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17 Lateral Skull Base Pathologies
187
hemorrhage → RBC breakdown → foreign body
reaction to cholesterol crystals [9]. Other features
include the following:
• Clinical ndings: Usually asymptomatic, it
may expand to compress CNs and brainstem.
• MRI ndings show nonenhancing lesion with
T1 and T2 hyperintensity from both high uid
and fat content (see Fig.17.8).
• Management:
– Observe if not causing symptoms.
– Surgical decompression for cranial neu-
ropathies, brainstem compression
– Transnasal approaches provide the wid-
est access for lesions with extension
medial to the carotid.
– Lateral approaches: Infracochlear and
infralabyrinthine afford only narrow
access but provides a route for aeration
and drainage through connection with
middle ear/mastoid.
17.3.2 Asymmetric Marrow
It is a variant of normal anatomy; it is found in
around 5–10% of individuals as an asymptomatic
imaging nding. It appears on MRI as nonenhancing T1 hyperintense asymmetry. CT scan
demonstrates normal, noneroded bone. No follow- up or treatment is required.
Fig. 17.7 MRI T1 with contrast shows dumbbell shape
meningioma of the right jugular foramen
Fig. 17.8 Axial CT and T1 MRI in two different patients
showing expansile lesion in the right and left petrous apices respectively displaying CT hypodensity and high
17.3.3 Eusion/Trapped Fluid
It occurs in a pneumatized petrous apex that
trapped effusion. It is seen on imaging studies
and in most cases is asymptomatic.
T1-WI signal intensity due to fatty contents representing
cholesterol granuloma
188
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Fig. 17.9 Axial HRCT and T2WI MR showing evidence of right-sided otomastoiditis with opacication of pneuma-
tized right petrous apex and erosion of its posteromedial wall denoting petrous apicitis
Z. Altamimi et al.
CT shows petrous apex air cell opacication
with present septations; MRI demonstrates a T1
hypointense, T2 hyperintense area with no
enhancement.
Most cases are asymptomatic with no required
intervention. For symptomatic patients, prolonged antibiotics with a corticosteroid can be
used, and rarely surgical drainage is required.
17.3.4 Cholesteatoma/Epidermoid
Cyst
Epithelial cyst within the petrous apex. Imaging
studies demonstrate bone destruction on CT and
restricted diffusion on DWI MRI.
Surgical excision is quite challenging in this
area, if patient has a dead ear. A
translabyrinthine
or transcochlear approach will give optimal
access for the eradication of the cholesteatoma.
17.3.5 Petrous Apicitis
with abscess; otherwise does not enhance; T2
high signal (see Fig.
17.9).
Treatment is achieved by antibiotics if no
improvement surgical drainage should occur by
mastoidectomy and drainage.
17.3.6 Chordoma
It is a malignancy of the primitive notochord that
usually arises from the midline with extension
from clivus to petrous apex. It has a locally
aggressive behavior. Skull base chordomas
account for only 0.1–0.2% of all intracranial
tumors [10]. CT shows a destructive lesion with
calcication foci and enhances on T1 with contrast, which may be difcult to differentiate from
chondrosarcoma.
The optimal treatment involves radical surgery plus adjuvant radiotherapy. Chordoma carries a poor prognosis with a high rate of
recurrence, even after extensive surgery and adjuvant radiotherapy [
10].
Petrous apicitis is a rare complication of otomastoiditis especially in individuals with a pneuma-
17.3.7 Chondrosarcoma
tized petrous apex. There is a classic triad of sixth
nerve palsy, deep facial pain, and ipsilateral otorrhea, which is referred to as Gradenigo syndrome,
although it may not be present in every patient [8].
CT scan demonstrates air cell coalescence; T1
intermediate signal may have an enhancing ring
It is a rare cartilaginous tumor. It arises from
skull base synchondroses, most commonly from
the petroclival region [10]. It presents as a
destructive lesion that invades bone and extends
into soft tissues and can manifest with headache
AL GRAWANY
17 Lateral Skull Base Pathologies
189
and diplopia. The lesion is located in the central
or paramedian skull base. The diagnosis of chondrosarcoma is radiological; CT shows irregular
bone destruction, may have “popcorn” calcications, and enhances on T1 with contrast.
Treatment is surgical resection; both radiation
therapy and chemotherapy are of no benet as
primary therapy, but radiotherapy (proton beam)
may be of benet in cases of subtotal resection
and recurrent tumor [11].
17.3.8 Metastasis
The petrous apex is the most common site of
metastatic spread within the temporal bone [8].
Breast cancer is the most common primary metastatic cancer, followed by lung, prostate, kidney,
and melanoma primary cancers.
17.4 Diuse Temporal Bone/
Other Skull Base Lesions
17.4.1 Fibrous Dysplasia
It is a focal condition where medullary bone is
replaced by bro-osseous tissue. Usually monostotic (localized to one site), progressive external
auditory canal occlusion with conductive hearing
loss rarely causes sensorineural hearing loss.
Diagnosis is usually made by CT scan, which
shows “ground glass” expansive mass; treatment
is mainly observation, may consider canaloplasty
for conductive hearing loss or cholesteatoma formation behind canal stenosis, and radiotherapy
should be avoided.
17.4.2 Eosinophilic Granuloma
It is the most common form of Langerhans cell
histiocytosis, known as the localized form, it carries the best prognosis [12]. It typically affects
mastoid, the external auditory canal (EAC), and
petrous apex, and may involve entire temporal
bone; it affects older children and young adults.
It presents as painful postauricular swelling, or
with granulation and otorrhea of EAC.CT scan
shows areas of bony destruction, and MRI T1
with contrast shows enhancement. Treatment is
conservative, surgical excision, or low-dose
radiotherapy for inaccessible or recurrent
lesions.
17.4.3 Rhabdomyosarcoma
It is the most common temporal bone malignancy
of children. It affects the middle ear and mastoid.
It is divided into four histologic types: embryonal, botryoid, alveolar, and pleomorphic. The
embryonal type is the most common. It presents
with chronic otalgia and otorrhea that fails to
respond to appropriate medical therapy.
Treatment includes limited surgical intervention,
external beam radiotherapy, and chemotherapy.
17.4.4 Endolymphatic Sac Tumor
It is a rare malignancy of the inner ear, originating from the endolymphatic sac on the posteromedial wall of the temporal bone. It is slow
growing, but locally destructive tumor with a low
risk of distant metastases.
It is histologically shown as papillary adenomas. It has an association with Von-Hippel–
Lindau (VHL) syndrome (seen in 10–30% of
VHL patients); therefore, these patients require
screening [10].
The diagnosis is mainly by imaging; CT scan
shows a soft tissue mass on the posterior petrous
face with a destruction of adjacent regions of the
temporal bone with a characterizing expansile
appearance. MRI shows retrolabyrinthine lesion
with hyperintense T1, heterogeneous T2 signal,
and T1 with contrast reveals heterogeneous
enhancement (see Fig.17.10).
The treatment is best achieved with early and
complete tumor resection. Different lateral skull
base approaches can be used according to tumor
localization, tumor size, and invasion. It is a
highly vascularized tumor with a higher risk of
bleeding. Radiotherapy can be utilized depending on the disease stage [10].
190
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Fig. 17.10 Axial and coronal MRI T1 with contrast reveals heterogeneous enhancement of right ear endolymphatic sac
tumor
Z. Altamimi et al.
17.4.5 Osteopetrosis
It is a rare disorder of bone remodeling with a
symmetrical increase in bone density because of
defective function of the osteoclasts. It presents
in two types, an autosomal dominant (AD) type
and an autosomal recessive (AR) type. The AD,
also known as Albers-Schonberg disease, is the
more common type, affecting the head and mandible including the temporal bone and ossicles
but it spars the otic capsule. It presents with cranial neuropathies due to compression at neural
foramina. The AR, also known as malignant
infantile osteopetrosis, is more severe with higher
morbidity and mortality.
The treatment focuses on symptomatic management, and decompression interventions of the
facial nerve and the cochlear nerve may be of
benet. Bone marrow transplantation also has
been described for malignant osteopetrosis.
Take-Home Messages
• Glomus tumors considered the most
common benign tumor of the temporal
bone and middle ear of adults. Glomus
jugulare is the most common type
involving the jugular fossa.
• Glomus tumors can present with different types of associated cranial nerve
syndromes, including Vernet syndrome,
Collet–Sicard syndrome, and Villaret
syndrome.
•
Jugular foramen lesions surgical exci-
sion is quite challenging and might
require advance approaches such as
transmastoid-transcervical, and infratemporal fossa approach.
• Cholesterol granuloma is the most common pathologic lesion found in the
petrous apex.
AL GRAWANY
17 Lateral Skull Base Pathologies
• Petrous apicitis can present with classic
triad of sixth nerve palsy, deep facial
pain, and ipsilateral otorrhea, which is
referred to as Gradenigo syndrome.
• The petrous apex is the most common
site of metastatic spread within the temporal bone, and most commonly metastasize from breast cancer.
• Fibrous dysplasia is characterized by
“ground glass” on CT scan. Radiotherapy
should be avoided as it carries a risk of
malignant transformation.
References
1. Ramina R, Maniglia JJ, Fernandes YB, Paschoal JR,
Pfeilsticker LN, Neto MC, Borges G.Jugular foramen
tumors: diagnosis and treatment. Neurosurg Focus.
2004;17(2):E5.
2. Borba LA, Araújo JC, de Oliveira JG, Filho MG,
Moro MS, Tirapelli LF, Colli BO. Surgical management of glomus jugulare tumors: a proposal for
approach selection based on tumor relationships with
the facial nerve. J Neurosurg. 2010;112(1):88–98.
3. Fish JH, Klein-Weigel P, Biebl M, etal. Systematic
screening and treatment evaluation of hereditary neck
paragangliomas. Head Neck. 2007;29(9):864–73.
191
4. Drovdlic CM, Myers EN, Peters JA, etal. Proportion
of heritable paraganglioma cases and assodated clinical characteristics. Laryngoscope. 2001;111:1822–7.
5. Fayad JN, Keles B, Brackmann DE.Jugular foramen
tumors: clinical characteristics and treatment outcomes. Otol Neurotol. 2010;31:299–305.
6. Weissman JL, Hirsch BE. Imaging of tinnitus: a
review. Radiology. 2000;216:342–9.
7. Willen SN, Einstein DB, Maciunas RJ, et al.
Treatment of glomus jugulare tumors in patients with
advanced age: planned limited surgical resection followed by staged gamma knife radiosurgery: a preliminary report. Otol Neurotol. 2005;26:1229–34.
8. Isaacson B, Kutz JW, Roland PS. Lesions of the
petrous apex: diagnosis and management. Otolaryngol
Clin N Am. 2007;40(3):479–519.
9. Jadder RK, Cho M. A new theory to explain the
genesis of petrous apex cholesterol granuloma. Otol
Neurotol. 2003;24:96–106.
10. Zanoletti E, Mazzoni A, Martini A, et al.
Surgery of the lateral skull base: a 50-year
endeavour. Acta Otorhinolaryngol Ital.
2019;39(Suppl 1):S1–S146. https://doi.
org/10.14639/0392-100X-suppl.1-39-2019.
11. Lustig LR, Sciubba J, Holliday MJ.Chondrosarcoma
of the skull base and temporal bone. J Laryngol Otol.
2007;121:725–35.
12. Bayazit Y, Sirikci A, Bayaram M, Kanlikama M,
Demir A, Bakir K.Eosinophilic granuloma of the temporal bone. Auris Nasus Larynx. 2001;28(1):99–102.
The Facial Nerve
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HassanHaidar andSuzanMohamed
18
18.1 Introduction
The facial nerve can be affected anywhere along
its course. A comprehensive assessment considering all differential diagnoses is critical to
optimal management, as prompt and appropriate therapy leads to better outcomes. The chapter
will cover the anatomy, pathology, investigation,
and intervention. Information is organized to
cover the most common pathology followed by
least common and then rare conditions.
18.2 Facial Nerve Anatomy
The facial nerve runs from the brain stem to facial
muscles, and it has seven segments: intracranial
→ meatal segment → meatal foramen → labyrinthine segment→ tympanic segment → mastoid
segment → extratemporal segment [1].
In the parotid, the facial nerve divides into
ve branches (extratemporal branches): temporal, zygomatic, buccal, marginal mandibular, and
cervical.
The Narrowest segment of nerve (0.68 mm)
occurs at meatal foramen [2] and is thepresumed
H. Haidar (*)
Hamad Medical Corporation, Doha, Qatar
S. Mohamed
Otolaryngology Department, Hamad General
Corporation, Doha, Qatar
e-mail: SMohamed50@hamad.qa
site of nerve injury in Bell’s palsy and therefore
is site of facial nerve decompression.
Dehiscence is the most common variation
of facial nerve, and the most frequent dehiscent
areas are: tympanic segment > geniculate (middle
fossa) > mastoid (adjacent to retrofacial cells).
In the brainstem, three nuclei give rise to the
facial nerve:
1. Facial motor (voluntary facial movement),
2. Superior salivatory (parasympathetic effer-
ents for tearing and salivation),
3. Nucleus of the solitary tract (sensory afferents
for taste).
The facial nerve trunk consists of approximately 10,000 nerve bers, approximately
7000 of which are myelinated motor bers.
The remaining 3000 bers are somatosensory
and secretomotor, and are known as the Nervus
Intermedius.
The facial nerve sheath consists of several
layers. The endoneurium, closely adherent to the
layer of Schwann cells of the axons, surrounds
each nerve ber. The perineurium, which is the
intermediate layer surrounding groups of fascicles, provides tensile strength to the nerve and is
believed to represent the primary barrier to the
spread of infection. The outermost layer of the
nerve is the epineurium. This outer layer contains
the vasa nervorum, which provides the blood
supply to the nerve.
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_18
AL GRAWANY
193
194
Sunderland Classification of Facial Nerve Injuries
° Class I: Neuropraxia; compression of axon, no axonal disruption
° Class II: Axonotmesis; disruption of axon; endoneurium, perineurium, and epineurium still intact
° Class III: Neurotmesis; disruption of endoneurium surrounding axon; perineurium and endoneurium
still intact, risk for synkinesis
° Class IV: Neurotmesis; disruption of perineurium and endoneurium, epineurium still intact
H. Haidar and S. Mohamed
18.3 House–Brackmann Scale
The House–Brackmann Facial Nerve Grading
System is widely used to characterize the degree
of facial paralysis. In this scale, grade I is assigned
to normal function, and grade VI represents complete paralysis. Intermediate grades vary according to function at rest and with effort (Fig.18.1).
18.4 Facial Nerve Injury
andRegeneration
18.4.1 Facial Nerve Injury
Classication (Fig.18.2)
1. Neuropraxia
(a) Axon and supporting tissues remain intact
(b) No Wallerian degeneration
(c) Complete recovery
2. Axonotmesis
(a) Loss of continuity of the axon
(b) Wallerian degeneration occurs
(c) Complete recovery, no synkinesis
3. Neurotmesis
(a) Injury involves endoneurium
(b) Wallerian degeneration occurs
(c) Increasing risk of synkinesis and incom-
plete recovery with increasing Sunderland
class
In facial palsy, there can be a combina-
tion of injuries occurring at the same time.
Electrodiagnostic testing is useful to demonstrate
the most prevalent degree of injury.
Electrodiagnostic testing can determine percentage of bers stimulable (neuropraxia) versus
non-stimulable (axonotmesis and neurotmesis).
Unfortunately, no current testing can distinguish between axonotmesis from neurotmesis.
More rapid degeneration indicates more severe
injury and most likely neurotmesis.
Wallerian degeneration is a process that occurs
before nerve regeneration and can be described as
a cleaning or clearing process that essentially prepares the distal stump for reinnervation. Schwann
cells proliferate and form endoneurial tubes with
the remaining connective tissues that guide regeneration of the axon to its nal destination.
Electrical stimulation can promote nerve
regeneration [3].
When nerve bers are damaged, they may
aberrantly regenerate. During regeneration,
excessive collateral branching of the axons
occurs, not only at the site of the lesion but also
along the entire course of the nerve. These extraaxons may result in synkinesis. An example of
abnormal neural regrowth is “crocodile tears,”
or increased lacrimation associated with eating. It
occurs when efferent bers normally targeted to
travel with the chorda tympani nerve to the submandibular and sublingual glands are misdirected
through the greater supercial petrosal nerve to
the lacrimal gland. This results in parasympathetic innervations of the lacrimal gland as well as
the normal target, the salivary glands. As a result,
Fig. 18.1 House–
Brackmann
classication of facial
palsy
Fig. 18.2 Sunderland classication of facial nerve injuries
° I: Normal function
° II: Slight weakness but symmetric at rest, good forehead motion
° III: Obvious weakness but symmetric at rest, impaired forehead motion,
able to close eye, may have synkinesis or contracture
° IV: Symmetric at rest, incomplete eye closure, no forehead motion
° V: Asymmetry at rest, barely perceptible movement
° VI: Asymmetry at rest, no movement
House–Brackmann Classification
18 The Facial Nerve
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195
when eating, instead of getting the normal salivary response to increase the salivation, the neuronal signal causes tearing of the lacrimal gland.
These abnormal movements can be more distressing than the facial palsy itself. Botulinum
toxin injection and facial reanimation are among
the proposed methods of treatment.
18.5 Facial Nerve Function Tests
It is used to assess integrity of nerve in cases of
complete facial paralysis (for paresis not used
because nerve is intact).
18.5.1 Electroneuronography (ENoG:
Evoked EMG)
It records facial muscle compound action potentials (CAP) in response to transcutaneous electrical stimulation (stimulating electrode placed at
the region of stylomastoid foramen).
It provides an objective measure of action
potential amplitudes from normal and paralyzed
sides.
It should NOT be done until 2–3days after
injury (wait for Wallerian degeneration to occur).
It predicts prognosis and determines the criteria for surgical intervention in traumatic/Bell’s
palsy (>90% denervation). In Bell’s palsy: middle
fossa decompression is suggested if >90% degeneration compared to normal side within 2weeks.
18.5.2 Electromyography (EMG)
It determines the level of spontaneous muscle
activity, and it is useful in predicting prognosis
for acute or long-standing paralysis.
Fibrillation → Seen in denervated muscle
~2weeks after injury.
Silence → Muscle atrophy (long-standing
denervation).
• Polyphasic potentials → seen with muscle
reinnervation ~6weeks after injury
• Normal voluntary action potentials indicate at
least partial nerve continuity.
18.5.3 Nerve Excitability Test (NET)
It compares the lowest current stimulation threshold required to cause minimal muscle contraction
on each side of the face (difference >3.5mA considered signicant); it requires subjective observation by tester.
18.5.4 Maximum Stimulation Test
(MST)
It compares muscle movement on each side of
face in response to suprathreshold current stimulation, stimulation probe placed in the region of
nerve branch to be tested; it requires subjective
grading by tester.
18.6 Unilateral Facial Nerve
Weakness (Fig.
18.3)
18.6.1 Congenital Facial Palsy
Congenital causes include obstetric, developmental facial paralysis, Möbius syndrome, and
idiopathic mandibular division palsy.
• Obstetric injury, often with forceps delivery,
is the commonest cause of congenital cause;
most recover within a month.
• Idiopathic marginal mandibular nerve palsy
(congenital unilateral lower lip palsy/CULLP)
causes unilateral weakness of depressor anguli
oris and is associated with other major congenital anomalies in 10% of children, most
commonly the cardiovascular system. It
affects about one in 160 live births.
• Möbius syndrome is a rare condition of
unknown origin. Children usually present at
an early age with facial and ocular symptoms
which include incomplete eye closure, masklike face, inability to follow gaze, drooling,
and difculty sucking. The facial nerve is
always involved, the abducens nerve is
involved in 75–100% of cases, and the hypoglossal nerve is commonly implicated. Other
cranial nerves may be involved. The condition
is often bilateral.
AL GRAWANY
196
weakness
H. Haidar and S. Mohamed
Unilateral facial weakness
Congenital Infectious
Mobius syndrome:
CN VII/VI palasies,
club foot, mental
retardation
Congenital lower lip
palsy:
Hypoplasia of
depressor anguli
oris muscle, cardiac
defects
Fig. 18.3 Causes of unilateral facial palsy
Bell’s palsy
Herpes zoster
oticus/Ramsay
Hunt syndrome
HIV
Lyme disease:
10 % develop
ipsilateral or
bilateral facial
Limb abnormalities may be present in up to
25% of cases.
• Goldenhar’s syndrome comprises hemifacial
microsomia, epibulbar dermoid cysts, and vertebral anomalies, and may have facial nerve
weakness.
18.6.2 Bell’s Palsy
It is the most common cause of unilateral facial
weakness/paralysis, and idiopathic but viral etiology is suspected.
Risk factors: Diabetes, pregnancy, and prior
history (10% recur).
18.6.2.1 Clinical
– Acute unilateral weakness or paralysis devel-
ops within 48h.
– May have viral prodrome, hyperacusis,
decreased tearing, numbness/pain of ear/face/
neck, and taste changes
Traumatic
TB fracture
latrogenic
Chronic
Cholesteatoma
Neoplastic:
Schwannom, glomus,
parotid tumor
Melkerson−Rosenthal
syndrome:
begins in childhood
recurrent facial edema
recurrent facial weakness
recurrent fissured tomgue;
treat with steroids
– ENoG can be considered for patients with
complete paralysis, and it is used to determine
candidacy for surgical intervention.
18.6.2.2 Treatment
– High-dose steroids (prednisone 1 mg/kg)
increase the rate of recovery.
– No evidence of improvement with addition of
antivirals to steroids [4]
– Eye care if difculty with eye closure to pre-
vent exposure keratitis (saline drops, lacrilube
ointment, and eye bubble)
– Surgery: Middle fossa decompression for
patients under 65 with >90% neuronal degeneration within 2weeks of onset
18.6.2.3 Prognosis
More than 90% of patients will completely
recover [5].
It shows poor prognosis with advanced age
and complete paralysis.
18 The Facial Nerve
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197
18.6.3 Traumatic Facial Palsy
Trauma is the second commonest cause and may
be due to temporal bone fracture, penetrating
wounds, or obstetric injury.
18.6.3.1 Blunt Trauma
• Longitudinal versus transverse (see chapter
TB fracture)
• Facial paralysis is more likely with transverse
fractures
• Most commonly injured at perigeniculate region
• Management analogous to Bell’s palsy
– Medical: High-dose steroids (prednisone
1mg/kg)
– Surgical: Consider decompression for
patients with immediate complete paralysis
and >90% neuronal degeneration on ENoG
within 2weeks of onset. If no hearing, perform translabyrinthine exploration; if hearing is still present, combined middle fossa/
transmastoid exploration is performed.
18.6.3.2 Penetrating Trauma
– Gunshots, knives, …
– High risk of nerve transection
– Nerve injury to facial nerve branches medial
to a line drawn vertically through the lateral
canthus of the eye may retain facial movement
because of the degree of arborization
– Injury to the frontal and marginal mandibular
nerves manifesting with weakness should
always be repaired as the likelihood of spontaneous recovery is poor. Nerve repair should
ideally be done within 72h to permit identication of the distal ends of the severed nerves
by electrical stimulation; beyond 72 h neurotransmitter stores may become depleted.
18.6.4 Herpes Zoster Oticus/Ramsay
Hunt Syndrome
Herpes zoster oticus: Reactivation of herpes
zoster virus (normally dormant in geniculate
ganglion) with cutaneous lesions in distribution
of nervus intermedius (CN VII).
Since the vestibulocochlear nerve is in proximity to the geniculate ganglion, it may also be
affected, and patients may also suffer from tinni-
tus, hearing loss, and vertigo. Involvement of the
trigeminal nerve can cause numbness of the face.
Ramsay Hunt syndrome: Herpes zoster oticus + facial paralysis, 18% of adult facial palsies.
18.6.4.1 Clinical
– Shingles in external auditory canal, pinna,
anterior 2/3s of tongue, and soft palate;
– Facial paresis/paralysis with Ramsey Hunt
syndrome,
– May have associated hearing loss (50% of
patients, due to involvement of CN VIII), also
tinnitus and vertigo/disequilibrium
18.6.4.2 Diagnosis
– Audiogram may show sensorineural hearing
loss;
– MRI to evaluate the course of facial nerve
18.6.4.3 Treatment
– Treatment with prednisone and acyclovir
800mg ve times a day started within the rst
3 days of facial paralysis may increase the
probability of complete recovery [6]
– Consider anticonvulsants (carbamazepine,
gabapentin, lyrica) for postherpetic neuralgia
Prognosis: Increased risk of residual facial
weakness compared to Bell’s palsy.
Surgical Pearl
At birth, the facial nerve exits in the stylomastoid foramen on the lateral aspect of the
skull, just inferior to the tympanic membrane and external ear canal. This makes
the facial nerve vulnerable to traumatic
injury during difcult delivery.
18.6.5 Acute Otitis Media
andMastoiditis
It is typically seen in children who appear toxic
with otoscopic ndings of middle ear empyema.
The palsy is often progressive in over a 2–3day interval.
AL GRAWANY
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