FACIAL NERVE.pptx

1. FACIAL NERVE
Marizen D. Lucas

2. The course and various fiber components of the facial nerve are shown schematically in
THE FIGURE AND The facial nerve can be divided into six segments:
• INTRACRANIAL
• INTRAMEATAL
• LABYRINTHINE
• TYMPANIC
• MASTOID
• EXTRACRANIAL
2

3. Intracranial
The frontal branch components of the facial nucleus, unlike the other motor components,
are innervated by the left and right corticonuclear tract. Before the facial nerve leaves the
brainstem, its motor fibers wind around the abducens nucleus and form the "internal genu"
of the nerve. After leaving the brainstem, the facial nerve enters the internal porus acusticus
along with the vestibulocochlear nerve.
Intrameatal
Accompanied by cranial nerve VIII, the facial nerve travels
through the internal auditory canal to the fundus; there it
passes anterosuperiorly through the meatal foramen,
leaving the meatus. This is the narrowest point in the bony
fallopian canal (facial canal) and is the site where the nerve
is most likely to become entrapped due to inflammatory
swelling.

4. Labyrinthine
After running a short distance anteriorly, the
facial nerve gives off the greater petrosal nerve
with its secretory fibers to the lacrimal glands
and nasal mucosal glands. The facial nerve
turns sharply downward and posteriorly at the
geniculate ganglion, forming the first genu.
Tympanic
This segment of the facial nerve runs
horizontally through the middle ear, passing
above the stapes, to the aditus ad antrum near
the lateral semicircular canal. The tympanic
nerve segment is covered by a thin bony
sheath.

5. Mastoid
The mastoid segment of the facial nerve forms
the second genu by the aditus ad antrum,
turning vertically downward at an
approximately 90-degree angle. It courses
through the mastoid and leaves its bony canal
at the stylomastoid foramen. Just before
exiting at this foramen, the facial nerve gives
off the chorda tympani, which runs back to the
middle ear and passes through it. It contains
sensory gustatory fibers.
Extracranial
After emerging from the stylomastoid
foramen, the facial nerve enters the parotid
gland, where it branches at the pes
anserinus. The individual branching pattern
within the gland is variable.

6. Function
6
Evaluation
The predominant and most important function of the facial nerve is supplying motor
innervation to the mimetic muscles of the face. It has secretory and sensory functions as
well.
Clinical Examination
History: The onset and course of facial nerve paralysis should be documented. The patient should be
questioned about:
·Otologic symptoms and diseases or previous ear surgery
·Trauma
·Neurologic disease
·Tick bites (borreliosis) or evidence of other infections
·Systemic diseases such as diabetes mellitus, cancer, autoimmune diseases, or sarcoidosis
The symptoms of a facial nerve lesion may also include hyperacusis (paralysis of the stapedius
muscle), otalgia (irritation of the sensory fibers), gustatory disturbances, and disturbances of
lacrimation (dryness, crocodile tears = gustatory lacrimation due to faulty neural regulation).

7. 7
Testing the motor function of the facial nerve should include the following:
 Frontal branch: wrinkling the forehead or looking upward. Intact function of the
frontal branch compared with the other facial nerve branches indicates a central
or supranuclear lesion when paresis is present.
 Ophthalmic branch: rapid blinking (slowed in mild paresis); eyelid closure,
spontaneous or against a resistance (weakened in mild paresis); or incomplete lid
closure (deficit measured in millimeters, seen in severe paresis or paralysis)
 Oral branch: baring the teeth, whistling, and inflating the cheeks; air will escape
even with mild paresis.
The examiner should also watch for synkinesis-an involuntary associated movement
of mimetic muscles accompanying the voluntary movement of other muscles, such as
an unintended movement of the oral commissure induced by closing the eyes.
This type of synkinesis generally persists as a residual defect following the complete
degeneration of nerve fibers (neurotmesis).
Inspection

8. 8
Lacrimal secretion can be tested by placing strips of filter
paper in the lower eyelid and comparing the sides
(Schirmer's test). The amount of tears produced can be
helpful in planning corneoprotective therapy.
Audiometric testing (pure-tone, speech and immittance
measurements) is necessary due to stapedius muscle
involvement and the close proximity of cranial nerve VIII

9. 9
Site-of-Lesion Determination and Imaging Studies
Today, the best and most widely used topodiagnostic tests are computed tomography (CT) and magnetic resonance
imaging (MRI). Inflammatory facial nerve lesions can be demonstrated by MRI after gadolinium contrast administration.
Otogenic and traumatic facial paralysis should always be evaluated by thin-slice bone-window CT scanning of the
temporal bone. If the site of the lesion is not visualized in one plane, scans should be acquired in a second plane (axial
and coronal; temporal bone CT)
Electrical and Magnetic Testing
The importance of electrical and magnetic testing lies in the objective detection and quantification of facial paralysis.
Repeated tests are useful for defining the degree of facial nerve damage and assessing the prognosis for recovery. From a
pathophysiologic standpoint. three degrees of facial nerve fiber injury are distinguished:
1. Neurproxia
2. Axonotmesis
3. Neuromesis

10. 10
Electroneurography (ENoG)
This test involves supramaximal stimulation of the nerve trunk and measuring the muscular response with surface
electrodes. The degree of degeneration is expressed as a percentage relative to the healthy side (= 100%). More than
90% degeneration of the nerve fibers is & poor prognostic sign in terms of complete recovery.
The electrical potentials of the mimetic muscles are measured with needle electrodes, Recordings are made during
spontaneous and voluntary muscular activity for the objective detection of paralysis and reinnervation, EMG is also used
for the intraoperotive monitoring of facial nerve function during parotid and otologic surgery and intracranial operations.
Electromyography (EMG):
Magnetic stimulation
The intracranial portion of the facial nerve can be stimulated with a magnetic coil to test function over the entire course
of the nerve. If the nerve is responsive to stimulation when facial paralysis is present, there is good prognosis for recovery.
If the nerve is unresponsive, a prognostic assessment cannot be made.

11. 11
Diagnosis and Management of
Facial Paralysis
Generally, it is easily determined from the history whether the paralysis is
traumatic or nontraumatic.
With nontraumatic paralysis, the function of the frontal branch can be
tested to determine whether the lesion is central (i.e., supranuclear) or
peripheral. This is followed by various diagnostic steps and considerations.
It is particularly important to differentiate between complete paralysis and
incomplete paralysis (paresis).

12. 20XX presentation title 12

13. CLINICAL ASPECTS
13

14. 14
Inflammatory Changes
Idiopathic Facial Paralysis (Bell's Palsy)
Synonyms: cryptogenic, rheumatic or ischemic facial paralysis
Definition: Bell's palsy is a unilateral, peripheral facial paralysis of acute onset that
has no discernible cause and does not involve any other cranial nerves.
Occurrence: Bell's palsy is the most common form of facial paralysis, The incidence is
approximately 20 per 100,000 population.
Pathogenesis: Unknown. Theories include infection and inflammation (viral,
autoimmune) vascular ischemia, and constitutional factors, Idiopathic facial paralysis
is more common in diabetic patients and in pregnancy (third trimester)
Symptoms: Often the initial symptom is retroauricular pain, followed by unilateral
peripheral facial paralysis in which the frontal branch is equally affected. The paralysis
is partial in 30% of cases and complete in 70% of cases. It develops within a few days
(2-5 days) and. Has 00 systemic manifestations. The clinical features may include
hyperacusis (stapedius muscle paralysis), dysgeusia, and decreased lacrimation.

15. 15
Idiopathic Facial Paralysis (Bell's Palsy)
Diagnosis: The diagnosis is one of excision based on the typical clinical course and the absence of an identifiable cause of
the paralysis.
Differential diagnosis: Otogenic and infectious causes of peripheral facial paralysis should be excluded. Bell's palsy requires
differentiation from Melkersson-Rosenthal syndrome (peripheral facial paralysis with recurrent swelling of the face and lips
and fissured tongue).
Course and prognosis: Partial paralysis always resolves completely within a few weeks. Recovery from complete paralysis
takes longer (months) and is complete in only about 60-70% of cases. Approximately 15% of patients are left with
troublesome residual palsy and/or synkinesis.
Complications: The most serious complication is corneal damage due to lagophthalmos, ectropion, and/or decreased
lacrimation. The best preventive measures are moisturization and ophthalmologic follow-up.
Treatment: Treatment with corticosteroids, occasionally combined with rheologic or antiviral agents, is generally
recommended although definite efficacy has not been confirmed. Surgical decompression of the facial nerve is also of
unproven benefit and carries a considerably higher risk. It is important to protect the cornea with a watch- glass eye
dressing, moisturizing eye drops and ointments, and if necessary by tarsorrhaphy or by placing a gold or titanium weight
in the upper eyelid.

16. Inflammatory Otogenic Facial Paralysis
Definition: This is type of facial paralysis caused by the
spread of an infectious or other inflammatory process
from the ear and temporal bone to the facial nerve.
Occurrence: Facial paralvsis can occur as a relatively
rare complication in all forms of otitis and
osteitis/osteomyelitis of the temporal bone,
particularly in cases with cholesteatoma, subacute
mastoiditis in pediatric patients, and advanced
necrotizing otitis externa (see p. 221)
Etiology. The functional damage is caused by a direct
toxic insult, inflammatory epineural edema and pres-
sure, and in some cases by osteitis.
Symptoms: Otologic symptoms are usually the
dominant findings, and facial paralysis occurs as a
complication. A chronic process (cholesteatoma) may
have an insidious onset.
Diagnosis: The otoscopic findings suggest the correct diagnosis.
Further investigation requires an audiologic examination and CT
scans of the temporal bone.
Differential diagnosis: Differentiation is required from infectious
diseases, especially herpes zoster oticus, and from tumors of the
lateral skull base, temporal bone, and parotid gland
Complications: The complications depend largely on the underlying
disease,
Treatment: Except for facial paralysis in the setting of acute otitis
media (antibiotics), treatment consists of prompt surgical exposure
of the nerve and appropriate antibiotic therapy. Corticosteroids are
also administered to reduce edema.
Course and prognosis: These depend on the degree of paralysis, the
underlying disease, and the timing of
treatment. The less complete and more acute the para- lysis and the
earlier treatment is initiated. the better the prognosis.

17. Traumatic Facial Paralysis
17
Definition: A complete or partial facial nerve injury may result from traumatic rupture or stretch injury, nerve compression
(by hematoma or bone fragments), trauma-induced swelling, or thermal injury (from a drill during otosurgery). The paralysis
may be immediate (a complete, instantaneous traumatic lesion) or delayed (progresses over several days following the
trauma).
Pathogenesis: Facial paralysis may be caused by a temporal bone fracture, facial trauma (sharp or blunt), surgical trauma
(surgery of the petrous bone or parotid gland), or obstetric trauma. Depending on the degree of the trauma, the effects can
range from transient conduction block (neurapraxia) or nerve damage with an intact perineurium (axonotmesis) to a
complete nerve transection (neurotmesis).
Symptoms: Traumatic facial paralysis does not occur in isolation but is accompanied by other symptoms relating to the
trauma.
Diagnosis: A history of trauma usually suggests the cause of the facial nerve paralysis. The paralysis is difficult to detect only
in patients who are comatose. In patients who have sustained a temporal bone fracture, facial nerve function should always
be tested and documented so that immediate paralysis can be distinguished from paralysis of delayed onset. Thereafter the
course is monitored by electrodiagnostic testing (neurography and EMG). It is also important to determine the site of the
lesion. This requires thin-slice CT scanning, especially in patients with a temporal bone fracture.

18. Traumatic Facial Paralysis
18
Course: The course depends on the extent of the injury. A nerve rupture causes immediate and complete paralysis that does
not tend to resolve over time. With milder injuries, the paralysis often increases over a period of several days and then tends
to resolve spontaneously. It is important, therefore, to document the course of traumatic facial paralysis clinically and by
electrodiagnostic testing. The indication for surgical decompression of traumatic facial paralysis depends on the course. For
this reason, the function of the facial nerve and the course of the paralysis should always be carefully documented in patients
with temporal bone fractures.
Complications: Complications may consist of corneal damage, residual palsy, and complications relating to the primary
trauma.
Treatment: Every case of immediate paralysis should be surgically explored. The timing depends on clinical circumstances. A
severed or badly damaged nerve is either directly reapproximated or microsurgically repaired with an interposed nerve graft
(great auricular nerve or sural nerve).
Delayed paralysis is treated initially with corticosteroids to reduce edema. If neurography indicates more than 90%
degeneration or if CT indicates compression by bone fragments, the nerve is surgically explored. This is also done if other
indications for temporal bone surgery exist (cerebrospinal fluid leak, ossicular chain disruption). It is usually sufficient to
decompress the nerve.

19. QUESTIONS
19
This is the narrowest point in the bony fallopian canal
(facial canal) and is the site where the nerve is most
likely to become entrapped due to inflammatory
swelling
• INTRACRANIAL
• INTRAMEATAL
• LABYRINTHINE
• TYMPANIC
• MASTOID
• EXTRACRANIAL
The initial symptom is retroauricular pain,
followed by unilateral peripheral facial
paralysis in which the frontal branch is
equally affected.
Idiopathic Facial Paralysis (Bell's
Palsy)
Inflammatory Otogenic Facial
Paralysis
Traumatic Facial Paralysis
NOTA

20. QUESTIONS
20
This is the narrowest point in the bony fallopian canal
(facial canal) and is the site where the nerve is most
likely to become entrapped due to inflammatory
swelling
• INTRACRANIAL
• INTRAMEATAL
• LABYRINTHINE
• TYMPANIC
• MASTOID
• EXTRACRANIAL
The initial symptom is retroauricular pain,
followed by unilateral peripheral facial
paralysis in which the frontal branch is
equally affected.
Idiopathic Facial Paralysis (Bell's
Palsy)
Inflammatory Otogenic Facial
Paralysis
Traumatic Facial Paralysis
NOTA

21. THANK YOU FOR
LISTENING!
20XX presentation title 21