Operative Techniques in Otolaryngology (2017) 28, 277–283

Temporal bone fracture requiring facial nerve

decompression or repair
Keonho Kong, MD Alexander Sevy, MD

From the Department of Otolaryngology-Head and Neck Surgery, Louisiana State University School of
Medicine, New Orleans, Louisiana

KEYWORDS Facial nerve paralysis is one of the complications with temporal bone fractures. Although most are
Temporal bone; treated medically with observation and steroids, we review the indications and surgical approaches to
Facial nerve; the facial nerve along its course within the temporal bone. It is important to get an examination as early
Fracture; as possible to determine immediate vs delayed, and complete vs incomplete paralysis. Patients with
Decompression; immediate onset, complete facial nerve paralysis should receive electrodiagnostic testing 3-7 days after
Perigeniculate; onset, to allow for Wallerian degeneration. If there is 490% electroneuronography degeneration within
Paralysis; 6 days or 495% degeneration within 14 days, surgical exploration is recommended. Exact surgical
Middle fossa; timing for decompression is controversial and definitive data is lacking but some authors have had
Transmastoid success even beyond 2 months postinjury and the risks and benefits should always be discussed with
each patient. The approach for surgical decompression of the facial nerve should be based on the site of
injury, if discernible, but most commonly involves transmastoid, middle fossa craniotomy, or a
combination of these approaches. The perigeniculate region is the most commonly injured portion of the
facial nerve with temporal bone fractures. If a transection is encountered, the nerve should be repaired
by either primary nerve repair if tension free, otherwise a secondary repair with a cable graft should be
performed.
r 2017 Published by Elsevier Inc.

Introduction life. Surgical management of facial nerve dysfunction in the

setting of trauma remains a controversial issue. In this
Temporal bone fractures are present in 14%-22% of article, we review the indications and detail the different
patients with skull fractures.1 Temporal bone fractures can surgical approaches or techniques of facial nerve decom-
cause significant morbidity to patients and can be associated pression.
with sensorineural hearing loss, conductive hearing loss,
facial paralysis, cerebrospinal fluid (CSF) fistula, vertigo or
meningitis. Approximately, 7%-10% of temporal bone Background
fractures are associated with facial nerve dysfunction.2
Depending on the degree of injury, facial nerve paralysis Temporal bone fractures
can cause significant morbidity and affect one's quality of
In a large retrospective series reported by Brodie et al, the
most common cause of temporal bone fractures was motor
Address reprint requests and correspondence: Alexander Sevy, MD,
Department of Otolaryngology-Head and Neck Surgery, Louisiana State
vehicle accidents (31%), followed by assault (17%), and
University School of Medicine, New Orleans, Louisiana. falls (16%).1 A 76% of the fractures in that study were in
E-mail address: asevy@lsuhsc.edu males and 22% were in patients 17 years or younger.1
http://dx.doi.org/10.1016/j.otot.2017.08.014
1043-1810/r 2017 Published by Elsevier Inc.
278 Operative Techniques in Otolaryngology, Vol 28, No 4, December 2017
Trauma to the facial nerve can result from complete
sectioning as well as tearing, compressing, torsion, traction,
or crushing injuries. Nerve injury can occur directly from
the trauma or indirectly as with formation of hematoma or
inflammation. Temporal bone fractures have traditionally
been classified into transverse, longitudinal, or mixed based
on its orientation in relation to the petrous axis, with
longitudinal fractures being more common but transverse
having a higher frequency of facial nerve injury. However,
modern nomenclature has shifted toward otic capsule
involving or otic capsule sparing based on whether or not
it involves the otic capsule because this has the most
relevance to clinical prognosis. Facial nerve injuries and
sensorineural hearing loss are more frequent with otic
capsule involving fractures, whereas otic capsule sparing
fractures are associated more with conductive or mixed
hearing loss. Approximately, 60% of temporal bone
fractures are open which increases the risk of meningitis.1
Facial nerve
Understanding anatomy is the key to any successful
surgery and in this case is particularly important to review
the course of the facial nerve as it runs within the temporal
bone (Figure 1). The cisternal segment (20-25 mm) of the
facial nerve spans from the brainstem pontomedullary
sulcus to the porus acusticus of the internal auditory
canal (IAC) where it enters to become the meatal segment
(7-9 mm), running superiorly to the cochlear nerve
and anteriorly to the superior vestibular nerve.4 The
Figure 1 Facial nerve anatomy. Course of the facial nerve
within the temporal bone is in yellow. (Color version of the figure
available online.)
intratemporal portion of the facial nerve begins at the
fundus as the meatal segment becomes the labyrinthine
segment (3-5 mm). In this segment, the fallopian canal is at
its narrowest. The first branch of the facial nerve, the greater
superficial petrosal nerve (GSPN), arises through the
Fallopian hiatus as the labyrinthine segment terminates at
the geniculate ganglion where it makes an acute 40°-80°
turn (first genu).4 Distal to the first genu is the tympanic
segment (10-12 mm), which courses posteriorly and inferi-
orly, superior and medial to the cochleariform process,
above the oval window, and then under the lateral
semicircular canal to the pyramidal process. A cadaveric
study (n ¼ 150) showed a 29.3% dehiscence in the fallopian
canal, the most common of which was in the portion
running above the oval window.20 As the nerve makes the
more obtuse (90°-125°) curve of the second genu, it
becomes to mastoid, or vertical, segment (10-15 mm). This
descending segment concludes the intratemporal portion of
the facial nerve at the stylomastoid foramen.4 Three
branches arise along the vertical segment: (1) nerve to the
stapedius muscle, (2) chorda tympani, and (3) Arnold's
(auricular branch of Vagus) nerve. Facial nerve injuries
through temporal bone fractures most commonly occur at
the geniculate ganglion followed by the mastoid (vertical)
segment.5-7,17,23
Work up or management
Physical examination
As with any trauma, initial management of temporal bone
fractures should always start with the A, B, C's: airway,
breathing, and circulation. Facial paralysis from temporal
bone trauma can be categorized as immediate or delayed.
It is critical for prognosis and management to distinguish
between a delayed onset of facial paralysis and a delayed
diagnosis of immediate paralysis. A facial nerve examina-
tion is often difficult to perform in the setting of trauma
where patients often have altered mental status or are
chemically sedated or paralyzed. The House Brackmann
(HB) scale is the standard for grading degree of facial
paralysis with a range from HB I representing full move-
ment to HB VI, complete paralysis with the notable
difference between III and IV of no longer being able to
close the eyelids, and paresis or incomplete paralysis
represented by the range of HB II-V. Electrodiagnostic
testing, discussed further below, is also often used to further
characterize facial nerve function and track recovery.
A delay in diagnosis is often common in trauma
situations due to altered mental status due to concomitant
injuries, patient intubation, and delay in consultation. Any
delayed diagnosis or paralysis with unknown onset may
need to be considered as an immediate onset paralysis in
discussing prognosis with the patient and to avoid under-
treatment. Any patient with delayed onset paralysis of any
kind (complete or incomplete) should be observed and
treated medically with steroids, unless contraindicated due
Kong and Sevy Temporal Bone Fracture
to other medical comorbidities. Any patient with acute onset
incomplete paralysis should also be observed focus on
nonsurgical treatment. In patients with acute onset complete
paralysis, further investigation with electrodiagnostic testing
should be sought out.
A thorough otologic examination should always be
performed. Important external ear findings may include
auricular lacerations or cartilage exposures, Battle's sign
(ecchymosis over mastoid prominence), Hitselberberger's
sign (posterior external auditory canal [EAC] paresthesia),
and auricular hematomas. The EAC should be inspected for
otorrhea (bloody or CSF), EAC stenosis or fracture,
lacerations, tympanic membrane perforation, or hemotym-
panum. Pneumatic otoscopy should be avoided as to not
introduce air or bacteria intracranially or to the inner ear. If
the patient is able to comply, a cursory bedside hearing test
with finger rubbing or masked whisper or tuning fork
examination should be performed. Hyperacusis may in-
dicate a stapedius nerve or muscle injury.
Surgical vs nonsurgical management of facial nerve paralysis
is based on prognosis of function recovery. Brodie et al showed
100% of patients (n ¼ 35) with incomplete paralysis eventually
recovered to a HB I or II.1 The same study also showed that
patients with complete paralysis had recovery to HB I or II in
only 50% (n ¼ 2) with immediate onset vs 100% (n ¼ 6) with
delayed onset.1 Adour et al8 showed that 100% (n ¼ 13) of
incomplete facial nerve paralysis patients recovered to normal
function within 8 weeks with steroid therapy. Adegbite et al9
showed that 62% (n ¼ 15) of patients with incomplete paralysis
had complete recovery in 4 months with no intervention, where
as 90% (n ¼ 10) of patients with complete paralysis did not
recover after 5 months. This study also showed that there was no
statistically significant difference in recovery of function
between immediate and delayed onset facial palsy.9
Electrodiagnostic testing
Electrodiagnostic testing can be a useful adjunct tool for
determining prognosis of a facial nerve paralysis. Wallerian
degeneration typically ranges from 3-7 days after a nerve
injury, however, ENoG responses have been shown to be
lost after 3-5 days with transected intratemporal facial
nerves.10 Options for electrodiagnostic testing include
Hilger facial nerve stimulator, facial electromyography
(EMG), and electroneuronography (ENoG). ENoG, also
called evoked EMG, records electrically elicited compound
muscle action potentials of the facial muscle. The facial
nerve is transcutaneously stimulated at the level of the
stylomastoid foramen using bipolar electrodes and electrical
activity is recorded with percutaneous needle electrodes at
the orbicularis oculi and orbicularis oris. Sillman et al11
performed ENoG within 2 weeks after onset of paralysis and
showed that there was no clinical association with an ENoG
decline 490% in traumatic patients (n ¼ 9). Totally, 66%
of the study subjects recovered to HBI or II, and 22%
recovered to HBIII or IV. However, they did not categorize
the patients into immediate or delayed onset and just
279
describes their patient's paralysis as “acute.” On the
contrary, Fisch states that a 95% degeneration by 2 weeks
reduces satisfactory spontaneous facial nerve recovery by
50%.12
Facial EMG measures electrical activity, spontaneous
and voluntary, of the facial musculature with percutaneous
needle electrodes. This test is often used in conjunction with
ENoG for prognostication of facial function after injury as
well as in tracking facial nerve recovery. Sillman et al11
showed that out of 8 patients with 490% ENoG
degeneration, but with presence of voluntary motor
potentials on EMG in 2 weeks all of them recovered to a
HB II or greater. Fibrillation potentials indicates degener-
ation of the lower motor nerve with muscle denervation and
is generally seen in 14-21 days after injury. Polyphasic
reinnervation with voluntary muscle contraction indicates
early evidence of nerve recovery and can be seen 6-12
weeks before clinical evidence of nerve recovery.
Although ENoG and EMG are objective, there are also
subjective measures used including the nerve excitability test
(NET) and maximum stimulation test (MST) performed with the
Hilger nerve stimulator in testing facial nerve function. The
facial nerve is transcutaneously stimulated at the stylomastoid
foramen or angle of the jaw. The benefit of these testing
methods is that it can easily be done at the bedside. The NET
measures current thresholds required to induce minimal muscle
contraction. The values are then compared between the affected
and unaffected sides of the face. The MST is similar to the NET
but measures thresholds required to induce maximal muscle
contraction. A difference in 3.5 mA or greater is considered
significant for the NET. The MST is expressed as the proportion
of facial muscle movement on the affected side compared to the
nonaffected side. The MST is considered to be a more sensitive
test compared to the NET,22 but the NET also has been found to
positively correlate with poor prognosis.21 Because the nature of
the test depends heavily on observer determination of muscle
twitching, there can be interobserver variability.
Other testing
A high-resolution computed tomography of the temporal
bone (with submillimeter cuts) should be obtained in the
setting of temporal bone trauma, particularly with acute
onset facial nerve paralysis.3 It can be useful in determining
the extent of the fracture and the type of fracture (otic-
sparing or otic-involving). However, it is often not definitive
in predicting the exact area of injury along the course of the
facial nerve.17
To help further localize a facial nerve injury, clinical
symptoms can help determine the location of the lesion in
the course of the facial nerve such as change in taste,
hyperacusis, numbness, and xerophthalmia. First described
in 1903 by a German ophthalmogist, Dr Schirmer's test has
been used as a topographical test to determine whether a
facial nerve injury is distal or proximal to GSPN as well as
the geniculate ganglion.19 The test traditionally uses filter
paper placed in the inferior conjunctival sac and measures
280 Operative Techniques in Otolaryngology, Vol 28, No 4, December 2017

the amount of lacrimation by the distance of paper that is insult is not identified in the setting of trauma, however,
soaked in 5 minutes. A study by Fisch showed that 92% caution should be taken prior to undertaking surgical repair
(n ¼ 13) of patients with facial paralysis from longitudinal determining a suspected area of nerve injury this is critical
temporal bone fracture had significant, unilateral or bilateral to choosing a surgical approach. The patient's hearing status
reduction of lacrimation compared to normal values.18 In a is also an important consideration for the approach that
study by Lambert and Brackmann,17 85% of patients (22 of should be selected. For example, if a patient already has
26) had a positive Schirmer test and out of those patients, all total sensorineural hearing loss from otic capsule involving
but one had an injury to the geniculate ganglion. Addition- temporal bone fracture, then a translabyrinthine approach
ally, salivary flow studies can be conducted by catheterizing can be considered.
Warthin's ducts bilaterally and administering a sialogogue,
such as lemon juice. Middle fossa approach
An audiogram should be obtained, as well, if at all
feasible. The patient's hearing level, or potential loss of The middle fossa approach is capable of exposing the
hearing, can help you determine the surgical approach that facial nerve in cistern, IAC and labyrinthine segments
should be taken, if necessary. Absent acoustic reflexes might (proximal to the geniculate ganglion). It is a useful approach
indicate a deficit in nerve to the stapedius or to the muscle to expose the proximal facial nerve segments without
itself, however, in the setting of a conductive hearing loss sacrificing sensorineural hearing, in contrast to the trans-
the reflex is commonly absent. A retrospective study (n ¼ labyrinthine approach. This approach can be combined with
467) by Ikeda et al21 showed a statistically significant the transmastoid approach to expose the entire intratemporal
positive correlation between absent stapedial reflex and poor length of the facial nerve. Either a curvilinear incision in the
prognosis of facial nerve paralysis. scalp that follows the periphery of the temporalis muscle
or a preauricular incision that extends into the temporal
scalp is made (Figure 2). The curvilinear incision can
Surgical management be extended into a more traditional mastoidectomy incision
for a combined approach. The incision is taken down to
Timing subcutaneous tissues and skin flaps are raised. With the
curvilinear incison,the temporalis muscle is incised around
Timing of facial nerve repair or decompression is its periphery and elevated inferiorly down to the root of the
controversial. Hato et al13 showed that patients that
underwent facial nerve decompression o2 weeks (n ¼ 14)
had a statistically significant increase in rate of complete
recovery compared to those that underwent surgical manage-
ment 42 weeks (n ¼ 52). This study included patients with
immediate facial paralysis due to temporal bone trauma
with HB IV-VI with 490% ENoG degeneration. Fisch
recommends that a delay in 3-4 weeks for surgery for patients
with complete facial paralysis with 490% ENoG degener-
ation within 6 days offers the best results (n ¼ 93).14
However, he does not provide specific results on level of
recovery in his paper. McCabe describes the physiologic
processes and lists the 20th day after injury to be the
most ideal time of repair as this is the time that “peak
proteosynthetic ability” has been reached.15 Sanus et al16
reports that 6 of 8 patients with HB VI that underwent late
decompression surgery recovered to a HB III with a mean
delay to operation of 70.1 ± 54.8 days after trauma. The other
2 subjects were at HB IV and VI at the end of their follow
ups. In a prospective study by Ulug et al, all patients with HB
VI (n ¼ 11) that underwent surgical decompression achieved
a recovery to HB I-III within 1 year with surgery ranging
from 14-75 days postinjury.23

Figure 2 Incisions for middle fossa, transmastoid, and

Surgical approaches
There are various approaches to expose the facial nerve
for decompression. An entire segment facial nerve explora-
tion and decompression may be required if the specific
combined approaches. Middle fossa: (red solid) preauricular, (blue
dash) curvilinear—can be extended into transmastoid incision for a
combined approach. Transmastoid: (green short dash)—can be
extended for combined approach. (Color version of the figure
available online.)
Kong and Sevy Temporal Bone Fracture
Figure 3 Middle fossa approach and facial nerve repair.
(A) Gentle retraction of temporal lobe allows exposure with a
diamond bur of the facial nerve from the cisternal to the tympanic
segment including the most often damaged perigeniculate
ganglion. The GSPN is identified then the IAC can be drilled
out (60° angle from the superior semicircular canal). (B) If the
facial nerve is only sectioned at one site or as in (A), at two sites,
and the two ends of the nerve can meet each other without any
tension, primary anastomosis with 9-0 or 10-0 monofilament
should be attempted. Mobiliziation of the facial nerve may provide
up to 1.5 cm to facilitate tension free closure. (C) If there is any
tension or the nerve ends do not meet, a cable nerve graft can be
performed. (Color version of the figure available online.)
zygoma. With the preauricular incision the temporalis can
be divided vertically, then elevated from the cranium and
spread to provide exposure for the craniotomy. A middle
fossa craniotomy is performed centered roughly over the
EAC. Although gently retracting the temporal lobe, the dura
is elevated from the floor of the middle fossa from lateral to
medial and posterior to anterior using an operative micro-
scope (Figure 3A). There are many structures a surgeon
should be careful not to injure, and can use as landmarks in
this area. The first, and most lateral, adhesion that will be
encountered will be at the petrosquamous suture line. From
there, one can identify the middle meningeal artery
anteromedially as it exits foramen spinosum. The arcuate
eminence, or the bony convexity of the superior semi-
circular canal, is located posterior or medially on the floor of
the middle fossa. The GSPN runs posterior to anteriorly as it
leaves the geniculate ganglion through the fallopian hiatus.
The petrous carotid artery runs just deep to the GSPN.
The arcuate eminence and GSPN are important landmarks
for identification of the IAC. There are 2 ways that are
commonly used to identify the IAC. First, the IAC can be
found running deep at about 60° from the arcuate eminence.
Second, the IAC can be traced anterograde from the GSPN
to the geniculate ganglion. The roof of the middle ear
(tegmen tympani) is opened to expose the tympanic
segment, head of the malleus and cochleariform process.
The perigeniculate region is fully decompressed via tracing
GSPN posteriorly and the tympanic segment proximally.
The labyrinthine segment is then exposed proximally toward
the IAC by unroofing the bone overlying it using a small
diamond burr. The upper basal turn of the cochlea is located
281
in very close proximity anterolaterally to the labyrinthine
segment, therefore, extra care should be used drilling this
segment. Once the entire facial nerve is exposed and
overlying bone is adequately drilled, dura of the IAC and
thickening around the meatal foramen can be incised. Under
binocular microscopy, sharply dissect with a fresh blade
using outward strokes from just under the edge of
perineurium and periosteum of the nerve is split to complete
the decompression. See later for description of nerve repair.
Bone wax should be used to seal any air cells drilled open to
prevent CSF leak. Fascia, abdominal fat, or temporalis
muscle may be placed over the repaired nerve as well as the
temporal bone drilling defect, and this can protect the nerve
from pulsations of the dura and further reduce risk of CSF
leak. Any retractors used are gently removed, craniotomy
flap is replaced, overlying temporalis is reapproximated, and
skin closure is performed to conclude the procedure.
Transmastoid approach
The transmastoid approach is capable of exposing the
mastoid and tympanic segments of the intratemporal facial
nerve (Figure 4). It allows for hearing preservation if not
extended to a translabyrinthine or transcochlear approach. A
standard complete, canal wall up mastoidectomy is
performed through a postauricular incision. Again, if being
combined with the middle fossa approach, the curvilinear
incision can be extended down for exposure. The lateral
semicircular canal is identified and exposure is extended
anterosuperiorly to find the body of the incus in epitympa-
num. The mastoid (vertical) segment of the facial nerve can
be found running lateral to the ampulla of the posterior
semicircular canal, inferior to the lateral semicircular canal,
and superior to the digastric ridge. The digastric ridge is
followed anteriorly toward the stylomastoid foramen where
the nerve can be found exiting the temporal bone. Once the
mastoid segment is found, attention is directed toward the
facial recess. The facial recess is a triangular space bounded
by the short process of the incus bone superiorly, the
tympanic segment medially and the chorda tympani
laterally. The facial recess is drilled out carefully using a
Figure 4 Transmastoid approach. A standard mastoidectomy is
performed to identify the vertical segment of the facial nerve. An
extended facial recess can be drilled and the incus removed for
additional exposure proximal to the second genu. (Color version of
the figure available online.)
282 Operative Techniques in Otolaryngology, Vol 28, No 4, December 2017
small diamond burr in a parallel fashion to the direction
of the nerve. Copious irrigation should be used to avoid
thermal damage to the nerve. The facial nerve is
skeletonized, leaving a thin bony shell covering. The nerve
is then decompressed starting in the mastoid segment
distally at the stylomastoid foramen. The segment of the
nerve between the lateral semicircular canal and the
stylomastoid foramen should be exposed 180° along its
posterior and superior surfaces. Damage to the lateral
semicircular canal should be avoided when exposing the
second genu and distal tympanic segments. This can be
accomplished by thinning the bony wall of the facial nerve
with the diamond burr in a posterior to the lateral and
anterolateral fashion along the nerve. The second genu and
distal tympanic segments are decompressed next. The incus
may be removed for improved exposure in some individuals
this can be replaced or reconstructed later with a prosthesis.
The proximal tympanic segment and perigeniculate
region can also be accessed with this approach. The
proximal tympanic segment is exposed by separating the
incudostapedial joint through the facial recess and rotating
the incus posteriorly using a 90° hook. Here, the nerve can
be seen running superiorly to the oval window and, more
proximally, between the cochleariform process (inferior)
and the transverse ridge (superior). The proximal tympanic
segment is decompressed to the level of the cocheariform
process. The head of the malleus may be removed with a
malleus nipper at this point and with further medial
dissection, the junction of the geniculate ganglion and
tympanic segment can be found.
More proximal dissection of facial nerve is inhibited at
this juncture due to the ampulla of the superior semicircular
canal. The transmastoid can be extended into the supra-
labyrinthine approach at this time for exposure of the
labyrinthine segment. However, this exposure is rarely used
as the exposure is limited should any nerve grafting or
repair be required. If the patient has ipsilateral profound
sensorineural hearing loss, the transmastoid can also be
extended to a translabyrinthine or transcochlear approach.
The translabyrinthine approach involves obliteration of
the Eustachian tube through the facial recess, the stapes is
removed from the already dislocated incudostapedial joint.
Labyrinthectomy is then performed with dissection
through the lateral semicircular canal superior to the second
genu. The labyrinthectomy is continued through the
vestibule and medial wall of the otic capsule and the IAC
can be accessed.
Facial nerve repair techniques
Primary repair
When a transected neve is encountered, repair of the
nerve to maintain continuity and restore function is
indicated. There are many ways to repair the facial nerve.
The approach is mainly dependent on the length of nerve
that needs to be repaired as it is important that it is done so
that there is absolutely no tension on the nerve. When
possible, primary repair is the preferred option but may
require extended dissection to allow for nerve rerouting—a
1.5 cm gain of length can be achieved by sacrificing the
GSPN and chorda tympani branches, and skeletonizing the
entire fallopian canal portion of the nerve. It is paramount to
create fresh nerve edges with a sharp fresh blade for
anastomosis. The most common anastomotic repair techni-
que is epineural repair. The epineurium is reapproximated
with 9-0 or 10-0 monofilament sutures (Figure 3B).
Alternatively, some surgeons prefer to use collagen sleeves
or fibrin glue for facial nerve repair.
Secondary repair
Should a tension-free repair be unachievable with the
methods described above, secondary repair via cable
grafting can be performed (Figure 3C). The most commonly
used nerves for cable grafting are the great auricular nerve,
sural nerve, and peroneal nerves. With discrepancies
between nerve diameters, the edges of the smaller nerve
may be beveled for reapproximation. The greater auricular
nerve provides up to 8 cm of potential length and is most
commonly used for short-segment repairs due to the
proximity in its location to the surgical field of facial nerve
exposure. It can be found along the posterior border of the
sternocleidomastoid at about the halfway point between the
mastoid tip and clavicle. The sural nerve provides the
greatest length (up to 40 cm) for grafting. It is capable of
being used for reconstructing the entire length of the facial
nerve. It is located deep or posterior to the saphenous vein
between the lateral malleolus and Achilles tendon.
It is important to discuss timing and expectations with the
patient, keeping in mind that it takes time for regeneration,
often 6 months for lesions proximal to the geniculate
ganglion all the way up to a year. Keep in mind the
possibility of 2 noncontinguous nerve injury sites. Through-
out any recovery for patients with at least HB IV, eye care is
paramount. However, without significant nerve regenera-
tion, it is important to work with our Facial Plastics
colleagues to consider eyelid gold weights, facial nerve
reanimation, that is, with CN V or XII, as well as Botox and
static procedures for our patients with facial nerve injuries.
Conclusion
Facial nerve paralysis is a potential complication of
temporal bone trauma. It is important to conduct an
examination including facial nerve function as early as
possible to determine immediate vs delayed, and complete
vs incomplete paralysis. Refer to Figure 5 for a summary of
the treatment algorithm for facial nerve injuries with
temporal bone trauma. Most patients with facial paralysis
can be treated nonsurgically with observation and steroids.
Eye care is paramount in the setting of incomplete eye
closure. Patients with immediate, complete facial paralysis
Kong and Sevy Temporal Bone Fracture
Figure 5 Treatment algorithm for facial nerve injury. Note on copyrights. Dr Sevy retains the copyright to the illustrations in this article.
The authors are pleased to extend copyright permission for use of our original illustrations for our chapter in all of its forms (print, online) but
reserve copyright ownership and privilege for future use.
should undergo ENoG 3-7 days after onset of deficits. If
there is 490% ENoG degeneration within 6 days or 495%
degeneration within 14 days, surgical exploration is
recommended. Exact surgical timing for decompression is
controversial and definitive data is lacking. Most plan for
surgery within the first month, but some authors have had
success even beyond 2 months postinjury and the risks and
benefits should always be discussed with each patient.
The surgical approach(es) should selected based on the
suspected location of lesion along course of facial nerve but
most commonly involve transmastoid, middle fossa cranio-
tomy or a combination of these. The perigeniculate region is
the most commonly injured portion of the facial nerve with
temporal bone fractures and is best accessed with the
middle fossa craniotomy. A transected facial nerve should
be repaired by primary nerve repair only if tension free,
which may be aided by mobilizing the nerve, otherwise
secondary repair should be performed using a cable graft.
It is important to counsel patients on the prognosis and
timing of their potential recovery and also to consider
further procedures with facial plastics when their recovery
of facial nerve function is incomplete.
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