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Trigeminal neuralgia



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)



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



Pain- From Symptom to Disease

Pain

Depression

Thinking negatively

Inactivity

Medical

Dependence

InsomniaSocially deprived



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



Anatomy



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)



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.



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



Etiology and Pathophysiology….

Older ideas

Epileptogenesis (seizures from the brain)

Newer theoriesEctopic nerve firing (seizures in the nerve)

Ephapsis (cross-wirednerves)



Types of Trigeminal Neuralgia

Typical TN

Atypical TN

Pre-TN

Multiple sclerosis-related TN

Tumor-related TN

Post-traumatic TN (trigeminal neuropathy)Failed TN



Diagnosis

Classic TN

Atypical or mixed TN

A persistent and dull ache between paroxysms or mild sensory loss



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.



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



Treatment

Medical treatment

Carbamazepine (Tegretol) – first line

Oxcarbazepine

Gabapentin (Neurontin)Lamotrigine

Baclofen

Phenytoin

ClonazepamValproate

Mexiletine

Topiramate

Second line

Others



Medical Treatment of TN



Mechanism of medical therapy



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 )



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



Microvascular decompression

(MVD)

TRIGEMINAL NEURALGIA



V

VIII

sca

aica

V

MRI T2 CISS sequence

Endoscope 4mm, 30°

TRIGEMINAL NEURALGIA



Superior cerebellar

artery



microscope endoscope


Glossopharyngeal neuralgia



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.



Radiofrequency

thermocoagulation (RFT)



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



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)



(a) Thermal lesion of trigeminal nerve. (b) Mislocation of the electrode.

(c) Expansion of thermal energy to neighboring neural structures.



Glycerol rhizolysis (GR)



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



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



Balloon compression(BC)



0.5~1 ml of contrast

Pear-shape balloon

Compression time:

1~7 min.



Stereotactic radiosurgery(SRS)



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



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



Peripheral procedures



In nerve blocks, a local anesthetic is injectednear the nerve.

Trigeminal Nerve Block





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



Ganglion level procedures vs



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



Flow chart of the current practice of surgery for TN at UCLA.

GIANT CELL ARTERITIS



66


(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




67


Presentation

Headache

Scalp tenderness

Thickened temporal

arteries Jaw claudication

Acute visual loss

Weight loss, anorexia,

fever, night sweats,malaise & depression



68


Ocular Complications Transient monocular

visual loss(amaurosis fugax)

Visual loss due toCentral retinal

artery occlusion(CRAO) or

Anterior ischaemicoptic neuropathy(AION)

Visual field defects




69


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



70


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



71


HistopathologyGranulomatous cell

infiltration

Giant cells

Disruption of internal

elastic lamina

Proliferation of

intima

Occlusion of lumen




72


Treatment

Intravenous and oral steroids – prolonged

course of steroids often necessary

Origin:



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)



Course:



Course:

- It leaves the skull through jugular foramen

- Descend between

(i t l C tid A t & i t l j l V i )



(internal Carotid Artery & internal jugular Vein)

Then it curve forwards with the stylopharyngeus Muscle between

(internal Carotid Artery

&

external Carotid Artery ).



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.



• Branches:

• 1. Motor branch; for one muscle(stylopharyngeus muscle).

• 2. Parasympathetic branch; for parotid gland

3. Sensorybranches:



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



Motor

parasympathetic

sensory



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.



Pathological case



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



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



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



T i l F i l P i



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



Typical Facial Pain

Vidian neuralgia

Glossopharyngeal neuralgia

Postherpetic neuralgia

Pain in the area of previous herpes zoster

outbreak

TMJ syndrome



Sphenopalatine Ganglion

Analgesia

Hi t



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



Indications

SPG neuralgia


Migraine

Cluster headache

Atypical facial pain

OthersBack pain, sciatica, angina, arthritis, herpes

zoster ophthalmicus, cancer pain



Methods



Methods

Local anesthetics

Steroids

Phenol

Radiofrequency thermocoagulation

(RFTC)

Electromagnetic field-pulsed

radiofrequency (EMF)

Capacitor

Techniques



Techniques

Intranasal topical application of localanesthetics

Techniques



Techniques

Greater palatine foramen approach

Techniques



Techniques

Infrazygomatic arch approach

Techniques



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



Complications

Infection

Epistaxis

Hematoma formation

Hypesthesia of the palate

Eagle syndrome



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

nevralgie trigeminala c[1]

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