Trigeminal neuralgia

1. TRIGEMINAL NEURALGIA
PRESENTATION BY-
SWALIHA ALTHAF

2. It usually presents with sharp,electric shock
like pain in the face or mouth,Pain is intense
,lasting for brief period of seconds to 1 min
,after which there is refractory period during
which pain cannot be reinitiated for a period
of time

3. SYNONYMS
• Trifacial neuralgia
• Fothergill’s disease
• Tic-doloureux (painful jerking)

4. ETOIOLOGY
• INTRACRANIAL CAUSES
1. Petrous ridge compression-internal carotid
artery pulsations
2. Multiple sclerosis
3. Intracranial tumors- at the cerebellopontine
angle
4. Intracranial vascular abnormalities-basilar
artery aneurysm, superior cerebellar artery
abnormality

5. EXTRACRANIAL CAUSES
1. Vascular factors
2. Dental etiology
3. Post traumatic neuralgia
4. Infections
5. Viral etiology

6. Other disorders that may affect the
trigeminal nerve include :
• Neuralgias and
neuritis
• Syphilis
• Tuberculosis
• Tumor of the brain
• Basilar meningitis
• Pontine diseases .
• Skull fracture
• Aneurysm of the
carotid artery or
circle of willis
• Psychoneuroses,and
• Cavernous
sinus
thrombosis

7. Atherosclerotic blood vessel pressing on the
root of Trigeminal nerve
Focal demyelination
Hyperexcitability of nerve fibres
Episodes of intense pain

9.  *Pre Trigeminal neuralgia
 *Idiopathic Trigeminal neuralgia
 Symptomatic neuralgia

10. • Pre trigeminal neuralgia:
Dull aching pain usually observed before
appearance of trigeminal neuralgia
• Idopathic neuralgia:
Where the etiology remains unknown
• Symptomatic neuralgia:
The type in which the etiology is known

11. CLINICAL FEATURES
 Incidence : 4 in 1,00,000
 Age : 4thto 5th decade
 Sex : F>M
 60% on the right side, 3% bilateral.
 Mean age of onset-52-58yrs

12.  Involvement :
 maxillary-60%
 mandibular-49%
 ophthalmic-16%
 all 3 divisions-1%

13.  Manifests as sudden, unilateral, intermittent,
paroxysmal, sharp, shooting, lancinating pain,
elicited by slight touch.
 Patient usually complains of electric
shock/lightening like pain
 Usually confined to one part.
 Lasts for few seconds to minutes.
 Motionless or mask like face.

14.  Rarely crosses the midline.
 Trigger points - Spontaneous attack or triggered
by trigger zone or movement of the face as in
chewing, talking, brushing or yawning
 This leads patient frequently go unshaven or
unwashed
 Paroxysms occur in cycles.
 Depression and weight loss

15. Trigger zones are usually located on vermillion border
of lip, ala of the nose, cheek, chin, and around the eye.

17. • There is generally no evidence of sensory or
motor impairment
• Apart from pain the other features are
itching & sensitivity of the face
• Rarely trigeminal neuralgia is associated
with hemi facial spasm- a condition called
TIC CONVULSIF that involves both V & VII
cranial nerves

18. DIAGNOSIS
• History
• Trigeminal nerve examination
• Diagnostic nerve blocking MRI (brain)
• EEG
• Microneurography

19.  Post herpetic
 neuralgia Dental pain
 Post traumatic neuralgia
 Multiple sclerosis
 Glossopharyngeal
 neuralgia Migraine
 SUNCT syndrome (sudden unilateral neuralgia type of
pain with conjunctival involvement)
 Migraine
 Tumors of nasopharynx( trotter`s syndrome)

20. MANAGEMENT
• PHARMACOLOGICAL
• SURGICAL
• OTHERS

21.  FIRST LINE OF APPROACH
 Carbamazepine 100, 200mg..
 SECOND LINE OF APPROACH
 Phenytoin 100mg Baclofen 5-80
mg/day
 Lamotrigine 25 mg/day THIRD
LINE OF APPROACH
 Clonazepam 4-8 mg Valproic acid
250-500 mg
 Oxcarbazepine 1200mg/day

22. Other methods used are :
 Trichloro ethylene inhalation
 Topical capsaicin cream application
 Proparacaine 0.5% anaesthetic drops in eye
 Anti inflammatory drug-Indomethacin & short
courses of steroids are found useful in some
cases

23. SURGICAL
 Stereo tactically controlled thermo coagulation of V
cranial nerve
 Vascular decompression
( through posterior fossa craniotomy)
 Repositioning of the basilar artery
( compressing the V nerve)
 Micro vascular decompression
 Gamma knife radio surgery
 Cryotherapy

24.  Injection of the nerve with alcohol
 Local anaesthetic injection of the nerve
 Nerve sectioning & avulsion
 Percutaneous radiofrequency trigeminal
neurolysis
 Bulbar trigeminal tractotomy
 Glycerol rhizotomy

25. POST HERPETIC NEURALGIA
 It is caused by reactivation of
varicella- zoster virus infection
 15-20% of cases of herpes zoster
invoule trigeminal nerve
 Majority cases affect ofhthalamic division
of 5th nerve

26.  Characterized by pain and lesions in the region of
eyes and forehead
 Infection of maxiilary and mandibilar divisions
cause facial and oral pain
 Pain resolves within month after the lesions heal
 Mostly affects elderly people.

27. PATHOGENESIS
 The vz virus injures the periphral nerve by
demyelination, wallerian degeneration and
sclerosis
 Atrophy of dorsal horn cells in the spinal
cord
 Patient exhibits painfull response to non
painfull stimuli

28.  Pain paresthesia Hyperesthasia and
alodynia persists months to years after
zoster lesions have healed
 Pain is accompanied by a sensory deficit in
the region of nerve distrubtion

29. TREATMENT
• Topical therapy: lidocaine,
capsaicin,EMLA cream.
• Tricyclic antidepressants: amitriptyline, nor
triptyline, doxepin, desiprimine
• Others: gabapentin, carbamazepine,
phenytoin

30. Surgery:
 nerve blocks peripheral nerve sresection,
dorsal root surgery
 Prevention:antiviral drug (famciclovir) and
corticosteroids

31. THANK YOU