Phẫu Thuật Tai Mũi Họng Và Phẫu Thuật Đầu Cổ

1348
Section 15
Temporal Bone
the dissection inferior to the cochlea and anteroinfe-
rior to the IAC.
The air cells lateral to the cholesterol granuloma
often appear dark. Once the cyst is entered, the char-
acteristic thick, yellow-brown fl uid and cholesterol crys-
tals are encountered. The fi stula opening into the cyst
is enlarged while keeping the carotid artery and jugular
vein in view. Cup forceps are used to remove some of
the lateral inferior lining of the cyst wall. The cavity is
evacuated of its fl uid contents. The size of the opening
is maximized by drilling to the limits of the carotid
artery, jugular bulb, and basal turn of the cochlea. The
cavity is irrigated with bacitracin-saline solution. If the
cyst is multiloculated and the surgical approach gives
limited exposure, endoscopy may be helpful. A sinus
(2.7 mm) or otologic (1.9 mm) endoscope may facili-
tate visualization of hidden parts of the cystic lesion. In
combination with suction and irrigation, endoscopy
facilitates débridement and effi cient drainage of sep-
tated cholesterol granuloma or eradication of choles-
teatoma limited to the inferior petrous apex.37
The area is stented and drained with silicone or
Silastic tubing. If not available, Silastic sheeting (0.02
inch) is cut in a rectangular shape and rolled to make
a cylinder (Fig. 126-13). The inferior and lateral aspect
of the Silastic tubing is trimmed so that it is contained
completely within the middle ear and hypotympanic
spaces. Gelfoam impregnated with an antibiotic suspen-
sion is placed in the newly created hypotympanum and
along the medial fl oor of the new bony EAC. The infe-
rior aspect of the tympanomeatal fl ap is returned to its
anatomic position. A small graft of fascia positioned
medial to the tympanomeatal skin fl ap and extended
laterally toward the ear canal may be needed to cover
a residual defect. Gelfoam with antibiotic suspension is
placed lateral to the tympanic membrane and along the
fl ap of the meatal skin. The auricle is returned to its
anatomic position while ensuring that the posterior
conchal skin fl ap is laid fl at against the posterior bony
canal wall. The lateral cartilaginous canal is packed with
lateral rosebud packing, Gelfoam, or a Merocel sponge.
The postauricular incision is closed with 4-0 resorbable
suture braided subcutaneously and 5-0 fast-absorbing
suture in the skin and covered with Steri-Strips, and a
sterile mastoid dressing is applied.
The transcanal infracochlear approach requires
exposure of the sigmoid sinus and drilling under the
cochlea, which can potentially lead to complications. A
modifi cation was proposed in which only exposure of
the ICA is required and a surgical window is drilled
anterior to the cochlea, thereby presumably reducing
the risk of injury to the jugular bulb and round window.
The tradeoff for increased safety is a smaller working
space averaging 4.7 × 3.2 mm instead of 7.3 × 9.4 mm
with a traditional infracochlear approach.38
Retrofacial Infralabyrinthine Approach
The patient is positioned supine on the table with the
head turned toward the contralateral ear. One centime-
ter of postauricular hair is shaved, and the ear is pre-
pared in usual fashion. Two percent lidocaine with
1:100,000 epinephrine is infi ltrated into the skin 2 cm
posterior to the postauricular sulcus. A curvilinear inci-
sion is made through the skin. Fibroperiosteal tissue is
elevated from the mastoid cortex, and self-retaining
retractors are placed.
A complete transcortical mastoidectomy is per-
formed. The sigmoid sinus is decompressed, and 1 cm
of bone posterior to the edge of the sinus is removed.
The horizontal semicircular canal is delineated. The
aditus ad antrum is opened as widely as possible to
maximize ventilation into the epitympanic and middle
ear spaces. Further ventilation through the middle ear
is accomplished by opening the facial recess if commu-
nication between the aditus ad antrum of the mastoid
and the epitympanum of the middle ear is insuffi cient.
A
B
Figure 126-13. A, A rolled Silastic sheet is placed in the opening of the fi stula from the cystic cavity to the hypotympanum. B, The Silastic
sheeting in place.

Chapter 126
Cholesterol Granuloma and Congenital Epidermoid Tumors of the Temporal Bone 1349
The posterior semicircular canal is outlined with a
diamond drill. The vertical portion of the facial nerve
is defi ned, and a thin covering of bone is left for protec-
tion. Additional bone is removed to expose the mastoid
tip and digastric ridge.
Using a cutting burr, drilling is continued through
the air cells posterior to the vertical portion of the facial
nerve. Dissection is carried in an anteromedial direc-
tion. The continuation of the sigmoid sinus into the
jugular bulb must be defi ned. To obtain adequate
access through this route, a high jugular bulb must not
be present. This anatomic variation would have been
identifi ed on preoperative bone-windowed CT scan-
ning. In patients with a high jugular bulb, the proce-
dure can be converted into an infracochlear approach.26
Posterior compression of the sigmoid sinus enhances
the exposure and angle necessary to gain access to the
petrous apex cyst. Once it is opened, the contents of
the cyst are evacuated. Cup forceps are used to com-
pletely remove the lining of the posterolateral cyst wall.
This opening is maximized through the confi nes of the
area limited by the facial nerve anteriorly, the ampulla-
ted end of the posterior semicircular canal superiorly,
the posterior fossa dura posteriorly, and the jugular
bulb inferiorly.
The cavity is irrigated with bacitracin solution. A
Silastic tube or sheeting rolled into a cylinder is placed
in the cavity and trimmed to an appropriate length so
that it lies within the inferior aspect of the mastoidec-
tomy (Fig. 126-14). The postauricular incision is closed
with 4-0 resorbable braided suture, and a sterile mastoid
dressing is applied.
Translabyrinthine Approach
The translabyrinthine approach for drainage of the
petrous apex is identical to that for resection of an
acoustic neuroma (Chapter 124). This approach is
undertaken if hearing is signifi cantly compromised or
absent. Bone is removed 1 cm posterior to the sigmoid
sinus, and the middle fossa tegmen is thinned. A com-
plete labyrinthectomy is performed. The IAC is care-
fully outlined while taking care to not enter the dura of
the IAC, the posterior fossa, or the middle fossa.
The incus is removed, and the fossa incudis is
drilled to maximize communication between the
mastoid and the epitympanic space. A trough is created
superior to the IAC if the bony anatomy permits.
Entrance into the petrous apex can be achieved through
suprameatal air cells, if present. Care must be taken to
avoid injury to the facial nerve in its labyrinthine
segment.
The bone inferior to the IAC is removed with a
diamond burr (Fig. 126-15). The location of the jugular
bulb is noted. Caution should be exercised when
working in the area superior to the jugular bulb and
inferior to the IAC. The cochlear aqueduct enters the
vestibule in this area, and entry into the cochlear aque-
duct results in leakage of CSF into the wound. This is
diffi cult to suture and may need to be plugged with fat
or muscle. If it cannot be occluded in watertight fashion
and sealed from potential communication with the cyst,
the cholesterol granuloma drainage procedure must be
terminated. Abdominal fat is packed into the cavity, and
muscle is plugged into the epitympanum.
Figure 126-14. Retrofacial infralabyrinthine approach. A transcor-
tical mastoidectomy is performed to identify the antrum, posterior
semicircular canal, facial nerve, digastric ridge, and jugular bulb. A
Silastic tube from the mastoid into the cyst provides drainage and
aeration.
Figure 126-15. Translabyrinthine approach to the petrous apex.
The IAC is skeletonized to create an inferior and superior trough
around the porus acusticus. Care is taken to avoid the cochlear aque-
duct and jugular bulb. The labyrinthine segment of the facial nerve
is noted.

1350
Section 15
Temporal Bone
The inframeatal exposure of the petrous apex
should drain and ventilate the cyst adequately. More
aggressive removal of cyst lining is possible with wider
exposure. Drainage with a catheter or Silastic sheeting
is unnecessary if a large opening in the fi stula is created.
The wound is copiously irrigated with bacitracin solu-
tion. The skin is closed in two layers, and a sterile
mastoid dressing is applied.
Transcochlear Approach
The transcochlear approach is reserved for patients
who have a large tumor of the petroclival region with
preexisting hearing loss. It is a modifi cation of the
translabyrinthine approach in which the cartilaginous
EAC is closed in a cul-de-sac. A canal wall down mas-
toidectomy is then performed with unroofi ng of the
sigmoid sinus and exposure of the dura of the posterior
and middle fossae. The IAC is identifi ed and the facial
nerve is decompressed from the stylomastoid foramen
to the IAC. The facial nerve is dissected free from the
fallopian canal and transposed posteriorly. This requires
identifi cation and sacrifi ce of the greater superfi cial
petrosal nerve (GSPN). After liberation of the genicu-
late ganglion, the labyrinthine, tympanic, and vertical
portions of the facial nerve are successively released and
transposed posteriorly toward the dura of the posterior
fossa. The nerve is immobilized with fi brin glue. The
cochlea and fallopian canal are then drilled to expose
the vertical portion of the ICA. Additional anterior
exposure requires drilling the anterior wall of the EAC
and displacing the mandibular condyle anteriorly. The
horizontal portion of the IAC is then exposed. At the
end of the procedure, the eustachian tube is plugged
with muscle, Surgicel, and fat harvested from the
abdomen, which is then covered with a temporalis myo-
fascial fl ap.
Although this approach is fairly safe and allows
good exposure, it is frequently complicated by cranial
nerve palsy. For instance, in a review of 66 cases, every
patient in whom the facial nerve was transposed had
facial nerve weakness, with only 5% of patients recover-
ing normal facial nerve function 1 year after the
procedure. Most of the patients (60%) recovered to
House-Brackmann grade III function. Other postopera-
tive defi cits included weakness of cranial nerves IV
(6%) and VI (9%).39
Tympanomastoid Exteriorization
A petrous apex epidermoid tumor or cholesterol granu-
loma can be marsupialized or drained directly into the
tympanic space. This approach almost always entails a
canal wall down mastoidectomy. Whether the ossicular
chain can be reconstructed depends on the location of
the disease, the status of the hearing preoperatively,
and the procedure that was performed.
The patient is positioned supine on the operating
table with the head turned toward the contralateral ear.
The supra-auricular and postauricular hair is shaved,
and the ear is prepared and draped in the usual sterile
fashion. A longer Koerner fl ap is made in the EAC in
anticipation of a canal wall down mastoidectomy. A
postauricular incision is made, and dissection is contin-
ued into the EAC. The posterior canal skin fl ap is ele-
vated and retracted into the ear canal with tracheotomy
tape. The auricle is retracted anteriorly. A transcortical
mastoidectomy is performed. Because the approach is
directed toward the anterior epitympanic area, creation
of a large mastoid cavity is to be avoided. Therefore,
bone from the mastoid tip and sinodural angle does not
have to be extensively removed unless the temporal
bone is pneumatized and mucosal disease is present.
The aditus ad antrum, horizontal semicircular
canal, and incus are identifi ed. Attention is then turned
to the EAC. A tympanomeatal fl ap is elevated to identify
and disarticulate the incudostapedial joint. The incus is
removed and saved if it is not involved with cholestea-
toma. The posterior bony canal wall is taken down, the
anterior and posterior buttress is removed, and the
facial ridge is lowered to the level of the EAC. Using a
malleus nipper through the neck of the malleus, the
head of the malleus is removed. Drilling and dissection
are continued anteriorly through the zygomatic route.
The geniculate ganglion is noted, and dissection is con-
tinued along the GSPN. If greater exposure is necessary
inferiorly, the malleus and tensor tympani tendon are
removed as well. Although it may permit drainage of a
cholesterol cyst, the tympanomastoid approach is pre-
dominantly used to marsupialize cholesteatoma located
in this area (Fig. 126-16).
The invasive and expansive nature of petrous apex
epidermoid tumors is likely to cause sensorineural
Figure 126-16. Tympanomastoid exteriorization. A canal wall
down mastoidectomy is used to expose the anterior epitympanum
and the cholesteatoma in the petrous apex. Dissection along the
greater superfi cial petrosal nerve opens the petrous apex through the
air cells of the zygomatic route.

Chapter 126
Cholesterol Granuloma and Congenital Epidermoid Tumors of the Temporal Bone 1351
hearing loss. If cochlear function has been compro-
mised preoperatively (speech reception threshold
>70 dB, discrimination <30%), greater exposure is
achieved by continuing the dissection through the
cochlea. The inferior limits of this opening are the
eustachian tube and genu of the carotid artery. Drilling
is continued through and parallel to the plane of the
cochlea. The proximal modiolus and lateral fundus of
the IAC should be avoided to prevent a CSF leak. The
contents of the petrous apex cholesteatoma are evacu-
ated with blunt instruments such as suction, cup forceps,
curettes, and smooth elevators. The epithelial matrix is
usually left intact (Fig. 126-17). The cavity is copiously
irrigated with bacitracin solution.
Despite the use of meticulous surgical technique
while removing or exteriorizing an epidermoid tumor
or cholesterol granuloma, CSF leakage may occur as a
result of attenuation of the dura. Another situation in
which a transepitympanic petrous apex exteriorization
approach may need to be converted to obliteration is
when the carotid artery becomes signifi cantly exposed.
Concern for desiccation of the adventitia of the carotid
artery in a marsupialized cavity demands soft tissue pro-
tection and coverage. This routinely entails obliteration
of the cavity with a temporalis muscle fl ap or abdominal
fat. If the cavity must be obliterated because of a CSF
leak, wide exposure of the carotid artery, or excessive
exposure of the dura, great effort is taken to completely
remove the wall of the granuloma or the epidermal
matrix lining. The external auditory meatus is closed in
a two-layer technique (see Chapter 125). An abdominal
fat graft is most effective in sealing the CSF leak and
obliterating the cavity. The posterior portion of the
temporalis muscle is divided, rotated inferiorly, and
sutured to the sternocleidomastoid muscle and subcu-
taneous tissue of the posterior skin.
If cochlear function was not sacrifi ced, reconstruc-
tion of the ossicular chain is undertaken. These tech-
niques are reviewed in Chapter 114. When performing
an exteriorization procedure, the epidermoid cavity is
packed with continuous gauze impregnated with anti-
biotic ointment. The packing is placed through the
external auditory meatus and positioned in the depth
of the epidermoid cavity. The packing is continued
through the epitympanic space and mastoid cavity to
secure the Koerner fl ap posteriorly. The postauricular
wound is closed with 4-0 resorbable braided suture sub-
cutaneously and 5-0 fast-absorbing suture in the skin
supported by Steri-Strips, and an external mastoid
dressing is applied.
Preauricular Subtemporal Infratemporal
Approach
This approach is used when complete excision of cho-
lesterol granuloma or epidermoid tumor of the petrous
apex is necessary. If normal cochlear function is present
preoperatively, a hearing conservation procedure is
warranted. The patient is positioned supine on the
table with the head turned toward the contralateral ear.
Should lateral neck rotation be limited, an ipsilateral
shoulder roll is placed to provide additional rotation. A
strip of hair is shaved from the lateral side of the scalp.
The head is placed in three-point fi xation with pins
using a Mayfi eld head holder. The preauricular incision
is outlined in curvilinear fashion toward the hairline of
the forehead (Fig. 126-18). A solution of 1% lidocaine
with 1 : 100,000 epinephrine is injected into the planned
incision. The skin is incised, and the dissection is taken
down to the level of the temporal fascia. Anterior and
posterior skin fl aps are elevated. Anteriorly, the frontal
or temporal branch of the facial nerve must be pre-
served by incising the deep temporalis fascia in the area
just superior to the temporal fat pad. Dissection is con-
tinued anteroinferiorly beneath the level of the deep
temporalis fascia to protect the frontalis branch within
the anterior skin fl ap from transection, although it is
still subject to being stretched (Fig. 126-19). The root
and arch of the zygoma are palpated and isolated by
incising the periosteal attachments superior and infe-
rior to the arch. Using a Freer or Adson elevator, the
medial surface of the zygomatic arch is freed of its mus-
cular attachments.
The attachment of the temporalis muscle is incised
along its borders of insertion. A margin of the fi brous
attachment along the superior temporal line is pre-
served to facilitate subsequent reapproximation and
wound closure. The temporalis muscle is incised poste-
riorly, superiorly, and anteriorly and elevated from the
temporal fossa. The inferiorly based temporalis muscle
fl ap is dissected well into the infratemporal fascia.
Figure 126-17. Transcochlear approach to the petrous apex. The
contents of the epidermoid tumor are removed while leaving the
matrix lining intact.

1352
Section 15
Temporal Bone
Figure 126-18. Incision for a preauricular subtemporal infratem-
poral fossa approach.
Figure 126-19. The anterior fl ap is elevated. The frontal branch
of the facial nerve is preserved by incising the superfi cial and deep
layers of the temporalis fascia superior to the level of the temporal
fat pad.
If access to the vertical portion and genu of the
carotid artery is necessary, resection of the mandibular
condyle is undertaken. Soft tissue surrounding the
mandibular condyle is elevated. Venous bleeding is
often encountered but is controlled with bipolar coagu-
lation. The neck of the condyle is freed of its perios-
teum, and the bone is cut with a reciprocating or sagittal
saw. If proximal exposure of the carotid artery is not
necessary, the capsule and meniscus of the temporo-
mandibular joint are dissected from the glenoid fossa,
and the condyle is retracted inferiorly.
The subtemporal approach is continued by per-
forming a temporal craniotomy centered over the infra-
temporal fossa. The inferior aspect of the craniotomy
should be made as low as possible (Fig. 126-21). The
base of the skull consisting of the inferior squamous
portion, part of the petrous portion, and the posterior
extent of the sphenoid bone is further removed with a
cutting burr. The middle fossa dura is elevated medially
in a posterior-to-anterior direction to the level of the
superior petrosal sinus. The temporal lobe is gently
elevated and retracted superiorly with a Greenberg
retractor. The middle meningeal artery is identifi ed
and divided via bipolar coagulation. The third or man-
dibular division of the trigeminal nerve is identifi ed.
Along the fl oor of the middle cranial fossa, the GSPN
is identifi ed and provides a landmark for the geniculate
ganglion. The geniculate ganglion also serves as a supe-
rior landmark for the cochlea. The GSPN is then tran-
sected to avoid traction injury to the facial nerve.
Further drilling in this area with cutting and then
diamond burrs provides initial exposure of the carotid
artery.
The horizontal portion of the carotid artery must
be dissected for identifi cation, retraction, or possibly
temporary clipping. Bone between the facial hiatus and
the foramen spinosum is removed with a drill and ron-
geurs to unroof the carotid artery. Dissection lateral to
The zygomatic arch containing the lateral glenoid
fossa and part of the body of the zygoma are removed
as one unit. This permits further retraction of the infe-
riorly pedicled temporalis muscle fl ap and provides
greater exposure of the infratemporal fossa (Fig.
126-20).
Figure 126-20. The zygomatic arch and glenoid fossa are removed.
The temporalis muscle, pedicled on its origin, is retracted
inferiorly.

Chapter 126
Cholesterol Granuloma and Congenital Epidermoid Tumors of the Temporal Bone 1353
the artery exposes the tensor tympani muscle and the
eustachian tube. The eustachian tube is transected, and
its cartilaginous portion is suture-ligated if the carotid
artery is mobilized anterolaterally.
Drilling is continued in the central aspect of the
petrous apex. An expansile tumor or cyst should be
readily apparent at this time (Fig. 126-22). The area is
entered, and its contents are evacuated. Once a cavity
has been created, meticulous dissection of the epider-
mal matrix or cyst wall is performed. Care must be
taken when the cyst lining is removed from the carotid
artery because of possible attenuation of the adventitia
and wall of the carotid artery. Attention is also given to
the dura from which the cyst wall lining was removed.
The integrity of the dura must be verifi ed to prevent
postoperative CSF leakage. When the entire cyst wall
has been removed, the cavity is copiously irrigated with
bacitracin solution. The residual cavity defect warrants
soft tissue obliteration with abdominal fat. The lateral
craniotomy bone fl ap is returned to its anatomic posi-
tion and secured with miniplates or 2-0 Vicryl sutures,
the temporalis muscle is reattached to its insertion with
multiple 2-0 Vicryl sutures, and the zygomatic arch is
secured in its original position with miniplates or
sutures. The skin is closed in three-layer fashion, and a
sterile pressure dressing is applied.
Expanded Endoscopic Transnasal Approach
Since writing of the fi rst edition of this textbook, sur-
geons at the University of Pittsburgh Medical Center
have developed and mastered transnasal endoscopic
procedures directed to the pituitary gland, anterior
skull base, anterior cranial fossa, infratemporal fossa,
and posterior fossa. These surgical techniques have
been adapted to gain access to the petrous bone from
an anterior approach despite development of the sphe-
noid sinus.32 The dissection through the sphenoid bone
is medial to the carotid artery. The petrous apex is the
point of entry for access and drainage of cholesterol
granuloma.
POSTOPERATIVE MANAGEMENT
The intensity of immediate postoperative care is deter-
mined by the extent of the operative procedure under-
taken and whether the cranial nerves, the carotid artery,
the dura, or the otic capsule were affected or compro-
mised by the procedure. Patients undergoing a drain-
age procedure for cholesterol granuloma via the
infracochlear or infralabyrinthine route can be dis-
charged from the hospital on the same or the following
day, depending on their tolerance for the procedure
and reaction to general anesthesia. Patients are seen 7
to 10 days postoperatively for ear canal packing and
removal of the postauricular Steri-Strips. If the medial
external canal covering the tympanomeatal fl ap was
fi lled with Gelfoam, antibiotic suspension drops are
prescribed twice daily. The patient is seen every 2 to 3
weeks to suction out the remaining Gelfoam and ensure
that healing of the inferior canal wall is taking place.
After a few weeks, the middle ear can be assessed. It
takes 4 to 6 weeks for the inferior canal and hypotym-
panum to heal. The patient’s middle ear is observed in
the interim to monitor for resolution of postoperative
serous effusion. Concern for compromised middle ear
aeration via the eustachian tube is managed by place-
ment of a myringotomy tube in the anterosuperior
quadrant. An audiogram is obtained after complete
healing to assess the status of postoperative hearing.
A pressure dressing is maintained over wounds
that were obliterated with fat or a transposed tem -
poralis muscle. Drains are not placed within the opera-
tive site routinely. However, if an abdominal fat graft
was obtained and a Penrose drain was placed in the
Figure 126-21. A frontotemporal craniotomy is performed to
provide access to the middle (subtemporal) and infratemporal
fossae.
Cyst
V3
Eustachian
tube
Internal
carotid
artery
GSPN
Figure 126-22. Bone separating the subtemporal dura from the
infratemporal fossa is removed to expose V3. The greater superfi cial
petrosal nerve (GSPN) has been divided to permit decompression of
the internal carotid artery. This exposure allows excision of a petrous
apex cholesterol granuloma if a drainage procedure is unsuccessful
or resection of an isolated epidermoid tumor if hearing is intact.

1354
Section 15
Temporal Bone
abdominal wound, the drain is removed once drainage
diminishes. In patients with congenital epidermoid
tumor who are able to have the disease exteriorized by
marsupialization, the mastoid dressing is removed the
day after surgery. A cotton ball placed in the external
auditory meatus is subject to serosanguineous drainage
and is changed frequently. When the patient is seen 7
to 10 days postoperatively, the postauricular Steri-Strips
and part of the continuous-strip gauze packing are
removed. The packing is withdrawn until there is sig-
nifi cant resistance to removal or mild bleeding is
encountered. Topical antibiotic ear drops are pre-
scribed, and the remainder of the packing is removed
the following week. Oral antibiotics are not prescribed,
although oral narcotic analgesics are provided for pain
relief.
Patients requiring extensive dissection or resection
are at risk for CSF leak and injury to the cranial nerves,
otic capsule, carotid artery, dura, and brain. Patients
are closely monitored for symptoms or signs related to
these neurovascular structures. The patient’s neuro-
logic status is monitored frequently when a CSF leak
is encountered or a subtemporal approach was per-
formed. Patients are evaluated for signs of mental status
change or evidence of meningitis. Those requiring
a transpetrous or subtemporal infratemporal fossa
approach for total resection of cholesterol granuloma
or epidermoid tumor are usually hospitalized for a few
days. The wound and patient are observed for infection,
subdural hematoma, and CSF accumulation, otorrhea,
or rhinorrhea. Further details regarding skull base
approaches are reviewed in Chapter 102.
The presence or development of facial nerve dys-
function requires supportive care. Particular attention
is devoted to protection of the cornea. Weakness of the
orbicularis oculi with symptomatic lagophthalmos is
managed by artifi cial tears during the day and ointment
at night. A clear moisture chamber is provided if topical
drops alone do not adequately relieve the dryness and
irritation. Placement of a gold weight within the upper
eyelid is recommended for assisted lid closure and
corneal protection if it is anticipated that facial paralysis
will be present for more than a brief time (see Chapter
121). Persistent erythema with eye irritation warrants
ophthalmic consultation.
Inadvertent or intentional entry into the otic
capsule usually results in vertigo if vestibular function
was present preoperatively. Supportive measures con-
sisting of antiemetic medications such as phenothiazine
or droperidol should be taken. Assisted ambulation will
enhance central vestibular recovery. The physical
therapy department is consulted to initiate a rehabilita-
tion treatment plan. Physiologically young patients will
adapt centrally to the unilateral vestibular loss. At our
institution, patients who continue to exhibit uncom-
pensated disequilibrium are subsequently referred to
the vestibular rehabilitation physical therapist for
ongoing outpatient care. Coping strategies and vestibu-
lar retraining exercises are the focus of their program.
If a hearing preservation procedure was performed,
a postoperative audiogram is obtained at approximately
1 month. Unless the procedure consisted of marsupial-
ization into a large mastoid cavity, it is necessary to
monitor for recurrence with radiologic imaging. Given
that the tumor or cystic lesion demonstrated bone
expansion with smooth remodeling, a CT scan can be
used to effectively evaluate changes in the cavity. Regard-
less of whether the procedure entailed drainage and
ventilation or resection with obliteration, a CT scan
obtained 3 months postoperatively will provide the
baseline for future comparisons. MRI does have a role
in postoperative monitoring (Fig. 126-23). If there is
concern for recurrence of pathology despite a stable
CT scan, MRI readily differentiates changes in tissue
density. If the cavity was obliterated with fat, fat suppres-
sion MRI techniques can be used to critically assess the
contents of the bony cavity. A subsequent scan is
obtained 1 year after the baseline scan. If the petrous
apex is found to contain air, adequate ventilation has
been achieved. If the cavity was obliterated and the
patient shows no new clinical signs or symptoms, a CT
scan is obtained 3 years later.
COMPLICATIONS
The problems and complications that arise after man-
agement of cholesterol granuloma and large epider-
moid tumors depend on the surgical approach and
completeness of the procedure. In addition to the
problem of persistent or recurrent disease, complica-
Figure 126-23. Postoperative magnetic resonance image of the
cholesterol granuloma shown in Figure 121-5. This non–contrast-
enhanced T1-weighted image demonstrates lack of signal in the
petrous apex (arrow), indicative of excellent aeration and resolution
of the cyst.

Chapter 126
Cholesterol Granuloma and Congenital Epidermoid Tumors of the Temporal Bone 1355
tions can be grouped by cranial nerve defi cits, central
nervous system sequelae, vascular injury and bleeding,
and problems related to the wound.
A preexisting conductive hearing loss may remain
or increase in magnitude, depending on the operative
management of the ossicular chain and tympanic mem-
brane. The fi rst goal of the procedure is to effectively
eradicate or exteriorize the pathologic process for
which the procedure was performed. This may require
radical mastoidectomy, which by defi nition may maxi-
mize a conductive hearing loss. Under this circum-
stance, the conductive hearing loss is an accepted
outcome from the procedure rather than a risk or
complication. However, if the ossicular chain was
reconstructed and a conductive hearing loss persists,
subsequent aural rehabilitation can be provided by revi-
sion surgery or hearing aid amplifi cation.
Despite normal cochlear function, the procedure
may occasionally require sacrifi ce of the otic capsule to
eliminate the cyst or tumor. Again, this would be not a
complication but rather a planned outcome. However,
if it was unplanned, sensorineural hearing loss may
result from inadvertent injury to the otic capsule or
ossicular chain. Planned or unintended entry into the
inner ear typically results in vestibular signs of nystag-
mus, vomiting, and postural instability and symptoms
of nausea, vertigo, and disequilibrium.
Middle ear effusion develops when the eustachian
tube is sacrifi ced during the subtemporal infratemporal
fossa approach. The resultant conductive hearing
loss is treated with a ventilation tube. It is best to
wait approximately 4 to 6 weeks before tube insertion
to allow complete healing of any potential dural
defects.
Resection of large tumors of the petrous apex
extending toward the cavernous sinus may also put the
third, fourth, fi fth, and sixth cranial nerves at risk.
Patients with petrous apex involvement occasionally
have preoperative symptoms of facial hypoesthesia.
Care should be taken to minimize further trauma to the
trigeminal nerve. Similarly, the immediate proximity of
the sixth nerve to Meckel’s cave requires that it be
identifi ed during intradural procedures to avoid exces-
sive manipulation. Injury to this nerve results in paresis
of the lateral rectus muscle. If the nerve was stretched
during the procedure, return of function can be
expected within a few months. Sacrifi ce of the sixth
cranial nerve or paralysis that does not resolve warrants
consultation with an ophthalmologist for corrective
muscle surgery.
Injury to the seventh cranial nerve may result in
paresis or paralysis of the facial musculature. If it is
known that dissection around the facial nerve left the
nerve anatomically intact, supportive care is provided
as described previously under “Postoperative Manage-
ment.” Sacrifi ce of the seventh nerve is corrected by
reconstruction with a hypoglossal-to-facial nerve anasto-
mosis if primary or cable graft repair could not be per-
formed at the time of the procedure.
The lower cranial nerves may also be affected by
large epidermoid cysts or cholesterol granuloma of the
petrous apex. However, direct invasion is relatively rare.
Intraoperative injury to these nerves results in dyspha-
gia, aspiration, hoarseness, and inanition. Temporary
dysfunction is managed by injection of Gelfoam into
the vocal cord and enteral supplementation via naso-
gastric feeding. Permanent injury to the vagus nerve
resulting in hoarseness, dysphagia, and aspiration is
managed by a type I thyroplasty and cricopharyngeal
myotomy.
Infralabyrinthine or infracochlear drainage proce-
dures require intimate dissection around the jugular
bulb. Intraoperative extradural venous bleeding can be
quite bothersome, but it is usually controlled with Sur-
gicel, bone wax, or bipolar cautery. Dissection of the
petrous apex requires careful attention to the carotid
artery. Preoperative testing with balloon occlusion pro-
vides an indication of how the patient will tolerate tem-
porary intraoperative occlusion to repair injury to the
ICA. It is best to avoid a potential injury to the carotid
artery by meticulous dissection and protection of the
vessel. If the dura into the posterior fossa is opened,
similar respect is given to the intracranial vessels. Repair
of these small vessels is technically most diffi cult, and
clipping or bipolar coagulation may be necessary. This
may result in serious central nervous system defi cits in
the cerebellum, midbrain, and brain stem.
Procedures in which resection or drainage is
attempted in an extradural fashion may still be compli-
cated by CSF otorrhea and rhinorrhea. Leakage around
the otic capsule into a closed middle ear space will be
manifested as CSF rhinorrhea. Canal wall down proce-
dures (radical mastoid cavity) in which tympanic mem-
brane reconstruction was not undertaken will have CSF
leaking directly through the aural wound. The risk for
meningitis demands repair of the fi stula. Lumbar drain-
age of CSF is rarely effective in controlling the leak once
a fi stula has developed in an open cavity. Operative
intervention requiring soft tissue obliteration with
wound compression is usually necessary for effective
control.
Wound infection is a rare complication of otologic
surgery. Soft tissue infection and cellulitis are treated
with systemic antibiotics. Formation of an abscess such
as in the epidural space requires drainage, culture for
an organism, and appropriate parenteral antibiotics.
Drainage procedures for cholesterol granuloma provide
a potential pathway for retrograde infection into the
cystic cavity. If the expansion process had thinned the
wall of the cavity and exposed the carotid artery, carotid
hemorrhage may result. A bacterial or fungal infection
may become established in the cancellous bone,
with the subsequent development of temporal bone
osteomyelitis.18
Excessive retraction of or direct injury to the tem-
poral lobe may occur from procedures directed at the
petrous apex via the subtemporal infratemporal fossa
or direct transtemporal approaches. Injury to the left
temporal lobe may result in expressive or receptive
aphasia. Though rare, ischemia and infarction may
produce temporary or permanent hemiparesis and
hypoesthesia.

1356
Section 15
Temporal Bone
6. Schick B, Brors D, Koch O, et al: Magnetic resonance imaging in
patients with sudden hearing loss, tinnitus and vertigo. Otol
Neurotol 22:808-812, 2001.
7. Politzer A: Uber bewegliche Exudate in der Trommelfellhohle
[The membrane in health and disease]. Vienna, Wien Med
Presse (Wm Wood), 1869.
8. Shambaugh GE: The blue drum membrane. Arch Otolaryngol
10:238-240, 1929.
9. House JL, Brackmann DE: Cholesterol granuloma of the cerebel-
lopontine angle. Arch Otolaryngol 108:504-506, 1982.
10. Graham MD, Kemink JL, Latack JT, Kartush JM: The giant cho-
lesterol cyst of the petrous apex: A distinct clinical entity. Laryn-
goscope 95:1401-1406, 1985.
11. Mosnier I, Cyna-Gorse F, Grayeli AB, et al: Management of cho-
lesterol granulomas of the petrous apex based on clinical and
radiologic evaluation. Otol Neurotol 23:522-528, 2002.
12. Jackler RK, Cho M: A new theory to explain the genesis of petrous
apex cholesterol granuloma. Otol Neurotol 24:96-106, discussion
106, 2003.
13. Gadre AK, Brodie HA, Fayad JN, O’Leary MJ: Venous channels
of the petrous apex: Their presence and clinical importance.
Otolaryngol Head Neck Surg 116:168-174, 1997.
14. Schuknecht H: Pathology of the Ear. Philadelphia, Lea & Febiger,
1993.
15. Von Remak R: Beitrag zur Entwicklungsgeschichte der kreb-
shaften Geschwulste. Dtsch Klin 6(170B):174, 1854.
16. Pyle GM, Wiet RJ: Petrous apex cholesteatoma: Exteriorization
vs. subtotal petrosectomy with obliteration. Skull Base Surg 1:97-
105, 1991.
17. Glasscock ME 3rd, Woods CI 3rd, Poe DS, et al: Petrous apex
cholesteatoma. Otolaryngol Clin North Am 22:981-1002, 1989.
18. Michaels L: An epidermoid formation in the developing middle
ear: Possible source of cholesteatoma. J Otolaryngol 15:169-174,
1986.
19. McGill TJ, Merchant S, Healy GB, Friedman EM: Congenital
cholesteatoma of the middle ear in children: A clinical and his-
topathological report. Laryngoscope 101:606-613, 1991.
20. Nager G: Epidermoids (Congenital Cholesteatomas). Baltimore,
Williams & Wilkins, 1992.
21. Yamakawa K, Shitara N, Genka S, et al: Clinical course and surgi-
cal prognosis of 33 cases of intracranial epidermoid tumors. Neu-
rosurgery 24:568-573, 1989.
22. Pisaneschi MJ, Langer B: Congenital cholesteatoma and choles-
terol granuloma of the temporal bone: Role of magnetic reso-
nance imaging. Top Magn Reson Imaging 11:87-97, 2000.
23. Van Havenbergh T, Koekelkoren E, De Ridder D, et al: Image
guided surgery for petrous apex lesions. Acta Neurochir (Wien)
145:737-742, discussion 742, 2003.
24. de Vries EJ, Sekhar LN, Horton JA et al: A new method to predict
safe resection of the internal carotid artery. Laryngoscope 100:85-
88, 1990.
25. Eisenberg MB, Haddad G, Al-Mefty O: Petrous apex cholesterol
granulomas: Evolution and management. J Neurosurg 86:822-
829, 1997.
26. Haberkamp TJ: Surgical anatomy of the transtemporal approaches
to the petrous apex. Am J Otol 18:501-506, 1997.
27. Brackmann DE, Toh EH: Surgical management of petrous apex
cholesterol granulomas. Otol Neurotol 23:529-533, 2002.
28. Thedinger BA, Nadol JB Jr, Montgomery WW, et al: Radiographic
diagnosis, surgical treatment, and long-term follow-up of choles-
terol granulomas of the petrous apex. Laryngoscope 99:896-907,
1989.
29. Cristante L, Puchner MA: A keyhole middle fossa approach to
large cholesterol granulomas of the petrous apex. Surg Neurol
53:64-70, discussion 70-71, 2000.
30. Montgomery WW: Cystic lesions of the petrous apex: Transsphe-
noid approach. Ann Otol Rhinol Laryngol 86:429-435, 1977.
31. DiNardo LJ, Pippin GW, Sismanis A: Image-guided endoscopic
transsphenoidal drainage of select petrous apex cholesterol gran-
ulomas. Otol Neurotol 24:939-941, 2003.
32. Kassam AB, Gardner P, Snyderman C, et al: Expanded endonasal
approach: Fully endoscopic, completely transnasal approach to
the middle third of the clivus, petrous bone, middle cranial fossa,
and infratemporal fossa. Neurosurg Focus 19(1):E6, 2005.
PEARLS
• Both CT and MRI are necessary for determining the
type of pathology affecting the petrous apex.
• Transnasal/transpetrous approaches to pathology
of the petrous apex should be considered when
reviewing images showing the anatomy of related
structures.
• Sacrifi ce of the eustachian tube results in middle ear
effusion when the tympanic membrane remains
intact or is reconstructed. Delayed ventilation of the
middle ear should be planned after extensive
procedures to avoid the risk of CSF otorrhea.
• Temporary or permanent injury to the facial nerve
requires early aggressive eye care to protect the
cornea from desiccation or further injury.
• Placement of a ventilation tube in the tympanic
membrane may obviate early occlusion of a Silastic
drainage tube positioned between the petrous apex
and the hypotympanum after an infracochlear
approach.
PITFALLS
• Underestimating the exposure necessary for
complete removal or creating suboptimal drainage
of pathologic processes of the petrous apex will
result in persistence or recurrence of disease.
• CSF otorrhea or rhinorrhea after approaches to the
petrous apex may not respond to lumbar drainage;
operative intervention will probably be necessary.
• Subtotal removal of the epithelial matrix of an
epidermoid cyst may be temporizing and represents
the fi rst stage of subsequent procedures.
• Performing a procedure that drains the petrous apex
and creation of a radical mastoid cavity without
coverage of an exposed carotid artery may result in
desiccation and rupture.
• A middle fossa approach to cholesterol granuloma
of the petrous apex may not afford adequate
drainage into the middle ear. The entire cyst and its
lining will need to be removed.
References
1. Chole RA: Petrous apicitis: Surgical anatomy. Ann Otol Rhinol
Laryngol 94:251-257, 1985.
2. Farrior JB: Anterior hypotympanic approach for glomus tumor
of the infratemporal fossa. Laryngoscope 94:1016-1021, 1984.
3. Giddings NA, Brackmann DE, Kwartler JA: Transcanal infraco-
chlear approach to the petrous apex. Otolaryngol Head Neck
Surg 104:29-36, 1991.
4. Muckle RP, De la Cruz A, Lo WM: Petrous apex lesions. Am J
Otol 19:219-225, 1998.
5. Terao T, Onoue H, Hashimoto T, et al: Cholesterol granuloma
in the petrous apex: Case report and review. Acta Neurochir
(Wien) 143:947-952, 2001.

Chapter 126
Cholesterol Granuloma and Congenital Epidermoid Tumors of the Temporal Bone 1357
33. Kaylie DM, Warren FM 3rd, Haynes DS, Jackson CG: Neuroto-
logic management of intracranial epidermoid tumors. Laryngo-
scope 115:1082-1086, 2005.
34. Fisch U: Infratemporal fossa approach to tumours of the tempo-
ral bone and base of the skull. J Laryngol Otol 92:949-967,
1978.
35. House WF, De La Cruz A, Hitselberger WE: Surgery of the skull
base: Transcochlear approach to the petrous apex and clivus.
Otolaryngology 86:770-779, 1978.
36. Selesnick SH, Abraham MT, Carew JF: Rerouting of the intratem-
poral facial nerve: An analysis of the literature. Am J Otol 17:793-
805, discussion 806-809, 1996.
37. Mattox DE: Endoscopy-assisted surgery of the petrous apex. Oto-
laryngol Head Neck Surg 130:229-241, 2004.
38. Gerek M, Satar B, Yazar F, et al: Transcanal anterior approach
for cystic lesions of the petrous apex. Otol Neurotol 25:973-976,
2004.
39. Sanna M, Zazzoni A, Saleh E, et al: The system of the modifi ed
transcochlear approach: A lateral avenue to the central skull base.
Am J Otol 19:88-98, 1998.

Chapter 127
Cerebrospinal Fluid Otorrhea and
Encephalocele
Elizabeth H. Toh
Temporal bone cerebrospinal fl uid (CSF) otorrhea
may occur from a variety of congenital or acquired eti-
ologies (Table 127-1). Leakage of CSF through the tem-
poral bone represents a fi stula from the fl uid-fi lled
subarachnoid space into the pneumatized temporal
bone. Subsequent egress of CSF through a defect in the
mastoid cavity, tympanic membrane, or external audi-
tory canal presents as otorrhea. Rhinorrhea represents
drainage of CSF through the eustachian tube and may
occur with or without otorrhea. An encephalocele is a
protrusion of the brain, with or without overlying dura,
beyond the confi nes of the cranial cavity into the
mastoid or middle ear. A true encephalocele contains
prolapsed brain tissue, whereas a meningoencephalo-
cele contains brain and meninges. The terms CSF otor-
rhea and encephalocele both imply an anatomic pathway
between the subdural space and the exterior. For this
reason, both have equal potential for central nervous
system complications and infections.
Gacek demonstrated that aberrant arachnoid gran-
ulations may occur in the vicinity of the temporal bone
as well as in other areas of the skull base.1 Unlike classic
arachnoid granulations, these aberrant structures do
not have an absorptive role associated with CSF.
Although arachnoid granulations of the middle or pos-
terior cranial fossa are not routinely encountered
during mastoid surgery, the incidence of these struc-
tures in temporal bone histopathologic studies of the
surface of the middle fossa is as high as 22%. The most
common locations of these aberrant arachnoid granula-
tions are lateral to the cribriform plate in the anterior
cranial fossa, and on the fl oor of the middle fossa.
Occasionally they may occur in the posterior fossa plate
between the sigmoid sinus and the bony labyrinth.
Intermittent increases in spinal fl uid pressure are
hypothesized to cause gradual increase in size of these
aberrant arachnoid granulations and erosive changes in
the underlying bone, with eventual protrusion through
the tegmen or posterior fossa plate. It is thought that
these granulations are the largest single cause of spon-
taneous CSF leaks in adults. The typical presentation of
spontaneous CSF leaks in adults is unilateral serous
otitis media with no preceding upper respiratory infec-
tion, which is refractory to decongestant and antibiotic
therapy. Myringotomy and ventilation tube placement
usually results in persistent clear watery drainage that
does not respond to conventional ototopical therapy. A
high index of clinical suspicion is necessary to diagnose
this entity.
Perilymphatic fi stulas are another potential source
of communication between the middle ear and the sub-
arachnoid space. These defects rarely result in any clini-
cally signifi cant accumulation of fl uid within the middle
ear and therefore typically do not present like other
causes of CSF otorrhea or rhinorrhea. Leakage typically
occurs from the otic capsule through a dehiscence in
the stapes footplate. The diagnosis is usually made in
childhood, and typically presents as recurrent meningi-
tis with hearing loss in the affected ear. Perilymphatic
fi stulas are discussed in detail in Chapter 119.
Spontaneous meningoencephaloceles of the skull
base have been reported since early in this century. The
most common location for encephaloceles of the tem-
poral bone is along the fl oor of the middle cranial fossa.
The posterior fossa of the temporal bone may also be
affected, although rarely. Defects are frequently identi-
fi ed in multiple locations at the time of presentation.
Congenital defects in the bone of the skull base predis-
pose to progressive formation of dural and arachnoid
herniations. Prolapse into the epitympanum and middle
ear may cause conductive hearing loss or present with
a mass in the middle ear (Fig. 127-1). Retrograde bacte-
1359

1360
Section 15
Temporal Bone
rial contamination from the nasopharynx, paranasal
sinuses, or middle ear may result in the development
of meningitis. Therefore this disorder occurs most fre-
quently in childhood.
Trauma to the temporal bone may occur as a result
of blunt head trauma or surgery of the temporal bone.
CSF otorrhea secondary to temporal bone fractures is
discussed in Chapter 128. Diagnosis is straightforward
in these cases, and the majority of these patients respond
to conservative management. Bed rest and head eleva-
tion results in spontaneous resolution in up to 90% of
patients with temporal bone fractures. Most of the
remaining cases can be controlled by intermittent or
continuous lumbar drainage, leaving only a few patients
who require surgical intervention.2 Iatrogenic trauma
to the dura during surgery of the temporal bone can
eventually lead to weakening of the dura with resultant
meningoencephalocele, encephalocele, and CSF otor-
rhea. Dural exposure alone, without violation, does not
usually result in herniation of brain tissue or CSF leak.
If CSF leak is noted at the time of iatrogenic trauma,
surgical repair should be performed immediately.
CSF otorrhea and encephaloceles related to chronic
otitis media may occur with or without cholesteatoma,
usually in patients with an antecedent history of oto-
logic surgery. Cholesteatomas may erode into the otic
capsule as well as through the middle or posterior
fossa plates. However, chronic otitis media and mastoid-
itis with granulation tissue alone may also lead to this
defect over a long period. The erosive process from
cholesteatoma and chronic infl ammation most com-
monly affects the horizontal semicircular canal, but may
extend superiorly to involve the mastoid and middle ear
tegmen.
Primary tumors or tumors metastatic to the tempo-
ral bone or areas adjacent to it may also cause bone
erosion, which may be associated with secondary CSF
otorrhea. The most common tumor in children is rhab-
domyosarcoma. The most common tumors in adults are
epithelial tumors and paragangliomas.
PATIENT SELECTION
CSF leak of otogenic origin may present in several ways.
If the tympanic membrane is violated, clear otorrhea is
noted. With an intact tympanic membrane, the patient
may complain of clear watery drainage from the nose,
which usually occurs when bending over or straining. If
leakage is minimal or intermittent, CSF may drain
directly into the pharynx and esophagus without being
noticed by the patient. The second clinical presentation
occurring in individuals with an intact tympanic mem-
brane, is hearing impairment and aural fullness as a
result of middle ear effusion. Even in the absence of an
antecedent upper respiratory infection, the diagnosis is
presumed to be serous otitis media, and a myringotomy
is often performed to drain the fl uid. Following this
procedure, the patient has continuous clear otorrhea,
which persists despite antibiotic, antihistamine, and
decongestant therapy. The latter presentation is typical
of spontaneous otogenic CSF leaks in adults and a high
index of suspicion is critical in making a timely diagno-
sis. The incidence of bilaterality in spontaneous oto-
genic CSF leaks may be up to 22%.3
Meningitis (single or repeated episodes) may be
the initial presentation of a CSF leak. This is more
common in children when they have been unaware of
any hearing loss or aural fullness in the affected ear.
Meningitis often leads to a profound sensorineural
hearing impairment, which may often be the present-
ing problem in children. Any patient presenting with
meningitis must be carefully evaluated for a potential
otogenic source.
Patients complaining of hearing impairment occa-
sionally will have a mass discovered within the middle
ear, with or without hearing loss (Fig. 127-2). High-
resolution computed tomography (CT) of the temporal
bone usually identifi es the origin of the soft tissue mass
and points to any defects in the bony plates of the
middle or posterior fossa. Anyone with previous tympa-
nomastoid surgery presenting with otorrhea, a middle
ear effusion, or rhinorrhea should be suspected of
having a defect in the dura as a result of the original
procedure. A history of prior trauma to the temporal
bone should alert the examiner to the potential diag-
nosis of encephalocele or meningoencephalocele.
Table 127-1
CAUSES OF CEREBROSPINAL FLUID
OTORRHEA
Congenital
Acquired
Spontaneous
Meningoencephalocele,
secondary to
congenital skull base
defects
Posttraumatic
(temporal
bone
fractures,
surgery)
Arachnoid
granulations
Perilymphatic fi stulas
Chronic otitis
media
Neoplasia
Postirradiation
Encephalocele
Figure 127-1. Herniation of brain tissue from the middle cranial
fossa into the epitympanum.

Chapter 127
Cerebrospinal Fluid Otorrhea and Encephalocele 1361
PREOPERATIVE PLANNING
Once CSF otorrhea, rhinorrhea, or encephalocele is
suspected, efforts must proceed quickly to confi rm the
presence of a dural defect and furthermore to locate
the defect precisely. The surgeon should attempt to
elicit the symptoms of rhinorrhea. This can often be
accomplished by having the patient bend forward and
place the head between the knees for several minutes.
It may also be accomplished by having the patient lie
in a head-down position and then turn to the prone
position to encourage active drainage. When CSF is
observed clinically, there is usually no question about
its origin. It appears as clear as water and is not cloudy
or sanguinous. Diffi culty in identifi cation may be
encountered only in trauma cases in which there is
concomitant bleeding. In these cases, a telltale ring of
CSF may be seen outside the stain left by blood and
serum on a dressing or bed linens (halo sign), which
may alert the physician to this problem.
Testing fl uid for the presence of glucose, usually
with a test strip, is notoriously unreliable and usually
requires large amounts of fl uid to produce consistent
results. It is therefore no longer used as a primary diag-
nostic modality for confi rmation of CSF. When the
origin or nature of the drainage is in question, we prefer
the technique of identifying β2-transferrin within the
fl uid using immunoelectrophoresis. This testing
requires remarkably scant quantities of CSF and may be
submitted to the laboratory as free fl uid or on a carrier
material such as Gelfoam or Merocel. β2-transferrin is
present only in CSF and perilymph, and is not found in
blood or serum. The sensitivity and specifi city of this
test is approximately 100% and 95%, respectively, and
is not infl uenced by contamination with blood or other
body fl uids.4
High-resolution CT imaging of the temporal bone
using a bone algorithm is the cornerstone of diagnosing
and localizing CSF leaks in the temporal bone. Coronal
cuts usually enable the examiner to identify the location
and number of bony defects in the petrous temporal
bone. CT imaging also helps in identifying soft tissue
within the middle ear and mastoid, erosion of the bone
of the otic capsule, or structural anomalies of the inner
ear (Fig. 127-3). Magnetic resonance imaging of the
brain plays a complementary role in determining the
nature and origin of soft tissue in the middle ear and
mastoid when a large defect in the tegmen is identifi ed
on CT imaging (Fig. 127-4). Neither radionuclide cis-
ternography or CT cisternography provides any addi-
tional diagnostic information in the evaluation of CSF
leaks.5
An audiogram should be obtained to evaluate the
presence and extent of hearing impairment in the
affected ear before surgical management. A hearing
preservation approach is preferred in the presence of
any aidable residual hearing in the operated ear.
SURGICAL APPROACHES
The surgical approach is dictated by the size, number,
and location of bony defects, as well as the status of the
hearing in the affected ear. Dehiscence of the posterior
fossa plate, as well as of the posterior and lateral por-
tions of the middle fossa plate, can almost always be
repaired through a transmastoid approach (Fig. 127-5).
Medial and anterior defects involving the tegmen
tympani and petrous apex, respectively, require a
Figure 127-2. Middle ear mass visualized on otoscopy.
Tegmen defect
Figure 127-3. High-resolution coronal computed tomography
scan of temporal bone showing the defect in the bone in the tegmen
tympani and soft tissue in the epitympanum and middle ear (arrow).

1362
Section 15
Temporal Bone
middle cranial fossa approach for repair. Large or mul-
tiple tegmen defects usually require a combined trans-
mastoid and middle cranial fossa approach. Patients
with chronic otitis media and defects eroding the otic
capsule may require a canal wall-down mastoidectomy
in order to obtain adequate exposure for surgical repair
and exteriorization of disease if extensive cholestea-
toma is identifi ed.
Details of the techniques for each of these
approaches are described in Chapters 115 and 124. The
transmastoid approach provides the distinct advantage
of extracranial visualization of the defect without tem-
poral lobe retraction. However, bony defects exceeding
2 cm in diameter are more reliably repaired from above
using a supplemental middle fossa approach. In these
cases, the postauricular incision is extended superiorly
and anteriorly, and a limited craniotomy is performed,
centered around the location of the defect identifi ed
from below. Similarly, in a patient with previous canal
wall-down mastoid cavity with residual hearing, the
defect in the tegmen and the encephalocele should
be repaired from above using the middle fossa
approach.6
When CSF otorrhea is copious, a lumbar drain is
placed at the time of surgery. During surgery, the drain
can be clamped to aid localization of the site of the leak.
The Valsalva maneuver, performed by the anesthetist,
may also be helpful, when necessary.
When brain herniation is encountered, there is
uniform agreement that this tissue is nonfunctional and
may be removed. This lack of function is assumed to be
the result of tissue strangulation, ischemia, and resul-
tant edema of this tissue. In general, broad-based
encephaloceles herniating through large bony defects
are considered viable and may be reduced back into the
cranial vault. Bipolar electrocautery is used to remove
nonviable tissue until the margins of the bony defect
through which it has extruded is well defi ned.
Many methods of repair of these defects have been
advocated over the years. A multilayer closure using a
combination of free grafts has remained the most reli-
able technique to repair the defects. A large variety of
materials including both biologic tissues and synthetic
materials have been used to repair the dura. Autolo-
gous temporalis fascia, pericranium, and fascia lata are
preferred when available because they are easy to
handle, nontoxic, inexpensive, and have favorable bio-
logic behavior. Fascia lata may be obtained if temporalis
fascia is lacking due to previous surgery, but obtaining
fascia lata requires additional surgery, operating time,
and donor site morbidity. The use of synthetic materials
is no longer widely used because of local tissue reac-
tions, excessive scar formation, meningitis, and hemor-
rhage. Solvent-preserved, gamma-sterilized Tutoplast
bovine pericardium has also been widely used for dural
substitution with favorable clinical outcomes.7,8 The use
of fi brin glue with primary closure alone does not
appear to have any additional benefi t.2 Hydroxyapatite
cement cranioplasty has been used in conjunction with
autologous fat for prevention of CSF leak following
vestibular schwannoma surgery and for primary repair
of small defects in the tegmen in spontaneous CSF
leaks.9
Encephalocele
Figure 127-4. T2-weighted magnetic resonance imaging (MRI) of
brain in coronal plane confi rming soft tissue seen in Figure 127-3 as
encephalocele (arrow).
Tegmen defect
with herniated
brain tissue
Figure 127-5. The transmastoid approach for repair of an enceph-
alocele (right ear).

Chapter 127
Cerebrospinal Fluid Otorrhea and Encephalocele 1363
Two layers of temporalis fascia are used with a trans-
mastoid approach, one on either side of the bony
defect. Following removal of all soft tissue around the
bony defect in the posterior or middle fossa, the intra-
cranial dura is dissected with a duckbill or hockey-stick
elevator until 1 cm of elevation is obtained circumfer-
entially around the bony defect. At this point, dried
temporalis fascia is placed within the bony defect and
spread out over the intracranial surface between the
dura and the tegmen (Fig. 127-6). Reexpansion of the
brain contents ensures the retention of the fascial graft.
The bony defect is then closed using a cancellous bone
graft taken from the mastoid process, retrosigmoid
area, or squamous portion of the bone, or using a
conchal cartilage graft. This provides additional support
for the primary graft material. When small bone defects
are present, the bone graft or cartilage graft can be
contoured to fi t tightly into the exact shape of the space
it is fi lling (Fig. 127-7). A tightly fi tting graft in a small
defect requires nothing further to keep it in place. A
second layer of temporalis fascia is then placed over the
bony defect on the mastoid side (Fig. 127-8), buttressed
in place by means of temporalis muscle or abdominal
fat.
Fascia on
intracranial
surface of
defect
Fascia
A
B
Figure 127-6. Use of fascia intracranially to form the fi rst layer of
repair of a dural defect.
Bone
graft
Bone graft
A
B
Second layer of fascia
Figure 127-7. A shaped bone graft placed into the tegmen
defect.
Figure 127-8. A second layer of fascia placed lateral to the bone
graft.

1364
Section 15
Temporal Bone
done by an intradural technique.10 Opening the dura
on the lateral surface of the temporal lobe permits ele-
vation of the brain from the underlying dura. This
allows for close inspection of the herniated contents as
well as the adjacent brain. Larger broad-based encepha-
loceles in uninfected fi elds may potentially be recranial-
ized using this technique. The graft is placed on the
dura, and the expanded brain then secures its fi xation.
In the rare case of a large defect with high-volume CSF
drainage, vascularized tissue such as a pedicled tempo-
ralis muscle fl ap or pericranial fl ap should be rotated
intracranially and secured to dura medial to the
defect.
Defects in the otic capsule or tegmen plate associ-
ated with chronic middle ear disease are approached in
the standard tympanomastoid fashion. In the absence
of any useful hearing in the affected ear, the eustachian
tube, mastoid, and middle ear may be obliterated and
the ear canal closed. The malleus, incus, tympanic
membrane, and skin of the medial external auditory
canal are removed. It is also necessary to carefully seal
the eustachian tube using bone and temporalis muscle
(Fig. 127-12). The external auditory meatus is oversewn
and closed in a layered fashion by means of absorbable
Dexon sutures medially and nylon sutures laterally (Fig.
127-13). Temporalis muscle and abdominal fat are used
to fi ll the bony defects (Fig. 127-14).
Following completion of repair and before wound
closure, the head is elevated 45 degrees; this is con-
tinued in the recovery room and throughout the
Bone defect
in tegmen
Figure 127-9. The middle fossa approach to repair showing the
defect in the bone after removal of herniated tissue.
A middle cranial fossa approach may be used as the
primary approach for repair when anterior, medial, or
multiple defects are present. Following extradural ele-
vation of the temporal lobe, soft tissue is once again
carefully removed from the bony defect (Fig. 127-9). A
large piece of dried temporalis fascia is next placed
across the fl oor of the middle cranial fossa (Fig. 127-
10), and the temporal lobe is allowed to reexpand and
hold this tissue in place. Larger defects should be sup-
ported using an additional bone or cartilage graft
placed over the fascial graft. In addition, an attempt is
made to close the dural defect responsible for the leak.
When this defect is small, it can be closed primarily by
suturing. When the defect is larger, a small piece of
temporalis muscle is oversewn with 6-0 Nurolon sutures
(Fig. 127-11). Alternatively, the entire repair can be
Figure 127-10. A large piece of dried temporalis fascia is used to
cover the defect in the bone.
Figure 127-11. The temporalis muscle oversewn on the dura to
repair the dural defect.

Chapter 127
Cerebrospinal Fluid Otorrhea and Encephalocele 1365
hospitalization. Because of the potential for intracranial
infection, a bolus of intravenous antibiotic is always
given perioperatively. We use third-generation cephalo-
sporins with broad-spectrum coverage. When purulent
exudate is encountered at the time of surgery, cultures
help determine the choice of antibiotic.
POSTOPERATIVE MANAGEMENT
Postoperatively, the head is elevated 45 degrees during
the hospital stay and patients are encouraged to con-
tinue this for 7 to 10 days at home. Patients who have
undergone craniotomy for repair of CSF leaks should
be observed in the hospital for at least 3 to 4 days. Those
who have undergone transmastoid surgery may gener-
ally be discharged home in 1 to 2 days. Antibiotic cover-
age is also continued intravenously until the patient is
discharged, and then a similar agent is given orally for
7 days. When lumbar drainage has been placed preop-
eratively, it is continued for 24 to 72 hours postopera-
tively, depending on the extent of CSF leakage and size
of defect repaired. The subarachnoid drain is then
clamped for an additional 24 hours to confi rm the
absence of any further CSF leak, and then removed.
Persistent CSF leak is the most common complica-
tion following surgery. Because of the blood within the
middle ear postoperatively, visualization of the tym-
panic membrane is not a good guide to successful ces-
sation of CSF leakage in the immediate postoperative
period. However, within 3 to 4 weeks, the middle ear
should be pneumatized and clearly visualized. The
patient is also questioned repeatedly and asked to
report any incidence of nasal or posterior pharyngeal
drainage, which might indicate continued CSF
Bone chips and
temporalis muscle
Figure 127-12. Obliteration of the eustachian tube with bone
chips and temporalis muscle.
A
B
Figure 127-13. A, Sealing of the external meatus by sewing a fi bro-
fascial fl ap to its medial surface. B, Completion of the meatal closure
with everting sutures placed.
Figure 127-14. Obliteration of the mastoid with a fat graft taken
from the abdominal wall.

1366
Section 15
Temporal Bone
otorrhea. Restraints against lifting, straining, and exer-
cise are encouraged for 2 weeks following surgery.
Although temporary aphasia and seizures are
potential postoperative complications from temporal
lobe resection or retraction, our patients have had no
problems related to the excision of nonviable brain
tissue. Neurologic defi cits are not expected postopera-
tively, and headache has not been a signifi cant problem.
Meningitis and brain abscess are potential complica-
tions, but these have usually been seen preoperatively
rather than postoperatively.
References
1. Gacek RR: Arachnoid granulation cerebrospinal fl uid otorrhea.
Ann Otol Rhinol Laryngol 99:854-862, 1990.
2. Savva A, Taylor MJ, Beatty CW: Management of cerebrospinal
fl uid leaks involving the temporal bone: Report on 92 patients.
Laryngoscope 113:50-56, 2003.
3. Lundy LB, Graham MD, Kartush JM, et al: Temporal bone
encephalocele and cerebrospinal fl uid leaks. Am J Otol 17:461-
469, 1996.
4. Skedros DG, Cass SP, Hirsch BE, et al: Beta-2 transferrin assay in
clinical management of cerebral spinal fl uid and perilymphatic
fl uid leaks. J Otolaryngol 22:341-344, 1993.
5. Stone JA, Castillo M, Neelon B, et al: Evaluation of CSF leaks:
High-resolution CT compared with contrast-enhanced CT and
radionuclide cisternography. AJNR Am J Neuroradiol 20:706-712,
1999.
6. McMurphy AB, Oghalai JS: Repair of iatrogenic temporal
lobe encephalocele after canal wall down mastoidectomy in the
presence of active cholesteatoma. Otol Neurotol 26:587-594,
2005.
7. Caroli E, Rocchi G, Salvati M, et al: Duraplasty: Our current
experience. Surg Neurol 61:55-59; discussion 59, 2004.
8. Filippi R, Schwarz M, Voth D, et al: Bovine pericardium for dura-
plasty: Clinical results in 32 patients. Neurosurg Rev 24(2-3):103-
107, 2001.
9. Kveton JF, Goravalingappa R: Elimination of temporal bone cere-
brospinal fl uid otorrhea using hydroxyapatite cement. Laryngo-
scope 110(10 Pt 1):1655-1659, 2000.
10. Jackson CG, Pappas DG Jr, Manolidis S, et al: Brain herniation
into the middle ear and mastoid: Concepts in diagnosis and surgi-
cal management. Am J Otol 18(2):198-205; discussion 205-196,
1997.
PEARLS
• The vast majority of traumatic CSF leaks resolve
with conservative management alone.
• Dural exposure alone without violation at the time
of otologic surgery does not lead to CSF leak.
• Due to a signifi cant incidence of multiple tegmen
defects in spontaneous CSF leaks, the middle fossa
approach allows for thorough inspection of the
middle fossa fl oor before surgical repair.
• The best results are obtained with multilayer closure
techniques using autologous tissue.
• In a nonhearing ear, obliteration of the middle ear
and mastoid with blind sac closure of the external
auditory canal offers the most effective and reliable
repair for CSF leaks and large encephaloceles.
PITFALLS
• Failure to recognize multiple defects on preoperative
CT imaging may lead to incomplete repair and
persistent postoperative CSF leak.
• Failure to circumferentially elevate dura around the
bony defect will not allow for reliable graft
placement and repair.
• Primary dural closure alone is usually not adequate
for repair of CSF leaks.
• The use of fi xatives, such as fi brin glue, does not
improve surgical success rates.
• With large tegmen defects, the weight of the
temporal lobe alone, without the use of a
supporting bone or cartilage graft, is not adequate
for supporting a soft tissue graft over the defect.

Chapter 128
Temporal Bone Trauma
Elizabeth H. Toh
Injuries resulting from trauma to the temporal bone
range from temporary and minor disorders to severe
and permanent ones. Identifi able fractures are usually
associated with more severe neurologic defi cits, but
even in the absence of a fracture, the auditory and ves-
tibular systems may have sustained concussive damage
resulting in clinically signifi cant functional sequelae.
Dysfunction of the facial nerve occasionally occurs even
in the absence of radiographically demonstrable frac-
ture. Blows to the side of the head or penetrating
trauma from foreign bodies introduced through the
external auditory canal may result in trauma to the
tympanic membrane, ossicular chain, inner ear, and,
rarely, the facial nerve. Injuries to the middle ear gener-
ally can be dealt with using the same techniques out-
lined in Chapter 114. The scope of this chapter is
restricted to management of the sequelae of temporal
bone fractures.
PATIENT SELECTION
Fractures of the temporal bone have traditionally been
classifi ed anatomically into longitudinal, transverse,
and mixed, based on their relationship relative to the
long axis of the petrous pyramid (Figs. 128-1 and
128-2). This traditional scheme of classifi cation has
been shown to be of limited value in reliably predicting
clinical complications resulting from injury to the tem-
poral bone. With the advent of high-resolution com-
puted tomography (HRCT) imaging, several authors
have proposed the use of “otic capsule sparing” and
“otic capsule violating” terminology to better defi ne
and prognosticate the clinical impact of these injuries.1,2
The most serious injuries, and those most often requir-
ing surgery, are the result of transverse or otic capsule–
violating fractures. Table 128-1 lists the most common
sequelae of temporal bone fractures. Facial nerve palsy
and the rare persistent cerebrospinal fl uid (CSF) leak
are the primary clinical conditions that require the
determination of suitability for surgical intervention in
the early postinjury setting. Hearing loss and dizziness
do not generally require early intervention; in many
cases, these conditions resolve spontaneously. Less
common symptoms, such as facial hypesthesia and
paresis of the abducens nerve, are also frequently self-
limited. Any associated lacerations of the external audi-
tory canal and violation of the tympanic membrane may
initially be managed conservatively with dry ear precau-
tions and ototopical antibiotics. Elective surgical repair
of persistent perforations of the tympanic membrane
may be offered for a safe dry ear or hearing improve-
ment following a 6- to 8-week trial of conservative man-
agement. The risk of delayed meningitis and secondary
cholesteatoma formation should be kept in mind in
patients with temporal bone fractures.
Facial Paralysis
Weakness of the facial nerve may be immediate or
delayed in onset, partial or complete. Although there
is universal agreement that delayed-onset facial paraly-
sis usually portends favorable clinical recovery and
should be managed conservatively, much controversy
surrounds the role and timing of surgery in the patient
with immediate-onset weakness.3-5 Most traumatic facial
palsies resolve without surgical intervention and the
decision to operate is usually based on predictors of
poor functional outcome. We agree with the otologic
consensus that surgical exploration is of benefi t in
patients with immediate-onset complete facial paralysis
because of the greater likelihood that the nerve has
been anatomically disrupted or is compressed by a bone
spicule. Surgery in these patients appears to facilitate
early recovery with minimal faulty regeneration.
1367

1368
Section 15
Temporal Bone
Table 128-1
SYMPTOMS AND SIGNS FOLLOWING
TEMPORAL BONE FRACTURE
Symptom/Sign
Treatment
Hearing loss
No immediate treatment necessary.
Dizziness
Vestibular suppression followed by
rehabilitation.
Facial weakness
Early determination of status is
necessary. Surgical exploration for
immediate onset paralysis with poor
prognostic indicators.
Cerebrospinal
fl uid otorrhea
Usually resolves spontaneously; not a
surgical consideration for at least 7
days.
A
B
Figure 128-1. A, Longitudinal temporal bone fracture (arrows)
sparing the otic capsule and internal auditory canal. B, Computed
tomography scan showing a longitudinal fracture (arrow).
A
B
Figure 128-2. A, Transverse temporal bone fracture (arrows) with
involvement of the otic capsule and the contents of the internal audi-
tory canal. B, Computed tomography scan showing transverse
fracture (arrow).
The following criteria form the basis for surgical
selection with respect to facial paralysis in temporal
bone trauma:
1. Immediate onset paralysis with progressive decline
of electrical responses on electroneuronography
(ENoG) to less than 10% of responses on the normal
side within the fi rst 14 days.
2. Immediate-onset paralysis with signifi cant disruption
of the fallopian canal demonstrated on HRCT.
The decision to intervene surgically is more chal-
lenging in patients with incomplete immediate-onset
facial paralysis. Conservative management is the general
rule when partial function remains. Aggressive eye care
is critical while awaiting functional recovery in all
patients. In the absence of any medical contraindica-
tions, the administration of a tapering course of sys-
temic steroids (prednisone 1 mg/kg body weight or
equivalent, tapered over 1 week) is generally thought
to be helpful in reducing any traumatic neural edema
and promoting early recovery. Care must be taken to
rule out extratemporal nerve injuries in patients in
whom only one or several branches are involved.

Chapter 128
Temporal Bone Trauma 1369
Cerebrospinal Fluid Leak
CSF leak associated with temporal bone fractures may
manifest as otorrhea, rhinorrhea, or otorhinorrhea. A
high percentage of CSF leaks associated with skull base
fractures resolve with conservative management within
a week. Strict bed rest, head elevation, and the admin-
istration of stool softeners usually suffi ce to control
these leaks. Lumbar drainage is used with an indwelling
catheter for approximately 3 to 4 days when spontane-
ous resolution does not occur within the fi rst 3 days of
bed rest and head elevation. When drainage persists
despite these measures or when HRCT identifi es obvious
severe bone disruption, surgery is indicated. The overall
incidence of meningitis following temporal bone
trauma with an associated CSF leak is less than 10%.3
The use of prophylactic antibiotics is recommended in
select patients with increased risk of meningitis, includ-
ing those with persistent CSF leaks beyond 7 days, those
with concomitant infections elsewhere, and those who
have a lumbar drain in place. Indiscriminate use of sys-
temic antibiotics may mask the early signs and symp-
toms of meningitis. White blood cell counts help in
early detection of meningitis, and diagnostic lumbar
puncture should be performed when any clinical suspi-
cion of infection arises.
PREOPERATIVE EVALUATION
Dedicated HRCT of the temporal bones at 1- to 1.5-mm
thickness intervals using bone algorithm is the best
imaging modality for evaluating temporal bone injury.
Axial and true or high-resolution reconstructed coronal
images should be requested. A routine CT scan of the
head obtained for the purpose of ruling out intracra-
nial trauma is inadequate for evaluating the intratem-
poral facial nerve and ossicular chain. When evaluating
the fallopian canal, one should look for multiple frac-
ture sites because this is more common than is usually
recognized.6 The status of the otic capsule and the
ossicular chain can be ascertained as well. Longitudinal
or otic capsule sparing fractures will most often com-
promise the facial nerve at or distal to the geniculate
ganglion. Conversely, transverse or otic capsule involv-
ing fractures usually injure the facial nerve medial to
the geniculate ganglion (Fig. 128-3). The degree of
pneumatization of the mastoid and level of the middle
fossa dural plate are of interest if surgical intervention
is contemplated. The signifi cance of these factors is
discussed later in the chapter. Magnetic resonance
imaging plays a complementary role in the evaluation
of associated intracranial trauma.
Topographic testing of facial nerve function, includ-
ing the Schirmer test, has been found to be unreliable
in localizing the site of lesion and has limited clinical
utility in this setting. Audiometric testing is a necessary
component of a full clinical evaluation and should be
obtained at the earliest feasible time. It is helpful not
only to determine the type of hearing loss but in the
case of sensorineural impairment, to decide whether
residual function is useful. Hearing results do not
dictate the necessity for surgery in the early posttrauma
period, but they do infl uence the selection of surgical
approach, when it becomes necessary. Conductive
hearing loss will often resolve spontaneously; hearing
losses that remain can be surgically corrected later. Sen-
sorineural hearing impairment is usually permanent,
although it sometimes improves slightly over time. Ves-
tibular testing plays no role in the early evaluation of
fractures of the temporal bone. The vast majority of
vestibular symptoms are expected to resolve and may,
in any case, be delineated later.
When the decision has been made to surgically
explore the facial nerve, empiricism dictates that undue
delay is counterproductive. Once the patient is neuro-
logically stable and the site of lesion identifi ed on
HRCT, surgery should proceed. The organization of
blood clot and the development of scar and fi brous
tissue can only affect results negatively. This active
approach to these injuries is obviously not always possi-
ble because some patients are seen for the fi rst time
after many weeks or months have elapsed. These
patients will nevertheless benefi t from exploration, as
long as they meet the criteria elaborated earlier.7 When
persistent CSF leak is the only indication for surgical
intervention, closure should proceed after 7 to 10 days
of conservative management because the risk of men-
ingitis increases signifi cantly thereafter.3
SURGICAL TECHNIQUES
Selection of surgical approach is dependent on both
site of injury and hearing status in the involved ear.
Injuries of the facial nerve at or distal to the geniculate
ganglion can be approached via a standard transmas-
toid exposure. Injuries medial to the geniculate gan-
glion may be approached in several ways, depending on
residual hearing in the affected ear and the degree of
G
FN
Figure 128-3. Superior view of a transverse fracture line (arrow)
involving the facial nerve (FN) medial to the geniculate ganglion
(G).

1370
Section 15
Temporal Bone
pneumatization of the temporal bone. Severe sensori-
neural hearing loss allows for translabyrinthine expo-
sure of the facial nerve. Conversely, when hearing
conservation is indicated, the middle cranial fossa
approach may be elected. In the case of a well pneuma-
tized epitympanum in which the middle fossa dural
plate is relatively high, the labyrinthine portion of the
facial nerve may be exposed via a transmastoid transepi-
tympanic approach (Fig. 128-4). This approach,
however, does not provide adequate exposure for the
meatal segment of the facial nerve.
Although repair of a disrupted tympanic membrane
and defects of the ossicles may be accomplished simul-
taneously, it is often necessary to delay these reconstruc-
tive efforts due to edema of the mucosa, bleeding, and
the friability of traumatized tissue within the middle
ear. In cases of severe bony tegmen disruption with
herniation of brain tissue, associated repair of the
encephalocele is indicated.
Transmastoid Approach for Facial
Nerve Injuries at or Distal to the
Geniculate Ganglion
A complete mastoidectomy (see Chapter 115) is per-
formed to access the mastoid antrum and locate the
lateral semicircular canal. Bony dissection is then con-
tinued anterosuperiorly toward the epitympanum until
the body of the incus is identifi ed. The parasagittal
plane of the incus is extrapolated posteriorly to identify
the level of the facial recess, which is then opened and
saucerized to delineate the vertical facial nerve within
the mastoid. The mastoid segment of the nerve may
also be identifi ed at its point of exit from the stylomas-
toid foramen by following the digastric ridge anteriorly
in the mastoid tip. Skeletonization of the fallopian
canal should be performed with care using 2- to 3-mm
diamond burrs and copious irrigation. In most cases,
the fracture line is often observed on the surface of the
mastoid cortex and can be followed medially to the site
of injury. Working alternately between the facial recess
and the epitympanum, the surgeon can remove thin
bone from the tympanic portion of the fallopian canal
if bony decompression of this segment is indicated (Fig.
128-5). If necessary, the incus can be removed in order
to improve exposure of the tympanic facial nerve. In
this case, the incudostapedial joint is separated through
the facial recess using a small sharp hook and the incus
retrieved through the epitympanum, taking care not to
sublux the stapes. Preserving a small bony bridge in the
fossa incudis for support of the short process of the
incus allows for easy replacement of the incus with little
or no hearing defi cit.
Injuries to the facial nerve produced by stretching
or compression are managed with decompression of
the fallopian canal proximal and distal to the injury
until normal nerve is identifi ed. The need for addi-
tional incision of the epineural sheath is controversial.
Any bone chips impinging on the nerve should be
removed. The integrity of the axonal bundles within the
nerve sheath must also be determined. Transection of
nerve fi bers by trauma may be total or partial. It is gen-
erally considered advantageous to preserve the facial
nerve when 50% or more of the diameter of the nerve
appears intact. Complete transection may be repaired
with primary end-to-end apposition. If tension-free
reapproximation or reanastomosis cannot be accom-
plished or maintained, facial nerve rerouting for
primary reanastomosis or interposition grafting should
be considered. Eliminating the second genu of the
facial nerve, for example, is an effective technique for
shortening the distance of proximal and distal nerve
segments lateral to the geniculate (Fig. 128-6A). Anas-
tomosis might also proceed directly from the internal
auditory canal (IAC) to the vertical segment of the
facial nerve by dividing the greater superfi cial petrosal
Figure 128-4. Transmastoid exposure of temporal bone that is
suitable for transepitympanic exploration (large arrow) of the facial
nerve because of a high middle fossa tegmen. (Arrow, level of middle
fossa dura.)
Figure 128-5. Exposure and decompression of the horizontal
portion of the facial nerve (arrow). (Incus removed.)

Chapter 128
Temporal Bone Trauma 1371
nerve at the geniculate ganglion, rerouting the intact
distal segment, and interposing a cable graft (see Fig.
128-6B). For interposition nerve grafting (Fig. 128-7),
the great auricular nerve is the preferred donor
site because of the nerve’s proximity and size com-
patibility. Epineurium must be carefully trimmed
back and nerve fascicles sharply sectioned for optimal
end-to-end contact. For both primary repair and inter-
position grafting of the labyrinthine, tympanic, and
mastoid segments, the fallopian canal provides an excel-
lent bed for anastomosis and usually the nerve does
not require any suturing. With repair of the nerve
within or medial to the IAC, one or two 8-0 monofi la-
ment sutures may be placed in the epineurium.
Standard layered mastoidectomy wound closure and
ear dressings are used.
Transmastoid Translabyrinthine Approach
for Facial Nerve Injuries Medial to the
Geniculate Ganglion without Useful Hearing
The procedure described in the preceding section is
carried out and followed by a complete labyrinthectomy
and skeletonization of the IAC from the porus acusticus
to the fundus (see Chapter 124). When drilling through
the semicircular canals, care should be exercised when
following the posterior semicircular canal anteriorly
under the second genu of the facial nerve to its ampulla.
The superior limit of the lateral IAC is defi ned by the
location of the superior vestibular nerve, which lies
immediately anterior to the ampulla of the superior
semicircular canal. The IAC is skeletonized laterally to
permit identifi cation of Bill’s bar (vertical crest), which
separates the facial nerve anteriorly from the superior
vestibular nerve posteriorly. Skeletonization of the facial
nerve is then continued anteriorly to the geniculate
ganglion using a small diamond burr. The entire intra-
temporal course of the facial nerve can then be exposed
(Fig. 128-8). If facial nerve rerouting is necessary to
achieve tension-free repair, the greater superfi cial
petrosal nerve is divided at the geniculate ganglion and
the facial nerve gently elevated out of the fallopian
canal. Grafting techniques are similar to those described
earlier, except the repair of a transected nerve is con-
siderably more diffi cult in the IAC because of gravity
and the presence of CSF pulsations. Collagen or Silastic
sleeves can add support to the anastomosis following
suturing and add greater strength to the graft sites.
Closure is similar to that described for translabyrinthine
removal of acoustic neuromas and requires the oblitera-
tion of the eustachian tube and middle ear with tempo-
ralis muscle, packing of the mastoid cavity with
abdominal fat, and layered wound closure. A pressure
dressing should be maintained over the operated ear
for 3 to 4 days to minimize the risk of postoperative CSF
leakage.
Transmastoid Transepitympanic Approach
for Facial Nerve Injuries Medial to the
Geniculate Ganglion with Useful Hearing
Following a complete mastoidectomy, the incus is
removed as described earlier under Transmastoid
Approach for Facial Nerve Injuries at or Distal to the
Geniculate Ganglion. The geniculate ganglion is identi-
fi ed and followed posteromedially, staying anterior to
the ampullated end of the superior semicircular canal
(Fig. 128-9). The superior semicircular canal is skele-
tonized, allowing for exposure of the labyrinthine
portion of the facial nerve. This portion of the nerve
can then be decompressed; in fact, CSF is routinely
encountered. Preoperative review of the HRCT scans
must ensure that injury is lateral to the meatal portion
of the nerve in order to achieve adequate exposure
using this approach. When adequate exposure is in
doubt, or if grafting of the meatal or proximal facial
nerve is anticipated, the middle fossa approach should
be used.
A
B
CAROTID
Figure 128-6. A, Reconstructive technique for gaining length and
avoiding an interposition graft by eliminating the second genu of the
facial nerve. (Arrow, transpositioned facial nerve.) B, Anastomotic
technique using an interposition graft and “short-circuiting.” (Large
arrows, normal course of the facial nerve; small arrow, shortened
course of the facial nerve.)

1372
Section 15
Temporal Bone
A
B
C
Figure 128-7. Use of an interposi-
tion graft for repair of a facial nerve
defect in the internal auditory canal
by the middle fossa approach. (Arrows,
site of nerve transection, freshening,
and repair.)
Middle Cranial Fossa Approach for Facial
Nerve Injuries Medial to the Geniculate
Ganglion with Intact Hearing
The superior surface of the temporal bone is exposed
extradurally as described in Chapter 124. The extent of
surgical exposure for decompression or repair of the
facial nerve in this context is identifi cation of the greater
superfi cial petrosal nerve at its take off from the genicu-
late ganglion anteriorly. The nerve can then be fol-
lowed proximally into the labyrinthine and IAC
segments, recognizing the proximity of the labyrinthine
facial nerve to the basal cochlear turn. Bone of the
tegmen tympani may be removed to expose the tym-
panic segment of the nerve, taking care to avoid drilling
directly on the head of the malleus and body of the
incus. The middle fossa approach may be combined
with a transmastoid exploration of the more distal nerve
segment when indicated (Fig. 128-10). In that case, the
transmastoid procedure should be completed fi rst in
order to fenestrate the middle fossa tegmen superior to
the geniculate ganglion, thereby simplifying identifi ca-
tion of the facial nerve and internal auditory canal
through the middle fossa craniotomy. This combined
exposure allows for surgical access to the entire intra-
temporal facial nerve from the cisternal segment to the
stylomastoid foramen, while preserving hearing in the
operated ear. Closure of the middle fossa craniotomy is

Chapter 128
Temporal Bone Trauma 1373
identical to that described for removal of tumor via the
middle fossa (see Chapter 124). The mastoidectomy
wound is closed in a standard layered fashion.
Repair of Cerebrospinal Fluid Leaks
Surgical techniques for the sole purpose of repairing
CSF leaks resulting from temporal bone trauma are
infl uenced by (1) site of leak, (2) hearing status of the
affected ear, and (3) presence of brain herniation
through the tegmen. For fractures through the tegmen
mastoideum with persistent CSF leak, “sandwich” grafts
consisting of fascia or freeze-dried dura are placed
intracranially and extracranially using a combined
transmastoid mini-middle fossa approach (see Chapter
127), and bone paté is placed along the fracture line.
Large dehiscences of bone may require bony autografts,
fashioned bone plugs, or microplating for temporal
lobe support (Fig. 128-11).
When there is signifi cant herniation of the tempo-
ral lobe through the fracture site, the devitalized brain
tissue is débrided through a transmastoid exposure,
and the viable brain and dura elevated back through
am extradural mini-middle fossa approach. The resul-
tant dural defect may be repaired using temporalis
fascia or freeze-dried dura. The bony defect is rein-
forced using autologous bone harvested from the cra-
niotomy fl ap to prevent further prolapse of brain tissue
into the mastoid or middle ear cavities.
In patients with anacusis following trauma, oblitera-
tion of the middle ear and mastoid with blind sac
closure of the external auditory meatus may be per-
formed using a standard two-layered technique. A
complete mastoidectomy is performed. The skin of the
external auditory canal, tympanic membrane, malleus,
and incus are removed, leaving the stapes intact. The
eustachian tube is obliterated with muscle, and the
Figure 128-8. Transmastoid translabyrinthine exposure of the
entire facial nerve. (Arrow, internal auditory canal.)
SSC
LSC
Figure 128-9. Transmastoid transepitympanic exposure of the
labyrinthine portion of the facial nerve (arrow). SCC, superior semi-
circular canal; LSC, lateral semicircular canal.
Figure 128-10. Combined middle fossa transmastoid approach to
the facial nerve for hearing preservation.
Figure 128-11. Bone grafting for repair of a middle fossa defect
using a microplate (arrow).

1374
Section 15
Temporal Bone
middle ear and mastoid cavities are packed with abdom-
inal fat.
POSTOPERATIVE MANAGEMENT
Postoperative management in these patients is similar
to that of chronic middle ear and mastoid surgery.
With the exception of translabyrinthine craniotomies,
mastoid dressings for all other cases are removed in 24
hours to check for hematoma, cutaneous CSF leaks, or
wound infection. The dressing is reapplied as necessary.
If the dura has been opened, perioperative antibiotic
coverage is used for 48 hours and consists of either
broad-spectrum cephalosporins or vancomycin in peni-
cillin-allergic patients. In addition to achieving a water-
tight wound closure, elevation of the head by 30 degrees
and use of stool softeners helps minimize postoperative
CSF leakage. Steroids are given in moderate doses and
tapered over 5 to 7 days unless medically contraindi-
cated. The use of steroids in these cases, as in acoustic
tumor surgery, has signifi cantly decreased postopera-
tive complaints of headache and neck pain. This is
probably due to suppression of infl ammation from the
breakdown of red blood cells in the CSF. Supportive
eye care is continued and varies greatly depending on
age, skin laxity, and anticipated time for return of facial
function. Young patients with good corneal coverage
may require nothing but lubricants and moisture cham-
bers. Others may require lateral tarsorrhaphy, gold
weights, or even oculoplastic procedures if severe ectro-
pion develops.
Early ambulation is encouraged for all the usual
reasons, in addition to the benefi ts obtained in
early vestibular compensation. Early enrollment in a
formal vestibular rehabilitative and physical therapy
program is helpful in older and multiply injured indi-
viduals. The early convalescent period is an appropriate
time for more in-depth investigation of auditory and
vestibular function in those who manifest persistent
symptoms.
When the nerve has been determined to be intact
or following adequate grafting, some return of function
is to be expected. The repaired or grafted nerve will
generally recover limited function with variable synki-
nesis. This is usually demonstrable within 6 months for
lesions distal to the geniculate ganglion but may take
up to 1 year for more proximal lesions. Failure of
expected return of function within 1 year should moti-
vate the surgeon to review the initial CT scan and
perhaps even to repeat the study. Facial paralysis may
persist in “old” temporal bone injuries long after spon-
taneous resolution should have occurred. Scarring
and degeneration of the proximal nerve segment in
these cases usually precludes successful primary repair.
Anastomosis of the facial and hypoglossal nerves or
nerve muscle pedicle reconstruction is advised in this
instance.
Pseudoaneurysms of the internal carotid artery are
very rarely seen following head trauma. These consist
of disruption of the intima of the artery with conse-
quent dissection of blood between the vessel wall and
the adventitial layer (Fig. 128-12). Stabilization may be
spontaneous, but continued dissection of the aneurysm
may require treatment. Following balloon occlusion
and xenon fl ow studies to determine contralateral fl ow,
balloons can be angiographically inserted proximal and
distal to the site by an interventional radiologist. Failure
of the contralateral fl ow testing would necessitate bypass
grafting of the carotid artery.
Figure 128-12. High-resolution computed tomography scan
showing a posttraumatic pseudoaneurysm (large arrow) of the internal
carotid artery. (Small arrow, normal carotid.)
PEARLS
• The primary indications for surgical intervention in
temporal bone fractures are immediate complete
facial paralysis with poor prognostic indicators, and
persistent CSF leaks.
• Newer spiral CT scanners offer the ability to
reconstruct high-resolution coronal images of the
temporal bone, thus obviating the need for extreme
neck extension needed to obtain true coronal
images in these patients.
• Surgical approach is determined by hearing status in
the affected ear and site of injury.
• When ENoG demonstrates less than 10% activity on
the affected side, the adjunctive use of facial muscle
electromyography to confi rm the absence of
electrical activity or appearance of fi brillation
potentials is helpful in identifying surgical
candidates for facial nerve decompression.8
• Facial nerve injuries distal to the geniculate ganglion
are best accessed using the transmastoid approach,
whereas facial nerve injuries medial to the geniculate
ganglion may typically be accessed using the middle
fossa approach in the hearing ear and using the
translabyrinthine approach in the nonhearing ear.

Chapter 128
Temporal Bone Trauma 1375
References
1. Ishman SL, Friedland DL: Temporal bone fractures: Traditional
classifi cation and clinical relevance. Laryngoscope 114:1173-1741,
2004.
2. Dahiya R, Keller JD, Litofsky SN, et al: Temporal bone fractures:
Otic capsule sparing versus otic capsule violating clinical and
radiographic considerations. J Trauma 47:1079-1083, 1999.
3. Brodie HA, Thompson TC: Management of complications from
820 temporal bone fractures. Am J Otol 18:188-197, 1997.
4. Nosan DK, Benecke JE, Murr AH: Current perspective on tempo-
ral bone trauma. Otolaryngol Head Neck Surg 117:67-71, 1997.
5. McKennan KY, Chole RA: Facial paralysis in temporal bone trauma.
Am J Otol 13:167-172, 1992.
6. Lambert PR, Brackmann DE: Facial paralysis in longitudinal tem-
poral bone fractures: A review of 26 cases. Laryngoscope 94:1022-
1026, 1984.
7. Quaranta A, Campobasso G, Piazza F, et al: Facial nerve paralysis
in temporal bone fractures: Outcomes after late decompression
surgery. Acta Otolaryngol 121:652-655, 2001.
8. Darrouzet V, Duclos JY, Liguoro D, et al: Management of facial
paralysis resulting from temporal bone fractures: Our experience
in 115 cases. Otolaryngol head Neck Surg 125:77-84, 2001.
PITFALLS
• Nerve repair under tension compromises
microvascular circulation at the site of repair,
resulting in scar formation, impaired axonal
penetration, and uniformly poor functional
outcome.
• Failure to recognize the presence of multiple sites of
injury along the facial nerve will result in persistent
facial paralysis following surgical decompression.
• Additional sensorineural hearing loss may result
from drilling on the ossicular chain or violating the
ampullated ends of the lateral and posterior
semicircular canals when exposing the perigeniculate
facial nerve through transmastoid approaches.
• Undue delay in surgical repair of persistent CSF leaks
beyond 7 days may increase the risk of meningitis.
• When the external auditory canal is severely
traumatized, cicatricial canal stenosis may develop
with cholesteatoma formation medial to the stenotic
segment.

Chapter 129
Cochlear Implantation
Yu-Lan Mary Ying and Elizabeth H. Toh
Cochlear implants are implantable electronic prosthe-
ses designed to convert mechanical sound energy into
electrical signals that directly stimulate the auditory
nerve in severely to profoundly deaf individuals. They
have become the standard of care for rehabilitating
deafened individuals who no longer benefi t from the
use of conventional hearing aids. The Food and Drug
Administration (FDA) approved the use of cochlear
implant devices in the United States for adults in 1985
and for children in 1990. Since then, more than 80,000
devices have been implanted in this country.
The functional anatomy of the inner ear as it applies
to cochlear implantation is briefl y reviewed here. The
cochlea consists of a central bony skeleton, the modio-
lus, and the surrounding bony otic capsule. Within the
modiolus lies the auditory nerve with bipolar primary
afferent neurons, their cell bodies (spiral ganglia), and
efferent nerve fi bers. The presence of at least 10,000
surviving cochlear neurons is vital for successful hearing
outcomes using a cochlear implant device. The spiral
ganglion neurons follow the spiral arrangement of the
cochlear duct with maximal ganglion cell density located
between the upper basal turn and lower middle turn of
the cochlear duct. This has clinical signifi cance in
cochlear implantation for placing the electrode array
close to the greatest density of cochlear neurons.
All cochlear implant systems have an externally
worn device and an implanted internal component.
The external hardware consists of an ear-level micro-
phone, an ear-level or body-worn speech processor, and
a transmitter placed behind the ear. The internal com-
ponent consists of a receiver/stimulator, linked to an
intracochlear electrode array via a lead wire. Sound
received by the microphone is transduced into electri-
cal signals, which are fi ltered, analyzed, and digitized
by the speech processor, and forwarded to the transmit-
ting coil. The encoded signals are then delivered to the
implanted receiver/stimulator by radio-frequency elec-
tromagnetic induction. This signal is reconverted to an
electrical signal, which is then delivered to the implanted
electrode within the scala tympani. Current applied to
the electrodes radiates into the fl uid of the scala
tympani, spreads through the habenula perforata of the
osseous cochlear modiolus, and stimulates the auditory
nerve.
Three implant systems (Nucleus Freedom system,
Harmony HiResolution Bionic Ear system, and Med-El
SonataTI
100 and PulsarCI100 systems) are currently FDA
approved for use in adults and children in the United
States. All are multichannel systems with 16 to 24 elec-
trodes designed to take advantage of the tonotopic orga-
nization of the cochlea. Incoming speech signals are
fi ltered into a number of frequency bands, each corre-
sponding to a given electrode in the array. The Nucleus
Freedom and HiResolution Bionic Ear systems use pre-
curved modiolar-hugging electrode arrays. The relative
proximity of these precurved electrode arrays to spiral
ganglion cells offers theoretical advantages of improved
sound quality, speech recognition, and power effi ciency.
By contrast, the longer tapered straight electrode of the
Med-El PulsarCI100 and SonataTI
100 systems are designed
for deep intracochlear insertion and electrical stimula-
tion of the full sound frequency range. Overall hearing
outcomes as refl ected by standard audiologic test scores
have been comparable using devices from all three man-
ufacturers. The selection of device to be implanted is,
in most practices, left to the patient.
PATIENT SELECTION
Candidacy criteria for cochlear implantation in adults
and children continue to evolve with advances in
1377

1378
Section 15
Temporal Bone
electrode design, surgical techniques for atraumatic
electrode insertion, and speech processing strategies.
Current devices use either precurved perimodiolar
electrode arrays or slim-profi le tapered arrays to mini-
mize trauma to surviving neural elements within the
cochlea. With the possibility of preserving residual
hearing in the implanted ear, candidacy criteria have
expanded to include individuals with more residual
hearing.
Adults
Current candidacy criteria for cochlear implantation in
adults are listed in Table 129-1. It is well established that
individuals who lose hearing after acquiring speech and
language skills (postlingually deafened) and those with
a shorter duration of deafness before implantation
perform better with cochlear implants. In fact, duration
of deafness has been found to be the only reliable
predictor of auditory performance.1 Other variables,
including age at implantation, age at onset of hearing
loss, age of deafness, hearing aid use, side implanted,
and preoperative audiologic test scores, have not con-
sistently correlated with postimplantation performance.
Prelingually deafened adults who have been habilitated
using aural and oral education may receive some benefi t
from a cochlear implant.2 There is no upper age limit
for implantation in adults with good health.
Children
The selection procedure for children is more complex
than for adults. In contrast to adults, both prelingually
and postlingually deafened children are candidates for
cochlear implantation. Research has shown that early
auditory experience is critical for the development of
central and peripheral auditory neural pathways. There
exists an early period of language development in
humans between ages 2 and 5, during which auditory
input is paramount. Therefore, early hearing habilita-
tion using a cochlear implant in children with congeni-
tal deafness and early profound acquired hearing loss
is critical. Early implantation signifi cantly improves the
chance for development of normal speech and lan-
guage in children.
Since the legislation of universal newborn hearing
screening across the United States, many more infants
with congenital hearing loss are being identifi ed within
the fi rst few months of life. Current FDA guidelines
permit implantation of children as young as 12 months
of age. Exceptions to this lower age limit may be made
in children with deafness resulting from meningitis.
Earlier implantation in these children may allow for
successful electrode insertion before the development
of intracochlear ossifi cation. Criteria for the pediatric
age group are listed in Table 129-2. Appropriate family
motivation, expectations, and support are also impor-
tant factors in determining suitability of the child for
implantation.
PREOPERATIVE EVALUATION
A complete history and physical examination are neces-
sary to detect problems that may contraindicate surgery,
or interfere with the patient’s ability to complete post-
implantation rehabilitation. Etiology of hearing loss is
rarely a contraindication to implantation. Profound
hearing loss associated with cochlear nerve aplasia is a
rare congenital anomaly, in which the lack of auditory
innervation obviates the option for cochlear implanta-
tion. Prior meningitis with cochlear ossifi cation or
fi brosis does not exclude a patient from implantation,
but may necessitate modifi cation of the surgical tech-
nique itself. The ear selected for implantation must be
free of infection and ideally have an intact tympanic
membrane.
An audiologic evaluation that characterizes hearing
loss in both unaided conditions and in best binaurally
aided conditions is performed. This includes measure-
ment of pure tone thresholds, word, and sentence
recognition testing. Aided speech recognition scores
are the primary audiologic determinants of cochlear
implant candidacy. Audiologic screening in children
requires auditory brain stem evoked response testing,
and otoacoustic emissions testing, in addition to con-
ventional behavioral audiometry. A 6-month trial period
Table 129-1
CANDIDACY CRITERIA FOR
COCHLEAR IMPLANTATION IN
ADULTS OLDER THAN 18 YEARS
• Bilateral severe to profound hearing loss: a three-
frequency pure-tone average (500, 1000, 2000 Hz)
unaided threshold in the better ear of greater than
70 dB
• Less than 20% word recognition score with consonant
nucleus consonant (CNC) words bilaterally
• Minimal benefi t from conventional hearing aids, as
defi ned by hearing in noise sentence testing (HINT)
recognition scores of less than 50% correct in the best
aided condition
• No medical contraindications
Table 129-2
CANDIDACY CRITERIA FOR
COCHLEAR IMPLANTATION
IN CHILDREN
Children age 12 to 24 months:
• Bilateral profound hearing loss
• Lack of auditory skills development and minimal
hearing aid benefi t
• No medical contraindications
• Enrollment in an education program emphasizing
auditory development
Children age 25 months to 18 years:
• Bilateral severe to profound hearing loss
• Lack of auditory skills development and minimal
hearing aid benefi t (open set word recognition scores
of less than 30% correct)
• No medical contraindications
• Enrollment in an education program emphasizing
auditory development

Chapter 129
Cochlear Implantation 1379
using appropriate amplifi cation, and intensive auditory
and speech training is an integral component of candi-
dacy assessment in children. The global evaluation of
cochlear implant candidacy in children is considerably
more challenging than in adults and is best approached
by a dedicated team comprising speech and hearing
professionals. The ultimate candidacy of a child is
determined not only by a demonstrated physiologic
need but also by the strength of the child’s social and
educational background.
Preoperative imaging necessarily includes a high-
resolution, thin-cut computed tomography (CT) scan
of the temporal bone in both the axial and coronal
planes. This is used to determine the presence and
patency of the cochlea, identify any congenital inner
ear malformations, assess the caliber of the internal
auditory canal, and assess the anatomy of the mastoid,
middle ear, and facial nerve. Congenital malformations
of the inner ear and cochlear ossifi cation per se are not
contraindications to cochlear implantation, although
modifi cations in surgical technique or the use of non-
standard implant electrodes may be necessary and
should be anticipated preoperatively. More recently,
some implant teams have advocated the routine use of
magnetic resonance imaging (MRI) of the internal
auditory canals as the preoperative imaging modality of
choice. In a retrospective review by Parry and colleagues,
MRI was found to be more sensitive and specifi c in
diagnosing soft tissue abnormalities in the inner ear
than high-resolution computed tomography in cochlear
implant candidates.3 Using high-resolution T2-weighted
sequences, MRI offers the capability for visualizing
intracochlear fl uid and is therefore more sensitive for
detecting both bony and soft tissue obliteration of the
cochlea. MRI can also be used to identify neural com-
ponents within the internal auditory canal on sagittal
reconstructions of the internal auditory canal to confi rm
the presence of a cochlear nerve.
In children, a comprehensive psychosocial evalua-
tion is performed to identify factors that may affect
subsequent adjustment to or benefi t from the implant.
Reasonable implant expectations and acceptance of the
child or adult recipient by family members are
addressed.
Several factors infl uence the selection of ear to be
implanted. Generally, the ear with the shortest duration
of deafness, the more consistent use of a hearing aid,
and the most radiographically favorable anatomy (well-
pneumatized mastoid, normal facial nerve anatomy,
normal inner ear development, and patent cochlea) is
selected for implantation. More recently, Friedland and
colleagues have suggested that cochlear implantation
of the poorer hearing ear does not compromise post-
operative performance as measured using standard
audiologic tests.1 While duration of deafness was still
the most consistent and signifi cant determinant of post-
operative speech recognition, the authors concluded
that the overall auditory experience of the individual,
rather than ear-specifi c criteria, was the best predicator
of postoperative cochlear implant performance in the
postlingually deafened adult. When both ears are
equally suitable for implantation, the ear on the side of
dominant hand is selected to facilitate usage of the
device.
Of the more than 80,000 patients worldwide who
have received cochlear implants, approximately 3500
have received bilateral cochlear implants.4 Given the
advantages of conventional binaural amplifi cation for
bilateral sensorineural hearing loss over monaural
amplifi cation, we should expect similar auditory perfor-
mance with bilateral cochlear implantation. The
reported benefi ts of bilateral implantation include sig-
nifi cant decrease in head-shadow effect, improved
speech understanding in noise, binaural summation,
and sound localization. Implants may be placed sequen-
tially at separate surgeries or simultaneously.
Children with cochlear implants have an increased
risk for Streptococcus pneumoniae meningitis compared
with children without cochlear implants. Routine pre-
operative pneumococcal vaccination is now recom-
mended for all patients.5 Guidelines for vaccination
vary by patient age and are listed in Table 129-3.
SURGICAL APPROACHES
Surgery is performed under general anesthesia with the
patient in the supine position. Continuous intraopera-
tive facial nerve monitoring is routinely employed. The
use of long-acting muscle relaxants is avoided for this
reason. A single dose of a broad-spectrum antibiotic
such as cefazolin (Ancef), 2 g, is administered at the
time of anesthesia induction.
Device templates provided by the manufacturer are
used to outline the position of the behind-the-ear (BTE)
processor, internal receiver, and surgical incision. The
internal receiver is placed above and behind the BTE
processor, avoiding any overlap between the two com-
ponents. The position of the internal receiver may be
Table 129-3
GUIDELINES FOR MENINGITIS
PROPHYLAXIS IN COCHLEAR
IMPLANT CANDIDATES
• Children who have completed the pneumococcal
conjugate vaccine (Prevnar) series should receive one
dose of the pneumococcal polysaccharide vaccine
(Pneumovax 23). If they have just received the
pneumococcal conjugate vaccine, they should wait at
least 2 months before receiving the pneumococcal
polysaccharide vaccine.
• Children between 24 and 59 months of age who have
never received either the pneumococcal conjugate
vaccine or pneumococcal polysaccharide vaccine
should receive two doses of pneumococcal conjugate
vaccine 2 or more months apart and then receive one
dose of pneumococcal polysaccharide vaccine at least 2
months later.
• Individuals age 5 years and older with cochlear
implants should receive one dose of pneumococcal
polysaccharide vaccine.
Source:
cochlear/dis-cochlear-hcp.htm

1380
Section 15
Temporal Bone
marked at this point using methylene blue and an 18-
gauge needle if desired. A variety of skin fl aps have
been described, most of which are some variation of the
standard postauricular incision used for routine mastoid
surgery with a posterosuperior extension to provide sur-
gical exposure for seating the internal receiver (Fig.
129-1). Minimal access approaches have been described
for cochlear implant insertion if cosmesis is of concern
to the patient. In this case, an oblique incision no
greater than 3 cm in length, approximately 0.5 cm
behind the postauricular crease, is made above and
behind the pinna (Fig. 129-2).6 After infi ltration of the
planned incision with 1% lidocaine with 1:100,000 epi-
nephrine solution, the skin and subcutaneous tissue are
incised down to the level of the temporalis fascia supe-
riorly and mastoid periosteum inferiorly (Fig. 129-3).
Skin fl aps are then developed anteriorly to the ear canal
and posteriorly to allow for placement of the internal
receiver. An anteroinferiorly based musculoperiosteal
fl ap is then created by incising the temporalis fascia,
muscle, and periosteum. Posterosuperiorly, this fl ap
should be long enough to completely cover the elec-
trodes as they emerge from the internal receiver. The
mastoid cortex and retromastoid cranium are exposed
by elevating this musculoperiosteal fl ap anteriorly until
the spine of Henle is visualized (Fig. 129-4).
A complete mastoidectomy is performed using a
combination of cutting and diamond drill burrs and
continuous suction irrigation, without saucerization of
the mastoid cavity. A bony overhang along the superior
and posterior margins of the mastoid cavity is preserved
for securing the electrode array within the cavity. Once
the mastoid antrum is entered, the lateral semicircular
canal is identifi ed and drilling continues anterosuperi-
orly until the body of the incus is identifi ed. The latter
is used to defi ne the level of the facial recess. Using 1- to
3-mm diamond burrs, the facial recess, bound by the
chorda tympani nerve, facial nerve, and incus buttress,
is carefully saucerized with copious irrigation to avoid
thermal injury to the facial nerve (Fig. 129-5). Removal
of bone anteromedial to the facial nerve in the facial
Figure 129-1. Implant template placement and surgical incision
marking (Nucleus Freedom device).
Figure 129-2. Minimal access incision for cochlear implantation.
(From O’Donoghue GM, Nikolopoulos TP: Minimal access surgery for pediat-
ric cochlear implantation. Oto Neurotol 23:891-894, 2002. Reprinted with
permission from Lippincott Williams & Wilkins, Optometry and Vision
Science.)
Figure 129-3. Skin incision and fl ap elevation.
Spine of
Henle
Figure 129-4. Musculoperiosteal fl ap elevated.

Chapter 129
Cochlear Implantation 1381
recess is sometimes necessary to visualize the round
window niche. When the facial recess is narrow, the
chorda tympani nerve may need to be sacrifi ced to gain
adequate exposure to the cochlea. In this situation,
extreme caution should be exercised when removing
bone lateral to the chorda tympani nerve to avoid violat-
ing the external auditory canal. Where a prominent
round window lip is evident and obscures visualization
of the round window membrane, the bony lip may be
carefully drilled down using a 1- to 1.5-mm diamond
burr. The mastoid cavity is then thoroughly irrigated
with bacitracin solution (50,000 units bacitracin powder
dissolved in 1000 mL normal saline solution) to remove
any bone dust. The epitympanum and facial recess are
plugged with Gelfoam or cotton prior to irrigation to
avoid dispersing bone dust into the middle ear.
The position of the internal receiver is then con-
fi rmed at this point using the BTE and device tem-
plates. A dummy internal receiver is used to mark out
the dimensions of the bony recess necessary to seat the
internal receiver. Cutting and diamond drill burrs are
used to develop this recess and the tunnel connecting
this recess to the posterosuperior limit of the mastoid
cavity. In pediatric patients, the limited thickness of the
skull may necessitate removal of bone down to dura,
leaving a central island of bone, to allow for adequate
recessing of the device. Several techniques are available
to secure the device within the bony recess, including
the use of nonabsorbable sutures with or without screws,
Gore-Tex strips, and microplates. We use four 4-0 silk
sutures placed through suture tunnels created along-
side the bony recess (Fig. 129-6).
Next, the cochleostomy is performed. Using a 1-
mm diamond burr, a small cochleostomy is made imme-
diately anterior and inferior to the round window
membrane (Fig. 129-7). This allows surgical access
directly into the scala tympani of the cochlear basal
turn. Placement of the electrode array into this location
is also possible directly through the round window
membrane.
The internal receiver is then placed in the bony
recess previously created. The magnet of the internal
device may be placed medial or lateral to the temporalis
muscle (Fig. 129-8). Once the receiver has been secured
in place, the electrode array is inserted into the scala
tympani of the cochlea (Fig. 129-9). A variety of
tools are provided by the implant manufacturers to
facilitate electrode insertion. Undue force should not
be used during electrode insertion to avoid electrode
kinking within the cochlea and minimize insertional
trauma to surviving neural elements within the cochlea.
The cochleostomy is then plugged with small pieces of
temporalis muscle or fascia. The ground electrode
is then buried under the temporalis muscle antero-
superiorly. Once the implant is in place, only bipolar
electrocautery should be used in order to minimize
the risk of electrical current conduction through the
device or into the cochlea. Intraoperative measure-
ments (neural-response telemetry and impedence
Incus
Round
window
niche
Lateral semicircular canal
Figure 129-5. Facial recess opened for surgical access to round
window.
Figure 129-6. Bony recess and tunnel drilled for internal receiver
and electrodes. Silk ties in place to secure internal receiver within
recess.
Promontory
Cochleostomy
Incudostapedial joint
Figure 129-7. Placement of cochleostomy anterior and inferior to
round window membrane.

1382
Section 15
Temporal Bone
testing) are obtained to confi rm proper functioning
of the device before or during wound closure. A plain
anteroposterior view radiograph of the skull may be
routinely or selectively obtained intraoperatively to
confi rm correct placement of the electrode array within
the cochlea (Fig. 129-10). The wound is closed in layers
without drainage. Care should be taken to ensure that
the musculoperiosteal fl ap completely covers the
mastoid cavity containing the electrode array. A mastoid
dressing is applied to the operated ear for 24 hours.
POSTOPERATIVE MANAGEMENT
The patient is discharged home on the day of surgery
with a 7-day course of oral antibiotics with antistrepto-
coccal coverage. The patient is instructed to remove the
mastoid dressing on postoperative day 1. The initial
follow-up visit is in 1 week. The patient is fi tted with a
signal processor 4 weeks after surgery, and individual
programming/rehabilitation begins. Regular follow-up
visits with the implant physician and audiologist for the
fi rst several years with objective assessment of perfor-
mance are planned.
COMPLICATIONS
Potential risks of the implant procedure are similar for
chronic ear surgery: infection, facial nerve paralysis,
dysgeusia, dizziness, cerebrospinal fl uid (CSF) drain-
age, meningitis, risks of general anesthesia, and
bleeding.
Wound infection that leads to failure of healing at
the incision site is the most common problem associ-
ated with implant surgery. Breakdown of the skin fl ap
with potential extrusion of the device can be prevented
by keeping the skin incision at least 1 cm away from the
edge of the internal receiver and maintaining a 6- to 7-
mm thick skin fl ap overlying the internal receiver and
magnet.7 Any sign of cellulitis warrants aggressive treat-
ment with broad-spectrum intravenous antibiotics. If
implant exposure results from necrosis of the overlying
skin fl ap, local rotational fl aps may be necessary to
cover the device (Fig. 129-11).
Facial nerve injury can occur as a result of surgery.
Although intraoperative facial nerve monitoring may
reduce this risk, a thorough knowledge of temporal
Figure 129-8. Device secured within bony recess and under tem-
poralis muscle.
Implant electrode
Implant electrode
Implant electrode
Incus
Incus
Lateral
Lateral
semicircular canal
semicircular canal
Lateral
semicircular canal
Cochleostomy packed
Cochleostomy packed
with muscle
with muscle
Cochleostomy packed
with muscle
Figure 129-9. Electrode placed in scala tympani through facial
recess.
Electrode in cochlea
Ground
electrode
Figure 129-10. Anteroposterior radiograph of the skull showing
good electrode placement within the cochlea.

Chapter 129
Cochlear Implantation 1383
Figure 129-11. Wound breakdown over internal receiver with early
extrusion of the device.
bone anatomy and meticulous surgical technique, along
with copious irrigation while drilling in and through
the facial recess, remain critical.
CSF leak has occurred when drilling the bony well
for the internal receiver in patients with thin temporal
squama. A small dural tear can be covered with tempo-
ralis fascia or repaired primarily. Firm packing of the
cochleostomy site with connective tissue prevents peri-
lymphatic fi stulae following electrode array insertion.
In patients with congenitally malformed inner ears, a
postoperative CSF leak is anticipated based on the pre-
operative imaging fi ndings. The eustachian tube should
be temporarily obliterated before the cochleostomy.
The elective placement of a lumbar drain in these cases
is optional. If a signifi cant postoperative CSF leak devel-
ops despite these measures, the eustachian tube and
middle ear may be obliterated.
Worldwide meningitis cases in children and adult
cochlear implant recipients reported in 2002 led the
FDA and Centers for Disease Control and Prevention
to develop recommendations for preoperative vaccina-
tion for all implant recipients. Studies have reempha-
sized the importance of packing the cochleostomy site
with soft tissue to prevent bacteria from entering the
inner ear and intracranial space.8,9
Intracochlear ossifi cation can be anticipated preop-
eratively on CT imaging of the temporal bone. Surgical
management options include drilling through the basal
turn of the cochlea with partial electrode insertion,10
insertion of a split electrode array through two separate
cochleostomies in the basal and apical cochlear turns,
respectively, to maximize the number of electrodes
implanted.11 The fi rst cochleostomy is created at the
standard site, just anterior to the round window mem-
brane. The second cochleostomy is created approxi-
mately 2 mm anterior to the oval window.12 An extensive
drillout procedure to gain access to the upper basal
turn has also been described by Gantz and colleagues
for the ossifi ed cochlea.13
PEARLS
• A limited cortical mastoidectomy with inferior
exposure down to the level of the inferior external
auditory canal is usually adequate for cochlear
implantation.
• A combined transmastoid/transcanal approach,
leaving the ear canal skin intact, may be helpful for
added surgical exposure of the cochlea when a
contracted mastoid is encountered.
• Removal of bone medial and anterior to the facial
nerve within the facial recess may be necessary for
exposure of the round window niche.
• Attention should be directed to inserting the
cochlear implant electrode into the scala tympani
with the electrode plates directed toward the
modiolus.
• The musculoperiosteal fl ap should be
reapproximated such that it completely covers the
mastoid cavity with the carrier and ground
electrodes within it.
PITFALLS
• Drilling lateral to the chorda tympani nerve when
opening the facial recess may result in violation of
the tympanic membrane or external auditory canal.
• Thermal injury to the facial nerve may occur while
drilling in the facial recess if continuous irrigation is
not applied.
• Inadequate surgical exposure and visualization of the
round window may result in erroneous placement of
the implant electrode within hypotympanic air cells.
• Suctioning at or within the cochleostomy may result
in trauma to the surviving intracochlear neural
elements, thus limiting postoperative auditory
function.
• The presence of congenital inner ear malformations
may increase the risk of postoperative CSF leak and
meningitis.
References
1. Friedland DR, Venick HS, Niparko JK: Choice of ear for cochlear
implantation: The effect of history and residual hearing on pre-
dicted postoperative performance. Oto Neurotol 24:582-589,
2003.
2. Waltzman SB, Cohen NL: Implantation of patients with prelin-
gual long-term deafness. Ann Otol Rhino Laryngol 108:84-87,
1999.
3. Parry DA, Booth T, Roland PS: Advantages of magnetic reso-
nance imaging over computed tomography in preoperative evalu-
ation of pediatric cochlear implant candidates. Oto Neurotol
26:976-982, 2005.
4. Lustig LR, Wackym PA: Bilateral cochlear implantation. Oper
Tech Otolaryngol 16:125-130, 2005.
5. Reefhuis J, Honein MA, Whitney CG, et al: Risk of bacterial men-
ingitis in children with cochlear implants. N Engl J Med 349:435-
445, 2003.

1384
Section 15
Temporal Bone
6. O’Donoghue GM, Nikolopoulos TP: Minimal access surgery for
pediatric cochlear implantation. Oto Neurotol 23:891-894,
2002.
7. Luxford WM, Mills D: Cochlear implantation in adults. In Jackler
RK, Brackmann DE (eds): Neurotology, 2nd ed. New York,
Mosby, 2004, pp 1309-1314.
8. Cohen NL, Roland JT Jr, Marrinan M: Meningitis in cochlear
implant recipients: The North American experience. Otol Neu-
rotol 25:275-281, 2004.
9. O’Donoghue G, Balkany T, Cohen N, et al: Meningitis and
cochlear implantation. Oto Neurotol 23:823-824, 2002.
10. Miyamoto RT, Kirk KI: Cochlear implantation. In Bailey BJ,
Johnson JT (eds): Head & Neck Surgery—Otolaryngology, 4th
ed. Philadelphia, Lippincott Williams & Wilkins, 2006, pp
2265-2277.
11. Millar DA, Hillman TA, Shelton C: Implantation of the ossifi ed
cochlea: Management with the split electrode array. Laryngo-
scope 115:2155-2160, 2005.
12. Lenarz T, Lesinski-Schiedat A, Weber BP, et al: The nucleus
double array cochlear implant: A new concept for the obliterated
cochlea. Oto Neurotol 22:24-32, 2001.
13. Gantz BJ, McCabe BF, Tyler RS: Use of multichannel cochlear
implants in obstructed and obliterated cochleas. Otolaryngol
Head Neck Surg 98:72-81, 1988.

Chapter 130
Microvascular Decompression of the
Seventh Cranial Nerve
Johnathan A. Engh, Amin B. Kassam,
Michael Horowitz, Jeffrey Balzer, and John Y. K. Lee
Hemifacial spasm (HFS) is a relatively uncommon
affl iction with an estimated yearly incidence of approxi-
mately 1 per 10,000.1 The disorder is characterized by
involuntary unilateral contractions and twitching of the
eye and face. The spasms are painless, yet they often
cause signifi cant social distress. In addition, many
patients with HFS have diffi culty reading, driving, or
working. Medications generally offer no relief of symp-
toms. Botulinus toxin (Botox, Allergan, Inc.) injections
have become increasingly popular as a temporizing
measure for HFS, but do not have long-lasting effi cacy.
As a result of the lack of response of HFS to these con-
servative therapies, surgical interventions for HFS have
emerged over the past half century.
The hypothesis that vascular compression of the
seventh cranial nerve (CN VII) causes HFS opened the
door for these surgical therapies. The theory was fi rst
proposed by Campbell and Keedy in 1947 as well as
Laine and Nayrac in 1948.2,3 Their proposal was based
on Dandy’s hypothesis that vascular compression of the
dorsal root of the trigeminal nerve causes trigeminal
neuralgia.4 Subsequently, Gardner and Sava published
their initial experience with decompression of the
seventh nerve for HFS in 1962.5,6 However, despite
these early reports, decades would pass before Jannetta
popularized microvascular decompression (MVD) of
CN VII as the defi nitive treatment for hemifacial
spasm.7,8 Today, microvascular decompression of the
seventh nerve stands alone as the single most effective
and long-lasting treatment for HFS.
PATIENT SELECTION
HFS is a purely clinical diagnosis and therefore a careful
history and physical examination must be obtained
before consideration of craniotomy and MVD. Typi-
cally, HFS manifests as unilateral intermittent twitching
of the facial muscles, usually beginning with orbicularis
oculi. Subsequently, spasms spread contiguously to the
other facial muscles. In atypical HFS, twitching begins
in the lower facial muscles and subsequently spreads
upward. The disease generally takes a relentless course
and over a variable period of time progresses to all of
the major muscles of one side of the face, including the
frontalis, platysma, and stapedius muscles. The latter
creates an odd clicking sound in the ipsilateral ear.
Severe spasms may lead to tonic facial contractures
(i.e., “tonus” phenomenon), which can be associated
with facial muscle paresis. The cosmetic deformity of
HFS is the most obvious concern for most patients,
prohibiting normal social interactions. Moreover, HFS
usually becomes a functional disability. Repetitive
closure of the eyelids, especially when associated with
tonus phenomenon, can impair vision and prohibit the
pursuit of both occupational and leisure activities,
including driving and reading.
HFS is slightly more common in women, and the
left side of the face is more often affected than the
right.8 Symptoms may be exacerbated by fatigue and
stressful activities. Although the spasms are involuntary,
voluntary movements such as talking and smiling can
1385

1386
Section 15
Temporal Bone
trigger contractions. Spasms continue during sleep,
and no known medical conditions are associated with
increased incidence of HFS. There is no apparent
genetic transmission of HFS, although rare familial
cases have been reported. No known toxin exposures
appear to increase the incidence of this condition.
The differential diagnosis of hemifacial spasm
includes postparalytic synkinesis, which occurs after
facial nerve trauma or Bell’s palsy. This phenomenon
is usually brought on by facial movement and rarely
occurs at rest. Other conditions that can be confused
with hemifacial spasm include blepharospasm, tics or
habit spasms, facial myokymia, Meige syndrome (com-
bination of oromandibular dystonia and blepharo-
spasm), and focal cortical seizures. Blepharospasm and
myokymia typically occur bilaterally, whereas bilateral
HFS is exceedingly rare. The distinguishing features of
HFS and similar conditions are outlined in Table
130-1.
PREOPERATIVE EVALUATION
Although preoperative imaging cannot make or support
the diagnosis of HFS, mass lesions such as neoplasms of
the cerebellopontine angle, posterior circulation aneu-
rysms, or arteriovenous malformations may be associ-
ated with HFS in 1% to 2% of cases. Therefore an
essential part of the patient’s preoperative evaluation is
magnetic resonance imaging (MRI) scan with and
without contrast to rule out the existence of such a mass
lesion. If a mass lesion is discovered, both the mass
lesion and the vascular compression source must be
treated in order to achieve a cure. However, MRI and
computed tomography (CT) scans should not be relied
upon to identify vessels responsible for compression. A
vessel (arterial or venous) of any size can be responsible
for the compression syndrome. If the MRI scan does
demonstrate a large vessel near the CN VII root exit
zone, the fi nding does not necessarily mean that this
vessel is the primary source of compression or the only
source of the compression. Thus, the role of preopera-
tive imaging is to rule out other sources of vascular
compression rather than guide the operative approach
in most cases.
Once a patient is diagnosed with HFS and obtains
adequate imaging, it is reasonable to refer the patient
to a neurologist or neurophysiologist for electroneuro-
physiologic testing. The routine battery of tests that are
performed includes baseline brain stem auditory evoked
responses (BAERs), facial electromyography (EMG),
and baseline lateral spread (LS) testing (see later text).
Abnormalities are noted before any operations. Such
testing is most critical in patients who have received
Botox injections before seeking surgical treatment,
because their baseline responses are often abnormal.
Patients with HFS have a characteristic electrophysi-
ologic anomaly termed the lateral spread response. An
understanding of the importance of this abnormal
muscle response is critical, both to the diagnosis of HFS
as well as the operation to cure it.9 The LS can be
evoked via percutaneous stimulation of one branch of
the facial nerve while recording stimulus-evoked EMG
from the various muscles of the face innervated by the
facial nerve. In patients with HFS, when one branch of
the facial nerve is electrically stimulated (e.g., zygo-
matic branch), not only do the muscles innervated by
that branch (e.g., orbicularis oculi) display an evoked
EMG response, but other facial muscles (e.g., mentalis)
not innervated by that branch also demonstrate evoked
EMG activity. This paradoxical EMG response can be
evoked in the operating room and consists of a triphasic
EMG potential followed by a series of after-discharge
Table 130-1
DISTINGUISHING FEATURES OF HEMIFACIAL SPASM AND SIMILAR CONDITIONS
Condition
Spasm Location
Spasm Pattern
Spasm Laterality
Pain
Hemifacial spasm
Orbicularis, with
spread to other facial
muscles
Arrhythmic and
intermittent, may
persist during sleep
Unilateral
Usually none
Blepharospasm
Orbicularis, may
spread to the rest of
the face
Symmetrical and
forceful
Bilateral
Usually none, but
may have
photophobia and/or
ocular dysesthesias
Post-paralytic
synkinesis
Anywhere in facial
nerve distribution
Associated with
movement
Usually unilateral
Varies
Facial myokymia
All facial muscles
Movements
exacerbated by
fatigue; fi ne and
continuous
Varies
Usually none
Tics and habit spasms
Usually outside the
facial nerve
distribution
Stereotyped and
simple
Often bilateral
Usually none
Focal seizure activity
Anywhere in facial
nerve distribution
Clonic, gross
movements
Unilateral unless
seizure generalizes
None

Chapter 130
Microvascular Decompression of the Seventh Cranial Nerve 1387
potentials most typically recorded at a latency of 10 to
12 milliseconds. This response is obliterated following
an adequate decompression of the seventh nerve (Fig.
130-1).
Most patients with hemifacial spasm are between
the fourth and sixth decades of life, and are reasonable
candidates for general anesthesia. Nonetheless, all of
these patients require a formal perioperative risk assess-
ment before any operation. Preoperative laboratory
evaluations including electrolytes, complete blood
counts, and coagulation profi les should be assessed.
Electrocardiography and chest roentgenography help
rule out occult cardiovascular disease. It is not necessary
to keep blood products on hold in most cases. Any
patient with a signifi cant cardiac or other medical risk
should have it addressed before craniotomy for MVD.
SURGICAL APPROACH
Patient Positioning and Preparation
The retrosigmoid or retromastoid approach is the stan-
dard surgical approach for MVD of the seventh nerve.
Once anesthetized, the patient is placed in three-point
head fi xation with pins in the ipsilateral frontotemporal
region and the contralateral mastoid. This approach
maximizes access to the mastoid region on the treated
side. When placing the pin fi xation, it is important to
keep the operative side pins anterior to a line running
superiorly from the earlobe. If the pin is placed too far
posteriorly, it will be diffi cult to insert the self-retaining
retractor, because the handles will contact the head
holder. In addition, the squamosal portion of the tem-
poral bone is to be avoided with the fi xation pins,
because this area of the skull is particularly thin and
pinning in this area can lead to an epidural hematoma.
Sixty pounds of pressure is usually adequate for rigid
head fi xation.
After pinning, the patient is rotated with the treated
side up into the lateral decubitus position. All pressure
points are padded, and an axillary roll is placed. The
patient is taped to the table securely at the hip and
underneath the axilla. In addition, the ipsilateral shoul-
der is pulled caudally with care not to stretch the bra-
chial plexus. The neck is gently fl exed and elevated
from the lateral position such that two fi ngerbreadths
are maintained between the chin and the sternum. This
maneuver is designed to minimize the risk of jugular
venous thrombosis. Proper patient positioning is dem-
onstrated in Figure 130-2.
A Doppler monitor should be secured to the ante-
rior chest wall in order to detect the occurrence of air
embolism during venous sinus exposure. While lumbar
cerebrospinal fl uid (CSF) drainage is not routinely
used, we do consider the use of CSF drainage if the
patient is especially young (in which case the posterior
fossa is fuller) or if the operation is a revision procedure
(in which case the cerebellum may be adherent to the
overlying dura). Furthermore, a lumbar drain is of addi-
tional value if the surgeon is less experienced at the
procedure: lumbar drainage creates early cerebellar
relaxation and minimizes the CSF pulsations that can
make microsurgical dissection in this region more
diffi cult.
Figure 130-1. Demonstration of the
“lateral spread” phenomenon as visualized
intraoperatively during an MVD for HFS.

1388
Section 15
Temporal Bone
Intraoperative Monitoring
Intraoperative BAERs are monitored, as are stimulus-
evoked EMG responses from the orbicularis and men-
talis muscle groups in response to stimulation of the
zygomatic branch of the facial nerve. In addition, spon-
taneous EMG from cranial nerves IX and X is recorded
to detect any injury potentials. The anesthesiologist
should use only short-acting muscle relaxation for
induction, thereby allowing for EMG monitoring and
assessment of the presence of a lateral spread response
before incision. The surgeon must ensure that an ade-
quate recording of the lateral spread response is present
before skin incision.
Surgical Exposure
A 3- × 5-cm area behind the ear is shaved. The mastoid
eminence, digastric groove, and inion should be identi-
fi ed externally. The line between the inion and the
external auditory meatus approximates the position of
the transverse sinus. The digastric groove overlies the
sigmoid sinus, and the junction of these two lines
defi nes the transverse-sigmoid junction. A vertical inci-
sion is drawn 3 to 5 cm long, approximately 0.5 cm
medial to the shaved hairline and parallel to it. A stan-
dard preoperative sterile skin preparation is applied.
During draping of the operative fi eld, the patient is
administered 12.5 to 25 g of intravenous mannitol to
facilitate cerebellar relaxation. Skin is opened with a
scalpel. Deeper dissection uses monopolar electrocau-
tery and bipolar sacrifi ce of the occipital artery. The
initial periosteal dissection should always proceed medi-
ally before completing the lateral dissection, because
the lateral periosteum is more loosely attached to the
skull than is the medial periosteum, and the muscle
thickness is greater medially than laterally. If the
surgeon performs the muscle and periosteal dissection
laterally (toward the ear) fi rst, there is usually not
enough tissue resistance to allow the Weitlaner retrac-
tor to force the medial tissue out of the surgical fi eld.
This situation makes visualization of the intracranial
contents more diffi cult. If one should make the mistake
of dissecting laterally fi rst, the problem can be over-
come in two ways: (1) by extending the incision superi-
orly and inferiorly to allow for more tissue mobilization
or (2) by substituting skin hook and spring retractors
for the Weitlaner self-retaining retractor.
Once the muscle and periosteum are mobilized
and retracted, the underlying bony anatomy should be
clearly identifi ed. The mastoid emissary vein, which
often marks the transverse-sigmoid sinus junction, will
almost always be encountered and will need to be fi lled
with wax for adequate hemostasis. The digastric groove
must also be visualized; drilling along its medial border
creates the dural exposure necessary for an adequate
brain stem view.
Following periosteal dissection, the overlying bone
may be removed via a craniectomy or craniotomy. Even
though bone removal can be minimized to only a few
centimeters, the authors prefer bone removal suffi cient
to expose the inferior edge of the transverse-sigmoid
junction and the medial edge of the sigmoid sinus down
to the level of the lower digastric groove. This 4- × 3-cm
ovoid opening provides adequate inferolateral expo-
sure to access the lateral cerebellomedullary cistern
without signifi cant cerebellar retraction. It is necessary
to remove a portion of the posterior mastoid air cells
in order to expose the edge of the sigmoid sinus. All
the air cells are thoroughly waxed in order to avoid a
postoperative CSF leak.10
Before dural opening, the Greenberg brain retrac-
tor system is attached to the three-point head holder in
case fi xed spatulas are required to control unforeseen
intracranial bleeding. The system is not used in the vast
majority of cases. The dura mater is then opened in a
curvilinear fashion and refl ected laterally with 4-0
monofi lament suture. The dural refl ection must lie
immediately parallel to the descending sigmoid sinus
so as to avoid a shelf of dura reducing subsequent lateral
visualization. The medial dural cuff is maintained to
allow for a watertight closure. A 3- × 0.5-cm rubber dam
cottonoid sponge is placed along the lateral aspect of
the cerebellar lobe to begin navigating around the cer-
ebellum (Fig. 130-3).
Nerve Exposure
At this point, the operating microscope with a 325-mm
objective lens is brought into the fi eld. Dissection pro-
ceeds laterally around the edge of the cerebellum
toward the lateral cerebellomedullary cistern, which
contains the 11th cranial nerve. The brain is gently
retracted with a cottonoid sponge. All cottonoids are
moistened with saline and placed over an appropriately
sized (0.5 × 3.0 cm) piece of latex (rubber dam) cut
from a sterile surgical glove. The latex prevents trauma
to the cerebellum and allows for easier advancement of
the cottonoids. A rubber dam cottonoid and Tefl on
pledgets are pictured in Figure 130-4. Whereas we favor
not using a retractor during the case, but rather retract-
Figure 130-2. Proper lateral decubitus positioning for a seventh
nerve decompression. This photograph and all subsequent operative
photographs depict a left-sided operation.

Chapter 130
Microvascular Decompression of the Seventh Cranial Nerve 1389
ing with a controlled sucker (no. 3-4F), a 60-degree
tapered retractor can be placed over the rubber dam
cottonoid against the inferolateral aspect of the cerebel-
lum. Following gentle navigation around the inferolat-
eral cerebellar edge, the petrous dura overlying the
11th cranial nerve is visualized. Safe exposure of this
landmark requires a dynamic dissection process with
intermittent adjustments of both the patient’s position
and the operating microscope. Dissection around the
lateral border of the cerebellum without adequate
adjustment of the patient’s position and/or the micro-
scope’s position may lead to cerebellar injury. This
injury can be profound enough to cause lateral cerebel-
lar infarction and brain herniation.
Beneath the petrous dura, the 11th nerve is visual-
ized. If necessary, a portion of the overlying bone can
be drilled off to facilitate cisternal visualization. The
arachnoid between the nerve and the cerebellar fl oc-
culus is opened with an arachnoid knife. At this point
the operator holds still, patiently allowing CSF egress
and cerebellar relaxation. The working zone of the pos-
terior fossa is markedly increased by this maneuver. In
addition, this maneuver allows for initial inspection of
the lower cranial nerves (CN IX through XI). An overly
superior approach to this cistern exposes the seventh
and eighth nerves prematurely without adequate CSF
drainage. An overly inferior approach to this cistern
leads to the cerebellar tonsils near their termination at
the foramen magnum.
Once CSF is drained and the cerebellum relaxes,
the arachnoid over the lower cranial nerves is opened
sharply with an arachnoid knife and microscissors (Fig.
130-5). The fl occulus of the cerebellum and the choroid
plexus protruding through the foramen of Luschka are
exposed and gently retracted. Retraction at this point
may result in changes in the BAER. If signifi cant BAER
changes occur (i.e., greater than 50% amplitude reduc-
tion or greater than 1 millisecond latency), retraction
should be relaxed and the surgeon should pause until
all responses return to their baseline confi guration.
Additional arachnoid around CN VIII may need to be
cut to reduce transmitted retraction forces from the
cerebellum as it is mobilized medially. It is important
to watch the retractor (if used) or cottonoid frequently
throughout the operative period because it is common
for one of them to move against the lower cranial nerves
and cause potential irreversible damage. Thorough,
sharp arachnoidal dissection helps prevent cranial
nerve injury during this portion of the procedure. In
particular, removal of arachnoidal adhesions around
the eighth nerve minimizes retraction injury to the
cochlear nerve and cochlear nucleus. Any injury poten-
tials are immediately reported to the surgeon during
this critical portion of the dissection.
The facial nerve must be exposed along its entire
course, especially at the brain stem root exit zone, the
most common site of vascular compression. To visualize
the root exit zone, it is important to completely dissect
the fl occulus and choroid plexus from the base of
cranial nerves VIII, IX, and X. Looking toward the
Figure 130-3. Rubber dam cottonoid placed on the lateral cerebel-
lum in preparation for navigation around the cerebellar hemisphere.
Figure 130-4. Patties and pledgets for microvascular decompres-
sion. Tefl on pledgets are visualized superiorly, and a rubber dam
cottonoid inferiorly.
Figure 130-5. Visualization of the ninth (IX), tenth (X), and elev-
enth (XI) cranial nerves following arachnoidal dissection.

1390
Section 15
Temporal Bone
brain stem (achieved by angling the microscope inward
and rotating the patient toward the surgeon), the
surgeon should focus just medial to the ninth and tenth
nerves. It is from this area that the facial nerve arises as
it runs rostrally to follow the course of CN VIII, deep
to it (Fig. 130-6). It is often necessary to work between
CN IX and X and between CN VIII and IX to get the
best view of the brain stem origin of the seventh
nerve.
Microvascular Decompression
The most common vessels compressing the facial nerve
are the posterior inferior cerebellar artery (PICA) and
anterior inferior cerebellar artery (AICA).8,11,12 Because
of the proximity of the PICA origin from the vertebral
artery (VA) to the compression site, the authors often
fi rst decompress the VA from the brain stem before
decompression of PICA from the seventh nerve root
exit zone. The VA is reliably located just medial to CN
XI. The VA is elevated from the brain stem and large
pieces of Tefl on felt are placed between the vessel and
the medulla so as to move the entire vascular complex
laterally. This maneuver shifts the PICA and other VA
perforators away from the brain stem as well as the CN
VII exit zone. Early mobilization shifts PICA distally,
reducing the need for neural tissue retraction during
subsequent decompression. Once the VA is mobilized
laterally, attention is turned to the CN VII root exit
zone. Any arteries compressing this site are mobilized
away from the brain stem and decompressed using
Tefl on pledgets (Fig. 130-7). At this point, the lateral
spreads often begin to change morphology and ampli-
tude or may even suddenly disappear. If they do not
fully disappear, additional arterial sources of compres-
sion are sought. Some may be quite small and may be
considered inconsequential to the spasm; however, by
decompressing them the lateral spreads often com-
pletely resolve. If the spreads remain, a search for veins
contacting the CN VII exit zone is carried out. Often
these veins can also be decompressed from the brain
stem using sharp dissection and small pieces of Tefl on.
In other instances they need to be divided using a
microknife, scissors, or hook. At no time should bipolar
cautery be used in the region of CN VII or the brain
stem; even small energy surges can lead to permanent
CN VII and VIII dysfunction. Hemostasis from divided
veins is readily achieved using gentle Tefl on tampon-
ade. When veins are found and eliminated, it often
takes several minutes for the lateral spreads to com-
pletely disappear or fall to negligible levels. The reason
for this delayed change is not clear; however, it is a reli-
able enough fi nding that the authors will wait several
minutes for the lateral spreads to abate before search-
ing for additional pathology. Such patience eliminates
unnecessary dissection, which puts the cranial nerves
and the brain stem at risk for iatrogenic injury.
Throughout the operation, close communication is
maintained with the neurophysiology team. Any change
in the BAER morphology mandates immediate action,
because the eighth cranial nerve is especially sensitive
to manipulation. If the amplitude drops by more than
50% or if the latency is increased by more than 1 milli-
second, surgical manipulation ceases, and the BAER
should be allowed to return to baseline. In less favor-
able circumstances, the surgeon should always wait until
the latency drops below a 0.5-millisecond delay and the
wave amplitude increases to at least 50% of baseline
before resuming manipulation. Occasionally, the BAER
will change after placement of a Tefl on felt, necessitat-
ing removal. Sudden loss of BAER usually denotes a
vascular injury to CN VIII either from vasospasm or
vessel loss. Small perforator injury can lead to such
changes, especially branches of AICA or the labyrin-
thine artery. Inadvertent spread of bipolar current
can also lead to irreversible injury. The authors
have frequently witnessed improvement of BAER
recordings following irrigation of the eighth nerve with
Figure 130-6. Visualization of the seventh nerve (VII) exiting the
brain stem anterior and deep to the superfi cial eighth nerve (VIII).
A small artery is compressing the nerve at its root exit zone.
Figure 130-7. Adequate decompression of the seventh nerve with
Tefl on pledgets.

Chapter 130
Microvascular Decompression of the Seventh Cranial Nerve 1391
papaverine, implying that improvement of local micro-
circulation can improve nerve function.
The neurophysiology team is essential for success-
ful performance of a microvascular decompression of
the seventh nerve. Accurate intraoperative monitoring
prevents iatrogenic injury. In addition, tracking the
lateral spread of impulses along the seventh nerve can
lead the surgeon to the critical pathology, and lateral
spread obliteration increases the surgeon’s confi dence
that the patient will be cured. In certain cases, decom-
pression of large vessels that appear to be clear culprits
may in fact have no effect on lateral spreads. Further-
more, fi nal decompression of small venules or arteri-
oles can lead to ultimate resolution of abnormal
electrical crosstalk and irritation. Therefore, neuro-
physiology input is critical to both novice and experi-
enced microsurgeons.
Closure
At the conclusion of the decompression procedure,
several Valsalva maneuvers to 40 mm Hg for 10 seconds
are performed to ensure hemostasis. It is important
to be sure the patient is pharmacologically paralyzed
before Valsalva maneuvers are requested. The region is
gently irrigated with warm saline bulb irrigation, and
the dura is closed. Dural closure must be watertight. If
the dura cannot be easily reapproximated, a small piece
of muscle is sewn over the opening to seal off the leak.
Larger defects are closed with a dural graft. Valsalva
maneuvers are again performed to ensure the adequacy
of the dural closure. If there is an inadvertent injury to
a dural venous sinus during closure, then the area of
the injury should be packed with hemostatic agents,
such as Avitene, and allowed to stop spontaneously.
Under no circumstances should such an injury be
directly repaired with suture or vascular clips, which
may worsen such an injury.
After dural closure, the bone edges of the mastoid
air cells are thoroughly waxed once again. A pad of
Gelfoam is placed over the dura to fi ll in any dead
space. Sometimes, fi brin sealant glue can be applied to
the dura as an additional barrier to CSF leakage. A wire
mesh with titanium screws (KLS Martin, Jacksonville,
FL) is fastened to the bony edges to reapproximate the
shape of the skull. Care must be taken to avoid plunging
into the subdural space with a slipped screw while
attaching the cranioplasty plate. The authors have
found that this technique prevents the adhesion of
nuchal muscles to the dura, which may cause chronic
postoperative headaches. The muscles are approxi-
mated with interrupted 2-0 absorbable sutures, and the
fascia is closed in a similar fashion. The subcutaneous
tissue and skin are closed with 3-0 absorbable sutures
and a running 4-0 nylon suture. A sterile bandage is
affi xed with paper tape.
POSTOPERATIVE MANAGEMENT
As with any other patient status postcraniotomy
with intradural manipulation, postoperative cardiac
telemetry and respiratory monitoring is essential. Fol-
lowing a postoperative neurologic examination and a
few hours of surveillance in the postanesthesia care
unit, patients are transferred to the neurologic step-
down unit for overnight observation. Postoperative
hypertension is to be avoided, because it entails an
increased risk of late hemorrhage. The authors use
intravenous short-acting antihypertensive agents (e.g.,
labetalol or hydralazine) to prevent elevation of the
systolic blood pressure above 160 mm Hg for 24 hours.
Postoperative nausea is treated with intravenous ondan-
setron, and other agents are added if necessary. Any
patient with a severe headache undergoes an immedi-
ate non–contrast-enhanced head CT scan to rule out
any postoperative hematoma. Patients with persistent
headache not alleviated by medication and a negative
scan undergo high-volume lumbar puncture. Approxi-
mately 15% to 20% of patients benefi t from this method
of treatment for mild postoperative intracranial hyper-
tension. The cause of the intracranial hypertension is
unclear, but it may be related to blood products and
bone dust within the subarachnoid space, impairing
CSF reabsorption.
Most patients are transferred from the stepdown
unit to a regular fl oor on postoperative day 1. Diet is
advanced, as well as activity. Most patients are ready to
leave the hospital within an average of 3 days. Following
discharge home, all patients are brought back to clinic
within 10 to 14 days of the procedure for a wound
check, neurologic examination, and audiogram. There
is no role for routine postoperative imaging. The major-
ity of patients are spasm-free at the time of discharge;
in addition, patients with residual postoperative spasm
tend to achieve delayed symptom resolution if the intra-
operative decompression was adequate.13-15 Cure rates
generally range from 80% to 90% in experienced
hands.
Complications include CSF leaks, wound infections,
and cranial nerve injuries. Postoperative CSF leaks can
present with rhinorrhea, otorrhea, or leakage directly
through the incision. A lumbar drain with aggressive
CSF drainage can eliminate an early postoperative leak,
but if this therapy fails, then the wound needs to be
revised in the operating room. Wound infections are
uncommon, but they also necessitate operative washout
and wound revision, along with appropriate antibiotics.
Cranial nerve injuries are usually managed expectantly
with two major exceptions: (1) patients with signifi cant
orbicularis weakness may require a gold weight for
corneal protection, and (2) patients with signifi cant
vocal cord dysfunction may require a vocal cord
injection.
MVD of the seventh nerve remains the gold stan-
dard therapy for hemifacial spasm. No other treatment
has comparable long-term results. However, the proce-
dure should not be taken lightly, because the complica-
tions of the operation can be serious. Results are best
in experienced hands. Careful patient selection, metic-
ulous operative technique, and reliable neurophysio-
logic monitoring are the three keys to successful
treatment.

1392
Section 15
Temporal Bone
References
1. Auger RG, Whisnant JP: Hemifacial spasm in Rochester and
Olmsted County, Minnesota, 1960 to 1984. Arch Neurol 47:1233-
1234, 1990.
2. Campbell E, Keedy C: Hemifacial spasm: A note on the etiology
in two cases. J Neurosurg 4:342-247, 1947.
3. Laine E, Nayrac P: Hemispasme facial gueri par intervention sur
la fossa posterieure. Rev Neurol 80:38-40, 1948.
4. Dandy WE: Concerning the cause of trigeminal neuralgia. Am J
Surg 24:447-455, 1934.
5. Gardner WJ: Concerning the mechanism of trigeminal neuralgia
and hemifacial spasm. J Neurosurg 19:947-958, 1962.
6. Gardner WJ, Sava GA: Hemifacial spasm—a reversible patho-
physiologic state. J Neurosurg 19:240-247, 1962.
7. Jannetta PJ, Abbasy M, Maroon JC, et al: Etiology and defi nitive
microsurgical treatment of hemifacial spasm: Operative tech-
niques and results in 47 patients. J Neurosurg 47:321-328, 1977.
8. Barker FG, Jannetta PJ, Bissonette DJ, et al: Microvascular decom-
pression for hemifacial spasm. J Neurosurg 82:201-210, 1995.
9. Moller AR, Jannetta PJ: Monitoring facial EMG responses during
microvascular decompression operations for hemifacial spasm.
J Neurosurg 66:681-685, 1987.
10. McLaughlin MR, Jannetta PJ, Clyde BL, et al: Microvascular
decompression of cranial nerves: Lessons learned after 4400
operations. J Neurosurg 90:1-8, 1999.
11. Fukushima T: Microvascular decompression for hemifacial spasm:
Results in 2870 cases. In Carter LP, Spetzler RF (eds): Neurovas-
cular Surgery. New York, McGraw-Hill, 1995, pp 1133-1145.
12. Huang CI, Chen IH, Lee LS: Microvascular decompression for
hemifacial spasm: Analyses of operative fi ndings and results in
310 patients. Neurosurgery 30:53-56, 1991.
13. Ishikawa M, Nakanishi T, Takamiya Y, Namiki J: Delayed resolu-
tion of residual hemifacial spasm after microvascular decompres-
sion operations. Neurosurgery 49: 847-854, 2001.
14. Gotu Y, Matsushima T, Natori Y, et al: Delayed effects of the
microvascular decompression on hemifacial spasm: A retrospec-
tive study of 131 consecutive operated cases. Neurologic Res
24:296-300, 2002.
15. Shin JC, Chung UH, Kim YC, Park CI: Prospective study of micro-
vascular decompression in hemifacial spasm. Neurosurgery
40:730-735, 1997.
PEARLS
• The preoperative decision to perform an MVD for
HFS is guided by clinical presentation, not by MRI.
• Correct preoperative patient positioning is critical to
adequate exposure of the CN VII-VIII complex and
minimization of brain retraction.
• The copious application of bone wax to the mastoid
air cells both before dural opening and after dural
closure prevents postoperative CSF leaks.
• Following dural opening, navigation around the
cerebellar lobe toward the seventh nerve exit zone is
a dynamic process with multiple adjustments of
both microscope and patient position. Patience and
sharp arachnoidal dissection facilitate safe CSF
egress to minimize retraction injury.
• Entry into the cerebellomedullary cistern (i.e., the
cistern of the 11th nerve) from below with
subsequent dissection upward is the safest way to
identify the eighth nerve (which runs quite
superfi cially) and thus prevent injury to it. Cerebellar
relaxation afforded by this maneuver facilitates
subsequent dissection.
PITFALLS
• Tearing of a venous sinus during dural opening or
closure can lead to signifi cant blood loss, and
hemostasis is diffi cult to obtain in this situation.
• Aggressive retraction of the lateral cerebellar lobe
can lead to a cerebellar infarction postoperatively
and, in rare cases, mass effect upon the brain stem.
• The eighth cranial nerve is extraordinarily sensitive to
manipulation; attempts to adequately decompress
the seventh nerve at the expense of eighth nerve
manipulation rather than extensive arachnoidal
dissection can lead to deafness.
• Attempts to directly coagulate small arterioles or
venules at the root exit zone of the seventh nerve
from the brain stem are prone to causing irreversible
neural injury.
• Failure to keep the hand steady while affi xing the
cranioplasty plate can cause the screw to plunge
into the subdural space, causing signifi cant bleeding
and necessitating redo wound closure.

Chapter 131
Surgery for Vertigo
William A. Wood and Elizabeth H. Toh
Vertigo may result from disorders of both the central
and peripheral vestibular systems. The majority of
patients may be managed conservatively with medical
therapy and vestibular rehabilitation therapy. Critical to
the management of patients with vertigo is the correct
diagnosis of the underlying pathology. Those with
peripheral vestibular disease who have symptoms refrac-
tory to medical management may benefi t from surgery.
Surgical options include those that address the specifi c
pathology of the disease and those that ablate the
peripheral vestibular organ. This chapter describes
operative techniques for posterior semicircular canal
occlusion (PSCO), endolymphatic sac decompression
with or without shunting, labyrinthectomy, vestibular
nerve section, and repair of superior semicircular canal
dehiscence. Repair of perilymph fi stulas is described in
Chapter 119.
PATIENT SELECTION
Several criteria should be met before considering
surgery for vestibular disease. First, a defi nitive diagno-
sis of a unilateral peripheral vestibulopathy should be
made. This can usually be established following a com-
prehensive history, physical examination, and vesti -
bular testing. The latter aids in localizing the site
of pathology and excluding any underlying central
vestibular problems that will impair vestibular com-
pensation following ablative surgery. Bilateral and
central vestibular dysfunctions are contraindications for
ablative surgery such as labyrinthectomy and vestibular
nerve section.
Next, graduated and comprehensive medical man-
agement of the vertigo should be instituted. This should
include a trial of pharmacotherapy and for uncompen-
sated peripheral vestibulopathy, a course of vestibular
rehabilitation therapy. If symptoms persist despite non-
surgical treatment and are disabling, surgical options
may be considered.
Last, the age, comorbidities, and overall physical
condition of the patient should be considered. In
general, central vestibular compensation following
ablative surgery is poorer in older individuals. Persistent
disequilibrium may render that individual more dis-
abled compared with their preoperative condition.
The most common peripheral vestibular disorders
amenable to surgical intervention include benign par-
oxysmal positional vertigo (BPPV), Meniere’s disease,
uncompensated peripheral vestibulopathy, perilymph
fi stula, and superior semicircular canal dehiscence
(SCDS) syndrome.
Benign Paroxysmal Positional Vertigo
The current canalolithiasis theory holds that the patho-
physiology of BPPV likely results from free-fl oating
otoconia within the posterior semicircular canal (PSC).
Intraoperative observations of particulate matter in the
PSC in some patients with BPPV support this hypothe-
sis.1 Positional changes cause movement of the otoconia
within the canal, which in turn produces endolymph
currents that deform the cupula and cause vertigo.
BPPV is usually idiopathic, but may also begin after
head trauma or vestibular neuritis. Patients often com-
plain of sudden, short-lived severe vertigo related to
changes in head position, particularly when going to,
rolling over in, or arising out of bed.
A variant of the theory of pathogenesis of BPPV
holds that these detached crystals adhere to either the
gelatinous cupula of the crista ampullaris (“cupuloli-
thiasis”). A competing theory is that there is loss of
inhibitory input from the damaged otoliths.2 Also, mag-
netic resonance imaging (MRI) of patients with perma-
nent or “atypical” BPPV has shown fractures or fi lling
1393

1394
Section 15
Temporal Bone
defects in the semicircular canals that are not seen in
control subjects.3,4
Particle repositioning is the mainstay of treatment
for BPPV. A recent meta-analysis of nine randomized
controlled trials with a total of 505 patients found that
canalith repositioning is very effective, while noting that
approximately one third of patients experience sponta-
neous resolution within 3 weeks.5 The most recent pub-
lished case series notes that in a practice with more than
3000 patients evaluated and treated for BPPV over a 7-
year period, less than 1% of patients required surgical
intervention.6
For the small subset of patients with intractable and
multiply recurrent BPPV, occlusion of the PSC is offered
(PSCO). Success rates for PSCO, as defi ned by signifi -
cant relief of symptoms, are greater than 90% in most,
if not all, series. Postoperative sequelae commonly
include unsteadiness that may persist for only a few
weeks to more than a year, and occasionally sensorineu-
ral hearing loss (SNHL), which some authors attribute
to comorbidities (e.g., coexisting Meniere’s disease and
previous otologic surgery). Division of the singular
nerve (singular neurectomy) that innervates the PSC is
no longer performed for BPPV. Preoperatively, the
patient should undergo an enhanced MRI scan of the
internal auditory canals to evaluate for the rare pres-
ence of a retrocochlear lesion that may present with
BPPV symptoms.7
Meniere’s Disease
Meniere’s disease is the traditional term for idiopathic
symptomatic endolymphatic hydrops. Some authorities
describe the classic constellation of symptoms—fl uctu-
ating hearing loss, vertigo, a sensation of aural fullness
and/or tinnitus—as Meniere’s syndrome and reserve the
term Meniere’s disease for the idiopathic form, because
the symptom complex may also result from, for example,
an infectious etiology such as syphilis.8 The aural symp-
toms typically make localization self evident for the
patient and physician, but the physician must elicit a
directed and detailed history to narrow the differential
diagnosis. The natural history of the disease varies
greatly. A number of studies report long-term follow-up
that seems to indicate some cases of Meniere’s progres-
sively worsen, whereas others stabilize. A number of
longitudinal studies have noted progression to bilateral
disease in one third or more of patients, increasing as
the disease progresses.
The majority of patients with Meniere’s disease
experience control of vestibular symptoms with medical
treatment alone, although hearing loss generally pro-
gresses with time. This includes a combination of dietary
salt and caffeine restriction, and diuretic therapy
(Dyazide). Other medications used with some success
in Meniere’s disease include vasodilators, histamines,
and steroids. When a 6-month trial of medical therapy
fails to adequately control vertigo attacks, treatment
options include surgery, intratympanic steroid or gen-
tamicin therapy, and use of the Meniett device. The
indications and techniques for intratympanic therapy
are discussed in Chapter 107. All of these invasive treat-
ment options aim to control the vertigo attacks only.
Relief of tinnitus and aural fullness, and hearing stabi-
lization or recovery is not consistently achieved. Surgi-
cal options for Meniere’s disease include endolymphatic
sac surgery, labyrinthectomy, and vestibular nerve
section.
Endolymphatic sac surgery for Meniere’s disease
remains controversial. Surgery theoretically modulates
endolymphatic sac function enough to control vertigo
in approximately 60% of patients. The risk of additional
hearing loss with sac surgery is minimal. Decompres-
sion alone is indicated for Meniere’s disease in an only
hearing ear because the theoretical risk of hearing loss
is less compared with decompression with opening of
the endolymphatic sac for shunt placement. One well-
known randomized controlled trial comparing endo-
lymphatic shunt placement with cortical mastoidectomy
failed to show any therapeutic benefi t of shunt surgery
over mastoidectomy alone.9 Subsequent statistical analy-
ses of the same data set argue that the results support
the effi cacy of the shunt and do not support the placebo
effect claimed by the original authors.10 A subsequent
randomized controlled study performed by Thomsen
and colleagues compared shunt surgery with insertion
of a tympanostomy tube and again failed to demon-
strate any advantage to shunt surgery.11
Vestibular nerve section denervates the vestibular
end organ with a small risk of additional hearing loss.
Vertigo control for Meniere’s disease alone using this
procedure is greater than 90%. There are three surgical
approaches for this procedure: retrolabyrinthine,
middle fossa, and translabyrinthine. The retrolabyrin-
thine approach is the preferred approach for a hearing
ear. The middle fossa approach is reserved for hearing
patients with persistent vertigo following a retrolabyrin-
thine nerve section due to the presence of persistent
vestibular nerve fi bers in the distal internal auditory
canal.
Labyrinthectomy involves surgical removal of the
sensory epithelium of all fi ve vestibular end organs and
results in the loss of input to the central nervous system.
The absence of this input facilitates better central
compensation, as compared to aberrant input from
an improperly functioning organ.12 The procedure is
offered only to patients with unilateral Meniere’s disease
and no useful residual hearing in the affected ear.
Vertigo control is greater than 90%, although all resid-
ual hearing in the operated ear is sacrifi ced. For rare
residual symptoms after labyrinthectomy, translabyrin-
thine vestibular neurectomy can be performed.
Surgery for Uncompensated
Peripheral Vestibulopathy
Uncompensated unilateral peripheral vestibulopathy
causes long-term persistence of disequilibrium and diz-
ziness following a unilateral peripheral vestibular insult.
Most cases result from trauma, Meniere’s disease, and
vestibular neuritis. Despite vestibular rehabilitation
therapy, these patients continue to experience disabling

Chapter 131
Surgery for Vertigo 1395
symptoms. Some patients develop concurrent or subse-
quent BPPV, which can usually be treated successfully
with repositioning.13 For patients with ongoing symp-
toms beyond the inciting episode who do not respond
adequately to medical management and vestibular
rehabilitation, vestibular ablation of the affected ear
should be considered. Treatment options include
chemical ablation with intratympanic gentamicin
therapy, vestibular neurectomy, and labyrinthectomy,
as described for Meniere’s disease.
Surgery for Superior Canal
Dehiscence Syndrome
In 1998, Minor described a new syndrome with vertigo
induced by sound (Tullio’s phenomenon) or aural
pressure (Hennebert’s sign), and computed tomogra-
phy (CT) evidence of dehiscent bone over the superior
semicircular canal (SSC).14 Valsalva maneuvers, sneez-
ing, and other activities that increase intracranial pres-
sure may produce vertigo. Offi ce pneumatic otoscopy
should elicit upward eye movement in the plane of the
SSC. If elicited, this provides suffi cient clinical suspi-
cion to proceed with a high-resolution CT scan of the
temporal bone. Additional testing may include vestibu-
lar evoked myogenic potentials (VEMPs), measured via
contractions of the tonically active sternocleidomastoid
muscle to loud click noises presented in the ipsilateral
ear. Audiometric testing in these patients may show a
conductive hearing loss with intact stapedial refl exes
resulting from an inner ear conductive loss created by
the dehiscent SSC segment behaving as a “third
window.”
Diagnosis of SCDS is confi rmed on high-resolution
CT imaging of the temporal bone in the coronal plane
using a bone algorithm (Fig. 131-1). There is no advan-
tage to additional Stenver and Pöschl views on CT
imaging, which are digitally reformatted in planes per-
pendicular and parallel to the SSC, respectively.15 One
recent retrospective review evaluating radiologic fi nd-
ings alone in more than 400 temporal bone CT scans
found evidence of a dehiscent-appearing SSC in 9% of
studies, indicating a high sensitivity but low specifi city
for imaging in SCDS, given the apparent rarity of the
clinical syndrome.16
Repair of the bony defect over the SSC may be
offered for relief of severe and disabling noise- and
pressure-induced vertigo. The SSC is surgically accessed
through a middle fossa approach. The SSC is either
plugged using a technique analogous to that used for
posterior canal occlusion in BPPV, or the dehiscent
canal is covered with a combination of fascia, bone, and
fi brinogen glue. Minor reported a case series of 20 sur-
gical repairs and found resolution of symptoms in 8 of
9 patients treated with plugging and 9 of 11 patients
treated with capping without plugging.17
PREOPERATIVE PLANNING
Following a complete medical evaluation, the patient’s
vestibular complaints can usually be localized to the
central or peripheral vestibular organs. In the case of
peripheral vestibular disease, when a reasonable trial of
medical therapy fails to control vertigo and the patient
is signifi cantly disabled as a result of ongoing vestibular
symptoms, the options for surgery and chemical abla-
tion of the vestibular labyrinth should be discussed. The
risks, complications, alternatives, and expected results
of each procedure appropriate for the clinical situation
are discussed with the patient.
A gadolinium-enhanced MRI scan of the brain and
internal auditory canals is obtained as part of the initial
diagnostic evaluation to exclude the presence of a
retrocochlear or intracranial tumor. Additional CT
imaging of the temporal bone as described earlier is
obtained if there is clinical suspicion of SCDS. Vestibu-
lar function testing is used to localize the side of
vestibular impairment and diagnose signifi cant bilateral
peripheral vestibular hypofunction or central vestibular
dysfunction. The presence of bilateral or central ves-
tibular dysfunction may signifi cantly impair post -
operative vestibular compensation and should therefore
be taken into consideration when determining candi-
dacy for vestibular ablation. The mobility and quality
of life in older individuals with preexisting disequilib-
rium are severely impacted following any ablative
procedure.
Preoperative hearing assessment is critical in select-
ing the appropriate surgical procedure and approach
for each individual. Functional hearing is typically
defi ned as a pure tone average of 50 dB or better and
a word recognition score of 50% or better. These scores
are used as general guidelines rather than absolute cri-
teria for hearing preservation in vestibular surgery. The
inability to perceive benefi t from conventional amplifi -
cation in the affected ear serves as an indicator of poor
functional hearing in that ear. The hearing status of
the contralateral ear is also assessed preoperatively. If
Figure 131-1. Coronal computed tomography of temporal bone
showing dehiscence of superior semicircular canal (arrow).

1396
Section 15
Temporal Bone
treatment is being offered for an only-hearing ear, con-
servatism is the preferred approach.
SURGICAL APPROACHES
Posterior Semicircular Canal Occlusion
The patient is positioned and prepped as for standard
mastoid surgery. Facial nerve monitoring is not rou-
tinely used. Broad-spectrum antibiotics may be admin-
istered intravenously at induction of general anesthesia.
Through a standard postauricular approach, the
surgeon performs a limited cortical mastoidectomy to
expose the mastoid antrum and lateral semicircular
canal (LSC) in the usual fashion. A saline-soaked
Gelfoam pledget is placed into the aditus ad antrum to
reduce the amount of blood and bone dust that enter
the middle ear space. The PSC lies posterior and per-
pendicular to the LSC. The surgeon uses a small
diamond burr to skeletonize and blue-line the PSC. A
1- × 3-mm oval window of bone over the mid portion of
the PSC is then carefully thinned using a small diamond
burr without violating the membranous labyrinth. The
lumen of the PSC may be occluded using bone wax,18
bone paste (bone dust mixed with fi brinogen glue),19
or soft tissue (Fig. 131-2). The selected material should
be prepared and ready for application before exposure
of the membranous labyrinth. Bone dust and bone wax
are applied to the PSC on the back of a duckbill elevator
(see Video 131-1). Suction should not be applied to the
opened canal because this may disrupt the membra-
nous labyrinth and cause SNHL. After occlusion of the
canal, the PSC defect may be covered with fascia, addi-
tional bone paste, and/or autologous blood. The surgi-
cal site is then closed in a layered fashion as described
in Chapter 115.
Most published reports describe mechanical plug-
ging as the mainstay of PSCO. The CO2 laser may also
be used for ablation of the membranous labyrinth as an
adjunct to mechanical plugging of the PSC.20 Either
technique should prevent circulation of endolymph
within the occluded membranous PSC and relieve the
disabling symptoms of BPPV.
Endolymphatic Sac Decompression or Shunt
The patient is positioned and prepped as for standard
mastoid surgery. Facial nerve monitoring is routinely
used. Perioperative antibiotics are not routinely admin-
istered. A postauricular incision is made approximately
1 to 2 cm posterior to a standard postauricular incision
for mastoid surgery because such an incision may be
used in the future to perform a retrolabyrinthine nerve
section for patients with persistent vertigo following
endolymphatic sac surgery. A complete mastoidectomy
is then performed. The mastoid antrum is entered and
the LSC is identifi ed. The sigmoid sinus is then skele-
tonized down to the proximal jugular bulb (Fig. 131-3).
A saline-soaked Gelfoam pledget is placed into the
aditus ad antrum to reduce the amount of blood and
bone dust that enter the middle ear space.
The endolymphatic sac lies deep to the posterior
fossa bone plate, between the PSC and the sigmoid
sinus. It is consistently inferior to “Donaldson’s line,”
an imaginary line extending posteriorly from the plane
of the LSC. The vertical facial nerve is identifi ed, using
the LSC as a landmark, and skeletonized, as is the PSC,
before opening the retrofacial air cells between the
facial nerve laterally and the posterior fossa plate medi-
ally. The retrolabyrinthine air cell tract over the poste-
rior fossa plate leads to the junction of the PSC and the
posterior fossa dura, and removal of these air cells
expose the operculum of the vestibular aqueduct (Fig.
131-4). Opening the retrofacial air cell tract exposes the
junction of the ampullated limb of the posterior semi-
circular canal and posterior fossa plate overlying the
endolymphatic sac.
A
B
C
D
Figure 131-2. Technique for posterior semicircular canal (PSC).
A, Skeletonization of midportion of PSC using small diamond burr.
B, PSC fenestrated without violating membranous labyrinth. C, Bone
wax, bone paste, or soft tissue is applied to the fenestrated portion of
the PSC using a duckbill elevator. D, The membranous labyrinth
within the PSC is compressed and occluded.
Retrofacial air
cell tract
Posterior
fossa
bone plate
Sigmoid
sinus
Retrolabyrinthine
air cell tract
Figure 131-3. Complete mastoidectomy with skeletonization of the
posterior semicircular canal, retrolabyrinthine and retrofacial air
cells, sigmoid sinus, jugular bulb, and posterior fossa bone plate.

Chapter 131
Surgery for Vertigo 1397
Once the posterior fossa plate has been thinned to
an eggshell thickness from the anterior border of the
sigmoid sinus to the PSC, the thin remaining bone over
the dura is removed using a Freer elevator or a large
diamond burr to widely expose the endolymphatic sac
(Fig. 131-5). The sac appears as a fan-shaped thickening
of the dura spreading out from just deep to the PSC,
posterolaterally toward the sigmoid sinus (Fig. 131-6).
The dura medial to the PSC can be palpated to defi ne
the operculum and endolymphatic duct (Fig. 131-7).
At this point, decompression of the sac is complete
and if shunting is not planned, the surgical wound is
closed in a standard layered fashion. To open the endo-
lymphatic sac, the surgeon carefully incises the lateral
wall of the sac in a radial direction using a Beaver no.
5940 blade from the sigmoid sinus toward the opercu-
lum (Fig. 131-8). The medial and lateral walls of the sac
are bluntly separated using an annulus elevator (Fig.
131-9). To place a shunt, the surgeon inserts a small
piece of 0.005-inch thick silastic sheeting into the lumen
of the sac (Fig. 131-10). The wound is then closed in
the standard layered fashion for mastoid surgery and a
mastoid dressing is applied for 24 hours.
Surgical Labyrinthectomy
For the patient with disabling vertigo or disequilibrium
resulting from a unilateral peripheral vestibulopathy
and with no useful hearing in the affected ear, vestibu-
lar ablation is the treatment of choice. This may be
done chemically using intratympanic gentamicin or sur-
gically through a standard transmastoid approach. The
neurosensory epithelium of the vestibular labyrinth is
systematically and completely removed. This reliably
Operculum of the
vestibular aqueduct
Posterior
fossa dura
Retrolabyrinthine
air cell tract
Figure 131-4. The retrolabyrinthine air cell tract is opened, leading
to the junction of the posterior semicircular canal and the posterior
fossa dura near the operculum of the vestibular aqueduct.
sigmoid sinus
endolymphatic sac
Figure 131-5. The dura of the posterior fossa is widely exposed.
The endolymphatic sac is visible as a thickening of the dura fanning
out from the posterior semicircular canal to the sigmoid sinus.
Figure 131-6. Location of the endolymphatic sac between the
posterior semicircular canal and sigmoid sinus.
Figure 131-7. The dura medial to the posterior semicircular canal
is palpated to defi ne the operculum and endolymphatic duct.
Posterior
semicircular
canal
Retrofacial
air cell tract
Posterior
semicircular canal
Sigmoid
sinus
Endolymphatic
sac

1398
Section 15
Temporal Bone
controls vertigo in most patients, but moderate to severe
postoperative disequilibrium may necessitate a course
of vestibular rehabilitation therapy to facilitate central
vestibular compensation.
A transmastoid labyrinthectomy begins with a com-
plete mastoidectomy through a standard postauricular
incision, with intraoperative facial nerve monitoring.
Perioperative antibiotics are not routinely administered
for this procedure. Once the mastoid antrum is entered
medially, the LSC is identifi ed and drilling is continued
anteriorly into the epitympanum until the body of the
incus is identifi ed. The perilabyrinthine air cells are
carefully removed to expose all three semicircular
canals. The surgeon should identify the course of the
tympanic and mastoid segments of the facial nerve, but
need not skeletonize it.
The semicircular canals are then opened sequen-
tially to maintain surgical orientation of the canals
during the labyrinthectomy. Using a 3-mm cutting burr
and copious suction irrigation, the LSC is fenestrated
superiorly along its entire length, beginning at the
ampullated end and progressing posteriorly toward the
PSC (Fig. 131-11). The inferior wall of the LSC protects
the second genu of the facial nerve and should be left
intact. The PSC is then fenestrated using the same size
drill burr. Dissection is continued inferiorly and anteri-
orly under the facial nerve to expose the ampulla of the
PSC. The inferior wall of the PSC should be left intact
because it protects a high-riding jugular bulb. The PSC
is then followed superiorly to the common crus, which
will lead to the SSC. The SSC lies perpendicular to both
the LSC and the PSC, on a deeper plane, and is care-
fully dissected in a posterior to anterior direction toward
the ampulla (Fig. 131-12). Care is taken not to violate
Figure 131-8. The lateral wall of the endolymphatic sac is
incised.
Figure 131-9. The medial and lateral walls of the endolymphatic
sac are bluntly separated.
Figure 131-10. A silastic shunt is inserted in the lumen of the
endolymphatic sac.
Figure 131-11. The superior wall of the lateral semicircular canal
is removed. The inferior wall is left intact to protect the facial
nerve.
Posterior
semicircular
canal
Superior
semicircular
canal
Lateral
semicircular
canal
Endolymphatic sac shunt
Endolymphatic sac shunt
Endolymphatic sac shunt
Endolymphatic sac opened