 1999 and includes contributions by experts in the
growing field of myofascial pain and dysfunction (33).
The second edition summarizes significant progress in
the understanding of the pathophysiological basis of the
clinical presentations associated with MTrPs. The
manuals have been translated into six different
languages, including Spanish. Several other MTrP
manuals have been published in Switzerland, the
United States and the UK (46, 55, 56).
Several assessment and treatment approaches
have emerged independently of each other both in
Europe and in the United States, including myofascial
trigger point therapy (USA), neuromuscular technique
or NMT (UK), neuromuscular therapy, also abbreviated
as NMT (USA), and manual trigger point therapy
(Switzerland). It is not a coincidence that these
approaches share many similarities and have common
goals and objectives (57). Recent insights in the nature,
etiology and neurophysiology of MTrPs and their
associated symptoms have propelled the interest in the
diagnosis and treatment of persons with MPS
worldwide (58).
Diagnostic Criteria
A diagnosis of MPS can be made only by
palpation. There are no laboratory tests, imaging
studies, or standardized diagnostic criteria to make an
initial diagnosis of MPS. While this may suggest, that
a diagnosis of MPS can not be established, clinical
evidence combined with multiple scientific studies and
case reports support the practice of evaluating patients
for the presence of MTrPs. In a survey of physician
members of the American Pain Society, 85% of 493
medical pain specialists, representing fourteen medical
specialties, agreed that MPS is a distinct syndrome
(59). MPS may actually be the most overlooked
diagnosis in chronic pain patients (60). The diagnosis
depends on the clinician’s skills, training and
experience in taking a patient’s history, performing a
comprehensive examination, and assessing patients for
MTrPs. Clinicians should not assume knowing how to
identify MTrPs without specific training (61, 62).
Unfortunately, few medical, dental and allied health
school curricula include education and training in the
assessment and treatment of MTrPs. Most clinicians
trained in the diagnosis and treatment of MTrPs have
been trained through post-graduate continuing
education programs, such as the Interessengemeinschaft
f!r Myofasziale Triggerpunkttherapie (Society for
Myofascial Trigger Point Therapy) in Switzerland
(www.imtt.ch) and the Janet G. Travell, MD Seminar
Seriessm
in the US (www.painpoints.com). The
International Myopain Society has established a
multidisciplinary international committee to design a
study model for validation of diagnostic criteria. The
4
committee aims to establish reliable methods for
diagnosis of MPS, determine the interrater reliability of
MTrP examination, and determine the sensitivity and
specificity with which classification criteria can
distinguish patients with MPS from healthy control
subjects (63).
Simons, Travell and Simons defined a MTrP
as a localized spot of tenderness in a nodule of a
palpable taut band of contractured muscle fibers (33).
Taut bands are examined by gently palpating a muscle
perpendicular to the direction of the muscle fibers.
Taut bands need to be differentiated from more
generalized muscle spasms, that can be defined as
electromyographic activity as a result of increased
neuromuscular tone of the entire muscle (64, 65). A
taut band feels like a rope or string of contractured
fibers, that may extend from one end of the muscle to
the other end. There are two basic palpation techniques
for the proper identification of MTrPs. A flat palpation
technique is used for example with palpation of the
temporalis and masseter muscles (Figure 1). A pincher
palpation technique is used for example with palpation
of the sternocleidomastoid and the upper trapezius
muscles (Figure 2).
Figure 1 – a. Flat palpation of the temporalis muscle
Figure 1 – b Flat palpation of the masseter muscle
Figure 1 – c. Intra-oral palpation of the masseter muscle
Figure 2 – a. Pincher palpation of the
sternocleidomastoid muscle
Figure 2 – b. Pincher palpation of the trapezius muscle
Two recent studies have established excellent
overall interrater reliability of the clinical examination
used to establish the presence of MTrPs (62, 66). To
make a diagnosis of MPS, the minimum essential
features that need to be present are a taut band, an
exquisitely tender spot or nodule in the taut band, and
5
the patient’s recognition of the pain complaint with
pressure on the tender nodule (62). Simons, Travell
and Simons add a painful limit to stretch range of
motion as the fourth essential criterion (33). Taut
bands and MTrPs are found in asymptomatic
individuals and are only considered clinically relevant
when the patient recognizes the elicited pain or when
the functional limitations imposed by the taut band
contribute to mechanical dysfunction secondary to
muscle shortening (61, 67). The presence of a local
twitch response, referred pain, and the
electromyographic demonstration of endplate noise
increase the certainty and specificity of the diagnosis.
Local Twitch Response
A local twitch response (LTR) is elicited by
either strong digital palpation or needling/injection of a
taut band or MTrP, that results in an involuntary brief
burst of motor action potentials propagated only by
fibers of that taut band or by fibers of a taut band from
another muscle (68-70). A LTR is a spinal cord reflex,
mediated through the spinal cord without supraspinal
influences (69). During the physical examination, a
LTR confirms the presence of a MTrP. Although the
LTR can occur during physical examination of MTrPs,
eliciting a LTR is not essential for making a diagnosis
of MPS. Eliciting a LTR manually or with needling
can be difficult and rather painful for patients, which
suggests that a LTR perhaps originates from
stimulation of sensitized nociceptors in the MTrP
region rather than exclusively from mechanical
stimulation (38). Eliciting a LTR during needling
procedures is critical for the successful treatment of a
MTrP (61, 71). Close proximity to the MTrP is
essential (68). Gerwin and Duranleau were able to
objectively visualize the LTR using diagnostic
sonography, following stimulation of a MTrP by
insertion of a hypodermic needle (72). High resolution
sonography was however, not sensitive enough to
visualize the actual MTrP (73).
Referred Pain
Since Kellgren’s early studies on referred pain
from muscle, multiple clinical reports have been
published on referred pain from MTrPs (74). Referred
pain is challenging for clinicians, as the patient’s
perception of localization of pain can be very different
from the original source of pain (75). To better
appreciate the clinical implications of referred pain
from MTrPs, a more extended review is included in this
chapter. Although Asina and colleagues did not
specifically mention MTrPs, they described many of
the symptoms commonly associated with MTrPs, such
as increased myofascial tenderness, hardness, referred
pain causing headaches, and central sensitization as a
result of persistent nociceptive input from pericranial
and extracranial muscles (76). Many case reports
describe that MTrPs can cause or contribute to
persistent headaches, facial pain, and
temporomandibular pain (50, 77-80). Carlson
demonstrated the clinical significance of referred pain
by eliminating pain of the masseter muscle by treating
MTrPs in the trapezius muscle (81).
Many scientific studies and review articles
have focused on muscle referred pain (12, 23, 44, 82-
93). Referred pain is not specific to MTrPs, but it is
more common and much easier to elicit over MTrPs
than over other structures (85). Hong found that all
subjects reported referred pain with pressure directly
over active MTrPs, but less than 50% of subjects
reported referred pain with pressure over latent MTrPs
(85). Compared to active MTrPs, latent MTrPs do not
produce spontaneous pain; they require more pressure
to elicit localized and referred pain (33). Normal
muscle tissue and other body tissues, including skin,
zygopophyseal joints, and internal organs may also
refer pain to distant regions with prolonged and
sufficient mechanical pressure (67, 89, 94-99). In the
orofacial region, it is relevant that the teeth can also
refer pain to other areas, including the TMJ and the
sinuses (75).
By mechanically stimulating an active MTrP,
patients often report the development of referred pain in
fairly consistent patterns, either immediately or after a
brief 10-15 second delay. Mechanical stimulation may
consist of manual pressure, needling of the MTrP,
movement of the involved body region, or even
prolonged postural strains, such as forward head
posture or prolonged mouth opening. Usually, pain in
reference zones is described as deep tissue pain of a
dull and aching nature. However, some patients report
burning or tingling sensations or other paresthesia (89,
100). In that sense, the term “referred sensation”
reflects the clinical condition sometimes more
accurately than the established term “referred pain.”
Common referred pain patterns for nearly all skeletal
muscles are documented by Travell and Simons (33,
53, 54). Dejung and colleagues have modified several
referred pain patterns in their recent publication on
MTrPs (55).
6
Neurobiology of Referred Pain
In recent years, much new information has
become available about the neurobiology of muscle
referred pain (23, 38). Although the majority of data
has been obtained from animal experiments, it is
probably applicable to patients. Mense and colleagues
have demonstrated that skeletal muscles have different
types of nociceptors (101-103). Under normal
conditions, skeletal muscle nociceptors require high
intensities of nociceptive stimulation involving high-
threshold mechanosensitive neurons, that do not
respond to moderate local pressure, contractions or
muscle stretches (65). Muscle nociceptors are activated
by endogenous pain-producing substances such as
bradykinin or serotonin. At least one of the muscle
nociceptors is specifically sensitive to ischemic
conditions (104).
Local ischemia is associated with MTrPs.
Looking at MTrPs from a biomechanical perspective, it
is conceivable that at the cytoskeletal level, myosin
filaments literally get stuck in the Z band of the
sarcomere. During sarcomere contractions, titin
filaments are folded into a gel-like structure at the Z
band. In MTrPs, gel-like titin appears to prevent the
myosin filaments from detaching. The myosin
filaments may actually damage the regular motor
assembly and prevent the sarcomere from restoring its
resting length (105). The contracted sarcomeres are
thought to reduce the local circulation by compressing
the capillary blood supply and thus cause a significant
lack of local oxygen. One study has shown that the
oxygen saturation in the center of a MTrP is less than
5% of normal (106). Histological studies also suggest
that MTrPs are ischemic: ragged-red and moth-eaten
fibers have been identified in myogeloses and MTrPs
(107-110). Moth-eaten fibers indicate a change in the
distribution of mitochondria or the sarcotubular system,
while ragged-red fibers reflect an accumulation of
mitochondria (111). Both are usually associated with
muscle ischemia, denervation, or strenuous exercise
(112). Simons suggested that myogeloses and MTrPs
may represent the same phenomenon (113).
Local hypoxia is associated with the release
of endogenous inflammatory substances, such as
prostaglandin, bradykinin, serotonin, capsaicin,
histamine, and interleukins. Activation and
sensitization of muscle nociceptors leads to
inflammatory hyperalgesia, an activation of high
threshold nociceptors associated with C fibers, and an
increased production of bradykinin. Furthermore,
bradykinin stimulates the release of tumor necrosis
factor (TNF-"), which in turn activates the production
of the interleukins IL-1#, IL-6 and IL-8. Especially IL-
8 can cause hyperalgesia that is independent from
prostaglandin mechanisms. Via a positive feedback
loop, IL-1 beta can also induce the further release of
bradykinin (114). Bradykinin triggers the release of
calcitonin gene related peptide (CGRP), which reduces
the effectiveness of acetylcholinesterase (115-117).
The combination of endogenous substances reinforces
the observed hyperalgesia. Injections of bradykinin and
serotonin into the temporal muscle of healthy
volunteers caused more severe pain than either
bradykinin or serotonin by itself (118). Following
muscle trauma multiple substances are released
simultaneously, which appears to occur in MTrPs as
well. In their studies of the neurochemical milieu of
MTrPs, Shah and colleagues at the U.S. National
Institute of Health have confirmed increased
concentrations of bradykinin, substance P, TNF-",
interleukins, CGRP, and norepinephrine in active
MTrPs when compared with latent MTrPs and healthy
control subjects (119). In addition, the pH of the MTrP
site was significantly lower in the active MTrP group.
The endogenous substances bind to specific
receptor molecules in the membrane of nociceptive
nerve endings, including the so-called purinergic and
vanilloid (VR-1) receptors. Purinergic receptors bind
adenosine triphosphate and stimulate nociceptors
accordingly. VR-1 receptors are especially sensitive
under conditions of lowered tissue pH and muscle
ischemia. Mense suggested that pain during tooth
clenching, bruxism, and tension-type headaches is
mediated by the VR-1 receptor molecule (44).
Bradykinin, serotonin and prostaglandin interact at
many levels at the vanilloid receptors (120).
Referred pain is generated by central
mechanisms dependent on peripheral input from the
referred pain area. MTrPs are a source of ongoing
peripheral nociceptive input. Long-term nociceptive
input into the spinal cord or brain stem causes changes
in function and connectivity of sensory dorsal horn
neurons or neurons in the trigeminal nucleus caudalis
respectively (21, 44, 121, 122). The ongoing afferent
barrage into the dorsal horn and the trigeminal nucleus
results in central sensitization, the unmasking of
sleeping receptors in the dorsal horn, referred pain, and
hyperexcitability (121, 123-125). There is considerable
evidence that both neurokinin and N-methyl-D-
aspartate (NMDA) receptors are involved in triggering
hyperalgesia and the MTrP-induced hyperexcitability
of dorsal horn cells and brainstem nociceptive neurons
(21, 44, 126).
7
In MTrPs, low-threshold mechanosensitive
neurons may also get activated (127). Strong or long-
lasting nociceptive input from damaged muscle tissue
or from MTrPs results in spatial summation in the
dorsal horn or brain stem and the appearance of new
receptive fields, which means that input from
previously ineffective regions can now stimulate the
neurons. In other words, the population of dorsal horn
sensory neurons responding to the MTrP afferent input
grows larger. As interneurons are located over various
segments, the expansion may reach sensory neurons
that supply peripheral areas outside the initial MTrP
area. The expansion of pain areas is commonly seen in
patients with headaches, whiplash, and other diagnoses
(128, 129). There is no nociceptor activity in the
referred pain area (44).
Masseter MTrPs can trigger maxillary and
mandibular tooth pain, TMJ pain, facial pain, including
pain commonly associated with sinusitis, deep ear pain,
tinnitus, and frontal and temporal headaches (Figure 3).
Figure 3 – a. Referred pain pattern of the deep masseter
muscle
Figure 3 – b. Referred pain pattern of the superficial
masseter muscle
Temporalis MTrPs can induce maxillary tooth pain and
temporal headaches (Figure 4).
Figure 4 – Referred pain pattern of the temporalis
muscle
Medial pterygoid MTrPs result in pain in the mouth,
tongue, pharynx, hard palate, and behind the
temporomandibular joint (Figure 5).
8
Figure 5 – Referred pain pattern of the medial
pterygoid muscle
Lateral pterygoid MTrPs cause TMJ pain and pain in
the maxillary sinus (Figure 6).
Figure 6 – Referred pain pattern of the lateral pterygoid
muscle
MTrPs in the posterior belly of the digastric muscle
refer pain to the upper part of the sternocleidomastoid
muscle, the front of the throat, and sometimes into the
occiput. MTrPs in the anterior belly of the digastric
muscle refer pain to the mandibular incisors, the
alveolar ridge, and the tongue (Figure 7).
Figure 7 – Referred pain pattern of the digastric muscle
MTrPs in the platysma muscle cause referred pain
sensations over the lateral surface of the mandible.
Most cervical muscle MTrPs have referred pain
patterns into the head and face regions (Figure 8) (33).
Simons, Travell and Simons described the formation of
so-called satellite MTrPs in referred pain areas (33).
Figure 8 – a. Referred pain pattern of the
sternocleidomastoid muscle, sternal portion
9
Figure 8 – b. Referred pain pattern of the
sternocleidomastoid muscle, clavicular portion
Figure 8 – c. Referred pain pattern of the trapezius
muscle
Electromyographic Findings
Hubbard and Berkhoff recorded both low-
amplitude continuous action potentials (10-50
microvolts), which they labeled “spontaneous
electrical activity,” and intermittent spikes (100-600
microvolts) from active MTrPs (130). The electrical
activity was only present in sites of active MTrPs and
was absent in adjacent non-tender muscle tissue.
Subsequent studies indicated that the low-amplitude
noise-like potentials represented grossly abnormal
endplate activity (EPN) as compared to the normal
miniature endplate potentials (MEPP) commonly
reported by electromyographers (131-134). In the
EMG literature, abnormal EPN is assumed to be
associated with normal motor endplates and normal
disease-free muscles (135). However, the physiology
literature indicates that EPN represents an abnormal
concentration of acetylcholine up to three times normal
levels (132, 134, 136, 137). Recent studies by Shah
and colleagues confirmed high concentrations of
acetylcholine at MTrP sites (119, 138).
EPN is not exclusive to MTrPs. Already in
1956, Liley reported that a normal endplate could
exhibit abnormal noise-like discharge patterns by
mechanically stressing the endplate (139). Simons
suggested that Liley’s observation may help to account
for the activation of MTrPs by mechanical overload or
mechanical trauma (34). In 1997, Maselli confirmed
that damage to the endplate caused by the tip of the
advancing EMG needle could convert normal miniature
endplate potentials (MEPP) to EPN, because of a
massive release of acetylcholine (140). Brown and
Varkey suggested that the spikes, that Hubbard and
Berkhof had observed in MTrPs, could also arise from
mechanical stimulation of the endplate, however,
Wiederholt had already provided evidence that the
spikes indeed originated in the neuromuscular junction
(130, 135, 141). In Maselli’s words, the origin of the
spikes “corresponds to single muscle fiber action
potentials postsynaptically activated by suprathreshold
end-plate noise” (140). By using a very slow
insertional technique as described by Simons and
colleagues, EPN from MTrP can be reliably observed
(132, 134).
10
Integrated Trigger Point Hypothesis
Combining all available supporting evidence
of the existence of MTrPs, Simons has recently
proposed a new “integrated trigger point hypothesis”
(33). The integrated trigger point hypothesis has
evolved through several steps of progress since its first
introduction as the “energy crisis hypothesis” in 1981
(142). The hypothesis builds on the finding that
excessive amounts of acetylcholine from the motor
nerve terminal cause miniature motor endplates
potentials that produce the endplate noise observed
with needle EMG of MTrPs. The excessive
acetylcholine maintains a sustained depolarization of
the postjunctional membrane, which in turn results in
an excessive release of calcium from the sarcoplasmic
reticulum and sustained sarcomeric contractions.
Shenoi and Nagler suggested that an impaired re-uptake
of calcium into the sarcoplasmic reticulum induced by
calcium channel blockers may cause MTrPs (143).
According to the integrated trigger point
hypothesis, the sarcomeric contractions cause local
hypoxia, reducing the available energy supply. The
combined decreased energy supply and increased
metabolic demand possibly may explain the common
finding of abnormal mitochondria in the nerve terminal,
referred to as “ragged red fibers” (Henriksson et al.
1993; Henriksson 1999). The local energy crisis would
also impair the calcium pump, which would provide
another mechanism of the sustained contractures. The
calcium pump is responsible for returning intracellular
calcium into the sarcoplasmic reticulum against a
concentration gradient, which requires a functional
energy supply.
As reviewed, hypoxia also stimulates the
release of endogenous substances, resulting in
hyperalgesia, central sensitization, and stimulation of
the autonomic nervous system, which has been shown
to increase endplate potentials. For example, an
increase in psychological arousal resulted in an
immediate increase of endplate spike rates (144, 145).
Autogenic relaxation and the administration of the
sympathetic blocking agents phentolamine and
phenoxybenzamine inhibited the autonomic activation
(146-148). Induced autonomic nerve activity would
explain autonomic phenomena commonly seen with
MPS, and further contribute to the abnormal release of
acetylcholine, possibly by increasing the permeability
of calcium channels in the cell membrane of the nerve
terminal (149, 150). A recent study examined the
effects of MTrP massage therapy on the cardiac
autonomic tone in healthy subjects. The researchers
observed that following MTrP therapy, there was a
significant decrease in heart rate, and systolic and
diastolic blood pressure, indicating a significant
increase in parasympathetic activity (151).
The integrated trigger point hypothesis is
summarized in figure 9. The hypothesis is a “work in
progress” that is beginning to be subjected to rigorous
scientific review and verification.
Figure 9 – Integrated trigger point hypothesis
It is likely that new studies will demonstrate that there
are many other factors to consider. For example,
preliminary data from current studies by Shah and
colleagues provide already new insights in the basic
pathophysiology of MTrPs (119). The finding of
increased levels of several endogenous substances in
the neurochemical milieu of MTrPs, including
bradykinin, serotonin, prostaglandin, and CGRP,
combined with the finding of a lowered pH may alter
the current understanding of motor endplate
dysfunction in relation to MTrPs. Both CGRP and a
lowered pH can effectively reduce the function of
acetylcholinesterase, which could cause an overall
increase of available acetylcholine (115-117). At the
same time, a lowered pH can activate peripheral
nociceptors and trigger capsaicin- sensitive afferents,
which in turn can release several of the endogenous
11
substances from their peripheral endings, including
CGRP (152-154). A pH of 6.1 resulted in a threefold
increase of the basal CGRP release, which was entirely
dependent on the presence of extracellular calcium
(155). Bradykinin caused a 50% increase of the basal
CGRP release which was also dependent on the
presence of extra-cellular calcium (155). Endogenous
substances such as bradykinin, serotonin and
prostaglandin, clearly interact at multiple levels,
including at the vanilloid receptors (120). Although
the relevance of these interactions has not been studied
specifically in relationship to MTrPs, it is likely that
future studies will reveal new aspects of their
pathophysiology. Interestingly, Shah and colleagues
established an immediate drop in the concentrations of
several substances with dry needling of a MTrP (119).
If the integrated trigger point hypothesis is basically
correct, MTrPs are primarily a muscle disease with
secondary but important sensory, motor and autonomic
phenomena (156).
Clinical Applications
MPS and MTrPs should be considered in the
differential diagnosis of craniomandibular pain and
temporomandibular joint dysfunction, migraines,
tension headaches, radiculopathies, complex regional
pain syndrome, whiplash injuries, and most other pain
syndromes. To diagnose and manage MPS, clinicians
must become well-trained in the identification of
MTrPs. Through inactivation of MTrPs, clinicians can
facilitate return to function and elimination of pain in
both acute and chronic pain patients. Together with the
patient, ultimate functional goals need to be discussed.
For some patients, eating solid foods may be the final
goal. For others, it may be restoring sleep, regaining
sexual activity, or returning to work. Treating MTrPs
is merely an effective tool to assist patients in regaining
lost function (157). There are many different manual
techniques, including myofascial release techniques,
compression, trigger point compression combined with
active contractions of the involved muscle, muscle
energy or post-isometric relaxation, connective tissue
stretches, and general massage therapy. Needling
techniques include superficial and deep dry needling,
and trigger point injections (61, 158). For persistent
cases, botulinum toxin can be used as it blocks the
release of acetylcholine (159, 160). Throughout the
treatment process, patients must be educated regarding
the etiology, perpetuating factors, and self-
management. Patients must learn to modify their
behaviors and avoid overloading the muscles without
resorting to total inactivity (161).
A sudden onset or a clear remembrance of the
onset of pain may indicate an acute activation of MTrPs
due to mechanical stress, but it may also indicate a
sudden change in the patient’s environment or habits.
The mechanical stress may be the result of sudden or
abrupt movements, motor vehicle accidents, falls,
fractures, joint sprains or dislocations, a direct blow to
a muscle, joint, or mandible, excessive exercise or
activity, or performing new or unusual activities. A
slow insidious onset is usually the result of chronic
overloading of tissue, such as habitual chewing gum or
tobacco, postural imbalances, poor body mechanics,
repetitive movements, and tension as a consequence of
psychological or emotional stress (57).
Clinicians should consider both the sensory
and mechanical aspects of MTrPs. The physical
examination must include a thorough evaluation of
MTrPs relevant to the patient’s current pain
presentation. The patient’s current area(s) of pain can
be visualized through patient pain drawings. While
patients communicate their pain patterns, the clinician
can begin identifying those muscles and active MTrPs
most likely involved in the pain problem. For example,
in a patient with complaints of temporal headaches, the
pain complaint may direct the clinician to the
sternocleidomastoid, trapezius, temporalis and inferior
oblique capitis muscles. The patient’s head posture in
slight side bending and rotation may implicate the
scalene muscles, although the referred pain pattern
from MTrPs in the scalene muscles does not include the
head region. If the patient in addition presents with a
paradoxical breathing pattern, it will be necessary to
examine and treat the accessory breathing muscles as
well, including the pectoralis minor, scalenes,
sternocleidomastoid and upper trapezius musculature
that may be overloaded due to increased demands.
Teaching the patient a normal diaphragmatic breathing
pattern and fostering awareness of relaxation
techniques for the upper chest and neck region will aid
in the long term management of the headaches.
Dentists should limit their direct treatment to muscles
cranially from the clavicles to stay within the scope of
dental practice.
Habitual postural patterns need to be assessed
(162-164). Does the patient have a forward head
posture? Are there certain work postures or habits that
maintain the head in an antero-position? Forward head
posture is associated with multiple static and dynamic
changes in total body alignment. Patients with forward
head posture present with posterior cervical rotation of
the upper cervical and subcranial motion segments, a
posteriorly displaced mandible, altered occlusion, as
12
well as shoulder girdle protraction, internally rotated
humeri, increased thoracic kyphosis, a loss of lumbar
lordosis, and an increase in posterior pelvic rotation.
Dentists need to be familiar with the consequences of
forward head posture. For example, if a patient with
forward head posture receives a splint, the dentist may
have to adjust the splint after the patient’s head posture
has been corrected by a physical therapist. Close
working relationships between dentists and physical
therapists are very important and benefit patients.
Simons, Travell and Simons advocated the
spray and stretch technique, which combines use of a
vapocoolant spray with passive stretching of the muscle
(33). Application of vapocoolant spray stimulates
thermal and tactile A-beta skin receptors, thereby
inhibiting C-fiber and A-delta fiber afferent nociceptive
pathways and muscle spasms, MTrPs, and pain when
stretching. Prior to applying the spray and stretch
method, the patient is positioned comfortably. The
muscle involved is sprayed with a few sweeps of a
vapocoolant spray, after which the muscle is stretched
passively. With the muscle in the stretched position, the
spray is applied again over the skin overlying the entire
muscle, starting at the trigger zone and proceeding in
the direction of and including the referred pain zone.
Following the stretch and spray, the area is heated with
a moist heat pack for 5-10 minutes. The patient is
encouraged to move the body part several times
through the full range of motion. The spray and stretch
technique can be used in physical therapy as a separate
modality or following myofascial trigger point
injections. Muscle stretching can be combined with
muscle energy techniques or post isometric relaxation,
during which the muscle is stretched after a brief sub-
maximal isometric contraction. All techniques are used
diagnostically and therapeutically (61, 158). Some
patients can learn to use spray and stretch techniques at
home. Self treatment programs can be very effective
(165).
Inactivation of MTrPs by injection or dry
needling appears to be the result of the mechanical
action of the needle, since it can be successfully
accomplished without the use of local anesthetics or
other materials. In 1979, Lewit confirmed that the
effects of needling were primarily due to mechanical
stimulation of a MTrP with the needle. Dry needling of
a MTrP using an acupuncture needle caused immediate
analgesia in nearly 87% of needle sites. In over 31% of
cases, the analgesia was permanent. Twenty percent
had several months of pain relief, 22% several weeks,
and 11% several days. Fourteen percent had no relief
at all (166).
When using injection needles, the use of a
local anesthetic is more comfortable for many patients
and results in a longer lasting reduction in MTrP pain
(167). The use of solid acupuncture needles versus
injection needles has not been examined at this time.
After identifying and manually stabilizing the tender
area in the taut band with the fingers, the needle is
quickly passed through the skin and then into the
trigger zone. A LTR or a report of referred pain
indicates that the trigger zone has been entered. A small
amount, usually 0.1 or 0.2 ml, of local anesthetic may
be injected into the trigger zone. There is no benefit to
adding steroids. The needle is withdrawn to just below
the skin, the angle of the needle changed, and the
needle is again passed through the muscle to another
trigger zone. A conical volume of muscle can thus be
examined for active trigger points without withdrawing
the needle through the skin. The trigger zone is
explored in this manner until no further LTRs are
obtained. Dry needling a MTrP is most effective, when
LTRs are elicited (71, 138). A LTR has been shown to
inhibit abnormal endplate noise. Current (unpublished)
research strongly suggests that a LTR is essential in
altering the neurochemical milieu of a MTrP (Shah,
2003, personal communication). Patients commonly
describe an immediate reduction or elimination of the
pain complaint after eliciting LTRs. Once the pain is
reduced, patients can start active stretching and
strengthening programs. Eliciting a LTR with dry
needling is usually a rather painful procedure. Post-
needling soreness may last for one to two days, but can
easily be distinguished from the original pain
complaint. At this point, the taut band is usually gone,
and the spontaneous pain of the trigger point has
subsided. Patients who have previously undergone
treatment can tell when MTrPs remain, and when they
have been sufficiently inactivated. A knowledgeable
patient will urge the clinician to continue in an area
until a key MTrP is inactivated, at which time there will
be a noticeable decrease in pain. The process is
repeated until the symptomatic MTrPs are treated
throughout the functional muscle unit (61).
There is no limit to the number of MTrP that
can be needled. Common sense and patient comfort
dictate restraint. Nevertheless, when treating a regional
MPS, a sufficient number of muscles in the region must
be treated to resolve the problem and allow effective
post-needling stretching. All the muscles in a functional
muscle unit must be released and returned to full
length, if possible, either by needling or by MTrP
compression and stretching. Inadequate treatment that
leaves critical MTrPs within a functional muscle unit
13
usually results in the recurrence of trigger points
throughout the muscles of the functional unit. Five to
ten different MTrP sites can readily be treated per
session, and some physicians and physical therapists
skilled in MPS management will treat considerably
more in one session. Repeat injections or dry needling
into the same area are best done after an interval of one
week to allow the muscle to recover. Muscles of the
affected functional unit must always be stretched, to
their full length if possible, after MTrP needling. Moist
heat is applied to the muscle to improve the local
circulation and to reduce post-injection soreness.
Otherwise, MTrPs will recur because of residual
muscle dysfunction. Local anesthetic patches can be
applied to reduce the superficial or cutaneous soreness
from needling.
Trigger point injections or dry needling are a
highly effective way to reduce the local pain and
contraction of the taut band. This does not, however,
constitute the whole treatment of MPS and MTrPs. The
causes that led to the condition must be corrected, when
possible. Mechanical, medical, and psychological
perpetuating factors must also be eliminated or
alleviated in order to reduce the chance of recurrence.
Inadequate attention to these aspects of treatment leads
to failure to relieve pain and restore function (61, 168).
Summary
Myofascial pain syndrome as defined by
Simons, Travell and Simons offers clinicians an
excellent entry point into patients’ acute and chronic
pain problems. Myofascial trigger points are a
common source or contributing factor to many
musculoskeletal disorders. In the craniomandibular
region, myofascial trigger points are frequently
responsible for local and referred pain patterns, causing
headaches, TMJ pain and dysfunction, tooth aches, and
facial pains. Clinicians should routinely incorporate
myofascial trigger points in their examinations and
differential diagnoses.
The results of many scientific studies are
beginning to validate several aspects of the integrated
trigger point hypothesis and refine others. A better
understanding and working knowledge of MTrPs and
MPS offers an effective approach to relieve pain,
restore function, and contribute significantly to
patients’ quality of life.
References
1. LeResche L. Epidemiology of temporomandibular
disorders: implications for the investigation of etiologic factors. Crit
Rev Oral Biol Med 1997;8:291-305.
2. Drangsholt M, LeResche L. Temporomandibular disorder
pain. In: Crombie IK, Croft PR, Linton SJ, LeResche L, Von Korff
M, editors. Epidemiology of pain. Seattle: IASP Press; 1999. p. 203-
233.
3. Elliott AM, Smith BH, Penny KI, Smith WC, Chambers
WA. The epidemiology of chronic pain in the community. Lancet
1999;354(9186):1248-52.
4. Buskila D, Abramov G, Biton A, Neumann L. The
prevalence of pain complaints in a general population in Israel and its
implications for utilization of health services. J Rheumatol
2000;27(6):1521-5.
5. Zondervan K, Barlow DH. Epidemiology of chronic
pelvic pain. Baillieres Best Pract Res Clin Obstet Gynaecol
2000;14(3):403-14.
6. Israel HA, Ward JD, Horrell B, Scrivani SJ. Oral and
maxillofacial surgery in patients with chronic orofacial pain. J Oral
Maxillofac Surg 2003;61(6):662-7.
7. Curtis AW. Myofascial pain-dysfunction syndrome: the
role of nonmasticatory muscles in 91 patients. Otolaryngol Head
Neck Surg 1980;88(4):361-7.
8. Kryshtalskyj B. The role of diagnostic arthroscopy in the
management of temporomandibular joint dysfunction. J Otolaryngol
1991;20(5):325-8.
9. Widmark G. On surgical intervention in the
temporomandibular joint. Swed Dent J Suppl 1997;123:1-87.
10. Velly AM, Gornitsky M, Philippe P. Contributing factors
to chronic myofascial pain: a case-control study. Pain
2003;104(3):491-9.
11. Laskin DM. The clinical diagnosis of temporomandibular
disorders in the orthodontic patient. Semin Orthod 1995;1(4):197-
206.
12. Fricton JR. Etiology and management of masticatory
myofascial pain. J Musculoskeletal Pain 1999;7(1/2):143-160.
13. Clarke NG. Occlusion and myofascial pain dysfunction: is
there a relationship? J Am Dent Assoc 1982;104(4):443-6.
14. Ito H, Okimoto K, Mizumori T, Terada Y, Maruyama T.
A clinical study of the relationship between occlusal curvature and
craniomandibular disorders. Int J Prosthodont 1997;10(1):78-82.
15. Denbo JA. Malocclusion. Dent Clin North Am
1990;34(1):103-9.
16. Kerstein RB. Treatment of myofascial pain dysfunction
syndrome with occlusal therapy to reduce lengthy disclusion time--a
recall evaluation. Cranio 1995;13(2):105-15.
17. Flor H, Birbaumer N, Schulte W, Roos R. Stress-related
electromyographic responses in patients with chronic
temporomandibular pain. Pain 1991;46(2):145-52.
18. Sieber M, Grubenmann E, Ruggia GM, Palla S. Relation
between stress and symptoms of craniomandibular disorders in
adolescents. Schweiz Monatschr Zahnmed 2003;113(6):648-654.
19. Moss RA, Garrett JC. Temporomandibular joint
disfunction syndrome and myofascial pain dysfunction syndrome: a
critical review. J Oral Rehabil 1984;11(1):3-28.
20. Ro JY. Contribution of peripheral NMDA receptors in
craniofacial muscle nociception and edema formation. Brain Res
2003;979:78-84.
21. Sessle BJ, Hu JW, Cairns BE. Brainstem mechanisms
underlying temporomandibular joint and masticatory muscle pain. J
Musculoskeletal Pain 1999;7(1/2):161-169.
14
22. Sessle BJ, Hu JW, Amano N, Zhong G. Convergence of
cutaneous, tooth pulp, visceral, neck and muscle afferents onto
nociceptive and non-nociceptive neurones in trigeminal subnucleus
caudalis (medullary dorsal horn) and its implication for referred pain.
Pain 1986;27:219-235.
23. Graven-Nielsen T, Mense S. The peripheral apparatus of
muscle pain: evidence from animal and human studies. Clin J Pain
2001;17(1):2-10.
24. Kraus SL. Cervical spine influences on the management
of TMD. In: Kraus SL, editor. Temporomandibular disorders. New
York: Churchill Livingstone; 1994. p. 325-412.
25. Fink M, Wähling K, Stiesch-Scholz M, Tschernitschek H.
The functional relationship between the craniomandibular system,
cervical spine, and sacroiliac joint: a preliminary investigation. J
Craniomandib Pract 2003;21(3):202-208.
26. Rocabado M, Tapia V. Radiographic study of the
craniocervical relation in patients under orthodontic treatment and the
incidence of skeletal symptoms. J Craniomand Practice 1987;5(1):36.
27. Rocabado M. Biomechanical relationship of the cranial,
cervical and hyoid regions. J Craniomandibular Pract 1983;3:62-66.
28. Dworkin SF, LeResche L. Research diagnostic criteria for
temporomandibular disorders: review, criteria, examinations and
specifications, critique. J Craniomandib Disord Facial Oral Pain
1992;6:301-355.
29. Rammelsberg P, LeResche L, Dworkin S, Mancl L.
Longitudinal outcome of temporomandibular disorders: a 5-year
epidemiologic study of muscle disorders defined by research
diagnostic criteria for temporomandibular disorders. J Orofac Pain
2003;17(1):9-20.
30. Dworkin SF, Turner JA, Mancl L, Wilson L, Massoth D,
Huggins KH, et al. A randomized clinical trial of a tailored
comprehensive care treatment program for temporomandibular
disorders. J Orofac Pain 2002;16(4):259-76.
31. Dworkin SF, Sherman J, Mancl L, Ohrbach R, LeResche
L, Truelove E. Reliability, validity, and clinical utility of the research
diagnostic criteria for Temporomandibular Disorders Axis II Scales:
depression, non-specific physical symptoms, and graded chronic pain.
J Orofac Pain 2002;16(3):207-20.
32. Dworkin SF, Huggins KH, Wilson L, Mancl L, Turner J,
Massoth D, et al. A randomized clinical trial using research
diagnostic criteria for temporomandibular disorders-axis II to target
clinic cases for a tailored self-care TMD treatment program. J Orofac
Pain 2002;16(1):48-63.
33. Simons DG, Travell JG, Simons LS. Travell and Simons'
myofascial pain and dysfunction; the trigger point manual. 2 ed.
Baltimore: Williams & Wilkins; 1999.
34. Simons DG. Review of enigmatic MTrPs as a common
cause of enigmatic musculoskeletal pain and dysfunction. J
Electromyogr Kinesiol 2004;in press.
35. Padamsee M, Mehta N, White GE. Trigger point injection:
a neglected modality in the treatment of TMJ dysfunction. J Pedod
1987;12(1):72-92.
36. Domnitz JM, Swintak EF, Schriver WR, Shereff RH.
Myofascial pain syndrome masquerading as temporomandibular joint
pain. Oral Surg Oral Med Oral Pathol 1977;43(1):11-7.
37. Svensson P, Graven-Nielsen T, Arendt-Nielsen L.
Mechanical hyperesthesia of human facial skin induced by tonic
painful stimulation of jaw muscles. Pain 1998;74(1):93-100.
38. Mense S, Simons DG. Muscle pain; understanding its
nature, diagnosis, and treatment. Philadephia: Lippincott Williams &
Wilkins; 2001.
39. Ayer WA, Machen JB, Getter L. Survey of myofascial
pain-dysfunction syndrome and pathologic bruxing habits among
dentists. J Am Dent Assoc 1977;94(4):730-2.
40. Kawazoe Y, Kotani H, Hamada T, Yamada S. Effect of
occlusal splints on the electromyographic activities of masseter
muscles during maximum clenching in patients with myofascial pain-
dysfunction syndrome. J Prosthet Dent 1980;43(5):578-80.
41. Arima T, Svensson P, Arendt-Nielsen L. Experimental
grinding in healthy subjects: a model for postexercise jaw muscle
soreness? J Orofac Pain 1999;13(2):104-14.
42. Abdel-Fattah RA. Preventing temporomandibular joint
(TMJ) and odontostomatognatic (OSGS) injuries in dental practice.
Boca Raton: CRC Press; 1993.
43. Svensson P, Burgaard A, Schlosser S. Fatigue and pain in
human jaw muscles during a sustained, low-intensity clenching task.
Arch Oral Biol 2001;46(8):773-7.
44. Mense S. The pathogenesis of muscle pain. Current Pain
and Headache Reports 2003;7(6):419-425.
45. Simons DG. Muscle pain syndromes - part 1. Am J Phys
Med 1975;54:289-311.
46. Baldry PE. Myofascial pain and fibromyalgia syndromes.
Edinburgh: Churchill Livingstone; 2001.
47. Stockman R. The causes, pathology, and treatment of
chronic rheumatism. Edinburgh Med J 1904;15:107-116.
48. Travell JG, Rinzler SH. The myofascial genesis of pain.
Postgrad Med 1952;11:452-434.
49. Steindler A. The interpretation of sciatic radiation and the
syndrome of low-back pain. J Bone Joint Surg Am 1940;22:28-34.
50. Travell J. Identification of myofascial trigger point
syndromes: a case of atypical facial neuralgia. Arch Phys Med
Rehabil 1981;62(3):100-106.
51. Travell J. Temporomandibular joint pain referred from
muscles of the head and neck. J Prosthet Dent 1960;10:745-763.
52. Travell J. Mechanical headache. Headache 1967;7:23-29.
53. Travell JG, Simons DG. Myofascial pain and dysfunction;
the trigger point manual. Baltimore: Williams & Wilkins; 1983.
54. Travell JG, Simons DG. Myofascial pain and dysfunction:
the trigger point manual. Baltimore: Williams & Wilkins; 1992.
55. Dejung B, Gröbli C, Colla F, Weissmann R.
Triggerpunkttherapie. Bern: Hans Huber; 2003.
56. Rachlin ES, Rachlin IS. Myofascial pain and
fibromyalgia, trigger point management. St. Louis: Mosby; 2002.
57. Dommerholt J, Issa T. Differential diagnosis: myofascial
pain. In: Chaitow L, editor. Fibromyalgia; a practitioner's guide to
treatment. Edinburgh: Churchill Livingstone; 2003. p. 149-177.
58. Bennett RM. The clinical neurobiology of fibromyalgia
and myofascial pain: therapeutic implication. Binghamton: Haworth
Press; 2002.
59. Harden RN, Bruehl SP, Gass S, Niemiec C, Barbick B.
Signs and symptoms of the myofascial pain syndrome: a national
survey of pain management providers. Clin J Pain 2000;16(1):64-72.
60. Hendler NH, Kozikowski JG. Overlooked physical
diagnoses in chronic pain patients involved in litigation.
Psychosomatics 1993;34(6):494-501.
61. Gerwin RD, Dommerholt J. Treatment of myofascial pain
syndromes. In: Weiner R, editor. Pain management; a practical guide
for clinicians. Boca Raton: CRC Press; 2002. p. 235-249.
62. Gerwin RD, Shannon S, Hong CZ, Hubbard D, Gevirtz R.
Interrater reliability in myofascial trigger point examination. Pain
1997;69(1-2):65-73.
63. Russell IJ. Reliability of clinical assessment measures for
the classification of myofascial pain syndrome. J Musculoskeletal
Pain 1999;7(1/2):309-324.
64. Janda V. Muscle spasm: a proposed procedure for
differential diagnosis. J Manual Med 1991;6:136-139.
65. Mense S. Pathophysiologic basis of muscle pain
syndromes. In: Fischer AA, editor. Myofascial pain; update in
diagnosis and treatment. Philadelphia: W.B. Saunders Company;
1997. p. 23-53.
15
66. Sciotti VM, Mittak VL, DiMarco L, Ford LM, Plezbert J,
Santipadri E, et al. Clinical precision of myofascial trigger point
location in the trapezius muscle. Pain 2001;93(3):259-66.
67. Scudds RA, Landry M, Birmingham T, Buchan J, Griffin
K. The frequency of referred signs from muscle pressure in normal
healthy subjects (abstract). J Musculoskeletal Pain 1995;3 (Suppl
1):99.
68. Hong C-Z, Torigoe Y. Electrophysiological characteristics
of localized twitch responses in responsive taut bands of rabbit
skeletal muscle. J Musculoskeletal Pain 1994;2::17-43.
69. Hong C-Z, Yu J. Spontaneous electrical activity of rabbit
trigger spot after transection of spinal cord and peripheral nerve. J
Musculoskeletal Pain 1998;6(4):45-58.
70. Wang F, Audette J. Electrophysiological characteristics of
the local twitch response with active myofascial pain of neck
compared with a control group with latent trigger points. Am J Phys
Med Rehabil 2000;79(2):203.
71. Hong CZ. Lidocaine injection versus dry needling to
myofascial trigger point. The importance of the local twitch response.
Am J Phys Med Rehabil 1994;73(4):256-63.
72. Gerwin RD, Duranleau D. Ultrasound identification of the
myofascial trigger point. Muscle Nerve 1997;20(6):767-768.
73. Lewis J, Tehan P. A blinded pilot study investigating the
use of diagnostic ultrasound for detecting active myofascial trigger
points. Pain 1999;79(1):39-44.
74. Kellgren JH. Observations on referred pain arising from
muscle. Clin Sci 1938;3:175-190.
75. Svensson P. Orofacial musculoskeletal pain. In:
Giamberardino MA, editor. Pain 2002 - An updated review: refresher
course syllabus. Seattle: IASP Press; 2002. p. 447-458.
76. Ashina S, Jensen R, Bendtsen L. Pain sensitivity in
pericranial and extracranial regions. Cephalalgia 2003;23(6):456-62.
77. Gupta MK, el-Sheikh MH, Sherif AM, el-Sharani F.
Temporomandibular joint (TMJ) myofascial pain dysfunction
syndrome (MPDS) non-surgical management. J Pierre Fauchard Acad
1993;7(3):101-6.
78. Mascia P, Brown BR, Friedman S. Toothache of
nonodontogenic origin: a case report. J Endod 2003;29(9):608-610.
79. Kleier DJ. Referred pain from a myofascial trigger point
mimicking pain of endodontic origin. J Endod 1985;11(9):408-11.
80. Dunteman E, Turner MS, Swarm R. Pseudo-spinal
headache. Reg Anesth 1996;21(4):358-60.
81. Carlson CR, Okeson JP, Falace DA, Nitz AJ, Lindroth JE.
Reduction of pain and EMG activity in the masseter region by
trapezius trigger point injection. Pain 1993;55(3):397-400.
82. Fricton JR, Kroening R, Haley D, Siegert R. Myofascial
pain syndrome of the head and neck: a review of clinical
characteristics of 164 patients. Oral Surg Oral Med Oral Pathol
1985;60(6):615-623.
83. Fricton JR. Management of masticatory myofascial pain.
Semin Orthod 1995;1(4):229-43.
84. Arendt-Nielsen L, Graven-Nielsen T, Svensson P, Jensen
TS. Temporal summation in muscles and referred pain areas: an
experimental human study. Muscle Nerve 1997;20(10):1311-3.
85. Hong C-Z, Chen Y-N, Twehous D, Hong DH. Pressure
threshold for referred pain by compression on the trigger point and
adjacent areas. J Musculoskeletal Pain 1996;4(3):61-79.
86. Hong CZ, Kuan TS, Chen JT, Chen SM. Referred pain
elicited by palpation and by needling of myofascial trigger points: a
comparison. Arch Phys Med Rehabil 1997;78(9):957-60.
87. Jaeger B. Myofascial referred pain patterns: the role of
trigger points. Cda J 1985;13(3):27-32.
88. Svensson P, Arendt-Nielson L. Clinical and experimental
aspects of temporomandibular disorders. Curr Rev Pain
2000;4(2):158-65.
89. Vecchiet L, Giamberardino MA. Referred pain: clinical
significance, pathophysiology and treatment. In: Fischer AA, editor.
Myofascial pain: update in diagnosis and treatment. Philadelphia:
W.B. Saunders Company; 1997. p. 119-136.
90. Mense S, Hoheisel U. New developments in the
understanding of the pathophysiology of muscle pain. J
Musculoskeletal Pain 1999;7(1/2):13-24.
91. Simons DG. Referred phenomena of myofascial trigger
points. In: Vecchiet L, Albe-Fessard D, Lindblom U, Giamberardino
MA, editors. New trends in referred pain and hyperalgesia.
Amsterdam: Elsevier Science Publishers; 1993. p. 341-357.
92. Arendt-Nielsen L, Svensson P. Referred muscle pain:
basic and clinical findings. Clin J Pain 2001;17(1):11-9.
93. Wright EF. Referred craniofacial pain patterns in patients
with temporomandibular disorder. JADA 2000;131:1307-1315.
94. Fukui S, Ohseto K, Shiotani M, Ohno K, Karasawa H,
Naganuma Y, et al. Referred pain distribution of the cervical
zygopophyseal joints and cervical dorsal rami. Pain 1996;68:79-83.
95. Hong CZ, Simons DG. Pathophysiologic and
electrophysiologic mechanisms of myofascial trigger points. Arch
Phys Med Rehabil 1998;79(7):863-872.
96. Torebjörk HE, Ochoa JL, Schady W. Referred pain from
intraneural stimulation of muscle fascicles in the median nerve. Pain
1984;18:145-156.
97. Dwyer A, Aprill C, Bogduk N. Cervical zygapophyseal
joint pain patterns. I: A study in normal volunteers. Spine
1990;15(6):453-457.
98. Neumann M. Trunk Pain. In: Raj PP, editor. Practical
management of pain. St. Louis: Mosby Year Book; 1992. p. 258-271.
99. Bellew JW. Lumbar facets: an anatomic framework for
low back pain. The Journal of Manual & Manipulative Therapy
1996;4(4):149-156.
100. Mense S. Nociception from skeletal muscle in relation to
clinical muscle pain. Pain 1993;54:241-289.
101. Mense S. Muscular nociceptors. J Physiol (Paris)
1977;73(3):233-40.
102. Diehl B, Hoheisel U, Mense S. The influence of
mechanical stimuli and of acetylsalicylic acid on the discharges of
slowly conducting afferent units from normal and inflamed muscle in
the rat. Exp Brain Res 1993;92(3):431-40.
103. Mense S, Meyer H. Different types of slowly conducting
afferent units in cat skeletal muscle and tendon. J Physiol
1985(363):403-417.
104. Mense S, Stahnke M. Responses in muscle afferent fibres
of slow conduction velocity to contractions and ischaemia in the cat. J
Physiol 1983;342:383-97.
105. Wang K, Yu L. Emerging concepts of muscle contraction
and clinical implications for myofascial pain syndrome (abstract). In:
Gerwin RD, editor. Focus on Pain; 2000; Mesa, AZ: Janet G. Travell,
MD Seminar Seriessm; 2000.
106. Brückle W, Sückfull M, Fleckenstein W, Weiss C, Müller
W. Gewebe-pO2-Messung in der verspannten Rückenmuskulatur (m.
erector spinae). Z. Rheumatol. 1990;49:208-216.
107. Henriksson KG, Bengtsson A, Larsson J, Lindstrom F,
Thornell LE. Muscle biopsy findings of possible diagnostic
importance in primary fibromyalgia (fibrositis, myofascial
syndrome). Lancet 1982;2(8312):1395.
108. Bengtsson A, Henriksson KG, Larsson J. Muscle biopsy
in primary fibromyalgia. Light-microscopical and histochemical
findings. Scand J Rheumatol 1986;15(1):1-6.
109. Windisch A, Reitinger A, Traxler H, Radner H, Neumayer
C, Feigl W, et al. Morphology and histochemistry of myogelosis. Clin
Anat 1999;12(4):266-271.
110. Reitinger A, Radner H, Tilscher H, Hanna M, Windisch
A, Feigl W. Morphologische Untersuchung an Triggerpunkten.
Manuelle Medizin 1996;34:256-262.
16
111. Henriksson KG, Bengtsson A, Lindman R, Thornell LE.
Morphological changes in muscle in fibromyalgia and chronic
shoulder myalgia. In: Værøy H, Merskey H, editors. Progress in
fibromyalgia and myofascial pain. Amsterdam: Elsevier; 1993. p. 61-
73.
112. Heffner RR, Barron SA. The early effects of ischemia
upon skeletal muscle mitochondria. J Neurol Sci 1978;38(3):295-315.
113. Simons DG. Triggerpunkte und Myogelose. Manuelle
Medizin 1997;35:290-294.
114. Poole S, de Queiroz Cunha F, Ferreira SH. Hyperalgesia
from subcutaneous cytokines. In: Watkins LR, Maier SF, editors.
Cytokines and pain. Basel: Birkhaueser; 1999. p. 59-87.
115. Kimura I, Okazaki M, Nojima H. Mutual dependence of
calcitonin -gene related peptide and acetylcholine release in
neuromuscular preparations. Eur J Pharmacol 1997;330:123–128.
116. Fernandez HL, Rossa GS, Nadelhaft I. Neurogenic
calcitonin gene-related peptide: a neurotrophic factor in the
maintenance of acetylcholinesterase molecular forms in adult skeletal
muscles. Brain Research 1999;844:83–97.
117. Fernandez HL, Chen M, Nadelhaft I, Durr JA. Calcitonin
gene-related peptides: their binding sites and receptor accessory
proteins in adult mammalian skeletal muscles. Neuroscience
2003;119:335–345.
118. Jensen K, Tuxen C, Pedersen-Bjergaard U, Jansen I,
Edvinsson L, Olesen J. Pain and tenderness in human temporal
muscle induced by bradykinin and 5-hydroxytryptamine. Peptides
1990;11(6):1127-32.
119. Shah J. The use of a microdialysis/acupuncture needle to
assess the neurochemical milieu in active and latent myofascial
trigger points in the upper trapezius muscle. In: Focus on Pain 2003;
2003; Orlando: Janet G. Travell, MD Seminar Series; 2003.
120. Vyklicky L, Knotkova Urbancova H, Vitaskova Z,
Vlachova V, Kress M, Reeh PW. Inflammatory mediators at acid pH
activate capsaicin receptors in cultured sensory neurons from
newborn rats. J Neurophysiol 1998;79:670–676.
121. Sessle BJ. Acute and chronic craniofacial pain: brainstem
mechanisms of nociceptive transmission and neuroplasticity, and
their clinical correlates. Crit Rev Oral Biol Med 2000;11(1):57-91.
122. Ellrich J, Andersen OK, Messlinger K, Arendt-Nielsen L.
Convergence of meningeal and facial afferents onto trigeminal
brainstem neurons: an electrophysiological study in rat and man. Pain
1999;82(3):229-37.
123. Marchettini P, Simone DA, Caputi G, Ochoa JL. Pain
from excitation of identified muscle nociceptors in humans. Brain
Res 1996;740(1-2):109-116.
124. Hoheisel U, Mense S, Simons D, Yu X-M. Appearance of
new receptive fields in rat dorsal horn neurons following noxious
stimulation of skeletal muscle: a model for referral of muscle pain?
Neurosci Lett 1993;153:9-12.
125. Arendt-Nielsen L, Graven-Nielsen T. Deep tissue
hyperalgesia. J Musculoskeletal Pain 2002;10(1/2):97-119.
126. Hu JW, Sessle BJ, Raboisson P, Dallel R, Woda A.
Stimulation of craniofacial muscle afferents induces prolonged
facilitatory effects in trigeminal nociceptive brainstem neurons. Pain
1992;48:53-60.
127. Bendtsen L, Jensen R, Olesen J. Qualitatively altered
nociception in chronic myofascial pain. Pain 1996;65:259-264.
128. Airaksinen O, Pontinen PJ. Effects of the electrical
stimulation of myofascial trigger points with tension headache.
Acupunct Electrother Res 1992;17(4):285-90.
129. Koelbaek Johansen M, Graven-Nielsen T, Schou Olesen
A, Arendt-Nielsen L. Generalised muscular hyperalgesia in chronic
whiplash syndrome. Pain 1999;83(2):229-34.
130. Hubbard DR, Berkoff GM. Myofascial trigger points
show spontaneous needle EMG activity. Spine 1993;18:1803-1807.
131. Simons DG, Hong C-Z, Simons L. Prevalence of
spontaneous electrical activity at trigger spots and control sites in
rabbit muscle. J Musculoskeletal Pain 1995;3:35-48.
132. Simons DG. Do endplate noise and spikes arise from
normal motor endplates? Am J Phys Med Rehabil 2001;80:134-140.
133. Couppé C, Midttun A, Hilden J, Jørgensen U, Oxholm P,
Fuglsang-Frederiksen A. Spontaneous needle electromyographic
activity in myofascial trigger points in the infraspinatus muscle: A
blinded assessment. J Musculoskeletal Pain 2001;9(3):7-17.
134. Simons DG, Hong C-Z, Simons LS. Endplate potentials
are common to midfiber myofascial trigger points. Am J Phys Med
Rehabil 2002;81(3):212-222.
135. Wiederholt WC. "End-plate noise" in electromyography.
Neurology 1970;20(3):214-24.
136. Ito Y, Miledi R, Vincent A. Transmitter release induced
by a 'factor' in rabbit serum. Proc R Soc Lond B Biol Sci
1974;187:235-241.
137. Heuser J, Miledi R. Effects of lanthanum ions on function
and structure of frog neuromuscular junctions. Proc R Soc Lond B
Biol Sci 1971;179(56):247-60.
138. Shah J, Phillips T, Danoff JV, Gerber LH. A novel
microanalytical technique for assaying soft tissue demonstrates
significant quantitative biomechanical differences in 3 clinically
distinct groups: normal, latient and active. Arch Phys Med Rehabil
2003;84:A4.
139. Liley AW. An investigation of spontaneous activity at the
neuromuscular junction. J Physiol 1956;132:650-666.
140. Maselli RA. End-plate electromyography: use of spectral
analysis of end-plate noise. Muscle Nerve 1997;20(1):52-8.
141. Brown WF, Varkey GP. The origin of spontaneous
electrical activity at the end-plate zone. Ann Neurol 1981;10(6):557-
60.
142. Simons DG, Travell J. Myofascial trigger points, a
possible explanation. Pain 1981;10(1):106-9.
143. Shenoi R, Nagler W. Trigger points related to calcium
channel blockers (letter). Muscle Nerve 1996;19(2):256.
144. Lewis C, Gevirtz R, Hubbard D, Berkoff G. Needle
trigger point and surface frontal EMG measurements of
psychophysiological responses in tension-type headache patients.
Biofeedback & Self-Regulation 1994;3:274-275.
145. McNulty WH, Gevirtz RN, Hubbard DR, Berkoff GM.
Needle electromyographic evaluation of trigger point response to a
psychological stressor. Psychophysiology 1994;31(3):313-316.
146. Banks SL, Jacobs DW, Gevirtz R, Hubbard DR. Effects of
autogenic relaxation training on electromyographic activity in active
myofascial trigger points. J Musculoskeletal Pain 1998;6(4):23-32.
147. Chen JT, Chen SM, Kuan TS, Chung KC, Hong CZ.
Phentolamine effect on the spontaneous electrical activity of active
loci in a myofascial trigger spot of rabbit skeletal muscle. Arch Phys
Med Rehabil 1998;79(7):790-794.
148. Hubbard DR. Chronic and recurrent muscle pain:
pathophysiology and treatment, and review of pharmacologic studies.
J Musculoskeletal Pain 1996;4:123-143.
149. Chen JT, Chen SM, Kuan TS, Hong C-Z. Inhibitory effect
of calcium channel blocker on the spontaneous electrical activity of
myofascial trigger point. J Musculoskeletal Pain 1998;6(Suppl. 2):24.
150. Hou CR, Chung KC, Chen JT, Hong CZ. Effects of a
calcium channel blocker on electrical activity in myofascial trigger
spots of rabbits. Am J Phys Med Rehabil 2002;81(5):342-9.
151. Delaney J, Leong KS, Watkins A, Brodie D. The short-
term effects of myofascial trigger point massage therapy on cardiac
autonomic tone in healthy subjects. J Adv Nurs 2002;37(4):364-371.
152. Geppetti P, Del Bianco E, Patacchini R, Santicioli P,
Maggi CA, Tramontana M. Low pH-induced release of calcitonin
gene-related peptide from capsaicin-sensitive sensory nerves:
17
mechanism of action and biological response. Neuroscience
1991;41(1):295-301.
153. Santicioli P, Del Bianco E, Geppetti P, Maggi CA.
Release of calcitonin gene-related peptide-like (CGRP-LI)
immunoreactivity from rat isolated soleus muscle by low pH,
capsaicin and potassium. Neuroscience Letters 1992;143:19-22.
154. Steen KH, Steen AE, Reeh PW. A dominant role of acid
pH in inflammatory excitation and sensitization of nociceptors in rat
skin, in vitro. J Neurosci 1995;15:3982–3989.
155. Averbeck B, Izydorczyk I, Kress M. Inflammatory
mediators release calcitonin gene-related peptide from dorsal root
ganglion neurons of the rat. Neuroscience 2000;98(1):135–140.
156. Borg-Stein J, Simons DG. Focused review: myofascial
pain. Arch Phys Med Rehabil 2002;83(3 Suppl 1):S40-7, S48-9.
157. Gerwin RD. Management of persons with chronic pain.
In: Ozer MN, editor. Management of persons with chronic neurologic
illness. Boston: Butterworth-Heinemann; 2000. p. 265-290.
158. Gröbli C, Dommerholt J. Myofasziale Triggerpunkte;
Pathologie und Behandlungsmöglichkeiten. Manuelle Medizin
1997;35:295-303.
159. de Paiva A, Meunier FA, Molgo J, Aoki KR, Dolly JO.
Functional repair of motor endplates after botulinum neurotoxin type
A poisoning: biphasic switch of synaptic activity between nerve
sprouts and their parent terminals. Proc Natl Acad Sci U S A
1999;96(6):3200-3205.
160. Freund B, Schwartz M, Symington M. Botulinum toxin:
new treatment for temporomandibular disorders. Br J Oral
Maxillofacial Surg 2000;38:466-471.
161. Simons DG, Simons LS. Chronic Myofascial Pain
Syndrome. In: Tollison CD, Satterthwaite JR, Tollison JW, editors.
Handbook of Pain Management. Baltimore: Williams & Wilkins;
1994. p. 556-577.
162. Passero PL, Wyman BS, Bell JW, Hirschey SA, Schlosser
WS. Temporomandibular joint dysfunction syndrome. A clinical
report. Phys Ther 1985;65(8):1203-7.
163. Mannheimer JS. Prevention and Restoration of Abnormal
Upper Quarter Posture. In: Gelb H, editor. New Concepts in
Craniomandibular and Chronic Pain Management. London: Mosby-
Wolfe; 1994. p. 93-161.
164. Paris SV. Cervical symptoms of forward head posture.
Top Geriatr Rehabil 1990;5(4):11-19.
165. Hanten WP, Olsen SL, Butts NL, Nowicki AL.
Effectiveness of a home program of ischemic pressure followed by
sustained stretch for treatment of myofascial trigger points. Phys Ther
2000;80(10):997-1003.
166. Lewit K. The needle effect in the relief of myofascial pain.
Pain 1979;6:83-90.
167. Hong C-Z. Considerations and recommendations
regarding myofascial trigger point injection. J Musculoskeletal Pain
1994;2:29-59.
168. Dommerholt J. Muscle pain syndromes. In: Cantu RI,
Grodin AJ, editors. Myofascial Manipulation. Gaithersburg: Aspen;
2001. p. 93-140.