Trigeminal neuralgia is characterized by brief, severe, stabbing pains in the face that are often triggered by trivial stimuli. It is mostly caused by blood vessel compression of the trigeminal nerve root. Diagnosis involves unilateral facial pain in the trigeminal nerve distribution that is provoked by triggers. Treatment options include carbamazepine medication or microsurgical decompression/ablative surgeries if drugs fail.

1. SYMPTOMATOLOGY
AND
PATHOPHYSIOLOGY
OF TRIGEMINAL
NEURALGIA
BY DR PRIYANKA.P.S
2ND YR PG SCHOLAR
PANCHAKARMA
DEPARTMENT
ALVAS AYURVEDA
MEDICAL COLLEGE

2. SUICIDE DIESEASE??????

3. HISTORY OF TRIGEMINAL
NEURALGIA
Early descriptions of TN can be inferred from the writings of galen, Aretaeus of
cappadocia and avicenna, the first accurate descriptions of TN were not officially
documented untill the 1700 AD.
In 1756 , Nicholas and re conceptualized TN in terms of convulsive behaviour.
In 1773, john fothergill presented his impression of TN to the medical society of
london” a painful affection of face”
In 1891, sir victor horsley proposed the first open surgical procedure of TN.
In 1932,Dandy theorized that trigeminal neuralgia was caused by a blood vessel
compressing the nerve
In 1967 peter jannetta was finally able to further confirm this theory

5. DIVISIONS OF TRIGEMINAL
NERVE

6. WHAT IS TRIGEMINAL NEURALGIA?

7. DEFINITION
• According to international association
for study of pain –
Sudden , usually unilateral, severe brief stabbing
recurrent pain in the distribution of one or more
branches of 5th cranial nerve

8. Acc to HIS (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.

9. Fothergills
disease
Trifacial
neuralgia
Tic
douloureux

10. PREVALENCE

11. ETIOLOGY
Trigeminal nerve
function is
disrupted
Because of artery
or blood vessel ,
nerve is
compressed
Occur due to aging
Surgical injuries
Also caused by
tumor –
compressing the
trigeminal nerve
Related to multiple
sclerosis
Facial trauma

12. TRIGGER ZONES
V1
• Supra orbital
ridge of
affected side
V2
• Skin oof upper
lip, cheeks
and upper
gums
V3
• Lower lip,
teeth or gums
of lower jaw.

13. TRIGGERING FACTORS

15. HOW IS THE DIAGNOSIS MADE????
Pain- paroxysmal
Pain provoked by light touch or
trigger zone
Pain unilateral
Pain confined to trigeminal nerve
distribution
Clinical sensory examination
normal

16. CLINICAL SYMPTOMS
• Paroxysmal pain felt within
one or more divisons of the
trigeminal nerve.
• Often triggered by triggered by
a sensory stimulus to the skin,
mucosa or teeth within the
area innervated by ipsilateral
rigeminal nerve.
• The trigger zone most
commonly occurs nears the
naso labial fold.
• The pain is described as electric
shock like, shooting or
lancinating.
• Each attack lasts only seconds,
but the pain may be repetative
at short intervals.
• After many attacks within few
hours ,the patient may
describe lingering facial pain.
• Attacks of TN are most
common in the second and
third divisons of the nerve.
• Tongue is supplied by the
mandibular division of the
nerve, but its uncommon for
the pain to spread into the
tongue, even when the lower
lip and mandible are involved.
• Attacks of pain during sleep
are uncommon but do occur.
• Frequent attacks may be
associated with weight loss ,
dehydration or depression

17. Unilateral orofacial pain
Pain distribution with the facial
or intraoral trigeminal territory
Possible TN
Possible neuropathic
pain
Pain triggered by typical
maneuers
Clinically established
TN,Probable
neuropathic pain
Diagnostic test confirming
lesion or disease that can
explain TN
Etiology established
TN,definite Neuropathic
pain
MRI showing neuro
vascular compression with
morphological changes of
trigeminal root
MRI or other diagnostictest
demonstrating major
neurological disease
Classical TN Secondary
TN
Idiopathic
TN

18. CLASSIFICATION
Etiology
primary
secondary
symptom
Typical
Atypical

19. CLASSICAL/PRIMARY/
IDIOPATHIC TRIGEMINAL
NEURALGIA

20. FEATURE EXPLANATION
Paroxysmal attacks of pain lasting from a
fraction of second to 2 minutes.
May affect one or more divisions of trigeminal
neuralgia
Pain characteristics
•Electrical , intense sharp or stabbing
•Precipitated from trigger areas by innocuos
stimuli
•Precipitated by trigger factors
Between attacks there is usualy no pain , but
some atypical patients have low grade
background pain or longer lasting attacks,
periods of remission from days to years may
occur.
Pain is mostly unilateral and does not cross
the midline, it is very raarely bilateral, b/l pain
may include disease like multipple sclerosis ,
most patients have pain in the distribution of
the 2nd or 3rd divison or both.
Pain may be accompanied by spasm of the
facial muscles , after an attack of refractory
period occurs where pain cannot be triggered.
Innocous stimuli include touch , wind, shaving
but also may include temperature, noise,
lights and taste, trigger points may change
location within the same patient. A short gap
between trigger and pain may be observed.

21. FEATURE EXPLANATION
Usually no clinically evident neurological
deficit
Particularly in long standing , sensory testin g
may reaveal mild deficit in the distribution of
the trigeminal nerve.
Compression of the nerve root by a vascular
malformation (tortous aberrent vessels) is
considered as classic trigeminal neuralgia

22. SECONDARY TRIGEMINAL
NEURALGIA

23. FEATURE EXPLANATION
Features are Very Similar As Those Of
Classic Trigeminal Neuralgia
•Paroxysmal attacks
•<2 min duration
•Affecting one or more divisions of
the trigeminal nerve
Pain characteristics
Electrical, intense, sharp , superficial
stabbing
Precipitated from trigger areas or
trigger factors
•Sensory dysfunction is usually
present but may be undetectable in a
small number of patients
There are more reports of background pain
than in classic TN.B/L pain may indicate
multipple sclerosis particularly in younger
patients.
Growths in the region of cerebellopontine
angle may induce TN,usually with cranial
nerve dysfunction, posterior fossa tumours
and menangiomas are most likely to cause TN
like symptoms
No refractory period occurs as in classic TN.
pain quality may also differ
Usually accompanied by other cranial nerve
dysfunction

24. TYPICAL TRIGEMINAL NEURALGIA:
• Most common form, previously termed CLASSICAL,
IDIOPATHIC .
• Nearly all cases of typical trigeminal neuralgia are caused
by blood vessel compressing the trigeminal nerve root
ATYPICAL TRIGEMINAL NEURALGIA:
It is characterized by a unilateral, prominent constant
and severe aching and burning pain superimposed
upon other typical symptom.

25. Sl no TYPICAL TGN ATYPICAL TGN
1 site Unilateral sharp,shooting,stabbing,
lingering after sensations
Unilateral,sharp,
shooting,stabbing, lingering
after sensations,burning
2 Duration of
pain
Few seconds at most Several seconds
3 Duration of
paroxysms
Seconds to minutes Seconds to minutes
4 Continous
pain
no Yes
7 Associated
Features
Vasodialation, swelling seen with
severe pain
Vasodialation, swelling seen
with severe pain
8 radiation None outside affected division None outside affected division
9 Provoking
factors
Touching, speaking , eating , drinking,
cold not heat, movements
Touching, speaking , eating ,
drinking, cold occasionally
heat, movements
10 Variability of
pain
Some variation Definite variation

26. Sl no Typical TGN ATYPICAL TGN
11 Sensory loss Not detectable with bedside tests QST
may be abnormal
May be detectable with
bedside tests QST usually
abnormal
12 Pain
behaviour
aversion to touch aversion to touch
13 Course of pain Early remissions,pre-TGN Early remissions ,previously
typical TGN

27. ANATOMICAL CONSIDERATIONS
• 5TH nerve supplies sensation to the skin of face and anterior half of
the head.
• Motor part- innervates the muscles involved in chewing.
• It exits in the lateral mid pons and traverses the middle cranial
fossa to the gasserian and trigeminal ganglion in meckels cave,
where the nerve divides into 3 divisons- opthalmic (v1), maxillary
(v2) and mandibular (v3)
• Trigeminal nerve is predominantly sensory and motor innervation
is exclusively carried in v3.
• Upon entering the pons, pain and temperature fibres descend
ipsilaterally to the upper cervical spinal cord as the spinal tract of
5th cranial nerve, before syapsing with the spinal nucleus of the 5th.
• This accounts for the facial numbness and pain that can occur with
spinal cord .

29. PATHO-PHYSIOLOGY
Ectopic generation of action
potentials in pain sensitive afferent
fibres of the 5th cranial nerve root
just before it enters the lateral
surface of the pons
Compression or other pathology in
the nerve leads to demyelination of
large myelinated fibres that do not
themselves carry pain sensation but
become hyperexcitable and elctrically
coupled with smaller unmyelinated
or poorly myelinated pain fibres in
close proximity.
This may explain why tactile stimuli
,conveyed via the larger myelinated
fibres can stimulate paroxysms of
pain.
Compression of the trigeminal nerve
root by a blood vessel, most often
the superior cerebellar artery is now
believed to be the source of
trigeminal neuralgia.

30. DIFFERENTIAL DIAGNOSIS
Condition Cluster
head ache
SUNCT CPH Cracked
tooth
syndrom
e
Jabs and
jolt
syndrom
e
Post
herpetic
neuralgia
Giant cell
arteritis
location of
pain
Retrobulb
ar cheek,
chin
Retrobul
bar,fore
head
Forehead,
retrobulbar
Upper
jaw ,
lower
jaw
Anywher
e in the
head
Forehead,
eye,
cheek
(rarely)
Forehead,
neck,tem
ple
Duration of
pain
20 min to
hrs
5 hrs to
several
minutes
2-45 min seconds seconds continous continous
Shooting
pain or
paroxysms
Only
superimos
ed on dull
deep pain
yes no yes yes Superimp
osed
backgrou
nd pain
none

31. COURSE AND PROGNOSIS
TN frequently has exacerbating an remitting course
over many years.
During exacerbations the painful attacks may occur
anytimes a day for weeks or months at a time
A spontaneous remission may occur at any time
and lasts for months or years.
The reasons for these fluctuations are unknown.

32. INVESTIGATIONS
XRAY
MRI

33. CURRENT TREATMENT MODALITIES
Examination-MRI-Classical tn, symptomatic TN
pharmacological surgical rx
treatment
surgical
RX
Microsurgical
decompression
Ablative surgery
Carbamazepine

34. WHAT ARE THE SURGICAL
TREATMENT OPTIONS???????
EXTRA CRANIAL
• Alcohol block in
pheripheral nerve
• Electrosurgery
• Cryosurgery
• Selective radiofrequency
thermocoagulation
INTRACRANIALLY
• Alcohol blockade at
gasserian ganglion
• Retro gasserian rhizotomy
• Medullary tractotomy
• Midbrain tractotomy
• Intra cranial decompression

35. SUMMARY POINTS
• Trigeminal neuralgia is a rare but characteristic pain
syndrome.
• Most cases are still reffered to as idiopathic ,although many
are associated with vascular compression of the trigeminal
nerve
• A minority of cases are symptomatic of multiple sclerosis or
nerve compression by tumour
• The condition is variable and patients may have just one
episode.
• Most patients respond well to drugs;carbamzepine is
usually the first lie of treatment.
• If drug treatment fails or is not tolerated,surgical
treatments are available