2. Facial nerve runs from pons to parotid.
It is a mixed nerve having motor and a sensory root.
The latter is also called the nerve of Wrisberg and carries
secretomotor fibres to the lacrimal gland and salivary
glands, and brings fibres of taste and general sensation.
Thus there are two efferent and two afferent pathways.
Components of the facial nerve include:
3. 1. Special visceral efferent –
- forms the motor root and supplies all the muscles
derived from the second branchial arch, i.e. all the
muscles of facial expression, auricular muscles (now
vestigial), stylohyoid, posterior belly of digastric and the
stapedius.
2. General visceral efferent-
supplies secretomotor fibres to lacrimal, submandibular
and sublingual glands and the smaller secretory glands in
the nasal mucosa and the palate.
4. 3. Special visceral afferent- brings taste from the
anterior two-thirds of tongue via chorda tympani and soft
and hard palate via greater superficial petrosal nerve.
- Taste is carried to the nucleus of tractus solitarius.
4. General somatic afferent brings general sensation
from the concha posterosuperior part of external canal
and the tympanic membrane.
-These fibres account for vesicular eruption in herpes zoster
infection of the geniculate ganglion.
-It also brings proprioceptive sensation from the facial
muscles.
5. NUCLEUS OF FACIAL NERVE
Motor nucleus of the nerve is situated in the pons.
It receives fibres from the precentral gyrus.
Upper part of the nucleus which innervates forehead muscles
receives fibres from both the cerebral hemispheres, while the
lower part of nucleus which supplies lower face gets only
crossed fibre from one hemisphere.
The function of forehead is preserved in supranuclear lesions
because of bilateral innervation.
Facial nucleus also receives fibres from the thalamus by
alternate routes and provides involuntary control to facial
muscles.
6.
7. The emotional movements such as smiling and crying are
thus preserved in supranuclear palsies because of these
fibres from the thalamus.
8. COURSE OF FACIAL NERVE
Motor fibres take origin from the nucleus of VIIth nerve, hook
round the nucleus of VIth nerve and are joined by the sensory
root (nerve of Wrisberg).
Facial nerve leaves the brainstem at pontomedullary junction,
travels through posterior cranial fossa and enters the internal
acoustic meatus.
At the fundus of the meatus (lateral most part of meatus), the
nerve enters the bony facial canal, traverses the temporal
bone and comes out of the stylomastoid foramen.
Here it crosses the styloid process and divides into terminal
branches.
The course of the nerve can thus be divided into three parts.
9. 1. Intracranial part- From pons to internal acoustic meatus
(15–17 mm).
2. Intratemporal part- From internal acoustic meatus to
stylomastoid foramen. It is further divided into
+(a) Meatal segment (8–10 mm)- Within internal acoustic
meatus.
+(b) Labyrinthine segment (4.0 mm)-From fundus of meatus
to the geniculate ganglion where nerve takes a turn posteriorly
forming a “genu.”
-The nerve in the labyrinthine segment has the narrowest
diameter (0.61–0.68 mm) and the bony canal in this segment is
also the narrowest.
-Thus oedema or inflammation can easily compress the nerve
and cause paralysis.
-This is also the shortest segment of the nerve.
10. (c) Tympanic or horizontal segment (11.0 mm)-From geniculate
ganglion to just above the pyramidal eminence.
- It lies above the oval window and below the lateral semicircular
canal.
(d) Mastoid or vertical segment (13.0 mm) –
From the pyramid to stylomastoid foramen.
Between the tympanic and mastoid segments is the second genu
of the nerve.
3. Extracranial part –
From stylomastoid foramen to the termination of its peripheral
branches.
11.
12. BRANCHES OF FACIAL NERVE
1. Greater superficial petrosal nerve-
It arises from geniculate ganglion and carries secretomotor fibres
to lacrimal gland and the glands of nasal mucosa and palate.
2. Nerve to stapedius. It arises at the level of second genu and
supplies the stapedius muscle.
3. Chorda tympani. It arises from the middle of vertical
segment, passes between the incus and neck of malleus, and
leaves the tympanic cavity through petrotympanic fissure.
It carries secretomotor fibres to submandibular and sublingual
glands and brings taste from anterior two-thirds of tongue.
13. 4. Communicating branch-It joins auricular branch of vagus
and supplies the concha, retroauricular groove, posterior
meatus and the outer surface of tympanic membrane.
5. Posterior auricular nerve. It supplies muscles of pinna,
occipital belly of occipitofrontalis and communicates with
auricular branch of vagus.
6. Muscular branches to stylohyoid and posterior belly of
digastric.
7. Peripheral branches. The nerve trunk, after crossing the
styloid process, forms two divisions, an upper temporofacial
and a lower cervicofacial, which further divide into smaller
branches.
-These are the temporal, zygomatic, buccal, mandibular and
cervical and together form pes anserinus (goosefoot).
They supply all the muscles of facial expression
14.
15.
16.
17.
18. BLOOD SUPPLY OF FACIAL NERVE
It is derived from four blood vessels
(i) Anterior-inferior cerebellar artery supplies the nerve in
cerebellopontine angle
(ii) labyrinthine artery, branch of anterior-inferior cerebellar
artery, which supplies the nerve in internal auditory canal
(iii) superficial petrosal artery, a branch of middle meningeal
artery, which supplies geniculate ganglion and the adjacent
region
(iv) stylomastoid artery, branch of posterior auricular artery,
which supplies the mastoid and tympanic segment.
All the arteries form an external plexus which lies in the
epineurium and feeds a deeper intraneural internal plexus
19.
20. SURGICAL LANDMARKS OF FACIAL NERVE
For middle ear and mastoid surgery-
1. Processus cochleariformis. It demarcates the
geniculateganglion which lies just anterior to it. Tympanic segment
of the nerve starts at this level.
2. Oval window and horizontal canal. The facial nerve runs above
the oval window (stapes) and below the horizontal canal.
3. Short process of incus. Facial nerve lies medial to the short
process of incus at the level of aditus.
4. Pyramid. Nerve runs behind the pyramid and the posterior
tympanic sulcus.
5. Tympanomastoid suture. In vertical or mastoid segment ,nerve
runs behind this suture.
6. Digastric ridge. The nerve leaves the mastoid at the anterior
end of digastric ridge.
21. For parotid surgery
1. Cartilaginous pointer. The nerve lies 1 cm deep and slightly
anterior and inferior to the pointer.
Cartilaginous pointer is a sharp triangular piece of cartilage of
the pinna and “points” to the nerve.
2. Tympanomastoid suture. Nerve lies 6–8 mm deep to this
suture.
3. Styloid process. The nerve crosses lateral to styloid process
4. Posterior belly of digastric. If posterior belly of digastric
muscle is traced backwards along its upper border to its
attachment to the digastric groove, nerve is found to lie
between it and the styloid process.
22.
23. VARIATION AND ANOMALIES OF FACIAL NERVE
1. Bony dehiscence. This is the most common anomaly.
Dehiscence (absence of bony cover) occurs most commonly
in tympanic segment over the oval window.
-It also occurs near the region of geniculate ganglion or in
the region of retrofacial mastoid cells.
-A dehiscent nerve is prone to injury at the time of surgery
or gets easily involved in mastoid and middle ear infections.
2. Prolapse of nerve. The dehiscent nerve may prolapse
over the stapes and make stapes surgery or ossicular
reconstruction difficult.
3. Hump. The nerve may make a hump posteriorly near the
horizontal canal making it vulnerable to injury while
exposing the antrum during mastoid surgery.
24. 4. Bifurcation and trifurcation. The vertical part of facial
nerve divides into two or three branches, each occupying a
separate canal and exiting through individual foramen.
5. Bifurcation and enclosing the stapes. The nerve divides
proximal to oval window—one part passing above and the
other below it and then reuniting.
6. Between oval and round windows. Just before oval
window the nerve crosses the middle ear passing between
oval and round windows
++Anomalies of the nerve are more common in congenital
ears; utmost care should be taken while operating cases of
microtia or other congenital conditions of the ear.
25.
26. Patterns of branching of Facial Nerve
Classified by Davis et al (1956)
1. Type I facial nerve (straight branching) with variations.
Type IA
I). Zygomatic sending a loop to itself
ii)Absent zygomatic loop
Type IB
Iii )Buccal nerve arising from upper division & mandibular
sending a loop to itself
iv) Mandibular loop is absent
27. Type II facial nerve
major connection between buccal & zygomatic nerves
28. Type III facial nerve with major connection between
buccal & any other nerve.
Type IIIA
i). Anastomosis between zygomatic & buccal nerve
ii). between buccal & upper division
iii). between buccal and lower division
Type IIIB iv). between buccal nerve (arising from mandibular)
&zygomatic nerve
Type IIIC
v) Connection between buccal & marginal mandibular
vi). Connection between buccal nerve arising fromupper division &
lower division .
vii). Type III C with additional anastomosis between upper & lower
divisions .
29. Type IV Complex branching pattern
Type IVA
i). Buccal nerve arising from upper division
ii). No anastomosis between buccal nerve & upper
division (V).
TYPE IVB
iii). Buccal nerve arising from both division.
iv). Buccal nerve arising from upper division only (V).
30. Type V Two main trunks
i). Type VA
upper & lower division arising from major trunk, buccal nerve
arises from both divisions, minor trunk joins lower division.
ii). Type VB
upper division from major & lower from minor trunk, buccal nerve
arises from both division.
iii). Type VC
upper & lower division both arise from the major trunk & minor
trunk enters the upper division as a separate branch.
31. Variation of Marginal Mandibular branch
I) The MMB showed one (28%), two (52%), three (18%), or
four branches (2%) where it exited the parotid gland.
+II) Type I (60%)
did not communicate with other branches.
+Type II (40%)
communicated with the buccal or cervical branches, or with
another branch of the MMB
III) The MMB pass the facial artery superficially (42%),
deeply in 4%, and on both sides of it in 54% of the facial
halves
32. Age Changes
child adult
Chorda tympani may exit
through Stylomastoid
Foramen
2nd genu is more acute and
lateral
Nerve trunk is more anterior
and lateral on exit through
Stylomastoid Foramen
Nerve very superficial over
angle of mandible
Chorda tympani exit
proximal to Stylomastoid
Foramen
2nd genu is less acute and
medial
Nerve trunk is less anterior
and deeper
Nerve less superficial over
angle of mandible
33. STRUCTURE OF NERVE
From inside out, a nerve fibre consists of axon, myelin sheath,
neurilemma and endoneurium.
A group of nerve fibres is enclosed in a sheath called
perineurium to form a fascicle and the fascicles are bound
together by epineurium
34.
35. SEVERITY OF NERVE INJURY
Degree of nerve injury will determine the regeneration of
nerve and its function. Earlier nerve injuries were divided into:
1. Neurapraxia, a conduction block, where flow of axoplasm
through the axons was partially obstructed.
2. Axonotmesis—injury to axons.
3. Neurotmesis—injury to nerve.
Sunderland classified nerve injuries into five degrees of
severity based on anatomical structure of the nerve and this
classification is now widely accepted.
36. 1°= Partial block to flow of axoplasm; no morphological changes are
seen. Recovery of function is complete (neurapraxia).
2°= Loss of axons, but endoneurial tubes remain intact. During
recovery, axons will grow into their respective tubes, and the result is
good (axonotmesis).
3°= Injury to endoneurium. During recovery, axons of one tube can
grow into another. Synkinesis can occur (neurotmesis).
4°= Injury to perineurium in addition to above. Scarring will impair
regeneration of fibres (partial transection).
5°= Injury to epineurium in addition to above (complete nerve
transection).
The first three degrees are seen in viral and inflammatory disorders
while fourth and fifth are seen in surgical or accidental trauma to the
nerve or in neoplasms.
37. ELECTRODIAGNOSTIC TESTS
These tests are useful to differentiate between neurapraxia and degeneration
of the nerve.
They also help to predict prognosis and indicate time for surgical decompression
of the nerve.
1. Minimal nerve excitability test.
The nerve is stimulated at steadily increasing intensity till facial twitch is just
noticeable.
This is compared with the normal side.
There is no difference between the normal and paralyzed side in conduction
block.
In other injuries, where degeneration sets in, nerve excitability is gradually
lost. When the difference between two sides exceed 3.5 m amp, the test is
positive for degeneration.
Degeneration of fibres cannot be detected earlier than 48–72 h of its
commencement.
38. 2. Maximal stimulation test (MST)
This test is similar to the minimal nerve excitability test but
instead of measuring the threshold of stimulation, the current
level which gives maximum facial movement is determined and
compared with the normal side.
Response is visually graded as equal, decreased or absent.
Reduced or absent response with maximal stimulation indicates
degeneration and is followed by incomplete recovery.
39. 3. Electroneuronography (ENoG)
It is a sort of evoked electromyography.
The facial nerve is stimulated at the stylomastoid foramen and
the compound muscle actionpotentials are picked up by the
surface electrodes.
Supramaximal stimulation is used to obtain maximal action
potentials.
The responses of action potentials of the paralyzed side are
compared with that of the normal side on similar stimulation
and thus percentage of degenerating fibres is calculated.
Studies reveal that degeneration of 90% occurring in the first 14
days indicates poor recovery of function.
Faster rate of degeneration occurring in less than 14 days has a
still poorer prognosis.
ENoG is most useful between 4 and 21 days of the onset of
complete paralysis.
40. 4. Electromyography (EMG)
This tests the motor activity of facial muscles by direct insertion of needle
electrodes usually in orbicular oculi and orbicularis oris muscles and the
recordings are made during rest and voluntary contraction of muscle.
In a normal resting muscle, biphasic or triphasic potentials are seen every
30–50 ms.
In a denervated muscle spontaneous involuntary action potentials called
fibrillation potentials are seen.
They appear 14–21 days after denervation.
With regeneration of the nerve after injury, polyphasic reinnervation
potentials replace fibrillation potentials.
They appear 6–12 weeks prior to clinical evidence of facial function and thus
provide the earliest evidence of recovery.
Voluntary contraction causes motor discharge. Diminished or no response to
voluntary contraction is seen after nerve injury.
41. Electromyography is useful in planning reanimation procedures.
Presence of normal or polyphasic potentials after 1 year of
injury indicates that reinnervation is taking place and there is
no need for reanimation procedure.
If fibrillation potentials are seen, it indicates intact motor end
plates but no evidence of reinnervation and need for nerve
substitution.
Electrical silence indicates atrophy of motor end plates and
need for muscle transfer procedures rather than nerve
substitution.
Thus ENoG and EMG are complimentary and help to
prognosticate in cases of facial paralysis and in deciding the
procedure for reanimation, i.e. nerve substitution versus
muscle transposition or sling operation.
42. CAUSES OF FACIAL PARALYSIS
The cause may be central or peripheral.
The peripheral lesion may involve the nerve in its intracranial,
intratemporal or extratemporal parts. Peripheral lesions are more
common and about two-thirds of them are of the idiopathic
variety.
Central
• Brain abscess
• Pontine gliomas
• Poliomyelitis
• Multiple sclerosis
44. iv)Trauma
– Surgical: Mastoidectomy and stapedectomy
– Accidental: Fractures of temporal bone
v) Neoplasms
– Malignancies of external and middle ear
– Glomus jugulare tumour
– Facial nerve neuroma
– Metastasis to temporal bone (from cancer of
breast,bronchus, prostate)
45. Extracranial part
• Malignancy of parotid
• Surgery of parotid
• Accidental injury in parotid region
• Neonatal facial injury (obstetrical forceps)
• Systemic diseases
• Diabetes mellitus
• Hypothyroidism
• Uraemia
• Polyarteritis nodosa
• Wegener’s granulomatosis
• Sarcoidosis (Heerfordt’s syndrome)
• Leprosy
• Leukaemia
• Demyelinating disease
46. A. IDIOPATHIC
1. BELL PALSY
Sixty to seventy-five per cent of facial paralysis is due to Bell
palsy.
It is defined as idiopathic, peripheral facial paralysis or paresis of
acute onset.
Both sexes are affected with equal frequency.
Any age group may be affected though incidence rises with
increasing age.
A positive family history is present in 6–8% of patients.
Risk of Bell palsy is more in diabetics (angiopathy) and pregnant
women (retention of fluid).
47. Aetiology
1. Viral infection –
-Most of the evidence supports the viral aetiology due to herpes simplex, herpes
zoster or the Epstein– Barr virus
-Other cranial nerves may also be involved in Bell palsy which is thus considered a
part of the total picture of polyneuropathy.
2. Vascular ischaemia –
-It may be primary or secondary.
- Primary ischaemia is induced by cold or emotional stress.
- Secondary ischaemia is the result of primary ischaemia which causes increased
capillary permeability leading to exudation of fluid, oedema and compression of
microcirculation of the nerve .
3. Hereditary-
The fallopian canal is narrow because of hereditary predisposition and this makes
the nerve susceptible to early compression with the slightest oedema.
Ten percent of the cases of Bell palsy have a positive family history.
48. 4. Autoimmune disorder. T-lymphocyte changes have been observed
49. Clinical Features
Onset is sudden.
Patient is unable to close his eye.
On attempting to close the eye, eyeball turns up and out (Bell
phenomenon).
Saliva dribbles from the angle of mouth.
Face becomes asymmetrical.
Tears flow down from the eye (epiphora).
Pain in the ear may precede or accompany the nerve paralysis.
Some complain of noise intolerance (stapedial paralysis) or loss of
taste (involvement of chorda tympani).
Paralysis may be complete or incomplete.
Bell palsy is recurrent in 3–10% of patients
50.
51. Diagnosis-
Diagnosis is always by exclusion.
All other known causes of peripheral facial paralysis should be
excluded.
This requires careful history, complete otological and head and
neck examination, X-ray studies, blood tests such as total
count, peripheral smear, sedimentation rate, blood sugar and
serology.
Nerve excitability tests are done daily or on alternate days and
compared with the normal side to monitor nerve degeneration.
Localizing the site of lesion (topodiagnosis) helps in
establishing the aetiology and also the site of surgical
decompression of nerve, if that becomes necessary.
52. TOPODIAGNOSTIC TESTS FOR LESIONS IN
INTRATEMPORAL PART
1. Schirmer test.
It compares lacrimation of the two sides.
A strip of filter paper is hooked in the lower fornix of
each eye and the amount of wetting of strip measured.
Decreased lacrimation indicates lesion proximal to the
geniculate ganglion as the secretomotor fibres to
lacrimal gland leave at the geniculate ganglion via
greater superficial petrosal nerve.
Sum of the lengths of wetted filter paper for both eyes
less than 25 mm
54. 2. Stapedial reflex.
Stapedial reflex is lost in lesions above the nerve to stapedius
. It is tested by tympanometry
Impedence audiometry can record the presence or absence of
stapedius muscle contraction to sound stimuli 70 to 100 db
above hearing threshold.
An absence reflex or a reflex less than half the amplitude is
due to a lesion proximal to stapedius nerve.
55. 3. Taste test.
It can be measured by a drop of salt or sugar solution
placed on one side of the protruded tongue, or by
electrogustometry.
Impairment of taste indicates lesion above the chorda
tympani
Compares amount of current require for a response each
side of tongue
Normal : difference < 20 uAmp (thresholds differening by
more than 25%= abnormal)
Total lack of Chorda tympani : No response at 300 uAmp
Disadvantage : False +ve in acute phase of Bell’s palsy
56. 4. Submandibular salivary flow test.
It also measures function of chorda tympani.
Polythene tubes are passed into both Wharton
ducts and drops of saliva counted during one
minute period.
Decreased salivation shows injury above the
chorda.
57. Treatment
General
1. Reassurance.
2. Relief of ear pain by analgesics
3. Eye care
4. Physiotherapy or massage of the facial muscles gives
psychological support to the patient.
- It has not been shown to influence recovery.
- Active facial movements are encouraged when there is
return of some movement to the facial muscles.
58. Medical management-
• Steroids.
Their utility has not been proved beyond doubt in carefully controlled
studies.
Prednisolone is the drug of choice.
If patient reports within 1 week, the adult dose of prednisolone is 1
mg/kg/day divided into morning and evening doses for 5 days.
Patient is seen on the fifth day.
If paralysis is incomplete or is recovering, dose is tapered during the
next 5 days. If paralysis remains complete, the same dose is continued
for another 10 days and thereafter tapered in next 5 days (total of 20
days).
Contraindications to use of steroids include pregnancy, diabetes,
hypertension, peptic ulcer, pulmonary tuberculosis and glaucoma.
Steroids have been found useful to prevent incidence of synkinesis,
crocodile tears and to shorten the recovery time of facial paralysis.
Steroids can be combined with acyclovir for Herpes zoster oticus or
Bell palsy.
59. Acyclovir 400 mg 5 times/day
Famciclovir and valacyclovir 500 mg bid
Other drugs. Vasodilators, vitamins, mast cell inhibitors
and antihistaminics have not been found useful.
Treatment consists of Infra-red radiation on affected
side of the face at 2 ft (60cm) ,followed by interrupted
galvanism on affected side.
60. Surgical treatment.
Nerve decompression relieves pressure on the nerve fibres and
thus improves the microcirculation of the nerve.
Vertical and tympanic segments of nerve are decompressed.
Some workers have suggested total decompression including
labyrinthine segment by postaural and middle fossa approach.
Facial nerve decompression
Indication:
-Completely paralysis
-ENoG less than 10% in 2 weeks
-Appropriate time for surgery is 2-3 weeks after paralysis
61. prognosis
Eighty-five to ninety per cent of the patients recover fully.
Ten to fifteen per cent recover incompletely and may be
left with some stigmata of degeneration.
Recurrent facial palsy may not recover fully.
Prognosis is good in incomplete Bell palsy (95% complete
recovery) and in those where clinical recovery starts
within 3 weeks of onset (75% complete recovery).
62. 2. MELKERSSON SYNDROME
It is also an idiopathic disorder consisting of a triad of facial paralysis,
swelling of lips and fissured tongue.
Paralysis may be recurrent.
Treatment is the same as for Bell palsy
• Recurrent facial palsy.
- Recurrent facial palsy is seen in Bell palsy (3–10% cases), Melkersson
syndrome, diabetes, sarcoidosis and tumours.
-Recurrent palsy on the same side may be caused by a tumour in 30% of cases
Bilateral facial paralysis.
- Simultaneous bilateral facial paralysis may be seen in Guillain-Barré
syndrome, sarcoidosis, sickle cell disease, acute leukaemia, bulbar palsy,
leprosy and some other systemic disorders.
63. B. INFECTIONS
HERPES ZOSTER OTICUS (RAMSAY–
HUNT SYNDROME)
There is facial paralysis along with
vesicular rash in the external
auditory canal and pinna .
There may also be anaesthesia of
face, giddiness and hearing
impairment due to involvement of
Vth and VIIIth nerves. Treatment Is
the same as for Bell palsy
64. C. TRAUMA
1. FRACTURES OF TEMPORAL BONE
-Fractures of temporal bone may be longitudinal, transverse or
mixed
-Facial palsy is seen more often in transverse fractures (50%).
- Paralysis is due to intraneural haematoma, compression by a
bony spicule or transection of nerve.
-In these cases, it is important to know whether paralysis was of
immediate or delayed onset.
- Delayed onset paralysis is treated conservatively like Bell palsy
while immediate onset paralysis may require surgery in the form
of decompression, re-anastomosis of cut ends or cable nerve graft
65. Differences in longitudinal and transverse fractures of temporal bone
Longitudinal
More common (80%) Less common (20%)
Type of injury Parietal blow Occipital blow
Fracture line Runs parallel to long axis of
petrous pyramid. Starts at squamous part
of temporal bone to end at foramen
lacerum
Bleeding from ear common d/t Common,
due to injury to tegmen and tympanic
membrane
Csf otorrhoea Present, often mixed with
blood
Structures injured Tegmen, ossicles and
tympanic membrane
Hearing loss Conductive
Vertigo Less often; due to concussion
Facial paralysis Less (20%), delayed onset.
Nerve is injured in tympanic segment,
distal to geniculate ganglion
Transverse
Less common (20%)
Occipital blow
Runs across the petrous. Starts at
foramen magnum or jugular foramen
towards the foramen spinosum
Absent because tympanic membrane is
intact. Haemotympanum may be seen
Absent or unmanifested
Labyrinth or CN VIII
Sensorineural
Severe, due to injury to labyrinth or CN
VIII
Most common (50%). Immediate onset.
Injury to nerve in meatal or
labyrinthine segment proximal to
geniculate ganglion
66.
67. 2. EAR OR MASTOID SURGERY
-Facial nerve is injured during stapedectomy, tympanoplasty
or mastoid surgery.
- Paralysis may be immediate or delayed and treatment is
the same as in temporal bone trauma
-Sometimes, nerve is paralyzed due to pressure of packing
on the exposed nerve and this should be relieved first.
-Operative injuries to facial nerve can be avoided if
attention is paid to the following:
-a) Anatomical knowledge of the course of facial nerve,
possible variations and anomalies and its surgical landmarks.
-Cadaver dissections should be an important part of the
training in ear surgery..
68. (b) Always working along the course of nerve and never across
it.
(c) Constant irrigation when drilling to avoid thermal injury.
Use diamond burr when working near the nerve.
d) Gentle handling of the nerve when it is exposed, avoiding
any pressure of instruments on the nerve.
(e) Not to remove any granulations that penetrate the nerve.
(f) Using magnification; never to work on facial nerve without
an operating microscope
69. 3. PAROTID SURGERY AND TRAUMA TO FACE
Facial nerve may be injured in surgery of parotid tumours
or deliberately excised in malignant tumours.
Accidental injuries in the parotid region can also cause
facial paralysis.
Application of obstetrical forceps may also result in facial
paralysis in the neonate due to pressure on the
extratemporal part of nerve.
70. D. NEOPLASMS
1. INTRATEMPORAL NEOPLASMS
-Carcinoma of external or middle ear, glomus tumour,
rhabdomyosarcoma and metastatic tumours of temporal bone, all
result in facial paralysis.
- Facial nerve neuroma occurs anywhere along the course of nerve
and produces paralysis of gradual or sudden onset.
-It is treated by excision and nerve grafting.
- High-resolution CT scan and gadoliniumenhanced
-MRI is very useful for facial nerve tumour.
2. TUMOURS OF PAROTID Facial paralysis with tumour of the
parotid almost always implies malignancy
71. E. SYSTEMIC DISEASES AND FACIAL PARALYSIS
Peripheral facial paralysis is mostly of idiopathic variety but
always needs exclusion of diabetes, hypothyroidism,
leukaemia, sarcoidosis, periarteritis nodosa, Wegener’s
granulomatosis, leprosy, syphilis and demyelinating disease
72. LOCALIZATION OF FACIAL LESION
A. CENTRAL FACIAL PARALYSIS
-It is caused by cerebrovascular accidents (haemorrhage,
thrombosis or embolism), tumour or an abscess.
-It causes paralysis of only the lower half of face on the
contralateral side. Forehead movements are retained due to
bilateral innervation of frontalis muscle.
- Involuntary emotional movements and the tone of facial
muscles are also retained.
73. B. PERIPHERAL FACIAL PARALYSIS
-All the muscles of the face on the involved side are paralyzed.
-Patient is unable to frown, close the eye, purse the lips or whistle.
-A lesion at the level of nucleus is identified by associated paralysis
of VIth nerve.
-A lesion at cerebellopontine angle is identified by the presence of
vestibular and auditory defects and involvement of other cranial
nerves such as Vth, IXth, Xth and XIth.
-A lesion in the bony canal, from internal acoustic meatus to
stylomastoid foramen, can be localized by topodiagnostic tests.
-A lesion outside the temporal bone, in the parotid area, affect
only the motor functions of nerve.
It may sometimes be incomplete as some branches of the nerve may
not be involved in tumour or trauma.
74. COMPLICATIONS FOLLOWING
FACIAL PARALYSIS
1. Incomplete recovery.
- Facial asymmetry persists.
- - Eye cannot be closed resulting in epiphora
- A weak oral sphincter causes drooling and difficulty in taking food
2. Exposure keratitis.
-Eye cannot be closed, tear film from the cornea evaporates causing dryness,
exposure keratitis and corneal ulcer.
-This is worse when tear production is also affected.
- It can be prevented by use of artificial tears (methylcellulose drops) every 1–2
h, eye ointment and proper cover for the eye at night.
-Temporary tarsorrhaphy may also be indicated.
-Eye closure can also be improved by using gold-weight implant sutured to the
tarsal plate deep to levator palpebrae muscle.
75. 3. Synkinesis (mass movement).
- When the patient wishes to close the eye, corner of
mouth also twitches or vice versa.
- It is due to cross innervation of fibres; there is no
treatment.
4. Tics and spasms.
-They are the result of faulty regeneration of fibres.
- Involuntary movements are seen on the affected side of
the face.
5. Contractures. They result from fibrosis of atrophied
musclesn or fixed contraction of a group of muscles.
-They affect movements of face but facial symmetry at rest
is good.
76. 6. Crocodile tears (gustatory lacrimation).
- There is unilateral lacrimation with mastication.
- This is due to faulty regeneration of parasympathetic
fibres which now supply lacrimal gland instead of the
salivary glands.
- It can be treated by section of greater superficial
petrosal nerve or tympanic neurectomy.
7. Frey’s syndrome (gustatory sweating).
- There is sweating and flushing of skin over the parotid area
during mastication.
-It results from parotid surgery.
8. Psychological and social problems.
- Drooling during eating and drinking and impairment of
speech cause social problems.
77. HYPERKINETIC DISORDERS OF
FACIAL NERVE
They are characterized by involuntary twitching of facial muscles on one or both
sides
1. Hemifacial spasm. It is characterized by repeated, uncontrollable twitchings
of facial muscles on one side
It is of two types (i) essential or idiopathic, where cause is not known and
(ii) secondary, where cause is acoustic neuroma, congenital cholesteatoma or
glomus tumour.
Many cases of hemifacial spasm are due to irritation of the nerve because of a
vascular loop at the cerebellopontine angle.
Microvascular decompression through posterior fossa craniotomy has met with
high success rate in these cases.
Idiopathic type has been treated by selective section of the branches of facial
nerve in the parotid or by puncturing the facial nerve with a needle in its
tympanic segment.
78. Botulinum toxin has been used in the affected muscle. It
blocks the neuromuscular junction by preventing release
of acetylcholine
2. Blepharospasm. Twitchings and spasms are limited to
orbiculars oculi muscles on both sides.
The eyes are closed due to muscle spasms causing
functional blindness.
The cause is uncertain, but probably lies in the basal
ganglia.
It is treated by selective section of nerves supplying
muscles around the eye on both sides.
Botulinum-A toxin injected into the periorbital muscles
gives relief for 3–6 months. Injection can be repeated, if
necessary.
79. SURGERY OF FACIAL NERVE
1. Decompression. The nerve may be compressed by oedema,
haematoma or a fractured bone in its intratemporal part.
-The bony canal is exposed and uncapped.
- The sheath of nerve is also slit to relieve pressure due to
oedema or intraneural haematoma
2. End-to-end anastomosis. This is done when the gap
between severed ends of the nerves is only a few millimetres.
-It is a suitable procedure for extratemporal part of the nerve.
-There should not be any tension in the approximated ends.
80. 3. Nerve graft (cable graft). When the gap between severed
ends cannot be closed by end-to-end anastomosis, a nerve graft
is more suitable than extensive rerouting or mobilization of
nerve.
- Nerve graft is taken from greater auricular, lateral cutaneous
nerve of thigh or the sural nerve.
- In the bony canal, the graft may not require any suturing.
4. Hypoglossal-facial anastomosis. Hypoglossal nerve is
anastomosed to the severed peripheral end of the facial nerve.
- It improves the muscle tone and permits some movements of
facial muscles, but at the expense of atrophy of tongue on that
side.
- -However, disability of tongue due to atrophy is not so severe
and patient adjusts to the difficulty in chewing and articulation
after a few weeks.
81. 5. Plastic procedures. They are used to improve cosmetic
appearance when nerve grafting is not feasible or has
failed.
-The procedures include facial slings, face lift operation or
slings of masseter and temporalis muscle.
- The latter also gives some movement to face in addition
to symmetry
