2. INTRODUCTION
• Trigeminal neuralgia is a neuropathic disorder of trigeminal nerve that causes
episodes of intense pain in eyes, lips, scalp, forehead and jaws
• It has been labeled as suicide disease due to insignificant number of people taking
their own life because they are unable to have their pain controlled by medication
or surgery
• Other names for the disease are Tic Douloureux/Trifacial neuralgia/Fothergill’s
disease
3. DEFINITIONS
“Trigeminal neuralgia (TN) is defined as sudden,
usually unilateral, severe, brief, stabbing,
lancinating, paroxysmal, recurring pain in the
distribution of one or more branches of 5th cranial
nerve”
(International Headache society)
Painful unilateral affection of the face,
characterized by brief electric shock like pain
limited to the distribution of one or more divisions
of 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;
terminations may remit for varying periods
4. TIC DOULOUREUX
Tic douloureux Painful jerking
It is a truly agonizing condition, in which the patient may clench the hand over the face
& experience severe, lancinating pain associated with spasmodic contractions of the
facial muscles during attacks – a feature that led to use of this term
5. HISTORY
• Aristaeus of Cappadocia –At the end of first century -1st clinical description of TN
• John Locke in 1677, gave the first full description with its treatment
• Nicholas Andre in 1756, coined the term ‘Tic Douloureux.’
• John Fothergill in 1773, published detailed description of TN, since then, it
has been referred to as ‘ Fothergill’s disease ’
• Sir Victor Horsley in 1891 , proposed first open surgical procedure for TGN
(sectioning of preganglionic roots)
• Walter Dandy in 1925 , advocated the partial sectioning of nerve in posterior
cranial fossa
• 1932 he proposed that TGN was caused by blood vessels compressing the nerve
which was confirmed in 1967 by Peter Janetta
6. GENERAL CHARACTERISTICS
• Incidence: It is a rare affliction, seen in about 4 in 100,000 persons
• Age of occurrence: Late middle age or later in life (5th or 6th decade)
• Sex predilection: With female predisposition (58%)
• Affliction for sides: Predilection for the right side is noted (60%)
• Division of trigeminal nerve involvement: V3 is more comm only involved
than V2 division. Very rarely V1 ophthalmic division is involved in about 5 percent
of cases (Only sensory division is affected) .
7. ETIOLOGY
• Dental etiology: According to Westrum and Black(1976), differentiation from loss
of teeth and degeneration of nerve is not restricted to peripheral parts of the
ganglia, but proceeds proximally to involve areas of spinal nucleus. This can partly
explain the affliction in the maxillary and mandibular divisions of 5th cranial nerve
• Infections: Various granulomatous and non granulomatous infections involving
the 5th cranial nerve can bring about neuralgic pain
• Ratner’s jaw bone cavities (1979): Cavities found in the alveolar and jaw bones are
the causative factor. Patients with neuralgia inducing cavitational osteonecrosis also
can be candidates
• Multiple sclerosis: Olfson (1966), suggested the presence of sclerotic plaque
located at the root entry zone of the trigeminal nerve. Usually patients will have
an established diagnosis of multiple sclerosis with demyelinating disease
• Petrous ridge (basilar) compression: Lee (1937), suggested that trigeminal
neuralgia may be caused by compression of the nerve at the Dural foramen or
over the petrous tip and advocated decompression by performing removal of the
bony rim of petrous bone.
8. ETIOLOGY (cont’d)
• Post traumatic neuralgia: The most common types of traumatic neuromas involving
the trigeminal branch, are those following trauma and those resulting from some
dental procedures. These may lead towards neuralgic pain
• Intracranial tumors: Many lesions such as epidermoid tumors, meningiomas of
cerebellopontine angle and Meckel’s cave, arteriovenous malformations,
aneurysms and vascular compression have been suggested as the causes. Trigeminal
neuromas in the middle cranial or the posterior fossa may be also the causative factor.
These intracranial tumors or vascular malformations may impinge on the nerve
• Intracranial vascular abnormalities: Compression – Jannetta et al showed that
vascular compression is a common finding in patients with TN and that surgical
decompression of the nerve root often effectively alleviates TN symptoms. Distortion
of the root entry zone of the trigeminal nerve at the pons by an arterial loop,
usually of the superior cerebellar artery, or by venous compression by
arteriovenous malformations, etc. Compression of the intracranial retrogasserian
portion of the 5th cranial nerve by a displaced vein or artery may be also a cause.
Aneurysm of the internal carotid artery may cause TN
• Viral etiology: Postherpetic neuralgia is seen in elderly patients. History of a previous
episode of infection by varicella zoster virus may be present in these patients. Viral
lesions of the ganglion can be the etiological factor
9. PATHOGENESIS
Classically, TN has been related to a neurovascular compression in the
prepontine cistern at the nerve root entry-zone due to an abnormal artery or
vein, arteriovenous malformation, vestibular schwannoma, meningioma,
epidermoid cyst, tuberculoma, various other cysts and tumors, aneurysm,
vessels aggregation, and arachnoiditis
10. TRIGEMINAL CONVERGANCE-
PROJECTION THEORY
In the trigeminal convergence-projection theory, it has been hypothesized that
continuous or recurrent nociceptive inputs from head and neck converge on spinal
trigeminal nucleus (sub nucleus caudalis), where the release of neurotransmitters and
vasoactive substances may be promoted. This release decreases the threshold of
adjacent second order neurons that receive input from sites other than nociceptive
sources. The signals from these excited second-order neurons may be transmitted to
the thalamus, limbic system, and somatosensory cortex and interpreted as pain
11. BIO RESONANCE HYPOTHESIS
Recently, the bio resonance hypothesis for TN pathogenesis has been proposed. This
theory states that when the vibration frequency of a structure surrounding the
trigeminal nerve becomes close to its natural frequency, the resonance of the
trigeminal nerve occurs. The bio-resonance can damage trigeminal nerve fibers and
lead to the abnormal transmission of the impulse, which may finally result in facial pain
12. IGNITION THEORY
The triggering of pain in TN may follow innocuous stimuli, a phenomenon that is
probably explained by postinjury changes in neuronal function After nerve injury, there
is an increased proportion of A-beta fibers with sub threshold oscillations that
ultimately generate ectopic Discharges These produce a Transient depolarization in
Neighboring passive C neurons in the same Ganglion These findings favor a
mechanism where afferent nociceptors could be stimulated by activity in injured low
threshold mechanoreceptors
13. CLASSIFICATION
TYPICAL TRIGEMINAL NEURALGIA
ATYPICAL TRIGEMINAL NEURALGIA
PRE- TRIGEMINAL NEURALGIA
MULTIPLE SCLEROSIS RELATED TRIGEMINAL NEURALGIA
SECONDARY OR TUMOR RELATED TRIGEMINAL NEURALGIA
TRIGEMINAL NEUROPATHY OR POST- TRAUMATIC
TRIGEMINAL NEURALGIA
FAILED TRIGEMINAL NEURALGIA
14. PRE- TRIGEMINAL NEURALGIA
Days to years before the first attack of TN pain, some sufferers experience odd
sensations of pain,( such as toothache) or discomfort( paresthesia )
15. TYPICAL TRIGEMINAL NEURALGIA
• Most common form, previously termed CLASSICAL, IDIOPATHIC and ESSENTIAL TN
• Nearly all cases of typical TN caused by blood vessel compressing the trigeminal
nerve root
• Pulsation of vessels upon the trigeminal nerve root do not visibly damage the
nerve
• However irritation from repeated pulsations may lead to changes of nerve function,
delivery of abnormal signals to the trigeminal nerve nucleus , this causes
hyperactivity of trigeminal nerve root leading to trigeminal nerve pain
16. ATYPICAL TRIGEMINAL NEURALGIA
It is 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
17. MULTIPLE SCLEROSIS RELATED TN
• Symptoms of MS related TN are identical to typical TN
• Bilateral TN is more commonly seen in people with MS
• MS involves formation of demyelinating plaques within the brain
18. SECONDARY OR TUMOR RELATED TN
• TN pain caused by a lesion, such as a tumor
• Tumor that severely compresses or distorts the trigeminal nerve may cause
numbness, weakness of chewing muscles or constant aching pain
19. FAILED TRIGEMINAL NEURALGIA
In a very small proportion of sufferers , all medications, surgical procedures prove
ineffective in controlling TN pain Such individual also suffer from additional trigeminal
neuropathy as a result of destructive intervention they underwent
20. CLINICAL FEATURES
• TN typically manifests as a sudden, unilateral, intermittent paroxysmal, sharp,
shooting, lancinating, shock like pain, elicited by slight touching superficial ‘trigger
points’ which radiates from that point, across the distribution of one or more branches
of the trigeminal nerve
• Pain is usually confined to one part of one division of trigeminal nerve—
mandibular or maxillary, but may occasionally spread to an adjacent division or rarely
involve all three divisions
• Pain rarely crosses the midline
• The pain is of short duration and lasts for a few seconds, but may recur with variable
frequency
• Even though there is a refractory period (complete lack of pain) between the attacks,
some patients report a dull ache in between the attacks
• During an attack, the patient grimaces with pain, clutches his hands over the affected
side of the face, stopping all the activities and holds or rubs his face, which may redden
or the eyes water until the attack subsides
• Male patients avoid shaving
• The oral hygiene is poor, as patient avoids brushing of teeth
21. CLINICAL FEATURES
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
In extreme cases, the patient will have a motionless face - the ‘frozen or mask
like face’
It is characteristic of the disorder, that attacks do not occur during sleep
Manypatients will leada very poor quality of life, because of excruciating pain
It is very common for these patients to undergo indiscriminate dental extractions
on the affected side without any relief from pain, because the pain of the trigger
zone and pain fiber distributions often mimic pain of odontogenic origin
More than50 percent of patients experience early remissions of greater than 6
months before return of active pain.
22. TRIGGER ZONE
• Presence of an intraoral or extraoral trigger points provocable by obvious
stimuli is seen in TN
• Trigger zone is an area of facial skin or oral mucosa,where low intensity
mechanical stimulation such as light touch, an air puff, or even touching face
at a particular site or by chewing or even by speaking or smiling, brushing,
shaving or even washing the face, etc. can elicit a typical pain attack
• The location of the trigger points depends on which division of
trigeminal nerve is involved
I. In V2—points are located on the skin of the upper lip, ala nasi or cheek or on the upper gums
II. In V3—this is the most frequently involved branch. Trigger points are seen over the lower lip, teeth
or gums of the lower jaw. Tongue is rarely involved
III. In V1—the trigger zone usually lies over the supraor bital ridge of the affected side.
23. CLINICAL SCENARIO
A 55-year-old woman presents with severe pain in her face and jaw. The pain seemed
to tear through her face like a lightning bolt. It was brief but excruciating pain which
came in repeated flashes when activated. She could not wash the right side of his face,
chew tough foods or talk for any length of time without triggering pain. She could not
even tolerate a light breeze blowing across her face
STEPS OF MANAGEMENT
Management of acute Pain
Ruling out other D/D
Proper diagnosis and confirmation of disease etiology
Treatment Options
24. MANAGEMENT OF ACUTE PAIN
Phenytoin has proven effective in managing neuralgia crisis in a small case series. A loading
dose of 14 mg/kg applied intravenously was required to relieve the pain for 1–2 days, which
is long enough for alternative oral drug therapy to kick in when initiated simultaneously
[Cheshire, 2001]
Intranasal administered lidocaine 8% was effective in temporarily relieving second-division
neuralgic pain [Kanai et al. 2006b]
Subcutaneous sumatriptan 3 mg was shown to be superior to placebo in providing prompt
and marked analgesia in 80% of patients in a double-blind, placebo-controlled study of 24
patients with refractory TN. The median duration of pain relief was 8 h [Kanai et al. 2006a]
A different approach could be ganglionic local opioid analgesia (GLOA) at the superior
cervical ganglion, which was evaluated retrospectively in 74 patients with neuropathic facial
pain
A clinically relevant pain reduction was observed in 73% of the patients. The proportion of
responders (pain reduction ≥50%) was 59% after the first blockade
25. DIFERENTIAL DIAGNOSIS
• MIGRAINE- severe type of periodic headache is persistent, at least over a period of
hours and it has no trigger zone
• SINUSITIS- pain is not paroxysmal, in this pain is persistent, associated nasal
symptoms.
• DENTAL PAIN- localized, related to biting or hot or cold foods, visible abnormalities
on oral examination
• Tumors of nasopharynx - in this similar type of pain is produced, manifested in the
lower jaw, tongue and side of the head with associated middle ear deafness. This
complex lesion is called TROTTER’S syndrome. Patient exhibit asymmetry and
defective mobility of the soft palate and affected side. As the tumor progresses,
trismus of internal pterygoid muscle develops, and patient is unable to open the
mouth. Here actual cause of pain is involvement of mandibular nerve in the
foramen ovale
• Post herpetic neuralgia- pain is usually involved in ophthalmic division. The history
of skin lesion prior to onset of neuralgia, pain is persistent, associated nasal
26. D/D
• TMJ PAIN : Often bilateral, may radiate around ear to the neck or temple region,
jaw opening may be limited and there may be an audible click
• Persistent idiopathic facial pain : Often bilateral and may extend out of trigeminal
territory , pain is continuous and mild to moderate & throbbing in nature
• Temporal arteritis : Constant pain often associated with jaw claudication , fever and
weight loss , temporal arteries may be firm , tender and non pulsatile on
examination
28. DIAGNOSIS
• Examination of clinical features and trigger zones
• CT and MRI
• OPG
• Diagnostic local Anesthetic Peripheral nerve Block
• Response to carbamazepine
29. CT SCAN AND MRI
To diagnose post operative causes , neuritis , vessel compression Lesions/ Tumors of
posterior cranial fossa
30. Diagnostic local Anesthetic Peripheral nerve
Block
Always begin injectionsat surface site of pain and then move proximally.
For example, if the pain is perceived in the lower lip, then inject lower lip, then mental
nerve and then inferior alveolar nerve
Inject 0.5 cc of normal saline at test site , Wait for 5 minutes. If pain is relieved, then
psychogenic pain is likely
If the pain persists, then inject 0.5ml of 2 percent lignocaine without adrenaline at
surface site and wait for 5 minutes. If pain is relieved, then direct therapy at small
nociceptor fibers
If the pain persists–inject little deeper and wait for 5 minutes. If pain is relieved,
then consider musculoskeletal origin of pain
If pain is not relieved, inject at more proximal portion of nerve—If pain is
relieved, direct therapy at site, when relief occurred
Thus, selective inferior alveolar, lingual, buccal, infra orbital, posterior superior
alveolar blocks can be given to know the involvement of the branch of the trigeminal
nerve
34. CARBAMEZAPINE
• Carbamazepine is highly specific in only relieving pain of TN and not any other type
of facial pain
• Carbamazepine 100 mg three times a day is introduced and titrated over 1
to 5 weeks period until either remission is achieved or side effects or toxicity are
unacceptable
• More of daily drug dosage should be taken at night, so that adequate serum
concentration can be present in early morning, when pain most occurs
• Complete blood count with platelet count, liver function screening should be done
prior to treatment, a month after treatment and at 3 to4 months intervals,
particularly, if patient continues to receive a high dose (1000 to 1500 mg/day)
• SIDE EFFECTS: Visual blurring, dizziness, somnolence, skin rashes and ataxia and in
rare cases hepatic dysfunction, leukopenia, thrombocytopenia—aplastic anemia
• Initial dose 100mg/BD
• Maximum dose 1600-1800 mg / day
35. OTHER DRUGS
CLONAZEPAM 0.5mg / TDS max: 20mg
Side effects : Drowsiness, fatigue, lethargy
Tab. Phenytoin 100mg/TDS
Side effects: Slurred speech, abnormal movements, swelling of lymph glands,
gingival hypertrophy, hirsutism, folate deficiency
Tab. Oxcarbazepine—1200 mg/day
Side effects: Hyponatremia , double vision
Valproic acid—600 mg/day
Side effects: irritability, tremors, confusion, hepatoxicity, weight gain
Baclofen (Lioresal)—10 mg tds
Side effects: fatigue, vomiting
37. EXTRACRANIAL APPROACH
• PERIPHERAL INJECTION
I. LONG ACTING ANAESTHETIC
II. ALCOHOL BLOCK
III. GLYCEROL BLOCK
• PERIPHERAL NEURECTOMY
• CONTROLLED RADIOFREQUENCY THERMOCOAGULATION
• CRYOSURGERY
38. LONG ACTING ANAESTHETIC
• The management of trigeminal neuralgia in older patients who do not want
neurolytic block and/or surgical treatment may be problematic
• This paper describes three patients who had first and/or second division trigeminal
neuralgia
• The analgesic effects of infraorbital nerve block using 0.5% bupivacaine or 1%
mepivacaine dissipated within a few days, however, the effects of nerve blocks
using 4% tetracaine dissolved in 0.5% bupivacaine lasts for around 3 months
• Hypesthesia was observed in two patients within a week following the block, but
sensory level returned to normal within 2 weeks and there were no further
complications in any patient
39. ALCOHOL BLOCK
• 0.5 – 2 ml of 75-95 % absolute alcohol can be used to block the peripheral
branches of the trigeminal nerve
• Aim is to destroy the nerve fibers
• It produces total numbness in the region of distribution of the nerve that was
anaesthetized
• Complication:
i. Necrosis of the adjacent tissue
ii. Fibrosis
iii. Alcohol induced neuritis
40. PERIPHERAL NEURECTOMY (NERVE
AVULSION)
• Oldest & most effective peripheral nerve destructive method Can be repeated &
relatively reliable technique
• It acts by interrupting the flow of a significant number of afferent impulses to
central trigeminal apparatus
• Performed commonly on infraorbital, inferior alveolar, mental and rarely lingual.
• Disadvantage: May produce full anesthesia / deep hypoesthesia
41. INFRAORBITAL
NEURECTOMY
Conventional intraoral approach
A. A ‘U’ - shaped Caldwell – Luc incision is made in the upper buccal
vestibule in the canine fossa region , Mucoperiosteal flap is
reflected superiorly to locate the infraorbital foramen
B. Once the nerve is exposed, all the peripheral branches are held
with the hemostat & avulsed from the skin surface intraorally
C. Then the entire trunk is separated from the skin surface is held
with the hemostat at the exit point from the foramen & is
removed by winding it around hemostat & pulling it out from the
foramen
D. Then it may be plugged with polyethylene plug
42. Braun’s transantral approach
• An intra oral incision is made from the maxillary tuberosity to the midline in the
maxillary vestibule
• The descending palatine branch of the trigeminal nerve is identified & traced to
the sphenopalatine ganglion
• The maxillary nerve is sectioned from the foramen rotundum to the inferior orbital
fissure
• The antral mucoperiosteal flap in the vestibule is repositioned & sutured back
• A 3 cm window is made in the anterolateral wall of the maxillary sinus
43. INFERIOR ALVEOLAR NEURECTOMY
Extra oral approach
Done through Risdon’s incision After reflection of
masseter, a bony window is drilled in outer cortex
& nerve is lifted with nerve hook & avulsed from its
superior attachment & mental nerve is avulsed
anteriorly through the same approach
44. Intra oral approach
Dr Ginwalla’s incision :
• Incision is made along with the anterior
border of ascending ramus, extending
lingually & buccally & ending in a fork like
an inverted Y
• Incision is then deepened on the medial
aspect of ramus
• The temporalis & medial pterygoid
muscles are split at their insertion &
inferior alveolar nerve is located.
• The nerve is ligated at two points in the
most superior part visible & divided
between the ligature
• The superior end is cauterized & the lower
end is held securely using a hemostat
• The mental nerve is also similarly ligated in
two points close to the mental foramen &
divided between two
• The remaining nerve is held at the inferior
alveolar end & wound around the
hemostat & excised from the canal.
45. LINGUAL NEURECTOMY
An incision is made in the anterior border of the ramus slightly towards the lingual side
The lingual aspect is exposed & the lingual nerve identified in the third molar region
just below the periosteum
The nerve can be either avulsed or ligated, cut and the ends may be cauterized.
46. CRYOSURGERY
• Barnard first used cryotheraphy in 1981 for the treatment of the trigeminal
neuralgia
• After identifying the affected nerve , it is then exposed to the cryoprobe intraorally
• Direct application of cryotheraphy probe at temperatures colder than -60 C are
known to produce Wallerian degeneration without destroying the nerve sheath
itself
• Nerve is exposed for 2 mm freeze followed by 5 mm thaw cycle
• The freeze – thaw cycle is repeated at least 3 times
48. PERCUTANIOUS
RHIZOTOMY
This is done on the Gasserian
ganglion which involve either
mechanically or chemically
damaging parts of the trigeminal
nerve
Technique of needle penetration:
The foramen ovale is best
visualize with the x – ray tube
placed for a submentovertex
position
Infiltration of the skin & cheek is
done with local anaesthetic agent
on the affected side
Three points of Hartel are marked
on the side of the face using
49. CONTROLLED RADIOFREQUENCY
THERMOCOAGULATION
It was first introduced by Kirschner (1931) & later modified by Sweet (1970)
Technique: The patient is sedated with a short acting sedative and vital signs
are monitored
The electrode is inserted through the cheek under fluoroscopy into foramen
ovale. The patient is awakened briefly to accurately locate the position of the
electrode.
Indication:
Toxicity of drugs
Failure of response to the other modalities
Dependence on the drugs for life time
Elderly patients
Medically compromised patients
Advantages: Comparative low rate of recurrence Zero mortality
Thermocoagulation preserves the motor function of the trigeminal nerve Can
avoid major surgical procedure
Disadvantage: May cause anaesthesia dolorosa loss of corneal reflex
Meningitis (rarely)
Lesion production: • Thermal lesion of 30-90 sec. duration are made at 65 to
75 degree centigrade. Power: 25 watt,voltage 40-45 volts.Current 120-140mA.
• Temp. 65-75 degrees. • 5mm bare tip electrode with 2mm diameter
Leison produced of 10*6mm within trigeminal ganglion root at temp. 75
degrees.
50. Percutaneous glycerol rhizotomy
Glycerol is a neurolytic alcohol which can be used
to chemically destroy the nerve root
Advantages: Simple technique Lower incidence of
anaesthesia dolorosa
Complication: Post operative headache, nausea,
vomiting Meningitis Post operative herpes
simplex
51. Percutaneous balloon compression
This is a mechanical means of destruction of the trigeminal nerve introduced by
Mullan & Lichtor in 1980
Technique: A no. 4 Fogarthy’s catheter is introduced with fluoroscopic guidance
A 0.7 mm balloon is inflated for 1 – 2 minutes
53. MICROVASCULAR DECOMPRESSION
Microvascular decompression achieves the most sustained pain relief with 90% of
patients reporting initial pain relief and over 80% still pain free after 1 year, with
75% after 3 years and 73% after 5 years remaining pain free
It is, however, a major surgical procedure that entails craniotomy to reach the
trigeminal nerve in the posterior fossa
The average mortality rate ranges from 0.2% to 0.5%, and up to 4% of patients
suffer from major problems such as cerebrospinal fluid (CSF) leakage, infarcts or
haematomas
The most common complications are aseptic meningitis (11%), sensory loss (7%)
and hearing loss (10%) as long-term complications
54. GAMMA KNIFE SURGERY
It is non invasive scalpel less radiosurgery
Based on the principle that radiation delivered precisely to a target will destroy the
cells in a particular area while minimizing injury to surrounding nerve and brain
tissue
Patient is fitted with collimater halmet secured with screws
The halmet has 201 separate small holes that aim ionizing radiation to a single
target
Procedure is performed under local anaesthesia with mild sedation and takes 15 –
45 mins for a single area
Procedure can be repeated until all required tissue is treated
55. GAMMA KNIFE SURGERY
• In gamma knife surgery, a focused beam of radiation is aimed at the trigeminal
root in the posterior fossa
• One year after gamma knife surgery, 69% of patients are pain free without
additional medication. At 3 years, 52% are still pain free
• The development of pain relief can be delayed (mean 1 month). Side effects are
sensory complications in 6% that may develop with a delay of up to 6 months,
facial numbness in 9–37% which improves over time and paresthesias in 6–13%
• Quality of life improves by 88%
• The main disadvantage of gamma knife surgery is the treatment expense that limits
widespread usage making it a reserve treatment option for patients that cannot
undergo open surgery or have blood coagulation problems (e.g. are receiving
warfarin)
56. Recent advances
• Transcranial magnetic stimulation
• Botulinum toxin in trigeminal neuralgia
Experts indicate that it has a antinociceptive effect with transitory effect
on trigeminal territory. It inhibits neurotransmitters and reduce peripheral and central
sensitization
• Psychologic inhibition by transcutaneous neural stimulation
• Accupuncture
• Psychologic : Biofeedback and Psychiatric councelling
57. Transcranial magnetic stimulation
• Repetitive transcranial magnetic stimulation (rTMS) is an emerging technology that
introduces the possibility of assessing whether patients with trigeminal neuropathic
pain will respond to direct epidural cortical stimulation by first measuring their
response to a trial of non-invasive cortical stimulation
• In a study of 24 TN patients given rTMS to the motor cortex at 20 Hz daily for 5
days, pain ratings decreased by approximately 45% for 2 weeks [Khedr et al. 2005]
• In a different study of 12 patients with chronic intractable TN who had failed
surgical treatment, 58% experienced a greater than 30% reduction in pain after
receiving repetitive TMS
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