Facial neuropathy

1. Neurologic disorders in
maxillofacial region
Dr. Simon

2. Outline
 Introduction
 Sensory disturbances of face
 Classifications of nerve injury
 Trigeminal neuralgia
 Motor disturbances of face and jaws
 Bells palsy
2

3. Introduction
 Anatomy of trigeminal nerve
3

4. Cont…
•Composed of mesoneurium, epineurium, perineurium and
endoneurium
4

5. Sensory disturbances of face and
jaws
 Impaired sensation
Allodynia
Analgesia
Anesthesia
Dysesthesia
Neuralgia
Neuritis
Protopathia
Causalgia
5

6. Etiology
 Surgical procedures
 Removal of impacted tooth
 Orthognathic surgery
 Endodontic and periradicular surgery
 Endosseous dental implant placement
 Salivary duct and gland surgery
 Treatment of benign and malignant lesions
 Facial trauma
6

7. Nerve injury classification
Seddon classification
 Neurapraxia:
Mild, temporary injury
Compression or retraction of nerve
No axonal degeneration
Rapid and complete recovery
No surgical intervention required
7

8. Cont…
 Axonotmesis:
Disruption or loss of continuity of some axons
 General structure of nerve remains intact
Prolonged conduction failure
 Initial signs of recovery > 3 months
Eventual recovery is often less than normal
(paresis, hypoesthesia)
8

9. Cont…
 Neurotmesis
Complete severance or disruption of all layers
Wallerian degeneration of all axons
Total permanent conduction block of all impulses
Likely subsequent neuroma formation
No recovery is expected without surgical
intervention
9

10. Cont…
Sunderland classification
 10 lesion (type I,II,III)
 20 lesion: axonal injury with subsequent degeneration
and regeneration
 30 lesion: endoneurial sheath is breached resulting in
intrafascicular disorganization
 40 lesion: disruption of axon, endoneurium and
perineurium with preservation of continuity of
epineurium
 50 lesion: severe disruption of connective tissue
10

11. Patient evaluation
 Patients history
 Clinical neurosensory testing
Brush directional discrimination
Two point discrimination
 Contact detection
Pinprick nociception, thermal discrimination
11

12. Cont…
12

13. Management
 Nerve regeneration in bony canals frequently
occurs
 Pharmacologic management
 Surgical intervention
Neurorrhaphy (if infection subsided)
All pathologic conditions of the nerve ends must
be resected (neuromas)
Nerve must be properly coapted13

14. Cont…
14

15. Cont…
 Indications for
microneurosurgery:
Observed nerve
severance
Total anesthesia beyond
3 months
Dysesthesia beyond 4
months
 Contraindications
microneurosurgery:
 Central neuropathic
pain
 Dysesthesia not
abolished by LA nerve
block
Improving sensation
Sensory deficit
acceptable to the
patient
Metabolic neuropathy15

16. Trigeminal neuralgia
 Neuropathic pain of trigeminal nerve origin, "tic
douloureux”
 Sudden, usually unilateral, severe, brief, stabbing,
lancinating, paroxysmal, recurring pain in the
distribution of one or more branches of TN
 Pain is intense, lasting for brief periods followed by a
refractory period
16

17. Epidemiology
 Over 50 years of age
 Incidence 8:100,000
 Female-to-male ratio 1.6:1
 Predilection for right side is noted (60%)
 V3 more involved than V2 and rarely V1
17

18. Etiology and Pathogenesis
 Usually idiopathic
 Probable etiologic factors
Dental etiology
Multiple sclerosis
Intracranial tumors
Infections
Post traumatic neuralgia
Petrous ridge (basilar) compression
18

19. Cont…
 Compression or other pathology in the nerve leads
to demyelination
 Fibers that do not themselves carry pain sensation
but become hyperexcitable and electrically
coupled with smaller unmyelinated or poorly
myelinated pain fibers in close proximity
 Ectopic generation of action potentials in pain-
sensitive afferent fibers19

20. Clinical characteristics
 No abnormal neurologic deficit
 Elicited by slight touch to trigger points
 Usually confined to one part of one division
 Pain rarely crosses the midline
 Pain is of short duration, but may recur with
variable frequency
20

21. Cont…
 Refractory period between attacks, some patients
report a dull ache
 Paroxysms occur in cycles, each cycle lasting for
weeks or months
 In extreme cases, patient will have a motionless
face—the ‘frozen or mask like face’
 Oral hygiene is usually poor
21

22. Cont…
 Trigger zones
Corner of lips
Cheek
Ala of nose
Supra orbital ridge
Any intraoral site
 Attacks do not occur during sleep
 Early remissions of greater than 6 months before
return of active pain in half of patient
22

23. DIAGNOSIS
 Well taken history
 Proper clinical examination
 Injections of local anesthetic agent into trigger
zone
 All patients should ideally have MRI or at least a
CT scan
23

24. Protocol for diagnostic local anesthetic
peripheral nerve blocks
 Often results in an immediate reduction in TN
attacks
 Allows the patient to talk and provides practical
way
 Eliminate the bouts of pain for prolonged time
 Material Required
3–1 cc syringes
3–25 gauge needles
24

25. Cont…
 Sweet Criteria
 Paroxysmal
 Provoked by light touch to face (trigger zones)
 Confined to trigeminal nerve distribution
 Unilateral
 Clinical sensory examination is normal
25

26. ICHD criteria for classical TN
A. Paroxysmal attacks of pain, lasting from a second
to 2 minutes, affecting one or more divisions and
fulfilling criteria B and C
B. Pain has at least one of the following
characteristics:
Intense, sharp, superficial or stabbing
Precipitated from trigger areas or by trigger
factors
26

27. ICHD criteria for symptomatic TN
A. Paroxysmal attacks of pain,lasting from a second
to 2 minutes, affecting one or more divisions and
fulfilling criteria B and C
B. Pain has at least one of the following
characteristics:
Intense, sharp, superficial or stabbing
Precipitated from trigger areas or by trigger
factors27

28. Differential diagnosis
 Primary somatic pain
 Migraine or cluster headache
 Temporal arteritis
 Multiple sclerosis
 Mass lesions: Aneurysms, neurofibromas, acoustic
schwannomas and meningioma
28

29. TREATMENT
Medical management
 Modification of the paroxysmal pain at cortical
level
 Antiepileptic drugs
Carbamezepin 400-1200
mg/day
Gabapentin 600-3200
mg/day
Baclofen 15-80 mg/day
Clonezepam 2-8 mg/day
Lamotrigine 50- 500 mg/day
Oxcarbazepine 300-2400
29

30. Diagnostic and treatment algorithm
30

31. Cont…
 Start with low dose of a single AED
 Gradually escalate over subsequent days
 Carbamazepine (Tegretol) primarily used- 100 mg
PO TID and titrated over 1 to 5 weeks period
 More of daily drug dosage should be taken at
night
 CBC, LFT should be done especially for high dose
taking patient31

32. Cont…
Multiple Drug therapy
 When a patient only partially responds to single
drug therapy
 There is little chance of success for additional third
drug
 Careful reappraisal, including a critical reevaluation
diagnosis
 If the diagnosis of TN is confirmed, such patients32

33. Surgical treatments
 Peripheral neurectomy
Simple, can be repeated and relatively reliable
It acts by interrupting flow of afferent impulses
Indicated in patients, in whom craniotomy, a
more extensive procedure is contraindicated
Nerve end should be cauterized or redirected
Disadvantages - Full anesthesia or deep
hypoesthesia, neuroma formation33

34. Recent surgical approaches
 Percutaneous stereotactic radiofrequency thermal
lesioning of trigeminal ganglion
 Posterior fossa exploration and microvascular
decompression of the trigeminal root, and
 Gamma knife radiation to trigeminal nerve root
entry zone
34

35. Motor disturbances of face and jaws
 Paresis: weakness of muscles to perform motor
functions
 Paralysis: total flaccidity of muscles to perform
motor functions
 Altered motor function of the lips, cheeks, forehead
and eyelids produces significant problems in the
affected individual
35

36.  Parotid plexus: five terminal branches
Facial nerve
36

37.  Facial palsy is commonly unilateral
 It may be either:
Peripheral: lesion of the facial nerve
Nuclear: destruction of the facial nucleus
Cereblar or supranuclear: injury to the brain or
from the injury to the face area of the motor
cortex itself
Cont…
37

38. House-Brackmann classification
Grade I : Normal function without weakness
Grade II : Mild dysfunction with slight facial
asymmetry
with a minor degree of synkinesis
Grade III : Moderate dysfunctions—obvious, but not
disfiguring, asymmetry with contracture or hemifacial
spasm, but residual forehead movement
38

39. Grade IV : Moderately severe dysfunction–
obvious, disfiguring asymmetry with lack of
forehead
motion and incomplete eye closure
Grade V : Severe dysfunction—asymmetry at rest
and only slight facial movement
Grade VI : Total paralysis—complete absence of
tone or motion
Prognosis is dependent on grade of severity39

40. Bell’s Palsy
 Acute peripheral facial nerve palsy of unknown
cause
 Sudden onset
 Not related to any other disease elsewhere in the
body
 Most common cause of unilateral facial paralysis
40

41.  Incidence: 13 to 34 cases per 100,000 population
 Sex predilection: More in female
3x more in pregnant women
 Age: middle aged people
 Positive family hx reported in about 8%
Epidemiology
41

42.  Viral hypothesis: subclinical herpes simplex or
herpes zoster
Combination of facial palsy and herpes is
known as the Ramsay Hunt syndrome
Herpetic eruptions may occur on the skin, ear,
tympanic membrane, palate, face, soft palate
and tongue
Etiology
42

43.  Ischemic hypothesis: ischemia from disturbed
circulation in the vasoneurosum
 Genetic predisposition
Cont…
43

44. Clinical Features
 Abrupt loss of muscular control on one side of the
face
 Usually after awakening early in the morning
 Unilateral involvement of entire side of the face
 Inability to smile, close the eye or raise the
eyebrow on the affected side
 Drooling of saliva
 Loss or alteration of taste
 Loss of blinking reflex44

45.  Paralysis of facial muscles, with or without loss of
taste or altered secretion
 Onset is acute; the course is progressive,
reaching maximal clinical weakness/paralysis
within three weeks or less and recovery or some
degree of function is present within six months
 Associated prodrome, ear pain, or dysacusis is
variable
Diagnosis
45

46.  Initially unilateral facial weakness affecting all
parts of the facial musculature
 Gradually worsens over 2 to 3 days, reaching a
maximum in about 2 weeks
 Remission begins within three weeks of onset in
85% of cases
 Spontaneous recovery is known to occur in Bell’s
palsy
Prognosis
46

47. Management
 Physiotherapy: indicated to maintain the
muscle tone and should be instituted as early
as possible
47

48.  Medication: within 2 to 3 weeks of onset of
symptoms prednisolone in doses of 1 mg/kg/d for
10 to 14 days with a gradual tapering
 If the patient is seen after 3 to 4 weeks, then
steroid therapy is of no use
 Antiviral therapy (optional)
Cont…
48

49.  If incomplete eye closure is present, artificial
lubrication, taping the eye, gold weight or
tarsorrhaphy might prevent visual loss from
exposure keratitis
Cont…
49

50.  Internal decompression—the nerve is exposed in
fallopian canal and pressure in canal is relieved
by exposing the nerve
 External decompression—is done by releasing of
epineural sheath from surrounding scar tissue,
bone or a foreign body
 Currently not recommended
Surgical decompression
50