A CASE REPORT

Trigeminal Neuralgia
ON TRIGEMINAL
The terrible journey of a
nerve impulse!
NEURALGIA
DR UNNIKRISHNAN
UNNIKRISHNAN P
P
DR
NEUROANAESTHESIA
NEUROANAESTHESIA
SCTIMST
SCTIMST
TRIVANDRUM
TRIVANDRUM
INDIA
INDIA

Dr. Manaswita Tripathy

 A 60 year old male reported to the department of Oral Medicine

& Radiology, KVGDC, sullia with a chief complaint of pain in
the right lower back teeth region since 10 days.
On eliciting the history of present illness same kind of pain was
present since past 20 years.

 Patient had taken medications for the same, following which

pain was under control but had reappeared 10 days back.

Pain was chronic in onset, severe & shooting type, intermittent

in nature, lasts for about 4-5 minutes followed by a period of
remission with 1 or 2 episodes per day.

 Pain aggravates on while speaking, eating, drinking but doesnt

disturb the sleep of the patient.
Medical history: patient had consulted a neurologist for the same
and had taken medications. Patient had also taken injection for
pain relief 3 times 9 years back.
History of snake bite 10 years back.

List of medications prescribed

previously

Tab Tegretal 400mg thrice daily

Tab Gabentin twice daily
Syp Balariohta three tsf twice daily
Cap Neuoden twice daily
Cap Renerve once daily
Cap Evion 400 mg once daily

 Dental history: patient had under gone removal of two teeth in rt

lower back teeth region 20 years back.
Habit index: habit of bidi smoking 4 times per day since 45
years.
Oral hygiene habits: brushes once daily using brush and paste
only on left side.
Diet : takes soft diet and chews only on left side.

 On Extra Oral Examination no

gross asymmetry was detected.
TMJ examination revealed bilaterally
synchronous movement, with out any
pain or clicking sound.
There was no trigger zone present
extra orally.

Intra oral examination

Grayish white palate was seen with small nodular excrescences
having small central red spots corresponding to inflamed orifices
of the minor salivary glands.

Intra oral trigger zone was present 1 cm

anterior to the right retro molar region.

Gingiva soft & edematous

Generalized recession

 Missing teeth wrt 17,18,46,47, 48

Generalized attrition
Moderate calculus & stains

Provisional diagnosis
Trigeminal Neuralgia of right mandibular branch
Chronic generalized periodontitis
Kennedys class II edentulous space in relation to
maxillary & mandibular arch.
Smokers palate

Differential diagnosis
1. Post traumatic neuralgia
2. Glossopharyngeal neuralgia
3. Migraine
4. Cluster headaches
5. Paroxysmal hemicrania syndromes

Investigations
OPG

MRI

Final diagnosis
Trigeminal Neuralgia of right mandibular branch
Chronic generalized periodontitis
Kennedys class II edentulous space in relation to
maxillary & mandibular arch.
Smokers palate

Treatment plan
Local anesthetic nerve block was given on right side.
(inferior alveolar nerve block)
Referred for surgical treatments.

Discussion

Wendy S. Hupp, Cranial Neuralgias, Dental clininics of noth america;

july 2013, vol 57, no 3

Wendy S. Hupp, Cranial Neuralgias, Dental clininics of noth america; july

2013, vol 57, no 3

Ophthalmic nerve
branches

A. Infratrochlear
B. Anterior Ethmoid
C. Posterior Ethmoid
D. Lacrimal
E. Supraorbital
F. Supratrochlear
G. Nasociliary

Maxillary nerve branches

A. Zygoticaticotemporal
B. Zygomaticofacial
C. Post. Sup. Alveolar Brs
D. Nasopalatine
E. Greater Palatine
F. Lesser Palatine
G. Mid. & Ant. Alveolar Brs
H. Infraorbital

Mandibular nerve branches

A. Auriculotemporal
B. Lingual
C. Inferior Alveolar
D. N. to the Mylohyoid
E. Mental
F. Buccal

 Three divisions of Trigeminal nerve

come together in an area called
Gasserion ganglion.
From there , the root continues back toward the side of the brain
stem & inserts into the pons.
Within the brain stem, the signals traveling through the trigeminal
nerve reach specialized clusters of neurons called Trigeminal nerve
nucleus.

Information brought to the brain stem by trigeminal nerve is then

processed before being sent to the brain and cerebral cortex, where a
conscious perception of facial sensation is generated

History
Aretaeus of Cappadocia at the end of 1st century - 1st clinical
description of TN
John Locke in 1677 (American physician & philosopher)
accurately identified clinical features
Nicolaus Andre in 1756 tic douloureux (painful jerking)
John fothergill in 1773- full & accurate description of TN
{OOO medical management update, Vol. 100, No. 5 Nov 2005}

Trigeminal neuralgia
Also called tic douloureux , Fothergills disease
Trigeminal neuralgia is diagnosed In 6 of every 100.000 persons
each year.
It is the most common of the cranial neuralgias and chiefly
affects individuals older than 50 years of age.
Sex predilection: female predisposition
Afflictions for sides: R>L

 Trigeminal neuralgia (TN) is defined by The International

Association for The Study of Pain (IASP), as sudden usually
unilateral severe, brief, stabbing, recurrent episodes of pain in the
distribution of one or more branches of the trigeminal nerve
The International Headache Society (IHS) divides Trigeminal
Neuralgia into two distinct categories: classical and
symptomatic (secondary) TN.

 Classical TN includes those patients in which no identifiable

cause can be found for their TN other than a vascular
compression of the trigeminal nerve.

Symptomatic TN describes those patients in which an

identifiable cause can be found, other than a vascular
compression, such as a tumour, arteriovenous malformation or
multiple sclerosis (MS).

The IHS diagnostic criteria

CLASSICAL Trigeminal neuralgia
A. Paroxysmal attacks of pain lasting from a fraction of a second to
2 minutes, affecting one or more divisions of the trigeminal
nerve and fulfilling criteria B and C.
B. Pain has at least one of the following characteristics:
1. intense, sharp, superficial or stabbing
2. precipitated from trigger areas or by trigger
factors

 C. Attacks are stereotyped in the individual patient

D. There is no clinically evident neurological deficit
E. Not attributed to another disorder

Symptomatic Criteria
A. Paroxysmal attacks of pain lasting from a fraction of a second
to 2 minutes, with or w/o persistence of pain between
paroxysms, affecting 1 or more divisions of the trigeminal nerve,
& fulfilling criteria B & C.
B. Pain has at least 1 of the following characteristics:
1. Intense, sharp, superficial, or stabbing
2. Precipitated from trigger zones or by trigger factors

 C. Attacks are stereotyped in the individual patient

D. A causative lesion, other than vascular compression, has

been demonstrated by special investigations &/or posterior
fossa exploration.

Etiology
The cause of classic TN remains controversial, but approximately
10% of cases are symptomatic and have detectable underlying
pathology, such as
Tumor of the cerebellopontine angle,
A demyelinating plaque of multiple sclerosis,
A vascular malformation.

The most frequent tumor is a meningioma of the posterior cranial fossa.

(a)

(b)
Anatomy Trigeminal nerve and Trigeminal neuralgia

(c)

Trigeminal neuralgia and its managementLuke Bennetto, Nikunj K Patel, Geraint

Fuller BMJ 2007;334:201-5

Pathophysiology
The Ignition Hypothesis as described by Devor et al is the most
widely accepted hypothesis for the pathophysiology of TN.

According to it, TN results from specific abnormalities of

trigeminal afferent neurons in the trigeminal root or ganglion.

Injury renders the axons hyperexcitable, resulting in paroxysmal

pain discharges.

 These partially injured sensory neurons thus become hyperexcitable

and exhibit a phenomenon known as After discharge.

These after discharge bursts may be triggered by an external

stimulus and extend beyond the duration of the stimulus.

 They can then also recruit additional neighbouring neurons,

leading to a rapid build up of electrical activity, which results in
a paroxsymal explosion of pain

Ephaptic Cross-talk that is, electrical cross-talk among neurons

also takes place and leads to further amplification.

 This is possible because the insulation has been eroded and the
fibers lie in close contact with each other.

Characteristically, TN attacks are rapid, and Devor et al explain

the Stop Mechanism as being due to post-burst hyperpolarisation,
which is due to influx of potassium ions into the channels, making
the nerve refractory to further excitation.

Joanna M Zakrzewska, Roddy McMillan, Postgrad Med J 2011;87:410e416.

 Additional evidence for this theory was obtained from a study

using tomographic magnetic resonance imaging (MRI), which
showed that contact between a blood vessel and the trigeminal
nerve root was much greater on the affected side.

 Evidence against this theory includes the finding by

neurosurgeons that manipulation of the area of the nerve root
may eliminate the painful episodes even when an atherosclerotic
vessel is not pressing on the nerve root.

Other investigators believe that a major factor in the etiology of

TN is a degeneration of the ganglion rather than the nerve root.

Clinical Features
Characterized by paroxysmal, severe, intense
pain that is almost always (95 %-97 %) unilateral.
Regional distribution limited to one or more
divisions of trigeminal nerve.
Most commonly involves the maxillary &
mandibular divisions, with opthalmic division
involved in < 5 % cases.

 Pain is frequently described as electric shock like, lancinating or

shooting, stabbing type with an abrupt onset and termination.

Pain is commonly triggered by minimal stimuli within the affected

area. (washing, shaving, chewing, talking, brushing teeth, and even
cold wind/drafts)

 The duration of attack usually ranges from a few seconds to 2

mins & may be either isolated or repetitive at short intervals so
that the individual attacks blend into one another.

Between attacks, patients report a burning or dull sensation,

which tends to subside in time.

 Periods of remission from attacks, ranging from several months

to years, occur in about 50 % of patients.

The clinical features of symptomatic TN is identical to classic

TN, except caused by a demonstrable structural lesion other than
vascular compression.

Wendy S. Hupp, Cranial Neuralgias, Dental clininics of noth america; july 2013, vol
57, no 3

 Pain in TN is precipitated by a light touch on a trigger zone

present on the skin or mucosa within the distribution of the
involved nerve branch.

Common sites for trigger zones include the nasolabial fold and the
corner of the lip.

Trigger zones are usually located on vermillion border of lip,

ala of the nose, cheek, chin, and around the eye.

 Just after an attack, there is a refractory period when

touching the trigger zone will not precipitate pain.

The number of attacks may vary from one or two per day to
several per minute.

There is often periods of exacerbations i.e. when painful attack

comes and periods of remission i.e. when no pain occurs

Fig. 4 Progression of Trigeminal Neuralgia

DIAGNOSIS
History
Trigeminal nerve examination
Diagnostic nerve blocking
MRI (brain)

The diagnosis of TN is usually based on the history of shooting pain

along a branch of the trigeminal nerve, precipitated by touching a
trigger zone, and possibly examination that demonstrates the shooting
pain.
A routine cranial nerve examination will be normal in patients with
idiopathic TN, but sensory and/or motor changes may be evident in
patients with underlying tumors or other CNS
pathology.

 Local anesthetic blocks, which temporarily eliminate the trigger

zone, may also be helpful in diagnosis.
Since approximately 10% of TN cases are caused by detectable
underlying pathology, enhanced MRI of the brain is indicated to
rule out tumors, multiple sclerosis, and vascular malformations.

Magnetic resonance angiography may also be needed to detect

difficult to visualize vascular abnormalities.

Differential Diagnosis
1. Dental pain
Post traumatic neuralgia
Paroxysmal hemicrania syndromes
TMD
Atypical facial pain
Temporal arteritis
2. Migraine and cluster headaches
Post herpetic neuralgia
Multiple sclerosis

Joanna M Zakrzewska, Roddy McMillan, Postgrad Med J 2011;87:410e416.

Luke Bennetto, Nikunj K Patel, Geraint Fuller, Trigeminal neuralgia and its
management, BMJ ; 27 jan 2007 : Volume 334

Treatment
PHARMACOLOGICAL
SURGICAL

Pharmacological Treatmen

Joanna M Zakrzewska, Roddy McMillan, Postgrad Med J 2011;87:410e416

Side effects of carbamazepine:

Drowsiness, mental confusion, dizziness, nystagmus (rapid
movements of the eye), ataxia (decreased coordination), diplopia
(double vision), nausea, and anorexia (loss of appetite).
Two to six percent of sufferers who take carbamazepine
develop blood disorders including leukopenia or agranulocytosis
or aplastic anemia.
Due to these complications, blood tests are usually conducted
before carbamazepine is started, and repeated intermittently.

Gabapentin (Neurontin)
Gabapentin is an anti-epileptic drug that is structurally related
to the neurotransmitter GABA.
The starting dose is usually 300mg three times a day and this
is increased to a maximal dose.
The most common adverse reactions include somnolence
(sleepiness), ataxia (decreased coordination), fatigue, and
nystagmus (rapid movements of the eye).
As with all of these drugs, rapid discontinuation should be
avoided as severe withdrawal reactions may occur.

 Topical injections of lidocaine into trigger points can provide

immediate but short-lasting pain relief.

Since TN may have temporary or permanent spontaneous

remissions, drug therapy should be slowly withdrawn if a patient
remains pain free for 3 months.

T. P. JORNS & J. M. ZAKRZEWSKA, Evidence-based approach to the medical management

of trigeminal neuralgia, British Journal of Neurosurgery, June 2007; 21(3): 253 261

Surgical Treatment
The interventions are performed at three target areas:

Peripheral - that is, distal to the Gasserian ganglion at

specified
trigger points

Gasserian ganglion level

Posterior fossa at the root entry zone.

Cryosurgery
Mental nerve - the third division
Infraorbital nerve - the second division.

This procedure is usually effective for 12 to 18 months, at which

time it must be repeated or another form of therapy must be
instituted.

Percutaneous radiofrequency thermocoagulation

A cannula is inserted into the trigeminal ganglion via the
foramen ovale.
The nerve is lesioned using heat (RFT), glycerol injection or
mechanical balloon compression.

 Pulsed radiofrequency thermocoagulation is a procedure

whereby the RFT is applied in pulses rather than a continuous
current.
surgical complication - Anesthesia Dolorosa, which is numbness
combined with severe intractable pain.

 The most extensively studied surgical procedure is Microvascular

Decompression of the nerve root at the brainstem.

It requires a craniotomy to be performed

in the post auricular region, thus exposing
the trigeminal root entry zone in the
posterior fossa.

 Any vessels impinging on the trigeminal nerve are identified

before being moved out of contact with the nerve and secured
using teflon tape or a vascular sling.
Complications were rare but included haematoma, infarcts, CSF
leak, transient diplopia, facial numbness, and facial weakness

 The most common complication is that of Aseptic Meningitis,

which occurs in roughly 11% of patients.

Sensory loss occurs in around 7% of patients.

The most significant long term complication is that of ipsilateral

hearing loss which occurs in as many as 10% of patients.

Gamma knife stereotactic radiosurgery

Minimally invasive technique for the treatment of TN.
Utilizes a cobalt-60 gamma emission source focused at the
trigeminal root entry zone.

Uses multiple beams of radiation, usually in doses of 70 to 90

Gy units, converging in three dimensions to focus precisely on
a small volume.

 The method relies on precise MRI sequencing that helps

localization of the beam and allows a higher dose of radiation to
be given with more sparing of normal tissue.

This technique is particularly helpful

for elderly patients with a high surgical risk.

 There are no guild lines for preventing g the development of

trigeminal neuralgia, but some steps can be taken to prevent the

attack.
1.EAT LUKEWARM FOODS AND DRINKS
2.EAT SOFT FOOD
3.AVIOD KNOWN TRIGGERS.
4.USE COTTON PADS WHEN WASHING YOUR FACE.

CONCLUSION
Trigeminal Neuralgia (TN) is neuropathic facial pain arising
from the trigeminal nerve.
It is a rare but debilitating condition that can initially be
treated in primary care by both medical and dental
practitioners, Currently, the guidelines and associated evidence
are insufficient to recommend definitive management, and
further high quality research is required.

References
T. P. JORNS & J. M. ZAKRZEWSKA, Evidence-based approach to the
medical management of trigeminal neuralgia, British Journal of
Neurosurgery, June 2007; 21(3): 253 261
Luke Bennetto, Nikunj K Patel, Geraint Fuller, Trigeminal neuralgia and its
management, BMJ ; 27 jan 2007 : Volume 334
Wendy S. Hupp, Cranial Neuralgias, Dental clininics of noth america; july
2013, vol 57, no 3
Joanna M Zakrzewska ,Journal of Neurology, Neurosurgery, and Psychiatry
1987;50:485-487
Oral & maxillofacial patholgy, Neville, 2nd edition.
Burkets 9th & 11th edition