17
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).

Myofascial Pain Syndrome in Craniomandibular Region

Embed Size (px)

Citation preview

Page 1: Myofascial Pain Syndrome in Craniomandibular Region

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).

Page 2: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 3: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 4: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 5: Myofascial Pain Syndrome in Craniomandibular Region

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).

Page 6: Myofascial Pain Syndrome in Craniomandibular Region

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).

Page 7: Myofascial Pain Syndrome in Craniomandibular Region

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).

Page 8: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 9: Myofascial Pain Syndrome in Craniomandibular Region

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).

Page 10: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 11: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 12: Myofascial Pain Syndrome in Craniomandibular Region

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

Page 13: Myofascial Pain Syndrome in Craniomandibular Region

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.

Page 14: Myofascial Pain Syndrome in Craniomandibular Region

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.

Page 15: Myofascial Pain Syndrome in Craniomandibular Region

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.

Page 16: Myofascial Pain Syndrome in Craniomandibular Region

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:

Page 17: Myofascial Pain Syndrome in Craniomandibular Region

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.