This document discusses trigeminal neuralgia, a neuropathic pain condition that causes severe, sporadic facial pain. It provides information on: 1) The etiology, including neurovascular compression as a common cause. 2) Symptoms like brief, severe facial pain that may be triggered by light touch. 3) Treatment options like carbamazepine, microvascular decompression surgery, and percutaneous radiofrequency thermocoagulation of the gasserian ganglion. 4) Imaging techniques like MRI that can identify compressive vascular structures.

1. The terrible journey of a
nerve impulse!
DR UNNIKRISHNAN P
NEUROANAESTHESIA
SCTIMST
TRIVANDRUM
INDIA

2. Demotivating , demoralizing..
one of the most painful neuropathic pains
IASP definition: Sudden, recurrent, severe pain in the
distribution of one or more branches of the fifth cranial nerve
no universal treatment is capable of reverting completely
impairment of daily functionality, reduced quality of life and
depression
overwhelming fear that pain can suddenly return again

3. Peculiar neuropathic pain
not accompanied by sensory deficit
Can be cured by a small nerve or root lesion
Cause ? Now… sound hypothesis of neurovascular conflict
(NVC) [ Are we still hearing sounds of conflict? ]
tic douloureux = since painful brief muscle spasms

4. EPIDEMIOLOGY
3-5/ one lac; 52- 69 years most common
More recent estimates suggest the prevalence is
approximately 1.5 cases per 10,000 population, with an
incidence of approximately 15,000 cases per year
Multiple sclerosis is found to be a risk factor; ?HTN
I‟m also having..[youngest 12m]
3.4/lac 5.9/lac

5. Anatomy - whereabouts
• Emerge as a larger sensory and smaller motor root
• Fibres in sensory root are axons of cells in
trigeminal ganglion which occupies Meckels cave
• Neurons of the unipolar cells of the ganglion
divides into central and peripheral processes
• Peripheral ophthalmic,maxillary and sensory part
of mandibular
• Central fibres of the sensory root

6. Whereabouts……

7. origin of the…..pain....nerve
.

8. Course and relevance in TN
 The sensory fibers arise from the gasserian ganglion (lying
near the petrous part of the temporal bone in the dura
matter), pass backward, enter the pons, and divide into
upper and lower roots.
 The upper roots end in the principal or superior sensory
nucleus and locus caeruleus.
 The lower roots descend through the pons and medulla
and terminate in the spinal tract nucleus, which consists of
subnucleus caudalis, subnucleus inter-polates, and
subnucleus oralis.
 The subnucleus caudalis serves as the principal brainstem
relay site for orofacial pain, and the superior sensory
nucleus and subnucleus oralis are sites relaying orofacial

9. No monopoly; already a lot
of members to control
• 1 motor and 3 sensory nuclei
• Motor upper pons
• Mesencephalic midbrain ; for proprioception
• Main sensory nucleus upper pons ; for touch
• Spinal nucleus in lower pons, medulla and upper cervical
spinal cord; for pain and temperature

10. Complex routes….
.

11. The Spinal Trigeminal
Nucleus
.

12. Principal brainstem relay
sites….
Subnucleus caudalis  orofacial pain
Superior sensory nucleus , subnucleus oralis
 Tactile information
The similarity….
Neurons in dorsal horn   Thalamus
Neurons in subnucleus caudalis   
Thalamus
Motor root….
Motor roots from the superior and lower
nucleus then joins the sensory root as it
emerges from the pons

13. Eagerly waiting for chaos..
Nociceptive neurons in subnucleus caudalis respond to
noxious stimulation of the 
Orofacial tissues
Tooth pulp
TMJ
Dura
Jaw
Tongue
Neck muscles
Mechanoreceptive neurons in the superior sensory nucleus

Light tactile stimuli to
Skin
Mucosa
teeth

14. Ophthalmic nerve

15. Maxillary nerve

16. Mandibular nerve

17. ETIOLOGY AND
PATHOPHYSIOLOGY
“Pain is temporary. Quitting lasts forever”…Lance Armstrong
His quotes also are loosing integrity...???

18. Central vs Peripheral
Central theories emphasize the role of deafferentation
(secondary to compression of the trigeminal roots or
ganglion) in the genesis of neural hyperactivity.
Peripheral theories note that changes in peripheral axons
and myelin may lead to altered nerve sensitivity to chemical
and mechanical stimuli.
Starts as a peripheral lesion; response of central synapses
to this sets stage for the war; SO BOTH MECHANISMS
PLAY

19. Painful and annoying
conflict…
In 85%, no structural lesion is seen
Classic [idiopathic] form: “Neurovascular conflict” i.e.
vascular compression of nerve most commonly @ its entry
into pons [REZ]
Significant NVC= an artery (not a vein), crossing (not
parallel to) the nerve and provoking displacement/grooving
of it (Casselman,2000)

20. Amplifying….
compression results in focal trigeminal nerve demyelination
leads to ephaptic transmission [action potentials jump from
one fiber to another]
A lack of inhibitory inputs from large myelinated nerve fibers
plays a role.
a reentry mechanism causes an amplification of sensory
inputs

21. Print master
Your Text here

22. Two types....One feature..
Trigeminal neuralgia is divided into classic [idiopathic] and
symptomatic types
The classic form includes the cases that are due to a normal
artery present in contact with the nerve, such as the SCA or
even a primitive trigeminal artery
Symptomatic forms can have multiple origins: Aneurysms,
tumors, chronic meningeal inflammation.An abnormal
vascular course of the superior cerebellar artery is often
cited as the cause
Uncommonly, an area of demyelination from multiple
sclerosis may be the precipitant

23. ETIOLOGY
• compression of nerve root [most common-vascular; rarely
tumor/vein/avm] usually when pain @ v2 / v3, compression
is by SCA ; pain @ v1  by AICA
• Inflammatory causes: multiple sclerosis [in1-5% of patients
with MS;more likely if patient with TN is 20-40ys] ; Damage
to myelin sheath [Myelin gone….signals blend….nerves
may sense light touch as pain!!!!!] ), sarcoidosis, and Lyme
disease neuropathy
• traumatic accidents
• unsuccessful dental work

24. ETIOLOGY
Tumor-related causes : (most commonly in the cerebello-
pontine angle) include acoustic neurinoma, chordoma at the
level of the clivus, pontine glioma or
glioblastoma,epidermoid, metastases, and lymphoma and
paraneoplastic etiologies.
Vascular causes include a pontine infarct and arteriovenous
malformation or aneurysm in the vicinity.
infections , varicella virus
foci of abscesses
bone resorption with irritation of the trigeminal nerve in the
maxilla or mandible

25. Print master
Your Text here

26. Print master
Your Text here

27. Don‟t get deceived by
imitations
DIFFERENTIAL DIAGNOSIS
variety of tumours and other lesions involving, or impinging
on, the trigeminal nerve, ganglion or sensory root 
tumours of the C-P angle, MCF, cranium or extracranial
tissues (often metastatic), and from the envelopes of the
Gasserian ganglion.
OTHERS
atypical facial pain syndromes
cluster headache
postherpetic neuralgia
geniculate neuralgia (Ramsay Hunt)
sphenopalatine ganglion neuralgia
glossopharyngeal neuralgia
dental disease, orbital disease
temporomandibular dysfunction
temporal arteritis

28. I doubt….you are having….
Headache Classification Subcommitee of the International
Headache Society. Cephalalgia 2004

29. Difficult to bear
Almost always u/l
Comes like electric shock
Brief; but will recur
„Paralysing‟
Light pressure on trigger points will trigger the attack
Unpredictable symptom free intervals
Atypical pain patterns are there
My patients‟ biggest ambitions:
Eating….
Shaving….
Make up face….

30. Please don‟t touch on these
areas ..Ok..?
.

31. DIAGNOSIS

32. Keep a low threshold for MRI
in
younger patients
atypical clinical features
sensory loss
dull burning pain between paroxysms
patients who do not respond to initial medical therapy

33. Imaging
C.T.
M.R.I. :
CONVENTIONAL: can rule out tumour / multiple sclerosis
3-D VOLUME ACQUISITION, with contrast injection and thin cuts
(ie, 0.8 mm) without gaps can see Trigeminal nerve and associated
blood vessels
The trigeminal nerve is easily observed in the axial plane when the
MRI series is centered at die midpoint of the 4th ventricle.
To ensure adequate evaluation, the nerve should be observed on 3
adjacent cuts.
when an offending vessel is present, it will be detected 80% of the
time
OTHERS: TOF, CISTERNOGRAPHY
Also look for tumours, multiple sclerosis, abnormalities of

34. Imaging
Meckel‟s cave, the cavernous sinus, the skull base
foramina, the pterygopalatine fossa and the peripheral
trigeminal nerve course
always look for a normal gray and white matter and
brainstem, a normal cisternal segment, a fluid fi lled
Meckel‟s cave, a homogeneously enhancing cavernous
sinus, a fat-filled superior orbital fissure and pterygopalatine
fossa, normal foramen rotondum and ovale, and a
symmetrical appearance of the masticator muscles with

35. DIFFERENTIATION
• paroxysms of pain last longer
• pain tends to be constant
• Involvement of forehead alone +/- autonomic symptoms
• neurologic deficit is often detected (cutaneous
hypoesthesia, loss of corneal reflex, masticatory muscle
weakness).

36. .
Treatment

37. PHARMACOLOGICAL
enormous belief in Carbamazepine
Phenytoin is the second treatment of choice
3 weeks over,adequate serum levels obtained…..but no relief
DISCONTINUE
because higher doses may lead to toxicity.
The short-term efficacy rate is 60%; decreases to 30% after 2 years
Lamotrigene useful in failure/intolerance with
Carbamazepine
Gabapentin : benign adverse effect profile, can be used as
adjuvant also
Topiramate: proved to be effective where combination
therapy fails

38. Treatment
Your Text here Take @ meals
Use long acting preparations
fewer drug interactions and side effects;
but cross reactivity with carbamazepine +

39. Treatment
Your Text here

40. SURGICAL Rx-FACTS
aimed at either destroying parts of nerve fibers or
decompressing the trigeminal nerve to relieve pain
although surgical treatment may initially be successful,
trigeminal neuralgia may recur retry medical therapy
[because drugs that were previously ineffective may
become effective later]
patients with classic trigeminal neuralgia, evidence of
vascular compression, shorter duration of disease, and no
previous surgery respond better to all treatment options.
In such patients, MVD can be considered the “gold
standard” surgical procedure, and it offers the best long
term cure rates.

41. SURGICAL Rx-FACTS
All procedures have high initial response rate, except for
stereotactic radiosurgery, which usually takes maximum
effect at one to two months
Ablative Rxs are used to a greater extent in patients with
high operative risk

42. Microvascular decompression
(MVD) of the posterior fossa
junction of the Vth nerve with the pons is explored
blood vessels and tumors removed from direct contact with
the nerve. The SCA, PICA, VA, and AICA (& small
branches) are separated from the nerve by a piece of
Dacron fabric
Efficacy is reported to be 85% initially, and 80% at 5 years.
carries a relatively low risk of pain
recurrence, dysthesia, corneal analgesia, and trigeminal
motor weakness

43. .

44. MVD-Risks
Risks higher in patients who have an ecstatic
(atherosclerotic) and a tortuous vertebrobasilar arterial tree
the risk for perioperative mortality [around 0.4%], serious
morbidity (eg, stroke, hemorrhage, venous occlussion,
M.I.,HCP), permanent hearing loss, and facial palsy is
higher after MVD than after percutaneous procedures.
But ablative procedures are less effective in the long term
and more likely to produce facial numbness and other minor
complications than MVD

45. MVD-Follow up
• OPERATIVE FINDINGS (97%)
• arterial channels 374 (80,3%) Russel R. Lonser and Ronald I. Apfelbaum
“Operative Neurosurgical Techniques”
• venous channels 65 (13,9%) Vol 2, pp 1531-1538 (2006)
• tumor 12 (2,6%)
• negative 15 (3,2%)
• total 466
• COMPRESSIVE ARTERY
• SCA – 80%
• SCA+AICA – 9%
• AICA – 8%
• Basilar – 2%
• Others--1%

46. MVD-Follow up
• INITIAL RESULTS
• complete relief – 91% Russel R. Lonser and Ronald I. Apfelbaum
“Operative Neurosurgical Techniques”
• pain reduced – 6% Vol 2, pp 1531-1538 (2006)
• pain not relieved – 2%
• death – 1%
• COMPLICATIONS
• cranial nerve dysfunction – 12,6%
• dizziness, ataxia – 3%
• infarction – 1,8%
• seizures – 1%
• death – 1%

47. MVD-Follow up
• LONG-TERM RESULTS
• no recurrence - 62% Russel R. Lonser and Ronald I. Apfelbaum
“Operative Neurosurgical Techniques”
• mild pain (no medication) - 5% Vol 2, pp 1531-1538 (2006)
• pain controlled with medication -14%
• severe pain not controlled “ - 18%
• died - 1%

51. PREOPERATIVE
SIMULATION
fusion imaging technique of three-dimensional (3-D) MR
cisternography and co-registered 3-D MRA
The presence of offending vessels and compressive site of
neurovascular conflict was assessed from the various
viewpoints within the cistern
surgeon's-eye view, bird's-eye view

53. PREOPERATIVE
SIMULATION
Presurgical Virtual Endoscopy: is a novel technique that
provides excellent visualization of the three-dimensional
relations between neurovascular structures and allows
simulation of MVD

54. Percutaneous radiofrequency
thermocoagulation of the gasserian
ganglion
A high-frequency current used to destroy precisely the A-
delta and C-fiber nociceptors
based on the theory that lower temperatures selectively
destroys the nociceptive unmyelinated C-fibers & the poorly
myelinated A-delta fibers while sparing the heavily
myelinated A-alpha & A-beta fibers which convey the touch,
proprioceptive & motor impulses.

55. Percutaneous radiofrequency
thermocoagulation of the gasserian
ganglion
Under fluoroscopic guidance, an insulated needle is passed
through the foramen ovale next to the gasserian ganglion
The initial efficacy ̴ 90%, with 80% patients remaining free of
pain at 1 year and 50% remaining pain free at 5 years.
appropriate for elderly and for those with poor medical
conditions
Risks : numbness, paresthesia, and anesthesia
dolorosa,corneal anesthesia [may develop after lesioning of
the ophthalmic division]

56. Percutaneous radiofrequency
thermocoagulation of the gasserian
ganglion
Under fluoroscopic guidance, an insulated needle is passed
through the foramen ovale next to the gasserian ganglion
Foramen ovale accessed under flouroscopy
Ensure CSF flow…
Needle advanced to petrous clivus junction
Test stimulus which will elicit the patients original neuralgic
pain
Thermocoagulation

57. .

58. Percutaneous radiofrequency
thermocoagulation of the gasserian
ganglion
A

59. Percutaneous
microcompression of the
gasserian ganglion
involves passing a fine balloon catheter through the foramen
ovale.
Inflation of the balloon produces an ischemic or mechanical
destruction of cells in the ganglion.38
associated with the highest risk for postoperative motor
trigeminal weakness.
the best choice for patients who have ophthalmic nerve pain
and who are not candidates for MVD

60. Gamma knife irradiation
[NIHCE,U.K. APPROVED]
radiation is aimed at the proximal nerve and root entry zone
in the pons
gamma knife projects 201 very fine beams of gamma rays
(generated by RA Cobalt) through the skull and brain.
The dose of radiation along any one beam is too small to
effect any change by itself
but when all 201 beams intersect, a very high dose of
radiation can be administered with little or no radiation to
surrounding tissue.41
has been shown to affect abnormal ephaptic transmission
but not normal axonal conduction

61. Glycerol injection
Injected behind the ganglion, which destroys small and large
myelinated and unmyelinated fibers.
Under fluoroscopic guidance, glycerol is injected into the
cistern of Meckle's cave.
OTHERS METHODS : Laser irradiation of the skin overlying
peripheral nerves with a heliium-neon laser

62. Weighing once more….
Your Text here

63. Proparacaine eye drops
Is a local anesthetic agent that anesthetizes the eye and
possibly the nerves around it.
It is shown that it can give short-term relief in some
instances
usually effective if the pain is in the distribution of the
ophthalmic division of the trigeminal nerve.
almost certainly ineffective for classic trigeminal neuralgia.
relatively harmless, but can damage the eye if used
extensively
So it cannot be considered a long-term treatment.

64. Final words….
patients with trigeminal neuralgia deserve an accurate and
dispassionate explanation of the merits and drawbacks of all
methods of treatment from the outset.

65. References
• Trigeminal neuralgia Pathophysiology and treatment A.
JOFFROY, M. LEVIVIER and N. MASSAGER
• Manish K Singh, MD; Chief Editor: Robert A Egan, MD[2012]
Medscape
• Pain Management: Trigeminal Neuralgia;Meraj N. Siddiqui,
Hospital Physician;Turner White;2003
• BMJ Luke Bennetto, Nikunj K Patel and Geraint Fuller ;2008
• John tew, Mayfield Clinic Update,2012
• review on the causes of trigeminal neuralgia symptomatic to
other diseases florin popovici1, ROMANIAN JOURNAL OF
NEUROLOGY – VOLUME X, NO. 2, 2011

66. HOPING FOR MORE AND MORE WAYS TO COOL THIS
HEAD
THANK YOU