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Introduction
Pain over the orofacial region can arise from disorders of the
nervous system, face, oral cavity, teeth and temporomandibular
joint (Table 11.01). Neuralgias such as cranial neuralgia and
postherpetic neuralgia have to be differentiated from other
organic causes such as tumour or infection. Headaches may be
referred to the facial region. e general approach to headache
has been described in Chapter 10.
Trigeminal Neuralgia
Nicholas Nadre, a Parisian surgeon, first described the pain
involving the trigeminal nerve as trigeminal neuralgia in 1756
and coined the name of tic douloureux. e International
Association for the Study of Pain (IASP) defines trigeminal
Orofacial Pain
11
Chi Tim HUNG, Theresa Tak Lai LI
INTRODUCTION
TRIGEMINAL NEURALGIA
POSTHERPETIC NEURALGIA
GLOSSOPHARYNGEAL
NEURALGIA
OTHER CRANIAL NEURALGIAS
ATYPICAL FACIAL PAIN
TEMPOROMANDIBULAR JOINT
DISORDERS
MYOFASCIAL PAIN SYNDROME
REFERENCES
Table 11.01 Causes of facial pain
Region/system Causes/syndromes
Diseases of nervous
system
Trigeminal neuralgia
Postherpetic neuralgia
Glossopharyngeal neuralgia
Other cranial neuralgias
Diseases of
musculoskeletal system
Temporomandibular joint
problem
Myofascial pain syndrome
Diseases of oral cavity Dental infection
Headache referred to
face
Temporal arteritis
Sinusitis
Miscellaneous Atypical facial pain
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182 Chi Tim HUNG, Theresa Tak Lai LI
neuralgia as “sudden, usually unilateral, severe brief
stabbing, recurrent pains in the distribution of one
or more branches of the Vth cranial nerve” [85].
Causes
Trigeminal neuralgia can be divided into three
types: idiopathic, atypical and secondary to organic
brain lesions. e commonest presentation is the
idiopathic type where no obvious cause can be
identified. e neurovascular conflict/compression
theory has been postulated to be a causative
factor [105]. e trigeminal root entry zone in
the posterior cranial fossa or the mid-third of the
trigeminal nerve is found to be compressed in 70–
96% of cases at craniotomy by a loop of artery or
vein, aneurysms, arteriovenous malformation or an
arachnoid cyst. e area of impingement correlates
with the site of pain. Posterior fossa exploration
for microvascular decompression of the trigeminal
nerve is based on the vascular compression theory.
One or several offending vessels may be identified;
the most common vessel is the superior cerebellar
artery [105]. A vein embedded in the nerve either
alone or in association with an artery is frequently
present. Under microscopic examination,
distortion of the nerve has been shown to be
present in half and marked indentation present in
one-third of patients [105].
Structural alteration of
the whole trigeminal nerve is frequently observed
with features such as global atrophy and local
thickening of the arachnoid membrane. However,
there is still debate on whether microvascular
compression alone is the cause for idiopathic
trigeminal neuralgia [18]. Hamlyn showed that it
is present in 14% of fresh cadavers not known to be
suffering from neurological diseases [42]. Recurrent
vascular compression was identified in 4–56% of
failed microvascular decompression presenting
again for posterior fossa exploration [61, 95]. e
microvascular compression also cannot explain
the effectiveness of other procedures apart from
decompression.
Apart from the idiopathic type, trigeminal neuralgia
can be secondary to organic diseases like trigeminal
tumours and acoustic neuroma. Multiple sclerosis
has been associated with trigeminal neuralgia (4–
18%) [11, 37, 47]. It causes a neuralgia picture
with or without evidence of compression at the
root entry zone. e incidence of trigeminal
neuralgia in multiple sclerosis is higher than in
the general population. In contrast to idiopathic
trigeminal neuralgia, neuralgia associated with
multiple sclerosis can be bilateral. It could be the
first symptom of multiple sclerosis, presenting at
early age and preceding other symptoms of multiple
sclerosis by 1 to 11 years [47].
Pathogenesis
e genesis of trigeminal neuralgia depends on
central and peripheral components [34]. Centrally
there is compression at the trigeminal root entry
zone and failure of central inhibitory mechanisms
[32]. e peripheral component consists of
trigeminal nerve demyelination [15]. Changes in
the myelin sheaths have been observed in patients
afflicted with the disorder. Demyelination most
often occurs at the cerebellopontine angle. e
pulsatile vessels on contacting the demyelinated
nerves cause ectopic firing of nociceptive action
potentials and produce the tic-like symptoms.
Pagni hypothesised trigeminal neuralgia as a kind
of sensory reflex epilepsy [88].
e compression
at the posterior root produces demyelination
and microneuromas which produce ectopic
discharges. e trigeminal ganglion also gives rise
to spontaneous impulse generation. Owing to the
chronic anomalous afferent barrage, an epileptic
subliminal focus is kindled in the trigeminal
nucleus. e pain paroxysms develop when the
subliminal activity is driven by prolonged seizures
in the periphery (trigger zone stimulation) or
others.
e recent “ignition hypothesis” of trigeminal
neuralgia is proposed and is based on the latest
advances in the understanding of abnormal
electrical behaviours in injured sensory neurones
and new histopathological observations of biopsy
specimens from patients with trigeminal neuralgia
undergoing microvascular decompression surgery
[25]. According to the hypothesis, injury renders
axons and axotomised somata of the trigeminal nerve
root or ganglion hyperexcitable. is, in turn, gives
rise to pain paroxysm as a result of synchronised
after-discharge activity which accounts for the signs
and symptoms of trigeminal neuralgia.
Clinical features
Trigeminal neuralgia is a disease of the elderly
affecting those more than 50 years of age [17,
60, 66]. Although rare, case reports of idiopathic
trigeminal neuralgia in children with documented
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Orofacial Pain 183
neurovascular compression have been reported
[22]. e disease has a female preponderance with
a female to male ratio of 2:1. e pain is unilateral
with the right side affected more often. e area of
pain conforms to the territory innervated by the
three branches of the trigeminal nerve (Fig. 11.1).
e most common clinical pain results from the
involvement of a combination of the second and
third divisions of the trigeminal nerve [66]. In
terms of the involvement of individual branches,
the mandibular branch is mostly affected, followed
by maxillary and ophthalmic branches. e pain
usually comes in paroxysms of brief episodes
lasting for seconds to minutes and is described as
severe, lancinating, stabbing, sharp, lightning-like
or shock-like. e patient is pain free between
such attacks but there are exceptions. Frequency
of attack ranges from several times a day to a few
times a month. e character of pain may change
over time with increase in frequency of attacks and
decrease in pain-free periods. Pain is provoked by a
minimal local stimulus on the affected or “trigger”
area. Triggering events include touching or washing
of the face, brushing teeth, exposure to cold, wind
blowing onto the face, shaving, eating, drinking
and simply talking. Most of the trigger areas lie in
the region of the face, lip, oral cavity and nose. A
classical clinical pattern is when the patient freezes
all motions including speech and articulation until
the pain has subsided during an acute episode of
attack. In order to avoid such pains, patients often
avoid pain triggering activities and may refrain
from eating or drinking. Bed rest and sleep with
the painful side up, to avoid touching the trigger
area, will usually bring about pain relief. Physical
signs are rare and sensory loss is not present. e
disease has spontaneous remissions.
Diagnosis and dierential
diagnosis
e diagnosis of trigeminal neuralgia is made on
symptomatology and exclusion of other differential
diagnosis. Since the character of pain may change
over time from lancinating pain to pain of a more
constant nature, the initial character of pain at
onset of disease is important. Atypical trigeminal
neuralgia is sometimes diagnosed when the pain
is constant, unresponsive to carbamazepine and
sometimes accompanied by facial hypoaesthesia. It
is highly controversial whether trigeminal neuralgia
and atypical trigeminal neuralgia are variants of the
same disease. Positive physical signs should prompt
the physician to search for organic causes of facial
pain or trigeminal neuralgia (Table 11.01) using the
appropriate investigations. A computed tomography
scan or magnetic resonance imaging of the brain
and skull base is also indicated when the pain is
atypical or not responsive to conventional drugs
to rule out organic causes. ese imaging studies
are also required when interventional treatments
are contemplated. e role of angiography in
diagnosing vascular compression is limited and
usually not indicated.
Cluster headache can be confused with trigeminal
neuralgia. e autonomic signs of a cluster headache
would be diagnostic. Postherpetic neuralgia
involving the trigeminal branches produces severe
constant burning pain in the trigeminal region.
A history of preceding herpes infection would be
diagnostic. However, sometimes the two diseases
may coexist, and the herpes eruption may not be
obvious in some patients. Dental pains associated
with infection are throbbing in character and
accompanied by local signs around the tooth
such as swelling and inflammation. Pain of
musculoskeletal origin such as temporomandibular
joint disease or myofascial pain has to be excluded.
Reader’s paratrigeminal syndrome is characterised
by unilateral head, face and retro-orbital pain
Figure 11.01 The innervation of the face by the
three branches of the trigeminal nerve.
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184 Chi Tim HUNG, Theresa Tak Lai LI
sometimes associated with oculomotor paresis.
Atypical facial pain is a diagnosis by exclusion.
Management
e management strategy for idiopathic trigeminal
neuralgia is broadly classified into pharmacological
and interventional, supplemented by psychological
approaches if necessary.
Pharmacotherapy
Pharmocotherapy is the mainstay of treatment for
trigeminal neuralgia.
1. First-line treatment
(a) Carbamazepine
Carbamazepine is the oldest anticonvulsant used for
treatment of trigeminal neuralgia and is considered
as the first-line treatment [1, 5, 27, 90, 112].
Crossover randomised controlled trials have found
that carbamazepine is effective against the neuralgia
but with notable adverse effects [136].
A start-low-
and-go-slow approach is favoured. Patients should
be started on an initial dose of 100 mg twice daily
and slowly stepped up to the therapeutic dose of
800–1200 mg daily. Although some studies have
shown that the therapeutic effect varies with the
plasma concentration, it is important to take into
account that carbamazepine is heavily protein
bound (75%) and thus the clinical effect depends
on the free drug concentration rather than the total
drug concentration as measured by drug assays [5,
118, 119]. A blood level of carbamazepine should
be measured to check for drug compliance if the
therapeutic effect is suboptimal.
ere are two preparations of carbamazepine, the
conventional and controlled-release preparations,
available in clinical practice. e conventional
carbamazepine is almost completely absorbed
from the gastrointestinal tract, albeit slowly. It can
be given twice daily although some patients may
benefit from a three-times daily dosing to reduce
the peak plasma concentration and associated side
effects [5]. In contrast, carbamazepine controlled-
release (CR) is usually given twice daily. e
bioavailability of carbamazepine CR is 15% less
than conventional carbamazepine and the plasma
concentration at the steady state is lower but more
stable [79]. e controlled-release preparation has
the advantage of maintaining a fairly constant drug
concentration, which is important for effective pain
management. e adverse effects of carbamazepine
are common and include dizziness, ataxia, vomiting,
allergic skin reaction (self-limiting increased
pigmentation in facial areas) and leucopenia. Rare
complications like aplastic anaemia, agranulocytosis
and dermatological reactions have been reported.
Life-threatening but rare dermatological reactions
such as Stevens-Johnson syndrome (SJS) and toxic
epidermal necrolysis (TEN) have also been reported.
According to the drug insert for carbamazepine
(Tegretol) issued by Novartis (April 2008), there
is a higher incidence of reported cases of SJS in
some Southeast Asian countries, such as Hong
Kong, the Philippines, ailand and Malaysia,
where there is a higher prevalence (10–15%) of
the HLA-B*1502 allele. us it is recommended
that testing for the presence of the HLA-
B*1502 allele should be considered in patients of
genetically at-risk populations before commencing
on carbamazepine therapy. For patients testing
positive, the use of carbamazepine should be
avoided and alternative treatment considered.
Screening is not recommended for patients who
are already on carbamazepine treatment, as the risk
of developing SJS or TEN is largely confined to
the first few months of therapy, regardless of HLA-
B*1502 status.
Carbamazepine should be used with caution in
the elderly. e free drug concentration may be
higher in the elderly because of reduced protein
binding and drug elimination [24, 59, 131].
Carbamazepine reduces tolerance to alcohol and
induces liver enzymes. Drug-induced hepatitis may
occur. Monitoring of haematological and hepatic
parameters should be performed before starting
carbamazepine therapy and repeated monthly in
the first 6 months of treatment, then every 6 to 12
months, or whenever necessary [79].
2. Second line treatment
e drugs described in the following section lack
systematic review or good quality randomised,
controlled trials and are considered as an alternative
option or add-on treatment to carbamazepine
[135].
(a) Gabapentin
Gabapentin is approved for partial seizures with
demonstrated clinical efficacy in the management
of neuropathic pain, especially for painful diabetic
neuropathy and postherpetic neuralgia [6, 19, 30,
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Orofacial Pain 185
77, 95, 96, 97, 100, 104, 107, 121]. Gabapentin
binds to the α-2-δ subunit of a voltage dependent
calcium channel at the dorsal horn of the spinal
cord and decreases the calcium-mediated synthesis
and release of excitatory neurotransmitters [77,
81]. It has gained popularity in the treatment of
neuropathic pain because of the low toxicity and the
favourable side-effect profile [70]. It is metabolised
and excreted unchanged by the kidneys and
hence preferred in the treatment of neuropathic
pain in the elderly [131]. Various case reports
have established the usefulness of gabapentin in
idiopathic trigeminal neuralgia and in refractory
trigeminal neuralgia associated with multiple
sclerosis [19, 53, 68, 69, 103, 107, 109]. Tremont-
Lukats et al. regarded gabapentin as the first choice
of therapy in neuropathic pain [120]. While it is
increasingly used in neuropathic pain, there is as
yet no evidence from published literature that it is
superior to carbamazepine [129]. A starting dose
of 300 mg at bedtime, then stepping up to 900
mg per day in three divided doses is recommended.
Patients with refractory pain may require 1800 mg
to 2400 mg per day in divided doses. Dizziness and
somnolence are the most common adverse effects.
If these adverse effects are severe, it is suggested to
commence at a lower dose, for example 100 mg
given daily, and slowly titrating to the effective dose
and at the usual dosing interval of every 8 hours.
(b) Phenytoin
Phenytoin is much less effective than carbamazepine
when used as a monotherapy and should be
considered as an add-on drug. It is started at a
single dose of 100 mg at bedtime and the usual
dose is 300 mg daily as an adjuvant therapy. Only
about 20% of patients obtain sustained relief from
phenytoin. Drowsiness, ataxia and diplopia are
common side effects. Phenytoin has the advantage
of being available intravenously for very severe pain
conditions that hinder oral intake. A loading dose
of 15 mg/kg
-1
may be used as for epilepsy and given
slowly at a rate of 25 mg/min
-1
or less [129].
(c) Baclofen
A few controlled trials have established the role of
baclofen in the management of trigeminal neuralgia
either alone or as an adjuvant to carbamazepine
[2, 33, 35, 39]. It acts by facilitating segmental
inhibition of the trigeminal complex [39]. e
starting dose is 5–10 mg three times daily. It can be
slowly increased to a daily maintenance dose of 50–
60 mg. Apart from the drowsiness and dizziness,
adverse effects are fewer than with carbamazepine.
ere is a potential for withdrawal syndrome
(hallucinations and seizures) and dose tapering has
to be slow [35].
(d) Tricyclic antidepressants
A tricyclic antidepressant such as amitriptyline is
not useful by itself as it seldom treats lancinating
pains well. Amitriptyline can be added on top of
the other anticonvulsants when the pain is difficult
to treat.
(e) Lamotrigine
Lamotrigine is an anticonvulsant that has been
reported to be useful for trigeminal neuralgia [68,
69, 78, 100, 106, 109, 121]. Experience is still
limited, but lamotrigine is a possibility as an add-on
treatment. Skin rash may develop in young patients
and mental confusion in elderly patients [69].
Interventional procedures
When drug therapy fails to relieve pain or when
a patient cannot tolerate the adverse effects of
drugs, interventional procedures, percutaneous
or open, should be considered. Percutaneous
procedures include local anaesthetic blocks,
gangliolysis, neuroablation and radiosurgery, while
surgical operations are neuroablative surgery or
microvascular decompression.
1. History [100]
Trigeminal neuralgia was treated for the first
time by alcohol injection into the nerve by Pitres
in 1902. A report by Cushing stated that Hartel
was the first to block the Gasserian ganglion itself
with alcohol. Kirschner applied diathermy on
the Gasserian ganglion in the early 1930s, while
Putnam and Hamptom introduced fluoroscopic
guidance during the procedure. Haakanson
advocated the use of glycerol instead of alcohol
for direct injection to the Gasserian ganglion in
1981. Sweet and Wepsic developed the technique
of percutaneous retrogasserian radiofrequency
thermal rhizotomy for the treatment of trigeminal
neuralgia from 1969 through 1986, which by and
large is used today.
2. Anatomy
e trigeminal nerve, the largest cranial nerve,
originates from the Gasserian ganglion, which lies
within the cranium in the Meckel’s cave close to the
apex of the petrous bone (Fig. 11.02). e ganglion
is bounded by the cavernous venous sinus, the
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186 Chi Tim HUNG, Theresa Tak Lai LI
inferior surface of the temporal lobe of the brain
inferiorly and the brain stem posteriorly.
e Gasserian ganglion gives off its three
branches intracranially (Fig. 11.03) and they
are somatotropically located on a plane running
from a superomedial to an inferolateral direction;
the ophthalmic branch is located dorsomedially,
the maxillary branch is intermediate, and the
mandibular branch lateroventrally and exits
through the foramen ovale.
All three branches carry sensory fibres providing
cutaneous and dermatomal innervation of the face
(Fig. 11.01), and sensory innervation of the nasal
and oral mucosae, the teeth and the anterior two-
thirds of the tongue. Motors fibres innervating
the masticatory muscles are contained only in the
mandibular branch.
3. Procedures
(a) Glycerol gangliolysis [14]
is is based on the rationale that glycerol acts
preferentially on small myelinated and unmyelinated
fibres, particularly on the damaged large myelinated
fibres. Glycerol gangliolysis is less dependent on
co-operation from the patient. e patient is better
sedated, making the procedure more comfortable.
e incidence of sensory dysaesthesia is low and
other complications are few. Glycerol gangliolysis
can be performed as a day procedure.
However, glycerol gangliolysis is not commonly
performed because it is technically difficult. e
needle has to enter the foramen ovale just anterior
to the geometric centre to enter the trigeminal
cistern. Placement at the anteromedial rim will
result in cavernous sinus bleeding.
e patient is premedicated with atropine and
placed supine. A 20G x 10-cm long needle enters
the Meckel’s cave under fluoroscopic guidance
and heavy sedation. After the needle position is
confirmed, a sitting position is assumed. e needle
is pushed in further until cerebrospinal fluid is seen
dripping from it. A radioactive contrast medium,
metrizamide, is injected in 0.2–0.4 ml increments
until the cistern fills and spills into the posterior
cranial fossa. e head is then positioned to remove
the metrizamide from the targeted nerve roots.
Glycerol is then injected and the nerve roots which
have been covered by metrizamide will be protected.
Facial pain may occur during glycerol injection and
can be controlled with opioids. e selected posture
is maintained for 1–2 hours. Usually the patient will
become pain free within the next 24 hours although
some may take days to weeks [17]. Patients may
report mild ipsilateral facial dysaesthesia following
glycerol injection procedure.
(b) Percutaneous radiofrequency rhizotomy
Radiofrequency rhizotomy produces neuroablation
by means of heat generated by the radiofrequency
current. An active electrode is placed where the
heat lesion is to be made. e size and consistency
of the lesion are dependent on temperature
generated; time for thermal equilibrium, which
Figure 11.02 The Gasserian ganglion in Meckel’s
cave filled with cerebrospinal fluid.
Figure 11.03 Diagram showing the Gasserian
ganglion located in the middle cranial fossa and the
course of the three branches.
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Orofacial Pain 187
is at 60 seconds; electrode size and configuration
(Fig. 11.04); and local tissue characteristics, such
as presence of cerebrospinal fluid or blood where
low electric resistance is encountered [92, 93, 102,
124]. e radiofrequency current heats the tissue
which in turn heats the electrode tip, thus enabling
accurate monitoring of tissue temperature. A series
of graded lesions of planned and reproducible size
is then produced.
Another observation of radiofrequency lesion-
making in the peripheral nervous system is the
highly selective destruction of pain-carrying nerve
fibres. Applying this observation specifically on
trigeminal ganglion, at temperatures near 60 to
70°C, the highly myelinated A-beta fibres can
survive better than the unmyelinated A-delta
and C fibres [93, 124]. Clinically, this results in
elimination of neuralgia with preservation of tactile
and motor innervations. Hence the advantages of
radiofrequency are the ability to accurately locate
the nerve fibres which cause pain before selectively
applying the lesion, a high chance of immediate
pain relief, low relapse rate and that the procedure
can be repeated. is is considered by many to
be the treatment of choice after failed medical
treatment [90, 114].
e organisation and function of the nerve block
facility prior to conduction of the radiofrequency
Figure 11.04 Enlarged view of radiofrequency
electrode tip showing the lesion size (circled
area) is related to the length and proportional
to the diameter (radius
2
) of the active tip of the
radiofrequency cannula at a given temperature. a
= length of active tip; b = lesion length; c = lesion
diameter.
Figure 11.06 A radiofrequency generator (with
permission of Baylis Medical Co Ltd).
Figure 11.05 A radiofrequency generator (with
permission of Neurotherm Ltd.
procedure is detailed in Chapter 26. A radiofrequency
generator capable of generating a 500MHz-
radiofrequency current with a stimulation mode
and a lesion mode must be available (Figs. 11.05
and 11.06). e TEW needle set has been used in
the past (Fig. 11.07). In current pain practice, the
disposable radiofrequency cannula 22G x 10 cm x
2 mm active tip (Fig. 11.08) a with corresponding
thermocouple electrode (Fig. 11.09) set is used to
produce a typical lesion size.
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188 Chi Tim HUNG, Theresa Tak Lai LI
e different techniques of percutaneous
radiofrequency rhizotomy are described
in elsewhere [92, 93, 102, 123, 124]. e
transforaminal approach is described below. e
intravenous access established. After antiseptic skin
preparation, the procedure is performed under
fluoroscopic guidance in a sterile manner. An
anteroposterior view of the skull is first obtained.
en a submentovertex projection of the skull is
obtained through a 30
° caudal inclination of the
fluoroscopy beam followed by a lateral inclination
of 15
° towards the side of the lesion in order to
view the foramen ovale (Figs. 11.11 and 11.12).
e patient is then administered monitored
anaesthetic care with intravenous propofol to
facilitate needle insertion. e point of skin needle
entry is 2–3 cm lateral to the corner of the mouth
and aimed at the intersection of the sagittal plane
through the pupil of the eye and the coronal plane
through the middle of the zygoma, 2 cm anterior
to the tragus. e trajectory of the cannula needle
should be in line with the axis of the fluoroscopy
beam directed towards the medial aspect of the
foramen ovale (Figs. 11.10, 11.13 and 11.14).
Caution has to be exercised in preventing the
cannula from entering the buccal mucosa. e
operator should place the index finger in the patient’s
mouth during advancement of the cannula. Sudden
contraction of jaw muscles or exacerbation of pain
heralds entry into foramen. A lateral fluoroscopic
view is obtained once the cannula has traversed the
foramen ovale. e lateral image should reveal that
the cannula is directed towards the angle formed
by the clivus and the petrous ridge of the temporal
Figure 11.07 TEW needle set.
Figure 11.08 Disposable radiofrequency cannula
(with permission of Baylis Medical Co Ltd).
Figure 11.09 Radiofrequency cannula with
connection to thermocouple electrode (with
permission of Baylis Medical Co Ltd)..
Figure 11.10 Photo of a spinal needle traversing
the foramen ovale at the skull base.
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Orofacial Pain 189
bone, and the tip must not exceed 2 mm in distance
from the plane of the clivus or above the crest of the
petrous ridge (Figs. 11.15 and 11.16).
Once the cannula position is confirmed, the
patient is allowed to emerge from anaesthesia and
stimulation is commenced to locate the desired
branch for lesioning at the following parameters.
Both sensory and motor stimulations are essential
to confirm accurately the position of the cannula
and to avoid injuring the motor component. e
usual stimulation parameters are as follows;
• Sensory stimulation at 50Hz. Paraesthesia
between 0.3 to 0.5 volt must be noted in the
Figure 11.11 Submental radiographic view with
the foramen ovale (arrow) seen medial to the medial
edge of the mandible.
Figure 11.12 Submental radiographic view (arrow)
of the foramen ovale.
Figure 11.14 Submental view with “tunnel view”
of the needle in the foramen ovale.
Figure 11.13 Submental radiograph with
radiofrequency needle at the foramen ovale.
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