Review Article

Facial Pain, Cervical

Address correspondence to
Dr Steven B. Graff-Radford,
The Pain Center at
Cedars-Sinai, 444 South

Pain, and Headache San Vicente Boulevard,

Suite 1101, Los Angeles, CA
90048, Steven.Graff-Radford
@cshs.org.
Steven B. Graff-Radford, DDS
Relationship Disclosure:
Dr Graff-Radford serves
as a member of the speakers’
ABSTRACT bureau or as a consultant
for Allergan, Inc.; MAP
Purpose of Review: This review discusses the role of musculoskeletal structures Pharmaceuticals, Inc.; Nautilus
of the jaw and neck in perpetuating or triggering primary headache. Because treat- Pharma; NuPathe, Inc.;
ments aimed at these structures often reduce headache, a better understanding of Pfizer, Inc.; and Zogenix,
Inc. Dr Graff-Radford has
their role in headache is needed. served as an expert witness
Recent Findings: Central sensitization may result in changes in the afferent path- and has performed medical
ways, making communication from cervical and temporomandibular nociceptive record review.
Unlabeled Use of
neurons to the trigeminal nucleus possible. This provides the pathophysiologic basis Products/Investigational
for directing therapy to the neck or temporomandibular joint to alleviate primary Use Disclosure:
headache. Dr Graff-Radford discusses
the unlabeled use of
Summary: Clinicians should recognize the significant role that musculoskeletal amitriptyline, selective
structures of the head and neck play in the perpetuation of headache and the im- serotonin-norepinephrine
portance of evaluating every patient for temporomandibular disorders and cervical reputake inhibitors, and
antiepileptic drugs
abnormalities. for the treatment of
temporomandibular disorders.
Continuum Lifelong Learning Neurol 2012;18(4):869–882. * 2012, American Academy of
Neurology.

INTRODUCTION tion between cervical dysfunction and

Pain presentations in the head and
neck may involve neurologic, vascular,
and musculoskeletal structures. These
structures influence each other, and
their interrelationships are not always
clear. Many patients have coexisting
chronic head, neck, and face pain be-
cause of the nociceptive barrage, cen-
tral sensitization may account for the
referral to distant sites. The close
proximity of the trigeminal nucleus
and upper cervical afferent pathways
may account for the cross-referral from
neck to face. As nociceptive inputs
become chronic, central neurons are
sensitized, reducing the threshold for
activation and thereby making the
response to afferent stimulation more
sensitive, which may cause the recep-
tive field to enlarge. Because of this in-
terrelationship, individualized care to
each pathologic system is necessary.
Reviews that have studied the associa-
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migraine, as well as between cervical dys-
function and temporomandibular disor-
ders (TMDs), find no clear cause-effect
relationship between these disorders.1,2
TEMPOROMANDIBULAR
DISORDERS
The relationship between TMD and
primary headache is important to under-
stand, as treating one may affect the
other (Case 9-1). TMD as a collective
term may include a number of different
clinical entities, including myogenous
and arthrogenous components. Pain in
the temporomandibular joint (TMJ)
may occur in 10% of the US population,
and TMD has been reported in 46.1%
of the US population.5,6 Studying the
epidemiology of TMD has not allowed
the differentiation of headache from fa-
cial pain. Very few patients with either
clicking or popping or intermittent pain
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 Facial and Cervical Pain

Case 9-1
A 56-year-old woman presented with jaw, neck, and head ache. Pain was localized to the right
temporomandibular joint (TMJ) radiating into the masseter. She described the pain as mostly dull and
achy with associated cracking in her jaw joint. At times she had limited mouth opening and had to make her
jaw click to open. She described this as locking. The pain worsened as the day progressed and caused
headache and neck pain. The pain radiated from the cervical region into the upper shoulder and down the
right arm and was associated with a sensation of tingling in her hand. She denied weakness in the upper
extremity. The arm pain was described as intermittent, achy, and dull. Headache was described as
intermittent with a throbbing quality and with tenderness over the left superficial temporal artery. No
associated nausea, vomiting, photophobia, or phonophobia was present. When having a headache, she
preferred to be sedentary. She reported that her jaw had made a clicking noise for years, accompanied
by pain that worsened with function such as chewing or talking. She also reported a history of migraine
with aura occurring 1 to 2 times per year. She used four hydrocodone and diazepam pills daily. Examination
showed limited jaw range of motion and pain on palpation over the TMJ. Her neck range of motion was
limited, and movement increased the neck pain and often triggered a headache. The superficial temporal
artery was very tender to palpation. Brain MRI was normal; MRI of the neck was positive for
facet arthropathy; and the temporomandibular MRI showed disk displacement without recapture. Further
testing included erythrocyte sedimentation rate and C-reactive protein, which were normal.
The patient was given tizanidine 4 mg at bedtime and advised to increase it to 8 mg after 4 days.
The diazepam was stopped, and the narcotic was placed on a time-contingent basis and reduced by one
pill every 4 days. An explanation about medication-overuse headache and narcotic-induced hyperalgesia
was provided as motivation. Because of the limited range of motion and the presence of disk
displacement (Figure 9-1) the patient was sent for arthrocentesis. Immediately after the procedure,
she was given anti-inflammatory medication and advised to stretch her jaw according to the exercises
she had been taught. The pain rapidly decreased, and a stabilization splint and an exercise program
maintained the
range of motion.
As the patient’s
jaw pain improved
a series of neck
stretches were
provided,
relieving the
generalized neck
pain and reducing
the headaches. If
the neck pain had
persisted, facet
blocks would have
been considered.
Comment.
Because the
patient is older
than age 50 and
has severe
temporal pain
FIGURE 9-1 A, Degenerative condyle disk displacement. The upper arrow points to the with temporal
degenerative condyle, and the lower arrow shows the disk deformed (not
bowtie-shaped) and forward of its normal position. B, Open disk, no capture. The tenderness to
arrow shows the disk pushed forward of the condyle. It is not able to relocate itself between palpation, giant
the condyle and temporal bone.
cell arteritis
Continued on page 871

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 Continued from page 870
should be considered. Giant cell arteritis (International Classification of Headache Disorders, Second
Edition 6.4.1)3 should be suspected in patients older than 50 years who present with persistent
headache centered on one or both temples that worsens with cold temperatures and is associated with
jaw claudication. The examination may reveal an enlarged, tender temporal artery. Laboratory
investigation should include erythrocyte sedimentation rate and/or C-reactive protein.4 A temporal
artery biopsy may be required to confirm the presence of giant cells. Treatment is usually with
corticosteroids and is urgent because blindness secondary to granulomatous occlusion of the vessels
may be rapid. This case illustrates the need to be aware that patients with primary headache may be
helped by being aware of the role temporomandibular disorders and cervical abnormalities may play in
perpetuating or triggering headache.

require treatment. It is estimated that
75% of the population has a sign or
symptom during their lifetime, but
fewer than 5% need therapeutic inter-
vention. Because both headache and
TMD are so common, they may be
reported as unified or separate entities.
The TMJ and associated orofacial struc-
tures can be considered as triggering
or perpetuating factors for migraine.
Ciancaglini and Radaelli7 report that
headache occurs significantly more fre-
quently in patients with TMD symptoms
(27.4% versus 15.2%). Ignoring the TMJ,
muscles, or other orofacial structures as
peripheral triggers of headache will
often result in a poor clinical outcome.
The trigeminal nerve is the final conduit
of face, neck, and head pain.8 Manage-
ment of pain in the first division may be
influenced by therapy aimed at struc-
tures innervated by the second or third
trigeminal divisions.
Etiology
Inflammation within the joint accounts
for TMD pain, and the dysfunction is
caused by a disk-condyle incoordina-
tion. The etiology for TMD may include
parafunctional behaviors, macrotrau-
mas or microtraumas, changes in the
occlusion, and behavioral influences.
Treatments aimed at the occlusion and
masticatory system have been success-
ful at treating the headache associated KEY POINTS
with TMD. However, the cause-and- h Because both headache
effect relationship remains unknown. and temporomandibular
disorder are common,
Randomized controlled trials in which
they may be reported as
headache is treated by modifying the
unified or separate
occlusion show no scientific support entities.
for this treatment. A literature meta-
analysis does not support occlusion as h Inflammation within
the temporomandibular
a factor in headache etiology. Sensory
joint accounts for
innervation of the TMJ is mediated tempomandibular
through the mandibular division of disorder pain; the
the trigeminal nerve. Pain-sensitive dysfunction is caused
elements within the TMJ include the by disk-condyle
joint capsule, the posterior attachment incoordination.
tissues, and the discal ligaments. The h A literature meta-analysis
posterior attachment is highly inner- provides no support for
vated, richly vascularized, and frequently occlusion as a factor in
implicated in the pathophysiology of headache etiology.
joint pain. In contrast, the intraarticular
disk is largely devoid of neural or
vascular tissue but plays a vital role in
maintaining condylar stability during
mandibular movement.
Trauma to the TMJ may result in acute
capsulitis, but this inflammatory process
tends to resolve quickly without com-
plication. Chronic joint disorders are
more frequently associated with pain-
ful derangement of the TMJ. Articular
disk displacement frequently underlies
the mechanism of joint derangement,
but the etiology is unclear. The remark-
able adaptive capacity of the TMJ is well
documented.8 Failure of this mecha-
nism may lead to tissue destruction

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 Facial and Cervical Pain

KEY POINTS
h The right and left
temporomandibular
joints move as a
functional unit and are
lined by a fibrous
connective tissue that is
more resistant to
degenerative change
and has a greater
capacity for repair.
h Articular disk
displacement is the
most common
temporomandibular
arthropathy and is
characterized by an
abnormal relationship
or misalignment of the
articular disk relative to
the condyle.
and disk displacement and may be af-
fected by age, stress, sex, systemic ill-
ness, and previous trauma. However,
acute and chronic disk displacement is
not always painful.
The TMJ has a bilateral location,
with an upper and lower compartment
separated by a fibrocartilaginous disk.
This diarthrodial structure allows for
both rotatory and translational move-
ment of the mandible. Although the
TMJ is subject to the same pathologic
disorders that affect other synovial
joints, it is unique in certain anatomic
aspects. Both joints move as a func-
tional unit and are lined by a fibrous
connective tissue that is more resistant
to degenerative change and has a
greater capacity for repair. The masti-
catory system includes the articulation
of the upper and lower dentition that
may limit or support joint function and
stability. Major components of TMD
are joint noise and incoordination of
the disk-condyle relationship, which
presents as noise in the joint with or
without locking or the inability to open
with a normal range of motion. This
condition is often referred to as an in-
ternal derangement. Known as a disk
derangement disorder, articular disk
displacement is the most common tem-
poromandibular arthropathy and is
characterized by an abnormal relation-
ship or misalignment of the articular
disk relative to the condyle.9 It is clas-
sified as disk displacement with reduc-
tion or disk displacement without
reduction (Table 9-1 and Table 9-2).10
In disk displacement with reduction,
during mouth opening, the disk that
begins in a misplaced position reduces
or improves its structural relationship
with the condyle. As it reduces, a sound
often described as clicking or popping
is heard. When the mouth closes, a sec-
ond sound called a reciprocal click may
be audible as the disk moves off the
condyle just before the teeth come
together. Usually the closing noise is of
less magnitude. Clicking sounds are
not necessarily a sign of degeneration
or an indication for treatment. More
than one-third of an asymptomatic sam-
ple can have moderate to severe de-
rangement as seen on imaging,11 and
as many as 25% of clicking joints show
normal or slightly displaced disks.12

TABLE 9-1 Diagnostica Criteria for Disk Displacement With

Reduction

b All of the Following Must Be Present

Reproducible joint noise that occurs usually at variable positions during
opening and closing mandibular movements
Displaced disk that improves its position during mandibular opening on
soft tissue imaging and absence of extensive degenerative bone changes
on hard tissue imagingb
b Any of the Following May Accompany the Preceding Criteria
Pain, when present, precipitated by joint movement
Deviation during opening movement coincidental with a click
Unrestricted mandibular movement
Episodic and momentary catching during opening (G35 mm) that
self-reduces with voluntary mandibular repositioning
a
Reprinted with permission from Okeson JP, Mosby.10 B 2003, Elsevier.
b
Although the diagnosis of disk displacement can only be confirmed with soft tissue imaging,
the self-limiting nature of the disorder does not warrant routine soft tissue imaging.

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Asymptomatic clicking does not require
treatment.
A disk displacement without reduc-
tion, also referred to as a closed lock,
occurs when the out-of-place disk re-
mains out of place during movement
of the mandible. This is usually associ-
ated with limited range of motion.
Myofascial Pain
Frequently pain associated with TMD
is muscular in origin. The most com-
mon diagnosis is myofascial pain. Char-
acterized by a regional muscle pain,
myofascial pain has been described as
dull or achy and is associated with the
presence of trigger points in muscles,
tendons, or fascia.13Y17 It is a common
cause of persistent regional pain in-
volving the neck, shoulder, head, and
orofacial regions. Although the precise
etiology of myofascial pain is unclear,
it may be associated with stress and
oral habits (developmental factors) or
poor sleep, postural abnormalities, and
depression (perpetuating factors).18,19
KEY POINTS
The major characteristics of myofascial h Asymptomatic clicking
pain include trigger points in muscles does not require
and local and referred pain. The trig- treatment.
ger points may present clinically as
h Frequently pain
active or latent. When active, digital associated with
palpation produces pain referral to a temporomandibular
distant site. When latent, local tender- disorder is muscular in
ness to palpation may be present, but origin.
no distant referral occurs. Myofascial
pain is not confined to a single derma-
tomal, myotomal, or visceral division
but may expand beyond these limits.
Clinically, the tender points appear in
tense muscles in which active or passive
stretching produces increased pain
associated with decreased motion. Max-
imal pain is produced when the muscle
is contracted against fixed resistance.
Clinical examination reveals a nodular
or ropelike band under the skin that is
associated with the tender points. Pal-
pation may result in a visible move-
ment by the patient called a jumps
sign.20 Moving the fingers over the
nodule in a direction opposite to the
muscle fiber orientation may elicit a

TABLE 9-2 Diagnostica Criteria for Disk Displacement Without

Reduction

b All of the Following Must Be Present

Persistent markedly limited mouth opening (G35 mm) with a history
of sudden onset
Deflection to the affected side on mouth opening
Markedly limited laterotrusion to the contralateral side
(if unilateral disorder)
Reproducible joint noise that occurs usually at variable positions
during opening and closing mandibular movements
Disk without reduction found on soft tissue imagingb
b Any of the Following May Accompany the Preceding Criteria
Pain precipitated by forced mouth opening
History of clicking that ceases with locking
Pain with palpation of the affected joint
Ipsilateral hyperocclusion
Absence of mild osteoarthritic changes with hard tissue imaging
a
Reprinted with permission from Okeson JP, Mosby.10 B 2003, Elsevier.
b
Although the diagnosis of disk displacement can be confirmed only with soft tissue imaging,
the self-limiting nature of the disorder does not warrant routine soft tissue imaging.

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 Facial and Cervical Pain
twitch called the twitch response. The
pain is elicited in a characteristic pattern
specific for each muscle. The referred
pain may be accompanied by referred
tenderness that may initiate further mus-
cle pain and satellite trigger points.
Imaging
Imaging may define the disk position
and its movement during function. Ini-
tially imaging is done with the mouth
closed; sequences are then repeated
with the mouth open. Evaluating how
the disk-condyle complex moves dur-
ing these excursions is useful. A num-
ber of imaging modalities can reveal
suspected pathology, and the type se-
lected should be based on the clinical
findings. Panoramic, transcranial, and
tomographic studies are used to eval-
uate the bone, and MRI can be used to
image soft tissues. Cone beam CT is
the newest imaging technique for the
face and jaws; it uses less radiation and
allows reconstruction into two- and
three-dimensional images. MRI remains
the gold standard of diagnostic imag-
FIGURE 9-2 A, Normal disk, closed mouth. The arrow points to the disk seen as a dark bowtie
shape. B, Normal disk, open mouth. The arrows point to the disk seen as a dark
bowtie shape.
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ing for soft tissues and the best
method to assess disk position.21
Figure 9-2 shows the normal anatomy
of the TMJ. The TMJ is located ante-
rior to the external auditory meatus
and comprises a socket in the tempo-
ral bone within which the mandibular
condyle functions. The condyle can
move in anterior, posterior, and lateral
directions. The fibrocartilaginous artic-
ular surfaces of the condyle and fossa
function against the fibrous interarticu-
lar disk, which is attached to the con-
dyle by the medial and lateral collateral
ligaments. Posteriorly, the disk attaches
to the posterior retrodiscal tissues,
which are highly vascularized and richly
innervated. This tissue is the source of
pain due to inflammation. Anteriorly,
the disk attaches to the lateral pterygoid
muscle, which serves to bring the con-
dyle forward and lateral. Normal disk
position with the mouth closed and the
mouth open can be seen in Figure 9-2.
Figure 9-1 demonstrates disk displace-
ment and failure of the disk to be
recaptured in opening. This explains
August 2012
 KEY POINTS

TABLE 9-3 International Classification of Headache Disorders,a,b h The potential for cervical
Second Edition, Criteria for Cervicogenic Headache dysfunction to manifest
as headache is
Diagnostic Criteria: recognized under the
A. Pain referred from a source in the neck and perceived in one or more classification of
regions of the head and/or face, fulfilling criteria C and D. cervicogenic headache.
B. Clinical, laboratory, and/or imaging evidence of a disorder or lesion within The pain is typically
the cervical spine or in the soft tissues of the neck known to be, or perceived within the
generally accepted as, a valid cause of headache. dermatomes of the
C. Evidence that the pain can be attributed to the neck disorder or lesion, trigeminal and upper
based on at least one of the following criteria:
cervical (C2, C3) nerves.
1. Demonstration of clinical signs that implicate a source of pain in the neck.
2. Abolition of headache following diagnostic blockade of a cervical h Diseases or dysfunctions
structure or its nerve supply using placebo or other adequate controls. of the cervical region
D. Pain resolves within 3 months after successful treatment of the causative may cause pain when
disorder or lesion. the pathology involves
a
Previously used terms for cervicogenic headache include cervical headache and headache
pain-sensitive structures
attributed to disorder of the cervical spine. that refer in a
b
Adapted from Headache Classification Subcommittee of the International Headache Society, physiologically
Cephalalgia.3 B 2004, with permission from SAGE. cep.sagepub.com/content/24/1_suppl/9.long.
based pattern.
h The structures known
to cause pain include
locking. Understanding the pathophysi- to 2.5% of the general population and the facet joints,
ology is important, as it will alter the increase to 15% to 20% in a population periosteum, ligaments,
treatment. with chronic headache. Cervicogenic muscles, cervical nerve
headaches affect women more often roots and nerves, and
than men in a 4:1 ratio. The average vertebral arteries.
CERVICOGENIC PAIN age of patients with cervicogenic head-
While cervical pain has been described ache is in the forties.25
in many primary headaches, some are
caused by cervical pathology. The po- Pathogenesis
tential for cervical dysfunction to cause Diseases or dysfunctions of the cervi-
headache is recognized under the clas- cal region may cause pain when the
sification of cervicogenic headache pathology involves pain-sensitive struc-
(Table 9-3), and the pain typically tures that refer in a physiologically
manifests within the dermatomes of based pattern. The local pain-sensitive
the trigeminal and upper cervical (C2, structures include the facet joints, peri-
C3) nerves.3 Cervical structures that osteum, ligaments, muscles, cervical
innervate the trigeminocervical com- nerve roots and nerves, and the verte-
plex or nucleus include the C1-C3 nerve bral arteries.26Y28 Cervical causes of
roots and their branches, the occiput- headache include developmental anom-
C3 joints, the alar and transverse alies of the craniovertebral junction and
ligaments, the prevertebral and post- upper cervical spine, tumors, Paget dis-
vertebral muscles, the trapezius, the ease, osteomyelitis, rheumatoid arthritis,
sternocleidomastoid muscles, the cer- ankylosing spondylitis, retropharyngeal
vical dura mater, and the vertebral and tendonitis, and cervical dystonias. Cer-
carotid arteries.1,22Y24 vical spina bifida does not cause head-
ache unless it is associated with other
Epidemiology anomalies, such as Chiari malforma-
Estimates of the prevalence of cervi- tions. Cervical disk disease is common
cogenic headache range from 0.4% but is not usually accepted as a cause
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 Facial and Cervical Pain

KEY POINT
h Response to neural
blockade does not
necessarily exclude the
facet joint as a pain
contributor.
of headache. Should they be impli-
cated, herniations involving the upper
cervical segments (C1-C3) would be
expected. Another controversial cause
of headache is cervical whiplash injury.
Pain is usually self-limiting, resolves
in weeks, and is likely due to injury of
ligaments and muscles. Evidence dem-
onstrates that chronic pain in this set-
ting may be secondary to shearing of
long axons in the brainstem and upper
cord that causes centrally mediated
pain and headache.29Y31 Sjaastad and
Bovim32 have suggested that patients
with cervicogenic headache report a
fairly uniform headache profile, with
the implication that the pain emanates
from cervical structures. They empha-
size that this is not a disease but rather
a reaction pattern. The profile they de-
scribe includes (1) unilaterality begin-
ning in the neck and radiating to the
oculofrontal area, (2) moderate non-
throbbing pain, intermittent or contin-
uous, and provoked by neck movement
or sustained awkward postures, (3) non-
radicular pattern, (4) reduced range
of motion in the cervical spine, (5) pre-
dominantly female, (6) history of trauma,
and (7) transient relief with cervical
block or C2 root block. Other migraine-
associated symptoms or autonomic fea-
tures are not necessary.32,33
Figure 9-3 depicts the degenerative
changes that can be associated with
facet joints. Blocking these facet joints
and determining the degree of pain re-
lief may be helpful in identifying a local
source of pain.
Response to neural blockade does
not necessarily exclude the facet joint
as a pain contributor.
Nerve Block
Peripheral nerve blocks have long been
used in headache management. The
most widely used procedure for this
purpose has been greater and lesser
occipital nerve blocks. The rationale for
blocking occipital nerves in headache
relates to the convergence of cervical

FIGURE 9-3 A, Cervical spine. B, Cervical spine showing facet arthropathy. The arrows point to
the facet joints.

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and trigeminal fibers in the trigeminal
nucleus caudalis. The region around
the nerve is usually infiltrated with a
local anesthetic (lidocaine, bupivacaine,
or both), and a corticosteroid is some-
times added. Several studies suggest
the efficacy of greater and lesser occipi-
tal nerve block in the treatment of mi-
graine, cluster headache, and chronic
daily headache. However, few of those
studies are controlled and blinded.34
Cervical nerve root blocks have been
performed since the late 19th century,
and with the improvement of imag-
ing, the procedure has been increasing
in popularity over the past decade.35,36
Cervical nerve root blocks are used to
manage or treat spinal pain, radicular
pain, and complex regional pain syn-
dromes. Such blocks are usually per-
formed in outpatient clinics, with or
without imaging guidance such as fluo-
roscopy or CT.
Diagnostic and therapeutic selective
nerve root blocks may be useful in the
diagnosis of patients with headache
and radiculopathy. A reduction in pain
after nerve block with local anesthetic
may indicate the irritated root is causing
the headache. Using local anesthetic
selective nerve root blocks, Persson
and colleagues37 concluded that a direct
relationship exists between degenera-
tive change causing nerve root compres-
sion in the upper and lower cervical
spine and headache.
It is common for cervical facet or
zygapophyseal joint pathology to con-
tribute to neck pain; therefore, man-
agement with intraarticular injections,
blocking the medial branches that in-
nervate the joint, or performing medial
branch neurolysis may successfully re-
duce chronic neck pain.
Neural Radiofrequency
Procedures
A review of the literature on interven-
tions aimed at the facet shows benefit
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KEY POINT
that may vary in duration.38 Boswell h Great caution should be
and colleagues38 concluded that there exercised in providing
was moderate evidence for neurotomy mobilization, and in
in short-term and long-term outcome, particular manipulation,
whereas the blocks alone produced because in rare cases
little, if any, long-term benefit. stroke and vertebral
artery dissection may
Physical Therapy occur.
Cervical manipulation and mobiliza-
tion have been evaluated for headache
management in several systematic re-
views, case series, and controlled stud-
ies. Mobilization and manipulation
are similar terms that are frequently
used interchangeably in the literature.
Both terms refer to passive movement
techniques used to restore normal mo-
tion to a joint. Manipulation occurs
when a high velocity thrust is applied
at the end range of motion. Mobiliza-
tion implies passive movement, usually
rhythmic in nature, that varies in am-
plitude but never exceeds the joint’s
normal motion.39 A Cochrane Database
Review40 reported high-quality evi-
dence for manipulation in the man-
agement of migraine compared with
amitriptyline. Generally the literature
does not support cervical manipula-
tion for the prevention or acute care
of migraine.41Y43 The mobilization of
the upper cervical joint using different
techniques seems to be relatively safe
and helpful for cervical headache, but
the small sample size (10 patients) and
length of follow-up (only 4 weeks) are
limitations of the study. Great caution
should be exercised in providing mobi-
lization, and in particular manipulation,
because in rare cases stroke and verte-
bral artery dissection may occur.
More than 100 cases of serious com-
plications from chiropractic manipula-
tion have been reported, and it can be
assumed that a fairly large number of
similar complications go unreported.44
The potential serious complications
are increased risk of vertebral artery
dissection and approximate sixfold
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 Facial and Cervical Pain

KEY POINT
h Temporomandibular increase in stroke or TIA. It is appro- to avoid chewy foods, especially chew-
disorders are priate to inform patients about these ing gum. They can be taught to avoid
self-limiting. potentially serious complications of cer- clenching their jaws during the day, to
vical chiropractic manipulation. apply heat or ice, and to perform jaw-
stretching exercises.

MANAGEMENT OF
TEMPOROMANDIBULAR
DISORDERS
The biggest gap in TMD-headache
studies is the lack of clear diagnosis.
Further, it is uncertain whether the
cause of headache can be connected
to or correlated with TMD if treating
the TMD reduces the headache. It is
clear that primary headache is a CNS
issue and that treating an existing TMD
in the presence of primary headache
may reduce the pain intensity and fre-
quency. This, however, should not be
misconstrued as cause and effect. The
five basic areas considered in TMD ther-
apy are summarized in Table 9-4.
Patient Education and Self-Care
It is essential to keep in mind that TMDs
are self-limiting. Because the TMJ is
covered with fibrocartilaginous mate-
rial, it has the propensity to remodel. In
most patients, the disorder will resolve
within 7 years.45,46 Typically, patients re-
spond to conservative, noninvasive in-
tervention unless nonreducing disk
displacements are limiting function. This
explanation lessens patient fear of the
disorder. Patients should be instructed
Cognitive-Behavioral
Interventions
Behavioral modification of maladaptive
habits is an important component in
the management of TMD. This may be
accomplished with simple exercises or
with the help of a structured program
facilitated by a specialist in behavioral
modification. This type of program
may include lifestyle counseling, pro-
gressive relaxation, biofeedback, and
hypnosis. Treatments should be indi-
vidualized to the patient.47
Pharmacologic Therapy
Pharmacology can promote patient com-
fort and healing when it is incorporated
as part of a comprehensive therapy. For
TMD, the most common medications
include nonsteroidal anti-inflammatory
drugs and muscle relaxants. The use
of tricyclic antidepressants, selective
serotonin-norepinephrine reuptake in-
hibitors, and antiepileptic drugs are also
important in pain management.48
Physical Therapies
Physical therapies include posture train-
ing, exercise, joint mobilization, and

TABLE 9-4 Basic Principles of Management of Temporomandibular

Disorders

b Patient education and self-care

b Cognitive-behavioral interventions
b Pharmacologic management (eg, analgesics, nonsteroidal
anti-inflammatory drugs, muscle relaxants, sedatives, and antidepressants)
b Physical therapies (eg, posture training, stretching exercises, mobilization,
physical modalities, appliance therapy, and occlusal therapy)
b Surgery

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the use of physical agents or modalities.
The goal is to reduce the pain and simul-
taneously improve the joint movement
by altering nociceptive input, reducing
inflammation, decreasing coordinating
and strengthening muscle activity, and
allowing regeneration of tissues. In
Case 9-1, physical therapy and appli-
ance therapy were initiated and were
recommended because of the locking
and arthrocentesis. The patient was
asked to continue with her stabilization
appliance, and stretching exercises
were provided along with the use of a
vapocoolant spray to maintain the gains
after arthrocentesis.
The type of splint used in TMD is
controversial. Fricton and colleagues49
reviewed 42 studies involving intraoral
splints. Generally, in patients with more
severe TMDs, splints are beneficial in
relieving TMD pain compared with pla-
cebo, and stabilization splints are the
most effective with the least potential
for adverse effects. Because many dif-
ferent splint designs are available, a
summary of the conclusions from this
review will provide a guideline for splint
use.
In severe TMDs, stabilization splints
(splints that cover all maxillary or man-
dibular teeth, do not alter the jaw pos-
ition, and are worn at night only) reduce
TMD pain when compared with non-
occluding splints. Studies of headaches
with specific diagnoses are limited, and
definitive conclusions cannot be con-
firmed. When compared to physical medi-
cine techniques, cognitive-behavioral
therapies, and acupuncture, stabiliza-
tion appliances are equivalent. One
study claims that splint therapy may
be better than pharmacotherapy.50
Evidence shows that anterior posi-
tioning splints (hard splints that cover
all the maxillary and mandibular teeth
and hold the lower jaw in a forward
position) and soft splints (splints that
cover all the maxillary and mandibular
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teeth and hold the lower jaw in a for-
ward position) reduce TMD when com-
pared with placebo.
Anterior positioning splints are
equally or more effective than stabili-
zation splints in the management of
TMJ clicking and locking. The use of
these appliances may lead to occlusal
changes, so they should be used with
caution.
Compared with stabilization appli-
ances, there is no evidence supporting
the use of anterior bite planes, such as
the nociceptive trigeminal inhibition
reflex device (NTI) (a hard splint that
covers only the central incisors on the
maxilla and central and lateral incisors
on the bottom, holding the mandible
forward), in headache. Potential side
effects, including swallowing, possible
aspiration, tooth movement, and bite
change, make this splint undesirable. A
comprehensive review of controlled
trials by Stapelmann and Turp51 con-
cluded that the NTI might be useful
in TMD and bruxism, but the potential
negatives should be carefully consid-
ered. Despite the evidence that splint
therapy is useful, splints should not be
used in isolation but rather as part of an
integrated therapy program.52
Occlusal adjustment was once con-
sidered beneficial for TMD; however, no
evidence supports its use. A Cochrane
Database review53 and other system-
atic reviews concluded that evidence is
insufficient to support ongoing use of oc-
clusal adjustment as a treatment of TMD.
Miscellaneous physical therapies.
Electrotherapy. Electrotherapy is pos-
tulated to modify muscle hyperactivity
and tissue swelling, change circula-
tion, and reduce trigger point activity.
Electrogalvanic stimulation uses a high-
voltage, low-amperage, monophasic
current of varied frequency. The use of
transcutaneous electrical nerve stimula-
tion (TENS) in the head is controversial
for the fear of creating epileptogenic
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 Facial and Cervical Pain
effects. TENS uses a low-voltage, low-
amperage, biphasic current of varied
frequency and is designed primarily for
sensory counterstimulation in painful
disorders. Little evidence is available for
its effectiveness in the head.
Ultrasound. When transmitted
through the tissue with a high-frequency
oscillating transducer head, ultrasound
produces heat that can reach a depth
of 5 cm. It is a frequently used physical
treatment modality for musculoskeletal
problems. When used to deliver medi-
cation into the tissue, the process is
called phonophoresis, although the
mechanism and efficacy of drug deliv-
ery are unknown.
Iontophoresis. Iontophoresis is a
technique to enhance the transport
of drug ions across the skin into the
deeper tissue using a weak current. Re-
cent studies question the efficacy of this
modality to provide pain relief.
Laser treatment. Low-level laser ther-
apy may have biostimulating (biostim-
ulation involves the modification of
the environment to stimulate existing
tissue capable of bioremediation) and
analgesic effects through direct irradia-
tion without causing a thermal response.
Several studies investigating the efficacy
of laser therapy in TMDs are inconclu-
sive because of poor methodology or
small sample size. Further research is
needed to support the use of low-level
laser therapy in TMD treatment.
Surgery. TMJ surgery is effective for
specific articular disorders and may in-
clude arthrocentesis, arthroscopy, ar-
throtomy, and joint replacement. Most
patients respond to simple intraarticular
irrigation with or without steroids. This
procedure is effective in patients with
acute closed lock and will likely result
in improved range of motion. It can
also be used for patients with degen-
erative arthritides. In patients with
disk displacement, arthrocentesis can
be helpful.
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