ISSN 0017-8748

Headache doi: 10.1111/head.12272

© 2013 American Headache Society Published by Wiley Periodicals, Inc.

Review Article
Orofacial Pain: A Guide for the Headache Physician
Martina K. Shephard, BDent(Hons), MBBS(Hons), FRACDS; E. Anne MacGregor, MD, FFSRH;
Joanna M. Zakrzewska, MD, FDSRCS, FFPMRCA

Orofacial pain represents a significant burden in terms of morbidity and health service utilization. It includes very common
disorders such as toothache and temporomandibular disorders, as well as rare orofacial pain syndromes. Many orofacial pain
conditions have overlapping presentations, and diagnostic uncertainty is frequently encountered in clinical practice. This review
provides a clinically orientated overview of common and uncommon orofacial pain presentations and diagnoses, with an
emphasis on conditions that may be unfamiliar to the headache physician. A holistic approach to orofacial pain management
is important, and the social, cultural, psychological and cognitive context of each patient needs to be considered in the process
of diagnostic formulation, as well as in the development of a pain management plan according to the biopsychosocial model.
Recognition of psychological comorbidities will assist in diagnosis and management planning.

Key words: cranial neuralgia, dental pain, headache, multidisciplinary management, orofacial pain, psychological comorbidity

Abbreviations: AAOP American Academy of Orofacial Pain, GCA giant cell arteritis, ICHD International Classification of
Headache Disorders, MMP masticatory myofacial pain, MRI magnetic resonance imaging, NVOP neurovas-
cular orofacial pain, RCT randomized controlled trial, RDCTMD Research Diagnostic Criteria for Temporo-
mandibular Disorders, TMD temporomandibular disorder, TN trigeminal neuralgia

(Headache 2014;54:22-39)

Orofacial pain may be defined as pain localized to
the region above the neck, in front of the ears and
below the orbitomeatal line, as well as pain within the
oral cavity.1 It includes pain of dental origin and
temporomandibular disorders (TMDs), and thus is
widely prevalent in the community. Up to a quarter of
the population reports orofacial pain (excluding dental
From the Oral Medicine Unit, Eastman Dental Hospital,
UCLH NHS Foundation Trust, London, UK (M.K. Shephard);
Centre for Neuroscience & Trauma, Blizard Institute of Cell
and Molecular Science, Barts and the London School of Medi-
cine and Dentistry, London, UK (E.A. MacGregor); Eastman
Dental Hospital, UCLH NHS Foundation Trust, London, UK
(J.M. Zakrzewska).
Address all correspondence to M.K. Shephard, Oral Medicine
Unit, Eastman Dental Hospital, UCLH NHS Foundation
Trust, London WC1X 8LD, UK.
pain), and up to 11% of this is chronic pain.2 Patients
with orofacial pain present to a variety of clinicians,
including headache physicians, dentists, maxillofacial
surgeons, otolaryngologists, neurologists, chronic pain
clinics, psychiatrists, and allied health professionals
such as physiotherapists and psychologists.3,4 Orofacial
pain is associated with significant morbidity and high
levels of health care utilization.5
This review presents a clinically orientated over-
view of orofacial pain presentations and diagnoses.
The scope of orofacial pain includes common dis-
orders such as dental pain and TMDs, as well as a
number of rare pain syndromes. Pain in the orofacial
region is derived from many unique tissues such as
teeth, meninges, and cornea. This results in several
unique physiological mechanisms that have been well

Conflict of Interest: No authors report a relevant conflict of

Accepted for publication September 30, 2013. interest.

22

Headache
Fig 1.—Classification of orofacial pain.
reviewed.6 Because of these unique mechanisms and
the requirement for specialist knowledge of the
complex anatomy and physiology of the orofacial
region, diagnosis may be difficult. Many patients have
consulted multiple clinicians for their condition yet
remain undiagnosed or with an incorrect diagnosis.7,8
Our aim is to provide the headache physician with a
guide to orofacial pain presentations and diagnoses
informed by our clinical experience in the fields of
medicine as well as dentistry, and to review the litera-
ture relevant to these conditions. We provide an over-
view of the common presentations of orofacial pain
including dental causes of pain, non-dental causes of
intraoral pain, and extraoral facial pain syndromes, as
the signs and symptoms of many of these conditions
can overlap significantly, causing diagnostic difficulty.
We also present a discussion of history, diagnosis,
and management considerations relating to the
biopsychosocial model of diagnostic formulation and
management.This approach is particularly relevant and
important in the field of orofacial pain given the signifi-
cant level of psychological distress and social dysfunc-
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
23
tion that is associated with these disorders.9,10 As with
other types of chronic pain, there is often a mismatch
between the patient’s expectation of a cure for their
pain, and the reality that for many types of chronic pain,
a cure is seldom possible. Medicine alone does not have
the tools to manage a condition that has a neurophysi-
ological cause but is also experienced emotionally,
socially,financially,and spiritually.11 Recognition of psy-
chological comorbidities is essential for appropriate
diagnosis and successful pain management.
METHODOLOGY
This is a narrative, clinically orientated review of
orofacial pain conditions encountered in a specialist
orofacial pain clinic, with references to relevant lit-
erature. Quotations from patients are included to
illustrate relevant points as these also form part of the
evidence base.12 The types of orofacial pain have been
divided into sections as shown in Figure 1. Informa-
tion regarding dental causes of orofacial pain is
included as this area is often unfamiliar to medical
practitioners. Evidence-based management options,

24
as far as possible, for the specific diagnoses are sum-
marized and presented in a tabulated form (Table). In
the second half of the paper, we discuss holistic man-
agement approaches to orofacial pain.
TYPES OF OROFACIAL PAIN
Dental Pain.—There are few causes for dental
pain; however, because of significant neural conver-
gence in the jaws and face, it may be referred, poorly
localized, or misdiagnosed. The 4 major causes of
dental pain are pulpitis, cracked tooth syndrome,
dental abscess, and dentine sensitivity.13 These are
often acute conditions, but because they are common,
they may coexist with other chronic pains.14
Both the dental pulp and periodontal ligament
contain nociceptors. Nociceptive output in these
areas is triggered by changes in pressure and the
effect of inflammatory mediators.
Pulpitis.—Pulpitis is the term used to describe pain
because of inflammation of the dental pulp, and it is
usually due to dental caries. Inflammation of the pulp
leads to accumulation of extracellular fluid, inflam-
matory mediator release, and vasodilatation, which
causes an elevation of pressure within the pulp
chamber, which is a non-compliant space. The pres-
sure increases further as venous stasis and eventually
pulp necrosis occur, with release of inflammatory
mediators and necrotic cell contents. Elevated pres-
sure and inflammatory chemicals activate nociceptors
in the pulp chamber causing pain.
Reversible pulpitis is defined as a transient pain
in response to specific stimuli (hot, cold, sweet), which
occurs when the pulp is inflamed. These symptoms
resolve when the cause of the inflammation is treated.
The pain of reversible pulpitis may be described as
fleeting, shooting, stabbing, or sensitive.
Irreversible pulpitis is characterized by spontane-
ous pain, which may be worsened by or persist fol-
lowing the removal of a stimulus such as heat or cold.
It is an indicator of incipient pulpal necrosis. The pain
of irreversible pulpitis is often described as persistent,
throbbing, dull, or aching. It may be worsened by
physical activity and head movement.
Pulpal pain is often poorly localized as the
inflammation is restricted to the pulp chamber and is
thus not affecting proprioceptive nerve fibers, which
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
are located in the periodontal ligament. It is common
for patients to be unable to localize the exact source
of the pain. Pulpal pain may respond to simple or
opioid-based analgesics, but the pain of irreversible
pulpitis will not resolve until pulpal necrosis has
occurred or the pulpal tissue has been mechanically
removed (by endodontic treatment).
If pulpal inflammation and infection reaches the
base of the pulp chamber, an area known as the apex
or root tip, it may extrude through the apical foramen
into the periodontal space (Fig. 2). This will cause
pain due to stimulation of nociceptors in the peri-
odontal ligament space, and the pain will be well
localized due to involvement of periodontal ligament
proprioceptive fibers. Extrusion of inflammatory fluid
and necrotic cell products into the periodontal space
causes pain because of pressure effects, and the tooth
will become exquisitely tender to touch or biting. This
leads to the pain becoming very well localized, and
the source of pain may be readily identified by gentle
tapping on the tooth. When inflammation and infec-
tion has progressed through the apical foramen, it is
described as a periapical abscess.
Dental infection may progress into the bone,
under the oral mucosa or into soft tissue spaces, and
form an abscess or spreading infection, with resultant
ongoing pain.
Cracked Tooth Syndrome.—Cracked tooth syn-
drome occurs when a crack has occurred in the dental
hard tissues and reaches the pulp chamber. The crack
is usually not visible to the naked eye. Pain because of
cracked tooth syndrome is classically intermittent,
provoked on biting or releasing biting on a hard
object, and is notoriously difficult to diagnose. It may
be described as sharp or sensitive, and is usually
related to mastication. The tooth may also become
sensitive to hot and cold stimuli. It is thought that the
pain is due to fluid shifts within the dentine tubules,
which are generated due to pressure differences as
the crack opens and closes during mastication. It can
be extremely difficult to diagnose.15
Dentine Sensitivity.—Pain because of dentine sen-
sitivity is classically stimulated by exposure to cold,
heat, sweet foods/drinks, and mechanical trauma such
as toothbrushing. The sensation is due to the move-
ment of fluid in dentinal tubules in response to

Headache
Fig 2.—Dental anatomy.
osmotic or temperature-related effects. Dentinal
tubules contain the processes of cells residing in the
dental pulp (odontoblasts), and fluid movement
appears to trigger nociceptive output by mechanisms
that are as yet unclear. Gingival recession can lead to
exposure of the endings of dentine tubules, as can loss
of enamel on the crown of the tooth. Dentinal sensi-
tivity is described as very rapid, fleeting, shooting
pain, or sensitivity, and is always in response to an
identifiable stimulus.
NON-DENTAL INTRAORAL PAIN
Intraoral pain may also arise from non-dental
structures.16 Oral mucosal malignancies such as squa-
mous cell carcinoma or salivary gland carcinoma may
be painful because of ulceration or perineural invasion.
Inflammatory oral mucosal diseases such as oral
lichen planus, recurrent aphthous stomatitis, vesi-
culobullous diseases, and oral mucosal infections such
as candidiasis or herpes viruses (herpes simplex, vari-
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
25
cella zoster) may all cause significant oral pain.
Patients with hematinic deficiencies, diabetes, hema-
tological malignancies, HIV/AIDS, and Behçet’s
disease may have significant oral mucosal pain and/or
ulceration. Examination will usually reveal the asso-
ciated oral mucosal abnormalities.17
Pain may be experienced in the oral cavity,face,and
neck because of salivary gland pathology. Blockage of a
major salivary gland duct may be due to infection,
mechanical obstruction by tumors, docholithiasis, or
ductal strictures. Obstruction of the duct will lead to
pain as the gland fills with saliva, which cannot be
released. Pain due to chronic ductal obstruction typi-
cally worsens preprandially or during meal times. Infec-
tion of the salivary glands will result in gland swelling,
pain, and erythema/warmth of the overlying skin.
Post-Traumatic Trigeminal Neuropathic Pain/
Atypical Odontalgia.—This definition encompasses
intraoral pain that is localized to a non-diseased den-
toalveolar structure, such as a tooth or an area of

26
alveolar ridge from which a tooth has previously been
extracted.18 The pain is often described as “burning,”
“shooting,” or “shock-like,” and there may be signifi-
cant hyperalgesia and allodynia of the affected
region, often with an associated area of hypoesthesia
or dysesthesia. The pain is usually continuous, with
some patients experiencing evoked severe episodes.
The area is usually clearly defined with little radia-
tion.19,20 Patients have described it as “nails being hit
the whole time” or “kicked in the face and left bruised
and burning.”
Controversy remains about nomenclature and
criteria for these conditions, and in this article, we
differentiate them by the presence or absence of a
precipitating event. It has been proposed that formal
neurophysiological testing would help distinguish
those with neuropathic pain compared with inflam-
matory causes.20-22 Patients with trigeminal neuro-
pathic pain have an identifiable traumatic episode
preceding the onset of the pain. The precipitating
event may include physical trauma such as facial
fractures, iatrogenic trauma such as restorative,
endodontic, or oral surgical procedures (apicectomy,
extraction, implant placement), prolonged severe
infection of dentoalveolar structures, or dental proce-
dures carried out with ineffective anesthesia.23 Tri-
geminal neuropathic pain is persistent and severe,
and associated with a high level of psychological dis-
tress and a risk of further iatrogenic harm because of
patients seeking ongoing dental or surgical interven-
tions for relief of pain.
Atypical odontalgia or persistent dentoalveolar
pain refers to a similar clinical presentation without a
clear precipitating event.24,25 “Persistent dentoalveo-
lar pain” is an ontological definition describing the
symptoms and signs without attributing a causation
or mechanism. Such definitions are developed using
analysis of patient interviews.26,27 These conditions are
usually managed along the same pathways as for
other neuropathic pain.28 Until there are internation-
ally agreed diagnostic criteria based on case–control
studies and more well-conducted trials have been
carried out, treatment of these conditions can vary
substantially between clinicians, leaving patients con-
fused and continually consulting in hope that a “cure”
will be found.
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
Burning Mouth Syndrome.—Burning mouth syn-
drome describes a collection of symptoms affecting
the oral cavity, including a “burning” or painful sen-
sation, often with an associated alteration in taste
sensation and an altered perception of the quality and
quantity of saliva. The symptoms are most commonly
localized to the tongue.29,30 On clinical examination,
the oral mucosa appears entirely normal. The area of
abnormal sensation does not typically follow ana-
tomic boundaries, is usually bilateral, and is continu-
ously present. Patients may describe their symptoms
as “discomfort” rather than pain. One patient
described their symptoms as a “Prickly feeling like an
injection wearing off,” and when choosing photo-
graphic images as representative of their symptom,
many choose images of fire.31 Other causes of oral
burning sensations such as hematinic deficiencies, dia-
betes, other systemic diseases, and oral infections
should be ruled out. The condition is most common in
perimenopausal or postmenopausal females, and is
strongly associated with psychological comorbidities
such as anxiety and depression.32 Patients often
report that their symptoms are worsened during
periods of psychological stress. The etiology of the
condition is unclear, although recent studies have sug-
gested the presence of a small-fiber sensory neuro-
pathy, thus suggesting it is a form of neuropathic
pain,33,34 but others propose a steroid dysregulation
mechanism.35 The condition can be difficult to
manage, and a variety of RCTs have been reported,
which include drug therapies and cognitive behavior
therapy.36-38 Research on this condition is difficult to
conduct in part due to its rarity and a lack of animal
models; however, studies are being undertaken that
indicate evidence of central changes on functional
magnetic resonance imaging (MRI), thus supporting
the hypothesis that there are definite neurophysi-
ological elements to this condition, rather than it
being a psychosomatic condition as has been previ-
ously suggested.
FACIAL PAIN WITH/WITHOUT
INTRAORAL PAIN
TMDs.—TMDs are the most common causes of
orofacial pain, affecting 10-15% of the population.39,40
Presenting features include pain localized to the

Headache
pre- and post-auricular areas, the angle and ramus of
the mandible, and the temporal region. There may be
associated clicking, sticking, or locking of the temporo-
mandibular joints. The pain may be intermittent or
continuous, and is usually described as dull, aching, or
throbbing, or in the words of patients: “weight on the
side of the face getting heavier and heavier,” “pressure
feeling,” “elastic band that is too tight,” or “needles
digging in.” Some patients experience pain that is sharp
or shooting in character, intermixed with dull continu-
ous pain. The pain commonly radiates into the tempo-
ral or occipital regions into the neck and across the
malar region of the face; it can be unilateral or bilat-
eral, and of varying severity. There may be an associ-
ated bruxing or clenching habit. The pain is typically
aggravated by opening the mouth wide, yawning, or
chewing. There may be limitation of mouth opening.41
TMD has historically been classified using the
Research Diagnostic Criteria into myofascial pain, disc
displacement, and other disorders,42,43 as the Interna-
tional Classification of Headache Disorders (ICHD)-II
of TMD was not useful in clinical settings.2 Newer clas-
sification criteria refer to myalgia, myofascial pain with
referral, and myalgia with disc involvement.41
A large prospective cohort study is currently
underway in the USA investigating the prognostic
factors related to the development of TMD.44-46 Par-
ticipants with and without TMD participate in a
battery of psychometric, biometric, and genetic tests.
Baseline data on the psychological characteristics of
the TMD cases demonstrate that this population
shows higher levels of distress, catastrophizing, and
increased somatic awareness compared with non-
TMD controls. A number of other studies have
reported similar findings.47-49
TMD has been linked with other psychological
and chronic pain conditions, including fibromyalgia,
back pain, headaches, chronic widespread pain, and
hypermobility.50-53 Degenerative temporomandibular
joint disease is rare but may occur in rheumatoid
arthritis. Interest has been raised recently in the pos-
sibility of TMD-related headache, which may involve
aspects of peripheral and central sensitization.54
Management of TMD is primarily conservative,
as in the majority of cases, the disorder is self-limiting.
Careful explanations are crucial as it has been shown
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
27
that patients experience a considerable amount of
uncertainty both in terms of diagnosis and then man-
agement, as dentists also often find it difficult to
manage.55-57 Approximately 10% of patients develop
chronic pain, and this has been linked to fibromyalgia,
depression, and chronic widespread pain.58 Therapies
used for TMD include simple analgesia, tricyclic anti-
depressants, occlusal splints or bite guards, diet modi-
fications, physiotherapy, cognitive behavioral therapy,
and surgery.59-61 Evidence for the majority of these
therapeutic options is poor, and there remains con-
siderable confusion about the best form of manage-
ment.7 Surgery is only indicated for TMD with
significant functional limitation or in cases with asso-
ciated degenerative joint disease or disc dysfunc-
tion.62 Education, psychological support and self-
management strategies are recommended as part of a
multidisciplinary approach to the management of
TMD, and these should be done early to reduce
costs.63-65 There remains considerable variation in the
way TMD is diagnosed and managed partly due to
conflicting evidence. It is anticipated that the large
US-based Orofacial Pain: Prospective Evaluation and
Risk Assessment (OPPERA) study will provide more
robust evidence, as it is a prospective study that has
enrolled asymptomatic participants.44-46
Giant Cell Arteritis.—Giant cell arteritis (GCA) is
an important differential diagnosis in any patient over
the age of 50 years presenting with temporal or pre-
auricular pain. This condition is potentially vision-
threatening and needs to be identified and treated
as a matter of urgency. The pain of GCA is often
described as “throbbing” and continuous, and may be
associated with jaw claudication, visual symptoms,
and systemic illness, including musculoskeletal pain in
the upper limbs (polymyalgia rheumatica). Clinical
examination may demonstrate a reduced pulse in a
tortuous temporal artery. Blood tests for erythrocyte
sedimentation rate and C-reactive protein (CRP)
should be performed urgently as these will assist in
confirmation of the diagnosis, followed by temporal
artery biopsy.66 If the clinical presentation is strongly
suggestive of GCA, treatment with high-dose cortico-
steroids should be commenced prior to the receipt of
test results, and urgent referral to ophthalmology
should be made to avoid loss of vision.67

28
Post-Herpetic Neuralgia.—Post-herpetic neuralgia
is a neuropathic pain arising after reactivation of
herpes virus species (most commonly varicella
zoster), which may involve branches of the trigeminal
nerve. The first division is most commonly affected;
however, involvement of the second or third divisions
may result in facial or intraoral neuropathic pain.
The pain is unilateral and restricted anatomically to
1 or more branches of the trigeminal nerve, and
is described as “burning” and continuous.18 History
often reveals an episode of herpes virus reactivation
including the presence of “blisters,” “ulcers,” or
vesicles on the skin or intraorally, associated with
extreme pain in the same region, which typically pre-
cedes the appearance of the vesicles. Pain may persist
for up to 6 weeks following an episode of herpes
virus reactivation, and allodynia is often present on
examination. Ongoing pain and neurological abnor-
malities 3-6 months following the acute episode is
classified as post-herpetic neuralgia and is common
in elderly patients, resulting in considerable impact
on quality of life.68 There is often a complaint of
severe itching. Management is as for other types of
neuropathic pain.69 However, it is important to treat
the acute episode with high-dose antiviral medica-
tions and even tricyclic antidepressants in elderly
patients as they are at higher risk of developing post-
herpetic neuralgia. Antiviral medication should be
commenced within 72 hours of the onset of rash/
vesicles but may be started up to 7 days following
onset, particularly in immunocompromised or older
individuals.70
Trigeminal Neuralgia.—Trigeminal neuralgia (TN)
is a condition characterized by episodic, usually
unilateral, severe attacks of facial pain, which are
often described as “shooting,” “electric shock-like,”
or “stabbing.” Metaphors used by patients include
“plugged into the mains and switched on and off” and
“rockets and explosions.” The pain attacks are of very
short duration (seconds) with a refractory period, and
periods of complete pain remission may occur, which
can last for months or even years.71 With time, the
remission periods tend to shorten. Some patients
describe a continuous dull ache or burning after an
acute attack, eg, “red hot iron being pushed and
turned inside the cheek,” and if this sensation persists,
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
it has variously been labeled as atypical TN, type 2
TN,72 or TN with concomitant pain.73 The pain is
restricted to the anatomical boundaries of divisions of
the trigeminal nerve and most commonly affects the
second and third divisions. The pain is triggered by
a variety of light touch stimuli, including talking,
eating or tooth-brushing, face-washing, or cold winds.
Patients will usually be able to identify a discrete
“trigger zone” within which sensory stimuli will
produce a pain attack. It is a severe and disabling
pain, and has a significant impact upon quality of life.
One of our patients described her TN experience as
follows: “My whole life was falling apart. My husband
was losing weight, everything was falling apart in our
house, my job and there was nothing I could do about
the pain.”
In some patients, there is an identifiable cause,
such as an intracranial lesion or a vascular compres-
sion of the trigeminal nerve.74 TN is reported in up to
3.8% of patients with multiple sclerosis.75 For this
reason, imaging (MRI) forms an essential part of
the work-up for TN. Management will depend on
whether there is an identifiable cause, but is primarily
medical, and aims to achieve symptom relief. Medical
management involves the use of anticonvulsants such
as carbamazepine or oxcarbazepine.74,76 Second line
agents include lamotrigine and baclofen. Because of
the increasing number of anticonvulsants now avail-
able, many patients are referred unnecessarily late for
surgical interventions that can offer the best quality-
of-life outcomes.77 Surgical procedures such as micro-
vascular decompression may be performed if there is
imaging evidence of a lesion affecting the trigeminal
nerve root, and the disease is causing a significant
impact on quality of life.78,79 Other less invasive sur-
gical procedures such as radiofrequency thermoco-
agulation, glycerol rhizotomy, balloon compression,
or gamma knife surgery tend to provide shorter
periods of pain relief and have a higher risk of sensory
loss. They are used in patients who are medically unfit
for major surgery such as microvascular decompres-
sion. It remains difficult for patients and clinicians to
make decisions about treatment due to a lack of high-
quality evidence. Some data suggest that many
patients prefer a surgical option rather than ongoing
medical management.80

Headache
Glossopharyngeal Neuralgia.—Glossopharyngeal
neuralgia has a similar presentation to TN, although
the location of the pain is different. Patients may
experience paroxysmal attacks of pain felt deeply in
the throat, ear, or posterior aspect of the tongue. The
triggers for pain attacks include chewing, talking,
drinking, and swallowing. The condition is usually
managed medically with anticonvulsant drugs.
Refractory cases may require surgery in the form of
microvascular decompression.81
Anesthesia Dolorosa.—Anesthesia dolorosa is a
condition arising from damage to the trigeminal
nerve, usually during surgery for TN. The condition
develops 3-6 months following the traumatic incident.
It is characterized by “painful numbness.” Patients
will report continuous facial pain in an area of numb-
ness, often described as “burning,” “pressure,” or
“stinging.” This is a typical patient description: “The
right side of my face, from my chin to above my right
eye, is numb and I frequently experience a ‘crawling’
sensation on the right side of my face and scalp. Also,
my face has quite a bit of pressure and feels as though
it is being pulled or tugged, as if in a visor.”
The pain is persistent, severe, and associated
with a high level of psychological distress and
comorbidity. It is often resistant to treatment. The
area involved may include all 3 divisions of the tri-
geminal nerve. Examination findings may include
objective sensory deficits, allodynia, and hyperalgesia
or hypoalgesia.82 Management options are as for
neuropathic pain, with psychological support playing
a significant role. In the new ICHD classification,
this entity has been named “painful post-traumatic
trigeminal neuropathy.”18
Persistent Idiopathic Facial Pain/Atypical Facial
Pain.—This term is used to describe a facial pain pre-
sentation that does not fit the clinical pattern for any
other diagnosis and is relatively rare.18,83 It is often
continuous, “nagging” and “dull” in nature, and is not
restricted by neurological anatomical boundaries.84,85
An example of a patient’s description of the pain is:
“Concrete poured into my head and then moving
around.”
There is a high level of associated psychological
comorbidity and a high prevalence of chronic pain
elsewhere in the body.5,32 It is often associated with
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
29
conditions such as irritable bowel syndrome and
chronic widespread pain. The etiology of the condi-
tion is unclear, although recent research has sug-
gested the possibility of a pathophysiology similar to
trigeminal neuropathic pain.86,87 There is often a
history of mental health problems that may predate
the pain. Management is often difficult and includes
medical and psychological input, using a multidisci-
plinary team approach.88-90 Because of the very broad
definition that has been proposed in the new ICHD
classification, this diagnosis will continue to be
applied to a very heterogeneous group of patients and
thus limit further research into the condition.18
HEADACHE-RELATED FACIAL PAIN
Migraine and Neurovascular Orofacial Pain.—
Migraine may manifest as facial pain either because
of referral or as a phenomenon referred to as atypical
or lower half migraine.91 Some authors have sug-
gested the presence of a separate entity that they
have named neurovascular orofacial pain (NVOP).92
This is a rare presentation and may mimic a number
of other orofacial pain diagnoses. The pain is usually
experienced in the distribution of the second or third
divisions of the trigeminal nerve and is episodic.
Attacks generally last for longer than 60 minutes. It is
often described as “throbbing” and may have accom-
panying autonomic signs or systemic symptoms such
as nausea. Patients may also complain of dental sen-
sitivity, which can introduce diagnostic difficulties as
patients pursue treatment for a perceived dental
source of pain. NVOP has features in common with
migraine as well as trigeminal autonomic ceph-
alalgias, and it is suggested that NVOP may represent
“relocated” migraine.93 It is important to differentiate
NVOP from dental pulpal pathology, with which it is
often confused due to the presence of dental sensitiv-
ity during attacks. A case series of 7 lower facial
migraines showed that all cases responded to triptans,
and 3 responded to migraine prophylactic measures.94
Case–control studies from a range of different clinical
settings are necessary in order to provide more evi-
dence for the presence of this entity, as its manage-
ment can be substantially different to other orofacial
pain diagnoses.

30
Trigeminal Autonomic Cephalalgias.—This group
includes cluster headache, paroxysmal hemicrania,
short-lasting unilateral neuralgiform headache
attacks with cranial autonomic features, and short-
lasting unilateral neuralgiform headache attacks with
conjunctival injection and tearing. These headaches
are characterized by unilateral head or facial pain
with cranial autonomic features that occur ipsilater-
ally and at the same time as the pain.18 Patients with
these disorders may present to facial pain clinics, as
the facial pain component may be more significant
than the headache. Accurate history-taking is essen-
tial in formulating this diagnosis, as patients may be
unaware of the autonomic symptoms unless specifi-
cally asked. Comprehensive discussion of these disor-
ders may be found in the literature. However, more
careful phenotyping and larger case series are neces-
sary to determine which of these diagnoses are
unique entities and which may represent a continuum
in the natural history of these disorders.95,96
TMD-Related Headache.—Recent studies have
described an association between TMD and head-
ache. Many patients with TMD also report headache,
and in some cases, there is a clear relationship
between temporomandibular joint-related triggers
and headache onset.97 TMD is also common among
migraine and tension-type headache sufferers.98
A HOLISTIC APPROACH TO FACIAL PAIN
The History.—Accurate and comprehensive
history-taking is essential in order to gather sufficient
information in order to formulate a diagnosis and
treatment plan.99 The medical consultation has been
described as “a transaction that involves translation,”
and further that “the physician’s concern is to trans-
late the subjective experience of illness into the rec-
ognizable discourse of medicine.”100 It has also been
suggested that we should not be “taking” a history but
“receiving it.”100 Inaccurate or inappropriate “transla-
tion” can lead to inaccuracy of diagnosis and impair
the therapeutic relationship.
Our unit advocates the use of a structured or
semistructured history in order to ensure consistency
in history-taking and documentation, and to assist in
diagnostic accuracy. An open-ended style of history-
taking, rather than an interrogative approach, often
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
yields important information and ensures that
patients feel they have been listened to and their
health beliefs understood.101,102 Building a therapeutic
relationship is essential in the assessment and man-
agement of chronic pain. Ensuring sufficient duration
for the initial consultation, allowing the patient time
to speak and express their ideas regarding the pain,
and eliciting and understanding patient expectations
are all essential for successful pain management.103 A
recent study of 12 patients interviewed preconsulta-
tion and post-consultation in a pain clinic, without the
knowledge of the clinicians involved, provided some
of these comments:
I guess what the appointment has done is
drawn a line under it and made me think, well,
that’s fine but nothing can be done about it so I
just need to get on with things.
Even though I haven’t come away with a
cure, I feel in a better position to cope with my
symptoms.
I felt xxx listened to me more than the other
healthcare professionals I have seen and took
into account the effects the pain was having on
my life in general, rather than just treating me as
a diagnosis.104
In addition to the standard pain history, psychiat-
ric comorbidities must be identified and addressed
early in the therapeutic relationship, as they may have
been present before the onset of the pain.15 It is also
essential to elicit detailed information regarding
social history, major life events, psychosocial stressors,
and the impact of pain on the patient’s ability to
participate in the activities of daily living. Many
patients with facial pain who present to secondary
care or pain clinics have attended consultations with a
large number of primary and secondary care provid-
ers, and may have had multiple investigations or inter-
ventions for their pain.7,102,105 This is illustrated by the
following patient quotation: “A lot of people would
think [that consulting a] dentist, max facs [maxillo-
facial surgery], neurologist was already over the top
but I wanted to be certain that I’d tried everything.”
These patients often have a significant level of
psychological distress, and this can impact negatively
on the therapeutic relationship and management
strategies. Understanding the patient’s expectations

Headache
and illness beliefs, and assessing negative prognostic
factors such as catastrophizing or low self-efficacy
levels is essential in order to formulate an appro-
priate treatment plan using the biopsychosocial
model that will then require a multidisciplinary team
approach.106
Psychological screening tools such as the
National Institutes of Clinical Excellence depression
screening questions, the Hospital Anxiety and
Depression Scale, Patient Health Questionnaire, and
the Beck Depression Inventory are useful for quan-
tifying the degree of psychological comorbidity.107 The
inclusion of an objective measure of pain impact on
quality of life is essential in every facial pain consul-
tation; the Graded Chronic Pain Scale, Brief Pain
Inventory (including the extended version),108 the
Pain Catastrophizing Scale, and the EuroQoL scale
are useful tools. However, these measures need to be
carefully interpreted in the context of the patient’s
comorbidities. As 1 patient commented: “And if
you’re very depressed and it’s hard to verbalize how
you feel about things, or whether you can’t just mark
on a scale between nought and ten what your pain is
like, you know, what’s your pain, is it nought or is it
ten?”31
Diagnostic Considerations.—There is also the pro-
pensity for clinicians to “label” patients with a diag-
nosis, with the expectation that this will enable the
patient to accept the condition and progress with
treatment. This approach may be helpful for some
patients – 1 patient stated: “I was quite relieved to
have a diagnosis . . . although I had hoped I would
come away with a solution for a cure, I am happy now
that I know the cause and that it is not serious.”104
However, our experience is that this is often not
the case. Some facial pain presentations are diagnos-
tically challenging, and the evolution of symptoms
over time may either clarify, or rule out, the diagnosis
initially given. Extant classification systems may also
hinder diagnosis or result in inaccurate labeling. It has
been found that the number of patients whose symp-
toms could not be classified as a specific diagnosis was
larger in ICHD-II than in ICHD-I, with particular
difficulty experienced in patients with persistent idio-
pathic facial pain.109 In a study examining the useful-
ness of the ICHD-II classification criteria, only 56% of
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
31
patients were successfully diagnosed with orofacial
pain using ICHD-II.2 Applying American Academy of
Orofacial Pain (AAOP)/Research Diagnostic Criteria
for Temporomandibular Disorders (RDCTMD) crite-
ria, a further 37% were diagnosed with masticatory
myofascial pain (MMP), and further published criteria
enabled the remaining patients to be allocated to other
predefined diagnoses. The authors concluded that
while MMP is clearly defined by AAOP and the
RDCTMD, expansion of ICHD-II was needed so as to
integrate more orofacial pain syndromes.
It may be better to give no diagnosis rather than
the wrong diagnosis, as revising a diagnosis that has
previously been presented to the patient as definitive
can be damaging to the therapeutic relationship and
the patient’s confidence in the clinician. The use of a
grading system such as “definite,”“probable,” or “pos-
sible” has been suggested for use when diagnosing
neuropathic pain.110 This classification could be
extended to other orofacial pain diagnoses as a means
of managing the uncertainty in providing diagnoses
for conditions that have varied clinical presentations.
Ontological approaches to the diagnosis and classifi-
cation of facial pain syndromes aim to reduce the
problems associated with “labeling” and focus on the
use of purely descriptive terms with no inferences
made regarding mechanism or etiology.27
“Labeling” or compartmentalizing patients into
diagnostic categories also ignores the multifaceted
nature of chronic pain syndromes, particularly
orofacial pain. The patient is not the diagnosis –
rather the pain condition has occurred in a patient
who exists within a milieu of social, cultural, psycho-
logical, and cognitive influences. Patients’ beliefs
about their condition will also affect their disability
and outcome,111 as the quote in Figure 3 illustrates.
Recognizing the significance of these contributory
factors to the overall presentation is essential for
effective therapeutic dialogue as well as good man-
agement of pain.
This concept has been further explored in a
recent series of qualitative studies examining
patients’ experience and perception of orofacial
pain.26,102,105 As with any other chronic pain psycho-
logical factors will increase pain disability.112
Orofacial pain syndromes often co-exist with signifi-

32
Fig 3.—Extract from a patient letter about treatment of her
orofacial pain.
cant psychological morbidity, probably more so than
other types of chronic pain,10,113 and are risk factors
for chronicity.114 Addressing these factors is essential
for appropriate management of the orofacial pain, as
treatment outcome has been shown to be related to
psychological comorbidity.49 Affective as well as inter-
pretative and cognitive factors play an important role
in the patient’s perception of pain. One small quali-
tative study found that their patients perceived their
orofacial pain to “have no limits and to repressively
permeate all aspects of their existence: social, practi-
cal, and emotional.”105 This illustrates the significant
impact that orofacial pain can have on quality of life,
and provides a focal point for assessment of pain
management outcomes. Patients need to know that
although the sensation of pain may not be completely
alleviated by treatment, the impact of pain upon their
daily life can certainly be modulated.
Management.—Chronic pain management should
be holistic in nature and approach, and involves
addressing all the factors that modulate the pain expe-
rience.7 Addressing unrealistic patient expectations is
important for setting achievable treatment goals.
There remains a common perception that pain should
always be curable, as demonstrated in this quote from
a patient:“Many don’t understand the pain I feel.They
think I should be over this pain by now. Others feel I
should seek other doctors. They feel there should be
something to relieve this terrible pain and ask me why
I’m not trying to find it, if it is so bad.”
Pain as defined by International Association for
the Study of Pain is both a “sensory and emotional
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
experience,” and it should be managed as such. A
recent study has shown that chronic musculoskeletal
pain can be experienced as a “constant adversarial
struggle,” and the researchers suggest that patient and
clinician expectations of a diagnosis and cure need
to be challenged.115 Beliefs, coping strategies, and
catastrophizing predict functioning in patients with
chronic pain, and this should be considered when
individualizing pain management programs.116 This
extends to patients’ beliefs about medication as these
will influence adherence.117
Successful pain management is also related to the
patient’s self-efficacy beliefs and ability to learn and use
positive coping strategies.118 Recognition of the contri-
bution of social, psychological, and lifestyle factors to
the pain experience, as expressed in the patient quote
earlier, is essential for taking the next steps in chronic
pain management and achieving a reduction in the
impact of pain on quality of life. The provision of
support for these next steps is a fundamental part of
multidisciplinary pain management. Pain management
programs delivered in group settings normalizes the
pain experience, and the concept of an improved pain
experience because of observation of others with a
similar complaint is also expressed by the patient
quoted earlier. Newer techniques such as an e-learning
cognitive behavioral therapy model can be helpful.119
Supported but self-directed pain management focused
around lifestyle change and reducing the impact of pain
on quality of life is a more effective management
approach in chronic pain than the traditional, didactic
biomedical model, but these strategies need to be tai-
lored appropriately.120
CONCLUSION
Orofacial pain in its fullest definition affects up to
a quarter of the population, and the associated mor-
bidity, social impact, and health costs can be high if
these conditions are not accurately diagnosed and
managed in a timely fashion. Recognition of the
significant contribution and high prevalence of psy-
chological distress and comorbidity is essential for
successful management. Multidisciplinary approaches
and a biopsychosocial model of pain management are
an essential adjunct to established evidence-based
medical and surgical management of these conditions.
 15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
Headache 33

Table.—Summary of Management

Management of dental pain

Pulpitis Removal of irritant, eg, dental caries and restorative or endodontic treatment, or extraction
Cracked tooth Reducing movement across crack, eg, full-coverage restoration of tooth, may require endodontic
treatment or extraction
Dentine sensitivity Desensitizing agent application, dental restoration to cover exposed dentine
Abscess Remove source of infection
Management of non-dental intraoral pain
Oral malignancy Surgical resection ± chemoradiotherapy
Opioid analgesia
Inflammatory oral Topical anti-inflammatory agents
mucosal disease Systemic and topical steroids
Systemic immunosuppressants (rarely)
Salivary duct blockage Sialography, irrigation, and ductal dilatation
Endoscopic removal of stone
Lithotripsy of stone
Antibiotics for infection
Surgical removal of gland
Trigeminal neuropathic Topical anesthetics
pain Tricyclic antidepressants
Anticonvulsants
Psychological approaches
Atypical odontalgia As above
Burning mouth Clonazepam
syndrome Tricyclic antidepressants
Psychological approaches
Management of facial pain with/without intraoral pain
Temporomandibular Conservative management and simple analgesia
joint disorder Surgical intervention (in specific scenarios)
Psychological approaches
Giant cell arteritis Early initiation of high-dose systemic steroids
Post-herpetic neuralgia Systemic antiviral medication
Tricyclic antidepressants
Anticonvulsants
Psychological approaches
Trigeminal neuralgia Carbamazepine/oxcarbazepine
Lamotrigine, pregabalin
Microvascular decompression and other ablative procedures
Glossopharyngeal As for trigeminal neuralgia
neuralgia Surgical management options include microvascular decompression
Anesthesia dolorosa Tricyclic antidepressants
Anticonvulsants
Pregabalin/gabapentin
or combinations of above drugs
Psychological approaches
Persistent idiopathic Tricyclic antidepressants
facial pain SNRIs
Cognitive behavioral therapy
Management of headache-related facial pain
Migraine/neurovascular Acute:
orofacial pain Simple analgesia/NSAIDs ± anti-emetics
Triptans
Preventative:
Beta-blockers
Tricyclic antidepressants
Topiramate/sodium valproate
Gabapentin
 15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
34 January 2014

Table.—Continued

Cluster headache Acute:

Oxygen
Triptans
Preventative:
Prednisolone (bridging)
Verapamil
Lithium
Methysergide
SUNCT/SUNA Lamotrigine
Oxcarbazepine
Topiramate
Gabapentin
Intravenous lidocaine
Paroxysmal hemicrania Indomethacin
TMD-related headache NSAIDs
Physiotherapy
Psychological approaches

NSAID = non-steroidal anti-inflammatory drug; SNRI = serotonin-norepinephrine reuptake inhibitor; SUNA = short-lasting uni-
lateral neuralgiform headache attacks with cranial autonomic features; SUNCT = short-lasting unilateral neuralgiform headache
attacks with conjunctival injection and tearing; TMD = temporomandibular disorder.

Acknowledgment: JZ undertook this work at UCL/ REFERENCES

UCLHT, who received a proportion of funding from 1. Zakrzewska JM, Hamlyn PJ. Facial pain. In:
the Department of Health’s NIHR Biomedical Research Crombie IK, Croft PR, Linton SJ, et al, eds. Epide-
Centre funding scheme. miology of Pain. Seattle, WA: IASP Press; 1999:
171-202.
STATEMENT OF AUTHORSHIP 2. Benoliel R, Birman N, Eliav E, Sharav Y. The
International Classification of Headache Dis-
Category 1 orders: Accurate diagnosis of orofacial pain?
(a) Conception and Design Cephalalgia. 2008;28:752-762.
Martina K. Shephard, Joanna M. Zakrzewska 3. Bell GW, Smith GL, Rodgers JM, Flynn RW,
(b) Acquisition of Data Malone CH. Patient choice of primary care practi-
Martina K. Shephard, Joanna M. Zakrzewska tioner for orofacial symptoms. Br Dent J. 2008;204:
(c) Analysis and Interpretation of Data 669-673.
Martina K. Shephard, E. Anne MacGregor, 4. Wirz S, Ellerkmann RK, Buecheler M, Putensen C,
Joanna M. Zakrzewska Nadstawek J, Wartenberg HC. Management of
chronic orofacial pain: A survey of general dentists
Category 2 in german university hospitals. Pain Med. 2010;11:
(a) Drafting the Manuscript 416-424.
Martina K. Shephard 5. Aggarwal VR, McBeth J, Zakrzewska JM, Lunt M,
(b) Revising It for Intellectual Content Macfarlane GJ. The epidemiology of chronic syn-
Martina K. Shephard, E. Anne MacGregor, dromes that are frequently unexplained: Do they
Joanna M. Zakrzewska have common associated factors? Int J Epidemiol.
2006;35:468-476.
Category 3 6. Hargreaves KM. Orofacial pain. Pain. 2011;152:
(a) Final Approval of the Completed Manuscript S25-S32.
Martina K. Shephard, E. Anne MacGregor, 7. Beecroft EV, Durham J, Thomson P. Retrospective
Joanna M. Zakrzewska examination of the healthcare “journey” of chronic

Headache
orofacial pain patients referred to oral and maxil-
lofacial surgery. Br Dent J. 2013;214:E12.
8. Rollman A, Visscher CM, Gorter RC, Naeije M.
Care seeking for orofacial pain. J Orofac Pain.
2012;26:206-214.
9. Reid KJ, Harker J, Bala MM, et al. Epidemiology
of chronic non-cancer pain in Europe: Narrative
review of prevalence, pain treatments and pain
impact. Curr Med Res Opin. 2011;27:449-462.
10. Sipila K, Ylostalo PV, Joukamaa M, Knuuttila ML.
Comorbidity between facial pain, widespread pain,
and depressive symptoms in young adults. J Orofac
Pain. 2006;20:24-30.
11. Schatman ME. Preface. In: Schatman ME, ed.
Ethical Issues in Chronic Pain Management. New
York: Informa Healthcare US; 2007:v-vii.
12. Morris DB. Intractable pain and the perception of
time: Every patient is an anecdote. In: Stannard C,
Kalso E, Ballantyne J, eds. Evidence-Based Chronic
Pain Managment, 1st edn. West Sussex: Blackwell
Publishing Ltd; 2010:52-58.
13. Hegarty AM, Zakrzewska JM. Differential diagno-
sis for orofacial pain, including sinusitis, TMD,
trigeminal neuralgia. Dent Update. 2011;38:396-
408.
14. Mitchell L, Mitchell DA. Oxford Handbook of
Clinical Dentistry, 5th edn. Oxford: Oxford Univer-
sity Press; 2009.
15. Banerji S, Mehta SB, Millar BJ. Cracked tooth syn-
drome. Part 1: Aetiology and diagnosis. Br Dent J.
2010;208:459-463.
16. Vickers ER, Zakrzewska JM. Dental causes of
orofacial pain. In: Zakrzewska JM, ed. Orofacial
Pain, 1st edn. Oxford: Oxford University Press;
2009.
17. Scully C. Oral and Maxillofacial Medicine: The
Basis of Diagnosis and Treatment, 3rd edn. London:
Churchill Livingstone c/o Elsevier Ltd; 2013.
18. Headache Classification Committee of the Interna-
tional Headache Society. The International Classi-
fication of Headache Disorders, 3rd edition (beta
version). Cephalalgia. 2013;33:629-808.
19. Baad-Hansen L, Leijon G, Svensson P, List T.
Comparison of clinical findings and psychosocial
factors in patients with atypical odontalgia and
temporomandibular disorders. J Orofac Pain. 2008;
22:7-14.
20. Benoliel R, Zadik Y, Eliav E, Sharav Y. Peripheral
painful traumatic trigeminal neuropathy: Clinical
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
35
features in 91 cases and proposal of novel diagnos-
tic criteria. J Orofac Pain. 2012;26:49-58.
21. Forssell H, Tenovuo O, Silvoniemi P, Jaaskelainen
SK. Differences and similarities between atypical
facial pain and trigeminal neuropathic pain. Neu-
rology. 2007;69:1451-1519.
22. Jaaskelainen SK, Teerijoki-Oksa T, Forssell H.
Neurophysiologic and quantitative sensory testing
in the diagnosis of trigeminal neuropathy and neu-
ropathic pain. Pain. 2005;117:349-357.
23. Renton T, Yilmaz Z. Profiling of patients present-
ing with posttraumatic neuropathy of the trigemi-
nal nerve. J Orofac Pain. 2011;25:333-344.
24. Baad-Hansen L, List T, Jensen TS, Svensson P.
Increased pain sensitivity to intraoral capsaicin in
patients with atypical odontalgia. J Orofac Pain.
2006;20:107-114.
25. Baad-Hansen L. Atypical odontalgia – Pathophysi-
ology and clinical management. J Oral Rehabil.
2008;35:1-11.
26. Durham J, Exley C, John MT, Nixdorf DR. Persis-
tent dentoalveolar pain: The patient’s experience. J
Orofac Pain. 2013;27:6-13.
27. Nixdorf DR, Drangsholt MT, Ettlin DA, et al. Clas-
sifying orofacial pains: A new proposal of tax-
onomy based on ontology. J Oral Rehabil. 2012;39:
161-169.
28. Napenas JJ, Zakrzewska JM. Diagnosis and man-
agement of trigeminal neuropathic pains. Pain
Manag. 2011;1:353-365.
29. Grushka M. Clinical features of burning mouth
syndrome. Oral Surg Oral Med Oral Pathol. 1987;
63:30-36.
30. Woda A, Grushka M. Burning mouth syndrome. In:
Zakrzewska JM, ed. Orofacial Pain, 1st edn.
Oxford: Oxford University Press; 2009:83-92.
31. Padfield D. MASK: MIRROR: MEMBRANE The
photograph as a mediating space in clinical and
creative pain encounters. PhD. London: University
of London; 2013.
32. Taiminen T, Kuusalo L, Lehtinen L, et al. Psychiat-
ric (axis 1) and personality (axis 11) disorders in
patients with burning mouth syndrome or atypical
facial pain. Scand J Pain. 2011;2:155-160.
33. Forssell H, Jaaskelainen S, Tenovuo O, Hinkka S.
Sensory dysfunction in burning mouth syndrome.
Pain. 2002;99:41-47.
34. Albuquerque RJ, de Leeuw R, Carlson CR,
Okeson JP, Miller CS, Andersen AH. Cerebral

36
activation during thermal stimulation of patients
who have burning mouth disorder: An fMRI study.
Pain. 2006;122:223-234.
35. Woda A, Dao T, Gremeau-Richard C. Steroid
dysregulation and stomatodynia (burning mouth
syndrome). J Orofac Pain. 2009;23:202-210.
36. Zakrzewska JM, Glenny AM, Forssell H. Interven-
tions for the treatment of burning mouth syn-
drome. Cochrane Database Syst Rev. 2005;(1)
CD002779.
37. Lewis MA, Sankar V, De Laat A, Benoliel R. Man-
agement of neuropathic orofacial pain. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod. 2007;
103(Suppl.):S32-S24.
38. de Moraes M, do Amaral Bezerra BA, da
Rocha Neto PC, de Oliveira Soares AC, Pinto LP,
de Lisboa Lopes Costa A. Randomized trials for
the treatment of burning mouth syndrome: An
evidence-based review of the literature. J Oral
Pathol Med. 2012;41:281-287.
39. Drangsholt M, LeResche L. Temporomandibular
disorder pain. In: Crombie IK, Croft PR, Linton SJ,
LeResche L, eds. Epidemiology of Pain, 1st edn.
Seattle, WA: IASP; 1999:203-233.
40. Janal MN, Raphael KG, Nayak S, Klausner J.
Prevalence of myofascial temporomandibular dis-
order in US community women. J Oral Rehabil.
2008;35:801-809.
41. Schiffman E, Ohrbach R, Truelove E, et al. Diag-
nostic criteria for temporomandibular disorders
(DC/TMD) for clinical and research applications:
Recommendations of the International RDC/
TMD Consortium Network and Orofacial Pain
Special Interest Group. J Orofac Pain. In press.
42. Dworkin SF, LeResche L. Research Diagnostic
Criteria for Temporomandibular Disorders:
Review, criteria, examinations and specifications,
critique. J Craniomandib Disord. 1992;6:301-355.
43. Hasanain F, Durham J, Moufti A, Steen IN, Wassell
RW. Adapting the diagnostic definitions of the
RDC/TMD to routine clinical practice: A feasibil-
ity study. J Dent. 2009;37:955-962.
44. Fillingim RB, Ohrbach R, Greenspan JD, et al.
Potential psychosocial risk factors for chronic
TMD: Descriptive data and empirically identified
domains from the OPPERA case-control study. J
Pain. 2011;12:T46-T60.
45. Fillingim RB, Slade GD, Diatchenko L, et al.
Summary of findings from the OPPERA baseline
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
case-control study: Implications and future direc-
tions. J Pain. 2011;12:T102-T107.
46. Slade GD, Bair E, By K, et al. Study methods,
recruitment, sociodemographic findings, and demo-
graphic representativeness in the OPPERA study.
J Pain. 2011;12:T12-T26.
47. Reissmann DR, John MT, Schierz O, Seedorf H,
Doering S. Stress-related adaptive versus maladap-
tive coping and temporomandibular disorder pain.
J Orofac Pain. 2012;26:181-190.
48. Turner JA, Dworkin SF, Mancl L, Huggins KH,
Truelove EL. The roles of beliefs, catastrophizing,
and coping in the functioning of patients with tem-
poromandibular disorders. Pain. 2001;92:41-51.
49. Gustin SM, Wilcox SL, Peck CC, Murray GM,
Henderson LA. Similarity of suffering: Equiva-
lence of psychological and psychosocial factors in
neuropathic and non-neuropathic orofacial pain
patients. Pain. 2011;152:825-832.
50. Wiesinger B, Malker H, Englund E, Wanman A.
Back pain in relation to musculoskeletal disorders
in the jaw-face:A matched case-control study. Pain.
2007;131:311-319.
51. Balasubramaniam R, de Leeuw R, Zhu H,
Nickerson RB, Okeson JP, Carlson CR. Prevalence
of temporomandibular disorders in fibromyalgia
and failed back syndrome patients: A blinded pro-
spective comparison study. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2007;104:204-216.
52. Slade GD, Sanders AE, Bair E, et al. Preclinical
episodes of orofacial pain symptoms and their asso-
ciation with health care behaviors in the OPPERA
prospective cohort study. Pain. 2013;154:750-760.
53. Abel MD, Carrasco LR. Ehlers-Danlos syndrome:
Classifications, oral manifestations, and dental con-
siderations. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2006;102:582-590.
54. Anderson GC, John MT, Ohrbach R, et al. Influ-
ence of headache frequency on clinical signs and
symptoms of TMD in subjects with temple head-
ache and TMD pain. Pain. 2011;152:765-771.
55. Durham J, Steele JG, Wassell RW, Exley C. Living
with uncertainty: Temporomandibular disorders. J
Dent Res. 2010;89:827-830.
56. Aggarwal VR, Joughin A, Zakrzewska JM,
Crawford FJ, Tickle M. Dentists’ and specialists’
knowledge of chronic orofacial pain: Results from
a continuing professional development survey.
Prim Dent Care. 2011;18:41-44.

Headache
57. Durham J, Exley C, Wassell R, Steele JG. “Man-
agement is a black art” – professional ideologies
with respect to temporomandibular disorders. Br
Dent J. 2007;202:E29.
58. Velly AM, Look JO, Schiffman E, et al. The effect
of fibromyalgia and widespread pain on the clini-
cally significant temporomandibular muscle and
joint pain disorders – a prospective 18-month
cohort study. J Pain. 2010;11:1155-1164.
59. List T, Axelsson S. Management of TMD: Evidence
from systematic reviews and meta-analyses. J Oral
Rehabil. 2010;37:430-451.
60. Fricton J, Look JO, Wright E, et al. Systematic
review and meta-analysis of randomized controlled
trials evaluating intraoral orthopedic appliances
for temporomandibular disorders. J Orofac Pain.
2010;24:237-254.
61. Mujakperuo HR, Watson M, Morrison R,
Macfarlane TV. Pharmacological interventions for
pain in patients with temporomandibular disorders.
Cochrane Database Syst Rev. 2010;(10)CD004715.
62. Guo C, Shi Z, Revington P. Arthrocentesis and
lavage for treating temporomandibular joint disor-
ders. Cochrane Database Syst Rev. 2009;(4)
CD004973.
63. Gatchel RJ, Stowell AW, Wildenstein L, Riggs R,
Ellis E III. Efficacy of an early intervention for
patients with acute temporomandibular disorder-
related pain: A one-year outcome study. J Am Dent
Assoc. 2006;137:339-347.
64. Michelotti A, Iodice G, Vollaro S, Steenks MH,
Farella M. Evaluation of the short-term effective-
ness of education versus an occlusal splint for the
treatment of myofascial pain of the jaw muscles. J
Am Dent Assoc. 2012;143:47-53.
65. Michelotti A, Steenks MH, Farella M, Parisini F,
Cimino R, Martina R. The additional value of a
home physical therapy regimen versus patient edu-
cation only for the treatment of myofascial pain of
the jaw muscles: Short-term results of a random-
ized clinical trial. J Orofac Pain. 2004;18:114-125.
66. Meisner RJ, Labropoulos N, Gasparis AP,
Tassiopoulos AK. How to diagnose giant cell arte-
ritis. Int Angiol. 2011;30:58-63.
67. Kale N, Eggenberger E. Diagnosis and manage-
ment of giant cell arteritis: A review. Curr Opin
Ophthalmol. 2010;21:417-422.
68. Bouhassira D, Chassany O, Gaillat J, et al. Patient
perspective on herpes zoster and its complications:
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
37
An observational prospective study in patients
aged over 50 years in general practice. Pain. 2012;
153:342-349.
69. O’Connor AB, Dworkin RH. Treatment of neuro-
pathic pain: An overview of recent guidelines. Am J
Med. 2009;122:S22-S32.
70. Dworkin RH, Johnson RW, Breuer J, et al. Recom-
mendations for the management of herpes zoster.
Clin Infect Dis. 2007;44(Suppl. 1):S1-26.
71. Katusic S, Beard CM, Bergstralh E, Kurland LT.
Incidence and clinical features of trigeminal
neuralgia, Rochester, Minnesota, 1945-1984. Ann
Neurol. 1990;27:89-95.
72. Limonadi FM, McCartney S, Burchiel KJ. Design
of an artificial neural network for diagnosis of
facial pain syndromes. Stereotact Funct Neurosurg.
2006;84:212-220.
73. Obermann M, Yoon MS, Ese D, et al. Impaired
trigeminal nociceptive processing in patients with
trigeminal neuralgia. Neurology. 2007;69:835-
841.
74. Cruccu G, Gronseth G, Alksne J, et al. AAN-EFNS
guidelines on trigeminal neuralgia management.
Eur J Neurol. 2008;15:1013-1028.
75. Foley PL, Vesterinen HM, Laird BJ, et al. Preva-
lence and natural history of pain in adults with
multiple sclerosis: Systematic review and meta-
analysis. Pain. 2013;154:632-642.
76. Gronseth G, Cruccu G, Alksne J, et al. Practice
parameter: The diagnostic evaluation and treat-
ment of trigeminal neuralgia (an evidence-based
review): Report of the Quality Standards Subcom-
mittee of the American Academy of Neurology and
the European Federation of Neurological Societ-
ies. Neurology. 2008;71:1183-1190.
77. Zakrzewska JM, Lopez BC, Kim SE, Coakham
HB. Patient reports of satisfaction after microvas-
cular decompression and partial sensory rhizotomy
for trigeminal neuralgia. Neurosurgery. 2005;56:
1304-1311.
78. Zakrzewska JM, Akram H. Neurosurgical inter-
ventions for the treatment of classical trigeminal
neuralgia. Cochrane Database Syst Rev. 2011;(9)
CD007312.
79. Zakrzewska JM, Coakham HB. Microvascular
decompression for trigeminal neuralgia: Update.
Curr Opin Neurol. 2012;25:296-301.
80. Spatz AL, Zakrzewska JM, Kay EJ. Decision
analysis of medical and surgical treatments for tri-

38
geminal neuralgia: How patient evaluations of ben-
efits and risks affect the utility of treatment
decisions. Pain. 2007;131:302-310.
81. Patel A, Kassam A, Horowitz M, Chang YF. Micro-
vascular decompression in the management of
glossopharyngeal neuralgia: Analysis of 217 cases.
Neurosurgery. 2002;50:705-710.
82. Headache Classification Subcommittee of the
International Headache Society (IHS). The Inter-
national Classification of Headache Disorders (2nd
edition). Cephalalgia. 2004;24:1-160.
83. Mueller D, Obermann M, Yoon MS, et al. Preva-
lence of trigeminal neuralgia and persistent idio-
pathic facial pain: A population-based study.
Cephalalgia. 2011;31:1542-1548.
84. Zebenholzer K, Wober C, Vigl M, Wessely P,
Wober-Bingol C. Facial pain and the Second
Edition of the International Classification of Head-
ache Disorders. Headache. 2006;46:259-263.
85. Pfaffenrath V, Rath M, Pollmann W, Keeser W.
Atypical facial pain – application of the IHS crite-
ria in a clinical sample. Cephalalgia. 1993;13(Suppl.
12):84-88.
86. Schmidt-Wilcke T, Hierlmeier S, Leinisch E.
Altered regional brain morphology in patients
with chronic facial pain. Headache. 2010;50:1278-
1285.
87. Jaaskelainen SK, Forssell H, Tenovuo O. Electro-
physiological testing of the trigeminofacial system:
Aid in the diagnosis of atypical facial pain. Pain.
1999;80:191-200.
88. Jensen R, Mitsikostas DD, Wober C. Persistent
idiopathic facial pain. In: Martelletti P, Steiner TJ,
eds. Handbook of Headache. Milan: Practical Man-
agement Springer; 2011:505-513.
89. Harrison SD, Glover L, Feinmann C, Pearce SA,
Harris M. A comparison of antidepressant medica-
tion alone and in conjunction with cognitive
behavioural therapy for chronic idiopathic facial
pain. In: Jensen TS, Turner JA, Wiesenfeld-Hallin
Z, eds. Proceedings of the Eighth World Congress
on Pain. Progress in Pain Research and Manage-
ment. Vol. 8. Seattle, WA: IASP Press; 1997:663-
672.
90. List T, Axelsson S, Leijon G. Pharmacologic
interventions in the treatment of temporoman-
dibular disorders, atypical facial pain, and burning
mouth syndrome. A qualitative systematic review. J
Orofac Pain. 2003;17:301-310.
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
January 2014
91. Yoon MS, Mueller D, Hansen N, et al. Prevalence
of facial pain in migraine: A population-based
study. Cephalalgia. 2010;30:92-96.
92. Benoliel R, Sharav Y. Neurovascular orofacial
pain. Cephalalgia. 2008;28:199-200.
93. Hussain A, Stiles MA, Oshinsky ML. Pain remap-
ping in migraine: A novel characteristic following
trigeminal nerve injury. Headache. 2010;50:669-
671.
94. Obermann M, Mueller D, Yoon MS, Pageler L,
Diener H, Katsarava Z. Migraine with isolated
facial pain: A diagnostic challenge. Cephalalgia.
2007;27:1278-1282.
95. Goadsby PJ, Cittadini E, Cohen AS. Trigeminal
autonomic cephalalgias: Paroxysmal hemicrania,
SUNCT/SUNA, and hemicrania continua. Semin
Neurol. 2010;30:186-191.
96. Goadsby PJ. Trigeminal autonomic cephalalgias.
Continuum. 2012;18:883-895.
97. Schiffman E, Ohrbach R, List T, et al. Diagnostic
criteria for headache attributed to temporoman-
dibular disorders. Cephalalgia. 2012;32:683-692.
98. Fernandes G, Franco AL, Goncalves DA, Speciali
JG, Bigal ME, Camparis CM. Temporomandibular
disorders, sleep bruxism, and primary headaches are
mutually associated. J Orofac Pain. 2013;27:14-20.
99. Blau JN. How to take a history of head or facial
pain. Br Med J. 1982;285:1249-1251.
100. Marshall RJ, Bleakley A. Lost in translation.
Homer in English; the patient’s story in medicine.
Med Humanit. 2013;39:47-52.
101. Kenny DT. Constructions of chronic pain in doctor-
patient relationships: Bridging the communication
chasm. Patient Educ Couns. 2004;52:297-305.
102. Wolf E, Birgerstam P, Nilner M, Petersson K.
Patients’ experiences of consultations for nonspe-
cific chronic orofacial pain: A phenomenological
study. J Orofac Pain. 2006;20:226-233.
103. Napenas JJ, Nussbaum ML, Eghtessad M,
Zakrzewska JM. Patients’ satisfaction after a com-
prehensive assessment for complex chronic facial
pain at a specialised unit: Results from a prospec-
tive audit. Br Dent J. 2011;211:E24.
104. Bonathan CJ, Zakrzewska JM, Love J, Williams
AC. Beliefs and distress about orofacial pain:
Patient journey through a specialist pain consulta-
tion. J Orofac Pain. (submitted).
105. Wolf E, Birgerstam P, Nilner M, Petersson K. Non-
specific chronic orofacial pain: Studying patient

Headache
experiences and perspectives with a qualitative
approach. J Orofac Pain. 2008;22:349-358.
106. Hals EKB, Stubhaug A. Mental and somatic
co-morbidities in chronic orofacial pain conditions:
Pain patients in need of multiprofessional team
approach. Scand J Pain. 2011;2:153-154.
107. Dworkin RH, Turk DC, Farrar JT, et al. Core
outcome measures for chronic pain clinical trials:
IMMPACT recommendations. Pain. 2005;113:9-
19.
108. Lee JY, Chen HI, Urban C, et al. Development of
and psychometric testing for the Brief Pain
Inventory-Facial in patients with facial pain syn-
dromes. J Neurosurg. 2010;113:516-523.
109. Zebenholzer K, Wober C, Vigl M, Wessely P,
Wober-Bingol C. Facial pain in a neurological ter-
tiary care centre – Evaluation of the International
Classification of Headache Disorders. Cephalalgia.
2005;25:689-699.
110. Treede RD, Jensen TS, Campbell JN, et al. Neuro-
pathic pain: Redefinition and a grading system for
clinical and research purposes. Neurology. 2008;70:
1630-1635.
111. Galli U, Ettlin DA, Palla S, Ehlert U, Gaab J. Do
illness perceptions predict pain-related disability
and mood in chronic orofacial pain patients? A
6-month follow-up study. Eur J Pain. 2010;14:550-
558.
112. Arnow BA, Blasey CM, Constantino MJ,
et al. Catastrophizing, depression and pain-related
disability. Gen Hosp Psychiatry. 2011;33:150-
156.
15264610, 2014, 1, Downloaded from https://headachejournal.onlinelibrary.wiley.com/doi/10.1111/head.12272 by UNIVERSIDAD DE VALPARAISO, Wiley Online Library on [01/05/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License
39
113. Sipila K, Maki P, Laajala A, Taanila A, Joukamaa
M, Veijola J. Association of depressiveness with
chronic facial pain: A longitudinal study. Acta
Odontol Scand. 2013;71:644-649.
114. Aggarwal VR, Macfarlane GJ, Farragher TM,
McBeth J. Risk factors for onset of chronic oro-
facial pain – Results of the North Cheshire oro-
facial pain prospective population study. Pain.
2010;149:354-359.
115. Toye F, Seers K, Allcock N, et al. A meta-
ethnography of patients’ experience of chronic non
malignant muskuloskeltal pain. Br J Pain. 2013;
7(Suppl. 1):84, abstract 104.
116. Turner JA, Jensen MP, Romano JM. Do beliefs,
coping, and catastrophizing independently predict
functioning in patients with chronic pain? Pain.
2000;85:115-125.
117. Rosser BA, McCracken LM, Velleman SC, Boichat
C, Eccleston C. Concerns about medication and
medication adherence in patients with chronic pain
recruited from general practice. Pain. 2011;152:
1201-1205.
118. Jensen MP. Psychosocial approaches to pain man-
agement: An organizational framework. Pain.
2011;152:717-725.
119. Macea DD, Gajos K, Daglia Calil YA, Fregni F.
The efficacy of Web-based cognitive behavioral
interventions for chronic pain: A systematic review
and meta-analysis. J Pain. 2010;11:917-929.
120. Vlaeyen JW, Morley S. Cognitive-behavioral treat-
ments for chronic pain: What works for whom?
Clin J Pain. 2005;21:1-8.