MEDICAMENTS MANAGEMENT OF THE

TRIGEMINAL NEURALGIA

Rahmat Babuta, drg

Asri Arumsari drg., SpBM
 INTRODUCTION

Trigeminal neuralgia : sudden attack of pain

--- facial spasm --- in few second

Incidence : 70 / 100.000 populations, mostly five

decade, no race predilection, Woman>men

Anamnesis
Clinical description
Diagnosis
Neurological examination
Supportive examination
 INTRODUCTION

Treatment :

Medicaments --- Failed --- Surgery

Medicaments of treatment : anti convulsant ---

effective 80% --- tolerance & side effect
(be careful!!!!!)
ANATOMY OF TRIGEMINAL NERVE
 ANATOMY

DIVISION AREAS AFFECTED FUNCTION

V1 : Ophthalmic Eye, forehead & nose Sensory

V2 : Maxillary Upper teeth, gums & lip, the Sensory

cheek, lower eyelid, & the
side of the nose
V3 : Mandible Lower teeth, gums & lip Sensory
Jaw Motoric
 PATHOPHYSIOLOGY

Pathophysiology etiology

1.Mechanic compression ---

blood vessel, lesion or tumor
2.Blood vessel malformation
ETIOLOGY 3.Sclerosis multiple
4.Physic trauma of the
trigeminal nerve --- surgery or
infections
5.No clear
 PATHOPHISIOLOGY

Compression of the trigeminal nerve

(Trigeminal nerve root ,portio minor)

Irritation from repeated pulsations ---

demyelinisation & changes of nerve function --
- delivery of abnormal signals --- trigeminal
nerve nucleus --- hyperactivity --- generation of
the trigeminal neuralgia
 PATHOPHISIOLOGY

Multiple sclerosis --- demyelinisation ---

hyperactivity of the trigeminal nerve nucleus
--- tend to be younger & bilateral --- trigeminal
neuralgia
Demyelinisation & axon change ---
depolarization & potential action --- excitatory
amino acid glutamate + glutamate receptor ---
central sensitization --- electric shock-like
interneuron nucleus trigeminus & neuron
trigeminothalamic activation
 CLASSIFICATION

Idiopathic Symptomatic
Anamnesis, clinical Anamnesis, clinical
presentation, presentation, neurological
neurological examination examination & supportive
& supportive examination --- clear etiology
examination --- no clear
etiology
 CLINICAL DESCRIPTION

-Multiple episodes of severe & spontaneous pain

--- lasting seconds

-The pain --- shooting, lancinating or shocklike

-The episodes frequently are triggered by

painless sensory stimuli to trigger zones

-Triggers include touch, certain head

movements, talking, chewing, swallowing, or
even cold draft
 CLINICAL DESCRIPTION

-The episodes may be repetitive, recurring &

remitting randomly
-Pain-free intervals typically grow shorter as
the disease progresses
-Some patients can have difficulty talking,
eating, & maintaining facial hygiene out of
fear of triggering the pain
 DIAGNOSIS

Anamnesis
Clinical description
Clinical assay

Supportive examination
To differentiate idiopathic or symptomatic
1.CT Scan
2.MRI
3.MRTA
 DIAGNOSIS

Fig 2 : MRI examination

 TREATMENT

Medicaments --- failed --- Surgery

Anti convulsant

Mechanism : inhibiting the neuronal sodium

channel activity --- reducing of nucleus
hyperactivities

As the disease progresses & pain becomes

more frequent & severe --- increased doses of
medications are required --- intolerable side
effects & inadequate pain control
 TREATMENT

-The starting daily dose is low --- increase until

the pain is completely alleviated or side effect
occur

-Once relief of the pain has been achieved, the

same dose is usually continued for at least
two weeks before trying to reduce to a
minimal dosage that provides pain relief

-Medications --- single dose or combination

 TREATMENT

1.CARBAMAZEPINE (TEGRETOL)
-The most effective medication
-Side effect >> : drowsiness, mental confusion,
dizziness, nystagmus, ataxia, diplopic,
nausea, allergic skin rash, blood defective ---
make it difficult to use in elderly patients
-The effective dose ranges from 600-1200mg/d
-The dose may be tapered once pain is
controlled, since remission may occur
 TREATMENT

2.OXYCARBAZEPINE (TRILEPTAL)

-Ketoderivat carbamezepine --- fewer side

effects & risk of toxicity, but must be taken in
higher doses to provide adequate pain control

-Side effect >> : dizziness, nausea, vomiting,

fatigue, tremor.

-Doses : 600-3000mg/d

-Increasing & decreasing the dose should be

gradual
 TREATMENT

3.PHENYTOIN (DILANTIN)
-Anti convulsion --- No CNS depression
-Mechanism : blocking of spread impulse
-Side effect >> : nystagmus, dysarthria,
ophalmoplegia, ataxia, drowsiness, gingival
hyperplasia, hypertrichosis
-Doses : 900-1500mg/day tid
-Phenytoin may be also be administered
intravenously to treat severe exacerbations of
TN
 TREATMENT

4.BACLOPHEN (LIORESAL)
-Baclophen is not as effective as
carbamazepine or phenytoin for TN, but may
be used in combination with these
medications
-Side effect >> : drowsiness, dizziness,
nausea, & leg weakness
-Doses : starting dose 5 mg 2 or 3 times a day
--- & may be gradually increased --- has a
short duration of function --- doses every 3 to
4 hours
 TREATMENT

5.GABAPENTIN (NEURONTIN)

-Is an anti-epileptic drug --- structurally related

to the neurotransmitter GABA --- almost as
effective as carbamazepine but fewer side
effects

-The starting dose : 300mg tid --- increased

maximal dose (3600mg)

-Side effect : somnolence, ataxia, fatique,

nystagmus
 CONCLUSION

Trigeminal neuralgia --- sudden attack of pain ---

facial spasm --- in few second --- decrease live
quality
Diagnosis : anamnesis, clinical presentation,
neurological examination, supportive
examination --- treatment
Treatment --- medicaments (first choice ---
successful 80%) --- failed --- surgery