DR GURCHAND SINGH

1. FACIAL
NERVE &
ITS
DISORDERS
BY—DR GURCHAND SINGH
ASSISTANT PROF
ENT DEPARTMENT

2.  "Bymeansof nerves,thepathwaysof thesensesare
distributedliketherootsandfibersof a tree."
--AlessandroBenedetti,1497

3. INTRODUCTION
 Facial nerve is a nerve of 2nd brachial arch.
 mixed nerve having 10000 fibers .
 70% (7000) are myelinated motor axons to
facial muscles.
 30% (3000) are sensory and
parasympathetic.
 Gabriel Fallopius described the
fallopian canal for the intra
temporal portion of the Facial
nerve which is 33mm long.

4. COURSE OF THE FACIAL NERVE
 INTRACRANIAL
 INTRATEMPORAL
 EXTRACRANIAL

5. INTRACRANIAL
 CORTEX
Facial motor nerves are
represented on the cortex with
the forehead being uppermost
followed by eyelids midface lips.

6. MOTOR CORTEX
INTERNAL CAPSULE
MID BRAIN
LOWER BRAIN
PONS

7.  Facial nerve hooks around nucleus of
abducens.(internal genu).
 Joined by nerve of Wriesberg and
emerge from the lower border of the
Pons between olive and inf cerebellar
peduncle.
 At the CP angle it is related to two
divisions of auditory nerve nervus
intermedius and post AICA.
 Segment from the pons to IAM is 15-
17mm

8.  The FN exits the pontomedullary
junction caudal to the trigeminal
nerve and superior to
vestibulocochlear nerve.

9. INTRATEMPORAL COURSE
 MEATAL SEGMENT 8-10mm
 LABRYNTHINE SEGMENT 4.0mm
diameter of 0.61-0.68mm
 TYMPANIC /HORIZONTAL SEGMENT
11.0mm
 MASTOID /VERTICAL SEGMENT
13.0mm

10. MEATAL SEGMENT
 8-10 mm in length.
 Enters the temporal bone via porus
acousticus lies in IAC
 Association – coclear nv,
-int.auditory vessels,
- NI

11. LABRYNTHINE SEGMENT
 From the fundus of the IAC continues
into the bony fallopian canal running
above the vestibule.
 Reaches the medial wall of
epitympanic recess where it bends
sharply
 Reddish gangliform swelling first
genu
 Narrowest portion of the canal
(0.68mm) with archanoid band –
Bottle neck.

12. Branches:
1)Greater Superficial Petrossal
Nerve
secretomotor fibers to lacrimal and
nasal mucosa.
2)Lesser superficial petrosal
nerve secretary fibers to parotid
gland.

13. TYMPANIC SEGMENT/HORIZONTAL
 From the genu nerve runs post and
inferiorly in the medial wall of
tympanum.
 Inf to horizontal semicircular canal
superior to oval window and
promontory.
 Processus cochlearformis-landmark

14. MASTOID SEGMENT/VERTICLE
 From the pyramidal eminence to the
stylomastoid foramen.
 Passes through the bony floor of the
aditus bends gradually forming the
second genu.
 Length- 13 mm

15.  Branches:
 -nerve to stapedius.
 Chorda tympani secretomotor
fibers to the submaxillary and
sublingual gland and taste sensation
from anterior 2/3rd of tongue.
 Auricular branch
of Vagus

17. EXTRACRANIAL COURSE
 As its exit from stylomastoid foramen
 1) Posterior auricular
 Auricularis posterior, occipitalis, intrinsic muscles on
the back of auricle
 2) Digastric branch
 post belly of digastric
 3) Stylohyoid branch-
 Stylohyoid muscle

18. PAROTID PLEXUS
 Course of the facial N through the
stylomastoid foramen to the
substance of the parotid gland.
Crosses the styloid proccess
Retromandibular vein
External carotid artery
To form pes anserinus

19. BRANCHES OF THE PAROTID
PLEXUS
TEMPORAL AURICULARIS ANT AND SUP.
INTRINSIC MUSCLE ON THE
LATERAL SIDE OF EAR.
OCCIPITOFRONTALIS.
ORBICULARIS OCULI
CORRUGATOR SUPERCILLI
ZYGOMATIC ORBICULARIS OCCULI
BUCCAL PROCERUS
ZYGOMATICUS MAJOR
LEVATOR LABI SUPERIORIS
LEVATOR ANGULI ORIS
ZYGOMATICUS MINOR
ALAEQUE NASI

20. MANDIBULAR BRANCH DEPRESSOR ANGULI ORIS
DEPRESSOR LABII INFIRIORIS
MENTALIS
ORBICULARIS ORIS
RISORIUS
CERVICAL BRANCH PLATYSMA

21. GVESVESVAGSA

22. PES ANSERIUS

25. EXTRAPYRAMIDAL SYSTEM
 Consists of Basal Ganglia and
descending motor projections other
than CST.
 Impulses are mediated through
cingulate orbital and other frontal
cortical areas and basolateral
portion of amygdala.

26.  Responsible for spontaneous
emotional facial expressions.
 Interplay between pyramidal and
extrapyramidal system Tonus
stabilizes motor response .
 E.g destruction: Parkinsonism.

28. Surgical landmarks
 Mastoid & middle ear surgery
1.) Processus cochlearformis(PC)
- GG lies just ant.to PC .
- tympanic segment start at this level
- useful landmark
2.) Oval window & horizontal canal(HC)
- FN runs above the oval window & below the HC
- Tympanic wall FC at this part is thin
- Fractured easily & dehiscence is frequent

30. Tympanomastoid suture line
- Lies ant. to nv & close to to the course
of CTN
- CTN & FN runs deep to this suture line.
6.) Digastric ridge
- Nv. leaves temporal bone through
SMF just ant. & lat. to sigmoid sinus
where digastric ridge turns.

31. Parotid surgery
 Tragal pointer
- Sharp triangular piece of cartilage of
pinna
- nv lies 1cm deep & slightly inf. to
pointer
 Post.belly of digastric muscle
- Nv. lies b/w digastric groove & styloid
process
 Styloid process -Nv. crosses the lat. to
it

33. Evaluation of facial nerve
 Blink test
 Testing of facial movement
 Wrinkling the forehead & elevate of
eyebrow (temporal)
 Wrinkling of nose (buccal)
 Showing of teeth & blowing of cheek
(mandibular)
 Grimacing (cervical)

34. Topographic testing
 Schimer ‘s test
 Paper strip over lower conjuctival fornix 5 min.
 Result – decrease in lacrimation of 75% or more
on affected side
 - b/l decrease in lacrimation (<10 mm
on both side at 5 min.
 Stapideal reflex
 Absent – lesion is b/w GG & stapedisus muscle
 Present – lesion is distil to stapedius muscle

35. Testing for taste
 Electrogaustetry method
 Electric current is applied lat.border of ant
2/3 part of tongue
 Metallic taste to patient
 Normal – 1mA raised up to 4mA if CTN is
involved
 Can be used for GSPN
 Submandibular gland flow
 Compare the two side
 Polythene tubes passed in Wharton’s duct
 Salivation – 6% citric acid

36. Electrophysiologic testing
 Minimal nerve excitibility
 Diffrentiate b/w neurapraxia & degenration of
nerve
 Conduction block- no difference b/w 2 sides
 Nerve degenration- nerve excitibility is
gradually lost
 Difference b/w 2 sides > 3.5mA
 Maximal stimulation test
 Evaluate facial nerve degenration
 Stimulate nerve 1mA,increased upto 5mA
 Absent,markedly decreased,minimally
decreased,equal

37. Electroneurography(ENoG)
 Amount of severe nerve fibre degeneration
 Useful b/w 4 -21 days (complete paralysis)
 Bell’s palsay,trauma, acute otitis media
 Objective recording of evoke compound muscle
action potential (CAMP = 5,320µv)
 Supramaximal stimulus for maximal amplitude
CAMP
 Degeneration >90% nerve fibre – first 14 days
- bad
 Prognosis depends on rate of degeneration
 Not useful in long standing > 3weeks & tumors

38. Electromyography (EMG)
 Record spontaneous activity of facial muscles
 At rest- muscle shows no electric activity
 Voluntry contraction – normal volitional motor
unit potential
 Denervated muscle- spontaneous electric
potential (fibrillation), appears after 10-21 days
 Adv : incomplete/complete paralysis
 : earliest sings of recovery/reinnervation

39. Supranuclear infranuclear
supranuclear infranuclear
Facial palsy of lower half
contralateral side
Ipsilateral Complete facial palsy.
Hemiplegia or hemiparesis ond/or
ataxia
No hemiplegia/ataxia
No muscle atrophy or
fasciculations
Muscle atrophy and fasciculations
Tone maintained flaccid

40. SUPRANUCLEAR INFRANUCLEAR

41. LAYERS OF THE FN.
AXON
MYLEIN SHEATH
CONNECTIVE TISSUES----ENDONEURIUM---TUBULE
MULTIPLE TUBULES COVERED BY PERINEURIUM----FASCICLE.
MULTIPLE FASCICLES COVERED BY EPINEURIUM.

42. PATHOLOGY OF NERVE INJURY
 Fate of a nerve depends upon its
degree of injury.
 NEUROPRAXIA: physiological
nerve conduction block with no
anatomical defect.
 AXONOTMESIS: Axon sheath is
intact but axon is divided .Distal
degeneration of nerve fibers occurs.
 NEUROTMESIS: Whole nerve is
severed.

44. CLASSIFICATION BASED ON NERVE
REGENERATION
 Sunderlands (1951) classification of
nerve injury.
 House Brackmann`s classification of
grades of facial nerve paralysis

45. DEGREE
OF
NERVE
INJURY
ETIOLOGy PATHOLOGY NEUROBIO
LOGY OF
RECOVERY
TIME
PERIOD
HOUSE
BRACKMAN
N GRADE
I bells palsy,
herpes
zooster
cephalicus.
NEUROPRAXIA NO
MORPHOLO
GICAL
CHANGES
1-4WEEKS GRADE I
COMPLETE
WITHOUT
EVIDENCE OF
FAULTY
REGENERATI
ON.
2 viral and
inflammato
ry disorder.
SOM CSOM
with
Cholesteat
oma.
AXONOTMESI
S
AXONS
GROW INTO
THE INTACT
MYLINE
TUBES
1-
2MONTHS
GRADE11
FAIR
SOME
NOTICEABLE
DIFFERENCE
WITH
SPONTANEOU
S
MOVEMENTS.
MINIMAL
EVIDENCE

46. DEGRE
E OF
NERVE
INJURY
ETIOLOGy PATHOLOGY NEUROBIO
LOGY OF
RECOVERY
TIME
PERIOD
HOUSE
BRACKMAN
N GRADE
3 CSOM with
cholesteato
ma,slow
growing
neoplasms.
NEUROTMESI
S
LOSS OF
ENDONEURI
UMAXONS
GROW INTO
OTHER
TUBULES.
SYNKINESIS
2-
4MONTHS
GRADE III
MODERATE
OBVIOUS
WEAKNESS
COMPLETE
EYE
CLOSURE
GRADE IV
OBVIOUS
DISFIGURIN
G WEAKNESS
WITH
INCOMPLETE
EYE
CLOSURE
4 surgical
transection,
trauma,rapi
dly growing
neoplasm.
PARTIAL
TRANSECTION
NEW AXONS
ARE
BLOCKED
BY
SCARRING
IMPAIRS
4-
18MONTHS
GRADE V
MOTION IS
BARELY
PERCEPTIBLE

47. DEGREE
OF
NERVE
INJURY
ETIOLOGy PATHOLOGY NEUROBIO
LOGY OF
RECOVERY
TIME
PERIOD
HOUSE
BRACKMAN
N GRADE
5 complete
transection
iartrogenic
trauma.
COMPLETE
TRANSECTION
EPINEURIU
M IS
DESTROYED
.
SCAR
FILLED
GAPS
WHICH
FORM
BARRIERS
NEVER GRADE VI
NONE

48. axoplasm is
gradually
depleated by
catabolism
If it is not
replenished
loss of
axon will
occur in 29

49.  IN CASE OF PRESSURE OR
SECTIONING: Axon of peripheral
segment of nerve are unable to
replenished by fresh axoplasm .
 Live for 2-3 days with continued
electrical excitablility but without
conduction of impulses across the
site of injury.

50. COMPLICATION OF NERVE
REGENERATION
 Hypokinesis: few fibers
reinnervate the muscle.
 Hyperkinesis : spasm of facial
muscles due to ephahtic
transmition.
Depolarisation at the site of injury
causes firing of adjascent neuron.

51. SYNKINESIS
 Abnormal synchronisation of
movement accuring with voluntary
and reflex activity of muscles that
normally do not contract together.
 Range from a tiny twich of the chin
along with blinking to inability to
move any muscle seperately.

52. ETIOLOGY
BB
NEUROLOGICAL
CONGENITAL
TRAUMA
INFECTIONS
NEOPLASTIC
MISCELLANEOUS

53. CONGENITAL
 BIRTH TRAUMA
-forceps delivery.
-prolonged labour.
-Evidence of echymosis , lacerations.
-I II III degree of injury.
-Synkinesis may be evident in years to
come.
-in EMG there will be progressive decline
in amplitude of action potential.

54. INHERITED:
- Myotonic dystrophy:
- -autosomal dominant
- -progressive muscle wasting and
mental impairment.
- -facial is among the first to be
affected.

55.  Albers schoenberg disease:
Autosomal recessive
pattern/mutation.
Disorder of bone metabolism.
Bone density increases and primary
bone resorbtion decreases.
Osteoporosis of bony canals.
Blindness deafness and facial
paralysis(III VIII VII nerve)

56.  DEVELOPEMENTAL
ABNORMALITIES
 Moebius syndrome:
 Multiple cranial nerve
involvement(III IV V VIII X XII)
 Thaliomides
 Unilateral/bilateral facial palsy lower
half less affected.

57.  CHARGE syndrome:
 Colobomata
 Heart defects
 Atresia choanae
 Retarded growth
 Genital hypoplasia
 Ear anomalies.
 Facial nerve dysfunction

58. •BACTERIAL:
•-Malignant otitis
externa.
•-Choleateatoma.
•-Botulism.
•-Lyme disease.
•-Mastoiditis
•VIRAL:
•-Herpes zooster
cephalicus(Ramsay
Hunt Syndrome)
•-poliomylities
•-Encephalitis.
•FUNGAL:
•-mucormycosis

59. Otitis media/otitis externa:
 Acute suppuration compression of
the facial nerve at the congenital
dehiscence or along neural and
vascular structure.
 Cholesteatoma granulations can
press upon the nerve.
 Treatment is primarily eradication of
infection.

60.  LYME DISEASE:
 Tick borne spirochaete.
 Facial nerve
palsy(unilateral/bilateral) is due to
bite on head or neck causes rash
headache fever.
 Confirmed ELISA, antibodies to
immunoglobulin G and M.
 Rx tetracyclines 3-4 weeks

61.  BELLS PALSY:
 Vascular ischemic theory.
 Hereditary theory.
 Viral theory.

62.  PRIMARY VASCULAR THEORY:
-Ischemia leading to vasoconstriction
of blood vessles.
 SECONDARY VASCULAR THEORY:
-arterial constriction
-cappilary dialitation
-increased permiability
-transudation
-compression

63.  TERTIARY:
 Long standing Bells palsy ischemia
leads to thickening of underlying
fascial nerve sheath.
 Strangulating effect.

64. VIRAL THEORY:
 Virus replicates in the ganglionic
cell.
 Local damage.
 Inflammation of schwan cell.
 Lymphocytic infilteration.
 Autoimmune response.
 Hypofunction of nerve

65.  HEREDIATARY:
Familial variation of the fallopian
canal.
Narrow diameter is more susceptible
for ischemia

66. NEOPLASTIC
 CP ANGLE:
-vestibular schwanoma.
-Facial nerve tumors.
-Cochlear tumors.
-Meningioma
-Arachnoid cyst

67.  TEMPORAL BONE TUMOR:
PRIMARY:
-glomus Jugulare
-Von Recklinghaunsens disease.
SECONDARY:
-Teratoma
-Leukemia
-sarcoma

68.  PAROTID TUMORS:
 BENIGN:
 Pleomorphic adenoma
 Adenolymphoma.
 MALIGNANT:
 Mucoepidermoid carcinoma.
 Acinic cell carcinoma.
 Adenocarcinoma.

69.  NEUROLOGICAL:
-Opercular syndrome.
-Millard gubbler syndrome.
-Encephalitis.
-Myasthenia gravis.
-Multiple sclerosis
 MISCELLANEOUS:
-Tetanus
-diptheria

71. THANK YOU