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190 Chi Tim HUNG, Theresa Tak Lai LI
target painful division
• Motor stimulation at 2Hz. Little or no motor
contraction of the masseter muscle must be
present with 0.6 to 1 volt for V3 branch. ere
will be no motor contraction when the tip of
the cannula is in either V1 or V2 branches.
After location of the target division, the patient is
given propofol anaesthesia again for radiofrequency
thermal lesioning at the following parameters.
However, profound anaesthesia should be avoided.
e usual lesioning sequence is as follows;
• First lesion at 60°C for 60 seconds. After
lesion is completed, check corneal reflexes and
pain sensitivity bilaterally
• Second lesion at 65°C for 60 seconds. Proceed
in a similar manner
• ird lesion at 65°C for 60 seconds. Proceed
in a similar manner.
Haemodynamic changes including hypertension
and bradycardia can occur during radiofrequency
heating of rootlets especially in the elderly with
ophthalmic branch involvement [111]. Persistent
sensory loss over the face is common (98%)
and the degree is associated with likelihood of
recurrence [62]. Masseter muscle weakness is
not uncommon (2–4%) but improves with time,
usually within 1 year. Annoying dysaesthesia or
unpleasant sensory disturbances (5.2–24.2%)
and anaesthesia dolorosa (0.1–1.8%) can occur.
Ophthalmic-related adverse effects including loss
of corneal reflex (7%), neurolytic keratitis (0.6–
1.8%) visual loss or retrobulbar haematoma have
been reported. It is sometimes difficult to make
an isolated ophthalmic branch lesion without
corneal anaesthesia. e incidence of infection
from the Sweet series was 24 cases of meningitis in
7,000 cases of trigeminal radiofrequency lesioning
[111]. Transient abducens nerve palsy for less
than 2 months has been reported in the elderly
with ophthalmic involvement [40, 44]. Ocular
motor nerve paralysis and cavernous sinus fistula
are possible. Misplacement of needles into the
incorrect skull base foramina can lead to vascular
damage and intracranial bleeding.
Percutaneous radiofrequency rhizotomy is the
most extensively studied modality for treatment
of trigeminal neuralgia [13, 16, 62, 64, 86, 113,
114]. Clinical experience from various centers in
treating over 14,000 patients have been reported
in 33 series. e efficacy for mandibular neuralgia
is best and that for ophthalmic neuralgia is least
favourable. Since there is contagious innervation
by the ophthalmic branch for maxillary branch
neuralgia, results of maxillary neuralgia are also
not so favourable [17]. Technical failure occurs in
6–7 % of patients. e low recurrence rate is at the
price of sensory deficit [62]. e recurrence rate of
those with marked skin analgesia and hypoalgesia
at 4.5 years was 13% and 26% respectively; and
Figure 11.15 Drawing of needle directed towards
the angle formed by the clivus and petrous bone.
Figure 11.16 Lateral radiograph showing needle
passing through the foramen ovale and directed
towards the angle formed by the clivus and petrous
bone.
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Orofacial Pain 191
at 9 years it was 7.5% and 41% respectively [13].
e recurrence rate for those patients with no
permanent deficit was 60%.
A 25-year review of a series of 1,600 idiopathic
trigeminal neuralgia patients who underwent
a single procedure showed complete pain relief
immediately, and at 5-year and 10-year follow ups
in 97.6%, 57.7% and 52.3% of patients respectively
[52]. For those patients who had received
multiple procedures, pain relief was observed in
over 90% at 5-, 10- and 20-year follow ups. Early
pain recurrence (less than 6 months) was seen in
7.7% and late pain recurrence in 17.4%. Taha et
al. conducted another prospective 15-year follow
up of 154 consecutive patients with trigeminal
neuralgia treated by percutaneous radiofrequency
rhizotomy and concluded that the procedure has
a high long-term success rate in patients with
trigeminal neuralgia [113]. Pain recurred in 25%
of patients within 14 years of treatment. ey
noted that the rate of recurrence and dysaesthesia
correlate with the extent of lesioning, and the
timing of pain recurrence correlates with sensory
deficit. e recommendation was that dense
hypoalgesia in the painful trigger zone, rather
than analgesia, should be the target lesion for
an effective and safe treatment for trigeminal
neuralgia.
(c) Percutaneous balloon compression
rhizotomy
is refers to the use of a balloon to induce ischaemia
and mechanical damage to rootlet and ganglion
cells. As with glycerol gangliolysis, no patient co-
operation is needed. It is technically easier for
the inexperienced hands. A general anaesthesia is
needed. e lesion cannot be confined to a single
division. Hypertension and bradycardia are more
pronounced during the procedure. Hypertension
has to be treated promptly and may require the use
of sodium nitroprusside.
e procedure involves inserting a 14G needle
under fluoroscopic guidance into the foramen
ovale. Such a large bore needle is often difficult to
cannulate. A 4FG Fogarty embolectomy catheter is
then advanced 15–20 mm beyond the needle and
the balloon inflated with non-ionic contrast, which
will appear as a pear on fluoroscopy if the balloon is
situated in the Meckel’s cave. e balloon inflation
is kept for a minute. Sensory deficit is related to
duration of compression.
Immediate pain relief is possible in 90–100% of
patients. According to Mullan, the long-term
relief is about 80% at 5 years and 70% at 10 years
[80].
e average time for recurrence ranges from
4.2 to 6.5 months. As many as 77% patients may
have recurrence of pain at 36 months. Most of
recurrences of pain occur before 48 months. e
pain that recurs after balloon compression can be
easily controlled with drugs.
Complications include sensory loss over the
mandibular branch, dysaesthesia (6.7–8.5%),
balloon rupture, herpetic eruptions and abducens
nerve palsy. Masticatory muscle weakness occurs
in nearly all patients. e muscle weakness usually
disappears in about 3 months. Sometimes it can last
up to a year and in 3% of patients it may become
permanent. Keratitis and corneal anaesthesia are
rare.
Please also refer to Chapter 31 for more neurosurgery
information.
Which procedure to choose?
An ideal treatment should eliminate the pain
with no sensory loss, with low treatment
related morbidity and virtually no mortality.
Microvascular decompression carries a small risk
of mortality. Incidences of facial numbness and
corneal anaesthesia are lowest, but cranial nerve
and hearing deficit can occur. Percutaneous
radiofrequency rhizotomy has the lowest
recurrence rate but at the cost of facial numbness
and possible corneal anaesthesia. Percutaneous
balloon compression rhizotomy has a higher
recurrence rate and masticatory dysfunction is
common. e initial success rate for glycerol
ganglionlysis is not as good as the other procedures
and the technique is more demanding. More
information about radiosurgery is needed before a
conclusion can be made about its role. No systemic
reviews or randomised controlled trials exist to
provide clinical evidence on the efficacy of these
interventional procedures for the management of
trigeminal neuralgia. e choice of technique will
hence depend on expertise and facilities available
and the theory combined with clinical experience
in the technique’s execution.
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192 Chi Tim HUNG, Theresa Tak Lai LI
Postherpetic Neuralgia
Facial pain may also occur due to postherpetic
neuralgia affecting the trigeminal nerve. Details of
postherpetic neuralgia can also be found in Chapter
15.
Glossopharyngeal Neuralgia
[74]
Glosspharyngeal neuralgia is quite similar to
trigeminal neuralgia except for the distribution of
pain. e condition is probably more common than
is recognised. It originates from a dysfunction of
the glossopharyngeal nerve that can be compressed
by an artery as it exits from the medulla to the
jugular foramen. Multiple sclerosis can give rise to
the same picture. It is characterised by lancinating
pain deep in the pharynx, base of the tongue and
tonsillar fossa (oropharyngeal form). e pain can
radiate to the ear (otitic form), angle of the jaw
and upper neck, where it can be confused with
trigeminal neuralgia. In fact, trigeminal neuralgia
can occur concurrently in approximately 10% of
patients afflicted with glossopharyngeal neuralgia.
Trigger areas can be identified in the same area of the
pain but not on the face. e disease affects those
aged 50 years or older (57%) and can be bilateral
in 12% of patients. Since the glossopharyngeal
nerve is involved in the regulation of heart
rate and blood pressure, cardiac arrhythmia or
asystole has been described during an attack. is
feature differentiates it from trigeminal neuralgia.
Diagnostic testing with local anaesthetics can
be done to relieve the pain. Local anaesthetics
can be injected into the trigger area, around the
glossopharyngeal nerve at the jugular foramen, or
topically onto the pharynx as appropriate.
e principle of treatment for glossopharyngeal
neuralgia follows that of trigeminal neuralgia.
Carbamazepine is the mainstay therapy. A recent
report on the use of pregabalin in a patient with
glossopharyngeal neuralgia described complete
pain relief with full tolerance of the drug; however,
more clinical trials are needed for clinical evaluation
[7, 72]. Interventional procedures involving
radiofrequency ablation of the glossopharyngeal
nerve can be performed. Operative procedures
including sectioning the glossopharyngeal nerve
and upper rootlets of the vagus nerve may give
good results [89].
Other Cranial Neuralgias
Other less commonly encountered neuralgia
syndromes in the face include the geniculate
neuralgia (Ramsay Hunt Syndrome),
sphenopalatine neuralgia and vidian neuralgia. e
area of pain is related to the nerve affected, e.g.
pain occurs around the ear and tonsillar regions in
geniculate neuralgia. Interested readers should refer
to standard textbooks for details.
Table 11.02 Comparison of trigeminal neuralgia and postherpetic neuralgia
Trigeminal neuralgia Postherpetic neuralgia
Branch of trigeminal nerve
commonly affected
V2, V3 V1
Trigger Localised trigger area or outside
the affected area
Non-noxious tactile trigger in the
affected area
Pain qualities Shock-like pain Shock-like pain, allodynia,
hyperaesthesia
Sensory loss No Yes
Pain-free intervals Yes No
Pathology Demyelination at nerve root Inflammatory damage to nerve
root, dorsal horn, spinal cord
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Orofacial Pain 193
Atypical Facial Pain [45, 49,
63, 110]
Atypical facial pain or atypical facial neuralgia is
a loose term used to encompass a large variety of
conditions that have common symptoms and signs
but unknown aetiology. Occasionally, there will
be a history of trauma to the peripheral branches
of the trigeminal nerve, or dental interventions.
Sometimes chronic infection of the nasal sinuses,
jaw or skull base may be found. Otherwise this is
a diagnosis by exclusion and hence it is difficult
to treat. Because of the lack of precision in the
terminology, the International Headache Society has
dropped atypical facial pain in its classification.
Clinical features
e condition usually affects middle-aged females
who may have shopped around many doctors.
e pain is usually unilateral. A bilateral variant
has been described which almost always affects
females. e area affected does not conform to
the anatomical innervation of the trigeminal
branches. Occasionally, the pain can extend into
the neck as well. In contrast to the brief lancinating
attacks with clear pain-free periods in trigeminal
or glossopharyngeal neuralgia, the pain in atypical
facial pain is constant, vague, wandering and poorly
localised. e pain can last for days and pain-free
periods are uncommon. e pain is burning or
aching in character. Physical examination may reveal
hypoaesthesia in the area of pain. Some patients
may also present with significant psychopathology
[43]. Patients may appear depressed, anxious and
emotional.
Diagnosis
is is a diagnosis by exclusion. A diligent search for
a treatable lesion such as malignancy and infection
must be made. Even when the patient presents
with overt psychological symptoms, it does not
mean that there is no underlying organic lesion. A
detailed psychological work-up is necessary and the
diagnosis has to be reviewed at intervals.
Treatment
Treatment outcome is in general unsatisfactory.
Reassurance and building a proper trusting doctor-
patient relationship is important. Many patients
find it difficult to accept that their pain is not
organic in origin; such a notion would imply a
disorder of their mind. It takes time and patience
to explain to the patient that pain has different
elements and dimensions. Absence of an organic
cause does not imply something wrong in the
mind. e pain should be acknowledged by the
physician as genuine and not imaginary. Indeed,
pain may arise from muscle cramping due to stress.
Patient should be reassured time and again that this
is a common disorder. ere is usually no serious
physical or progressive disorder associated with
it. Once a trusting relationship has been built up,
patients will stop shopping around for doctors.
ey can then comply with the treatment regime.
Drug treatment with tricyclic antidepressants may
help. It is important to explain to the patient before
commencing treatment that the antidepressant is
used for the central analgesic effect and not for
the antidepressant effect. Antiepileptic agents like
gabapentin and carbamazepine may also be of
benefit.
Interventional procedures, especially the
neuroablative procedures, should not be undertaken
lightly in any patient with atypical facial pain. It
might be better to regard atypical facial pain as
a contraindication to interventional treatment
unless there is a clearly surgically treatable lesion.
Interventional procedures in atypical facial pain
rarely yield good results and may bring on new
symptoms.
Temporomandibular Joint
Disorders
Temporomandibular disorders have been
collectively grouped as myofascial pain dysfunction
syndrome or temporomandibular joint (TMJ)
dysfunction syndrome [43]. ese terms have
been used interchangeably in the past. However,
it is probably justified to segregate the myofascial
pain dysfunction into two subgroups on the basis
of psychometric differences, clenching habits and
masseter muscle electromyogram levels. ese are
namely the myogenic facial pain group and the
TMJ internal derangement group.
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194 Chi Tim HUNG, Theresa Tak Lai LI
Patients with internal derangement of the TMJ
usually present with pain localised to the joint
[26]. e articular disc of the joint is usually
the culprit and it may become displaced during
TMJ movements. Initially, the displacement can
be reduced spontaneously resulting in a click
on opening of the mouth and a reciprocal click
on closing the mouth. As the disease advances,
intermittent locking of the jaw may occur. When
disc displacement occurs without reduction, a
closed lock with reduced mouth opening will
result. An arthrography of the TMJ can be
performed to evaluate the displacement. Magnetic
resonance imaging is noninvasive and permits
displacements to be imaged in all directions. ere
is also increased incidence of osteoarthrosis of
TMJ in patients with TMJ disc displacement. e
relationship of TMJ disc displacement to the pain
and joint dysfunction needs to be further clarified.
Not all patients with TMJ disc displacements will
complain of pain. Apart from disc displacements,
primary and secondary degenerative diseases of the
TMJ such as rheumatoid arthritis could also give
rise to localised pain.
Treatment
Treatment modalities include physical methods
such as transcutaneous electrical nerve stimulation,
ultrasound, muscle relaxation techniques,
acupuncture and trigger point injections.
Physiotherapy such as postural awareness and range
of motion exercises will help. Occlusal appliances
are necessary for intracapsular dysfunction or
myogenic dysfunction [23]. Surgery on the TMJ
may be indicated for treatment of intra-articular
biomechanical dysfunction where there is evidence
that surgical correction will restore function
and decrease symptoms [75]. Such procedures
include arthrocentesis, arthroscopic surgery and
arthrotomy.
Myofascial Pain Syndrome
Myofascial pain syndrome is believed to be a
muscle disorder characterised by the presence of
hypersensitive points called trigger points within
the muscles affected [108]. Apart from the pain,
there is also tenderness, muscle spasm and reduced
range of movement of the nearby joint. When the
trigger points are activated, local pain can be felt
in the muscle as well as distant pain. Activating
such trigger points often reproduces the symptoms
the patient has been suffering. Although the distal
pain does not follow a dermatomal pattern, the
referral pattern is fairly constant for the structure
stimulated. Many confusing terms have been used
in the past, including myalgia, myositis, fibrositis
and myofascitis. Fibromyalgia probably represents a
more generalised disorder affecting multiple groups
of muscles in the body [132]. Myofascial pain
syndrome behaves very similarly to fibromyalgia
except for the magnitude of the muscle group
involvement. However, there are problems with
the constructs of myofascial pain syndrome and
fibromyalgia, and doubts exist as to whether these
two conditions are valid diagnosis entities. Details
can be found in Chapter 14.
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Introduction
Neck pain is defined as pain perceived dorsally in the cervical
region of the spinal column, between the superior nuchal line
and an imaginary transverse line through the spinous process
of T1 [35]. However, referred pain towards the shoulders,
trapezius and interscapular regions is not uncommon. is is
described in patterns relative to the cervical root distributions
over relevant cervical facet joints as described by Dwyer [16].
However, it should be noticed that this referral pain is not
the same as radicular pain caused by nerve root compression.
Radicular pain is sharp and, in general, marks a narrow band
of pain path down the upper limb. Referred pain is dull and
poorly localised towards the shoulder and upper back.
Neck pain is one of the most common musculoskeletal
disorders, second only to low back pain. Bogduk called it “the
poor cousin of low back pain” [7]. It is poorer in terms of
prevalence as well as having much less literature and fewer
studies relevant to its cause, diagnosis and management.
Neck pain also differs from low back pain in having a higher
proportion of cases with definite cause relationship to known
trauma incidence, most notably the infamous “whiplash
injury” after road traffic accidents.
In practice, though the cause and outcome of neck pain is also
much related to psychosocial factors, a higher proportion of
neck pain patients, relative to low back pain patients, have no
history of definite occupational mishap.
With these differences, it is necessary to be very careful and
selective in directly extrapolating the knowledge on low back
pain to the management of neck pain. is strategy is tempting
Neck Pain
12
Ping Hong CHIN
INTRODUCTION
EPIDEMIOLOGY
RISK FACTORS
LOOKING FOR A CAUSE
ASSESSMENT OF
COMPLICATIONS
TREATMENT OPTIONS
CONCLUSION — PROBLEM
SOLVING APPROACH
REFERENCES
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