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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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C L I N I C A L
CLINICAL CHARACTERISTICS
P R A C T I C E
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P R A C T I C E
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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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C L I N I C A L
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
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TABLE 2
DOSAGE
7-12 liters/minute
for 15-30 minutes
ROUTE OF
ADMINISTRATION
Inhalation (with
nonrebreathing
face mask)
Subcutaneous
injection
CLASS OF
MEDICATION
Not listed
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6 milligrams
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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
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
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
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
Frequency
15-180
minutes
1-8/day
Autonomic
Yes
Yes
Yes
No/very rare
Trigger
Alcohol,
nitrates
Mechanical
Cutaneous
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.
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