C L I N I C A L

P R A C T I C E

Trigeminal autonomic cephalalgias

A review and implications for dentistry
Ramesh Balasubramaniam, BDSc, MS; Gary D. Klasser, DMD;
Robert Delcanho, BDSc, MS, FFPMANZCA

IO
N

Background. The authors review the epidemiology, clinical features, pathophysiology, diagnosis,
treatment, orofacial presentations and dental implicaN
C
U
A ING EDU 2
tions of trigeminal autonomic cephalalgias (TACs):
RT
ICLE
cluster headache (CH), paroxysmal hemicrania (PH) and
short-lasting unilateral neuralgiform headache attacks with conjunctival
injection and tearing (SUNCT).
Types of Studies Reviewed. The authors conducted PUBMED
searches for the period from 1968 through 2007 using the terms trigeminal
autonomic cephalalgias, cluster headache, paroxysmal hemicrania,
short-lasting unilateral neuralgiform headache attacks with conjunctival
injection and tearing, epidemiology, pathophysiology, treatment,
oral, facial and dentistry. They gave preference to articles reporting
randomized, controlled trials and those published in English-language
peer-reviewed journals.
Results. TACs refers to a group of headaches characterized by unilateral
head pain, facial pain or both with accompanying autonomic features.
Although their pathophysiologies are unclear, CH, PH and SUNCT may be
differentiated according to their clinical characteristics. Current treatments
for each of the TACs are useful in alleviating the pain, with few refractory
cases requiring surgical intervention. Patients with TACs often visit dental
offices seeking relief for their pain.
Clinical Implications. Although the prevalence of TACs is small, it is
important for dentists to recognize the disorder and refer patients to a neurologist. This will avoid the pitfall of administering unnecessary and
inappropriate traditional dental treatments in an attempt to alleviate
the neurovascular pain.
Key Words. Trigeminal autonomic cephalalgias; cluster headache;
paroxysmal hemicrania; short-lasting unilateral neuralgiform headache
attacks with conjunctival injection and tearing.
JADA 2008;139(12):1616-1624.
T

ABSTRACT
CON

rigeminal autonomic
cephalalgias (TACs) is a
collective term that
refers to a group of
headaches characterized
by unilateral head pain, facial pain
or both, with accompanying autonomic features.1,2 The International
Classification of Headache Disorders II (ICHD-II)2 classifies TACs as
follows:
depisodic or chronic cluster
headache (CH);
depisodic or chronic paroxysmal
hemicrania (PH);
dshort-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT).
The aim of this article is to
increase awareness and provide
information regarding TACs,
because patients often consult dentists regarding symptoms associated
with these types of headaches.3 It is
important for dentists to understand these disorders so that unnecessary and inappropriate invasive
dental procedures will be avoided in
this patient population.4 We discuss
briefly each of the TACs, specifically
their clinical characteristics, pathophysiology, diagnosis and treatment. In addition, we explore orofacial presentations and the dental
implications of TACs.

When this review was conducted, Dr. Balasubramaniam was a fellow, Department of Oral Medicine, University of Pennsylvania, School of Dental Medicine,
Philadelphia. He now is a clinical associate professor, School of Dentistry, University of Western Australia, Perth, and codirector, Perth Orofacial Pain and Oral
Medicine Centre, St. John of God Hospital, Subiaco Clinic, Suite 319, 25 McCourt St., Subiaco, Western Australia 6008, Australia, e-mail ramesh.
balasubramaniam@uwa.edu.au. Address reprint requests to Dr. Balasubramaniam.
Dr. Klasser is an assistant professor, Department of Oral Medicine and Diagnostic Sciences, University of Illinois at Chicago, College of Dentistry, Chicago.
Dr. Delcanho is a clinical associate professor, School of Dentistry, University of Western Australia, Perth, and codirector, Perth Orofacial Pain and Oral Medicine
Centre, St. John of God Hospital, Subiaco Clinic, Western Australia, Australia

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CLINICAL CHARACTERISTICS

Cluster headache. The prevalence of CH is

between 120 and 300 per 100,000 people in the
general population.5-8 CH has a male preponderance, with a male-to-female ratio of 2.5-3.5:1.9,10
The age at onset of CH typically is between 20
and 29 years.11,12 The likelihood of a family history
in a patient with CH is between 3 and 20
percent.11,13,14
CH is characterized by severe, mainly unilateral pain attacks usually localized to orbital,
supraorbital or temporal sites or combinations of
these sites, accompanied by ipsilateral autonomic
features.1,2 These pains may radiate to the maxilla, nostril, gingiva, palate, jaws, teeth and neck
region, thus confusing the dentist as to the true
source of the pain.15-18
Pain. The pain is excruciating, with patients
often describing it as constant, boring and
burning or with phrases such as hot, burning
poker in the eye or eye is being pushed out.10,19
Not surprisingly, approximately 93 percent of
patients with CH report being restless during
attacks, resulting in behaviors such as pacing,
head banging and other physical activity.9,19,20
Patients with CH may find some relief from the
pain by pressing on the superficial temporal
arteries, applying heat or cold over the site of
pain, pacing, isolating themselves from people or
even getting fresh air.20-22 CH has a significant
socioeconomic burden, which includes restrictions
in daily living, social activities, family life and
housework.23
Almost all CH attacks involve ipsilateral cranial autonomic features such as conjunctival
injections, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis,
eyelid edema and facial flushing or pallor.
These features are considered pathognomonic for
CH.9-11,19,24 Apart from miosis, ptosis or both,
which may persist after a CH attack, autonomic
features tend to cease with the pain.25 Less commonly, migrainelike features such as an aura
(visual, sensory or motor) may develop before a
CH attack, and photophobia, phonophobia, osmophobia, nausea and vomiting may occur during an
attack.9,10,26
Frequency of attacks. The frequency of CH
attacks can vary from one to three times daily
(and in some cases up to eight times in a 24-hour
period), with peaks at 1 a.m., 2 p.m. and 9 p.m.12,27
The attack usually begins abruptly without

P R A C T I C E

warning, lasting between 15 and 180 minutes

(and in some cases up to eight hours) and terminating abruptly or dissipating slowly.10,22,28 As
noted above, the International Headache Societys
ICHD-II has classified CH into two forms:
episodic and chronic.2 The more common episodic
form occurs in bouts, with periods of complete
remission.1,2 The chronic form represents 10 percent of cases of CH and is either continuous or
occurs with brief periods of remission.1,2,29
Paroxysmal hemicrania. Approximately 1 in
50,000 people in the general population has some
form of PH diagnosis.22 Contrary to CH, PH has a
greater female preponderance, with a female-tomale ratio of 1.6-2.36:1.30,31 The typical age at
onset of PH is between 20 and 30 years.31,32 A
familial link for PH is rare, and further investigation into genetic predisposition is required.33
Pain. PH is characterized by severe, shortlasting, strictly unilateral pain attacks localized
to orbital, supraorbital or temporal sites or combinations of these sites, accompanied by one or
more ipsilateral autonomic features.1,2 However,
the pain also may involve the maxilla and frontal
regions,2,22 neck and occiput,22,32 as well as orofacial structures,17,34-40 thereby making the separation from an odontogenic diagnosis somewhat difficult. The pain is excruciating, with patients
typically describing the quality as boring or stabbing at peak intensity.1,41 One-third of patients
with PH report experiencing pain or discomfort
between PH attacks.31
Almost all PH attacks involve ipsilateral cranial and facial autonomic features, with lacrimation, conjunctival injection, nasal congestion and
rhinorrhea observed most frequently.2,22,31 Similar
to CH, migrainelike features, as described above,
may occur during a PH attack.22,30,31
Most PH attacks are spontaneous; however, certain triggers such as glyceryl trinitrate, alcoholic
drinks and mechanical rotation or manipulation of
ABBREVIATION KEY. CH: Cluster headache.
ICHD-II: International Classification of Headache
Disorders II. NSAID: Nonsteroidal anti-inflammatory
drug. PH: Paroxysmal hemicrania. SUNA: Shortlasting unilateral neuralgiform headache attacks with
cranial autonomic symptoms. SUNCT: Short-lasting
unilateral neuralgiform headache attacks with conjunctival injection and tearing. TACs: Trigeminal autonomic cephalalgias. TMDs: Temporomandibular disorders. V2/V3 > V1: Maxillary/mandibular division
greater than ophthalmic division of the trigeminal
nerve.
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P R A C T I C E

the head and/or neck may precipitate an

attack.31,42,43 The attacks in PH are shorter-lasting
(typically two to 30 minutes) than those in CH, but
they can last up to two hours.1,2,31 PH attacks occur
between one and 40 times per day,31 with a mean
of six to 14 attacks per day30,44; they also may occur
regularly at all hours of the day and night.
Forms of PH. The International Headache
Societys ICDH-II has classified PH into two
forms: episodic and chronic.2 Most patients (80
percent) experience the chronic form of PH, which
essentially is unremitting. However, 20 percent of
patients have the episodic form, which involves
bouts of PH ranging from two weeks to 4.5
months, accompanied by periods of remission
lasting between one and 36 months.31,45 Typically,
episodic PH progresses to chronic PH.41 The hallmark of PH is absolute cessation of the headache
with indomethacin therapy, and, hence, it is distinguishable from the other TACs.1,2
Short-lasting unilateral neuralgiform
headache attacks with conjunctival injection and tearing. SUNCT is extremely rare,
with approximately 80 reported cases in the literature; however, because the classification is new
and previously was not well-defined, it is likely to
be more common than the literature suggests.46 It
has a male-to-female ratio of 1.3:1 based on 50
patients with an onset at between 35 and 65
years of age (mean age, 50 years).47 To our knowledge, there has been only one report of SUNCT in
a family and, hence, the possibility of a familial
link is undetermined.48
Pain. SUNCT is a syndrome characterized by
strictly unilateral and intense pain attacks localized to orbital, supraorbital, temporal and frontal
areas or combinations of these sites, and it is
accompanied by cranial and facial autonomic features. The pain occasionally may involve the
neck, other areas of the head, ear, nose, cheek,
palate and throat.2,47,49-52 Of particular interest to
dentists, 33 and 21 percent of patients with
SUNCT reported experiencing pain localized to
the maxillary branch of the trigeminal nerve and
teeth, respectively.53 The pain intensity of SUNCT
varies from moderate to excruciating47,49; however,
84 percent of patients with SUNCT reported
experiencing pain as 10 of 10 (most severe pain
imaginable) on a verbal rating scale.53
Features. Almost all SUNCT attacks involve
ipsilateral cranial and facial autonomic features,
namely conjunctival injection (100 percent of
patients) and tearing (94 percent),2,22,47 although
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rhinorrhea, nasal congestion, eyelid edema,

ptosis, miosis and facial sweating or redness are
reported infrequently.47 The autonomic features
occur one to two seconds after the onset of an
attack and abort within a few seconds of the
pains ceasing.49 Unlike in CH and PH, migrainelike features are not associated with SUNCT
attacks.47,53
The majority of SUNCT attacks occur spontaneously or are triggered by an innocuous mechanism, as in trigeminal neuralgia (TN).47 Common
precipitants include touching or washing the face
or scalp, shaving, eating, brushing teeth, talking
and coughing.46,49 A SUNCT attack usually begins
abruptly, with maximum intensity occurring
within two to three seconds, and it may persist
for between two and 600 seconds (mean duration,
49 seconds).49,51,54-56 Despite almost neuralgialike
triggers in SUNCT, there are no refractory
periods, as are seen in TN.49
The frequency of attacks varies from less than
once a day to more than 60 attacks per hour, and
they may last for days.55,57-59 SUNCT attacks have
a bimodal distribution, occurring in the morning
and afternoon or evening, but they rarely are nocturnal.53,60 The ICHD-II criteria do not distinguish
between the chronic and episodic forms of
SUNCT, as is the case for the other TACs2; however, reports suggest that a chronic form of
SUNCT does exist.47,49,53
PATHOPHYSIOLOGY OF TRIGEMINAL
AUTONOMIC CEPHALALGIAS

Despite ongoing research, the exact pathophysiology of the various TACs remains unclear. The
anatomical distribution of the pain suggests
involvement of a central pain generator mediated
by the first division of the trigeminal nerve and
supported by neurogenic inflammatory mechanisms involving the intracranial and extracranial
vasculature (trigeminovascular activation).61
Patients response to indomethacin therapy in
PH, but not in CH and SUNCT, suggests a different pathophysiology between the subtypes.
Indeed, although all three conditions can be considered phenotypically related in terms of symptomatology, they differ significantly in terms of
frequency and duration of attacks, response to
various medications and triggers. Furthermore,
the associated autonomic phenomena, found both
clinically and experimentally in subjects with different TACs, vary widely between patients, suggesting that a number of possible mechanisms

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P R A C T I C E

TABLE 1
are at play.
62
Drummond recently
Medical conditions with symptoms similar to those
reviewed the autonomic
of TACs.*
mechanisms related to
CLUSTER HEADACHE
PAROXYSMAL
SUNCT
CH, which possibly are
HEMICRANIA
applicable to PH and
Other TACS
SUNCT. These mechaParoxysmal hemicrania
Cluster SUNCT
Cluster paroxysmal hemicrania
nisms include massive
SUNCT
trigeminal-parasympaOther Primary Headache
thetic discharge63; cenHypnic headache, hemicrania
Hypnic headache, hemicrania
Primary stabbing headache
trally mediated hypothalcontinua, SUNA, primary
continua, SUNA, primary
stabbing headache, primary
stabbing headache, primary
amic disturbance64; and
cough headache, migraine
cough headache, primary
sympathetic dysfunction
with or without aura
exertional headache, primary
headache associated with sexual
secondary to trigeminal
activity
parasympathetic activaVascular Disorders
tion during attacks and/or
Carotid artery dissection or
Middle cerebral artery infarct,
Cerebellopontine arterioinjury to the pericarotid
aneurysm, vertebral artery
collagen vascular disease,
venous malformation,
dissection or aneurysm, giant
parietal arteriovenous
cavernous hemangioma
plexus of sympathetic
cell (temporal) arteritis
malformation
65
nerve fibers.
Tumors
Further evidence from
65
Pituitary adenoma,
Pancoast tumor, pituitary
Posterior fossa, pituitary lesions
animal studies docunasopharyngeal carcinoma,
microadenoma,
mented that stimulation of
sphenoidal meningioma
macroprolactinoma
trigeminal efferents can
Orofacial Conditions
result in cranial autonomic
Pulpal pain, periodontal pain,
Pulpal pain, periodontal pain,
Pulpal pain, periodontal pain,
outflow (that is, the
TMDs
TMDs
TMDs
trigeminal-autonomic
Trigeminal neuralgia
Trigeminal neuralgia
Trigeminal neuralgia
reflex). This presumably

Maxillary sinusitis

occurs via brain-stem conHead

and
neck
trauma
nections between the
trigeminal nucleus cau* TACs: Trigeminal autonomic cephalalgias.
SUNCT: Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing.
dalis and the superior sali SUNA: Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms.
1,65,66
vatory nucleus.
In fact,
TMDs: Temporomandibular disorders.
Dash: Not applicable.
cranial autonomic symptoms appear as a normal
DIAGNOSIS
physiological response to strong trigeminal noci67,68
69
ceptive input.
Benjamin and colleagues also
suggested that cranial autonomic symptoms may
The key to diagnosing a TAC is based on the
be prominent in TACs owing to central disinhibipatients history of experiencing attacks. These
tion of the trigeminal-autonomic reflex by the
features include the rapid onset and location of
hypothalamus. These processes or combinations
the pain; quality, duration and temporal patterns
of the above are responsible for the autonomic
of episodes; triggering factors; and associated
features manifested by patients with TACs. The
autonomic features.2,9,19 Clinicians must make a
finding of hypothalamic activation on functional
differential diagnosis before establishing a
imaging studies for all of the TACs points clearly
working diagnosis for TACs, because many other
to the hypothalamus as a generator or facilitator
conditions can mimic these headaches (Table 1).
of these attacks and, therefore, a target for
Because a dentist may be the first health care
treatment.
practitioner visited by a patient with a TAC, denTherefore, pain attacks in patients with TACs
tists should have the diagnostic skills to differenare thought to be initiated by hypothalamic distiate these symptoms from those of an odontocharge,70-72 although what actually triggers this
genic source. For example, a patient may report
discharge remains unknown. Clearly, further sciexperiencing unilateral boring pain localized to
entific research is required to elucidate the pathothe orbit that is triggered by alcohol consumption,
physiology of the various TACs.
which is highly suggestive of a CH rather than of

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TABLE 2

Abortive treatments for cluster headache.

TREATMENT
First Tier
100% Oxygen

DOSAGE

7-12 liters/minute
for 15-30 minutes

ROUTE OF
ADMINISTRATION
Inhalation (with
nonrebreathing
face mask)
Subcutaneous
injection

CLASS OF
MEDICATION
Not listed

unremitting headache, poor response to

standard treatment, presence of
abnormal physical findings and
abnormal cranial nerve examination
results (except for miosis and ptosis).73,74
MEDICAL TREATMENT

Successful treatment of TACs includes

various forms of therapy. These include
Second Tier
nonpharmacological therapies that
20 mg
Nasal spray
Triptan
Sumatriptan
encompass behavioral and lifestyle
5 or 10 mg
Nasal spray
Triptan
Zolmitriptan
1 mg (two sprays
Nasal spray
Alkaloid
Dihydroergotamine
interventions; pharmacological theraeach nostril); may
vasoconstrictor
pies involving abortive strategies, prerepeat once, if
needed
ventive strategies or both; and nonsurIntravenous or intra- Alkaloid
0.5-1 mg
gical and surgical procedures. Clinimuscular injection
vasoconstrictor
Ergotamine
1-2 mg (maximum, Oral tablets
Alkaloid
cians may administer these therapies
6 mg/day)
vasoconstrictor
as single interventions or in combinaNasal spray/solution Anesthetic
Lidocaine (4%-6%)
Four sprays
ipsilaterally
tion. We present below brief descriptions of the various treatment options
TABLE 3
for each TAC.
Preventive treatments for cluster headache.
Cluster headache. Altering
TREATMENT
DOSAGE
ROUTE OF
CLASS OF
lifestyle habits,9,75 such as cigarette
ADMINISTRATION
MEDICATION
smoking10,76 and alcohol intake,10 and
First Tier
treating obstructive sleep apnea77
Verapamil
360-720
Oral
Calcium channel
should be considered in CH managemilligrams/day
blocker
Lithium
300-1,200 mg/day
Oral
Anticonvulsant
ment. The clinician directs abortive
Corticosteroid 60-80 mg/day (taper Oral
Steroid
pharmacological treatment toward
(prednisone;
across one to four
short-term
managing the attack. This is achieved
weeks)
use)
by administering 100 percent oxygen,
Second Tier
triptans, ergot derivatives or intranasal
Valproic acid
1,000-2,500 mg/day Oral
Anticonvulsant
lidocaine (Table 2). In some cases, pracTopiramate
50-200 mg/day
Oral
Anticonvulsant
Melatonin
3-10 mg at night
Oral
Hormone
titioners administer preventive pharGabapentin
300-900 mg/day
Oral
Anticonvulsant
macological treatment, including cortiCapsaicin
Place via cotton
Intranasal
Capsaicinoid
(0.025%)
swab in ipsilateral
(active compound in
costeroids, verapamil and lithium, to
nostril twice a day
chili peppers)
reduce the duration and frequency of
for seven days
the attacks12 (Table 3). Investigators
odontogenic pain. Similarly, odontogenic pain typhave studied numerous medications to treat
ically is not associated with ipsilateral cranial
patients with refractory cases of CH, with varying
autonomic features observed in patients with
results.22 Clinicians also have used peripheral
TACs, such as conjunctival injections, lacrimanerve blocks78 and surgical approaches for refraction, nasal congestion and rhinorrhea.
tory cases and medically complex patients.79-84
Dentists should refer a patient to a neurologist
Paroxysmal hemicrania. The medical treatfor a diagnostic workup if he or she has symptoms
ment for patients with PH is prophylactic use of
that are not representative of an odontogenic
indomethacin, which is considered pathognomonic
problem. Although the diagnosis of a TAC often is
for this type of headache. However, although rare,
straightforward and usually does not require
cases of indomethacin-resistant PH have been
extensive diagnostic tests, a neurological examireported.30,85 Anecdotal evidence and case
nation supplemented with neuroimaging studies,
reports86,87 suggest that patients whose symptoms
such as computed tomography and magnetic resoare refractory or whose conditions are nonresponnance imaging, may be warranted to rule out censive may be treated with other medications or
tral nervous system pathology. Clinicians may
anesthetic blockades (Table 4).
need to address several red flags to rule out an
Short-lasting unilateral neuralgiform
underlying pathology. These include a chronic
headache attacks with conjunctival injecSumatriptan

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Triptan

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C L I N I C A L

tion and tearing. SUNCT is considered to be relatively refractory to treatment.88 Nevertheless, clinicians have
tried pharmacological approaches
(Table 5), as well as several surgical
approaches involving local anesthetic
blockades, invasive procedures
involving the trigeminal nerve and
neurosurgical procedures. Some case
reports51,89-93 indicate that the anticonvulsant drug lamotrigine has been
highly effective in a number of patients
with SUNCT. However, other case
reports54,94,95 indicate a lack of effectiveness with lamotrigine.
IMPLICATIONS FOR DENTISTRY

P R A C T I C E

TABLE 4

Treatments for paroxysmal hemicrania.

TREATMENT
First Tier
Indomethacin

DOSAGE

ROUTE OF
ADMINISTRATION

CLASS OF
MEDICATION

75-150
milligrams/day

Oral

NSAID*

Oral

NSAID

Verapamil

Varying dosages
studied
240-320 mg/day

Oral

Acetazolamide

750 mg/day

Oral

Sumatriptan

6 mg

Topiramate
Corticosteroid
(prednisone)
Greater occipital
nerve block

150 mg/day
Varying dosages
studied
Varying dosages
studied

Subcutaneous
injection
Oral
Oral

Calcium channel
blocker
Carbonic anhydrase
inhibitor (diuretic)
Triptan

Second Tier
NSAID

Nerve-block
injection

Anticonvulsant
Steroid
Local anesthetic

Dentists often are faced with the diffi* NSAID: Nonsteroidal anti-inflammatory drug.
cult task of diagnosing odontogeniclike
TABLE 5
pain emanating from various anatomical structures. TACs may present a
Treatments for short-lasting unilateral
challenge for the dentist because of
neuralgiform headache attacks with
their often overlapping and similar preconjunctival injection and tearing.
sentations to true odontogenic pain.
Dentists need to keep in mind that the
TREATMENT
DOSAGE
ROUTE OF
CLASS OF
ADMINISTRATION
MEDICATION
oral cavity is not the source of all odontogenic pain but may merely be a site of First Tier
Lamotrigine
100-300
Oral
Anticonvulsant
pain.96 The key to discerning source
milligrams/day
versus site of pain is to take a thorough
Lidocaine
1.5-3.5 mg/kg*/hour Intravenous
Anesthetic
medical history and perform a compreSecond Tier
Gabapentin
800-2,700 mg/day
Oral
Anticonvulsant
hensive clinical examination. Failure to
Topiramate
50-300 mg/day
Oral
Anticonvulsant
complete these steps increases the risk
Third
Tier
of misdiagnosis, which may lead to
Corticosteroid
Varying dosages
Oral
Steroid
unnecessary, inappropriate and irre(prednisone,
studied
prednisolone,
versible dental procedures.
methylpredPatients often describe the pain due
nisolone)
Carbamazepine 600-1,200 mg/day
Oral
Anticonvulsant
to CH as emanating from the midfacial
Oxcarbazepine 600 mg/day
Oral
Anticonvulsant
region, which may be interpreted as
Lidocaine
Varying dosages
Intranasal,
Anesthetic
pain originating from the teeth, jaws or
studied
mouthwash
temporomandibular joints.15-17 There* kg: Kilogram.
fore, it is not uncommon for people to
seek care from dentists. Bahra and Goadsby4
dental procedures. Some investigators have posreported that 230 (45 percent) of 511 subjects
tulated that dental extractions may be a precipiwith CH were examined by a dentist before
tating factor for CH. In a study of 54 subjects
receiving the correct diagnosis. (We should point
with CH, Penarrocha and colleagues98 found that
out that subjects also visited a mean of three
tooth extraction or endodontic treatment had
physicians before receiving a correct diagnosis.)
been performed in the pain-affected quadrant in
These authors also found that misdiagnosis often
31 (57 percent) of the subjects and in the conled to unnecessary and inappropriate dental
tralateral quadrant in 18 (33 percent) of the subprocedures.
jects. In addition, they found that in 24 (44 perIn another study, Bittar and Graff-Radford97
cent) of the 54 subjects, tooth extraction had been
found that 14 (42 percent) of 33 subjects with CH
performed after the onset of pain in an attempt to
underwent some form of invasive and irreversible
resolve the problem; however, only one subject
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TABLE 6

Differentiating features of trigeminal autonomic cephalalgias,

trigeminal neuralgia and odontogenic pain.
FEATURE

CLUSTER
HEADACHE

PAROXYSMAL
HEMICRANIA

SUNCT*

TRIGEMINAL
NEURALGIA

ACUTE PULPAL
PAIN

CHRONIC
PULPAL
PAIN

PERIODONTAL
PAIN

Sex (Maleto-Female)

5:1

1:2

2:1

1.6:1

1:1

1:1

1:1

Age (Years)

20-40

30

40-70

50

Any age

Any age

Any age

Throbbing or
aching
Mild-to-severe
Tooth

Tender or
aching
Mild
Tooth

Tender or aching

Seconds to all day

Varies

Constant

Mild
Tooth, gingivae,
bone
Varies

Daily

Daily

No

No

Inconsistent

Apical or lateral
tooth pressure

Pain
Type

Boring

Boring

Electriclike

Electriclike

Severity
Location

Very severe
Orbital

Very severe
Orbital

Severe
Orbital

Very severe
V2/V3 > V1

Duration

2-30 minutes
2-40/day

15-240
seconds
3-200/day

< 1-30 seconds

Frequency

15-180
minutes
1-8/day

Autonomic

Yes

Yes

Yes

No/very rare

Trigger

Alcohol,
nitrates

Mechanical

Cutaneous

Mucocutaneous Electric and

thermal
stimulation, tooth
percussion

Any
No

* SUNCT: Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing.
V2/V3 > V1: Maxillary/mandibular division greater than ophthalmic division of the trigeminal nerve.

reported having experienced improvement. These

authors concluded that the onset of pain after a
dental procedure might suggest a relationship
between nerve damage and the development of
CH, but we also must consider the possibility that
dental extraction and endodontic procedures were
performed in response to CH.
Because of the short duration of attacks, frequent recurrences, excruciating intensity and pulsatile pain quality found in patients with PH, it is
possible that this disorder may be mistaken for
dental pulpitis.40 It also is not uncommon for PH
to manifest in the maxillary region, thereby being
mistaken for tooth pain.31 Benoliel and Sharav35
reported on seven cases of PH, four of which had
been confused with pain of dental origin. Two of
these patients received irreversible dental treatments. Other studies have reported similar occurrences whereby the spectrum of failed dental
treatment ranged from pharmacological
approaches to full-mouth reconstruction.17,34,36,38
The literature also contains case reports in
which patients with SUNCT, in addition to experiencing facial pain, complained of pain radiating
to adjacent teeth.99-101 This resulted in clinicians
delivering therapeutic interventions for tooth
pain such as extraction, occlusal splints and
incorrect drug treatment. PH also may be misdiagnosed as pain associated with temporomandibular disorders. The manifestation of PH in
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the temporal, maxillary and ear regions along

with ipsilateral masticatory muscle tenderness
may contribute to the misdiagnosis.35,36,38,40 Again,
this may lead to unnecessary treatments such as
inappropriate pharmacological approaches and
surgical interventions.40
Differences in the quality and intensity of pain
described for PH (throbbing and excruciating) and
in musculoskeletal pain (mild-to-moderate aching
pain) should assist practitioners in making the
correct diagnosis. Another pain condition that
may be confused with PH or SUNCT is TN. The
common features of all three disorders, such as
the excruciating pain, intermittent temporal pattern, unilaterality, frequency of attacks and lancinating nature, may be partially responsible for
the misdiagnoses. In addition, there are reports
in the literature of the coexistence of TN and
SUNCT, suggesting a pathophysiological relationship between these short-lasting unilateral
disorders.100,102,103
Because of these similarities, it is important
for dentists to recognize and understand some differentiating features among these disorders. A
major difference between TN, PH and SUNCT is
that a TAC always is associated with autonomic
features, whereas TN usually occurs without any
such features,104 except in rare circumstances and
only in the ophthalmic branch.105 In addition, it is
rare for TN attacks to disturb the patients sleep,

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C L I N I C A L

whereas sleep disturbance may occur in patients

with PH, but it is rare in patients with SUNCT.
Another differentiating feature between PH and
TN involves the much shorter duration of the
attack in TN, which often is triggered by an
innocuous stimulation. However, this manifestation, although not consistent for patients with
PH, is similar to that observed in patients with
SUNCT. Finally, treatment of TN with carbamazepine often is considered pathognomonic for
this disorder. Similarly, treatment of PH with
indomethacin is considered pathognomonic; however, indomethacin will not alleviate TN nor will
carbamazepine alleviate PH. SUNCT is relatively
refractory to most medications, with the possible
exception of lamotrigine and intravenous lidocaine. Table 6 summarizes the clinical characteristics of TACs, TN and odontogenic pain.
CONCLUSION

TACs are painful and disabling primary

headaches. Dentists may be the first practitioners
visited by patients with these disorders, and,
therefore, it is essential that they recognize and
understand the characteristics of TACs to avoid
making an incorrect diagnosis. This will prevent
unnecessary and inappropriate traditional dental
treatments. Ultimately, with this knowledge, dentists will be in a position to refer patients for
appropriate care.
Disclosure. The authors did not report any disclosures.
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