Phẫu Thuật Tai Mũi Họng Và Phẫu Thuật Đầu Cổ

Chapter 121
Tumors of the Facial Nerve 1245
diagnosis is based on the interpretation of radiologic
imaging.
The status of the patient’s hearing must also be
considered. It must be anticipated that a patient will
probably lose residual hearing if the tumor erodes into
the otic capsule or is causing retrocochlear hearing loss.
In patients with poor contralateral hearing, removal of
an ipsilateral tumor of the facial nerve should not be
recommended if injury to the cochlear nerve or otic
capsule is likely. In this situation, surgical decom-
pression, stereotactic radiosurgery (SRS), or watchful
waiting is suggested unless the tumor has imminent
potential to create other signifi cant neurologic sequelae.
Similarly, if tumor growth results in severe ipsilateral
sensorineural hearing loss, resection is undertaken and
amplifi cation or cochlear implantation is performed on
the contralateral side.
The physician may be faced with various options
that require careful deliberation regarding the optimal
management of facial nerve tumors. The most straight-
forward situation occurs in a patient with symptoms of
slowly progressive facial paralysis and evidence of synki-
nesis, hemifacial spasm, or a tic developing over a
period of a few weeks to months. Similarly, a patient
with complete facial paralysis in whom Bell’s palsy is
diagnosed and who fails to demonstrate any return of
motor function within 6 months should be presumed
to have a tumor.
Recurrent episodes of Bell’s palsy should also
arouse suspicion of a tumor of the facial nerve, espe-
cially when complete return of function does not occur
and each episode results in subsequent worsening or
permanent dysfunction. Patients often experience
twitching, tics, or fasciculations with concomitant synki-
nesis and mass movement and may complain of eye
symptoms because of an inability to blink or close the
eye. The patient’s facial nerve function grade is
recorded.
The ideal surgical candidate is a patient who has
slowly progressive facial paresis with House-Brackmann
grade III or worse and normal hearing on the contra-
lateral side. Assuming that the patient has no medical
conditions posing unacceptable surgical risks or contra-
indications to a potentially lengthy general anesthetic,
the patient is a candidate for surgical removal of the
tumor. The radiographic size, location, and involve-
ment of nearby structures will dictate the most advanta-
geous surgical approach.
One of the more diffi cult decisions to be made is
recommending treatment of a presumed tumor of the
facial nerve when a patient has normal facial function
or is presenting with subtle facial paresis, synkinesis, or
fasciculations. This situation arises when a patient is
scanned for other symptoms, such as sensorineural
hearing loss, unrelenting pain, pulsatile tinnitus, or
atypical vestibular complaints. If a tumor of the facial
nerve is presumptively diagnosed because of its location
and enhancement characteristics, a comprehensive dis-
cussion of treatment options, risks, and benefi ts should
take place with the patient and family. When the tumor
is small, there is a greater likelihood of complete
removal with anatomic preservation of the facial nerve.
This affords the patient the greatest chance of normal
or nearly normal facial function. A small hemangioma
located in the area of the labyrinthine segment, genicu-
late ganglion, or horizontal segment can frequently be
removed with preservation of the underlying facial
nerve. However, both the patient and the surgeon must
be prepared for the possibility that the tumor has infi l-
trated the facial nerve and requires resection and nerve
grafting. This would obviously result in complete paraly-
sis, which is a marked change requiring psychological
adjustment in view of the fact that minimal dysfunction
was present preoperatively. Larger hemangiomas fi lling
the IAC are more likely to require facial nerve sacrifi ce
and repair.
Thus, patients with normal facial function and a
presumed tumor of the facial nerve must decide whether
they wish to proceed with surgical removal or wait until
facial paresis/paralysis develops. It must be emphasized
to such patients that the longer facial paralysis has been
present, the poorer the outcome after primary nerve
repair. The timing for intervention is infl uenced by the
surgeon’s technical skills and experience in managing
tumors in this site. Special mention should be made of
the rare cystic facial neuroma. Rapid growth of the cyst
can make facial weakness worse or accentuate other
symptoms. A recent publication advocates drainage and
marsupialization of the cyst through a retrosigmoid
approach to manage this subset of patients.15
The surgeon may incidentally discover a primary
tumor of the facial nerve when surgery is being carried
out for other indications. Otologic procedures during
which the horizontal or vertical segments of the facial
nerve may be visualized include exploratory tympanot-
omy, tympanomastoidectomy, and cochlear implanta-
tion. In this situation, the planned procedure should
be completed if the anatomy permits. Rather than
removing the tumor in a patient with normal preopera-
tive facial function, the fi ndings and subsequent evalu-
ation should be discussed once the patient is fully
awake. Although there are rare exceptions to this prin-
ciple, the patient and family should understand the
nature of the pathology and participate in the subse-
quent course of management given the potential for
facial nerve paralysis.
Medium to large primary tumors of the facial nerve
are frequently accompanied by facial weakness. Occa-
sionally, in a patient with normal facial function pre-
operatively, a tumor of the facial nerve is identifi ed
intraoperatively during surgery for a posterior fossa
tumor. In particular, during surgery for an enhancing
IAC and CPA tumor presumed to be an acoustic
neuroma, it may be discovered that the tumor is indeed
a neuroma or, less likely, a hemangioma of the facial
nerve. It is usually well into the tumor removal stage
that the origin of the tissue is clearly identifi ed. Decom-
pression may buy additional time for paralysis to occur,
but once the tumor is partially resected, facial paresis
will probably result. Because facial paralysis is a known
risk and complication of acoustic neuroma surgery, the
surgeon should proceed with tumor removal. In this

1246
Section 14
Facial Nerve
situation, the patient is informed after tumor resection
and reconstruction have been completed. However, if
it can be demonstrated early in the procedure that a
small tumor originates from the facial nerve, decom-
pression of the surrounding bone provides additional
time for less restricted tumor growth. Retrospective
review of the radiologic images may demonstrate fi nd-
ings that in the future would raise suspicion of a primary
facial nerve tumor.
Dissatisfaction with the possibility of worsening
facial weakness after microsurgical resection has led to
a search for treatment alternatives for facial nerve
neuroma. Recent reports in the literature have dis-
cussed the use of SRS for nonacoustic schwannomas,
including facial nerve neuroma. SRS has been well
established as a treatment modality for acoustic neuroma
that affords excellent tumor control with a low rate of
new cranial nerve defi cits. Several publications have
discussed the use of both gamma knife– and linear
accelerator–based radiosurgery to treat nonacoustic
neuromas. Pollock and colleagues reported on the
treatment of 11 patients with either trigeminal or
jugular foramen schwannomas.16 Tumor growth was
controlled in 100% of patients with trigeminal schwanno-
mas and 75% of patients with jugular foramen schwanno-
mas at mean follow-ups of 21 and 10 months, respectively.
None of the patients experienced worsening of cranial
nerve defi cits after treatment. Mabanta and associates
published a series of 18 patients with nonacoustic
schwannomas who were treated with linear accelerator
SRS.17 Two of the 18 patients had a facial neuroma; the
remaining patients had a trigeminal or jugular foramen
tumor. The authors reported a 100% control rate.
Three patients suffered complications, including pro-
gression of preexisting facial weakness, new hearing
loss, and ataxia. However, fi ve patients experienced
improvement in neurologic symptoms. A French series
of nine patients with facial neuroma treated with gamma
knife radiosurgery was published in 2004.18 Follow-up
ranged from 2 to 7 years, during which time no patient
experienced worsening of facial function. Additionally,
two case reports from the Japanese literature discuss the
use of SRS for facial neuroma.19,20
PREOPERATIVE PLANNING
Complete examination of the head and neck with atten-
tion directed to facial nerve function is performed. The
House-Brackmann grading system is used to record the
degree of facial nerve weakness or paralysis. The patient
is instructed to attempt complete and forceful eye
closure. If the patient demonstrates a poor Bell phe-
nomenon and is unable to adequately protect the
cornea, the benefi t of insertion of a gold weight should
be addressed. Various gold weights are temporarily
taped to the upper eyelid to determine whether
improved eye closure and comfort are achieved. If
ectropion is present, a lower lid–tightening procedure
should be planned. The ear is inspected with an operat-
ing microscope. The status of the external auditory
canal, tympanic membrane, and middle ear is noted.
Audiometric analysis will determine the hearing status
of both ears. Identifi cation of ipsilateral conductive
hearing loss suggests that ossicular chain involvement
may require disarticulation and reconstruction and that
the middle ear will require exploration. If poor hearing
is identifi ed in the contralateral ear and it is anticipated
that hearing will be compromised on the side with the
tumor, careful deliberation must be given to the options
of tumor management. In this situation, observation,
radiation therapy, or surgical decompression to provide
more room for tumor growth are all reasonable man-
agement alternatives.
Stapes refl ex testing may be helpful in determining
the site of the lesion. An intact stapes refl ex in the pres-
ence of facial paralysis would indicate facial nerve
involvement in the distal vertical segment or its extra-
temporal course. Vestibular testing does not provide
enough information to alter the treatment strategy.
Preoperative electrophysiologic facial nerve tests
are occasionally helpful. When facial paresis is present,
electroneuronography (ENoG) demonstrates decreased
responses. The ENoG data obtained from patients with
normal facial function or minimal paresis may occasion-
ally be of benefi t. Elicitation of 50% or greater reduc-
tion in the ENoG amplitude provides additional support
demonstrating compromised neural integrity. Patients
with normal facial function and surgeons may be more
willing to entertain surgical excision when objective
verifi cation of facial nerve involvement is established.
However, ENoG is rarely useful when complete facial
paralysis has been present for more than a few weeks.
In the setting of facial paresis or paralysis, facial elec-
tromyography of the peripheral facial muscles may
provide evidence of fi brillation (denervation) and poly-
phasic voluntary motor unit (reinnervation) potentials.
This provides confi rmatory evidence that an ongoing
destructive and reparative process is occurring.
Preoperative diagnosis of a presumed tumor of the
facial nerve depends on radiologic imaging. The
surgeon must carefully review the scans to ensure that
complete data have been compiled. Both contrast-
enhanced CT and MRI are often needed to determine
the extent and size of the lesion, whether the otic
capsule is eroded, and which segments of the facial
nerve are affected. Facial nerve neuromas are prone to
multiple areas of involvement. Imaging will identify
whether the labyrinthine segment of the nerve enhances
or is widened, whether the greater superfi cial petrosal
nerve is involved, and whether middle ear growth has
affected the ossicular chain. The MRI or CT scanning
protocol should extend beneath the skull base to trace
the course of the facial nerve through the parotid. This
information is needed to determine which operative
approach is most appropriate, who should be part of
the surgical team, what surgical and ancillary equip-
ment is necessary (such as facial nerve monitoring),
and whether other autologous tissue is needed for nerve
repair and wound closure. These latter areas include
the neck for a greater auricular nerve graft, the lateral
lower part of the leg for a sural nerve graft, or the
abdomen for a free fat graft.

Chapter 121
Tumors of the Facial Nerve 1247
The appropriate surgical approach is dictated by
the size and location of the tumor and the type and
degree of hearing loss. Although unusual and diffi cult
to diagnose, presumed tumors of the facial nerve iso-
lated to the CPA are removed through a retrosigmoid
craniotomy. The more common location for these
tumors is between the lateral IAC and the vertical
segment of the facial nerve. A middle fossa approach is
necessary for tumors of the facial nerve in the IAC,
labyrinthine segment, and geniculate ganglion areas if
hearing is to be preserved. Tumors confi ned to the
horizontal or vertical fallopian canal are managed by a
transmastoid approach. A combined middle fossa–trans-
mastoid approach is necessary for larger tumors cen-
tered around the geniculate ganglion because access to
the proximal and distal nerve stumps for repair will be
needed. When hearing in the ipsilateral ear is compro-
mised (speech reception threshold >50 dB, discrimina-
tion
<50%), a translabyrinthine or transcochlear
approach permits direct access to the tumor and facili-
tates primary repair of the facial nerve.
Hemangiomas of the facial nerve are, by defi nition,
vascular tumors. However, they rarely achieve suffi cient
size to warrant arteriography and embolization. Never-
theless, blood typing and screening are performed
when an intracranial procedure is planned.
A comprehensive discussion of the natural course
of the tumor and the risks and benefi ts of surgical resec-
tion must take place with the patient and signifi cant
family members. The patient should understand that
temporary or permanent facial paralysis will probably
occur and that subsequent care will be dictated by the
intraoperative management of the tumor. Unilateral
complete hearing loss may result despite undertaking a
hearing preservation approach.
SURGICAL TECHNIQUES
All procedures are performed with the patient under
general endotracheal anesthesia with inhalational and
intravenous narcotic agents. In patients with preopera-
tive facial function, muscle relaxants are avoided to
permit facial nerve monitoring. The patient is placed
in the supine position with the head turned toward the
contralateral ear when undergoing transmastoid, trans-
labyrinthine, middle fossa, or a combined procedure.
The more medial access needed for the retrosigmoid
approach often requires placement of support rolls
beneath the patient’s shoulder and hip to rotate the
patient into a semidecubitus position. A Mayfi eld head
holder and pins are secured to the patient and the table
when a retrosigmoid approach is used (Fig. 121-6A and
B). The upper part of the neck is included in the opera-
tive fi eld to provide access to the greater auricular
nerve. The ipsilateral leg is also prepared and draped
if the tumor is known to be extensive and could require
a longer nerve graft. The left lower quadrant of the
abdomen is prepared for a fat graft when a translaby-
rinthine or middle fossa approach is planned. Periop-
erative antibiotics are given when opening the dura is
anticipated.
Transmastoid Approach
A curvilinear incision is made 1 cm posterior to the
postauricular sulcus through the skin, subcutaneous
tissue, and fi broperiosteal layer over the mastoid cortex.
The periosteum is elevated posteriorly and anteriorly
until the level of the bony external auditory canal is
encountered. Self-retaining retractors are placed, and
a transcortical mastoidectomy is performed. The antrum
and horizontal semicircular canal serve as important
initial surgical landmarks for this approach. The sino-
dural angle is delineated. Bone over the sigmoid sinus
and posterior bony canal wall is thinned to provide the
necessary exposure to the vertical portion of the facial
nerve.
The short process of the incus is identifi ed. It serves
as a helpful landmark for the facial recess, which must
be surgically defi ned. Regardless of whether the tumor
is located in the horizontal or vertical portion of the
facial nerve, the middle ear and mastoid portions are
exposed to obtain access to the margins. The tumor
should be evident at this time. Using continuous suction
A
B
Figure 121-6. A, Positioning of a patient for a retrosigmoid
approach to the posterior fossa. B, Photograph of a patient in a three-
pin Mayfi eld head holder.

1248
Section 14
Facial Nerve
irrigation and diamond burrs, the bone overlying the
facial nerve and tumor is thinned. Access to the hori-
zontal (tympanic) segment of the facial nerve often
requires removal of the incus (Fig. 121-7), which is
accomplished through the facial recess unless the tumor
is so large that it obliterates this space. In this situation,
the ear is returned to its anatomic position and a tym-
panomeatal fl ap is elevated through the ear canal. Bone
from the posterosuperior canal wall is removed by
curette to provide exposure of the incudostapedial
joint. The joint is separated and the incus is removed
(see Chapter 117) (see Video 121-1).
This approach provides access to the facial nerve
from the geniculate ganglion to the stylomastoid
foramen. If additional exposure is necessary at the
proximal horizontal segment of the facial nerve, the
head of the malleus is removed. The eggshell-thinned
bone of the fallopian canal is removed. If the tumor
extends toward the distal aspect of the vertical segment
of the facial nerve, the chorda tympani nerve is sacri-
fi ced and dissection of the facial recess is extended. The
tumor is removed with a 59S Beaver blade by sharply
dividing the tumor from the nerve. Fine spring scissors
facilitate this dissection. If the tumor cannot be sepa-
rated from the nerve, sharp transection is performed to
remove the nerve segment and tumor together (see
Videos 121-2 and 121-3). Frozen section examination is
used to examine the margins of resection and histologi-
cally confi rm complete removal of the tumor. The
nerve is repaired with an interposition graft from the
greater auricular nerve (see the next section, “Greater
Auricular Nerve Graft”). The graft is carefully posi-
tioned in the fallopian canal without tension, between
the remaining segments of the facial nerve. It is diffi cult
and unnecessary to suture the ends together. A small
piece of fascia or fi brin glue may be placed over each
anastomosis to minimize mobility. If the head of the
malleus has not been removed, the incus can be
returned to its anatomic position and supported by
Gelfoam. Absence of the head of the malleus requires
ossicular chain reconstruction by means of an incus
interposition. This procedure is detailed in Chapter
114. If the ear canal was entered for exposure or ossicu-
lar chain reconstruction, the tympanic membrane is
returned to its anatomic position and supported with a
silk sleeve or Gelfoam. The postauricular incision is
closed in the usual fashion, and a sterile dressing is
applied to the mastoid and neck.
Greater Auricular Nerve Graft
Various characteristics of the greater auricular nerve
make it an ideal donor for facial nerve repair. The
nerve is in close proximity to the surgical fi eld. Although
it supplies sensation to the pinna and preauricular area,
sacrifi ce of this nerve leaves only a small area of anes-
thesia. The anatomy of the nerve is relatively constant,
thus providing consistent localization.
Two methods are used for localizing the greater
auricular nerve (Fig. 121-8). Dividing the sternocleido-
mastoid (SCM) muscle into thirds, the nerve is identi-
fi ed at the posterior border of the SCM, between the
upper and the middle thirds. The other method locates
the nerve midway along a line connecting the mastoid
tip and the angle of the mandible. An incision in a skin
crease over this area is taken through subcutaneous
Figure 121-7. A complete mastoidectomy via a facial recess
approach provides exposure of the epitympanum and the vertical
segment of the facial nerve. The incus has been removed to reveal
the tumor. The head of the malleus is intact.
Figure 121-8. Methods for identifying the greater auricular nerve
with pertinent anatomic landmarks. The greater auricular nerve exits
posterior to the sternocleidomastoid muscle at the junction of its
upper and middle thirds. The greater auricular nerve can also be
found midway between the angle of the mandible and the mastoid
tip.

Chapter 121
Tumors of the Facial Nerve 1249
tissue. This may be incorporated with the mastoid inci-
sion or, preferably, through a separate incision. The
greater auricular nerve is found lying lateral to the
SCM, exiting from its posterior surface. Retrograde dis-
section along the nerve by retracting the SCM anteri-
orly permits more proximal harvesting of the nerve
from its origin in the cervical plexus.
Translabyrinthine Approach
A postauricular curvilinear incision is positioned
approximately 3 to 4 cm posterior to the postauricular
crease. A transcortical mastoidectomy is performed as
described previously. Similar to the approach for an
acoustic neuroma, bone posterior to the sigmoid sinus
is removed and the sigmoid sinus is skeletonized. This
facilitates retraction of the posterior fossa dura and
sigmoid sinus. A labyrinthectomy is performed to expose
the IAC. The bone surrounding the IAC and porus is
removed. Tumor extending distal to the labyrinthine
segment is exposed (Fig. 121-9). Involvement of the
horizontal segment may require removal of the head of
the malleus and the incus to get to the distal tumor
margin. The facial nerve is decompressed beyond the
area of enlargement. All drilling should be completed
before opening the dura of the IAC and posterior
fossa.
The posterior fossa and IAC dura are opened. The
labyrinthine segment of the facial nerve is a critical
anatomic landmark in translabyrinthine surgery.
However, it may not be evident when the nerve is
encased by tumor. Its location in the anterosuperior
quadrant of the IAC and medial to the eighth nerve
complex in the CPA is traced proximally and confi rmed
with a nerve stimulator if facial function was present
preoperatively. The vestibular nerves are sharply divided
and sacrifi ced. Tumor that is extrinsic to the nerve
is sharply dissected from the underlying facial nerve.
Hemangioma of the facial nerve is vascular with a gritty
texture because of the bony trabeculations that are
often present in the labyrinthine segment and genicu-
late ganglion areas. Sacrifi ce of the facial nerve is neces-
sary if the tumor cannot be sharply dissected from the
nerve. The tumor is removed and the margins checked
by frozen section examination.
The method of nerve repair depends on the length
of facial nerve graft resected. If a small section of nerve
has been sacrifi ced, primary repair is accomplished by
mobilizing the horizontal and vertical portions of the
facial nerve from the fallopian canal. This posterior
transposition provides 1 to 2 cm of additional length to
perform the anastomosis (Fig. 121-10). The proximal
nerve stump is supported with Gelfoam. Placement of
9-0 or 10-0 nylon suture may be diffi cult near the porus
or CPA. Satisfactory reapproximation with one suture
is suffi cient. Because of the lack of epineurium covering
the proximal facial nerve, a single suture passed through
the diameter of the nerve stabilizes the anastomosis.21
Resection of a larger segment of the facial nerve may
require a cable graft. The greater auricular nerve usually
provides both adequate length and similar diameter to
that of the facial nerve. If there is a noticeable differ-
ence in diameter between the two ends of the nerve
graft, with the proximal end being larger, the distal end
of the nerve graft is sutured to the proximal end of the
Figure 121-9. Translabyrinthine approach to a tumor of the facial
nerve proximal to the geniculate ganglion. An island of bone remains
over the sigmoid sinus. The dura of the internal auditory canal is
intact. The tumor extends from the fundus to the second genu.
Facial nerve
anastomosis
CN IX, X, XI
CN VIII
Brain stem
CN V
Gelfoam
Figure 121-10. Horizontal and vertical segments of the facial nerve
mobilized to permit primary repair of the facial nerve (cranial nerve
[CN] VII). The brain stem, trigeminal nerve (CN V), cochleovestibu-
lar nerves (CN VIII), and lower cranial nerves (CN IX, X, XI) are
demonstrated. Gelfoam supports the proximal nerve for suturing.

1250
Section 14
Facial Nerve
facial nerve to ensure that all graft fascicles at this
anastomosis are present in the distal nerve. The distal
anastomosis is secured with 8-0 nylon suture and
has the additional support of the fallopian canal (Fig.
121-11).
Fat is harvested from the left lower quadrant of the
abdomen. The abdominal wound should be closed over
a Penrose drain. The abdominal fat is soaked in baci-
tracin solution, and the wound is copiously irrigated
with bacitracin solution. Strips of abdominal fat are
placed around the nerve to support the anastomosis.
The remainder of the cavity is fi lled with abdominal fat.
The wound is closed in three-layer fashion, and a sterile
mastoid pressure dressing is applied.
Middle Fossa Approach
Detailed surgical techniques involving the middle fossa
approach are comprehensively described in Chapter
124. The patient is placed in a supine position on the
operating table with the head fully turned toward the
contralateral ear. A preauricular incision begins in a
skin crease anterior and superior to the tragus. The
incision is gently curved to the superior temporal line
to expose the temporal fascia. The skin fl aps are under-
mined posteriorly and anteriorly, and a self-retaining
retractor is placed. A temporalis muscle fl ap pedicled
on its inferior origin is elevated to the level of the zygo-
matic root. A middle fossa temporal craniotomy mea-
suring 4 × 5 cm is created, and the bone fl ap is removed.
The middle fossa dura is elevated from the temporal
bone. It is typically necessary to remove additional bone
inferiorly to a level fl ush with the fl oor of the middle
fossa. When the fl oor of the middle fossa is reached, it
is safer to elevate the dura in a posterior-to-anterior
direction to avoid injury to the greater superfi cial petro-
sal nerve. Hemangiomas of the facial nerve involving
the geniculate ganglion should be evident at this time.
Another important landmark is the arcuate eminence.
Unfortunately, this structure is inconsistently present
and may be confused with other ridges on the fl oor of
the middle fossa. Drilling medially over the meatal
plane toward the superior petrosal sinus is safe and
avoids injury to the otic capsule. Drilling with suction
irrigation is directed inferiorly until the roof of the IAC
is encountered. The underlying periosteum and dura
are left intact until all bone work is completed. The IAC
is demarcated laterally to expose its roof until the laby-
rinthine segment of the facial nerve is identifi ed. Tumor
extending distal to the geniculate ganglion requires
further bony dissection. The tegmen tympani is removed
with caution because of the underlying ossicular chain.
If additional access to the epitympanum and horizontal
facial nerve is needed, a transmastoid approach should
be performed as well. Preoperative imaging should
have prepared the surgeon to anticipate the need for a
combined approach.
Once adequate bone exposure is achieved, the IAC
dura is opened to expose the tumor and proximal facial
nerve (Fig. 121-12). The tumor is sharply dissected from
the underlying facial nerve, if possible. Often during
removal of a hemangioma, a plane can be developed
between the facial nerve and the tumor. Sometimes a
neuroma of the facial nerve, if located eccentrically,
may be excised while continuity of the underlying nerve
is maintained. If the nerve must be sacrifi ced because
of tumor involvement, reconstruction will require a
graft. For this short distance, the greater auricular nerve
is readily accessible and of appropriate length and
diameter.
If there is a minimal weakness of facial nerve func-
tion, decompression of the involved segment of the
nerve is a treatment strategy. The overlying bone of the
Cable graft to
facial nerve
Figure 121-11. Greater auricular nerve interposition cable graft to
the facial nerve from the porus to the distal vertical segment.
Arcuate
eminence
Malleus, incus
GSPN
Figure 121-12. Middle fossa approach to a tumor of the facial
nerve located at the geniculate ganglion. The labyrinthine and proxi-
mal horizontal segments are exposed. GSPN, greater superfi cial
petrosal nerve.

Chapter 121
Tumors of the Facial Nerve 1251
IAC, labyrinthine segment, and geniculate ganglion is
drilled to eggshell thickness and carefully removed.
Despite bleeding that may occur from a hemangioma,
the use of bipolar cautery should be avoided around
the facial nerve.
Proximal anastomosis of the facial nerve is techni-
cally challenging through a middle fossa approach. Size
9-0 or 10-0 nylon suture is secured to the proximal end
of the nerve graft. A single suture is then passed into
the cut end of the proximal facial nerve. The distal end
of the nerve graft is positioned without tension next to
the distal facial nerve. If the tumor is located laterally
in the fundus and geniculate ganglion areas, the greater
auricular nerve graft is placed in a bone trough con-
necting the labyrinthine and proximal horizontal seg-
ments of the fallopian canal. Suturing in this area is
usually unnecessary (Fig. 121-13). Either a free tempo-
ralis muscle graft or a small piece of abdominal fat is
used to plug the IAC to prevent a cerebrospinal fl uid
(CSF) leak.
During closure, attention must be focused on the
tegmen tympani. If it is absent, support is provided by
sagittally splitting the craniotomy bone plate and posi-
tioning a bone segment over the epitympanum. The
dura is tacked with 4-0 Nurolon to the edges of the
craniotomy defect. The craniotomy bone plate is
replaced and secured with 2-0 absorbable suture or
miniplates. The temporalis muscle is returned to its
anatomic position and secured with 2-0 and 3-0 absorb-
able suture. The skin is closed in two layers, and a
compression dressing is applied.
Combined Middle Fossa–Transmastoid
Approach
This approach is used when a tumor of the facial nerve
is proximal to the geniculate ganglion and distal to the
head of the malleus in the horizontal segment of the
nerve. This approach is also undertaken if hearing is to
be preserved. Otherwise, a translabyrinthine approach
is more direct and effi cient. The incision for the com-
bined approach is the standard postauricular one. The
superior limb extends beyond the route of the helix to
the preauricular area. The incision continues anteriorly
and superiorly, parallel to the hairline toward the tem-
poral area. The incision courses superiorly and curves
posteriorly, parallel to the superior temporal line. It
forms the shape of a question mark (Fig. 121-14). The
posteriorly based temporal skin fl ap is retracted with
either suture or large self-retaining retractors. This
combined approach provides additional access to the
horizontal and vertical portions of the facial nerve, as
described in the section “Transmastoid Approach,”
earlier in this chapter.
The choice of donor nerve is dictated by the length
of the resected facial nerve. Usually, the greater auricu-
lar nerve provides adequate length for repair. However,
should a longer segment be needed, a sural nerve is
harvested (see the next section, “Sural Nerve Graft”).
The surrounding areolar and adventitial layers should
be débrided from the end of the nerve graft and the
thin epineurium left for suturing (see Video 121-4).
In this combined approach the tegmen tympani is
removed to expose the tumor and the course of the
facial nerve. As mentioned in the previous section, this
area is repaired with bone taken from the middle fossa
craniotomy plate. Care must be taken to not compress
Figure 121-13. Interposition cable graft repair from the facial
nerve in the distal internal auditory canal to the horizontal
segment.
Figure 121-14. Incision for a combined middle fossa–transmastoid
approach.

1252
Section 14
Facial Nerve
the facial nerve graft or to impede ossicular chain
reconstruction. Again, the IAC must be diligently
packed with fat or muscle to prevent leakage of CSF
from the IAC into the middle ear space. Wound closure
follows as described in the previous section.
Sural Nerve Graft
The sural nerve is a cutaneous sensory nerve that inner-
vates the posterolateral aspect of the foot and back of
the leg (Fig. 121-15). It is identifi ed 2 cm posterior to
the lateral malleolar process and deep to the lesser
saphenous vein. The sural nerve is of greater diameter
than the auricular nerve and has a higher neural popu-
lation. There are two methods for harvesting the nerve.
The fi rst is by multiple stepped transverse incisions over
the posterolateral aspect of the leg and blind dissection
of the nerve with a vein stripper (Fig. 121-16A and B).
The other technique dissects the nerve with a continu-
ous vertical incision. This method creates more postop-
erative morbidity but provides better control of bleeding
and minimizes trauma to the nerve.
Retrosigmoid Approach
It is unusual to preoperatively diagnose a neuroma of
the facial nerve that is isolated to the posterior fossa and
IAC. An enhancing tumor in this area would be most
consistent with an acoustic neuroma. The operative
approach and techniques are detailed in Chapter 124.
Primary anastomosis is not feasible when surgical expo-
sure is limited to the posterior fossa. A translabyrinthine
approach would be required to mobilize the facial nerve
in the temporal bone. Cable nerve grafting in this area
is also technically diffi cult, especially when tumor
extends out to the fundus, and may necessitate a com-
bined transmastoid and retrosigmoid approach.
Stereotactic Radiosurgery
Fractionated external beam radiation therapy has been
the conventional method for radiation treatment.
Newer techniques using a frame-based linear accelera-
tor, gamma radiation from cobalt delivered through a
gamma knife, or electron beam from a mobile linear
accelerator such as the CyberKnife are available for
single or multiple focused treatments (fractions) and
provide millimeter accuracy in delivery of treatment.
We prefer the CyberKnife system for various reasons. It
is a mobile linear accelerator that delivers photon
beams measured in megavolts (Fig. 121-17). It is a frame-
less system that avoids the minor morbidity of placing
a head frame on the patient, thus making it ideal for
fractionated treatment. More important, the system
allows treatment of tumors that extend below the skull
Sural nerve
Lesser
saphenous
vein
Figure 121-15. Landmarks and anatomy of the sural nerve. Note
the relationship to the lesser saphenous vein and lateral malleolus.
B
A
Figure 121-16. A, Surgical exposure for harvesting a sural nerve
graft. B, Closure of incisions with a stair-step approach.

Chapter 121
Tumors of the Facial Nerve 1253
base. The gamma knife system has its fi eld of delivery
limited to the head and skull base.
Both CT and MRI are performed, fused, and dis-
played by overlapping the images. The tumor map is
contoured so that the fi eld of interest is outlined by
using information from both the CT and MRI scans,
although treatment is based on CT confi rmation. The
soft tissue signal from MRI allows the tumor to be out-
lined. The bony anatomy of the temporal bone is also
used to verify the location of the tumor and identify
other important structures to be protected from the full
dose of delivered radiation. These are termed critical
structures. At our institution, this process of contouring
the tumor is done jointly by both the surgeon and the
radiation oncologist. The planned treatment is then
reviewed with the radiation physicist. The tumor is irra-
diated with 18 to 21 Gy to the 80% isodose line in three
fractions. For 18 Gy, each treatment fraction would be
6 Gy given during three sessions delivered every other
day. The dose at the margin of the tumor is usually close
to the prescription dose of 18 to 21 Gy, unless there is
a critical structure immediately adjacent to the tumor.
Minimizing treatment to a critical structure would lower
the dose at the margin of the tumor. The maximum
tumor dose is 22.5 to 26.25 Gy at the 100% dose. A mask
made of Aquaplast is fi t tightly to the patient’s head,
face, and neck to provide immobilization. Each treat-
ment is given for approximately 30 minutes delivered
every other day. No sedation, intravenous fl uids, or hos-
pitalization is necessary.
Conventional external beam radiation therapy may
incur long-term complications such as osteonecrosis,
chronic otitis externa, breakdown of skin, eustachian
tube dysfunction, and the potential development of a
malignant tumor. Acute cranial nerve dysfunction
(hearing loss, imbalance or vertigo, facial paresis, vocal
fold weakness, dysphagia) can occur and may be tran-
sient. The use of focused stereotactic radiation therapy
should minimize these risks.
POSTOPERATIVE MANAGEMENT
Unless medical conditions indicate otherwise, patients
undergoing transmastoid or extratemporal surgery do
not require intensive care management in the postop-
erative period. In contrast, patients undergoing a trans-
labyrinthine, suboccipital, or middle fossa approach
should be observed in an intensive care setting. Neuro-
logic symptoms and potential complications are moni-
tored for 24 hours. The compression dressing is
maintained for 3 days. If an abdominal drain was placed
at the site of a fat graft, it is removed when drainage is
minimal.
Patients are relatively immobilized when a sural
nerve graft is taken. An elastic wrap is left in place for
approximately 1 week. Active ambulation in the imme-
diate postoperative period is uncomfortable and dis-
couraged. Physical therapy consultation and the use of
a walker are most helpful for early rehabilitation.
Sutures or staples are removed 7 to 10 days after
surgery.
Paresis or paralysis of the face is often present post-
operatively. Critical attention is directed toward protec-
tion of the cornea during the recovery period.
Lubrication with artifi cial tears during the day and oint-
ment at night is prescribed. A moisture chamber is also
benefi cial to maintain humidity around the eye. If a
nerve-grafting procedure was undertaken, facial recov-
ery is not anticipated for at least 6 months, depending
on the site of nerve sacrifi ce and repair. The patient is
asked to attempt eye closure while noting the degree of
scleral and corneal show (Fig. 121-18). If eye symptoms
are bothersome and corneal protection is compro-
mised, a gold weight is temporarily affi xed to the upper
lid to determine whether lid closure is facilitated and
irritation is alleviated. A variety of gold weights (0.6 to
Figure 121-17. CyberKnife Robotic Radiosurgery system manufac-
tured by Accuray, Sunnyvale, CA.
Figure 121-18. Left facial paralysis with incomplete eye closure. A
good Bell phenomenon is present, with the lower cornea just
visible.

1254
Section 14
Facial Nerve
1.6 g) are sampled to determine the optimal size (Fig.
121-19). Insertion of the gold weight is subsequently
performed during the hospital stay. Topical tetracaine
hydrochloride (Pontocaine) ophthalmic drops are
placed in the eye. A scleral shield is placed over the
cornea for protection. Intravenous sedation is given,
and a local anesthetic is injected into the upper
eyelid.
The incision in a supratarsal crease is taken through
the skin and orbicularis oculi muscle. Westcott scissors
are used to dissect a plane deep to the orbicularis oculi
muscle and superfi cial to the tarsal plate. A pocket is
created to insert the appropriate size of gold weight, as
determined preoperatively (Fig. 121-20). A 1.2-g gold
weight is well tolerated by most patients. The gold
weight is sutured to the tarsal plate with 8-0 nylon.
The orbicularis oculi muscle is reapproximated with
6-0 Dexon, and the skin is closed with running fast-
absorbing catgut. A 1/8-inch Steri-Strip is applied over
the incision.
Patients not complaining of or demonstrating pre-
operative vestibular symptoms may experience acute
nausea and become vertiginous if the vestibular nerve
has been sacrifi ced or the otic capsule is entered during
the procedure. Supportive care is provided over the
fi rst few days, pending central compensation for the
unilateral vestibular injury.
Patients who are stable and able to ambulate are
discharged within 2 to 6 days postoperatively, depending
on whether an intracranial approach was undertaken.
Hearing is preliminarily assessed by gross measures such
as whispering or using a telephone. Tuning forks are also
useful. If the middle ear was not involved but surgery was
in close proximity to the cochlear nerve or artery or the
otic capsule, an audiogram is obtained while the patient
is in the hospital. If ossicular chain reconstruction was
performed, a formal audiogram is obtained 4 to 6 weeks
after surgery. Sutures are removed from the operative
site 7 to 10 days after surgery.
There are several choices regarding the optimal
radiologic method for monitoring the tumor postoper-
atively. If details regarding the bony anatomy need to
be critically assessed, CT scanning is appropriate. Oth-
erwise, MRI provides important information on soft
tissue densities. Fat suppression techniques will reduce
the signal of adipose tissue and more readily differenti-
ate tumor from a fat graft. A baseline scan is obtained
3 months postoperatively and repeated 1 year later. Any
postoperative changes should be less intense and con-
tracted than on the baseline scan. The schedule for
future scans is based on whether complete tumor
removal was achieved and the fi ndings on the 15-month
postoperative scan.
Hearing status is assessed during the postoperative
period. An audiogram is performed to determine
whether a conductive, sensorineural, or mixed hearing
loss remains. Signifi cant conductive loss can be repaired
electively if the middle ear space was not obliterated
during wound closure. Hearing aid amplifi cation may
also be offered for conductive or sensorineural loss if
word recognition is good.
Return of facial function is monitored over time.
Evidence of reinnervation is initially manifested by an
increase in facial tone and redefi nition of the nasolabial
fold. Recovery may occur within 6 weeks if tumor
removal permitted preservation of the facial nerve.
Facial recovery can take 12 to 15 months if nerve or
cable grafting was performed in the IAC/CPA region.
When return of function is delayed close to one year,
needle electromyographic recordings may demonstrate
polyphasic potentials indicating that reinnervation is
taking place. This reassures both the surgeon and the
patient that more time is needed to observe for ongoing
recovery.
Figure 121-19. A gold weight (1.2 g) is taped to the upper eyelid
to provide complete eye closure.
Figure 121-20. A pocket is created deep to the orbicularis oculi
muscle and superfi cial to the tarsal plate for insertion of a gold
weight.

Chapter 121
Tumors of the Facial Nerve 1255
COMPLICATIONS
Vascular Injury
Intraoperative arterial or venous bleeding should be
readily recognized and managed. The surgeon should
be aware of the anatomic variability of the sigmoid sinus
and jugular bulb. The sigmoid sinus may be located
extremely laterally or anteriorly within the mastoid as
the facial nerve is approached. This applies to any trans-
mastoid procedure. Furthermore, approaches that
require dissection medial to the plane of the vertical
segment of the facial nerve may encounter the jugular
bulb. Constant awareness of this structure will minimize
inadvertent damage. Injury to the sigmoid sinus usually
responds to local compression with Surgicel and neu-
roplasty. The carotid artery should not be subject to
injury with any of the approaches described unless the
cochlea has been extensively eroded by tumor. This
would be evident on preoperative images, and appro-
priate meticulous surgical technique should be used.
During a translabyrinthine or retrosigmoid approach,
the anterior inferior cerebellar artery should be identi-
fi ed and protected. Injury to this vessel results in anacu-
sis, vertigo, facial paralysis, hemiparesis, and possibly
death.
Cerebrospinal Fluid Leak
The potential morbidity of CSF otorrhea, rhinorrhea,
or a cutaneous fi stula is the development of meningitis.
Meningitis is a serious complication that if not recog-
nized and treated early, may prove fatal. High clinical
suspicion for a leak or meningitis is maintained through-
out the postoperative period. The patient is instructed
to avoid straining or sneezing with a closed mouth and
to report any suspicious watery drainage. A leak through
the wound is repaired by placing interrupted sutures
across the dehiscent site. Topical collodion liquid is
another adjunctive method for sealing the incision. A
compression dressing is reapplied. If the wound is not
ballotable and rhinorrhea is present, a subarachnoid
lumbar drain is placed for 3 to 5 days. Drainage is main-
tained at 6 to 10 mL/hr (~150 to 240 mL/day). Almost
all CSF leaks respond to this regimen. Failure to stop
the leak will require re-exploration and possible oblit-
eration of the eustachian tube.
Hearing Loss and Vertigo
Depending on the location of the tumor and the opera-
tive approach used, hearing loss may occur. Complete
sensorineural loss (anacusis) is a known risk rather than
a complication when a tumor is located in the IAC and
CPA. Similarly, if the CT scan demonstrates otic capsule
erosion, there is a greater likelihood of hearing com-
promise. Persistent conductive hearing loss would occur
from unrecognized ossicular chain involvement, unsuc-
cessful ossicular chain reconstruction, or persistent
fl uid in the middle ear space.
Unless there has been ongoing vestibular loss,
sudden sacrifi ce of the vestibular nerves or injury to the
labyrinth results in acute vestibular vertigo. Supportive
measures are provided, and assuming that complete
denervation has occurred, central compensation should
provide return of balance function over the next 6
weeks. Patients experiencing diffi culty in recovery of
balance are referred to a physical therapist trained in
vestibular rehabilitation.
Facial Nerve Repair
Certain principles must be adhered to when facial nerve
repair is undertaken. The ends of the nerve or cable
graft should be sharply freshened before anastomosis.
The proximal end of the facial nerve in the CPA, bathed
in CSF, is not likely to become desiccated. Immediately
after tumor removal, if the facial nerve is resected, iso-
lating plus wrapping the proximal stump in moistened
Gelfoam protects the nerve and eliminates confusion
regarding its true identity when the anastomosis is per-
formed. There should be no tension on the anastomo-
sis. If during a translabyrinthine approach a transposed
nerve is reapproximated, it should be further supported
with the fat used for obliteration and packing. Mono-
fi lament nylon suture (9-0 or 10-0) is used for the proxi-
mal neurorrhaphy when the dural extension or
epineurium is absent. An epineurium-to-epineurium
repair is performed more peripherally with 8-0 suture.
PEARLS
• Up to one half of all patients with primary tumors
of the facial nerve will have normal facial nerve
function.
• Both CT and MRI with gadolinium enhancement
are essential in establishing the diagnosis of primary
tumors of the facial nerve.
• Resection of the nerve and cable grafting are often
required to achieve complete tumor resection, and
the surgeon should always be prepared for this
possibility.
• MRI with fat suppression should be used
postoperatively to evaluate for tumor recurrence.
• Stereotactic radiosurgery appears to be an effective
means of tumor control for facial nerve neuromas
and should be considered in elderly patients,
patients who are higher surgical risks, patients with
good facial nerve function, and those with only one
hearing ear.
PITFALLS
• Patients with a primary tumor of the facial nerve
and good preoperative facial function present a
diffi cult management problem, and consideration
should be given to surgical decompression,
stereotactic radiosurgery, or observation.
• Attempts to resect a tumor of the facial nerve in an
only-hearing ear should be avoided if the tumor
involves the IAC or cochlea.

1256
Section 14
Facial Nerve
7. Fagan PA, Misra SN, Doust B: Facial neuroma of the cerebello-
pontine angle and the internal auditory canal. Laryngoscope
103:442-446, 1993.
8. Isaacson B, Telian SA, McKeever PE, et al: Hemangiomas of the
geniculate ganglion. Otol Neurotol 26:796-802, 2005.
9. Asaoka K, Sawamura Y, Tada M, et al: Hemifacial spasm caused
by a hemangioma at the geniculate ganglion: Case report. Neu-
rosurgery 41:1195-1197, 1997.
10. Friedman O, Neff BA, Willcox TO, et al: Temporal bone heman-
giomas involving the facial nerve. Otol Neurotol 23:760-766,
2002.
11. Martin N, Sterkers O, Nahum H: Haemangioma of the petrous
bone: MRI. Neuroradiology 34:420-422, 1992.
12. Fisch U, Ruttner J: Pathology of intratemporal vascular tumors.
Laryngoscope 91:867-876, 1981.
13. House JW, Brackmann DE: Facial nerve grading system. Otolar-
yngol Head Neck Surg 93:146-147, 1985.
14. Prasad S, Myers EN, Kamerer DB, et al: Neurilemmoma
(schwannoma) of the facial nerve presenting as a parotid mass.
Otolaryngol Head Neck Surg 108:76-79, 1993.
15. Rodrigues SJ, Fagan PA, Biggs ND: Management of cystic facial
neuromas: An alternative approach. Otol Neurotol 25:183-185,
2004.
16. Pollock BE, Kondziolka D, Flickinger JC, et al: Preservation of
cranial nerve function after radiosurgery for nonacoustic
schwannomas. Neurosurgery 33:597-601, 1993.
17. Mabanta SR, Buatti JM, Friedman WA, et al: Linear accelerator
radiosurgery for nonacoustic schwannomas. Int J Radiat Oncol
Biol Phys 43:545-548, 1999.
18. Mdarhri D, Touzani A, Tamura M, et al: [Gamma knife surgery
for VII nerve schwannomas.] Neurochirurgie 50:407-413, 2004.
19. Hasegawa T, Kobayashi T, Kida Y, et al: [Two cases of facial neu-
rinoma successfully treated with gamma knife radiosurgery.] No
Shinkei Geka 27:171-175, 1999.
20. Isono N, Tamura Y, Kuroiwa T, et al: [Combined therapy with
surgery and stereotactic radiosurgery for facial schwannoma:
Case report.] No Shinkei Geka 30:735-739, 2002.
21. Brackmann DE, Hitselberger WE, Robinson JV: Facial nerve
repair in cerebellopontine angle surgery. Ann Otol Rhinol Lar-
yngol 87:772-777, 1978.
• Resection of a hemangioma of the facial nerve may
involve signifi cant bleeding, but use of bipolar
cautery should be avoided near the facial nerve.
• A primary tumor of the facial nerve may be
identifi ed intraoperatively after having been
diagnosed preoperatively as an acoustic neuroma; in
this case, the surgeon should notify the patient’s
family and proceed with tumor resection.
• Failure to plug the IAC with fat or muscle during a
middle fossa approach may lead to CSF rhinorrhea
or otorrhea.
• Tumor may involve a long length of the nerve not
detected by MRI.
References
1. Fisher BJ, Dennis KE: Malignant epithelioid cranial nerve sheath
tumor: Case report of a radiation response. J Neurooncol 78:173-
177, 2006.
2. Selesnick SH, Burt BM: Regional spread of nonneurogenic
tumors to the skull base via the facial nerve. Otol Neurotol
24:326-333, 2003.
3. Suryanarayanan R, Dezso A, Ramsden RT, et al: Metastatic carci-
noma mimicking a facial nerve schwannoma: The role of com-
puterized tomography in diagnosis. J Laryngol Otol 119:1010-1012,
2005.
4. Cawthorne T: Bell’s palsies. Ann Otol Rhinol Laryngol 72:774-
779, 1963.
5. Lipkin AF, Coker NJ, Jenkins HA, et al: Intracranial and intra-
temporal facial neuroma. Otolaryngol Head Neck Surg 96:71-79,
1987.
6. O’Donoghue GM, Brackmann DE, House JW, et al: Neuromas of
the facial nerve. Am J Otol 10:49-54, 1989.

Chapter 122
Facial Nerve Decompression
Yu-Lan Mary Ying and Elizabeth H. Toh
Facial paralysis causes signifi cant functional and aes-
thetic defects that often lead to great psychosocial dis-
tress. The potential causes of acute facial paralysis are
numerous and listed in Table 122-1. This chapter
focuses on management of the most common causes of
facial paralysis that are amenable to surgical decom-
pression, including Bell’s palsy, facial paralysis associ-
ated with acute and chronic otitis media, and facial
paralysis resulting from surgical trauma. Facial paralysis
associated with temporal bone trauma is discussed in
Chapter 128.
The goal of management in patients with facial
paralysis of any etiology is to maximize functional recov-
ery and minimize cosmetic deformity. In an effort to
improve our understanding of neural injury and recov-
ery, Sunderland introduced a histopathophysiologic
classifi cation system for nerve injuries that remains
widely used today.1 Injuries that induce only a conduc-
tion block within the nerve (neuropraxia, fi rst-degree
injury) do not disrupt axoplasmic continuity, and neural
discharges can still be conducted if an electrically
evoked stimulus is presented distal to the conduction
block. The gross nerve structure remains intact. Second-
degree injury involves axonal disruption (axonotmesis),
without disruption of surrounding Schwann cell and
neural connective tissue integrity. Full recovery usually
occurs with the fi rst two degrees of injury. Third- and
fourth-degree injuries involve damage to the endoneu-
rium and perineurium, respectively. The most severe
forms of injury are characterized by complete neural
tube disruption (neurotmesis, fi fth-degree injury). In
second- to fi fth-degree injuries, the facial nerve under-
goes distal wallerian degeneration. As a result, these
nerves are not able to propagate electrically generated
evoked potentials distal to the site of injury.
During recovery, if the axon regenerates through
an intact neural tubule, complete return of motor func-
tion occurs without synkinesis. However, any violation
of the neural support structures (endoneurium, peri-
neurium, and epineurium) will result in misdirection
of the regenerating neural fi bers and cause synkinesis
and incomplete motor recovery. When complete paral-
ysis is due to either anatomic discontinuity or irrevers-
ible neural degeneration, the facial nerve requires
repair or decompression for the most optimal func-
tional and aesthetic results. Nonetheless, with com-
pletely severed nerves, some residual weakness and
synkinesis are to be expected, even with the best surgi-
cal outcomes.
PATIENT SELECTION
Electrical Testing
Electrical testing constitutes the primary diagnostic
modality for surgical decision making in patients with
facial paralysis. Surgical management of a patient with
facial paralysis is based on the premise that decompres-
sion or repair of the injured nerve will lead to better
long-term functional outcomes than is the case with
spontaneous recovery in a conservatively managed
patient. Several electrical tests are available to evaluate
the status of the facial nerve, estimate the severity of
nerve injury, and prognosticate spontaneous recovery.
Because most injuries to the facial nerve affect the intra-
temporal portion of the nerve, which is not usually
readily accessible for evaluation, assessment of injury is
based on measuring downfi eld potentials in the degen-
erating distal nerve. The extent and rate of progression
of wallerian degeneration after injury are used as rela-
tive indicators of the severity of neural injury. Rapid
wallerian degeneration is associated with neurotmesis,
whereas nerves that degenerate more slowly are more
likely to exhibit axonotmesis. The two most reliable and
objective electrical tests for facial nerve assessment are
electroneuronography (ENoG) and facial muscle elec-
tromyography (EMG). Because complete or nearly
complete recovery is to be expected with incomplete
1257

1258
Section 14
Facial Nerve
Table 122-1
DIFFERENTIAL DIAGNOSIS OF FACIAL PARALYSIS
Birth
Traumatic vaginal delivery
Myotonic dystrophy
Möbius’ syndrome (facial diplegia associated with other
cranial nerve defi cits)
Traumatic
Cortical injuries
Basilar skull fractures
Brain stem injuries
Penetrating injury to the middle ear
Facial injuries
Barotrauma
Neurologic
Opercular syndrome (cortical lesion in the facial motor
area)
Millard-Gubler syndrome (abducens palsy with
contralateral hemiplegia because of a lesion in the base
of the pons involving the corticospinal tract)
Infectious
Malignant otitis externa
Acute or chronic otitis media
Cholesteatoma
Meningitis
Parotitis
Chickenpox
Herpes zoster oticus (Ramsay Hunt syndrome)
Encephalitis
Poliomyelitis (type I)
Mumps
Mononucleosis
Leprosy
Human immunodefi ciency virus and acquired
immunodefi ciency syndrome
Infl uenza
Coxsackievirus
Malaria
Syphilis
Tuberculosis
Botulism
Mucormycosis
Lyme disease
Genetic and Metabolic
Diabetes mellitus
Hyperthyroidism
Pregnancy
Alcoholic neuropathy
Bulbopontine paralysis
Oculopharyngeal muscular dystrophy
Neoplastic
Facial nerve neuroma
Facial nerve hemangioma
Vestibular schwannoma
Glomus jugulare tumor
Meningioma
von Recklinghausen’s disease
Cholesterol granuloma
Carcinoma (invasive or metastatic from the breast, kidney,
lung, stomach, larynx, prostate, or thyroid)
Toxic
Thalidomide (Miehlke’s syndrome: involvement of cranial
nerves VI and VII with atretic external ears)
Tetanus
Diphtheria
Carbon monoxide
Lead intoxication
Iatrogenic
Mandibular block anesthesia
Antitetanus serum
Vaccine treatment of rabies
Otologic, skull base, and parotid surgery
Embolization
Idiopathic
Bell’s palsy
Melkersson-Rosenthal syndrome (recurrent facial palsy,
furrowed tongue, fasciolabial edema)
Hereditary hypertrophic neuropathy (Charcot-Marie-Tooth
disease, Dejerine-Sottas disease)
Autoimmune syndromes of temporal arteritis, periarteritis
nodosa, and other vasculitides
Guillain-Barré syndrome (ascending paralysis)
Multiple sclerosis
Myasthenia gravis
Sarcoidosis (Heerfordt’s syndrome, uveoparotid fever)
Wegener’s granulomatosis
Eosinophilic granuloma
Amyloidosis
Hyperostoses (e.g., Paget’s disease, osteopetrosis)
Kawasaki disease (infantile acute febrile mucocutaneous
lymph node syndrome)
Vascular
Benign intracranial hypertension
Intratemporal aneurysm of the internal carotid artery
Data modifi ed from May M: Differential diagnosis by history, physical fi ndings and laboratory results. In May M (ed): The Facial Nerve.
New York, Thieme-Stratton, 1986.
facial paralysis, electrical testing is of value only in
assessing a patient with complete facial paralysis.
ENoG measures facial motor activity in response to
a suprathreshold electrical stimulus applied to the facial
nerve distal to the site of injury. Compound muscle
action potentials are measured with surface electrodes
placed in the nasolabial fold. The amplitudes of com-
pound muscle action potentials elicited on the normal
and involved sides are compared. In the fi rst 3 days after
the onset of complete facial paralysis, the distal facial
nerve will continue to stimulate normally until wallerian
degeneration occurs. ENoG testing is therefore delayed
until at least 3 days after the onset of acute facial paraly-
sis and continued every second or third day until day
14. Reduction of the ENoG response relative to the
unaffected side correlates with the degree of facial

Chapter 122
Facial Nerve Decompression 1259
muscle denervation, which in turn refl ects the extent
of neural degeneration on the paralyzed side. Because
severe neural degeneration is associated with poor
functional recovery, surgical decompression is offered
when ENoG testing indicates greater than a 90%
decrease in function on the affected side versus the
normal side.
EMG with needle electrodes placed within the facial
musculature measures spontaneous and voluntary elec-
trical activity in the facial muscles. It is useful for assess-
ing the presence and extent of muscle denervation and
reinnervation. EMG testing is a necessary adjunct to the
interpretation of ENoG results if surgical decompres-
sion is being considered. Deblocking of the regenerat-
ing nerve fi bers results in asynchronous fi ring of
electrical potentials and therefore the absence of mea-
surable compound action potentials on ENoG testing
with skin surface electrodes. Because voluntary motor
unit action potentials measured on needle EMG testing
do not require synchronous electrical activity, they may
be detected early in the recovery of facial nerve func-
tion and indicate a favorable prognosis. In addition,
polyphasic action potentials on voluntary facial muscle
contraction indicate muscle reinnervation and may
precede clinical signs of recovery by 6 to 12 weeks.
Spontaneous fi brillation potentials detected 2 to 3
weeks after injury indicate signifi cant muscle denerva-
tion and poor recovery.
Bell’s Palsy
Bell’s palsy, by far the most common cause of acute
facial paralysis, accounts for approximately 70% of
cases.2 There is enough evidence to support the concept
that the facial paralysis associated with Bell’s palsy is the
result of an infl ammatory response to herpes simplex
virus type 1 that induces edema and vascular compro-
mise, which results in functional impairment.3,4 This
entrapment neuropathy is believed to occur in the laby-
rinthine segment of the facial nerve, where the fallo-
pian canal is narrowest in diameter.
Unilateral facial paralysis affecting all branches of
the nerve begins suddenly over the course of 24 to 48
hours and may progress to complete paralysis within 3
to 7 days. Symptoms may be preceded by otalgia on the
affected side. With the exception of facial dysfunction
and, rarely, an erythematous chorda tympani nerve, no
other abnormalities are typically detected on clinical
examination of these patients. Hearing and balance are
not affected. Progressive loss of facial function beyond
2 weeks, absence of recovery by 4 months, fl uctuating
function, ipsilateral recurrence, and the presence of
facial twitching should alert the physician to the possi-
ble presence of an underlying tumor and prompt early
imaging of the facial nerve. Bell’s palsy may recur in up
to 15% of patients, although it more commonly occurs
on the contralateral side.
Sixty-fi ve percent to 85% of these patients regain
good facial function with medical treatment alone con-
sisting of systemic steroids with or without antiviral
therapy. The prognosis for satisfactory recovery of
women in whom Bell’s palsy with complete facial paraly-
sis develops during pregnancy is signifi cantly worse.5
Facial movement usually begins in these patients
approximately 3 weeks after onset of the paralysis. Per-
manent residual weakness or secondary abnormalities,
such as synkinesis or facial spasm, occur in 15% to 35%
of patients. In patients with electrical tests indicating
severe neural degeneration, surgical decompression
may offer improved recovery of facial function. In a
multicenter prospective clinical trial involving individu-
als with Bell’s palsy who had 90% or greater degenera-
tion on ENoG testing within the fi rst 14 days of onset
of complete paralysis and absence of motor unit poten-
tials on voluntary EMG testing, surgical decompression
of the facial nerve at the meatal foramen, labyrinthine
segment, and geniculate ganglion resulted in a 91%
chance of good outcome 7 months after paralysis as
opposed to a 42% chance of good recovery in patients
with the same ENoG and EMG parameters who were
treated with steroids only.6 The results of this study
suggest that surgical decompression of the labyrinthine
facial nerve may be benefi cial for a select group of
patients with Bell’s palsy who meet electrical test criteria
for unfavorable recovery. However, some controversy
remains regarding the benefi t of surgical decompres-
sion for these patients.7
All patients seen within the fi rst 2 weeks after the
onset of acute facial paralysis should be treated with
systemic steroid therapy (prednisone, 1 mg/kg/day for
10 days with an additional 5-day taper). Additionally, a
10-day course of antiviral therapy may be prescribed
(acyclovir, 800 mg fi ve times a day, famciclovir, 500 mg
three times a day, or valacyclovir, 1 g two times a day).8,9
Antiviral therapy should preferably be commenced
within 72 hours of the onset of symptoms.10,11 With the
exception of protective eye care, no additional treat-
ment is necessary for patients with incomplete paralysis.
Those who progress to complete paralysis should
undergo electrical testing beginning 3 days after com-
plete loss of clinical function. If ENoG testing indicates
greater than 90% degeneration within the fi rst 2 weeks
after the onset of paralysis, the patient has a 50% chance
of residual facial weakness and synkinesis. Surgical
decompression may be offered to these patients if addi-
tional EMG testing fails to reveal any evidence of neural
regeneration.
Herpes Zoster Oticus
Herpes zoster oticus (Ramsay Hunt syndrome) is a syn-
drome of acute peripheral facial paralysis associated
with otalgia and varicelliform lesions of the auricle and
external auditory canal. It is distinguished from Bell’s
palsy by the characteristic viral eruptions, a higher inci-
dence of associated cochlear and vestibular dysfunc-
tion, and a poorer prognosis for recovery of facial
function. Primary treatment of herpes zoster oticus is
antiviral agents such as acyclovir or famciclovir and
high-dose systemic corticosteroids. Unlike Bell’s palsy,
there is no literature to support surgical decompression
of the facial nerve in these patients.

1260
Section 14
Facial Nerve
Acute Facial Paralysis Resulting from
Surgical Trauma
Traumatic injuries to the facial nerve from temporal
bone fractures, penetrating trauma, and iatrogenic
injury represent the second most common cause of
facial paralysis. The facial nerve is at risk for injury
during surgery on the parotid gland, temporal bone,
and cerebellopontine angle. Complications from
parotid gland or temporomandibular joint surgery can
result in injuries that affect the facial nerve from the
stylomastoid foramen to the facial musculature. In the
cerebellopontine angle, facial nerve disruption gener-
ally results during removal of an acoustic neuroma. The
lack of a tough epineural sheath and anatomic distor-
tion by the tumor make the nerve particularly prone to
injury in this site.12
Within the temporal bone, iatrogenic injuries to
the facial nerve occur most commonly during middle
ear and mastoid surgery. The incidence of unexpected
injury to the facial nerve as a result of an operative
procedure is highest during surgery for chronic otitis
media with or without cholesteatoma, and such injury
occurs in up to 2% to 4% of cases. In surgery for chronic
ear conditions, the facial nerve is most vulnerable to
injury at three sites: the tympanic segment, the second
genu, and the mastoid segment. The facial nerve is
especially vulnerable in the tympanic segment because
the fallopian canal is naturally dehiscent at this site in
up to 30% of individuals.13 Furthermore, this site is fre-
quently involved with granulation tissue or cholestea-
toma, which can cause erosion of the fallopian canal. If
the fallopian canal is dehiscent or eroded, dissection of
diseased mucosa or cholesteatoma from the nerve
sheath can injure the nerve. The tympanic segment of
the facial nerve is also at risk for injury caused by drill-
ing, especially during removal of the posterior canal
wall in a canal wall down mastoidectomy. The vertical
portion of the facial nerve can be injured during drill-
ing of the mastoid when the posterior canal wall is taken
down, when the facial recess is opened, or when the
retrofacial air cell tracts are opened. The key to avoid-
ing iatrogenic injuries in temporal bone surgery is thor-
ough knowledge of facial nerve anatomy within the
temporal bone.14
Iatrogenic facial nerve trauma is best prevented by
acquiring a thorough understanding of the course of
the nerve through the temporal bone and by clearly
identifying landmarks within the middle ear and
mastoid that relate closely to the nerve. Injuries to the
facial nerve detected at the time of surgery should be
addressed immediately whenever possible. Surgical
decompression of the fallopian canal 1 cm proximal
and distal to the site of an injury is usually adequate if
the nerve is intact but contused. The epineurium may
be incised if the nerve is signifi cantly edematous or
contused. By contrast, if more than 50% of the nerve
has been transected, repair by primary neurorrhaphy
or interposition grafting is warranted. If facial nerve
paralysis is unexpected and noted immediately in the
recovery room, any packing in the ear should be
removed, and the patient should be observed for 2
hours to allow any effect of the lidocaine used during
the procedure to dissipate. Operative trauma to the
facial nerve must be suspected if the facial paralysis
persists. Neural integrity can also be confi rmed by the
presence of voluntary motor unit action potentials on
needle EMG testing in the immediate postoperative
period. Surgery to explore and repair the facial nerve
should be arranged within 24 to 48 hours. Delayed
facial paralysis may also occur after mastoid surgery and
is generally a result of neural edema and secondary
entrapment neuropathy after mild manipulation of the
facial nerve in a dehiscent segment. Packing should be
removed from the mastoid and ear canal, and serial
ENoG testing should be performed to detect any signifi -
cant neural degeneration. All patients with facial paraly-
sis resulting from surgical trauma should be treated
with high-dose systemic corticosteroids (prednisone,
1 mg/kg/day for 10 days with an additional 5-day
taper).
Acute Facial Paralysis Associated with Acute
and Chronic Otitis Media
Facial paralysis associated with acute suppurative otitis
media is typical in children or young adults who have
clinical signs and symptoms of a middle ear abscess.
The facial paralysis usually progresses rapidly over a
period of 2 to 3 days and is associated with the acute
onset of otalgia and otorrhea. The pathophysiology
appears to be related to the presence of natural bony
dehiscences in the fallopian canal along the tympanic
segment of the facial nerve that allow infl ammatory
products to produce infl ammation and edema of the
nerve.
Management of facial paralysis associated with
acute otitis media should be aggressive. Myringotomy is
performed immediately to drain the purulent exudate
and to obtain material for culture and sensitivity testing.
A ventilation tube is placed to maintain aeration of the
middle ear. Intravenous broad-spectrum antibiotics are
begun empirically and may be modifi ed when the
results of the culture and sensitivity testing are available.
Topical antibiotic otic drops are started, and daily aspi-
ration of the middle ear is performed. Corticosteroids
(prednisone, 1 mg/kg/day) are prescribed for 10 days.
If computed tomography (CT) of the temporal bone
reveals coalescent mastoiditis or intracranial extension
of the infection, a cortical mastoidectomy should be
performed. Patients with intracranial complications
should be managed in consultation with the neurosur-
gical service. The prognosis for recovery of function in
those with facial paralysis secondary to acute otitis
media is good without surgical decompression.15
In chronic otitis media, facial nerve paralysis is most
commonly associated with cholesteatoma or chronic
infl ammatory granulation tissue involving the tympanic
and vertical segments of the facial nerve.16 As with acute
otitis media, facial nerve dysfunction may be caused by
infl ammation, edema, and subsequent entrapment
neuropathy. Alternatively, extraneural and intraneural

Chapter 122
Facial Nerve Decompression 1261
compression may also result from an enlarging choles-
teatoma or abscess. Chronic otitis media complicated
by facial paralysis is usually managed surgically. Removal
of cholesteatoma, with or without surgical decompres-
sion of the affected facial nerve segment, intravenous
antibiotics, and corticosteroid therapy usually result in
favorable functional recovery. Patients with chronic
suppurative otitis media without cholesteatoma appear
to have a better functional outcome than do those with
cholesteatoma.17 The prognosis for recovery of facial
function in these patients is related to the time of
intervention.18
Acute Facial Paralysis Associated
with Tumors
The most common neoplasms causing facial paralysis
are malignant tumors of the parotid gland. Facial nerve
neuroma, acoustic neuroma, and primary brain tumors
are less common causes of facial paralysis. Surgical man-
agement is dictated by tumor pathology and is described
in detail in other chapters of this textbook.
PREOPERATIVE PLANNING
Electrical tests, including ENoG and EMG, are used to
determine surgical candidacy when no clinical function
is observed. General guidelines for offering surgical
decompression include 10% or less muscle function on
the affected side versus the normal side as determined
by ENoG performed between days 3 and 14 after the
onset of complete facial paralysis, along with the absence
of motor unit action potentials on EMG testing.
High-resolution axial and coronal CT scanning of
the temporal bone using a bone algorithm should be
performed if surgery is planned. This is of particular
value in patients with facial paralysis resulting from
otitis media and trauma. CT enables the surgeon to
localize the site of pathology preoperatively. Magnetic
resonance imaging will demonstrate enhancement of
the labyrinthine facial nerve in all cases of Bell’s palsy
but is not routinely performed before surgical decom-
pression unless there is clinical suspicion of underlying
neoplastic disease.
Audiometric testing should be performed in all
cases of facial nerve paralysis to detect any associated
hearing loss, which may aid in the diagnosis, especially
of any injury to the cochlea, and help dictate the surgi-
cal approach. It also provides a baseline for monitoring
recovery in the postoperative period.
Determination of which regions of the facial nerve
require exploration and the approach to be used is
based primarily on the cause of the facial paralysis and
the expected site of injury. In Bell’s palsy, the labyrin-
thine segment and perigeniculate region are decom-
pressed via a middle fossa approach. In facial paralysis
caused by acute or chronic otitis media, the mastoid
and tympanic segments are explored, depending on
the site and extent of disease. Canal wall down mastoid-
ectomy may be required to properly exteriorize a cho-
lesteatoma involving the facial nerve. Surgery for facial
paralysis secondary to intraoperative injury is directed
at the site of surgical injury.
Lubrication and protection of the affected eye
should be instituted at the time of initial diagnosis and
continued until adequate eye closure is achieved. An
ophthalmologic opinion should be obtained if expo-
sure keratitis is present.
SURGICAL APPROACHES
Selection of the surgical approach is determined by the
location of the facial nerve injury and hearing status in
the affected ear (Fig. 122-1).
Transmastoid Approach
This approach is used when facial nerve injury is limited
to the tympanic and mastoid segments of the intratem-
poral facial nerve. The mastoid cortex is exposed
through a standard postauricular incision and soft
tissue dissection as described in Chapter 115. A com-
plete mastoidectomy is performed until the mastoid
antrum is entered medially. The lateral semicircular
canal is identifi ed and bone dissection is continued
anterosuperiorly to expose the body of the incus in the
epitympanum. Great care should be taken to avoid
inadvertently drilling on the ossicular chain and violat-
ing the tegmen when drilling in the epitympanum.
The mastoid segment of the facial nerve is identi-
fi ed by two important surgical landmarks: the lateral
semicircular canal superiorly and the digastric ridge
inferiorly (Fig. 122-2). The lateral semicircular canal is
the most important landmark for the facial nerve
because it defi nes both the anteroposterior and the
mediolateral location of the facial nerve at the second
genu. As the digastric ridge is followed anteriorly, the
underlying fascia spirals to form the sheath of the facial
nerve at the stylomastoid foramen. Thus, the course of
the mastoid segment of the facial nerve can be pre-
dicted by visualizing a line connecting the lateral semi-
circular canal and the anterior aspect of the digastric
ridge.
ANTERIOR
Geniculate ganglion
Mastoid segment
of facial nerve
MEDIAL
Labyrinthine
segment of
facial nerve
LATERAL
POSTERIOR
Figure 122-1. Anatomic course of the facial nerve.

1262
Section 14
Facial Nerve
Once the course of the mastoid segment of the
facial nerve is identifi ed, the facial recess is opened with
1- to 3-mm diamond burrs (Fig. 122-3). Drilling should
be carried out parallel to the course of the nerve with
the use of copious irrigation to minimize the risk of
thermal injury to the nerve. A narrow bridge of bone is
preserved along the inferior border of the fossa incudis
to protect the incus. Bone is removed over the lateral
surface of the facial nerve until a thin shell of bone
remains. Inferior and lateral exposure of the facial
recess is limited by the chorda tympani nerve. Anterior
and slightly medial to the facial nerve, additional bone
removal is often necessary to maximize exposure within
the facial recess.
At this point, exposure of the facial nerve is suffi -
cient to allow decompression of the mastoid segment,
second genu, and distal tympanic segment. Decompres-
sion begins by exposing the thick periosteum of the
stylomastoid foramen with a 2- to 2.5-mm diamond burr
while leaving the thick fi brous sheath around the facial
nerve intact in this location. The circumference of the
facial nerve should be exposed for 180 degrees along
its posterior and superior surface, between the lateral
semicircular canal and the stylomastoid foramen
(Fig. 122-4).
A small diamond drill burr is then used to decom-
press the second genu and distal tympanic segment of
the facial nerve by rotating the diamond burr from the
posterior surface of the nerve to the lateral and antero-
lateral surface of the nerve. This maneuver, called barber
poling, prevents fenestration of the lateral semicircular
canal (Fig. 122-5).
Depending on the position of the incus, the distal
tympanic segment and second genu of the facial nerve
may be decompressed with a microdrill and microcu-
rette while leaving the incus intact in some individuals
(Fig. 122-6). If the relative proximity of the incus to the
fallopian canal does not allow safe dissection of the
nerve, the incus should be removed for exposure and
replaced at the completion of the procedure.
The ability to expose the perigeniculate region via
the transmastoid approach depends on the position of
Facial nerve
Digastric
ridge
Digastric
muscular
insertion
Fossa
incudis
Lateral
semicircular
canal
Posterior
semicircular
canal
Figure 122-2. Surgical landmarks for the mastoid segment of the
facial nerve.
Figure 122-3. The facial recess is opened.
Figure 122-4. The mastoid segment of the facial nerve is
decompressed.
Figure 122-5. The second genu and distal tympanic segment of the
facial nerve are decompressed.

Chapter 122
Facial Nerve Decompression 1263
the middle fossa plate within the epitympanum and
requires removal of the incus and occasionally the head
of the malleus. The incudostapedial joint is separated
through the facial recess, and the incus is rotated pos-
teriorly out through the epitympanum by placing a 90-
degree hook under the incus body. The tympanic facial
nerve lies superior to the oval window and then courses
between the cochleariform process inferiorly and the
cog superiorly before diving medially toward the genic-
ulate ganglion. The proximal tympanic segment is
decompressed up to and beyond the cochleariform
process with a microdrill and microcurette. The junc-
tion of the facial nerve and geniculate ganglion is
reached with further anterior and medial dissection
under the head of the malleus (Fig. 122-7).
The facial nerve turns abruptly posterior, medial,
and inferior at the geniculate ganglion as it enters the
labyrinthine segment. The ampulla of the superior
canal blocks further exposure of the labyrinthine facial
nerve through the transmastoid approach. Complete
exposure of the labyrinthine segment of the facial nerve
requires a middle fossa approach (if hearing is present)
or a translabyrinthine approach (if hearing is absent).
Once the fallopian canal in the tympanic and
mastoid segments has been exposed, any residual
impinging bony spicule is removed. The nerve sheath
is opened at the site of injury and for a short distance
proximal and distal to the site of injury to assess the
severity of injury to the fascicles. If the fascicles are
intact, the decompression procedure is complete. If
more than 50% of the nerve fascicles have been violated
or the nerve is completely transected, primary neuror-
rhaphy or cable grafting is indicated.
The removed incus is replaced at the end of the
procedure and supported in place with saline-soaked
Gelfoam pledgets. If removal of the malleus head was
necessary for surgical exposure, the incus may be
sculpted and interposed between the stapes capitulum
and malleus handle. The postauricular wound is closed
in layers with absorbable suture, and a mastoid dressing
is applied to the operated ear for 24 hours. Postopera-
tive hospitalization for transmastoid decompression
alone is not necessary.
Translabyrinthine Approach
This approach is used to decompress the facial nerve
proximal to the geniculate ganglion in a nonhearing
ear. The surgical technique is identical to that used for
translabyrinthine removal of acoustic neuromas and is
detailed in Chapter 124.
Middle Fossa Approach
The primary advantage of the middle fossa approach is
that it provides optimal exposure of the perigeniculate
and labyrinthine facial nerve while preserving residual
hearing in the operated ear. This is the approach used
for surgical decompression of carefully selected patients
with Bell’s palsy and temporal bone fracture. It may also
be used in combination with a transmastoid approach
if complete intratemporal facial nerve decompression
is necessary.
The patient is positioned supine with the head
turned so that the operated ear is facing up. Intraopera-
tive facial nerve monitoring is established at the begin-
ning of the procedure. Paralytic agents are not used
after induction of general anesthesia. Although the
facial nerve is paretic, direct electrical stimulation of
the intratemporal facial nerve during surgery may
sometimes identify the site of conduction block. Brain
stem auditory evoked responses are also monitored
routinely because hearing preservation is desired.
Perioperative
medications
administered
include
broad-spectrum antibiotics with good cerebrospinal
fl uid (CSF) penetration (ceftriaxone), furosemide
(Lasix), 20 mg mannitol, 0.5 gm/kg, and dexame-
thasone, 10 mg. Bacitracin (50,000 units/L of saline
solution) is used in the irrigation fl uid.
An incision is made in the preauricular crease,
starting at the level of the lower border of the zygoma
and extending superiorly above and behind the auricle
to form a reverse question mark (Fig. 122-8). Anterior
Figure 122-6. The proximal tympanic segment is decompressed
with the incus in place if space permits.
Figure 122-7. The perigeniculate and distal labyrinthine segments
of the facial nerve are decompressed.

1264
Section 14
Facial Nerve
and posterior skin fl aps lateral to the temporalis fascia
are elevated to expose the temporalis muscle. An
anteroinferiorly based temporalis muscle fl ap is created
by incising the muscle along linea temporalis with
Bovie electrocautery. A 4- × 5-cm craniotomy centered
two thirds anterior and one third posterior to the exter-
nal auditory canal and inferiorly based at the root of
the zygoma is created with a 4-mm cutting burr (Fig.
122-9). The bone fl ap is carefully elevated from under-
lying dura with a dural elevator, removed, and soaked
in bacitracin solution until the end of the procedure.
Any bleeding from the dura may be controlled with
bipolar electrocautery. The inferior border of the cra-
niotomy is then lowered to the level of the middle fossa
fl oor. Dura is carefully elevated off the middle fossa
fl oor in a posterior-to-anterior direction to expose the
anatomy of the fl oor of the middle fossa (Fig. 122-10).
The limits of exposure are the middle meningeal artery
anteriorly, the sulcus of the superior petrosal sinus
medially, and the arcuate eminence overlying the dome
of the superior semicircular canal posteriorly. Dura
over the greater superior petrosal nerve (GSPN) tends
to be densely adherent to the nerve. Great care is
needed in dissection at this point because of the possi-
bility of injuring a dehiscent geniculate ganglion. The
dura is elevated in a posterior-to-anterior direction to
minimize injury to the GSPN and geniculate ganglion
(Fig. 122-11). Once exposure of the fl oor of the middle
fossa is complete, the tongue of the middle fossa self-
retaining retractor is secured at the sulcus of the supe-
rior petrosal sinus to retract the temporal lobe (Fig.
122-12).
The GSPN is used as the primary anatomic land-
mark for locating the facial nerve along the middle
fossa fl oor. The arcuate eminence overlying the dome
of the superior semicircular canal is located, and the
positions of the cochlea, facial nerve, internal auditory
canal (IAC), and middle ear ossicles are estimated. The
location of the IAC is determined by bisecting the angle
formed by the GSPN and arcuate eminence (Fig.
122-13). The roof of the middle ear is opened to iden-
tify the head of the malleus and the cochleariform
process. The perigeniculate region is exposed by follow-
ing the GSPN posteriorly and the tympanic segment of
the facial nerve anteriorly into the geniculate ganglion
with a 1-mm diamond burr (Fig. 122-14).
Bone over the labyrinthine facial nerve is then care-
fully removed by following the nerve from the genicu-
late ganglion posteriorly and medially into the IAC
(Fig. 122-15). The labyrinthine facial nerve lies imme-
diately lateral to the upper basal turn of the cochlea.
The diameter of the fallopian canal in the labyrinthine
segment is less than 1 mm, and it runs between the
upper basal turn of the cochlea and the ampulla of the
superior semicircular canal. The distance between
the upper basal turn of the cochlea and the ampulla of
the superior semicircular canal is 5.5 ± 1.0 mm (Fig.
122-16). A 1-mm diamond burr is used to uncover the
superior surface of the labyrinthine segment. To prevent
inadvertent fenestration of the cochlea, the area imme-
diately anterior to the labyrinthine segment is closely
observed for the blue line of the upper basal turn of
the cochlea. Similarly, the area posterior to the labyrin-
thine segment is observed for the blue line of the
ampulla of the superior semicircular canal. If the
cochlea is inadvertently fenestrated, suctioning should
be avoided in the area and the bone defect immediately
plugged with bone wax. Bone over the tegmen tympani
Figure 122-8. Skin incision for the middle fossa approach.
Figure 122-9. Temporal craniotomy used in the middle fossa
approach.

Chapter 122
Facial Nerve Decompression 1265
V3 division of trigeminal nerve,
foramen ovale
Greater superficial petrosal nerve
Foramen for
middle
meningeal
artery
External
auditory
canal
Petrosquamous
suture
Arcuate eminence
(superior semicircular
canal)
Superior
petrosal sinus
Petrous
carotid artery
Trigeminal
ganglion
Figure 122-10. Anatomy of the
fl oor of the middle fossa.
Greater
superficial
petrosal
nerve
Figure 122-11. The greater superfi cial petrosal nerve is identifi ed
and preserved.
Greater
superficial
petrosal
nerve
Cochlea
Malleus
Incus
Ampulla of
superior
semicircular
canal
Internal auditory canal
Tympanic segment of
the facial nerve
Figure 122-12. The fl oor of the middle fossa is exposed, and the
self-retaining middle fossa retractor is secured.

1266
Section 14
Facial Nerve
60°
60°
Greater
superficial
petrosal
nerve
Internal
auditory
canal
Arcuate
eminence
Figure 122-13. The position of the internal auditory canal is iden-
tifi ed by using the anatomic relation of the greater superfi cial petrosal
nerve and the arcuate eminence.
Cochleariform
process
Malleus
Incus
Geniculate
ganglion
Figure 122-14. The tegmen tympani is unroofed to identify the
malleus, incus, and cochleariform process. The geniculate ganglion
is exposed. The perigeniculate and labyrinthine segments of the
facial nerve are identifi ed.
Cochleariform
process
Malleus
Greater
superficial
petrosal nerve
Internal
auditory
canal
Labyrinthine
segment
Figure 122-15. The labyrinthine segment of the facial nerve is
exposed.
is removed to complete bony decompression of the
perigeniculate facial nerve. Once bony exposure of the
facial nerve has been achieved, the dura of the IAC and
any dural thickening surrounding the meatal foramen
are incised. The periosteum and perineurium of the
facial nerve are split to a point just distal to the genicu-
late ganglion (Fig. 122-17).
Before closure, any open mastoid air cells are
occluded with bone wax and the resultant epitympanic
defect covered with temporalis fascia. The roof of the
IAC is sealed with a small abdominal fat graft. A free
bone graft is harvested from the temporal craniotomy
fl ap for placement over the fascia to provide additional
structural support and prevent herniation of dura/
brain into the middle ear. The middle fossa retractor is
released and removed to allow the temporal lobe to
expand back over the middle fossa fl oor. The remain-
der of the craniotomy fl ap is replaced and secured by
reapproximating the overlying temporalis muscle. The
skin fl ap is then reapproximated in two layers without
the use of any drain. A mastoid dressing is placed over
the operated ear for 3 days postoperatively, and the
patient is hospitalized for 4 to 5 days. The patient is
monitored postoperatively in routine manner for intra-
cranial surgery, with attention paid to CSF leakage from
the wound or nose. Placement of a lumbar drain usually
resolves this problem.
Facial Nerve Repair
Restoration of anatomic continuity of the facial nerve
without tension is the primary goal of facial nerve
repair. In general, the earlier that repair of the injured
facial nerve takes place, the better the functional
outcome. In patients with neural transection from
surgery or trauma, immediate exploration and primary
repair are advocated. If not possible, delayed explora-
tion and repair should be performed as soon as medi-
cally feasible (within 30 days) for the best functional
outcome.9 The transected ends of the facial nerve
should preferably be tagged to facilitate identifi cation
of the nerve endings at the time of secondary surgery.
Three anastomotic techniques have been reported
in the literature. Epineural nerve repair is the most
common anastomosis technique. It involves placing
nonabsorbable suture through the epineurium on each
side of the anastomosis and reapproximating the ends.
The potential disadvantage is that it fails to approxi-
mate the individual nerve fascicles. Perineural repair
consists of suturing the individual perineurium of each
fascicle. The epineurium is sutured as a second layer.
The advantage of this technique is that better contact
of individual nerve fascicles may be achieved. Fascicular
and interfascicular nerve repair involves individually
approximating the fascicles. Natural fi ber, fi brinogen
adhesives, or fi ne sutures (10-0 or 11-0 nylon) are used
to coapt the individual fascicles. To date, no defi nitive
studies have documented the superiority of tubuliza-
tion or enclosing the anastomosis to prevent tissue inva-
sion and abnormal axon growth.9 Accurate surgical
approximation remains the primary goal. It is impor-

Chapter 122
Facial Nerve Decompression 1267
1.5 mm
±0.5 mm
3.0 mm
±1.0 mm
5.5 mm
±1.0 mm
Labyrinthine
segment of
facial nerve
Figure 122-16. Average anatomic measure-
ments between the labyrinthine segment of the
facial nerve, the upper basal turn of the cochlea,
and the ampulla of the superior semicircular
canal.
Figure 122-17. The dura of the internal
auditory canal and the periosteum and perineu-
rium of the facial nerve are incised.
tant to remember that the working portion of the nerve
is the endoneural surface and not the nerve ends.
Therefore, epineurium needs to be trimmed back to
uncover the endoneural surface for good axonal volume
match at the anastomotic sites.
In general, partial or complete transaction of the
facial nerve should be repaired by primary neurorrha-
phy or cable grafting when the proximal and distal ends
of the facial nerve are accessible.
Primary Repair
Primary repair is the ideal surgical option whenever
feasible because there will be only one anastomosis and
minimal size incongruency of the reapproximated
nerve endings. For this reason, some surgeons prefer
nerve mobilization and primary anastomosis over other
techniques.
Intratemporal rerouting of the distal nerve segment
involves a translabyrinthine exposure, sectioning of the
GSPN and chorda tympani branches, and complete
skeletonization of the facial nerve within the fallopian
canal to gain another 1.5 cm in length for tension-free
anastomosis. The disadvantage of this approach is that
the blood supply to the distal nerve segment may be
disrupted and lead to further neural injury. The cut
endings of the nerve are freshened by sharply trimming
the endings back to normal-appearing nerve tissue. Any
excess surrounding soft tissue is trimmed to allow
proper identifi cation of the nerve sheath. In delayed
repairs, fi brous scarring or traumatic neuromas at the

1268
Section 14
Facial Nerve
proximal end of the cut nerve should be excised before
repair. Suture anastomosis of the nerve is generally
unnecessary within the temporal bone. When outside
the fallopian canal, one to two 9-0 monofi lament sutures
are used to reapproximate the epineural layer. At the
cerebellopontine angle, the lack of a resilient epineural
layer may necessitate a single through-and-through
suture to secure the cut ends of the nerve together. The
suture is passed through the distal end fi rst to avoid
placing tension and traction on the proximal end,
which may lead to tearing of the proximal end. After
suture repair, the anastomosis may be further rein-
forced with fi brinogen. Use of nerve tubes and conduits
is unnecessary.
Cable Grafting
Cable or interposition grafting involves placing a free
nerve graft between the proximal and distal segments
of the facial nerve. This procedure provides a conduit
for growth of axons to the facial musculature. It is indi-
cated when tension-free primary anastomosis cannot be
performed. Disadvantages of this technique are the
requirement for two anastomoses and decreased axon
availability.
The great auricular nerve is the most widely used
donor nerve in the head and neck for most short-
segment facial nerve defects because of its close proxim-
ity to most surgical fi elds, excellent size match, and
limited donor site morbidity. Its limitations are its rela-
tively short length (up to 8 cm), restricted branching
pattern, and potential for involvement by malignant
disease. The great auricular nerve is located midway
between the mastoid tip and clavicle along the posterior
border of the sternocleidomastoid muscle.
The sural nerve is the second most popular donor
nerve for facial nerve reconstruction. It provides excel-
lent size match, is available in lengths of up to 40 cm
for grafting, and has an extensive arborization pattern.
It is an ideal choice for near-total facial nerve recon-
struction after oncologic procedures, as well as for
cross-facial grafting. Harvesting of the sural nerve
requires a second operative site. The sural nerve is
located between the lateral malleolus and Achilles
tendon, deep or posterior to the saphenous vein.
Details on the technique of harvesting great auricu-
lar and sural nerve grafts are provided in Chapter 121.
Neural anastomosis is accomplished in a fashion similar
to primary anastomosis. Cable grafts laid within the fal-
lopian canal may be supported with Gelfoam alone
without suture approximation (Fig. 122-18).
POSTOPERATIVE MANAGEMENT
Patients undergoing transmastoid exploration of the
facial nerve are discharged home on the same day. If a
craniotomy is performed, the patient will require hospi-
talization for several days for close observation. Periop-
erative antibiotics are routinely administered for all
craniotomy cases. The patient is instructed about eye
protection, and this is reinforced until good eye closure
is restored. Static reanimation of the eye with an upper
eyelid gold weight or palpebral spring is recommended
at the time of facial nerve repair or grafting in patients
requiring neurorrhaphy, because recovery of facial func-
tion is not anticipated for 6 to 12 months. Reanimation
is also recommended for patients with facial paralysis
who lack a normal Bell phenomenon and those with a
decreased or absent corneal refl ex in the affected eye.
COMPLICATIONS
Potential complications of transmastoid facial nerve
decompression include further surgical trauma to the
facial nerve, hearing loss (either conductive or sensori-
neural), vertigo, CSF leak, and wound infection. All
drilling along the facial nerve should be performed
with a diamond burr and copious irrigation to prevent
thermal injury. The inner ear is most at risk at the
lateral semicircular canal during decompression of
the mastoid segment and second genu of the nerve.
The ampullated ends of the superior and lateral canals
are at risk during exposure of the perigeniculate region
from the transmastoid approach. It is important to rec-
ognize inadvertent fenestration of the inner ear as soon
as it occurs and to seal the fenestration with bone wax.
Sensorineural hearing loss can also occur from inadver-
tently drilling on the ossicular chain. This injury is pre-
vented by disarticulating and removing the incus if
there is not enough room to safely decompress the
tympanic segment without touching the incus. Care
should be taken to avoid trauma to the middle fossa
dura to prevent CSF leakage. To minimize trauma to
the dura, it is important to use the properly sized burr,
watch all edges of the burr while drilling, and switch to
a diamond burr when in tight areas or when the dura
has been exposed. If the dura is violated, repair with
fascia, muscle, bone, or any combination of these tissues
is necessary. Techniques for repair of dural and tegmen
defects are described in Chapter 127.
Figure 122-18. Interposition nerve graft laid in the mastoid
segment of the fallopian canal.

Chapter 122
Facial Nerve Decompression 1269
Potential intraoperative and postoperative compli-
cations of the middle fossa approach include sensori-
neural hearing loss, vertigo, edema of the temporal
lobe or contusion, subdural hematoma, CSF leak, and
meningitis. Sensorineural hearing loss and vertigo
result from inadvertent fenestration of the cochlea and
vestibular labyrinth during exposure of the labyrinthine
facial nerve and IAC. Should fenestration occur, the site
should be immediately occluded with bone wax. Tem-
poral lobe edema or contusion (or both) and subdural
hematoma may occur as a result of direct injury during
craniotomy or temporal lobe retraction. These compli-
cations are avoided by taking steps to reduce intracra-
nial pressure at the start of surgery (e.g., reducing Pco2;
administering intravenous mannitol, furosemide, and
dexamethasone). If the temporal lobe is tight, a small
incision in the dura can be made to release CSF before
retracting the temporal lobe. If injury to the temporal
lobe is suspected, a CT scan of the head should be per-
formed postoperatively to assess the degree of edema,
and a neurosurgeon should be consulted.
Although functional outcome does not seem to be
related to the length of the nerve graft, nerve grafts
placed distal to the meatal foramen appear to do better.
Timing of repair after injury is also a critical factor in
determining recovery. The best functional recovery
after nerve repair or grafting still results in mild to
moderate facial weakness with synkinesis. Facial move-
ment may not be clinically evident until at least 6 months
after surgery and may continue to improve for 2 years
or more after neurorrhaphy. Therefore, adjuvant facial
reanimation procedures (see Chapter 88) may be indi-
cated if poor oral and ocular sphincter control is
bothersome.
References
1. Sunderland S: Nerves and nerve injuries. Baltimore, Williams &
Wilkins, 1968.
2. Niparko JK: The acute facial palsies. In Jackler R, Brackman D
(eds): Neurotology. St Louis, Mosby–Year Book, 1994.
3. Burgess RC, Michaels L, Bale JF Jr, et al: Polymerase chain reac-
tion amplifi cation of herpes simplex viral DNA from the genicu-
late ganglion of a patient with Bell’s palsy. Ann Otol Rhinol
Laryngol 103:775-779, 1994.
4. Murakami S, Mizobuchi M, Nakashiro Y, et al: Bell palsy and
herpes simplex virus: Identifi cation of viral DNA in endoneurial
fl uid and muscle. Ann Intern Med 124:27-30, 1996.
5. Gillman GS, Schaitkin BM, May M, et al: Bell’s palsy in pregnancy:
A study of recovery outcomes. Otolaryngol Head Neck Surg
126:26-30, 2002.
6. Gantz BJ, Rubinstein JT, Gidley P, et al: Surgical management of
Bell’s palsy. Laryngoscope 109:1177-1188, 1999.
7. Friedman RA: The surgical management of Bell’s palsy: A review.
Am J Otol 21:139-144, 2000.
8. Adour KK, Ruboyianes JM, Von Doersten PG, et al: Bell’s palsy
treatment with acyclovir and prednisone compared with predni-
sone alone: A double-blind, randomized, controlled trial. Ann
Otol Rhinol Laryngol 105:371-378, 1996.
9. Axelsson S, Lindberg S, Stjernquist-Desatnik A: Outcome of treat-
ment with valacyclovir and prednisone in patients with Bell’s
palsy. Ann Otol Rhinol Laryngol 112:197-201, 2003.
10. Alberton DL, Zed PJ: Bell’s palsy: A review of treatment using
antiviral agents. Ann Pharmacother 40:1838-1842, 2006.
11. Hato N, Matsumoto S, Kisaki H, et al: Effi cacy of early treatment
of Bell’s palsy with oral acyclovir and prednisolone. Otol Neu-
rotol 24:948-951, 2003.
12. Fucci MJ, Buchman CA, Slattery WH: Neurorrhaphy techniques
for facial paralysis. Facial Plast Surg Clin North Am 5:223-240,
1997.
13. Di Martino E, Sellhaus B, Haensel J, et al: Fallopian canal dehis-
cences: A survey of clinical and anatomical fi ndings. Eur Arch
Otorhinolaryngol 262:120-126, 2005.
14. Weber PC: Iatrogenic complications from chronic ear surgery.
Otolaryngol Clin North Am 38:711-722, 2005.
15. Redaelli de Zinis LO, Gamba P, Balzanelli C: Acute otitis media
and facial nerve paralysis in adults. Otol Neurotol 24:113-117,
2003.
16. Harker LA, Pignatari SS: Facial nerve paralysis secondary to
chronic otitis media without cholesteatoma. Am J Otol 13:372-
374, 1992.
17. Makeham TP, Croxson GR, Coulson S: Infective causes of facial
nerve paralysis. Otol Neurotol 28:100-103, 2007.
18. Quaranta N, Cassano M, Quaranta A: Facial paralysis associated
with cholesteatoma: A review of 13 cases. Otol Neurotol 28:405-
407, 2007.
PEARLS
• Incomplete facial paralysis portends a favorable
prognosis and should be managed conservatively.
• ENoG and EMG testing should be used to identify
patients who would potentially benefi t from surgical
decompression of the facial nerve.
• Thorough understanding of temporal bone anatomy
and the intratemporal course of the facial nerve is
critical in preventing iatrogenic trauma to the nerve.
• Tension-free anastomosis is critical for the best
functional results after neurorrhaphy.
• Static facial reanimation procedures should be
considered after facial nerve repair if signifi cant oral
or ocular sphincter defi ciencies are encountered.
• Temporal lobe retraction is poorly tolerated in
elderly individuals and results in an unacceptably
high risk of intracranial complications.
• Inadvertent drilling on the incus or stapes during
decompression of the distal tympanic facial nerve
will result in postoperative sensorineural hearing
loss.
• Thermal injury to the facial nerve may occur if
inadequate irrigation is used while decompressing
the fallopian canal with a diamond drill burr.
• Mobilization of the facial nerve from the fallopian
canal to gain nerve length for primary anastomosis
entails a moderate risk of further nerve
devascularization and trauma.
PITFALLS
• ENoG results alone may underestimate the extent of
recovery in a regenerating nerve and should therefore
never be used independently to determine candidacy
for surgical decompression.

section 15
Temporal Bone
Chapter 123
Carcinoma of the Temporal Bone
Barry E. Hirsch, C. Y. Joseph Chang, and Stephanie Moody Antonio
Primary malignant tumors arising in the temporal bone
are rarely seen in the typical community practice of
otology. The external auditory canal (EAC) is the most
common site of origin. Squamous cell carcinoma of the
EAC has a reported incidence of about 1 per one million
per year and is the major focus of this chapter. Primary
malignancies of the temporal bone may also arise in the
middle ear and mastoid and rarely in the jugular
foramen and petrous apex. Secondary tumors of the
temporal bone commonly develop as a result of spread
from adjacent structures such as the concha, pinna, and
parotid gland. Metastasis to the temporal bone from
distant sites can also occur, often at the petrous apex.
Each region of the temporal bone is affected by unique
tumor types, clinical manifestations, and examination
fi ndings. Because it is common for a tumor to involve
overlapping anatomic regions, no area can be consid-
ered in isolation, and broad understanding of the tem-
poral bone and its surrounding structures is vital.
Basal cell carcinoma is the most common tumor of
the pinna and concha and occurs four times as fre-
quently as squamous cell carcinoma. Melanoma and
Merkel cell cancer are less common. Melanoma of the
pinna and EAC account for about 10% of head and
neck melanomas.1 Malignancies arising from the medial
EAC and middle ear include squamous cell carcinoma,
adenocarcinoma, adenoid cystic carcinoma, and rarely,
Merkel cell carcinoma, lymphoma, and malignant
melanoma. Rhabdomyosarcoma originates in the
middle ear and mastoid and is the most common malig-
nancy of the temporal bone in children. Other tumor
types occurring in the middle ear and mastoid include
melanoma, squamous cell carcinoma, endolymphatic
sac tumor (papillary adenocarcinoma), adenocarci-
noma, and lymphoma. Malignant schwannomas and
neuromas have been identifi ed in the middle ear and
jugular foramen. Unique tumor types in the petrous
apex include chondrosarcoma, neuroendocrine carci-
noma, meningioma, and hemangiopericytoma. Adenoid
cystic carcinoma, mucoepidermoid carcinoma, sarcoma,
plasmacytoma, fi brosarcoma, multiple myeloma, and
osteosarcoma have also been reported in the temporal
bone. Metastasis to the temporal bone from breast,
colon, and renal cell carcinomas have all been
reported.
A patient with long-standing otorrhea, otalgia, or a
mass in the EAC should be presumed to have carci-
noma until proved otherwise. Bleeding, hearing loss,
facial paralysis, a periauricular swelling or mass, lymph-
adenopathy of the parotid or upper part of the neck,
and lower cranial nerve palsies may indicate a cancer
lesion in the temporal bone. It is important to be
mindful of the possibility of malignant otitis externa
because its clinical picture is very similar to cancer in
this site.
Sun exposure contributes to the development of
basal cell and squamous cell carcinomas of the pinna
and lateral EAC. A genetic predisposition to skin cancer
1271

1272
Section 15
Temporal Bone
may also exist and is manifested by the development
of skin cancer in sites not exposed to sunlight, as
well as in sun-exposed areas. Chronic otitis media
and cholesteatoma are common in patients with cancer
of the temporal bone and have been implicated as
etiologic factors. Squamous metaplasia resulting
from chronic infl ammation could result in dysplastic
changes and lead to cancer.2-4 Human papillomavirus
has been implicated in squamous cell carcinoma of the
middle ear.5-7 Included in these series are cases of tem-
poral bone cancer induced by radiation exposure.
Patients with these cancers had a particularly poor
outcome.
PERTINENT TEMPORAL BONE ANATOMY
The pinna and temporal bone have traditionally been
divided into anatomic subunits that correspond to the
depth of resection of the various procedures used for
surgical correction. The EAC is divided into cartilagi-
nous (lateral) and bony (medial) portions. The carti-
laginous portion is a poor barrier against the spread of
neoplasm. Tumors in this area can erode through skin,
cartilage, and soft tissue to invade the parotid gland
anteriorly or the concha and postauricular sulcus pos-
teriorly (Fig. 123-1A and B [1 and 2]). The fi ssures of
Santorini are vertical fi ssures in the cartilaginous EAC
that allow direct access of cancer from the skin of the
EAC to periparotid tissues (Fig. 123-2). In contrast, the
bony canal provides a more resistant barrier to direct
invasion. Cancer in this area tends to track medially
through the tympanic membrane into the middle ear
and mastoid spaces (see Fig. 123-1A and B [3]). The
foramen of Huschke provides a potential pathway
between the bony EAC and the soft tissues of the parotid
area and temporomandibular joint (TMJ). This struc-
ture is a defect in the anterior inferior tympanic ring
that usually closes by 5 years of age but persists in 7%
of adults (Fig. 123-3).8
The middle ear and mastoid cavities provide
minimal resistance to the spread of cancer. Anteriorly,
cancer may invade through tissue surrounding the
eustachian tube and involve the internal carotid artery
(ICA), Meckel’s cave, and the cavernous sinus (see Fig.
123-1A and B [5]). Superiorly, cancer can penetrate the
tegmen tympani and tegmen mastoideum to involve the
middle fossa dura and temporal lobe (see Fig. 123-1A
and B [4]). Medially, the otic capsule provides a good
barrier to the spread of cancer, but several areas are
vulnerable. The round and oval windows can be pene-
trated and result in invasion through the vestibule into
the internal auditory canal (IAC) and posterior fossa
(see Fig. 123-1A and B [6]). In addition, the facial nerve
can provide a pathway for the spread of cancer intra-
cranially through the petrous apex, as well as into the
infratemporal fossa (ITF) through the stylomastoid
foramen (see Fig. 123-1A and B [7]). Posteriorly, cancer
can invade the posterior fossa plate, dura, and sigmoid
sinus (see Fig. 123-1A [8]). Finally, the air cell system
of the temporal bone provides a multidirectional
highway for the spread of cancer. Cancer within the
middle ear and mastoid follows air cells as a pathway
into the petrous apex and IAC and inferiorly into the
jugular bulb and can penetrate the ITF and posterior
fossa (see Fig. 123-1A and B [5, 6, and 9]).
Lymphatic drainage of the EAC extends anteriorly
to the parotid and periparotid lymph nodes, inferiorly
to the internal jugular lymph nodes, and posteriorly to
the mastoid lymph nodes. The lymphatic drainage
pathways from the middle ear and mastoid have not
been well elucidated, but they are believed to be of only
minor importance, because nodal metastasis from a
malignancy limited to the middle ear and mastoid is
rare.
STAGING OF TEMPORAL
BONE MALIGNANCIES
A systematic and useful staging system for cancer of the
temporal bone has not been universally accepted. A
major obstacle to the development of a useful preopera-
tive staging system in the past was the diffi culty of cancer
mapping because the medial portion of the cancer
could not be visualized and spread to the skull base
and intracranial cavity was diffi cult to evaluate. The
development of multiaxial imaging modalities such as
computed tomography (CT) and magnetic resonance
imaging (MRI) has helped overcome this problem. A
useful system proposed by the University of Pittsburgh
uses imaging to determine the extent of tumor involve-
ment and has become widely accepted for squamous
cell carcinoma.9-14
The staging system for cancer of the temporal bone
involves the same tumor-node-metastasis (TNM) model
used for staging cancers in other anatomic sites. Tumor
extent is defi ned as T1 through T4, depending on the
degree of bone, cartilage, and soft tissue involvement
of the ear canal and tympanic, mastoid, and petrous
bones (Table 123-1). The N and M portions of the clas-
sifi cation and the staging system follow the same format
as for other sites according to the American Joint Com-
mittee on Cancer.15 In our recent series of patients with
squamous cell carcinoma of the temporal bone staged
in this manner, the 2-year disease-free survival rate was
100% for T1, 100% for T2, 56% for T3, and 17% for
T4, thus demonstrating that this staging system can be
predictive of outcome.9 We modifi ed the Pittsburgh
staging system after further review of patients from an
extended series.16 In the modifi ed staging system, facial
nerve weakness is considered an indicator of T4 cancer
and has a worse prognosis than T3 cancer. We observed
that facial nerve paresis did not occur in cancers classi-
fi ed as limited T1, T2, or T3 lesions. Involvement of the
facial nerve would otherwise be classifi ed as T4 based
on the anatomic area of involvement, including the
medial wall of the middle ear (horizontal segment),
extensive bony erosion in the mastoid (vertical segment),
or involvement of the stylomastoid foramen. In the T4
group, survival was similar in patients with and without
facial paralysis. A few reports have used the modifi ed
staging system,16,17 but further study on the importance
of facial paralysis in cancer of the temporal bone is

Chapter 123
Carcinoma of the Temporal Bone 1273
A
B
Figure 123-1. Axial (A) and coronal (B)
temporal bone anatomy identifying path-
ways of the spread of cancer. Cancer can
spread (1) anteriorly through the cartilagi-
nous ear canal into the parotid gland; (2)
through the concha into the postauricular
sulcus; (3) through the tympanic membrane
into the middle ear; (4) posteriorly into the
mastoid; (5) into the anterior mesotympa-
num to the carotid artery and eustachian
tube; (6) into the inner ear through the
round window or otic capsule; (7) along the
facial nerve into the infratemporal fossa; (8)
through the mastoid, posterior fossa dura,
and sigmoid sinus; and (9) beneath the skull
base to the jugular fossa, carotid artery, and
lower cranial nerves.
needed to support standardization of this staging
system.
TREATMENT
The fi rst systematic discussion of the management of
cancer of the temporal bone was presented by Politzer
in 1883.18 Refi nements in this approach have evolved
over the past century. Radical mastoidectomy with radi-
ation therapy was previously the recommended treat-
ment, but cure rates were quite low. In 1954, Parsons
and Lewis described the technique of en bloc subtotal
temporal bone resection.19 Lederman presented
the fi rst large series of patients treated by radiation
therapy in 1965 and espoused the concept of com -
bined therapy at a time when the role of radiation in
treating cancer of the temporal bone was not yet well
accepted.20 In 1984, Graham and colleagues reported

1274
Section 15
Temporal Bone
was 18%, but the operative mortality rate was 27%.22
Lederman reported a cure rate of 33% at 5 years for
combined surgical and radiation treatment versus 11%
for radiation alone.20 Despite advocating en bloc subto-
tal temporal bone resection and occasional adjuvant
radiation therapy, Lewis and Page achieved a 28% cure
rate.23 The cure rate remains low despite the innovative
work of surgeons and radiation oncologists and the use
of aggressive therapy. Patients with cancer limited to
the EAC have been reported to have an 85% to 100%
disease-free survival rate with surgery with or without
radiation therapy.10,16,24,25 Cancer extending to the
middle ear, mastoid, and soft tissues is associated with
a poor outcome, and even with extensive surgery and
radiation therapy, the survival rate is little more than
50%.
It has not been clearly established what treatment
modalities provide the best outcome given the extent
of disease. The relatively low incidence of cancer of the
temporal bone makes randomized clinical trials impos-
sible. As a consequence, every published study is essen-
tially an analysis of a case series, with inconsistent
treatment protocols often being used. This, along with
the lack of a universal staging system and variability in
surgical nomenclature, limit making use of published
data in a meaningful analysis.
Surgical Therapy
Primary surgical therapy should be performed to
remove the cancer in its entirety. The issue of whether
piecemeal resection as opposed to en bloc resection
compromises survival has not been resolved. It is clear
that piecemeal resection of the temporal bone medial
to the EAC is a more controlled operation than the en
bloc technique is. Once the cancer has spread to the
medial wall of the middle ear and invades the mastoid
air cells, the prognosis becomes quite poor unless clear
margins are achieved with radical therapy. A positive
margin is associated with a very poor chance of cure.
The treatment program depends primarily on the
extent of the cancer. The margins of resection for
Table 123-1
CARCINOMA OF THE TEMPORAL
BONE: TUMOR STAGING SYSTEM
T1
Tumor limited to the EAC; no bone erosion or
soft tissue extension
T2
Tumor with limited bone erosion to the EAC
or <0.5 cm of soft tissue involvement
T3
Tumor with full-thickness EAC bone erosion,
<0.5-cm soft tissue involvement, or tumor in the
middle ear or mastoid
T4
Tumor eroding the cochlea, petrous apex,
medial wall of the middle ear, carotid canal,
jugular foramen, or dura; or >0.5-cm soft tissue
involvement; or facial nerve paresis
EAC, external auditory canal.
Sebaceous gland
Ceruminous gland
Fissure of Santorini
Hyaline cartilage
Parotid gland
Figure 123-2. The fi ssures of Santorini are vertical fi ssures in the
cartilaginous external auditory canal. Tumor spreads easily through
these pathways into the periparotid soft tissues.
Tympanic incisure
Parts of
temporal bone:
Squamous
Petrous
Tympanic
Spine of
sphenoid bone
Foramen of Huschke
External acoustic meatus
Lesser tympanic spine
Greater tympanic spine
Figure 123-3. Foramen of Huschke.
During development, two prominences
(greater and lesser tympanic spines)
extend from the tympanic ring and
separate the space into the external
auditory canal and the foramen of
Huschke. These processes approach
each other and fuse during the fi rst
year of life. With continued growth of
bone from the inferior part of the tym-
panic bone, the foramen eventually fi lls
with bone. Occasionally, the foramen
remains patent. (Adapted from Anson BJ,
Donaldson JA: Surgical Anatomy of the
Temporal Bone. The Middle Ear. Philadel-
phia, WB Saunders, 1967, p 122.)
total en bloc resection of the temporal bone, including
the ICA.21
Historically, overall 5-year survival with temporal
bone cancer was low. In Conley and Novack’s series of
patients undergoing surgical resection, the cure rate

Chapter 123
Carcinoma of the Temporal Bone 1275
A
B
Figure 123-4. Axial (A) and coronal
(B) illustrations demonstrating (1) lateral
resection of the temporal bone, (2) subto-
tal resection of the temporal bone, and
(3) total resection of the temporal bone.
The carotid artery is preserved in this
illustration.
lateral, subtotal, and total temporal bone resection are
illustrated in Figure 123-4. Cancer limited to the EAC
(T1, T2) should be treated by lateral temporal bone
resection with superfi cial parotidectomy and preserva-
tion of the facial nerve. Rarely, the cancer may be small,
isolated in the lateral cartilaginous aspect of the EAC,
and not eroding bone, thereby permitting sleeve resec-
tion of the external canal skin, lateral to the tympanic
membrane. In practice, sleeve resection is probably not
oncologically adequate. Cancer that has invaded the
middle ear and mastoid cavities (T3) should be
addressed by subtotal temporal bone resection. Total
temporal bone resection (sometimes called radical tem-
poral bone resection) is performed when cancer extends
to the petrous apex. Cancer extending to the TMJ,
neck, dura, or ITF (T4) will require resection of these

1276
Section 15
Temporal Bone
structures. Although involvement of dura and brain is
considered by some to indicate unresectable disease,
Moffat and coauthors reported on two patients with
squamous cell cancer involving the brain who survived
after resection and radiation therapy.13
Adjuvant Therapy
Radiotherapy as a single modality has not been very
successful in curing any stage of carcinoma of the tem-
poral bone. Although the additional benefi t of postop-
erative radiation therapy has been questioned for
limited tumors excised with adequate margins and for
larger tumors with positive margins,26 it is generally
believed that combined therapy consisting of primary
surgical resection followed by radiation therapy pro-
vides the best chance to control the cancer and improve
survival.10,13,16 We routinely recommend postoperative
radiation therapy unless the cancer is well isolated in
the EAC with very little bone erosion. Fifty to 60 Gy are
delivered to the primary site, parotid region, ITF, and
ipsilateral neck.
The role of chemotherapy is evolving. Tradition-
ally, it has not been effective for primary treatment. A
group of patients treated by preoperative chemoradia-
tion therapy and temporal bone resection had better
survival than did patients treated by surgery or radiation
therapy alone.27 In cases in which medical conditions
preclude a safe procedure or the extent of disease
prohibits a reasonable chance of adequate resection,
palliative radiation therapy and chemotherapy may be
offered.
Management of the Parotid Lymph Nodes
Parotidectomy is routinely performed in conjunction
with temporal bone resection. In this way, the fi rst
echelon of lymphatic drainage for the anterior EAC
may be reviewed. Ideally, the parotid is resected en bloc
with the temporal bone. However, for T1 and T2
cancers, superfi cial parotidectomy is suffi cient. For T3
and T4 cancers and if the facial nerve is to be resected,
total parotidectomy is performed.
Neck Dissection
Supraomohyoid neck dissection is performed in most
cases. The lymphatic drainage of pinna and EAC lesions
is not entirely predictable but will often extend to the
upper jugular nodal chain. Also, exposure of cervical
structures provides safe control of the great vessels, if
needed. In a clinically N0 neck, neck dissection can be
done as a staging procedure to assist in the decision as
whether to proceed with postoperative radiation
therapy. The survival benefi t provided by elective neck
dissection is unclear. Metastasis to the lymph nodes is
a signifi cant indicator of a poor prognosis. In Moffat
and associates’ report of 39 patients with squamous cell
carcinoma of the temporal bone, 9 (23%) had positive
nodes in the neck. All these patients succumbed to the
disease within 27 months.13 In our experience, neck
dissection and parotidectomy are commonly carried
out at the time of temporal bone resection, which pro-
vides good local/regional control but does not seem to
affect survival.16
PATIENT SELECTION
In general, less extensive cancers are more readily cured
than advanced cancers that have invaded the middle
ear and mastoid. A major diffi culty in the management
of cancer of the temporal bone has been the small
percentage of patients in whom the diagnosis is made
early in the course of their disease. Because chronic
otitis media or otitis externa with purulent otorrhea is
very common, otorrhea caused by cancer is often
assumed to be secondary to infl ammatory disease.
Other symptoms of hearing loss and tinnitus are not
specifi c to cancer of the temporal bone. All too fre-
quently, biopsy is delayed until the disease is no longer
limited to the EAC (Fig. 123-5).
The signs and symptoms of cancer arising in the
temporal bone, especially early in its course, may be
diffi cult to distinguish from those of chronic otitis
externa and otitis media. However, the presence of per-
sistent, deep-seated, unrelenting pain may be a differ-
entiating symptom because appropriate treatment of
routine chronic ear infections usually provides relatively
rapid relief of discomfort. Chronic petrositis (Gradeni-
go’s syndrome) is associated with deep chronic pain
and otorrhea, although a mass lesion is absent. Sponta-
neous bleeding is also an unusual feature in purely
infectious ear disease unless canal cholesteatoma has
caused bone erosion with neovascularization. Malig-
Figure 123-5. This patient with pathology of the right external
auditory meatus failed to respond to medical therapy. Early biopsy in
this case is warranted.

Chapter 123
Carcinoma of the Temporal Bone 1277
nant external otitis, which can closely mimic the signs
and symptoms of malignancy, can be diffi cult to distin-
guish from cancer. Cases of malignant external otitis
that were eventually diagnosed as cancer have been
reported, thus underscoring the importance of early
biopsy in suspicious cases.28 In summary, any condition
of the EAC that does not respond to topical and sys-
temic antibiotic treatment should be suspected of har-
boring a malignancy, and biopsy should be performed
early. Biopsy is performed by direct incision; a staging
mastoidectomy is not appropriate because it reduces
the reliability of staging radiography and may compro-
mise the surgical margins of resection.
Depending on the stage of disease, surgical treat-
ment of cancer arising in the temporal bone is poten-
tially a major undertaking. The risk of morbidity and
mortality increases with factors such as advanced age
and medical conditions such as coronary artery disease,
pulmonary disease, diabetes mellitus, and peripheral
vascular disease. However, because combined-modality
therapy that includes major surgery appears to be the
only treatment that offers any reasonable chance of
control of cancer, there is no absolute medical contra-
indication to surgical treatment. Aggressive preopera-
tive, perioperative, and postoperative care must be
given to minimize the chance of a major medical com-
plication. Each patient and physician will need to decide
whether the proposed treatment and its potential
benefi t are worth the risk. For example, a patient with
cancer of the temporal bone who has a life expectancy
of less than one year for other medical reasons will
probably derive minimal benefi t from aggressive
treatment.
The second issue regarding the decision to proceed
with treatment is the extent of the cancer. Extension
into certain areas such as the cavernous sinus and brain
parenchyma makes total tumor extirpation nearly
impossible,29 and the possibility of cure becomes
unlikely, even with the addition of aggressive adjuvant
radiation therapy and chemotherapy. In these cases
there is little potential for improving the patient’s prog-
nosis. Involvement of the internal carotid canal is also
problematic but it is not an absolute contraindication
to total resection of cancer. Some patients will be able
to tolerate resection of the ICA but will require preop-
erative studies to determine eligibility, as described in
a later section.
PREOPERATIVE PLANNING
History, physical examination, and radiologic imaging
remain the most important methods of determining
the extent of the cancer. Evidence of the spread of
cancer beyond the anatomic limits of the EAC is evalu-
ated. The cancer and associated infl ammation often
obliterate the EAC, thereby restricting examination of
the tympanic membrane and middle ear. However, the
presence of severe conductive hearing loss, unilateral
sensorineural hearing loss, otitis media, vertigo, taste
dysfunction, or facial nerve paralysis may indicate inva-
sion into the middle ear, eustachian tube, and otic
capsule. The presence of Horner’s syndrome, transient
ischemic attacks, or syncope may indicate involvement
of the ICA. Trismus, TMJ dysfunction, and lower cranial
nerve palsies suggest the spread of cancer into the
jugular foramen ITF. The presence of seizures, dyspha-
sia, and other cognitive defi cits warrant investigation
for intracranial spread of tumor. The patient should be
examined carefully for physical evidence of a mass in
the neck, parotid gland, soft palate, and postauricular
region. An audiogram is obtained to establish the type
and degree of hearing loss. The status of the hearing is
important because preservation of hearing is possible
only if lateral resection of the temporal bone is per-
formed. However, the amount of resection is deter-
mined by the extent of the cancer and not by the degree
of residual hearing function.
The full extent of the cancer should be mapped in
accordance with physical fi ndings and multiaxial
imaging consisting of CT for delineation of the bony
anatomy of the temporal bone and MRI for visualiza-
tion of soft tissues and intracranial structures. The
initial radiologic study for defi nition of the tumor is
high-resolution CT with and without contrast enhance-
ment. It can accurately map tumors in the temporal
bone and predict invasion of cancer outside the EAC.
CT is especially well suited for detecting bony abnor-
malities. Extension of tumor into the bone of the EAC,
middle ear, mastoid, labyrinth, eustachian tube, carotid
canal, sigmoid sinus, ITF, and intracranial cavity can be
seen (Fig. 123-6). MRI with gadolinium enhancement
is superior to CT in certain respects, especially in
delineating soft tissue detail. MRI is more accurate in
differentiating effusion in the middle ear and mastoid
Figure 123-6. Computed tomography scan of extensive squamous
cell carcinoma of the temporal bone with erosion through the bone
of the right external auditory canal into the anterior soft tissue
(arrow), middle ear, and mastoid (arrowheads). (Courtesy of M. Arriaga,
M.D.)

1278
Section 15
Temporal Bone
from cancer, although such differentiation may be dif-
fi cult with either modality. MRI is signifi cantly better
than CT in determining the interface between cancer
and normal tissue. Therefore, MRI is quite sensitive in
detecting invasion of cancer into the dura and soft
tissues of the ITF (Fig. 123-7) and temporomandibular
region (Fig. 123-8). Usually, both MRI and CT will be
required to adequately stage the disease process.
Once a tumor map has been created, the need for
further studies will become apparent. Encroachment of
cancer in the region of the ICA should be investigated
with angiography to help determine whether invasion
into the vessel has occurred. Because there is a signifi -
cant risk of injury to the carotid artery if tumor resec-
tion is performed near this vessel, the patient’s tolerance
of permanent occlusion of the ICA should be deter-
mined preoperatively by balloon test occlusion with
xenon/CT.30 The venous phase of the angiogram dem-
onstrates the venous anatomy of the brain. Specifi cally,
the location of the vein of Labbé and the dominance
of the ipsilateral sigmoid and jugular drainage are
noted. In a few patients, the ipsilateral venous drainage
is so dominant that sacrifi ce of the jugular vein or
sigmoid sinus on this side can lead to venous cerebral
infarction. Thus, careful consideration of the patency
of the contralateral side must be undertaken if it is
anticipated that the sigmoid sinus or jugular vein may
be sacrifi ced.
The presence of metastatic cancer, especially in the
neck, should be detected before therapy. Metastasis to
the neck is unusual in cancer of the temporal bone, but
a thorough physical examination and CT or MRI with
contrast enhancement should detect lymph node
Figure 123-7. Magnetic resonance image of the same patient as in
Figure 123-2 with carcinoma of the temporal bone. A T1-weighted
contrast-enhanced image demonstrates enhancement of the middle
ear and infratemporal fossa (arrows). (Courtesy of M. Arriaga, M.D.)
B
A
Figure 123-8. Sagittal T1-weighted magnetic resonance image of
the temporomandibular joint (TMJ). A, There is a normal soft tissue
interface between the external auditory canal (dashed arrow) and the
condyle (solid arrow). B, Tumor from the external canal extends
through the bony canal into the glenoid fossa (arrow).
involvement. Spread of cancer to the lymph nodes in
the superfi cial lobe of the parotid gland is more
common, so the superfi cial lobe of the parotid gland is
usually removed during surgery with preservation of the
facial nerve. If the pathology is squamous cell carci-
noma, a metastatic evaluation consisting of chest radi-
ography and liver function testing is adequate. In
malignant tumors with a high predilection for systemic
spread such as melanoma, CT scanning of the chest,
abdomen, and pelvis, as well as whole-body bone scan-
ning, should be performed. The recent introduction of
positron emission tomography (PET)/CT scanning has
made identifi cation of metastasis more accurate.
Preoperative staging determines the scope of the
planned procedure and the necessity for a team
approach. Neurosurgical participation is appropriate
when surgery requires intracranial resection. Similarly,
wound closure after tumor removal may necessitate
transfer of regional or distant tissue, thus warranting
consultation with a reconstructive surgeon.

Chapter 123
Carcinoma of the Temporal Bone 1279
Surgical treatment of cancer of the temporal bone
usually requires a long duration of anesthesia and can
entail major blood loss and fl uid shifts, intracranial
manipulation, and postoperative stress, including fl uid
and electrolyte abnormalities, pulmonary and cardiac
stress, coagulation abnormalities, and the possibility of
aspiration. The patient’s medical status should be opti-
mized before surgery. Signifi cant conditions such as
coronary artery disease, chronic obstructive pulmonary
disease, diabetes mellitus, bleeding disorders, and
malnutrition
should
be
identifi ed
and
treated
preoperatively to minimize potential major medical
complications.
SURGICAL TECHNIQUES
The surgical approach is dictated by the location and
extent of cancer relative to the temporal bone. Lateral
resection of the temporal bone is performed for cancer
limited to the EAC (T1, T2). Subtotal resection of the
temporal bone is performed for cancer that has pene-
trated into the middle ear and mastoid cavities (T3).
The medial extent of resection incorporates the otic
capsule. Extratemporal dissection is dictated by the
areas of cancer infi ltration and is specifi cally focused
toward the ITF, jugular bulb, or dura, as indicated.
Invasion into the petrous apex by cancer is managed by
total resection of the temporal bone.
General oral endotracheal anesthesia is achieved
with inhalational agents, intravenous narcotics, and
hypnotics. Neuromuscular blocking agents are avoided
during the procedure to permit monitoring of motor
nerve activity. A short-acting agent, such as succinylcho-
line, is frequently used at the start of the procedure for
safe induction and intubation. The patient is placed
supine with the head turned toward the contralateral
ear. Sequential compression stockings are worn to
prevent deep venous thrombosis. Cranial nerves VII,
IX, X, and XI are monitored if they need to be identi-
fi ed and preserved. Monitoring for cerebral and brain
stem traction or injury during subtotal or total temporal
bone resection is achieved with somatosensory evoked
potentials and contralateral auditory brain stem
response recordings, respectively. Regions to be pre-
pared include not only the primary surgical site but also
any areas needed to provide graft material, such as the
abdomen for fat; neck or leg for nerve grafts; and chest,
abdomen, or back for pedicled or free fl aps. A third-
generation cephalosporin with cerebrospinal fl uid
(CSF) penetration, such as ceftriaxone, is administered
perioperatively. Furosemide (Lasix), 10 mg, and man-
nitol, 0.25 to 0.5 g/kg, are given intravenously 30
minutes before the intracranial portion of the
procedure to decompress the subarachnoid space if
retraction of the temporal lobe or cerebellum is
anticipated.
Lateral Temporal Bone Resection
The anatomic unit removed with lateral resection of the
temporal bone is the EAC. Boundaries of resection
include the middle ear cavity medially, the TMJ capsule
anteriorly, the zygomatic root superiorly, the mastoid
cavity posteriorly, and the ITF inferiorly. Laterally, the
resection can include the concha, as well as portions of
the pinna, depending on the extent of the cancer.
Occasionally, the entire pinna must be removed. Lateral
resection of the temporal bone is appropriate for cancer
limited to the EAC without penetration medially
through the tympanic membrane. Spread of cancer
anteriorly or inferiorly into the TMJ or ITF can be
treated by extension of the surgical resection into these
areas. Signifi cant spread of cancer into the middle ear
or mastoid cavity requires more extensive resection of
the temporal bone.
The lateral margins of resection depend on the
location of the cancer. In general, if the cancer is situ-
ated within the EAC, only the conchal bowl is included.
The proposed incision sites are injected with 2% lido-
caine with 1:100,000 epinephrine for hemostasis. A cir-
cumferential incision is made around the concha for
cancer involving only the EAC, and the tragus is left
with the skin fl ap if the cancer does not involve the
lateral and anterior external auditory meatus. Other-
wise, the tragus is included with the lateral circumfer-
ential skin margin (Fig. 123-9). If the subcutaneous
layer of the concha, tragus, and antihelix is involved by
cancer, more of the central portion of the pinna is
resected (Fig. 123-10). If a substantial portion of the
pinna is involved, the entire pinna is resected.
Figure 123-9. Postauricular and meatal incisions for resection of
the temporal bone. This illustration demonstrates inclusion of the
tragus with the specimen.

1280
Section 15
Temporal Bone
A postauricular incision is made 3 cm behind the
postauricular sulcus and extended superiorly toward
the temporal area and inferiorly over the mastoid tip
into a high cervical skin crease. The neck incision is
brought more inferiorly if neck dissection is anticipated.
The postauricular skin incision is raised a short distance
anteriorly. The dissection is then directed medially
through the fi broperiosteal layer over the mastoid
cortex. This facilitates obtaining a tight three-layer
closure if CSF is encountered. The soft tissue fl ap is
dissected in a subperiosteal plane until the posterior
part of the conchal incision is reached. To avoid inad-
vertent entry into the EAC, a hemostat is placed through
the posterior aspect of the conchal incision into the
postauricular wound. Once this plane of dissection has
been established, the conchal incision is connected
circumferentially with the postauricular wound, thus
isolating the conchal bowl, EAC, and tumor from the
skin fl ap containing the remainder of the pinna (Fig.
123-11). If there is any doubt about the adequacy of the
lateral skin margin, a crescent-shaped segment of skin
from the conchal bowl of the pinna is sent for frozen
section analysis. The lateral part of the EAC is sutured
closed to prevent tumor spillage. The skin fl ap is dis-
sected anteriorly while staying superfi cial to the deep
temporalis fascia superiorly, the sternocleidomastoid
fascia inferiorly, and the parotid fascia anteriorly (Fig.
123-12) until the masseter muscle is identifi ed. This
develops an anterior-based skin fl ap that is retracted
forward to expose the entire parotid gland (Fig.
123-13). The skin fl ap is secured with sutures and rubber
bands.
Using a large cutting burr, a complete mastoidec-
tomy is performed to expose the sinodural angle poste-
riorly, the tegmen mastoideum superiorly, the bony ear
canal anteriorly, and the digastric ridge inferiorly. Care
is taken to not thin the bony ear canal to the point of
exposing the cancer. The horizontal semicircular canal
is identifi ed for orientation, and the bone of the zygo-
Figure 123-10. Skin incision when tumor infi ltrates the tragus and
conchal bowl.
Figure 123-11. The anteriorly based skin fl ap containing the pinna
is separated from the core of the external auditory meatus. The
meatus has been oversewn to prevent tumor spillage.
Figure 123-12. The anteriorly based skin fl ap containing the pinna
(black arrow) is refl ected anteriorly, with the external auditory canal
(white arrow) and surrounding soft tissue left behind.
Figure 123-13. Most of the pinna remains with the specimen (see
Fig. 123-10). The skin fl ap is secured anteriorly to expose the parotid
gland (arrow). The superior limb of the incision is extended toward
the forehead in preparation for an infratemporal fossa approach.

Chapter 123
Carcinoma of the Temporal Bone 1281
matic root is drilled to expose the epitympanum and
bony plate of the tegmen tympani. Drilling in this area
is directed anteroinferiorly toward the posterior aspect
of the glenoid fossa. Dissection directed anteriorly poses
the risk of penetrating the dura of the middle fossa. The
anterior limit of this dissection is the capsule of the
TMJ.
A large diamond burr is used to identify the vertical
portion of the facial nerve from the second genu to the
stylomastoid foramen while maintaining the horizontal
semicircular canal and digastric ridge as landmarks.
Once the facial nerve has been identifi ed, the facial
recess is opened with a small cutting burr, followed
by a diamond burr (Fig. 123-14). The middle ear is
inspected through the facial recess to verify the absence
of penetration of the cancer through the tympanic
membrane. The incudostapedial joint is disarticulated
and the incus is removed. The tensor tympani tendon
is transected. The facial recess is then extended inferi-
orly by sacrifi cing the chorda tympani nerve to expose
the posterior portion of the hypotympanum. Using a
cutting burr, the inferior portion of the tympanic ring
is drilled toward the anterior wall of the EAC (Fig. 123-
15). Care is taken to not thin the bony EAC extensively
to avoid exposure of the cancer. The more medial ori-
entation of the anterior tympanic membrane requires
infratympanic drilling directed anteromedially to avoid
inadvertent entry into the anterior sulcus of the EAC.
This is accomplished by continuing the dissection of
the facial recess anteromedially while always keeping
the hypotympanum in view. The anterior limit of this
dissection is the periosteum between the temporal
bone, the ITF, and the capsule of the TMJ. In this area,
the surgeon must remain oriented to the location of
the eustachian tube orifi ce to avoid injury to the carotid
artery.
Once this bony dissection has been completed, the
EAC is attached anteriorly by anteromedial section of
bone just lateral to the eustachian tube. A superfi cial
parotidectomy is performed by identifying the facial
nerve distal to its exit from the stylomastoid foramen.
After retracting the tail and body of the parotid gland,
the main trunk of the facial nerve is traced peripherally
to isolate the lateral or superfi cial portion of the gland.
Details of this technique can be found in Chapter 62.
Dissection of the facial nerve in the stylomastoid
foramen can be diffi cult because the nerve is sur-
rounded by a thick cuff of fi brous tissue. Meticulous
dissection in this area and isolation of the nerve often
result in facial paresis or paralysis, which is usually tem-
porary. It is preferable to maintain this cuff of tissue
lateral to the facial nerve because less aggressive dissec-
tion can allow preservation of facial function. Once the
superfi cial lobe of the parotid gland has been dissected,
the EAC and parotid specimens are removed in conti-
nuity with the extratemporal portion of the facial nerve
under direct vision.
An osteotome is inserted through the extended
facial recess to the bone just lateral to the eustachian
tube orifi ce. A few gentle taps on the osteotome will
complete the osteotomy, and the EAC can be dissected
from the TMJ capsule (Fig. 123-16). During this maneu-
ver care must be taken to avoid injury to the ICA by the
osteotome, which lies just medial to the eustachian
tube. At this point the specimen is attached only to the
parotid gland, the superfi cial lobe of which can be
removed in continuity with the specimen and the facial
nerve preserved.
If the operative resection creates a large and deep
cavity, the posterior one half of the temporalis muscle
is rotated into the surgical defect and secured with 2-0
absorbable suture (Fig. 123-17). The skin fl ap is
Figure 123-14. The facial recess is dissected to expose the chorda
facial angle and the incudostapedial joint.
Extend
facial
recess
Figure 123-15. The operative fi eld is demonstrated. The facial
recess is extended inferiorly and then anteriorly by dissecting medial
to the tympanic annulus. The stylomastoid foramen is exposed, but
the nerve is not dissected free from its surrounding fascia and fi brous
tissue.

1282
Section 15
Temporal Bone
returned to its anatomic position. Hemovac drains are
placed both superiorly and inferiorly while avoiding
suction trauma to the facial nerve (Fig. 123-18). Small
to medium defects are closed with a split-thickness skin
graft that is secured with bolster packing consisting of
silk ligatures tied over a Xeroform bolster. This tech-
nique is described under “Reconstruction” later in this
chapter. Larger skin and cavity defects are closed with
free or pedicled myocutaneous fl aps. A compression
dressing is applied unless microvascular anastomosis
has been performed.
Subtotal Temporal Bone Resection
Cancer extending medial to the tympanic membrane
and invading the middle ear, hypotympanum, otic
capsule, facial nerve, or mastoid is managed by subtotal
resection of the temporal bone. In the past, an en bloc
technique of resection was advocated to encompass the
tumor. It has been noted that en bloc resection of the
EAC with surrounding soft tissue structures followed by
piecemeal resection of tumor and structures medial to
the middle ear provides better operative control and
probably does not negatively infl uence the cure rate.24
The strategy is to perform a largely extradural and sub-
periosteal resection of the temporal bone with margins
at the middle fossa dura superiorly, the posterior fossa
dura and sigmoid sinus posteriorly, the ICA anteriorly,
the base of the skull and jugular bulb inferiorly, and
the petrous apex medially. Extension of cancer beyond
these boundaries signifi es a grave prognosis, but the
resection can be extended in certain cases, as discussed
later.
The approach for lateral resection of the temporal
bone is performed as described previously, with exami-
nation of the middle ear through the facial recess and
mastoid cavity for cancer. If cancer is present, the more
encompassing resection is warranted. If facial nerve
function is normal preoperatively and it is visibly clear
of tumor as noted during the procedure, a decision is
made, based on the extent of cancer, whether the nerve
should be sacrifi ced and included with the specimen. If
the nerve is to be preserved, piecemeal resection of the
cancer is planned. If the facial nerve is uninvolved, it
will be mobilized and preserved as the dissection pro-
ceeds. Bone is removed over the sigmoid sinus and
posterior fossa dura. The tegmen and posterior fossa
plates of bone are fi rst thinned with a cutting burr and
then resected piecemeal after dural elevation. These
segments of bone are sent for permanent section. Care
is taken to not injure the superior petrosal sinus at this
Figure 123-16. The remaining anterior bony attachment is freed
with a small osteotome positioned medial to the anterior tympanic
annulus.
Figure 123-17. A superfi cial parotidectomy is performed to remove
the parotid with the lateral temporal bone specimen. The posterior
one half of the temporalis muscle is rotated into the mastoid cavity.
Figure 123-18. Skin closure with Hemovac drains in place. The
central cavity defect will be closed with a skin graft.

Chapter 123
Carcinoma of the Temporal Bone 1283
stage. Translabyrinthine dissection exposes the IAC and
jugular bulb. If cancer is not present at the jugular bulb,
no further resection is performed in this area.
If the facial nerve is to be preserved, it is skeleton-
ized along the labyrinthine, geniculate, horizontal, and
vertical segments down to the stylomastoid foramen.
The eggshell-thin pieces of bone on the anterior, lateral,
and posterior aspects of the nerve are removed with a
dissector. The dura of the IAC is opened to allow mobi-
lization of the facial nerve at the porus acusticus. The
greater superfi cial petrosal nerve is transected from the
geniculate ganglion, and the facial nerve is gently dis-
sected out of its bony canal and mobilized posteriorly
(Fig. 123-19). If the facial nerve is to be sacrifi ced, the
dissection and mobilization are omitted, but the IAC is
still opened. Both the facial and the vestibulocochlear
nerves are transected, and the proximal ends of these
nerves are examined by frozen section analysis to ensure
a tumor-free medial margin of resection. The remain-
ing tympanic ring inferiorly is then drilled to the peri-
osteum of the skull base. This periosteum protects
vascular and neural structures in the ITF and is not
resected unless cancer is identifi ed in this area. Bone
resection continues along the periosteum anterosupe-
riorly until the capsule of the TMJ is encountered.
Medially, bone dissection is continued until the vertical
portion of the ICA is encountered. Care is taken to keep
the periosteal covering over this artery intact while drill-
ing with a diamond burr.
If cancer has not infi ltrated into the protympanum,
the anterior limit of resection can be performed without
resection of the mandibular condyle. Absence of cancer
in this area can be confi rmed intraoperatively by obtain-
ing a frozen section of the mucosal edge near the eusta-
chian tube orifi ce. The bone lateral and posterior to
the vertical portion of the ICA above the jugular bulb
is drilled with a diamond burr to isolate the artery from
the otic capsule. Once this has been accomplished, the
remainder of the otic capsule containing the cochlea is
drilled (Figs. 123-20 and 123-21). The vaginal process
between the jugular bulb and the ICA is also drilled out,
with only the petrous apex remaining.
Dissection of the Jugular Foramen
If cancer has infi ltrated into the jugular bulb, total
removal of the cancer requires resection of the sigmoid
sinus. If only the lateral aspect of the sigmoid sinus or
jugular bulb is involved, resection can be achieved
without much added morbidity. Resection of cancer
involving the medial wall or pars nervosa of the jugular
foramen results in injury to the lower cranial nerves and
possibly a larger dural defect.
Figure 123-19. The facial nerve, if it is to be preserved, is mobi-
lized by transecting the greater superfi cial petrosal nerve and trans-
posing the facial nerve posteriorly. The vestibular nerves are divided
to gain access to the facial nerve. The cochlear nerve remains
intact.
Extratemporal
facial nerve
V3
Proximal
facial nerve
Figure 123-20. Subtotal resection of the temporal bone with the
medial margin through the internal auditory canal and cochlea. The
vertical portion and genu of the carotid artery are dissected. The
vaginal process between the jugular bulb and the carotid artery has
been drilled. The extratemporal facial nerve is intact.
Figure 123-21. Intraoperative dissection through the internal
auditory canal and cochlea modiolus for subtotal resection of the
temporal bone.

1284
Section 15
Temporal Bone
For cancer that involves only the lateral wall of the
sigmoid sinus and jugular bulb, total resection of tumor
can be achieved with an ITF approach similar to the
Fisch type A. The subtotal temporal bone resection is
completed after dissection and isolation of the internal
jugular vein (IJV) and cranial nerves IX, X, XI, and XII
in the neck. The facial nerve has been either transected
or mobilized out of the way. The soft tissues between
the posterior belly of the digastric muscle and the IJV
are dissected in layers to expose the vein from the skull
base to the jugular bulb. The IJV is doubly ligated in
the neck with 2-0 silk and divided. The sigmoid sinus
inferior to the takeoff of the superior petrosal sinus is
tied with 2-0 silk by making stab incisions in the dura
on either side of the sigmoid sinus, passing a curved
aneurysm needle into and out of the dural opening,
and passing the tie around the sigmoid sinus (see
Chapter 125, Figs. 125-10 and 125-11). The dural inci-
sions are repaired primarily or with plugs of muscle
secured with 4-0 Nurolon. The sigmoid sinus can also
be controlled proximally by extraluminal packing with
oxidized cellulose.
The retrosigmoid dura is decompressed to the
jugular foramen with a diamond drill. The vaginal
process has already been resected during the subtotal
temporal bone resection. The cancer in the region of
the jugular bulb is debulked without entering the
lumen. To resect the lateral wall of the sigmoid sinus
and jugular bulb, the inferior petrosal sinus feeding
into the lumen must be controlled. A large incision is
made on the lateral aspect of the jugular bulb, and the
medial wall is quickly packed with oxidized cellulose to
control bleeding. Once adequate hemostasis has been
achieved, the lateral wall of the sigmoid sinus from the
superior ligation to the jugular foramen is removed
along with the IJV. The medial wall of the lumen is
inspected for residual cancer, and the packing in the
jugular bulb is reinforced as needed (Fig. 123-22).
If cancer is present on the medial wall of the jugular
bulb, the resection must be extended into the pars
nervosa. If a decision is made to do this, the medial wall
of the jugular bulb is removed, and the contents of the
par nervosa are resected, including cranial nerves IX,
X, and XI. The adequacy of margins of resection of
these nerves proximally and distally is verifi ed by frozen
sections, and further resection is completed as
necessary. A positive margin proximally will require
nerve resection in the posterior fossa, which can be
performed through a retrosigmoid approach or through
the exposure created by resection of the jugular bulb.
The residual bone anteromedial to the jugular foramen
can be drilled to the ICA anteriorly and the hypoglossal
canal anteromedially. The inferior petrosal sinus may
need to be packed again during this maneuver. Any
dural defects should be repaired with fascia or
pericranium.
If the lower cranial nerves were functional preop-
eratively and required transection intraoperatively, a
tracheotomy is performed for pulmonary toilet and
care of aspiration, and a nasogastric feeding tube is
placed. Medialization of the vocal cord via a type I thy-
roplasty or arytenoid adduction can also be performed
intraoperatively (see Chapter 41).
Dural Resection
If inspection of the dura reveals residual cancer after
subtotal resection of the temporal bone, resection of
the dura is performed in collaboration with a neurosur-
geon. For cancer in the subtemporal dura, an incision
is made in the dura laterally while being careful to not
injure the vein of Labbé. The temporal lobe is retracted
superiorly to expose the involved dura inferiorly, which
is excised with adequate margins. The defect is closed
with a fascial or pericranial graft. The presence of inva-
sion into brain parenchyma should have been detected
preoperatively. Resection of involved brain tissue may
be technically possible, but the probability of cure is
exceedingly low.
Involvement of the posterior fossa dura by cancer
is treated similarly. Adequate exposure can frequently
be obtained through a presigmoid dural incision. The
cerebellum is retracted, and the involved dura is excised
with appropriate margins. If the medial wall of the
sigmoid sinus is involved, the craniectomy is extended
posteriorly with a drill to make a retrosigmoid opening
in the dura. The lateral wall of the sigmoid has already
been resected, and hemostasis at the inferior petrosal
sinus has been achieved. The cerebellum is retracted,
the involved dura is resected with margins, and the
defect is repaired with a fascial or pericranial patch.
Infratemporal Fossa Resection
When cancer infi ltrates into the protympanum, addi-
tional anterior exposure is needed to transpose the
Proximal facial nerve
Eustachian
tube
Carotid artery
Figure 123-22. Dissection of the jugular foramen when cancer
invades the hypotympanum and vaginal process. Resection of the
inferior sigmoid sinus and lateral jugular bulb is demonstrated. Oxi-
dized cellulose is packed in the openings in the inferior petrosal
sinus. The facial nerve has been resected proximally to the labyrin-
thine segment. The cochlea has been partially removed. The eusta-
chian tube can be seen.

Chapter 123
Carcinoma of the Temporal Bone 1285
carotid artery and excise soft tissue around the eusta-
chian tube. The superior portion of the incision is
extended anterosuperiorly toward the frontotemporal
hairline to expose the temporalis muscle. Elevation of
the skin fl ap is performed superfi cial to the deep tem-
poral fascia until the region of the frontal branch of the
facial nerve is reached, at which point the dissection is
carried deep to the fascia in the superfi cial temporal fat
pad while avoiding injury to the frontal branch of the
facial nerve. This dissection is carried to the lateral rim
of the orbit anteriorly and the zygomatic arch inferiorly.
Using electrocautery, the periosteum is incised along
the lateral edge of the orbital rim and the superior edge
of the zygomatic arch. The soft tissue lateral, medial,
and inferior to the zygomatic arch is dissected in a sub-
periosteal plane to release it from the masseter muscle.
A V-shaped osteotomy is made in the malar eminence,
which consists of the anterior zygoma and lateral
maxilla. The zygomatic arch is removed and saved after
the osteotomy is completed in the posterior zygomatic
root. The temporalis muscle is then dissected off the
underlying bone and remains pedicled on the coronoid
process of the mandible (Fig. 123-23).
Total parotidectomy is performed by dissecting out
the branches of the facial nerve. If the nerve is to be
sacrifi ced and included with the temporal bone dissec-
tion, the peripheral branches are identifi ed, tagged,
and transected. The superfi cial temporal artery is
divided and the soft tissues overlying the condylar
portion of the mandible are resected. Using an oscillat-
ing saw, the mandibular condyle is transected at the
level of the coronoid notch. The frontal branch of the
facial nerve may require transection to provide access
to the mandible.
With the temporalis muscle refl ected inferiorly, the
contents of the ITF are separated from the skull base
by dissection in a subperiosteal plane starting anteri-
orly. The lateral pterygoid plate is encountered fi rst.
The foramen ovale is located approximately 1 cm pos-
terior and just medial to this structure, and the foramen
spinosum is situated about 0.5 cm posterior to the
foramen ovale (Fig. 123-24). The middle meningeal
artery is coagulated with bipolar cautery and transected.
Now, with the vertical portion of the ICA in view at the
skull base, the periosteum of the skull base is elevated
in a posterior-to-anterior direction to connect to the
dissection at the foramen ovale.
If any tumor is seen within the ITF, it may be
resected at this time because the important structures
in the region have been identifi ed. The lateral ptery-
goid muscle is transected in the region of the mandibu-
lar osteotomy. The dissection is performed in layers
while taking care to not lacerate the internal maxillary
artery inadvertently. Any vascular structures that are in
the way can be divided and controlled with ties or
clips. The venous plexus in the pterygoid region can be
the source of signifi cant bleeding, which must be con-
trolled by bipolar cautery and packing with oxidized
cellulose.
Figure 123-23. Infratemporal fossa approach for cancer invading
the eustachian tube and petrous apex. The zygomatic arch has been
removed, and the temporalis muscle has been mobilized inferiorly.
The mandibular condyle and the parotid gland remain intact.
Facial nerve
Middle meningeal
artery
V3
Figure 123-24. Exposure of the petrous apex and infratemporal
fossa. A total parotidectomy has been completed. The middle men-
ingeal artery is divided, and the trigeminal nerve (V3) is exposed.

1286
Section 15
Temporal Bone
A temporal craniotomy is performed to provide
access to the fl oor of the middle fossa. The middle fossa
dura is elevated to expose the IAC posteriorly, the supe-
rior petrosal sinus medially, and the foramen ovale
and V3 anteriorly. The fl oor of the middle fossa is
then resected posterior to V3 and medial to the eusta-
chian tube with a cutting burr or rongeurs. If tumor
invades the eustachian tube with extension into the
petrous apex, total resection of the temporal bone is
performed.
Total Temporal Bone Resection
Total en bloc resection of the temporal bone with clear
margins is conceptually the procedure needed for
oncologic control. The vital structures that surround
the temporal bone demand that a meticulously con-
trolled approach be performed to avoid catastrophic
vascular and neurologic consequences. Even if the
carotid artery is to be sacrifi ced with the specimen,
proximal and distal control must be achieved. Similarly,
the brain, dura, and cranial nerves must be dissected
and isolated. Although a “no-touch” tumor approach
remains the technique to which we aspire, it is often
not accomplished to safely obtain access to the petrous
portion of the temporal bone.
After completion of subtotal temporal bone dissec-
tion, proximal control of the ICA is obtained either at
the skull base or in the neck. Distal control is achieved
in the fl oor of the middle cranial fossa via middle fossa
craniotomy. The carotid artery posterior to V3 is
exposed so that a clip can be placed on it for distal
control if necessary. The bone lateral to the ICA at the
genu is removed, and the ICA is dissected free from its
canal from the skull base to the foramen ovale. A thick,
fi brous ring of tissue surrounds the ICA at the carotid
foramen. When mobilizing this portion of the ICA, it is
safer to fi rst dissect circumferentially around the fi brous
tissue rather than along the carotid itself because the
risk of carotid laceration is high. The fi brous ring can
be left intact while the ICA is mobilized. Once adequate
exposure has been achieved, the remainder of the otic
capsule containing the cochlea is drilled. Anteriorly,
the petrous apex is drilled to complete total resection
of the temporal bone (Fig. 123-25). The eustachian
tube lies inferolateral to the carotid canal at the genu
and travels anteromedially. The eustachian tube can be
resected anteriorly to the level of the foramen ovale. If
cancer is found anterior to this area, nasopharyngeal
resection and possibly cavernous sinus dissection will
be necessary to achieve total resection, which is beyond
the scope of this chapter. The transected end of the
eustachian tube is sutured closed to prevent CSF
rhinorrhea.
Reconstruction
The goals of soft tissue reconstruction after temporal
bone resection include alleviation of cosmetic defor-
mity, prevention of CSF leak, and promotion of ade-
quate healing. In most cases, these objectives are best
accomplished with a vascularized fl ap. To prevent com-
munication between the nasopharynx and the middle
ear space after lateral temporal bone resection, the
eustachian tube is obliterated by scarifying the mucosa
and fi lling the lumen with ossicles, bone dust, Surgicel,
or a plug of muscle.
The resultant defect after lateral resection of the
temporal bone is similar to that after radical mastoid-
ectomy, and there is usually little risk of CSF leak, so
adequate tissue coverage can be accomplished with a
split-thickness skin graft to create a mastoid cavity.
However, because most patients require radiation
therapy after surgery or have previously undergone
radiation therapy, we believe that a vascularized fl ap to
promote adequate healing provides the optimal result.
The posterior one half of the temporalis muscle is sepa-
rated from the anterior portion, and while pedicled
inferiorly, the posterior portion of the muscle is rotated
into the mastoid cavity.
The surgical defect after subtotal temporal bone
resection extends medially through the otic capsule
and poses a greater likelihood of a CSF leak. If ITF dis-
section has not been performed, the resultant defect is
not signifi cantly larger than one resulting from lateral
temporal bone resection. Usually, a pedicled posterior
temporalis fl ap provides adequate coverage. Other
options include a lower island trapezius or pectoralis
major myocutaneous fl ap. If these fl aps cannot be
mobilized superiorly to cover the temporal bone defect
adequately, a free fl ap with microvascular anastomosis
to the superfi cial temporal or facial artery system can
be used. The most commonly used free fl ap is the rectus
abdominis, although a scapular or latissimus dorsi free
fl ap can also be used. The TMJ is not reconstructed
routinely.
If the facial nerve has been resected and there is an
adequate proximal stump, it is reconstituted with a
V3 divided
Eustachian tube
Figure 123-25. Total temporal bone resection. The mandibular
condyle is resected. The carotid artery has been spared and is retracted
to provide safe access to the petrous apex. Removal of the otic capsule
has left a large dural defect. V3 has been divided and the eustachian
tube has been suture-ligated. The infratemporal fossa is dissected
down to the pharyngobasilar fascia.

Chapter 123
Carcinoma of the Temporal Bone 1287
cable nerve graft. Most frequently, we use the sural
nerve (see Chapter 121). The greater auricular nerve
can be used if the length required is less than 6 cm.
Otherwise, a sural nerve graft is necessary to obtain a
longer donor graft for anastomosis between the proxi-
mal and distal ends of the facial nerve (Fig. 123-26). If
facial nerve resection has been performed distal to the
pes anserinus, both the upper and lower branches are
reconstructed. If the proximal stump of the facial nerve
has been resected at the brain stem with an inadequate
length left for anastomosis, a hypoglossal-to-facial (XII
to VII) nerve anastomosis can be performed.
If a CSF leak is a potential problem, the wound
should be closed in at least three layers with two layers
of 2-0 Vicryl or Dexon for the deep tissues followed by
a running and locking horizontal mattress suture con-
sisting of 4-0 Surgilon for the skin. If a conchal defect
is closed with a skin graft, this area must be isolated
from the remainder of the wound before skin grafting
by completely obliterating the space between the pinna
fl ap and the underlying muscle fl ap with 2-0 and 3-0
absorbable suture.
A split-thickness skin graft (0.015 inch) is secured
to 180 degrees of the pinna defect. Sutures of 3-0 silk
are kept long to serve as bolster ties. A piecrust tech-
nique is used, similar to that for grafting oral cavity
lesions. The central aspect of the skin graft is contoured
within the cavity defect, and the remaining skin is
trimmed to the appropriate size and further secured to
the wound margins (Fig. 123-27). The graft is usually
packed with Xeroform gauze and secured with a tie-
over bolster dressing (Fig. 123-28).
After wound closure, a mastoid dressing is placed
and the patient is extubated before transport to the
recovery area. Unless a watertight CSF closure has
been achieved, drains for the wound are placed to
gravity drainage. Continuous suction is applied when
the likelihood of CSF permeating the wound is
negligible.
POSTOPERATIVE MANAGEMENT
Most patients who undergo lateral resection of the tem-
poral bone require postoperative care comparable with
that after routine mastoidectomy, except that the fl ap
requires monitoring. The head should be elevated 30
degrees, and diet and ambulation are advanced as toler-
ated. The mastoid dressing is removed on the fi rst post-
operative day, and any skin graft bolsters are removed
on the fi fth day. The remaining pinna may have a
tenuous blood supply, especially if a large, anteriorly
based skin fl ap was raised. This is usually manifested by
increased venous congestion, which can compromise
the auricle and the remainder of the wound. If the
pinna appears to be in jeopardy, we have used medical-
Figure 123-26. Right total temporal bone resection, including the
condyle of the mandible. The facial nerve is repaired with a long sural
nerve graft (arrows at the upper and lower divisions of the remaining
nerve).
Figure 123-27. A split-thickness skin graft is sutured to the poste-
rior skin margins with 3-0 silk.
Figure 123-28. The skin graft is contoured to the cavity, immobi-
lized with Xeroform gauze, and secured with 3-0 silk sutures tied over
the packing.

1288
Section 15
Temporal Bone
grade leeches to assist venous decompression and mobi-
lization of fl uid (Fig. 123-29).
If a signifi cant dural defect was created or a consid-
erable amount of brain retraction was necessary during
surgery, the patient is managed in a monitored care
situation for the fi rst 24 hours for frequent neurologic
evaluation and monitoring of vital signs. The level of
care needed, which is similar to that after translabyrin-
thine acoustic tumor surgery, can be given in an inten-
sive care unit or a step-down unit. The patient’s intake
and output, as well as blood count and electrolytes, are
monitored. The mastoid dressing is kept in place for 3
to 5 days, although on the second postoperative day the
dressing is removed to check the wound and then
replaced. The patient is monitored for CSF rhinorrhea
or CSF leak through the wound, and any suspicious
fl uid is sent for β2-transferrin testing. The patient is
instructed to not strain or perform a Valsalva maneuver
for 3 weeks. We do not routinely place a lumbar drain
intraoperatively, although it has been done on occasion
if a large dural defect is expected or if neck dissection
has been performed and there is possible communica-
tion between the neck wound and the subarachnoid
space. The patient can be transferred to surgical fl oor
care if no signifi cant intracranial complications have
occurred.
If ITF dissection with resection of the mandibular
condyle has been performed, the patient is encouraged
to mobilize the mandible as soon as possible to promote
maintenance of a proper occlusal relationship and to
decrease the risk of fi brous ankylosis. Our colleagues in
oral surgery are consulted to oversee this aspect of the
patient’s recovery.
If a free fl ap has been performed, the patient and
wound are closely monitored by clinical fi ndings and
Doppler ultrasound examination of the vascular anas-
tomosis. Care is taken to not place any ties around the
patient’s neck that could potentially constrict the vas-
cular pedicle to the fl ap. Any evidence of signifi cant
fl ap ischemia should be detected early so that interven-
tion to salvage the fl ap, which may include revising the
anastomoses, can be performed immediately.
Patients who have facial nerve palsy or paralysis
postoperatively are treated with eye drops during the
day and ointment at night to avoid exposure keratitis
and corneal ulceration. A plastic eye shield (moisture
chamber) is useful in protecting the eye. If facial nerve
function is expected to return within 4 to 6 weeks, as
occurs after facial nerve transposition, the patient
usually requires no further treatment. If recovery from
facial nerve dysfunction is expected to take longer or if
the dysfunction may be permanent, a gold weight is
placed in the upper eyelid and a lateral tarsal strip is
performed if ectropion becomes a problem. These pro-
cedures are performed in the early postoperative period
(see Chapter 121). If facial nerve function fails to
recover, a hypoglossal-to-facial (XII to VII) nerve anas-
tomosis can subsequently be performed.
A patient with new iatrogenic lower cranial nerve
palsy or paralysis is at signifi cant risk for aspiration and
resultant pulmonary infection. The patient should be
placed in a step-down unit for frequent suctioning
through the tracheostomy. Nutrition is provided
through a feeding tube while the patient undergoes
swallowing rehabilitation coordinated by a speech
pathologist. This rehabilitation includes clinical assess-
ment as well as evaluation by modifi ed barium swallow
and performance of various swallowing exercises cus-
tomized for each patient. Once the patient is handling
secretions adequately with competent glottic function,
the tracheotomy tube is removed to enhance recovery
of deglutition. The feeding tube is removed when the
patient is able to ingest adequate nutrition by mouth.
If adequate swallowing function cannot be attained, a
gastrostomy tube is placed.
Immediate postoperative scans are not performed
unless the patient is showing evidence of an intracranial
complication such as hemorrhage, abscess, hydroceph-
alus, or pneumocephalus. Baseline postoperative scans
consisting of MRI or CT, or both, are obtained within
3 months after surgery to help monitor for recurrent
disease. These scans are repeated every 6 months for
the next 2 years and yearly thereafter.
Reconstruction with a split-thickness skin graft over
a vascularized muscle fl ap creates minimal cosmetic
deformity (Fig. 123-30). If the entire pinna has been
resected, reconstruction options are a prosthetic ear or
multistaged procedures in a surgical bed that is com-
promised. Given the problems inherent in reconstruc-
tion of the pinna, our preference is for a prosthesis.
Using either the preoperative ipsilateral ear or a reverse
moulage of the contralateral ear, a synthetic prosthesis
Figure 123-29. Severe venous congestion compromises the auricle.
Options for management include stab incisions or leeches, as
demonstrated.

Chapter 123
Carcinoma of the Temporal Bone 1289
can be created that is both functionally and cosmeti-
cally acceptable (Fig. 123-31).
Radiation treatment is begun approximately 6
weeks after surgery, when adequate wound healing has
occurred. The most common area of recurrence of
cancer is locally, in the skull base, dura, or ITF, so these
areas are treated specifi cally. The neck is also treated,
especially zones II and III, although the risk of failure
here is much less than the risk of failure locally.
COMPLICATIONS
The goal of surgical treatment of cancer of the tempo-
ral bone is to achieve total removal of the cancer with
minimal morbidity. Avoidance of complications is criti-
cal to successful rapid rehabilitation of the patient post-
operatively. Aggressive temporal bone resection may be
associated with major intracranial complications. Exten-
sive brain retraction can result in lower cranial nerve
palsy with aspiration, cerebellar or temporal lobe edema
and dysfunction, and cerebral infarction. The vein of
Labbé is particularly vulnerable, and compression of
this vein can lead to temporal lobe venous infarction.
Dissection of the ICA can result in embolic stroke,
injury with bleeding, and stroke. The dura must be
carefully reconstructed because CSF leaks in this setting
can be diffi cult to control and are a major risk for
meningitis.
Vascular
Major arterial injuries can cause disastrous conse-
quences, and all precautions should be taken to prevent
these injuries. Most moderate-sized vessels such as
branches of the internal maxillary artery can be con-
trolled adequately, even in the event of inadvertent
laceration. However, the ICA requires more complex
management. The need for possible surgical dissection
near the ICA should be ascertained preoperatively by
CT and MRI and by angiography if necessary. If it is
determined that carotid mobilization or dissection may
be required, preoperative balloon test occlusion with
xenon/CT is performed. The data obtained provide an
estimate of ipsilateral regional cerebral blood fl ow while
the carotid is temporarily occluded for 15 minutes.
These results place patients in one of three risk groups
for the development of major cerebral ischemia in the
event of abrupt carotid interruption: high, intermedi-
ate, and low. Approximately 80% of patients will be in
the low-risk group, and these patients are likely to toler-
ate permanent carotid occlusion. About 10% will be in
the high-risk group. These patients will not tolerate any
duration of carotid occlusion, so operative therapy
involving carotid manipulation should be avoided
unless bypass to the middle cerebral artery is performed
initially. The remaining 10% of patients will be in the
intermediate-risk group. These patients require carotid
revascularization if the ICA is sacrifi ced and the use of
adjuvant methods to minimize cerebral ischemia,
such as induced hypertension, barbiturate coma, and
hypothermia.30
Intraoperatively, before manipulation of the ICA,
proximal control of the vessel in the neck or at the skull
base and distal control in the horizontal portion of the
intrapetrous carotid artery should be obtained. In this
way, should an inadvertent injury to the ICA occur,
Figure 123-30. A well-healed split-thickness skin graft at the meatal
opening. The size of the defect does contract to provide an acceptable
cosmetic appearance.
A
B
Figure 123-31. A, Total auricu-
lar
resection
with
only
the
tragus remaining. B, A prosthetic
pinna provides excellent cosmetic
appearance and function.

1290
Section 15
Temporal Bone
rapid control of the situation can be achieved so that
the injury can be managed in an expeditious and con-
trolled fashion. If a laceration of the ICA occurs, it is
managed by either primary repair, repair with a patch,
bypass grafting using the saphenous vein, or sacrifi ce of
the ICA without reconstruction.
Venous complications are also possible after tem-
poral bone resection, especially if manipulation or
resection of the sigmoid sinus is performed. The vein
of Labbé is an important route of venous outfl ow from
the temporal lobe, and damage to this vein can lead to
signifi cant temporal lobe infarction with aphasia if
on the dominant side and seizures. The best strategy
for managing this complication is prevention. When
packing or ligating the sigmoid or transverse sinus it is
important to stay far anterior to the insertion of the vein
of Labbé into the transverse sinus. Once an infarct
occurs, therapy consists of speech and language reha-
bilitation, neurologic support, and administration of
antiseizure medications such as phenytoin (Dilantin)
and phenobarbital.
Cerebrospinal Fluid Leak
The main morbidity of a CSF leak is increased risk for
the development of meningitis. Because meningitis can
be a life-threatening condition, prevention plus control
of CSF leaks is very important. CSF leaks occur when
there is inadequate closure of the dura in conjunction
with a path for egress of CSF through the soft tissues to
the external environment. The usual sites of leakage are
the eustachian tube, incision site, and remnant of the
EAC.
Prevention is the most effi cacious method of man-
agement. All dural closures should be made as water-
tight as possible. Any potential dead spaces should be
obliterated by placement of muscular fl aps or autolo-
gous fat grafts. The fi nal barriers to CSF fl ow, skin
closure and the eustachian tube, should be closed or
obliterated in watertight fashion. A drain is not placed
in the wound. Postoperatively, the patient’s head is kept
elevated and the patient is instructed to avoid straining
or performing a Valsalva maneuver. A pressure dressing
is maintained for 5 days.
Despite preventive treatment, CSF leaks can occur,
and when they do, prompt management can prevent
serious consequences. The critical factor is early diag-
nosis. The patient should be instructed to report any
egress of clear fl uid from the nose or any drip down the
nasopharynx. Oftentimes, the diagnosis is obvious and
no further testing is required. β2-Transferrin testing of
fl uid will identify CSF.31 However, if the physician is
clinically suspicious that a CSF leak has occurred, action
must be taken despite test results to the contrary.
If the leakage occurs through an incision, the area
of dehiscence is reinforced with horizontal mattress
sutures. Topical collodion liquid is also useful. Most
CSF leaks that persist for more than 24 hours despite
maintenance of a pressure dressing and head elevation
can be controlled with the placement of a lumbar drain.
The lumbar drain is allowed to drain approximately
150 mL/day, or 50 mL per 8-hour shift. Care must be
taken to not overdrain CSF, because severe headaches
may develop and there is the potential that the negative
pressure may permit air and other nonsterile fl uids to
enter the subarachnoid space from the wound. The use
of antibiotics prophylactically in the setting of a CSF
leak is controversial. In the event of a CSF leak into a
clean surgical wound, the authors think that antibiotic
prophylaxis does not reduce the incidence of meningi-
tis and may in fact increase the risk of having a resistant
organism in patients in whom bacterial meningitis does
develop.
If the CSF leak persists after 3 to 5 days of lumbar
drainage, a surgical procedure to stop the leak is indi-
cated. Usually, the uncontrolled CSF leak is through
the eustachian tube. A transmastoid procedure through
the previous incision is performed to access the eusta-
chian tube and obliterate it in a more complete fashion.
This can be accomplished by further scarifi cation of the
mucosa followed by insertion of bone dust, Surgicel,
and muscle plugs. Occasionally, the source of a CSF
leak in the dural repair will be visible. In such cases, the
dural closure can be reinforced with patches of fascia
or muscle sewn over the dural defect. The wound is
closed in multiple layers, as described previously, in
watertight fashion, and a mastoid dressing is placed for
5 days. Lumbar drainage is continued for the next 3
days and the drain removed if there is no further CSF
leak.
A very diffi cult problem occurs if an extensive neck
procedure is performed at the time of temporal bone
resection with dural resection. Because the neck
requires drainage temporarily after surgery, a CSF leak
into the neck can occur quite readily. This becomes a
potentially serious problem when a tracheostomy is in
place. Great effort is necessary to ensure that the tra-
cheostomy wound does not communicate with the neck
dissection. Otherwise, CSF will readily pass subcutane-
ously through the neck into the trachea and exit out
the tracheotomy wound. Similarly, tracheal secretions
colonized with bacteria can infect the neck and CSF
space by retrograde contamination and create a very
serious infection.
Infection
Wound infections occur infrequently after resection of
the temporal bone. Appropriate treatment is no differ-
ent from treatment elsewhere in the head and neck. A
more feared complication is meningitis or other intra-
cranial infection such as a brain abscess. The risk of
meningitis developing after resection of the temporal
bone and requiring intracranial surgery is low in the
absence of a CSF leak, so prompt and effective treat-
ment of such leaks is critical. Symptoms of meningitis
include fever, severe headache, backache, and altered
sensorium. There may or may not be focal neurologic
defi cits. The diagnosis is made by lumbar puncture. A
third-generation cephalosporin is administered intrave-
nously after samples are obtained for culture. A CT scan
with contrast enhancement is obtained to rule out an

Chapter 123
Carcinoma of the Temporal Bone 1291
intracranial abscess. It is diffi cult to differentiate aseptic
meningitis from bacterial meningitis based on clinical
fi ndings and laboratory values, so antibiotics are contin-
ued until culture results are available in 2 days. If the
cultures are negative and clinical suspicion of bacterial
meningitis is not high, the antibiotics are stopped and
steroids (dexamethasone [Decadron], 4 mg intrave-
nously every 6 hours) are given and tapered over a
period of several weeks. If the cultures are positive or
the patient’s clinical status is suggestive of bacterial
meningitis, the antibiotics are tailored to the culture
results and continued for 10 to 14 days.
Aspiration pneumonia is a possible complication
after temporal bone resection, especially if previously
functional lower cranial nerves are sacrifi ced or injured
during surgery. In these cases, a type I thyroplasty with
or without vocal cord medialization and a tracheotomy
are usually performed at the time of surgery. The
patient is fed through a feeding tube until aspiration
stops and the patient is able to swallow. Aggressive pul-
monary toilet is provided while the patient undergoes
rehabilitation for deglutition and airway protection.
Aspiration pneumonia is treated with culture-specifi c
antibiotic therapy and further aggressive pulmonary
toilet.
Intracranial Hemorrhage and Hypertension
Although neurosurgical procedures have become rela-
tively safe, there is still a risk of acute intracranial com-
plications after temporal bone resection involving
intradural manipulation. One of the most rapidly pro-
gressive and potentially fatal complications is acute
intracranial hemorrhage, which if not treated promptly
can lead to irreversible cerebral injury with uncon-
trolled cerebral edema or brain stem herniation and
even death. Preventing this complication obviates the
urgent management necessary for this event. All patients
should be screened by history and physical examination
for bleeding disorders. If detected, the disorder should
be treated adequately before surgery. Intraoperatively,
all bleeding sites must be well controlled before closure
of the wound. Postoperatively, the patient should
remain normotensive and refrain from vigorous
activities.
The signs of acute intracranial hemorrhage are due
to increased intracranial pressure, as manifested by
altered sensorium or loss of consciousness. Focal neu-
rologic defi cits, including fi xed and dilated pupils and
systemic signs such as bradycardia and hypertension,
can also occur, but lack of these changes does not rule
out an intracranial hemorrhage. The location of hem-
orrhage can be extradural, subdural, or intraparenchy-
mal. Most extradural hematomas are due to bleeding
from dural vessels or dural sinuses. Subdural hemor-
rhage occurs as a result of dural bleeding, as well as
uncontrolled bleeding from intracranial vessels. Intra-
parenchymal hemorrhage is rare after the resection of
extra-axial lesions.
Once an intracranial hemorrhage is suspected, a
CT scan without contrast enhancement is performed to
confi rm the diagnosis. The patient’s condition is
temporized by the administration of mannitol, 0.25 to
0.5 g/kg intravenously, and hyperventilation after intu-
bation. If the patient’s vital signs are unstable or there
is evidence of brain stem herniation, the patient is
brought directly to the operating room without scan-
ning. A lumbar puncture should never be performed
in this setting for fear of inducing brain stem herniation
through the foramen magnum. A ventriculostomy can
be performed to rapidly decompress the increased
intracranial pressure. The craniectomy or craniotomy
is reopened, and the blood clot is evacuated. The source
of bleeding is sought and controlled.
Postoperatively, the patient is monitored in an
intensive care unit setting with maintenance of ventric-
ulostomy pressure under 15 mm Hg. A CT scan is
obtained to rule out further hematoma, and the patient
is allowed to recover.
Wound
Management of wound complications after temporal
bone resection is similar to that in other areas of the
head and neck, except that CSF leak is a potential
problem, as discussed previously. The integrity of the
fl ap used to obliterate the operative defect is vital to
keep the subarachnoid space separated from the outside
environment. Complications that can compromise this
function are ischemia and separation of the fl ap from
the wound.
It is unusual for ischemia to develop in pedicled
fl aps, but it occurs occasionally if the fl ap is stretched
too far or if strangulation of the vascular pedicle occurs
as a result of signifi cant constriction placed inadver-
tently around the neck. Injury to the vascular pedicle
intraoperatively can also occur but is rare. If the pedi-
cled fl ap becomes nonviable, it should be replaced
immediately with an alternative fl ap, whether it is
another pedicled fl ap or a free fl ap. Free fl aps are more
susceptible to ischemic complications than pedicled
fl aps are, and careful monitoring in the postoperative
period by clinical evaluation and Doppler ultrasound is
performed to detect any impending vascular pedicle
compromise. If vascular compromise does occur, the
patient is taken back to the operating room to revise
the vascular anastomosis.
Flap separation leading to wound dehiscence occurs
most frequently at the distal edge of a pedicled fl ap.
The cause is usually placement of the fl ap under too
much tension or local necrosis of the distal portion of
the fl ap. If an intact bed of granulation exists within the
wound and there is no evidence of a CSF leak, conserva-
tive wound management with dressing changes to allow
healing by secondary intention is adequate. In the pres-
ence of a CSF leak, the wound should be revised imme-
diately. If the tip of the fl ap is necrotic but an adequate
extra length of fl ap is available, the fl ap revision is per-
formed by advancing the new distal end to cover the
entire wound. If there is not enough length, a second
pedicled or free fl ap should be used to either close the
residual wound or replace the old fl ap entirely.

1292
Section 15
Temporal Bone
SUMMARY
Cancer of the temporal bone is a challenging disease
to treat effectively. Modern management of this disease
consists of combined-modality therapy, including
surgery to remove all evident disease and radiation
therapy to treat the margins of resection. The surgical
procedure of choice depends on the extent of disease
and consists of lateral resection of the temporal bone;
subtotal resection of the temporal bone; subtotal resec-
tion of the temporal bone with extension to the ITF,
jugular foramen, or dura; and total resection of the
temporal bone, which also includes removal of the
petrous apex. In the event of facial nerve sacrifi ce,
primary reconstruction with a cable graft is performed.
Postoperative radiation therapy should encompass the
resection margins, residual parotid gland, ITF, and
ipsilateral neck.
2. Kenyon GS, Marks PV, Scholtz CL, et al: Squamous cell carci-
noma of the middle ear. A 25-year retrospective study. Ann Otol
Rhinol Laryngol 94:273-277, 1985.
3. Lim V, Danner C, Colvin GB, et al: Primary basal cell carcinoma
of the middle ear presenting as recurrent cholesteatoma. Am J
Otol 20:657-659, 1999.
4. Takahashi K, Yamamoto Y, Sato K, et al: Middle ear carcinoma
originating from a primary acquired cholesteatoma: A case
report. Otol Neurotol 26:105-108, 2005.
5. Jin YT, Tsai ST, Li C, et al: Prevalence of human papillomavirus
in middle ear carcinoma associated with chronic otitis media. Am
J Pathol 150:1327-1333, 1997.
6. Lim LH, Goh YH, Chan YM, et al: Malignancy of the temporal
bone and external auditory canal. Otolaryngol Head Neck Surg
122:882-886, 2000.
7. Lustig LR, Jackler RK, Lanser MJ: Radiation-induced tumors of
the temporal bone. Am J Otol 18:230-235, 1997.
8. Donaldson JA: Surgical Anatomy of the Temporal Bone, 4th ed.
Philadelphia, Lippincott Williams & Wilkins, 1992.
9. Arriaga M, Curtin H, Takahashi H, et al: Staging proposal for
external auditory meatus carcinoma based on preoperative clini-
cal examination and computed tomography fi ndings. Ann Otol
Rhinol Laryngol 99:714-721, 1990.
10. Austin JR, Stewart KL, Fawzi N: Squamous cell carcinoma of the
external auditory canal. Therapeutic prognosis based on a pro-
posed staging system. Arch Otolaryngol Head Neck Surg 120:1228-
1232, 1994.
11. Gillespie MB, Francis HW, Chee N, et al: Squamous cell carci-
noma of the temporal bone: A radiographic-pathologic correla-
tion. Arch Otolaryngol Head Neck Surg 127:803-807, 2001.
12. Leonetti JP, Smith PG, Kletzker GR, et al: Invasion patterns of
advanced temporal bone malignancies. Am J Otol 17:438-442,
1996.
13. Moffat DA, Wagstaff SA, Hardy DG: The outcome of radical
surgery and postoperative radiotherapy for squamous carcinoma
of the temporal bone. Laryngoscope 115:341-347, 2005.
14. Zhang B, Tu G, Xu G, et al: Squamous cell carcinoma of tem -
poral bone: Reported on 33 patients. Head Neck 21:461-466,
1999.
15. American Joint Committee on Cancer Staging: Manual for
Staging of Cancer, 3rd ed. Philadelphia, JB Lippincott, 1988.
16. Moody SA, Hirsch BE, Myers EN: Squamous cell carcinoma of
the external auditory canal: An evaluation of a staging system.
Am J Otol 21:582-588, 2000.
17. Nyrop M, Grontved A: Cancer of the external auditory canal.
Arch Otolaryngol Head Neck Surg 128:834-837, 2002.
18. Politzer A: A Textbook of Diseases of the Ear. London, Baillier
Tindadl & Cox, 1883.
19. Parsons H, Lewis JS: Subtotal resection of the temporal bone for
cancer of the ear. Cancer 7:995-1001, 1954.
20. Lederman M: Malignant tumours of the ear. J Laryngol Otol
79:85-119, 1965.
21. Graham MD, Sataloff RT, Kemink JL, et al: Total en bloc resec-
tion of the temporal bone and carotid artery for malignant
tumors of the ear and temporal bone. Laryngoscope 94:528-533,
1984.
22. Conley JJ, Novack AJ: The surgical treatment of malignant tumors
of the ear and temporal bone. Part I. Arch Otolaryngol 71:635-
652, 1960.
23. Lewis JS, Page R: Radical surgery for malignant tumors of the ear.
Arch Otolaryngol 83:114-119, 1966.
24. Kinney SE: Squamous cell carcinoma of the external auditory
canal. Am J Otol 10:111-116, 1989.
25. Spector JG: Management of temporal bone carcinomas: A thera-
peutic analysis of two groups of patients and long-term followup.
Otolaryngol Head Neck Surg 104:58-66, 1991.
26. Prasad S, Janecka IP: Effi cacy of surgical treatments for squamous
cell carcinoma of the temporal bone: A literature review. Otolar-
yngol Head Neck Surg 110:270-280, 1994.
27. Nakagawa T, Kumamoto Y, Natori Y, et al: Squamous cell carci-
noma of the external auditory canal and middle ear: An opera-
tion combined with preoperative chemoradiotherapy and a free
surgical margin. Otol Neurotol 27:242-248, discussion 249,
2006.
PEARLS
• Always consider the possibility of cancer in a patient
with chronic otorrhea, especially if the patient has
severe pain, a mass or ulcer, or facial paralysis or if
the patient does not respond appropriately to
medical management.
• Perform both CT and MRI to assess the bone and
soft tissue anatomy and the extent of disease.
• Management of temporal bone cancer includes
adequate resection, usually with lateral or subtotal
temporal bone resection, and in most cases,
postoperative radiation therapy.
• The cure rate is 80% to 100% for T1 and T2 cancers
but remains limited for late-stage disease, with a
mortality rate of 50% or higher.
• Compromise of facial nerve function requires
diligent care of the eye.
PITFALLS
• Performance of a mastoidectomy for staging or
biopsy is never appropriate.
• Failure to achieve adequate margins will probably
ultimately result in treatment failure.
• Large defects should not be closed by local tissue
advancement; free fl aps are more appropriate in
selected patients.
• Failure to obliterate the eustachian tube may result
in nasopharyngeal refl ux and infection or CSF
rhinorrhea when the dura is incompletely closed.
• Insuffi cient venous drainage may compromise the
vascular integrity of the remaining pinna.
References
1. Devaney KO, Boschman CR, Willard SC, et al: Tumours of
the external ear and temporal bone. Lancet Oncol 6:411-420,
2005.

Chapter 123
Carcinoma of the Temporal Bone 1293
28. Grandis JR, Hirsch BE, Yu VL: Simultaneous presentation of
malignant external otitis and temporal bone cancer. Arch Oto-
laryngol Head Neck Surg 119:687-689, 1993.
29. 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.
30. Ariyan S, Sasaki CT, Spencer D: Radical en bloc resection of the
temporal bone. Am J Surg 142:443-447, 1981.
31. 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.

Chapter 124
Acoustic Neuroma
Barry E. Hirsch, Michele St. Martin, and Amin B. Kassam
Acoustic neuroma (AN) is the most common benign
tumor arising in the posterior cranial fossa. The term
acoustic neuroma is a misnomer, in that the tumor typi-
cally arises from the vestibular rather than the auditory
division of the eighth cranial nerve and is of Schwann’s
cell origin. Thus the proper nomenclature would be
vestibular schwannoma. These tumors are thought to
originate near Scarpa’s ganglion where the density of
Schwann’s cells is greatest. The origin of the tumor is
equally divided between the superior and the inferior
divisions of the vestibular nerve. Typically, these tumors
are benign and slow growing, increasing in size, on
average, from 1 to 2 mm a year; however, more rapid
or slower growth characteristics are also observed. The
consistency can be soft, fi rm, or mixed, with cystic com-
ponents as well.
HISTORY
Surgery of AN was fi rst described in the late 19th
century. Early successful surgical resection was accom-
plished through a suboccipital craniotomy, removing
the tumor by fi nger dissection.1 Surgical mortality was
unacceptably high owing to the fact that many patients
were moribund preoperatively. Two of the early pio-
neers in AN surgery were Harvey Cushing and his
protégé, Walter Dandy. During the fi rst 3 decades of
the 20th century, Cushing refi ned his philosophy of
management of AN to recommend a bilateral suboc-
cipital craniectomy approach and advocated unhurried
resection and meticulous hemostasis. He also employed
partial cerebellar resection when necessary. His tech-
niques for hemostasis included the use of bone wax,
silver clips, and electrocautery.2,3 Unfortunately, he
gutted only the core of the tumor; thus many patients
subsequently died of tumor regrowth.
The concept of total tumor removal was advanced
by Dandy, who reintroduced a unilateral suboccipital
approach with gentle but complete resection of the
tumor capsule.4 The fi rst translabyrinthine craniotomy
was performed by F. H. Quix in 1911.5 This approach
was condemned by the neurosurgical community
until the early 1960s when the translabyrinthine
approach was perfected by William House in conjunc-
tion with his neurosurgical colleague, William Hitsel-
berger. Their use of an operating drill and microscope
to directly access the tumor with preservation of
the facial nerve set the stage for the new era of surgery
for AN.6
Methods for diagnosing AN have signifi cantly
improved over the past century. Tomography has
enabled the identifi cation of enlargement of the inter-
nal auditory canal (IAC). Myelography required injec-
tion of contrast material into the subarachnoid space;
the contrast was fl oated into the IAC by patient posi-
tioning. Contrast-enhanced computed tomography
(CT) eliminated much of the morbidity associated with
myelography, reduced the amount of radiation expo-
sure, and increased the sensitivity of diagnostic radio-
graphic tests. Since the mid-1980s, magnetic resonance
imaging (MRI) has become the state-of-the-art in diag-
nosing ANs. Tumors as small as 1 to 2 mm may be
readily identifi ed on MRI.
Audiometric tests have undergone similar sophisti-
cated improvements over time. A battery of special tests,
including Bekesy’s audiometry, alternating binaural
loudness balance test, short-increment sensitivity index,
and tone decay, are now of only historical importance
for use in categorizing cochlear or retrocochlear
hearing loss. Identifying decay of the acoustic refl ex
or reduced word discrimination at higher presenta -
tion levels (rollover) is suggestive of retrocochlear
1295