This document provides an overview of neurologic disorders that can affect the maxillofacial region. It discusses sensory disturbances such as trigeminal neuralgia and various classifications of nerve injuries. It also covers motor disturbances like Bell's palsy. Trigeminal neuralgia is characterized by intense, stabbing pain in the face that is triggered by light touch. Bell's palsy causes sudden, unilateral facial paralysis of unknown cause. The document outlines evaluation, diagnosis, and management approaches for various neurologic conditions affecting the face and jaws.

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