nevralgie trigeminala c[1]
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Trigeminal neuralgia
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Introduction
Neuralgia
Unexplained peripheral nerve pain
The most common site: head and neck
The most frequently diagnosed form:
trigeminal neuralgia (TN)
Fothergill’s disease
Tic douloureux (painful jerking)Mean age: 50 y/o
Female predominance (male : female = 1:2 ~2:3)
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Epidemiology
Incidence, approximate at 5 in every 100 000
Gender ratio of 2 female : 1 male
Right sided 56% of the time
Maxillary (V2) > Mandibular (V3) > Ophthalmic
(V1)
Mean age at diagnosis is 60 years-old
It occurs mostly after 5th decade.↑ frequencywith age, highest at >80 years old
10-15% of patients seeking care at dental
specialty
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Pain- From Symptom to Disease
Pain
Depression
Thinking negatively
Inactivity
Medical
Dependence
InsomniaSocially deprived
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Characteristics of trigeminal neuralgia
paroxysms of severe, lancinating,
electric shock-like bouts of pain
restricted to the distribution of the
trigeminal nerveUnilaterally (right side)
The mandibular (V3) and/or maxillary (V2)
branch or, rarely, the ophthalmic (V1) branch
Spontaneously attack or triggered bytrigger zone & movement of the face
Seconds to minutes
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Anatomy
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Pathogenesis of trigeminal neuralgia
Uncertain
Traumatic compression of the trigeminal
nerve by neoplastic (cerebellopontine angle
tumor) or vascular anomalies
Infectious agents
Human herpes simplex virus (HSV)
Demyelinating conditionsMultiple sclerosis (MS)
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Etiology and Pathophysiology
TN may be idiopathic (primary) or symptomatic
(secondary).
Most cases of idiopathic TN are the result of
vascular compression of V nerve, near its entry
into the pons Symptomatic causes include: multiple sclerosis,
tumors, basilar artery aneurysm (an outpouching
of a blood vessel) and by a traumatic event
such as a car accident.Compression or other pathology in the nerve
leads to demyelination of large myelinated
fibers.
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Etiology and Pathophysiology….
Demyelinative lesions of trigeminal fibersappear to set up ectopic generation of
spontaneous nerve impulses and their
ephaptic conduction to adjacent fibers.
This can lead to pain attacks at the slightest
stimulation of any area served by the nerve .
It also hinder the nerve's ability to shut off thepain signals after the stimulation ends
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Etiology and Pathophysiology….
Older ideas
Epileptogenesis (seizures from the brain)
Newer theoriesEctopic nerve firing (seizures in the nerve)
Ephapsis (cross-wirednerves)
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Types of Trigeminal Neuralgia
Typical TN
Atypical TN
Pre-TN
Multiple sclerosis-related TN
Tumor-related TN
Post-traumatic TN (trigeminal neuropathy)Failed TN
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Diagnosis
Classic TN
Atypical or mixed TN
A persistent and dull ache between paroxysms or mild sensory loss
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DiagnosisTN is often misunderstood as pathology
of dental origin. Many patients may gountreated for long periods of time beforea correct diagnosis is made.
TN remains a clinical diagnosis.
MRI and MRA can be performed if there issuspicion of underlying pathology.
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Diagnostic Clues in Facial Pain
Diagnosis Pain
Character
Pain
Distribution
Pain
Triggers
Other clues
Trigeminalneuralgia
Paroxysmal,lancinating
Trigeminal only
V2 most frequent
Touch, chewing,talking, etc
Glossopharyn
geal neuralgia
Paroxysmal,
lancinating
Ear, throat Swallowing
Trigeminal
neuropathicpain
Constant, burning,
dull throbbing
Trigeminal only None Hx of trigeminal
nerve injury
Postherpetic
neuralgia
Constant, crawling
May have
paroxysmal
component
Trigeminal only
V1 most frequent
Touch Hx of herpes zoster
ophtalmicus
Anesthesiadolorosa
Constant, burning,
itching in aninsensate region
Trigeminal only None Hx of trigeminal
nerve lesion
Malignancy Constant
May have
paroxysmal
component
In area of neoplasm
or referable to nerve
compression
Possible if trigeminal
nerve involved
Head/neck neoplasm
Atypical facial
pain
Constant Nonanatomic, often
bilateral
None Prominent psychiatric
component
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Treatment
Medical treatment
Carbamazepine (Tegretol) – first line
Oxcarbazepine
Gabapentin (Neurontin)Lamotrigine
Baclofen
Phenytoin
ClonazepamValproate
Mexiletine
Topiramate
Second line
Others
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Medical Treatment of TN
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Mechanism of medical therapy
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Advantages and Disadvantages Advantages
The benefits of this medical treatment option include
avoiding the risks involved with the invasive surgical
treatments
Disadvantages
These drugs provide complete or acceptable relief of pain
in 69% of patients with TN.
Many patients cannot tolerate medications for years.
Drug Interactions ( As the treatment is Chronic)
Unacceptable side effects (ataxia, memory disturbance,
skin rash , neutropeania )
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SURGICAL TREATMENT
Gasserian ganglion-level procedures
Microvascular decompression (MVD)
Ablative treatments
• Radiofrequency thermocoagulation (RFT)
• Glycerol rhizolysis (GR)
• Balloon compression (BC)
• Stereotactic radiosurgery (SRS)Peripheral procedures
Peripheral neurectomy
Cryotherapy (cryonanlgesia)
Alcohol block
Neuro-destructive
procedure
Surgical
decompress
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Microvascular decompression
(MVD)
TRIGEMINAL NEURALGIA
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V
VIII
sca
aica
V
MRI T2 CISS sequence
Endoscope 4mm, 30°
TRIGEMINAL NEURALGIA
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Superior cerebellar
artery
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Trigeminal neuralgia
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microscope endoscope
Trigeminal neuralgia
Glossopharyngeal neuralgia
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Microvascular Decompression
Involves a craniotomy via the posterior
fossa
High long-term success rate (above 70%)
has been reported
Morbidity includes facial dysaesthesia,
cerebellar injuries and hearing loss.
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Radiofrequency
thermocoagulation (RFT)
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CSF flow when entry Mechel’s cave 45~90 sec. cycles of 60~90℃
Perceiving a sharp pinprick as a light touch (hypalgesia)
Divisional cutaneous facial flushing
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Most commonly used
Needle is introduced percutaneously and
passed through the foramen ovale
Then RF lesion is applied (Heating or
Pulsed lesion)
Percutaneous Radiofrequency Rhizotomy
(Gasserian Ganglion Block)
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(a) Thermal lesion of trigeminal nerve. (b) Mislocation of the electrode.
(c) Expansion of thermal energy to neighboring neural structures.
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Glycerol rhizolysis (GR)
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Glycerol Rhizotomy
Injection of 0.1 - 0.2 ml of glycerol into theMeckel’s cave, through a percutaneousneedle placement.
High success rate with low morbidity hasbeen reported
This procedure has a relatively highrecurrence rate
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Test dose: 0.1-0.15 ml
0.05~0.1 ml at 3~5 min. intervals
Total dose: 0.1~0.4 ml
Sensory changes: pain, burning or paresthesia
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Balloon compression(BC)
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0.5~1 ml of contrast
Pear-shape balloon
Compression time:
1~7 min.
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Stereotactic radiosurgery(SRS)
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Gamma Knife
Single high dose radiotherapy delivered
with exquisite precision to a
radiographically defined target, at the
junction of trigeminal nerve and brainstem.
Success rate is 70%
Ad t d Di d t f
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Advantages and Disadvantages of
Surgical Intervention
Advantages
• Less neurological morbidity
Less recurrence
No vascular morbidity Results are better
Avoid years of medication and intermittent pain
Disadvantages
The risks of "anesthesia dolorosa“ - feeling sensation inpart of the face is reduced or eliminated entirely, while
the sense of pain remains
Risk of infection, facial weakness, facial numbness,
double vision, reduced hearing, and alterations in
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Peripheral procedures
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In nerve blocks, a local anesthetic is injectednear the nerve.
Trigeminal Nerve Block
Peripheral neurectomy
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Peripheral neurectomy
Alcohol block0.5~1.5 ml of 80~100%
alcohol
Whole branch & smaller
peripheral nerve branches
External approach &
intraoral method
CryotherapyExposed surgically and
direct application of a
cryoprobe -50~-140℃
3 cycles of 2 min. with a 5
min. thawing period in
between
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Ganglion level procedures vs
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Ganglion-level procedures vs.
Peripheral procedures
Ganglion-level ablative procedures
Similar long-term success rate
Varying degrees of sensory loss
Balloon compression: least likely to impair corneal sensation or to cause anesthesia
dolorosa
Peripheral proceduresHigh recurrence rates
No benefit over ganglion-level procedures
Reserved for emergency use
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Flow chart of the current practice of surgery for TN at UCLA.
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
(Temporal or Cranial Arteritis)
Idiopathic vasculitis
Same disease spectrum as polymyalgia
rheumatica
Mainly women 65-80 years old
Medium and large arteries in head & neck
involved
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Presentation
Headache
Scalp tenderness
Thickened temporal
arteries Jaw claudication
Acute visual loss
Weight loss, anorexia,
fever, night sweats,malaise & depression
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GIANT CELL ARTERITIS
Ocular Complications Transient monocular
visual loss(amaurosis fugax)
Visual loss due toCentral retinal
artery occlusion(CRAO) or
Anterior ischaemicoptic neuropathy(AION)
Visual field defects
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Management
ESR if suspected
Start high dose steroids immediately to
prevent stroke or second eye involvement
Temporal artery biopsy within a week of
starting steroids
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GIANT CELL ARTERITIS
Temporal Artery Biopsy Arteries have skip
lesions
ultrasound/Doppler
may help identifyinvolved areas
If positive, confirmsdiagnosis – helpful inmanagement of future
disease If negative, doesn’t
exclude diagnosis, butneed to think about analternative diagnosis
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GIANT CELL ARTERITIS
HistopathologyGranulomatous cell
infiltration
Giant cells
Disruption of internal
elastic lamina
Proliferation of
intima
Occlusion of lumen
GIANT CELL ARTERITIS
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GIANT CELL ARTERITIS
Treatment
Intravenous and oral steroids – prolonged
course of steroids often necessary
Origin:
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g
from the
brain stem
(medulla)by 3 nuclei ;
1)Sensory
(so l i tary nuc leus)
2)Motor
( nucleus
ambiguus ) in medul la
SVE
&
3)Parasympathetic (inferio r salivary nucleus)
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Course:
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Course:
- It leaves the skull through jugular foramen
- Descend between
(i t l C tid A t & i t l j l V i )
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(internal Carotid Artery & internal jugular Vein)
Then it curve forwards with the stylopharyngeus Muscle between
(internal Carotid Artery
&
external Carotid Artery ).
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The nerve enters
the pharynx in the
2nd gap
(between
super ior & m iddle
constr ic tor
musc le )
then it passes
deep to hyoglossus
muscle & dividesinto its branches.
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• Branches:
• 1. Motor branch; for one muscle(stylopharyngeus muscle).
• 2. Parasympathetic branch; for parotid gland
3. Sensorybranches:
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A- .
B- Lingual br ; for
the general sensation
and taste of the
posterior 1/3 of tongue.
C-
D- Carot id b r ; supply
carotid sinus and
carotid body.
Pharyngeal br ; for
mucosa of
oropharynx.
Tonsi l lar b ranch ;
for palatine tonsil
and soft palate
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Motor
parasympathetic
sensory
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Foramen of Exit From Skull
Branches Area Supplied and Function
jugular
foramen
muscular branches
lingual branch
branch to carotid body and
sinus
tympanic branch
lesser petrosal
general motor to
stylopharyngeusmuscle,
special sensation of taste from
posterior 1/3 of tongue,
general sensation from the
posterior 1/3 of tongue,,
sensation from pharyngeal
mucosa, special sensation from
carotid body and sinus.
parasympathetic to the otic
ganglion for parotid gland
secretion.
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Pathological case
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Glossopharyngeal neuralgia :
severe pain in (back of the throat, area near tonsils, back of tongue,
and part of the ear).
rare disorder
begins after age 40 and occurs more in men
its cause is unknown.
Rarely, the cause is a tumor in the brain or neck
Pathological case
Diagnosis and Treatment
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DIAGNOSE: For the test, a doctor touches the back of the
throat with a cotton-tipped applicator. If pain results, the
doctor applies a local anesthetic to the back of the throat.
DRUGS
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If these drugs are ineffective, applying a local
anesthetic (such as cocaine) to the back of the
throat (temporary relief).
(permanent relief), surgery may be needed. Theglossopharyngeal nerve is separated from the artery
that is compressing it by placing a small sponge
between them.
DRUGS
Ex. TEGRETOL
NEURONTIN DILANTIN
LIORESAL
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T i l F i l P i
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Typical Facial Pain
Sphenopalatine neuralgia A unilateral, constant, boring pain,
predominantly located retroorbital and referred
to the nose, maxillary teeth, zygoma, mastoid,and ear
Associated parasympathetic symptoms
T i l F i l P i
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Typical Facial Pain
Vidian neuralgia
Glossopharyngeal neuralgia
Postherpetic neuralgia
Pain in the area of previous herpes zoster
outbreak
TMJ syndrome
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Sphenopalatine Ganglion
Analgesia
Hi t
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History
First described by Sluder in 1908Sphenopalatine neuralgia
Spread of infection from the paranasal sinus
Eagle, in early 1940Intranasal deformities
A reflex vasomotor change
The pathophysiology remainscontroversial
JAMA, 1913, 61:1201-1216
Arch Otolaryngeal, 1942, 35:66-84
I di ti
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Indications
SPG neuralgia
Trigeminal neuralgia
Migraine
Cluster headache
Atypical facial pain
OthersBack pain, sciatica, angina, arthritis, herpes
zoster ophthalmicus, cancer pain
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Methods
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Methods
Local anesthetics
Steroids
Phenol
Radiofrequency thermocoagulation
(RFTC)
Electromagnetic field-pulsed
radiofrequency (EMF)
Capacitor
Techniques
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Techniques
Intranasal topical application of localanesthetics
Techniques
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Techniques
Greater palatine foramen approach
Techniques
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Techniques
Infrazygomatic arch approach
Techniques
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Techniques
RFTC80℃, 70~90 sec, 2 lesions
EMF
42 ℃, 120 sec, 2~3 lesions
Others
Stereotactic radiosurgical treatment
One case report of SPG neuralgia
J Neurosurg, 1997, 87:450-453
Complications
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Complications
Infection
Epistaxis
Hematoma formation
Hypesthesia of the palate
Eagle syndrome
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Eagle syndrome
Elongation of the styloid process or mineralization of the stylohyoid ligament complex
Adults, Most commonly unilateral
Vague, radiated facial pain while swallowing, turning
the head or opening the mouth Classic Eagle syndrome – After tonsillectomy
Stylohyoid syndrome – impinge on the internal or
external carotid arteries and associated sympathetic
nerve fibers
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