2. Terminologies
PAIN : an unpleasant sensory and emotional experience associated with actual or
potential tissue damage or described in terms of such damage
NOCICEPTION: noxious stimulus originating from the sensory receptor
SUFFERING: refers to how human reacts to perception of pain
NEURALGIA : actual pain in a nerve, several nerves or groups of nerves
NEUROPATHY : disturbance in function or damage to the nerves
NEUROPATHIC PAIN: any abnormality in components of the nervous system itself
rather than to noxious stimulation of otherwise normal neural structures as with
superficial & deep somatic pain disorders
PAROXYSMAL : sudden recurrence or intensification of symptoms, such as
a spasm or seizure. These short, frequent, and stereotyped symptoms
NEUROPATHIC FACIAL PAIN : pain around the mouth or face that arises from a
primary lesion or dysfunction of the nervous system
4. Trigeminal Neuralgia : ‘sudden,
usually unilateral, severe, brief,
stabbing, recurrent episodes of pain
in the distribution of one or more
branches of the trigeminal nerve.
The International Association for the Study of Pain
DEFINITION
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
5. Painful unilateral affliction of the face, characterized by brief electric
shock like pain limited to the distribution of one or more divisions of
the trigeminal nerve. Pain is commonly evoked by trivial stimuli
including washing, shaving, smoking, talking, and brushing the teeth,
but may also occur spontaneously. The pain is abrupt in onset and
termination and may remit for varying periods.
Indian Headache Society
DEFINITION
7. Synonyms
Tic Douloureux
Tic: A repetitive
movement that is
difficult, if not
impossible to
voluntarily control
Douloureux- pain
French word
8. HISTORY
Aretaeus of Cappadocia is credited with the
first clinical description - described ‘‘spasm
and distortion of the countenance take place”
1677 John Locke, recognized that her facial
pain was not caused by dental pathology but
rather by neuralgia of the trigeminal nerve
In 1756, Nicolaus Andre - tic
douloureux
John Fothergill in 1773 also outlined the
major clinical features of TN
9. INCIDENCE
(Penman, 1968).
(Katusik et al., 1990 ;
Rothman and Monson,
1973).
Bennetto L, Patel NK, Fuller G. Trigeminal neuralgia and its management. BMJ. 2007;334:201-20
10. Etiology
Dental pathosis- loss of teeth
and degeneration of nerve.
Allergic
Mechanical factors
Anomalies of superior
cerebellar artery
Secondary lesion
Joffroy A, Levivier M, Massager N. Trigeminal neuralgia Pathophysiology and treatment. Acta neurol. belg., 2001, 101, 20-2
11. Pathophysiology
Ectopic action potential generated in the
pain sensitive afferent fibres of 5th cranial
nerve – produce symptoms
Compression leads- demyelination of large
myelinated fibres( does not carry pain)
Demylinated - hyperexcitable
Convey tactile stimuli when
electrically coupled with small
unmyelinated fibres in close
proximity
Nurmikko TJ, Eldridge PR, Trigeminal neuralgia- pathophysiology, diagnosis and current treatment. Br J Anaesth 2001; 87: 117-
32.
12. Pathophysiology
These findings
favor a
mechanism
whereby afferent
nociceptors
could be
stimulated by
activity in injured
low-threshold
mechanorecepto
rs.
These
produce a
transient
depolarizatio
n in
neighboring
passive C
neurons in
the same
ganglion
After nerve
injury, there is
an increased
proportion of A-
beta fibers with
subthreshold
oscillations that
ultimately
generate ectopic
discharges.
The triggering of
pain in TN may
follow innocuous
stimuli, a
phenomenon that
is probably
explained by
postinjury
changes in
neuronal function.
Ignition
theory
Devor and
colleagues
13. International headache society
Types
CLASSICAL
TN
A)Paroxysmal attacks of
pain lasting from fraction of
a second to 2 mins
affecting one or more
divisions of Tn and fulfilling
criteria B) and C)
B)Pain has atleast one of the
following characteristics:
1) intense, sharp, superficial or
stabbing
2) Precipitated from trigger areas or
by trigger factors
C)Attacks are
sterotyped in the
individual patient
D)No clinical
evident of
neurologically
deficit
SYMPTOMATI
C TN
A)Paroxysmal attacks of pain
lasting from fraction of a
second to 2 mins, with or
without persistence of aching
between paroxysms affecting
one or more divisions of Tn
and fulfilling criteria B) and C)
B)Pain has atleast one of the
following characteristics:
1) intense, sharp, superficial or
stabbing
2) Precipitated from trigger areas or
by trigger factors
C)Attacks are
sterotyped in the
individual patient
D)A causative
lesion other than
vascular
compression
15. ATYPICALTRIGEMINAL NEURALGIA:
characterized by a unilateral, prominent constant
and severe aching and burning pain superimposed
upon otherwise typical symptom.
Some believe that atypical TN is due to vascular
compression upon specific part of the trigeminal
nerve( the portio minor) while other theorize atypical
TN as more severe progression of typical TN
18. CLINICALFEATURES
Age of occurrence- late middle age. Female predilection.
Usually unilateral can be bilateral. Predilection for right side
Sudden, intermittent paroxysmal, sharp, shooting, lancinating, shock like pain,
elicited by slight touch – trigger points- which radiates from that point, across
the distribution of one or more branches.
Maxillary > Mandibular > Ophthalmic
Pain rarely crosses midline. Lasts for few secondsbut recur at variable
frequency.
During attack: patient grimaces with pain, clutches his hands over the affected
side of face, stopping all the activities and holds or rubs face, which may redden
or eyes may be filled with tears until the attack subsides
Attacks do not occur during sleep
Extreme cases- motionless face- frozen/ mask like face
19. washing
the face
brushing
teeth
shaving
applying
make up
going out
in cold
wind
vibrations
from
walking
Trigger factorsTrigger zones and trigger points
V2- skin of upper lip, ala,
cheeks & upper gums
V3- lower lip, teeth or gums
of lower jaw
V1- supraorbital ridge of
affected side
20.
21.
22. ‘Ice pick, shocks,
live 300-volt
current, electric
shock-like pains’
‘Constant hot knife
jabbing volts or
stabs in my right
cheek area’
‘Shooting jolts of
electricity
directly into the
raw nerves’
‘While brushing
my teeth one
morning I got a
bolt of lightning
exploded in my
face.’
‘The pain was sharp
stabbing, electrical
shock-like pains that
would last for only
seconds; however, there
would be a dull
sensation after the pain
subsided.’
Patient’s description of pain
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
23. WHITE AND SWEET DIAGNOSTIC CRITERIA FOR TRIGEMINAL
NEURALGIA
Pain-
paroxysmal
Pain-
provoked by
light touch to
trigger
zones
Pain-
confined to
trigeminal
distribution
Pain-
unilateral
Clinical
sensory
examination-
normal
26. Well taken history
Classic clinical
pattern
Response to
treatment with
carbamazepine –
universal in TN.
Diagnostic nerve
blocks- 2%
lignocaine
without
adrenaline
MRI
MRI showing neurovascular
compression of right trigeminal
nerve. Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
27. Differentialdiagnosis
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
28. SYMPTOM TRIGEMINAL NEURALGIA PULPITIS
CHARACTER Shooting, stabbing, sharp, electric Sharp, aching, throbbing
SITE/ RADIATION Trigeminal nerve distribution only,
intraoral and extraoral
Around a tooth, intraoral
SEVERITY Moderate to severe Mild to moderate
DURATION 1-60 s Refractory period Rapid but no refractory
period
PERIODICITY Rapid onset and termination, complete
periods of remission weeks to months
Unlikely to be more than 6
months
PROVOKING
FACTORS
Light touch, non- nociceptive
No change on postural changes
Hot/ cold applied to teeth
Increases on lying down
position
RELIEVING
FACTORS
Keeping still, drugs Avoid eating on that side,
drugs
ASSOCIATED
FACTORS
LA placed in trigger area relives pain,
severe depression and weight loss
Decayed tooth, exposed
dentine
29. SYMPTOM TRIGEMINAL NEURALGIA NEUROPATHIC TRIGEMINAL
PAIN
CHARACTER Shooting, stabbing, sharp, electric Aching, throbbing
SITE/ RADIATION Trigeminal nerve distribution only, intraoral and
extraoral
Around a tooth or area of past
trauma/ dental surgery or facial
trauma
SEVERITY Moderate to severe Moderate. Continuous soon after
surgery
DURATION 1-60 s Refractory period Continuous soon after injury
PERIODICITY Rapid onset and termination, complete periods
of remission weeks to months
Continuous
PROVOKING
FACTORS
Light touch, non- nociceptive Light touch
RELIEVING
FACTORS
Keeping still, drugs Avoid touch
ASSOCIATED
FACTORS
LA placed in trigger area relives pain, severe
depression and weight loss
History of dental treatment or
trauma in the area, may be loss of
sensation, allodynia near pain, LA
relives pain
30. SYMPTOM TRIGEMINAL NEURALGIA TMD
CHARACTER Shooting, stabbing, sharp, electric Dull, aching, nagging, sharp at
times
SITE/ RADIATION Trigeminal nerve distribution only, intraoral and
extraoral
Pre- auricular, radiates down
mandible, temple area, may be
postauricular or neck
SEVERITY Moderate to severe Mild to severe
DURATION 1-60 s Refractory period Lats for hours, mainly continuous
can be episodic
PERIODICITY Rapid onset and termination, complete periods
of remission weeks to months
Tends to build up slowly and
diminish slowly, lasts for years
PROVOKING
FACTORS
Light touch, non- nociceptive Clenching teeth, prolonged
chewing, yawning
RELIEVING
FACTORS
Keeping still, drugs Rest, decrease mouth opening
ASSOCIATED
FACTORS
LA placed in trigger area relives pain, severe
depression and weight loss
Muscle pain in other parts of the
body, limited opening, clicking on
wide opening
31. SYMPTOM TRIGEMINAL NEURALGIA SHORT UNILATERAL
NEURALGIFORMWITH
AUTONOMIC SYMPTOMS OR
CONJUNCTIVAL TEARING
CHARACTER Shooting, stabbing, sharp, electric Burning, stabbing, sharp
SITE/ RADIATION Trigeminal nerve distribution only, intraoral
and extraoral
Periorbital but can affect
maxillary division
SEVERITY Moderate to severe Severe
DURATION 1-60 s Refractory period Episodic 5-240s
PERIODICITY Rapid onset and termination, complete
periods of remission weeks to months
Numerous, can be periods of
complete remission
PROVOKING
FACTORS
Light touch, non- nociceptive Light touch
RELIEVING
FACTORS
Keeping still, drugs Nil
ASSOCIATED
FACTORS
LA placed in trigger area relives pain,
severe depression and weight loss
Often restless
32. SYMPTOM TRIGEMINAL NEURALGIA PAROXYSMAL HEMICRANIA
CHARACTER Shooting, stabbing, sharp, electric Throbbing, Boring
SITE/ RADIATION Trigeminal nerve distribution only, intraoral and
extraoral
Orbit, temple
SEVERITY Moderate to severe Severe
DURATION 1-60 s Refractory period Episodic 2-30 min
PERIODICITY Rapid onset and termination, complete periods
of remission weeks to months
1-40 a day, can be periods of
complete remission
PROVOKING
FACTORS
Light touch, non- nociceptive Nil
RELIEVING
FACTORS
Keeping still, drugs Indometacin
ASSOCIATED
FACTORS
LA placed in trigger area relives pain, severe
depression and weight loss
May have migrainous features
33. • Often preceded by aura, severe unilateral
headache often associated with nausea,
photophobia, phonophobia and neck stiffness
MIGRAINE
• History of herpes zoster or vesicular outbreak
POST HERPETIC NEURALGIA
• Common in elderly people, temporal pain should
be constant and associated with jaw claudication,
fever, weightloss.temporal arteries may be firm,
tender and nonpulsatile on palpation
TEMPORAL ARTERITIS
36. Drug Daily dose Mechanism Use Side effects
Carbamazepin
e
TEGRETOL,
CARBATOL
200- 1000 mg in
2 divided doze
Slows recovery rate of
voltage- gated sodium
channels, modulates
activated calcium channel
activity and activates
descending inhibitory
modulation system
Begin with small
doses, depending
on tolerability,
retard version
useful at night
Nausea,
drowsiness,
fatigue, dizziness,
memory problem,
diplopia,
nystagmus, liver
dysfunction
Oxcarbazepin
e
300 – 1800 mg
daily in 2 divided
doses
- “ - Use on a four
times daily bases
Decreased blood
sodium level,
dizziness, fatigue,
headache, tremors,
drowsiness,
dimished
concentration,
diplopia and
stammering
Gabapentin
NEURONTIN
1200- 3600 mg
daily in 3-4
divided dose
Unknown. But possibly
includes blockage of
voltage- gated calcium
channels by binding to
alpha subunits
Injected weekly
into trigger zones
Fatigue, dizziness,
ataxia, nystagmus
and tremor
Pharmacological treatment
37. Drug Daily dose Mechanism Use Side effects
Phenytoin
EPILEPTIN
EPTOIN
300- 500 mg
daily
Promotes
sodium efflux
from neurons
Along with
carbamazepine
Nystagmus,
ataxia, slurred
speech,
decreased
coordination,
mental
confusion
Lamotrigine
LAMITOR
100- 150 mg
daily in 2
divided doses
Decreases
repetitive firing
of sodium
channels by
slowing the
recovery rate of
voltage- gated
channels.
Initially very slow
escalation.
Can use along
with
carbamazepine
Decreased
blood sodium
level, dizziness,
fatigue,
headache,
tremors,
drowsiness,
dimished
concentration,
diplopia and
stammering
Pharmacological treatment
38. Surgical treatment
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
39. PERIPHERAL TECHNIQUES
Cryotherapy
Neurectomies
Peripheral radiofrequency thermocoagulations
(RFT’ s)
Injections- alcohol, phenol & streptomycin
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
J 2011;87:410 - 416
44. Take a dose 30-45 min prior to activities that involve light touch
Space out the doses evenly throughout the day
Avoid rapid escalation; often one dose escalation every 3 days is sufficient
Take a larger dose at night especially if pain does not wake at night
Expect to get side effects; reduction of dose can sometimes help
Stop the drug if a rash develops
Return to the general practitioner for blood test monitoring, especially in the first
few months of use
Inform any other prescribers that the patient is using these drugs, because
possible drug interactions are common (eg, carbamazepine and warfarin)
Once all pain has stopped and it can no longer be triggered, consider slow
reduction and eventual cessation of drug
restart the drug if any pain returns
Keep pain diaries in order to aid accurate evaluation of drug efficacy.
PATIENT INFORMATION
Zakrzewska JM, McMillan R. Trigeminal Neura;gia: the diagnosis and
management of this excruciating and poorly understood facial pain.Postgrad Med
47. 1. Gronseth G, Cruccu G, Alksne J, et al. Practice parameter: the diagnostic evaluation
and treatment of trigeminal neuralgia (an evidence-based review): report of the Quality
Standards Subcommittee of the American Academy of Neurology and the European
Federation of Neurological Societies. Neurology 2008;71:1183e90.
2. Nurmikko TJ, Eldridge PR, Trigeminal neuralgia- pathophysiology, diagnosis and
current treatment. Br J Anaesth 2001; 87: 117-32.
3. Joffroy A, Levivier M, Massager N. Trigeminal neuralgia Pathophysiology and
treatment. Acta neurol. belg., 2001, 101, 20-25.
4. Zakrzewska JM, Linskey ME. Trigeminal neuralgia. Clin Evid (Online);2009:1207.
5. Tyler-Kabara EC, Kassam AB, Horowitz MH, et al. Predictors of outcome in surgically
managed patients with typical and atypical trigeminal neuralgia: comparison of results
following microvascular decompression. J Neurosurg 2002;96:527e31
6. Gupta A, Singh SK, Sahu R. Trigeminal Neuralgia – A review Journal of dentofacial
sciences 2012; 1(1): 27-31
REFERENCES
48. REFERENCES
7. Bennetto L, Patel NK, Fuller G. Trigeminal neuralgia and its management. BMJ.
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8. Zakrzewska JM, Linskey ME. Trigeminal neuralgia. In: Zakrzewska JM, ed. Orofacial
Pain. New York: Oxford University Press; 2008, pp 119-134.
9. Love S, Coakham HB. Trigeminal neuralgia: pathology and pathogenesis. Brain
2001;124:2347e60.
10. Cruccu G, Gronseth G, Alksne J, et al. AAN-EFNS guidelines on trigeminal neuralgia
management. Eur J Neurol 2008;15:1013e28.
11. Weigel G, Casey KF. Striking Back. The Trigeminal Neuralgia Handbook. Barnegat
Light: The Trigeminal Neuralgia Association, 2000
12. Wiffen P, Collins S, McQuay H, et al. Anticonvulsant drugs for acute and chronic pain.
Cochrane Database Syst Rev 2005;(3):CD001133
13. Tolle T, Dukes E, Sadosky A. Patient burden of trigeminal neuralgia: results from a
cross-sectional survey of health state impairment and treatment patterns in six
European countries. Pain Pract 2006;6:153e60
49. 14. B D Chaurasia. Human Anatomy Regional and Applied Dissection and Clinical Vol.3 CBS
Publishers & Distributers;2004.
15. Okeson JP. Bell’s Orofacial pains. 6th edition. 2005.
16. www.teachme anatomy.com
17. Greenberg, Glick.,BURKETS Oral Medicine 12th Edition: 2012, CBS Publishers
18. Laskin MD, strauss RA. Oral and maxillofacial surgery clinics. 2003
19. Textbook of Oral & Maxillofacial Surgery by Neelima Anil Malik, 2 nd Edition 2008, Jaypee
Publishers
20. Pereira EAC. Trigeminal Neuralgia-Divided but Not Classified.Anesth Pain. 2012;2(2):101-2.
21. Serivani SJ, Mathews ES, Maciewicz RJ. Trigeminal Neuralgia. Oral surg Oral Med Oral
Pathol Oral Radiol Endod 2005; 100:527-38
22. Rothman KJ, Monson RR. Survival in trigeminal neuralgia. J Chronic Dis 1973;26:303e9.
REFERENCES
The trigeminal nerve, CN V, is the fifth paired cranial nerve. It is also the largest cranial nerve.TN is the nerve responsible for most of the sensation in the face. It is bilaterally present. The motar component supplies masticatory muscles, mylohyoid, anterior belly of digastric tensor tympani, tensor veli palatine
Sensory root comprises of y ganglion is present on the termporal bone or the meckels cave.
From there, it divides into 3 branches
First division is known as V1 provides sensation to the eye, upper eyelid and forehead
V2 provides sensation to the cheek, lower eyelid, nostril, upper lip and gum
V3 providessensation to the area of the jaw, lower lip and gum. Also controls muscles responsible for chewing
It is named so because pain paroxysm are usually accompanied by spasm of the ipsilateral facial muscles.
Dental pathosis – is belived by some investigators to be involved with the onset of trigeminal neuralgia
Allergic- it can be secondary to an allergic and hypersensitivity reaction causing edema of the trigeminal nerve root
Mechanical factors – like pressure due to aneurysms of the intrapetrous portion of the ICA tat may erode through the floor of the intracranial fossa to exert a pulsatile irritation on the ventral side of te trigeminal ganglion
Anomalies of superior cerebellar artery – most recently blamed cause of trigeminal neuralgia. It lies in contact with te sensory root of the nerve and implicated as a cause of demyelnation
Secondary lesion – conditions such as carcinoma of the maxillary antrum, nasopharyngeal carcinoma, tumors of peripheral; nerve root, intracranial vascular anomalies, and multiple sclerosis may be presented with TN
Classic TN- pain is generated because of compression of the trigeminal nerve most commonly at the root entry zone by an artery or vein.
Compression of the trigeminal root can be caused by superior cerebellar artery or tortuous vein
It is likely that both central and peripheral changes occur, which would explain why not all patients with a treated compression of the nerve get permanent relief
THOSE WITH SYMPTOMATIC TRIGEMINAL neuralgia have either a compression of Tn caused by tumors or other structural abnormalities such as artieriovenous malformations, of multiple sclerosis
Clasical TN includes all cases with no definitive etiology identified apart from vascular compression of trigeminal nerve
Quality of tn PAIN TYPICALLY ARISES IN THE PERSONS, WHO HAVE NO ABNORMAL NEUROLOGIC DEFICIT SUCH AS LOSS OF CORNEAL REFLEXES, ANESTHESIA, PARESTHESIA, MUSCULAR ATROPHY OR WEAKNESS ETC
Even though there is a refractory period ie complete lack of pain between the attacks, some patients report a dull ache inbetween the attack
The paroxysms occur in cycles, each cycle lasting for weeks or months and with time the cycle appears closer and closer.with each attack the pain seems to become more intense and unbearable.
The pain is provoked by light touch- trigger zones is an area of facial skin or oral mucosa where low intensity mechanical stimulation (light touch,an air puff, or even hair bending can elicit typical facial pain). Reported trigger factors are:
specific area that, when stimulated by touch, pain, or pressure, excites an attack of neurologic pain.
Patient’s description of pain that are pathognomic for TN
These descriptors imply not only the sharpness of the pain but also its rapidity and severity. Many patients vividly remember their first attack, and surgeons have gone so far as to say that patients who have a memorable onset are more likely to have good outcomes.13 The pain develops rapidly and lasts for no more than 2 min. Sometimes it is difficult for patients to appreciate that there are very short breaks between each attack of pain. Characteristically there is a refractory period. The severity of the pain varies from mild to extremely severe, resulting in weight loss and inability to maintain good oral hygiene
NEURALGIA : actual pain in a nerve, several nerves or groups of nerves
NEUROPATHY : disturbance in function or damage to the nerves
Neuropathic facial pain (NFP) is defined as pain around the mouth or face that arises from a primary lesion or dysfunction of the nervous system
Neuralgia is a symptom of nerve dysfunction present within the brain stem or within the nerve segment running to the trigeminal ganglion located within the base of the middle cranial fossa
Insuuficient evidence to support use of peripheral treatments
Under heavy sedation/ short GA
Ganglion is then lesioned under heat(RFT)
INJ OF GLYCEROL
Mechanical compression by use of a balloon
Ablative procedure
Targets the trigeminal root entry zone in post cranial fossa
Focuses a beam of radiation at this point
Gamma Knife contains 192- 201 cobalt-60 sources of approximately 30 curies
MVD is a surgical procedure to relieve the symptoms (pain, muscle twitching) caused by compression of a nerve by an artery or vein. MVD involves surgically opening the skull (craniotomy) and exposing the nerve at the base of the brainstem to insert a tiny sponge between the compressing vessel and the nerve. This sponge isolates the nerve from the pulsating effect and pressure of the blood vessel.
As well as knowing the optimal drugs to use, it is important
that doctors understand how patients can maximise the effects
of these drugs. We provide information leaflets, which include
some of the following instructions:
President of the Confederate States of America [47] American politician who was a U.S. Representative and Senator from Mississippi, the 23rd U.S. Secretary of War, and the President of the Confederate States of America during the American Civil War.
One of India's biggest film stars, Salman Khan, was diagnosed with TN in 2011. He underwent surgery in the US
All-Ireland winning Gaelic footballer Christy Toye was diagnosed with the condition in 2013. He spent five months in his bedroom at home, returned for the 2014 season